Hypovolaemic & Haemorrhagic Shock

Overview & definition

Hypovolaemic / haemorrhagic shock is blood loss reducing venous return (preload) and cardiac output. It is the leading cause of preventable trauma death. Modern management is damage control resuscitation: permissive hypotension until bleeding is controlled, 1:1:1 massive transfusion, damage control surgery, and TXA.[1][1]

Hypovolaemic shock is the archetype of the low-preload / high-SVR / low-CO shock phenotype. The central problem is loss of circulating volume, not pump failure (cardiogenic) or vasodilation (distributive). Everything else follows from that single defect: reduced venous return reduces stroke volume (Frank-Starling), the sympathetic nervous system compensates, and a series of clinical signs unfold in a predictable, examinable order. Recognition of the compensated phase — before blood pressure falls — is the single most important skill, because by the time a trauma patient is hypotensive they have lost at least 30% of their blood volume and the mortality curve has steepened.[1]

The four ATLS classes of haemorrhagic shock

The ATLS classification stratifies haemorrhagic shock by percentage blood volume lost (adult blood volume ≈ 70 mL/kg, so a 70 kg adult has ~5 L). Each class has a recognisable clinical signature. The examinable point — repeated below because it is the single most tested concept — is that blood pressure is maintained (compensated) until class III, so a normal blood pressure does NOT exclude significant blood loss.[1][1]

Class I — under 15% blood loss (compensated, minimal)

Loss of up to 750 mL in a 70 kg adult. The body tolerates this without any measurable physiological compromise — this is the volume given in a standard blood donation. Heart rate is under 100, blood pressure normal, pulse pressure normal, mental state normal, urine output normal (above 30 mL/h, or above 0.5 mL/kg/hr). Capillary refill may be slightly prolonged. Management is to identify and stop the source of bleeding; fluid resuscitation is rarely required beyond what is needed to maintain the circulating volume, and the patient can usually be managed with crystalloid if needed. The trap is assuming the well-looking trauma patient is fine — class I can silently progress to class IV if an occult source (intra-abdominal, retroperitoneal, pelvic) is missed.[1]

Class II — 15-30% blood loss (compensated, mild)

Loss of 750-1500 mL. This is where compensation becomes clinically visible but blood pressure is still maintained. Heart rate rises to 100-120 (early tachycardia is the first detectable sign). Pulse pressure narrows because diastolic pressure rises from catecholamine-driven vasoconstriction while systolic is preserved — a narrowed pulse pressure is a more sensitive marker of significant volume loss than the absolute systolic pressure. The patient is anxious/hostile (mild CNS hypoperfusion), urine output falls to 20-30 mL/h. Management: give 1-2 L warmed balanced crystalloid bolus and reassess; identify and control bleeding.[1][1]

Class III — 30-40% blood loss (decompensated, moderate)

Loss of 1500-2000 mL. This is the decompensation threshold — the point at which sympathetic compensation is exhausted and blood pressure finally falls. Most patients are hypotensive by this stage (typically 30% of patients are hypotensive at 30% loss; virtually all by 40%). Heart rate 120-140, pulse pressure markedly narrowed then systolic falls, the patient is confused, oliguric (5-15 mL/h). Class III shock is a surgical / MTP emergency — this is the patient who needs blood, not crystalloid, and immediate bleeding control. Delays here are lethal.[1]

Class IV — above 40% blood loss (decompensated, severe)

Loss of more than 2000 mL (above 2 L). The patient is lethargic or obtunded, markedly hypotensive, heart rate above 140 (or paradoxically bradycardic in the pre-arrest agonal phase), negligible urine output, cold and mottled peripheries. This is imminent cardiac arrest from exsanguination — activate the massive transfusion protocol immediately, take to theatre / angioembolisation without delay. Mortality is high; survival depends on the speed of haemorrhage control and prevention of the lethal triad.[1][1]

Pathophysiology

Blood loss reduces venous return (preload) and stroke volume (Frank-Starling). Compensatory sympathetic mechanisms (tachycardia, vasoconstriction) maintain blood pressure initially (classes I-II). Decompensation (classes III-IV) occurs once loss exceeds about 30 per cent — BP falls, perfusion is compromised, and shock ensues.[1][1]

