Podcast
Questions and Answers
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) presents to the emergency department with acute onset palpitations. An ECG confirms PSVT originating from the AV node. Considering the electrophysiological mechanisms targeted by antiarrhythmic drugs, which of the following agents is MOST likely to terminate the acute episode while minimizing the risk of inducing ventricular arrhythmias?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) presents to the emergency department with acute onset palpitations. An ECG confirms PSVT originating from the AV node. Considering the electrophysiological mechanisms targeted by antiarrhythmic drugs, which of the following agents is MOST likely to terminate the acute episode while minimizing the risk of inducing ventricular arrhythmias?
- Intravenous verapamil, given its selective blockade of L-type calcium channels in the AV node. (correct)
- Intravenous lidocaine, which primarily targets sodium channels in ventricular tissue and has minimal effect on AV nodal conduction.
- Oral flecainide, as it can terminate re-entrant tachycardias.
- Intravenous amiodarone, due to its broad-spectrum effects on multiple ion channels and prolonged refractoriness.
A patient with atrial fibrillation and rapid ventricular response is being considered for rate control therapy. The patient also has a history of heart failure with reduced ejection fraction (HFrEF). Which of the following rate-controlling agents should be AVOIDED due to the potential for exacerbating the patient's heart failure?
A patient with atrial fibrillation and rapid ventricular response is being considered for rate control therapy. The patient also has a history of heart failure with reduced ejection fraction (HFrEF). Which of the following rate-controlling agents should be AVOIDED due to the potential for exacerbating the patient's heart failure?
- Digoxin, due to its positive inotropic effects and ability to enhance vagal tone.
- Amiodarone, for its sympatholytic action and potential to improve ejection fraction.
- Atenolol, a beta-blocker with minimal negative inotropic effects.
- Diltiazem, a non-dihydropyridine calcium channel blocker. (correct)
A patient with a history of frequent premature ventricular contractions (PVCs) is started on mexiletine. After several weeks, the patient reports new-onset paresthesias, tremor, and nausea. Which of the following is the MOST appropriate next step in managing this patient?
A patient with a history of frequent premature ventricular contractions (PVCs) is started on mexiletine. After several weeks, the patient reports new-onset paresthesias, tremor, and nausea. Which of the following is the MOST appropriate next step in managing this patient?
- Discontinue mexiletine due to the high likelihood of drug-related neurotoxicity and/or gastrointestinal toxicity. (correct)
- Increase the dose of mexiletine to achieve therapeutic drug levels.
- Add a beta-blocker to reduce the frequency of PVCs, while continuing mexiletine at the same dose.
- Prescribe an antiemetic to manage the nausea, while continuing mexiletine at the same dose.
A patient with persistent atrial fibrillation undergoes successful electrical cardioversion to restore sinus rhythm. However, within a week, the atrial fibrillation recurs. Considering the electrophysiological mechanisms involved in maintaining sinus rhythm and preventing recurrence of atrial fibrillation, which of the following antiarrhythmic drug classes is MOST effective at preventing atrial remodeling and subsequent recurrence?
A patient with persistent atrial fibrillation undergoes successful electrical cardioversion to restore sinus rhythm. However, within a week, the atrial fibrillation recurs. Considering the electrophysiological mechanisms involved in maintaining sinus rhythm and preventing recurrence of atrial fibrillation, which of the following antiarrhythmic drug classes is MOST effective at preventing atrial remodeling and subsequent recurrence?
A clinician is treating a patient with Wolff-Parkinson-White (WPW) syndrome who presents with atrial fibrillation with rapid ventricular pre-excitation, resulting in hemodynamic instability. Which of the following antiarrhythmic medications is CONTRAINDICATED in this clinical scenario due to the risk of accelerating conduction over the accessory pathway and potentially causing ventricular fibrillation?
A clinician is treating a patient with Wolff-Parkinson-White (WPW) syndrome who presents with atrial fibrillation with rapid ventricular pre-excitation, resulting in hemodynamic instability. Which of the following antiarrhythmic medications is CONTRAINDICATED in this clinical scenario due to the risk of accelerating conduction over the accessory pathway and potentially causing ventricular fibrillation?
Given the increased mortality observed in clinical trials with antiarrhythmic drug (AAD) use due to proarrhythmic adverse medication reactions and limited efficacy, what advanced electrophysiological intervention has emerged as a more definitive treatment strategy, particularly for paroxysmal supraventricular tachycardia (PSVT)?
Given the increased mortality observed in clinical trials with antiarrhythmic drug (AAD) use due to proarrhythmic adverse medication reactions and limited efficacy, what advanced electrophysiological intervention has emerged as a more definitive treatment strategy, particularly for paroxysmal supraventricular tachycardia (PSVT)?
A patient with a history of atrial fibrillation and heart failure presents to the emergency department with symptomatic, rapid ventricular response. Considering the risks and benefits of AADs, which initial intervention strategy reflects current best practices?
A patient with a history of atrial fibrillation and heart failure presents to the emergency department with symptomatic, rapid ventricular response. Considering the risks and benefits of AADs, which initial intervention strategy reflects current best practices?
Considering the limitations and toxicities associated with long-term amiodarone use, what proactive monitoring protocol is most critical for detecting early signs of pulmonary fibrosis in an asymptomatic patient?
Considering the limitations and toxicities associated with long-term amiodarone use, what proactive monitoring protocol is most critical for detecting early signs of pulmonary fibrosis in an asymptomatic patient?
A patient with a history of structural heart disease develops sustained monomorphic ventricular tachycardia (VT) refractory to initial antiarrhythmic interventions. Beyond acute management, what long-term strategy provides the most robust protection against sudden cardiac death?
A patient with a history of structural heart disease develops sustained monomorphic ventricular tachycardia (VT) refractory to initial antiarrhythmic interventions. Beyond acute management, what long-term strategy provides the most robust protection against sudden cardiac death?
In a patient presenting with atrial fibrillation and a contraindication to anticoagulation, which intervention offers the most comprehensive approach to stroke risk reduction while mitigating the need for chronic antithrombotic therapy?
In a patient presenting with atrial fibrillation and a contraindication to anticoagulation, which intervention offers the most comprehensive approach to stroke risk reduction while mitigating the need for chronic antithrombotic therapy?
A patient with known Brugada syndrome experiences a syncopal episode. What is the most appropriate next step in management?
A patient with known Brugada syndrome experiences a syncopal episode. What is the most appropriate next step in management?
Which of the following statements correctly describes the mechanism of action of adenosine in terminating paroxysmal supraventricular tachycardia (PSVT)?
Which of the following statements correctly describes the mechanism of action of adenosine in terminating paroxysmal supraventricular tachycardia (PSVT)?
A patient with a history of long QT syndrome presents with Torsades de Pointes. Which immediate treatment is most appropriate to stabilize the patient?
