Shock and Haemorrhage Control

Advanced Paramedic Study Guide

The Pathophysiology of Shock: A Cellular Crisis

Beyond Hypotension: The Cellular Cascade

Shock is not merely low blood pressure; it is a failure of oxygen delivery ($DO_2$) to meet cellular metabolic demand ($VO_2$). When perfusion fails, the following cascade occurs:

  1. Anaerobic Shift: Cells switch from aerobic to anaerobic metabolism. This produces only 2 ATP (energy) molecules compared to 36 ATP in aerobic metabolism, creating an energy deficit.
  2. Lactic Acidosis: The byproduct of anaerobic metabolism is lactate. As lactate accumulates, the blood pH drops (metabolic acidosis). Acidosis inhibits enzymatic reactions necessary for clotting and myocardial contraction.
  3. Ion Pump Failure: The Na⁺/K⁺ pump requires ATP. As ATP fails, Sodium (Na⁺) and Water influx into the cell, while Potassium (K⁺) leaks out.
    • Result: Cellular swelling (intracellular oedema) and intravascular volume loss.
  4. Lysosomal Rupture: As intracellular acidosis worsens, lysosomal membranes rupture, releasing digestive enzymes that autodigest the cell and damage surrounding tissue. This triggers the systemic inflammatory response (SIRS).

The "Trauma Diamond of Death"

The traditional "Lethal Triad" has evolved. Recent literature (Dawkins) identifies Hypocalcemia as a critical fourth pillar that exacerbates mortality.

Component Pathophysiology Paramedic Intervention (Impact)
1. Hypothermia
(<35°C)		 Enzymes required for the clotting cascade are temperature-dependent. Platelet function is inhibited. Shifts oxyhemoglobin curve to the left (O₂ trapped on RBC). (+) Early exposure control, warm blankets, warm fluids (if given), cabin heat.
(-) Cutting clothes off without covering, cold IV fluids.
2. Acidosis
(pH <7.35)		 Result of anaerobic metabolism (lactate) and excessive crystalloids (NaCl is acidic). Acidosis reduces clot strength and myocardial contractility. (+) Optimise oxygenation/perfusion. Limit crystalloids.
(-) Excessive saline resuscitation (hyperchloremic acidosis).
3. Coagulopathy
(TIC)		 Trauma Induced Coagulopathy (TIC): Occurs within minutes. Driven by protein C activation, consumption of factors, and hemodilution. (+) Mechanical haemorrhage control, TXA, permissive hypotension (prevents clot blowout).
(-) Hemodilution with fluids.
4. Hypocalcemia
(iCa <1.0 mmol/L)		 Calcium is Factor IV. It is essential for the clotting cascade, platelet adhesion, and heart contractility. Citrate in blood products binds calcium. (+) Identification of risk. Administration of Calcium Gluconate/Chloride (if in scope/consult).
(-) Massive transfusion without calcium replacement.
Reflective Practice: You cannot "fix" the Diamond of Death once established; you can only prevent it. Early warmth, restrictive fluids, and hemorrhage control are the only pre-hospital tools to break this cycle.

Assessment: Recognizing Decompensation

The "Hateful Eight" Signs of Shock

Reliance on BP alone is dangerous. Young patients compensate until collapse. Look for these 8 signs (Leech et al.):

  • 1. Air Hunger (Tachypnoea fighting acidosis)
  • 2. Low EtCO₂ (Poor perfusion)
  • 3. Sweaty/Clammy (Sympathetic drive)
  • 4. Pallor (Vasoconstriction)
  • 5. Venous Collapse (Flat EJVs)
  • 6. Abnormal Pulse (Weak/Thready)
  • 7. Hypotension (Late sign)
  • 8. Altered Mental Status (Agitation/Confusion)

Note: Severe haemorrhage can cause a "Biphasic Response" where vagal tone leads to paradoxical bradycardia rather than tachycardia.

The COAST Score

A predictive tool for Trauma Induced Coagulopathy (TIC). If score ≥3, aggressive coagulopathy management is indicated.

