,""'.
[DNLM: I ..... rrh)'lhmlas. cardlac-
dlagoosJs--.Probiems and E1erdses.
2. Electrocardiography-Problems and
E1erds .... WG 18.2]
RC685.A65H842012
616.1 '2807547076---<Ic23
2011014268
"
Preface
f.CG I~o'froul: Exerdsa;/I Arrhythmia Interpretation, Sb:lh Edition, was written 10 MMst
physicians. nurse!, medical and nursinl! 5I:udenls. paramedics, tmell/ency medial teetmi-
cians. telemetry tethnictans. and other allifd health ~nonnel in ;w;quirinQ the knowledile
and skills essential for ldentilyina twit arrhythmias. It may also bt used as a rderenct for
electrocardiogram (ECC) review lor those already knowled2eable in ECG interpretation.
The text is writt~n in a simple manner and lUwtrated \!lith tiguru. tables, boxes, and ECC
tracinas. Each chapler is designed to build on the know\edae base I'rom the previous cIla!ten 50
that the beJlinnillJl stu:knl can quickly understand and I/I'35P lhe ba5k cmcepll of electrocardiOll-
Ji\Pt\y. An etrort has been made ('(It only to proYide good quoN/y ECG trocirtgs, but abo to provide
a 5I.Ifticient number and \Wiety of EGC practice strips 50 the Iwner retls confident In arrhythmia
inlerpretllion. There are I.lI.I?r fn) proclice strips - more than any book on /he mQrlrel.
Chapter I provides a disculoSion ofbaJic anatomy alld p/ly$IoJO\IYol the heart. The electri-
cal basis of t lectrocardiolOi is disCl.l!sed In Chapter 2. The components of the ECC traclnl!
twawforrns, intervals. sellmenl5, and complexes) are described in Chapter 3. Thischaplfr also
includes pndice tr.w:inlZS on w3wform identification. Cardiac monitol"$, lead JystflTl.'i, lead
placement ECC artifacts.:uld troubleshootinllllXlnllor probltmJ art discu!Sed in Chapter 4.
Astep-by-step lIuide to rhythm Jtritt :ulalysiJ is provided in Chapter 5. in addition to practice
tracin(lS on rhythm strip analYJis. The Indi\'itlual rhythm chapters (Chapter$ 6 throullh 9)
iocludt 3 description of each arrllythmia. arrhythmia uampltJ. causes. and ~ment
protocols. Current .ld'Janced cardiac life support (ACLS) Iluidelines are incorporated into each
arrhythmia chapter as awllcable to Ihe rh>thm discunion. Eadl arrhythmia chapttr abo
locludes approximately 100 !trips for self-evaluation. CIlapter 10 presents a \ltlleral discussion
of cardiac pacemakel"$ (twes. indications. function, pacemaker terminololZY, rmifimctions.
and PJCemaktr analYJ]J), alo~with practice tracinlU. Chapkr II is a postle!! comistinll ofa
mix 0( rhythm strips that can bt used as a stlf-evaluation tool or for ttstinll purpOstl.
The text has ~n thou!!htfully revisedartd I!QWIded to include nt.'WfiJlures. updated boxes
and tables, additional llIossary terms, and evtn more pr.w:tice rhythm 5trips. SkiJlbulfder
rhythm stripj. which are new to this edition. appear inunediate)y IOliowil1ll the practice
rhythm strips in Chapters 7. 8. and 9. Each Skillbuilder section provides a mix of strips that
test not onlY)IOUr urnknblldinQ. of Information It<lmW in that arrhythmia chapter but also
the concepts:uld skills learned in the chapter{s) immnHatdy precedinll il. For uample. the
Skill builder strips in Chapter 7 (Atrial arrhythmias) includr atrial rhythm strips as wt'll as
strips on sinw arrhythmias (Covtrtd in Chapter 6): Chapter 8 (Junctional arrhythmias and
AV blocksi includesjWlCtionalarrhythmias and AV blocks. as well as atrial and sinus arrhyth-
mias: and Chaplt'r 9 (Ventricular arrll).-thmias and bundle-brandl block), a mix of all of thf:o
arrhythmias c!7.'tred In Chapters 6 throuall 9. Such practice wilh mixed !trips will enhallCe
your ability to differentiate ~!Y.'ttn rhythm I/TOIlPS as you prol/Tl'SS throUllh the book - a
definite adYanl:alle ...."hen you \Itt to the Posttest. A handy pull-out section consistin!! of 48
individual ~hcards further challell>!es )'OUr ability to identity different types of arrhythmias..
The ECC tracinlti included in this book are actual Jlrips from patients. Above each rhythm
strip are J...5OOd indic3tors for rapid-rate calculation. For precise rate calculation. an ECC con-
IX'TSian table fOr heart rate is printed 011 the inside back COYer. For COII\'ef\ience. a rerrJOv.Ible pJas...
ticversion is also attached to the inside backcOl'eT. The heart rates for Tq/IIIar rhythms listed in the
anlWer keys were determined by the proci.le rate calculation method and ....;11 not a/y,'IYS coincide
....ith the rapid-rale calculation method. Rate calculation methods are disawed in Chapter 5.
The author and publisher Ilaw made every attempt to check the content. especially di'UII
dosages and man.1Ilement protocoll. for accuracy. Medicine is continually c~l1II. and
the reader has the responsibility to keep informed of local care protocols and chanlles in
emerjlency ~ procedures.
Iv
This hook is dedicated to
NO/Jell Grace, a "busy" little girl.
Anatomy and physiology
of the heart
EndocaJdium --~<"c..'
-f1------ P~~c~
++-_____ Parietallaye.
'" S810US pllricardum
Alveolus 01 lung ~
~~\
Pulmonary anerl'"
(to lungs)
--_-1 \\
~-'-'-_~ Aona (to body)
relaxation (diastole), the valve cU5~ close. BackHow of Blood flow through the
-
blood into the ventricles is prevented because ofthe cus~'
fibrous strength, their dose approximation. and their
heart and lungs
5hilpe. The second heart 50und (s.,) is produced by closure Blood How through the heart ilfId lungs is traditionally
of the aortic and pulmonic SL valws. It is best heard over described by tracing the How as blood returns from the sys-
the second intercostal space on the left or right side of the temic veins to the right side of the heart, to the lungs, back
sternum. to the left side of the heart. and out 10 the arterial vessels
"~.""m' ----------~~
Descendingaorla. - - - - - - - - - - - . . J
Figure 1-6. Papillary muscles and chordae tendheae.
Coronary circulation 5
of the systemic circuit (Figure I-S). The right atrium right coronary artery supplies the right side of the heart and
receives venous blood from the Ixxly via two of the bodys the left coronary artery supplies the left side of the heart.
largest veins (the superior vena cava and the inferior vena The right coronary artery arises from the right side
cava) and from the coronary sinus. The superior vena cava of the aorta and consists of one long artery that travels
returns venous blood from the upper body. The inferior downward and then posteriorly. The major branches of the
vena cava returns venous blood from the lower Ixxly. The right coronary artery are:
coronary sinus returns venous blood from the heart itself. conus artery
As the right atrium fills with blood. the pressure in the sinoatrial (SA) node artery (in 55% of population)
chamber increases. When pressure in the right atrium anterior right ventricular arteries
exceeds that of the right ventricle. the tricuspid valve acute marginal artery
opens, allowing blood to flow into the right ventricle. As AV node artery (in 90% of population)
the right ventricle fills with blood, the pressure in that posterior descending artery with septal branches
chamber increases, forcing the tricuspid valve shut and the (in 90% of population)
pulmonic valve open. ejecting blood into the pulmonary posterior left wntricular arteries (in 90% of population).
arteries and on to the lungs. In the lungs, the blood picks Dominance is a term commonly used to describe coro-
up oxygen and excretes carbon dioxide. nary vasculature and refers to the distribution of the terminal
The left atrium receives arterial blood from the pulmo- portion of the arteries. The artery that gives rise to both the
nary circulation via the pulmonary veins. As the left atrium posterior descending artery with its septal branches and the
fills with blood, the pressure in the chamber increases. posterior left ventricular arteries is considered to be a "domi-
When pressure in the left atrium aceeds that of the left nant' system. In approximately 90% of the population, tI-.e
wntricle, the mitral valw opens, allowing blood to flow into right coronary artery (RCA) is dominant. The term can be
the left ventricle. As the left ventricle fills with blood. the confusing because in most people the left coronary artery is of
pressure in that chamber increases, forcing the mitral valve wider caliber and penuses the largest percentage of the myo-
shut and the aortic valve open. ejecting blood into the aorta cardium. Thus, the dominant artery usually does not perfuse
and systemic circuit, where the blood releases oxygen to the the largest proportion of the myocardium. The left coronary
organs, tissues, and cells and picks up carbon dioxide. artery arises from the left side of the aortaand consists of the
Although hlood flow om he Imeed fmm th ... right. sid ... of left m~in cnmn","y ",1,,-1)'. ~ _.hmt .t... m. ",hich dividp_. into
the heart to the left side of the heart, it is important to realize the left anterior descendingilrtery and the circumflexilrtery.
that the heart worhas tv.o pumps (the right heart and the left The left anterior descending (LAD) travels downward over
heart) working simultaneously. As the right atrium receives the anterior surface of the left ventricle, circles the apex, and
venous blood from the systemic circulation. the left atrium ends behind it. The major branches of the lAD are:
receives arterial blood from the pulmonary circulation. As diagonal arteries
the atria fill with blood, pressure in the atria aceeds that of right ventricular arteries
the ventricles, forcing the AV valves open and allowing blood septal perforator arteries.
to flow into the wntricles. Toward the end of ventricular fiJI- The circumfla art~ry travels along the latual aspect of
ing, the tv.o atria contract, pumping the remaining blood the left ventricle and ends posteriorly. The major branches
into the ventricles. Contraction of the atria during the final of the circumflex are:
phase of diastole to complete ventricular filling is called the SA node artel)' (in 45% of population)
atrial kick. The ventricles are 70% filled before theatria con- anterolateral marginal artery
tract. The atrial kick adds another 30% to ventricular capac- posterolateral marginal artel)'
ity. In nomtal heart rhythms, the atria contract before the distal left circumflex artery.
wntricles. In abnormal heart rh}1hms, the loss of the atrial In 10% of the population, the circumflex artery gives
kick results in incomplete filling of the ventricles, causing a rise to the posterior descending artery with its septal
reduction in cardiac output (the amount of blood pumped branches, terminating as the posterior left ventricular
out of the heart). Once the ventricles are filled with blood, arteries. A left coronary artery with a circumflex that gives
pressure in the ventricles increases. forcing the AV valves rise to both the posterior descending artery and the pos-
shut and the SL valves open. The ventricles contract simul- terior left ventricular arteries is considered a "dominant"'
taneously, ejecting blood through the pulmonary artery into left system. When the left coronary artery is dominant, the
the lungs and through the aortic valve into the aorta. entire interventricular .septum is supplied by this artery.
lithl ... 1_1 'lJmmari?p-. the cnron~I)' ~rI ... ry di,trihlJlion 10
the myocardium and the conduction system.
Coronary circulation The right and left coronary artery branches are intercon-
The blood supply to the heart is supplied by the right cor- nected by an exlel15ive network of small arteries that provide
onary artery. the left coronary artery, and their branches the potential for cross flow from one artery to the other.
(Figure \-7). There is some individual variation in the These small arteries are commonly called roUa/eral vessels
""llnll of ~uruJldry "rl~ry br,,"d,iuK.. bul ill 1!~""r.. J, lI,,, ur wUa/t:TU/ c;;n;u/aliu .. Cundl~rdl cin;uldliul' ""i.l. ill birlh
6 Ana toOlYand physiology of the heart
lib.. ! ! .
Coronary arteries
COronary.n.ry Inclltl bllllCll" PortIon of lI'II'ocardlUm I~plld Portion 01 condut::tlon . ysttm IUPpl'"
Righi Corona"f artlllY
RighI atrium SinoIriaI (SAl node (55")'
RigIt wnlridt AbiIJoientricul. (AV) rIXIe and bundle ollis (90%)'
~Ieriof wall 0I1eIt ventricle (90%)'
Poaeriof ooe-titd of ~ sepllm (9O%f
'" of popula~
Cardiac innervation 7
Cardiac innervation
The heart is under the control of the autonomic nerv-
ous system located in the medulla oblongata, a part of
the brain stem. The autonomic nervous system regu-
lates functions of the body that are involuntary, or not
under conscious control. such as blood pressure and
heart rate. It includes the sympathetic nervous system
and the parasympathetic nertJOus system, each produc-
ing opposite effects when stimulated . Stimulation of
the sympathetic nervous system results in the release
of norepinephrine, a neurotransmitter, which acceler-
ates the heart rate. speeds conduction through the AV
node, and increases the force of ventricular contrac-
tion . This system prepares the body to function under
stress ("fight-or-flight" response ). Stimulation of the
parasympathetic nervous system results in the release
of acetylcholine, a neurotransmitter, which slows the
heart rate, decreases conduction through the AV node,
and causes a small decrease in the force of ventricular
contraction. This system regulates the calmer functions
of the body (" rest-and-digest " response). Normally a bal-
ance is maintained between the accelerator effects of
the sympathetic system and the inhibitory effects of the
parasympathetic system.
Electrophysiology
Cardiac cells
waler, producing posi tively and negatively charged ions_
The heart is compostd of thousands of cardiac cells. The An ion with a positive charge is called aealioll . An ion with
cardiac ceUs are long and narroY.\ and di\ide at their ends II negative charge is called an anion. Potassium (K') is the
into branches. These branches conned with branches of primary ion imide the cell and sodium rNa') is the primary
adjacent cells, forming a branching and anastolTlO5ing ion outside the cell.
network of cells. At the junctions where the branches join A memb rane separates the inside of the cardiac cell
togethe r is a spedal~ed cellular membrane of low electri (intracellular) from the outside (extracellular). llwre is a
cal resistance, which permits rapid conductionol electrical constant movement of ions across the cardiac ctll mem-
impulses from one cell to another throughout the cell net- brane. Differences in concentrations of these iom deter-
work. Stimulation of one cardiK cell initiates stimula.tion mine the celis electric dwge. The distribution of iom
of adjacent cells and ultimately leads to cardiac muscle on either side of the membrane is determined by several
contraction. faclors:
Thne are two basic kinds of cardja(: cells in the heart: f.lembrane channels (pores) - The cell memb rllJle hu
the m!lOcuniidl cefts (or "working" cells) lIfId the PUCil- openings through which ions pass back and forth between
maker cells. The myocardial cells are contained in the the extracellular and intracellular spaces. Some channels
muscular layer of the walls of the atria and ventricles. The are always open; others am be opened or closed; still others
myocardial "'Working" cells art permeated by contractile can be selectr.-e. allowing one kind ol ion to pass through
filaments which, when electrically stimulated. produce and excluding al l others.. Membrane channels open and
myocardial mu~cJe controction. The primary function of close in responst to a stimulus.
the myocardial cells is cardiac muscle contraction, fol- Concentration gradient - Particles in solution move.
lowed by relaxation. The pacemaker cells are found in the or diffuse. from areas of higher concentration to areas of
electrical conduction system of the heart and are primar- lowtr concentration. In the case of uncharged particles.
ily responsible for the spontaneous generation of electrical lllOI.-ement proceeds until the particles are uniformly dis-
impulSl$. tri buted within the solution.
Cardiac cells have four primary cell characteristics: Electrical gradient - Charged particles also diffuse. but
Qutomaticit!l - the ability of the pacemaker cells to the diffusion of charged particles is influenced not only by
generate their own electrical impulses spontane(lusly; this the concentration gradient. but abo by an electrical gradi.
characteristic is specific to the pacemaker cells. ent. Like charges repel: opjXlSite charges attr",t. TIlerefore.
uritability- the ability of the cardiac cells 10 respond positively charged particles tend to flow toward negatively
to an eleclrkal impulse: this characteristic is shared by all chlarged particles and negativdy charged particles toward
cardiac cells. positively charged pa rt icles.
conductitity - the ability of cardiac cells 10 conduct Sodium-potassium pump - The sodium-potassium
an electrical impulse: this characteristic is shared by all pump is a mechanism that actively transports ions an05$
cardiac cells. the cell membrane against its electrochemical gradient.
contractih"ty - the ability of cardiac cells to cause car- This pump helps to reestab lish the resting concentrations
di<w:: mu.scle contraction: this charocteristic is specific to of sodium and potassium after card~ depolarization.
myocardial cells. Electrical impulses are the result olthe flow of ions (pri-
marily sodium and potassium) back and forth across the
cardiac cell membrane (Figure 2-1). Normally there is an
Depolarization and repolnrizatlon ionic diffe rence between the two sides. In the resting CaT-
Cardiac cells aJ"e surrounded and filled with an electrolyte diac cell, there a.re more negative ions inside the cell than
lution. An electrolyte is a substance whOH molerules outside the cell. When t~ ions are 50 aligned. the rest-
dissociate into charged particles (ions) when placed in ing cell is called polarized. During this time. no electrical
8
- Electrical conduction system of th e h eart 9
AVnodo
"":'i--i- -t,,-Interventriculaf ...ptum
,
Bundle 01 His
Mter the delay in the AV node. the impulse moves because atrial repolaril.ation occurs during ventricular
through the bundle of His. The bundle of His divides into depolarization and is hidden in the QRS complex. The PR
two important conductil1ll pathways called the right bundle interval represents the time from the onset of atrial depo-
branch and the left bundle branch. The right bundle branch larization to the onset ofwntricular depolariution. The PR
conducts the electrical impulse to the right ventricle. The segment. a part of the PR interval. is the short isoelectric
left bundle branch divides into two divisions: the anterior line betv,'een the end of the P wave to the beginning of the
fascicle, which carries the electrical impulse to the anterior QRS complex. It is used as a baseline to evaluate elevation
wall of the left ventricle. and the posterior fascicle. which or depression of the ST segment. The QRS complex depicts
<:arrie.! the electrical impulse to the posterior willi of the wntricular depolari1.<ltion, or the spread of the impulse
left ventricle. Both bundle branches terminate in a new,'ork throughout the wntricles. The ST segment represents
of conduction fibers <:ailed Purkinje fibers. These fibers early ventricular repolariution. The T wave represents
make upan elaborate web that <:arTY the electrical impulses
directly to the ventricular muscle cells. The ventricles are
capable of serving as a backup pacemaker at a rate of 30 to
40 beats per minute (sometimes less). Transmission of the
,
electrical impulses through the conduction system is slow-
ed in the AV node and fastest in the Hi. Purkinje system
(bundle of His. bundle brunches. and Purkinje fibers).
The heart's electrical activity is represented on the
,:. .:,
,PR IntelWl
monitor or ECG tracing by three basic wawforms: the
P wave, the QRS complex. and the T u'(we (Figure 2-3).
ST segment
,
A U waw is sometimes present. Between the waveforms ," ,
are the follo\,>;nll sellments and intervals: the PR intervill, , ,
the PR segment. the ST segment. and the QT interval.
Although the letters themselves have no special signifi- : :0 :
cance. each component represents a particular event in the
depolariution- repolaril.ation cycle. The P waw depicts
:-:"~-"''-",cc-c-~:
PR ""gment aT Int .......
:
atrial depolarization, or the spread of the impulse from Rgure 2-3. Relatlonshp 01 the electrical conduction system to
the SA node throughout the atria. A waveform represent- the ECG.
ing atrial repolilrimtion IS usually not seen on the ECG
Refrac to ry a nd s uperno nual periods of the cardi ac cycle 11
Negative Positive
wntricular repolari1.ation. The U wave, which isn't always deftection deIkK:tion
present. represents late ventricular repolarization. The QT
interval represents total ventricular activity (the time from
the oru;et of ventricular depolarization to the end of ven_ Figure 2-6. RelaUOOshlp between current now and waYlllorm
dellecUons.
tricular repolari1.ation).
~
PositIVe defle<:tion
FIgure 2-5.
line.
T
NlIlIative deflection +
Biphaslc dene<:tion
OAS complex
~" V......
abwUII
;:;:toty fIlati;
Altract
porl'" FIgure :Z 7. Refractory and S!.p9mOnl1al periods.
Ab.soJute refractory period - During this period the Supernormal period - During this period the cardiac
cells absolutely cannot respond to a stimulus. This period cells will respond to a Wfilker than normal stimulus. This
extends from the onset of the QRS com pia to the peak of period occu rs during a short portion near the end of the
th~ T wav~. During this tim~ th~ cardiac c~lIs hav~ d ~polar T wave. just before th~ cells have completely repolarized.
ized and ar~ in th~ process of ~polarizing. Because the car-
diac cells have not repolari~ed to their threshold potential
(Ihe le~1 at which a cell must be repolarized before it can
ECG graph paper
be depolarized again) they cannot be stimulated to depolar- The PQRST sequence is recorded on special graph paper
ize. In other words. th~ myocardial cells cannot contract, made up of horizontal and vertical lines (Figure 2-8). The
and the cells of the elect ri cal conduction system cannot horizonlllilines meilSure the duration of the waveforms in
conduct an electrical impulse during the absolute refrac- seconds of time. Each small square measured hori~ontally
tory period . repr~nts 0.04 second in time. The width oflh~ QRS com-
Relative refractory period - During this period the plex in Figure 2-9 extends across for 2 small squares and
cardiac cells have repolarized sufticiently to respond to represents 0.08 second (0.04 second x 2 squilres). The ver_
a strong stimulus. This period begiru at the peak of the ticallinu measure the voltage or amplitude of the wave-
T wave and ends with the end of the T wave. The relative form in millimeters (mm). Each small square meilSured
refractory period is also called Ihe vulnerable period of vertically represents I mm in height. The height of Ihe
repo/arization. A strong stimulus occurring during the QRS complex in Figure 2-9 extends upward from baseline
vulnerable period may usurp the primary pacemaker of 16 small $quares and represents 16 mm volti\ge (I mm x
the heart (usually the SA node) and take over pacemaker 16squaru).
control. An example mighl be a prellUllure ventricular con-
traction (We ) that falls during the vulnerable per iod and
takes over control of the heart in the form of ventricular
tachycard ia.
Figure 2-8. EIec1rOCMdlographk: paper. Figure 2- 9 . ORS width: 0.08 second; ORS height: 16 mm.
Waveforms, intervals,
segments, and
complexes
Much of the information that the ECG tracing provides is and peaked. 'Ole abnormal P wave in right atrial enlarge-
obtained from the examination of the three prindpall<.<lVe. ment is sometimes referred to asp pulmonale because the
forms (the P wave, the QRS compler. and the T wave) lind atrial enlargement that it signifies is common with severe
their associated segments and intervals. Assessment of this pulmonary disease (for example, pulmonary stenosis and
data provides the facts necessary for an ao;urate ~rdial; insufficiency. chronic ob$troctive pulmonary disease.
rhythm interpretation. acute pulmonary embolism. and pulmonary edema).
Impulses traveling through an enlarged left atrium (left
atrial h}Pt'rtrophy) result in P waves that are: wide and
Pwave notched. The tenn p mitrale is used to describe the abnormal
The first deflection of the cardiac cycle, the P waw, P WiI\1eS seen in left atrialmJargement because they"''ere first
is ClIusd by depolarization of the right lnd left otrill seen in patients with mitral valve stenosis and iO$ufficielK)'.
(Figure 3-1). The fint part of the P wave represents depo- Left atrial enlargement can also be seen in left heart failure.
lari7.alion of the right atrium: the second part represents Edopic P u-'Ilce - The term ectopic means away from its
depolarization of the left atrium. The waveform begins as nonTIIIllOCiltion. Therefore, an ectopic P wave arises from a
the deflection leaves baseline and ends when the defledioo site other than the SA. node. AbnoTffiilI sites include the atria
returns to baseline. A normal sinus P wave originates in and theAV junction. P waves from the atria lTIlI,y be positive
the sinus node and travels through normal atria, resulting or negative: some are small. pointed. Rat. w;.wy. or sawtooth
in normal depolarization. Normal Pw/!ves /lrt smooth and in appearance. Pwaves from theAV junction are atways neg-
round, positive in lead II (a positive lead). 0.5 10 2.5 mm atillf (inverted) and may precede or follow the QRS complex
in height. 0.10 second or leu in width. with one P wallf or be hidden within the QRS complex and not visible.
to each QRS complex. More than one P wave before a Examples of P waves are shown in Figu re 3-2.
QRS complex indicates a conduction disturbance. such 115
that which occurs in second and third-degree heart block PR In terval
(discussed in Chapter 8).
There are two types of abnormal Pwaves: The PH interval (sometimes abbreviated PRJ) represents
Abnormal sinUJ P wove - An abnormal sinus P wallf the time from the onset of atrial depolariz.ation to the onsd
originates in the sinus node and tTilVels through enlarged of \'entricular depolarization. The PH interval (Figure 3-3)
atri.!r.. resulting in ahnorcml depobriwtion of the atria. indudes a P I<o'a~ and the short isoel~ctric line (PR seg-
Abnormal atria depolarization results in abnormal-lookinlt ment) that follows it. The PR interval is meatu red from the
P waves. beginning of the P wave as it leaves baseline to the begin-
Impulses traveling throogh lin enlarged right atrium ning of the QRS complex. The duration of the normal PR
(right atrial hypertrophy) result in P waves that are tall intel'llal is 0.12 to 0.20 seconds.
Abnormal PH intervals may be short or prolonged:
Short PR in/enoal - A short PR interval is less than
0.12 seconds lind may be seen if the electrical impulse
originates in an ectopic site in the AV junction. A short-
ened PH inte~l may also occur if the electrical impulse
progresses from the atria to the ventricles through one
of several abnormal conduction pathways (called acces-
, sory pilthwa)l5) that b}'pilS5 a part or all of the AV node.
Wolff-Parkinson-White syndrome (WPW) is an example of
such an acceswry pathway.
Pro/OI1ged PR in/errol - A prolonged PR interval is
Fillure 3-1 . Tte P waWl. greater than 0.20 seconds and indicates that the impulse
13
14 Wa\'eforms, intervals, segments, and co mplexes
Q S
Allure 3-3. TIle PR nlllYal.
Figure 3-5. lhe ORS compleX.
A B c
Normal PR Werval 01 0.20 Short PR inle<val Long PR inhtrva l 010.38
second (0.04 second ~ 5 01 O.eII slCord second (OJ)( secord"
squa .... ). (0.04 secord x 9i!z squares)
2aqu"'''') Flilure 3-4. PR Irterval ~Ies.
16 Waveforms, inte rval s, segments, and co mplexes
the baseli ne. A wave that cha nges direction but doesn't
crOM the baseline is Cillied a notch. (Figure 3-6. example E.
shows a notched R and Figure 3-6. example K. sho.,.,'S a
notched S.)
C~pital letters are used to designllte waves of large
amplitude (5 mm or more) and lowercase letters are used
" Nolchad A to designate waves of small amplitude (less than 5 mm ).
01- 1r,
a
,
H
,
f s
0.12 second or more. An abnormally wide QRS complex
may result from:
a block in the conduction of impulses through the right
or left bundle branch (bundle_branch block)
an electrical impulse that has arrived early (as with pre-
1\-,V"",,",,
mature beats) at the bundle branches before repolariza-
tion is complde. allowing the electrical impulse to initiate
depolarization of the ventricles earlier than usual. result-
ing in abnormal (aber rant) ventricular conduction lind
causing a wide QRS complex
J S s' K an electrical impulse thaI has been conduded from
the atria to the ventricles through an abnormal accessory
Figu re 3-6, DRS Vil"latlons. conduction pathway that bypasses the AV node. allow-
ing the electrical impulse to initiate depolari7.ation of
the wnlricles earlier than usual. resulting in abnormal Imnt may be displaced abow baseline (elet'Oteti ST seg-
(aberrant) vtntricular conduction and causing a wide QRS men/) or below baseline (depressed ST segment ). The PR
complex segment is normally used as II baseline reference to evalu-
an electrical impulse that has originated in an ectopic ate the degree of displacement of the ST segment from
site in the vtntricles. the ~lectric Hne. An 51 segment illlbnormal .... hen it is
Examples of QR5 complexes are shown in Figure 3-7. elevated or depressed 1 mm or more. measured at II point
0.04 second past the J point (the point where the QR5 com-
plex and the 5T segment meet).