Trauma-induced coagulopathy (TIC) is an endogenous coagulopathy of severe trauma (tissue-factor release, protein-C activation, hyperfibrinolysis), compounded by resuscitation (dilution, acidosis, hypothermia).[2][8]

The compensation cascade — the order of signs

The body defends blood pressure through a stereotyped, ordered sequence of sympathetic and neuroendocrine responses. Understanding the ORDER is the key to recognising compensated shock:[1][1]

1. Tachycardia (earliest sign) — reduced venous return reduces stroke volume; baroreceptors sense the fall and drive sympathetic output. Heart rate rises to maintain cardiac output (CO = HR × SV). This appears before any blood pressure change.
2. Vasoconstriction (increased SVR) — catecholamines constrict arterioles and venules, raising systemic vascular resistance and venous tone (the venous side mobilises the unstressed volume into the circulation). This is why diastolic pressure rises early.
3. Narrowed pulse pressure — because diastolic rises (vasoconstriction) while systolic is relatively preserved, the pulse pressure (systolic − diastolic) narrows. A narrowed pulse pressure is a sensitive marker of significant volume loss that precedes the fall in systolic pressure.
4. Hypotension (LATE sign) — once loss exceeds ~30%, compensation is exhausted; systolic pressure falls. By now the patient is in class III-IV shock. A normal systolic pressure does not mean the patient is well-resuscitated.
5. End-organ hypoperfusion — oliguria, altered mental state, cold peripheries, raised lactate. These are the markers of tissue-level shock regardless of the blood pressure number. [1]

[1] [1] [1]

The lethal triad

Three interlocking processes worsen coagulopathy and mortality:[2][1]

• Acidosis (pH below 7.2 → reduced coagulation-factor enzyme activity, impaired fibrin polymerisation).[2]
• Hypothermia (core below 35 → slowed coagulation cascade, impaired platelet function).[2]
• Coagulopathy (dilutional plus TIC, plus consumption).[2]

Each worsens the others in a vicious cycle; prevention is central.[2] Once the lethal triad is fully established (pH under 7.2, temperature under 35°C, INR above 1.5), mortality approaches 100%. The triad is far easier to prevent than to reverse — the entire damage-control philosophy is built on this premise.[7]

Fluid resuscitation — the initial approach and the response paradigm

The initial fluid strategy depends on whether the bleeding is controlled or uncontrolled. This distinction is the foundation of modern trauma resuscitation and was established by the landmark Bickell (1994) trial.[3]

Controlled haemorrhagic shock (non-trauma, or bleeding already stopped)

Give a 1-2 L warmed balanced crystalloid bolus (Hartmann / compound sodium lactate, or Plasma-Lyte — NOT normal saline, which causes hyperchloraemic acidosis that worsens coagulopathy), then reassess the response:[1][1]

• Rapid response — vital signs normalise and stay normal: the patient had a volume deficit and bleeding has stopped. Continue maintenance, investigate the cause.
• Transient response — vital signs improve then deteriorate again as the bolus wears off: this indicates ongoing haemorrhage. This is the trigger to activate the massive transfusion protocol (MTP), switch to blood-based resuscitation, and achieve definitive bleeding control (surgery / endoscopy / angioembolisation).
• No response / minimal response — severe ongoing loss or a different shock phenotype (cardiogenic from myocardial contusion/tamponade, distributive from neurogenic shock in spinal injury). Reassess the diagnosis with point-of-care ultrasound (FAST, RUSH/E-FAST); the "non-responder" to crystalloid in trauma is bleeding until proven otherwise. [1]

Uncontrolled haemorrhagic shock (active trauma bleeding)

In the actively bleeding trauma patient, aggressive crystalloid is harmful — it dilutes clotting factors, dislodges clots ("pop the clot"), worsens acidosis, and causes a lethal triad. The strategy is damage control resuscitation (below): permissive hypotension, minimise crystalloid, resuscitate with blood in 1:1:1 ratio, achieve bleeding control.[3][9]

[1] [1] [3] [9]

Damage control resuscitation (DCR)

