Escape rhythms
Impulse initiated by a latent pacemaker because the SA node rate has slowed is called
an escape beat
Persistent impairment of SA nodeseries of escape beats called escape rhythm
o Enhanced automaticity of latent pacemakers
Latent pacemakers can assume control of impulse formation if its intrinsic rate is higher
than that of the SA node
Ectopic beatectopic rhythm
o Abnormal automaticity
Cardiac tissue injury leads to cells outside the conduction system acquiring automaticity
If the pace outruns the SA node, these cells become the source of an abnormal ectopic
rhythm
o Triggered activity
Action potentials can trigger
abnormal depolarizations that
lead
to extra heart beats or
tachyarrhythmias
First action potential
leads to oscillations of
membrane voltage
called
afterdepolarizations
Two types of
afterdepolarization
Early: during repolarization phase of inciting beat
o Can occur during phase 2 or 3.
Phase 2: mostly inward calcium current
Phase 3: mostly sodium channels
o More likely in conditions that prolong QT interval
o Could be the initiating mechanism of torsade de pointes
Delayed: after repolarization has
completed
o Develop in states of high
intracellular calcium
Digitalis
intoxication
Catecholamine
stimulation
o Intracellular calcium
accumulation activates
chloride currents or Na/Ca
exchanger
Altered impulse conduction
o Conduction block
Propagating impulse is blocked when It encounters a region of the heart that is
electrically unexcitable
Can be:
Transient
Permanent
Unidirectional
Bidirectional
Conditions that cause this:
o
Ischemia
Fibrosis
Inflammation
Certain drugs
Functional blocks occur when a propagating impulse encounters cardiac cells that are
still refractory
Fixed blocks occur when a block is caused by a barrier imposed by fibrosis or scarring
that replaces myocytes
AV block removes normal overdrive suppression
Unidirectional block and reentry
o Electric impulse circulates repeatedly around a reentry path, recurrently depolarizing a region of
cardiac tissue
o Normally, refractory period of each
cell prevents immediate reexcitation
from adjacent cells
o Conduction block that prevents rapid
depolarization of parts of the
myocardium can create an
environment for continued
propagation and reentry
o action potential can conduct in a
retrograde direction, but not an
anterograde direction
o 2 conditions required:
unidirectional block
slowed conduction through
reentry path
usually appears as monomorphic tachycardia on ECG
polymorphic tachycardia is where the QRS shape varies
Bad news bears if you go polymorphic VTVF
Accessory pathways and Wolff-Parkinson-White Syndrome
o Affects 1 in 1,500 people
o Additional accessory pathway between ventricle
and atrium
Bypasses the AV node
Bundle of Kent
Spans the AV groove somewhere along the
mitral or tricuspid annuli
Accessory tissue conducts impulses faster
than the AV node
Leads to pre-excitation
o Signs on EKG
Shortened PR
Delta wave
Widened QRS
Physiologic basis of Antiarrhythmic therapy
o Bradyarrhythmias
Doesnt always require treatment
Transient pharmacotherapy
Anticholinergic drugs
1-blockers
Implanted pacemakers for sustained therapy
o Tachyarrhythmias
Goals:
Protect the patient from consequences of arrhythmia
Correct mechanism responsible for abnormality
Pharmacologic agents
To eliminate rhythms from increased automaticity:
o Reduce slope of phase 4 spontaneous depolarization
o Make the diastolic potential more negative (hyperpolarize)
o Make threshold potential less negative
To interrupt reentrant circuits:
o Inhibit conduction o reentry circuit to the point that conduction fails
o Increase refractory period within reentrant circuit
o Suppress premature beats
To eliminate triggered activity:
o Shorten AP duration
Prevent EAD
o Correct conditions of calcium overload
Prevent DAD
Vagotonic maneuvers
Carotid sinus massage
Rub firmly for a few seconds over the carotid sinus
parasympathetic
sympathetic
due to stretching of carotid baroreceptors
o i.e. the carotid body thinks the pressure is too high and baroreflex adjusts
autonomics accordingly
Electric cardioversion and defibrillation
Cardioversionterminate SVT or VT
Sedate the patient
Defibrillationterminate VF
CLEAR!!
