1: Cardiac Electrophysiology

Electrical signals generated by the heart muscle, responsible for heart contractions. They last longer than nerve and skeletal muscle action potentials.

Types of heart cells that have a true resting membrane potential. These cells are responsible for contracting the atria and ventricles, and transmitting electrical signals. Examples include atrial and ventricular myocytes, and Purkinje fibers.

Types of heart cells that lack a true resting membrane potential and spontaneously initiate electrical signals. These cells are responsible for setting the heart's rhythm. Examples include the sinoatrial and atrioventricular nodes.

The process of creating an electrical signal across the cell membrane of heart cells. It's caused by the movement of ions (Na+, K+, Ca++) across the membrane due to concentration gradients and channel openings.

The difference in electrical charge between the inside and outside of a cell membrane at rest. In heart cells, it's maintained by ion transport pumps that actively pump ions across the membrane.

The controlled movement of ions across the cell membrane through channels. These currents are responsible for the creation and propagation of electrical signals in the heart.

The pacemaker current, also known as the funny current (If), is responsible for initiating spontaneous depolarization in pacemaker cells. It is primarily driven by a slow inward sodium current. This current is crucial for establishing the heart's intrinsic rhythm.

This phase is characterized by a gradual depolarization of the membrane potential, leading to the triggering of an action potential. This spontaneous depolarization is primarily driven by the pacemaker current (If).

This phase is characterized by a rapid depolarization of the membrane potential, primarily driven by an influx of calcium ions through L-type calcium channels. This phase is responsible for the upward swing of the action potential.

This phase is characterized by a gradual repolarization of the membrane potential, primarily driven by an efflux of potassium ions. It allows the membrane potential to return to its resting state.

This phase refers to the resting membrane potential of non-pacemaker cells. During this phase, potassium permeability is high, and the cell is ready to be stimulated.

This phase initiates a rapid depolarization in non-pacemaker muscle cells. It is triggered by a sudden influx of sodium ions through fast sodium channels, leading to a rapid increase in membrane potential.

This phase is characterized by a brief repolarization, primarily driven by an efflux of potassium ions. It follows the rapid depolarization of Phase 0.

This phase represents a plateau period where calcium permeability is high. It contributes to the prolonged depolarization of the action potential in non-pacemaker cells.

The sinoatrial node (SAN) is the primary pacemaker of the heart, initiating the electrical impulse that triggers each heartbeat. It's located in the right atrium.

Specialized pathways within the atria (internodal tracts) carry the electrical impulse from the SAN to the AV node, ensuring synchronized atrial contraction.

The atrioventricular node (AVN) acts as a gatekeeper, delaying the impulse before it reaches the ventricles. This delay allows the atria to contract fully before the ventricles begin.

The bundle of His is a specialized pathway that rapidly conducts the electrical impulse from the AV node to the ventricles.

These branches extend from the bundle of His, carrying the electrical impulse to the left and right ventricles, ensuring simultaneous contraction.

These fibers distribute the electrical impulse throughout the ventricle walls, facilitating rapid and uniform ventricular contraction.

Autonomic nerve activity can influence heart conduction velocity. Sympathetic activation (via β1 receptors) increases conduction speed (positive dromotropy), while parasympathetic (vagal) activation (via M2 receptors) decreases conduction speed (negative dromotropy) primarily at the AV node.

Circulating catecholamines, like adrenaline, also influence conduction velocity. They increase conduction speed (positive dromotropy) by acting on β1 receptors.

Changes in phase 0 slope of the action potential can alter conduction velocity. Decreased phase 0 slope in AVN cells reduces conduction velocity, often caused by calcium channel inactivation or blockade, while decreased phase 0 slope in non-nodal cells is primarily due to sodium channel dysfunction.

Conduction blocks occur when the electrical impulse is interrupted or delayed, hindering the signal flow through the heart. Ectopic foci are abnormal pacemaker cells that initiate electrical activity outside the normal SAN, leading to irregular heartbeats.

Hyperkalemia can depolarize cells, causing a decrease in conduction velocity. It also alters the phase 0 of the action potential, leading to a slower upstroke and a decrease in conduction velocity.

Beta-blockers reduce heart rate and conduction velocity by blocking the effects of norepinephrine and epinephrine, which are sympathetic neurotransmitters. This slowing effect is a key mechanism for their use in treating arrhythmias.

Abnormal pacemaker sites, such as ectopic foci, can disrupt the normal conduction pathways and lead to irregular heartbeats, such as premature contractions (PVCs). These are localized regions within the heart that spontaneously generate action potentials independently of the SA node.

A complete AV block, also known as 3rd-degree AV block, is a complete dissociation between atrial and ventricular contractions due to a complete blockage of action potential transmission through the AV node. This results in a slow, chaotic, and irregular heart beat.

Reentry circuits can create local or global tachyarrhythmias. A reentry circuit is when an impulse circulates within the heart, leading to a rapid heart rate. The requirements for reentry include a partial depolarization of the conduction pathway, a unidirectional block, and critical timing.

The Wolff-Parkinson-White syndrome (WPW) is a type of global reentry. It involves an accessory pathway between the atria and ventricles that bypasses the AV node, leading to rapid and potentially dangerous heart rate. This results in a premature contraction of the ventricles, which can cause palpitations and dizziness.