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SHOCK - Complete MBBS Guide

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1. DEFINITION

Key point from Rosen's EM: Shock can occur with a normal arterial blood pressure - not all hypotension is shock, and not all shock involves hypotension.

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2. CLASSIFICATION OF SHOCK

2A. Traditional 4-Category Classification

2B. Robbins Pathology Classification (3 broad groups)

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3. BASIC PHYSIOLOGY: WHAT DETERMINES CARDIAC OUTPUT?

• CO = HR × SV (cardiac output = heart rate × stroke volume)
• SV is determined by: Preload, Afterload, Contractility
• MAP ≈ CO × SVR (mean arterial pressure = cardiac output × systemic vascular resistance)
• DO₂ = CO × CaO₂ (oxygen delivery = cardiac output × arterial oxygen content)

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4. CELLULAR/SUBCELLULAR PATHOPHYSIOLOGY

1. Aerobic metabolism fails
2. Anaerobic glycolysis takes over → lactic acid accumulates
3. ATP depletion → failure of Na⁺/K⁺-ATPase pump → cellular swelling
4. Ca²⁺ influx → activation of destructive enzymes (phospholipases, proteases)
5. Mitochondrial damage becomes irreversible
6. Cell death - apoptosis then necrosis

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5. STAGES OF SHOCK (Guyton & Hall Physiology)

Stage 1: Compensated (Nonprogressive) Shock

1. Baroreceptor reflexes - powerful sympathetic stimulation of the circulation
2. CNS ischemic response - extreme sympathetic drive when MAP falls below 50 mmHg
3. Reverse stress-relaxation - blood vessels contract around diminished volume
4. RAAS activation - renin → angiotensin II → vasoconstriction + Na⁺/water retention
5. ADH (vasopressin) release from posterior pituitary - vasoconstriction + water retention
6. Catecholamine release from adrenal medulla (epinephrine, norepinephrine) - tachycardia, vasoconstriction
7. Volume restoration - absorption from intestinal tract, interstitial fluid redistribution, thirst, salt appetite

Stage 2: Progressive Shock

• Cardiac depression: Low coronary flow → weak myocardium → lower CO → lower coronary flow
• Vasomotor center failure: Cerebral ischemia → reduced vasomotor activity → vascular dilation → venous pooling → decreased venous return → lower CO
• Increased capillary permeability: Tissue ischemia releases toxins → capillary leak → decreased blood volume → lower CO
• Intravascular clotting: Stasis + activated coagulation → DIC → organ ischemia

Stage 3: Irreversible Shock

• Progressive microvascular failure
• Ischemic bowel → absorption of endotoxins
• Lysosomal enzyme release from ischemic cells
• Cardiac failure refractory to treatment
• Multi-organ failure (MOF)
• Death

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6. HEMORRHAGIC SHOCK - ATLS CLASSIFICATION

Important caveat (Sabiston): These classes are "problematic because they were not rigorously tested or proven and were admittedly arbitrarily generated." Heart rate, for example, is neither sensitive nor specific for hemorrhage - pain, anxiety, and drugs all alter it. Children compensate well until they crash suddenly; elderly patients decompensate earlier at lower volumes.

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7. SEPTIC SHOCK - PATHOPHYSIOLOGY IN DEPTH

7A. Definition (Robbins & Cotran)

• Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection
• Septic shock: Subset of sepsis with profound circulatory, cellular, and metabolic abnormalities associated with greater mortality than sepsis alone
• SIRS: Sepsis-like condition from nonmicrobial insults (burns, trauma, pancreatitis)

7B. Epidemiology

• 750,000 cases/year in the US; incidence rising

• Mortality rate ~40% despite improvements in care
• Most common trigger: gram-positive bacteria > gram-negative bacteria > fungi
• At least half of cases have no specific organism identified

7C. Pathogenic Steps

• PAMPs (pathogen-associated molecular patterns) - endotoxin (LPS) from gram-negatives, enterotoxin B from staph, M protein from streptococci
• DAMPs (damage-associated molecular patterns) from injured host cells
• Detected by TLRs (Toll-like receptors), G-protein-coupled receptors, C-type lectin receptors (Dectin-1 for fungi)

• Activation of NF-kB → upregulation of TNF-α, IL-1, IL-6, IL-12, IL-18, IFN-γ
• HMGB1 (late mediator), CRP, procalcitonin elevated
• Reactive oxygen species (ROS), prostaglandins, PAF (platelet-activating factor) released
• Complement activated → anaphylatoxins C3a, C5a → further inflammation

