Pharmacology II: Antiarrhythmic Agents

The regular heartbeat rhythm, usually between 60 and 100 beats per minute (bpm), which originates from the electrical impulses in the sinoatrial (SA) node.

A disruption in the normal rhythm of the heart, ranging from minor and asymptomatic to life-threatening.

Heart rhythm abnormalities can be caused by problems with the generation or conduction of electrical impulses within the heart. These include automaticity and conduction.

Refers to the ability of heart cells to spontaneously generate electrical impulses. Abnormal automaticity can lead to faster or slower heartbeats.

Abnormal electrical activity that occurs in the heart, leading to extra heartbeats or abnormal rhythms. This can occur even when the heart is not actively generating its own impulses.

A disturbance in the normal conduction pathway of electrical impulses within the heart, resulting in a delay or block in the transmission of electrical signals.

The electrical activity in the heart slows down or is interrupted, leading to incomplete or absent heartbeats.

A circular pathway for electrical impulses in the heart causing a rapid, repetitive beating.

A classification system for antiarrhythmic drugs based on their primary electrophysiological effects. It categorizes drugs based on how they modify heart muscle action potentials and conduction.

Antiarrhythmic drugs primarily block sodium (Na+) channels in the heart, slowing down the speed of electrical signals through heart muscle.

These drugs have an intermediate effect on sodium channels, blocking them for a moderate duration.

These drugs exhibit a fast on-and-off effect on sodium channels, quickly blocking and releasing them.

These drugs have a slow on-and-off effect on sodium channels, blocking them for a longer period.

These drugs primarily block beta-receptors in the heart, indirectly affecting calcium (Ca++) channels and slowing heart rate.

Decreased conduction velocity through the heart, often combined with increased AV nodal refractoriness, resulting in bradycardia or heart block.

Antiarrhythmic agents typically exert multiple actions, often affecting more than one class of Vaughan Williams classification.

Class I antiarrhythmics block sodium channels during the action potential (AP), specifically during phases 0 and 2.

They bind preferentially to activated or inactivated sodium channels, not to resting channels. This means they have a greater effect on the heart when it's beating faster.

Class Ia drugs have a slower recovery from block (around 1-10 seconds), leading to a prolonged AP duration.

Class Ib drugs have a much faster recovery from block (within hours), leading to minimal effect on AP duration.

Class Ic drugs have a very slow recovery from the block (several hours), leading to a significant prolongation of the AP duration.

Flecainide, a Class Ic antiarrhythmic, is used primarily for supraventricular arrhythmias in patients with structurally normal hearts.

Flecainide is known to block both sodium and potassium channels, but it only weakly prolongs the QT interval.

Flecainide is generally well-tolerated, but dose-related side effects like blurred vision, arrhythmias, and worsening heart failure can occur.

Sympathetic nervous system (SNS) stimulation triggers the release of norepinephrine (NE), which activates beta-1 adrenergic receptors in the heart.

Norepinephrine (NE) binding to beta-1 adrenergic receptors opens L-type Ca++ channels, leading to increased intracellular calcium.

Increased intracellular calcium results in enhanced heart rate, faster conduction, and a shorter refractory period.

Beta-blockers block the effects of norepinephrine on beta-1 adrenergic receptors, ultimately reducing heart rate and slowing conduction.

Beta-blockers reduce heart rate by decreasing automaticity in the SA node, slowing conduction through the AV node, and prolonging the AV nodal refractory period.

Beta-blockers decrease intracellular calcium overload, which is protective against myocardial infarction and ischemic tissue.

Beta-blockers are used in various forms (oral, IV), with different agents having varying selectivity and properties.

Beta-blockers can cause adverse effects like bradycardia, heart block, bronchospasm, cold extremities, and impotence.

The inward movement of positively charged calcium ions (Ca++) into a cardiac cell, causing a depolarization (change in electrical potential). This depolarization is a key step in the heart's electrical cycle.

The process by which a cardiac cell returns to its resting electrical potential after depolarization. This happens due to efflux (outward movement) of potassium ions (K+) and inactivation of calcium channels, which are responsible for the initial depolarization.

The ability of certain cardiac cells to generate their own electrical impulses (action potentials) without external stimulation. This property is crucial for maintaining a regular heartbeat.

Group of specialized cells located in the right atrium of the heart. They function as the primary pacemaker of the heart, initiating electrical impulses that travel throughout the heart, causing contractions.

Specialized group of cells located in the junction between the atria and ventricles of the heart. It acts as a relay, slowing down the electrical impulse from the SA node, allowing the atria to contract before the ventricles.

Network of specialized conducting fibers in the ventricles of the heart that rapidly transmit electrical signals from the AV node to the ventricular muscle, ensuring coordinated contraction.

The speed at which pacemaker cells can spontaneously initiate action potentials (electrical impulses). The higher the rate, the faster the heart will beat.

The electrical activity of the heart, recorded as a waveform on an electrocardiogram (ECG). These waveforms are the graphical representation of the electrical impulses traveling through the heart.

A drug used to treat atrial fibrillation and atrial flutter. It works by blocking potassium, sodium, and calcium channels, and also has beta and alpha blocking properties.

A drug used to treat ventricular and supraventricular arrhythmias. It works by blocking potassium channels and also has beta-blocking properties.

A class of medications that block the effects of the sympathetic nervous system, often used to treat high blood pressure, heart rhythm problems, and other cardiovascular conditions.

A measure of how well the kidneys are filtering waste products from the blood.

A serious heart rhythm problem that can be fatal. It occurs when the heart beats too quickly and irregularly, which can lead to a sudden loss of consciousness.

A common measure of liver function. It tests the levels of certain enzymes in the blood, which can be elevated if the liver is damaged.

A measure of how quickly a drug is eliminated from the body.

A drug that is poorly soluble in water. It needs a solvent to be administered, and its accumulation in tissues can lead to potential side effects.

The initial dose of medication given to a patient to achieve a therapeutic effect rapidly.

A group of enzymes in the liver responsible for metabolizing drugs. They can be inhibited by some medications, leading to potential drug interactions.