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What is shock types of shock details of all types sign symptoms features ane management for MD anaesthesia exam 50 marks

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types of shock hemodynamic classification cardiogenic hypovolemic distributive diagram

Summary : This figure presents the updated SCAI SHOCK classification pyramid, which stratifies patients with acute myocardial infarction (AMI), cardiogenic shock (CS), and heart failure (HF) into five stages (A–E) based on severity, with an additional modifier for anoxic brain injury. Each stage is defined by clinical criteria related to hemodynamic stability and evidence of shock. pyramid diagram: # Overall Structure : • Five-tiered pyramid labeled from bottom (A) to top (E), each tier representing a stage of shock severity. • Left side: Each tier is labeled with a letter (A–E) and a corresponding color gradient from dark blue (A) to dark red (E). • Right side: Each tier is named and described with clinical criteria. • Top left: Box indicating "(A) Modifier: CA with concern for anoxic brain injury". # Stages & Descriptions : ## AT RISK (A, bottom tier) : • "A hemodynamically stable patient who is NOT experiencing signs or symptoms of CS, but is at risk for its development (i.e. large AMI or decompensated HF)." • Color: Dark blue. ## BEGINNING (B, second tier) : • "A patient who has clinical evidence of hemodynamic instability (including hypotension, tachycardia or abnormal systemic hemodynamics) without hypoperfusion." • Color: Medium blue. ## CLASSIC (C, middle tier) : • "A patient who has clinical evidence of hypoperfusion that initially requires pharmacologic or mechanical support. Hypotension is usually present." • Color: Light blue. ## DETERIORATING (D, fourth tier) : • "A patient who has clinical evidence of shock that worsens or fails to improve despite escalation of therapy." • Color: Light grey. ## EXTREMIS (E, top tier) : • "A patient with refractory shock or actual/impending circulatory collapse." • Color: Dark red. # Modifier : • "(A) Modifier: CA with concern for anoxic brain injury" is shown in a separate box, indicating an additional classification for patients with cardiac arrest and possible brain injury. # Design Encodings : • Pyramid shape with color gradient from blue (least severe) to red (most severe). • Each stage is labeled with a large letter (A–E) and a descriptive name in colored text matching the tier. • Descriptions are provided in smaller text to the right of each tier. • Modifier box is purple with white text. # Analysis : • The pyramid visually emphasizes increasing severity from bottom (A, at risk) to top (E, extremis). • The color gradient reinforces the escalation in clinical urgency. • The modifier box highlights the importance of considering anoxic brain injury in classification. • The structure allows rapid identification of patient status and guides clinical decision-making based on stage.

Summary : This figure presents the updated SCAI SHOCK classification pyramid, which stratifies patients with acute myocardial infarction (AMI), cardiogenic shock (CS), and heart failure (HF) into five stages (A–E) based on severity, with an additional modifier for anoxic brain injury. Each stage is defined by clinical criteria related to hemodynamic stability and evidence of shock. pyramid diagram: # Overall Structure : • Five-tiered pyramid labeled from bottom (A) to top (E), each tier representing a stage of shock severity. • Left side: Each tier is labeled with a letter (A–E) and a corresponding color gradient from dark blue (A) to dark red (E). • Right side: Each tier is named and described with clinical criteria. • Top left: Box indicating "(A) Modifier: CA with concern for anoxic brain injury". # Stages & Descriptions : ## AT RISK (A, bottom tier) : • "A hemodynamically stable patient who is NOT experiencing signs or symptoms of CS, but is at risk for its development (i.e. large AMI or decompensated HF)." • Color: Dark blue. ## BEGINNING (B, second tier) : • "A patient who has clinical evidence of hemodynamic instability (including hypotension, tachycardia or abnormal systemic hemodynamics) without hypoperfusion." • Color: Medium blue. ## CLASSIC (C, middle tier) : • "A patient who has clinical evidence of hypoperfusion that initially requires pharmacologic or mechanical support. Hypotension is usually present." • Color: Light blue. ## DETERIORATING (D, fourth tier) : • "A patient who has clinical evidence of shock that worsens or fails to improve despite escalation of therapy." • Color: Light grey. ## EXTREMIS (E, top tier) : • "A patient with refractory shock or actual/impending circulatory collapse." • Color: Dark red. # Modifier : • "(A) Modifier: CA with concern for anoxic brain injury" is shown in a separate box, indicating an additional classification for patients with cardiac arrest and possible brain injury. # Design Encodings : • Pyramid shape with color gradient from blue (least severe) to red (most severe). • Each stage is labeled with a large letter (A–E) and a descriptive name in colored text matching the tier. • Descriptions are provided in smaller text to the right of each tier. • Modifier box is purple with white text. # Analysis : • The pyramid visually emphasizes increasing severity from bottom (A, at risk) to top (E, extremis). • The color gradient reinforces the escalation in clinical urgency. • The modifier box highlights the importance of considering anoxic brain injury in classification. • The structure allows rapid identification of patient status and guides clinical decision-making based on stage.

