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Questions

 

A.1. What is the differential diagnosis of low CO following cardiac surgery?

Answer:

CO is the product of stroke volume (SV) and HR:

CO = HR × SV

According to this relationship, low SV and/or low HR result in a low CO state. However, rapid HR of either ventricular or atrial origin (ie, atrial fibrillation) can also cause a low CO state because diastolic filling time is decreased or the atrial contribution to ventricular filling is reduced. Preload, afterload, and contractility all contribute to SV and their alteration can also reduce CO (Table 12.1). A decrease in preload will decrease SV if the ventricle is underfilled. An increase in preload can also decrease SV if it causes ventricular overdistension, thereby stretching ventricular myocytes beyond the working limits of the length-tension relationship. A decrease in myocardial contractility can compromise CO. Finally, in a ventricle with systolic dysfunction, an increase in afterload can further impair ventricular ejection and SV. A combination of these hemodynamic disturbances can coexist in the same patient. For example, a patient can have both a decrease in contractility and reduced preload, thereby resulting in low CO. Therefore, correcting one problem alone might not optimize hemodynamic conditions.

Table 12.1: Differential Diagnoses of a Low Cardiac Output

ParameterChangeExamples
Heart rateDecreaseBradycardia
Heart block causing loss of AV synchrony
IncreaseAtrial fibrillation
Ventricular tachyarrhythmias
PreloadDecreaseHypovolemia
Mitral stenosis
IncreaseVentricular overdistension and systolic dysfunction
Mitral regurgitation
AfterloadIncreaseEmbolism
Outflow tract obstruction
ContractilityDirect decreaseRight and/or left ventricle
  • Ischemia/infarction

  • Stunning/hibernation

Indirect decreaseCardiac tamponade
Embolism
Negative inotropic agents
Toxins (endotoxin, inflammatory cytokines)

AV, atrioventricular.


References