2.2 Shock States

Key Takeaways

  • Hypovolemic and cardiogenic shock share high SVR and low cardiac output, but hypovolemic shows LOW filling pressures while cardiogenic shows HIGH PAWP and CVP.
  • Distributive (septic, anaphylactic, neurogenic) shock is defined by LOW SVR with normal or high cardiac output in its early phase.
  • Neurogenic shock uniquely pairs hypotension with BRADYCARDIA and warm, dry skin from loss of sympathetic tone (spinal cord injury above T6).
  • Cardiac tamponade produces Beck's triad: hypotension, jugular venous distention/elevated CVP, and muffled heart tones, with pulsus paradoxus.
  • Obstructive shock (tamponade, massive PE, tension pneumothorax) raises CVP and requires mechanical relief, not fluids or inotropes, as definitive therapy.
Last updated: July 2026

Shock: A Failure of Perfusion

Shock is inadequate tissue perfusion that starves cells of oxygen, forcing anaerobic metabolism and rising lactate. Regardless of cause it evolves through initial, compensatory, progressive, and refractory stages; the compensatory stage (tachycardia, vasoconstriction, oliguria) is where early recognition saves lives, while the refractory stage brings irreversible organ failure. The CCRN organizes shock into four categories, and the exam rewards you for matching a hemodynamic profile to its category.

Hypovolemic Shock

Caused by loss of intravascular volume — hemorrhage (trauma, GI bleed), or non-hemorrhagic losses (vomiting, diarrhea, burns, DKA, third-spacing). The body clamps down: CVP low, PAWP low, cardiac output/index low, SVR high (compensatory), SvO2 low. Hemorrhage is graded Class I-IV; Class III-IV (>30-40% loss) brings frank hypotension. Treatment: control the source, restore volume with crystalloid and blood products, and in trauma use permissive hypotension and massive transfusion 1:1:1 (RBC:plasma:platelets) until bleeding is controlled.

Cardiogenic Shock

The pump fails — most often a large anterior MI (>40% of LV), but also myocarditis, arrhythmia, or acute valve failure. The heart cannot eject, so blood backs up: PAWP high (often >18), CVP high, cardiac index low (<2.2), SVR high. The patient is "cold and wet" (poor perfusion + pulmonary congestion). Treatment: support perfusion pressure, then add an inotrope (dobutamine) to improve contractility; avoid large fluid boluses that worsen pulmonary edema; consider mechanical support (IABP, Impella — covered in ch-03) and urgent revascularization.

Distributive Shock

Pathologic vasodilation drops SVR and pools blood peripherally. Early distributive shock is warm — low SVR with normal or high cardiac output, bounding pulses, warm skin — progressing to a cold, low-output late phase. Three subtypes:

  • Septic (most common): infection triggers vasodilation and capillary leak. Profile: SVR very low, CO high or normal, PAWP low/normal. First-line pressor is norepinephrine; add vasopressin and pursue source control (detailed in ch-13).
  • Anaphylactic: IgE-mediated mast-cell degranulation releases histamine, causing vasodilation, bronchospasm, and airway edema. Treatment: intramuscular epinephrine 0.3-0.5 mg (1:1000) first, plus airway, fluids, antihistamines, and steroids.
  • Neurogenic: cervical/high-thoracic spinal cord injury above T6 severs sympathetic outflow. Its signature triad — hypotension WITH bradycardia and warm, dry skin — distinguishes it from every other shock (which brings tachycardia). Treatment: fluids, vasopressors (phenylephrine or norepinephrine), and atropine for symptomatic bradycardia. Do not confuse it with spinal shock (transient loss of reflexes/flaccidity below the injury), which is a neurologic, not hemodynamic, phenomenon.

Obstructive Shock

A mechanical barrier blocks filling or ejection; cardiac output falls and CVP rises. Definitive therapy is to relieve the obstruction — fluids and pressors only buy time.