Two black-and-white clinical photographs showing peripheral vasodilatation in patients with distributive shock. The top image displays a supine patient (BP 85/35 mmHg) with prominent, distended superficial veins across the upper arm and chest wall. The bottom image shows a second patient (BP 55/30 mmHg) with similar marked venous engorgement in the forearm, with superficial veins appearing highly visible and distended despite severe systemic hypotension. These visual findings demonstrate the paradoxical clinical presentation of distributive shock—often seen in severe organophosphate poisoning—where pathological peripheral vasodilation occurs instead of the expected compensatory vasoconstriction typical of hypovolemic or cardiogenic shock. Key concepts illustrated include the assessment of peripheral vascular tone, venous distension, and the recognition of warm shock/low systemic vascular resistance in an emergency clinical setting.

Two black-and-white clinical photographs showing peripheral vasodilatation in patients with distributive shock. The top image displays a supine patient (BP 85/35 mmHg) with prominent, distended superficial veins across the upper arm and chest wall. The bottom image shows a second patient (BP 55/30 mmHg) with similar marked venous engorgement in the forearm, with superficial veins appearing highly visible and distended despite severe systemic hypotension. These visual findings demonstrate the paradoxical clinical presentation of distributive shock—often seen in severe organophosphate poisoning—where pathological peripheral vasodilation occurs instead of the expected compensatory vasoconstriction typical of hypovolemic or cardiogenic shock. Key concepts illustrated include the assessment of peripheral vascular tone, venous distension, and the recognition of warm shock/low systemic vascular resistance in an emergency clinical setting.

Summary : This figure presents a pyramid diagram illustrating the classification of cardiogenic shock (CS) into five progressive stages (A–E), from "At Risk" to "Extremis," with detailed descriptions for each stage. pyramid diagram: # Structure & Levels : • The diagram is a five-level pyramid, with each level labeled from bottom (A) to top (E). • Each level represents a stage of cardiogenic shock, with increasing severity from A (base) to E (apex). • Levels are color-coded in gradients of blue, with darker shades at the base and lighter at the apex. ## Stages & Descriptions : • Stage A "At Risk": – Patients not currently experiencing signs or symptoms of cardiogenic shock, but at risk for its development. – Includes those with acute myocardial infarction, acute and/or acute on chronic heart failure symptoms. • Stage B "Beginning" Cardiogenic Shock: – Patients with clinical evidence of relative hypotension or tachycardia without hypoperfusion. • Stage C "Classic" Cardiogenic Shock: – Patients manifesting with hypoperfusion requiring intervention (inotrope, pressor, mechanical support, ECMO) beyond volume resuscitation. – Typically present with relative hypotension. • Stage D "Deteriorating or Doom": – Patients similar to category C but getting worse. – Failure to respond to initial interventions. • Stage E "Extremis": – Patients with circulatory collapse, often in refractory cardiac arrest with ongoing CPR or multiple simultaneous acute interventions (including ECMO-facilitated CPR). – Multiple clinicians at bedside due to lack of clinical stability. ## Design Encodings : • Each stage is labeled with a large letter (A–E), stage name, and a detailed description. • The pyramid shape visually emphasizes progression and severity. • The base (A) is widest, indicating the largest population at risk; the apex (E) is narrowest, indicating the most severe and least common stage. ## Caption & Source : • Figure is labeled as "FIGURE 1 The pyramid of CS classification" at the bottom. # Analysis : • The pyramid visually communicates the increasing severity and decreasing prevalence of cardiogenic shock stages from A (at risk) to E (extremis). • The detailed descriptions provide clear clinical criteria for each stage, supporting rapid classification and intervention planning. • The structure emphasizes that as patients progress upward, interventions become more urgent and complex, with the top stage (E) representing critical instability requiring maximal support.

