Shock

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See:
- Sepsis
- Acute Heart Failure
- Approach to Undifferentiated Shock: a case-based tutorial for final year medical students

Definition

Physiologic state characterised by a systemic impairment in oxygen delivery as a result of reduced tissue perfusion, almost universally mediated by low blood pressure ( $D O_{2} < \dot{V} O_{2}$ )

Pathophysiology

Perfusion Pressure MAP - CVP = CO \times SVR

MAP = mean arterial pressure
CVP = central venous pressure (pressure in the vena cava)
CO = cardiac output
- $CO = HR \times SV$
- Stroke volume is dependent upon preload, contractility and afterload
SVR = systemic vascular resistance
Low perfusion pressure must therefore be due to:
- Low preload ⇒
  - hypovolaemic (e.g. trauma, GI haemorrhage, severe diarrhoea)
  - obstructive ∵ of obstruction to venous return to the LV (e.g. massive PE, pericardial tamponade, tension pneumothorax)
  - tachycardic arrythmogenic shock because of short diastolic filling time
- Low contractility ⇒ cardiogenic (e.g. Acute MI, severe heart failure exacerbation, viral myocarditis)
- Low heart rate ⇒
  - Bradycardic arrhythmogenic shock
- Low systemic vascular resistance ⇒ distributive (e.g. sepsis, anaphylaxis, spinal cord trauma)
- Other types:
  - Toxin-mediated shock (e.g. cyanide and carbon monoxide)

Classification

Cardiogenic shock
- Depressed contractility: ACS, myocarditis, myocardial contusion, cardiomyopathy, drug overdose (e.g. CCB or beta-blocker)
- Acute valvular dysfunction: Papillary muscle or chordae tendinae rupture, infective endocarditis, severe aortic stenosis or mitral stenosis
- Arrhythmia: Tachycardia (e.g. VT, AF, SVT), bradycardia (e.g. heart block)
Hypovolaemic shock
- Haemorrhagic
  - Traumatic: external or internal (e.g. haemothorax, haemoperitoneum, retroperitoneal haemorrhage)
  - Non-traumatic: external (e.g. haemoptysis, haematemesis, PV bleeding) or internal (e.g. haemothorax, ruptured AAA, bleeding diathesis)
- Non-haemorrhagic
  - External (e.g. GI losses from diarrhoea and vomiting, burns, hyperthermia, high-output fistulae)
  - Internal (e.g. bowel obstruction, pancreatitis)
Obstructive shock
- Intrinsic to cardiovascular system
  - Pulmonary embolism
  - Air embolism
  - Myxoma
  - Amniotic fluid embolism
- Extrinsic to cardiovascular system
  - Tension pneumothorax
  - Cardiac tamponade
  - Abdominal compartment syndrome
  - Dynamic hyperinflation: Excessive ventilation with severe bronchospasm (Asthma Exacerbation, COPD)
Distributive shock
- Anaphylaxis
- Sepsis
- Neurogenic: Loss of sympathetic tone from high spinal cord trauma or epidural anaesthesia
- Drug related: Vasodilator antihypertensive agents, nitrates, strong analgesics
- Acute adrenal insufficiency: Addison’s disease, discontinuing long-term steroids
The mnemonic CHOD can be used to remember the above, however a better framework may be PROVED?:
- Cardiogenic (Pump)
- Rhythm abnormalities
- Obstructive
- Hypovolaemia (Volume)
  - In the trauma patient consider: SCALPeR: scalp/street, chest, abdomen, long bones, pelvis and retroperitoneum
    - Steet refers to external blood loss at the scnes and other pre-hospital haemorrhage
- Endocrine (these often cause a mixed classification, but its inclusion ensures things like Adrenal Crisis, hypo/hyperthyroidism, Diabetic ketoacidosis, severe acidosis/alkalosis are not missed)
- Distributive
- ?: is it real (check the BP measurement, is the arterial line really in an artery and is the transducer at the correct height)

