Dysrhythmias: Table 33-13

CHAPTER 33 Cardiovascular Emergencies 477
Table 33-13 OVERVIEW OF GLYCOPROTEIN IIB/IIIA INHIBITORS

Glycoprotein IIB/IIIA
inhibitor Dosage Potential side effects
Abciximab (ReoPro) 0.25 mg/kg over 10-60 min Potential for increased bleeding, hypotension, bradycardia, nausea and
0.125mg/kg/min for 12 hr vomiting, diarrhea
Eptifibatide (Integrilin) 180 mcg/kg over 1 to 2 min Potential for increased bleeding, hypotension
2 mcg/kg/min for up to 72 hr
Tirofiban HCL (Aggrastat) 0.4 mcg/kg/min for 30 min Potential for increased bleeding, nausea, bradycardia
0.1 mcg/kg/min for 12-24 hr
Another aspect of management of non-ST elevation acute

coronary syndromes is the use of glycoprotein IIB/IIIA in- Box 33-3 SYSTEMATIC EVALUATION
hibitors. Platelet adhesion, activation, and aggregation play OF CARDIAC RHYTHMS
major roles in development of thrombus, which can potenti-
ate evolution of these acute coronary syndromes into an RATE
AMI. Glycoprotein IIB/IIIA inhibitors antagonize or inhibit Bradycardia: 60 beats/min
the receptor sites, which inhibits platelet aggregation. It has Normal rate: 60 to 100 beats/min
been demonstrated that these reduce risk for development of Tachycardia: 100 beats/min
thrombus independent of aspirin and heparin therapies. Re-
fer to Table 33-13 for an overview of these agents.4,17,22,31,34
RHYTHM
Is the rhythm regular or irregular?
Dysrhythmias P WAVES
Are P waves present? Does one P wave appear before each
Blood flow deprivation to the myocardium as a result of QRS? Is P wave deflection normal?
AMI can affect the heart’s electrical conduction system,
causing various dysrhythmias. Table 33-14 summarizes dys- QRS COMPLEX
rhythmias and categories of antidysrhythmics according to Normal is 0.06 to 0.12 second. Are the QRS complexes nor-
modified Vaughan-Williams classification schema. By un- mal shape and configuration?
derstanding drug classifications, the emergency nurse can
anticipate expected action of the drug and nursing implica- P/QRS RELATIONSHIP
tions for drug administration and patient assessment.17,22,34 Does QRS complex follow every P wave?
PVCs are the most common dysrhythmia associated with PR INTERVAL
cardiac ischemia and AMI, occurring in approximately 85%
Normal is 0.12 to 0.2 second. Is the interval prolonged?
of patients with AMI. After initiation of oxygen therapy, li- Shortened?
docaine is the drug of choice for symptomatic PVCs. Lido-
caine may be used prophylactically for AMI patients, even
without PVCs, because of the high incidence of ventricular
tachycardia and ventricular fibrillation that occurs without tion, infection, degenerative changes in the conduction sys-
warning dysrhythmias. Some studies suggest that prophy- tem, rheumatic heart disease, and medications such as beta
lactic use of lidocaine in patients with AMI may increase blockers, calcium channel blockers, and cardiac glycosides.
mortality; therefore, lidocaine use must be considered with Management of symptomatic bradycardias and heart blocks
respect to potential adverse effects. PVCs may also be includes drugs such as atropine and epinephrine. An exter-
caused by hypoxemia, acidosis, alkalosis, electrolyte imbal- nal pacemaker or transvenous pacemaker may also be used.
ances, digoxin toxicity, and bradycardia.6 The underlying Second-degree Mobitz I heart block, associated with a con-
mechanism responsible for the patient’s PVCs should be duction defect through the AV node, is usually benign and
evaluated and treated. transient. This rhythm is commonly associated with inferior
Bradycardia is defined as a heart rate less than 60 beats infarction because the right coronary artery supplies this
per minute and occurs in approximately 65% of AMI pa- area and the AV node. Second-degree Mobitz II AV block
tients, particularly those with inferior wall infarction. occurs when conduction through the bundle branches is im-
Bradycardic dysrhythmias include AV blocks. Four different paired, usually because of blockage of the left coronary
types occur, depending on area and degree of damage to the artery, which supplies the anterior wall and bundle
conduction system. These AV blocks are referred to as first- branches.6 This form of second-degree block is more likely
degree, second-degree Mobitz I (Wenckebach), second-de- than the other form to progress to third-degree block.
gree Mobitz II, and third-degree or complete heart block. Other dysrhythmias that commonly occur are supra-
Blocks in conduction may be caused by myocardial infarc- ventricular tachycardias, which may be indicative of
Copyright © 2007 by Emergency Nurses Association. Published by Mosby, Inc., an affiliate of Elsevier Inc.
478 CHAPTER 33 Cardiovascular Emergencies
Table 33-14 ANTIDYSRHYTHMIC PHARMACOLOGIC AGENTS AS CLASSIFIED BY MODIFIED