Summary : This figure presents a pyramid diagram illustrating the classification of cardiogenic shock (CS) into five progressive stages (A–E), from "At Risk" to "Extremis," with detailed descriptions for each stage. pyramid diagram: # Structure & Levels : • The diagram is a five-level pyramid, with each level labeled from bottom (A) to top (E). • Each level represents a stage of cardiogenic shock, with increasing severity from A (base) to E (apex). • Levels are color-coded in gradients of blue, with darker shades at the base and lighter at the apex. ## Stages & Descriptions : • Stage A "At Risk": – Patients not currently experiencing signs or symptoms of cardiogenic shock, but at risk for its development. – Includes those with acute myocardial infarction, acute and/or acute on chronic heart failure symptoms. • Stage B "Beginning" Cardiogenic Shock: – Patients with clinical evidence of relative hypotension or tachycardia without hypoperfusion. • Stage C "Classic" Cardiogenic Shock: – Patients manifesting with hypoperfusion requiring intervention (inotrope, pressor, mechanical support, ECMO) beyond volume resuscitation. – Typically present with relative hypotension. • Stage D "Deteriorating or Doom": – Patients similar to category C but getting worse. – Failure to respond to initial interventions. • Stage E "Extremis": – Patients with circulatory collapse, often in refractory cardiac arrest with ongoing CPR or multiple simultaneous acute interventions (including ECMO-facilitated CPR). – Multiple clinicians at bedside due to lack of clinical stability. ## Design Encodings : • Each stage is labeled with a large letter (A–E), stage name, and a detailed description. • The pyramid shape visually emphasizes progression and severity. • The base (A) is widest, indicating the largest population at risk; the apex (E) is narrowest, indicating the most severe and least common stage. ## Caption & Source : • Figure is labeled as "FIGURE 1 The pyramid of CS classification" at the bottom. # Analysis : • The pyramid visually communicates the increasing severity and decreasing prevalence of cardiogenic shock stages from A (at risk) to E (extremis). • The detailed descriptions provide clear clinical criteria for each stage, supporting rapid classification and intervention planning. • The structure emphasizes that as patients progress upward, interventions become more urgent and complex, with the top stage (E) representing critical instability requiring maximal support.

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Here is the full, exam-ready answer for MD Anaesthesia - 50 marks.

SHOCK: Definition, Classification, Types, Features, and Management

[MD Anaesthesia - Long Essay, 50 Marks]

I. DEFINITION

Shock is defined as inadequate tissue perfusion resulting in insufficient oxygen delivery (DO₂) relative to oxygen demand (VO₂), causing cellular hypoxia and organ dysfunction.
The classic Gross definition (1872): "A manifestation of the rude unhinging of the machinery of life."
From the anaesthesia perspective (Miller's Anesthesia, 10e):
Shock is the inability to provide adequate oxygen to the tissues. The condition depends on the balance between oxygen supply (DO₂) and oxygen demand (VO₂).
Key equations:
  • CaO₂ (mL/dL) = (1.34 × Hb × SaO₂) + (PaO₂ × 0.003) → normal ≈ 20 mL/dL
  • DO₂ (mL/min) = CaO₂ × CO × 0.01
  • VO₂ = DO₂ × O₂ Extraction (CaO₂ - CvO₂)/CaO₂
When DO₂ falls below the critical threshold, VO₂ becomes delivery-dependent → anaerobic metabolism → lactic acidosis.

II. CLASSIFICATION OF SHOCK

Four major classes (Harrison's 22e, Miller's 10e, Sabiston Surgery):
TypePrimary MechanismCVPPCWPCOSVR
HypovolemicReduced preload↓↓↓↑
CardiogenicPump failure↑↑↓↑
DistributiveVasodilation / maldistribution↓↓↑↓↓
ObstructiveExtracardiac outflow block↑↓/↑↓↑
Source: Harrison's Principles of Internal Medicine 22e, Table 314-2
Schwartz Surgery further subdivides to 6 types: hypovolemic, septic (vasodilatory), neurogenic, cardiogenic, obstructive, and traumatic shock.

III. STAGES OF SHOCK

All types progress through three phases:
  1. Compensated (early) shock: Neurohumoral responses maintain BP via sympathoadrenal activation, tachycardia, increased SVR, ADH/RAAS activation. BP maintained; subtle signs only.
  2. Decompensated (progressive) shock: Compensatory mechanisms fail; progressive hypotension, anaerobic metabolism, lactic acidosis, organ hypoperfusion.
  3. Irreversible (refractory) shock: Irreversible cell death, mitochondrial failure, multiple organ dysfunction syndrome (MODS), death inevitable despite resuscitation.

