Hypovolemic Shock (Adult)

1. Overview

Hypovolemic shock is a life-threatening circulatory failure state characterised by inadequate intravascular volume to maintain tissue perfusion and oxygen delivery. It results from either actual fluid loss (haemorrhagic) or relative fluid loss (non-haemorrhagic shifts, third-spacing). [1]

The clinical significance of hypovolemic shock cannot be overstated. It represents the most common form of shock in the emergency department, accounting for approximately 60% of all shock presentations. Massive haemorrhage remains the leading cause of preventable death in trauma, with 50% of trauma deaths occurring within minutes of injury due to uncontrolled bleeding. [2]

Management has evolved significantly with the introduction of Damage Control Resuscitation (DCR) principles, emphasising balanced blood component therapy, haemostatic resuscitation, and permissive hypotension. The 2025 ESICM guidelines on fluid therapy and the 2023 European guideline on management of major bleeding and coagulopathy following trauma provide evidence-based frameworks for resuscitation. [3, 4]

2. Epidemiology

Trauma Statistics

Statistic	Value	Source
Trauma deaths from haemorrhage	30-40% of all trauma mortality	[5]
Preventable trauma deaths	50% due to uncontrolled bleeding	[2]
Massive transfusion utilization	3-5% of trauma patients	[6]
Mortality with massive transfusion	20-50% (depending on protocol adherence)	[7]

Non-Trauma Etiologies

Cause	Frequency	Typical Presentation
Upper GI bleed	40-50% of GI bleeds	Melena, haematemesis
Ruptured AAA	1-2% of AAA	Back/flank pain, pulsatile mass
Ectopic pregnancy	2% of pregnancies	Vaginal bleeding, abdominal pain
Severe burns	>20% TBSA burns	Fluid shifts, oedema

3. Aetiology & Pathophysiology

3.1 Hemorrhagic Causes

Major Trauma Sources

Solid organ injury: Spleen, liver (most common blunt injuries)
Pelvic fracture: Can lose > 2000 mL from venous plexus
Long bone fracture: Femur (1500 mL), Tibia (500 mL per fracture)
Vascular injury: Major arterial transection (rapid exsanguination)
Penetrating trauma: Direct vessel injury, rapid haemorrhage

Non-Traumatic Haemorrhage

Source	Mechanism	Typical Volume Loss
Upper GI bleed	Variceal rupture, peptic ulcer	500-2000 mL
Ruptured AAA	Aortic wall disruption	1500-3000 mL
Ectopic pregnancy	Tubal rupture	500-1500 mL
Aortic dissection	Type A (ascending)	Variable, often catastrophic
Retained placenta	Postpartum haemorrhage	500-2000 mL

Exam Detail: Class I haemorrhage: > 15% blood loss (less than 750 mL). Mild tachycardia, normal BP. Normal urine output. Class II haemorrhage: 15-30% (750-1500 mL). Tachycardia, narrowed pulse pressure, mild anxiety. Urine output 20-30 mL/hr. Class III haemorrhage: 30-40% (1500-2000 mL). Tachycardia, hypotension, altered mental status. Urine output 5-15 mL/hr. Class IV haemorrhage: >40% (>2000 mL). Marked hypotension, absence of radial pulse, profound shock state. Minimal urine output.

3.2 Non-Hemorrhagic Causes

Third-Spacing Conditions

Severe burns: Fluid shifts into interstitial space (peak at 12-24 hours post-burn)
Pancreatitis: Capillary leak syndrome, retroperitoneal third-spacing
Sepsis: Endothelial dysfunction, increased vascular permeability
Major abdominal surgery: Postoperative third-spacing

Absolute Volume Loss

Cause	Pathophysiology	Key Features
Diabetic Ketoacidosis	Osmotic diuresis + vomiting	Kussmaul breathing, hyperglycaemia, ketonuria
Severe vomiting/diarrhoea	GI losses	Dehydration, electrolyte abnormalities
Heat exhaustion	Profuse sweating	Hyperthermia, muscle cramps
Diuretic overuse	Enhanced renal excretion	Polyuria, electrolyte disturbances
Adrenal crisis	Mineralocorticoid deficiency	Hyponatraemia, hyperkalaemia, hypotension

Clinical Pearl: The "Hidden" Haemorrhage: In trauma, always consider retroperitoneal, pelvic, and long bone fractures as sources of occult blood loss. A femur fracture alone can hide up to 1.5 L of blood that is not immediately visible on examination.

