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Emergency and Acute Medicine - Shock
Shock is a state of inadequate tissue perfusion in which blood flow is insufficient to meet cellular metabolic demands. As a result, tissues do not receive enough oxygen and are unable to clear toxic metabolic byproducts. If untreated, shock progresses from impaired perfusion to organ dysfunction and ultimately death. Major categories include hypovolemic shock, cardiogenic or obstructive shock, septic shock, neurogenic shock, anaphylactic shock, and pharmacologic shock. Although the mechanisms differ, all forms lead to impaired oxygen delivery and end-organ injury.
Hypovolemic shock results from decreased intravascular volume, most commonly from hemorrhage or severe fluid loss. Acute onset should raise concern for bleeding, while a more progressive course with elevated hematocrit, blood urea nitrogen, and creatinine may suggest dehydration. Common causes include trauma, gastrointestinal bleeding, ruptured ectopic pregnancy, postpartum hemorrhage, vomiting, diarrhea, burns, ruptured aneurysm, and retroperitoneal bleeding. Cardiogenic or obstructive shock occurs when cardiac output is inadequate despite sufficient intravascular volume. It may result from myocardial infarction, cardiomyopathy, arrhythmias, myocarditis, valvular disease, tamponade, pulmonary embolism, or tension pneumothorax. Septic shock begins with overwhelming infection that triggers release of inflammatory mediators, producing vasodilation, capillary leak, and reduced systemic vascular resistance, later followed by myocardial depression. Neurogenic shock occurs when spinal cord injury disrupts sympathetic tone, leading to vasodilation and sometimes bradycardia, especially with lesions above T4. Anaphylactic shock results from massive mast cell degranulation after allergen exposure, leading to vasodilation, capillary leak, and airway compromise. Pharmacologic shock may result from drug-induced vasodilation or myocardial depression.
Patients in shock commonly present with hypotension, weak peripheral pulses, tachycardia, tachypnea, decreased urine output, diaphoresis, lethargy, or obtundation. History should focus on identifying the likely cause, including trauma, infection, allergic exposure, medication use, cardiac symptoms, or fluid loss. Physical examination should be targeted to the likely type of shock. In hypovolemic shock, neck veins are typically flat, mucous membranes are dry, and extremities are cold. In cardiogenic shock, jugular venous distention is often present, mucous membranes are moist, and extremities are cold. Early septic shock may show flat neck veins, dry mucous membranes, and warm extremities, though later patients can become cold and mottled. Additional findings such as wounds, urticaria, cellulitis, cardiac murmurs, or pelvic instability may help establish the diagnosis.
The workup of shock aims to identify both the type of shock and its underlying cause. Laboratory studies usually include hemoglobin and hematocrit, white blood cell count, electrolytes, glucose, coagulation studies, cardiac enzymes, urinalysis, pregnancy testing when appropriate, and serum lactate, which is a useful marker of tissue hypoperfusion. Imaging often includes chest radiograph, electrocardiogram, abdominal ultrasound, and sometimes computed tomography once the patient is stabilized. Electrocardiography may reveal ischemia, tamponade with electrical alternans or low voltage, or right-heart strain with pulmonary embolism.
Initial management centers on aggressive stabilization of airway, breathing, and circulation. Large-bore IV access is essential, and central venous access may be needed in severe cases. Oxygen should be administered, and fluid resuscitation should begin promptly in most noncardiogenic forms of shock. Active bleeding should be controlled immediately, including the use of direct pressure and pelvic stabilization when indicated. Hypovolemic shock requires rapid crystalloid resuscitation, typically 2 to 3 liters initially, followed by blood products if blood pressure does not improve. Definitive control of bleeding is crucial. Cardiogenic shock requires treatment of the specific cause, such as reperfusion for myocardial infarction, pericardiocentesis for tamponade, or treatment of dysrhythmias, with vasopressors such as norepinephrine or dopamine as needed. Septic shock requires aggressive crystalloid administration, early antibiotics, maintenance of urine output above 30 mL/hour, and vasopressor support, with norepinephrine preferred as first-line therapy. Anaphylactic shock requires prompt airway management, epinephrine, antihistamines, corticosteroids, and bronchodilators if bronchospasm is present. Pharmacologic shock may require decontamination, antidotes, and inotropic support. Neurogenic shock is treated supportively, with spinal stabilization and hemodynamic support.
All patients with shock require admission, and most with persistent shock need ICU-level monitoring. A small number whose shock is completely and definitively reversed in the emergency department may be managed outside the ICU, but no patient actively in shock should be discharged home. Important clinical priorities are to identify the cause quickly, begin aggressive fluid resuscitation early, and add vasopressors when indicated to minimize prolonged tissue hypoxia.
