Cardiac Arrhythmias - Berger/Rubinstein Flashcards Preview

M2 Cardiovascular > Cardiac Arrhythmias - Berger/Rubinstein > Flashcards

Flashcards in Cardiac Arrhythmias - Berger/Rubinstein Deck (29)

What disorders give rise to bradyarrhythmias?


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.


In AV Nodal reentrant tachycardia, two AV pathways are present. Generally, one is fast with a unidirectonal block. The other has slowed conduction.

What is the most typical pathway traced by the reentry?

How does it present on ECG?

Usuually, anterograde (A>>V) is over the slow pathway, with retrograde over the fast/unidirectional pathway.

P waves become superimposed on QRS. (In reverse, P waves are inverted)


AV reentrant tachycardia, a bypass tract is present that bridges the AV groove. Name an example of this condition...

What is a "concealed" AV reentrant tachycardia?

Wolff-Parkinson-White syndrome.

Concealed means that the bypass tract can only conduct retrograde potentials (promotes supraventricular tachycardia).


Describe the ECG findings in SINUS RHYTHM Wolff-Parkinson-White syndrome.

Distinguish between antidromic and orthodromic tachycardias.

The PR segment shortens, QRS widens, and a delta wave is present. 

Orthodromic: Anterograde impulse is through the AVN (bypass is retrograde), so no delta wave. Antidromic is reversed; anterograde through bypass and retrograde through AVN.


Why is atrial fibrillation dangerous for WPW patients?

If atrial impulses are allowed to bypass the AVN, ventricular tachycardia will develop.


How is Wolff-Parkinson-White syndrome treated?

Amiodarone or procainamide. Cardioversion in acute episodes. Catheter ablation as definitive therapy to destroy the bypass tract.

Avoid drugs that shorten ERP (Digoxin, beta blockers, CCBs).


Describe how ventricular premature beats are analogous to atrial premature beats.

When is treatment of PVCs necessary? With what?

Both result from ectopic focal activity. Both are often benign and seen in healthy hearts. They do not always cause contraction of the other compartment.

If PVCs are frequent (>20% of complexes, "high density"), treat with beta blockers and/or ablation of the active sites.


What defines a ventricular tachycardia? A sustained VT?

What are the two subtypes of VT?

At least 3 PVCs; sustained if occurring for >30sec. HR > 100bpm, QRS widening.

Monomorphic, and polymorphic.


How does a monomorphic VT appear on ECG?

How does a polymorphic VT appear on ECG?

Identical and regular QRS complexes, generally widened.

Wildly changing shape and rate of QRS complexes. 


What causes sustained monomorphic VT?

What causes polymorphic VT?

Reentry, usually resulting from a myocardial scar or structural disease.

Multiple ectopic foci or changing reentrant circuit. Long QT, acute ischemia/infarction, abnormalities of structure and channels...


Where is Torsades de Pointes seen?

How is it treated?

What are its symptoms?

In patients with QT prolongation (due to drugs, bradycardia, metabolic disturbances, or congenital)

Cardioversion, IV magnesium, and correction of underlying abormalities (eg QT shortening with beta agonists/pacing)

Syncome, lightheadedness, and cardiac death.


Describe the pathophysiology of congenital long QT syndrome.

Mutations in ion channels that prolong the action potential, allowing EADs:

Mutations of potassium channels (decrease outward flow >> slower repolarization)

Mutation in sodium channel (failure of inactivation >> longer AP)


How should a patient with unstable VT be treated?

What are the long-term treatments for VT?

Electrical cardioversion. Zap-zap!

Implantable cardioversion, ablation, antiarrhythmic drugs.


Why is V-fib immediatley lfe-threatening?

How does it appear on ECG?

How is it treated?

Lack of coordinated ventricular contraction means that cardiac output is zero.

No QRS complexes at all, just apparent noise.

Treat with immediate defibrillation. IV amiodarone? Implantable cardiodefibrillator thereafter.


Try to diagnose some of these, for practice:

Broad complex QRS at regular intervals.

Narrow complex QRS without normal rhythm. "Irregularly irregular"

1:1 P/QRS relationship with long PR interval.

Abscence of some QRS complexes following P waves.

Sinus rhythm, HR 80, with small bump preceding R wave.

Ventricular tachycardia, or SVT "with aberrancy".

Atrial fibrillation