Overview

This lecture reviews Chapter 9 of Chitin and Hall's "Mythical Physiology," covering heart anatomy, cardiac muscle properties, electrical activity, the cardiac cycle, heart valves, and regulation of heart function.

Heart Anatomy & Chambers

• The heart has four chambers: right atrium, left atrium, right ventricle, and left ventricle.
• Atria receive blood and empty it into the ventricles, which pump blood to the lungs (pulmonary artery) or body (aorta).
• Three muscle types: atrial muscle, ventricular muscle, and conductive fibers for electrical signaling.

Cardiac Muscle Structure & Function

• Cardiac muscle is striated and forms a syncytium, allowing coordinated contraction through intercalated discs.
• Intercalated discs enable ion flow between cells, propagating contraction.
• Atrial and ventricular syncytia are separated by a fibrous layer.

Cardiac Action Potential & Refractory Periods

• Cardiac action potential has a plateau phase due to prolonged calcium (L-type channel) influx.
• Four phases: rapid depolarization (Na+ influx), brief K+ efflux, plateau (Ca2+ influx), repolarization (K+ efflux).
• Absolute refractory period prevents immediate re-excitation; relative refractory period allows early contraction if stimulus is strong.

Excitation-Contraction Coupling

• Action potential triggers Ca2+ influx via T-tubules, larger in cardiac muscle than skeletal.
• Ca2+ from extracellular fluid opens ryanodine receptors in the sarcoplasmic reticulum (SR), causing further Ca2+ release.
• Contraction uses actin-myosin cross-bridges; relaxation occurs by pumping Ca2+ back into SR and out via Na+-Ca2+ exchanger.

Cardiac Cycle & Wiggers Diagram

• The cardiac cycle includes atrial contraction, ventricular contraction (systole), relaxation (diastole), and filling.
• Increased heart rate shortens the cardiac cycle, especially diastole.
• Wiggers diagram shows electrical, pressure, volume, and sound changes through the cycle.
• Systole: ventricular contraction/ejection; diastole: relaxation/filling.
• Isovolumic contraction/relaxation phases: pressure changes without volume change.

Heart Valves & Function

• Atrioventricular (AV) valves: between atria and ventricles, supported by chordae tendineae and papillary muscles.
• Semilunar valves (aortic, pulmonic): at exits of ventricles, prevent backflow under high pressure.

Pressure-Volume Relationships & Frank-Starling Law

• Volume-pressure diagrams show phases: diastole (filling), isovolumic contraction, ejection, isovolumic relaxation.
• Stroke volume = end diastolic volume - end systolic volume.
• Frank-Starling mechanism: increased filling increases contraction strength.
• Overstretching reduces contractility due to suboptimal filament alignment.

Regulation of Heart Function

• Parasympathetic (vagus) activity slows heart rate, mainly at the SA/AV nodes.
• Sympathetic activity increases rate and contractility in all heart parts.
• Potassium excess causes flaccid, slow heart; calcium excess causes spasticity; calcium deficit weakens contraction.
• Higher temperatures increase heart rate; arterial pressure affects afterload but cardiac output stays steady up to 160 mmHg.

Key Terms & Definitions

• Syncytium — Network of cardiac cells enabling coordinated contraction.
• Intercalated discs — Junctions between cardiac muscle cells for ion exchange.
• Action potential — Electrical impulse causing muscle contraction.
• Systole — Period of ventricular contraction and blood ejection.
• Diastole — Period of ventricular relaxation and filling.
• Isovolumic contraction/relaxation — Phases with pressure change but no volume change.
• Frank-Starling mechanism — Increased ventricular filling leads to stronger contraction.
• Afterload — Pressure the heart must overcome to eject blood.

Action Items / Next Steps

• Review diagrams of heart anatomy, Wiggers diagram, and pressure-volume loops.
• Study definitions of systole, diastole, and excitation-contraction coupling.
• Prepare for questions on electrical and mechanical coordination in the cardiac cycle.