STsegment Elevated 5T segments may be horizontal (straight
The ST segment represents earl y vtntricular repolariza- across), con"," (rounded upward), or concave (rounded
tion. The 51 segme nt is the flat line between the QRS com- inward). Common causes include 51 elevation myocardial
plexand the Twave (Figure 3-8). Normally the S1 segment infarction (STEMI ). coronary artery spasm (prirwnetars
is positioned at baseline (the isoelectric line). The ST seg.. angi~), acute IX'ricarditis, ventricular aneurysm, early
repolarization p.atlern (a form of myocardial repolariza-
tion sn in normal healthy individuals that produces
51-segment elevation closely mimicking that of acute
myocardial infarc tion (M11or pericarditis), hyperkalemia.
and h~'pDthermia.
Jpolnt Depressed ST segments may be horiwntal. downsJop-
ing. upsloping, or sagging. Common causes include
myocardial ischemia. non-ST elevation MI (non-
STEM!). reciprocaJ ECG changes associated with STEM!.
hypokalemia. and digitalis effect. Digitalis causes a sagging
ST-segment depression. ~;th a characteristic "scooped-
Figure 3-8. The ST segmect. out~ appearancr. Examples of ST segments are shown in
Figurr 3-9.
18 Waverorms, inte rval s, segm e m s, a nd complexes
G ~d&p", ..",
Twave
Th~ T wav~ represents v~ntricular r~polari1.ation. Th~ no r
mal T wave begins as th~ deflection gradually slopes upward
from the ST segment. and end. when the waveform returns
to baseline (Figure 310). Nonnal T waves ar~ rounded and
slightly asymmetrical (with th~ first part ofth~ T wave grad -
ually sloping to the peak and returning more abruptly to
baseline). positive in lead II (a positive lead). with an ampli
tud~ less than 5 mm. The T wave always follow. the QRS
Rgure3-10 . Th8TW3Y11.
complex ( r~polarization always foll<Mls depolarization) .
E Flat T wavs
A 1. Numbe, 01 .mall squares belwoon R wav... '" 31. Hall 01 B 1. Numbe, 01 small squarllll beIw""" R WIW8S" 38. Hall DI
31", 15. 38" 19.
2. Numbe,oI small squ ares in aT Inlerval" 11 2. Numbe, 01 small squar .... in aT inl"",al" 13
3. Compare the dilfe,80C9: aT inlerval " lass Ihan hal! the 3. Compare the dilfemnc:a : aT interval 10 Ie than hall the
RR Interval (11 small squa,es a,e I.... lhan 15small R-R int"",aI (13 sma! square. araless than 19 .mal
squar... ); aT inlerval is ,..,,,,,,,110,Il-0l0 heart mta. squares): aT inWNaI" """"allor ltd" heart rale.
(Dumtion of aT i1Ierval: 11 qUa'lIII x 0.04 ~"0.44 (OoJUl.tlon 01 aT intorval: 13 small IiqUB'1III x 0.04
""""'.) ....,end" 0.52 secend.)
Types ofECG monitoring middavicular line), one below the left clavicle (2nd inter-
spa~, Idt midclavkular line), one on the right lower rib
There are t~'O types of ECG monitoring: hordwirtl 4Ild cage (8th intenp.xe, right midclavicuJar lint), one on the
telemetry. With hardwire monitoring (bedside monitor- left lov.-er rib cage (8th interspace, Jdt midclavicular line),
ing), electrode pads (conductive gel diKS) a re placed and one in achest lead position fY, to V.). The SDc chest lead
on the patient's chut and attached to a lead-cable sys- positions (Figure 4-2) include:
tem and then connected to a monitor at the bedside. V, - 4th intercostal space. right sternal border
With telemetry monitoring (portable monitoring). elec- V, _ 4th intercostal sPi\te, left stunal border
trode pads are attached to tht patient's ches t and con- V.-midv.-aybetweenVzandV,
nected to leads that are attached to a portable monitor V, - 5th intercostal space, left midclavicular line
transmitter_ V. _ 5th intercostal space, left anterior Miliary line
Haruwire motliton"ng - Hardwire monitoring uses V. - 5th intercostal space, left midaxillary line
either a filJf!-leadwire system or a three-leadwire system_ lhe right arm (RA) lead is attached to the eledrode pad
With the fiw,-Ieadwire S)'!i tem (Figure 4- IJ. five elee. below the right clavicle: the left arm (LA) lead to the elec-
trode pads and five leadwires are used. One electrode trode pad below the left clavicle; the right leg (RL) lead
is placed below the right clavicle (2nd interspace. right to the electrode pad on the right lowe r rib cage; the left
25
26 Cardiac monitors
J J
flgLlre 4-2, Chest load posKIons, RIILl re 4-3. HardW __e monKorhg - ThrOO-lerulWire system.
lhls IIklslraUon shoWs you where to place the electrodes II1d attach
leadwlres using a three-leadWlre system. The lead wires are color-
coded as Iollows:
leg (LL) lead to the electrode pad on the left lower rib cage:
and the chest lead to the electrode pad of the specific chest white - right arm (RAj
position desired (V, through V,l. black -left arm (LA)
With the five-leadwire system for hardwire monitor- red -left leg (LL).
Leads placed in this position will allow you to monitor leads I,
ing, you can continuously monitor two l~ads using a
lead selector on the monitor. Leads placed in the arm II, or III using the lead selector on the mon~or.
and leg positions allow you to view leads I, II, III, AVR,
AVL, and AVF (Figure 4-1). To view chest lead V, to V" the LA lead is attached to the electrode pad below the left
the chest lead must be placed in the specific chest lead clavicle, and the LL lead is attached to the electrode pad on
position desired. Generally, a limb lead (usually I, II. or the left loy,-er rib cage. You can monitor either limb leads
III) and a chest lead (usually V, or V,) are cho~n to be I. II. or III by turning the lead ~Iector on the monitor.
monitored. Although you can't monitor chest leads (V, to V,) with a
With the three-leadwire system (Figure 4-3), three elec- three-leadwire system, you can monitor modified chest
trode pads and three leadwires are used. One electrode pad leads that provide similar infonnation. To monitor any of
is placed below the right clavicle (2nd interspace, right these leads. reposition the LL lead to the appropriate posi-
midclavicular line), one below the left clavicle (2nd inter- tion for the chest lead you want to monitor, and turn the
space, left midclavicular line), and one on the left lower rib lead ~Iector on the monitor to lead III. Examples of modi-
cage (8th interspace. left midclavicular line). The RA lead fied chest lead V, (HCL,) and modified chest lead V, (HCL, )
is attach~d to th~ electrode pad below the right clavicle, are shown in Figur~ 4-4.
Figure iI-il. HardWlra monnor1ng - Tllree-leadwlre system: Leads MCL, and MCt... Modified chest leads can be monitored with tho three-
leadW __o system by reposRlon1ng tho len leg (U) lead to the chest position desired and tumlng the lead selector on tho monttor to lead III.
Troub lesh ooting monitor problems 27
G G G
lead II Lead III
Negative lead - 2nd Interspace N"9IIti.... lead - 2nd Intonp""" N&gative lead - 2nd inlelSplOCe
right midclavicula, line right midclavicular Ii"" lelt midclavicula, line
Podive load - 2nd Interspace Positive klad -11th Interspa::e Positil'll Iliad - 8111 Inl9f&paoo
left midcIDVic .... a' Ii"" left midclavicular II"" lelt midclavicula, line
Ground load - 8th InllH'ap""" Ground lead - 8th interspace Ground lead - 8111 Interspace
right midclavicula, line right midclavlc:ular Ii"" 'ight midclavicular ina
and acti"ate the high rate alarm. Most high voltage arti gel, a loo"e electrode, or a disconnected lead wire. Low
facts are related to muscle movements from the piltient voltage QRS complexes can also activate the low-rate
turning in bed or moving the extremities (Figure 4-7). alarm; if the ventricular waveforms aren't tall enough.
Seizure activity can also produce high-voltage artifact the monitor detects no electrical activity and will sound
potentials (Figure 4-8) . the low-rate alarm.
False low-rate alamu - Any disturbance in the trans- Muscle tremors - Muscle tremors (Fil/ures 4-13 and
mission of the electrical signal from the skin electrode to 4-14) can occur in tense, nervous patients or those shiver-
the monitoring system can activate a false low-rate alarm ing from cold or having a chill. The ECG baseline has an
(Figures 4-9, 4-10, 4-11. and 4-12 ). This problem is usu- uneven, coarsely jagged appearance, obscuring the wave-
ally caused by ineffective contact bd""een the skin and the forms on the ECG tracing. The problem may be continuous
electrode-Ieadwire system, resulting from dried conductive or intermittent.
Trouble shooting monitor problems 29
Figure 4-7. Patient movement cause: str1ps above shoW pallent turning In bed Of extremity movement. SOIUtIm: Problem Is usually
Intermittent and no corractlon Is necesay. Movement tRact C~ be reduced by avoiding placement 01 electrode pads In areas where
extremity movemenlls greatesl (bony areas such as the davldes).
FIgure 4- 8. Setzln actlVlly C<rL activate the high-rate alarm on the monitor.
30 Ca rdiac lllonilOrs
Figuf1l 4 9, cont~uous straight Ina, QIJs,: DI18C1 conciJc1tt'a gaI, dl!ro"tl8Ctad lead wire, or dlsconn8cted el8ctrooa pad, sotJItm: Qlack
ellM:trode-lead syslem; re-prep alii fe-altach electrodes .nI1oacIs as necessary. fJie: A straight line may also h:llcali! the msenc:a 01
electrical acttvfty ~ thell8llt; the patJant must be avaIual9d Immediately !of the presenca 01 a pulse.
Figure 4 1O. ~termttblnt straIgIIt line. GaUS8: r.ef1actNe contact betWiIen SkIn and electrooa pac:!. SDIIIt/on: Make sure hair Is Clpped
.nI electrode pad Is pI;Qd on clean, dry skin; " dlaph:lresls Is a problem, prep skin SII1'ace wtth Unctln 01 benZoin solIIIon.
Figure 4 11 . conUrwus low waveform 'I1tagi. GaUS8:LowYOIIage QftS compleJDIIS. so.tstIon:lUm ~ amplItUde (gain) knob on monlor
or change lead positions.
Troubleshooting monilor proble ms 31
Fillure 4-12. Intermment loW waveform YO!t<Qe. ClIusfllntarmtttent 1oW-~e OIlS COOlplexes ara seen In both strtps aOOe.
SO/uI1on: Uthe pr~ Is frequent and acttvates the loW-rate alann, c:tmge lead posttlons.
Figure 4-13. contlnuollS musde tremor. cause: Muscle tremorn are usually related to tense or nenoos patients or Ihosa sIllYer1ng from
cold or a chili. SOlt/ltln: lI"eat cause.
32 Cardiu c monilOrs
Figure 4-14. .,lBrmltlenl musde 1r1lfl1CX. caUSI1: Muscle trernon thaI ClCClI' nlefmlllenlly. Sdu/fa!: correction Is usually unllBalSSal)'.
Nol6: In this str~, the palleR lias two p waves precedtrY;j each ORS complex \S8COOO-degrae atTklVenIrt:utaf block, MOOIIZ 11).11 the muscle
trem!n went continUOUS (as In Agulfl 4-13). yQJ wOUlCl be unable 10 identity this S8f1OUS IITt1ythmla.
Figure 4-15. Telemetry-rlllated Interference. cause: ECG sI!1lals 1I"e poorly received ~er the telemetry system causing sharp spIIes
nI someUmes kiss 01 signal recepllon. ThIs problem Is usually lfllated to wmk batteries or the transmltlef being usalin the outer fI1nges 01
Ihe ~11on lI"ea lor the base stallon receiver. SdutJon: Ctlange batteries; keep pall8nlln recepUon area 01 base station receivers
Telemetry-related interference - Te lemetry-related of the base station receiYer, resulting in sharp spikes or
artifacts occur ",-hen the ECG signals are poorly received straight lines on the ECC tracing .
owr a telemetry monitoring 5)'Stem (Figure 4-15). Weak Ekdrical interference lAC intmerence) - Electrical
ECC signals are caused by weak batteries or by the trans- interference (Figure 4-16) can occur ",-hen mUltiple pieces
mitter being used in the outer fringes of the reception area of electrical equipment are in use in the patient's room;
Trouble shooting monit o r problems 33
FIgure 4-17. wandertng baseline. CBUS8: Exaggerated resp~atory movements usually swn In paUents In respiratory distress (paUents
with chronic obstructlvo pulmonary disease). So/uIIon: AYOId placing electrode pads In lI'BaS where mOYOOler1ts 01 the accessory muscles 1I'lI
most exaggerated (Which can be anyw1lere on the <rltertf chest wal~. Ploc:e the pads on the uwer bock IX Iql 01 the shoolders " neceswy.
There are filii! basic steps to be fonowed in analyzing II calipers. a variation in the R-wave regularity may be noted,
rhythm strip. ~h step should Ix followed in sequence. but without marking and measuring between the short-
Eventually this will become II habit and \\;11 enable you to est and longest R-wave variation, there is no way to deter-
identify II strip quickly and accurately. mine how irregular the rhythm is, Examples of rhythm
measurement are shown in Figures 5-2. 5-3. and 5-4.
Step 1: Determine the regularity
(rhythm) ofthe R waves Step 2: Calculate th e heart rate
Starting at the left side of the rhythm drip. place an inda This measurement will al ....<l)'S refer to the ventricular rate
card above the first two R waves (Figure 5-1). Using a sharp unless the atrial and ventritular rates differ, in which case
pencil. mark on the index card .bove the tv.'O R waves. both will be given. The ventricular rate is usually deter-
Measure from R wave 10 R wave acro" the rhythm strip. mined by looking at a S-second rhythm strip. The top of the
marking on the index card any variation in R wave regular- electrocardiogram paper is marked at 3-second intervah;
ity. If the rhythm varies by 0.12 ~nd (3 small squares) two intervals equal 6 seooods (Figure 5-5). Several methods
or more between the mortesl and longest R wave variation tan be used to calculate heart rate. These methods differ
marked on the index card. the rhythm is irregular. If the according to the regularity or irregularity of the rhythm,
rhythm doesn't vat'}' or lIaries by Ius than 0. 12 second. the
rhythm is considered regular. Regular rhythms
Calipers may abo be used, instead of an index card. to Two methods can be used to talculale heart rate in regular
determine regularity olthe rhythm strip. R waw regularity rhythms;
is assessed in the same manner as with the index card, by Rapid rate calculution - Count the numberofR WiIVU
placing the two caliper points on top of two consetutive R in a &-second strip and multiply by 10 (6 secondS)( 10 = 60
waves and proceeding left to right across the rhythm strip. seconds. or the heart rale per minute). This method pro-
noting any variation in the R-R regularity vides an approximate heart rate in beats per minute, is
The author prefers the index tard method, because eath fast and simple. and tan be used with both regular and
Rwave variation (however slight) can be IJUIrked and meas- irregular rhythms .
ured to determine if a 0_12-second or greater VilTiante e:J[ists Prf!CiSIl rate rulculution - Count the number of small
between the shorter and longer R-wave variatiom, With .squares between two coMeCutive R wave.s (Figure 5-6) nnd
refer to the conversion table printed on the inside back
coverof the book. A remowble com'usion table is also pro-
vided.Although this method is accurate. it can be used only
for regular rhythms. If a conversion table isn't available.
divide the number of small squares be!>..'een the two con-
secutive R waves into 1500 (the number of small squares
in a I-minute rhythm ~trip). The heart rates ror regular
rhythms in the answer keys were determined by the precise
rate calculation method.
Irregular rhythms
Only rapid rate calculation is used to calculate hurt rate
in irregular rhythms, Count the number of R WilVes in a
6-second strip and multiple by 10 (Figure 5-7). or count
the number of R waves in a 3-second strip and multiply
Figure 5- 1. Index ca-a. by 20 (3 seconds )( 20 = 60 seconds, or the heart rate per
minute),
34
Step 2: Calcul a te the heart ra te 35
Figure So6. Regular rhy1tV1I; 25 small squares between Rwaves '" 60 heart rate.
Therefo re , you can't determine if the rhythm is regular or As you hav'e seen. rh~1hm strips may have one rhythm
irregular. In this situation. multiply the two R waves by or sevoeral rhythms. Therefore, each rhythm stTip may
40 (I Yi second x 40 '" 60 seconds. or the heart rate per havoe one ans ....-er or several al1SY>ers. Figures 5-8, 5-9, and
minute) to obtain an approximate heart rale of 80 beats 510 have two different rhythms and thus MOO different
per minute. The second rhythm is regular. with a heart answers. Each rhythm on the strip must be analyzed sepa-
rate of 167 beats per minute (9 small squares between R rately. When interpreting a rhythm strip. describe the basic
waves '" 167). underlying rh~thm first. then add additional information.
Step 2: Cnlcul nte the henrt rIl te 37
Agure 5-10. calculallng rate wtIen a mytlvn COYen less IIIan 3 seconds.
38 Analyzing a rhythm strip
Figure 5- 13. PR Ilterval 0.16 second. Flgure 5-14. aRS complex 0.12 seo:.od.
Box 5-1.
Rhythm strip analysis such as normal sinus rhythm with one premature ventric-
ular contraction (PVC) (Figure 5-8).
1. De1ermlne regula~ty (rhythm).
Z. C~k:U1iI1I! Hill!. Stl!P 3: Idl!nlify amll!xaminl! P wavl!s
3. examine P waves.
4. Measure PR In1erval. Analyze the P waves; one P wave should precede each
5. Measure aRS complex. QRS complex. All P waves should be identical (o r near
identical) in size. shape, and position. In Figure 5-11
Step 5: Mellsure the QRS complex 39
Overview
Since th is rate is faster than other pacemaker sites in the
The term arrhythmia (abo called dysmythmia ) is very conduction system, the SA node retains control as the pri-
general. rderriog to all rhythms other than the nor- mary pa.cemaker of the heart. Sinus rhythm originates in
ITIlIl rhythm of the heart (normal sinus rhythm). Sinus the SA node and the impulse follows the normal Induc-
arrhythmias (Figu re &-1) result from disturbances in tion pa.thway through the atria, the AV node, the bundle
impulse discha rge or impulse conduction from the sinus branches, and the ventricles, resulting in normal atrial and
node. The sinus node retains its role as pacemaker of the ventricular depolarization.
heart. but discharges impulses 100 fast (sinus tachycar-
dia) or too slow (sinus bradycardia); discharges impulses 80a i-1.
irregularly (sinus arrhythmia); fails to discharge an
..
Normal sinus rhythm: Identifying ECG features
impulse (sinus arrest ); or the impulse discharged is
blocked as it exits the sinoatrial (SA) node (SA exit block).
Sinus bradycardia. sinus tachycardia. sinus arrhythmia.
sinus arrest, and sinus block are all considHed arrhyth -
Rhythm:
"".
PW''IIiII:
"'
60 to 100 tJeallolmlllJle
Normal In stze. sIlape, and tinction:posltlYe In
mias. However, sinus bradycardia at rest. sinus tachycar- 1eaCI1: one P WlIYfI!r9CEide5 each ORS complex
dia with aen:ist, and sinus arrhythmia associated with PH IntiIn'aI: Normal (0.12" 0.20 second)
the phases of respiration are considered normal responses QRS comple.: Normal (0.10 sean:! or less)
of the heart
44
Sinus loc hrca rdio 45
-
Figure 6-3.
Rb)'Ulm:
PWI'I'9S:
PR InIlIrYaI:
Sinus tacllycartlla.
"""",,
115 beatsJrnhuto
"'"to
0.16 to 0.18 sean:I
DRS complex: 0.08 0.10 secood.
46 Sinus nrrhylhmins
heart rate slows down. Sinus tachycardia begins and ends du ring diastole), Sinus tachy<:ardia that persisb may be
gradually in contrast to other tachycardias ...... hich begin one of the first signs of early heart failure .
and end suddr:nly.
Sinus tachycardia can be caused by anything that Sinus bradycardia
increases sympathetic lone or anything thai decreases
pal'Mympathelic lone. Factors commonly associated with Sinus bradycardia (Figure 6-4 and Box 6-3) is a rhythm
sinus tachycardia are: that originates in the SA node and discharges impulses
anxiety. ucitement. stress. exertion. exercise regularly at a rate between 40 and 60 beats per minute.
fewr. nnemia. shock The P waves are nonnal in size, shape, and dirtction: posi-
hypoxia. hypovolemia. hypotension. heart failure. tive in lead II (a positive lead), with one P wave preceding
hyperthyroidism each QRS complex. The duration of the PR interval and the
pain, pulmonary embolism (sinus tachycardia is the QRS complex is within nonnallimits. The distinguishing
most common arrhythmia seen with pulmonaryemboJism) feature of this rhythm is the sinus origin and a heart rate
myocardi;lJ ischemia. myocardial infarction (M!) (sinus between 40 and 60 beats per minute.
tachyeardia persisting after an &cute infarct implies exten-
sive heart damage and is generall y a bad prognostic sign) ao. ...3,
drogs that increase sympathetic tone (epinephrine, Sinus bradycardia: Identifying ECG leaba'es
nortpinephrine, dopamine. dobutamine, tricyclic antide-
prtS5ants, isoproterenol. and nitroprusside) Rhylhm: R....
drogs that dec re;ue parasympathetic tone (atropine) Rot. 40 to 60 bealsImlnuls
use of substances such as caffeine, cOGline, and nicotine. p.,.",..: Normal In sue, sI\ap&, and ttr9ctkln: posltlYe In
Sinus tachycardia is usually a benign arrhythmia and lead I: one P WW1I ~ecalBS each ORS complex
treatment is directed at correcting the underlying cause Pft IlItan'aI: Normal (0.121D 0.20 S8IXJId)
ORS compleX: Normal (0.10 sec::ooo or less)
(relief of pain, fluid replacement, rtmoval of offending
medications or substances, and reducing fever or anxiety).
Ho.....ever, persistent sinus tachycardia should never be Sinus brady<:ardia is tht: normal response of the heart
ignored in any patient, especially the cardiac p.1lient. A to rtlaxation or ~leeping ...ntn the parasympathetic tffect
rapid heart rate increases the workload of the heart and on cardiac automaticity dominates over the sympathetic
ib oxygen requ irements and IT\iJ)' cause a decr\\il$ed stroke effect. It's ,ommon among trained athletes who may have_
volume leading to a decrease in cardiac output. In addi tion, resting or sleeping pulse rate as 10was35 beats per minute.
heart rates higher than norm;lJ decrease the amount of Mild bradycardia may actually be beneficial in some
time the heart spends in diastole, leading to a decrease in patients (for uample, awte loll) bec:ause of tht: decrease in
coronary artery pe rfusion (coronary arteries are perfused wo rkload on the heart,
RllyItIm:
R...
P WaY": " ...
Sinus -
Figure 6-4. Sinus bradycardia,
Regula'
Sinus bradycardia can be caused by anything that common and often the earl iest manifestation of sick sinus
incrtases potrMympathetic tont or anythinQ that decrtastS synd rome, Sick sinus synd rome is a dysfunctioning sinus
sympotthetic t~. It commonly OCCUI1l with the following: node ...... hich is manifested on the ECG by marked bradyar-
during sleep and in athldes rhythmias al ternating with episodes of tachyarrhythmias
in acute inftrior waH!>!1 involving the right coronuy and is commonly accompotnied by symptoms :ltJch!lS dizzi-
artery. which usually supplies blood to the SA node ness. fainting episodes, chest pain. shortnen ofbnath. and
as a reperfusion rhythm after coronary angioplasty or heart failure. This syndrome has also been called tachy-
afte r treatment with thrombolytics brady sfI71drome. Permanent pacemaker implantation is
v&gal stimulation from vomiting, bearing down recomm~nded once patients become symptomatic.
(VaJsalva's maneuwr), or carotid sinus pressure Sinus bradycardia doesn't require treatment unless the
!IS a vasovagal reaction. A vasovagal reaction is an patient becomes symptomatic. Some cliniCllI silins lind
utrtme body rtsponse that causes a marked decrease in symptoms requiring treatment include cold. clammy skin:
neart rate (due to vagal stimulation) and a marked decrease hypotension: shortness of breath, chest pain, changes in
in blood presw re (due to vasodilation), This reaction may menta l status. decrease in urine output, and heart failure.
ocaJr with potin, nausea. vomi ting, fright. or :ltJdden stres.s- If sinus bradycardia persists, the treatment of choice is
ful situations. The combination of extreme bradycardia and atropine, a drug that increases the heart rate bydecrea!iing
hypotension may re:ItJlt in fainting (vaKIYagal syncope). p.1rllSympathetic tone. 'l'ht usual dost is 0,5 rug IV push
The situation is usually reversed ..... hen the individual every 5 minutes unti l the bradyca rdia is resolved or a maxi-
is placed into a reaJmbent position, thertby increasing mum dose of3 mg is given. Atropine must beadministered
venous return to the heart. If fainting occu rs ..... ith the indi- correctly; atropine administered too slowly or in d05e5 less
vidual in a recumbent position. it can usually be revel1loed than 0.5 mg can further decrease the heart rate instead of
with leg elevation. ifl(:re.uing it. If the rhythm still doesn't resolve lifte r the
carotid sinus hypersensitivity syndrome. sleep apnea atropine is administertd. 11 tran scutaneous (external) or
decreased metabolic rate (hypothyroidism. hypother- transvenous potcemaker may be needed. All medications
mia); hyperkalemia that cause a decrease in heart rate shou ld be reviewed lind
sudden movement from recumbent to an upright posi- disoontinued if indicated. For chronic bradycardia. perma-
tion (common in the elderly) nent pacing may be indicated.
inc reased intracranial pressure (II. sudden appea rance
of sinus bradycardia in 11 pottient with cerebra l edema or Sinus arrhythmia
subdural hematoma is an important clinical obselVation)
drugs such .s digoxin, ca lcium channel blockel1l, lind Sinus arrhythmia (Figure 6-5 and Box 6-4) is a rhythm that
beta blockers originates in the sinus node and discharges impulses irreg-
degenerative disease of the sinus node (sic k sinus ularly. The heart rate may be normal (60 to 100 beats per
synd rome), Pel1listent sinus brAdycardia is the most minute) or slow (commonly associated with a brMlycardic
-
Allure 6-5.
RII)'II1m:
P waws:
PIt ln18rYaI:
SInus arrflrthmla
negular
SO beal&mloote
Normal In ron1Iguratloo; precede eadI 0fIS
0.12 to 0.1 4 second
ORS complex: 0.06 to 0.08 second
48 Sinus arrhythmias
Box , ..... sinus arrest and sinus exit block. Sinus arrest and sinus
Sinus arrhythmia: Identifying ECG features exit block. two separate arrhythmias with different patho-
physiologies (Figur~ 6-6. 6-7. and 68 and Box 6-5), are
Rhythm: Irregular discuned together because distinguishing between them is
Ratl: Normal (60 to 100 beats/mtlute) or SlOW ~ess \han at times difficult. and because Iheir treatment and clinical
60 bealslmlnute) significance are the same.
Pwaves: Normal., slm, shape.1Ild d ~ ectlon; posRIvo In
lead II; OI1e Pwave precedes each OAS complex Box 6-5.