A patient with a history of long QT syndrome presents with Torsades de Pointes. Which immediate treatment is most appropriate to stabilize the patient?
In the management of atrial fibrillation, what is the primary rationale for performing electrical cardioversion?
In the management of atrial fibrillation, what is the primary rationale for performing electrical cardioversion?
Considering the complex interplay between efficacy, safety, and non-pharmacological alternatives in arrhythmia management, under what specific clinical circumstances would the initiation of amiodarone therapy be most justifiable, despite its known risks, in a patient presenting with symptomatic, recurrent atrial fibrillation?
Considering the complex interplay between efficacy, safety, and non-pharmacological alternatives in arrhythmia management, under what specific clinical circumstances would the initiation of amiodarone therapy be most justifiable, despite its known risks, in a patient presenting with symptomatic, recurrent atrial fibrillation?
In a patient with chronic atrial fibrillation and concomitant moderate hepatic dysfunction, what specific alterations to sotalol dosing and monitoring would be most critical to implement, considering both its renal and potential hepatic clearance pathways, to mitigate the risk of proarrhythmia and other adverse effects?
In a patient with chronic atrial fibrillation and concomitant moderate hepatic dysfunction, what specific alterations to sotalol dosing and monitoring would be most critical to implement, considering both its renal and potential hepatic clearance pathways, to mitigate the risk of proarrhythmia and other adverse effects?
Considering the limitations and potential for increased mortality associated with antiarrhythmic drugs, in which specific patient population with atrial fibrillation would a rhythm control strategy employing AADs be most likely to demonstrate a clinically significant improvement in long-term outcomes, outweighing the inherent risks of the medication?
Considering the limitations and potential for increased mortality associated with antiarrhythmic drugs, in which specific patient population with atrial fibrillation would a rhythm control strategy employing AADs be most likely to demonstrate a clinically significant improvement in long-term outcomes, outweighing the inherent risks of the medication?
In a patient with HFrEF and recurrent symptomatic AF, who has failed treatment with an ARNI, SGLT2i, and has a CIED in place with optimized settings, what pharmacologic approach would be most appropriate to reduce early AF recurrence post-ablation, considering the potential adverse electrophysiological remodeling caused by long term use of AADs?
In a patient with HFrEF and recurrent symptomatic AF, who has failed treatment with an ARNI, SGLT2i, and has a CIED in place with optimized settings, what pharmacologic approach would be most appropriate to reduce early AF recurrence post-ablation, considering the potential adverse electrophysiological remodeling caused by long term use of AADs?
Given the increasing reliance on non-pharmacological interventions for arrhythmia management, under what specific circumstances would pharmacological cardioversion with intravenous ibutilide be most appropriate as a first-line strategy in a hemodynamically stable patient presenting with new-onset atrial flutter?
Given the increasing reliance on non-pharmacological interventions for arrhythmia management, under what specific circumstances would pharmacological cardioversion with intravenous ibutilide be most appropriate as a first-line strategy in a hemodynamically stable patient presenting with new-onset atrial flutter?
In the management of atrial fibrillation, considering the limitations of the AFFIRM trial, what specific advancement in understanding the pathophysiology of HFrEF challenges the notion that maintenance of sinus rhythm is not always necessary and supports a rhythm control strategy?
In the management of atrial fibrillation, considering the limitations of the AFFIRM trial, what specific advancement in understanding the pathophysiology of HFrEF challenges the notion that maintenance of sinus rhythm is not always necessary and supports a rhythm control strategy?
Considering the complex pharmacological properties of amiodarone and its effects on multiple ion channels and receptors, what specific electrophysiological mechanism is most likely responsible for its efficacy in both supraventricular and ventricular arrhythmias, while also contributing to its proarrhythmic potential under certain clinical conditions?
Considering the complex pharmacological properties of amiodarone and its effects on multiple ion channels and receptors, what specific electrophysiological mechanism is most likely responsible for its efficacy in both supraventricular and ventricular arrhythmias, while also contributing to its proarrhythmic potential under certain clinical conditions?
A patient with a history of sustained ventricular tachycardia is prescribed an antiarrhythmic drug. Post-administration, the patient's QRS interval widens significantly, and atrial refractoriness increases. Based on the Vaughan Williams classification, which class of antiarrhythmic drug is most likely responsible for these effects?
A patient with a history of sustained ventricular tachycardia is prescribed an antiarrhythmic drug. Post-administration, the patient's QRS interval widens significantly, and atrial refractoriness increases. Based on the Vaughan Williams classification, which class of antiarrhythmic drug is most likely responsible for these effects?
A cardiologist is treating a patient with atrial fibrillation and a rapid ventricular response. The selected antiarrhythmic agent prolongs the AV nodal refractory period and slows conduction velocity specifically within the AV node. According to the Vaughan Williams classification, which class of drug is the cardiologist most likely using?
A cardiologist is treating a patient with atrial fibrillation and a rapid ventricular response. The selected antiarrhythmic agent prolongs the AV nodal refractory period and slows conduction velocity specifically within the AV node. According to the Vaughan Williams classification, which class of drug is the cardiologist most likely using?
An electrophysiologist is performing an ablation procedure for a patient with recurrent ventricular tachycardia. During the procedure, they administer a drug that markedly prolongs the action potential duration in ventricular myocytes with reverse use-dependence. According to the Vaughan Williams classification, which drug is most likely being used?
An electrophysiologist is performing an ablation procedure for a patient with recurrent ventricular tachycardia. During the procedure, they administer a drug that markedly prolongs the action potential duration in ventricular myocytes with reverse use-dependence. According to the Vaughan Williams classification, which drug is most likely being used?
A patient with a history of both atrial fibrillation and heart failure is prescribed an antiarrhythmic drug. The chosen agent exhibits properties of all four Vaughan Williams classes but is known to have significant extracardiac effects and a complex pharmacokinetic profile. Which drug is most consistent with this description?
A patient with a history of both atrial fibrillation and heart failure is prescribed an antiarrhythmic drug. The chosen agent exhibits properties of all four Vaughan Williams classes but is known to have significant extracardiac effects and a complex pharmacokinetic profile. Which drug is most consistent with this description?
In a patient with Wolff-Parkinson-White (WPW) syndrome presenting with atrial fibrillation, which Vaughan Williams class of antiarrhythmic drugs is generally contraindicated due to the risk of paradoxical increase in ventricular rate?
In a patient with Wolff-Parkinson-White (WPW) syndrome presenting with atrial fibrillation, which Vaughan Williams class of antiarrhythmic drugs is generally contraindicated due to the risk of paradoxical increase in ventricular rate?
A patient undergoing treatment with a Class III antiarrhythmic agent develops Torsades de Pointes. Which specific mechanism associated with this class of drugs is most directly implicated in the genesis of this arrhythmia?
