Antidysrhythmic Drugs Quiz

An abnormal rhythm of the heartbeat. This disturbance can be mild, with a modest effect on the heart's ability to pump blood, or severe, rendering the heart unable to pump.

Drugs used to treat dysrhythmias (irregular heartbeats). They work by influencing the heart's electrical activity.

Fast heart rhythm, a type of dysrhythmia.

Slow heart rhythm, a type of dysrhythmia.

The ability of antidysrhythmic drugs to create or worsen existing dysrhythmias. This adds risk to their use, underscoring the importance of a careful evaluation of the benefits versus risks.

The SA node is responsible for initiating and regulating the heartbeat; it is the heart's natural pacemaker.

The AV node acts as a gatekeeper, slowing down electrical impulses before they reach the ventricles, allowing time for the ventricles to fill with blood.

The His-Purkinje system rapidly conducts electrical impulses to the ventricles, ensuring synchronized and strong contraction to pump blood effectively.

A fast potential is an action potential that occurs in the His-Purkinje system, atrial, and ventricular muscle, enabling rapid conduction of electrical impulses through the heart.

Sodium influx is responsible for the rapid depolarization phase (phase 0) of a fast potential, influencing the speed of electrical impulse conduction.

The phase of the cardiac action potential where rapid repolarization occurs, caused by potassium leaving the cell. Drugs that block potassium channels can delay this phase, which has implications for antidysrhythmic drug action.

The ability of cardiac cells to initiate an action potential through self-excitation. This is driven by spontaneous depolarization during phase 4 of the action potential. Pathological conditions can enhance this process and lead to dysrhythmias.

The interval between the start of atrial depolarization (P wave) and ventricular depolarization (QRS complex) on an electrocardiogram (ECG). A longer interval suggests slowed conduction through the AV node.

The phase of the cardiac action potential where calcium enters the cell and triggers muscle contraction. Drugs that affect calcium influx during this phase can reduce myocardial contractility but won't directly alter heart rhythm.

The time during which a cell is unable to respond to excitation or generate another action potential. Extending this period can help prevent dangerous dysrhythmias by preventing rapid, chaotic heartbeats.

The SA node, AV node, and His-Purkinje system are the heart's natural pacemakers, responsible for initiating and regulating the heartbeat.

When cells normally capable of automaticity discharge faster or slower than usual, it disrupts the normal heart rhythm, leading to dysrhythmias.

This occurs when tissues that typically don't have automaticity (atrial and ventricular muscle) develop spontaneous depolarization, causing irregular heartbeats.

This type of block occurs when impulse conduction through the AV node is delayed but not completely blocked.

Impulses are blocked but not completely, resulting in certain heartbeats being skipped.

This is when all impulses are blocked from passing through the AV node, leading to a complete disconnect between atrial and ventricular rhythms.

A reentrant circuit is a self-sustaining electrical loop that causes repetitive cardiac stimulation, resulting in various dysrhythmias. It occurs due to a one-way block, where an impulse can travel up a branch but not down.

A type of atrial dysrhythmia caused by an ectopic atrial focus discharging at a rapid rate (250 to 350 times per minute).

The preferred treatment for atrial flutter is DC cardioversion, which can almost always restore normal sinus rhythm.

Drugs that suppress AV conduction, like verapamil, diltiazem, or β-blockers, are used to control ventricular rate in atrial flutter.

Sustained SVT is typically caused by an AV nodal reentrant circuit, leading to a significantly increased heart rate (150 to 250 beats per minute).

Increasing vagal tone, such as via carotid sinus massage or the Valsalva maneuver, can be effective treatment for SVT.

Ventricular dysrhythmias can disrupt cardiac pumping, unlike atrial dysrhythmias, which are generally benign.

Ventricular tachycardia (VT) stems from a rapidly firing ectopic focus in the ventricle, typically at the site of an old infarct.

Ventricular fibrillation (VF) is a life-threatening condition characterized by asynchronous electrical activity in the ventricles, leading to complete loss of heart function.

Premature ventricular complexes (PVCs) are ectopic beats occurring before the normal beat in the cardiac cycle.

Class I antidysrhythmic drugs primarily act by blocking sodium channels, reducing the speed of electrical impulses through the heart.

Beta-blockers reduce the heart rate by blocking the effects of adrenaline and noradrenaline, which speed up the heart. They are considered Class II antidysrhythmic drugs.

Class III antidysrhythmic drugs like amiodarone prolong the action potential, delaying the repolarization of the heart's cells, thus slowing down the heart rate.

Class IV antidysrhythmic drugs (calcium channel blockers) like verapamil and diltiazem reduce heart rate and contractility by blocking calcium channels, which are responsible for muscle contraction.

