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: Uses norepinephrine at cardiac targets, acting on β1-adrenergic receptors to increase heart rate, contractility, and conduction velocity.

• Parasympathetic Pathway: Uses acetylcholine at cardiac targets, acting on muscarinic (M2) receptors to decrease heart rate and conduction.

• Autonomic Ganglia: Sympathetic preganglionic neurons release acetylcholine onto nicotinic receptors; parasympathetic preganglionic neurons also release acetylcholine onto nicotinic receptors.

• Effects: Sympathetic stimulation increases cardiac output; parasympathetic stimulation slows the heart.

• Example: During exercise, sympathetic activity predominates, increasing 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 and effective blood pumping.

• Autorhythmic Cells: Generate spontaneous action potentials; found in the SA node, AV node, and conduction system.

• 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.

• Sequence and Timing: Ensures atria contract before ventricles, optimizing blood flow.

• Example: The delay at the AV node allows ventricular filling before contraction.

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), 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 slope and heart rate; parasympathetic input decreases slope and heart rate.

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

From Electrical Activity to Contraction

Action potentials in contractile cardiomyocytes trigger contraction through excitation–contraction coupling, involving Ca2+ entry and release.

• 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 and handling.

• 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. Changes in chamber pressures drive valve movements and blood flow.

• 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 and close valves, direct blood flow.

• 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 determined by heart rate (HR) and stroke volume (SV). It is regulated by autonomic activity, venous return, preload, and contractility.

• Cardiac Output Formula:

• Regulatory Factors: Autonomic input, heart rate, venous return, preload, contractility.

• Frank–Starling Mechanism: Increased ventricular filling (preload) enhances contraction force and stroke volume.

• Example: During exercise, increased venous return raises EDV, boosting SV and CO.

Key Definitions and Calculations

Unit-Wide Integration

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

• Scenario Example: In heart failure, reduced contractility lowers SV and CO, despite normal HR.

• Clinical Application: Beta-blockers decrease HR and contractility, lowering CO for hypertension management.