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Chapter 9: Heart Anatomy, Physiology, and Function

Based on Chitin and Hall's Mythical Physiology

1. Introduction

This chapter explores the heart’s anatomy, the properties of cardiac muscle, the electrical activity that controls heartbeats, the cardiac cycle, heart valves, pressure-volume relationships, and regulation of heart function.

2. Heart Anatomy and Chambers

• The heart consists of four chambers:

  • Right atrium (receives deoxygenated blood from the body)
  • Left atrium (receives oxygenated blood from the lungs)
  • Right ventricle (pumps blood to the lungs via the pulmonary artery)
  • Left ventricle (pumps blood to the body via the aorta)

• Blood flows from atria to ventricles, then out to lungs or body.

• The heart muscle includes three types of fibers:

  • Atrial muscle fibers
  • Ventricular muscle fibers
  • Conductive muscle fibers (specialized for electrical signal propagation, not contraction)

3. Cardiac Muscle Structure and Syncytium

• Cardiac muscle is striated and organized as a syncytium, meaning cells are connected to function as a unit.
• Muscle cells are connected by intercalated discs, which allow ions to flow freely between cells, enabling coordinated contraction.
• The atrial and ventricular syncytia are separated by a fibrous layer, preventing direct electrical conduction between atria and ventricles except through specialized pathways.

4. Cardiac Action Potential

• The cardiac action potential differs from skeletal muscle by having a plateau phase due to prolonged calcium influx.

• Phases of cardiac action potential:

  • Phase 0: Rapid depolarization via sodium (Na⁺) influx through sodium channels.
  • Phase 1: Brief potassium (K⁺) efflux causing a small dip.
  • Phase 2 (Plateau): Calcium (Ca²⁺) influx through L-type calcium channels prolongs depolarization.
  • Phase 3: Repolarization via potassium efflux returning membrane potential to resting state.
  • Phase 4: Resting membrane potential maintained.

• The plateau phase allows sustained contraction necessary for effective pumping.

• Refractory periods:

  • Absolute refractory period: No new action potential can be initiated.
  • Relative refractory period: A stronger-than-normal stimulus can trigger an early contraction (premature beat).

5. Excitation-Contraction Coupling in Cardiac Muscle

• Action potential spreads across the membrane and down T-tubules, which are larger in cardiac muscle than skeletal muscle.
• T-tubule membranes contain negatively charged mucopolysaccharides that help store extracellular calcium.
• Calcium influx from extracellular fluid triggers opening of ryanodine receptors on the sarcoplasmic reticulum (SR), releasing more calcium inside the cell.
• Unlike skeletal muscle, cardiac muscle depends heavily on extracellular calcium for contraction.
• Calcium binds to troponin, enabling actin-myosin cross-bridge formation and contraction.
• Relaxation occurs by:
  • Pumping calcium back into the SR.
  • Extruding calcium out of the cell via the sodium-calcium exchanger (Na⁺/Ca²⁺ counter-transporter), which uses the sodium gradient maintained by the sodium-potassium ATPase.

6. The Cardiac Cycle

• The cardiac cycle includes all events from one heartbeat to the next:

  • Atrial contraction
  • Ventricular contraction (systole)
  • Ventricular relaxation (diastole)
  • Ventricular filling

• Increasing heart rate shortens the cardiac cycle, especially diastole, reducing filling time.

• The Wiggers diagram illustrates:

  • Electrical activity (ECG waves: P wave, QRS complex, T wave)
  • Heart sounds (lub-dub)
  • Pressure changes in atria, ventricles, and aorta
  • Volume changes in ventricles

7. Electrical and Mechanical Events in the Cardiac Cycle

• P wave: SA node fires, atrial depolarization, atrial contraction increases atrial pressure and pushes blood into ventricles.
• AV node delay: Allows ventricles to fill before contraction.
• QRS complex: Ventricular depolarization, triggers ventricular contraction.
• Ventricular pressure rises, closing AV valves (mitral and tricuspid) to prevent backflow.
• When ventricular pressure exceeds aortic/pulmonary artery pressure, semilunar valves open, ejecting blood.
• Ventricular volume decreases during ejection.
• After ejection, ventricles relax, pressure falls, semilunar valves close to prevent backflow.
• AV valves open when ventricular pressure falls below atrial pressure, allowing filling.

