- Understanding cardiovascular dysfunction in a critically ill patient requires consideration of cardiac function and systemic vascular factors controlling venous return.
- Compression by surrounding structures (cardiac tamponade) and increased afterload must be considered as external causes or contributors to cardiac dysfunction.
- Decreased ventricular pump function may be due to decreased systolic contractility, increased diastolic stiffness, abnormal heart rate and rhythm, or valvular dysfunction.
- Management of ventricular dysfunction aims to reverse the cause by optimizing preload and afterload and correcting abnormalities in heart rhythm, valve function, and contractility.
- Acute reversible contributions to depressed contractility result from ischemia, hypoxemia, acidosis, ionized hypocalcemia and other electrolyte abnormalities, myocardial depressant factors, and hypo- and hyperthermia.
- Management of acute-on-chronic heart failure progressively includes oxygen; optimizing preload with diuretics, morphine, and nitrates or fluid infusion for hypovolemia; afterload reduction; increasing contractility using catecholamines or phosphodiesterase inhibitors; antiarrhythmic drugs and resynchronization using biventricular pacing; intraaortic balloon counterpulsation; and cardiac transplantation.
This chapter reviews the etiology and management of circulatory disturbances arising in critically ill patients whose primary cause for ventricular dysfunction is more related to complications of other multisystem organ failures without diminishing the possibility that occult ischemic heart disease (see Chap. 25) might be unmasked by the stress imposed by multisystem organ failure or its diverse treatments. I emphasize how critical illness disturbs ventricular function and the systemic factors governing venous return and refer the reader to Chap. 25 for the detailed diagnosis and management of ischemic heart disease. To avoid redundancy, I refer liberally to other chapters in this book that discuss mechanisms for ventricular dysfunction in the context of other diseases (see Chaps. 20, 21, 26, 28, and 29).
Cardiac pump function can be defined by the relation of the heart's output to its input.1 Cardiac output is the most important output of the entire heart, and right atrial pressure (Pra) is an easily measured input of the entire heart. Cardiac output is initially assessed as high, adequate, or inadequate by cardiovascular examination and by clinical evaluation of perfusion. Later, after placement of a central venous catheter to allow measurement of central venous pressure (CVP) and central venous oxygen saturation, after placement of a pulmonary artery catheter, or after echocardiography, cardiac output can be more accurately quantitated. Pra is initially evaluated by clinical examination of distention of the jugular veins and later may be more accurately measured as the CVP. Other outputs, such as stroke work, and other inputs, such as pulmonary artery occlusion (or wedge) pressure (Ppw), serve to quantitate cardiac dysfunction and to determine the specific cause of cardiac dysfunction.
Depressed cardiac function may be due to left ventricular dysfunction, right ventricular dysfunction, external compression (cardiac tamponade), or excessively elevated right or left ventricular afterload. I focus on left ventricular and right ventricular dysfunction because cardiac tamponade is discussed in Chap. 28 and pulmonary embolism in Chap. 27. Yet in every case one ...