Shock States Overview

Shock is not simply low blood pressure. It is a state of cellular hypoxia in which oxygen delivery to tissues is insufficient to meet metabolic demand, regardless of the cause.

Key features shared across all shock types:

• Hypotension (MAP < 65 mmHg) — though early compensated shock may preserve BP
• Signs of impaired perfusion: altered mental status, oliguria, skin changes, elevated lactate
• Compensatory mechanisms: tachycardia, vasoconstriction, increased respiratory rate

Elevated serum lactate (> 2 mmol/L) is a key indicator of tissue hypoperfusion even when BP appears normal.

Mechanism: Inadequate circulating volume leads to decreased preload, stroke volume, and cardiac output. The body compensates with tachycardia and vasoconstriction (high SVR), but ultimately cannot maintain perfusion.

Causes: Hemorrhage (trauma, GI bleed, surgical), severe dehydration, burns, third-spacing (pancreatitis, bowel obstruction), vomiting/diarrhea.

Clinical findings: Tachycardia, hypotension, cool/pale/clammy skin, decreased capillary refill, flat neck veins, decreased urine output, thirst, anxiety.

Treatment priorities: Identify and control the source of volume loss. Fluid resuscitation with isotonic crystalloids or blood products (hemorrhagic). Vasopressors only after adequate volume replacement.

Mechanism: The heart fails as a pump, resulting in low cardiac output despite adequate (or excessive) filling pressures. Backup of fluid causes pulmonary congestion and further impairs oxygenation.

Causes: Massive MI (most common), acute decompensated heart failure, severe cardiomyopathy, myocarditis, severe valvular dysfunction, dysrhythmias with hemodynamic compromise.

Clinical findings: Tachycardia, hypotension, cool/clammy skin, distended neck veins (JVD), pulmonary crackles, S3 gallop, frothy sputum, decreased urine output. Pulmonary edema distinguishes from hypovolemic shock.

Treatment priorities: Inotropes (dobutamine) to improve contractility. Vasopressors (norepinephrine) if profoundly hypotensive. Careful fluid management — avoid fluid overload. Treat underlying cause (reperfusion for MI). Mechanical circulatory support may be needed.

Mechanism: Massive vasodilation distributes blood away from vital organs despite normal or increased cardiac output. Tissue perfusion is impaired due to maldistribution rather than low volume or pump failure.

Treatment priorities (septic): Fluids, vasopressors (norepinephrine first line), antibiotics, source control. For anaphylaxis: epinephrine, airway management. For neurogenic: fluid resuscitation, vasopressors, spinal stabilization.

Mechanism: A mechanical obstruction prevents adequate cardiac filling or outflow, reducing cardiac output. The heart itself is structurally intact but unable to pump effectively against the obstruction.

Causes and key features:

• Tension pneumothorax: Mediastinal shift compresses the heart and great vessels. Tracheal deviation, absent breath sounds, JVD, tachycardia, hypotension. Immediate needle decompression.
• Cardiac tamponade: Pericardial fluid compresses the heart. Beck's triad: hypotension, JVD, muffled heart sounds. Pulsus paradoxus. Emergency pericardiocentesis.
• Massive pulmonary embolism: Large clot obstructs pulmonary vasculature, causing right heart strain and reduced left heart filling. Sudden hypoxia, tachycardia, RV strain on ECG. Anticoagulation, thrombolytics, or embolectomy.

Treatment priorities: Relieve the obstruction — this is the definitive treatment. Supportive care buys time but does not reverse obstructive shock without addressing the cause.