Cardiac Physiology Notes

Heart Anatomy

  • Figure 18.4e: Frontal section of the heart.

    • Key structures include:
      • Aorta
      • Left pulmonary artery and veins
      • Left atrium and ventricle
      • Mitral (bicuspid) valve
      • Aortic and pulmonary valves
      • Papillary muscle
      • Interventricular septum
      • Epicardium, myocardium, and endocardium
      • Superior and Inferior vena cava
      • Right pulmonary artery and veins
      • Right atrium and ventricle
      • Fossa ovalis
      • Pectinate muscles
      • Tricuspid valve
      • Chordae tendineae
      • Trabeculae carneae

  • Figure 18.4d: Posterior surface view of the heart.

    • Key structures include:
      • Aorta
      • Left pulmonary artery and veins
      • Auricle of left atrium
      • Left atrium and ventricle
      • Great cardiac vein
      • Posterior vein of left ventricle
      • Apex
      • Superior and Inferior vena cava
      • Right pulmonary artery and veins
      • Right atrium
      • Right coronary artery (in coronary sulcus)
      • Coronary sinus
      • Posterior interventricular artery (in posterior interventricular sulcus)
      • Middle cardiac vein
      • Right ventricle

Microscopic Anatomy of Cardiac Muscle

  • Figure 18.11a: Cardiac muscle cell structure.

    • Features include:
      • Nucleus
      • Gap junctions
      • Desmosomes
      • Intercalated discs

  • Figure 18.11b: Detailed cardiac muscle cell.

    • Key components:
      • Nucleus
      • I band and A band
      • Sarcolemma
      • Z disc
      • Mitochondria
      • T tubule
      • Sarcoplasmic reticulum
      • Intercalated disc

Cardiac Muscle Contraction

  • Figure 18.12: Action potential and tension development in cardiac muscle.

    • Phases:
      • Depolarization (1): Na+ influx through fast voltage-gated Na+ channels; positive feedback cycle.
      • Plateau phase (2): Ca2+ influx through slow Ca2+ channels; maintains depolarization.
      • Repolarization (3): Ca2+ channels inactivate, K+ channels open, K+ efflux returns membrane potential to resting voltage.

  • Ca2+ influx triggers opening of Ca2+ -sensitive channels in the SR, releasing bursts of Ca2+.

  • E-C coupling occurs as Ca2+ binds to troponin, initiating filament sliding.

  • Duration of action potential (AP) and contractile phase longer in cardiac muscle than skeletal muscle.

  • Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels.

Heart Physiology: Electrical Events

  • Intrinsic cardiac conduction system: Network of noncontractile (autorhythmic) cells that initiate and distribute impulses, coordinating depolarization and contraction.

Autorhythmic Cells

  • Unstable resting potentials (pacemaker potentials or prepotentials) due to open slow Na+ channels.

  • At threshold, Ca2+ channels open.

  • Explosive Ca2+ influx causes the rising phase of the action potential.

  • Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels.

  • Figure 18.13: Pacemaker potential and action potential in autorhythmic cells.

    • Pacemaker potential (1): Slow depolarization due to opening of Na+ channels and closing of K+ channels.
    • Depolarization (2): Action potential starts when pacemaker potential reaches threshold; Ca2+ influx through Ca2+ channels.
    • Repolarization (3): Ca2+ channels inactivate, K+ channels open, K+ efflux returns membrane potential to negative voltage.

Intrinsic Conduction System

  • Figure 18.14a: Anatomy and sequence of electrical excitation.
    • Sinoatrial (SA) node (pacemaker) (1): Generates impulses.
    • Impulses pause (0.1 s) at the atrioventricular (AV) node (2).
    • Atrioventricular (AV) bundle connects atria to ventricles (3).
    • Bundle branches conduct impulses through the interventricular septum (4).
    • Purkinje fibers depolarize contractile cells of both ventricles (5).

