CV Pharmacology: Antiarrhythmics Overview

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Questions and Answers

What is a common adverse effect associated with sodium channel blockers?

Improved contractility

Oedema in feet and ankles (correct)

Increased alertness

Increased heart rate

Which class of drugs is combined with K+ channel blocking effects to lengthen action potentials?

Beta blockers

Class Ib drugs

Calcium channel blockers

Class Ia drugs (correct)

What is the mechanism by which sodium channel blockers affect action potentials?

They speed up the conduction through conductive tissue

They increase the rate of depolarization

They activate the sodium channels more quickly

They slow down generation of action potentials (correct)

What does the term 'negative inotropic effect' refer to?

Decreased muscle contraction strength Signup and view all the answers

Which Class Ia drug is considered obsolete due to its high risk of TdP?

Quinidine Signup and view all the answers

What is one common cause of tachycardias related to myocytes?

Ectopic pacemaker activity Signup and view all the answers

Which phenomenon refers to impulse re-exciting previously active tissue?

Re-entry Signup and view all the answers

What physiological change can trigger ectopic beats?

Abnormally high intracellular calcium concentration Signup and view all the answers

During which phases do early afterdepolarizations primarily occur?

Phase 2 and 3 Signup and view all the answers

What underlying condition is often associated with re-entry phenomena?

Damaged heart tissue Signup and view all the answers

What is the main characteristic of torsade de pointes (TdP) related to electrical activity in the ventricles?

Involves delayed afterdepolarisations during phase 4 Signup and view all the answers

What occurs during the re-entry phenomenon in the myocardium?

Electrical activity being blocked in part of the myocardium Signup and view all the answers

Which syndrome is characterized by a bypass of the AV node leading to re-entry tachycardias?

Wolfe-Parkinson-White syndrome Signup and view all the answers

What is the primary cause of abnormal automaticity in pacemaker cells?

Increase in phase 4 depolarisation Signup and view all the answers

Which class of the Vaughan-Williams classification includes voltage-gated Na+ channel blockers?

Class I Signup and view all the answers

What type of medications are classified under Class II of the Vaughan-Williams classification?

Anti-sympathetics (beta blockers) Signup and view all the answers

In the context of abnormal automaticity, what can lead to decreased action potential threshold?

Increased excitatory neurotransmitter levels Signup and view all the answers

Which class of the Vaughan-Williams classification is primarily associated with voltage-gated K+ channel blockers?

Class III Signup and view all the answers

Which Class 1b drug is most commonly used for emergency treatment of ventricular tachycardia?

Lidocaine Signup and view all the answers

What is a prominent risk associated with using Flecainide after a myocardial infarction (MI)?

Sudden death Signup and view all the answers

Which class of drugs is characterized by slow dissociation and is used for both atrial fibrillation and some ventricular tachycardias?

Class 1c Signup and view all the answers

Which of the following is a common side effect of beta-blockers?

Dizziness Signup and view all the answers

What mechanism do Class III drugs primarily utilize?

Block K+ channels Signup and view all the answers

Which of the following beta-blockers is β1-selective and preferred for general use?

Atenolol Signup and view all the answers

How do beta-blockers reduce arrhythmias due to excessive sympathetic activity?

Antagonizing β receptors Signup and view all the answers

What significant risk may occur if Class 1c drugs are used in patients with a weak heart?

Heart failure Signup and view all the answers

Which of the following options is a potential treatment for paroxysmal atrial fibrillation?

Beta-blocker Signup and view all the answers

Which class of anti-arrhythmic medications primarily works by lengthening action potentials in cardiac nodes?

Class 4: Calcium channel blockers Signup and view all the answers

What pharmacological agents are preferred for cardioversion in a haemodynamically stable ventricular tachycardia?

Amiodarone, then flecainide Signup and view all the answers

The 'pill in the pocket' approach is associated with which of the following therapies?

Single-dose antiarrhythmic for paroxysmal atrial fibrillation Signup and view all the answers

In the context of cardiac action potentials, which of the following is a general negative chronotropic effect of anti-arrhythmics?

