Once volume, rate and rhythm have been addressed, one is left with contractility as the only remaining determinant of cardiac output which is possible to manipulate.
The choice of inotrope in this situation has never been a topic for which there is a widespread consensus.
Luckily, there are only a few to chose from.
Dobutamine and milrinone seem to be the two popular choices. A comparison of the hemodynamic effects of milrinone with dobutamine has found that they are essentially the same when hemodynamic outcomes are concerned.
Milrinone and dobutamine are important enough to have their own pages, and in the table below I will summarise their distinct advantages and disadvantages.
| Dobutamine | Milrinone | |
| Contractility increase | Equipotent | Equipotent |
| Heart rate increase | Significantly increased | Mildly increased, mainly as a response to vasodilation |
| Myocardial relaxation | Unchanged; thus a poor choice for severe diastolic failure | Mildly increased |
| Pulmonary artery pressure and right ventricular afterload | Unchanged; thus a poor choice for severe pulmonary hypertension | Potent pulmonary vasodilator |
| Systemic vascular resistance, left ventricular afterload | MAP and SVR remain largely unchanged over a range of doses | Moderately potent arterial and venous vasodilator |
| Myocardial oxygen consumption | At least moderately increased | Mildly increased, and sometimes not at all (due to vasodilation and decreased myocardial workload) |
| Cardiac output | Significantly increased (due to increase in heart rate) | Moderately increased |
| Change in pharmacodynamics post cardiopulmonary bypass | Decreased catecholamine sensitivity, thus decreased dobutamine effect | Unchanged sensitivity to milrinone |
| Clearance | Hepatic, very rapid | Renal; prolonged |
Historically, IABP has also been offered to this sort of hemodynamically unstable patient. The abovementioned textbook recommends its use as a means of ameliorating the effects of inotropes on the oxygen demand of the stressed ventricle, and as a technique for improving coronary flow in situations where there is evidence of post-operative ischaemia. Certainly there seems to be at least physiological data that good diastolic augmentation improves coronary flow.
As for empirical outcomes data - most of it comes from the period spanning the late 1970s to mid 1990s.
There was a lot of early interest in this, and initially favourable outcomes were achieved, particularly in patients who failed to separate from bypass postoperatively (the mortality in this group being notoriously high at this stage). Today, this recommendation remains, largely because of inertia in this field. Strong evidence is lacking. However, some evidence is available for the preoperative use of IABP in patients with poor systolic function; in a retrospective audit the mortality of these patients halved (from 20% to 10%) in association with pre-operative IABP use.
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