Cardiac Muscle Physiology

Action Potentials in Cardiac Muscle Cells

Cardiac muscle cells (cardiomyocytes) generate action potentials that differ significantly from those in skeletal muscle. These differences are crucial for the heart's function as a rhythmic pump.

• Resting Membrane Potential: Cardiac myocytes have a resting potential of approximately -90 mV, which is more negative than that of skeletal muscle cells.

• Depolarization: Initiated by voltage-gated sodium channels, causing a rapid influx of Na+ and a sharp rise in membrane potential.

• Initial Repolarization: Fast-opening potassium channels briefly open, causing a small repolarization.

• Plateau Phase: Voltage-gated L-type (long-lasting) calcium channels open, allowing Ca2+ influx, which maintains depolarization and creates a plateau. This phase is unique to cardiac muscle and prolongs the action potential.

• Final Repolarization: Calcium channels close, and slow-opening potassium channels open, returning the cell to resting potential.

• No Hyperpolarization: Unlike neurons and skeletal muscle, cardiac myocytes do not exhibit an undershoot or hyperpolarization phase.

Example: The plateau phase prevents rapid re-excitation, ensuring the heart muscle relaxes before the next contraction, which is essential for effective pumping.

Comparison: Cardiac vs. Skeletal Muscle Action Potentials

• Skeletal Muscle: Short action potential, rapid contraction, allows summation and tetanus (sustained contraction).

• Cardiac Muscle: Long action potential with plateau, contraction occurs during the action potential, preventing summation and tetanus.

Additional info: This mechanism ensures the heart cannot enter tetanus, which would be fatal.

Excitation-Contraction Coupling in Cardiac Muscle

Cardiac muscle contraction is triggered by the influx of calcium ions, involving both extracellular and intracellular sources.

• T-tubules: Present but smaller than in skeletal muscle due to smaller cell size.

• L-type Calcium Channels: Located in the T-tubule membrane; open during the action potential, allowing extracellular Ca2+ to enter.

• Calcium-Induced Calcium Release (CICR): Influx of Ca2+ binds to ryanodine receptors on the sarcoplasmic reticulum (SR), triggering a large release of Ca2+ from the SR ("calcium sparks").

• Troponin Binding: Ca2+ binds to troponin, initiating cross-bridge cycling and contraction (similar to skeletal muscle).

• Relaxation: Ca2+ is removed by:

  • SERCA (SR Ca2+-ATPase): Pumps Ca2+ back into the SR (primary active transport).

  • Sodium-Calcium Exchanger (NCX): Exports Ca2+ in exchange for Na+ (secondary active transport).

  • Sodium-Potassium ATPase: Maintains Na+ gradient for NCX function.

Additional info: The large Ca2+ influx is measurable and termed "calcium sparks" in cardiac physiology literature.

Cardiac Conduction System

Autorhythmic Cells and Pacemaker Activity

The heart's rhythm is set by specialized autorhythmic cells that spontaneously depolarize, generating action potentials without external stimuli.

• Locations: Sinoatrial (SA) node, Atrioventricular (AV) node, Purkinje fibers.

• Pacemaker Potential: No true resting potential; after repolarization, the membrane potential immediately begins to depolarize again.

• Funny Channels (If): Open at hyperpolarized potentials (~-60 mV), allowing Na+ influx and initiating depolarization.

• Voltage-Gated Calcium Channels: Open as the membrane depolarizes, causing further depolarization and triggering the action potential.

• Repolarization: Slow-opening potassium channels allow K+ efflux, returning the cell to the trough potential.

Example: The SA node typically sets the pace at ~70 beats per minute. If the SA node fails, the AV node (~50 bpm) or Purkinje fibers (~30 bpm) can take over, though at slower rates.

Conduction Pathway of the Heart

• SA Node: Located in the right atrium; initiates the heartbeat and sets the pace.

• Internodal Pathways: Conduct impulses rapidly from the SA node to the AV node.

• Atrial Muscle: Impulse spreads through atrial muscle, causing atrial contraction (atrial systole).

• AV Node: Delays the impulse, allowing atrial contraction to complete before ventricular contraction begins.

• AV Bundle (Bundle of His): Conducts the impulse from the AV node down the interventricular septum to the apex of the heart.

• Purkinje Fibers: Distribute the impulse upward through the ventricular myocardium, causing ventricular contraction (ventricular systole).

Additional info: The delay at the AV node ensures proper coordination between atrial and ventricular contractions.

Electrocardiogram (ECG/EKG)

ECG Waves and Their Significance

An ECG records the electrical activity of the heart and is used to assess heart rate, rhythm, and conduction abnormalities.

• P Wave: Atrial depolarization (SA node firing and atrial contraction).

• QRS Complex: Ventricular depolarization (ventricular contraction); Q is downward, R is the large upward peak, S is a small downward deflection.

• T Wave: Ventricular repolarization (return to resting state).

Example: A normal ECG shows regular P, QRS, and T waves, indicating coordinated atrial and ventricular activity.

Common ECG Pathologies

Additional info: ECGs are essential for diagnosing arrhythmias, conduction blocks, and other cardiac pathologies.

Regulation of Heart Rate and Cardiac Output

Cardiac Output

Cardiac output (CO) is the volume of blood pumped by the heart per minute. It is determined by heart rate (HR) and stroke volume (SV).

• Formula:

• Normal Value: At rest, CO is typically about 5 liters per minute in adults.

Autonomic Regulation of Heart Rate

• Parasympathetic (Vagus Nerve): Releases acetylcholine, increases K+ permeability, hyperpolarizes pacemaker cells, slows heart rate.

• Sympathetic: Releases norepinephrine/epinephrine, increases Na+ and Ca2+ permeability, depolarizes pacemaker cells, increases heart rate.

• Mechanisms:

  • Parasympathetic: Opens K+ channels, lowers membrane potential, slows depolarization (shallower slope).

  • Sympathetic: Increases sensitivity and duration of funny channels, raises membrane potential, steepens depolarization slope.

Additional info: Changes in heart rate are primarily due to changes in the rate of depolarization of pacemaker cells before threshold is reached.

Regulation of Stroke Volume

• Intrinsic Control (Frank-Starling Law): Increased venous return stretches ventricular muscle, increasing force of contraction and stroke volume.

• Venous Tone: Constriction of veins increases return of blood to the heart, raising end-diastolic volume (EDV) and stroke volume.

• Frank-Starling Mechanism: The greater the stretch (EDV), the greater the force of contraction, up to an optimal point.

Graphical Representation:

• Sympathetic Stimulation: Increases contractility (force of contraction) by increasing Ca2+ availability, leading to more cross-bridge formation and higher stroke volume at any given EDV.

Summary Table: Cardiac Muscle vs. Skeletal Muscle