Sequence of Excitation

  • Sinoatrial (SA) node (pacemaker):
    • Generates impulses ~75 times/minute (sinus rhythm).
    • Depolarizes faster than any other part of the myocardium.
  • Atrioventricular (AV) node:
    • Smaller diameter fibers; fewer gap junctions.
    • Delays impulses ~0.1 second.
    • Depolarizes 50 times per minute without SA node input.
  • Atrioventricular (AV) bundle (bundle of His):
    • Only electrical connection between atria and ventricles.
  • Right and left bundle branches:
    • Carry impulses toward heart apex.
  • Purkinje fibers:
    • Complete pathway into apex and ventricular walls.
    • AV bundle and Purkinje fibers depolarize ~30 times per minute without AV node input.

Electrocardiography

  • Electrocardiogram (ECG or EKG): Composite of all action potentials generated by nodal and contractile cells at a given time.

  • Three waves:

    • P wave: Depolarization of SA node.
    • QRS complex: Ventricular depolarization.
    • T wave: Ventricular repolarization.

  • Figure 18.16: ECG components.

    • Includes P wave, QRS complex, T wave, P-Q interval, S-T segment, and Q-T interval.

  • Figure 18.17: Correlation of ECG waves with cardiac events.

    • P wave corresponds to atrial depolarization initiated by the SA node.
    • QRS complex corresponds to ventricular depolarization, with atrial repolarization occurring.
    • T wave corresponds to ventricular repolarization.

  • A prolonged QRS complex may indicate AV bundle damage.

ECG Anomalies

  • Figure 18.18:
    • Normal sinus rhythm.
    • Junctional rhythm: SA node nonfunctional; absent P waves; heart paced by AV node at 40-60 beats/min.
    • Second-degree heart block: Some P waves not conducted through AV node; more P waves than QRS waves (e.g., 2:1 ratio).
    • Ventricular fibrillation: Chaotic, grossly irregular ECG deflections; seen in acute heart attack and electrical shock.

Heart Sounds

  • Two sounds (lub-dup) associated with closing of heart valves.

    • First sound: AV valves close; beginning of systole.
    • Second sound: SL valves close; beginning of ventricular diastole.

  • Heart murmurs: Abnormal heart sounds; often indicate valve problems.

  • Figure 18.19: Auscultation points for heart valves.

    • Aortic valve sounds: 2nd intercostal space at right sternal margin.
    • Pulmonary valve sounds: 2nd intercostal space at left sternal margin.
    • Mitral valve sounds: Over heart apex (5th intercostal space) in line with middle of clavicle.
    • Tricuspid valve sounds: Typically heard in right sternal margin of 5th intercostal space.

Mechanical Events: The Cardiac Cycle

  • Cardiac cycle: All events associated with blood flow through the heart during one complete heartbeat.

    • Systole: Contraction phase.
    • Diastole: Relaxation phase.

  • Figure 18.20: Phases of the cardiac cycle.

    • Ventricular filling (mid-to-late diastole): AV valves open.
    • Atrial contraction.
    • Isovolumetric contraction phase: Aortic and pulmonary valves closed.
    • Ventricular ejection phase.
    • Isovolumetric relaxation (early diastole).
    • Includes ECG, heart sounds, atrial systole, dicrotic notch, and ventricular volume/pressure changes.

Regulation of the Cardiac Cycle

  • Heart rate and blood volume pumped change to meet requirements.
  • Cardiac center in medulla oblongata performs neural regulation of heart.
  • SA node (pacemaker) normally controls heart rate.
  • Sympathetic and parasympathetic fibers modify heart rate based on:
    • Physical exercise
    • Body temperature
    • Fight-or-flight response
    • Concentration of various ions

Parasympathetic and Sympathetic Regulation

  • Parasympathetic impulses:
    • Reach heart via vagus nerves.
    • Lower SA node rate from 100 beats/min to 60-80 beats/min.
    • Decrease heart rate via influence on SA and AV nodes.
  • Sympathetic impulses:
    • Reach heart on accelerator nerves.
    • Increase heart rate via influence on SA and AV nodes, atrial and ventricular myocardium.
  • Baroreceptor reflexes:
    • Involve cardiac control center in medulla oblongata.
    • Balance inhibitory and excitatory effects.
    • Contain cardioinhibitor and cardioaccelerator reflex centers.