400

Clinical Features

Haemodynamics
- Hypotension (MAP < 65 mmHg or significant drop from baseline)
- Elevated shock index (HR/SBP) >0.8
- Urine output < 0.5 mL/kg/hour
- Dark urine
- ↑ troponin
Skin perfusion
- Cool hands and knees are an early sign of vasoconstriction with reduced cardiac output
- Mottling
  - Suggests active endogenous vasoconstriction, implying that the patient would benefit from ionotropy not vasopressors
- Capillary refill time (>5 seconds)

Neurological
- Altered mental status (agitation → delirium → solmnolence), generally more of a sign of septic shock
Respiratory
- ↑ respiratory rate
- ↓ oxygen saturation
Hepatological
- ↑ bilirubin, AST, ALT
Nephrology
- ↓ Urine output
- ↑ Creatine
Haematological
- ↑/↓ platelets
- ↑ INR which can lead to DIC
- ↑ lactate and ↓ $HCO X_{3} X^{-}$

Approach to Undifferentiated Shock

Primary Survey

Call early for a senior doctor to help
Assess airway patency
- Exclude airway obstruction and asphyxia
Start monitoring (pulse oximetry, ECG, BP)
Assess breathing:
- Oxygenation (saturation probe)
- Ventilation (end tidal CO2, chest auscultation)
- Exclude tension pneumothorax and massive haemothorax
Assess circulation
- Peripheral and central temperature/capillary refill
- Vital signs (heart rate, blood pressure)
- Equipment check
  - Exclude artifactual shock and equipment failure as the cause of shock, e.g. IABP malfunction, ECMO circuit problems, vasopressor infusion drug error.
- Head-to-toe exposure
  - Exclude externally obvious haemorrhage
  - Exclude anaphylaxis/angioedema
- 12-lead ECG
- Point of care TTE: rapid assessment with cardiac echo and RUSH exam
  - Exclude cardiac tamponade
  - Exclude massive PE

Main Assessment Factors to Differentiate Shock Types

Peripheral perfusion (as a measure of TPR)

Heart rate

Preload status using JVP, CVP, PPV or response to passive leg raise

Overview of RUSH Exam

Heart: LV function, RV dilation, pericardial effusion/tamponade

IVC: size and collapsibility (volume responsiveness)

Lungs: B-lines (pulmonary oedema), pneumothorax (absence of sliding)

Abdomen: free fluid (haemoperitoneum, ruptured AAA)

Aorta: AAA

Lower limbs: DVT (if PE suspected)

Can use the mnemonic HI-MAP (Heart, IVC, Morrison’s pouch, Aorta, Pneumothorax) or alternatively go in the approach of pump (heart), tank (IVC, Morison’s pouch), and pipes (aorta, DVT)

Establish venous access
Collect a series of generic laboratory investigations, most importantly an ABG
Mobile Chest X-ray
Assess neurology (i.e. spinal injury)
- Exclude neurogenic (“spinal”) shock

Approach to Undifferentiated Shock

Empirical Resuscitation

Ventilate the intubated patient with low-moderate PEEP (0.1 cm $H X_{2} O$ /kg)
Commence fluid bolus: 10 ml/kg
- Generally 30 mL/kg within the first 3 hours for sepsis
- Give as a fluid challenge: 250-500mL over 10-15 minutes
  - Assess MAP response and dnyamic predictors (PP variations, PLR)
- Balanced crystalloid (hartmann’s or plasmalyte) generally preferred to normal saline unless:
  - Hypochloraemic alkalosis (e.g. vomiting, NGT losses)
  - Hyperkalaemia
  - Traumatic brain injury
  - Meningitis
- Albumin
  - Albumin 4% reasonable alternative to crystalloid in large-volume resuscitation in septic shock
  - Albumin 20% used in hepatic failure/spontaneous bacterial peritonitis, hepatorenal syndrome
If the patient appears peri-arrest with life threatening hypotension give adrenaline 0.1 mg boluses to buy time and set up a vasopressor infusion
Commence/escalate vasopressor infusion (see below)
- The optimal initial vasopressor is unknown as is the optimal MAP
  - In septic shock, it appears the initial pressor of choice is noradrenaline
Antibiotics after peripheral cultures are obtained if sepsis is possible
Steroids in patients with suspected adrenal crisis
- When in doubt about adrenal insufficiency, a reasonable approach is to give 6 mg dexamethasone and check a cortisol level simultaneously¹

