SHOCK
Shock = Failure of oxygen delivery relative to demand
Not hypotension
Not MAP <65
Not vasopressor deficiency
Core equation: DO₂ = CO x CaO₂
Shock = FLOW failure ± CONTENT failure → tissue hypoxia
Pressure opens the gate. Flow saves organs. Microcirculation proves it.
WHEN SHOCK EXISTS?
Shock is present if ANY of the following are seen (BP irrelevant):
Lactate ≥ 2 mmol/L or rising
CRT > 3 seconds
Cold/mottled extremities
Altered mentation
U OP < 0.5 ml/kg/hr
Normal BP does NOT exclude shock
OXYGEN DELIVERY — PRIORITY LADDER
Determinants of tissue oxygenation (in order of importance):
Cardiac Output (FLOW)
Hb
SaO₂
PaO₂ (minimal contribution)
Lungs don’t deliver oxygen. Blood flow does.
SHOCK MANAGEMENT — PHASED, IN ORDER
PHASE 1 — OPEN THE PRESSURE GATE (MACRO, ENTRY ONLY); Timeframe: first 30–60 min
Goal: allow perfusion to occur
Targets (not endpoints):
MAP ≈ 65 mmHg
SBP ≥ 90 mmHg
Tools: Fluids (guided), Norepinephrine, Early blood if clearly needed
MAP is a gatekeeper, not the destination
PHASE 2 — RESTORE FLOW (CORE PHASE)
This is where shock is won or lost
FLOW = Cardiac Output, NOT EF
CO = HR × Stroke Volume
Stroke Volume depends on: 1. Preload, 2. Contractility, 3. Afterload, & 4. Rhythm
Bedside assessment of FLOW (no calculations needed)
A. Clinical
Narrow pulse pressure → low SV
Cold extremities, prolonged CRT
Oliguria, altered mentation
B. Echo (answer ONE question only): Is forward flow adequate?
Patterns:
Hyperdynamic + small LV → preload failure
Hyperdynamic + normal LV → distributive / high VO₂
Sluggish LV → contractility failure
RV dilated, LV compressed → obstructive
C. ScvO₂ trend
<60% → delivery failing
Rising after intervention → flow/content improved
Falling despite MAP → pressor-induced flow strangulation
FLOW FAILURE — FOUR MECHANISMS
Preload failure → fluids (stop if no perfusion response)
Contractility failure → inotrope
Excess afterload → reduce pressor + add inotrope
Rhythm failure → fix rhythm first
You cannot resuscitate shock through an arrhythmia
PHASE 3 — FIX CONTENT (CaO₂ = OXYGEN CARGO)
Priority order:
Hemoglobin
SaO₂
PaO₂ (least important)
Transfuse when:
Hb < 7
Hb < 8 with ongoing shock, rising lactate, MI, TBI, persistent tachycardia
One unit of blood often improves DO₂ more than FiO₂ 100%
Avoid hyperoxia → causes vasoconstriction → worsens microflow
PHASE 4 — TRUST MICRO-PERFUSION (FINAL JUDGE)
If microperfusion is bad, shock is ongoing — MAP be damned
Primary endpoints (trend, not single value):
CRT < 3 sec (best bedside marker)
Lactate ↓ ≥10–20% in 2–4 hours
Warm extremities
Improving mentation
Improving urine output
Adjuncts:
Temperature gradients
Mottling score (knee window)
PPI (if available)
ACID–BASE AND SHOCK (CRITICAL ADDITION)
Acidosis kills shock resuscitation even if MAP is “normal”
pH < 7.25 → catecholamine failure
pH < 7.15 → myocardial depression
pH < 7.10 → mitochondrial failure
Mechanisms:
Capillary shutdown
RBC rigidity → micro-shunting
Mitochondrial inhibition
If lactate isn’t clearing, shock is ongoing — regardless of pressure
DO₂–VO₂ PHYSIOLOGY (WHY LACTATE RISES)
Lactate rises when:
DO₂ < VO₂ (true hypoxia)
β-adrenergic drive (aerobic glycolysis)
Mitochondrial dysfunction
Two zones:
Supply-independent: lactate normal
Supply-dependent: lactate rises steeply (true shock)
Resuscitation can work by:
Increasing DO₂ (flow, content)
OR decreasing VO₂ (often missed)
VO₂ MANIPULATION — THE MISSING HALF
Ways to reduce VO₂ :
Fever control (biggest lever)
Analgesia + sedation
Control work of breathing (ventilation)
Treat agitation, seizures, and shivering
Sedation in shock is metabolic resuscitation, not comfort care
SHOCK PHENOTYPES (FICK-BASED, NOT MAP-BASED)
1. Cold shock (low flow)
CO ↓, ScvO₂ ↓, lactate ↑
Cardiogenic, hypovolemic, obstructive, late sepsis
Treat: flow (fluids/inotrope), avoid vasoconstrictor overkill
2. Warm shock (extraction failure)
CO ↑/N, ScvO₂ ↑, lactate ↑
Early sepsis
Treat: source control, NE, time
3. Hypoxic/content shock
CO may be normal
Hb / SaO₂ low
Treat: blood, oxygen, and remove toxins