  • C - Chest or Abdominal Injury (Open/Trapped)
  • O - Open fracture or Pelvic fracture
  • A - Age < 35 years (Young patients mount stronger inflammatory response)
  • S - Systolic BP < 100 mmHg
  • T - Temperature < 35°C (or poor exposure)

Fluid Resuscitation & Permissive Hypotension

Permissive Hypotension Strategy

Goal: Maintain perfusion to vital organs without "popping the clot" or diluting clotting factors.

Target: Palpable radial pulse OR Systolic BP 70-90 mmHg (depending on local guidelines).

Fluid Choice: Blood is ideal. If unavailable, use small boluses (e.g., 250ml) of warmed crystalloids only to maintain the target. Avoiding excessive fluid is more important than the type of crystalloid.

CRITICAL CONTRAINDICATION: Traumatic Brain Injury (TBI)

Why? The injured brain loses autoregulation. Perfusion becomes entirely dependent on Mean Arterial Pressure (MAP). Hypotension in TBI doubles mortality.

TBI Target: Systolic BP >110-120 mmHg. In these patients, you must resuscitate to a higher pressure to ensure Cerebral Perfusion Pressure (CPP).

Clinical Decision Making

Scenario: Patient with a stab wound (shock) AND a head strike (TBI).

Dilemma: Permissive hypotension vs. TBI targets?

Resolution: The brain takes priority. Hypotension causes secondary brain injury. Aim for SBP >110 mmHg, but prioritize rapid transport and hemorrhage control to minimize fluid volume needed.

Tranexamic Acid (TXA)

Mechanism of Action

TXA is a synthetic derivative of the amino acid lysine. It acts as an antifibrinolytic by blocking the lysine binding sites on plasminogen. This prevents plasminogen from converting to plasmin, thereby inhibiting the breakdown of fibrin clots (fibrinolysis).

Evidence & Administration (CRASH-2 & PATCH)

  • Indication: Suspected significant internal or external haemorrhage (HR >110, SBP <90).
  • Timing is Critical: Must be given within 3 hours of injury.
    Risk: Administration >3 hours after injury is associated with increased mortality due to disseminated intravascular coagulation (DIC) phases.
  • Dose: 1g IV slowly over 10 minutes (Rapid push causes hypotension and seizures). Followed by 1g infusion over 8 hours.
  • PATCH-Trauma Trial (2023): Confirmed survival benefit in severe trauma but noted no significant improvement in "good functional outcome" at 6 months. It remains standard of care for survival.

Haemostatic Wound Packing

Indicated for life-threatening haemorrhage in junctional areas (groin, axilla, neck) where tourniquets cannot be applied.

Haemostatic Agents

  • Kaolin (e.g., QuikClot): Inert mineral. Activates Factor XII (Intrinsic pathway). Promotes rapid clotting.
  • Chitosan (e.g., Celox-A): Derived from shellfish. Bonds with red blood cells to form a gel-like plug. Independent of the body's clotting cascade (works in hypothermic/heparinized patients).

Procedure

  1. Expose: Fully expose the wound. Wipe away pooled blood.
  2. Identify: Locate the exact source of bleeding (artery/bone).
  3. Pack: Feed gauze directly onto the vessel. Pack tightly towards the bone. Fills the cavity.
  4. Pressure (CRITICAL): Apply firm manual pressure for 3-5 minutes (agent dependent). Do not release to "check".
  5. Bandage: Apply pressure dressing. If bleeding continues, remove and repack once, or apply second dressing on top (check local protocol).

Pelvic Binders (T-POD)

Pathophysiology of Pelvic Ring Injuries

"Open book" fractures increase the volume of the pelvic cavity. Venous plexuses and arteries shear, causing massive retroperitoneal haemorrhage. A pelvic binder reduces this volume, providing a tamponade effect.

Application & Logistics

  • Placement: Centred over the Greater Trochanters (Not the iliac crests!).
  • Priorities (Polytrauma):
    1. Pelvic Binder (Highest bleeding risk, reduces volume).
    2. Femoral Splinting (Anatomical splinting preferred).
    Note: Traction splints are contraindicated in suspected pelvic fractures as the counter-pressure transmits force to the pelvic ring.
  • Risks of Log-Rolling: Rolling can dislodge clots and exacerbate "open book" fractures.
    Alternative: Use a Scoop Stretcher to lift the patient and slide the binder under, or slide sheets. Minimize movement.