Cardiovascular failure is deterioration of cardiac function or vascular tone that results in impairment in end-organ perfusion. Collapse of the cardiovascular system can be either the end result of multisystem organ failure (MOF) or a manifestation of impaired cardiac function. In the acute phase of trauma, most shock is due to hemorrhage. Hemorrhagic shock leads to decreased preload or decreased right heart filling volumes, which is compensated by tachycardia and then may progress to hypotension and end-organ hypoperfusion. Cardiogenic shock alone stems from impaired myocardial contractility resulting in impairment of end organ perfusion with elevated cardiac filling pressures and low cardiac output.1 Unlike hemorrhagic shock, cardiogenic shock often does not respond simply to volume/blood product resuscitation and control of hemorrhage.2,3 Cardiogenic shock solely from impaired contractility is most often due to an acute myocardial infarction or acute on chronic heart failure.4 Therapy to support the failing cardiovascular system is directed at the etiology of the shock state and includes fluid resuscitation (preload) as well as pharmacologic modulation of vascular tone (afterload), contractility (with inotropes), and heart rate (with chronotropes). This chapter will explain the physiologic components of cardiovascular failure, assessment of patients with cardiovascular failure, treatment and monitoring (Fig. 56-1).5
Algorithm for the approach to the patient in the SICU with cardiovascular failure.
DETERMINANTS OF CARDIAC OUTPUT
Cardiac output is defined as the quantity of blood ejected into the aorta by the heart each minute and is calculated as heart rate multiplied by stroke volume (CO = HR × SV). This is the quantity of blood that flows through the circulation and is responsible for oxygen and nutrient transport to the tissues. The primary determinants of cardiac output are preload (the venous return to the heart), afterload (the resistance against which the heart must pump), contractility (the extent to which the myocardial cells can contract), and heart rate. The primary determinant of cardiac output is the filling of the heart and the ability to pump that volume effectively. Accordingly, the majority of therapies for augmenting cardiac output aim to restore filling pressures and support ineffective contractility.
Typically, 5.6 L/min is considered a normal resting cardiac output as measured in young, healthy males. However, cardiac output varies with activity, and is influenced by level of metabolism, exercise state, age, size of the individual, and other factors. Cardiac output in women is generally stated as being 10–20% lower than in men. Additionally, when factoring in age, the average cardiac output for adults is approximated as 5 L/min. Laboratory and clinical research have demonstrated that cardiac output increases in proportion to increasing body surface area. Therefore, to standardize cardiac output measurements between individuals, cardiac index (defined as cardiac output divided by body surface area in m2) is ...