A patient undergoing treatment with a Class III antiarrhythmic agent develops Torsades de Pointes. Which specific mechanism associated with this class of drugs is most directly implicated in the genesis of this arrhythmia?
A researcher is studying the effects of a novel antiarrhythmic drug on myocardial cells. The data indicate that the drug significantly prolongs the effective refractory period (ERP) without altering conduction velocity. Based on the Vaughan Williams classification, which class does this drug most likely belong to?
A researcher is studying the effects of a novel antiarrhythmic drug on myocardial cells. The data indicate that the drug significantly prolongs the effective refractory period (ERP) without altering conduction velocity. Based on the Vaughan Williams classification, which class does this drug most likely belong to?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) is being treated with verapamil. Which electrophysiological property of verapamil, as defined by the Vaughan Williams classification, contributes most to its efficacy in terminating PSVT?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) is being treated with verapamil. Which electrophysiological property of verapamil, as defined by the Vaughan Williams classification, contributes most to its efficacy in terminating PSVT?
An experimental drug is found to selectively block late sodium channels ($I_{NaL}$) without affecting other ion channels. How would this drug be classified within the Vaughan Williams framework, considering its impact on action potential duration and refractoriness?
An experimental drug is found to selectively block late sodium channels ($I_{NaL}$) without affecting other ion channels. How would this drug be classified within the Vaughan Williams framework, considering its impact on action potential duration and refractoriness?
A patient with known structural heart disease and frequent premature ventricular contractions (PVCs) is being considered for antiarrhythmic therapy. Given the increased risk of proarrhythmia, which Vaughan Williams class of drugs should be generally avoided?
A patient with known structural heart disease and frequent premature ventricular contractions (PVCs) is being considered for antiarrhythmic therapy. Given the increased risk of proarrhythmia, which Vaughan Williams class of drugs should be generally avoided?
Considering the historical progression of arrhythmia diagnostics and therapeutics, which of the following statements most accurately reflects the historical trajectory of advancements in this field?
Considering the historical progression of arrhythmia diagnostics and therapeutics, which of the following statements most accurately reflects the historical trajectory of advancements in this field?
Despite initial optimism regarding antiarrhythmic drug development, the clinical landscape has shifted towards non-pharmacological interventions. Which of the following best encapsulates the primary reasons for this paradigm shift?
Despite initial optimism regarding antiarrhythmic drug development, the clinical landscape has shifted towards non-pharmacological interventions. Which of the following best encapsulates the primary reasons for this paradigm shift?
The identification of genetic abnormalities in ion channels has significantly advanced our understanding of inherited arrhythmia syndromes. How has this discovery most profoundly impacted the clinical management of patients with arrhythmias?
The identification of genetic abnormalities in ion channels has significantly advanced our understanding of inherited arrhythmia syndromes. How has this discovery most profoundly impacted the clinical management of patients with arrhythmias?
Considering the evolution of arrhythmia management strategies, which statement best characterizes the current comparative roles of pharmacological and non-pharmacological therapies?
Considering the evolution of arrhythmia management strategies, which statement best characterizes the current comparative roles of pharmacological and non-pharmacological therapies?
The phenomenon of antiarrhythmic drug-induced proarrhythmia represents a significant clinical challenge. Which of the following mechanisms is LEAST likely to contribute to AAD-associated proarrhythmia?
The phenomenon of antiarrhythmic drug-induced proarrhythmia represents a significant clinical challenge. Which of the following mechanisms is LEAST likely to contribute to AAD-associated proarrhythmia?
While the surface electrocardiogram (ECG) remains fundamental in arrhythmia diagnosis, what is its most significant limitation when compared to intracardiac electrograms in elucidating complex arrhythmia mechanisms?
While the surface electrocardiogram (ECG) remains fundamental in arrhythmia diagnosis, what is its most significant limitation when compared to intracardiac electrograms in elucidating complex arrhythmia mechanisms?
The sinoatrial (SA) node's preeminence as the primary cardiac pacemaker is attributed to its intrinsic automaticity. Which of the following statements most accurately describes the physiological basis of this automaticity?
The sinoatrial (SA) node's preeminence as the primary cardiac pacemaker is attributed to its intrinsic automaticity. Which of the following statements most accurately describes the physiological basis of this automaticity?
For patients at high risk of life-threatening ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs) are often favored over antiarrhythmic drugs (AADs) as first-line therapy. Under which of the following clinical scenarios might AAD therapy be preferentially considered, despite the availability of ICDs?
For patients at high risk of life-threatening ventricular arrhythmias, implantable cardioverter-defibrillators (ICDs) are often favored over antiarrhythmic drugs (AADs) as first-line therapy. Under which of the following clinical scenarios might AAD therapy be preferentially considered, despite the availability of ICDs?
The text suggests that molecular biology and genomics hold promise for future advancements in arrhythmia therapies. Which of the following represents the most plausible and impactful application of these fields in the coming decades?
The text suggests that molecular biology and genomics hold promise for future advancements in arrhythmia therapies. Which of the following represents the most plausible and impactful application of these fields in the coming decades?
Despite the decline in antiarrhythmic drug (AAD) usage, there remain specific clinical contexts where AADs are considered indispensable. Which of the following scenarios best exemplifies a situation where AAD therapy remains a crucial component of arrhythmia management?
Despite the decline in antiarrhythmic drug (AAD) usage, there remain specific clinical contexts where AADs are considered indispensable. Which of the following scenarios best exemplifies a situation where AAD therapy remains a crucial component of arrhythmia management?
A novel antiarrhythmic drug selectively enhances the activity of the sodium-potassium pump in cardiomyocytes. Considering the pump's role in maintaining resting membrane potential (RMP), what would be the MOST likely electrophysiological consequence of this drug's action on the RMP and subsequent action potential characteristics?
A novel antiarrhythmic drug selectively enhances the activity of the sodium-potassium pump in cardiomyocytes. Considering the pump's role in maintaining resting membrane potential (RMP), what would be the MOST likely electrophysiological consequence of this drug's action on the RMP and subsequent action potential characteristics?
An experimental drug is found to selectively inhibit the transient outward potassium current ($I_{Kto}$) in ventricular myocytes. Given the role of $I_{Kto}$ in action potential repolarization, which of the following effects would be MOST anticipated on the action potential duration (APD) and the effective refractory period (ERP)?
An experimental drug is found to selectively inhibit the transient outward potassium current ($I_{Kto}$) in ventricular myocytes. Given the role of $I_{Kto}$ in action potential repolarization, which of the following effects would be MOST anticipated on the action potential duration (APD) and the effective refractory period (ERP)?
A patient with a genetic mutation has cardiomyocytes that exhibit a significantly reduced density of functional sodium channels. Considering the role of sodium influx in action potential generation, which of the following would be the MOST likely consequence of this channelopathy on the cardiac action potential?
