Cardiac Physiology: Electrical and Mechanical Events, Cardiac Output, and Regulation

Cardiac Physiology

Overview

Cardiac physiology explores the functional mechanisms of the heart, focusing on the sequence of electrical and mechanical events that drive blood flow. Understanding these processes is essential for comprehending how the heart maintains circulation and responds to physiological demands.

Electrical and Mechanical Events of the Cardiac Cycle

Components of the Cardiac Cycle

• Electrical Events: Initiated by the heart's conducting system, these events trigger contraction of cardiac muscle cells.

• Mechanical Events: The contraction (systole) and relaxation (diastole) of the atria and ventricles, resulting in blood movement.

• Blood Flow Direction: Blood flows from areas of higher pressure to lower pressure, moving through the heart chambers and valves in a coordinated sequence.

Example: During ventricular systole, the ventricles contract, increasing pressure and forcing blood into the arteries.

Electrical Activity: Pacemaker vs. Contractile Cells

• Pacemaker Cells: Located in the sinoatrial (SA) node, these cells spontaneously depolarize due to slow Na+ influx and Ca2+ entry, generating action potentials that set the heart rate.

• Contractile Cells: These cells respond to action potentials from pacemaker cells. Their depolarization is due to rapid Na+ influx, followed by a plateau phase from Ca2+ entry and K+ efflux.

Comparison: Pacemaker cells have unstable resting potentials and initiate impulses, while contractile cells have stable resting potentials and contract in response to impulses.

Excitation-Contraction Coupling in Cardiac Muscle

• Action potentials open voltage-gated Ca2+ channels in the sarcolemma.

• Ca2+ enters from the extracellular fluid and triggers further Ca2+ release from the sarcoplasmic reticulum (SR).

• Ca2+ binds to troponin, initiating contraction.

Comparison to Skeletal Muscle: In skeletal muscle, most Ca2+ comes from the SR; in cardiac muscle, both extracellular and SR Ca2+ are essential.

Electrocardiogram (ECG) Components

• P wave: Atrial depolarization (leads to atrial contraction).

• QRS complex: Ventricular depolarization (leads to ventricular contraction); atrial repolarization occurs here but is masked.

• T wave: Ventricular repolarization (leads to ventricular relaxation).

• Intervals and Segments: PR interval, ST segment, QT interval—each relates to specific phases of contraction and relaxation.

Application: Abnormalities in ECG waves can indicate arrhythmias or conduction blocks.

Phases of the Mechanical Cardiac Cycle

• Atrial Systole: Atria contract, topping off ventricular filling.

• Ventricular Systole: Ventricles contract, AV valves close (first heart sound), blood is ejected into arteries.

• Ventricular Diastole: Ventricles relax, semilunar valves close (second heart sound), ventricles fill with blood.

Pressure Changes and Heart Sounds

• AV Valves: Close when ventricular pressure exceeds atrial pressure ("lub" sound).

• Semilunar Valves: Close when arterial pressure exceeds ventricular pressure ("dub" sound).

Heart Sounds: S1 (AV valves close), S2 (semilunar valves close).

Pressure and Volume Changes During the Cardiac Cycle

• Atrial Pressure and Volume: Increase during atrial contraction, decrease as blood flows into ventricles.

• Ventricular Pressure and Volume: Pressure rises during systole, volume decreases as blood is ejected; pressure falls during diastole, volume increases as ventricles fill.

• Aortic Pressure: Rises during ventricular ejection, falls during diastole.

Regulation of Cardiac Output

Key Definitions

• Heart Rate (HR): Number of heartbeats per minute.

• Stroke Volume (SV): Volume of blood ejected by one ventricle per beat.

• Cardiac Output (CO): Volume of blood pumped by each ventricle per minute.

Formula:

$CO = HR \times SV$

Autonomic Innervation of the Cardiovascular System

• Sympathetic Stimulation: Increases HR and contractility via norepinephrine.

• Parasympathetic Stimulation: Decreases HR via the vagus nerve and acetylcholine.

Intrinsic vs. Extrinsic Controls

• Intrinsic Control: Regulation originating within the heart (e.g., Frank-Starling law).

• Extrinsic Control: Regulation by external factors (e.g., autonomic nervous system, hormones).

Factors Affecting Heart Rate

• Autonomic nervous system activity

• Hormones (e.g., epinephrine)

• Body temperature

• Electrolyte balance

Frank-Starling Law of the Heart

• The greater the ventricular filling (end-diastolic volume, EDV), the stronger the contraction and the greater the stroke volume.

$SV \propto EDV$

Factors Affecting Stroke Volume

• Preload: Degree of stretch of cardiac muscle before contraction (related to EDV).

• Contractility: Strength of contraction at a given preload.

• Afterload: Pressure the ventricles must overcome to eject blood.

Additional Key Terms

• Systole: Contraction phase of the heart.

• Diastole: Relaxation phase of the heart.

• Mean Arterial Pressure (MAP): Average pressure in the arteries during one cardiac cycle.

• Pulse Pressure: Difference between systolic and diastolic pressures.

$MAP = \frac{1}{3} (Systolic\ Pressure - Diastolic\ Pressure) + Diastolic\ Pressure$

$Pulse\ Pressure = Systolic\ Pressure - Diastolic\ Pressure$

Preload and Afterload

• Preload: Related to venous return and EDV; increased preload increases SV.

• Afterload: Increased afterload (e.g., high blood pressure) decreases SV and increases cardiac workload.

Variables Affecting Cardiac Output: Flow Chart

Variable	Effect on CO
Heart Rate (HR)	Directly proportional
Stroke Volume (SV)	Directly proportional
Preload (EDV)	Increases SV and CO
Afterload	Increases decrease SV and CO
Contractility	Increases SV and CO
Sympathetic Activity	Increases HR and SV
Parasympathetic Activity	Decreases HR

Predicted Effects on Cardiac Output

Change	Predicted Effect on CO
Decreased heart rate	Decreases CO
Increased EDV	Increases SV and CO
Decreased EDV	Decreases SV and CO
Increased sympathetic activity	Increases HR, SV, and CO
Decreased parasympathetic activity	Increases HR and CO
Decreased afterload	Increases SV and CO
Increased SV	Increases CO
Increased parasympathetic activity	Decreases HR and CO
Increased afterload	Decreases SV and CO
"Leaky" right AV valve	Decreases CO (inefficient ventricular filling)
"Leaky" left AV valve	Decreases CO (inefficient ventricular filling)
"Leaky" right semilunar valve	Decreases CO (backflow into ventricle)
"Leaky" left semilunar valve	Decreases CO (backflow into ventricle)
Thrombus in right pulmonary artery	Decreases CO (obstructs pulmonary circulation)
Thrombus in right external iliac vein	May decrease venous return and CO

Additional info: Cardiac output is a critical determinant of tissue perfusion and is tightly regulated by neural, hormonal, and intrinsic mechanisms to meet the metabolic demands of the body.