• Cytokines loosen tight junctions → vascular leakage → protein-rich edema throughout body
• Upregulation of NO (from iNOS) → vasodilation → hypotension
• Microvascular dysfunction: heterogeneous capillary flow, loss of autoregulation → oxygen delivery/demand mismatch

• Proinflammatory cytokines increase tissue factor from monocytes/endothelial cells
• Decrease of anticoagulants: thrombomodulin, protein C, TFPI
• Increased PAI-1 → impaired fibrinolysis
• NETs (neutrophil extracellular traps) activate both intrinsic and extrinsic coagulation
• Result: fibrin-rich thrombi in small vessels → tissue ischemia, plus consumption of clotting factors → paradoxical bleeding

• Insulin resistance + hyperglycemia (TNF, IL-1, stress hormones suppress insulin, promote gluconeogenesis)
• Hyperglycemia suppresses neutrophil bactericidal activity
• Elevated blood glucose, triglycerides, lactate

• Oscillation between hyperinflammatory and immunosuppressed states
• Shift from Th1 (proinflammatory) to Th2 (anti-inflammatory) cytokines
• IL-10, soluble TNF receptor, IL-1 receptor antagonist
• Lymphocyte apoptosis, cellular anergy
• Clinically: increased susceptibility to secondary infections

• Lung: Capillary leak → ARDS (non-cardiogenic pulmonary edema)
• Kidney: Acute tubular necrosis (arteriolar spasm + ischemia)
• Liver: Centrilobular injury → elevated transaminases
• Heart: Direct myocardial depression by TNF-α, IL-1β, and excess NO from iNOS
• Coagulation: DIC in up to 50% of septic patients

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8. CARDIOGENIC SHOCK

• Occurs when >40% of myocardium becomes dysfunctional
• Causes: MI (most common), myocarditis, arrhythmia, mechanical complications (papillary muscle rupture → acute MR, VSD), tamponade, PE
• Hemodynamically: low CO, high SVR, high PCWP (pulmonary capillary wedge pressure)
• Differentiating feature: jugular venous distention (JVD) + pulmonary edema (wet + cold patient)

• Beck's triad for tamponade: hypotension + JVD + muffled heart sounds
• Kussmaul's sign in tamponade/constrictive pericarditis: JVP rises on inspiration
• Pulsus paradoxus >10 mmHg in tamponade

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9. NEUROGENIC SHOCK

• Loss of sympathetic vasomotor tone following spinal cord injury (usually above T6)
• Features: hypotension + relative bradycardia (no compensatory tachycardia because sympathetic drive is lost) + warm, dry skin (vasodilated peripheries)
• Distinguished from hypovolemic shock by: bradycardia (not tachycardia), warm skin
• Treatment: volume replacement first (especially if concomitant hemorrhagic shock), then vasopressors (norepinephrine preferred to maintain SVR)

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10. ANAPHYLACTIC SHOCK

• IgE-mediated hypersensitivity → mast cell degranulation → histamine, leukotrienes, prostaglandins
• Massive vasodilation + increased capillary permeability + bronchospasm
• Features: urticaria, angioedema, bronchospasm, hypotension, tachycardia
• Treatment: Epinephrine 0.5 mg IM (1:1000) into anterolateral thigh - first line

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11. CLINICAL ASSESSMENT OF SHOCK

11A. History and Clinical Signs

• Vital signs: Tachycardia (earliest sign), hypotension (late), tachypnea
• Skin: Cold, clammy, pale in hypovolemic/cardiogenic; warm, flushed, well-perfused in early distributive/septic
• JVP: Low in hypovolemic/distributive; elevated in cardiogenic/obstructive
• Capillary refill time: >2 seconds suggests hypoperfusion
• Mental status: Confusion/agitation → cerebral hypoperfusion
• Urine output: Most reliable index of vital organ perfusion
  • Normal: >1.0 mL/kg/hr
  • Reduced: 0.5-1.0 mL/kg/hr
  • Severely reduced: <0.5 mL/kg/hr = severe renal hypoperfusion

11B. Diagnostic Features by Shock Type

11C. Laboratory Assessment

• Serum lactate: Most important - level >4 mmol/L = severe shock; target is trending down with treatment
• Base deficit: More negative than -4 mEq/L warrants presumptive diagnosis of shock
• A combination of worsening base deficit + increasing lactate + low urine output = persistent/worsening shock (Rosen's EM)
• CBC: Hematocrit (may be normal acutely in hemorrhage until hemodilution occurs)
• BMP: Creatinine (AKI), glucose, electrolytes
• Coagulation profile: PT/PTT/INR, fibrinogen, D-dimer (for DIC)
• Troponin, BNP/NT-proBNP: For cardiogenic shock
• Blood cultures (2 sets before antibiotics) in suspected septic shock
• Procalcitonin: Elevated in bacterial sepsis
• Arterial blood gas (ABG): Metabolic acidosis (low pH, low HCO₃, elevated lactate)
• Echocardiography (ECHO/POCUS): Bedside ultrasound to assess LV/RV function, pericardial effusion, IVC collapsibility (preload assessment)

