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  1. Early and adequate resuscitation of patients with acute circulatory failure is important to restore the balance between oxygen needs and delivery. Effective resuscitation can result in improved outcomes.

  2. Fluid resuscitation should be guided by repeated fluid challenges. Signs of fluid responsiveness can be explored in mechanically ventilated patients who are sedated. Passive leg raising is a relatively complex procedure.

  3. If fluid administration is insufficient to rapidly restore an adequate tissue perfusion pressure, vasopressors may be required even transiently; norepinephrine is currently considered the best first-line choice.

  4. Inotropes or vasodilator drugs may be needed to improve myocardial contractility and cardiac output. Dobutamine remains the inotropic agent of choice.

  5. Hemodynamic support should be titrated to the individual patient according to global parameters of hemodynamic and oxygenation status, supported by regional parameters when available.


The most common cause of organ failure in the critically ill patient is inadequate tissue perfusion related to acute circulatory failure. This is believed to result primarily from alterations in regional blood flow and/or tissue oxygen utilization. Early and adequate hemodynamic support of these patients is crucial if organ function is to be preserved and multiple-organ failure, a common cause of death in critically ill patients, prevented. In this chapter, we briefly review the main causes and symptoms of acute circulatory failure before focusing on the hemodynamic support of such patients.



Circulatory shock can be considered as a state of generalized circulatory failure resulting in inadequate oxygen utilization by the cells.1,2 It is a major cause of organ failure. A diagnosis of shock can be based on a combination of various clinical, hemodynamic, and biochemical signs, which can be broadly summarized as follows:

  1. Arterial Hypotension. Hypotension is perhaps the hallmark of acute circulatory failure, but may be only moderate, especially in patients with chronic hypertension. Usually the systolic arterial pressure is <90 mmHg or the mean arterial pressure (MAP) is <70 mmHg.

  2. Signs of Tissue Hypoperfusion. These are usually recognized at three levels: (a) cutaneous—the skin is usually vasoconstricted, cold, and clammy; (b) renal—a reduction in renal perfusion is manifested by a fall in urine output below 0.5 mL kg–1 hour–1 and, in more severe cases, below 20 mL kg–1 hour–1 in adults; (c) neurologic—this can, of course, be appreciated only in the nonanesthetized, unsedated patient. Decreased cerebral perfusion is demonstrated by an altered intellect, with disorientation and confusion, and lack of collaboration; there is often obtundation, without real coma.

  3. Biologic Signs of Altered Cellular Oxygen Availability. The development of hyperlactatemia is a hallmark of shock. The normal blood lactate level is around 1 mEq/L (or 1 mmol/L) but is typically increased above 2 mEq/L in acute circulatory failure.

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