A patient with a genetic mutation has cardiomyocytes that exhibit a significantly reduced density of functional sodium channels. Considering the role of sodium influx in action potential generation, which of the following would be the MOST likely consequence of this channelopathy on the cardiac action potential?
A pharmaceutical company is developing a novel antiarrhythmic drug that aims to selectively enhance calcium influx during Phase 2 of the cardiac action potential. What is the MOST likely electrophysiological consequence of this drug's action on the action potential duration and contractility?
A pharmaceutical company is developing a novel antiarrhythmic drug that aims to selectively enhance calcium influx during Phase 2 of the cardiac action potential. What is the MOST likely electrophysiological consequence of this drug's action on the action potential duration and contractility?
During an electrophysiology study, a researcher observes that localized application of a specific compound to the sinoatrial (SA) node significantly reduces the amplitude of the action potential upstroke without affecting the resting membrane potential. Which ionic current is MOST likely being directly affected by this compound?
During an electrophysiology study, a researcher observes that localized application of a specific compound to the sinoatrial (SA) node significantly reduces the amplitude of the action potential upstroke without affecting the resting membrane potential. Which ionic current is MOST likely being directly affected by this compound?
A patient with a history of structural heart disease and refractory ventricular tachycardia is being evaluated for antiarrhythmic therapy. Electrophysiological mapping reveals regions of slow conduction velocity within the ventricular myocardium. Considering the underlying ionic mechanisms, which alteration in ion channel function would MOST likely contribute to this slow conduction?
A patient with a history of structural heart disease and refractory ventricular tachycardia is being evaluated for antiarrhythmic therapy. Electrophysiological mapping reveals regions of slow conduction velocity within the ventricular myocardium. Considering the underlying ionic mechanisms, which alteration in ion channel function would MOST likely contribute to this slow conduction?
A novel genetic therapy aims to correct a mutation that disrupts the normal function of the cardiac sodium-calcium exchanger (NCX). Assuming the therapy successfully restores normal NCX function, what would be the MOST likely effect on intracellular calcium concentration and myocyte contractility under conditions of rapid, repetitive depolarization?
A novel genetic therapy aims to correct a mutation that disrupts the normal function of the cardiac sodium-calcium exchanger (NCX). Assuming the therapy successfully restores normal NCX function, what would be the MOST likely effect on intracellular calcium concentration and myocyte contractility under conditions of rapid, repetitive depolarization?
A patient with a history of structural heart disease and severely depressed left ventricular ejection fraction (LVEF <30%) develops atrial fibrillation with rapid ventricular response. Given the complexities of antiarrhythmic pharmacology and the need to minimize adverse hemodynamic effects, which of the following intravenous antiarrhythmic agents would be the MOST judicious choice for acute rate control, considering its impact on conduction velocity, refractoriness, and automaticity, as delineated in the Vaughan Williams classification?
A patient with a history of structural heart disease and severely depressed left ventricular ejection fraction (LVEF <30%) develops atrial fibrillation with rapid ventricular response. Given the complexities of antiarrhythmic pharmacology and the need to minimize adverse hemodynamic effects, which of the following intravenous antiarrhythmic agents would be the MOST judicious choice for acute rate control, considering its impact on conduction velocity, refractoriness, and automaticity, as delineated in the Vaughan Williams classification?
An electrophysiologist is preparing to perform an ablation procedure targeting a left atrial flutter circuit. The patient has a history of mild, well-controlled asthma. Considering the potential impact of antiarrhythmic drugs on atrial refractoriness and conduction velocity, which of the following pre-procedural antiarrhythmic agents would be MOST cautiously approached or avoided due to its potential to exacerbate the patient's underlying respiratory condition?
An electrophysiologist is preparing to perform an ablation procedure targeting a left atrial flutter circuit. The patient has a history of mild, well-controlled asthma. Considering the potential impact of antiarrhythmic drugs on atrial refractoriness and conduction velocity, which of the following pre-procedural antiarrhythmic agents would be MOST cautiously approached or avoided due to its potential to exacerbate the patient's underlying respiratory condition?
A patient with persistent atrial fibrillation and a history of significant structural heart disease is being considered for long-term antiarrhythmic therapy. The selection of an appropriate agent must balance efficacy in maintaining sinus rhythm with the risk of inducing proarrhythmia, particularly Torsades de Pointes. Which of the following Class III antiarrhythmic drugs would generally be considered to have the HIGHEST risk of QT prolongation and subsequent Torsades, necessitating meticulous monitoring and consideration of alternative agents?
A patient with persistent atrial fibrillation and a history of significant structural heart disease is being considered for long-term antiarrhythmic therapy. The selection of an appropriate agent must balance efficacy in maintaining sinus rhythm with the risk of inducing proarrhythmia, particularly Torsades de Pointes. Which of the following Class III antiarrhythmic drugs would generally be considered to have the HIGHEST risk of QT prolongation and subsequent Torsades, necessitating meticulous monitoring and consideration of alternative agents?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) is being evaluated for long-term management. The patient has contraindications to adenosine and calcium channel blockers. Considering the electrophysiological properties of Class Ia antiarrhythmic drugs, which of the following effects on conduction velocity, refractoriness, and automaticity is MOST responsible for their efficacy in suppressing PSVT?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) is being evaluated for long-term management. The patient has contraindications to adenosine and calcium channel blockers. Considering the electrophysiological properties of Class Ia antiarrhythmic drugs, which of the following effects on conduction velocity, refractoriness, and automaticity is MOST responsible for their efficacy in suppressing PSVT?
A patient with a history of frequent premature ventricular contractions (PVCs) and no structural heart disease is being considered for antiarrhythmic therapy to alleviate symptomatic burden. Given the nuanced risk-benefit profiles of different Vaughan Williams classes, which of the following approaches represents the MOST appropriate initial pharmacotherapeutic strategy, weighing efficacy against the potential for proarrhythmia and other adverse effects?
A patient with a history of frequent premature ventricular contractions (PVCs) and no structural heart disease is being considered for antiarrhythmic therapy to alleviate symptomatic burden. Given the nuanced risk-benefit profiles of different Vaughan Williams classes, which of the following approaches represents the MOST appropriate initial pharmacotherapeutic strategy, weighing efficacy against the potential for proarrhythmia and other adverse effects?
A patient with a history of concealed Wolff-Parkinson-White (WPW) syndrome is undergoing an electrophysiological study. During the procedure, a Class Ic antiarrhythmic drug is administered, paradoxically increasing the ventricular rate during induced atrial fibrillation. Based on the provided information regarding re-entrant circuits and proarrhythmia, what is the MOST likely mechanism by which the Class Ic agent exacerbates the arrhythmia in this specific scenario?
