Question 15

Outline the cardiovascular changes associated with morbid obesity

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College Answer

Many candidates did not include enough detail in their answers.  Higher scoring answers included more depth such as the following: blood volume, left ventricular changes, arterial blood pressure, pulmonary artery pressures, risks of ischaemia, 
arrhythmias etc. 


Though this SAQ obviously did not go well for 58% of the candidates, it is remarkable that 42% of them managed to assemble enough obesity-related information into some kind of precariously teetering answer structure. The remarks of the examiners here were not entirely informative as to what level of detail was expected, other than to say that whatever the trainees wrote was not enough. What follows is an attempt to bring together enough information to give the impression of depth, into a format which gives the impression of order.

  • Total body oxygen demand is increased
    • Oxygen requirement and CO2 production are increased by about 150%
    • This equates to approximately 300-350ml/min of O2, as compared to 200ml/min for non-obese patients
    • This is mainly because of increased lean body mass (adipose tissue has low metabolic demand)
    • In conscious obese patients, the effort of breathing is a major source of increased oxygen consumption
  • Cardiac output is increased
    • Stroke volume is increased by about 1.25ml per every 1kg/m2 BMI
    • Heart rate remains stable, or increases only slightly
    • The increase in cardiac output (approximately 1L//min for every 12.5 BMI is mainly due to an increase in stroke volume
  • Cardiac preload is increased
    • Total blood volume is increased
    • Thus, MSFP and CVP are increased
    • This increase in preload causes the increase in stroke volume
    • It is due to neurohormonal changes in obesity, which are mediated by the endocrine function of adipose tissue:
      • Sympathetic stimulation and thus RAAS activation by leptin
      • Angiotensinogen synthesis by leptin
    • These cause salt and water retention
    • Left and right atrial pressure increases, which increases the propensity to develop atrial arrhythmias
  • Cardiac afterload can be increased or decreased
    • Normotensive obese patients usually have decreased peripheral vascular resistance
    • However, the prevalence of hypertension in obesity is ~60%
    • This is mainly due to chronic sympathetic activation, which is attributed to the chronic hypoxia of OSA.
  • LV contractility is often stable
    • In response to increased preload and afterload, remodelling occurs:
      • Increased LV wall thickness
      • Increased LV chamber volume
      • As the result, LV diastolic function is often impaired
      • Response to exercise is affected by this: stroke volume in the extremely obese is peak at rest, and no major increase in stroke volume with exercise is possible
    • LV remodelling increases the propensity to develop ventricular arrhythmias, and increased LV mass predisposes the LV to ischaemia
  • There is increased RV afterload and preload
    • Preload is increased by the global circulating volume expansion
    • Afterload is increased because of:
      •  LV diastolic failure
      • Chronic hypoxia due to OSA or obesity hypoventilation, resulting in chronic  hypoxic pulmonary vasoconstriction


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