Introduction

Cardiac surgical patients often present for surgery with impaired ventricular contractility owing to chronic ischaemia or valve lesions. The heart is then subjected to a surgical procedure, which produces a period of global ischaemia and a massive, whole-body inflammatory response. The deleterious effects of cardiopulmonary bypass (CPB) are due to activation of the coagulation, fibrinolytic and complement pathways. This may lead to postoperative adverse effects, including extravascular fluid accumulation or ‘third spacing,’ coagulopathy and haemorrhage, and pulmonary, renal, cardiac and vasomotor dysfunction.

The perioperative period is often a time of significant haemodynamic and vasomotor instability. Ventricular contractility is usually impaired for up to 24 hours, which may respond to simple supportive measures such as fluid administration. When more severe, there may be a reduction in blood pressure and cardiac output (CO) associated with end-organ dysfunction. Under these circumstances, haemodynamic support is required.

Optimize the heart rate

The CO is a product of stroke volume (SV) and heart rate (HR). Generally, a postoperative HR of 80 to 100 beats per minute is regarded as optimal. The most frequent postoperative rhythm problem is bradycardia. This may be related to preoperative β-blockade or postoperative nodal dysfunction.

Increasing the HR in bradycardic patients improves CO. In addition, by decreasing diastolic filling time and reducing the end-diastolic volume (EDV), left ventricular (LV) wall tension is reduced and the perfusion of the subendocardium is improved, reducing the potential for ischaemia.