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Shock & Resuscitation

Name: Shock & Resuscitation
Creator: Veli Bakalov, MD

Read the SVR, pick the pressor, clear the lactate

Emergency & Critical Care·Resuscitation & Airway·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Four shocks (hypovolemic, cardiogenic, distributive, obstructive) are separated by preload (CVP/PCWP), cardiac output, and SVR.
Distributive shock (septic, anaphylactic, neurogenic) is the only warm shock: low SVR, and in sepsis high or normal cardiac output and high mixed venous O2 from impaired extraction; the other three raise SVR and lower output.
Cardiogenic shock = high PCWP, low output, high SVR with crackles and JVD → dobutamine (β1) plus norepinephrine for MAP, revascularization, and mechanical support; avoid fluid boluses (except RV infarct).
Neurogenic shock (cord injury above T6) = hypotension with bradycardia and warm, dry skin → fluids, vasopressors, and atropine.
Obstructive shock has JVD with low output: tamponade → pericardiocentesis, tension pneumothorax → needle decompression, massive PE → thrombolysis.
Septic shock: about 30 mL/kg crystalloid, then norepinephrine first-line (vasopressin second, epinephrine third) to MAP ≥65; dopamine is no longer first-line.
Hemorrhagic shock: blood products 1:1:1 with permissive hypotension until surgical control, not large crystalloid volumes.
Hour-1 sepsis bundle: lactate, blood cultures, broad-spectrum antibiotics within 1 hour, fluids, vasopressors, and early source control.
Resuscitation endpoints: MAP ≥65, lactate clearance (≥10% fall or normalization), urine output, and mental status, not blood pressure alone.

Shock and its four hemodynamic profiles

Definition. Shock is inadequate tissue perfusion and oxygen delivery; hypotension is a late sign, not the definition. There are four categories:

Hypovolemic: lost volume from hemorrhage or dehydration.
Cardiogenic: pump failure from MI, arrhythmia, or cardiomyopathy.
Distributive: vasodilation from sepsis, anaphylaxis, or neurogenic injury.
Obstructive: a mechanical block to flow from tamponade, tension pneumothorax, or massive PE.

Read the profile. SVR is LOW only in distributive shock and HIGH in hypovolemic, cardiogenic, and obstructive shock. Cardiac output is HIGH in distributive shock and LOW in the others. PCWP is HIGH in cardiogenic shock and LOW in hypovolemic and distributive shock.

Hemodynamic profiles of shock

Type	Preload (CVP, PCWP)	Cardiac output	SVR	Mixed venous O₂	Bedside clue
Hypovolemic	↓	↓	↑	↓	Cold, clammy skin; flat neck veins
Cardiogenic	↑	↓	↑	↓	Cool extremities, crackles, JVD
Distributive (septic)	↓ or normal	↑ or normal	↓	↑	Warm, flushed skin early
Neurogenic	↓	↓	↓	Variable	Warm, dry skin with bradycardia
Obstructive	CVP ↑; PCWP variable	↓	↑	↓	JVD plus cause-specific signs

A high mixed venous O₂ saturation in sepsis reflects impaired tissue extraction, not good perfusion.

The individual shock states

Hypovolemic shock from hemorrhage or fluid loss has low CVP and preload, low cardiac output, and a compensatory HIGH SVR (cold, clammy, vasoconstricted skin). Tachycardia and a narrowed pulse pressure precede hypotension, which in hemorrhage usually signals loss of about 30% of blood volume.

Cardiogenic shock, often after MI, is pump failure: filling pressures (PCWP) are HIGH, cardiac output is LOW, and SVR is high. Findings are cool extremities, pulmonary edema with crackles, and elevated JVD. Mortality is high.

The exception is right ventricular infarction: the preload-dependent RV needs fluids, and nitrates can precipitate hypotension.

Distributive shock is the odd one out: massive vasodilation drops SVR, so cardiac output is HIGH or normal and the skin is warm early. Mixed venous O₂ saturation is HIGH because tissues cannot extract oxygen. Sepsis, anaphylaxis (treated first with IM epinephrine), and neurogenic injury all cause it.

