Physiology
What structure normally sets the heart’s intrinsic rate at 60–100 bpm and initiates organized atrial depolarization?
SA Node
Fibrosis or dilation of this chamber predisposes to atrial fibrillation.
Left Atrium
Major ECG risk associated with sotalol.
torsades de pointes
This noninvasive ultrasound is first-line for evaluating atrial size and valvular disease.
transthoracic echocardiogram echocardiogram (TEE)
Cardiac biomarkers are negative in both stable and unstable angina because this does NOT occur.
The AV node has slow conduction velocity primarily because phase 0 depolarization depends on this channel type.
Loss of this mechanical event in AF contributes to decreased cardiac output, especially in diastolic dysfunction.
Atrial Kick
AF with a ventricular rate >200 bpm and delta waves on prior ECG is a contraindication to this medication class.
AV nodal blockers (beta-blockers, CCBs, digoxin, adenosine)
In WPW, there is an accessory pathway (Bundle of Kent) that bypasses the AV node. The AV node contributes a refractory period. If you use AV nodal blockers, you will block the AV node and not the accessory pathway, therefore increasing the HR as all electrical impulses are now being channeled through the accessory pathway.
This imaging modality is used before cardioversion to rule out left atrial appendage thrombus.
transesophageal echocardiogram (TEE)
4–24 hours: coagulative necrosis with infiltration of these cells begins.
Neutrophils
In atrial fibrillation, the ventricular rate is determined primarily by the refractory properties of this structure, not by atrial firing rate.
AV Node
AF results from multiple re-entrant circuits causing chaotic atrial depolarization at rates of this range.
300-600 bpm
This antiarrhythmic blocks potassium channels and prolongs phase 3 repolarization.
Amiodarone
Polymorphic VT following initiation of sotalol in an AF patient is due to prolongation of this interval.
QT Interval
A patient develops fever, pleuritic chest pain, and pericardial friction rub weeks after MI due to this immune-mediated complication.
Dressler syndrome
Increased vagal tone prolongs this ECG interval.
PR Interval
Histologically, long-standing AF is associated with increased deposition of this extracellular matrix protein, disrupting conduction pathways.
collagen (atrial fibrosis)
These four clotting factors are inhibited by warfarin.
II, VII, IX, and X
An ECG shows AF plus broad, notched P waves in previous tracings. This structural abnormality likely preceded development of AF.
Left atrial enlargement.
Unfractionated heparin works by potentiating this endogenous anticoagulant.
Antithrombin III
The His-Purkinje system conducts impulses rapidly due to high density of these channels and large fiber diameter.
Fast sodium channels
A 72-year-old man with hypertension and diabetes presents with new AF of unknown duration. He is hemodynamically stable. ECG shows irregularly irregular rhythm at 120 bpm. Echo shows left atrial enlargement.
Before rhythm control is attempted, management must prioritize prevention of this complication due to stasis in the left atrial appendage.
Thromboembolic Stroke
A patient with AF has a ventricular rate of 160 bpm. After IV diltiazem, the rate slows to 90 bpm but the atrial rate remains >300 bpm. This demonstrates that the drug primarily acts on this phase of the nodal action potential.
Phase 0 calcium-dependent depolarization in AV nodal cells
A 26-year-old man presents with sudden palpitations and lightheadedness. Blood pressure is 108/64 mmHg.
ECG shows:
Irregularly irregular rhythm
Ventricular rate varying between 180–240 bpm
QRS complexes are wide and vary in morphology beat-to-beat
No identifiable P waves
Prior ECG (1 year ago) showed a short PR interval and delta waves
What is the most appropriate next step in management?
A) IV diltiazem
B) IV metoprolol
C) IV adenosine
D) IV procainamide
E) IV digoxin
IV procainamide
A patient 5 days after a transmural MI suddenly develops hypotension and a new systolic murmur. Echocardiogram shows severe mitral regurgitation. The most likely underlying pathologic event is necrosis and rupture of this structure.
Posteromedial papillary muscle