Prodysrhythmic effects occur when antidysrhythmic drugs worsen existing heart rhythm problems or even create new ones. This is a significant risk associated with their use.

Ventricular dysrhythmias, arising from the ventricles of the heart, pose a greater danger than supraventricular dysrhythmias, originating in the upper chambers.

Treatment for dysrhythmias often involves two phases: initial termination of the arrhythmia followed by long-term suppression with drugs or other therapies.

Atrial fibrillation, the most common sustained dysrhythmia, is characterized by chaotic atrial activity leading to irregular heartbeats. It can increase the risk of stroke.

Vagotonic maneuvers, DC cardioversion, and specific drugs, such as beta-blockers, calcium channel blockers, adenosine, and digoxin, are commonly used to treat acute supraventricular dysrhythmias.

A specialized area in the heart responsible for initiating and regulating the heartbeat. It's the heart's natural pacemaker.

A critical structure in the heart that acts as a gatekeeper, slowing down electrical impulses before they reach the ventricles to allow adequate time for the ventricles to fill with blood.

The SA node is the natural pacemaker of the heart, controlling the rhythm by spontaneously generating electrical impulses.

The effective refractory period (ERP) represents the time during which a cardiac cell is unable to respond to excitation or generate another action potential. It's a vital protective mechanism against chaotic heartbeats.

During this phase, calcium enters the cell and promotes the contraction of atrial and ventricular muscle.

The ability of heart cells to spontaneously create electrical impulses, which is crucial for maintaining the rhythm of the heartbeat.

Drugs that block sodium channels to slow down electrical impulses in the heart.

A disturbance in the heart's rhythm caused by an abnormality in the heart's natural pacemaker, the SA node.

A disturbance in the heart's rhythm caused by an abnormality in the heart's electrical conduction system, specifically the AV node.

A disturbance in the heart's rhythm that occurs when an electrical impulse travels in a loop, causing repetitive and uncontrolled stimulation of the heart muscle.

Class I antidysrhythmic drugs work by blocking sodium channels, thus reducing the speed of electrical impulses through the heart.

Class II antidysrhythmic drugs, also known as beta-blockers, work by blocking the effects of adrenaline and noradrenaline, which speed up the heart.

Class III antidysrhythmic drugs prolong the action potential, effectively delaying the repolarization of the heart's cells and slowing down the heart rate.

Class IV antidysrhythmic drugs, calcium channel blockers, work by blocking calcium channels, which are critical for muscle contraction, thereby slowing down the heart rate and reducing contractile force.

Class I antidysrhythmic drugs, like lidocaine and procainamide, primarily work by blocking sodium channels. This reduces the speed of electrical impulses throughout the heart, helping to regulate an abnormal heartbeat.

Beta-blockers, like propranolol and metoprolol, act by reducing the effects of adrenaline, the 'fight-or-flight' hormone. By doing so, they slow down the heart rate and reduce its force of contraction, helping to control dysrhythmias.

Drugs belonging to Class III, such as amiodarone, extend the action potential duration, effectively delaying the repolarization phase of the heart's electrical cycle. This slows down the heart rate and helps regulate irregular rhythms.

These drugs, like verapamil and diltiazem, act by blocking calcium channels in the heart cells, reducing the strength of contractions and slowing the heart rate. They effectively manage dysrhythmias by controlling overactive hearts.

A significant risk associated with antidysrhythmic drugs is their potential to worsen existing heart rhythm problems or even create new ones. These are known as prodysrhythmic effects.

Ventricular tachycardia is a life-threatening condition in which the ventricles beat too fast, often between 150 and 250 times per minute. This rapid beating is caused by a single, rapidly firing focus within the ventricle.

Ventricular fibrillation (VF) is a life-threatening emergency that requires immediate treatment via electrical defibrillation. During VF, the heart's ventricles quiver randomly, causing complete loss of cardiac function and blood flow to the body.

Digoxin toxicity can mimic a wide range of heart rhythm problems, from mild AV block to severe ventricular flutter or fibrillation. It acts by disrupting the heart's electrical activity.

Cardioversion, a medical procedure involving electrical shock, is used to eliminate fibrillation and restore normal cardiac function in cases of ventricular fibrillation.

Atrial flutter is a type of atrial dysrhythmia where an ectopic focus in the atrium discharges rapidly, causing a rapid heartbeat. Though the atrium beats rapidly, the ventricles usually beat at a slower rate.

Sustained supraventricular tachycardia (SVT) is a condition involving a rapid heart rate (150-250 beats per minute) caused by a reentrant circuit in the AV node, an area near the heart's upper and lower chambers.

Ventricular dysrhythmias are serious heart rhythm problems originating in the ventricles, which can disrupt the heart's pumping function. In contrast, atrial dysrhythmias, often benign, originate in the atria.