Do not wait for hypotension to diagnose shock.
Early identification and initiation of aggressive therapy can significantly improve patient survival.
Initiate early goal-directed therapy in patients with septic shock.
Early revascularization is key to improving outcome in patients with cardiogenic shock.
More than 1 million patients present to U.S. emergency departments annually with shock, and despite continued advances in critical care, mortality rates remain very high. Shock occurs when the circulatory system is no longer able to deliver enough O2 and vital nutrients to adequately meet the metabolic demands of the patient. Although initially reversible, prolonged hypoperfusion will eventually result in cellular hypoxia and the derangement of critical biochemical processes. From a clinical standpoint, shock can be divided into the following subtypes: hypovolemic, cardiogenic, obstructive, and distributive. Hypovolemic shock results from an inadequate circulating blood volume owing to either profound dehydration or significant hemorrhage. Traumatic hypovolemia is the most common type of shock encountered in patients <40 years of age. Cardiogenic shock occurs when the heart is unable to provide adequate forward blood flow secondary to impaired pump function or significant dysrhythmia. Myocardial infarction is the leading cause of cardiogenic shock and typically occurs once ~40% of the myocardium is dysfunctional. Obstructive shock results from an extracardiac blockage of adequate venous return of blood to the heart (eg, pericardial tamponade, tension pneumothorax, and massive pulmonary embolism [PE]). Finally, distributive shock occurs secondary to an uncontrolled loss of vascular tone (eg, sepsis, anaphylaxis, neurogenic shock, and adrenal crisis). Neurogenic shock most commonly occurs in trauma patients with high cervical cord injuries and a secondary loss of sympathetic tone and should always be considered a diagnosis of exclusion. Classically these patients will present with hypotension and a paradoxical bradycardia. Suspect septic shock in elderly, immunocompromised, and debilitated patients who are toxic appearing despite only vague symptoms. The prognosis for patients with cardiogenic and septic shock remains grave, with mortality rates between 30% and 90%.
The pathophysiology of shock can be divided into 3 basic categories: a systemic autonomic response, endorgan cellular hypoxia, and the secretion of proinflammatory mediators. The autonomic system initially responds to widespread tissue hypoperfusion by globally increasing the overall cardiac output. As tissue perfusion continues to decline, the body shunts circulating blood away from less vital structures including the skin, muscles, kidneys, and splanchnic beds. Reflexively, the kidneys activate the renin-angiotensin axis, prompting the release of various vasoactive substances, with the net effect to preserve perfusion to the most critical organs, namely the brain and the heart.
When the preceding response is inadequate despite maximal tissue O2 extraction, cellular hypoxia forces a conversion from aerobic to anaerobic metabolism. By nature, anaerobic metabolism cannot produce enough adenosine triphosphate to maintain regular cellular function. Tissue lactate accumulates, resulting in systemic acidosis, and eventually this breakdown in cellular metabolism leads to widespread tissue death. Injured ...