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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.
Fluid resuscitation should be guided by repeated fluid challenges.
If fluid administration is insufficient to restore an adequate tissue perfusion pressure, vasopressors may be required; norepinephrine is currently considered the best first-line choice.
Inotropes or vasodilator drugs may be needed to improve myocardial contractility and cardiac output. Dobutamine remains the inotropic agent of choice.
Hemodynamic support should be titrated to the individual patient according to global parameters of hemodynamic and oxygenation status, supported by regional parameters when available.
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The most common cause of organ failure in the critically ill patient is inadequate tissue perfusion related to acute circulatory failure. This may result from persistent fluid deficits and/or alterations in regional blood flow or tissue oxygen utilization. Whatever the cause, 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.
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Clinical Signs of Shock
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Circulatory shock can be considered as a state of generalized circulatory failure resulting in tissue hypoxia. 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 broadly be summarized as follows:
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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 less than 90 mm Hg or the mean arterial pressure is less than 70 mm Hg.
Signs of tissue hypoperfusion: These are usually recognized at 3 levels: (a) cutaneous: the skin is usually vasoconstricted, cold, and clammy; (b) renal: a reduction in renal perfusion is manifested in adults by a fall in urine output below 0.5 mL/kg/h and, in more severe cases, below 20 mL/kg/h; (c) neurologic: This can of course be appreciated only in the unanesthetized, unsedated patient. Decreased cerebral perfusion is demonstrated by an altered intellect, with disorientation and confusion, and lack of collaboration; there is often obtundation, but coma develops only in advanced stages of multiple organ failure.
Biologic signs of altered cellular oxygen availability: The development of anaerobic metabolism is manifest by the development of hyperlactatemia. The normal blood lactate level is around 1 mEq/L (or 1 mMol/L) but is usually increased above 1.5 mEq/L in acute circulatory failure.
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Pathophysiologic Classification of Shock
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Shock can essentially be classified according to 4 pathophysiologic mechanisms1: hypovolemic, cardiogenic, obstructive, or distributive. Many patients with acute circulatory failure have a combination of 2 or more of the 4 mechanisms. For ...