Cardiac Physiology: Stroke Volume, Cardiac Output, and Autonomic Regulation

Cardiac Physiology

Stroke Volume, Cardiac Output, and Related Volumes

The heart's pumping efficiency is measured using several key parameters, including stroke volume, cardiac output, systolic volume, and end diastolic volume. Understanding these terms and their relationships is essential for analyzing cardiac function.

• Stroke Volume (SV): The amount of blood ejected by a ventricle during each heartbeat. It is calculated as the difference between end diastolic volume and end systolic volume.

• Cardiac Output (CO): The total volume of blood pumped by each ventricle per minute. It is calculated as the product of stroke volume and heart rate.

• End Diastolic Volume (EDV): The volume of blood in a ventricle at the end of filling (diastole), just before contraction.

• End Systolic Volume (ESV): The volume of blood remaining in a ventricle after contraction (systole).

• Systolic Volume: This term is often used interchangeably with stroke volume, but technically refers to the volume ejected during systole.

Key Equations:

• Stroke Volume: $SV = EDV - ESV$

• Cardiac Output: $CO = SV \times HR$

Example: If EDV = 120 mL, ESV = 50 mL, and HR = 70 bpm: $SV = 120\,\text{mL} - 50\,\text{mL} = 70\,\text{mL}$ $CO = 70\,\text{mL} \times 70 = 4900\,\text{mL/min}$

Comparison of Cardiac Output: Right vs. Left Ventricles

The right and left ventricles both pump blood, but to different circuits: the right to the pulmonary circulation and the left to the systemic circulation. Their cardiac outputs are normally equal to maintain balanced blood flow.

• Right Ventricle: Pumps deoxygenated blood to the lungs.

• Left Ventricle: Pumps oxygenated blood to the body.

• Comparison: Under normal conditions, the cardiac output of both ventricles is the same. If one side pumps more than the other, it can lead to congestion or edema in the respective circuit.

Additional info: The left ventricle generates higher pressure due to greater resistance in the systemic circuit, but the volume output remains matched to the right ventricle.

Preload, Contractility, and Afterload: Impact on Stroke Volume

Three major factors influence stroke volume:

• Preload: The degree of stretch of cardiac muscle fibers at the end of diastole (related to EDV). Increased preload increases stroke volume (Frank-Starling law).

• Contractility: The intrinsic strength of cardiac muscle contraction, independent of preload. Increased contractility increases stroke volume.

• Afterload: The resistance the ventricles must overcome to eject blood. Increased afterload decreases stroke volume.

Example: High blood pressure increases afterload, which can reduce stroke volume if not compensated by increased contractility.

Autonomic Control of the Heart: Sympathetic and Parasympathetic Systems

The heart is regulated by the autonomic nervous system (ANS), which includes the sympathetic and parasympathetic divisions. These systems modulate heart rate and contractility through specific neural pathways and target cells.

• Sympathetic Nervous System (SNS): Increases heart rate and contractility. Preganglionic neurons originate in the thoracic spinal cord and synapse in sympathetic ganglia. Postganglionic fibers innervate the SA node, AV node, and ventricular myocardium.

• Parasympathetic Nervous System (PNS): Decreases heart rate. Preganglionic fibers travel via the vagus nerve (cranial nerve X) and synapse on ganglia near or within the heart. Postganglionic fibers primarily innervate the SA and AV nodes.

• Innervated Cells: SNS innervates both nodal and myocardial cells; PNS mainly innervates nodal cells.

Additional info: The balance between SNS and PNS activity determines the resting heart rate and the heart's response to stress or relaxation.

Autonomic Innervation of the Heart: Receptors, Reflex Centers, and Effects

Autonomic regulation involves specific receptors, central reflex centers, and defined physiological effects on the heart.

• Receptor Types and Locations:

  • Beta-1 adrenergic receptors: Located on cardiac muscle and nodal cells; activated by norepinephrine (SNS).

  • Muscarinic (M2) receptors: Located on nodal cells; activated by acetylcholine (PNS).

• Reflex Centers:

  • Cardiac center: Located in the medulla oblongata; integrates sensory input and modulates ANS output to the heart.

  • Cardioacceleratory center: Stimulates SNS activity.

  • Cardioinhibitory center: Stimulates PNS activity.

• Targets: SA node, AV node, and ventricular myocardium.

• Effects:

  • SNS: Increases heart rate (positive chronotropy), increases contractility (positive inotropy), increases conduction velocity (positive dromotropy).

  • PNS: Decreases heart rate (negative chronotropy), little effect on contractility.

Example: During exercise, increased SNS activity raises heart rate and contractility to meet metabolic demands.

Division	Neurotransmitter	Receptor	Main Effect on Heart
Sympathetic	Norepinephrine	Beta-1 adrenergic	Increases HR & contractility
Parasympathetic	Acetylcholine	Muscarinic (M2)	Decreases HR