Perspective:

The following are 10 points to remember about circulatory shock:

1. Shock is the clinical expression of circulatory failure that results in inadequate cellular oxygen utilization.

2. Shock results from four potential, and not necessarily exclusive, pathophysiological mechanisms: hypovolemia (from internal or external fluid loss), cardiogenic factors (e.g., acute myocardial infarction, end-stage cardiomyopathy, advanced valvular heart disease, myocarditis, or cardiac arrhythmias), obstruction (e.g., pulmonary embolism, cardiac tamponade, or tension pneumothorax), or distributive factors (e.g., severe sepsis or anaphylaxis from the release of inflammatory mediators).

3. Septic shock, a form of distributive shock, is the most common form of shock among patients in the intensive care unit, followed by cardiogenic and hypovolemic shock; obstructive shock is relatively rare. The type and cause of shock may be obvious from the medical history, physical examination, or clinical investigations.

4. Early, adequate hemodynamic support of patients in shock is crucial to prevent worsening organ dysfunction and failure. Resuscitation should be started even while investigation of the cause is ongoing. Once identified, the cause must be corrected rapidly (e.g., control of bleeding, percutaneous coronary intervention for coronary syndromes, thrombolysis or embolectomy for massive pulmonary embolism, and administration of antibiotics and source control for septic shock).

5. 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.

6. Fluid therapy to improve microvascular blood flow and increase cardiac output is an essential part of the treatment of any form of shock. Even patients with cardiogenic shock may benefit from fluids, since acute edema can result in a decrease in the effective intravascular volume. However, fluid administration should be closely monitored, since too much fluid carries the risk of edema with its unwanted consequences.

7. 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. Norepinephrine is the vasopressor of first choice; it has predominantly α-adrenergic properties, but its modest β-adrenergic effects help to maintain cardiac output.

8. Dobutamine is the inotropic agent of choice for increasing cardiac output, regardless of whether norepinephrine is also being given. With predominantly β-adrenergic properties, dobutamine is less likely to induce tachycardia than isoproterenol.

9. The primary goal of resuscitation should be not only to restore blood pressure, but also to provide adequate cellular metabolism, for which the correction of arterial hypotension is a prerequisite. Restoring a mean systemic arterial pressure of 65-70 mm Hg is a good initial goal, but the level should be adjusted to restore tissue perfusion, assessed on the basis of mental status, skin appearance, and urine output.

10. 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 minimum blood pressure and cardiac output compatible with immediate survival. 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. In the third (stabilization) phase, the goal is to prevent organ dysfunction, even after hemodynamic stability has been achieved. 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.