Recognize shock
- Confirm hypotension or clear hypoperfusion
- Brain, kidney and skin perfusion windows
- Exclude measurement error and immediately reversible threats
Rapid bedside hemodynamic categorization: confirming MAP < 65 mmHg, assessing peripheral perfusion, POCUS cardiac/IVC profiling, and differentiating hypovolemic, distributive, cardiogenic, and obstructive etiologies.
Acute hypotension (Mean Arterial Pressure [MAP] < 65 mmHg or Systolic Blood Pressure [SBP] < 90 mmHg, or a drop > 40 mmHg from baseline) in the ICU signals inadequate tissue perfusion until proven otherwise. The immediate objective is not to normalize blood pressure mechanically, but to screen for immediately treatable life threats, categorize the physiological shock phenotype (distributive vs hypovolemic vs cardiogenic vs obstructive), and initiate phenotype-directed resuscitation.
Caution
Dangerous Diagnosis Not to Miss: Tension Pneumothorax, Cardiac Tamponade, Massive Pulmonary Embolism, Catastrophic Internal Hemorrhage (retroperitoneal/GI), and Acute STEMI / Cardiogenic Shock. Perform a rapid ultrasound screen (RUSH protocol) within minutes.
Undifferentiated shock: identify the physiology while resuscitation is already underway
Do not equate shock with a fixed fluid bolus. Reassess perfusion, preload responsiveness and cardiac function after every major intervention.
Verify Arterial Line / Cuff: Check arterial line transducer level (phlebostatic axis), zero reference, and flush test (damped waveform gives false hypotension); verify with manual cuff.
Rapid Perfusion Screen: Assess the 3 clinical windows of perfusion: (1) Brain (altered mental status, agitation, coma); (2) Kidneys (oliguria < 0.5 mL/kg/hr); (3) Skin (cool clammy extremities, mottled knees, capillary refill time > 3 seconds).
First-Line Vasopressor: Start Norepinephrine infusion (titrated to defend MAP ≥ 65 mmHg) via central venous or dedicated peripheral IV while diagnostic workup proceeds.
Passive Leg Raise (PLR) Test: Perform a 1-minute PLR test (legs elevated 45°, torso flat) to assess dynamic preload responsiveness before administering unguided fluid boluses.
Distributive Shock (Warm shock, bounding pulses, wide pulse pressure, hyperdynamic LV, collapsible IVC): Septic shock (most common), anaphylaxis, neurogenic shock, acute adrenal crisis, post-cardiac arrest vasoplegia.
Hypovolemic Shock (Cool extremities, flat neck veins, hyperdynamic collapsing LV, flat IVC): Hemorrhagic shock (GI bleed, trauma, retroperitoneal hematoma), dehydration, burns, third-spacing.
Cardiogenic Shock (Cool extremities, elevated JVP, pulmonary crackles, dilated poorly contracting LV, plethoric IVC): Acute myocardial infarction, acute decompensated heart failure, severe myocarditis, acute valvular catastrophe.
Obstructive Shock (Elevated JVP, severe hypotension, distinct mechanical blockage):
Caution
Common Diagnostic Trap: Reflexively administering repeated 1–2 liter crystalloid boluses for all hypotensive patients. If the patient has acute RV failure, cardiogenic shock, or severe capillary leak, excess fluid worsens ventricular interdependence, causes cardiorenal venous congestion (VExUS grade 3), and dramatically increases mortality.
Shock: Hemodynamic classification, oxygen delivery equations, and perfusion endpoints.
Septic Shock: SSC 2026 antimicrobial-timing framework, individualized fluids, vasopressor algorithms, and source control.
Cardiogenic Shock: SCAI shock staging, inotropes, and mechanical circulatory support.
Obstructive Shock: Pulmonary embolism, tamponade, and tension pneumothorax.
Hemodynamic Monitoring: Arterial line damping, stroke volume variation, and PAC indices.
Evidence status
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From recognizing hypoperfusion and initial crystalloid bolus to dynamic fluid responsiveness assessment and vasopressor targets.
From first-line norepinephrine titration to multi-agent vasopressor escalation and inotrope selection.
From multi-vasopressor failure to rescue non-adrenergic agents and mechanical circulatory support.
From confirming true hypotension to recognizing shock and its likely category.
Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.
The subset of sepsis with profound circulatory and cellular/metabolic abnormality — clinically identified by a vasopressor requirement to maintain MAP ≥ 65 mmHg plus lactate > 2 mmol/L despite adequate fluid resuscitation.
Primary pump failure, SCAI staging (A–E), PAC hemodynamics (CPO, PAPi), inotrope selection, emergent revascularization, and mechanical circulatory support.
Extracardiac mechanical barriers to filling or ejection: Massive PE, Cardiac Tamponade, Tension Pneumothorax, and Auto-PEEP.
RV anatomy and ischemia spiral, ventricular interdependence (D-sign), echocardiographic metrics (TAPSE, S', PAPi, VExUS), and the 4-pillar resuscitation strategy.
Patient-specific RBC transfusion thresholds, current platelet/procedural thresholds, plasma/cryoprecipitate use, and the TRALI vs TACO diagnostic matrix.