Critical Care & Anaesthesiology — Model Q&A
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CRITICAL CARE ANAESTHESIOLOGY — COMPREHENSIVE MODEL ANSWERS
Sepsis, Septic Shock and Shock — Complete Guide (Definitions • Pathophysiology • Diagnosis • SSC 2025 Guidelines • All Types of Shock • Evidence-Based Protocols)
Define Sepsis and Septic Shock. Describe the pathophysiology of sepsis highlighting key features. Discuss the diagnosis and management according to latest 2025 guidelines.
Sepsis is no longer simply "infection + SIRS criteria" — the landmark SEPSIS-3 consensus (Singer et al., JAMA 2016) redefined it as a SYNDROME OF LIFE-THREATENING ORGAN DYSFUNCTION caused by a DYSREGULATED HOST RESPONSE to infection. This paradigm shift — from an inflammation-centric to an organ-dysfunction-centric view — underpins every aspect of modern diagnosis and management. The Surviving Sepsis Campaign (SSC) 2025 Guidelines build on the 2021 framework, incorporating the latest evidence on fluid resuscitation, vasopressor selection, antibiotic stewardship, metabolic control, and adjunctive therapies.
1 Definitions (Sepsis-3 Consensus, JAMA 2016)
| Term | Formal Definition | Operational Criteria | Significance |
|---|---|---|---|
| INFECTION | Pathological process caused by invasion of normally sterile tissue, fluid, or body cavity by pathogenic microorganisms. | Clinical suspicion + supporting microbiological or radiological evidence. | The prerequisite for ALL sepsis definitions — without infection, organ dysfunction is not sepsis. |
| SEPSIS | "Life-threatening organ dysfunction caused by a dysregulated host response to infection" (Sepsis-3). | SOFA score ≥2 from baseline, attributable to infection. (In non-ICU, qSOFA ≥2 serves as screening). | Replaces SIRS definition. SOFA captures true organ-level consequences and mortality risk. |
| SEPTIC SHOCK | "Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to increase mortality." | Sepsis + (1) Vasopressor requirement for MAP ≥65 mmHg AND (2) Serum Lactate >2 mmol/L despite fluid resuscitation. | Identifies highest risk patients (mortality ~40%). Lactate criterion identifies cellular hypoxia/metabolic failure. |
format_list_numbered SOFA Score — Sequential (Sepsis-related) Organ Failure Assessment
| System | Score 0 | Score 1 | Score 2 | Score 3 | Score 4 |
|---|---|---|---|---|---|
| Respiratory (PaO₂/FiO₂) | >400 | 300–400 | 200–300 | 100–200 + MV | <100 + MV |
| Coagulation (Platelets ×10³/μL) | >150 | 100–150 | 50–100 | 20–50 | <20 |
| Liver (Bilirubin μmol/L) | <20 | 20–32 | 33–101 | 102–204 | >204 |
| Cardiovascular (MAP/Vasopressors) | MAP ≥70 | MAP <70 | Dopamine ≤5 | Dopamine 5.1–15 / NE ≤0.1 | Dopamine >15 / NE >0.1 |
| CNS (GCS) | 15 | 13–14 | 10–12 | 6–9 | <6 |
| Renal (Creatinine μmol/L) | <110 | 110–170 | 171–299 | 300–440 / UO <0.5 | >440 / UO <0.3 |
* SOFA ≥2 indicates confirmed organ dysfunction; each additional point adds ~10% mortality risk.
2 Pathophysiology of Sepsis — Key Features
| Pathophysiological Feature | Mechanism | Clinical Consequence |
|---|---|---|
| A. Innate Immune Activation & Cytokine Storm | PAMPs (LPS, peptidoglycan) bind PRRs (TLR-4) on macrophages → NF-κB activation → massive transcription of TNF-α, IL-1β, IL-6, IL-8. | Systemic vasodilation, capillary leak, fever, acute phase reactants (CRP, procalcitonin). Late phase causes CARS & immunoparalysis. |
| B. Endothelial Dysfunction & Microvascular Failure | Shedding of endothelial glycocalyx gel layer → massive protein-rich fluid leak into interstitium. iNOS upregulation → Nitric Oxide → profound vasodilation. | Distributive shock (low SVR), generalized edema, intravascular volume depletion, and microvascular thrombosis (DIC). |
| C. Cytopathic Hypoxia & Mitochondrial Dysfunction | NO and ROS directly inhibit Complex I & IV of mitochondrial electron transport chain. Cells cannot utilize O₂ despite normal delivery. | Lactate accumulation due to anaerobic glycolysis. Organ failure occurs at metabolic level ("cytopathic hypoxia"). |
| D. Organ-Specific Dysfunction | SA-AKI (tubular cell injury), SICM (sepsis cardiomyopathy from TNF-α), SA-ARDS (alveolar capillary leak), SAE (encephalopathy from BBB leak). | Multiorgan dysfunction syndrome (MODS), acute kidney injury requiring CRRT, mechanical ventilation dependency. |
3 Management — 2025 Surviving Sepsis Campaign (SSC) Guidelines
timer SSC Hour-1 Resuscitation Bundle
Define Shock. Classify all types of shock. For each type, describe the key features, pathophysiology, diagnosis, and management in detail.
