Shock - definition , classification, pathophysiology , sign and symptoms, investigation & management Recent guidelines for management of septic shock MD anaesthesia pg exam answer

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SHOCK

MD Anaesthesia PG Exam Answer

1. DEFINITION

Goldman-Cecil Medicine (22nd Ed.): Shock is an acute circulatory dysfunction that results in inadequate tissue perfusion - a medical emergency requiring prompt diagnosis and intervention to prevent circulatory collapse, multisystem organ failure, and death.

Miller's Anaesthesia (10th Ed.): Shock is the inability to provide adequate oxygen to the tissues that require it - a fundamental imbalance between oxygen delivery (DO₂) and oxygen demand (VO₂).

Key physiological principle:

O₂ Delivery (DO₂) = CO × CaO₂ × 10 = CO × (1.34 × Hb × SaO₂ + PaO₂ × 0.003) × 10
Normal DO₂ ≈ 1000 mL/min; Normal VO₂ ≈ 250 mL/min
When VO₂ becomes supply-dependent (i.e., falls below the critical DO₂ threshold), anaerobic metabolism and lactic acidosis ensue - this is the hallmark of shock.

2. CLASSIFICATION

Primary Classification (4 Types)

Type	Mechanism	CO	SVR	PCWP	Examples
Hypovolemic	Decreased preload/circulating volume	↓	↑	↓	Hemorrhage, burns, dehydration, vomiting, diarrhea
Cardiogenic	Pump failure (↓ contractility or obstruction)	↓	↑	↑	AMI, arrhythmia, myocarditis, valvular disease
Distributive	Loss of vasomotor tone / maldistribution	↑/N	↓↓	↓/N	Sepsis, anaphylaxis, neurogenic, adrenal insufficiency
Obstructive	Mechanical obstruction to flow	↓	↑	↑/↓	Tension pneumothorax, cardiac tamponade, massive PE

Sub-classification by Stage

Stage	Description	Key Features
Compensated (Stage I)	Normal BP maintained by neurohumoral mechanisms	Tachycardia, cool peripheries, anxiety, mild ↓ urine output
Decompensated (Stage II)	Compensatory mechanisms overwhelmed	Hypotension, oliguria, confusion, lactic acidosis
Irreversible (Stage III)	Cellular damage beyond recovery; MODS	Refractory hypotension, anuria, coma, DIC

ATLS Classification of Hemorrhagic Shock (Hypovolemic)

Class	Blood Loss (mL)	Blood Loss (%)	HR	BP	RR	Mental Status
I	<750	<15%	<100	Normal	14-20	Anxious
II	750-1500	15-30%	100-120	Normal	20-30	Mildly anxious
III	1500-2000	30-40%	120-140	↓	30-40	Confused
IV	>2000	>40%	>140	↓↓	>35	Lethargic/comatose

3. PATHOPHYSIOLOGY

A. Macrocirculatory Changes

Hypovolemic shock: Decreased circulating volume → ↓ venous return → ↓ preload → shift left on Frank-Starling curve → ↓ SV → ↓ CO → ↓ MAP. Compensatory sympathoadrenal activation → tachycardia, vasoconstriction (↑ SVR), venoconstriction (↑ venous return).

Cardiogenic shock: Primary pump failure → ↓ SV → ↓ CO → ↓ MAP. LV failure → ↑ LVEDP → pulmonary congestion. Baroreceptors trigger compensatory vasoconstriction → ↑ afterload → worsens LV failure (vicious cycle).

Distributive (Septic) shock: Inflammatory mediators (TNF-α, IL-1, IL-6, NO) → massive vasodilation → ↓ SVR → relative hypovolemia → ↑ CO (but ineffective). Capillary leak → absolute hypovolemia. Direct myocardial depression despite hyperdynamic state. Maldistribution of microvascular flow → cellular dysoxia even at normal DO₂.

