SHOCK — Complete Master Guide

THE MASTER MNEMONIC: "DISH — 3P Rule"

"D.I.S.H. needs 3 Ps to fix it: Pump it, Pour it, or Push it open"

HOW TO EXPAND THIS INTO FULL PARAGRAPHS

1. DEFINITION & CELLULAR BASIS

• Ill appearance / altered mental status
• HR >100, RR >20, PaCO₂ <32 mmHg
• Lactate >4 mmol/L or base deficit < −4 mEq/L ← most important
• Urine output <0.5 mL/kg/h (normal = 1.0 mL/kg/h)

Key point: Shock can occur with normal BP (compensatory adrenergic reflexes maintain pressure while organs are already underperfused).

2. THE FOUR TYPES — EXPANDED FROM "D.I.S.H."

D — DISTRIBUTIVE SHOCK (Tank too big)

• Microbial PAMPs (LPS, peptidoglycan, fungal glucans) activate TLRs, G-protein receptors, C-type lectin receptors on macrophages, neutrophils, dendritic cells, and endothelium
• Massive release of TNF, IL-1, IL-12, IL-18 → reactive oxygen species, prostaglandins
• Result: arterial vasodilation, vascular leakage, venous pooling, DIC, metabolic derangements → organ failure
• Organisms: Gram-positive bacteria (most common) > Gram-negative > fungi

SIRS (systemic inflammatory response syndrome) = same picture triggered by non-microbial insults: burns, trauma, pancreatitis.

1. Crystalloid 30 mL/kg; titrate by dynamic indices / urine output
2. Norepinephrine 0.5 mcg/min if volume fails
3. Antibiotics STAT; surgical source control
4. PRBC transfusion if Hgb <7 g/dL

I — INTRINSIC PUMP FAILURE = CARDIOGENIC SHOCK (Pump broken)

• Intrinsic myocardial damage: MI (most common), myocarditis, toxic cardiomyopathy
• Arrhythmias: ventricular tachycardia/fibrillation
• Extrinsic compression: Cardiac tamponade (pericardial fluid compresses ventricles)
• Outflow obstruction: Massive pulmonary embolism (right heart can't eject)

1. PEEP/oxygen for pulmonary edema
2. Norepinephrine 0.5 mcg/min + Dobutamine 5 mcg/kg/min
3. Reverse the insult: PCI, thrombolysis
4. Intra-aortic balloon pump (IABP) for refractory shock

Note: Cardiac tamponade and PE are sometimes classified separately as obstructive — but they both cause cardiogenic physiology.

S — STARVATION OF VOLUME = HYPOVOLEMIC SHOCK (Tank empty)

• Hemorrhage (trauma, GI bleed, ruptured AAA) — most studied
• Plasma loss: Burns (lose protein-rich fluid through denuded skin), intestinal obstruction (fluid shifts into bowel wall with high protein content)
• Dehydration: Vomiting, diarrhea, excessive sweating

• Crystalloid (10–20 mL/kg) as bridge
• If massive hemorrhage: balanced transfusion — PRBC : FFP : Platelets (1:1:1 ratio)
• If hemorrhage uncontrolled: REBOA (resuscitative endovascular balloon occlusion of aorta) while arranging surgery

H — HINDERED OUTFLOW = OBSTRUCTIVE SHOCK (Pipes blocked)

3. STAGES OF SHOCK (Guyton & Hall — applies to ALL types)

Compensatory mechanisms timeline: Catecholamines = 30 seconds; Angiotensin/ADH = 10–60 min; Fluid absorption/oral intake = 1–48 hours

4. HEMODYNAMIC FINGERPRINT — MASTER TABLE

5. PATHOLOGICAL CONSEQUENCES OF SHOCK (Robbins)

6. THE TRICK — QUICK RECALL CARD

        D  I  S  H
        ↓  ↓  ↓  ↓
      TANK PUMP EMPTY BLOCKED
      BIG  BROKEN TANK  PIPE

Vasopressors | Dobutamine+NE | Blood/fluids | Pericardio/needle/embolectomy

All share: ↓tissue perfusion → mitochondrial hypoxia → lactate → ATP depletion
           Compensated → Progressive → Irreversible

1. D — Is the patient warm, vasodilated, with bounding pulse? (Distributive — call sepsis/anaphylaxis/neuro)
2. I — Any MI, arrhythmia, tamponade? Wet lungs? (Intrinsic pump — call cardiology)
3. S — Trauma, bleeding, burns, vomiting? Dry, empty veins? (Starved of volume — pour blood/fluid)
4. H — Distended neck veins + no breath sounds / signs of PE? (Hindered outflow — unblock urgently)

7. SEPTIC SHOCK SPECIAL FEATURES (Robbins Deep Dive)

1. Triggers: PAMPs (LPS/endotoxin from gram-negatives; teichoic acid/peptidoglycan from gram-positives; glucans from fungi; superantigens like staphylococcal enterotoxin B)
2. Sensors: TLR4 (LPS), TLR2 (peptidoglycan), C-type lectins (fungi)
3. Mediators: TNF + IL-1 → neutrophil/endothelial activation → microvascular injury + DIC + vasodilation
4. Counterregulatory failure: Anti-inflammatory mediators (IL-10, TGF-β) create immune paralysis → opportunistic infections
5. Metabolic effects: Hyperglycemia → insulin resistance; impaired mitochondrial function; lactic acidosis
6. End result: MODS (Multi-Organ Dysfunction Syndrome) — the final common pathway of all shock

• Robbins, Cotran & Kumar — Pathologic Basis of Disease, pp. 134–136
• Robbins & Kumar Basic Pathology, pp. 134–140
• Rosen's Emergency Medicine, pp. 1391–1660
• Guyton and Hall Textbook of Medical Physiology, pp. 301–305
• Sabiston Textbook of Surgery, pp. 563–566

Hemodynamic Parameters & Clinical Findings — All Shock Types

TABLE 1 — HEMODYNAMIC PARAMETERS

Key PCWP rule: PCWP ↑ = left-sided congestion (cardiogenic). PCWP ↓ + CVP ↑ = right-sided obstruction (PE, tension PTX). Both ↓ = empty tank or vasodilated.

TABLE 2 — CLINICAL FINDINGS AT BEDSIDE

TABLE 3 — ECG & IMAGING CLUES

TABLE 4 — FIRST-LINE VASOPRESSORS & TREATMENT

Dopamine doses (Washington Manual): <5 mcg/kg/min = vasodilator (renal); 5–10 = inotrope; >10 = vasopressor. Higher arrhythmia risk than norepinephrine.

ONE-LINE MEMORY RULE FOR EACH

SUMMARY MATRIX — AT A GLANCE

                 CO    SVR   CVP   PCWP  Skin    JVP
Distributive:    ↑     ↓     ↓     ↓     WARM    flat
Hypovolemic:     ↓     ↑     ↓     ↓     cold    flat
Cardiogenic:     ↓     ↑     ↑     ↑↑    cold    RAISED
Obstructive:     ↓     ↑     ↑     ↓/↑   cold    RAISED

• Warm skin → Distributive
• Flat JVP + cold → Hypovolemic
• Raised JVP + wet lungs → Cardiogenic
• Raised JVP + clear lungs + specific sign (wheeze absent / muffled heart / S1Q3T3) → Obstructive