Electrical and Mechanical Events of the Heart: Cardiac Physiology and Regulation

Electrical Events of the Heart

Intrinsic Conduction System

The heart's rhythmic contractions are coordinated by an intrinsic conduction system composed of specialized cardiac muscle cells that generate and distribute electrical impulses. This system ensures the heart beats in a synchronized manner, independent of direct nervous system input, though it can be modulated by autonomic signals.

• Gap Junctions: Allow direct electrical communication between cardiac cells, enabling coordinated contraction.

• Autorhythmic Cells: Noncontractile cells that initiate and propagate action potentials throughout the heart.

• Pacemaker Cells: Located primarily in the sinoatrial (SA) node, these cells have unstable resting membrane potentials, leading to spontaneous depolarization (pacemaker potential).

Action Potential in Pacemaker Cells

Pacemaker cells generate action potentials in three main phases:

• Pacemaker Potential: Slow depolarization due to opening of Na+ channels and closing of K+ channels.

• Depolarization: At threshold (~–40 mV), Ca2+ channels open, causing rapid influx and the rising phase of the action potential.

• Repolarization: Ca2+ channels inactivate, K+ channels open, and K+ efflux returns the cell to its most negative voltage.

Sequence of Excitation

The electrical impulse travels through the heart in a precise sequence, ensuring efficient contraction:

1. Sinoatrial (SA) Node: Pacemaker in the right atrial wall; initiates impulses (~75/min).

2. Atrioventricular (AV) Node: Located in the inferior interatrial septum; delays impulse by ~0.1 s to allow atrial contraction.

3. Atrioventricular (AV) Bundle (Bundle of His): Only electrical connection between atria and ventricles.

4. Right and Left Bundle Branches: Conduct impulses through the interventricular septum toward the apex.

5. Purkinje Fibers (Subendocardial Conducting Network): Spread the impulse throughout the ventricular walls, causing contraction from apex upward.

Action Potentials of Contractile Cardiac Muscle Cells

Phases of Cardiac Muscle Action Potential

Contractile cardiac muscle fibers generate action potentials with distinct phases, resulting in prolonged contraction compared to skeletal muscle:

• Phase 0 (Depolarization): Rapid Na+ influx through voltage-gated channels.

• Phase 1 (Initial Repolarization): Na+ channels close, K+ channels briefly open.

• Phase 2 (Plateau): Ca2+ influx through slow channels balances K+ efflux, maintaining depolarization and triggering contraction.

• Phase 3 (Repolarization): Ca2+ channels close, K+ efflux restores resting potential.

• Phase 4 (Resting Potential): High K+ permeability maintains resting state.

Key Differences: Cardiac muscle action potentials and contractions are much longer than those in skeletal muscle, preventing tetanus and ensuring efficient blood ejection.

Electrocardiography (ECG/EKG)

Principles and Main Features

An electrocardiogram (ECG) records the electrical activity of the heart using electrodes placed on the body. It is a composite of all action potentials occurring in the heart at a given time.

• P wave: Atrial depolarization (SA node and atria).

• QRS complex: Ventricular depolarization and atrial repolarization.

• T wave: Ventricular repolarization.

• P-R interval: Start of atrial excitation to start of ventricular excitation.

• S-T segment: Entire ventricular myocardium depolarized.

• Q-T interval: Start of ventricular depolarization to end of repolarization.

Normal and Abnormal ECG Patterns

ECG analysis can reveal arrhythmias, conduction blocks, and other cardiac abnormalities. For example, a prolonged Q-T interval indicates a repolarization abnormality, increasing the risk of ventricular arrhythmias.

Mechanical Events of the Heart: The Cardiac Cycle

Phases of the Cardiac Cycle

The cardiac cycle describes the sequence of mechanical events during one heartbeat, including periods of contraction (systole) and relaxation (diastole):

1. Ventricular Filling (Mid-to-Late Diastole): Blood flows passively into ventricles; atrial contraction delivers the final volume (end diastolic volume, EDV).

2. Isovolumetric Contraction: Ventricles contract with all valves closed, increasing pressure until semilunar valves open.

3. Ventricular Ejection: Blood is pumped into the aorta and pulmonary trunk.

4. Isovolumetric Relaxation (Early Diastole): Ventricles relax, semilunar valves close, and the heart prepares for the next cycle (end systolic volume, ESV).

Heart Sounds

Two main heart sounds are produced by valve closures:

• First sound (lub): Closing of AV valves at the start of ventricular systole.

• Second sound (dup): Closing of semilunar valves at the start of ventricular diastole.

Regulation of Cardiac Output

Cardiac Output (CO)

Cardiac output is the volume of blood pumped by each ventricle per minute. It is calculated as:

Formula:

$\text{CO} = \text{HR} \times \text{SV}$

• HR: Heart rate (beats per minute)

• SV: Stroke volume (volume ejected per beat)

At rest, typical values are HR = 75 bpm, SV = 70 mL/beat, so CO ≈ 5.25 L/min.

Regulation of Stroke Volume

Stroke volume is determined by:

• Preload: Degree of stretch of cardiac muscle before contraction (Frank-Starling law).

• Contractility: Strength of contraction at a given muscle length, influenced by sympathetic stimulation and inotropic agents.

• Afterload: Pressure the ventricles must overcome to eject blood (mainly arterial pressure).

Formula:

$\text{SV} = \text{EDV} - \text{ESV}$

Regulation of Heart Rate

Heart rate is modulated by:

• Autonomic Nervous System: Sympathetic stimulation increases HR and contractility; parasympathetic (vagus nerve) decreases HR.

• Chemicals: Hormones (epinephrine, thyroxine) and ions (Ca2+, K+) affect HR and rhythm.

• Other Factors: Age, gender, exercise, and body temperature.

Clinical Considerations and Homeostatic Imbalances

Arrhythmias and Conduction Defects

• Arrhythmias: Irregular heart rhythms due to defects in the conduction system.

• Fibrillation: Rapid, uncoordinated contractions; requires defibrillation to restore normal rhythm.

• Heart Block: Impaired conduction through the AV node; may require artificial pacemaker.

Congestive Heart Failure (CHF)

CHF is a progressive condition where the heart cannot pump sufficient blood to meet tissue needs, often due to coronary artery disease, hypertension, myocardial infarcts, or cardiomyopathy. It can lead to pulmonary or peripheral congestion depending on which side of the heart is affected.

Developmental and Age-Related Aspects

Development of the Heart

The heart develops from mesoderm, forming a single pumping chamber by day 22 of embryonic development. Structural changes create a four-chambered heart by day 35, with fetal shunts (foramen ovale, ductus arteriosus) closing at or after birth.

Age-Related Changes

• Sclerosis and thickening of valve flaps

• Decline in cardiac reserve

• Fibrosis of cardiac muscle

• Atherosclerosis