Neurogenic shock follows spinal cord injury above T6. Loss of sympathetic outflow produces hypotension with warm, dry skin and, distinctively, BRADYCARDIA from unopposed vagal tone, rather than the tachycardia of other shocks. Treat with fluids, vasopressors, and atropine for bradycardia.

Bradycardia with hypotension after trauma separates neurogenic from hemorrhagic shock. Do not confuse it with spinal shock, the temporary flaccid areflexia below a cord injury.

Obstructive shock is a mechanical barrier with high CVP (JVD) and low output: fix the blockage, not the tank.

Tamponade: Beck triad and pulsus paradoxus → pericardiocentesis.
Tension pneumothorax: tracheal deviation and absent breath sounds → needle decompression.
Massive PE: right heart strain → thrombolysis may be needed.

Fluids, pressors, and inotropes

Crystalloid first, blood for bleeding. Begin resuscitation with balanced crystalloid; septic shock usually receives about 30 mL/kg IV within 3 hours (a weak SSC 2021 suggestion), with reassessment of fluid responsiveness. Hemorrhage needs blood products instead (massive transfusion at 1:1:1 RBC:plasma:platelets) with permissive hypotension until surgical control. Reassess perfusion after every intervention, not just the blood pressure.

Norepinephrine leads in septic shock. It is the FIRST-LINE vasopressor in septic and distributive shock (α > β, raising SVR and MAP); add vasopressin second and epinephrine third. Dopamine causes more arrhythmias and is no longer preferred first-line. Hydrocortisone is added when shock remains vasopressor-dependent.

Dobutamine drives the failing pump. Cardiogenic shock needs inotropy: dobutamine (a β₁ agonist) increases contractility and cardiac output, usually with norepinephrine to maintain MAP. Consider mechanical support (intra-aortic balloon pump, Impella) and urgent revascularization when ischemia is the cause. Aggressive fluid boluses worsen pulmonary edema.

Vasoactive agents

Agent	Receptors	Main role
Norepinephrine	α₁ > β₁	First-line in septic and distributive shock
Vasopressin	V₁	Second agent added in septic shock
Epinephrine	α and β	Third-line septic pressor; first-line for anaphylaxis
Dobutamine	β₁	Inotrope for cardiogenic shock
Dopamine	Dose-dependent D₁, β₁, α₁	No longer first-line; more arrhythmias
Phenylephrine	Pure α₁	Raises SVR; may cause reflex bradycardia

Sepsis bundle and resuscitation endpoints

Definitions. Sepsis is life-threatening organ dysfunction from a dysregulated response to infection. Septic shock is sepsis requiring vasopressors to keep MAP ≥65 mmHg with a lactate above 2 mmol/L despite adequate fluids.

Lactate and blood culturesDraw cultures before antibiotics; remeasure lactate if it is elevated.
Broad-spectrum antibioticsWithin 1 hour.
Crystalloid 30 mL/kgFor hypotension or lactate ≥4 mmol/L, within 3 hours (weak SSC 2021 suggestion); reassess fluid responsiveness.
NorepinephrineIf hypotension persists despite fluids, target MAP ≥65.

Sepsis hour-1 bundle

Source control (draining an abscess, removing an infected line) is essential to survival and should happen as early as is practical; antibiotics alone rarely sterilize an undrained focus.

Target a MAP of 65. A mean arterial pressure of at least 65 mmHg is the standard perfusion target in most shock states; higher targets are not routinely better. Titrate fluids and vasopressors to it while following lactate, urine output (at least 0.5 mL/kg/h), capillary refill, and mental status.

Clear the lactate. Lactate marks anaerobic hypoperfusion; a rising or persistently high level (>4 mmol/L) predicts worse outcomes. Lactate clearance (a fall of ≥10% or normalization) is a better sign that resuscitation is working than any single blood pressure.

Lactate can lag behind restored perfusion, so trend serial values rather than acting on one number.