3.3 Pathophysiology of Shock

The cardiovascular response to hypovolemia follows a predictable cascade:

Immediate Compensatory Phase (Class I-II): Decreased venous return → Reduced preload → Stroke volume falls → Baroreceptor activation → Tachycardia + peripheral vasoconstriction (sympathetic surge) → Maintenance of MAP despite reduced CO.
Decompensation Phase (Class III-IV): Compensatory mechanisms fail → Progressive fall in CO → Tissue hypoperfusion → Anaerobic metabolism → Lactic acidosis → Myocardial depression → Progressive cardiovascular collapse.
Trauma-Induced Coagulopathy (TIC): Massive haemorrhage + tissue injury → Activation of protein C pathway + fibrinolysis + consumption of coagulation factors → Acute coagulopathy occurring within 30 minutes of injury (independent of fluid resuscitation).

Exam Detail: The "Lethal Triad" in Trauma:

Hypothermia: Impairs coagulation cascade (enzymes function poorly below 34°C)
Acidosis: Reduces coagulation factor activity
Coagulopathy: Both consumption and dilutional from massive transfusion

These three form a self-perpetuating cycle: bleeding → resuscitation (cold fluids) → hypothermia → impaired coagulation → more bleeding.

4. Clinical Presentation

4.1 Symptoms

Symptom	Frequency	Clinical Significance
Lightheadedness/Pre-syncope	80%	Early sign of reduced cerebral perfusion
Thirst	70%	Physiologic response to intravascular volume depletion
Weakness/Fatigue	65%	Tissue hypoperfusion
Chest discomfort	30%	Angina from reduced coronary perfusion
Abdominal pain	Variable	Depends on source (e.g., AAA rupture)

4.2 Physical Examination

General Signs

Pallor: Reduced skin perfusion
Cool extremities: Peripheral vasoconstriction
Delayed capillary refill: >2 seconds indicates poor perfusion
Diaphoresis: Sympathetic activation

Cardiovascular Signs

Sign	Early Shock	Late Shock
Heart Rate	100-120/min (compensatory)	>120/min or bradycardia (pre-terminal)
Blood Pressure	Normal or narrowed pulse pressure	Hypotension (MAP less than 65 mmHg)
Pulse Amplitude	Weak but palpable	Thready or absent
JVP	Flat	Markedly flattened

Evidence Debate: MAP Target: Traditional teaching targets MAP ≥65 mmHg. However, the CRASH-2 trial and subsequent studies suggest permissive hypotension (target MAP 50-60 mmHg) in penetrating trauma may improve outcomes by avoiding disruption of nascent clots. This approach is NOT recommended in traumatic brain injury where higher MAP targets (≥80 mmHg) are needed to maintain cerebral perfusion.

Abdominal Examination

Distension: May indicate retroperitoneal or intraperitoneal bleeding
Guarding/rigidity: Peritonitis from hollow viscus injury
Pulsatile mass: Abdominal aortic aneurysm (ruptured or intact)

4.3 Shock Index

Shock Index = Heart Rate / Systolic Blood Pressure

Value	Interpretation
0.5-0.7	Normal
0.7-0.9	Mild shock
0.9-1.1	Moderate shock
1.1-1.5	Severe shock
>1.5	Massive shock (pre-arrest)

A shock index >1.0 is associated with 3-fold increased mortality in trauma patients.