I'A InteMI: Normal (0,12 to 0,20 second)
Sinus arrest and sinus ellit block: Identifying
QAS complex: Normal (0.10 secooo or less)
ECG leabJres
Rhythm: Bask: rhythm usually I"lIgular; there Is a sudden
rate). The P wav~ are normal in sne. shape. and direction: pause In the bask: rhythm (causing Irregularity) with
positive in lead II (a positive lead). with one P wave pre one or mol"ll missing beals; neart rate may slOW
ceding each QRS complex. The duration of the PR interval dOWn lor seY9r81 beats aner paJS8 ~ernporay rate
and the QRS complex is with in normal limits. The distin suppression) 001 returns 10 bask: rate
guishing feature of this rhythm is the sinus origin ood the Rate: lhal oIl.11derlyllg rhythm. usually stlus
rhythm irregularity. P Way": Sinus P waY9S with bask: rhythm; absenl dlSlng
Sinus arrhythmia is commonly lWOCiated with the
phas~ of respiration, During inspiration. the sinus node
P1Itnt,rval: ""~
Normal (0.12 to 0.20 second) with DaSI& rl'ly1hm:
absent during pause
fires faster; during expiration. it slows down. This rhythm
QRS complex: Normal (0.10 second or less)wllh basic rhythm;
is an extremely conunon finding among infants. children. absent during pause
and young adults. but may occur in any agegroup. Sinus
arrhythmia is a normal phenomenon that usually doesn't DlffMM tlarlffj fH fU" $
require treatmenl unlen it iSilccompanied bya bradycardia SinUI~; Basic rhythm (R-R regJlarlty) I"lIsumes 011 Urns alter
rate that causes symptoms.
SInus Irmt: "'"~
Bask: rhythm (R-R regJlarlty) doesn't resume on
Sinus pause (sinus arrest and sinus Ume alter pause
exit block)
Sinus pause is II broad term used to describe rhythms in Both sinus arr~t and ~inus e)lit block originate in the
which there is a sudden failure of the SA node to initiate or sinus node and are characterized by a sudden pause in the
conduct an impulse, Two rhythms fall under this category: sinus rhyl hm in which one or more beats (cardiac cycles)
Rgure 6-8. Normal sinus rhythm wllh sinus arras!; rale suppression Is presenlloltowlng pause.
Rhythm: BasIc rhythm regutar; Irregutar <lJ~ng pause
Rate: BasIc rhythm rale 84 beatslmnute; rate slows to 56 boatslmlrule loIlowlng pause (temporll)' rate suppression may occur
lollowlng a pause In the bask: rhythm)
P waygs: Sllus In baste rhythm; absent during pause
PfIlnl9rYat: 0.16 to 0.18 second In basic rhythm; absent during pause
DRS complex: 0.08100.10 second In basic rhythm; absent du~ng pause.
an: missing. The P waves in the underlying rhythm will ~ the timing of the sinus node discharge, and the underlying
nonnal in size. shape. and direction; positive in lead II (a rhythm won't resume on time after the pause.
positive lead). with one Pwave pre\:eding each QRS complex. With sinus exit block. an electrical impulse is initiated
The duration of the PR interval and the QRS complex in the by the SA node. but is blocked as itexils the sinus node.
underlying rhythm is within normallimils. The distinguish- preventing conduction of the impulse to the atria. Thus.
ing feature of both rhythms is the abrupt pause in the under- SA exit block is a disorder of conductivity. Because the reg-
lying sinus rhythm in which one or more beats are missing. ularity of the sinus node discharge isn't interrupted (just
followed by a resumption of the basic rhythm after the pause. blocked), the underlying rhythm will resume on time after
Sinus arrest is caused by a failure of the SA node to ini- the pause. Once the rhythm resumes after the pause (in
tiate an impulse and is therefore a disorder of automatic- both sinus arrest and sinus exit block) it's common for the
ity. This failure in the automaticity of the SA node upsets rate to be slower for several cycles (rate suppression). Rate
50 Sinus arrhythmias
suppression is temporary and will cause a brief irregularity Th e patient may become symptomatic if the pauses
in the underlying rhythm. but after sewral cycles the basic associated with sinus arrest or sinus exit block are fre-
rate and rhythm will return. An example of rate suppres quent or prolonged. Another danger is that the SA node
sion is shown in Figure 6-8. may lose pacemake r cont rol. 'Nhen the sinus node sl<p.ys
Differentiating bet'o\'een the two rhythms involves com down below its minimum firing rate of60 beats per minute
paring the length of the pause with the underlying pop becau~ of bradycardia or II pause in the underlying
or R-R interval to determine if the underlying rh}-1hm rhythm. an opportunity is provided for pacemaker cells
resumes on time after the pause. This can be determined in other areas of the conduction system to usurp cont rol
only if the underlying rhythm is regular. If the underlying from the sinus node and become the dominant pacemaker
rhythm is irregular. as in sinus arrhythmia (Figure 6-9). of the heart. T~ term ectopic is commonly applied to
it's impossible to distinguish sinus "rrest from sinus ait rhythms that originate from any si te other than the SA
block. In this case, the rhythm would best be interpreted node. Ectopic sites in the atria. AV node. or ventricl~ may
using the broad term sinus pause. indicating thilt either assume pacemaker control for one beat. ~ral beaU. or
rhythm could be present. Froma clinical viewpoint. distin- continuously.
guishing belY.-een sinus arrest and sinus exit block usually If symptomatic. the rhythm is treated the same lIS in
isn't essential. symptomatic sin us bradycardia. In addition. all medica-
Sinus a rrest or sinus exit block can be caused by numer- tions that depress sinus node discharge or conduction
ous factors. including: should be stopped.
increase in vagal (parasympathetic) tone on the SA node A summary of the identifying ECG features of sinus
myocardial ischemia or infarction arrhythmias can be fOllnd in Table 6-1.
use of certain drugs such as digoxin. beta blocken, or
calcium channel blockers.
Sinus pause (sillus arrest and sillus exit bloc k) 51
Table 6-1.
Sinus arrhythmias: Summary 01 Identifying ECG features
Normal sinus
rhythm
R~'" 6010 100 Positive in lead II; nonnal
in sim, shape, and
direction; 0IIII P wave
Normal (0.12 to
0.20 second) ....,
Normal (0.10second
Sinus
bradycardia
R~"" 40"60
"""""
Positive in lead II; nonnal Normal (0.12 to
....,
Normal (0.10 second
in sim, shape, and 0.20 second)
dirvction; 0IIII P wave
precedes each CfIS
Sinus
tachycardia ""... 100 to 160 """""
Positive in lead II; nonnal
in sim, shape, and
Normal (0.12 10
o.20second) ....,
Normal (0.10second
"""""
Sinus
alThytlvnia
trreg ..... 6010 tOO(nonnaI)
or< 60 (slow)
Pooitive in tead II; norm.1
in sim, shape, and
direction; 0IIII P wave
Norm31 (0.12 to
0.20 second) ....,
Nonn3I (0. to .cond
Ddfersntiatirtg
fealUrBII
Sirusbio:k: Basic ~ resumes on
time after pause
Sirusarrest
..
Basic ~ does not
resume on time after
~
Nuts: Hthe basic rhythm is iITll9Uar (sinus alThythmia~ sinus arrest cant be differentiated lrom sinus block. and !he rhythm is
interpretoo as sinus arrhythmia with sirllS pause.
52 Sinus arrhythmias
Strip6-7.RhyIIvn: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ Pwave: _ _ _ __
PR inleMll: ORS complex:_ _ _ _ __
IIlythm Interp-etmon:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Rhythm interpretatm:' _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
""""',."" .. ORScomplex:_ _ _ _ __
,,,,,- - - - - - - - - - - - - - - - - - - -
""' . ,,._-------- -
11ft inIeMII:
-------
CAS CGmp6lx:,_ _ _ __
Pwa....: _ _ _ _ __
1ItIytIIn.'''''ubdlon:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Mechan1sms of arrhythmias
continues as long as it encounters receptive cells, Reentry
Under certain drcumstances cardiac cells in any part Qfthe (like triggered activity) may result in atrial. junctional. or
heart may lake on the role of pacemaker of the heart. Such ventricular beats occurringsin!!ly. in pairs, in runs, or as
II pacemaker i5 called an ectopic pacelJl1lker (a pacemaker a sustained ectopic rhythlIL Common causes of reentry
other than the sinu~ node). The result can be ectopic beaU; indude myocardial ischemia or injury, hyperkalemia. and
or rhythms. These rhythms llrt identified according to the presence of an accessory conduction pathway between
the location of the ectopic pacemake r (for example. at rial. the atria and the ventricles.
junctional. or ventritular). Ttw three basic mechanisms Atrial arrhythmias (Figure 7-1) originate from edopic
that are responsible for ectopic beau and rhythms art sites in the atria. Ectopic P waves from the atrium differ
oltered automaticity, tn"ggered aclivif!l. and reentry: in morphology (snape) from the normal sinus P waves
Altel't'd ~utomilt icity- NOT1T\alIIy the automaticity of the (Figure 7-2). For example, in slower atrial rhythms (pre-
sinus node exceeds that of all other parts oftht conduction mature atrial contractions, wandering atrial p;teemaker)
system, allm.ing il to control the heart rate and rhythm. the P wave may appear as a small, pointed. and upright
Pacemaker cells in other areas of the heart also have the ....avtform; a small squiggle that is barely visible; or it may
property of automaticity, including cells in the atria, atrio- be inverted if the impulse originates (rom a site in the
ventricular (AV) junction, and the ventricles. The rates of lov.'er atrium near the AV junction. In faster atrial rhythms.
these other pacemaker sites ore slower. Therefore, they're the ectopic P wave is either superimposed on the preceding
suppressed by the sinus node under normal circumstances. T wave. appears in a sa ....tooth p4ttem (atrial flutter). or ill
Because the inherent firing rate of the pacemaker cells of seen as a ....avy baseline (atrial fibrillation).
the sinus node ill faster than the other pacemaker situ. it Some atrial arrhythmias may be associated with rapid
is the dominant and primary pacemaker of the heart. An ventricular rates. Increases in heart rate decrease the
ectopic pacemaker site can take O\'er the role of pacemaker length of time spent in diastole. If diastole is shortened.
either because it usurps control from the sinus node by thtre is leu time for coronary artery perfusion and le u
accelerating its own automaticity (enhanced automaticity) time for adequate ventricular tilling. Thul, an aceuively
or because the sinus node relinquishes its role by decreas-- rapid heart rale may lead to myocardial ischemia and may
jng its automaticity. Conditions that may predispose compromise cardiac output.
cardiac cells to altered automaticity include myocardial
ischemia or injury, hypoxia, an increase in sympathetic
tone, dillitalis toxicity. hypokalemia, and hypocalcemia.
Wandering atrial pacemaker
1'riggered activ ity - Triggered activity results from A ....anderinS atrial pacemaker (WAPj (Figure 7-3 and
abnormal electrical impulses that occur during repolariz.a... Box 7-1) occurs ....tlen the pacemaker site shifts back and
tion when cells are normally quiet. The ectopic pacemaker
cells may depolarize more than once aftu stimulation by Box 7-1.
a single electrical impulse. Triggered activity may result in Wandering atrial pacemaker: Identifying ECG
atrial, junctional, or ventricular btats occurring singly. in features
pairs, in runs (3 or more beats), or as a sustained ectopic
rhythm. CaUSt$ of triggered activity may include myocar_ Rllrthm: R9jlular or Ir!"9glfar
dial ischemia or injury, hypoxia, an increase in sympathetic Rllt: U5uaItf normal (60 to 100 bea1slmlrul9) 1M may be
tone, and digitalis toxicity. stow tIIan 60 beatslmlnUls)
P wa'lllS: VIIy In size, shape, and dlrictIon across rITytIlm
Reentry _ Normally an impube spreads through strip; one P wa'I9 ~ 9ach ORS cunplex
the heart only once. With reentry. an impulse can tra\'el P1ilntemt: USU/IIt)' normal IlnUon, but may be 8llrKm\aI
through an area of myocardium. depolarize it. and then d9p9ndhg on dmglng pacemaker Iocalloo
reenter that s.a.me area to depolarize it again. Reen- ORS compleX: Normal (0.10 sec:ord or less)
try involves a circular movement of the impulse, which
85
86 Atrial arrhythmi as
PoIntod Squiggle
T.p wave
w""
Figur.1-2. Atr1a1 Pwaves.
forth ~ho.een the sinus node and edopic atrial sites. The three different P-wave morphologies should be identified
P wave morphology will vary across the rhythm strip as ~fore making the diagnosis ofWAP.
the pacemaker "wanders" ~tween the multiple sites. The heart rate is usually normal. but may be slow.
The ectopic P wave may appear as a small. pointed. and The rhythm may be regular or irregular (each impulse
upright waveform; a small squiggle that is barely visible; or travels through the atria via a slightly different route).
it may be inverted if the impulse originates from a site in The PR interval is usually normal, but may be abnormal
the lower atrium near the AV junction. Generally, at least because of the different sites of impulse formation. The
Prema lllre atrial contraction 87
-
Agutl 73.
Rhrtllm:
P "....:
PRIn'aval:
Wanderklg atr1 al pacemaker.
lITegular
60 beatslmln!1le
Vary In sIZe, shape, across fhylhm str1p
0.1010 0.14 second
ORS COOlpla: 0.114 to 0.08 second.
QRS complex is normal in duration. Th~ distinguishing be reviel'.'ed and discontinued if po!ISibk If the heart rate
f~ature of th is rhythm is the changing P_wave morphology is slow and the patient is symptomatic, treatment of the
atnlS5 the rhythm strip. rhythm is the samt as (or symptomatic sinus bradycardia.
WAf> may be a normal phenomenon seen as a result of When WAP is associated with a heart rate greater than
increased vagal effect on the 5inoo.trial (SA) node, slow- 100 beats per minute, the rhythm is called multifOCflI
ing the si nus rate and allol'.ing other pactmaker sites atriol tuc:l!ycurdia (MAT) (Figure 7-4). MAT is a relatively
an opportunity to comlXte for control of the heart rate. infrequent arrhythmia and is most commonly observed in
h tan al50 occur due to f nhanctd automatici ty of atrial patients with RVert chronic obstructive pul monary dista.w.
pacemaker cells that usu rp pacemaker control from the
SA node. WAP is comfTM)nly seen in patients with chronic
P rematu re a t ria l co n tract ion
obstruc tive pulmonary disease,
WAf> usually isn't clinically s ign ificant, and treatment is A premature atrial contraction (PAC) (Figu res 7-5 through
not indicated. If the heart rate is slow, medications should 7-12 and Box 7-2) is an early beat originating from an
Figure 7-5. Normal si nus rhythm with pre matu re atr1al contraction (PAC).
Rhythm: Basic rhylhm r69Jla'; 1'r69J1a' with PAC
Ratl: Basic rhylhm rate 72 beats/mllllle; rale slows to 60 beal~mlnute following PAC (Tempol'MY rate suppression Is common
lailowlng a pause In the basic rhythm; alter several cardiac cycles the rale usually returns to the basic rhylhm rate.)
Pwaves: Sinus P waves with basic rhythm; P wave assoclaled with PAC Is premalure and closely resembles thai 01 the sinus P waves
In the unclertylng rhylhm.lndlca.Ung tho ectopic atrial patenlOOJr site Is close 10 the SA node
PR Internt 0.12 second (basic rhythm and PAC)
otiS oomplex: 0.08 second (basic rhythm and PAC).
Figure 7-G. Normal sinus rhythm with premature atrial contraction (PAC).
Rhythm: Basic rhythm regulM; l'regulM with PAC
Rate: Basic rhythm rale 88 beats/mllllle
P WaYss: Sinus P waves with basic rhylhm; premature. Inverted Pwave with PAC
PR Interval: 0.14 to 0.16 second (basic rhylhm); 0.14 second (PAC)
QRS complex: 0.Q410 0.06 second (basic rhylhm); 0.06 second (PAC).
Box 7-2. ectopic site in the atrium. which interrupts the regular-
Premature atrial contraction (PAC): Identifying ity of the basic rhythm (usually a sinus rhythm). The pre-
ECG features mature beat occurs in addition to the basic underlying
rhythm. PACs may originate from a singl~ ectopic pace-
Rhythm: ~ng rhylhm usualtj regOO'; I'regularwllh PACs maker site or from multiple sitel; in the atria. The early
Rate: That oIl1lC1er1yhg rhythm beat is characterized by a premature, abnormal P wave
P WaYlS: P wave associated with PAC Is premature and and a premature QRS complex that's identical or similar
abnormal In size. shape. in:! direction (com- to the QRS complex of the normally conduded beats. and
monly appeln small. upright. and pointed; may be is follol't~d by a pause.
Inverted); abnormal P wave commonly loond hidden
P-wav~ morphology differs from sinus beats and varies
In preceding T wave. dlstOfUng tho T-wave COIllou'
depending on th~ origin of th~ impulse in th~ atria If th~
PR Int,rval:
,-,
Usualtj normal; not measurable" hidden In
-
Allure 1-1. Hormal sinus rhythm wIIll prematul'l atrial contraction (pAC).
RhyttIm: BasIc rtr,'ltllllll9ular, mtgular wlltl PAC
BasIc rhytlVn rata 84 beatslmnute
'WIV": stlUS Pwaves wlltl basic rhythm; ~maturo, rtmormal PW;Ne w!Ih PAC (The P waYS Glthe PAC IS hmIIfl n IIle pr8C8dlng
T wave,!IstDrtIng the T-wave ccnru. [T wave IS taller and ITIOIlI pJlntBd.])
PR InlllVaI: 0.12 to 0.14 second (baSIC rhythm): no! measLniblEl with PM;
ORS complex: 0.06 to 0.08 second (baSt: rhythm); 0.06 S8COIld (PAC).
Allure 1-8. Hormal sinus rhythm wIIll one premature atrial con1ractlon (PAC) wnh aberrant ventricular condllellolt
Rhytnm: BasIc rhythm regular; lri1gularwntl MC
Rate: BasIc rtr,'ltlll rata 68 beatslmnute
P waves: stlUS In basic rhythm; premature, abnormal Pwave with PM;
PR InlefVaI: 0.18 to 0.18 second (baSIC rhythm): 0.24 98CCIIld (PAC)
OKS complex: 0.08 second (basic rhyIflm); 0.12 second (PAC).
l"1owevu, the P wave is different from the sinus P waves. In unmea:lurable if the abnormal P wave is obscured in the
lead II (a positive lead). it's generally upright and pointed preceding T wave.
(Figure 7-9). o r it may Ix inverted (Pigure 7-6) if the pace- lhe QRS of the PAC usually resembles that of the under-
maker site is near the AV junction. If the premature beat lying rhythm becau:14: the impulse is conducted normally
occurs very early, the abnormal P wave can be found hid- through the bundle branches into the ventricles. The
den in the preceding T wave, causing a distortion of the ventricles depolarize simultaneously, resulting in a nor-
T-wave contour (Figure 7-7). mal duration QRS complex. If the PAC occurs very early.
The PR intervals of the PACs are usually normal. simi- it is possible the bundle branches may not be repolarized
lar to tho:14: of the unde rlying rhythm . Occasionally the sufficiently to conduct the premature electrical impulse
PR interval may be prolonged if the PAC is very early and normally. If the bundle branches are not sufficiently repo-
finds the AV junction still partially refractory and unable larized. the electrical impul:14: is conducted down one bun-
to conduct at a normal rate. The PR interval will be dle branch (usually the left because it repolarizes quicke r)
90 i\lrlnl nrr hylhmlns
Figure 1-9. NOmJal sinus rhythm with premature atrial contraction (PAC).
Rhythm: Basic rtr,'thm regul...; Hegul... \\11th PAC
Aat.: Basic rtr,'thm rate 60 beatslmloote
PWlI'I'tS: Sinus Pwaves \\11th basic rhythm; premature. abnOrmal Pwave \\11th PAC
PR Interval: 0.12 to 0.16 second (basic rhythm); 0.16 second (PAC)
QRS compIIx: 0.08 second (basic rhythm and PAC)
Commen!: To determine the type 01 pause arter prematLra beats, measure Irom the ORS complex betore the premature beat to the
ORS complex arter the premature beat. It the meauement eqJ8ls two R-R InteJVals. the paJS9ls compensatory. II the mea-
surement equalS leSS lhIrilWO R-R IntervalS. the pause IS noncompensatory. ST-sllgmont dep'esSIOn IS present.
and not conduded down the other. The left ventricle is substances such as alcohol, caffeine, or tobacco. Other
depolarized first, followed by depolarization of the right causes include hypoxia, electrolyte imbalances. myocardial
ventricle (sequential depol1lriz.alion). Sequential ventricu- ischemia or injury, atrial enlargement, congestive heart
lar depolarization is slower, resulting in a wide QRS com- failure. and the administration of certain drugs, such as
plex of 0.12 5econd or greater. APAC associated with a wide epinephrine or nonepinephrine, that increase sympathetic
QRS complex is called a PAC with aberrancy, indicating tone. PACs may also occur without apparent cause.
that conduction through the ventricles is abnormal (aber- Infrequent PACs require no treatment. Frequent PACs
rant). Figure 7-8 shows a PAC with aberrant ventricular are treated by correcting the underlying cause: reducing
conduction (the QRS is wide) and a long PR interval, indio stress: reducing or eliminating the consumption of alco-
cating conduction through the AV node was also delayed. hol, caffeine, or tobacco; administering oxygen: correcting
Aberrantly conducted PACs must be differentiated from a electrolyte imbalances: treating congestive heart failure, or
premature vt!ntricular contraction (PVC), especially if the discontinuing certain drugs. If needed, frequent PACs may
abnormal P wave associated with the PAC is obscured in be treated with beta blockers. calcium channel blockers. or
the preceding T wave. PVCs are discussed in Chapter 9. antianxiety medications. Runs of PACs may require ami-
The pause associated with the PAC is usually a noncom- odarone to prevent more serious atrial arrh}1hmias from
pensatory pause (the measurement from the R wave before developing.
the premature beat to the R wave after the premature beat Occasionally, an ectopic atrial beat will occur late
is less than two R-R intervals of the underlying regular instead of early. This beat is called an atrial escape beat
rhythm) (Figure 7-9). This pause is C<lJled an incomplete (Figure 7-13). Atrial escape be<lts usually occur during a
pause because it doesnt equal two R-R intervals. Less com- pause in the underlying rhythm when the sinus node fails
monly, the PAC may occur with a wmpensatory pause (a to initiate an impulse (sinus arrest) or when conduction
pause that is equal to two R-R intervals), but this is usually of the sinus impulse is blocked for any reason (sinus exit
seen with the PVC. The compensatory pause is called a com- block. non conducted PAC, or Mobitz I second-degree AV
plete pause because it equals two R-R intervals. To differen- block). The pause in the rhythm allows an ectopic pace-
tiate between a complete pause and an incomplete pause, maker site in the atria to assume control of the heartbeat.
the underlying rhythm must be regular. Rarely, the PAC The morphologic characteristics of the late beat will be the
may occur with a pause that is longer than compensatory. same as the PAC. Escape beats act as an electrical backup to
PACs may appear as a single beat (Figure 7-9). every maintain the heart rate and require no treatment.
other beat (bigeminal PACs, Figure 7-10). every third beat,
(trigeminal PACs ), every fourth beat (quadrigeminal PACs,
Fi j!ure 7-11). in pairs (also called couplets. Fij!ure 7-12).
Nonconducted PAC
or in runs of three or more. Frequent PACs may initiate A nonconducted PAC (Figures 7-14 through 7-16 and
more serious atrial arrhythmias, such as paroxysmal atrial Box 7-3) results when an ectopic atrial focus occurs so
tachycardia (PAT ), atrial Hutter, or atrial fibrillation. Three early that it finds the AV node refractory and the impulse
or more beats ofPACs in a row at a rate of 140 to 250 beats! isnt conducted to the ventricles. This results in a prema-
minute constitute a run of PAT. ture. abnormal P wave not accompanied by a QRS complex,
Premature atrial beats are common. They can occur but followed by a pause (Figure 7 1-1.).
in individuals with a normal heart or in those with heart Like the conducted PAC, the P wave associated with the
disease. PACs may be seen with emotional stress (due to nonconducted PAC will be premature and abnormal insiz.e,
an increase in sym[Xlthdic tone), or ingestion of certain shape, or direction. The P wave is commonly found hidden
92 Atri al arrhyth mias
FiRure 7-13. Normal sinus rhythm with sinu s arrest and atrial escape beal
Rhythm: Basic rhythm regul.'l'; lrregul1l' dur~ pausa
Ratl: Basic rhythm rate 63 bealslmlflJle; ralll slows to 58 bealslmlnulll aner paJSe due to temporay rate SLp'esslon (common
loIlow~ pauses nthe basic rhylhm)
PWavH: Sinus P waves: P waves are notched In basic rhythm which could be duo to len atrial enlargement; peaked P WlJole with
escape beat
PH Intlrval: 0.1810 0.20 second (basic rhylhm and escape beal)
QRS compln: 0.08 second (basic rhylhm); 0.06 second (escape beal).
FiRlire 7-14. Normal sinus rhythm with nonc:onducllld premature atrial contraction (PAC).
Rhythm: Basic rhythm regul1l'; Irregul.'l' with noncon<iJcllld PAC
Rate: Basic ralll60 beatstmlnute; rate slows Iollowlng nonconclJcllld PAC (Rate suppression can !lCClJ' Iollowlng a paJSe In the
basic rhythm; aner several cycles, the rate will relum to the basic rhythm rate.)
PWa'lH: Sinus P waves with basic rhythm; premature. abnormal P wave with noncon<iJcted PAC
PR Interval: 0.20 second
ORS oompIex: 0.06 to 0.08 second
COmment: AU wlJoIels present
Box 7-3.
in the preceding T wave. distorting the T-wave contour
Nonconducted PACs: Identifying ECG features (Figure 7-15). and the pause that follows is usually non-
compensatory. The nonconducted PAC is th~ most com-
Rhythm: Underlying rhythm usually regular; Irregular wtth mon cause of unexpected piluses ina regular sinus rhythm.
nonconducted PACs The nonconduded PAC can be confused ....;th sinus
Rate: That oIlJ'ldefly~ rhylhm arrest or block (especially if the P wave of the PAC occurs
P waves: P wave assoclallld wtth the nonconducted PAC ~drly ~JluuKl' lu b~ hj<.l<.l~" ill Ih~ I'",~~<.li"l! T WdV~). All
Is premature. and abnormal In size. shape. or
three produce a sudden pause in the rhythm without QRS
d ~ectlon; onen 10lJId hidden In preceding T wave .
distorting the T wave contour complexes. To differentiate between these rhythms, one
PR Interval: Absentwtth nonconducted PAC must examine and compare T-wave contours (Figure 7-16).
QRS compllll: Absentwtth rxn:onducted PIC, The early, abnormal P wave of the nonconducted PAC will
distort the preceding T wave. In sinus arrest or sinus block.
No nconducted PAC 93
Figure 7- 15. Sinus rhythm with nonconducl9d premature atr1a1 contraction (PAC).
Rhythm: Basic rhythm regular. Irregular wlll1 nonconducted PACs
Rata: BasIc rhythm rata 88 beatstml1ute
Pwaves: Sl1us P WlMn wlII1 basic rhythm; P wave of nonconducted PAC Is premalu's. mnormal. and hkklen In the prec9CIlng T wave
(T wave Is taller and mOfS pol1led thM Ihos8 01 undertjlng rhythm.)
PfllnlllrYaI: 0.16 to 0.18 second (basic rhythm); not presenl with IIIIIICOOi:lJcted PAC
DRS compl8J.: 0.06 to 0.08 second (basic rhythm); nol present with nonconducted PAC.
Figure 7- 16. Dlfferentlallon of sinus alTllst or block from the nonconducted premature atrial contraction (PAC).
A Sinus arrest or blcx;k
1. Sudcloo pauoo In tho ba&1c rhythm
2. No Pwave present
3. T-WiJo/e contour occurring during pause remains unchalged
B Nonconducted PAC
1. Sudden paise In the basic rhythm
2. Abnormal. prema\u'8 Pwave present and oRen IolJId hidden In T wave
3. T-WiJo/9 contour OCCIITlng during pause will be different from the conloln of the basic rhythm.
94 Atrilll ll rrhythmi as
Figure 7-18. Normal sinus rhythm wlUl premature atrial contraction (PAC) and btwSt 01 paroxysmal atrial tachycardia {pAT}.
Rhythm: Basic rhy1!1m regu~ IrregtU w1th PH: and lust 0/ PAT
Rata : Basic rhy1!1m rate 94 beatsA'nlnute; PAT rate 167 beals/minute
P waYIII : ~us P waves w1th basic rhythm: premature, pOOIBd P waves wI1h PAC and PAT (P waves ;J"e supef1mposed on preceding
TwaYes.)
