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Heart Function Review

by bmahato1

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Cardiac cycle

  • ECG
    • p wave
    • QRS complex
    • T wave
  • Ventricular pressure vs time tracing
  • Aortic pressure vs time tracing
  • Atrial pressure vs time tracing
    • a wave: atrial contraction
    • c wave: AV valve closure
    • v wave: atrial filling
  • Ventricular volume vs time tracing
  • Heart sounds
    • S1: AV valves closure
    • S2: Semilunar valves (pulmonic & aortic valves)¬†closure
    • S3: Early diastolic
    • S4: Late diastolic
Cardiac output
CO = HR x SV
SV PAC: Stroke volume depends on three factors–preload (+), after load (-), and contractility (+)
Preload
  • Frank-Starling law: SV vs EDV/EDP graph
  • Pressure – volume loop: increase in preload leads to increase in SV by the same amount, i.e. ESV does not change
  • Preload can increase in aortic regurgitation or mitral regurgitation during diastole
Afterload
  • BP, aortic stenosis, vasoconstrictors (phenylephrine: alpha-1 agonist)
  • wall stress (=Pr/2w)
  • Pressure-volume loop: reduced SV–> increased ESV. Aortic valve opens and ejection starts at higher pressure. Less energy left for ejection after spending energy to overcome afterload.
  • ESVPR line: higher the afterload, greater the ESV (and so lower the SV)
Contractility
  • Strength of contraction after taking preload & afterload into account
  • Reflects chemical/hormonal stimulation of the heart: increase in actin-myosin interaction rate
  • Increase in contractility shifts Frank-Starling curve upward to the left: greater SV at any given preload (EDV/EDP)
Diastolic Disfunction
  • Heart failure with preserved ejection fraction
  • Non-compliant ventricle–>reduced filling–>reduced stroke volume
  • High diastolic ventricular pressure–>pulmonary HTN–>pulmonary edema
  • Causes: HTN, fibrosis, amylodosis, transient ischemia (since relaxation is active process)
Compensatory mechanisms if reduced CO
  • increased sympathetic flow
    • increase HR
    • increased contractility
    • vasoconstriction
      • arteries: increase SVR & BP: increase perfusion (but also afterload)
      • veins: increase venous return: increase preload: increased SV (but also excessive volume retention: edema)
  • RAS
    • AII
      • vasoconstrictor: see above
      • aldosterone: Na+ & water retention: increased venous return to heart: increased preload
  • ADH: water retention: increase preload

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