Physiology of the Heart

Review of Action Potentials

• Action Potential in Skeletal Muscle:
  • Opening of voltage-gated sodium channels → Na+ influx → depolarization
  • Channels close after 3ms → voltage-gated potassium channels open → K+ efflux → repolarization
  • Result: All-or-none event with a wave of depolarization along the muscle
  • Role in skeletal muscle: Depolarization travels down T-tubules → opens voltage-gated Ca2+ channels on sarcoplasmic reticulum → Ca2+ release

Differences in Cardiac Muscle

• Plateau Potential in Cardiac Muscle:
  • Depolarization: Na+ influx
  • Plateau phase: Balance between K+ efflux and sustained Ca2+ influx
  • Results in a longer depolarization phase, longer refractory period (~250ms vs. 3ms in skeletal muscle)
  • Prevents tetanus and fatigue in cardiac muscle
  • Contraction: Two sources of Ca2+ (sarcoplasmic reticulum and extracellular)

Cardiac Muscle Contraction

• Differences with skeletal muscle:
  • Requires extended refractory period to prevent tetanus
  • Uses plateau action potentials instead of spiked
  • External Ca2+ source augments the contraction
• Consequence: Stronger contractions and prolonged muscle action

Role of Pacemaker Cells

• Pacemaker Cells:
  • Located mainly in Sinoatrial (SA) Node and Atrioventricular (AV) Node
  • Self-excitable, no need for motor neuron stimulation
  • Generate rhythmical electrical activity called pacemaker potentials
  • Electrical signal conducted via gap junctions for synchronized contraction
  • Pacemaker potential drifts to threshold due to Na+ leakage and slower K+ leakage channels → opens voltage-gated Ca2+ channels

Heart Rate Modulation

• Sympathetic (fight/flight): Norepinephrine increases heart rate
• Parasympathetic (rest/digest): Acetylcholine slows heart rate
• Pacemaker cells can self-regulate but can be influenced by neurotransmitters

Conduction Pathway

• Sequence of excitation:
  1. SA Node (fastest pacemaker cells)
  2. AV Node (delays impulse)
  3. Bundle of His
  4. Right and Left Bundle Branches
  5. Purkinje Fibers
• Role of gap junctions: Faster, synchronized contraction across the heart

Cardiac Cycle

• Phases:
  1. Mid-to-late ventricular diastole: AV valves open, semilunar valves closed, ventricular filling
  2. Ventricular systole:
     • Isovolumetric contraction: Both AV and semilunar valves closed, pressure increases
     • Ventricular ejection: Semilunar valves open, blood ejected
  3. Early diastole: Ventricles relax, semilunar valves close
• Heart Sounds: "Lub" (AV valves closing), "Dub" (Semilunar valves closing)
• Cardiac Output (CO): CO = Stroke Volume (SV) x Heart Rate (HR)
  • SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)

Heart Pathologies

• Heart Attack (Myocardial Infarction): Death of heart muscle cells
  • Diagnosed by presence of cardiac enzymes (creatine kinase, troponin) in the bloodstream
• Arrhythmia: Uncoordinated heart contractions, diagnosed via EKG
• Congestive Heart Failure: Heart's inability to pump sufficiently
• Congenital Defects:
  • Ex: Patent ductus arteriosis (failure of fetal circulatory connection to close after birth)
• Age-related Changes:
  • Sclerosis of AV valves
  • Decline in cardiac reserve
  • Fibrosis in conduction pathways

Miscellaneous Notes

• Parasympathetic innervation through vagus nerve inhibits heart rate
• Sympathetic stimulation increases heart rate via norepinephrine
• Calcium channel blockers can regulate heart rate by affecting Ca2+ influx
• Pacemakers maintain heart rhythm without external stimulation
• Hormones like thyroxine and epinephrine can influence heart rate