After improvement in the first hour after bypass, myocardial function declines to a nadir at 4 to 5 h postoperatively before returning to preoperative levels at 24 h. This depression, which is seen even in those with good preoperative ventricular performance, is more severe in those with poor ventricular function or chronic heart failure, and may result in a low cardiac output syndrome requiring intervention with mechanical or pharmaceutical support.
Risk factors for a low cardiac output syndrome include low ejection fraction, cardiac enlargement and high baseline and postcontrast left ventricular end-diastolic pressure at cardiac catheterization, old age, and female sex. Cardiopulmonary bypass itself impairs ventricular function by a combination of reperfusion injury, the effects of cardioplegia solution, and some degree of ischemic damage which varys with the adequacy of myocardial protection. Myocardial 'stunning' refers to the myocardial dysfunction following ischemia and reperfusion, which is reversible and responsive to inotropic support in contrast with ongoing ischemia where inotropes may cause further injury.
Low cardiac output syndrome can be defined as a cardiac index of 2 l/min/m2 or less and is associated with increased risk of in-hospital death and multiple organ failure. Poor myocardial function decreases coronary perfusion pressure which reduces coronary blood flow leading to worsening cardiac function. The cycle can only be broken by improving myocardial performance by optimizing myocardial blood flow, increasing contractility, and reducing afterload with inotropic or vasodilator drugs or intra-aortic balloon counterpulsation.
Since inotropes act by raising calcium levels which may be increased already in stunned myocardium, there are good theoretical reasons for using mechanical assist devices rather than excessive doses of inotropes early in the low cardiac output syndrome after cardiac surgery. Inotrope regimens must be tailored individually and guided by invasive monitoring. Myocardial dysfunction is both systolic and diastolic so that the lusitropic effects of inotropic agents are important in this context. Apart from the adrenergic agonists norepinephrine (noradrenaline), epinephrine (adrenaline), dobutamine, and dopamine, the phosphodiesterase II inhibitors milrinone and enoximone may have a place acting as inodilators, increasing contractility, and reducing afterload while avoiding the problems associated with adrenergic receptor downregulation. Dopexamine is also an inodilator, although largely a b 2 agonist.
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