ICU Map

Shock

Initial resuscitation and classification once shock is established.

RecognizeAssessDecideDifferentialInterveneReassess
Confirmed Shock
Assessment StepConfirm shock physiology
Hypotension or normotensive hypoperfusion — elevated lactate, altered mentation, oliguria, cool and mottled skin.
Assessment StepEstablish access and send initial labs
Two large-bore IVs; lactate, CBC, chemistry, coagulation panel, and type & screen.
Assessment StepAssess volume responsiveness
A passive leg raise or fluid challenge with a dynamic measure, where feasible, before committing to large-volume fluid resuscitation.
Decision PointClassify shock type
The four categories are not mutually exclusive — critically ill patients often have more than one mechanism at once.
Differential Branches (4)
1Branch
Physiologic MechanismDistributive (e.g. septic)Explore Topic
Vasodilation with preserved or increased cardiac output; sepsis is the most common cause in the ICU.
2Branch
Physiologic MechanismCardiogenic
Acute MI, decompensated heart failure, or a new arrhythmia — pump failure with elevated filling pressures.
3Branch
Physiologic MechanismHypovolemicExplore Topic
Hemorrhagic or non-hemorrhagic volume loss outstripping intake.
4Branch
Physiologic MechanismObstructive
Tension pneumothorax, cardiac tamponade, or massive pulmonary embolism physically limiting filling or output.

An educational representation of clinical reasoning, not a diagnostic algorithm or personalized medical advice — always apply clinical judgment and institutional protocols.

Caution

Escalate — Red Flags & Critical Warnings

  • Shock with a fixed, dilated pupil or an asymmetric neurologic exam — consider a primary neurologic catastrophe rather than a purely hemodynamic cause.
  • No response to an adequate fluid bolus and vasopressor initiation — reassess the working diagnosis rather than continuing to escalate fluids alone.

Related Bedside Clinical Problems (23)

Bedside Presentations
Sudden Hypoxemia

Bedside triage of acute desaturation: signal verification, immediate danger screening (DOPE / tension pneumothorax), oxygen escalation ladder, and mechanism-based differential.

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Sudden Ventilator Deterioration & High Airway Pressures

Algorithmic troubleshooting of acute patient-ventilator collapse: the DOPE framework, peak vs plateau pressure differentiation, auto-PEEP evaluation, and manual bagging separation.

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Acute Hypotension & Undifferentiated Shock

Rapid bedside hemodynamic categorization: confirming MAP < 65 mmHg, assessing peripheral perfusion, POCUS cardiac/IVC profiling, and differentiating hypovolemic, distributive, cardiogenic, and obstructive etiologies.

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Linked Deep-Dive Topics (7)

Reference Knowledge
Shock: Foundational Critical Care Frameworkcardiovascular

Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.

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Septic Shockcardiovascular

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.

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Cardiogenic Shockcardiovascular

Primary pump failure, SCAI staging (A–E), PAC hemodynamics (CPO, PAPi), inotrope selection, emergent revascularization, and mechanical circulatory support.

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Obstructive Shockcardiovascular

Extracardiac mechanical barriers to filling or ejection: Massive PE, Cardiac Tamponade, Tension Pneumothorax, and Auto-PEEP.

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Acute Right Ventricular Failurecardiovascular

RV anatomy and ischemia spiral, ventricular interdependence (D-sign), echocardiographic metrics (TAPSE, S', PAPi, VExUS), and the 4-pillar resuscitation strategy.

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Sepsisinfectious-disease

Life-threatening organ dysfunction caused by a dysregulated host response to infection — recognized by an acute rise in SOFA score, not by infection plus fever alone.

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Major Bleeding, Hemorrhagic Shock, & Damage Control Resuscitationhematology

The trauma lethal diamond (hypothermia, acidosis, coagulopathy, hypocalcemia), 1:1:1 massive transfusion (PROPPR trial), early TXA (CRASH-2), and TEG/ROTEM algorithms.

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