Obstructive shock: Mechanical obstruction → prevents adequate cardiac filling or ejection → ↓ CO despite normal/elevated preload.

B. Microcirculatory & Cellular Changes

Sympathetic activation: Catecholamine release → vasoconstriction, tachycardia, redistribution of blood to vital organs (brain, heart); non-essential organs (gut, kidneys, skin) sacrificed
Neurohormonal: RAA activation → ↑ aldosterone, ADH → Na⁺ and water retention
Cellular hypoxia: Mitochondrial failure → shift to anaerobic glycolysis → lactic acidosis → ATP depletion
Reperfusion injury: Free radical generation, calcium influx, membrane pump failure
Inflammatory cascade: Complement, cytokines, PAF, arachidonic acid metabolites → endothelial injury, capillary leak
Coagulopathy: DIC triggered by tissue factor release, endothelial injury
MODS: Sequential organ failure - lungs (ARDS) → kidneys (AKI) → liver → gut (bacterial translocation) → brain

C. Oxygen Delivery-Consumption Relationship

Above critical DO₂ threshold: VO₂ is independent of DO₂ (adequate extraction compensates)
Below critical DO₂ threshold: VO₂ becomes supply-dependent → anaerobic metabolism
O₂ Extraction Ratio (O₂ER) = (CaO₂ - CvO₂) / CaO₂; normal 25-30%; can increase to 60-70% in shock

4. SIGNS AND SYMPTOMS

General (Common to All Shock Types)

System	Features
Cardiovascular	Tachycardia (>100/min), hypotension (SBP <90 or MAP <65 mmHg), weak/thready pulse, ↓ pulse pressure
Respiratory	Tachypnoea, Kussmaul breathing (metabolic acidosis compensation)
Skin	Cold, clammy, pale, mottled skin (except distributive - may be warm/flushed early)
Neurological	Altered sensorium, confusion, agitation → stupor → coma
Renal	Oliguria (<0.5 mL/kg/hr), rising creatinine
Metabolic	Lactic acidosis, high anion gap metabolic acidosis
GI	Nausea, vomiting, ileus, bowel ischemia

Distinguishing Features by Type

Feature	Hypovolemic	Cardiogenic	Distributive (Septic)	Obstructive
JVP	↓	↑	↓/N	↑ (tamponade, PE)
Extremities	Cold	Cold	Warm (early), cold (late)	Cold
Lung sounds	Clear	Crackles (APO)	Clear/crackles	Clear
History	Bleeding/dehydration	Chest pain, cardiac Hx	Fever, infection	Trauma, tachypnoea
Beck's triad	-	-	-	Tamponade only

5. INVESTIGATIONS

Immediate (Bedside)

ABG: pH, PaCO₂, PaO₂, lactate, HCO₃⁻, base excess - assess acid-base status, tissue perfusion
Serum lactate: >2 mmol/L indicates inadequate perfusion; >4 mmol/L = high mortality risk
Blood glucose: Hyperglycemia common in stress; hypoglycemia in adrenal crisis
ECG: Arrhythmia, MI (cardiogenic), right heart strain (PE), low voltages (tamponade)
Bedside ECHO (POCUS): Volume status, LV/RV function, tamponade, wall motion abnormalities

Laboratory

Test	Purpose
CBC	Hb/hematocrit (hemorrhage), leukocytosis/leukopenia (sepsis), platelets (DIC)
Coagulation (PT/APTT/INR/fibrinogen/D-dimer)	DIC, coagulopathy
Urea, Creatinine, Electrolytes	AKI, electrolyte disturbances
LFTs	Hepatic hypoperfusion ("shock liver")
Troponin, BNP/NT-proBNP	Myocardial injury, cardiogenic shock
Blood cultures (×2)	Before antibiotics in sepsis
Procalcitonin, CRP	Sepsis/infection markers
Serum cortisol	Adrenal insufficiency
Type and crossmatch	Pre-transfusion
Urine output monitoring	Renal perfusion (Foley catheter essential)

