Cardiovascular Physiology

Autonomic Control of the Heart

The autonomic nervous system regulates heart function through sympathetic and parasympathetic pathways, each using distinct neurotransmitters and receptors to modulate cardiac activity.

• Sympathetic Pathway: Originates from thoracic spinal segments; preganglionic neurons release acetylcholine at autonomic ganglia, postganglionic neurons release norepinephrine at cardiac targets, acting on β1-adrenergic receptors.

• Parasympathetic Pathway: Originates from the vagus nerve; pre- and postganglionic neurons release acetylcholine, acting on muscarinic (M2) receptors at the heart.

• Effects: Sympathetic activity increases heart rate, contractility, and conduction velocity; parasympathetic activity decreases these parameters.

• Example: During exercise, sympathetic tone increases, raising heart rate and contractility.

Cardiac Muscle and the Conduction System

Cardiac muscle consists of two main cell types: autorhythmic (pacemaker) cells and contractile cardiomyocytes. Their structural and electrical properties enable coordinated contraction.

• Autorhythmic Cells: Generate spontaneous action potentials; found in the SA and AV nodes.

• Contractile Cells: Respond to action potentials by contracting; make up the bulk of the myocardium.

• Electrical Conduction Pathway: SA node → atria → AV node → bundle of His → bundle branches → Purkinje fibers → ventricles.

• Coordination: Sequential activation ensures atrial contraction precedes ventricular contraction for efficient blood flow.

Generating and Regulating the Heartbeat

Pacemaker cells generate spontaneous action potentials, setting the heart rate. Their activity is modulated by autonomic input, and their action potentials differ from those of contractile cells.

• Pacemaker Action Potentials: Characterized by slow depolarization ("funny" current, If), rapid upstroke (Ca2+ influx), and repolarization (K+ efflux).

• Contractile Cell Action Potentials: Rapid depolarization (Na+ influx), plateau phase (Ca2+ influx), repolarization (K+ efflux).

• Autonomic Modulation: Sympathetic input increases pacemaker activity (faster heart rate); parasympathetic input decreases it (slower heart rate).

• Example: β1-adrenergic stimulation increases SA node firing rate.

From Electrical Activity to Contraction

Action potentials in contractile cardiomyocytes trigger contraction via calcium dynamics and excitation–contraction coupling.

• Ca2+ Entry: Action potential opens voltage-gated Ca2+ channels.

• Calcium-Induced Calcium Release: Ca2+ influx triggers further Ca2+ release from the sarcoplasmic reticulum.

• Excitation–Contraction Coupling: Increased intracellular Ca2+ binds to troponin, enabling actin–myosin interaction and contraction.

• Contractile Force: Depends on Ca2+ availability; reduced Ca2+ impairs contraction.

• Example: Digitalis increases intracellular Ca2+, enhancing contractility.

Electrical Activity and the Cardiac Cycle

The cardiac cycle is reflected in the electrocardiogram (ECG), which records electrical events, and is governed by changes in chamber pressures and valve movements.

• ECG Waves: P wave (atrial depolarization), QRS complex (ventricular depolarization), T wave (ventricular repolarization).

• Cardiac Cycle Events: Atrial systole, ventricular systole, diastole; pressure changes open/close valves and move blood.

• Key Volumes: End-Diastolic Volume (EDV): Volume at end of filling; End-Systolic Volume (ESV): Volume after contraction; Stroke Volume (SV): Amount ejected per beat.

• Formula:

• Example: If EDV = 120 mL and ESV = 50 mL, then SV = 70 mL.

Integrating Cardiac Output and Its Regulation

Cardiac output (CO) is the volume of blood pumped per minute, determined by heart rate (HR) and stroke volume (SV). It is regulated by autonomic activity, venous return, preload, and contractility.

• Formula:

• Regulatory Factors: Increased sympathetic activity raises HR and SV; increased venous return/preload enhances SV via the Frank–Starling mechanism.

• Frank–Starling Mechanism: Greater ventricular filling stretches muscle fibers, increasing contraction force and SV (within physiological limits).

• Example: During exercise, increased venous return and sympathetic tone elevate CO.

Unit-wide Integration

Effective cardiac function requires integration of autonomic regulation, electrical activity, excitation–contraction coupling, and pumping mechanics. Understanding these interactions is essential for predicting physiological and clinical outcomes.

• Scenario Example: In heart failure, reduced contractility lowers SV and CO, triggering compensatory sympathetic activation.

Key Table: Cardiac Volumes and Output

Additional info: Academic context and examples were added to expand brief learning objectives into comprehensive study notes.