A patient with a history of concealed Wolff-Parkinson-White (WPW) syndrome is undergoing an electrophysiological study. During the procedure, a Class Ic antiarrhythmic drug is administered, paradoxically increasing the ventricular rate during induced atrial fibrillation. Based on the provided information regarding re-entrant circuits and proarrhythmia, what is the MOST likely mechanism by which the Class Ic agent exacerbates the arrhythmia in this specific scenario?
An electrophysiologist is evaluating a patient with recurrent atrial flutter and suspects a macro-reentrant circuit in the right atrium. Considering the principles of functional re-entry, which of the following statements BEST describes the mechanism by which the re-entrant circuit is maintained?
An electrophysiologist is evaluating a patient with recurrent atrial flutter and suspects a macro-reentrant circuit in the right atrium. Considering the principles of functional re-entry, which of the following statements BEST describes the mechanism by which the re-entrant circuit is maintained?
A patient with known structural heart disease develops a wide-complex tachycardia. Initial treatment with amiodarone is ineffective, and the patient's condition deteriorates. Considering the mechanisms of proarrhythmia related to re-entrant circuits, which of the following scenarios MOST accurately describes how amiodarone might paradoxically worsen the arrhythmia?
A patient with known structural heart disease develops a wide-complex tachycardia. Initial treatment with amiodarone is ineffective, and the patient's condition deteriorates. Considering the mechanisms of proarrhythmia related to re-entrant circuits, which of the following scenarios MOST accurately describes how amiodarone might paradoxically worsen the arrhythmia?
A researcher is investigating a novel antiarrhythmic peptide that selectively targets gap junction conductance in a canine model of atrial fibrillation. Assuming the peptide effectively reduces lateralization of excitation, which of the following effects on functional re-entry would be MOST likely to contribute to arrhythmia termination?
A researcher is investigating a novel antiarrhythmic peptide that selectively targets gap junction conductance in a canine model of atrial fibrillation. Assuming the peptide effectively reduces lateralization of excitation, which of the following effects on functional re-entry would be MOST likely to contribute to arrhythmia termination?
A patient with a history of ischemic cardiomyopathy and inducible ventricular tachycardia (VT) undergoes programmed electrical stimulation (PES) during an electrophysiology study. The cardiologist observes that VT is easily induced and sustained. Based on the information provided, which of the following interventions would MOST directly address the underlying substrate sustaining the re-entrant VT?
A patient with a history of ischemic cardiomyopathy and inducible ventricular tachycardia (VT) undergoes programmed electrical stimulation (PES) during an electrophysiology study. The cardiologist observes that VT is easily induced and sustained. Based on the information provided, which of the following interventions would MOST directly address the underlying substrate sustaining the re-entrant VT?
A patient with persistent atrial fibrillation and underlying structural heart disease is being considered for pharmacological cardioversion. Pre-procedure TEE reveals no atrial thrombus. Intravenous administration of which antiarrhythmic drug carries the HIGHEST risk of precipitating Torsades de Pointes (TdP) due to reverse use-dependence, particularly in the presence of prolonged QT intervals and bradycardia?
A patient with persistent atrial fibrillation and underlying structural heart disease is being considered for pharmacological cardioversion. Pre-procedure TEE reveals no atrial thrombus. Intravenous administration of which antiarrhythmic drug carries the HIGHEST risk of precipitating Torsades de Pointes (TdP) due to reverse use-dependence, particularly in the presence of prolonged QT intervals and bradycardia?
During an electrophysiology study, a patient with a history of recurrent atrial tachycardia undergoes adenosine administration. The tachycardia terminates transiently with recurrence upon adenosine washout. What is the MOST likely mechanism of the transient termination observed in this scenario?
During an electrophysiology study, a patient with a history of recurrent atrial tachycardia undergoes adenosine administration. The tachycardia terminates transiently with recurrence upon adenosine washout. What is the MOST likely mechanism of the transient termination observed in this scenario?
A patient with a history of hypertrophic cardiomyopathy (HCM) presents with symptomatic non-sustained ventricular tachycardia (NSVT). Given the arrhythmogenic substrate in HCM, which of the following drug classes would be MOST appropriate for long-term suppression of ventricular ectopy, while simultaneously addressing the underlying pathophysiology of HCM?
A patient with a history of hypertrophic cardiomyopathy (HCM) presents with symptomatic non-sustained ventricular tachycardia (NSVT). Given the arrhythmogenic substrate in HCM, which of the following drug classes would be MOST appropriate for long-term suppression of ventricular ectopy, while simultaneously addressing the underlying pathophysiology of HCM?
A 68-year-old male with a history of myocardial infarction and reduced left ventricular ejection fraction (HFrEF) is initiated on sotalol for symptomatic atrial fibrillation. After several days, he develops marked QT prolongation and polymorphic ventricular tachycardia. Beyond immediate defibrillation, what is the MOST appropriate next step in managing this patient's proarrhythmic complication of sotalol therapy?
A 68-year-old male with a history of myocardial infarction and reduced left ventricular ejection fraction (HFrEF) is initiated on sotalol for symptomatic atrial fibrillation. After several days, he develops marked QT prolongation and polymorphic ventricular tachycardia. Beyond immediate defibrillation, what is the MOST appropriate next step in managing this patient's proarrhythmic complication of sotalol therapy?
A clinical trial is evaluating a new antiarrhythmic drug that selectively blocks late sodium channels ($I_{NaL}$) in patients with long QT syndrome (LQTS). Which of the following outcomes would provide the STRONGEST evidence that the drug is effective in reducing the risk of Torsades de Pointes (TdP) in this patient population?
A clinical trial is evaluating a new antiarrhythmic drug that selectively blocks late sodium channels ($I_{NaL}$) in patients with long QT syndrome (LQTS). Which of the following outcomes would provide the STRONGEST evidence that the drug is effective in reducing the risk of Torsades de Pointes (TdP) in this patient population?
In the context of triggered activity and afterdepolarizations, which of the following statements BEST delineates the mechanistic distinction between early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) in the genesis of arrhythmias, considering their ionic current dependencies and pharmacological modulations?
In the context of triggered activity and afterdepolarizations, which of the following statements BEST delineates the mechanistic distinction between early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) in the genesis of arrhythmias, considering their ionic current dependencies and pharmacological modulations?
Given a patient presenting with polymorphic ventricular tachycardia (PVT) linked to acquired long QT syndrome following initiation of a Class III antiarrhythmic, which intervention strategy would MOST effectively address the underlying electrophysiological derangement, considering the nuances of EAD formation at varying heart rates and action potential durations?
Given a patient presenting with polymorphic ventricular tachycardia (PVT) linked to acquired long QT syndrome following initiation of a Class III antiarrhythmic, which intervention strategy would MOST effectively address the underlying electrophysiological derangement, considering the nuances of EAD formation at varying heart rates and action potential durations?
