Circulatory shock is present when physical signs and changes in laboratory values suggest tissue hypoperfusion. This article in our Critical Care Medicine series reviews the diagnosis and treatment of various forms of shock.
Shock is the clinical expression of circulatory failure that results in inadequate cellular oxygen utilization. Shock is a common condition in critical care, affecting about one third of patients in the intensive care unit.
• How is circulatory shock diagnosed?
A diagnosis of shock is based on clinical, hemodynamic, and biochemical signs, which can broadly be summarized into three components. First, systemic arterial hypotension is usually present, but the magnitude of the hypotension may be only moderate, especially in patients with chronic hypertension. Typically, in adults, the systolic arterial pressure is less than 90 mm Hg or the mean arterial pressure is less than 70 mm Hg, with associated tachycardia. Second, there are clinical signs of tissue hypoperfusion, which are apparent through the three “windows” of the body: cutaneous (skin that is cold and clammy, with vasoconstriction and cyanosis, findings that are most evident in low-flow states), renal (urine output of <0.5 ml per kilogram of body weight per hour), and neurologic (altered mental state, which typically includes obtundation, disorientation, and confusion). Third, hyperlactatemia is typically present, indicating abnormal cellular oxygen metabolism. The normal blood lactate level is approximately 1 mmol per liter, but the level is increased (>1.5 mmol per liter) in acute circulatory failure.
• What are the principles of ventilatory support in managing circulatory shock?
The administration of oxygen should be started immediately to increase oxygen delivery and prevent pulmonary hypertension. Pulse oximetry is often unreliable as a result of peripheral vasoconstriction, and precise determination of oxygen requirements will often require blood gas monitoring. Mechanical ventilation via a mask rather than endotracheal intubation has a limited place in the treatment of shock because technical failure can rapidly result in respiratory and cardiac arrest. Hence, endotracheal intubation should be performed to provide invasive mechanical ventilation in nearly all patients with severe dyspnea, hypoxemia, or persistent or worsening acidemia (pH, <7.30). Invasive mechanical ventilation has the additional benefits of reducing the oxygen demand of respiratory muscles and decreasing left ventricular afterload by increasing intrathoracic pressure. An abrupt decrease in arterial pressure after the initiation of invasive mechanical ventilation strongly suggests hypovolemia and a decrease in venous return.
Morning Report Questions
Q: When are vasopressors indicated in circulatory shock, and what is the most appropriate vasopressor to use?
A: If hypotension is severe or if it persists despite fluid administration, the use of vasopressors is indicated. It is acceptable practice to administer a vasopressor temporarily while fluid resuscitation is ongoing, with the aim of discontinuing it, if possible, after hypovolemia has been corrected. Adrenergic agonists are the first-line vasopressors because of their rapid onset of action, high potency, and short half-life, which allows easy dose adjustment. The authors consider norepinephrine to be the vasopressor of first choice; it has predominantly (alpha)-adrenergic properties, but its modest (beta)-adrenergic effects help to maintain cardiac output. Administration generally results in a clinically significant increase in mean arterial pressure, with little change in heart rate or cardiac output. Dopamine has predominantly (beta)-adrenergic effects at lower doses and (alpha)-adrenergic effects at higher doses, but its effects are relatively weak. Dopaminergic effects at very low doses (<3 microg per kilogram per minute, given intravenously) may selectively dilate the hepatosplanchnic and renal circulations, but controlled trials have not shown a protective effect on renal function, and its routine use for this purpose is no longer recommended. In a recent randomized, controlled, double-blind trial, dopamine had no advantage over norepinephrine as the first-line vasopressor agent; moreover, it induced more arrhythmias and was associated with an increased 28-day rate of death among patients with cardiogenic shock. Administration of dopamine, as compared with norepinephrine, may also be associated with higher rates of death among patients with septic shock.
Q: What are the four phases in the treatment of shock?
A: There are essentially four phases in the treatment of shock, and therapeutic goals and monitoring need to be adapted to each phase. In the first (salvage) phase, the goal of therapy is to achieve a blood pressure level and cardiac output compatible with immediate survival. Minimal monitoring is needed; in most cases, invasive monitoring can be restricted to arterial and central venous catheters. Lifesaving procedures (e.g., surgery for trauma, pericardial drainage, revascularization for acute myocardial infarction, and antibiotics for sepsis) are needed to treat the underlying cause. In the second (optimization) phase, the goal is to increase cellular oxygen availability, and there is a narrow window of opportunity for interventions targeting hemodynamic status. Measurements of central venous oxygen saturation and lactate levels may help guide therapy, and monitoring of cardiac output should be considered. In the third (stabilization) phase, the goal is to prevent organ dysfunction, even after hemodynamic stability has been achieved. Oxygen supply to the tissues is no longer the key problem, and organ support becomes more relevant. Finally, in the fourth (de-escalation) phase, the goal is to wean the patient from vasoactive agents and promote spontaneous polyuria or provoke fluid elimination through the use of diuretics or ultrafiltration to achieve a negative fluid balance.