---

SHOCK - Complete Review

---

PART A: DEFINITION & CLASSIFICATION OF SHOCK

Definition

• CaO2 = (Hb × 1.34 × SaO2) + (PaO2 × 0.003)

---

Classification of Shock

---

---

PART B: HYPOVOLAEMIC SHOCK (Haemorrhagic Shock ★★★★)

Definition

• Haemorrhagic (most common): Trauma, GI bleeding, ruptured ectopic pregnancy, ruptured AAA
• Non-haemorrhagic: Vomiting, diarrhoea, burns, polyuria (DKA, DI), third-spacing (bowel obstruction, pancreatitis, burns)

---

ATLS Classification of Haemorrhagic Shock (4 Classes)

Key memory points: BP drops only in Class III/IV. Pulse pressure narrows from Class II. Urine output is the most sensitive early indicator of organ hypoperfusion.

---

Pathophysiology of Hypovolaemic/Haemorrhagic Shock

1. Initiating Event

2. Compensatory Phase (Neuroendocrine Response)

• Baroreceptors in the aortic arch, carotid bodies, and atria detect the fall in pressure.
• Inhibition of parasympathetic discharge + stimulation of sympathetic outflow.
• Release of norepinephrine and epinephrine → activation of adrenergic receptors on myocardium and vascular smooth muscle.
• Result: ↑HR, ↑contractility, ↑peripheral vascular resistance → attempted restoration of BP.
• Blood is selectively shunted AWAY from skin, skeletal muscle, and splanchnic circulation TOWARD brain, heart, and kidneys.

• Renal juxtaglomerular apparatus detects ↓ renal perfusion → secretes renin.
• Renin converts angiotensinogen → angiotensin I → (pulmonary ACE) → angiotensin II.
• Angiotensin II: vasoconstriction + stimulates adrenal medulla (catecholamine release) + stimulates adrenal cortex zona glomerulosa to release aldosterone.
• Aldosterone → ↑renal Na+ reabsorption (↑K+ excretion) → ↑water retention → ↑intravascular volume.

• Carotid baroreceptors signal hypothalamus (supraoptic & paraventricular nuclei).
• ADH released from posterior pituitary → free water retention at kidney collecting ducts.
• Also recruits extravascular and intracellular fluid into the vascular compartment.

• Fall in capillary hydrostatic pressure (precapillary sphincters constrict more than postcapillary) → net movement of interstitial fluid into capillaries (transcapillary refill).

• Catecholamine release → hepatic glycogenolysis → elevated glucose (early warning sign of hemodynamic instability).

3. Cellular/Metabolic Effects

• Cells switch from aerobic to anaerobic metabolism → lactic acid production → metabolic acidosis (high anion gap).
• ↓ATP production → failure of Na+/K+-ATPase pump → cellular swelling.
• Ischaemia-reperfusion → free radical generation and inflammatory cascade activation.

4. The "Lethal Triad"

5. Progression to Irreversible Shock

• Renal failure (ATN from ischaemia)
• ARDS (lung capillary leak + inflammation)
• Gut ischaemia → bacterial translocation → secondary sepsis
• Hepatic failure, DIC

---

Clinical Features (C/F) of Hypovolaemic Shock

• Thirst, anxiety, restlessness
• Dizziness, syncope (postural)
• Cold, clammy skin
• Oliguria/anuria
• Confusion, altered sensorium (late)

---

Investigations

• Pulse oximetry, continuous ECG monitoring, urinary catheter (hourly urine output)
• Blood glucose

• FBC/CBC: Haemoglobin, haematocrit (may be normal initially - dilutional fall takes hours)
• Blood group & crossmatch - urgent
• Coagulation profile: PT, aPTT, INR, fibrinogen, D-dimer (for DIC)
• Serum electrolytes: Na+, K+, Cl-, HCO3-
• Urea & Creatinine: Assess renal function
• Liver function tests
• Blood cultures (if septic component suspected)

• Arterial Blood Gas (ABG): pH, PaCO2, HCO3-, base excess (base deficit >-6 = significant shock); lactate
• Serum lactate: Best marker of tissue hypoperfusion - >4 mmol/L = severe shock, high mortality
• Base excess: Correlates with severity of haemorrhage

• CXR, FAST ultrasound (Focused Assessment with Sonography in Trauma)
• CT scan (haemodynamically stable patients only)
• eFAST for pneumothorax/haemothorax

• CVP (central venous pressure)
• Arterial line for continuous BP monitoring
• Pulmonary artery catheter (Swan-Ganz) in refractory cases
• Point-of-care coagulation (TEG/ROTEM in massive haemorrhage)

---

Management of Hypovolaemic/Haemorrhagic Shock

Step 1: Immediate Resuscitation (ABC approach)