Imaging

CXR: Cardiomegaly, pulmonary oedema, pneumothorax, widened mediastinum
CT thorax/abdomen: Source of sepsis, aortic dissection, PE (CTPA), trauma
Echocardiography (TTE/TOE): Gold standard for cardiac function in ICU
FAST scan: Abdominal/pericardial fluid in trauma

Haemodynamic Monitoring

Invasive arterial line: Continuous BP, waveform analysis
Central venous catheter: CVP (limited utility alone), drug delivery
Pulmonary artery catheter (Swan-Ganz): PCWP, CO, SVR (now selective use)
Cardiac output monitoring: PiCCO, LiDCO, oesophageal Doppler
ScvO₂/SvO₂: Target ScvO₂ >70%; low = inadequate DO₂
Dynamic fluid responsiveness markers: Pulse pressure variation (PPV >13% = fluid responsive in ventilated patients), stroke volume variation (SVV)

6. MANAGEMENT - GENERAL PRINCIPLES

A. Initial Stabilisation (ABC)

Airway & Breathing:

High-flow O₂ via face mask (target SpO₂ 94-98%)
Intubation and mechanical ventilation if: GCS <8, respiratory failure, refractory shock
RSI with haemodynamically stable induction agents (e.g., ketamine preferred in shock)

Circulation:

Two large-bore IV cannulae (14-16G) or IO access
Intra-arterial line for continuous monitoring
CVC if vasopressors needed

B. Fluid Resuscitation

Crystalloids first line: Balanced crystalloids (Ringer's Lactate, Plasmalyte) preferred over 0.9% NaCl (avoids hyperchloraemic acidosis)
Initial bolus: 30 mL/kg IV crystalloid within first 3 hours (septic shock)
Reassess after each bolus: Dynamic markers (PPV, SVV, PLR test) guide further fluids
Avoid fluid overload: Serial lactate clearance guides adequacy; avoid indiscriminate boluses
Albumin: Consider when large volumes of crystalloid required (4% or 20%)
Avoid: Hetastarch (HES) - associated with AKI and increased mortality in sepsis

C. Vasopressors (for MAP <65 mmHg despite adequate volume)

Agent	First-line / Role	Dose
Norepinephrine	First-line vasopressor	0.05-0.5 mcg/kg/min IV infusion
Vasopressin	Add-on to NE; spares NE dose; 1st-line in vasodilatory shock	0.03-0.04 units/min
Epinephrine	Low CO + septic shock	0.05-0.5 mcg/kg/min
Dopamine	Avoid in most; consider bradycardic patients only	5-20 mcg/kg/min
Phenylephrine	Tachyarrhythmia with septic shock	0.5-5 mcg/kg/min
Dobutamine	Cardiogenic shock / low CO despite fluids	2.5-20 mcg/kg/min

Start vasopressors peripherally to avoid delays (SSC 2026 recommendation) while central access obtained
MAP target: 65 mmHg (60-65 mmHg in elderly ≥65 years)

D. Type-Specific Management

Hypovolemic/Hemorrhagic Shock:

1:1:1 damage control resuscitation: PRBCs : FFP : Platelets
Tranexamic acid within 3 hours of trauma (1g IV bolus + 1g over 8 hours)
Target Hb 7-9 g/dL (transfusion trigger Hb <7 g/dL in stable patients)
Permissive hypotension (MAP 50-65) until surgical haemostasis in penetrating trauma
Early surgical haemostasis / intervention

Cardiogenic Shock:

Intra-aortic balloon pump (IABP), Impella, ECMO (VA-ECMO)
Dobutamine or milrinone for inotropy
Early coronary revascularization (PCI) in STEMI with cardiogenic shock
Avoid aggressive fluids (worsens pulmonary oedema)

Distributive (Septic) Shock: (See Section 7 below)