IV. TYPES OF SHOCK - DETAILED

1. HYPOVOLEMIC SHOCK

Definition: Shock due to absolute reduction in circulating blood/fluid volume causing decreased preload and CO.
Causes:
  • Hemorrhagic: Trauma (most common), GI bleeding (upper > lower), surgical blood loss, ruptured ectopic pregnancy/AAA
  • Non-hemorrhagic: Vomiting, diarrhea, osmotic diuresis (DKA, DI), burns (fluid redistribution), severe pancreatitis, nephrotic syndrome
ATLS Classification of Hemorrhagic Shock:
ClassBlood LossHRBPRRUrine OutputCNS
I<15% (<750 mL)<100Normal14-20>30 mL/hNormal
II15-30% (750-1500 mL)100-120Normal20-3020-30 mL/hAnxious
III30-40% (1500-2000 mL)120-140↓30-405-15 mL/hConfused
IV>40% (>2000 mL)>140↓↓>35<5 mL/hLethargic/Unconscious
Signs & Symptoms:
  • Hypotension, tachycardia, narrow pulse pressure
  • Cold, clammy, pale skin (vasoconstriction)
  • Decreased urine output (oliguria <0.5 mL/kg/h)
  • Altered consciousness: anxiety → confusion → coma
  • Increased respiratory rate (compensatory)
  • Collapsed JVP/neck veins
  • Dry mucous membranes (non-hemorrhagic)
  • Metabolic acidosis (elevated lactate)
Pathophysiology:
  • Volume loss → ↓ venous return → ↓ preload → ↓ SV → ↓ CO
  • Baroreceptor activation → sympathoadrenal surge → tachycardia, vasoconstriction
  • RAAS activation → aldosterone → Na⁺ and water retention
  • ADH release → water conservation
  • If untreated: microcirculatory failure → cellular hypoxia → lactic acidosis → MODS
Management:
  1. Airway & Breathing: Secure airway; O₂ supplementation; intubate if needed
  2. Hemorrhage control: Direct pressure, tourniquet, surgical intervention; damage control surgery principle
  3. IV access: Two large-bore peripheral IVs (14-16G); intraosseous if needed
  4. Fluid resuscitation:
    • Class I/II: Crystalloid (0.9% NaCl or Ringer's Lactate) 1-2 L bolus
    • Class III/IV: Massive transfusion protocol - 1:1:1 ratio (PRBC: FFP: Platelets)
    • Permissive hypotension (MAP 50-65 mmHg) in penetrating trauma until surgical hemostasis
  5. Vasopressors: Norepinephrine if fluid-unresponsive (secondary measure)
  6. Tranexamic acid: 1 g IV within 3 hours of traumatic hemorrhage (CRASH-2 trial evidence)
  7. Warming: Prevent/treat hypothermia (lethal triad: hypothermia + coagulopathy + acidosis)
  8. Monitor: Urine output, BP, HR, lactate clearance, ABG

2. CARDIOGENIC SHOCK

Definition: Shock due to primary cardiac pump failure resulting in reduced CO despite adequate preload. CO decreased, SVR increased, PCWP elevated.
Causes:
  • Myocardial: AMI (most common - especially large anterior STEMI), myocarditis, dilated cardiomyopathy, post-cardiac surgery low output syndrome, Takotsubo (stress) cardiomyopathy
  • Mechanical: Acute mitral regurgitation (papillary muscle rupture), acute VSD (post-MI), aortic stenosis, acute aortic insufficiency
  • Arrhythmia: Sustained VT, complete heart block, severe bradyarrhythmia
  • Obstructive (intrinsic): Critical AS, severe MS
Signs & Symptoms:
  • Hypotension (SBP <90 mmHg), narrow pulse pressure
  • Tachycardia (compensatory; may be absent if arrhythmia is causative)
  • Cold, clammy extremities (↑ SVR, vasoconstriction) - "cold and wet" pattern
  • Elevated JVP/distended neck veins (elevated PCWP/CVP)
  • Pulmonary crackles/rales (pulmonary edema from elevated LVEDP)
  • S3 gallop, new murmur (mechanical cause)
  • Oliguria (<0.5 mL/kg/h)
  • Altered mental status (cerebral hypoperfusion)
  • Elevated NT-proBNP, troponin
  • CXR: pulmonary congestion, cardiomegaly
  • ECG: ST changes, arrhythmia
Vicious Cycle of Cardiogenic Shock: Myocardial dysfunction → ↓ CO → ↓ coronary perfusion pressure → further ischemia → more myocardial dysfunction (the "death spiral")
SCAI Classification (2022):
  • Stage A: At risk
  • Stage B: Beginning (hemodynamic instability without hypoperfusion)
  • Stage C: Classic cardiogenic shock
  • Stage D: Deteriorating/Doom
  • Stage E: Extremis/cardiac arrest
Management:
  1. Revascularization: Urgent PCI for AMI-related cardiogenic shock (door-to-balloon <90 min)
  2. Vasopressors/Inotropes:
    • Norepinephrine - first-line vasopressor (MAP target ≥65 mmHg)
    • Dobutamine - inotrope for low CO; add to norepinephrine when EF reduced
    • Dopamine - alternative (higher arrhythmia risk)
    • Milrinone (PDE-III inhibitor): inodilator; useful post-cardiac surgery; dose 25-75 mcg/kg load then 0.25-0.75 mcg/kg/min
    • Levosimendan - calcium sensitizer; improves contractility without increasing myocardial O₂ consumption; 6-12 mcg/kg load then 0.1-0.2 mcg/kg/min
  3. Mechanical Circulatory Support (MCS):
    • IABP (Intra-aortic Balloon Pump): Counterpulsation; deflates systole (↓ afterload), inflates diastole (↑ coronary perfusion)
    • Impella (pLVAD): Microaxial pump; provides up to 5.5 L/min support
    • VA-ECMO: Maximum support for refractory cardiogenic shock/cardiac arrest
    • TandemHeart: Transseptal LA-to-aorta support
  4. Treat cause: Percutaneous/surgical repair of mechanical defects, cardioversion for arrhythmia
  5. Avoid excessive fluids (worsens pulmonary edema)
  6. Pulmonary artery catheter: Guides hemodynamic optimization in refractory cases
  7. Avoid/caution: BBs, CCBs acutely (worsen contractility)

