A 43-year-old man is evaluated for occasional palpitations provoked by anxiety. The patient describes a sudden-onset pounding sensation in the chest followed by lightheadedness and shortness of breath. He has never had syncope. The patient has no history of heart disease, and family history is unremarkable. After initial evaluation, he is treated with verapamil and reports marked improvement in the frequency of palpitation episodes. The tracing below shows the electrical activity of a specific type of cardiac cell in the patient's heart. Which of the following effects would verapamil administration most likely have on these cells?

Question

A 43-year-old man is evaluated for occasional palpitations provoked by anxiety.  The patient describes a sudden-onset pounding sensation in the chest followed by lightheadedness and shortness of breath.  He has never had syncope.  The patient has no history of heart disease, and family history is unremarkable.  After initial evaluation, he is treated with verapamil and reports marked improvement in the frequency of palpitation episodes.  The tracing below shows the electrical activity of a specific type of cardiac cell in the patient's heart.  Which of the following effects would verapamil administration most likely have on these cells?

Quizplus · Accepted Answer

11ec160b_3c84_2fe9_9249_474ef89fd878_MD0001_00 The above tracing demonstrates the action potential of cardiac pacemaker cells in cardiac slow-response tissues such as the sinoatrial (SA) and atrioventricular (AV) nodes. The pacemaker action potential includes the following phases: Phase 4 (spontaneous depolarization) begins after hyperpolarization triggers the opening of HCN channels that allow slow influx of Na⁺ ("funny current"). T-type (transient) Ca²⁺ channels then open once the membrane potential becomes more positive, allowing Ca²⁺ influx to contribute to depolarization. As the pacemaker cell approaches threshold, L-type (long-lasting) Ca²⁺ channels begin to open, which further increases Ca²⁺ influx and significantly decreases the time until threshold is reached. Phase 0 (upstroke) is characterized by continued opening of L-type Ca²⁺ channels. In cardiac slow-response tissues, the action potential upstroke is much slower and transitions gradually from phase 4 due to the relatively slow influx of Ca²⁺ into the cell. Phase 3 (repolarization) is characterized by the opening of K⁺ channels and efflux of K⁺ from the cell in conjunction with the closure of L-type Ca²⁺ channels. This patient's anxiety-provoked episodes of sudden-onset palpitations associated with lightheadedness and shortness of breath are consistent with paroxysmal supraventricular tachycardia. Class IV antiarrhythmics (eg, verapamil, diltiazem) are commonly used to prevent recurrent nodal tachyarrhythmias such as PSVT. They work by blocking L-type calcium channels in cardiac slow-response tissues, which causes slowing of phase 4 depolarization and reduced conduction velocity in the SA and AV nodes. (Choice A) Verapamil decreases the amount of intracellular calcium available for excitation-contraction coupling within cardiac myocytes. This reduces myocardial contractility, which can be harmful in patients with impaired ventricular function. However, the tracing shown in the question stem corresponds to pacemaker action potentials, not cardiac myocyte action potentials. (Choices B and C) The threshold potential refers to the amount of depolarization required to initiate an action potential. Class I (sodium channel blockers) and class IV (calcium channel blockers) antiarrhythmics raise the threshold potential of cardiac fast- and slow-response tissues, respectively, by blocking the channels that trigger an action potential. This effect also results in reduced action potential amplitude, decreased upslope, and reduced impulse conduction speed within the respective tissues. (Choice D) Verapamil's calcium blocking activity reduces the action potential duration in nodal tissues, but it also increases the refractory period by slowing the recovery of inactivated calcium channels. Class IA (eg, quinidine) and class III (eg, amiodarone) antiarrhythmics also increase the refractory period by blocking potassium channels and prolonging repolarization. Educational objective: Class IV antiarrhythmics (eg, verapamil, diltiazem) are commonly used to prevent recurrent nodal arrhythmias (eg, paroxysmal supraventricular tachycardia). They work by blocking calcium channels in slow-response cardiac tissues, slowing phase 4 (spontaneous depolarization) and phase 0 (upstroke). This reduces impulse conduction velocity in the sinoatrial and atrioventricular nodes. __________ References: Class IV antiarrhythmic agents: new compounds using an old strategy. (http://www.ncbi.nlm.nih.gov/pubmed/25354181) Antiarrhythmic and anti-ischemic properties of calcium-channel antagonists. (http://www.ncbi.nlm.nih.gov/pubmed/8689275)

A 43-Year-Old Man Is Evaluated for Occasional Palpitations Provoked by Anxiety