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KEY POINTS
Cardiac output (heart rate × stroke volume) is determined by rate, preload, afterload, and contractility.
Ventricular filling determines left ventricular end-diastolic volume, which in turn determines the force of ventricular contraction.
Hemodynamic transesophageal echocardiography (TEE) is performed with a miniaturized two-dimensional monoplane disposable TEE probe that can be left in place for up to 72 hours.
Right heart failure is characterized by increased right ventricular (RV) afterload (increased pulmonary resistance), which decreases the ability of the RV to pump blood forward to the left heart, thus decreasing left ventricular preload.
In valvular aortic stenosis, symptoms of left heart failure include dyspnea on exertion, angina, lightheadedness, and syncope.
Management of myocardial dysfunction includes vasopressors (eg, norepinephrine, vasopressin, phenylephrine), inotropes (eg, epinephrine, dobutamine, milrinone, dopamine, digoxin), and intra-aortic balloon pump counterpulsation.
A low mixed venous oxygen saturation occurs with decreased oxygen delivery (decreased hemoglobin, oxygen saturation, or flow) or increased oxygen demand (hyperthermia, pain, seizure, or shivering).
In the management of acute heart failure, nitroprusside reduces afterload by acting on arteriolar smooth muscle and has a rapid onset of action, and its effects cease within minutes of stopping the infusion.
In diastolic dysfunction, β-adrenergic blockade or calcium channel blockade reduces heart rate and increases left ventricular filling, which reduce mortality.
Cardiac death or a myocardial infarction occurs in 1% to 5% of unselected patients undergoing noncardiac surgery, and this concern is the most common indication for a preoperative cardiac evaluation.
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Cardiovascular failure is deterioration of cardiac function or vascular tone that results in impaired end-organ perfusion. In the acute phase of trauma, most shock is due to hemorrhage. Hemorrhagic shock causes decreased preload and thus decreased heart filling volumes, which are compensated by tachycardia. Without appropriate volume resuscitation and control of bleeding, hemorrhagic shock may progress to hypotension and end-organ hypoperfusion. In contrast, cardiogenic shock is due to impaired myocardial contractility with elevated cardiac filling pressures and low cardiac output that progresses to end-organ hypoperfusion.1 Unlike hemorrhagic shock, cardiogenic shock often does not respond simply to volume/blood product resuscitation and control of hemorrhage, and may often worsen as the patient is “driven off” the Starling curve.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 management (optimize preload) as well as pharmacologic modulation of vascular tone (optimize afterload), contractility (with inotropes), and heart rate (with chronotropes). This chapter will explain the physiologic components of cardiovascular failure and the evaluation, treatment, and monitoring of patients with cardiovascular failure (Fig. 58-1).5
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