PR tntllrYlI: 0.16 second
ORS compl8ll: 0.08 second
COmment: Arun oIlhroe or more con:sec:utlwl PIC!.Is conskIered PAT.
At rial flutter 95
is often precipitated by a PAC and commonly starts and dose is ineffective after 2 minutes. repeat a 12-mg dose of
stops abruptly, occurring in bursts or paroxysms (thus the adenosine in the same manner.
name paroxysmal atrial tachycardia), By definition, three If the patient doesn't respond to vagal maneuvers or to
or more con~cutive PAGs (at a rate of 140 to 250 beatsl the administration of three doses of adenosine. attempt rate
minute) is considered to be atrial tachycardia (Figure control using a calcium channel blocker (such as d iltiazem)
7-18), This rhythm may be due to enhanced automatic- or a beta blocker. These drugs act primarily on nodal tissue.
ily uf dlridl pi1\;erndkn ldb, r!:luUill!! ill rdvi~ firin!! of 411 either lu ~Iuw lhe Vl:lIlri~uI4r Tt:lpUIl:.t: by blulkill!! lOll-
e\:topic atrial focus, or to an atrial reentry circuit in which duction through the AV node or to terminate the reentry
an impulse travels rapidly and repeatedly around a circular mechanism that depends on conduction through the AV
pathway in the atria, node . In the setting of significantly impaired left ventricu -
The P waves associated ",ith atrial tachycardia are lar (LV) function (clinical evidence of congestive heart fail-
abnormal (commonly pointed), but may be difficult to ure or moderately to severely reduced LV ejection fraction),
identify because they're usually hidden in the preceding caution should be exerci~d in administering drugs with
T wave (the T wave and P wave appear as one ddled:ion negative inotropic effects. These include beta blockers and
called the T-P wave), One P wave precedes each QRS com- calcium channel blockers, with the exception of diltiazem
plex, unless AV block is present. The PR interval is usually (a calcium channel blocker that exhibits less depression of
not measurable, The duration of the QRS complex is nor- contractility when compared with similar drugs) .
maL Atrial tachycardia is characterized by regular, narrow When AV nodal agents are unsuccessful, cardioversion
QRS complexes, occurring at a rate of 140 to 250 beats per should be used to terminate the rhythm. Once the rhythm
minute, and ~parated by the T- P wave, is terminated . antiarrhythmics may be effective in con-
Atrial tachycardia may occur in people with healthy trolling the rhythm . Radiofn:quency catheter ablation of
hearts as well as those with diseased hearts , Atrial tachycar- the e\:topic focus or reentry circuit is successful in many
dia has been associated with ingestion of substances such ca~s.
\','hile the atria can tolerate the extremely high heart only one is followed by a QRS complex). Even ratios (2:1.
rate reasonably well, the 10,,",'l:r chambers (wntricles) can- 4:1 ) are more common than odd ratios (3:1, 5:1). If the
not. Fortunately. the AV node is present to slow down conduction ratio remains constant (2:1 ). the ventricular
and diminish the number of impulses that pass through rhythm will be regular. and the rhythm is described as
to the wntricles. The AV node conducts the impulses in atrial flutter with 2:1 conduction. If the conduction ratio
various ratios. For example. the AV node might allow every varies (from 4:1 to 2:1 to 6:1 ). the ventricular rhythm will
second impulse to travel through the AV junction to the be irregular. and the rhythm is described as atrial Hutter
wntricles. resulting in a 2:1 AV conduction ratio (a 2:1 with variable AV conduction. Conduction ratios are shown
conduction ratio indicates that for every two flutter waves, in Figures 7-19 and 7-20. In atrial flutter, the ventricular
Atrial flutter 97
B
Figure 7- 21 . COmpar1son of alr1a1 nuttarwlth 2:1 AV conducUon and paroxysmal alr1a1 tachycardia (pAT).
Example A.The rhythm shoWs PAT. This str~ shoWs the T-P W3VO (the T .on:! Pwaves appell' as one denectlon). An Isoolec-
IrIc line Is present after 1118 T-P wave.
Example B. The rhythm shows atrial fkJIIer with 2:1 AV conduction. This strip shows two nutter (sawtoo1l1) waves belOfa each
ORS complex. There Is no Isoolectrk: line.
HR - 149 50 JOULES
Figure 7-22. ClI'dloverslon 01 atrial nutter wl1I12:1 alrloYenlrtculll' conduction 10 normal sinus rhythm using 50 joules electrical energy.
rate is slower than the atrial rat~. with th~ rale depending the5\: impulses. a ventricular rale of 150 beats per minute
on the number of impul.u conduded through the AV node is common (a 2:1 AV condudion ratiol. Atrial flutter with
10 the wntricles. 2:1 AV condudion may be difficult 10 differentiate from
Becaus~atrial flutlerusually occurs at a rale of300beats atrial tachycardia. especially if the heart rate in both
per minute and the AV node usually blocks at least half of rhythms is 150 b~ats per minute. Th~se tv.o arrhythmias
98 Atrilll llrrh)'thmias
tan be differentiated by closely examining the baseline. with conversion to sinus rhythm is a risk unless the
In atrial tachycardia. an isoeledric line can usually be patient has been adequately anticoagulated. In this silu-
$een. whereas in atrial flutter the isoelectric line is absent. ation. attempl$ 10 convert the rhythm with cardioversion
A comparison of atrilll flutter with 2:1 AV conduction and or an antiarrhythmic should be delayed until the patient is
PAT is shown in Figure 1- 2l. adequately anticoagulated.
Atrial flutte r is rarely seen in people with a normal One method of anticoagulation involves placing the
htart. This arrhythmia most often occun in patients with patient on an oral anticoagulant at home for several weeks.
mitral or tricuspid vall.-e disea$e. Atrial flutter is common then itdmitting the patient tothe hospital for a tnnsesopha-
af\:er ca rdiac surgery. It may also occur in isdlemic heart geal echocardiogram (TEE). If the TEE is negative for atrial
disease. pulmol'l1lry embolism. and in alcohol intoxication. clots, the patient can safely have the rhythm electrically car-
Like PAT. the wntricular rate in atrial flutter may be dioverted, The palient is then discharged home on an oral
rapid. increasing my()(ardial ollYllen requirements and tar- anticoagu lant for several more weeks. Some physicians pre-
di.x: workload and decreasing cardiac output. In addition. fer a quicke r approach, using IV heparin or subcutaneous
the atria do not contract strongly enough to empty all the enoxaparin (Ulvenox) or datteparin (Fragmin) in a hospital
blood from the atrial (hambers into the ventricles. This setting, If the TEE is negative for mural thrombi. c:ardiover-
rtsults in a loss of the atrial kick, ....t.ich further decreases sion may be attempted .....ithin 24 hours. The patient is dis-
cardiac output. Over time some blood in the at ria may charged home on an oral anticoagulant for several weeks,
stagnate and mural thrombi (clots in the atrial chambt-rs) Unstable atrial flutter should be treated immediately
may form. Pieces of the clot may break off. leading to a risk with cardioversion, regardless of the duration of the
of systemic or pulmonary emboli. arrhythmia, Figure 7-22 is an example of atrial flutter con-
Prioritiu of trtatment include controlling the wntric- wrting to sinus rhythm after cardioversion
ubr rate. assessing anticoagulation needs. and restoring Antiarrhythmics art useful in maintaining sinus rhythm
sinus rhythm. As with PAT, controlling the ventricular rate after conversion. RadiofTequency catheter ablation of the
should be attempted first using a calcium channel bl()(ker. flutter reentry drcuit is becoming the treatment of choice
such as diltiazem, or a bt-ta bl()(ker. using caution in thost for chronic or recurrent atrial flutter.
patients with impaired left ventricular function. Before
attempting conversion of the rhythm, it's essential to know Atrial fibrillation
the approximate onsel of the arrh}thmia. If atrial flutte r
has been present for less than 48 hours, it's safe to con- Atrial fibrillation (Figures 7-23 through 7-26 and Box
vert the i'h)'thmwith cardioversion or lIIlliodarone, If atrial 7-6) is a rapid and highly il'Tegular heart rhythm caused
flulter has betn present for mort lhan 48 hours (o r the by chaotic electrical impulses that arise from an ectopic
onset is unknown), pulmonary or systemic embolization site in the atria. depolarizing at a rate greater than
Rgure 7 25. A111a1l'b1la1lonwltfll WiMS so small they appear tel be almost a nat line between ORS complexes.
Rgure 7 26. Cll'dkMnlm of alr1al flbrlllalion kJ sinus ItlyUlm; ):n:IIonaI escape beat (discussed ~ ~tar 8) Iollows 1118 initial slrus Ileat.
100 Atrial arrhyt hmias
...Nom.-...
Atlial arrhythmias: Summary of Identifying ECG features
W...seringlltrill
"""","
Premahxe aflat
RegIA.OI' iTegular
""""""
Thai of basic Itrjtlm
'hIy in ~. npe. and ctnc-
lion: 0I'III PWlMI precedes
ed1 QRS CIlIIIJMl
Ing on dlanging
pilcemaker location
-~""
premalul'll atrill
Basic rf?t1hm usualtt
regular; irregular with
That of basic Itrjtlm Premalln P _e that is
atrJormai il sim. shape. 01'
AbiseIt with norcort-
....,PAC
-..,
""""""'" PM;
~- """"""'" PM; di"ection; commonly kM1d il
preceding Twaw. distorting
T-wave conbJr
ParmysmaI atill
t\lI::hyellrdi. (PAl)
"".w 140-250 AOOormal P wa't'e (commoNy
panted~ usually hidden il
UuIy IIDI rneasurabIII Nom-
(O.10S&COlldor
tntt<Ilng Twaw SO thaI
T and P _ appear as one
'NaW defleeton (T -P _I;
"'"
one P WlWlIO fIlCh ORS
complex uressAV block is
.-
AnaI'utter ReglAar 01' iTegular Atrial: 250-400 Sawtooth deleclioro .ffdlg Not measu'able Nom.
(depencIt on abi<Mtl- V1tieu11t: 'Ia'iII with entire IlIRMe (O.10.teeOnd or
triclAar [AW) conduc-
lion reIiat)
number of impulses
~fvoL9:1AV
node (wi. be las !han
"'"
niall1.le)
Anal fibrillation
=_. . .
Gross/y~r
(unless wmicular
rate is rapid. in which
m~_
Atrial: 400 01' more
(can" be cotnted)
Ventricular: 'I3ias with
number of impulses
~fInIlqlAV
node (wiI be less than
a1rial11.\e; controlled if
Wavy de~ections affecting
entire baseline
Nol meastl'able
""""
(O. IOsecoodor
"'"
ram < loo.lrICOO-
.oIled if > 100)
102 Atrial arrhythmias
Rhythm interpretaoon:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
II Skillbuilder practice
This section contains mixed sinus and atrial rhythm strips, allowing the student to practice differentiating between
two rhythm groups before progressing 10 a new group. As before, analyze the rhythm strips using the five-step process.
i nterepret the rhythm by comparing the data collected with the ECC characteristics for each rhythm . All strips are lead II.
a positive lead. unless otherwise noted . Check your answers with the answer key in the appendix .
Overview
depolarization that spreads backward (retrograde) into the
The atrioventricular (AVl node is located in the lower atria as well as forward (antegradel into the ventricles. The
portion of the right atrium. The bundle of His conoects location of the Pwave relative to the QRS complex depends
the AV node to Ihe two bundle branches. Together, the AV on the speed of antegrade and retrograde conduction:
node and the bundle of His are called Ihe AV junction. The If the electrical impulse from the AV junction depolar
AV node doesn't contain pocemaker cells. The main fune- ius the atria first and then depolarizes the ventricles, the
lion of the AV node is to slow conduction 01 the electric.aJ P waw will be in front of the QRS complex.
impulse through the AV node to allow the atria to contract If the electrical impulse from the AV junction depolar
and complete tilling of the ventricles prio r to vt:ntricular izu the ventriclu first and then depolllrizes the atria, the
contraction. Pacemaker cells nearest the bundle of His in P Wil\'t ....ill bt alter the QRS complex.
the AV junction are responsible for secondary pacing func. If the electrical impulse from the AV junction depolar-
tion. Ar rhythmias originating in the AV junction are called ius both the atria and the ventriclu simultaneously, the P
junctional rhythms (Figure 8- 1). wave will be hidden in the QRS compla.
The inhertnt firing nle of the junctional pacemaker Retrograde stimulation of the at ria is ju.st opposite
celts is 40 to 60 beats pt r minute. A rhythm OCCUlTing the direction of atrial depolarizat ion when normal sinus
al this rate is called ajunetwool rhythm. Other rhythms rh}-1:hm is present and produces negative P waves (i nstead
originating in the AV junctional area include prellUlture of upright) in lead II (a positive lead). The PR interval is
junctionaJ contraclion./lCcelu atedjunc tional rhythm. and short (0. 10 second or less). The ventricles are depolarized
junctional tachycardia. normally. resulting in a normal duration QRS complex.
When the AV junction is functioning as the pacemaker Identifying featu res of junctional rhythms are summarized
of the heart. the electrical impulse produces a wave of in Figure 8-2.
First-degree AV block
Second-degree AV block, MobilZ I
Second-degree AV block, Mobitz II
Third-degree AV block
138
Premature junctional co ntrac tio n 139
8018-1.
Premature )mctlonal contraction (PJC):
Identifying ECG features
Allure 83, Pr&meture jUnctXlnaI CUlb'actlons ~I appear es a
Rh,-lhm: Lrldarlyhg rIlyIhm usually r~lar; Irragutar ~th
sIngIB bealln ~ ollhe aboY81tree pattarns. ,.Ie
Rate: Thal oIlhe \Ild9rIylng rtlyttvn
P w.wet: Pwaves associated WIth the PJC WIll be premature.
Premature junctional contraction IrMifted kllead I. n wi occur Immediately belore
A premature junctional contraction (PJC) (Figures 8-3 It1a ORS CCfl1IIBX. Immedlalel~ aner thB ORS, or be
through 8.8 and Box 81) is an early beat that originates hidden wlltln the ORS
in an ectopic pac~maker site in the AV jUllCtion. Lik~ the PH Intarra t SI10rt (0.10 secmd or less)
premature atrial contraction (PAC), the premature junc_ QRS compln: Premature; fQ11lal duratlm (0.10 $&Com or less)
Fillure 8-4. Hormal sinus rhythm with one premature Junctional contraction (pJC).
Rh,-lhm: Baslc rhy\tI1I regular, lmigular with PJC
Rate: Baslc rtlyttvn rate 94 beaWmlnute
P waves: Si-.us P waves with bask: rhythm; lnYerted P wave with PJC
PH InllfYaI: 0.1 4 to (l. 16 !IIICOIld (basic rhythm); 0.08 second (l'JC)
QRS complel: 0.08 secon:I
COIn""nt ST-segment !lepresslor1ls present.
140 Ju nclionalllrrhYl hrnias lUld AV blocb
Figure 8-5. Normal sinus roythm with 0l1li Pl9lllabJrtI Junctional contmctlon (pJC).
RhyIIIm: Basic rtr,1IVn regul; ~ with P.IC
Rift: Basic rtr,1IVn rate 72 beatslmlrute
P W8U; ~us P waves wllI1 basic rflythm; merted P waYII alter PJC (4111 ORS CO!!IPIIlQ
PH ~ltml; 0.14 to 0.16 second (basic: rflythm); 0.06 to D.OS SIIIXIfId (PJC)
ORS comp...: 0.06 to 0.08 second (basic rIl:;1hm); 0.08 second (PJC)
comlll8n1; AUwavelsJUSenl
Figure 8-S. Normal sinus ltIythm with 0l1li premabJrtI Junctional contraction (PJC).
,'...
...... Basic rtr,1IVn regula";"'~ with P.IC
Basic rtr,1IVn rate 63 beatsfmlllJle; ralll slows to 56 beatstmDlle lolloWlng P.IC due to rate suppression (commm llIilowlng
a pause In 'he basic rIIyIhm)
P W8U; Sinus Pwaves wllI1 basic rflyJhm; PWlVe assodalllcl with P.IC IS hldOOn In the CRS complllx
PH Inltml; 0.16 to 0.18 second (basic rflythm)
ORS comple x: 0.06 to 0.08 second (basic rIl:;1hm); 0.10 second (PJC)
comment; AUwavelsJHSi!nl
complex. The PR interval will be mrt (O.10 5eCond or less). differentiating PJCs from PACs. keep the following in
Figure 8-4 shows a PJC with the P wave before the QRS mind: PACs an much more common than PJCs. As a
complex; Figure 8-5 shows a PJC with the P wave after Ih~ result. narrow complex premature beats are more likely to
QRS complex;and in Figure8-6 the Pwave is hidden within be PACs. A comparison of ectopic atrial beats and ectopic
the QRS. PJCs are less common than PACs or premature junctional beats is shown in Figun 8-7. PJCs occur in addi-
ventricular contractions (PVCs) (discussed in Chapter 9). tion to the underlying rhythm. They occur in the same pat.
Inverted P waves in lead II may also occur with PACs terru as PACs; as asingle beat; in bigeminal, trigeminal, or
arising from the lower atria. but the associated PR inter quadrigeminal patterns; or in pairs (Figure 8-8). A series of
val is usually normal. If difficulty is encounte red in thru or more consecutive junctional beats is considered
Premature junctional contraction 141
RlJure B-7. Normal sinus rhythm WIth two pramaturli atrtal contractions (PACs) (4th and 8th complaJ.as) and OIlQ Junctional
escape beat (5th complex)
Rhythm: Regular (basic rhythm); Irregular with PACS and Junctional escape beat
Rate: 75 beatstmlnute (basic rhythm)
P waves: Sl1us (basic rhythm); pointed P waves with PACS; Inverted P waves with Junctional escape beat
PR Interval: 0.14 second (basic rhythm); 0.12 second (PACs); 0.08 second gunctlonal escape beal)
DRS ~omplel: 0.08 to 0.10 second (basic rhythm. PACS.lIld):llctlonal escape beat).
a rhythm (junctional rhythm. accelerated junctional imbalances; h}llOxia: congestive heart failure: coro-
rhythm. or junctional tachycardia). Differentiation of the nary artery disease: and enhanced automaticity of the AV
rhythm depends on the heart rate. junction caused by digitalis toxicity (the most common
Like PACs, the premature junctional impulse may cause). PJes may also occur without apparent cause.
(rarely) be conducted to the ventricles abnormally Frequent PJCs are best treated by correcting the under-
(ilbemmtly). Thi.:! results in a wide QRS complex. A P]C lying CaU5e: decreasing or eliminating the cOf15umption
associated with a wide QRS complex is called a PJC of caffeine. alcohol. or tobacco; correcting electrolyte
with aberrancy. indicating that conduction through the imbalances: administering oxygen; treating congestive
ventricles is aberrant. Because of the wide QRS complex. heart failure; and assessing digitalis levels. Frequent PJes
PJCs with aberrancy must be differentiated from PVCs. (more than 61minute) may precede the development of a
Conditiof15 associated with PJCs include ingestion of more serious junctional arrhythmia such as junctional
substances such as caffeine, alcohol, or tobacco: electrolyte tachycardia.
Agure 8-8. Normal sinus rhythm with paired premature Junctional contractions (pJCs).
Rhythm: BasIc rhythm regular; Irregular loIlowhg paired PJCS
Rata: BasIc rhythm rate 100 beatslmlnute
P waves: Sl1us P waves wlll1 basic rhythm: Inverted P waves with PJCs
PR Inmal: 0.12 to 0.14 second (basic rhythm); 0.08 second \WIth PJCS)
QRS ' III npl&~ : 0.06 to 0.08 S8&OIld (basic rIlythm and PJCs).
142 lun ctiollll l llrrh ythmills lind AV blocks
fi~ure8-B. Normal sinus rhythm with a pause followed by a Junctional escape beat.
Rhythm: Bast rtTfIhm regul.Y; lrregul.Y \\11th escape Ileat
Aal.: Bast rITfInm 60 tleats/mloole; rate sloWs to 45 Deats/minute alter es:ape Ileat (Aate suppression can occur folloWing any
pause In the baSiC rtTfIhm. Aller sewral cycles tile rale \\llIlIlIUn to the basIC rate.)
P Wav.l: Sinus P waws \\11th basic rhythm; hklllen P wwe with escape boat
PRlntlrva l: 0.16second
OAS complu: 0.06 second
COmment: ST-segment depresslon!llG a UWiNe am present.
The slow rate and loss of nol'ffiill atrial contraction Accelerated junctional rhythm
(atrial kick) secondary to retrograde atrial depolarization
may cause a decrease in cardiac output. Treatment for Al:celerated junctional rhythm (Figures 8--14 through
symptomatic junctional rhythm inc ludes following the 8-16 and Box 8-3) is an arrhythmia originating in the AV
protocols for significant bradycardia (atropine, pacing, junction with a rale between 60 and 100 beats per minute.
dopamine, or epinephrine infusions to increase blood pres- The term "acceleraled" denotes a rhythm that occurs at a
sure). Treatment should also be direded at identifying and rate that exceeds the junctional escape rale of 40 to 60. bu t
correcting the underlying cause of the rhythm if possible. isn't fast enough to be junctional tachycardia.
All medications should be revie\\led and discontinued if Accelerated junctional rhythm is regular wilh a heart
indicated. rate between 60 and 100 bfau per minute. The Pwaves are
BOI8-3.
Accelerated Junctional rhythm: Identifying ECG
features
lead II Rhythm:
Rate:
""".,
60 to 100 beats/minute
P wans: Inverted In lead II and occtn Immediately before
the ORS complex, immediately aner the ORS
FIIlU re 8-14. Acceleraled )jncUOnai rtlythm will appear as a complex, or Is hidden within the ORS complex
oootInuous rhylhm at a rale 0160 to 100 beatslmloote In any olllle PH Interval: Sh:lrt (0.10 socond or less)
allow II1ree patterns. QRS complex; Normal (0.10 second or less)
Junctionallachycardia may result from enhanced auto- that the PR interval is the key to identifying the type of
ITUllicity of the AV junction caused by digitalis toxicity (the block present. The width of the QRS complex and the
most common cause). Olher causes include damage to the ventricular rate are keys to differentiating the location
AV junction from MI (usually inferior-wall MI ) and heart of the block (the lower the location of the block in the
failure. conduction system. the wider the QRS complex and the
Junctional tachycardia may lead to a decrease in cardiac slower the ventricular rate ).
output related 10 the faster heart rate as well as the lo~ In first-degree AV block (the mildest form), the electri-
of the atrial kick s&ondary to retrograde depolarization cal impulses are delayed in the AV node longer than nor-
of the atria. Treatment is directed at re~rsing the conse- mill. but all impulses are conducted to the ventricles. In
quences of reduced cardiac output. as well as identifying second-degree AV block (type I and II). some impulses are
and correcting the underlying cause of the rhythm. Symp- conducted to the ~ntricles and some are blocked. The
tomatic junctionol tachy~~rdi~ m"}' respond to diltill.Zem. mo.t extrcme form ofhc;>.rt block i. third-degree AV bloc~.
beta blockers (use caution in patients with pulmonary in which no impulses are conducted from the atria to the
disease or heart f<lilure). or amiodarone. ~ntricln. The clinkal signifiQme of an AV block depends
on the degree of block. the ~ntricular rate. and patient
AV heart blocks response.
The ability to accurately diagnose AV blocks depends on
The term heart block is used to describe arrhythmias in a systematic approach. The following steps are suggested:
which there is delayed conduction or failed conduction of Look for the P wave. Is there one P wave before each
impulses through the AV node into the ~ntricles. Nor- QRS or more than one?
mally the AV node <lets as a bridge between the atria and Measure the regulilTity of the atrial rhythm (the pop
the ventricles. The PR interval is primilrily a measure of interval) and the ventricular rhythm (the R-R interval).
conduction between the initial stimulation of the atria and Measure the PR interval. Is the PR interval consistent
the initial stimulation of the ~ntricles. This measurement or does it vary? Remember, the PR interval is the key to
i. norITllllly 0.12 to 0.20 ""cond. identifying tho. type ofAV bled- present.
The site of pathology of theAV blocks may be at the level Look at the QRS complex. Is it narrow or wide?
of the AV node. the bundle of His. or Ihe bundle branches.
'Mten located at the level of the AV node or bundle of His, First-degree AV block
the QRS complexes will be nonnal duration. The QRS com-
plex will be wide if the site of pathology is located in the In first-degree AV block (Figure 8-19 and Box 8-5), the
bundle branches. sinus impulse is normally conducted to the AV node.
AV blocks are classified into first-degree. second- where it's delayed longer than usual before being con-
degree (type I and 11). and third -degree. This classifica- ducted to the ~ntricles. This delay in the AV node results
tion system is based on the degree (type) of block and in a prolonged PR interval (> 0.20 second). This rhythm
the location of the block. It is important to remember is reflected on the ECG by a regular rhythm (both atrial
Second-degree AVblock, type 1 (Mo bitz 1 or Wenckebach) 147
and ventricular l, one P wave preceding each QRS complex, Second-degree AV block, type I
a consistent but prolonged PR interval, and a narrow QRS
complex. Thi5 conduction disorder is located at the level
(Mobitz I or Wenckebach)
of the AV node (thus the narrow QRS complex) and isn't a Second-degree AV block, type I is commonly known
serious form of heart block. as !>Iobilz I or Wenckebach (for the early 20th century
The underlying sinus rh}thm is usually identified along physidan who discovered it) . This rhythm (Figures 8-20
with theAV block when interpreting the rhythm (for exam- through 8-23 and Box 8-6) is characterized by a failure of
pie, normal sinus rhythm with first-degree AV block). some of the sinus impulses to be conducted to the ventri-
First-degree AV block may occur from ischemia or cles. In !>Iobitz I, the sinu5 impulse is normally conducted
injury to the AV node or junction secondary to acute !>II to the AV node, but each successive impulse has increas-
(usually inferior-wall MI l. increased parasympathetic ing difficulty passing through the AV node, until finally
(vagal ) tone, drug effects (beta blockers, calcium channel an impulse does not pass through (isn't conducted ). This
blockers, digitalis, ilIlliodarone l, hyperkalemia, degenera- rhythm is reflected on the ECG by P waves that occur at
tion of the conduction pilthways associated with aging, and regular intervals across the rhythm strip and PR intervals
unknown causes. that progressively lengthen from beat to beat until a P wave
First-degree AV block produces no symptoms and appears that is not followed by a QRS complex, but instead
requires no treatment. Because first-degree heart block bya piluse. Themissing QRScomplex (dropped beat) causes
can progress to a higher degree of AV block under cutain
conditions, the rhythm should continue to be monitored BOI 8-6.
until the blo;;k resolves or stabilil.es. Drugs causing AV Second~egree AV block (Mobltz I): Identifying
block should be revie",'e(] and discontinued if indicated.
