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Critically ill patients are frequently encountered in the emergency department (ED) and intensive care unit (ICU), such that practitioners in both locations are required to quickly identify and resuscitate unstable patients. Additionally, with the problems of hospital overcrowding and subsequent boarding of critical patients in the ED, hemodynamic management after the initial resuscitation is prudent and mandatory in the ED.

Hemodynamic monitoring is an integral part of the management of critically ill patients, having a diagnostic, therapeutic, and resuscitation role. The analysis of hemodynamic variables beyond traditional vital signs allows the clinician to differentiate various causes of hemodynamic instability and intervene appropriately. This chapter will discuss hemodynamic monitoring methods.


Arterial blood pressure is a measure of the force exerted by circulating blood through a blood vessel. It is regulated via changes in the α-adrenergic tone of afferent vessels and varies in the different organs. For example, cerebral and coronary vessels have few α-adrenergic receptors, thus tissue perfusion depends directly on perfusion pressure in these vessel beds. However, tissue perfusion pressure cannot be measured directly, and arterial blood pressure has been used as a surrogate.1

Cardiac output (CO) and vascular tone are controlled via autoregulation, and hypotension reflects a failure of these mechanisms. Hypotension can result from severe cardiogenic or hemorrhagic shock (decreased CO) despite preserved vasomotor tone, or from a primary loss of vasomotor tone independent of CO, as in spinal cord trauma and septic shock. Normal blood pressure does not equate with cardiovascular stability, since it can occur in the setting of circulatory shock if systemic vasomotor tone proportionally increases. As a result, hypotension is always pathologic and reflects a failure of normal circulatory homeostatic mechanisms.

Autoregulation is determined by mean arterial pressure (MAP), and the normal range for most tissues is 65 to 120 mm Hg, keeping in mind that the contributors to MAP are CO and systemic vascular resistance (MAP = CO × SVR). As MAP decreases below 60 mm Hg, organ perfusion pressure is compromised and, if sustained, results in organ failure and death.2 Thus, one target of hemodynamic monitoring is to keep the MAP higher than 65 mm Hg. However, the optimal MAP varies according to the underlying cause of hemodynamic instability. For example, in septic shock, increasing MAP greater than 65 mm Hg with fluids and vasopressors increases oxygen delivery, but does not improve indices of organ perfusion or 28- and 90-day mortality.3,45 In fact, use of vasopressors to increase MAP higher than 65 mm Hg may actually result in increased mortality.6 In post-cardiac arrest patients, ACC/AHA guidelines recommend a systolic blood pressure (SBP) of greater than 90 mm Hg and MAP greater than or equal to 65 mm Hg.7,8 In traumatic brain injury, observational studies suggested that an SBP less than 90 mm Hg was an ...

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