A 62-year-old woman comes to the emergency department due to palpitations and shortness of breath that began an hour ago. Medical history includes hypertension, coronary artery disease, and paroxysmal atrial flutter. Blood pressure is 108/76 mm Hg and pulse is rapid. ECG shows atrial flutter with a ventricular rate of approximately 150/min. The estimated atrial rate based on ECG flutter waves is 300/min. Which of the following is most likely responsible for the rate difference between the atria and the ventricles?
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Atrial flutter usually involves a reentrant circuit that develops around the cavotricuspid isthmus of the right atrium, resulting in rapid atrial conduction at a rate of approximately 300/min (ie, flutter waves on ECG). Transmission of all of these electrical impulses to the ventricles would be highly problematic as a ventricular rate of 300/min would allow little time for diastolic filling, causing a profound drop in cardiac output and likely leading to sudden cardiac arrest. However, the atrioventricular (AV) node reduces the transmission of impulses from the atria to the ventricles due to the slow inward calcium current that drives the phase 0 depolarization phase of action potentials through the AV node.
A similar AV node slowing effect occurs with atrial fibrillation, which can have atrial rates up to 500-600/min.
(Choice B) A slow inward calcium current also controls the phase 0 depolarization of action potentials in the sinoatrial node. However, the sinoatrial node is suppressed during atrial flutter (and atrial fibrillation) as atrial impulses are driven by abnormal foci of conduction.
(Choices C, D, and E) Fast inward sodium channels control the phase 0 depolarization of both the atrial and the ventricular myocardium, allowing for rapid conduction speeds to be generated. However, the slow calcium channels in the AV node act as a buffer, preventing the transmission of rapid impulses from the atria to the ventricles. Some patients can have an abnormal accessory pathway (driven by fast sodium channels) that directly connects the atria to the ventricles and bypasses the AV node (ie, Wolff-Parkinson-White syndrome). In such patients, rapid atrial arrhythmias can generate dangerously high ventricular rates.
Educational objective:
The slow inward calcium current within the atrioventricular node decreases the transmission rate of rapid impulses generated by the atrial myocardium (eg, atrial fibrillation/flutter), acting as a conduction rate buffer between the atria and the ventricles.