Damage control resuscitation is the integrated package that replaced the old "give two litres of saline and run to theatre" approach. Its rationale: aggressive crystalloid and normotension in the actively bleeding patient deepen the lethal triad and worsen mortality. DCR instead buys time and physiology until the bleed is definitively controlled.[2][9]

1. Permissive hypotension.[1][2][10]

• Target MAP 50-65 (or SBP 80-90) until bleeding is controlled. Avoid normotension, which dislodges clots and dilutes clotting factors.[1]
• Restrict fluids; allow permissive hypotension to minimise clot disruption.[2]
• Do NOT use permissive hypotension in TBI — the brain-injured patient needs a CPP (MAP minus ICP) above 60, so maintain normotension (SBP above 110).[1][7]

2. 1:1:1 massive transfusion.[1][4]

• RBC : FFP : platelets 1 : 1 : 1 (the PROPPR trial showed equivalent overall mortality but earlier haemostasis and fewer deaths from exsanguination at 24h).[4]
• Give cryoprecipitate / fibrinogen to keep fibrinogen above 2 g/L.[7]
• TXA 1 g IV within 3 hours of injury (CRASH-2 — reduces mortality; after 3 hours there is no benefit and possible harm).[5][6]

3. Damage control surgery.[2]

• Rapid control of bleeding (packing, ligation, balloon tamponade, temporary vascular shunt).[2]
• Not definitive repair — stabilise first, then return to theatre (typically 24-48 h) for definitive surgery once stable.[2]

4. Warming and correction of acidosis.[2][1]

• Warmed IV fluids, forced-air warming, and body-cavity lavage as needed.[2]
• Empiric calcium (citrate in stored blood chelates Ca²⁺) — CaCl₂ 10 mmol per ~4 units blood products.[7]

Permissive hypotension in depth

Permissive hypotension means deliberately tolerating a sub-normal blood pressure in the actively bleeding patient, on the principle that restoring full pressure before haemostasis mechanically disrupts clots and accelerates bleeding. The evidence base is Bickell (1994): in penetrating torso trauma, delaying fluid resuscitation until operative control of bleeding improved survival (70% vs 62%) compared with immediate aggressive fluids.[3] Dutton (2002) showed that titrating to a lower target SBP (~70 mmHg) versus conventional (~100 mmHg) during active haemorrhage was safe and did not increase mortality.[10]

[3] [10] [7]

Tranexamic acid (TXA) — CRASH-2 and the 3-hour rule

Tranexamic acid is an anti-fibrinolytic (lysine analogue blocking plasminogen activation) that counteracts the hyperfibrinolytic component of trauma-induced coagulopathy. The dose is 1 g IV over 10 minutes, then 1 g over 8 hours.[5]

CRASH-2 (2010, 20,211 patients) showed TXA reduced all-cause mortality (14.5% vs 16.0%) and bleeding death, with no increase in thromboembolism.[5] The crucial refinement came from the time-window analysis (2011): benefit is greatest within 1 hour of injury, present within 3 hours, but TXA increases mortality when given more than 3 hours after injury.[6]

[3] [5] [6] [4]

Resuscitation endpoints — what to target

The goal of resuscitation is restoration of tissue oxygen delivery and the clearance of oxygen debt, not a particular blood pressure number. Resuscitating to a "normal" blood pressure alone is inadequate — a patient can be normotensive and still in shock at the tissue level (ongoing anaerobic metabolism, rising lactate). The validated endpoints are:[1][1]