Baroreceptor Reflex Example

  • Baroreceptors in aortic arch and carotid artery sinuses detect blood pressure.
  • Increased pressure stretches receptors.
  • Parasympathetic cardioinhibitory reflex lowers heart rate and blood pressure.
  • Stretch receptors in venae cavae:
    • Increase in blood pressure stretches receptors.
    • Sympathetic cardioaccelerator reflex increases heart rate and contraction force to lower venous pressure.
  • Other factors affecting heart rate:
    • Impulses from hypothalamus and cerebrum.
    • Body temperature.
    • Levels of ions.

Cardiac Output (CO)

  • Volume of blood pumped by each ventricle in one minute.
  • CO = HR eq SV
    • HR = heart rate (beats per minute).
    • SV = stroke volume (volume of blood pumped per beat).
  • At rest:
    • CO (ml/min) = HR (75 beats/min)
      eq SV (70 ml/beat) = 5.25 L/min
  • Maximal CO:
    • 4-5 times resting CO in non-athletes.
    • May reach 35 L/min in trained athletes.
  • Cardiac reserve: Difference between resting and maximal CO.

Regulation of Stroke Volume

  • SV = EDV - ESV
  • Factors affecting SV:
    • Preload.
    • Contractility.
    • Afterload.

Preload

  • Preload: Degree of stretch of cardiac muscle cells before contraction (Frank-Starling law).
  • Cardiac muscle exhibits length-tension relationship.
  • At rest, cardiac muscle cells shorter than optimal length.
  • Slow heartbeat and exercise increase venous return.
  • Increased venous return distends ventricles, increasing contraction force.

Contractility

  • Contractility: Contractile strength at a given muscle length, independent of stretch and EDV.
  • Positive inotropic agents increase contractility:
    • Increased Ca2+ influx due to sympathetic stimulation.
    • Hormones (thyroxine, glucagon, epinephrine).
  • Negative inotropic agents decrease contractility:
    • Acidosis.
    • Increased extracellular K+.
    • Calcium channel blockers.

Afterload

  • Afterload: Pressure that must be overcome for ventricles to eject blood.
  • Hypertension increases afterload, increasing ESV and reducing SV.

Regulation of Heart Rate

  • Positive chronotropic factors increase heart rate.
  • Negative chronotropic factors decrease heart rate.

Autonomic Nervous System Regulation

  • Sympathetic nervous system:
    • Activated by emotional or physical stressors.
    • Norepinephrine increases pacemaker firing rate and contractility.
  • Parasympathetic nervous system:
    • Opposes sympathetic effects.
    • Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels.
    • Heart at rest exhibits vagal tone (parasympathetic).

Chemical Regulation of Heart Rate

  • Hormones:
    • Epinephrine from adrenal medulla enhances heart rate and contractility.
    • Thyroxine increases heart rate and enhances norepinephrine/epinephrine effects.
  • Ion concentrations (Ca2+, K+) must be maintained for normal heart function.

Other Factors

  • Age.
  • Gender.
  • Exercise.
  • Body temperature.

Homeostatic Imbalances

  • Tachycardia: Abnormally fast heart rate (>100 bpm); may lead to fibrillation if persistent.
  • Bradycardia: Heart rate slower than 60 bpm; may result in inadequate blood circulation; may be desirable in endurance training.

Congestive Heart Failure (CHF)

  • Progressive condition where CO is too low to meet tissue needs.
  • Caused by:
    • Coronary atherosclerosis.
    • Persistent high blood pressure.
    • Multiple myocardial infarcts.
    • Dilated cardiomyopathy (DCM).

Age-Related Changes

  • Sclerosis and thickening of valve flaps.
  • Decline in cardiac reserve.
  • Fibrosis of cardiac muscle.
  • Atherosclerosis.