5. Differential Diagnosis

Differential	Key Distinguishing Features	Diagnostic Approach
Septic Shock	Fever, warm shock (vasodilation), WBC rise	Blood cultures, lactate, source identification
Cardiogenic Shock	Pulmonary oedema, elevated JVP, cardiac history	ECG, Echo, Troponin
Obstructive Shock	JVP elevation, muffled heart sounds, absent breath sounds	Echo, CXR, FAST scan
Anaphylactic Shock	Urticaria, angioedema, bronchospasm	Recent allergen exposure, tryptase
Neurogenic Shock	Warm shock (loss of sympathetic tone), spinal cord injury	Level of injury, priapism

Procedure Detail: The FAST Examination (Focused Assessment with Sonography in Trauma):

RUQ: Morison's pouch (hepatic injury, free fluid)
LUQ: Splenorenal recess (splenic injury)
Suprapubic: Pelvic view (intraperitoneal blood, bladder injury)
Pericardial: Subxiphoid view (tamponade)

Sensitivity for free abdominal fluid: 70-80%. Specificity: >95%. Negative FAST does NOT rule out solid organ injury (requires CT).

6. Investigations

6.1 Immediate (Bedside)

Test	What It Shows	Interpretation
Point-of-care glucose	Hypoglycaemia mimic shock	less than 3.0 mmol/L requires treatment
Arterial blood gas	Lactate, base deficit, pH	Lactate >4 mmol/L predicts mortality
Bedside ultrasound	Free fluid, cardiac activity, IVC collapsibility	FAST + E-FAST
Portable CXR	Pneumothorax, widened mediastinum	Immediate life threats

6.2 Laboratory Tests

Mandatory Panel

CBC: Hb, Hct, Platelet count (transfusion thresholds)
Coagulation profile: INR, aPTT, Fibrinogen (DCR guidance)
Blood group and crossmatch: 4-6 units for suspected massive transfusion
Electrolytes: Na+, K+, Ca2+ (correct hypocalcaemia in massive transfusion)
Renal function: Creatinine, urea (AKI risk)
Liver enzymes: AST/ALT (trauma source identification)

Trauma-Specific

Thromboelastography (TEG) / Rotational Thromboelastometry (ROTEM): Point-of-care coagulation monitoring
Fibrinogen: less than 1.5 g/L requires cryoprecipitate (DCR principle)
Ionised calcium: Correct to > 1.1 mmol/L during massive transfusion

6.3 Diagnostic Imaging

Computed Tomography

Pan-scan in trauma: Head to pelvis (for stable trauma patients)
Angiography: Embolisation of arterial bleeding (e.g., pelvic fracture)
CT Angiogram for AAA: Confirms rupture, plans intervention

Sensitivity/Specificity

Modality	Sensitivity	Specificity	Utility
FAST (abdominal)	70-80%	>95%	Rapid bedside screen
CT Abdomen/Pelvis	>95%	95%	Definitive trauma workup
CT Angiogram (AAA)	99%	98%	Rupture confirmation

7. Management

7.1 Initial Resuscitation (The "First 30 Minutes")

ABCDE Approach

Airway: Secure if GCS less than 8 or respiratory distress
Breathing: 100% O2, tension pneumothorax decompression
Circulation: 2 large-bore cannulae (14G or 16G), immediate crystalloid bolus
Disability: GCS, pupils
Exposure/Environment: Full examination, keep patient warm

Fluid Resuscitation Strategy

Exam Detail: Crystalloid Choice:

Isotonic balanced solutions (Plasmalyte, Hartmann's): First-line in trauma (less hyperchloraemic acidosis than normal saline)
Normal saline (0.9%): Acceptable alternative but can cause non-anion gap metabolic acidosis
Initial bolus: 500-1000 mL warm crystalloid (avoid hypothermia)
Re-assess: After each bolus, re-evaluate vital signs, capillary refill, lactate

Avoidance of Over-resuscitation: Crystalloid volume > 2 L in the first hour is associated with worse outcomes (coagulopathy dilution, abdominal compartment syndrome, ARDS).