ECG features
BoI8-5. Rhythm: Regular alrlal rhythm ; Irregular ventricular rhythm
First-degree AV block: Identifying ECG Rata : Atrial: That of tho lJlCIorlyllg sinus rhythm
features Ventrfcula': Vartes depending on number of Im-
pulses conducted through AV node (will be less than
Rhythm: Regular IhII alrlal rate)
Rate: ThaI 01 tho underlying slllls rhythm: both atrial P waY1lS : Sllus
and vootrtculM rates will be tho same PRlntervll: Varies; progressively lengthens until a P wave Isn1
P waves: Sinus; one P w;Jo/e to each ORS complex conducted (P wave OCCII"S wlthoullho ORS com-
Pfl lnlerYaI: Prolonged (> 0.20 second): remains consistent plex); a pauselollows the !topped ORS complex
QRS complex: Normal (0.10 second or less) OIlS complex: Normal (0.10 second or less)
148 Juncliomli arrhyt hmias M d AV blocks
tht ventricular rhythm to be irregular. After each dropptd Mobiu. I can be confused with the nonconducted PAC
beat the cycle repeats itself. The ovrrall a~arance of Ihe (Figun 8-23). Both rhythms have episodes where P waves
rhythm demoru;trates group beating (groups 01 beats .sepa- are not followed by a QRS romplex. but instead by /I pau.'Se.
rated by P,"Ull_) and is a dL~tinguishing characteristic of To differentiate Mm.een the two rhythrru, one must txlIm-
J'.10bitz. I. Escape beats (atrial. junctional. or ventricular) ine the configuration of the P waves and measure the pop
may occasionally oo::cur du ring the pause in the ventricular regularity. The nonconducted PAC will have an abnormal P
rhythm. and may obscure the diagnosis because they inter- wave and will occur prematurely. In Mobiu. I. the P wave is
rupt Ihe group beating pattern (Figure 8-22 ). The location normal and occurs on schedule. nol prematurely.
of the conduction disturban<:e is at the level of the AV node Mobiu. , is common following acute inferior-wall MI
lind therefore the QRS complex will be narrow. due to AV node ischemia. Other causes include increased
Pause I rhythm
pop rEgularity I.IlCh~Bd (P wave occurs on lime)
P wave conIlguratlon same as $1M beats
PR Interval 01 basic rtlythm YllteS
rtr,'ttIm remains constant
Figure 8-23. DllTerentlalton 01 the nonconductad pl"BmabJ'e atrial cootractton from Mobitz I.
ISO Junctio na l a rrhythmias a nd AV bl ocks
limits (rare). the patient may be asymptomatic. More com- little or no warning. Treatment is required immediately
monly. the ventricular rate is extremely slow, cardiac out- for symptomatic Mobitz II and for asymptomatic Mobitz
put is decreased. and symptoms are present (hypotension. II with wide QRS complexes in the setting of acute ante-
shortness of breath. heart failure. chest pain. or syncope). rior-wall MI. An external pacemaker should be applied
The syncopal episodes (called Slokes-Adams attacks or "'nile preparations are made for insertion of a temporary
Stokes-Adams syncope) are caused by a sudden slowing or trall5venous pacemaker. Atropine is usually not effectivt in
stopping of the heartbeat. reversing Mobitz. II second-degree AV block and mayactu -
Mobilz II is less common but more serious than Mobitz I. ally worsen the conduction disturbance. A dopamine infu-
Mobitz II has the potential to progress suddenly to third- sion may be used to increase blood pressure. Unresolvtd
degree AV block or ventricular standstill (asystole) with Mobitz II will require II permanent pacemaker.
Rgufll 8-26. Mobltz 1. This strtp shows a typical Weockebach pattern durtng the nrst part of the strtp changing to a 2:1
oonduclJon rallo alllM! and ofllM! strtp. Evon though 2:1 conducllon Is saan (common wllh MobltZ II), 1119 prasallCQ 01 a Wanckabach
pattern conllrms tIM! diagnosis 01 Mobltz I.
Rhythm : Atrial (regular); ventricular (Irregular)
Rate: Atrial (100 beatstmlnute); ventriculii' (60 bealstmlnute)
P wallS: Sl1us
Pfllnl9rYaI: ProgesslYely lengthens from 0.24 to 0.36 second
DRS complOJ : 0.06 to 0.08 socond.
152 Junctional arrhythmia s a nd AV blocks
ventr icles a re paced by a junctional pacemaker with nar- pacemaker. Third-degree AV block with narrow QRS
row QRS compl exes and a ventricular rate of 40 to 60 complexes may occasionally respond to atropine. Hypo-
!>fau per minute. Third -deg ree AV block associated with t~nsion should !>f treated ....ith vasopressOT$. Unresolved
an inferior-wall MI often resolves on iu own. Complete complete heart block will require a pennanent pacemaker.
heart block associated with an anterio r-wall MI is usu -
ally a result of a blod .... ithin the bundle branches. The
rhythm is usually unstable and the ventricles are paced
Tips on heart blocks
by a ventricular pacemaker with wide QRS compteJIes To distinguish one heart block from another, remember
and a ventricular rate of 40 !>fats per minute or less_ the~ important tips:
Third-degree AV block a5S0ciated with an anterior MI ,,1easure the poP interval. The poP interval is regular in
often does not resolve on its own and may require per- all the blocks. If you measure the pop interval. you ....ill be
manent pacing. Complete heart block can al50!>f seen in able 10 track the P waves, This is very important in finding
older patients who h,we chronic degene rat ive changes in hidden P waves ~en in third-degree AV block or Mabib: II
their conduction system not related to acute Mi. It h;u with higher condu,tion ratios (3: 1 or more).
also been reported with Lyme disease. Complete heart "leasure the R-R interval. First-degree and third-degree
block may occur with digitalis toxicity. AV block have a regular ....entricular rhythm. Habib: I has
The patient's response: to complete heart block is usu- an irregular ventricular rhythm. The ventricular rhythm
ally related to the ventricular rale. I(the ventricular rale is in "lOOitz II may be regular or irregular. depending on
within normal limits. the patient may be relatively a5)'1llP- conduction ratios.
lomatic with minor symptoms such as weakness, fatigue, "leasure the PR interval. If the PR interval is con-
dizziness. or I!l(ercise intolerance. More commonly, theven- sistent, choose be""een fi rst-degree and Mobilz II AV
tricuJar rate is extremely slow, cardiac output is decreased, block. First-degree AV block has one P wave to each QRS
and symptoms are present (hypotension. dyspnea. heart while Mobitz II AV block has ""0
or more P waves to
failure, chest pain, or SIokes-Adams s~cope). each QRS. If the PR interval is nol consistent, choose
Regardless of its cause, complete hear! block is a serious between Mob itz I AV block and third-degree AV block. In
and potentially life-threatening arrhythmia. Third-degree Mobib: I the PR interval is not consistent and the ven-
AVblock. like Mobitz II. can quickly progress to ven tricular tricular rhylhm is irregular. In third-degree AV block
standstill (asystole) with little or 00 warning. Treatment is the PR interval is not consistent and the ventricular
required immediately for symptomatic third-degree heart rhythm is regular.
block and for iU)'Illptomatic third-degree heart block with Table 8-1 compares the ECG characteristics of each
wide QRS complexes in the ~tting of acute anterior-wall type of AV block. A summary of the identifying ECG fea-
MI. An external pacemaker should be applied while prepa- tures of junctional rhythms and AV blocks can be found in
rations are made for in~rtion of a temporary lTansvenous Table 8-2.
154 Junctional arrhythmias andAVblocks
Table B-1.
AV block comparisons
Pft constant
(Rrst-tgrH)
PH constant PR varies
PR _ _
PR prt98SSively gilts longer
One P wave to each aIlS lIltil a ORS is dropped
PR varies
Talll, S-l.
Junctional arrhythmias and AV blocks: Summary of Identifying ECG features
,,~
"""" ..
jun:tional
cmtraction
Rh,II'"
Basic rhythm
usually regular;
ilTl9lla- with
Rata (bIIatstrnlnutl)
0.10second er less
QRS compIeJ
Premalure CfIS
complex;
~,
....,
Ikration
-
after the ~RS, or be hidden (0.10 second
within the ORS
JlIICtionai
.""" .,.60 merted in lead II and Short (0.10 socond or
kcelerated
jun:tional
....,. 6010100 merted in lead II and
will OCCll" immediately
Short (0.1 0 socond or
'=1 """"
(O.IOseconder
JlIICtionai
tachyc3"dia .""" ,100 merted in lead II and
will OCCll" immediately
Short (0.1 0 second or
'=1
N~'
(O.IOseconder
bafore the ORS COff1lIm:: II" "'I
immediately after the DRS,
II" be hidden wilhi1 the ORS
".- ."""
First-degree That of underlying sirIJs Sinus origi1; one P wave to Prolonged (more N~'
atriownlricuar rhythm; both atrial and each CflS compex than 0.20 second); (O.IOseconder
ventricular rates will be the remaillll consislllnt "')
A~
Second-degree AUlal: regual Atrial: thai 01 unda1ylng Sinus orIgn Varies; progressively N~'
-,
AV_ Venlricuar:
ilTl9lla-
sinus rhylhm
Vlllbicular. depends on rlJm-
ba" of impulses conducled
lengthens lI"Itil a P
wave isn'l corducIed
(P wave occurs
(0.10 second er
"'I
Ihrol9l AV oode; will be less wilhout the DRS
than atriallare complex); a pausa
follows the d'opped
DRS complex
Second-degree
AV_
MoI!itz II
Atrial: reguar
VelllricUar. usu-
ally regular. but
Atrial: thai of underlying
sinus rhythm
Vlllbicular. depends
Sinus orIgi1; I'MJ or 111"00
P waves (sometimes mora)
bafore each ORS complex
Normal or prolonged;
mmains consistmt .....
Nmnal n tkd<.
Iuda ollis;
may be ilTl9llar
~ conduction
ratios vary
on number of impulses
cordJcted thfOll\t1 AV node;
will be less than alriallal8
............
wide n tm:k in
Third-rIewM Atrial: reguar Atrial: thai of undB1ying Sinus P waves with no Varies~1Iy Normal if block
AVbIocl< Venlricuar. sinus rhylhm consmt relationship to allewl of AV
RhyttrnintMFetaOOn _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Pwave: _ _ _ _ __
Strip 8-59 . Rhythm: _ _ _ _ _ _ _ _ _ _ .... _ _ _ _ _ _ __
Pft interval: OOScomplex:_ _ _ _ _ __
~ i nt~o ~ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
176 Junctional arrh ythmias nnd AV blocks
Pwa'o'e: __________
Strip 8-71 . FIlythm: ___________________ ..'" ______________
11ft interval: ORScomplelC _ _ _ _ _ __
~im~ort _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
180 Junclionnl nrrh ythmias and AV blocks
Stripl-n.lllyttlm: _ _ __ __ _ _ _ _ _ __ __ _ __ Pwaw: _ __ __
PfI irftMII: QRS c:ompIa:,_ _ _ __
~~.On ___ _ _ _ _ _ __ _ _ _ _ _ _ _ __ _ __
IE Skillbuilder practice
This section contains mixed sinus, atrial, andjunctiollal and AV block rhythm strips, allowing the student to practice dif-
ferentiating betv.~en two rIlythm groups before progressing to a new group. As ~fore, analyze the rIlythm strips using the
five-step process. Interpret the rhythm by comparing the data collected with the ECG characteristics for each rhyt hm. All
strips are lead II. a positive lead. unleu otherwise noted. Check ~r answers with the lInswer key in the appendix.
197
198 Ven tri cular arrhythmias an d bundl e-branch block
the right bundle branch and the left bundle branch and its Box 9-1 .
fascicles at the same time, caming simultaneous depolari- Bundle-branch block: Identifying ECG features
zation of the right and left ventricles, resulting in normal
depolarization and a QRS duration of 0.10 second or less. Rhythm : Regular
'Nhen one of the bundle branches is blocked. the electrical Rate: lhal oIlhe underlying r11ythm (Usually sinus)
impulse trilVels down the intact bundle. depolarizing that P WIY8S: Sinus
wntricJe first, then the impulse progresses through the PI! InllllrYaI: Normal (0.12 to 0.20 socond)
interventricular septum to depolarize the othu ventricle. QRS complex: Wkle (0.12 second or grealer)
Depolarization of one ventricle before the other is called
sequential depolarization. Depolarization of the ventri-
cles is dela~d. resulting in a wide QRS complex of 0.12 by a monitoring lead. Differentiating between right and left
second or greater. The presence of a bundle-branch block bundle-branch block requires a 12-lead electrocardiogram
(Figures 9-2 through 9-4 and Box 9-1 ) can be recognized (EeG).
Right bundle-brnm:h block (REBEl may be pr.-sent in temporary or ,hroni,. and may be rate-related. The most
healthy individuals with no apparent underlying heart disease. common cause is hypertensive heart disease. Other causes
but more commonly occurs in the pr.-sence of coronary artery are the same as with RBBB.
disease (the most common cause). RBBB may be temporary or Specific treatment is usually not indkated for a
chronic. Oc=ionally, RBBB may appear only when the heart bundle-bran,h block. Cardiac pacing may be indicated if
rate exceeds a certain critical level (rule-related BBB). Com- the bundle-branch block develops as a result of acute MI or
mon causes include anteroseptal myocardial infarction (MD. in the presence of AV block.
pulmonary embolism. congestive heart failure. peril:aTditis.
~-pertensi~ heart disease. cardiolJl)ql<l~, congenital RBBB,
and degenerative disease of the electrical conduction system.
Premature ventricular contractions
Left bundle-branch block (LBBB ) is rarely seen in indi- A premature ventricular contraction (PVC) (Figures 9-5
viduals with healthy hearts. It appears most commonly through 9-14 and Box 9-2) is a premature, ectopic impulse
in elderly individuals with diseased hearts . LBBB may be thai arises below the bundle of His in the ventricles. PVCs
Figure 1-&. SIIlIIS P waves occulTIng belora and aflllt' premature YIIntJ1cular contractions (PVCs).
The snus P waves of lIle tn:Ie~ytng mythm CIrl be seen Just belOl'8 the PVC ., example A Md aIt9r Iha PVC In 'tie ST sao-
rnenlln IIKllmple B. These P waves are assocIattld with the tnIer1yI~ Iflythm (not the PIlI:) and usualy ~e hlalen wIlI*l the
WkIe ORS oIlha premall.re venlrlcular tooIracUoo.
EXamp19 A: Normal sinus rflythm with nrsl-de!Jee AV block !lid one PVC.
EXam~ B: Snus iWfhythmla wllh btnIle-bl'cn:h bIod( and one PVC.
occur as a result of reentry in the ventricles, enhanced lhe QRS is wide (0. 12 second or greater) and the
automaticity of a focus in the ventricles, or triggered activ- morphology is different from the QRS complexes of the
ity occurring during ventri cular repolarization. PVCs have underlying rhythm.
the following characteristics: lhe ST segment and T wave slope in the opposite
The QRS is premature. direction from the main QRS deflection (if the ectopic
A P wave isn't a!oSOCiated with the PVC. Normally the QRS complex is predominantly negative, the ST segment
P wave of the underlying rhythm (usually sinus) is obscured is usually ele\"ilted and the T waves positive: if the ectopic
within the PVC, but sometimes it appears just before or QRS complex is predominantly positive. the ST segment is
after the PVC in the ST segment orTwave (see Figure 9.6). usually depressed and the T wave negative).
202 Ventricular arrhythmias and bundle-branch block
Th~ paus~ associatd with th~ PVC is usually compensa- in runs (Figure 9-11). A run of three or more consecutive
tory (th~ m~asur~ment from the ~at before the PVC to NCs constitutes a rhythm. The rate will determine which
the ~at after the PVC is equal to two R-R intervals of th~ rhythm is present (idioventricular rhythm, accelerated idi-
underlying rhythm, Figure 9-5). The underlying rhythm oventricular rhythm, or VT).
must be regular to determine a compensatory pause. PVCs that look the same in the same lead are Cillled uni-
PVCs may occur in various patterns. They may appear Focal PVCs. These PVCS originate from a single ectopic
as a single beat (Figure 9-5), every other ~at (bigeminal focus in the wntricles. PVCS that appear different from
pattern. Figure 9-7), every third beat (trigeminal pattern, one another in the same lead are Cillled multifocal PVCS
Figure 9-8), every fourth beat (quadrigeminal pattern, (Figure 9-12). These PVCS lJSlIa!Jy originate from different
Figure 9-9), in pairs (also called COllplets, Figure 9-10), or ectopic sites, but sometimes Il"Iil}' fire from a single site and are
Box 9-2.
Premature ventricular contraction (PVC):
Identifying ECG features
Rhythm: lnIErtyIng rl"rflhm usually regula"; negular with PVC
Rata: Thai oIl.1lC1ertytng rflylhm (usually stl1JS)
P waves: None assoctated with PVC; P waves associated
with the underlying sJoos rflythm cal occastonally
be seen )Jst belore the PVC or alter the PVC In
the ST segment or T wave; usually these P WaYes
Me hidden In the ORS complex
PR Interval: Not measurwle
QRS compleX: Premature ORS complex; wide (0.12 second or
Figure 9-13. Interpolated premature ventricular contraction. grBaler)
Pre m a ture ve ntricular con tractions 203
conducted along different routes in the ventricles. resulting angioplasty: or following insertion of invasive catheters into
in a QRS that differs in morphology in the same lead. the heart. such as pacing leads or a pulmonary artery catheter.
A PVC sandwiched between two normally conducted Treatment of PVCs depends on the cause. the patient's
sinus beats. without greatly disturbing the regularity symptoms, and the clinical setting. Because occasional
of the underlying rhythm. is called an interpolated PVC PVCs are a normal finding in healthy individuals, no treat-
(Figure 9-13). The compensatory pause. usually associated ment may be indicated. especiilHy if the per5<ln is asymp-
with the PVC. is absent. tomatic. Initially. a search should be made for possible
R _an_ T PVC (Figure 9_14) is a term used to describe a reversible causes (such as oxygen for hypoxia; replacement
PVC which falls on the down slope of the preceding T wave. of electrolytes: diuretics for heart failure; elimination of
This period corresponds to the relative refractory period of certain drugs; avoidance of alcohol. caffeine. or tobacco;
ventricular repolariz.ation when the myocllrdium is in its and administration of antianxiety if indicated). Significant
most vulnerable state electrically. During this period. the PVCs (more than 6 per minute. multifocal PVCs, paired
myocardial cells havt repolarized enough to respond to a PVCs. R-on-T PVCS. or PVO; in runs of3 or more) should
strong stimulus. Stimulation of the ventricle at this time be treated with an antiarrhythmic medication. eSpe\:iaJly in
may precipitate repetitive ventricular contractions. result- the setting of acute MI or following cardiac surgery because
ing in VI or fibrillation. of the increased risk of VI and VF in this setting.
PVCS are among the most commonly s~n arrhythmias. On some occasions a ventricular beat may occur late
PVCs may occur in individuals with a healthy heart, but are instead of early. A late ectopic ventricular beat usually
more common in people with coronary heart disease. PVCs occurs after a pause in the underlying rhythm in which the
ar~ commonly caused by an increase in SYmpilth~tic tone dominant pacemilku (usll<lHy th~ sinus node) filils to initiilte
from emotional stress: ingestion of substances such as alco- an impulse. If the ventricles are not activated by the sinus
hol. caffeine. or tobacco: mitral valve prolapse, myocardial node. atria. or AV junction within a certain period of time.
ischemia or infarction; cardiomyopathy; congestive heart a focus in the ventricles may ~escape" and pace the heart .
failure; hypoxia: electrolyte imbalances (especially hypoka- These are called venfricufarescapebeats (Figure 9-15). The
lemia); drug effects (digitalis. epinephrine, norepinephrine): ventricular escape beat is a protective mechanism. protect-
as a reperfusion arrhythmia after thrombolytic thera~ or ing the heart from slow rates. and no treatment is required .
ST segment and T wave slope in the opposite direction Treatment protocols: Stable monomorphic
from the main QRS deflection. 'MIen the QRS complexes Vfwlthpulse
are of the same morphology in the same lead. the rhythm Amiodarone (150 rug in 100 mL D,W) is lIiwnas an intra
is termed monomorphic lIT. When the QRS complexes venous pi~back (IVPB) bolus over 10 minutes. An addi-
differ in morphology in the same lead. the VT is called tional150 rug NPB bolus dose can be repeated in 10 minutes
polymorphic VT. for resistant VT. Once the rhythm converts to a stable rhythm,
VT may occasionally occur at rates greater than 250 beatsl an amiodarone maintenance infusion should be started to
minute. At such extreme rates the QRS complexes appear prewnt reoccurrence of VT. The amiodarone maintenance
sa\\1:ooth in appearance and the rhythm is commonly referred infusion (900 mil in 500 rnL D,W in a IIlass bottle) is started
to as ventricular Rutter (Figure 9-17). Ventriwlar flutter is at 1 mg per minute for 6 hours. then decreased to 0.5mg per
so rapid that there is virtually no cardiac output. Ventricular minute for 18 hours. The total dose of amiodarone (NPB bolus
flutter is often a precursor to wntricular fibrillation. doses plus maintenance infusion) should not exceed 2.211 in
VT usually occurs in patients with underlying heart 24 hours. Oral amiodarone can be started once the mainte-
disease. It may be preceded by significant PVC. (more than nance infusion is completed. Elimination of the drug from
6 per minute. paired PVCs. multifocal PVCs), but often the body is extremely lonll (half-life lasts up to 40 days).
occurs without preexisting or precipitating PVC . The If the rhythm is un ..... pomive to amiodarone. sedate the
most common cause of sustained VT is coronary artery patient and perform synchronized cardioversion bellinning
disease with prior MI. Other causes include myocardial at 100 joules biphasic energy dose. increasinll in a stepwise
ischemia. acute MI, cardiomyopathy, conllestive heart fail - fashion with subsequent attempts.
ure, mitral valve prolapse. valvular heart disease, digitalis Some physicians prefer to skip drug therapy and go
toxicity, electrolyte imbalances (especially hypokalemia directly to synchroniud cardioversion. Figure 920 shows
and hypomallnesemia). myocardial contusion. mechanical cardioversion ofVT to sinus rhythm.
stimulation of the endocardium by a pacinll catheter or
pulmonary artery catheter, as an effect of reperfusion fol- Treatment protocols: Unstable
lowing thrombolytic therapy or angioplasty, and drulls that monomorphic vr with pulse
increase sympathetic tone (epinephrine. norepinephrine, Sedate the patient (if conscious).
dopamine). Certain medications or conditions may pro- Convert the rhythm using synchronized cardioversion
long the QT interval, causing the vt!ntricles to IN! particu- beginning at 100 joules biphasic energy dose, inmas
larly vulnerable to a!)'pe of polymorphic VT called torsade ing in stepwise fashion with subsequent attempts. Once
de pointes (Figure 9-19). cardioversion has converted the rhythm, a maintenance
When VT lasts for less than 30 seconds it is called non- infusion of amiodarone is usually started at I mg per
sustained VT. VT occurring in short runs of three or more minute for 6 hours, then decreased to 0.5 mg per min-
consecutive PVCs at a rate of 140 to 250 beats per minute is ute for 18 hours, followed by oral amiodarone once the
considered a "run" or "burst" of nonsustained VT (Figures maintenance infusion is completed.
9-11 and 9-18). Nonsustained VT, unless frequent, usually Treatment of chronic, re,urrent VT usuaJly includes
doesn't cause symptoms, but it can progress into sustained therapy y,;th an oral antiarrhythmic. Patients who are
VT. When VT lasts longer than 30 seconds, it is considered refractory to a pharmacologic approach may require further
sustained VT. Sustained VT is a life threateninll arrhythmia evaluation, which could include specialized electrophysi
for two major reasons: ologic testing and endocardial mapping with longterm
1. The rapid ventricular rate and loss of atrial kick reduce options including the use of an implantable cardiowrter
cardiac output. This reduction in cardiac output often defibrillator (ICD ) or reentry circuit ablation. The ICD is
compounds the alreildy low I:<Irdiac output frequently seen a surllically implanted devi,e developed to deliver an ele,
in the diseased hearts in y,-hich VT tends to occur. tric shock directly to the heart durinll a lifethreateninll
2. The rhythm may dellenerate into VF or asystole. tachycardia. Ablation (destruction) of the reentry circuit
Treatment is based on the patient's presentation. An involves delivering short pulses of radiofrequency current
';unstable" patient refers to an individual who presents through an intracardiac catheter. It produces a small burn
with symptoms such as hypotension, chest pain, shortness that effectively blocks the part of the circuit supportinl( the
of breath. signs of decreased perfusion (cool. clammy skin; reentranttype wave.
peripheral cyanosis; decreased level of consciousness; or a
decrease in urine output). A "stable" patient refers to an
Torsade de pointes ventricular
individual with normal blood pressure, no chest pain. and
no shortness of breath or signs of decreased perfusion. As tachycardia
part of the initial a ..essment you should check for a pulse. Tornade de pointe. (TdP) (Figure 9 19) i. a form of poly
lf there is not a pulse (pulseless VT ), the rhythm must be morphic VT. This name is deriwd from a French term
treated as VF. If there is a pulse, protocols for stahle VT and meaninll '"twisting of the points," which describes a QRS
unstable IT are followed. complex that changes polarity (from negative to positive
Ventricular fibrillation 207
and positive to negative) as it twists around the isoelec- results from diuretic therapy, diabetic ketoacidosis, severe
tric line. TdP is an intermediary arrhythmia between VT diarrhea, or inadequate replacement during prolonged
and VF. parenteral nutrition therapy. Dosage of potassium depends
TdP typically occurs when the QT interval of the under- on the serum potassium level, hospital protocols. and
lying rhythm is abnormally prolonged, usually 0.5 second physician orders.
or greater. A prolonged QT interval or long QT syndrome Removing or correcting precipitating factors:
(LQTS) is an abnormality of the hearfs electrical system. 1. Bradycardia-induced - Discontinue drugs that decreil..'ie
Although the mechanical function of the heart is entirely heart rate: overdrive pacing or isoproterenol infusion may
normal. the electrical problem is thought to be caused by be used to increase heart rate.
changes in the cardiac ion channels that affect repolaril.a- 2. Drug-induced - Discontinue drugs that prolong QT
tion, causing a lengthened relative refractory period (vul- interval.
nerable period) that puts the Vl:ntrides at risk for TdP and 3. Electrol}1e-induced - Correct electrolyte abnormalities:
may result in sudden death. magnesium and potassium are considered first-line therapy.
Some causes of TdP VT include bradyarrhythmias In treatment of congenital prolonged QT syndrome or
(marked sinus bradycardia. third-degree AV block with a recurrent TdP VT, an implantable defibrillator ICD can be
slow ventricular response): excessive administration of used as prophylaxis.
antiarrhythmics (quinidine, procainamide. disopyramide.
amiodarone, soblol): phenothiazines (prochlorperazine,
chloropromazine, thioridazine); psychotropic medica-
Ventricular fibrillation
tions (haloperidol, amitriptyline): electrolyte imbalances In ventricular fibrillation (VF) (Figures 9-21 and 9-22
(especially hypokalemia, hypomagnesemia, hypocalce- ilIld Box 9-4) a disorganized, chaotic, electrical focus in
mia); liquid protein diets; central nervous system disorders the ventrides takes over control of the heart. Organized
(subarachnoid hemorrhage or intracranial trauma); and ventricular depolarization and contraction do not occur
congenital LQTS. (there is no QRS complex), but instead the wntricular
The ventricular rate in TdP VT is extremely rapid and muscle quivers and is often described as resembling a "bag
the patient usually becomes unstable very quickly. Rec- of worms. The ECG in VF shows characteristic fibrillatory
ognition of TdP is critical not only because of the rapid waves that vary in shape and amplitude in an irregular and
deterioration of the patient but also because the treatment chaotic pattern.
plan differs greatly from the treatment of monomorphic VF with large amplitude waves is called coarse J1F
VT. Amiodarone, a drug used in treating monomorphic VT, (Figure 9-21). If the VF waves are small, the rhythm is
can prolong the QT interval and make matters worse in called line ]IF (Figure 9-22). Coarse VF waves are gen-
this situation. erally more irregular than fine VF waves. Fine VF may
resemble ventricular asystole and should be confirmed
Treatment protocols: TdP vr by eJt1lmining the rhythm in different leads. The distinc-
The initial treatment should be immediate un.synchro- tion between fine VF and coarse VF is significant because
nized shock at 200 joules biphasic energy dose. Due to the coarse VF usually indicates a more recent onset and is
variability in the QRS complexes in TdP, it might be dif- more likely to be reversed by early defibrillation. Fine
ficult or impossible to reliably synchronize to a QRS com- VF usually indicates that the rhythm has been present
plex. Although TdP is responsive to electrical therapy. the longer and may require drug therapy and cardiopulmo-
rhythm has a tendency to recur unless the precipitating nary resuscitation (CPR) before defibrillation can be
factors are eliminated. effective. Fine VF will progress to asystole unless the
Hagnesium is the pharmacologic treatment of choice rhythm is treated.
for TdP VT. Magnesium is usually very effective even in
patients with normal magnesium levels. Magnesium acts as 8019-4.
an antiarrhythmic and may terminate or prevent recurrent Ventricular fibrillation (VF): Identifying ECG
episodes of TdP. Give a loading dose of 1 to 2 g N diluted features
in 10 mL D,W slowly over 5 minutes. This is followed by a
0.5 to 1 g/h~ur IV drip. Aside effect of magnesium is hypo- Rhythm : None (P wtmJ .wi CRS complex are It>sent)
tension, especially if administered rapidly. Magnesium also Rate : None (P wtmJ .wi CRS complex are It>sent)
reduces neuromuscular tone and dose monitoring of deep Pwaves: Absent: wavy,lrregulM deflections seen, varying
tendon reflexes is suggested. In slze,~, and height and representatIYe 01
Potassium chloride (like magnesium) is a first-line qulverDJ oIlhe YOOtrlcles Instead 01 contraction:
therapy for TdP. Pota.. ium is e..ential for maintenance !!eRectionS may be small (described as fIn6 W) or
I.Yge (desalbed as coarse W)
of intracellular tonicity: transmission of nerve impulses: Pfllnterval: Not meastnble
contraction of cardiac, skeletal, and smooth muscles; and QflS complox: Absent
maintenance of normal renal function. Depletion usually
208 Venlricul nr nrrhyth minsllnd bundle- bru nch block
VF is the most common cause of cardiac death in becomes unconscious immediately, Cyanosis and ui zure
patients with <Kule MI. Other causes include myocardial adivity may also be present. Death is imminent unless the
ischemia. hypoxia, cardiomyopathy, electrolyte imbalances rhythm is treated immediately.
