Katzung - Chapter 14

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Questions and Answers

What is the normal frequency at which the sinoatrial (SA) node fires?

100-140 bpm

80-120 bpm

40-60 bpm

60-100 bpm (correct)

Which arrhythmia was documented in the patient presented in the case study?

Sinus bradycardia

Atrial flutter

Ventricular fibrillation

Atrial fibrillation (correct)

What medication was initiated for the patient to help manage her condition?

Atenolol

Sustained-release metoprolol (correct)

Amiodarone

Digoxin

What is the ventricular response rate observed in the patient's ECG?

88–114 bpm Signup and view all the answers

Which structural change is indicated by the echocardiogram in the patient?

Left ventricular hypertrophy Signup and view all the answers

Why might some arrhythmias require intervention with medication?

They can reduce cardiac output Signup and view all the answers

What is the potential consequence of early premature ventricular depolarizations?

Ventricular fibrillation Signup and view all the answers

What percentage of patients treated with digitalis may experience cardiac arrhythmias?

25% Signup and view all the answers

Which structure normally acts as the sole conduction pathway between the atria and ventricles?

Atrioventricular (AV) node Signup and view all the answers

Which drug has a significant effect on the AV nodal refractory period as indicated by an increase?

Amiodarone Signup and view all the answers

Which antiarrhythmic drug typically has a half-life of less than 10 minutes?

Esmolol Signup and view all the answers

Which medication is associated with a prolonged QRS duration?

Disopyramide Signup and view all the answers

Which of the following drugs demonstrates a variable effect on the SA nodal rate?

Amiodarone Signup and view all the answers

Which agent does not affect the QT interval?

Esmolol Signup and view all the answers

Which drug's primary utility is in supraventricular arrhythmias but has limited effects on ventricular arrhythmias?

Diltiazem Signup and view all the answers

What is the primary cause of the action potential plateau phases 1 and 2 in cardiac cells?

Turning off of most sodium current Signup and view all the answers

Which event marks the final repolarization phase (phase 3) of the action potential?

Completion of sodium and calcium channel inactivation Signup and view all the answers

What is the resting potential range for SA and AV nodal tissues?

−50 to −70 mV Signup and view all the answers

What primarily occurs during depolarization if the resting potential exceeds −55 mV?

Inactivation of all sodium channels Signup and view all the answers

What contributes to the 'slow responses' of cardiac action potentials?

Calcium inward current Signup and view all the answers

Which potassium current is rapidly activating and involved in phase 3 repolarization?

IKr Signup and view all the answers

In what condition do cells with severely depolarized membrane potentials exhibit special action potentials?

When calcium permeability is increased Signup and view all the answers

What does the slow reduction of the resting potential generally result in?

Depressed sodium currents Signup and view all the answers

Which is a characteristic of the slowly activating potassium current?

IKs Signup and view all the answers

What is the term used for depolarizations that arise during or after a normally evoked action potential?

Triggered automaticity Signup and view all the answers

How does ischemic cell damage affect the resting potential?

It causes prolonged depolarization Signup and view all the answers

What phenomenon occurs if conduction is too rapid around an obstacle?

Bidirectional conduction Signup and view all the answers

What can cause slowing of conduction in the heart?

Depressed sodium current Signup and view all the answers

What type of impulses can be generated from a circulating impulse in the heart?

Daughter impulses Signup and view all the answers

What is expected to occur in an area of unidirectional block?

Retrograde impulse may be propagated Signup and view all the answers

What is a potential consequence of circulation of multiple reentry circuits through the heart?

Random meandering of impulses Signup and view all the answers

In what area is calcium current particularly important for conduction depression?

AV node Signup and view all the answers

What is the effect when impulses collide in a normal conduction pathway?

The impulses become extinguished Signup and view all the answers

What term describes the situation when an impulse travels through the site of block due to shorter refractory period?

Retrograde transmission Signup and view all the answers

What is typically necessary for triggered automaticity to occur?

A normal action potential Signup and view all the answers

What is the primary action of Class 1 antiarrhythmic drugs?

Sodium channel blockade Signup and view all the answers

Which subclass of Class 1 drugs prolongs the action potential duration (APD)?

