Cardiovascular failure can be either the end result of multisystem organ failure (MOF) or a precursor to shock and MOF (see Chapter 61). Most often cardiovascular collapse will manifest itself with clinical signs and symptoms of cardiac failure. In trauma, the most common cause of shock is acute blood loss (hypovolemia), which results in decreased preload or decreased right heart filling volumes and manifests as tachycardia and hypotension (see Chapter 12). Although this is the most common type of shock occurring after injury, cardiogenic shock, resulting from impaired myocardial contractility, and septic shock, characterized by failure of the heart to overcome decreased vascular tone and failure of end-organ utilization of delivered oxygen, are also seen. As our population ages, the number of elderly patients in the intensive care unit (ICU) will increase. In fact, the number of elderly patients (>65 years old) is expected to double in the next three decades. With an aging population, there are age-related changes in physiology, exacerbations of chronic illnesses, and effects of therapeutic drugs, which need to be taken into consideration when caring for the traumatically injured patient.1–3 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) (Fig. 56-1).
Clinical decision tree for the diagnosis and management of cardiovascular failure.
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 therapeutic modalities aimed at augmenting cardiac output focus on restoring filling pressures and augmenting ineffective contractility.
Multiple studies and textbooks cite 5.6 L/min as a “normal” resting cardiac output as measured in young, healthy males. However, cardiac output varies with the level of activity of the body, and is influenced by level of metabolism, exercise state, age, size of the individual, and other factors. Accordingly, 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 ...