(especia lly hypokalemia and hypomagnesemia), digi-
talis toxicity. excessive doses of antiarrhythmics, cardiac Treatment protocols: VF
trauma, and mitral valve prolapse. VF may be preceded by Check the pulse 8nd rapid ly IIMUS the patient. If there is
significant PVCs or VT. but it may also occur spontaneously a pulse and the patient is conscious. VF im't the proble m.
without precipitating rhythms. VF may also occur during ECG artifacts produced by loose or dry electrodes. patient
anesthesia, cardiac catheteriution procedures, pacemaker mOllement, or muscle tremors may resemble VF.
implantat ion. placement of a pulmonary artery catheter, or If there is 00 pulse and the patient is unconscious, defi-
after accidental electrocution. brillate al 200 joules biphasic energy dose. If the 8rrest is
Once VF occurs there is no cardillC output, peripheral unwitnessed. perform CPR for 5 cycles (2 minutes) before
pulsel and blood pressure are absent, and the patient the ini tial shock.
the cardiac rh}1hm present just before the appearanceofthe beats per minute, but isn't fast enough to be Vr. AIVR has
final rhythm. wntricular standstill (asystole ). Continuous the same ECG charucteristics as NR (no P waws. wide QRS
IVR is generally symptomatic due to the slow rute and the complex. regular rhythm ), but is differentiated by the heart
loss of the atrial kick. The rhythm must be treated promptly rate. AIVR can occur as a continuous rh}thm (Figure 9-25 )
following the protocols for significant bradycardia (atropine. or in short runs of 3 or more consecutive ventricular beats
pacing, and vasopressors to increase blood pressure). at a rate of 50 to 100 beats per minute (Figure 9-26).
If the rate of NR falls below 20 beats per minute and the AIVR is common after acute inferior-wall MI and is fre-
QRS complexes deteriorate into irregular, wide. indistin- quentlya reperfusion rhythm following thrombolytic ther-
guishable waveforms. the rhythm is commonly referred to apy. angioplasty. or spontaneous reperfusion. AIVR may
as an agonal rhythm or "dying heart"(Figure 9-24 ). Treat- also be seen with digitalis toxicity.
ment is usually ineffectiw at this point. AIVR is usually well tolerated and is rarely associated
with symptoms. If the patient is symptomatic. it is usu-
ally related to a decrease in cardiac output from a loss of
Accelerated idioventricular rhythm the atrial kick and not because of the heart rate. which is
Accelerated idioventricular rhythm (AlVR ) (Figures 9-25 within a normal range.
and 9-26 and Box 9-6) originates in an ectopic pacemaker Treatment of AIVR with antiarrhythmics is not rec-
site in the ventricles with a rate bern.een 50 and 100 beats ommended. Abolishing the wntricular focus may lead to
per minute. The term accelerated denotes a rhythm that a less desirable rate and rhythm. This rhythm is usually
~ceeds the inherent idioventricular ncape rate of30 to 40 tramient, requires no specific therapy. and spontam:ously
Figure 1-2&. Nanna! sinus rtlyttlm WItt1 episode 01 accelerated kIIo8f1trlctJlar rtlythm (lJYR).
Rhythm: BasIc: rhy'lhm regular; AIVR basIcaIy IlI\IUlar (011 by 2 SQIJI'nSl
RIte:: 79 beaWmloota basic r1lyIvn; a-lUId 80 b8at~nunul8 AIYR mte
p wa_ sms PW3YIIS wID1 basic r1lythm; nane with AMI
PAl"."...: 0.12t10.16sean:1
ORS complu: 0.0611 0.08 sec:md (basi: fIlyt!lm); 0.12 S8C(III(I WVI\I.
""-
occurred during the paU!>C following a PAC.
ORS cunpIex 01' a straglt IN
Conditions contributing to the dewlopmrnt of ventric- PR 1ntIn"1I:
ular standstill include extensive lIl)'QCilTdiai damage (from ORS complex:
""'"
212 Ventricular a rrhythmias and bundle- branch block
figure 9-21. Normal sinus rflythm with one premature atr1al contraction changing to ventricular standstill.
Rhythm: Basic rhythm regulM
Rail: Basic rhythm 100 beaWmlnute
P wIVes: Sinus P waves am present
PR lnten"al: 0.16 to 0.18 second (basic rhythm)
QRS complllJ:: 0.06 second (basic rhythm).
Pulseless electrical activity (PEA) are the same as asystole. PEA has a poor prognosis unless
the underlying cause can be quickly identified and man-
Pulseless electrical activity (P EA) is a clinical situation aged appropriately.
(not a specific arrhythmia) in which an organized cardiac A summary of the identifying ECC features ofventricu-
rhythm (excluding pulseless VT) is observed on the moni- lar arrhythmias and bundle-branch block can be found in
tor, but no pulse is palpated. Causes and treatment of PEA Table 9-1.
Table 9-1 .
Ventricular arrhythmias and bundle-branch block: Summary of Identifying ECG features
... ..
,, ~ Rhythm Rate (beals/minute) P waYlS (IIad II) PR Interval DRS complH
Basic rhythm That oIlJ1der1ying Nona associated with PVC; P Not measurable PrematlR ORS
ventricuar usually rl9llar, rIrftIm (usualy silllS) WlIV8S associated with under- complex; abnormal
"""'''"'
(I'Iq
imlguar with
PIC
lying sillJl rhythm can some-
times be soon just belore PVC
shape; wide
(0.12 second or
or after PVC in ST segment or greater)
TWlII'II, but these waves ara
usually hidden within I'IC
Vmlricular
tachyC3"dia
Reguar (can be
sl911iy irregular)
140 to 250 Nona associated lith vr Not measurable
"..
(0.12 second or
..."
(VT) greater)
Vmlricular None (P wave and None (P '#me and DRS Absm~ wavy, i-reopar deftac- Not measurable
fibrilation (VF)
-,
DRS complex are complex are absent) tions seen in various sims,
shapes, and he91t1, ropresen-
tatil'll oIvenbicuiar ~iVllling
instead of contraction; dellac-
tions may be small (described
as fine ].F) or large (described
as coarse IIF)
Idiovenlricuar
rf1yIhm (IVR)
Reguar 30 to 40 (sometimes
I~I
..."
"'-""' " ..
(0.12 second or
"..
greater)
Vmlricular
slaldstil
(YenIriruar
AIriaI: ffPWlIYeS
present, wil hal'll
allial rhythm
Allial: if P waYeS
present. wil hal'll
allial rate
Tracing wi. show eithar
P waves wiIhaJl a (JIS
compl81 or a strai~t line
Not measurable
..."
_I Ventriwlar: None Ventricular: None
2 14 Ventricular arrhythmias and bundle-branch block
Slrip9-25_RhyIhm: _ _ _ _ _ _ _ _ _ _ - , _ _ _ _ _ _ _ _ PwaY8: _ _ _ _ __
PR 1n1&Mll: ORS c:omplex:_ _ _ _ __
"""m'_'____________________
R"""'_ -'____________________
PR Interval: ORS cornplex:_ _ _ _ __
, "I'-t-+++-t+lb-HHI-t-++++-'l'-H--f4t-+-+-lI+
' j!-H-tl I
~ rnu"I.'~' ~
1 ~ututut~~U;~~1
strip 9-58_ 1IlyIhm: _ _ _ _ _ _ _ _ ..'" _ _ _ _ _ __ Pwaw: _ _ _ _ __
11ft interval:_ _ _ _ _ _ _ _ OftScomplex:_ _ _ __
RhyIhm Int8fJ)fetation: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Rhythm interpretation:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
, I
I I
;;
II Skillbuilder practice
This section contains mixed sinus. atrial. andjunctioTUlI ondAV block. and ventricular rhythm strips. allowing the student
to practice differentiating betv,~n two rhythm groups before progressing to the Posttest As before. analyze the rhythm
strips usingthe five-step process. Interpret the rhythm by comparing the data collected with the ECG crurncteristiCl; for each
rhythm . All strips are lead II. a positive lead. unless otherwise noted. Check your answers with the answer key in theap~ndix.
Overview
Pulse generator - The pulse generator houSl.'S a bat-
An ~rti1icial pactlTl4ker is an electronic device that gener- tery, a lead conntctor, and electronic circuitry for pace-
ales and transmih an electrical stimulus to the atria. the maJrer sell ings.
wntrides. or both. resulting in depolari!;illion. followed Picing lead _ The pacing lead has one or twQ metal
by muscle contraction. The use of artificial pacemakers poles (electrodts) at the tip of the catheter that come in
may be necessitated wmn there is a significant ffiillfunc- contact with the endocardium (Figure 101). A lead with
tion of the heart's electrical system, usually inyolving the only one electrode at its tip is called II unipolar pacing
sinus node, the atria. or the atriOl.'enlricular (AV) conduc- system. A lead with two electrodts at its tip is called a
tion pathways. The result may be a slow, fast. or irregular bipolar pacing system. The pacing lead serves as a Irans-
rhythm. whkh can affect the heart's pumping ability and mis.5ion line between the pulse generator and the endo-
may lead toa decrease in cardiac output and in the quality C4l rd ium. Electrical impulses are transmitted from the
of life. Some indications for pacing include: pulse generator (through the pacing lead) to the endocar-
Sinoatrial d)'dunction dium, while information about intrinsic electrical activ-
I. Sinus bradycardia ity is relayed from the electrooe tip (through the pacing
2. Sinus alTl.'st lead) back to Ihe generator. If the generator responds by
3. Sinus exit block sending a pacing impulse to the heart, it is called trig
4. Atrial flutte r or fibri llation gering. If a pacing impulse is not sent 10 the hurt, this
5. Sick sinus syndrorrre (rhythms in which there is is called inhibition. Many permanent pacing leads are
markd bradycardia alternating with periods of tachy- constructed with fixation devicn (screws, tines, or barbs)
cardia, especially atrial flutter or fibrillation: abo called thai help guarantee long-term contact with the endocar-
tachy-brady syndrome). dium. Temporary pacing leads are not constructed with
6. Chronotropic incompetence {sinllS node is not Cllpa fixation devices 50 they can be easily removed ...men pilc-
ble of incrusing its rate in response to <tCtivity ing is no longer required.
AVblock Pacemakers can function in a fixed rate mode or a
I. Seconddegree AV block, Mobitz II demand mode:
2. Third-dq:jree AV block Fixed rate mode (asynchronous) - Fixed rate pace-
H y~r!;e'nsitive carotid sinus _ Stimulation of the makers initiate impulses at a set rate, regardless of the
carotid sinus that causes episodes of asystole resulting in patient's intrinsic heart rate. This moxie of pacing is
recurrent synco~: stimulators may include turning the knOYoll as asynchronous pacing because it's not syn-
head from side 10 side. or wearing a tight necktie or collar. ch ronned to $eose the patient's own heart rhythm. This
Pacemakers may be inserted on II temporary or perma may result in competition be""'een the patient's natural
nent basis depending on the clinical situation. Temporary (inlrinsic) rhythm and that produced by the pacemaker.
piKing is appropriate in emergent situations (transient Ventricular tachycardia or ~ntricular fibrillation may be
symptomatic bradycardias or AV block lISSOCiated ",ith induced if the pacing stimulus falls during the vulner-
myocardial ischemia or drug toxicity). Temporary pacing able period of the cardiac cycle. Fixed rale pacemakers are
may also be used to provide prophylactic therapy for high. rarely used today.
risk patients during cardiac C4ltheterization, during and Oemand mode (sync hronous) - A demand pace-
after cardiac surgery. and to override liKhyarrhythmias maker paces only when the heart fails to depolariz.e on
(~rdrive piKing). Permanent pacemaker implantation is its own (fires only "on demand"). Demand pacemakers
considered for unresoilltd rhythms or conditions in which are designed with a $ensing mechanism that inhibits
clinical symptoms are present and for which long-term discharge when the patient's heart rate is adequale and
piKing is indicated. a pacing mechanism that triggers the pacemaker to fire
A pacemaker system (Figures 10-5 and 10-6) consists of when no intrinsic activity occurs within a preset period.
a pulse generator and a pacinillead: This mode of pacing is called synchronous pacing because
256
Overview 257
it is synchronized to sense the patient's cardiac rhythm. If a single-chamber vent ricular pacemaker senses
Demand pacing is the most commonly u~d pacemaker a QRS complex, the pacemaker is inhibited from fir-
mode today. ing an electrical stimulus. If it does not sense a QRS
A pacemaker system may be single- or dual-chamber: complex. the pacemaker sends an electrical stimulus
Single-c hamber - A single-chamber pacemaker system to the ventricle. Stimuliltion of the ventricle produces
uses one lead inserted into either the right atrium or the a pacemaker spike followed by a wide QRS complex.
right ventricle. This pacemaker can sense and pace only resembling a ventricular ectopic beat (Figure 10-2,
the chamber into which it is inserted. example B). Single-chamber ventricular pacing is the
If a single-chamber atrial pacemaker senses a P wave. most commonly used temporary type of pacing and
the pacemaker is inhibited from firing an electrical stim- is also frequently used for permanent pacing. Single-
ulus. If it does not sense a P wave. the pacemaker sends chamber atrial or ventricular pacing can be used with
an electrkal stimulus to the atrium. Stimulation of the epkardial pacing wires.
atrium produces apacemalcer spike (a vertical line on the DUill-chim.ber - A dualo.Chamber pacemaker system
ECG), followed by a P wave (Figure 10-2, example A). uses ""'0 leads, one going to the right atrium and the other
to the right IIfntricie. 1he dual-chamber pacemaker can cardiac situations. External pacemakers are noninvasive.
sense and pace in both chambers. effectiw. lind quick and easy to apply. rcp provides only
If a duakhamber pacemaker senses a P waw, the pace ventricular pacing.
maker is inhibited from firing an electrical stimulus. If the TCP is indiCllted a.s a treatment for symptomatic
pacemaker does not sense a P wave. the pacemaker sends bradyarrhythmias (sinus bradycardia. slow atrial Hutter
an electrical stimulus to the atrium. Stimulation of the or fibrillation, Mobil1. [I second-degree AV block. or
atrium produces a pacemaker spike. followed by a P "'ave. third-degree AV block). TCP is not effective in rhythms
The pacemaker is programmed to wait, simulating an elec- without meaningful contractile activity such as wntricu-
tronic PR interval. In pacing terminology the artificial PR lar stands till and pulseless electrical activity (PEA) that
interval is called the AV interval. If a dual-chamber pace- occur in the setting of cardiac arrest. This is because the
maker senses a QRS complex. it is inhibi ted from liring an primary problem in these situations is the inability of the
electrical stimulus. If the pacemaker does not sense a QRS myocardium to contract when appropriately stimulated.
complex. the pacemaker will send an electrical stimulus to External pacemakers should not be relied upon for an
the wntricle. Stimulation of the ventricle producs a pace extended period of time. They should be used only as a
maker spike followed by a wide QRS complex. Figu re 10-2, temporary measure in emergency situations until trllns-
example C, snows stimulati on of the atria and the ventricle venous access is available or the c.ause of the bradyarrhyth-
by a dual chamber pacemake r. mia is resolved. Transvenoos pacing is still the treatment of
Dual-chamber pacemakers lin oCten called AV sequen- choice for patients requiring a temporary but longer period
tial pacemakers becaust of their ability to stimulate the of pacemaker support
atria and ventricles in sequence (first the atria, then the The technique of rcp involves:
ventriclu), mimicking normal htart physiology and thus I. Attach plICing pads toches!. rcp involves attaching two
preserving the atrial kick. large pacing pads to the skin surface of the patient's chest.
Dual _chambe r pacemakers are frequently used with Multifunction pads have the capability to monitor the heart
permanent pacing and can also be used with epicardial rhythm, externally pace. and defibrillate through one set of
pacing. DuaI-chamber temporary pacing can be done, but pads. The pads have conductive gel on the inner surface to
it is difficult to place temporary atrial wires and it is not as help transmit the electrical current through the chest wall.
reliable u ventricula r pacing. The large surface IIrea of the pad and the conductive gel
also help minimize the possibility of skin bums from the
procedure. If po$Sible. eJlCS5 hair should be clipped before
Temporary pacemakers the pads are appli ed to maximize contact with the skin
Temporary pacing can be accomplished with transcutane surface.
ous (tlCIernal), transvenoos, or epicardial methods: Most manufacturers recommend the pads be placed in
Transcutaneouspacing(TCP)- TCPreters to the deliv- an anterior-posterior pos.ition. The anterior pad (labeled
ery of II pacing stimulus to the heart through pads placed "front") is placed to the left of the sternum, halfway
on tht patient's outer chest (Figure 10-3). Requirements betv.'Un the Kiphoid process and the left nipple. In the
for Tep include pacing pads, a pacing cable. and a deli- female patient. the anterior pad shoul d be positioned under
brillator monitor with pacing capabilities. TCP is recom- the left breast. The posterior pad (labeled ~backW) is placed
mended as the initial IWICing method of choice in emergent on the left posterior chest directly behind the anterior pad.
Successful TCP requires a higher electric.al current
output (mA) than conventional transvenous pacing to
overcome the resistance oc the chest wall. Placement of
the pacing pads affects the amount of current required
to depolarize the ventricle. The placement that offers the
'''''''' I ~ ~.i--
, .,'" most direct pathway to the heart usually requires the low-
est rnA in order to pace the heart. Currents of 50 rnA or
~
more may be associated with discomfort and sedation may
_--l ...- ~ be required.
, I, '
I 2. Connect pacing pads to defibrillator or monitor. Con-
ned the pacing pads to a pacing cable and a defibrillator
( ,~ \~, \ i
monitor system v.ith pacing capabilities.
J. Initiate pacing. Set the defibrillator or monitor to pace
setting. Set the pacing rate first (usually 70). then slowly
increase the rnA until consistent ventricular capture is
-,.
Figne 1 0-3. External pacing pad placement (anteoo--posterD seen on the monitor (a pacing spike followed bya wide QRS
complex. Figure 104). If capture is lost during pacing, the
mA may have to be increased.
Temporary pacemakers 259
Verify that electrical capture (seen on the monitor) is at the tip of the pacing catheter is inflated and the wire
associat~d with mechanical capture (verified by palpa- is floated through th~ tricuspid valve into the apex of th~
ble pulses). Evalu<lte pulses on the patient's right side to rightventride for single-chamber ventricular pacing. Even
avoid confusion between the presence of an actual pulse though single-chamber atrial pacing and dual-chamber
and skeletal muscle contractions caused by the external pacing can be done. single-chamber wntricular pacing
pacemaker. is the most reliable and prderred choice for transwnous
Transvenous pacing - Transwnous pacing rders to pacing. Onc~ proper placement is wrified. the balloon is
the deliwry of a pacing stimulus to the heart through a deflated. The distal tail of the pacing catheter is connected
vein (tr~n""'-no". ~l"l"ro~ch ) _ Re'l,,;remenl., for tr~n-",e_ to thl'. ne~~t;ve connec.t;on of the hr;dp;;np; CJlhle and thl'.
nous pacing indude <In external pulse gener<ltor. a pac- proximal t.:lil is connected to the positive connection of the
ing lead wire, and a bridging cable to connect the two bridging cable.
(Figure 10-5). Using the dials on the external pulse generator. adjust
Some indications for transvenous pacing include the pacemaker sdtings:
symptomatic bradyarrhythmias (sinus bradycardia. 1. Determine voltage threshold. This is the smallest
Mobitz II second-degree AV block. and third-degr~e AV amount of voltage (rnA) required to pace the heart. 'Nhile
block). prophylactic therapy during cardiac catheteri- watching the cardiac monitor. gradually turn down the rnA
zation for high-risk patients. <lnd overdrive pacing of until capture is lost (usually 0.7 to 1.0 mAl <lnd thengradu-
tachyarrhythmias. Transvenous pacing is usually not ally turn up the rnA until capture is regained. The point at
effective when meaningful contractile activity is abs~nt y,-h.ich capture is regained is the threshold. Set the rnA at
(wntricular standstill and PEA). For significant unre- twice threshold level.
solved rhythm or conduction disorders. permanent 2. Set Pilcing rate. This is determined by the physician
pacing is requird. (usually 70 beats per minute).
Temporary pulse generators are externally controlled by 3. Set sensitivity. Sensitivity is usually maintained at maxi-
manipulating dials on the face of the unit. Removable bilt- mum clockwi~e position (5 oclock).
teries are contained within the generator housing. Prior to The number of temporary transwnous pacing leads
insertion of a pacing lead. prepare the equipment. Insert a being placed is decreasing, largely due to the improwd
new 9-volt batt~ry into the battery compartment; set pac- reperfusion management of acute MI and improved access
ing rate at 100 beats per minute. the rnA to 5. and the sen- to permanent pacing systems .
sitivity knob to trnXimum clockwise position for demand Epicarclial pacing - Epicardial pacing refers to the
(synchronous) pacing. Insert the end of the bridging cable delivery of a pacing stimulus to the heart through wires
into matching terminals on the pulse generator, and turn placed on the epicardial surface of the atrium, wntricle, or
1"111"" gl'.ner~tor on to verify pro[ll'r f"nct;on;n!! of thl'. hoth, during Qlrd;~c. _""I!ery_ 'lWo w;re., are ~ttach~d to the
battery and unit. atrium for singl~-chamber atrial pacing (one wire serws as
The prderred routes of access for transvenous pacing ground) or to the wntricle for single-chamber ventricu-
are the right internal jugular win. the right subclavian. and lar pacing. or two wires are attached to both chambers for
the right femoral win. The pacing lead is inserted into the dual-chamber pacing. The wires are loosely sutured to the
win of choice and guided into the heart using fluoroscopy. outer surface of the heart and pulled through th~ chest
Once- the- w;re- ;s v;,ullliz.cd in thc right ~tr;um. ~ bll.lloon wall where they Ilre Ilttll<:hed to a bridging coble II.Ild lIll
260 Pacem akers
Bridgi"ll cable
I.!..
"'o,tPU~~ ..oRa
te .. B
."
A
0' ,..
, "
c ':"Q'~' ~"CD "
. ~,""''-L D
A
BatieI)'
Pulse generator
Figure 1 0-5, Tempol3)' tI31svenoos pacemaker system.
A. Output or rnA dial
1. controls the amount 01 electrical energy delivered to endocardium.
2. Incroase rnA by turnhg dial cklckWlse to higher rumber; decreasa rnA by turning dial COlJItereiockWlsa to lower number.
B, Rata dial
1. Ootormh9S th9 hoa"t rata In boolslmlnuta a1 which tho stimulus Is to b9 dGllv9rod.
C, sensltlvtty or mY dial
1. controls the ability oflhe generator to sooselhe electrical actlvtty.
2. In maximum cIocI(\YIse position (5 o'dock), provides demllld (synchronous) pacing.
3. In maximum counterclockWise posttlon (7 o'clock), provides fixed rate (asynchronous) pachg.
4. Increase sooslUYity (mY) by turning mY dial cIockwtse to lower rumber, decrease senslUVIty by turning dial COUlIerdod<wtse to higher
number.
D, Onfotl control
1. AcIIyat~actlYates the pulse generator.
Pulse generator
r:::::~:t""'~dC~~f
E!ecrrical Battery ~
ClfCUI /
the passage of the lead wire. After satisfactory placement of and performing appropriately. This can be done in the
the pacing lead is confirmed, the lead is connected to the physician's office or owr the phone (remote monitor-
pacemaker generator. The generator is placed in the subcu- ing). Most pacemakers are programmable, enabling the
taneous tissue just below the left or right clavicle. Gener- physician to adjust pacing therapy.
ally the patient's nondominant side is chosen to minimize 2. Pilcemilker Silfety ~ Built-in filters protect pacemakers
interference with the patient's daily activities. from electrical interference from most devices encoun-
The major reason for implanting a pacemaker is the tered in daily life, including microwave owns. Security
presence of a symptomatic bradycardia. Symptomatic devices at airports should not cause any interference to
bradycardia is a term used to define a bradycardic rhythm the normal operation of the pacemaker; however, they may
that is directly responsible for symptom.! such as syncope, detect the metal in the pacemaker. In this situation, the
transient dizziness, confusion, fatigue, exercise intoler- pacemaker wearer can present an ID card indicating they
ance, congestive heart failure, dyspnea, and hypotension. have a pacemaker. Cell phones do not seem to damage or
Permanent pacemaker technology has undergone affect how the pacemaker works. Any activity that involves
major advances since pacemakers were first introduced in intense magnetic fields (such as arc welding) should be
the 1950s. Early pacemakers paced a single chamber (the avoided. Medical tests involving the use of magnetic res-
right ventricle) at a futed rate. Today', pacemaker< func_ onance im"lling (MRI ) are usually n,]ed out for patients
tion as demand pacemakers, sensing the patient's natural with pacemakers.
beats and pacing the heart "on demand" (pacing only when 3. Pacemaker replacement ~ The life of a pacemaker
needed). Most of the permanent pacemakers used today is affected by the type of pacemaker and how it is pro-
are the dual-chamber demand type. Although these dual- grammed to pace the heart. Today's pacemakers usually
chambu models are more expensive, they maintain AV contain lithium-iodine batteries, which are d~igned to
synchrony (the atria pace first, then the ventricles), pre- last many years. Pacemakers have a built-in indicator
serving the atrial kick and often providing patients with a to signal when the battery is approaching depletion.
higher quality of life. Studies have shown that unnecessary Most refled baltery depletion by a gradual decrease in
pacing of the right ventricle can lead to heart failure and an the pacing rate. The pacemaker is designed to operate
increased incidence of atrial fibrillation. The new~r dual- for several months to allow adequate time to schedule
chamber devices can keep the amount of right wntricular a replacement procedure. Because the batteries are per-
pacing to a minimum and thus prevent worsening of the manently sealed inside the pacemaker, the entire pace-
heart disease. maker is replaced when the battery runs down. Device
Permanent pacemakers are also available for specific replacement is usually a simpler procedure than the
conditions or needs: original insertion as it does not normally require leads
Rate-responsiw pacemilker ~ This pacemaker has to be replaced.
sensors that detect changes in the patient's physical activ-
ity and automatically adjust the pacing rate to meet the Permanent pacemaker
body's metabolic needs, Rate-responsive pacing mimics the
heart's normal rhythm, enabling patients to participate in identification codes
more activit ie5. A universal coding system is used to describe the func-
BiventricuJar pacemaker ~ A biwntricular pacemaker, tion of single- and dual-chamber pacemakers (Table 10-1).
also known as cardiac resynchroni1.ation therapy (C RT), The code is comprised of fiw positions. Various leiters are
stimulates both the right and left ventricles. By pacing both used for each position to describe a pacemaker function or
wntricles, the pacemaker can resynchronize a heart whose characteristic. Only one letter is used per position:
opposing walls do not contrilct in sym;hrony (/I problem First position ~ Identifies the chamber paced,
that occurs in 25% to 50% of heart failure patients). CRT Second position ~ Identifies the chamber where intrin-
devices have been shown to reduce mortality and improw sic electrical activity is sensed.
quality of life in patients with an ejection fraction of 35% Third position ~ Indicates how the pacemaker will
or less or in patients with heart failure symptoms. respond when it senses intrinsic electrical activity.
