BackCardiovascular Physiology: Structure, Function, and Regulation
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Cardiovascular Physiology
Introduction to Cardiovascular Function
The cardiovascular system is responsible for transporting blood throughout the body, delivering oxygen and nutrients, and removing waste products. Blood flow is driven by pressure gradients generated by the heart.
Pressure Gradient: Blood flows from areas of higher pressure to areas of lower pressure.
Pressure: The force exerted by a fluid on its container, measured in mm Hg in the cardiovascular system.
Driving Pressure: Created by ventricular contraction, it propels blood through the vessels.
Volume-Pressure Relationship: Pressure and volume are inversely related; as volume increases, pressure decreases, and vice versa.
Flow and Resistance: Blood flow is inversely proportional to resistance. Resistance is the opposition to flow within the vessels.
Factors Affecting Resistance
Viscosity: Increased viscosity (thicker blood) raises resistance and slows flow. Decreased viscosity lowers resistance.
Vessel Length: Longer vessels increase resistance; shorter vessels decrease resistance.
Vessel Diameter: Wider diameter reduces resistance and increases flow; narrower diameter increases resistance and decreases flow.
Vasodilation: Increase in vessel diameter.
Vasoconstriction: Decrease in vessel diameter.
Key Hemodynamic Terms
Flow Rate (Q): Volume of blood passing a point per unit time.
Velocity of Flow: Speed at which blood moves past a point.
Mean Arterial Pressure (MAP): The main driving force for blood flow, determined by cardiac output and peripheral resistance.
Cardiac Structure and Circulation
The heart is a four-chambered organ with specialized structures to ensure unidirectional blood flow and its own blood supply.
Chambers: Atria (upper), Ventricles (lower)
Pericardium: Protective sac surrounding the heart.
Myocardium: Muscular layer responsible for contraction.
Coronary Arteries and Veins: Supply and drain blood from the heart muscle itself.
Heart Valves
Atrioventricular (AV) Valves: Between atria and ventricles; include the tricuspid (right) and bicuspid/mitral (left) valves. Supported by chordae tendineae and papillary muscles.
Semilunar Valves: Between ventricles and major arteries; include the aortic and pulmonary valves.
Coronary Circulation
Right Coronary Artery: Marginal and posterior interventricular branches.
Left Coronary Artery: Anterior interventricular (LAD) and circumflex arteries.
Coronary Veins: Drain into the coronary sinus.
Cardiac Muscle Physiology
Cardiac muscle is specialized for continuous, rhythmic contraction and can generate its own action potentials.
Autorhythmic (Pacemaker) Cells: 1% of cardiac cells; initiate and conduct action potentials.
Contractile Cells: 99% of cardiac cells; responsible for contraction. Contain intercalated disks, gap junctions, desmosomes, abundant mitochondria, and less sarcoplasmic reticulum (SR) than skeletal muscle.
Excitation-Contraction Coupling
Action potentials from pacemaker cells spread via gap junctions to contractile cells.
Voltage-gated Ca2+ channels open, allowing Ca2+ influx, which triggers further Ca2+ release from the SR.
Graded Contractions
Cardiac muscle contractions are graded, not all-or-none, depending on Ca2+ availability and sarcomere length (degree of stretch).
Cardiac Action Potentials
Cardiac muscle cells have unique action potentials that prevent tetanus and allow rhythmic contractions.
Contractile Cells: Rapid Na+ influx causes depolarization; prolonged Ca2+ influx extends depolarization (plateau phase), preventing tetanus by extending the refractory period.
Autorhythmic Cells: Have an unstable resting membrane potential (pacemaker potential) due to "funny channels" that allow slow Na+ influx. When threshold is reached, Ca2+ channels open for depolarization; K+ efflux repolarizes the cell.
Electrical Conduction System of the Heart
The heart's electrical system coordinates contraction for efficient pumping.
Sinoatrial (SA) Node: The primary pacemaker, sets the heart rate.
Internodal Pathway: Conducts impulses from SA node to AV node.
Atrioventricular (AV) Node: Delays the impulse, allowing atrial contraction before ventricular contraction.
AV Bundle (Bundle of His): Connects atria to ventricles.
Bundle Branches: Carry impulses down the interventricular septum.
Purkinje Fibers: Distribute impulses to ventricular contractile cells.
Pacemaker Dysfunction
Complete Heart Block: Disruption of conduction from atria to ventricles.
Electrocardiogram (ECG)
An ECG records the electrical activity of the heart and is used to assess cardiac function.
P Wave: Atrial depolarization.
QRS Complex: Ventricular depolarization and atrial repolarization.
T Wave: Ventricular repolarization.
The Cardiac Cycle
The cardiac cycle describes the sequence of events in one heartbeat, including contraction (systole) and relaxation (diastole).
Diastole: Ventricular relaxation; AV valves open, semilunar valves closed, blood flows into ventricles.
Atrial Systole: Atria contract, pushing additional blood into ventricles.
Ventricular Systole: Ventricles contract, pressure rises, AV valves close (first heart sound), isovolumic contraction occurs.
Ventricular Ejection: Pressure exceeds that in arteries, semilunar valves open, blood is ejected.
Ventricular Relaxation: Ventricles relax, semilunar valves close (second heart sound), isovolumic relaxation occurs until AV valves open again.
Key Volumes and Formulas
End-Diastolic Volume (EDV): Blood in ventricles at end of diastole.
End-Systolic Volume (ESV): Blood in ventricles at end of systole.
Stroke Volume (SV): Blood ejected per beat.
Cardiac Output (CO): Blood pumped per minute.
Formulas:
Stroke Volume:
Cardiac Output:
Example:
Autonomic Regulation of Heart Rate
The autonomic nervous system modulates heart rate through parasympathetic and sympathetic pathways.
Parasympathetic Control: Increases K+ permeability (hyperpolarization) and decreases Ca2+ permeability in pacemaker cells, slowing heart rate.
Sympathetic Control: Increases Na+ and Ca2+ influx, speeding up depolarization and increasing heart rate.
Tonic Control: At rest, parasympathetic influence predominates; increased heart rate requires decreased parasympathetic and/or increased sympathetic activity.
Regulation of Stroke Volume
Stroke volume is influenced by the degree of ventricular stretch, contractility, and afterload.
Frank-Starling Law: Greater ventricular stretch (from increased venous return) leads to greater stroke volume.
Venous Return: Enhanced by skeletal muscle pump, respiratory pump, and sympathetic venous constriction.
Contractility: Increased by positive inotropic agents (e.g., sympathetic stimulation, certain hormones).
Afterload: The combined load of EDV and arterial resistance during ventricular contraction.
Ejection Fraction: Percentage of EDV ejected per beat: (e.g., )
Parameter | Definition | Typical Value |
|---|---|---|
End-Diastolic Volume (EDV) | Volume in ventricle at end of diastole | ~135 ml |
End-Systolic Volume (ESV) | Volume in ventricle at end of systole | ~65 ml |
Stroke Volume (SV) | EDV - ESV | ~70 ml |
Cardiac Output (CO) | SV x HR | ~5040 ml/min |
Ejection Fraction | SV / EDV | ~52% |
Examples and Applications
Exercise: Increases venous return, heart rate, and contractility, leading to higher cardiac output.
Heart Failure: Reduced contractility and ejection fraction.
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