8. Heart Sounds

• First heart sound (lub): Closure of AV valves at start of systole.
• Second heart sound (dub): Closure of semilunar valves at start of diastole.
• Occasionally, third and fourth heart sounds can be heard, related to rapid filling and atrial contraction.

9. Phases of the Cardiac Cycle

• Systole: Period of ventricular contraction and blood ejection.
• Diastole: Period of ventricular relaxation and filling.
• Isovolumic contraction: Ventricles contract with no volume change (all valves closed).
• Isovolumic relaxation: Ventricles relax with no volume change (all valves closed).

10. Diastolic Filling Phases

• Phase 1: AV valves open as atrial pressure exceeds ventricular pressure, rapid filling occurs.
• Phase 2: Passive filling continues as blood flows from veins to atria and ventricles.
• Phase 3: Atrial contraction actively pushes additional blood into ventricles.

11. Heart Valves

• Atrioventricular (AV) valves:

  • Mitral (left side) and tricuspid (right side) valves.
  • Supported by chordae tendineae and papillary muscles to prevent valve prolapse during ventricular contraction.
  • Close when ventricular pressure rises above atrial pressure.

• Semilunar valves:

  • Aortic and pulmonic valves at ventricular exits.
  • More robust to withstand high pressure.
  • Prevent backflow during ventricular relaxation.

12. Pressure-Volume Relationships and the Frank-Starling Mechanism

• Pressure-volume loops show phases of the cardiac cycle:

  • Diastole (filling) with increasing volume and low pressure.
  • Isovolumic contraction with rising pressure but constant volume.
  • Ejection phase with decreasing volume and high pressure.
  • Isovolumic relaxation with falling pressure and constant volume.

• Stroke volume = End diastolic volume (EDV) - End systolic volume (ESV).

• External work of the heart is the area within the pressure-volume loop.

• Frank-Starling law: Increased ventricular filling (preload) stretches cardiac muscle fibers, increasing contraction strength and stroke volume.

• Overstretching reduces contractility due to suboptimal actin-myosin overlap.

13. Regulation of Heart Function

• Autonomic nervous system:

  • Parasympathetic (vagus nerve):
    • Innervates SA and AV nodes.
    • Decreases heart rate (negative chronotropic effect).
    • Slightly reduces contractility.
  • Sympathetic:
    • Innervates entire heart.
    • Increases heart rate and contractility (positive chronotropic and inotropic effects).

• Ionic effects:

  • Potassium (K⁺): Excess causes flaccid, slow heart by blocking conduction and reducing resting membrane potential.
  • Calcium (Ca²⁺): Excess causes spastic contraction; deficiency weakens contraction.

• Temperature: Increased temperature raises heart rate up to a point; excessive heat can weaken the heart.

• Arterial pressure (afterload):

  • Increased arterial pressure increases afterload.
  • Cardiac output remains stable up to ~160 mmHg mean arterial pressure.
  • Beyond this, cardiac output decreases due to excessive workload.

14. Summary

• The heart functions as a mechanical pump controlled by electrical signals.
• Cardiac muscle’s unique action potential and excitation-contraction coupling enable sustained contractions.
• The cardiac cycle involves coordinated electrical and mechanical events to efficiently pump blood.
• Heart valves ensure unidirectional blood flow.
• The Frank-Starling mechanism and autonomic nervous system finely regulate cardiac output.
• Ionic balance and temperature also influence heart function.

Suggested Study Actions

• Review heart anatomy diagrams and Wiggers diagram.
• Understand phases of cardiac action potential and refractory periods.
• Study pressure-volume loops and Frank-Starling mechanism.
• Learn autonomic regulation and ionic effects on the heart.

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