Mortality and morbidity in cardiac surgery have continued to decline despite increases in patient age, comorbid conditions, and procedure complexity. Much of this success can be attributed to advances in critical care. This chapter will outline some strategies and principles of modern postoperative care.
Assessment and optimization of hemodynamics is a principle focus of care following cardiac surgery. Appropriate management requires knowledge of preoperative cardiac function and an appreciation of the impact of intraoperative events. The goal of postoperative hemodynamic management is the maintenance of adequate oxygen delivery to vital tissues in a way that avoids unnecessary demands on a heart recovering from the stress of cardiopulmonary bypass (CPB), ischemia, and surgery.
A basic initial hemodynamic assessment includes a review of current medications, heart rate and rhythm, mean arterial pressure (MAP), central venous pressure (CVP), and an ECG analysis to exclude ischemia and conduction abnormalities. The presence of a pulmonary artery catheter enables the measurement of pulmonary artery pressures, left-sided filling pressures (pulmonary capillary wedge pressure (PCWP)), and mixed venous oxygen saturation (MVO2). Cardiac output (CO), as well as pulmonary and systemic vascular resistances (SVRs) can also be calculated when a PA catheter is present. CO is determined utilizing thermodilution or by using the Fick equation. CO, blood pressure (BP), and SVR are related to each other using Ohm’s law (Table 17-1). Reasonable minimum goals for most patients include an MVO2 of about 60%, MAP > 65 mm Hg, and a cardiac index (CI) > 2 L/min/m2. Goals should be individualized. Patients with a history of hypertension or significant peripheral vascular disease will benefit from higher BP; patients who are bleeding or who have suture lines in fragile tissue are best served with tighter control. Strategies designed to produce a supra-normal CI or MVO2 have failed to demonstrate a survival advantage.1
Failure to achieve adequate CO and end-organ oxygen delivery can be caused by many co-dependent factors. These include volume status (preload), peripheral vascular tone (afterload), cardiac pump function, heart rate and rhythm, and blood oxygen carrying capacity.
Volume status can be estimated using invasive monitoring. CVP, unless it is very low, is an unreliable indicator of left ventricular end-diastolic volume. An elevated CVP can be seen in volume overload, right heart failure, tricuspid and mitral regurgitation, pulmonary hypertension, cardiac tamponade, tension pneumothorax, and pulmonary embolism. Pulmonary artery diastolic pressure correlates with left-sided filling pressures ...