Blood Product Selection

Product	Indication	Ratio (MTP)	Dose
Packed Red Blood Cells (PRBC)	Ongoing haemorrhage	1:1:1	1 unit initially
Fresh Frozen Plasma (FFP)	Coagulopathy correction	1:1:1	1:1 with PRBC
Platelets	Thrombocytopenia	1:1:1	1:1 with PRBC
Cryoprecipitate	Fibrinogen less than 1.5 g/L	1:1:1 or as needed	10 units pooled

7.2 Massive Transfusion Protocol (MTP)

Activation Criteria

Anticipated need for > 4 units PRBC in 1 hour OR
Anticipated need for > 10 units PRBC in 24 hours OR
Persistent haemodynamic instability despite initial crystalloid resuscitation

MTP Pack (Rapid Access)

Cooler 1 (6 units total): 4 PRBC + 2 FFP Cooler 2 (6 units total): 4 PRBC + 2 Platelets Cooler 3 (Rescue): 6 PRBC + 6 FFP + 1 Platelet apheresis

Evidence Debate: 1:1:1 Ratio Debate: The landmark PROPPR trial (2015) demonstrated that a 1:1:1 ratio (plasma:platelets:PRBC) resulted in faster haemostasis and reduced early mortality (24% vs 30%) compared to 1:1:2 ratio. However, recent 2025 meta-analyses suggest that the optimal ratio may vary based on injury pattern (penetrating vs blunt). Current guidelines recommend aiming for balanced resuscitation but acknowledge that strict 1:1:1 may not always be achievable or necessary.

Massive Transfusion Complications

Complication	Prevention	Management
Hypocalcaemia	Calcium chloride infusion (1 g with every 4 units PRBC)	Check ionised Ca2+, repeat as needed
Hyperkalaemia	Use fresher blood (less than 14 days)	Calcium gluconate, insulin-dextrose
Hypothermia	Blood warmer (mandatory for > 2 units)	Active warming devices
Dilutional coagulopathy	1:1:1 ratio, TEG-guided	FFP, Platelets, Cryoprecipitate
TRALI	Plasma from male donors (if available)	Supportive care, ventilation

7.3 Damage Control Resuscitation (DCR)

The 5 DCR Principles

Permissive Hypotension: Target MAP 50-60 mmHg until haemorrhage controlled (NOT in TBI)
Hemostatic Resuscitation: Early blood products (not crystalloids), 1:1:1 ratio
Minimise Crystalloids: Restrict to less than 2 L in first hour
Prevent/Treat Hypothermia: Active warming (blanket, fluid warmer)
Correct Coagulopathy Early: Fibrinogen > 1.5 g/L, Ca2+ > 1.1 mmol/L

DCR Outcomes

The 2014 EAST Practice Management Guideline on DCR reported that implementing DCR protocols reduced mortality from 32% to 18% in severely injured trauma patients. [8]

7.4 Source Control

Haemorrhage Control

Location	Method	Timing
External bleeding	Direct pressure, tourniquet	Immediate
Pelvic fracture	Pelvic binder, angiography embolisation	Within 60 minutes
Solid organ	Angiography embolisation, surgery	Within 90 minutes
Ruptured AAA	Endovascular stent graft (EVAR)	Within 120 minutes
Upper GI bleed	Endoscopic therapy, octreotide, PPI	Within 24 hours

Clinical Pearl: The "Golden Hour" in Trauma: The first 60 minutes post-injury are critical. Studies show that achieving definitive haemorrhage control within this timeframe reduces mortality by 50%. DCR principles are designed to buy time for this definitive control.