Approach to Undifferentiated Shock

Secondary Survey

Focused history:
- Immediate events preceding the collapse
- Drug administration history
- Recent interventions
- Relevant background history
- Collateral from recently attending staff/family
- Important history points:
  - ? chest pain/diaphoresis
  - Fevers, rigors, immunosuppression
  - Allergen exposure
  - Trauma/blood loss
  - Known cardiac disease, new dyspnoea
  - Chest procedure
  - Malignancy (PE)
  - Exogenous steroid use or adrenal disease
Focused examination and investigations
- ECG
- CXR
- ABG with special attention to lactate
- Head to toe examination
  - Fluid status (JVP, skin, mucous membranes, heart sounds, lung sounds, CRT, HR, SBP, urine output, IVC and collapsability)
  - Sources of sepsis
  - Toxidromes
  - Abdominal examination, looking for AAA, retroperitoneal haematoma and pancreatitis
- Bedside abdominal and chest ultrasound, looking for collections
- Formal (skilled) TTE, looking for valvular dysfunction, LVOT obstruction, regional wall motion abnormalities and septal defects
Labs
- FBC
- UEC
- LFT
- Inflammatory markers (CRP and procalcitonin)
- Blood cultures x 2
- Troponin and BNP
- Coagulation studies and D-dimer
- Cortisol level
- TSH and free T4 level

More than one type of shock may co-exist in the same patient for example:
- Sepsis + hypovolaemia
- Sepsis + sepsis induced cardiomyopathy

Approach to Refractory Shock

Diagnostic tests:
- Cardiac imaging:
  - Repeat POCUS
  - Formal echocardiography
  - Review CT imaging if available
  - Evaluate for unsual forms of shock (e.g. LVOT obstruction)
- Laboratory investigations:
  - ABG/VBG and EUCs
  - Glucose level
  - CMP
  - TSH and FT4
  - CRP, procalcitonin and blood cultures
- Pulmonary artery catheters
  - Guidelines and scientific statements suggest using pulmonary artery catheters early in the treatment course for selected patients who do not have a response to initial therapy or in cases of diagnostic or therapeutic uncertainty, such as in mixed shock
Treatment options:
- Optimise MAP target
  - Central arterial line (femoral or axillary) as opposed to radial artery
  - Reducing MAP target
- Review medications and stop hypotension inducing medications
  - Haemodynamically stable analgosedation (e.g. ketamine infusion)
  - Discontinue alpha-blockers being used for BPH
- Optimise pre-load
  - Reduce PEEP
  - Evaluate for auto-PEEP
  - Re-evaluate fluid status and consider volume administration if appropriate
- Metabolic optimisation
  - Temperature management
  - Intravenous calcium in patients with low ionised calcium
  - pH optimisation:
    - Bicarbonate
    - Ventilator management
    - Dialysis
  - IV thiamine for beriberi
  - Steroids may enhance vascular responsiveness to vasopressors
  - Thyroid hormone replacement for decompensated hypothyroidism
    - Probably treat with T3 to achieve more rapid improvement
- Vasopressor optimisation
  - High dose noradrenaline
  - Can consider second vasopressor (e.g. terlipressin)
  - If mottling present: pivot from vasopressors to inotropes
  - Consider right heart catheterisation for refractory or diagnostically unclear shock
- RV optimisation
  - Correct all reversible causes of elevated PVR: hypoxia (target SaO₂ >92%), hypercapnia, acidosis, over-distension on the ventilator
  - Pulmonary vasodilators: inhaled nitric oxide, nebulised iloprost (prostacyclin analogue)
  - Milrinone is the preferred inotrope when there is combined LV + RV failure — it reduces PVR while supporting both ventricles
  - Prone positioning reduces PVR in ARDS with cor pulmonale
- Heart rate optimisation
  - Atropine
  - Isoprenaline
  - Pacing
- Mechanical circulatory support
  - Invasive aortic balloon pump
  - Impella
  - VA-ECMO