Slowed action potential generation Signup and view all the answers

What is the primary mechanism of action for Class 3 anti-arrhythmics?

Delay repolarisation Signup and view all the answers

What is the role of digoxin in treating heart conditions?

Sedate an active lifestyle Signup and view all the answers

Which of the following drugs is typically NOT used in the management of haemodynamically stable ventricular tachycardia?

Adenosine Signup and view all the answers

What effect does increased ACh release have on M2 receptors in nodal cells?

Increased K+ efflux leading to hyperpolarisation Signup and view all the answers

Which treatment is first line for bradycardia?

IV Atropine Signup and view all the answers

What is the primary action of adenosine in treating supraventricular tachycardias?

Activates A1 receptors to increase K+ permeability Signup and view all the answers

What characterizes the effect of digoxin on myocytes?

Inhibition of Na+/K+ pump leading to increased intracellular calcium Signup and view all the answers

What is the main purpose of rate control in atrial fibrillation?

To prevent transmission of tachycardia to the ventricles Signup and view all the answers

Which of these is a potential side effect of adenosine administration?

Nausea Signup and view all the answers

What might result from increased intracellular Na+ levels due to digoxin?

Increased intracellular Ca2+ Signup and view all the answers

Which of the following is NOT a negative chronotropic agent?

IV Atropine Signup and view all the answers

Study Notes

CV Pharmacology: Arrhythmias

The lecture covers the electrophysiology behind the cardiac action potential.
It outlines how antiarrhythmic drugs alter ion flux and electrical properties of heart cells.
Specific targets are sodium channel blockers, beta-blockers, potassium channel blockers, and calcium channel blockers.
The therapeutic uses and adverse effects of these antiarrhythmic drugs are also addressed.

Cardiac Electrical Activity

The heart's electrical activity is controlled by the sino-atrial node, atrio-ventricular node, and Purkinje fibres.

Cardiac Syncytium

The heart's syncytium is a network of cells connected by gap junctions.
Electrical signals, in the form of action potentials, directly pass through these junctions to synchronise muscle contraction.
A histological picture of cardiac myocytes with intercalated disks are included. A schematic diagram of cardiac myocytes is also shown.

Cardiac Myocyte Action Potential (AP)

The cardiac myocyte AP includes rapid depolarisation (VG Na+), partial repolarisation (VG K+), a plateau phase (L-type VG Ca2+ vs. K+), repolarisation (VG K+), and rest (leak K+).
The effective refractory period (ERP) is a crucial phase in the AP.

Cardiac Nodal AP

Nodal APs have distinct phases: depolarisation (T/L-type VG Ca2+), repolarisation (VG K+), and pacemaker depolarisation (leak K+ & leak Na+).
Sympathetic (β1/2) and vagal (parasympathetic; mAChR) innervation play a role.

Electrocardiogram (ECG)

The ECG displays the electrical activity of the heart over time.
Key components are P-wave (atrial depolarisation), QRS complex (ventricular depolarisation), and T-wave (ventricular repolarisation).

Dysrhythmia Classifications

Arrhythmias are categorized by their location (e.g., superventricular, atrial, junctional, ventricular).
Arrhythmias are also categorized by their rate (tachycardia or bradycardia) and patterns (e.g., fibrillation, flutter).

Terminology

Chronotropic: altering the heart rate.
Inotropic: altering the strength of heart contractions.
Automaticity: the property of heart cells to spontaneously generate action potentials.
Ectopic beats: action potentials generated in the wrong place or phase compared to the normal electrical conduction pathway.

Common Causes of Tachycardias

After-polarization: high [Ca2+], triggering trains of APs and causes ectopic beats.
Re-entry: impulse re-excites previously active tissue, often associated with damaged heart tissue.
Ectopic pacemaker activity: excessive automaticity in nodes or activity outside normal nodes.

Triggered Activity

Early afterdepolarisations occur during phase 2/3 of the cardiac action potential, mediated by elevated Ca2+
Delayed afterdepolarisations occur during phase 4, potentially initiating arrhythmias.