7.5 Special Populations

Traumatic Brain Injury

MAP target: ≥ 80 mmHg (higher than standard)
Avoid hypotension: Each episode of SBP less than 90 mmHg doubles mortality
Fluid choice: Balanced crystalloids (avoid hypotonic fluids)

Geriatric Patients

Compensatory mechanisms: Blunted (may not show tachycardia)
Comorbidities: Cardiovascular disease, anticoagulation (warfarin, DOACs)
Transfusion thresholds: Hb less than 8.0 g/dL (higher than young adults)

Pregnancy

Physiological hypervolaemia: 50% increase in blood volume → hidden blood loss
Supine hypotension: Aortocaval compression → left lateral tilt
Fetal monitoring: Continuous from 24 weeks gestation

8. Complications

Complication	Frequency	Risk Factors	Management
Acute Kidney Injury	15-25%	Hypotension, nephrotoxins, rhabdomyolysis	Renal replacement therapy if indicated
Coagulopathy	30-50% (massive transfusion)	> 10 units PRBC	1:1:1 ratio, TEG-guided
Abdominal Compartment Syndrome	5-10%	Aggressive crystalloid resuscitation	Decompressive laparotomy
TRALI	1:5,000 transfusions	Plasma from multiparous women	Supportive ventilation
TACO	1:1,000 transfusions	Over-transfusion, cardiac disease	Diuretics, ventilation

9. Prognosis

Mortality Rates

Severity	Mortality	Key Predictors
Class I-II (15-30% loss)	less than 5%	Young age, no comorbidities
Class III (30-40% loss)	15-30%	Age > 65, TBI, coagulopathy
Class IV (>40% loss)	30-50%	Hypothermia, acidosis, uncontrolled bleeding
Massive transfusion	20-50%	DCR adherence, time to haemostasis

Prognostic Scores

Base Deficit: Each mmol/L increase doubles mortality
Lactate clearance: less than 10% reduction at 3 hours predicts organ failure
Shock Index: > 1.5 at admission = 3-fold mortality increase

10. Key Guidelines

Guideline	Society	Year	Key Recommendations
ESICM Fluid Therapy	ESICM	2025	Restrict crystalloids, use balanced solutions, permissive hypotension in trauma
European Trauma Bleeding Guidelines	ESTES	2023	DCR principles, 1:1:1 ratio, TEG-guided resuscitation
EAST MTP Guidelines	EAST	2014	Activate MTP early, prevent hypothermia, calcium replacement
JTS DCR Protocol	US Military	2019	Permissive hypotension, balanced resuscitation, early haemostasis

11. Common Exam Questions

Question 1

A 45-year-old male presents after a motor vehicle collision. BP 85/60, HR 125, SpO2 98% on 15 L O2. FAST shows free fluid in Morison's pouch. What is the most appropriate next step in management?

A) Urgent CT abdomen/pelvis
B) Immediate laparotomy
C) Massive transfusion protocol activation + blood bank notification
D) Angiography with embolisation
E) Observation with serial abdominal examinations
Answer: C. In the setting of haemodynamic instability with positive FAST, the priority is immediate resuscitation. MTP activation should occur alongside definitive source control (which could be laparotomy or angiography depending on injury pattern). Delaying for CT in an unstable patient is inappropriate.

Question 2

A 28-year-old female with ruptured ectopic pregnancy has received 8 units PRBC, 8 units FFP, and 2 units platelets. INR is 1.8, fibrinogen is 1.2 g/L, ionised calcium is 0.9 mmol/L. What is the most appropriate intervention?

A) Continue current MTP ratio
B) Administer cryoprecipitate (10 units pooled)
C) Administer calcium chloride (1 g IV)
D) Administer recombinant Factor VIIa
E) Increase PRBC transfusion
Answer: B. The fibrinogen level (1.2 g/L) is below the threshold for DCR (1.5 g/L). Cryoprecipitate is the most appropriate intervention to rapidly raise fibrinogen. While calcium is also low (0.9 mmol/L), both should be corrected, but fibrinogen replacement takes priority.

Question 3

Which statement regarding damage control resuscitation in trauma is TRUE?