  • Cardiac tamponade: pericardial fluid compresses the heart. Beck's triad — hypotension, jugular venous distention/elevated CVP, and muffled heart tones — with pulsus paradoxus and equalization of diastolic pressures. Treat with pericardiocentesis.
  • Massive pulmonary embolism: acute RV strain. Elevated CVP and PAP, clear lungs, severe hypoxia, and RV failure. Treat with anticoagulation or thrombolysis.
  • Tension pneumothorax: air trapped under pressure. Absent breath sounds, tracheal deviation away from the affected side, distended neck veins/high CVP, hypotension. Treat with immediate needle decompression (2nd intercostal space midclavicular line or 5th ICS), then chest tube.

Hemodynamic Profiles of Shock

Shock typeCardiac output/CISVRPAWP (LV preload)CVP
HypovolemicLowHighLowLow
CardiogenicLowHighHighHigh
Distributive (early)High/normalLowLow/normalLow/normal
Obstructive (tamponade/PE/tension)LowHighVariableHigh

Reading the Table Under Pressure

The fastest exam strategy is to ask two questions: Is the SVR high or low? and Are the filling pressures high or low? Low SVR isolates distributive shock. High SVR narrows it to hypovolemic (low filling pressures), cardiogenic (high PAWP), or obstructive (high CVP with variable PAWP). Then a distinguishing sign clinches the answer: bradycardia points to neurogenic, Beck's triad to tamponade, muffled versus absent breath sounds separates tamponade from tension pneumothorax, and a big anterior MI with a high wedge marks cardiogenic. Anchor every scenario to this two-step and the table above.

The Four Stages of Shock

Every shock, regardless of cause, progresses through predictable stages, and the CCRN expects you to intervene early:

  1. Initial stage: cardiac output has fallen but no visible signs; cells switch to anaerobic metabolism and lactate begins to rise.
  2. Compensatory stage: baroreceptor and sympathetic reflexes kick in — tachycardia, vasoconstriction (cool skin), tachypnea, and oliguria maintain a near-normal blood pressure. This is the window where recognition prevents deterioration.
  3. Progressive stage: compensation fails; hypotension, worsening acidosis, altered mental status, and organ hypoperfusion appear.
  4. Refractory stage: profound, unresponsive hypotension with irreversible multi-organ failure.

Because blood pressure is preserved during compensation, a normal blood pressure does not exclude shock — trend the heart rate, lactate, urine output, and mental status.

Worked Scenario

Consider a post-operative patient: heart rate 128, BP 92/70 (narrow pulse pressure), cool mottled skin, urine output 10 mL/hr, lactate 4.2 mmol/L, CVP 2 mmHg. The narrow pulse pressure, low CVP, tachycardia, and compensatory vasoconstriction all point to hypovolemic shock from occult bleeding. The correct action is source control and volume resuscitation, not a vasopressor — giving a vasoconstrictor to an empty tank raises the pressure number while worsening tissue perfusion. Contrast this with a warm, flushed, hypotensive patient with bounding pulses and a wide pulse pressure, whose low SVR marks early distributive shock. The bedside picture (skin temperature, pulse character, pulse pressure) often reveals the category before any invasive number returns.

Test Your Knowledge

A 26-year-old with a C6 spinal cord injury is hypotensive (BP 84/48) with a heart rate of 46, and the skin is warm and dry. Which shock state does this presentation MOST strongly suggest?

A
B
C
D
Test Your Knowledge

A patient develops hypotension, jugular venous distention with a CVP of 19 mmHg, muffled heart tones, and CLEAR bilateral breath sounds shortly after central line placement. What is the most likely diagnosis and definitive treatment?

A
B
C
D
Test Your Knowledge

A hypotensive patient has warm extremities, bounding pulses, cardiac index of 5.4 L/min/m2, and SVR of 420 dynes/sec/cm-5. This hemodynamic profile is characteristic of which shock category?

A
B
C
D