Considering the three essential electrophysiological requisites for the establishment of a stable reentrant circuit—two distinct conduction pathways, unidirectional block, and slow conduction—how would an adenosine-sensitive form of paroxysmal supraventricular tachycardia (PSVT) MOST likely fulfill these criteria, considering the specific anatomical and electrophysiological properties of the AV node?
Considering the three essential electrophysiological requisites for the establishment of a stable reentrant circuit—two distinct conduction pathways, unidirectional block, and slow conduction—how would an adenosine-sensitive form of paroxysmal supraventricular tachycardia (PSVT) MOST likely fulfill these criteria, considering the specific anatomical and electrophysiological properties of the AV node?
A patient with known structural heart disease and inducible ventricular tachycardia (VT) undergoes electrophysiological (EP) study. During programmed stimulation, VT is initiated, demonstrating a localized area of slow conduction and a critical isthmus within a scar region. Which of the following pharmacological interventions would MOST effectively target the underlying mechanism maintaining this reentrant VT circuit, considering the limitations of individual antiarrhythmic agents?
A patient with known structural heart disease and inducible ventricular tachycardia (VT) undergoes electrophysiological (EP) study. During programmed stimulation, VT is initiated, demonstrating a localized area of slow conduction and a critical isthmus within a scar region. Which of the following pharmacological interventions would MOST effectively target the underlying mechanism maintaining this reentrant VT circuit, considering the limitations of individual antiarrhythmic agents?
In a scenario involving a patient with recurrent atrial fibrillation (AF) and a history of heart failure with preserved ejection fraction (HFpEF), which of the following antiarrhythmic drug (AAD) regimens would be MOST judicious, considering the potential for adverse hemodynamic effects and the need for concomitant rate control, while also accounting for the impact on AV nodal function?
In a scenario involving a patient with recurrent atrial fibrillation (AF) and a history of heart failure with preserved ejection fraction (HFpEF), which of the following antiarrhythmic drug (AAD) regimens would be MOST judicious, considering the potential for adverse hemodynamic effects and the need for concomitant rate control, while also accounting for the impact on AV nodal function?
How should pharmacotherapy address the potential for Torsades de Pointes (TdP) in a patient with congenital long QT syndrome (LQTS) who requires antiarrhythmic therapy for recurrent symptomatic ventricular arrhythmias, considering the differential effects of various antiarrhythmic drugs on the QT interval and the underlying genetic mutation?
How should pharmacotherapy address the potential for Torsades de Pointes (TdP) in a patient with congenital long QT syndrome (LQTS) who requires antiarrhythmic therapy for recurrent symptomatic ventricular arrhythmias, considering the differential effects of various antiarrhythmic drugs on the QT interval and the underlying genetic mutation?
Given the established role of reentry as a fundamental mechanism for various cardiac arrhythmias, what intervention would MOST effectively prevent the initiation and perpetuation of atrial fibrillation (AF) in a patient with structural heart disease and a history of paroxysmal AF, considering the complex interplay between atrial remodeling, autonomic tone, and underlying substrate?
Given the established role of reentry as a fundamental mechanism for various cardiac arrhythmias, what intervention would MOST effectively prevent the initiation and perpetuation of atrial fibrillation (AF) in a patient with structural heart disease and a history of paroxysmal AF, considering the complex interplay between atrial remodeling, autonomic tone, and underlying substrate?
How would the presence of an accessory pathway in Wolff-Parkinson-White (WPW) syndrome modify the pharmacological management of atrial fibrillation (AF), particularly concerning the selection of antiarrhythmic agents to control ventricular rate, and what electrophysiological parameters dictate the choice of agents in this clinical context?
How would the presence of an accessory pathway in Wolff-Parkinson-White (WPW) syndrome modify the pharmacological management of atrial fibrillation (AF), particularly concerning the selection of antiarrhythmic agents to control ventricular rate, and what electrophysiological parameters dictate the choice of agents in this clinical context?
In the context of myocardial ischemia and reentry, which of the following best describes the sequence of events that facilitates the formation of a reentrant circuit?
In the context of myocardial ischemia and reentry, which of the following best describes the sequence of events that facilitates the formation of a reentrant circuit?
Given the limitations of current antiarrhythmic drug (AAD) therapies, what future direction in arrhythmia management holds the GREATEST promise for MECHANISTICALLY targeted and personalized interventions, minimizing off-target effects and maximizing efficacy in preventing sudden cardiac death?
Given the limitations of current antiarrhythmic drug (AAD) therapies, what future direction in arrhythmia management holds the GREATEST promise for MECHANISTICALLY targeted and personalized interventions, minimizing off-target effects and maximizing efficacy in preventing sudden cardiac death?
A patient with known structural heart disease develops sustained monomorphic ventricular tachycardia (VT). Acute management with intravenous amiodarone is initiated but proves ineffective in terminating the arrhythmia. Considering the mechanism of action and electrophysiological effects of amiodarone, which of the following factors is MOST likely contributing to the drug's failure in this scenario?
A patient with known structural heart disease develops sustained monomorphic ventricular tachycardia (VT). Acute management with intravenous amiodarone is initiated but proves ineffective in terminating the arrhythmia. Considering the mechanism of action and electrophysiological effects of amiodarone, which of the following factors is MOST likely contributing to the drug's failure in this scenario?
A patient presents with recurrent episodes of narrow QRS complex tachycardia. During an electrophysiology study, the cardiologist attempts to induce the tachycardia. Which of the following observations would be MOST suggestive of an atrioventricular nodal reentrant tachycardia (AVNRT)?
A patient presents with recurrent episodes of narrow QRS complex tachycardia. During an electrophysiology study, the cardiologist attempts to induce the tachycardia. Which of the following observations would be MOST suggestive of an atrioventricular nodal reentrant tachycardia (AVNRT)?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) undergoing an electrophysiology study is found to have dual AV nodal physiology. Given this finding, which of the following procedural strategies would MOST definitively address the underlying mechanism of the patient's arrhythmia?
A patient with a history of paroxysmal supraventricular tachycardia (PSVT) undergoing an electrophysiology study is found to have dual AV nodal physiology. Given this finding, which of the following procedural strategies would MOST definitively address the underlying mechanism of the patient's arrhythmia?
A researcher is investigating the effects of a novel compound on atrial electrophysiology. The compound prolongs the atrial effective refractory period (AERP) and slows atrial conduction velocity. Which of the following mechanisms is MOST likely responsible for these effects?
A researcher is investigating the effects of a novel compound on atrial electrophysiology. The compound prolongs the atrial effective refractory period (AERP) and slows atrial conduction velocity. Which of the following mechanisms is MOST likely responsible for these effects?
