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Haemorrhagic (Hypovolaemic) Shock - Complete Notes

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1. Causes in Case of an Accident (Trauma)

• Scalp lacerations (highly vascular; can lose >500 mL)
• Limb amputations or major vessel lacerations
• Open fractures

• Chest (haemothorax): Rib fractures, aortic or great vessel injury - up to 2-3 L can accumulate
• Abdomen (haemoperitoneum): Splenic laceration (most common solid organ injury), hepatic injury, mesenteric vessel tears, bowel injury
• Pelvis: Pelvic ring fractures - can accommodate 3-4 L of blood; associated with massive venous plexus bleeding
• Long bone fractures: Femur fracture - approximately 1-1.5 L; tibia - 0.5 L; each humerus - 0.3 L
• Retroperitoneum: Aortic or vena cava injury

• Tension pneumothorax (obstructive component)
• Cardiac tamponade (haemopericardium from penetrating injury)
• Spinal cord injury (superimposed neurogenic shock)
• Burns (plasma loss, not blood loss - hypovolaemic but not haemorrhagic)

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2. Stages of Haemorrhagic Shock

ATLS Classification (by volume of blood loss)

Note: The ATLS thresholds are recognised as somewhat arbitrary. Children compensate more effectively (higher cardiac reserve) and decompensate suddenly. Elderly patients decompensate at lower volumes due to reduced cardiac reserve and baseline use of beta-blockers/antihypertensives.

Pathophysiological Stages (Robbins & Kumar)

1. Nonprogressive (Compensated) Stage
   • Reflex compensatory mechanisms activated
   • Vital organ perfusion is maintained
   • Reversible with correction of cause
2. Progressive Stage
   • Compensatory mechanisms overwhelmed
   • Widespread tissue hypoperfusion
   • Anaerobic glycolysis → lactic acidosis → metabolic acidosis
   • Arteriolar dilation, microvascular pooling
   • Risk of DIC from endothelial injury
   • Vital organs (kidney, gut, brain, heart) begin to fail
3. Irreversible Stage
   • Cellular injury so profound that survival is impossible even if haemodynamics are corrected
   • Lysosomal enzyme leakage worsens shock
   • Myocardial contractility deteriorates (↑ nitric oxide synthesis)
   • Ischaemic gut allows translocation of intestinal bacteria → superimposed septic shock
   • Acute kidney injury from ischaemia
   • Death from multiple organ failure

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3. Compensatory Responses in the Nonprogressive (Compensated) Stage

Overview of Compensatory Mechanisms

• Venous return → ↓ preload → ↓ cardiac output → ↓ blood pressure
• Renal perfusion pressure
• Oxygen delivery to tissues

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A. BARORECEPTOR REFLEX - Flowchart

HAEMORRHAGE / BLOOD LOSS
        |
        ↓
↓ Mean Arterial Pressure (MAP) + ↓ Cardiac Output
        |
        ↓
AORTIC ARCH & CAROTID SINUS BARORECEPTORS
(mechanoreceptors detect ↓ wall stretch)
        |
        ↓
↓ Inhibitory afferent signals to cardiovascular centre
(↓ firing of glossopharyngeal CN IX and vagus CN X)
        |
        ↓
MEDULLARY CARDIOVASCULAR CENTRES ACTIVATED
(vasomotor centre + cardioacceleratory centre)
        |
    ____↓____
   |         |
   ↓         ↓
SYMPATHETIC    PARASYMPATHETIC
ACTIVATION     WITHDRAWAL
(↑ noradrenaline)   (↓ vagal tone)
   |         |
   ↓         ↓
• Tachycardia       • Further tachycardia
• ↑ Myocardial contractility
• Peripheral vasoconstriction
  (skin, gut, muscle → blood shunted
   to brain & heart)
• Adrenal medulla → ↑ Adrenaline + Noradrenaline
        |
        ↓
NET EFFECT:
↑ Heart Rate + ↑ Stroke Volume → ↑ Cardiac Output
↑ SVR → Restore MAP
Cutaneous vasoconstriction → Cold, clammy, pale skin