ImplantiJble cardiowrter-defi.brillators (JCDs) - These Fourth position ~ Identifies prOJ!rammablefunctions, the
devices haw the ability to pace for bradycardia, and over- capability for transmitting and receiving data (corrununica-
driw pace for tachycardia (anti tachycardia pacing) and tion), and the availability ofrate responsiwness.
shock therapy (cardioversion and defibrillation). They are Fifth position ~ Identifies antitachycardia functions:
used in the treatment of patients at risk for sudden cardiac 1. Antitachycardia pacing (ow rdrive pacing) ~ this func-
death. tion paces the heart faster than the intrinsic rate to convert
Once the pacemaker i. implanted, the following infor the tachycardia
mation is helpful to share with the patient: 2. Shock (synchronized cardioversion and defibrillation)
I. Periodic pacemaker checkups ~ The pacemaker is 3. Dual ~ performs both a pacing function and a shock
periodically checked to ensure the device is operational function.
262 Pucemukers
Tlble 1(J.1.
FlveleHer pacemaker Identification code
Arstlethlr SIeond Ieller Third I1I18r fourth tetter f1nhtaller
Ch/mber paced Ch/mber SIlnSlld RBBpOfISIl 10 IIIifIS~ ProgrammM1le hncIions Artill/ClrpurJia ~rn1ions
A:Alrium A:Alrium I '" IrtJibits pacing P '" Simple prOlJ"ammable P "Antitachycarda !llcing
V_ Ventricle V_ Ventricle T.. Triggers pacing M .. Multiprogfllmmeble S .. Shock
o" Duat {A and 'vi 0", Duat {Aand\? D" Duat (I aod T) C", Communication o '" Ouat (P and 5)
A = Rate rflSpor16iYe
Pacemaker terms dium (the negative pole) to the pacemaker generator located
in soft tissue (the positi~ pole). Because of the greater dis-
Pacemaker firing tance between the two poles. the ECC tracing will show a
A pacemaker produces a programmed current (stimulus) at tallle. easily visible pacing spike (Figure 10-7, example
a set rate to the myocardium. This enellly tra~ls from the A). Pacemaker systems utilizing bipolar pacing involve a
pacemaker generator through the lead wires to the myocar- small electrical circuit. The current travels between the elec-
dial m1.lS(:le. This is knownaspacem~ker firing and produces trode on the distal tip of the pacing lead (negative pole) to
a pacemaker spike (a vertical line) on Ihe ECG tracing. the proximal electrode located a few millimeters above the
Basic pacemaker operation consists of a closed-loop cir- distal tip (the positi~ pole). Because of the smaller dit lilnce
cuit in which electrical current flov,s betv,~en tv,o metal betv,een the ty,,o poles. the ECG tracing will show a small
poles (one negati~. the othe r positi~). The stimulating spike (Figure 10- 7, example B) or may not be visible in some
pube i, de1i~red through the ntgative electrode. Pace- leads on an ECG (Figure 10-7. example C).
rlUIker 'ystems may be either unipolar or bipolar. Unipolar
pacing has one pole (electrode) wilhin the heart. with the Capture
other pole being the metal case of the pulse generator. Pace- The term capture refers to the successful stimulation of
maker systems utilizing unipolar padng involve a large elec- the myoc .. rdium by a pacemaker stimulus. resulting in
trical circuit. The circuit tra~ls between the electrode on depolarization. Capture is evidenced on the ECG by a p.1ce-
the distal tip of the pacing lead in contact with the rTlyOC<lr- maker spike followed by either a.n atrial complex (P wave).
A. Unipolar pacing system (I""d II) B. Bipolar pacing Iyst"'" (lead III) c. Bipolar P""ing system (lead II)
Figure 1 0-7. Unlpotar and bipolar pac~ spikes. (AI Largo pactng spikes 11"9 soon wtth a unlpotar pacing system. (8) Small p;rlng
spikes 11"0 seen with a blpol1l" pactng system. (C)"The electrtcal clrcun Is so small n a bipolar systom that som9 leads may not show a pac~
spike.
Pacemaker terms 263
A B c
FIgure 10-8. Examplesor atrral caplurll.
(A) Atrral capture wtth normal-lookIllQ P waves conducted wrth IoIlQ PR nleml.
(8) Atrial capture with abnormar-Iooklng P waves.
(C) Atrrar capture with smarl. pointed P waves not Immedlatetj rorlowllg the atrial spike.
a ventricular complex (Q RS). or both, depending on the resultin g in normal depolarization and a narrow QRS
chambers being pilced. Capture beats are nOrJllill. compl ex.
Atrial depolaril.ation from a pacing stimulus results
in ~ p;lcing ."ike follov"ed hy "lr;,,1 "ct;vity (P w"",,) . The Sensing
morphology of the P waves produced may resemble that of Sensing is the ability of the pacemaker to detect intrinsic
sinus beats and be normal looking, or may be abnormal in electrical impulses (the patient's awn electrical activity)
appearance and so small that they are difficult to see. The P or electrical impulses produced by a pacemaker (paced
waws may not immediately follow the atrial pacing spike. activity) . If the pacemaker detects electrical activity, it is
The P waves may also be associated with a long PR interval. inhibited from delivering a stimulus. If the pacemaker does
Examples are shown in Figure 10-8. not detect electrical activity, it is triggered to initiate an
Normal ventricular depolarization is simultaneous electrical stimulus.
(both ventricles depolarize at the same time), resulting
in a narrow QRS complex of 0.10 second or less in dura- Intrinsic beat
tion. Ventricular depolarization from a pacing stimulus An intrinsic beat (also called native beat) is produced
is sequential (one ventricle depolarizes, then the other), by the patient's natural electrical system (Figure 10-9,
prolonging the duration of depolarization, resulting example B). Intrinsic beats are normal.
in a wide QRS complex of 0.12 second or greater. The
wide QRS complex immediately follows the pacing spike Automatic interval (pacing interval)
(Figure 10-9, example A). An exception to the wide The automatic interval refers to the heart rate at which
QRS rule is the biventricular pacemaker. This pace- the pacemaker is set. This interval is measured from one
maker simultaneously paces the right and left ventricle, pacing spike to the next consecutive pacing spike. For
Flllure 10-9, W ~lcular capture ooat, (B) na1lV9 beat, (e) fUsion beat
264 Pacemakers
atrial pacing. measure from one atrial pacing spike to the other. In Figure 10-9, example C, the fusion beat has
next consecutive atrial pacing spike. This is called the A-A more characteristics of the patient's paced beats than his
interval. analogous to the Pop interval of intrinsic wave- intrinsic beats. In Figure 10-10. example B. the fusion beat
fonus. For ventricular pacing. measure from one ven- has more characteristics of the patient's intrinsic beats
tricular pacing spike to the next consecutive ventricular than his paced beats. Fusion beats are normal and are
pacing spike (Figure 10-10. example A). This is called the usually seen only with ventricular pacing.
V-V interval. analogous to the R-R interval of intrinsic
wavdorms. Pseudofusion beat
A pseudofusion beat occurs when the pacemaker fires an
Fusion beat electrical stimulus after the patient's spontaneous impulse
A fusion beat occurs when the pacemaker fires an electri- has already started depolarizing the ventricle. The pac-
cal stimulus at th~ sam~ time the patimt's own electrical ing stimulus has no effect since the ventricle is already
impulse fires an electrical stimulus. This results in part being depolarized. The pseudofusion beat is evidenced on
of the ventricle being depolarized by the pacemaker and the monitor by a pacemaker spike occurring at the pro-
part by the patient's own intrinsic impulse. The fusion grammed rate (occurs on time). along with a native QRS
beat is evidenced on the ECG by a pacemaker spike that complex. The intrinsic QRS is not altered in height or
occurs at the programmed rate (occurs on time ). followed width (Figure 10-11 ). P~udofusion beats are normal and
by a QRS that is different in height or width from the are usually seen only with ventricular pacing.
paced beats and the patient's intrinsic beats (Figures 10-9
and 10-10). Pacemaker rhythm
The fusion beat has characteristics of both pacemaker Stimulation of the atria for one beat is called an atrial
and patient forces. although one usually dominates the paced beat. Continuous stimulation of the atria (all P waves
Figure 10-11 . Psoodolnluslon beat. The pacing spike Is located I1 Ih9 middle 01 Ih9 CRS In complex7.
Pacemaker mlllrunctiollS 265
are pacemaker induced) is clliled an atrial paced rhythm. demand pacemakers since nurses can interact more
Stimulntion of the ventricle for one btat is called a ven- directly with them than with permanent pacemakers. The
tricular paced beat. Continuous stimulation of the ventri- same concepts apply to permanent pacemakers. but co r-
de (all QRS complexes are pacemaker induced) is called a rection of malfunctions requires the use of a pacemaker
ventricular paced rhythm (Figure 10-12). Stimulati on of programmer or an actual surgical procedure to reposition
the atrin and the ventricle for one btat is called an AV paced the pacing lead or replace the generator.
beat. Continuous stimulation of the atria and ventricles
(all P waves and QRS complexes are pacemaker induced) is Failure 10 fire
called an AV paced rhythm. With fail ure to fire, the pacemaker does not discharge
a stimulus to the myocardium. Failure to tire wi ll be
evidenced on the ECC by an absence of a pacemaker
Pacemaker malfunctions spike where expected (Figure 10-13). Failure to ti re is
Basic functions of all pacemakers include the ability to fire abnormal.
(stimulus release). to sense electrical activity (intrinsic CIUiM'S lnd interventions for failure to fire:
and paced).llIId to capture (depolarize the chambers being 1. B~lIery depletion - Replace the battery.
paced). M05t malfunctions can be traced to problems with 2. Disc onnection in the system - Check the connections
the generator (parameter settings, battery failure), the lead between the generator, bridging cable. and lead: reconnect
(problems at the interface bety,'een the catheter tip and the or tighten connections.
endocardium. fracture in the lead or its insulating surface). 3. Fracture of INd or lead in sulltion - Do an overpen-
or to a disconnection in the system. etrated chest X-ray to detect fractures: have the physic~'n
This section includes a description of pacemaker mal- replace the lead.
functions. common causes. and interventions. It is directed o!.. ElectromAgnetic interference (EMJ) - Exposure of a
primarily toward temporary transvenou5 ven tricular pacing un it to such sources as electrocautery devices or
1>lRI may result in inhibition of the pacing stimulus. Avoid does not respond to a stilTJ.llus. Do an overpenelratfd chest
expo5ure. X'1'iI)' to determine the catheter po5ition. If the catheter is
5. Pacemake r is turned off ~ Make sure the pacemaker is out of position. a temporary maneuver is to tu m the patient
turned on: the generator should be secured awll)' from thf on his left side (gravity may allow the catheter loconlact lhe
patient. endocardium).A physician will have to reposition the lead.
J. Electrolyte imbalance ~ Electrolyte imbalances can
FaJlure to ca pture alter the abi lityof the heart to rtspond to a p-'cing stimu Ius.
With failure to capture. the pacemaker deliYers a pacing Check serum electrolyte levels and replace if needed.
stimulus. but electrical stimulation of the myocardium
(depolarization) does oot occur. This is evidenced on the Sensl ng failure
F.cc. by f"'Cemllker "(>ik... thilt ( I t t. . . at the programmed So>:Ming fail"re occ""" ..-hen the f'IICtmilker either dOB
rate. but are not followed by a P wave (for atrial pacing) or no t sense m)'OCllrdial electrical activity or the pacemaker
a QRS (for vtntricular p-'cing). Figure 1014 shows loa of OvtT5tnse5 the wrong signals. Sensing failure falls into two
capture with ventricular piKing. Lossof capture is abnorma.l. categories: undersensing and oversensillll.
CauSl'$ and in terventions for bilure 10 cilliure
I. rnA output is too low - Increase the mAon the genera- UluleNe/lsillg
lor by turning the rnA dial clockwise to a higher number The most common cause of sensing failure is undersensing.
(Figure 1(}'5). Over a period of days. inflammation or fibrin The ~maker does not sense (does not "seel myocardial
formation at the calheter tip may raise the stimulation electrical activity (eithe r intrinsic or paced) and fires earlier
thresho ld. requiring a highe r rnA output. than it should. Undersensing is recognized on the ECG by a
2. ltad is 01.11 of pos itiOIl or I}ing in infarcted tissue - The [Cing spike that occurs earlier than expected. It can occur
eltctrode tip must be in contact with the endocardium for the with capturt (Figure 1(}. IS. examples B and C) or without
electrical stimulus to cause depolarization. Infarcted tissue (Figu re 1015. example A).
Cluses and intelVentions {or undersensing than it should. Oversensing is recognized on the ECC by a
I. Se nsitivity sd too low - Increase sensitivity by turning paced beat that occurs later than ex~cted. (Figure 10-\6).
sensitivity dial clockwise to a 10l'>"l:r number. CIUseS il nd interventions {or oversensing
2. Pie ing catheter out o{ pos ition or lying in infarcted I . Sensitivity set too high - Decrease sensitivity by turn-
tissue - The electrode tip must be in contact with the ing the sensitivity dial counterclockwise to higher number.
endocardium to sense appropriately. Infarcted tissue does
not haw the ability to sense. Do an overpc!netrated chest
X-ray to determine catheter position. If the catheter is
Analyzing pacemaker strips
out of position, a temporary maneuver is to turn the patient
(ventricular demand type)
on his left side, which may allow migration of the catheter When analyzing pacemaker rhythm strips, you will again
into a beller position. A physician will have to reposition need to use either cali~rs or an index card. The following
the lead. steps should be helpful.
3. PACemaker set on lS}'I1c hronou s (fixed rate) mode - Step one - Place an index card above two consecutively
With asynchronous pacing, the sensing circuit is off. Turn pilced beats. Mark the autornatic intelVa!. 'Left mark and
the sensitivity dial to synchronous (demand) pacing mode. "right mark' mentioned in the steps below refer to marks
on the index card. The automatic interval measurement
Oversellsillg will assist you in determining if the pacemaker fired on
The pacemaker is too sensitiw ("sees too much) and is time, too early, too late, or not at all.
sensing the wrong signals (large P waves, large T waves, Step two - Starting on the left side of the strip. analyze
muscle mowment), causing the pacemaker to fire later each pacing spike you see. The patient"s intrinsic beats
,
Rgurll lD-t6. OWroorr.:;lrl\l.
Example k. Pacemaker Is s911Slng a age T wave.
Example B: Pacemaker Is sensing a low wave/orm artIlact Note: Using the automaUc InterwllM"ks on hclex card, place
- right mark on spike 01 late paclld beat. The len mark will malch whatEl't'er pacemaker Is sensing.
268 Pacemakers
do not need analyzing. but you need 10 bt able to identify R wave oflhe n.a.live beat immediately preceding the pacing
them from the paced beaU. spike being analyzed.
Step three - Ident ify the pacing spike to be analyzed S tep four - Ob5erve the relationship of the right mark
(only analyze one spike at a lime). Using the marked index with the spike being an.a.Iyzed to determine the answu:
card, place the left mark on the spike of the paced but or
Ventricular capture beat (normal)
Fusion beat (normal)
Undersensing (abnormal)
P~udofusion beal (normal)
Failure to capture (abnormal)
~~~~: ------------------------------------------------
Slrlp11J-2. Analysis :, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
~erpretation : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Strip11J-3. Analysis:, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
~erpretation : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Rhythm slrip prllclke: Pllcemakers 271
..
Strip 111-4. AnaIysis:_ _ _ _ _ __ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
, '.' '"",, ______________________
I~~~: _ _- - - - - - - - - - - - - - - - - - - - - - - -
~~-------------------------------------------
~~----------------------------------------
~ --------------------------------------
Rhythm strip prtu::lice: Pacemakers 2 73
,"""""..,,,- - - - - - - - - - - - - - - - - - - -
Strip 10-13. ANIysis:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
-""",,,- - - - - - - - - - - - - - - - - - - -
Strip 1O-19 . ~: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
lmerpretalion: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
~~~,----------------------------------------
Strip 1G-32.Analysls: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
~etat ion : _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Rhythm strip practice: Pacemakers 281
Strlp10-34. AnalysIs: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Irtl!fPretation:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
strip10-36.Ana/ysis:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
trterpretaioo:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
282 11llccmllkcrs
Slrip11-7. Analysis:, _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Interpretalion: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Strip11-4S. Analysis:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Inlerprelalion:_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Strip11-46. AnaIysis :, _ _ _ _ _ _ _ _ _ _~ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Inlerpretalion: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Strip 1'-68.Anaysis: _ _ _ _ _ _ _ _~ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
~e~ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Posttest: All rhythm groups 3 07
Smpll - D . M~~ _ _ _ _ _ _ _ ~_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
IlII8rpretation: _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
3 12 POSllest
PR Interval: ORScomplex:_ _ _ _ __
RhyItlm IntlNpl"etatiort_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Glossary
Index
321
Answer key to Chapter 3
Strip 3-2.
Strip 3-1.
322
Answer key to Chapter 3 323
Strip 3-11.
324 Answer key IQ Chllpter 3
Sbip 3-14.
Answer key to Chapters 5 through 11
325
326 AnswerkeytoChupters5lhrough II
""'" ...,
P waves: Sinus; P wa~ hidden with
Strip 1159
QRS compla: 0.06 to 0.08 second PIoIaWS: SiOOll (basic rh)1.hm); notched Rhythm: Regular (atrial and
Rhythm interpreilltion: Normal Pwavt$ u$WI1y indicate Itft atrial h)'- ventricular)
sinus rhythm with junclioTIIII ucape p!'rtrophy: no P __ e 5HIlwith fourth Rate: 93 beats/minute (alrill):
beat (fifth complex) after II pause complex: fifth COlT1lia has a P wave on 31 buWminute (ventricular)
in the basic rhythm: a U 'o\"1IYe is top oftht preceding T wa~ P WIVes: Three linus waws to
present. PR interval: 0.20 second (basic tach QRS comple)! (one hidden in
mythm) T wave)
S trip 85 1 QRS complex: 0.06 to 0.08 second PR interval: 0.32 to 0.36 second
Rhythm: Regular (atrial) but off by Rhythm interpretation: Sinus QRS complex: 0.08 second
two squares: irregular (~ntricular) bradycardia with a paU5e followed Rhythm interprelMion: Second
Rate: 60 to 65 beal&iminute (atrial): by a junclion.l tstape beat (fourth degree AV block. Mobil.1l1;
50 beats/minute (ventricuL!lr) complex) and a PAC (tifth complex); STsegment depre$5ion i. present.
P wa~s: Sinus IIbnorrMl P wa~ al5O(:iated 'o\ith
PR interval: Lengthens from 028 to PAC is obJtTYtd in preceding T wa~. Strip 8-60
0.40 second (not consistent) Rhythm: Regular (buic rhythm):
QRS complex: 0.08 iltcond Siri p 8-56 irregular (premature beats)
Rhythm interprttation: Mobiul Rhythm: Regular (lirst and second Rate: 60 bnt"minute (basic
second-degrH AV block myth~) rhythm)
Rate: 72 braWminute (first rhythm); P W/IYes: Sinus (basic rhythm);
Strip 852 obout 140 lxaUlminute (second prermture and abnormal (prtfl"\llture
Rhythm: Regular mythm) ""'u)
Ralt: 63 buts/minute P waves: Sinus (first rhythm): PR inte~l: 0.12 second (wic
P WiveS: Hidden in the QRS in~rted (second rhythm) rhythm): 0. 12 SKOI'Id (PAC): 0.08 to
comple! PR interval: 0.12 second (first rhythm): 0.10 second (pJCs)
PR interval: Not measurable 0.08 to 0.10 5tCOOd (second rh)Ithm) QRS complex: 0.08 second
QRS compla: 0.08 second QRS complex: 0.08 second Rhythm interprttlltion: Normal
Rhythm interpretation: Accelerated Rhythm interpretation: Normal sinus I'h)thm with one PAC (third
junctional rhythm sinllll rhythm cm.ng;ng to junctiOOllt complex) and paired Plel (Iixth and
tachycardia: STsegment depression seventh complexe$)
Strip 8 53 is pl'"esent.
Strip 8-61
Rhythm: Regular (atrial) but of( by
two squares: irregular (~ntricuL!lr) Rhythm: Regular
S tnp 857
Rate: 84 beats/minute (atrial): Rhythm: Regular
Rate:"7 beats/minute
P waves: Hidden in the QRS
40 beats/minute (ventricu L!lr) Rate: 84 beats/minute
P waves: Sinus (two or three P W/lWS P waves: Sinus complex
PR inlerval: Not measurable
before each QRS complex) PR interval: 0..30 to 0.32 second
QRS complex: 0.08 second
PR interval: 0.12 second (consistent) (remains constant)
QRS complex: 0.12 second QRS complex: 0.04 to 0.06 second Rhythm interprelati on: Junctional
mythm
Rhythm interpretation: Mobiu II Rhythm interpretation: Normal sinus
seconddegrH AV block with 2:1 and rhythm with lirst--degree AV block;
3:1 AV conduction STsegment elevation is present.
Answer key to Chapters 5 through II 345
Strip 111 03
Rhythm: Regular
Rate: 214 beats/minute
P waws: None identified
PR interval: Not measurable
QRS complex: 0.16 second or greater
Rhythm interpretation: Ventricular
tachycardia
Strip 11 \0<1
Rhythm: Irregular
Rate: 60 beats/minute
P waws: Fibrillatol)' waves
PR interval: Not measurable
QRS complex: 0.06 to 0.08 second
Rhythm interpretation: Atrial
fibrillation
Strip 11 105
Rhythm: Regular (basic rhythm)
Rate: 72 beats/minute (basic rhythm)
P waws: Sinus
PR interval: 0.16 to 0.18 second
QRS complex: 0.06 to 0.08 second
(basic rhythm): 0.12 second (PVC)
Rhythm interpretation: Normal sinus
rhythm with one interpolated PVC;
STsegment depression is present.
Glossary
Aberrant - Abnormal immediately after the QRS, or hidden reopen the artery br inflating the bal-
within the QRS complex with a short loon, compressing the atherosclerotic
Abcrr",ntly concluded ~upr.vcn PR intetval of 0.10 =ond or 1=; a ploque. and dilating the lumen of the
tricular premature beats - A pre- normal duration QRS complex; and a artery. Often followed by insertion of
mature electrical impulse ori{!inatinll rate between 60 and 100 beats/minute. a coronary artery sten!. Also known as
in the atria or AV junction may occur The rate is faster than the inherent fir- percutanrous trllTlSluminal coronary
50 early that the impulse arrives at ing rate of the AV junction. but slower angiop/asty or P1t:4.
the bundle of His before the bundle than junctional tachycardia.
branches have been sufficiently repo- Anion ~ An ion with a negative
larized. Becau.\e the right bundle Accessory conduction pathways - chaflle
branch is 5Jo~r to repolariz.e, the Several abnormal electrical conduction
impulse traV\!ls down the left bundle pathwa~'s within the heart that allow Antegrade conduction ~
branch first, and then stimulates the electrical impulses to bypass the atrio- Conduction ofthe electrical impulse in
right bundle branch. Because of this ventricular node before entering the a forward direction
delay in ventricular depolarization the ventricles.
QRS complex will be wide. Premature Aortic valve ~ One of two semilunar
atrial contractions (PACs) associated Acetylcholine ~ The chemical neu- valves; located between the left ven-
with a wide QRS complex are called rotransmitter for the parasrmpathetic tricle and the aorta.
PACs wilb aberrant ventricular con- nelVOUS s~'stem.
duction, indicating thai conduction Apex of th~ heart ~ The bottom of
through the ventricles is abnormal. Acutr myocardial infarction - the heart formed by the tip of the left
Premature junctional contractions Necrosis of the mrocardium caused by ~entricle; located to the left of the
(PJCs) lmOCiated with a wide QRS prolonged and complete interruption sternum at approximately the fifth
complex are called PJCs with aberrant of blood ftow to an area of the m)lOC4r- intercostal space. midclavicular line.
ventricular conduction. Also known u di.>.l mwdcm=.
PACs or PJCs with aberrancy. Arrhythmia ~ A general term refer-
Agonal rhythm ~ A rh~1hm seen in ring to any cardiac rh~1hm other than a
Absolutr refractory period ~ The a dying heart, in which the QRS com- sinus rh)'lhm. Often used interchange-
period of time during ~ntricular plexes deteriorate into irregular. wide, ably with dysrhythmia, a more appro-
depolarization and most of repolar- indistinguishable waveforDl.! just prior priate term. but one used less often.
il.iltion when cardiac cells cannot be to ventricular standstill.
stimulated to conduct an electrical Artifacts ~ Distortion of the ECG
impulse. This period be(!ins with the A1VR ~ aMr accelerated idioven- tracing by activity that is noncardiac in
onset of the QRS complex and ends at tricular rh~1hm origin. such as patient movement, elec-
the peak of the T waw. trical interference, or muscle tremors.
Amplitude - The height or depth Also knov.n as interferimCe or noise.
Accderated idiowntricular rhytbm ~ of a wave or complex on the ECG
An arrhrthmia originating in an ectopic measured in millimeters (mm). Also As~stole ~ Absence of ventricular
site in the wntricles characterized by a known as voltage. electrical activity. Tracing will show
re(!ular rhythm, an absence of P waves, P waves only or a straight line. Also
ond wide QRS complexe. at 0 rote of SO Angino ~ The term .... ed to ducribc colled ventricular standstill.
to 100 beats/minute. The rate is faster the pain that results from a reduction
than the inherent tiring rate of the ven- in blood supply to the m)lOC4rdium. Atria ~ The two thin-walled upper
tricles. but is slower than ventricular The pain is typically described as chest chambers of the heart. The right and
tachycardia. Also known as AIVR. heaviness, pressure, squee1:ing, or con- left atria are separated from the ~entri
striction. Associated srmptoms include cles by the mitral and tricuspid valws.
Accelerated junction,l rhythm ~ An nausea and diaphoresis.
orrhythmilt origi""ting in the otrio- Atrial fibrillation ~ An arrhyth-
ventricular (AV) junction character- Angjoplasty ~ The insertion of a mia originating in an ectopic site
ized by a regular rhythm; irwerted P balloon-tipped catheter into an occlud- (or numerous sites) in the atria
waves immediately before the QRS, ed or narrowed coronary artery to characterized by an atrial rate of 400
369
370 Glossary
beats/minute or more: atrial waveforms control). Includes the sympathetic junctional. or ventricular). Also knOv,,,
appearing as an irrejlular, wavy baseline: and parasympathetic nervous systems. as sallJ() or run.
a normal QRS duration: a grossly irreg- each producing opposite effects when
ular ventricular rh~1hm:.md a rate that stimulated. Calcium chinrnd blockers ~A
may be fiLIt or slow depending on the group of drugs that block entry of cal-
number of impulses conducted through AV ~ abbr atrioventricular cium ions into cells, especially those of
the atrioventricular node. cardiac and vascular smooth muscle.
Bachma.nn's bundle ~ A branch of U~d to treat hypertension, angina.