3. DISTRIBUTIVE SHOCK

Definition: Shock due to pathological vasodilation with maldistribution of blood flow, causing relative hypovolemia despite normal or elevated CO. SVR markedly reduced.
Three main subtypes:

3A. SEPTIC SHOCK (most common distributive shock)

Definition (Sepsis-3, 2016): Sepsis with persistent hypotension requiring vasopressor support to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate fluid resuscitation.
Pathophysiology:
  • Pathogen recognition (LPS, gram+/- bacteria, fungi, viruses) → pattern recognition receptors (TLRs) → massive cytokine release (TNF-α, IL-1, IL-6)
  • Endothelial activation → ↑ vascular permeability → "third spacing"
  • iNOS upregulation → excessive NO → profound vasodilation
  • Myocardial depression (sepsis-induced cardiomyopathy in ~40%)
  • Microcirculatory dysfunction → oxygen extraction failure
  • Coagulation activation → DIC possible
Hemodynamics: "Warm/hyperdynamic" initially - ↑ CO, ↓ SVR, ↓ CVP, bounding pulses; later "cold/hypodynamic" if myocardial depression develops.
Signs & Symptoms:
  • Fever (>38°C) or hypothermia (<36°C) - sepsis
  • Tachycardia (HR >90 bpm)
  • Tachypnea (RR >20 or PaCO₂ <32)
  • Leukocytosis (>12,000) or leukopenia (<4,000)
  • Warm, flushed skin (vasodilation; "warm shock")
  • Bounding pulses; wide pulse pressure
  • Hypotension despite fluid resuscitation
  • Oliguria, rising creatinine
  • Altered mentation, encephalopathy
  • Petechiae/purpura (meningococcemia, DIC)
  • Elevated lactate (>2 mmol/L = organ hypoperfusion)
  • SOFA score ≥2 (organ dysfunction)
Surviving Sepsis Campaign 2021 - Key Management (Hour-1 Bundle):
  1. Measure lactate (re-measure if >2 mmol/L)
  2. Blood cultures ×2 BEFORE antibiotics
  3. Antibiotics: Broad-spectrum within 1 hour of recognition (MANDATORY - each 1 h delay → 7-8% ↑ mortality)
  4. Fluid resuscitation: 30 mL/kg IV crystalloid within 3 hours for hypoperfusion (liberal vs. restrictive trial CLOVERS showed equipoise; current SSC favors 30 mL/kg then reassess)
  5. Vasopressors:
    • Norepinephrine (1st line) - target MAP ≥65 mmHg
    • Vasopressin 0.03 units/min (2nd line, add to NE; may improve kidney outcomes)
    • Epinephrine (3rd line)
  6. Corticosteroids: Hydrocortisone 200 mg/day IV if ongoing vasopressor requirement (refractory septic shock)
  7. Source control: Drain abscess, remove infected catheter/device; surgical debridement as needed
  8. Add dobutamine to norepinephrine OR switch to epinephrine if septic shock + reduced LVEF
  9. Antibiotic stewardship: Reassess and narrow at 48-72 h based on cultures
  10. Supportive: LPV for ARDS (6 mL/kg IBW), glucose control (target <180 mg/dL), VTE prophylaxis, early enteral nutrition
Sepsis Biomarkers: PCT (procalcitonin), CRP, lactate, IL-6