A patient with a history of atrial flutter develops atrial fibrillation (AF) following treatment with a Class IC antiarrhythmic drug. Which electrophysiological mechanism is MOST likely responsible for this transition?
A patient with a history of atrial flutter develops atrial fibrillation (AF) following treatment with a Class IC antiarrhythmic drug. Which electrophysiological mechanism is MOST likely responsible for this transition?
A patient with a history of ischemic cardiomyopathy and recurrent episodes of ventricular tachycardia (VT) is being considered for antiarrhythmic therapy. Given the underlying substrate for VT in this patient population, which of the following electrophysiological targets would be the MOST effective for preventing recurrent VT?
A patient with a history of ischemic cardiomyopathy and recurrent episodes of ventricular tachycardia (VT) is being considered for antiarrhythmic therapy. Given the underlying substrate for VT in this patient population, which of the following electrophysiological targets would be the MOST effective for preventing recurrent VT?
A pharmacologist is developing a novel antiarrhythmic drug designed to selectively target atrial fibrillation. Which of the following cellular mechanisms would be the MOST appropriate target to achieve this goal while minimizing ventricular effects?
A pharmacologist is developing a novel antiarrhythmic drug designed to selectively target atrial fibrillation. Which of the following cellular mechanisms would be the MOST appropriate target to achieve this goal while minimizing ventricular effects?
A patient with a history of atrial fibrillation and heart failure with reduced ejection fraction (HFrEF) is initiated on dofetilide, an antiarrhythmic agent known to prolong the QT interval. Which of the following monitoring parameters and management strategies is MOST critical to minimize the risk of Torsades de Pointes in this patient?
A patient with a history of atrial fibrillation and heart failure with reduced ejection fraction (HFrEF) is initiated on dofetilide, an antiarrhythmic agent known to prolong the QT interval. Which of the following monitoring parameters and management strategies is MOST critical to minimize the risk of Torsades de Pointes in this patient?
A patient with known structural heart disease and recurrent episodes of sustained monomorphic ventricular tachycardia (SMVT) is being evaluated for implantable cardioverter-defibrillator (ICD) placement. Despite optimal medical therapy, the patient continues to experience breakthrough VT episodes. In addition to ICD implantation, which of the following adjunctive strategies would be MOST appropriate to reduce the frequency of VT events?
A patient with known structural heart disease and recurrent episodes of sustained monomorphic ventricular tachycardia (SMVT) is being evaluated for implantable cardioverter-defibrillator (ICD) placement. Despite optimal medical therapy, the patient continues to experience breakthrough VT episodes. In addition to ICD implantation, which of the following adjunctive strategies would be MOST appropriate to reduce the frequency of VT events?
Flashcards
Antiarrhythmic Drugs (AADs)
Antiarrhythmic Drugs (AADs)
Drugs used to treat arrhythmias, but their use has declined due to increased mortality from proarrhythmic effects and limited efficacy.
Nonpharmacologic Arrhythmia Treatments
Nonpharmacologic Arrhythmia Treatments
Non-drug methods like ablation and ICDs that are increasingly used instead of AADs for managing arrhythmias.
Amiodarone
Amiodarone
A common AAD effective for various arrhythmias, but has frequent adverse effects requiring close monitoring. Pulmonary fibrosis is a major concern.
Atrial Fibrillation (AF) Treatment Goals
Atrial Fibrillation (AF) Treatment Goals
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AFFIRM Trial
AFFIRM Trial
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AADs in AF Post-Ablation
AADs in AF Post-Ablation
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AAD Monitoring
AAD Monitoring
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Supraventricular Tachycardia (SVT)
Supraventricular Tachycardia (SVT)
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Catheter Ablation
Catheter Ablation
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Proarrhythmic Effect
Proarrhythmic Effect
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Implantable Cardioverter Defibrillator (ICD)
Implantable Cardioverter Defibrillator (ICD)
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Pulmonary Fibrosis (as related to Amiodarone)
Pulmonary Fibrosis (as related to Amiodarone)
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AV Nodal Blocking Medications
AV Nodal Blocking Medications
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Adenosine
Adenosine
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Surface Electrocardiogram (ECG)
Surface Electrocardiogram (ECG)
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Automaticity
Automaticity
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Proarrhythmia
Proarrhythmia
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Radiofrequency Ablation
Radiofrequency Ablation
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SA Node
SA Node
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Cardiac Conduction System
Cardiac Conduction System
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SA Node Firing Rate
SA Node Firing Rate
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Heritable Long QT Syndrome
Heritable Long QT Syndrome
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Non-DHP CCB Antiarrhythmic Mechanism
Non-DHP CCB Antiarrhythmic Mechanism
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Non-DHP CCB Arrhythmia Target
Non-DHP CCB Arrhythmia Target
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Dihydropyridine (DHP) CCBs & Arrhythmias
Dihydropyridine (DHP) CCBs & Arrhythmias
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AADs & Heart Failure (HFrEF)
AADs & Heart Failure (HFrEF)
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Mexiletine's Side Effects
Mexiletine's Side Effects
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Vaughan Williams Classification
Vaughan Williams Classification
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Class Ia Antiarrhythmics
Class Ia Antiarrhythmics
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Class Ib Antiarrhythmics
Class Ib Antiarrhythmics
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Class Ic Antiarrhythmics
Class Ic Antiarrhythmics
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Class II Antiarrhythmics
Class II Antiarrhythmics
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Class III Antiarrhythmics
Class III Antiarrhythmics
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Class IV Antiarrhythmics
Class IV Antiarrhythmics
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↑HV Interval (Amiodarone)
↑HV Interval (Amiodarone)
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↑QRS Duration (Amiodarone)
↑QRS Duration (Amiodarone)
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Amiodarone's Multi-Class Action
Amiodarone's Multi-Class Action
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Cardiac Conduction Branches
Cardiac Conduction Branches
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Refractory Period
Refractory Period
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Resting Membrane Potential (RMP)
Resting Membrane Potential (RMP)
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Sodium-Potassium Pump
Sodium-Potassium Pump
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Action Potential (AP)
Action Potential (AP)
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Action Potential Phase 0
Action Potential Phase 0
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Action Potential Phase 1
Action Potential Phase 1
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Afterdepolarizations
Afterdepolarizations
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Early Afterdepolarizations (EADs)
Early Afterdepolarizations (EADs)
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Delayed Afterdepolarizations (DADs)
Delayed Afterdepolarizations (DADs)
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TdP Cause by Drugs
TdP Cause by Drugs
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DADs Precipitation
DADs Precipitation
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DADs Suppression
DADs Suppression
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Reentry
Reentry
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Reentry Requirements
Reentry Requirements
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Reentry Initiation
Reentry Initiation
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Reentrant Tachycardia
Reentrant Tachycardia
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Initiating Event
Initiating Event
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Tachycardia Initiation/Termination
Tachycardia Initiation/Termination
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Atrial Fibrillation (AF)
Atrial Fibrillation (AF)
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Atrial Flutter (AFl)
Atrial Flutter (AFl)
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AV Nodal Reentrant Tachycardia (AVNRT)
AV Nodal Reentrant Tachycardia (AVNRT)
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AV Reentrant Tachycardia (AVRT)
AV Reentrant Tachycardia (AVRT)
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Recurrent Ventricular Tachycardia (VT)
Recurrent Ventricular Tachycardia (VT)
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Hypoxia/Ischemia Effect
Hypoxia/Ischemia Effect
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Potassium Release
Potassium Release
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Reentry Factors
Reentry Factors
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Proarrhythmia Mechanism
Proarrhythmia Mechanism
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Functional Reentry
Functional Reentry
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Reentrant Loop Core
Reentrant Loop Core
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Functional Reentry Edge
Functional Reentry Edge
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Reentry Location
Reentry Location
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Purkinje System & Reentry
Purkinje System & Reentry
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Reentry Models & Drugs
Reentry Models & Drugs
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Critical Balance
Critical Balance
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Microreentrant Loops
Microreentrant Loops
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Study Notes
Arrhythmias
- In September 2023, Table 40-7 regarding dose adjustments for sotalol was corrected for patients with atrial fibrillation/flutter with chronic kidney disease, additionally, recommendations were added for hepatic dysfunction.