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B. RAAS (Renin-Angiotensin-Aldosterone System) - Flowchart

HAEMORRHAGE
        |
        ↓
↓ Renal perfusion pressure
(↓ stretch of afferent arteriole)
        |
        ↓  Also triggered by:
JUXTAGLOMERULAR CELLS ← Sympathetic β₁ stimulation
        |                ← ↓ NaCl delivery to macula densa
        ↓
RENIN SECRETION
        |
        ↓
ANGIOTENSINOGEN (produced by liver)
        | (cleaved by Renin)
        ↓
ANGIOTENSIN I (Ang I)
        | (ACE - Angiotensin Converting Enzyme)
        | (mainly in pulmonary endothelium)
        ↓
ANGIOTENSIN II (Ang II)
        |
    ____↓_______________
   |                   |
   ↓                   ↓
ADRENAL CORTEX    VASCULAR SMOOTH MUSCLE
(Zona glomerulosa) (AT₁ receptors)
   |                   |
   ↓                   ↓
ALDOSTERONE       VASOCONSTRICTION
SECRETION         (↑ SVR → ↑ MAP)
   |
   ↓
RENAL DISTAL TUBULE & COLLECTING DUCT
   |
   ↓
↑ Na⁺ reabsorption → ↑ Water retention
↑ K⁺ excretion
   |
   ↓
↑ Blood volume → ↑ Preload → ↑ Cardiac Output

ADDITIONAL Ang II EFFECTS:
• Stimulates ADH (vasopressin) from posterior pituitary
• Stimulates thirst centre (hypothalamus)
• Noradrenaline release potentiation
• ↑ Splanchnic vasoconstriction

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C. ADH (Vasopressin) Response

↓ Blood volume / ↓ BP detected by
hypothalamic osmoreceptors + baroreceptors
+ Ang II stimulation
        |
        ↓
POSTERIOR PITUITARY → ↑ ADH (Vasopressin) secretion
        |
    ____↓___________
   |               |
   ↓               ↓
RENAL COLLECTING  VASCULAR
DUCT (V2 receptor) (V1 receptor)
   |               |
   ↓               ↓
↑ Water retention  Splanchnic &
(aquaporin-2)      peripheral
↑ Concentrated urine vasoconstriction

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D. Other Compensatory Mechanisms

• Tachycardia (most sensitive early sign)
• Normal or slightly reduced BP (pulse pressure narrows first)
• Cool, pale, clammy skin (peripheral vasoconstriction)
• Oliguria (renal conservation of fluid)
• Anxious/restless mental state

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4. Other Types of Shock

A. Cardiogenic Shock

B. Extracardiac Obstructive Shock

C. Distributive Shock (the "warm shocks")

• Most common form of distributive shock
• Triggered by gram-positive bacteria (most common now), gram-negative, fungi
• Mechanism: Pattern recognition receptors (TLRs) detect PAMPs (LPS, peptidoglycan) → massive cytokine release (TNF-α, IL-1, IL-6) → ↑ NO synthesis → profound vasodilation → ↓ SVR → distributive hypoperfusion
• Also: endothelial activation, microvascular thrombosis (DIC), capillary leak
• Early presentation: WARM skin, flushed, bounding pulse (high CO initially) - distinguishes from other shocks
• Late: cardiovascular collapse, myocardial depression, MODS
• Haemodynamics: ↑ CO, ↓ SVR, ↓ PAOP initially; later ↓ CO as myocardium fails

• Spinal cord injury above T6 → loss of sympathetic vasomotor tone below lesion
• Mechanism: Loss of sympathetic efferents → profound vasodilation + bradycardia (unopposed vagal tone)
• Classic triad: Hypotension + Bradycardia + Warm dry skin (unlike all other shocks where skin is cold and clammy)
• Mechanism differs from haemorrhagic: it is NOT volume depletion, but redistribution
• Haemodynamics: ↓ CO, ↓ SVR, normal/↓ CVP
• Treatment: vasopressors (noradrenaline) + cautious fluids + spinal stabilisation