3B. ANAPHYLACTIC SHOCK

Definition: Severe, life-threatening systemic IgE-mediated hypersensitivity reaction causing massive histamine/mediator release.
Causes: Medications (penicillin, NSAIDs, contrast media, neuromuscular blockers - most common in OR), latex, insect stings, food (nuts, shellfish)
Anaphylaxis is HIGHLY RELEVANT for anaesthesiologists - NMBAs account for ~60% of perioperative anaphylaxis.
Pathophysiology:
  • IgE cross-linking on mast cells/basophils → degranulation → histamine, tryptase, leukotrienes, prostaglandins
  • Profound vasodilation + increased vascular permeability (up to 35% of plasma volume can extravasate within 10 min)
  • Bronchospasm (histamine, leukotrienes on airways)
  • Urticaria, angioedema
Signs & Symptoms (Triad: Cardiovascular + Respiratory + Cutaneous):
  • Cardiovascular: Hypotension, tachycardia, distributive shock, cardiovascular collapse
  • Respiratory: Bronchospasm (wheezing), laryngeal edema, stridor, respiratory distress, hypoxia
  • Cutaneous: Urticaria, angioedema, flushing, pruritus (may be absent in ~20%)
  • Nausea, vomiting, abdominal cramps
  • Under anaesthesia: sudden bronchospasm + hypotension + ↑ airway pressures may be only clues
NAP6 Grading (Ring & Messmer):
  • Grade I: Cutaneous only
  • Grade II: Mild systemic (hypotension + tachycardia + bronchospasm)
  • Grade III: Severe life-threatening (cardiovascular/respiratory collapse)
  • Grade IV: Cardiac arrest
Management:
  1. REMOVE TRIGGER (stop offending drug, remove latex)
  2. Epinephrine IM 0.5 mg (1:1000) - absolute first-line; IM into lateral thigh; repeat every 5 min if needed
    • IV epinephrine 0.1-1 mcg/kg/min infusion for severe/refractory cases
  3. Position: Supine with legs elevated (Trendelenburg); if airway compromise - semi-recumbent
  4. Airway: High-flow O₂; early intubation if airway edema (before it closes)
  5. IV fluids: Rapid bolus 1-2 L crystalloid (massive third-spacing)
  6. Antihistamines: Chlorphenamine 10 mg IV (H1 blocker) + ranitidine/famotidine (H2 blocker)
  7. Corticosteroids: Hydrocortisone 200 mg IV (prevents biphasic reaction; NOT acute emergency treatment)
  8. Bronchospasm: Salbutamol nebulization/IV; MgSO₄ if severe
  9. Vasopressors: Norepinephrine or vasopressin for refractory hypotension
  10. Glucagon: 1-5 mg IV if on beta-blockers (epinephrine-resistant anaphylaxis)
  11. Post-event: Serum tryptase at 1h, 4h, 24h; allergy/immunology referral

3C. NEUROGENIC SHOCK

Definition: Shock from loss of sympathetic tone below the level of a spinal cord injury (typically T6 and above), causing vasodilation and bradycardia without compensatory tachycardia.
Causes: High spinal cord injury, spinal anaesthesia (high spinal block), autonomic neuropathy
Differentiate from Spinal Shock: Spinal shock = loss of all spinal cord function (motor, sensory, reflexes) below injury - not the same as neurogenic shock.
Hemodynamics: ↓ SVR, ↓ HR (bradycardia - loss of cardiac accelerators T1-T4), ↓ CO → hypotension
Signs & Symptoms:
  • Hypotension + Bradycardia (classic triad differentiates from hypovolemic shock where tachycardia predominates)
  • Warm, dry skin (no vasoconstriction despite hypotension - paradoxical; no sweating below injury)
  • Neurological deficits (paraplegia/quadriplegia, sensory loss)
  • Priapism (males - loss of sympathetic inhibition)
  • Loss of temperature regulation (poikilothermia)
  • Absent reflexes below injury (flaccid paralysis acutely)
  • Diaphragmatic breathing only (if above C4)
Management:
  1. Airway/Immobilization: Cervical spine immobilization; intubation with inline stabilization if needed
  2. IV fluids: Cautious crystalloid (avoid over-hydration - pulmonary edema risk)
  3. Vasopressors:
    • Phenylephrine (pure alpha agonist) for hypotension without bradycardia
    • Norepinephrine (alpha + beta) if bradycardia present
    • Atropine 0.5-1 mg IV for symptomatic bradycardia
    • Dopamine as alternative
  4. MAP target: ≥85-90 mmHg for 7 days post-SCI (to optimize spinal cord perfusion - ASIA/ACS guidelines)
  5. Temperature regulation: Active warming (no shivering)
  6. Methylprednisolone: Controversial; no longer routinely recommended for acute SCI
  7. DVT prophylaxis (paralyzed limbs → high risk)
  8. Bladder/bowel management: Urinary catheter, bowel care