Shock is a state of acute circulatory failure with inadequate tissue perfusion resulting in generalized cellular hypoxia (Vincent JL, NEJM 2013). Oxygen delivery equation: DO₂ = CO × CaO₂. Shock occurs when DO₂ falls below critical threshold (~330 mL/min/m²) or when cellular metabolism fails to utilize delivered O₂, leading to anaerobic glycolysis and lactate accumulation.
1 Mechanistic Classification of Shock Types
| Shock Type | Primary Mechanism | Cardiac Output (CO) | SVR | PCWP / Preload | ScvO₂ |
|---|---|---|---|---|---|
| 1. Distributive (Septic, Anaphylactic, Neurogenic) | Profound vasodilation (↓↓SVR); maldistribution of blood flow. | ↑ High (hyperdynamic) | ↓↓ Very Low | Low / Normal | ↑ High / Normal (impaired extraction) |
| 2. Hypovolaemic (Haemorrhagic, Dehydration) | Severe intravascular volume depletion (↓Preload). | ↓ Low | ↑↑ High (compensatory) | ↓↓ Very Low | ↓ Low (increased extraction) |
| 3. Cardiogenic (MI, Heart Failure, SICM) | Primary myocardial pump failure. | ↓↓ Very Low | ↑↑ High (compensatory) | ↑↑ High (>18 mmHg) | ↓ Low |
| 4. Obstructive (Tamponade, Massive PE, Tension PTX) | Physical obstruction to cardiac filling or outflow. | ↓↓ Very Low | ↑↑ High | ↑ Elevated (Tamponade) / ↓ (PE) | ↓ Low |
2 ATLS Classification of Haemorrhagic Shock (70 kg Adult)
| Parameter | Class I (<15%, <750 mL) | Class II (15–30%, 750–1500 mL) | Class III (30–40%, 1500–2000 mL) | Class IV (>40%, >2000 mL) |
|---|---|---|---|---|
| Heart Rate (bpm) | <100 | 100–120 | 120–140 | >140 |
| Blood Pressure | Normal | Normal / ↓ | ↓↓ Decreased | ↓↓↓ Severely Low |
| Urine Output | >30 mL/hr | 20–30 mL/hr | 5–15 mL/hr | Negligible |
| Fluid Resuscitation | Crystalloid ± Blood | Crystalloid + Blood | Urgent Blood + MTP | Massive Transfusion (1:1:1) |
Viva Corner — Top Examiner Questions & Exam Pearls
Frequently asked in DNB & MD Anaesthesiology Viva / OSCE Stations
help Q. A patient has suspected sepsis with SOFA ≥2 but has a lactate of 1.8 mmol/L and MAP of 70 mmHg on no vasopressors. Does this patient have septic shock?
NO — By Sepsis-3 definition, septic shock requires BOTH (1) vasopressor requirement to maintain MAP ≥65 mmHg AND (2) serum lactate >2 mmol/L despite fluid resuscitation. This patient meets neither. They have SEPSIS (SOFA ≥2 + infection). They should receive the Hour-1 bundle and close monitoring.
help Q. Why does a patient with septic shock have a HIGH cardiac output but still have tissue hypoxia (elevated lactate)?
This is due to DISTRIBUTIVE SHOCK and CYTOPATHIC HYPOXIA. High CO reflects the hyperdynamic state due to vasodilation. However, microvascular flow is maldistributed (functional AV shunting), and mitochondrial electron transport chain (Complex I/IV) is inhibited by Nitric Oxide, preventing cells from using O₂.
SEPSIS-3: Sepsis = organ dysfunction (SOFA ≥2). Septic shock = vasopressor + lactate >2. SSC 2025: Hour-1 Bundle (Lactate, Cultures, 1h Antibiotics, 30 mL/kg Balanced Crystalloid, Norepinephrine MAP ≥65). Corticosteroids: Hydrocortisone 200 mg/day ONLY in vasopressor-refractory shock. Glucose: 7.8–10 mmol/L (NICE-SUGAR). ARDS: TV 6 mL/kg, Prone >16h if PaO₂/FiO₂ <150 (PROSEVA NNT 6).
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