Implantable cardioverter-defibrillators
Device continually monitors cardiac activity
Applies therapeutic countershock when needed
Escape rhythms
o SA node activity is impaired or a block
o AV node or His-Purkinje system takes overlatent pacemakers
o Junctional escape rhythms arise form AV node or proximal bundle of His
Normal, narrow QRS complex
40-60 bpm
no P waves because impulse originates below the atrium
retrograde P waves may be observed after QRS
Second-degree AV block
Mobitz type 1 (Wenckebach) block
Degree of AV delay (i.e. PR interval) increases gradually until a QRS gets
dropped
vagal tone
ischemia of AV node
-blockers
CCBs
Digitalis
Structural causes:
MI
Chronic degeneration
Third-degree AV block
Complete heart blockcomplete failure of AV conduction
Complete dissociation of P wave from QRS
Tachyarrhythmias
Supraventricular arrhythmias
Sinus tachycardia
Atrial flutter
Rapid regular atrial activity
180-350 bpm
many impulses reach the AV node during refractory period and dont conduct
o slower ventricular rate
Sawtooth appearance on EKG
To fix it:
o Electrical cardioversion
o Rapid atrial stimulation
o Pharmacologic intervention
-blockers
CCBs (verapamil, diltiazem)
Digoxin
Atrial fibrillation
Very fast atrial rate (350-600 /min)
Distinct P wave not discernible on EKG
Average ventricular rate in untreated AF is ~140-160 bpm
Mechanism is probably multiple wandering reentrant circuits within the atria
Things to worry about:
o Rapid ventricular rates could compromise cardiac output
LV hypertrophy
Pulmonary edema
o Stasis of blood within the atria
Formation of thrombusstroke
Treatment:
o Ventricular rate control
-blockers
CCBs (diltiazem, verapamil)
Digitalis is NOT effective unless ventricular contractile function is
concomitantly impaired
o Try to restore sinus rhythm
Chemical or electrical cardioversion
Maze procedure
Multiple incisions to prevent formation of reentry circuits
Percutaneous catheter ablation
Cauterize left atrium around pulmonary veins
Last resort is catheter ablation of AV node
o Prevention of thromboembolism
Terminate reentry
o Valsalva
o Carotid sinus massage
o IV adenosine
o IV CCBs
o IV -blockers
Preventative:
Oral -blockers, CCBs or digoxin
Catheter ablation if those dont work
Treatment:
o Greater caution is needed than with AVNRT
o Same drugs block conduction in normal AV node,
but often do not work on accessory pathways
Sometimes they even shorten refractory
period on accessory pathway and lead to
even faster rates of ventricular tachycardia
o Preferred drugs:
Sodium channel blockers (Class IA and IC
antiarrhythmics)
Class III antiarrhythmics
These slow conduction in the accessory
pathway
o If accompanied by hemodynamic collapse, wide
QRS tachycardia must be cardioverted
If hemodynamically stable:
IV procainamide (class IA)
Ibutilide (class III)
Lown-Ganong-Levine syndrome
o Short PR, but normal, narrow QRS
No delta wave
PSVT from concealed accessory pathway
Can result in orthodromic AVRT under the right conditions
Management is the same as for patients with AVNRT
Focal atrial tachycardia
Results from automaticity of atrial ectopic site or reentry
Looks like sinus tachycardia, but P wave has a different morphology
o Suggests atopic depolarization
Can be caused by digitalis toxicity
Can be exaggerated during sympathetic elevation
Vagal maneuvers have no effect on these
Treatment:
o -blockers
o CCBs
o Class IA, IC, III antiarrhythmics
o Catheter ablation as last resort
Multifocal atrial tachycardia
EKG shows irregular rhythm with multiple (>3) P wave morphologies
Average atrial rate is >100 bpm
o
Ventricular arrhythmias
Ventricular premature beats
AP from ectopic ventricular focus
EKG:
o Widened QRS not related to P wave
Can occur in:
o Bigeminyevery 2 beats
o Trigeminyevery 3 beats
o Quadrigeminyevery 4 beats
o Couplets2 in sequence
o Triplets3 in sequence
Ventricular tachycardia
Series of 3 or more VPBs
2 flavors:
o Sustained VT
> 30 seconds
produces syncope
requires cardioversion or drugs
o Non-sustained VT
Self-terminating
Both commonly found in patients with structural heart disease
EKG:
o Wide QRS (>0.12 sec)
o 100-200 bpm or faster
Can be categorized by QRS
o Monomorphictheyre all the same
Structural abnormality that supports reentry circuit
Maybe from old infarction/scar
o Polymorphictheyre not the same
Multiple ectopic foci
Most commonly caused by
Acute myocardial ischemia/infarction
Torsades de pointes
Management
o Cardioversion
o Antiarrhythmic drugs
Torsades de Pointes
Polymorphic VT
Varying amplitudes of QRS
Causes:
o EAD with QT prolongation
Can result from hypokalemia or hypomagnesemia
Can result from persistent bradycardia
Can result from drugs that block potassium currents
o
Ventricular fibrillation
Immediately life-threatening arrhythmia
Disordered, rapid stimulation of ventricles with no coordinated contractions
Must cardiovert, or patient dies