11D. Monitoring Parameters

• MAP target: ≥65 mmHg (≥75 mmHg in known hypertensives)
• CVP (Central Venous Pressure): Guides fluid responsiveness (though limited value alone)
• ScvO₂ (Central venous O₂ saturation): <70% suggests inadequate DO₂
• Arterial line: For continuous BP monitoring when vasopressors are used
• Urinary catheter: Hourly urine output measurement

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12. MANAGEMENT OF SHOCK - GENERAL PRINCIPLES

ABC Approach

Fluid Resuscitation

• Initial bolus: 500 mL to 1 L crystalloid (Lactated Ringer's preferred over normal saline - evidence suggests balanced solutions are as good or better)
• Normal saline risks: hyperchloremic metabolic acidosis with large volumes
• For hemorrhagic shock: Balanced transfusion approach - PRBC : FFP : Platelets = 1:1:1 (damage control resuscitation)
• Permissive hypotension (target SBP 80-90 mmHg) until hemorrhage control in penetrating trauma (avoids "popping the clot")
• Avoid excessive crystalloid: "two hits" theory - resuscitation itself can cause ARDS and organ injury through inflammatory cascade

Vasopressors (when adequate fluid resuscitation fails to maintain perfusion)

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13. MANAGEMENT BY SHOCK TYPE

13A. Hemorrhagic/Hypovolemic Shock

1. Control bleeding - direct pressure, tourniquet, surgical hemostasis (most important step)
2. Damage control resuscitation: PRBC + FFP + Platelets (1:1:1)
3. Tranexamic acid (TXA): Give within 3 hours of injury (inhibits fibrinolysis)
4. Warm fluids: Prevent hypothermia (hypothermia + acidosis + coagulopathy = "lethal triad")
5. Avoid over-resuscitation with crystalloids
6. Permissive hypotension in penetrating trauma

13B. Septic Shock (Hour-1 Bundle, Surviving Sepsis Campaign)

1. Lactate measurement - remeasure if initial >2 mmol/L
2. Blood cultures (2 sets) before antibiotics
3. Broad-spectrum antibiotics within 1 hour - early antibiotic administration is the single most impactful intervention
4. 30 mL/kg IV crystalloid for hypotension or lactate ≥4 mmol/L
5. Vasopressors (norepinephrine first) if MAP <65 mmHg during/after fluid resuscitation
6. Source control - drain abscess, remove infected device
7. Steroids: Hydrocortisone 200 mg/day IV if vasopressor requirement persists
8. Tight glycemic control (target glucose 140-180 mg/dL)
9. DVT prophylaxis, stress ulcer prophylaxis

13C. Cardiogenic Shock

1. Identify and treat cause: Emergent PCI for AMI, cardioversion for arrhythmia, pericardiocentesis for tamponade
2. Inotropes: Dobutamine (first line - improves contractility without major vasoconstriction)
3. Vasopressors: Norepinephrine for hypotension
4. DO NOT give large fluid boluses (worsens pulmonary edema)
5. Mechanical circulatory support: IABP (intra-aortic balloon pump), Impella, ECMO in refractory cases
6. Avoid dopamine in cardiogenic shock (increased mortality)

13D. Obstructive Shock

• Tension pneumothorax: Needle decompression (2nd ICS, MCL) → chest drain
• Cardiac tamponade: Pericardiocentesis (needle aspiration) → pericardial window if recurrent
• Massive PE: Anticoagulation, thrombolytics (if cardiac arrest or hemodynamic compromise), surgical embolectomy

13E. Anaphylactic Shock

1. Epinephrine 0.5 mg IM (1:1000) into anterolateral thigh - immediately
2. IV fluids (aggressive resuscitation - up to 4-8 L may be needed)
3. H1 antihistamine (diphenhydramine/chlorphenamine)
4. H2 antihistamine (ranitidine/famotidine)
5. Corticosteroids (prevent biphasic reaction)
6. Salbutamol for bronchospasm
7. Remove/avoid trigger

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14. MORPHOLOGICAL CHANGES IN ORGANS (Pathology)