Anaphylactic Shock:

Adrenaline 0.5 mg IM (1:1000) immediately
IM preferred over IV (except cardiac arrest)
Antihistamines (chlorpheniramine) + corticosteroids (hydrocortisone) adjuncts
IV fluids, bronchodilators (salbutamol nebulisation)

Obstructive Shock:

Tension pneumothorax: Immediate needle decompression (2nd ICS MCL) → chest drain
Cardiac tamponade: Pericardiocentesis or surgical pericardial window
Massive PE: Systemic thrombolysis (alteplase 100mg IV) or catheter-directed thrombolysis / surgical embolectomy

E. General Supportive ICU Care

Ventilation (if intubated): Lung-protective (TV 6 mL/kg IBW, plateau pressure <30 cmH₂O, PEEP 5-10 cmH₂O)
Blood glucose: Target 140-180 mg/dL; insulin infusion if >180 mg/dL
Blood transfusion: Restrictive strategy, Hb trigger <7 g/dL (stable), <8 g/dL (cardiac)
VTE prophylaxis: LMWH preferred over UFH (unless contraindicated)
Stress ulcer prophylaxis: PPI or H₂ blocker in ventilated/coagulopathic patients
Nutritional support: Early (within 72h) enteral nutrition when haemodynamically stable
Sodium bicarbonate: Only if pH ≤7.2 + AKI (AKIN stage 2-3)

7. SEPTIC SHOCK - RECENT GUIDELINES (SSC 2026 + S3 2025)

Definition (Sepsis-3, JAMA 2016 - still current)

Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA score ≥2)
Septic shock: Subset of sepsis with circulatory, cellular, and metabolic abnormalities profound enough to substantially increase mortality, clinically defined as:
- Persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg, AND
- Serum lactate >2 mmol/L despite adequate fluid resuscitation
- Hospital mortality >40%

SSC 2026 Key Updates (Prescott et al., Crit Care Med 2026)

The 2026 guidelines include 129 statements (46 new); co-published March 2026 with broad global representation (23 countries).

A. Screening & Diagnosis

Screen ALL hospitalized patients for sepsis using validated tools
Obtain blood cultures (≥2 sets) before antibiotics whenever possible (without delaying antibiotics)
Measure serum lactate - guide resuscitation; repeat if initial lactate >2 mmol/L

B. Antimicrobial Therapy (URGENT)

Recommendation	Evidence
Administer antimicrobials immediately (within 1 hr) of recognition of septic shock	Strong
Use empiric broad-spectrum antibiotics covering all likely pathogens initially	Strong
Reassess/de-escalate based on cultures + clinical improvement (stewardship)	Strong
Do NOT use procalcitonin alone to start antibiotics (may use to stop/shorten course)	Conditional
Source control within 6-12 hours (drain abscesses, remove infected devices)	Strong

C. Fluid Resuscitation

Recommendation	Evidence
Crystalloids first-line; balanced crystalloids over 0.9% saline	Strong
Initial bolus: 30 mL/kg IV crystalloid in first 3 hours	Conditional
Start crystalloid bolus followed by vasopressors if hypotension persists	Conditional
Consider albumin addition when large crystalloid volumes required	Conditional
Do NOT use HES (hydroxyethyl starch)	Strong
Use dynamic measures (PPV, PLR) to guide further fluids - avoid over-resuscitation	Conditional
Active fluid removal (diuresis/ultrafiltration) once patient stabilized and hemodynamics improved	Conditional (NEW 2026)

D. Vasopressors

Recommendation	Evidence
Norepinephrine - first-line vasopressor	Strong
MAP target 65 mmHg	Strong (Moderate)
For elderly ≥65 yrs: MAP target 60-65 mmHg (not higher)	Conditional (NEW)
Start vasopressors peripherally to restore MAP - don't delay for central line	Conditional
Add vasopressin (0.03 units/min) to norepinephrine to achieve MAP target or reduce NE dose	Conditional
Consider epinephrine if MAP target not achieved with NE + vasopressin	Conditional
Avoid dopamine (except selected bradycardic patients)	Strong
Avoid terlipressin as vasopressor	Strong

