Mechanical Events of the Cardiac Cycle – Key Vocabulary

Cardiac Cycle as a Repeating Loop

  • The heart cycle can be described from any point because it is continuous; in this video the description begins late in diastole (the pause between beats).
    • All four chambers (atria + ventricles) are relaxed ➜ pressures are low.
    • Blood flows passively from veins → atria → ventricles because \Delta P = P{veins}-P{ventricles} > 0 (no ATP required by myocardium).

Electrical Triggers & Their Mechanical Outcomes

  • SA-node firing
    • Initiates atrial depolarization (P-wave on ECG, shown later).
    • Leads to atrial systole (active filling).
  • AV-node delay (~0.1 s)
    • Ensures atria finish contracting before ventricles start.
    • Fibrous skeleton electrically insulates atria from ventricles.
  • Impulse travels through Bundle of His → bundle branches → Purkinje fibers ➜ ventricular depolarization and contraction.

Phase-by-Phase Mechanical Events

1. Passive Ventricular Filling (late diastole)

  • P{ventricles} < P{atria} ➜ AV valves open.
  • Gradual rise in both atrial & ventricular pressures as volume increases.
  • Ventricular volume tracing: gentle upward slope.

2. Active Filling (atrial systole)

  • Atria contract, expend ATP ➜ final “atrial kick.”
  • Sharp bump in both pressures and ventricular volume.
  • Contributes a minority of total ventricular filling (majority is passive).

3. Isovolumetric Ventricular Contraction (first half of ventricular systole)

  • Ventricular myocardium begins to contract ➜ rapid pressure rise.
  • Valve status:
    • AV valves snap shut when P{ventricles} > P{atria} (no further filling).
    • Semilunar valves still closed because P{ventricles} < P{artery}.
  • All four valves closed ⇒ ventricular volume constant (horizontal line on V-volume graph).
  • Produces S₁ ("lub") heart sound (turbulent back-flow through narrowing AV valves).

4. Ventricular Ejection (second half of ventricular systole)

  • Continues contraction ➜ P{ventricles} > P{artery}.
  • Semilunar valves open → blood exits to aorta/pulmonary artery.
  • Ventricular pressure slightly > arterial throughout ejection.
  • Ventricular volume falls steeply; end-systolic volume remains (cannot eject 100 %).

5. Isovolumetric Relaxation (early ventricular diastole)

  • Ventricular muscle begins relaxing ➜ pressure drops fast.
  • Semilunar valves close instantly when P{ventricles} < P{artery}.
  • AV valves still closed because P{ventricles} > P{atria}.
  • Volume constant again (horizontal segment) ➜ defines isovolumetric relaxation.
  • Generates S₂ ("dub") as semilunar valves shut; sound limited to early part of phase.

6. Return to Passive Filling

  • Complete relaxation ⇒ P{ventricles} < P{atria}.
  • AV valves reopen; cycle restarts with passive filling.

Interpreting Pressure–Volume & Pressure–Time Graphs

  • Top panel: Pressures (mm Hg)
    • Green = left ventricular
    • Purple = left atrial
    • Blue = aortic (arterial)
  • Bottom panel: Ventricular volume (mL)
  • Key observations:
    • Passive filling: green < purple; both slopes up.
    • Atrial systole: small spike in both pressures & volume.
    • Isovolumetric contraction: green rises steeply; no change in volume.
    • Ejection: green just above blue; volume declines.
    • Isovolumetric relaxation: green falls below blue; volume plateau.
    • Aortic pressure rises during ejection then decays (to be addressed in vascular unit).

Valve Dynamics Summarized

PhaseAV ValvesSemilunar Valves
Passive fillingOpenClosed
Active filling (atrial systole)OpenClosed
Iso-vol. contractionClosedClosed
EjectionClosedOpen
Iso-vol. relaxationClosedClosed
Return to passive fillingOpenClosed

Origin of Normal Heart Sounds

  • Mechanism: Turbulent blood flow through a narrowing orifice under high pressure → tissue vibrations → sound waves.
  • Materials: Valves = fibrous connective tissue (flexible, not rigid); sound is NOT valves “slamming.”
  • Timing
    • S₁: during closure of AV valves (early isovolumetric contraction).
    • S₂: during closure of semilunar valves (early isovolumetric relaxation).
  • Sounds fade quickly once valves fully shut and turbulence stops.

Abnormal Sounds: Heart Murmurs

  • Defined as a sound outside S₁–S₂ windows.
  • Always indicate turbulent flow through an inappropriate narrow opening.
  • Common anatomical causes:
    • Valvular stenosis (doesn’t open fully) or insufficiency/regurgitation (doesn’t close fully).
    • Congenital septal defects (interatrial or interventricular holes).
  • Clinical importance: location in cycle pinpoints defect (systolic vs diastolic murmurs).

Practical / Clinical Connections

  • Understanding pressure relationships guides stethoscope auscultation, Doppler studies, and interpretation of pressure–volume loops used in cardiology.
  • Quantities such as stroke volume = EDV - ESV and ejection fraction = \frac{SV}{EDV} derive from these mechanical events.
  • AV-node delay and fibrous skeleton are crucial; damage (e.g., ischemia, fibrosis) can lead to atrioventricular block and disrupt the precise sequence, reducing cardiac efficiency.
  • Recognition of murmurs assists early detection of congenital heart disease, valvular degeneration, rheumatic fever sequelae, etc.
  • Energy-saving design: majority of ventricular filling is passive, minimizing myocardial oxygen demand.

Key Numerical/Formula References

  • Typical left-side pressures (rest):
    • P_{atria}^{max} \approx 10\,\text{mmHg}
    • P_{ventricle}^{systole} \approx 120\,\text{mmHg}
    • P_{aorta}^{rest} \approx 80\,\text{mmHg} diastolic → 120\,\text{mmHg} systolic.
  • Normal end-diastolic volume (EDV): \sim 120\,\text{mL}; end-systolic volume (ESV): \sim 50\,\text{mL}.
  • Stroke volume: SV = 70\,\text{mL} (illustrative average).
  • Flow principle: \text{Flow} = \dfrac{\Delta P}{R} (Ohm’s law analogy for fluids).

Conceptual Take-Aways

  • The heart functions as a pressure pump; valve status is entirely dictated by instantaneous pressure gradients.
  • Iso-volumetric phases are "all-valves-closed" intervals critical for pressure transitions.
  • Atrial contribution is small but significant for maximal ventricular preload, especially when heart rate is high or in certain pathologies.
  • Heart sounds are hemodynamic, not mechanical “clicks;” any extra sound reflects pathology.
  • Graphical literacy (pressure-time, pressure-volume) is essential for higher-level cardiovascular physiology and clinical practice.