4. OBSTRUCTIVE SHOCK

Definition: Shock due to a mechanical obstruction to blood flow extrinsic to the heart, impairing ventricular filling or outflow, resulting in reduced CO.
Causes:
  • Impaired venous return (inflow obstruction):
    • Tension pneumothorax
    • Cardiac tamponade
    • Constrictive pericarditis
    • Severe positive-pressure ventilation (↑ intrathoracic pressure)
  • Outflow obstruction:
    • Massive pulmonary embolism
    • Severe pulmonary hypertension
    • Aortic dissection
    • Air embolism, fat embolism
Signs & Symptoms:
Cardiac Tamponade (Beck's Triad):
  • Muffled heart sounds
  • Elevated JVP (↑ CVP)
  • Hypotension
  • Pulsus paradoxus (>10 mmHg drop in SBP during inspiration)
  • Tachycardia
  • ECG: Electrical alternans, low voltage
  • Echo: Pericardial effusion, diastolic RV collapse
Tension Pneumothorax:
  • Respiratory distress, tachypnea
  • Absent breath sounds ipsilateral
  • Tracheal deviation (contralateral - late sign)
  • Hypotension, tachycardia, elevated JVP
  • Haemodynamic collapse (obstructive shock)
Massive Pulmonary Embolism:
  • Acute dyspnea, pleuritic chest pain, hemoptysis
  • Hypotension, tachycardia, tachypnea
  • Elevated JVP, signs of RV failure (right heart strain)
  • ECG: S1Q3T3 pattern, right heart strain, sinus tachycardia
  • Echo: dilated RV, D-sign (septal flattening)
  • CTPA: confirmatory
Management:
CauseImmediate Treatment
Tension PTXNeedle decompression (2nd ICS MCL) → chest drain
Cardiac TamponadePericardiocentesis (or surgical pericardial window)
Massive PESystemic thrombolysis (rtPA 100 mg over 2h), ± surgical embolectomy, catheter-directed therapy
Constrictive PericarditisPericardiectomy (surgical)
Air EmbolismLeft lateral Trendelenburg (Durant's maneuver), aspirate via CVP
  • All obstructive shock: IV fluids cautiously (increase preload to maintain CO), vasopressors (norepinephrine), O₂/intubation
  • Do NOT use vasodilators (worsen hypotension)
  • Inotropes for RV failure in massive PE (dobutamine)

V. MIXED SHOCK

Mixed shock occurs when a patient has more than one type simultaneously. Example:
  • Septic shock can involve distributive (vasodilation) + cardiogenic (sepsis-induced cardiomyopathy) + hypovolemic (third spacing) components
  • Harrison's 22e: "The types of shock are not mutually exclusive - not uncommonly a patient will present with more than one type"

VI. GENERAL PRINCIPLES OF SHOCK MANAGEMENT

Immediate Assessment (ABC)

  1. Airway: Secure patent airway; intubate if GCS <8 or respiratory failure
  2. Breathing: O₂ supplementation; mechanical ventilation if needed; treat tension PTX
  3. Circulation: IV access × 2 large bore; fluid bolus; assess hemodynamics
  4. Disability: GCS, pupils, glucose
  5. Exposure: Look for source, injuries, rashes, temperature

Monitoring in Shock

ParameterTarget
MAP≥65 mmHg (≥85-90 in neurogenic SCI)
Heart RateTrend toward normal (<100/min)
Urine Output≥0.5 mL/kg/h
Lactate<2 mmol/L; clearance >10%/2h
CVP8-12 mmHg (not reliable sole guide)
PCWP12-15 mmHg (cardiogenic: 15-18)
ScvO₂>70%
Arterial pH≥7.35

Diagnostic Evaluation

  • Lactate - marker of tissue hypoperfusion; serial measurement guides therapy
  • ABG - metabolic acidosis (pH, base deficit, lactate)
  • ECG - AMI, arrhythmia, PE (S1Q3T3), tamponade (electrical alternans)
  • CXR - pulmonary edema (cardiogenic), PTX, effusion, infiltrates (sepsis)
  • POCUS/Echo - most rapid bedside tool:
    • RUSH protocol (Rapid Ultrasound for Shock and Hypotension)
    • ACES protocol (Abdominal and Cardiothoracic Evaluation)
    • Assess LV/RV function, pericardial effusion, IVC collapsibility, PTX
  • CBC, BMP, coags, cultures, troponin, BNP, procalcitonin

