Cardiac Physiology: Cardiac Action Potentials & Contraction

Cardiac Physiology: Cardiac Action Potentials & Contraction

Objectives

This section covers the generation of cardiac action potentials and the mechanisms underlying heart contraction. Understanding these processes is essential for grasping how the heart maintains rhythmic pumping and responds to physiological demands.

• Generation of Cardiac Action Potentials: The heart's electrical activity originates from specialized cells that do not require nervous system input.

• Description of Heart Contraction: The coordinated contraction of cardiac muscle ensures effective blood circulation.

Cardiac Autorhythmic Cells

Characteristics and Function

Autorhythmic cells are specialized cardiac cells responsible for initiating and regulating the heart's electrical impulses. Unlike contractile cells, they do not contribute to the force of contraction but are essential for setting the heart's rhythm.

• Generation of Action Potentials: Autorhythmic cells spontaneously generate action potentials, independent of nervous system stimulation.

• No Contractile Function: These cells do not contract but activate adjacent contractile cells.

• Key Locations: The sinoatrial (SA) node, atrioventricular (AV) node, and the bundle of His are major sites of autorhythmic cells in the heart.

Example: The SA node, located in the right atrium, acts as the primary pacemaker, setting the pace for the entire heart.

Pacemaker Potential

Definition and Mechanism

The pacemaker potential refers to the gradual depolarization of autorhythmic cell membranes, leading to the threshold required for action potential generation. This process is distinct from the stable resting membrane potential seen in nerve and skeletal muscle cells.

• Slow Drift to Threshold: The membrane potential of autorhythmic cells slowly rises toward threshold due to specific ion channel activity.

• Self-Induced Action Potentials: Unlike other excitable cells, autorhythmic cells do not require external stimuli to reach threshold.

Comparison Table:

Cell Type	Resting Membrane Potential	Action Potential Initiation
Nerve/Skeletal Muscle	Stable	Requires stimulus
Cardiac Autorhythmic	Pacemaker potential (slow drift)	Self-induced

Ion Mechanisms in Pacemaker Potential

Multiple ionic mechanisms contribute to the pacemaker potential, resulting in rhythmic action potential generation.

• Na+ Influx: Sodium ions enter the cell through If (funny) channels, causing initial depolarization.

• K+ Efflux: Potassium ions exit the cell, but the efflux gradually decreases, contributing to depolarization.

• Ca2+ Influx: Transient and long-lasting calcium channels open as the membrane approaches threshold, further depolarizing the cell.

Example: The opening of voltage-gated Ca2+ channels at threshold leads to a rapid upstroke in the action potential.

Phases of Pacemaker Potential

The pacemaker potential consists of several phases, each characterized by specific ion channel activity.

• Initial Depolarization: Net Na+ influx through If channels moves the membrane potential toward threshold.

• Threshold Achievement: Transient Ca2+ channels open, allowing brief Ca2+ influx and further depolarization.

• Rapid Depolarization: Long-lasting Ca2+ channels open, causing a steep rise in membrane potential.

• Repolarization: K+ channels open, allowing K+ efflux and returning the membrane potential to its starting value.

Equation:

$\text{Pacemaker Potential} = \text{Net Na}^+ \text{influx} + \text{Reduced K}^+ \text{efflux} + \text{Ca}^{2+} \text{influx}$

Key Ion Channels in Pacemaker Cells

• If (funny) channels: Permeable to Na+, responsible for initial depolarization.

• Transient (T-type) Ca2+ channels: Briefly open near threshold, allowing Ca2+ influx.

• Long-lasting (L-type) Ca2+ channels: Open at threshold, causing rapid depolarization.

• K+ channels: Open during repolarization, restoring membrane potential.

Additional info: The interplay of these channels ensures rhythmic, spontaneous action potentials in the heart's pacemaker cells.