VAUGHAN-WILLIAMS CLASSIFICATION SCHEMA
Pharmacologic Electrophysiologic Drug
Class action effects Indications examplars Comments
I Sodium channel Decreases conduction ve- Ventricular Moricizine Risk of proarrhyth-
blockade (stabi- locity; prolongs PR and dysrhythmias (Ethmozine) mia potential
lizes cell mem- QRS intervals
brane)
IA Blocks and delays repo- Atrial and Quinidine sulfate Observe for heart
larization, thereby ventricular (Quinidex) block, hypotension,
lengthening the action dysrhythmias Procainamide HCL prolonged PR/
potential duration and (Pronestyl) QRS/QT intervals
the effective refractory Disopyramide
period (Norpace)
IB Shortens the action of po- Ventricular Lidocaine HCL Potential toxicity:
tential duration dysrhythmias (Xylocaine) Dizziness, vertigo,
Tocainide HCL confusion, seizures
(Tonocard)
Mexilitene HCL
(Mexitil)
IC Slows conduction of Ventricular Flecainide acetate Risk of proarrhyth-
electrical impulses in dysrhythmias (Tambocar) mia potential
atria, AV node, and Propafenone
ventricular/His
(Rhythmol)
Purkinje fibers
II -adrenergic Inhibition of the sympa- Supraventricular Propranolol HCL Observe for hypoten-
blockade thetic stimulation— & ventricular (Inderal) sion, bradycardia,
reducing heart rate and dysrhythmias Esmolol HCL heart block
decreasing myocardial (Brevibloc)
irritability and shortens Acebutolol
action potential (Sectral)
III Potassium channel Delayed repolarization Ventricular Amiodarone HCL Observe for exacer-
blockade and prolongation of the tachycardia (Cordarone) bation of dysrhyth-
action potential, thus de- and ventricular Dofetilide mias, hypotension
creasing myocardial irri- fibrillation (Tikosyn)
tability Ibutilide fumarate Pulmonary fibrosis
(Corvert) may occur with
amiodarone use
IV Calcium channel Slows conduction of elec- SVT and atrial Verapamil (Calan) Observe for hypoten-
blockade trical impulses and de- dysrhythmias Diltiazem sion, bradycardia,
creases rate of impulse (Cardizem) heart block
initiation Nifedipine
(Procardia)
Unclassified Potassium channel Slows conduction through SVT Adenosine Has very rapid effect,
opener AV node and increases (Adenocard) short half-life
refractory period in AV
node
HCL, Hydrochloride; AV, atrioventricular; SVT, supraventricular tachycardia.
myocardial ischemia or anterior wall infarct. Often asso- rapamil, and procainamide, and vagal maneuvers or syn-
ciated with chest pain, tachycardias are dangerous be- chronized cardioversion.
cause they increase myocardial oxygen consumption and Evaluation of dysrhythmias requires a systematic ap-
may extend the infarct. Treatment depends on clinical proach (Box 33-3). An overview of each rhythm is pre-
findings. For hemodynamically unstable patients, therapy sented, including rhythm strip in lead II, significance of the
may include pharmacologic agents such as adenosine, ve- rhythm, and therapeutic interventions for adults.
Impulse travels from

