Week 11 Physiology

Effects of gravity.

  • Mean arterial pressure at heart is 100mmHg
  • This increases by 0.77mmHg for every centimetre below the heart and the same increases with every cm above heart
  • Similar effect on venous pressure
  • Standing increases HR


Effects of exercise (popular question).

  • Increases HR, SV, SBP, mean arterial pressure
    • Venoconstriction –> increase pre load
    • Increased action of the muscle pump –> increased preload
    • Increased respiration rate –> increased thoracic pump –> increase venous return
    • Blood flow = pressure difference/resistance so during exercise SBP increasing increases P difference therefore blood flow increases, and also resistance decreases to increase flow
  • Adrenaline(sympathetic tone) + lactic acid (vasoactive metabolite)–> increased HR and cause skeletal vasodilation and constriction of non vital organ blood supply.
  • VO2 = CO x O2 required to supply muscles
  • Skeletal muscle flow increases from 20% at rest to 80-85% in exercise
    • Sympathetic tone causes venous contraction in skeletal muscles –> increase preload(when capacitance vessels contricted)
  • Numbers
    • SV increases during exercise until 40% of VO2max, rising from approximately 80 mL/beat to 120 mL/beat.
    • HR increases with intensity until VO2max is reached, rising from approximately 70 bpm to 200bpm.
    • Cardiac output increases with intensity until VO2max is reached, rising from approximately 5 L/min to approximately 25-30 L/min.
    • The arterial-venous oxygen difference is the amount of oxygen extracted from the blood rises from approximately 4 mL of oxygen per 100 mL of blood at rest to 18 mL of oxygen per 100 mL of blood during high-intensity aerobic exercise.
    • VO2 – the average person aged 20 years are 37-48 mL/kg/min.
      • CO is a major determinant of VO2
      • Declines with age as max HR declines
    • One metabolic unit (MET) equals the VO2 at rest. The estimate of the value of one MET is 3.5 mL of oxygen per kg/min.



  • When tissue perfusion is unable to match tissue’s metabolic demands for oxygen and other nutrients.
  • Clinical syndrome of hypotension, oliguria and poor peripheral perfusion
  • Types.
    • Cardiogenic
      • Heart failure due to MI, arrhythmias, valvular pathology
    • Hypovolaemic
      • Haemorrhage, trauma, dehydration
      • commonest
    • Distributive
      • Septic shock
      • Anaphylactic
    • Neurogenic
  • The body’s response depends on degree of volume loss
    •  10% well tolerated (tachycardia)
    • 20 – 25% failure of compensatory mechanisms (hypotension, orthostasis,
    • decreased CO)
    • > 40% loss associated with overt shock (marked hypotension, decreased CO,
    • lactic acidemia)


  • Stages of shock
  • Compensated
    • Tachycardia, renin-angiotensin system activated, Na and H2O retention, vasopressin, thirst, neurogenic vasoconstriction to maintain BP. Increase HR, contractility and resistance.
    • Pronounced tachycardia.
  • Progressive shock
    • when the initial cardiovascular insult is so large the normal compensatory mechanisms cannot cope –> either needing iatrogenic support or decent into vicious cycle of decreased CO and BP –> decreased myocardial and cerebral perfusion –> decreased cardiac contractility and neurological BP control –> vasodilation and venous pooling, hypoxia and acidosis leads to oedema and clotting –> decreased myocardial filling –> decreased CO.
    • Iatrogenic support will help restore normal circulation
  • Refractory (irreversible) shock.
    • Without intervention progressive shock goes into irreversible shock and the cerebral and cardiac function are so compromised that no intervention will be able to restore normal cardiovascular function.


Hypertension.- causes (Good MCQ or viva question).

  • Primary – Genetic and lifestyle factors – account for 90-95%
  • Genetic
    • Usually multi focal
    • Rarely unifocal eg ion channelopathy
  • Lifestyle
    • Sedantary lifestyle
    • Obesity
  • Secondary causes
    • CKD
    • Polycystic kidneys
    • Bilateral renal artery stenosis
    • Phaeocytochroma
    • Cushings syndrome
    • Coarctation of aorta
    • OSA
      hyper and hypothyroidism


Pathogenesis of CHF

  • HTN
  • Iscahemic
  • Valvular pathology
  • Dilated cardiomyopathy – pregnancy
  • Can be due to systolic or diastolic dysfunction (systolic has all the evidence for ‘SAAB’ meds, diastolic doesn’t have the evidence
  • Adaptations
    • Frank starling curve –> increase preload to increase Cardial contractility and CO
    • ANP – promote vasodilation and naturesis
    • Altered myocyte regeneration and death
    • Myocardial hypertrophy
    • Neurohormonal response via increased sympathetic tone via baroreceptors(dec SV)–> increased HR, contractility and vasoconstriction, stimulate renin angiotensin, aldosterone
    • Issues – contractile dysfunction, impaired filling, increased pressures, volume loading, dysrythmias, ventricular remodelling


Viva questions:

  1. Tell me the immediate compensatory mechanisms which operate upon assuming the upright posture.
  2. What types of shock are you familiar with?
  3. What is the body’s response to the rapid loss of 1500 mls. of circulating blood volume ?
  4. What is the body’s response to exercise