Cardiac Physiology is the study of the functions of the heart, including the electrical impulses that regulate heartbeat and the mechanics of blood circulation.
Dr. Matt Parker, University of Surrey, explores how cardiac action potentials are essential for heart function and rhythm.
Heart muscle is innervated by both the autonomic nervous system and intrinsic pacemaking cells, demonstrating automaticity (self-excitability). This allows the heart to initiate its own contractions without external stimulus.
The cardiac muscle contracts as a functional syncytium, meaning that individual muscle cells work in unison due to the presence of intercalated discs that facilitate electrical coupling through gap junctions.
Cardiac muscle has a long absolute refractory period, approximately 250 ms, which prevents tetany (sustained contraction) and allows the heart to fill with blood properly before the next contraction.
The contraction mechanism of cardiac muscle resembles that of skeletal muscle but is unique due to its pacemaker cells and the calcium-induced calcium release mechanism that sustains muscle contraction.
The SA node, located in the right atrium, generates approximately 75 impulses per minute, serving as the primary pacemaker of the heart, influencing heart rate and rhythm.
The AV node plays a crucial role in the conduction system by delaying the electrical impulse for about 0.1 seconds, allowing time for the atria to empty blood into the ventricles before they contract.
The Bundle of His carries impulses from the atria into the ventricles and splits into right and left bundle branches that run down the interventricular septum, ensuring simultaneous contraction of both ventricles.
These fibers conduct impulses rapidly to the apex of the heart and spread throughout the ventricular walls, causing a coordinated contraction from the bottom up, enabling efficient blood ejection.
These specialized cells in the heart initiate action potentials and possess pacemaker potentials. They have unstable resting potentials and rely on calcium influx instead of sodium for generating the rising phase of action potentials, which allows the heart to maintain a rhythm independent of external inputs.
Each phase of the action potential has critical implications for myocardial contractility and heart rhythm.
A rapid influx of Na+ ions into the cardiac cells, triggered by nearby depolarization, results in a substantial rise in membrane potential and initiates the contraction.
Following depolarization, a transient outflow of K+ ions begins, marking the initial phase of repolarization and contributing to the cellular recovery.
This phase is characterized by a prolonged period of depolarization where Ca²⁺ ions enter the cells through L-type calcium channels while K⁺ channels remain open, creating a plateau in the action potential and allowing for sustained contraction.
Rapid efflux of K+ ions resumes as Ca²⁺ influx diminishes, which leads to the restoration of resting membrane potential and prepares the cells for the next cycle of activation.
In this phase, the heart muscle cells remain in a stable negative resting state until the next action potential is triggered by the SA node, ensuring readiness for the next heartbeat.
The ECG provides a graphical representation of the electrical activity of the heart and correlates to various phases of the cardiac action potential:
QRS Complex: Corresponds to the depolarization phase, representing ventricular contraction.
T Wave: Represents the repolarization phase of the ventricles, indicative of relaxation and recovery.
Understanding cardiac action potentials is crucial for comprehending heart behavior. Significant fluctuations in Ca²⁺ and K⁺ conductance directly impact cardiac function, influencing how the heart responds to different physiological demands.
The normal heart rate is approximately 75-80 action potentials per minute, regulated by external factors:
Sympathetic Activation: Increases heart rate (cardioacceleratory), preparing the body for stress or activity.
Parasympathetic Activation: Decreases heart rate (cardioinhibitory), promoting rest and recovery.
The generation of action potentials is intrinsically managed by the SA node, emphasizing the heart's independence from nervous system stimulation for rhythm generation, although the autonomic nervous system can modulate its rate.
Introduction
Cardiac Action Potential
Heart Muscle Characteristics
Stimulation
Contractility
Refractory Period
Comparison
Heart Physiology: Sequence of Excitation
Sinoatrial (SA) Node
Atrioventricular (AV) Node
Pathway of the Electrical Impulse
Bundle of His
Purkinje Fibers
Intrinsic Conduction System
Autorhythmic Cells
Phases of the Cardiac Action Potential (AP)
General Overview
Phase 0: Depolarization
Phase 1: Early Repolarization
Phase 2: Plateau Phase
Phase 3: Rapid Repolarization
Phase 4: Resting Potential
Electrocardiogram (ECG) Correlation
Summary of Cardiac Action Potentials