Trauma Related Shock

Haemorrhagic Shock

Assessing severity
- Hypotension is a late sign, particularly in young patients who compensate with tachycardia and vasoconstriction
- Shock index (HR/SBP) and pulse pressure can be used to assess the degree of hypovolaemic shock²
Stop the bleeding
- Identifying the cause of bleeding and controlling it as soon as possible is essential³; fluids and blood products only buy time until this happens
Permissive hypotension
- Restricted volume replacement with a target SBP of 80–90 mmHg until major bleeding has stopped, in patients without clinical evidence of brain injury²
- Severe TBI (GCS ≤ 8): maintain MAP ≥ 80 mmHg²
- If restricted volume replacement doesn’t achieve the target, add noradrenaline to fluids²
Fluids
- 0.9% saline or balanced crystalloid can be started²
- Avoid hypotonic solutions such as Ringer’s lactate (i.e. Hartmann’s) in severe head trauma²
- Restrict colloids due to their adverse effects on haemostasis²
Major haemorrhage protocol (MHP)³
- Institutions should use an MHP that covers haemorrhage control, correction of coagulopathy and normalisation of physiological derangement
- A high ratio of RBC:FFP:PLT may be beneficial, but there is insufficient evidence for 1:1:1 over 2:1:1
  - Ratio should be no lower than 2:1:1, achieved as soon as possible and maintained until bleeding is controlled
  - Initial doses: at least 1 unit FFP with every 2 units RBC, and at least 1 adult unit of platelets with every 8 units RBC
  - 1 adult unit of platelets in Australia = platelets from 4 whole blood donors, so 1:1:1 = 4 RBC : 4 FFP : 1 adult platelets
- Fibrinogen replacement: 3–4 g as fibrinogen concentrate or cryoprecipitate (e.g. 3 units of apheresis cryoprecipitate)
- Measure early and frequently: temperature, acid–base status, ionised calcium, Hb, platelets, PT/INR, APTT and fibrinogen; consider repeating after every 4 units of RBC
- Values indicating critical physiological derangement:
  - Temperature < 35 °C
  - pH < 7.2, base excess < –6 mmol/L, lactate > 4 mmol/L
  - Ionised calcium < 1 mmol/L
  - INR > 1.5, PT or APTT > 1.5 × ULN
  - Fibrinogen < 2.0 g/L
- Give RBC through a blood warmer and keep core temperature ≥ 35 °C
- Correct hypocalcaemia with calcium chloride²
- Switch to group-specific blood components as soon as possible, and cease the MHP once critical bleeding is controlled
Tranexamic acid
- 1 g IV over 10 minutes, then 1 g over 8 hours²
- Give as soon as possible and within 3 hours of injury²³; don’t wait for viscoelastic testing²
- CRASH-2 showed a reduction in all-cause mortality (14.5% vs 16.0%)⁴; the benefit appears confined to patients treated within 3 hours of injury, with possible harm after this⁵
- Insufficient evidence to recommend it in critical GI bleeding³

Trauma Related Shock

Neurogenic Shock

Loss of sympathetic tone, typically after spinal cord injury at or above T6⁶
- Hypotension (SBP < 90 mmHg) from loss of vascular tone and pooling of blood in the limbs
- Bradycardia and reduced contractility from unopposed vagal activity
In multitrauma, consider other causes of shock (particularly haemorrhage) before attributing hypotension to the spinal injury⁶
Management⁶
- Fluid resuscitation, balanced against the risk of fluid overload
- Vasopressors/inotropes second line, targeting MAP 85–90 mmHg in the acute phase

Vasopressors and Ionotropes

Start noradrenaline early — don’t wait for large volumes of fluid; fluid overload is harmful
Peripheral vasopressor use (short-term, large proximal vein) is acceptable to avoid delaying treatment while CVC inserted
Corticosteroids for vasopressor-refractory septic shock: hydrocortisone 200 mg/day IV (APROCCHSS, ADRENAL trials)
Titrate to MAP 65 (not higher in most cases — SEPSISPAM trial: no benefit at MAP 80–85)

