Management of Low Cardiac Output Post Cardiac Surgery

Abstract

Recognition and preemptive action against low cardiac output is one of the major challenges in cardiac surgery. Low cardiac output can be simply defined as inability of the heart to pump enough blood to meet the metabolic requirements of the body. Cardiac output can be recognized at various stages and it is critical to prevent and treat it in time to prevent a spiraling cycle which will be fatal; Prevention of low output starts from the preoperative period and extends well into the postoperative period. • CI < 2.4L/m2 • Increasing Lactate > 4mmol/L • MVO2 <65 % • Venous pO2 < 27 mm Hg • Increasing Toe core difference (Delta T) • Urine output < 1ml/Kg/Hr The aetiology of a low cardiac output following heart surgery is diverse. The most common causes include: • Intravascular volume depletion • Systolic heart failure • Pericardial tamponade. Transient, reversible myocardial depression may follow an episode of acute ischemia (preoperative or intraoperative) and is especially problematic where intraoperative myocardial protection has been difficult or suboptimal. Establish the diagnosis, including aetiology. Distinguishing tamponade from heart failure may require cardiac imaging with transthoracic or transesophageal echocardiography. Tamponade may not be detectable using transthoracic echocardiography in the early phase after surgery. The principal role of echocardiography is thus the investigation of possible alternative diagnosis. Management of low cardiac output post cardiac surgery includes Correction of all easily reversible factors, including hypovolaemia, tamponade, electrolyte abnormalities and dysrhythmias. Theoretically, inotropic agents can improve hemodynamic parameters increasing cardiac output and reducing left and right ventricular filling pressures. The basis of the acute inotropic response to an increased adrenergic drive is the rapid increase in the tissue levels of the second messenger, cyclic AMP. Pharmacologically, acute inotropic support uses the same principles, either by administration of exogenous catecholamines, which stimulate the beta receptor or by inhibition of the breakdown of cyclic AMP by phosphodiesterase (PDE) inhibitors Inotropic support includes Adrenaline, Dopamine, Dobutamine, Noradrenaline and Levosimendan… • In case of myocardial dysfunction, consider the following three options either alone or combined: • Among catecholamines, consider low-to-moderate doses of dobutamine and epinephrine: they both improve stoke volume and increase heart rate while PCWP is moderately decreased; catecholamines increase myocardial oxygen consumption. • Milrinone decreases PCWP and SVR while increasing stoke volume; milrinone causes less tachycardia than dobutamine it is potent vasodilators that cause reductions in cardiac filling pressures, pulmonary vascular resistance and SVR they are commonly used in combination with β1-adrenergic agonists. Compared to dobutamine in postoperative low CO, phosphodiesterase III inhibitors caused a less pronounced increase in heart rate and decreased the likelihood of arrhythmias also, the incidence of postoperative myocardial infarction was significantly lower with amrinone compared to dobutamine (40%). • Levosimendan, a calcium sensitizer, increases stoke volume and heart rate and decreases SVR Levosimendan has been recommended for the treatment of acute HF and was recently used for the successful treatment of low CO after cardiac surgery. The effects of levosimendan have been compared to those of dobutamine and milrinone. Levosimendan has been shown to decrease the time to extubation compared to milrinone. Compared to dobutamine, levosimendan decreases the incidence of postoperative atrial fibrillation and myocardial infarction, ICU length of stay, acute renal dysfunction, ventricular arrhythmias, and mortality in the treatment of post-operative LV dysfunction. Levosimendan showed little change in MVO2 and improved early heart relaxation after aortic valve replacement.