A.1. What is the differential diagnosis of low CO following cardiac surgery?
Answer:
CO is the product of stroke volume (SV) and HR:
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
| Parameter | Change | Examples |
|---|---|---|
| Heart rate | Decrease | Bradycardia |
| Heart block causing loss of AV synchrony | ||
| Increase | Atrial fibrillation | |
| Ventricular tachyarrhythmias | ||
| Preload | Decrease | Hypovolemia |
| Mitral stenosis | ||
| Increase | Ventricular overdistension and systolic dysfunction | |
| Mitral regurgitation | ||
| Afterload | Increase | Embolism |
| Outflow tract obstruction | ||
| Contractility | Direct decrease | Right and/or left ventricle |
| Indirect decrease | Cardiac tamponade | |
| Embolism | ||
| Negative inotropic agents | ||
| Toxins (endotoxin, inflammatory cytokines) |
References