• IgE-mediated type I hypersensitivity → mast cell degranulation → histamine, leukotrienes, prostaglandins
• Mechanism: Massive vasodilation + ↑ capillary permeability + bronchospasm
• Triggers: bee stings, peanuts, latex, penicillin, contrast dye
• Features: urticaria, angioedema, bronchospasm, ↓ BP, ↑ HR
• Treatment: Adrenaline (IM) is the cornerstone

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5. Treatment of Haemorrhagic Shock - With Physiological Basis

Treatment Flowchart

PATIENT WITH SUSPECTED HAEMORRHAGIC SHOCK
(trauma victim: hypotension, tachycardia, pale, cold, clammy)
                |
                ↓
        PRIMARY SURVEY (ABCDE)
      Airway → Breathing → Circulation
                |
         _____ ↓ _____
        |             |
    EXTERNAL        INTERNAL
    HAEMORRHAGE     HAEMORRHAGE
        |             |
   Direct pressure   Identify source:
   Tourniquets       • FAST ultrasound
   Wound packing     • CXR / Pelvis XR
   Haemostatic       • CT Angiography
   dressings
                |
                ↓
      DEFINITIVE HAEMORRHAGE CONTROL
      (surgery, interventional radiology,
       pelvic binder, wound packing)
                |
                ↓
      ESTABLISH IV ACCESS (2 large-bore IVs)
      Baseline bloods: FBC, U&E, LFT, coagulation,
      Group & Crossmatch, ABG, Lactate
                |
         _____ ↓ ______
        |               |
    Class I-II         Class III-IV
    (Crystalloid)      (Blood products)
        |               |
   Warmed lactated  Activate MASSIVE
   Ringer's or      TRANSFUSION PROTOCOL
   Normal saline    1:1:1 ratio:
   1-2 L bolus      PRBC : FFP : Platelets
                |
                ↓
        PERMISSIVE HYPOTENSION
        (target SBP 80-90 mmHg until
         definitive haemostasis achieved)
         [Not in TBI or pregnancy]
                |
                ↓
        PREVENT "LETHAL TRIAD"
        Acidosis + Hypothermia + Coagulopathy
                |
       _________↓_________
      |          |         |
   Treat      Warm        Treat
   acidosis   patient +   coagulopathy
   (fix        fluids      (FFP, platelets,
   perfusion)              cryoprecipitate,
                           TXA)
                |
                ↓
        MONITOR ENDPOINTS
        • Urine output >0.5 mL/kg/hr
        • MAP >65 mmHg
        • ↓ Lactate / lactate clearance
        • Base deficit normalising
        • SvO₂ > 65%
        • Coagulation studies normalising

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Treatment in Detail with Physiological Basis

A. Haemorrhage Control (Source Control)

• External: Direct pressure, tourniquets, haemostatic dressings (kaolin-based, e.g., QuikClot)
• Internal abdominal/thoracic: Emergency surgery (laparotomy, thoracotomy)
• Pelvic fractures: Pelvic binder (reduces pelvic volume, tamponades venous bleeding), angioembolisation
• Damage control surgery: Abbreviated initial surgery to stop haemorrhage and contamination, then ICU resuscitation, then definitive repair

B. Fluid Resuscitation

• Physiological basis: Replace depleted interstitial and intravascular fluid compartments. Only ~25% of infused crystalloid remains intravascular (remainder enters interstitium due to colloid osmotic pressure difference).
• Lactated Ringer's is preferred over normal saline to avoid hyperchloraemic metabolic acidosis.
• LR does NOT worsen lactic acidosis - lactate is metabolised to bicarbonate in the liver.
• Limitation: Large-volume crystalloid infusion causes dilutional coagulopathy, hypothermia, ARDS, abdominal compartment syndrome.