• Lactate clearance — serum lactate reflects the magnitude of anaerobic metabolism (oxygen debt). The target is lactate returning to normal (under 2 mmol/L), ideally with a fall of at least 10% per hour (or 50% in the first 6 hours, analogous to the Jansen lactate-clearance concept). A rising or static lactate signals ongoing hypoperfusion. Lactate is the single best global marker of adequacy of resuscitation.
• Urine output above 0.5 mL/kg/hr — renal perfusion is a sensitive, real-time, bedside index of adequate cardiac output and tissue perfusion. Oliguria (under 0.5 mL/kg/hr) signals under-resuscitation. A catheter and an hourly urine measure are mandatory in any shocked patient.
• Normal mental state — the brain is the most perfusion-sensitive organ; a clear sensorium indicates adequate cerebral perfusion (and by inference adequate cardiac output). Confusion, agitation, or lethargy = ongoing shock.
• Base deficit / bicarbonate — a base deficit worse than −5 mmol/L (or worsening trend) reflects metabolic acidosis from hypoperfusion; it should normalise with adequate resuscitation.
• Central venous oxygen saturation (ScvO₂) — above 70% indicates adequate oxygen delivery relative to extraction (the principle from early goal-directed therapy).
• Capillary refill time under 2 seconds and warm, well-perfused peripheries — a return of the vasoconstricted, mottled periphery to normal indicates SVR normalising as shock resolves.
• Resolution of metabolic acidosis (pH above 7.35, normal strong ion difference). [1]

[1] [1]

Prognosis

Mortality depends on the speed of bleeding control and prevention of the lethal triad. Damage control resuscitation reduces mortality compared with traditional aggressive fluid resuscitation.[1][2][1] Trauma-induced coagulopathy on arrival multiplies mortality by 3-4 times; the lethal triad, once established, carries a mortality approaching 100%. Early recognition (class II, before hypotension), prompt MTP activation, and rapid definitive bleeding control are the modifiable determinants of survival.[8]

Special populations and pitfalls

[1] [1]

Differential diagnosis of shock that is NOT responding

A trauma patient who fails to respond to adequate resuscitation may have an alternative or additional cause of shock — mechanical, cardiogenic, or obstructive. Point-of-care ultrasound (E-FAST / RUSH) is the key diagnostic tool:[1]

• Tension pneumothorax — hypotension, distended neck veins, unilateral absent breath sounds, tracheal deviation. Needle/finger thoracostomy immediately.
• Cardiac tamponade — Beck's triad (hypotension, muffled heart sounds, raised JVP), pulsus paradoxus. Pericardiocentesis / thoracotomy.
• Myocardial contusion / cardiogenic shock — blunt cardiac injury can cause pump failure; echocardiography shows reduced contractility.
• Neurogenic shock (spinal cord injury) — hypotension with bradycardia (unlike the tachycardia of hypovolaemia), warm peripheries (loss of sympathetic tone).
• Missed source of bleeding — pelvic fracture, retroperitoneal haematoma, intrathoracic, long-bone fracture (each femur fracture can hold 1-2 units). Re-survey the patient. [1]

Monitoring the resuscitating patient

[1] [7] [1]

Red flags

Exam practice

[1] [1] [4] [5] [1] [1] [1]

Clinical pearls

References

1. [1]Boutros A, et al. Resuscitation for Hypovolemic Shock Surg Clin North Am, 2017.PMID 29132511
2. [2]Duchesne JC, et al. Damage control resuscitation Blood Rev, 2015.PMID 25631636
3. [3]Bickell WH, Wall MJ Jr, Pepe PE, et al. The use and clinical importance of a substrate-specific electrode for rapid determination of blood lactate concentrations JAMA, 1994.PMID 7966896
4. [4]Holcomb JB, Tilley BC, Baraniuk S, et al. (PROPPR Study Group) Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial JAMA, 2015.PMID 25647203
5. [5]CRASH-2 trial collaborators Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial Lancet, 2010.PMID 20554319
6. [6]CRASH-2 collaborators The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH-2 randomised controlled trial Lancet, 2011.PMID 21439633
7. [7]Spahn DR, Bouillon B, Cerny V, et al. The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition Crit Care, 2019.PMID 30917843
8. [8]Brohi K, Singh J, Heron M, Coats T Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis J Trauma, 2008.PMID 18469643
9. [9]Cannon JW, Khan MA, Raja AS, et al. Damage control resuscitation in patients with severe traumatic hemorrhage: A practice management guideline from the Eastern Association for the Surgery of Trauma J Trauma Acute Care Surg, 2017.PMID 28225743
10. [10]Dutton RP, Mackenzie CF, Scalea TM Molecular Mechanisms in Root Nodule Development J Plant Growth Regul, 2000.PMID 11038225