Re-entry

Action potentials blocked in part of the myocardium (cells in refractory period). Refractory cells may be activated by backpropagation.
APs pass through myocardium from node to node, leading to synchronised depolarisation in normal conditions. In re-entry, the signal may backpropagate out of phase, causing additional contractions.

Slow-Fast AVN Path

A discussion of the electrical pathways through the atrioventricular node (AVN). The schematic diagrams show the slow and fast pathways, highlighting the differences in conduction velocity and their clinical relevance.

Wolfe-Parkinson-White Syndrome

Re-entry occurs in Wolfe-Parkinson-White syndrome with an accessory pathway bypassing the AV node.
This pathway can transmit atrial tachycardias to ventricles.

Abnormal Automaticity

Pacemaker cells are excessively active, increasing phase 4 depolarisation and lowering the AP threshold.
This can lead to tachycardia.

Vaughan-Williams Classification

This system classifies antiarrhythmic drugs based on their electrophysiological effects. It is clinically outdated, but useful for learning purposes.

Class 1: Sodium Channel Blockers

Block sodium channels to slow or prevent the generation of action potentials in myocytes.
Adverse effects include oedema (feet/ankles), dizziness.

Class 1A, 1B, and 1C Drugs

Detailed information on different types of sodium channel blockers, their mechanisms of action, therapeutic uses, side effects and ECG characteristics.

Class II: Beta-blockers

Antagonise adrenergic beta receptors. Reducing sympathetic nervous system activity and preventing tachycardia.
Specific drugs like atenolol, bisoprolol, metoprolol, and propranolol are discussed.

Class III: Potassium Channel Blockers

Prolong the refractory period in nodal and myocardial tissues through blocking potassium channels. Amiodarone is heavily highlighted as a prominent drug in this Class, as well as its therapeutic and potential toxicities.

Class IV: Calcium Channel Blockers

Block calcium channels (L-type) to decrease nodal action potential amplitude and increase length of the nodal AP.
Verapamil and Diltiazem are key drugs in this category.

Digoxin

Digoxin inhibits the Na+/K+ pump in myocytes.
This increases intracellular calcium levels, leading to a positive inotropic effect but a negative chronotropic effect, particularly on nodes.

Adenosine

Emergency medication for superventricular tachycardias.
Activates A1 receptors in the AV node causing hyperpolarisation and slowing conduction rates.

Drugs for Bradyarrhythmias

Atropine, and sympathomimetic agents (adrenaline, dopamine, dobutamine) are mentioned as drugs to treat bradyarrhythmias through increasing heart rate.

Atrial Tachycardias

Focuses on maintaining orderly ventricular activation to prevent the conduction of atrial tachycardia.
Discussion of rate control and rhythm control strategies in the treatment of atrial tachycardias.

A-fib: Rate and Rhythm Control

Details about strategies for treating atrial fibrillation (A-fib), including rate and rhythm control interventions. Discussing the relevant drugs and procedures.

Ventricular Tachycardias

Discusses non-heamodynamically stable ventricular tachycardias and treatment strategies.
Strategies for management when haemodynamically stable.

Summary

Antiarrhythmics modify cardiac action potentials.
General negative chronotropic effects slow AP generation and lengthen the refractory period.
Various drug classes (1-4) with their mechanisms are summarized.

Pictorial Summary

A visual representation of the various drug classes and their effects on different aspects of cardiac action potentials.

Sicilian Gambit

A detailed table outlining a variety of antiarrhythmic drugs, their mechanisms of actions, and various other factors.

MBBS Learning Outcomes

Indicates the importance of the topic in relation to broader medical education.

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Description

This quiz explores the electrophysiology of cardiac action potentials and the role of antiarrhythmic drugs. It covers sodium channel blockers, beta-blockers, potassium channel blockers, and calcium channel blockers, discussing their mechanisms, therapeutic uses, and side effects. Additionally, it touches on cardiac electrical activity and syncytium, enhancing your understanding of cardiac function.