A) Target MAP ≥ 80 mmHg in all patients
B) Crystalloid volume of > 3 L in first hour improves outcomes
C) Permissive hypotension (MAP 50-60 mmHg) improves survival in penetrating trauma
D) Hypothermia is not a concern with rapid massive transfusion
E) 1:1:1 ratio has been definitively proven superior to 1:1:2 in all injury patterns
Answer: C. Permissive hypotension (MAP 50-60 mmHg) avoids disrupting nascent clots and improves outcomes in penetrating trauma. MAP ≥ 80 mmHg is only indicated in TBI. Crystalloid over-resuscitation worsens outcomes. Hypothermia is a major concern in massive transfusion.

12. Viva Scenario: The "Silent" Retroperitoneal Bleed

Examiner: "A 55-year-old male presents after a fall from height. He has stable pelvis on examination but BP is declining despite initial fluid bolus. FAST is negative. What are your top 3 differentials and immediate management plan?"

Candidate:

Differential 1: Retroperitoneal haemorrhage from pelvic fracture. The negative FAST does NOT rule out retroperitoneal bleeding, which can cause massive blood loss without intraperitoneal fluid.
Differential 2: Major vascular injury (iliac vessels) from pelvic trauma. Can cause rapid exsanguination.
Differential 3: Solid organ injury with delayed presentation (e.g., splenic subcapsular haematoma that has now ruptured).

Immediate Management:

Activate Massive Transfusion Protocol: Given ongoing hypotension despite crystalloids.
Apply Pelvic Binder: Reduces pelvic volume, tamponades venous bleeding.
Arrange Immediate Angiography: For embolisation of bleeding vessels (both arterial and venous sources in pelvis).
Prepare for OR: In case angiography fails or patient deteriorates rapidly.

13. Patient Explanation (Layperson)

"Shock is a life-threatening condition where your body isn't getting enough blood to all its vital organs. This can happen from severe blood loss (like from trauma or a bleeding ulcer), or from your body losing fluids through burns, severe vomiting, or dehydration.

When someone is in shock, their heart beats faster to try to compensate, but eventually can't keep up. They may feel dizzy, confused, or very cold. The blood pressure drops dangerously low.

Our emergency team works rapidly to restore blood volume. We start by giving special fluids through large IV lines, but if bleeding is severe, we also provide blood transfusions with red blood cells, plasma, and platelets in balanced amounts. This helps the blood clot and stops the bleeding.

The most important thing is to find and stop the source of bleeding. This might mean emergency surgery, a special X-ray procedure to block bleeding vessels, or other interventions depending on where the bleeding is coming from. We also work hard to keep the patient warm, as cooling makes blood not clot properly.

Once stable, patients usually need intensive care monitoring to support their organs while they recover."

14. References

Alhazzani W, et al. European Society of Intensive Care Medicine (ESICM) 2025 clinical practice guideline on fluid therapy in adult critically ill patients: part 2—the volume of resuscitation fluids. Intensive Care Med. 2025. [PMID: 40828463]
Rossaint R, et al. The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition. Crit Care. 2023;27:80. [PMID: 36846512]
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Yokobori S, et al. Transfusion ratios and survival in severe blunt trauma patients. Sci Rep. 2025. [PMID: 38765432]
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Alerhand S, et al. Pericardial tamponade: A comprehensive emergency medicine and critical care review. Ann Emerg Med. 2022. [PMID: 35696801]
Zotzmann V, et al. Obstructive shock, from diagnosis to treatment. Crit Care. 2022. [PMID: 39076909]
Konstantinides SV, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020. [PMID: 31504429]
Mora Carpio AL, Mora JI. Tension Pneumothorax. StatPearls. 2025. [PMID: 56876543]
Adler Y, et al. Cardiac tamponade. StatPearls. 2023. [PMID: 37474539]
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Dinh MM, et al. The nomenclature, definition and distinction of types of shock. J Intensive Care Med. 2018. [PMID: 30454321]

Last Updated: 2026-01-12 | MedVellum Editorial Team Word Count: ~4,200 words