Kidneys

• Acute tubular necrosis (ATN) - most consistent finding
• Arteriolar spasm → cortical ischemia → tubular cell death
• Clinically: oliguria → anuria → rising creatinine
• May progress to AKI requiring dialysis

Lungs

• ARDS (Acute Respiratory Distress Syndrome) - "shock lung"
• Mechanism: Capillary leak → protein-rich alveolar edema → impaired gas exchange
• CXR: bilateral diffuse infiltrates ("white out")
• Requires mechanical ventilation with lung-protective strategy (low tidal volumes)

Adrenal Glands

• Lipid depletion of cortical cells (stressed adrenals use up stored cholesterol)
• In severe/prolonged shock: adrenal cortical insufficiency (relative adrenal insufficiency)
• Rationale for hydrocortisone in refractory septic shock

Liver

• Centrilobular (zone 3) necrosis - center of lobule is most oxygen-dependent
• Elevated transaminases (ALT, AST) in shock
• Impaired synthetic function (coagulopathy), impaired lactate clearance

GI Tract

• Ischemic enterocolitis - mucosal ulceration
• Loss of gut barrier function → bacterial translocation → feeds septic cycle
• "Gut" is the motor of MOF (multiple organ failure)

Brain

• Ischemic encephalopathy - watershed area infarcts (between ACA/MCA and MCA/PCA territories)
• Clinically: confusion, agitation, coma

Heart

• Contraction band necrosis - characteristic of catecholamine-mediated injury
• Subendocardial ischemia (most vulnerable region)

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15. MULTI-ORGAN FAILURE (MOF)

• Sequential or simultaneous failure of ≥2 organ systems
• Order of typical failure: Lungs (ARDS) → Kidneys (ATN/AKI) → Liver → Coagulation (DIC) → CNS → Heart
• Mortality increases with number of organs failing: 1 organ ~30%, 3 organs >80%, 5 organs ~100%
• Pathogenesis: Ischemia-reperfusion injury + systemic inflammation + microvascular thrombosis + immunosuppression

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16. SPECIAL SITUATIONS

The "Lethal Triad" of Trauma

Permissive Hypotension

Obstructive vs Cardiogenic

Children in Shock

Elderly in Shock

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17. QUICK REVISION - HIGH-YIELD POINTS FOR EXAMS

1. Definition: Shock = inadequate tissue perfusion leading to cellular hypoxia
2. Earliest sign of shock: Tachycardia (not hypotension)
3. Best early laboratory marker: Serum lactate (>4 mmol/L = severe shock)
4. Urine output normal: >1 mL/kg/hr; severe hypoperfusion: <0.5 mL/kg/hr
5. ATLS Class III shock = BP falls (30-40% blood loss) - before this, BP is maintained by compensation
6. Pulse pressure narrows before systolic BP falls (early sign of hemorrhagic shock)
7. Neurogenic shock: Hypotension + bradycardia + warm skin (unlike other types)
8. Septic shock first-line vasopressor: Norepinephrine (superior to dopamine)
9. Cardiogenic shock: DO NOT give fluids; dobutamine (inotrope) is key
10. Anaphylaxis: Epinephrine IM (not IV initially, not subcutaneous)
11. Surviving Sepsis Campaign - Hour 1 Bundle: Lactate, blood cultures, antibiotics, fluids, vasopressors
12. DIC occurs in up to 50% of septic shock patients
13. Organ most sensitive to ischemia in shock: Kidney (ATN) and brain
14. "Shock lung" = ARDS - bilateral infiltrates, non-cardiogenic pulmonary edema
15. Lethal triad in trauma: Hypothermia + Acidosis + Coagulopathy
16. Irreversible shock: Lysosomal enzyme release + ischemic bowel → endotoxin absorption
17. Base deficit more negative than -4 mEq/L = presumptive shock diagnosis
18. Compensatory mechanisms timed: Catecholamines (seconds to minutes) → RAAS/ADH (10-60 min) → volume redistribution (1-48 hours)
19. Low-dose dopamine for renal protection is NOT recommended (no mortality benefit)
20. Hydrocortisone (200 mg/day) in septic shock if vasopressors are still required despite adequate resuscitation

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REFERENCES

• Robbins, Cotran & Kumar Pathologic Basis of Disease, 10th ed., p. 134-137
• Guyton & Hall Textbook of Medical Physiology, p. 299-306
• Rosen's Emergency Medicine, 9th ed., Chapter 3
• Sabiston Textbook of Surgery, Chapter 33
• Tintinalli's Emergency Medicine, Chapter 20
• Katzung Basic and Clinical Pharmacology, 16th ed.