Cardiac Arrhythmias - Berger/Rubinstein Flashcards
What disorders give rise to bradyarrhythmias?
Tachyarrhythmias?
Impaired impulse formation or conduction.
Increased automaticity, triggering, and re-entry.
What are some physiological causes for sinus bradycardia?
What are some pathological causes for it?
In resting athletes, and during sleep, heart rate can drop below 60bpm. This is not abnormal.
Sick sinus syndrome
Distinguish between a ventricular and junctional escape rhythm.
Junctional: Faster (40-60bpm), with either no P wave or an inverted, retrograde one.
Ventricular: Slower (30-40bpm), with QRS widening.
What is the defining characteristic of a first-degree AV block?
What are some potential causes of it?
PR prolongation, otherwise normal sinus rhythm.
ANS activity, drugs, transient ischemia (all reversible), damage from MI, degeneration from aging (irreversible).
How does a Mobitz I AV block appear on ECG?
How does a Mobitz II AV block appear on ECG?
Which is also termed “Wenckebach”?
PR duration lengthening until a QRS complex is dropped, then repeat.
Intermittent loss of QRS without PR lengthening. QRS widening.
Mobitz I = Wenckebach.
In Mobitz II AV block, where is the block located?
How should it be treated?
What can cause it?
Distal to the AV node (hence QRS widening).
Implantation of a pacemaker (may progress to third degree block).
Product of scar/infarct, or degeneration of conduction system.
Describe the appearance of third-degree AV block on ECG.
Why does it look this way?
Dissociation of the P and QRS wave rhythms. Some widening of QRS.
In a complete block, the latent pacemakers handle ventricular contraction, which happens at a slower pace than the atria. QRS widening of escape occurs distal to AVN.
What are some physiological causes of sinus tachycardia?
Exercise, stress, fever, anemia, hypoxia, hypovolemia, hyperthyroidism.
What can cause atrial premature beats?
How does it present on ECG?
Automaticity in an ectopic locus.
Extra or early P waves, which may be conducted to the ventricles.
Describe the reentry pattern seen in atrial flutter.
Describe its appearance on ECG.
Usually counterclockwise around the right atrium. Sometimes clockwise.
A “saw tooth” pattern with extra P waves. Sometimes 1:1 AV involvement.
How is atrial flutter treated?
What are its predisposing factors?
Rate control (beta blockers, CCBs, digoxin) and rhythm control (electrical cardioversion, pace termination, catheter ablation, class I/III antiarrhythmics). Avoid drugs that slow atrial conduction?
Prior heart surgery, coronary disease, cardiomyopathy.
What is the primary complication of Atrial flutter/fibrillation?
How is it avoided?
Stroke from atrial thrombus formation.
Assessment with CHADS2VASc scoring, oral aspirin/anticoagulants (dabigatran, warfarin, rivaroxaban, apixaban)
Describe the pathophysiology of atrial fibrillation.
How does it appear on ECG?
Chaotic, rapid (>400/min) discharges in various atrial loci disorganized muscle activity, which is occasionally transmitted to the ventricles.
“Irregularly Irregular” QRS complexes, abscence of clear P waves.
Besides stroke, what complications can result from atrial fibrillation?
How is A-fib treated?
Involvement of the ventricles can result in systemic symptoms; hypotension or heart failure.
Anticoagulation to avoid stroke, rate control (beta blockers, CCBs, digoxin), and restoration of normal sinus rhythm (cardioversion, catheter ablation, antiarrhythmics)
Distinguish between the pathophysiologies of AV nodal reentrant tachycardia and AV reentrant tachycardia.
In AV nodal reentrance, the abnormal pathway is within the AV node.
In AV reentrance, the abnormal pathway crosses the AV groove.