Shock is a state of inadequate tissue perfusion in which blood flow is insufficient to meet cellular metabolic demands. As a result, tissues do not receive enough oxygen and are unable to clear toxic metabolic byproducts. If untreated, shock progresses from impaired perfusion to organ dysfunction and ultimately death. Major categories include hypovolemic shock, cardiogenic or obstructive shock, septic shock, neurogenic shock, anaphylactic shock, and pharmacologic shock. Although the mechanisms differ, all forms lead to impaired oxygen delivery and end-organ injury.
Hypovolemic shock results from decreased intravascular volume, most commonly from hemorrhage or severe fluid loss. Acute onset should raise concern for bleeding, while a more progressive course with elevated hematocrit, blood urea nitrogen, and creatinine may suggest dehydration. Common causes include trauma, gastrointestinal bleeding, ruptured ectopic pregnancy, postpartum hemorrhage, vomiting, diarrhea, burns, ruptured aneurysm, and retroperitoneal bleeding. Cardiogenic or obstructive shock occurs when cardiac output is inadequate despite sufficient intravascular volume. It may result from myocardial infarction, cardiomyopathy, arrhythmias, myocarditis, valvular disease, tamponade, pulmonary embolism, or tension pneumothorax. Septic shock begins with overwhelming infection that triggers release of inflammatory mediators, producing vasodilation, capillary leak, and reduced systemic vascular resistance, later followed by myocardial depression. Neurogenic shock occurs when spinal cord injury disrupts sympathetic tone, leading to vasodilation and sometimes bradycardia, especially with lesions above T4. Anaphylactic shock results from massive mast cell degranulation after allergen exposure, leading to vasodilation, capillary leak, and airway compromise. Pharmacologic shock may result from drug-induced vasodilation or myocardial depression.
Patients in shock commonly present with hypotension, weak peripheral pulses, tachycardia, tachypnea, decreased urine output, diaphoresis, lethargy, or obtundation. History should focus on identifying the likely cause, including trauma, infection, allergic exposure, medication use, cardiac symptoms, or fluid loss. Physical examination should be targeted to the likely type of shock. In hypovolemic shock, neck veins are typically flat, mucous membranes are dry, and extremities are cold. In cardiogenic shock, jugular venous distention is often present, mucous membranes are moist, and extremities are cold. Early septic shock may show flat neck veins, dry mucous membranes, and warm extremities, though later patients can become cold and mottled. Additional findings such as wounds, urticaria, cellulitis, cardiac murmurs, or pelvic instability may help establish the diagnosis.
The workup of shock aims to identify both the type of shock and its underlying cause. Laboratory studies usually include hemoglobin and hematocrit, white blood cell count, electrolytes, glucose, coagulation studies, cardiac enzymes, urinalysis, pregnancy testing when appropriate, and serum lactate, which is a useful marker of tissue hypoperfusion. Imaging often includes chest radiograph, electrocardiogram, abdominal ultrasound, and sometimes computed tomography once the patient is stabilized. Electrocardiography may reveal ischemia, tamponade with electrical alternans or low voltage, or right-heart strain with pulmonary embolism.
Initial management centers on aggressive stabilization of airway, breathing, and circulation. Large-bore IV access is essential, and central venous access may be needed in severe cases. Oxygen should be administered, and fluid resuscitation should begin promptly in most noncardiogenic forms of shock. Active bleeding should be controlled immediately, including the use of direct pressure and pelvic stabilization when indicated. Hypovolemic shock requires rapid crystalloid resuscitation, typically 2 to 3 liters initially, followed by blood products if blood pressure does not improve. Definitive control of bleeding is crucial. Cardiogenic shock requires treatment of the specific cause, such as reperfusion for myocardial infarction, pericardiocentesis for tamponade, or treatment of dysrhythmias, with vasopressors such as norepinephrine or dopamine as needed. Septic shock requires aggressive crystalloid administration, early antibiotics, maintenance of urine output above 30 mL/hour, and vasopressor support, with norepinephrine preferred as first-line therapy. Anaphylactic shock requires prompt airway management, epinephrine, antihistamines, corticosteroids, and bronchodilators if bronchospasm is present. Pharmacologic shock may require decontamination, antidotes, and inotropic support. Neurogenic shock is treated supportively, with spinal stabilization and hemodynamic support.
All patients with shock require admission, and most with persistent shock need ICU-level monitoring. A small number whose shock is completely and definitively reversed in the emergency department may be managed outside the ICU, but no patient actively in shock should be discharged home. Important clinical priorities are to identify the cause quickly, begin aggressive fluid resuscitation early, and add vasopressors when indicated to minimize prolonged tissue hypoxia.
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