• Apply direct pressure to external bleeding wounds
• IV access: Two large-bore (14-16G) peripheral cannulae
• Send bloods (FBC, U&E, LFTs, coagulation, crossmatch, ABG, lactate)
• Fluid warming to prevent hypothermia

Step 2: Fluid Resuscitation

• Initiate with 1-2L of crystalloid (warm Ringer's lactate or Hartmann's solution)
• Balanced crystalloids (Ringer's lactate, PlasmaLyte) preferred over normal saline - lower chloride load reduces risk of hyperchloraemic acidosis
• Normal saline acceptable but large volumes cause hyperchloraemic metabolic acidosis
• Avoid hetastarch/HES - associated with worse outcomes (renal failure, increased mortality)

• Packed red blood cells (PRBC): Target Hb ≥7-8 g/dL
• Fresh Frozen Plasma (FFP): Replaces clotting factors; target INR <1.5
• Platelets: Target >50,000/mm3 (>100,000 in CNS injury)
• Massive Transfusion Protocol (MTP): PRBC:FFP:Platelets in ratio of 1:1:1 - improves survival in massive haemorrhage
• Tranexamic acid (TXA): 1g IV loading dose within 3 hours of injury - reduces mortality in traumatic haemorrhage (CRASH-2 trial). Additional 1g IV over 8 hours.
• Cryoprecipitate: For fibrinogen <1.5 g/L

• In penetrating trauma without TBI: target SBP 80-90 mmHg until surgical haemorrhage control.
• Avoids "popping the clot" and dilutional coagulopathy.
• Target MAP >65 mmHg once haemorrhage controlled.

Step 3: Vasopressors

• Norepinephrine (first-line): α1 and β1 activity, maintains MAP
• Dopamine (second-line)

Step 4: Source Control (Definitive)

• Surgical haemorrhage control in trauma (damage control surgery)
• Endoscopy/intervention for GI bleeding
• Embolization for pelvic/hepatic bleeding
• Correction of fractures, tourniquet for limb haemorrhage

Step 5: Monitoring Endpoints of Resuscitation

---

---

PART B (OR): SEPTIC SHOCK ★★★★

Definition (Sepsis-3, 2016)

• Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection (SOFA score increase ≥2 from baseline).
• Septic Shock: A subset of sepsis with persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate volume resuscitation. Mortality ~40%.

• Temperature >38°C or <36°C
• HR >90 bpm
• RR >20/min or PaCO2 <32 mmHg
• WBC >12,000 or <4,000 cells/μL or >10% bands

• Altered mental status
• RR ≥22/min
• SBP ≤100 mmHg (≥2 criteria = high risk, investigate for sepsis)

---

Pathophysiology of Septic Shock

1. Trigger & Microbial Factors

• Any microorganism can trigger septic shock (no organism identified in ≥50% of cases).
• Gram-negative bacteria: Lipopolysaccharide (LPS/endotoxin) in outer membrane is a classic trigger - activates TLR-4 on macrophages.
• Gram-positive bacteria (now leading cause in hospitalised patients): cell wall components (peptidoglycan, teichoic acid) trigger via TLR-2.
• Fungi, viruses also implicated.

2. Systemic Inflammatory Response

• TNF-α and IL-1β (primary mediators): cause fever, vasodilation, myocardial depression
• IL-6, IL-8, IL-12: amplify inflammation
• Activation of complement system, coagulation cascade
• Endothelial activation → upregulation of adhesion molecules → neutrophil margination and tissue infiltration

3. Three Primary Hemodynamic/Physiologic Effects

• Absolute: GI fluid losses, sweating, tachypnoea, decreased intake
• Relative: Massive vasodilation (↓SVR) → venous pooling; increased venous capacitance
• Markedly increased capillary permeability → fluid leak into third spaces (interstitium)

• Direct myocardial depression by TNF-α, IL-1β
• Inducible nitric oxide synthase (iNOS) → excess nitric oxide (NO) production → vasodilation + direct myocardial toxicity
• Impaired mitochondrial oxidative phosphorylation → cellular energy failure
• Echocardiography shows impaired global longitudinal strain even before reduction in EF

• Maldistribution of blood flow at microvascular level
• Arteriovenous shunting → cells receive blood but cannot extract O2 ("cytopathic hypoxia")
• Mitochondrial dysfunction → impaired O2 utilization despite adequate delivery
• Results in high ScvO2 paradoxically in late septic shock
• Widespread endothelial damage → DIC, ARDS, AKI, hepatic failure

4. Phases of Septic Shock

---

Clinical Features (C/F) of Septic Shock

• Known/suspected source of infection (UTI, pneumonia, abdominal, wound, line)
• Fever, rigors, malaise
• Altered sensorium, confusion

• Fever (or hypothermia in severe/elderly)
• Warm, flushed skin
• Bounding, fast pulse; tachycardia
• Hypotension (SBP <90 mmHg or MAP <65 mmHg)
• Wide pulse pressure initially
• Hyperventilation (compensatory respiratory alkalosis)