Vasopressors and Inotropes Summary

DrugReceptorsUseKey Points
Norepinephrineα1>β11st line most shockVasoconstriction, mild inotropy
VasopressinV1R2nd line septic shockAdd to NE; 0.03 units/min; steroid-sparing
Epinephrineα+β1+β2Anaphylaxis (1st line), 3rd vasopressorBronchodilation, tachycardia, ↑ lactate
DopamineDA, β1, αAlternative vasopressorHigher arrhythmia risk vs NE
Dobutamineβ1>β2Cardiogenic shock low COInotrope/chronotrope, vasodilation
Phenylephrineα1Neurogenic, high-spinalPure vasopressor; no inotropy; bradycardia
MilrinonePDE-IIIPost-cardiac surgeryInodilator; avoid if hypotensive
LevosimendanTroponin CCardiogenic, post-cardiac surgeryNo ↑ myocardial O₂ consumption

VII. SHOCK IN ANAESTHESIA - SPECIAL CONSIDERATIONS

  1. Perioperative Anaphylaxis: Most common triggers: NMBAs (rocuronium > suxamethonium), latex, antibiotics (penicillin), colloids; NAP6 (UK audit) - 1:10,000 anaesthetics; management as above
  2. High Spinal/Epidural: Neurogenic shock - treat with ephedrine/phenylephrine; atropine for bradycardia; position supine + legs elevated
  3. Anaesthetic agents in shock: Ketamine preferred (sympathomimetic), etomidate (hemodynamically stable); reduce doses of propofol/thiopentone (vasodilatation worsens); volatile agents reduce SVR and CO - use with extreme caution
  4. Goal-Directed Therapy (GDT): Intraoperative optimization of DO₂ using fluid responsiveness (PLR, SVV, PPV) and targeted vasopressor/inotrope therapy - reduces postoperative morbidity
  5. Intraoperative monitoring: Invasive arterial line (gold standard for BP in shock), CVP, pulmonary artery catheter (selected cases), cardiac output monitoring (LiDCO, PiCCO, PAC)
  6. TEG/ROTEM: Guide coagulation management in hemorrhagic/traumatic shock
  7. Lethal Triad in Trauma: Hypothermia + Acidosis + Coagulopathy - break this cycle; DCR + DCS

VIII. ENDPOINTS OF RESUSCITATION

  • Lactate clearance (≥10% per 2 hours) is more reliable than static hemodynamic parameters
  • Normalization of base deficit (target BD > -6)
  • ScvO₂ >70% (or SvO₂ >65%)
  • Urine output ≥0.5 mL/kg/h
  • Normothermia, INR, and platelet count normalization in hemorrhagic shock

IX. COMPLICATIONS OF SHOCK

  • Acute Kidney Injury (AKI) - most common
  • ARDS - acute respiratory distress syndrome
  • MODS (Multiple Organ Dysfunction Syndrome)
  • DIC - especially septic and traumatic shock
  • Intestinal ischemia - bacterial translocation → further sepsis
  • Acute Liver Failure - "shock liver" (centrilobular necrosis)
  • Myocardial Ischemia - demand-supply mismatch
  • Adrenal Insufficiency - relative, in critical illness

SUMMARY TABLE

FeatureHypovolemicCardiogenicSepticAnaphylacticNeurogenicObstructive
HR↑↑↑↑↑↑↓ or N↑
BP↓↓↓↓↓↓
SVR↑↑↑↑↓↓↓↓↓↓↑
CO↓↓↓↓↑↑↓↓↓
CVP/JVP↓↑↓↓↓↑
SkinCold/clammyCold/clammyWarm/flushedFlushed/urticariaWarm/dryCold
1st RxFluids + control bleedInotropes + revascularizeAbx + fluids + NEEpinephrine IMNE/phenylephr.Treat cause
SCAI Cardiogenic Shock Classification Pyramid
SCAI staging of cardiogenic shock (A-E)
References (Authoritative Textbooks):
  • Harrison's Principles of Internal Medicine 22e (2025), Chapter 314-315 (Shock and Sepsis)
  • Miller's Anesthesia 10e, Chapter 75 (Shock)
  • Sabiston Textbook of Surgery - Chapter on Shock
  • Surviving Sepsis Campaign Guidelines 2021 (Evans L et al, Crit Care Med 2021)
  • Fuster & Hurst's The Heart 15e - Cardiogenic Shock Chapter
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