Atrial flutter ~ An arrh~1:hmia origi- the internodal atrial conduction tracts. and as an antiarrhythmic.
nating in an ectopic site in the atria Conducts the electrical impulses from
characterized by an atrial rate between the sinoatrial node to the left atrium. Cudiac cells ~ Cells of the heart con-
250 and 400 beatyminute: atrial wave- sisting of the myocardial cells responsi-
forms appearing in a sav,10oth pattern: Ba.seUne ~ The straight line between bl~ for contraction of the heart muscle
a nonnal QRS duration: a regular or E:CG wavdonns when no electrical and the pacemaker cells of the electri-
irregular ventricular rh~1:hm: and a activity is detected. cal conduction system, which spontane-
rate which may be fast or slow depend- ously generate electrical impulses.
ing on the number of impulses con- Base of the heirt ~ Top of the heart
ducted through the AV node. located at approximately the level of CardiiC cycle ~ Consists of one
the second intucostal space. heartbeat or one PQRST sequence.
Atrial kick ~ Blood pushed into the Represents atrial contraction and
ventricles 11.1 a result of atrial contrac- Ikta blockers - A group of drugs relaxation follov.~d by l'entricular con-
tion to complete filling of the ventri- that block sympathetic activity. Used traction and relaxation.
cles just before the ventricles contract to treat tachyarrh~1:hmias, MI, angina.
and hypertension. Cardiac ta.mpolude ~ Compression
Atrioventricular block (AV block) ~ of the heart due to the effusion of Huid
A delay or failure of conduction of elec- Bigeminy ~ An arrhythmia in which into the pericardial cavity (as occurs
trical impulses thr~ the AV node. every other ""lIt i. ~ premature eetopic in ["O'.ricarditi<) or the ac.mm"l.tion of
beat. The premature beat may be blood in the pericardium (11.1 occu~ in
Atrioventricular junction IAV atrial, junctional. or ventricular in heart rupture or penetrating trauma).
junction) - Consists of the AV node origin (i.e., atrial bigeminy, junctional
and the bundle of His. bigeminy, ventricular bigeminy). Cardiomyopathy ~ A disease of the
hurt muscle. Characterized by cham-
AtrioventricuJiT n<><k IAV node) ~ Biphasic deflection ~ A waveform ber dilation, wall thickening, decreased
Located in the lov.~r portion of the that is part positive and part negative. contractility, and conduction distur-
right atrium near the interatrial sep- bances. End result is usually severe
tum: only normal pathway for conduc- Bradycardil -An arrhythmia with a dysfunction of the heart muscle,
tion of atrial impulses to the ventricles: rate of less than 60 beats/minute. resulting in terminal heart failure.
primary function is to slov. conduction
of electrical impulses through the AV Bundle-brancb block - A block of CardiO\ersion ~ An electric shock
node to allow the atria to contract conduction of the electrical impulses synchronized to fire during the QRS
(atrial kick) and complete filling the through either the right or left bundle complex: used to terminate rh~1:hms
\entride.s. branch, resulting in a right or left such as atrial fibrillation or Hutter,
bundle-branch block. paroxysmal atrial tachycardia. and ven-
Atrioventricular valves (AV tricular tachycardia to normal sinus
valves) ~ The two valves located Bundle branches ~ A part of the rhythm: uses lov,~r joules of electric-
between the atria and the ventricles. electrical conduction system consisting ity. Also known as synchronized shock.
The tricuspid separates the right atri- of the right and left bundle branches that
um from the right ventricle, the mitral conducts the electrical impulses from the C~tion ~ An ion with a positive
separates the left atrium from the left bundle r:i His to the Purkinje network. charge.
ventricle.
Bundle of His ~ A part of the Cbordae tendineal! ~ Thin strands of
Automlticity ~ Ability of a cell to electrical conduction system that con- fibrous connective tissue that extend
spontaneously generate an impulse. nects the atrioventricular node to the from the cusps of the atrimentricular
bundle branches. valves to the papillary muscles and
Autonomic nelVOUS system ~ prevent the AV valves from bulging
Regulates functions of the body that Bunts ~ Thre~ or more conse,utive biKk into th~ atria during ventricular
are involuntary (not under conscious premature ectopic beats (atrial, contraction.
Glossary 371
of the bundle of His, the bundle Ion - Electrically charl!ed particle. Monomorphic - Refers to QRS com-
branches, and the Purkinje fibers. plexes of the same morphology in the
Ischemiil - Reduced blood flow to same lead.
Hypertrophy - An increase in the tissue caused by narrowing or occlu-
thickness of a heart chamber because sion of the artery supplying blood to it. Morphology - The shape of II
of a chronic increase in pressure waveform.
amVor volwne within the chamber. boelectric line - See baseline.
H~-pertrophy may occur in both the Multifocll - Indicates an arrhythmia
atria and the ventricles. IVR - abbr idioventricular rhythm originating in multiple pacemaker
sites.
Idioventriculu rhythm - An J point - The point where the QRS
arrhythmia arising in an ectopic site in complex and ST segment meet. Multifocll premillure ventricular
the ventricles characterized by a regu- contractions - l'Yes originating in
lar rh~thm; an absena! of P waves; wide Junctional rh)thm - An arrhythmia multiple paa!maker 5ites in the ventri-
QRS complexes; and a rate between arising in the atrioventricular (AY) cles having different QRS morphology
30 and 40 (sometimes lessl beats/ junction characterized by a rel/ular in the same lead.
minute. This is the inherent rh~thm of rh~thm; inverted P waves immediately
the ventricles. Also known as IVR. before the QRS, immediately after the Mural thrombi - Clots in the cham-
QRS, or hidden within the QRS com- bers of the atria caused by ineffective
Infarction - Death (necrosis) of plex, with a short PR interval of 0.10 atrial contraction (may occur in atrial
tissue caused by an interruption of second or less; a normal-duration QRS fibrillation or flutter)
blood supply to the affected tissue. complex; and a rate betl\"een 40 and 60
beats/minute. Junctional rhythm is the Myocilrdium ~ The middle and
lnkrior ven ~ cavil - One of two inherent rhythm of the AY node. thickest la~"er of the heart composed
large ~"eins that empty venous blood primarily of cardiac muscle cells and
into the right atrium. Junctional tachycardia - An responsible for the hearts ability to
arrhythmia arising in the atrioven- contract.
Inherent firing rate - The normal tricular jundion characteri~ed by
rate at which electrical impulses are a regular rhythm; inverted P waves Nf"gativ( deflection - A wa~efonn
generated in a pacemaker. whether immediately before the QRS. imme- that is below baseline.
it is the sinoatrial node or an ectopic diately after the QRS, or hidden
pacemaker. Also known as the intrin- within the QRS complex, with a short Noncompensatory pilU ie - A pause
sic firing rote. PR interval of 0.10 second or less; a following a premature beat. A noncom-
normal -duration QRS complex; and a pensatol)' pause is identified on the
Interatrial s~ptum - The I\-all sepa- rate greater than 100 beats/minute, ECG by measuring from the R Wllve
rating the right and left atria. before the premature heat to the R
rnA - abbr milliampere wave following the premature beat; if
Internodal atriill conduction that measurement is less than two car-
trilds - Part of the electrical con- Mediastinum - Located in !"he middle diac cycles (less than the sum of two
duction system. Consists of three of the thoracic cavity. Contains the R-R intervals), the pause is considered
pathways of specialized conducting heart, trachea, esophagus, and great ve5- noncompensatory. A noncompensa-
tissue JOCllt~d in th~ walb ofthe right sels (pulmonary arteries and veins, aorta, tory pause (annot be identified if the
atrium. Conducts impulses from the and the superior and inferior vena cava). underlying rhythm is irregular. Also
sinoatrial node to the atrioventricular known as incomplete pame.
node. Ml - abbr myocardial infarction
Nonconducted prematul"( atrial
Interpolated PVC - A premature Milliampere - Unit of measure cOlltnction - A premature abnormal
~entricular contraction (IVe) that falls of electrical current needed to P wa~"e not accompanied by a QRS
between two QRS complexes without cause depolarization of the myocar- complex, but follOl\"ed by a piluse.
a pause. dium. A tenn used most often with
pacemakers. Nomlll sinus rhythm - The nonnal
IntTilventriculiT ~ptum - The wall rh~1hm of the heart originating in
separating the right and left ventricles. Mitral valve - One of ""0 atrioven- the sinoatrial node characterized by a
tricular valves. Located bet",-een the regular rhythm; normal P waves,
Intrinsic beat - Beats produced by left atrium and left ventricle. Similar PR interval. and QRS duration;
the heart's own electrical conduction in structure to the tricuspid valve, but and a rate be""een 60 and 100 beats!
system. Also known as IUltive beat. has only two cusps. minute.
Glossary 373
Overdrive pacing ~ Pacing the heart Premature iltrial contraction - An pulse less ventricular tachycardia) is
at a rate faster than the tachycardia to early beat originating in the atria. char- observed on the ECC, but no pulse is
terminate the tachyarrhythmia. acterized by a premature, abnormal P palpated. Treatment protocols are the
wave (usually upright); a PR interval same as for wntricular standstill.
PAC ~ abbr premature atrial that may be normal or abnormal; and a
contraction normal-duration QRS complex followed PUTkinje fibers - A network of fibers
by a pause. Also knO\'ln asPAC. that carry electrical impulses directly
Pacemaker ~ A device that deliv to ventricular muscle cells.
ers an electric current to the heart to Premilure junctional contraction -
stimulate depolarization. An early beat originating in the atrio- P wave - The waveform represent
\~ntricular junction characterized by ing depolarization of the right and left
Papillary muscles ~ Projections of a premature inverted P wave occur- atria.
myocardium arising from the walls ring inunediately before the QRS,
of the ventrides connected to fibr0U5 immediately after the QRS, or hidden Q wilve~ The negative deflection of
cords called chordae tendineae, which within the QRS complex with a short the QRS complex that precedes the
are attached to the valve leaflets. PR interval of 0.10 second or les,s and R wa\~.
During ventricular contraction the a normal-duration QRS complex fol-
papillary muscles contract and pull on lowed by a pause. Also known as PJC. QRS complex - The waveform that
the chordae tendineae. thus prevent- represents depolarization of the ventri-
ing inversion of the atrioventricular Premature ventricular contr~c cles; consists of the Q, R and S waves.
valve leaflets into the atria, lion - An early beat originating Normal duration is 0,10 second or less,
in the ventricles characterized by a
Para.~ymrathetic n ~\"Vnll~ .<ydem ~ rrem.tur~, wide QR.'; cnml'lu with QT inte\"Val _ The portinn nf thp.
A part of the autonomic nervous no associated P wave and an ST seg ECC between the onset of the QRS
system. Stimulation of this sys- ment and T wave that slope opposite complex and the end of the T waw,
tem decreases the heart rate. slows the main QRS deflection followed by representing ventricular depolarization
conduction through the atrioventricu - a pause. Also known as PVC. and repolarization.
lar node, decreases the force ofven-
tricular contraction. and causes a drop PR interval - The period of time Rate suppnssion - A decrease in the
in blood pressure. from the beginning of atrial depolar- heart rate for several cycles following a
ization (P wave) to the beginning of pause in the basic rh~1:hm.
Paroxysmal ~ A term used to \~ntricular depolaril.ll.tion (QRS com-
describe the sudden onset or cessation plex). The normal PR interval duration RecipTOCill change - A change
of an arrhythmia. is 0.12 to 0.20 second. detected by the ECC in an area of the
heart opposite the site of a myocardial
Paroxysmal IITial tachycardia ~ An Prinzmetal's angina - A type of infarction.
arrhythmia originating in the atria angina occurring when the coronary
characterized by abnormal P wave! arteries experience spasms and Relative refnctory period - The
that are u.lUally hidden in the preced- constrict. period oftime during ventricular
ing T waws; a normal QRS duration; repolarization during which the ven
and a regular rhythm betv.~en 140 and Proarrhythmic - The effect of tricles can be stimulated to depolarize
250 beats/minute, certain drugs (especially antiarrhrth - by an eiearical impulse stronger than
mics) to induce or wo ... en wntricular u,,,al. Thi, period beWn, at the peak
PAT - abbr paroxysmal atrial arrh~1:hmias. of the T waw and ends with the end
tachycardia of the T waw. Also known as the tul
PR segment ~ The portion of the nerable period of lIentricular repo/ar-
PJC ~ abbr premature junctional ECC betv.~en the end of the P wave ization.
contraction and the beginning of the QRS complex.
Reperfusion Thythnu ~ Rh)'lhms
PolymoTphic - Refers to QRS com- Pulmonic valve. - One of two semilu- that may occur following reperfu-
plexes of different morphology in the nar valves. Located between the right sion therapy. Examples of reperfusion
same lead. wntricle and the pulmonary artery. rhythms include sinus bradycardia.
accelerated idiowntricular rhythm,
Positive deflection - A waveform Pulseles,s electrical activity - premature wntricular contractions,
that is above baseline. A clinical situation in which an ventricular tachycardia, and wntricu-
organized cardiac rh~thm (excluding lar fibrillation.
374 Glossary
Reperfusion ther,py ~ Treatment intervals with two, three, or more P of the electrical impulse from the
to reopen an occluded coronary artery waves before each QRS complex; a ven- sinoatrial node to the atria (a disor-
using a thrombol~1:ic agent or coro- tricular rhythm that may be regular or der of conduction). The ECG tracing
llary interventions. such as balloon irregular depending on the number of ""ill show a sudden pause in the sinus
angioplasty, coronary artery stenting, impulses conducted to the ventricles; rh~1hm in which one or more beats
or atherectomy. and a QRS complex that may be nar- are missing. The underlying rh~1:hm
row or wide depending on the site of resumes on time following the pause.
Repolarization ~ An electrical the conduction disturbance.
process by which a depolarized cell Sinus nod ~ The dominant pace-
returns to its resting state (negative Sequential ventricular depoliriza - maker of the heart located in the wall
charge) due to the mmement of ions tion ~ One ventricle depolarizes of the right atrium close to the inlet of
acr05.! a cell membrane. The repolar- before the other (instead of simul- the superior vena cava.
ization process produces the ST seg- taneously), resulting in a wide QRS
ment, the T waw, and the U waw. complex. Sinus tachycardiA ~ An arrh~1hmia
originating in the sinus node
Retrograde ~ "'oving backward or in Sick sinu& s~Tldrome ~A characterized by a regular rhythm;
the oppo.lite direction to that which is degenerative disease of the sinus node normal P wa~'es, PR interval, and QRS
considered normal. resulting in bradyarrh~1:hmias alter- duration; and a rate betl'..~en 100 and
nating with tachyarrhythmia_. _ Thi. 160 Iw.llt<lminnte.
R-on -T premillure ventricular s~Tldrome is often accompanied by
contnction (PVC) ~A PVC that falls symptoms such as dizzinm, faint in!!, ST segment ~ The Hat line between
on the down slope of the preceding chest pain, dyspnea, and congestive the QRS complex and the T wave that
T wave. Stimulation of the ventricle heart failure. Permanent pacemaker represents early ventricular repolariza-
at this time may precipitate repetitive implantation is recommended once tion. The ST segment is nonnaUy at
ventricular contractions, resulting in the patient becomes s)'lllptomatic. Also baseline.
ventricular tachycardia or fibrillation. known as tachy-brady syndrome.
Stoku-Ad,ms iltKla ~ Fainting
R-R interval ~ The period of time Sinus i1JTest ~ An arrhythmia ",used episodes that oo;ur when the heart
from one R wave to the next consecu- by a failure of the sinoatrial node to rate suddenly slows or stops momen-
tive Rwa~~. initiate an impulse (a disorder of auto- tarily; common with second..degree
maticity). The ECG tracing will show atrio~~ntricular (AY) block, Mobitz II.
R wive ~ The positive wave in the a sudden pause in the sinus rhythm and third-degree AV block.
QRS complex. in which one or more beats are mm-
ing. The underl~ing rhythm does not Superior vena cava ~ One of two
SA ~ abbr sinwtnal resume on time following the pause, lar~ veins that empty venous blood
into the right atrium.
Second-degn atrioventricular (AV) SinU& ,rrhythmia ~ An alTh~1hmia
block Mobilz I ~ An arrhythmia in originating in the sinoatrial (SA) node Supemonnal period - The last
which there is prO{lre!sive delay in that occurs ""tten the SA node discharges phase of repolarizatiOil during which
the conduction of electrical impulses impulses irregularly. Sinus arrhythmia the cardiac cell ",n be stimulated to
through the AV node until an impulse is a normal phenomenon associated with depolarize by a weaker than nonnal
is blIKked and not ,onducted to the th\: phases 0( mpiration, This rh)thm electrical stimulus, This period oo;urs
ventricle!. Characterized by regularly is characterized by an irregular rhythm near the end of the T waw just before
occurring P waves; progressive length- normal P waves, PR interval, and QRS the cells have completely repolariz.ed.
ening of the PR interval until a P wave duration, and may be associated ""iih a
appears without a QRS. but is followed normal or bradycardic rate. Supraventriculu ~A general tenn
by a pause; normal QRS duration: and used to describe arrhythmias that
<II, irr~J!uldr v~"lri~uldr rhyllllll. Ab" Sinus br...JYHr~i. ~AJl drrhyllt- "rilli''''l~ ill .il~ ...b""" lh~ bWldl~
known as Wenckebach. mia originating in the sinus node branches (i.e., sinus node , atria, and
characterized by a regular rhythm; atrioventricular junction).
Second-degree atrioventricular normal P waves, PR interval, and QRS
block Mobitz " - An arrhythmia in duration; and a rate between 40 and S Wive - The negative deflection of tile
which some electrical impulses are 60 beats/minute. QRS complex that follows the R waw.
conducted to the ventricle., but mo.t
are blocked. Characterized by regularly Sinus exit block ~ An arrhythmia Sympilhetic nervous system - A
occurring sinus P waves; consistent PR caused by a block in the conduction part of the autonomic nervous system.
Glossary 375
Stimulation of this system increases inserted into a large vein and posi- Ventricle, - The two thick-walled
heart rate, speeds conduction through tioned in the right wntride. Electrical lower chambers of the heart; they
the atrioventricular node, increases the impulses are conducted from an exter- receive blood from the atria and pump
force of ventricular contraction, and nal power source (pacing generator) it inlo the pulmonary and systemic
causcs an incrca:;c in blood prcssurc, through thc lcad wire to thc right circulation. The ventricle. an: scporatcd
ventricle. from the atria by the mitral and tricus-
Syncope - Fainting, U.!ual1y result- pid valves.
ing from cardiac or neurologic events, Tricuspid valve - One of two atrio-
ventricular valves. Located between VentricullT fibriJlillion - An
TCP - aM, transcutaneous pacing the right atrium and the rightventri- arrhythmia arising from a disorga-
de. Similar in structure to the mitral nized, chaotic electrical focus in Ihe
TdP -obb, torsade de pointes valve, but has three cusps. ventricles in which the ventricles
quiver inslead of contracting effec-
Third-Ikgret atriovtntricular (AV) Trigemin~ - An arrh)ll:hmia in tivtly. The ECG tracing sho ....'S an
block -An arrhythmia in which which every third beat is a premature irregular, wavy baseline without QRS
there is no conduction of electrical ectopic beat. The premature beals complexes.
impulses through the AV nook There may be atrial, junctional, or ventricu-
is independent beating of the atria lar in origin ( i.e., atrial trigeminy, "fntricullT standstill - An arrhyth-
and ventricles, The atria are paced by junctional trigeminy, ventricular mia in which there is an absence of
the sinoatrial node at a rate of 60 to trigeminy). all ventricular acti~'ily. The ECG trac-
100 beats/minute and the ventricles ing Will5how either P waves without
are paced either by the AV junction T wave - A wa~'e that follows the QRS complexes or a straight line. Also
at a rate of 40 to 60 beats/minute ST segment. Represents ventricular knO ....T1 as ventricula, asystole.
or by the ventricles at a rate of 30 repolarization.
to 40 beats/minute, This rh~1hm is Ventricular hchycardia - An
characterized by sinus P waves that Unifoul PVCS - Premature arrhythmia arising from an ectopic
have nn cnn.,i,tp.nt relatinn.,hi" to the ventricular c.nntr.ctinn., (PVc.,) origi_ .,ite in the wntride,- On the F.Cc, the
QRS complexes (variable PR inter- nating in the same site in the ventricle rh,1:hm appears a5 a 5eries of wide
vals); P waves found hidden in the having the same QRS morphology in QRS complexes with no associated P
QRS complexes, ST segments, and T the same lead. waves; a regular or slightly irregular
waves; a regular atrial and ventricular rhythm; and a rate of 140 to 250 beats/
rh~1hm; a narrow QRS complex if the U wave - A wave that sometimes minute.
wntricles are paced by the AV junc- follows the T wave. Represents late
tion; and a wide QRS if paced from a ventricular repolarization. Vulnerable period - The period of
wntricular site, Also known as com- time during ventricular repolariz.a-
plete hea,t block. Vagal maneuvers - Methods used tion in which the ventricles can be
to stimulate vagal (paras~mpathetic) stimulated to depolarize by a strong
Torude de pointes - A form of tone in an attempt to slow the heart electrical stimulus. This period
wntricular tachycardia associated with rate. Methods include coughing, corresponds to the do",,, slope of the
a prolonged QT interval. The name bearing down (Valsalva maneuwr), T wave (relative refractory period).
is derived from a French term mean- squatting, breath-holding, carotid Electrical stimuli occurring during
ing "twisting of the points," I'lhich sinus pressure, stimulation ofthe the vulnerable period may lead to
describe. a QRS complex that changes gag reflex, and immersion of the face ventricular tachycardia or wntricular
polarity (from negative to positive and in ice water. fibrillation.
positive to negative) as it twists around
the isoelectric line. Also knol'tTI as TdP. Valsaln maneuver - Forceful act of Wandering atrial pilcemaker - An
expiration with mouth and nose closed arrhythmia arising from multiple
Transcutaneous pacing (TCP) - producing a "bearing down" action. pacemaku sites in the atria. The ECG
External Qrdiac pacin~, Consists of two One of sewral ViI~alllliLlleuvers, tracin~ will show a normal or slow
large electrode pads commonly placed rate; a regular or irregular rhythm;
in an anterior-posterior position on the Vasovagal ruction - An extreme P waves thai vary in size, shape, and
patient's chest to conduct electrical body response that causes marked bra- direction across the rhythm strip; a
impulses through the skin to the heart. dycardia (due to vagal stimulation) and PR interval that is usually normal, but
marked hypotension (due to vasodila- may be abnormal because of the differ-
Transvenous pacing - Cardiac tion). A vasovagal reaction may result ent sites of impulse formation; and a
pacing through a win. A lead wire is in fainting (vasovagal s~ncope,. normal QRS duration.
Index
376
Index 377
s u
Second-del!~t. type J heart blocks. UndtrStnsinl!. 266-267. 2661
147-1 50.1471.148.,149. U _ve. 21-22. 21 . 375
Second-del!~" type II hu.rt blo<:ks.
150-152. 15Oi. lSOt.15 1i V
Semilunar val ...... 3-4. 4i Vallal man.u ........ 375
Sequenlial IkJ)Olarization. 198. 374 V.balva, ~r.47. 95.375
s;.:k sinus .yndrome. 47.374 V~.I reaction. 375
Sinoatrial (SA), 374 V.ntric"".375
Sinoatrial dysfuotlion. 256 Ventricula'lIrrl'o-thmias
Sinw arrest.48-50. 49i. 511. 374 buls lAd rhythms. 197. 197i
5inw arrhythmia... 47-18.47i. Sit 374 rilfthm .Irip practice for.2 14-255i
ECG f\'.ll.tu~ 48t. 511 Ventricular t.tape beals. 203. 203;
rhythm strip practice, 52-84i Ventricular fibrilLltion. 2<17-2119. 208~
with sinus po""". 48--50, SOi 213t.375
Sinw bmlyocardi ... 46-47.46i, Sit 374 treatment protocol. 20S-209
Sinw ait block, 48-50. 481, Sit. 374 Ventricular (luuer. 204i. 206
Sinus n<><k. 374 Ventricular .tm<ktill. 211- 212. 212i.
Sinw paUst. 48--50. 50~ Sit 213t.375
Sinw Ulchycardia. 45-16,45i. Sit. 374 Ventrkular tac~rdil. 204-206. 204i,
Sodiurn--pobMium pump. 8-9. 9i 205,. 21lt, 375
StoIcfS,AIbnu attacks. 151.374 IUlhIe monomorphic. wilh
StoIcfS-Adamuyncopto.15L 153 pulst.2(16
srsqlm~nt. ]7. 17i. 18i.374 Wl5U1ble monomorphic, wilh pul..,.
51 H1Iment dev.tion myoQrdial
infarction (STEMI), 17
2"
Vul,",rablt J'Kriodofrtpo~riulion.l2.
5~rior ....... cava. 374 375
5~roorlTllOJ Pfriod. 374
S.... TI"Itntncul.u arrhythmiu. 197 W
5 ....ve.374 WanderinQ al rial paoemaktr, 85-87. 871,
$ympathdk '"'NOW syslffll. 7. 374 101t.375
Syncope. 375 Wandering bastlint. 33. 33.
Systo:mic circu't. blood fIowand. 2 Waveforms, cum:nt tI!M and, I I. Iii
$yawle.7 practice slriPJ for labe liflll. 23-24;
Weotktbach. U7-ISO. 148i. 149i
T
T~hybrady .yndrome. 47
Telemetry monitorinll. 27. 27i
fi .... -leadwire system. 27, 27i
Ihret-leadwir. syslem, 27. 28i
Ttmporary pattlNktrs
rpicard,al pacing. 2S--260
TCP lhniQun. 258-259. 258,. 2591
traru .... now pacinI!. 259. 260i
Third-degree heart blocks. 152- 153.
152i. 1521. 153i
Torsade d. poinl.. (TdP),2t 205,.
206--207, 375
I~tm.nl protocols. 207
TramctltmtoUO PKino: (TeP). 258-259,
258i. 2591, 375
Transt50phaj/eaJ cchOCllrdioilram (TEE),
98
T""'-"""nous pacinQ. 259. 2fj{Ii. 375
Tricw.pid valve, 375
Tril!cminy.375
Tr~redacl'vity, 85
T ....ve. 19--20, ]9i. 375
2
3
Answer: Normal sinus rhythm
Nonnal sinus rhythm: Identifying ECG features
Rhythm: Regular
Rate: 60 to 100 Deats/minute
P waves: Normal In size, shape, direction; positive illead II, a positive lead ; one P wave precedes each DRS
complex
PR Interval: Normal (0.12 to 0.20 second)
QRS complex: Normal (0.10 second or less)
6
4
9
7
11
12
10
11
12
Answer: Sinus bradycardia with one PAC (abnormal Pwave associated with
PAC Is hidden In preceding T wave, distorting T-wave contour)
Premature atrial contraction: Identifying ECG features
Rhythm: Underlying rtlythm usually regular; irregular with premature beat
Rate: That of underlying rhythm
P waves: Pwave associated with PAC is premature, abnormal (commonly appears small, upright, and pointed,
but may be inverted or a squiOOIe); abnormal P wave is onen fOlJld hidden in preceding T wave, distorting
T-wave contour
PR Interval: Usually normal, but may be abnormal
ORS complex: Premature, normal duration ORS (0.10 second or less); followed by a pause
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Answer: Normal sinus rhythm with one nonconducted PAC (abnormal P wave associated with PAC is
hidden in preceding T wave, distorting T-wave contour)
Nonconducled PACs: Idenlifying ECG fealures
Rhythm: Underlying rhythm usually regular; Irregular with nooconducted PACs
Rate: That of underlying rhythm
P waves: Premature and abnormal; otten found hidden In preceding T wave, distorting T-wave contour;
a pause follows the noncon<i.Jcted Pwave
PR Interval: Absent with nonconducted PAC
QRS complex: Absent with nonconwcted PAC
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,.
Answer: Atrial flutter wtth 4:1 AV conduction
Atrial flutter. Identifying ECG features
Rhythm: Regular or irregular (depends on AV conduction ratios)
Rate: Atrial: 250 10 400 beals/minute
Ventricular: Varies wiltl number of impulses conducted through AV node; will be less Ihan
the atrial rate
P waves: Sawtooth wave deflectioos affecting Itle entire baseline
PR Interval: Not measurable
QRS complex: Normal (0.10 second or less)
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Answer: Second-degree AV block., Mobitz II with 3:1 AV conduction (one P wave hidden on top ofT wave)
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4e