• Cold, clammy, mottled skin
• Absent peripheral pulses
• Oliguria → anuria
• Confusion → stupor → coma
• Features of multi-organ failure (jaundice, haematuria, ARDS)

• Respiratory: ARDS - bilateral infiltrates, PaO2/FiO2 <200
• Renal: Rising creatinine, oliguria
• Hepatic: Jaundice, raised transaminases
• CNS: Encephalopathy, delirium
• Haematological: Thrombocytopaenia, DIC

---

Management of Septic Shock

"Hour-1 Bundle" (Sepsis Bundle - complete within 1 hour)

1. Measure serum lactate - if >2 mmol/L, high risk; re-measure if initial >2 mmol/L
2. Obtain blood cultures (at least 2 sets) BEFORE antibiotics if not significantly delayed
3. Administer broad-spectrum IV antibiotics (within 1 hour of recognition)
4. IV fluid resuscitation: ≥30 mL/kg crystalloid IV within 1 hour for hypotension OR lactate ≥4 mmol/L
5. Vasopressors if hypotension persists despite fluids - maintain MAP ≥65 mmHg

A. Resuscitation

• 30 mL/kg IV crystalloid (IBW) within first hour
• Balanced crystalloids (Ringer's lactate/PlasmaLyte) preferred over normal saline - associated with lower renal dysfunction and improved mortality
• Albumin: NOT superior to crystalloid; not routinely recommended
• Reassess volume responsiveness continuously (avoid overload)

• Norepinephrine - FIRST LINE: α1 + β1 activity, potent vasoconstriction; superior to dopamine (fewer arrhythmias)
• Vasopressin - SECOND LINE: adjunct to norepinephrine; potential benefit in less severe septic shock (NE dose 5-14 μg/min)
• Epinephrine - third-line or for refractory shock; can be added to norepinephrine
• Dopamine: Use only in selected patients (bradycardia, low arrhythmia risk); more adverse events than NE
• Angiotensin II: Investigational; raises MAP in vasodilatory shock via RAAS

• Dobutamine: Add if myocardial dysfunction with persistent hypoperfusion despite adequate preload and MAP; increases CO but risk of arrhythmias

• MAP ≥65 mmHg
• Urine output ≥0.5 mL/kg/hr
• Lactate normalization (clearance target: >10% decrease per 2 hours)
• ScvO2 ≥70% (SvO2 ≥65%)

B. Antimicrobials

• Start within 1 hour of recognition - each hour of delay increases mortality
• Empiric broad-spectrum antibiotics covering likely organisms based on source:
  • Community-acquired: 3rd/4th gen cephalosporin + metronidazole, or piperacillin-tazobactam
  • Hospital/ICU: Meropenem/imipenem ± antifungal (fluconazole/echinocandin) if Candida risk
  • Suspected MRSA: Add vancomycin/linezolid
• De-escalate based on cultures/sensitivities (antibiotic stewardship)
• Duration: Typically 7-10 days; use procalcitonin to guide de-escalation

C. Source Control

• Identify and remove/drain infectious source as soon as possible
• Remove infected lines/catheters
• Drain abscesses, debride necrotizing infections
• Operative intervention for perforation, ischaemic bowel, necrotizing fasciitis

D. Adjunctive Therapies

• Hydrocortisone 200 mg/day IV infusion (50 mg q6h or 200 mg continuous infusion)
• Indicated in septic shock refractory to fluid resuscitation AND vasopressors
• Not for patients who are adequately responding to fluids/vasopressors
• Mechanism: Relative adrenal insufficiency is common in septic shock; steroids restore vascular responsiveness

• Target Hb ≥7 g/dL in septic shock (restrictive strategy)
• No benefit of transfusing to Hct of 30% (original EGDT target) - abandoned

• Target blood glucose 140-180 mg/dL (7.8-10 mmol/L)
• Avoid hypoglycaemia - more harmful than moderate hyperglycaemia

E. Organ Support

• Mechanical ventilation if ARDS: Lung protective strategy (tidal volume 6 mL/kg IBW, plateau pressure <30 cmH2O, PEEP)
• Renal replacement therapy (RRT): CRRT for AKI with severe oliguria, acidosis, or fluid overload
• Prone positioning for severe ARDS (PaO2/FiO2 <150)

---

Summary: Comparison - Hypovolaemic vs Septic Shock

---

• Bailey & Love's Short Practice of Surgery, 28e
• Harrison's Principles of Internal Medicine, 22E
• Sabiston Textbook of Surgery (Biological Basis of Modern Surgical Practice)
• Rosen's Emergency Medicine (Concepts and Clinical Practice)
• The Washington Manual of Medical Therapeutics
• Goldman-Cecil Medicine, International Edition