• Packed Red Blood Cells (PRBCs): Restore haemoglobin - directly increases oxygen-carrying capacity (CaO₂). Each unit raises Hb by ~1 g/dL.
• Fresh Frozen Plasma (FFP): Replaces all coagulation factors (I, II, V, VII, VIII, IX, X, XI). Physiological basis: massive haemorrhage + dilution consumes/dilutes clotting factors → consumptive and dilutional coagulopathy.
• Platelets: Dilutional thrombocytopenia occurs; platelets <50,000/mL impairs surgical haemostasis.
• Massive Transfusion Protocol (1:1:1): Evidence-based ratio of PRBC:FFP:Platelets mimics whole blood. Prevents "resuscitation coagulopathy."
• Cryoprecipitate: Concentrated source of fibrinogen and Factor VIII when FFP is insufficient.

• Physiological basis: Inhibits fibrinolysis by blocking plasminogen and plasmin binding to fibrin. Shock activates the fibrinolytic system → clots are lysed before haemostasis is established.
• Effective when given within 3 hours of injury.
• Primarily beneficial in severe haemorrhagic shock.
• Source: Mulholland's Surgery - "Recent support has emerged to suggest the addition of tranexamic acid (TXA) for patients suffering from exsanguinating haemorrhage."

C. Permissive Hypotension (Hypotensive Resuscitation)

• Physiological basis: Aggressive fluid resuscitation before haemostasis raises BP → dislodges soft clots → worsens bleeding. Maintaining SBP 80-90 mmHg (MAP ~50 mmHg) until surgical haemostasis is achieved reduces re-bleeding.
• Contraindicated in traumatic brain injury (TBI), spinal cord injury, and pregnancy (these organs require higher perfusion pressure).

D. Treating the "Lethal Triad"

          LETHAL TRIAD
         _____|_______
        |      |      |
   Acidosis  Hypo-  Coagulopathy
             thermia
        |      |      |
        ↓      ↓      ↓
   Fix    Warm   FFP + platelets
   source  IV    + cryoprecipitate
   of shock fluids + TXA
   (not    + forced
   bicarb  air
   alone)  warming

• Acidosis: Best treated by restoring perfusion (fixing cause). Sodium bicarbonate corrects pH but does NOT fix the underlying problem; can paradoxically worsen intracellular acidosis. THAM (tromethamine) is an alternative buffer that buffers CO₂ without generating it.
• Hypothermia: Room-temperature crystalloids + open body cavities = rapid heat loss. Use warmed fluids, forced-air warming blankets. Hypothermia worsens coagulopathy (enzyme function is temperature-dependent).
• Coagulopathy: Dilutional + consumptive. Correct with 1:1:1 resuscitation, TXA, avoid excessive crystalloids.

E. Vasopressors

• Used when volume resuscitation alone is insufficient to restore MAP
• Noradrenaline (norepinephrine): First-line vasopressor - acts on α₁ receptors → vasoconstriction → ↑ SVR → ↑ MAP
• Vasopressin (ADH): Adjunct vasopressor; acts on V1 receptors; endogenous levels are depleted in prolonged shock; "vasopressin-deficiency" state
• Physiological basis: Vasopressors restore perfusion pressure to vital organs when CO is being restored; they do NOT replace volume.

F. Monitoring Endpoints

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Radiology of Hypovolaemic Shock (CT findings)

• Flat/slit-like IVC (↓ preload, volume depletion)
• Small-calibre, hypo-enhancing aorta (in traumatic haemorrhagic shock)
• "Shock bowel" - hyperenhancing bowel wall with dilated fluid-filled loops
• Adrenal hyperenhancement (stress response)

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Summary: Physiological Basis of Each Treatment

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• Robbins, Cotran & Kumar: Pathologic Basis of Disease - Shock, Stages, Morphology
• Sabiston Textbook of Surgery - ATLS Classes, Haemorrhagic Shock, RAAS
• Mulholland and Greenfield's Surgery (7e) - Neuroendocrine Response, Fluid Therapy, Lethal Triad
• Robbins & Kumar Basic Pathology - Shock Types and Pathogenesis