Cardiac Muscle, Conduction System, and Cardiac Cycle

Cardiac muscle histology, action potential, refractory periods, conduction pathway, cardiac cycle, stroke volume, cardiac output, and preload/afterload/contractility.

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Cardiac Muscle, Conduction System, and Cardiac Cycle

Cardiac Muscle Histology

Cardiac muscle fibers, compared to skeletal muscle, are:

  • Shorter in length
  • Less circular in transverse section
  • Branching with a "stair-step" appearance
  • Typically 50–100 μm long and about 14 μm in diameter
  • Connected by gap junctions, allowing the myocardium to contract as a single, coordinated unit

The Action Potential

The action potential is an electrical current that travels across the cell membranes of the heart, causing contraction. It is caused by the interaction of three ions: potassium (K+), calcium (Ca2+), and sodium (Na+).

Key Terms

TermDefinition
PolarizedInside of cell is more negative than the outside
DepolarizationMovement of charged particles across the membrane making the inside positive
RepolarizationMovement of ions restoring the inside of the cell to its negative charge
Resting Membrane Potential (RMP)Electrical charge difference across the fibers of the heart cell at rest (~ -90 mV)

Five Phases of the Action Potential

PhaseNameKey Events
Phase 0DepolarizationThreshold reached at -70 mV; Na+ moves rapidly into the cell through voltage-gated fast Na+ channels, causing a spike; Ca2+ moves in slowly through Ca2+ channels (causes contraction); K+ is leaving the cell
Phase 1Early repolarizationNa+ channels partially close, slowing Na+ inflow; voltage-gated K+ channels open; decreased positive ions create a negative deflection
Phase 2Plateau phaseSustained contraction; Ca2+ slowly enters through Ca2+ channels (shifts graph positive); K+ continues to slowly leave through K+ channels (shifts graph negative)
Phase 3Final repolarizationK+ flows out rapidly through K+ channels; Na+ and Ca2+ channels close, stopping entry
Phase 4Resting stateRMP returns to -90 mV; voltage-sensitive ion channels return to pre-depolarized permeability; excess Na+ inside returns to normal; K+ inside returns to normal; additional Na+/Ca2+ pump removes extra Ca2+

Refractory Periods

PeriodDescriptionPhases
Absolute Refractory Period (ARP)Cell will not respond to further stimulationPhase 0, 1, 2, and part of 3
Relative Refractory Period (RRP)Some cells repolarized to threshold; can respond to a stronger than normal stimulusLate phase 3
Effective Refractory Period (ERP)Includes ARP and first half of RRP; a conducted action potential cannot be generatedThrough first half of RRP
Supranormal Period (SNP)Weaker than normal stimulus can cause depolarization; extends from end of phase 3 to beginning of phase 4; can cause R on T phenomenon and dysrhythmiasEnd of phase 3 to beginning of phase 4

Cardiac Conduction System Terminology

TermDefinition
AutomaticityAbility of SA node cells to generate an action potential without being stimulated
ExcitabilityAbility of a cell to reach threshold potential and respond to a stimulus (irritability)
ConductivityAbility of a cardiac cell to receive and conduct an electrical impulse to an adjoining cell
ContractilityAbility of myocardial cells to shorten, causing contraction in response to electrical stimulus

Cardiac Conduction System

The conduction system is composed of autorhythmic fibers that are self-excitable and repeatedly generate action potentials to trigger heart contractions.

Pathway and Components

ComponentLocationFunctionIntrinsic Rate
Sinoatrial (SA) NodeRight atrial wall, inferior and lateral to SVC openingLead pacemaker; repeatedly depolarizes to threshold spontaneously (pacemaker potential)60–100 bpm
Bachmann's BundleFrom SA node to LAConducts impulses directly to the left atrium, causing simultaneous atrial contraction
Internodal Tracts (anterior, middle, posterior)Right atriumConduct electrical impulse from SA node to AV node
Atrioventricular (AV) NodeInteratrial septum, anterior to coronary sinus openingDelays impulse to allow atria to empty blood into ventricles, increasing stroke volume40–60 bpm
AV Bundle (Bundle of His)Fibrous skeleton insertionOnly site where action potentials can conduct from atria to ventricles
Right and Left Bundle BranchesInterventricular septum toward apexConduct impulses to Purkinje fibers
Purkinje FibersFrom apex upward to ventricular myocardiumRapidly conduct action potential from apex upward, causing contraction to begin at the apex20–40 bpm

AV Node Functional Regions

  • Atrionodal (AN) — transitional zone
  • Nodal (N) — midportion
  • Nodal-His (NH) — lower region merging with Bundle of His

The Cardiac Cycle

One cardiac cycle includes the systolic and diastolic phases of both the atria and ventricles. At a heart rate of 75 bpm, one cycle lasts 0.8 seconds.

Key Acronyms

AcronymDefinition
EDVEnd-diastolic volume (~130 mL) — blood volume at end of relaxation period
SVStroke volume (~70 mL) — volume ejected per beat from each ventricle
ESVEnd-systolic volume (~60 mL) — blood remaining after contraction

SV = EDV - ESV

Atrial Systole (0.1 sec)

  • SA node depolarization causes atrial depolarization (P wave on ECG)
  • Atria contract, forcing blood through open AV valves into ventricles
  • Contributes a final ~25 mL to the ventricular volume
  • At the end: each ventricle has ~130 mL (EDV)

Ventricular Systole (0.3 sec)

  • AV node depolarization causes ventricular depolarization (QRS complex)
  • Ventricles contract; pressure rises, forcing AV valves closed
  • Isovolumetric contraction (~0.05 sec) — all four valves closed; muscle fibers contract but don't shorten
  • When LV pressure exceeds aortic pressure (~80 mmHg) and RV pressure exceeds pulmonary trunk pressure (~20 mmHg), SL valves open
  • Ventricular ejection (~0.25 sec): LV reaches ~120 mmHg, RV reaches ~25-30 mmHg
  • Each ventricle ejects ~70 mL into aorta/pulmonary trunk
  • T wave marks ventricular repolarization

Ventricular Diastole (0.4 sec)

  • Ventricles relax; pressure falls
  • Blood in aorta/pulmonary trunk flows backward, closing SL valves
  • Dicrotic notch — rebound of blood off closed aortic valve cusps
  • Isovolumetric relaxation — brief period with all four valves closed
  • When ventricular pressure drops below atrial pressure, AV valves open
  • Ventricular filling begins; majority of blood rushes in rapidly

Cardiac Output

Cardiac output (CO) is the volume of blood ejected from the ventricle per minute.

CO = SV × HR

In a typical resting adult male:

  • SV = 70 mL/beat, HR = 75 bpm
  • CO = 70 mL × 75 bpm = 5,250 mL/min = 5.25 L/min

Cardiac Reserve

The difference between maximum CO and resting CO. Average person has a cardiac reserve of 4–5 times resting value. Top endurance athletes may have 7–8 times. Severe heart disease may result in little to no cardiac reserve.

Regulation of Stroke Volume

FactorDescription
PreloadDegree of stretch on the heart before contracting (at end of diastole). Frank-Starling law: greater stretch = larger volume = stronger contraction
ContractilityForcefulness of contraction of individual ventricular muscle fibers. Positive inotropic agents (e.g., increased Ca2+) increase contractility; negative inotropic agents (e.g., calcium channel blockers) decrease it
AfterloadPressure that must be exceeded before ejection can occur. RV overcomes pulmonary artery pressure (~20 mmHg); LV overcomes aortic pressure (~80 mmHg). Increased afterload (hypertension, atherosclerosis) decreases stroke volume