SA to AV node
through His bundle
to Purkinje fibers
Sympathetic
stimulation
SA node originates
impulses at regular
rate of greater
than 100/minute
can lead to fur-
Vagus nerve
SA node originates
impulses at a regular rate
of less than 60/minute
can eradicate the

can decrease cardiac output.
SA node rate varies

with respiration
Atrial origin of
abnormal impulse
Impulse travels from

site above ventricles
through HIS bundle to
Purkinje fibers
Pacemaker
site varies
in the atria
Circus movement
in atria; variable
degree of block
Chaotic impulses from atria;

variable degree of block
can cause congestive heart failure.
High nodal impulse:

inverted P wave
before QRS complex
Middle nodal impulse:

P wave hidden in
QRS complex
Low nodal impulse:

inverted P wave
after QRS complex
SA node originates
impulse; partial block
at AV node.
SA node originates impulse;

partial block at AV node
and temporary pacing.
Partial intermittant
block at AV node.
Complete block at AV node;

may have nodal or ventricular
independent pacemaker
can be used until pacing unit is available. Be prepared to
Ventricular bigeminy
Ventricular trigeminy
Couplet
amiodarone may be used. After ectopy is resolved, IV drip of effective
One ventricular
pacemaker fires
rapidly
lidocaine, or
Ventricular ectopic
sites firing so fast that
quivering results
Slow impulses
from ectopic site
in ventricle
No electrical activity
Pacemakers Two major reasons for lack of capture are acidosis and hy-
Temporary pacing is used when a patient’s condition deteri- poxemia. Evaluate the patient’s oxygen saturation and acid-
orates secondary to a bradycardic or tachycardic dysrhyth- base levels to determine appropriate interventions for such
mia unresponsive to other therapy. Indications for pacing disorders. Another reason for lack of capture is related to the
include severe bradycardia, high-degree AV blocks, atrial external pacing device and pacing electrodes. Check all con-
tachycardia, atrial flutter, and recurrent ventricular tachy- nections. Consider repositioning the posterior electrode to the
cardia. fifth intercostal space, midaxillary line (V6 chest lead posi-
Three methods can be used for pacing—transthoracic, tion). Replace dry pacing electrodes. Make sure contact be-
transvenous, and external (transcutaneous) methods. The tween external pacing electrodes and skin surface is adequate.
transthoracic approach is not used in the ED because of as- Skin should be clean and dry before electrode application;
sociated risks, time required to complete the procedure, and benzoin may be used to improve adherence to the skin.
interference with chest compressions. The transvenous
method involves inserting a catheter electrode percuta- Implanted Cardioverter Defibrillator Therapy
neously into the right atrium or ventricle via the subclavian, The implanted cardioverter defibrillator (ICD) is a device
internal jugular, brachial, or femoral vein. The procedure is that may be used as a treatment modality to reduce the inci-
guided by the changes in the ECG or fluoroscopy. Atrial dence of sudden death from AMI. Approved in 1985, the
pacing is used to suppress atrial tachycardia, whereas ven- ICD monitors the patient’s cardiac rhythm and provides pac-
tricular pacing suppresses ventricular ectopy by overdrive ing or defibrillation to the patient depending on program-
pacing. ming. Newer models can deliver multiple or tiered therapies,
Transcutaneous or external pacing is used more often in antitachycardia pacing (fast pacing), single-chamber ven-
the ED. A negative electrode is placed posteriorly at tricular demand pacing for bradycardia (slow pacing), car-
midthoracic level of the spine with a positive electrode dioversion, or defibrillation shocks.
placed anteriorly at the chest lead V3 position. This posi- ICD generators are implanted under skin and subcuta-
tion provides a lower pacing threshold and is away from neous tissue. Depending on device, the ICD generator may
large skeletal muscles, thus decreasing muscle stimulation. be implanted in the abdomen or upper chest. Older ICD de-
Electrode placement should not interfere with defibrilla- vices require a surgical approach for applying electrodes to