Class 1A Signup and view all the answers

What effect does procainamide have on the upstroke of the action potential?

Slows the upstroke Signup and view all the answers

Which subclass of Class 1 drugs dissociates from the sodium channel with rapid kinetics?

Class 1B Signup and view all the answers

What additional effect does procainamide exhibit aside from sodium channel blockade?

Potassium channel blockade Signup and view all the answers

Which class of antiarrhythmic drugs is recognized for having minimal effects on the APD?

Class 1C Signup and view all the answers

Which class of drugs is considered sympatholytic?

Class 2 Signup and view all the answers

What is the primary mechanism by which Class 3 antiarrhythmic drugs work?

Blocking potassium channels Signup and view all the answers

Which of the following drugs is more effective than procainamide in suppressing abnormal ectopic pacemaker activity?

Quinidine Signup and view all the answers

What is the effect of procainamide on the QRS duration in an ECG?

Prolongs the QRS duration Signup and view all the answers

Study Notes

Case Study Overview

A 69-year-old woman experiences palpitations, shortness of breath, and fatigue.
History of hypertension; ECG shows paroxysms of atrial fibrillation with heart rates of 88-114 bpm.
Echocardiogram reveals a left ventricular ejection fraction of 38% and signs of left ventricular hypertrophy.
Patient was anticoagulated with warfarin; sustained-release metoprolol was initiated at 50 mg/d.
After 7 days, normal sinus rhythm returns spontaneously.

Arrhythmias in Clinical Practice

Cardiac arrhythmias affect up to 25% of digitalis-treated patients, 50% of anesthetized patients, and over 80% of those with acute myocardial infarction.
Arrhythmias can lead to reduced cardiac output and possible fatal rhythm disturbances, needing prompt treatment with antiarrhythmic drugs.

Cardiac Electrical Activity

The electrical impulse originates in the sinoatrial (SA) node, typically at 60-100 bpm.
The impulse rapidly spreads through the atria to the atrioventricular (AV) node, the main conduction pathway to the ventricles.
Abnormal rhythms can disrupt cardiac function and require intervention.

Calcium Channels and Depolarization

Calcium channels (especially the "L" type) have slow activation and inactivation compared to sodium channels.
Depolarization affects sodium currents and can alter action potentials, with hyperkalemia or ischemia impacting cardiac function.
Phase 3 repolarization involves inactivation of sodium and calcium channels, leading to increased potassium permeability.

Reentry Circuits and Arrhythmias

Reentry circuits can form due to abnormal electrical conduction, with impulses propagating through excitable tissue.
These circuits can generate arrhythmias, with altered conduction velocities giving rise to multiple daughter impulses.

Antiarrhythmic Drug Classes

Antiarrhythmic drugs are categorized into four classes based on their mechanism of action:
- Class 1: Sodium channel blockers, affecting action potential duration.
- Class 2: Sympatholytic agents reducing β-adrenergic activity.
- Class 3: Prolonging action potential duration through potassium current blockade.

Specific Antiarrhythmic Agents

Procainamide (Class 1A): Slows action potential upstroke, prolongs QRS duration and APD, slightly less effective than quinidine for suppressing ectopic activity.

Pharmacologic Properties of Antiarrhythmic Drugs

Various antiarrhythmic agents have distinct effects on SA node rate, AV nodal refractory period, QRS duration, and QT interval, influencing their use in supraventricular and ventricular arrhythmias.
Adenosine: Decreases SA nodal rate, significantly increases AV nodal refractory period.
Amiodarone: Reduces SA rate, variable effects on AV refractory period, prolongs QT interval.
Diltiazem: Modulates SA/AV nodal activity without affecting QRS duration; useful in SV arrhythmias.
Flecainide: Affects AV refractory period with significant impact on ventricular arrhythmias.

Key Points on Drug Selection

Drug choice should consider the type of arrhythmia, cardiac status, and specific effects on heart rhythm parameters.
Antiarrhythmic agents have varying half-lives and need careful management due to potential side effects and interactions.

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Description

Explore a detailed case study focusing on agents used in cardiac arrhythmias. This chapter discusses the symptoms and ECG findings of a patient experiencing palpitations and shortness of breath. Gain insights into the management and treatment options for cardiac conditions.