Action Potentials
- Electrical stimulation causes changes in membrane potential over time, resulting in a characteristic action potential (AP) curve, results from transmembrane movement of specific ions, and is divided into different phases.
- Phase 0 (rapid depolarization): Abrupt increase in membrane permeability to sodium influx.
- Phase 1 (initial repolarization): Transient and active potassium efflux (Ito current).
- Phase 2 (plateau phase): Calcium influx balanced by potassium efflux.
- Phase 3 (cellular repolarization): Membrane remains permeable to potassium efflux.
- Phase 4 (gradual depolarization): Constant sodium leak into the intracellular space is balanced by decreasing potassium efflux.
Sodium Channels
- Sodium channels cycle between resting, activated, and inactivated states depending on membrane potential and time.
- Activation of SA and AV nodal tissue is dependent on slow depolarizing current through calcium channels, whereas atrial and ventricular activation depends on rapid depolarizing current through sodium channels.
Abnormal Conduction
- Tachyarrhythmias result from abnormalities in impulse generation (automatic tachycardia and triggered automaticity) or impulse conduction (reentrant tachycardias).
- Triggered automaticity refers to transient membrane depolarizations during repolarization (EADs) or after repolarization (DADs).
Reentry
- Necessitates two pathways for conduction, a unidirectional block, and slow conduction in the other pathway.
- Key is crucial discrepancies in the electrophysiologic characteristics of the two pathways.
- Reentrant focus may excite surrounding tissue faster than the SA node, leading to tachycardia.
Drug Classes
- Class Ia drugs (quinidine, procainamide) slow conduction and prolong refractoriness by blocking sodium and potassium channels.
- Class Ib drugs (lidocaine, mexiletine) generally facilitate conduction by shortening refractoriness.
- Class Ic drugs, (flecainide & propafenone) are potent sodium channel blockers that slow conduction.
- Class III drugs (amiodarone, dronedarone, sotalol, ibutilide, dofetilide) delay repolarization by blocking potassium channels.
EADs and DADs
- Experimentally, EADs may be precipitated by hypokalemia, class 1a AADs, or slow stimulation rates.
- Medication such as DADs may be precipitated by digoxin or catecholamines and may be suppressed by non-dihydropyridine (non-DHP) calcium channel blockers (CCBs).
Additional Mechanisms
- Medications can depress automatic properties, alter reentrant loop conduction, or reverse responsible heart disease.
- Proarrhythmia can occur through anatomic re-entry in the anatomic model of reentry.
- A functional reentrant loop may be caused by non-transmural block.
- The length of the circuit may vary with conduction velocity and impulse recovery, continually exciting tissue.
Amiodarone Specifics
- Half life is approximately 60 days and a large volume of distribution and is a substrate of the cytochrome P450 (CYP) 3A4 isoenzyme, inhibition of P-gp, amiodarone can increase digoxin concentrations.
- Reducise dose by 50% when initiating amiodarone, empiric warfarin dose reduction is necessary
Dronedarone Specific
- Increased dabigatran concentrations in patients with renal impairment to minimize bleeding, the dose of dabigatran should be reduced to 75 mg twice daily.
- Modifications to the chemical structure of dronedarone result in it being less lipophilic than amiodarone and less likely to accumulate in tissues causing organ toxicities.
Prevention
- Stroke risk is increased five-fold with annual attributable risk increasing from 1.5% in individuals 50 to 59 years of age to almost 24% in those 80 to 89 years of age and antithrombotic recommendations used in patients with AF should also be applied to those with AFL.
- When starting AF, the CHEST and American College of Cardiology (ACC)/American Heart Association (AHA) guidelines recommend assessing the patient's risk for stroke and bleeding before selecting the most appropriate regimen.
- No antithrombotic therapy is recommended for males with CHA2DS2-VASc score of 0 & CHA2DS2-VASc score of 1. and females with a No antithrombotic therapy and for for Patients with one non-sex CHA2DS2-VASc stroke risk factor (ie, CHA2DS2-VASc score of 1 & CHA2DS2-VASc stroke for pts with 2. or more non sex risk factors.
Novel Agents
- Over the past decade, the Food and Drug Administration (FDA) has approved several oral antithrombotic therapies for stroke prevention in patients with AF not due to valvular heart disease (moderate-to-severe mitral stenosis or mechanical heart valve).
- SAMe-TT2R2 to assist in the identification of patients who are likely or not likely (TTR >65% for antithrombotic therapy.
- The left atrial appendange may be viable therapy with the watchman.
Atrial Flutter Treatment
- Patients with known cardiovascular or comobidity of more weight, hypertension, diabetes, and sleep apnea are at higher risk as well.
- Patients with hypertension should be ≤130/80 mm Hg.
- Roughly 50% of patients with AF have sleep apnea. When managed with continuous positive airway pressure, the recurrence of AF may be ameliorated and controlling these disease states reduces the risk of developing AF.
AVNRT Mechanism
- PSVT generated by reentrant mechanisms includes AV nodal reentry (ie, AVNRT), AV reentry incorporating an accessory pathway (ie, AVRT), SA nodal reentry, and intra-atrial reentry. AVNRT and AVRT
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Description
These questions cover the selection of appropriate antiarrhythmic drugs based on specific arrhythmia types and patient comorbidities. Includes scenarios involving PSVT, atrial fibrillation, and PVCs. Focuses on drug mechanisms and contraindications.