tion. The rate of pacing impulses may be “fixed” (asyn- the epicardial surface of the heart. Newer devices allow sub-
chronous, competitive, or nondemand) or set to fire on de- cutaneous or submuscular insertion of the ICD patch along
mand. A fixed rate delivers electrical current at regular the left anterior axillary line, left midaxillary area, or left
intervals and is usually used when patients have bradycar- posterior area. The lead is then tunneled along the left ante-
dia causing hemodynamic instability; for example, com- rior chest wall and connected to the ICD generator.
plete heart block. The demand pacing mode senses the pa- If the patient requires defibrillation, external defibrilla-
tient’s own QRS complexes and generates an impulse only tion can still be performed. Defibrillator paddles should not
if the patient does not have an intrinsic QRS generated dur- be placed over the ICD generator. If defibrillation attempts
ing a set time frame. Fixed-rate pacing is rarely used be- are unsuccessful, consider anterior-posterior placement of
cause of potential competition with the patient’s own paddles to improve conduction of electrical current around
rhythm or ventricular fibrillation if the pacer discharges on ICD electrodes on the chest wall. Anyone in physical con-
the T wave (relative refractory period) of the patient’s own tact with the patient when the ICD device fires may experi-
cardiac cycle.6 ence a harmless, slight tingling sensation. If the ICD fires in-
Successful pacing depends on condition of the myo- appropriately, the physician can deactivate the device by
cardium. Patients with severe bradycardia, heart block, or placing a magnet over the ICD generator.6
idioventricular rhythm who can generate a pulse with each
QRS complex usually respond to cardiac pacing and have a
better outcome. Patients in asystole are less likely to respond
Acute Ischemic Heart Failure
to pacing. Heart failure (HF) occurs when the myocardium fails to
Factors that indicate successful pacemaker capture—that function adequately as a pump. This inadequacy results in
is, successful electrical stimulation followed by mechanical venous congestion, decreased stroke volume, decreased
response—include combined pacing spike and QRS com- cardiac output, and increased peripheral systemic pres-
plex 0.14 seconds in duration and resolution of the dys- sure. Onset may be gradual or sudden. The primary pre-
rhythmia being treated. Mechanical capture occurs when the cipitating event for HF is some type of myocardial dam-
heart responds to pacing with effective contractions. Me- age that activates many compensatory mechanisms. Over
chanical capture is evaluated by the presence of a pulse con- time, compensatory mechanisms are exhausted and cause
sistent with paced beats. Both types of capture (electrical adverse events. HF rarely occurs at the same time as AMI.
and mechanical) must be present for effective pacing. Assess Development is generally more insidious, occurring over
the patient’s hemodynamic and neurologic response by pal- time. HF may be seen alone or in conjunction with pul-
pating the carotid or femoral pulse, obtaining vital signs, monary edema. The onset of HF is a symptom of an un-
and evaluating the level of consciousness. derlying problem such as AMI, hypertension, fluid overload,

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CHAPTER 33 Cardiovascular Emergencies 477

Table 33-13 OVERVIEW OF GLYCOPROTEIN IIB/IIIA INHIBITORS

Another aspect of management of non-ST elevation acute

Table 33-14 ANTIDYSRHYTHMIC PHARMACOLOGIC AGENTS AS CLASSIFIED BY MODIFIED

HCL, Hydrochloride; AV, atrioventricular; SVT, supraventricular tachycardia.

Impulse travels from

can lead to fur-

can eradicate the

SA node rate varies

Impulse travels from

Chaotic impulses from atria;

can cause congestive heart failure.

High nodal impulse:

Middle nodal impulse:

Low nodal impulse:

SA node originates impulse;

and temporary pacing.

Complete block at AV node;

can be used until pacing unit is available. Be prepared to

amiodarone may be used. After ectopy is resolved, IV drip of effective

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