Neurogenic & Obstructive Shock

Neurogenic shock is a form of distributive shock resulting from loss of sympathetic tone, most commonly after spinal cord injury at T6 or above. Without sympathetic input, vessels dilate massively and the heart loses its compensatory tachycardia. The signature triad is hypotension, bradycardia, and warm/dry skin below the level of injury — the opposite of every other shock type where you expect cool, clammy skin and tachycardia. Treatment targets the missing sympathetic response: vasopressors (phenylephrine or norepinephrine) to restore vascular tone and atropine for symptomatic bradycardia. Aggressive fluid resuscitation alone won't fix it because the problem is a dilated vascular bed, not volume loss. Note: neurogenic shock (hemodynamic instability) is distinct from spinal shock (temporary areflexia below the lesion). Obstructive shock occurs when blood physically cannot fill or leave the heart. The three classic causes are tension pneumothorax, cardiac tamponade, and massive pulmonary embolism. Each creates a mechanical barrier. In tension pneumothorax, look for tracheal deviation, absent breath sounds, and JVD. In cardiac tamponade, Beck's triad — hypotension, muffled heart sounds, and JVD. In massive PE, sudden dyspnea, hypoxia, and right heart strain. Obstructive shock is a surgical or procedural emergency: needle decompression, pericardiocentesis, or thrombolytics respectively. Fluids and vasopressors are temporizing — they cannot fix the obstruction.