E. Corticosteroids (2024 Focused Update + 2026)

Recommendation	Evidence
Hydrocortisone 200 mg/day IV (50 mg q6h or continuous infusion) if shock persists despite adequate fluids + vasopressors	Conditional FOR
Do NOT use high-dose/short-course corticosteroids (e.g., methylprednisolone pulse)	Strong AGAINST

F. Monitoring & Resuscitation Targets

Parameter	Target
MAP	≥65 mmHg (60-65 in elderly)
Serum lactate	Normalize (lactate clearance ≥10% per 2 hours)
ScvO₂	≥70%
Urine output	≥0.5 mL/kg/hr
Blood glucose	140-180 mg/dL (insulin if >180)
ICU admission	Within 6 hours of diagnosis
Sodium bicarbonate	Only if pH ≤7.2 + AKI AKIN stage 2-3

G. Mechanical Ventilation in Sepsis-Induced ARDS

Lung-protective: TV 6 mL/kg IBW, plateau pressure ≤30 cmH₂O
Prone positioning ≥12 hours/day for moderate-severe ARDS
PEEP titrated to oxygenation; avoid aggressive weaning
Head of bed elevation 30-45°
Avoid routine PA catheters
ECMO (VV) as rescue in refractory ARDS if experienced team available

H. Additional SSC 2026 Updates (NEW)

Domain	New Recommendation
Enteral nutrition	Early (within 72h) enteral nutrition in mechanically ventilated patients
VTE prophylaxis	LMWH preferred over UFH (Strong)
Transfusion	Restrictive strategy (Hb trigger 7 g/dL)
Post-sepsis care	12 new recommendations on structured follow-up, medication reconciliation at discharge, screening for economic/social needs
Goals of care	Discuss prognosis and integrate palliative care principles when appropriate

8. HAEMODYNAMIC PROFILES SUMMARY (Quick Revision)

Parameter	Hypovolemic	Cardiogenic	Septic	Obstructive (Tamponade)
CO/CI	↓	↓↓	↑ (early) / ↓ (late)	↓
SVR	↑	↑↑	↓↓	↑
CVP/PCWP	↓	↑	↓/N	↑
SvO₂	↓	↓	↑ (maldistribution)	↓
Pulse pressure	↓	↓	↑ (early)	↓ (pulsus paradoxus)

References

Goldman-Cecil Medicine, 22nd Ed. (2025) - Chapter 92: Approach to the Patient with Shock
Miller's Anaesthesia, 10th Ed. - Classification and Pathophysiology of Shock
Barash's Clinical Anaesthesia, 9th Ed. - Table 57-4: Management of Sepsis and Septic Shock
SSC 2026: Prescott et al. Crit Care Med 2026 - Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026
S3 Guideline 2025 (Brunkhorst et al., Med Klin Intensivmed Notfmed, 2025) [PMID: 40824313] - German S3 guideline update targeting SSC 2021 adaptations
Sepsis-3 Definitions: Singer M, Deutschman CS et al. JAMA 2016;315(8):801-810

Exam Tip for MD Anaesthesia: Key differentiators examiners look for - (1) oxygen delivery equation and the critical DO₂ concept, (2) haemodynamic profiles across shock types, (3) ATLS haemorrhagic shock classes, (4) SSC 2026 - peripheral vasopressor initiation, MAP 65 vs. 60-65 in elderly, active fluid removal in de-escalation phase, and the strong recommendation AGAINST high-dose pulse corticosteroids. The Sepsis-3 clinical definition of septic shock (MAP <65 + lactate >2 despite resuscitation) is non-negotiable in any examiner's question.

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