Noradrenaline

0.01-3 mcg/kg/min IV infusion (central line preferred)

First line vasopressor in distributive and most forms of shock

Predominantly $α_{1}$ agonist with some $β_{1}$ ⇒ ↑ SVR and mild ↑ HR/CO

Can be run peripherally short-term (forearm or antecubital) at low doses while CVC inserted

Metaraminol

Bolus: 0.5-2 mg IV PRN | Infusion: 15-30 mg in 500 mL at 15-60 mL/hr

Predominantly $α_{1}$ agonist; also causes indirect noradrenaline release

Used widely in peri-operative setting and as bridge vasopressor pre-noradrenaline

Can be given peripherally; suitable in ward or theatre setting

Tachyphylaxis with prolonged use

Reflex bradycardia can occur - treat with atropine

Less titratable than noradrenaline infusion

Adrenaline

Anaphylaxis: 0.3-0.5 mg IM (thigh) | Shock infusion: 0.01-1 mcg/kg/min IV

Anaphylaxis: IM adrenaline (Epipen 0.3 mg or ampoule 1:1000) is the drug of first choice

Septic shock: Second agent alongside noradrenaline when additional inotropic support needed; associated with increased lactate that does not reflect true worsening

Cardiogenic shock: Adrenaline has more arrhythmogenic risk than other inotropes

Cardiac arrest: 1 mg IV every alternate loop

Terlipressin

Bolus: 0.85–2.5 mg IV bolus q4–6h | Infusion: 1.3–5 mg/24h

$V_{1}$ receptor agonist (smooth muscle vasoconstriction)

Hepatorenal syndrome type 1: terlipressin + albumin is first line

Variceal bleeding: 2mg IV bolus then 1 mg q4-6h for up to 5 days

Used in refractory septic shock as noradrenaline-sparing agent (off-label in Australia)

Risk: digital/skin ischaemia, bradycardia, mesenteric ischaemia — monitor carefully

Avoid in ischaemic heart disease, peripheral vascular disease

Dobutamine

2–20 mcg/kg/min IV infusion

$β_{1}$ and $β_{2}$ agonist - positive inotropy, chronotropy; reduces SVR (vasodilatory)

Used in cardiogenic shock with adequate MAP (often combined with noradrenaline)

Risk of tachycardia and arrhythmia; may worsen hypotension in true hypovolaemia

Milrinone

0.125–0.75 mcg/kg/min IV (load: 25–50 mcg/kg over 10 min, often omitted)

Used in cardiogenic shock, especially post-cardiac surgery or when β-receptor downregulation limits dobutamine effect

Useful in pulmonary hypertension (reduces PVR)

Longer half-life — effects accumulate, harder to titrate; prolonged hypotension if overdosed

Renally cleared — dose-reduce in AKI

Phenylephrine

Bolus 50–200 mcg IV | Infusion 10–300 mcg/min

Pure α₁ agonist — vasoconstriction without inotropic effect

Useful in tachycardia-associated shock where noradrenaline’s β₁ effect is undesirable (e.g., HOCM, AF with fast ventricular rate)

Reflex bradycardia — use cautiously in bradycardic patients

Can worsen cardiogenic shock by increasing afterload without supporting cardiac output

Situation	First agent	Add / escalate to	Avoid
Undifferentiated shock	Noradrenaline	Fluid trial first; escalate based on 6-step framework	—
Septic shock (vasodilatory)	Noradrenaline	Terlipressin (refractory); hydrocortisone; adrenaline if inotrope also needed	Excess fluid, dopamine
Cardiogenic shock (LV)	Noradrenaline (MAP support)	Dobutamine or milrinone (inotropy); IABP/Impella/VA-ECMO escalation	Dopamine, excessive adrenaline
RV failure	Noradrenaline	Milrinone (reduces PVR + inotrope); adrenaline; inhaled iloprost/NO	Vasodilators, aggressive fluid loading in RV dilation
Anaphylaxis	Adrenaline 0.5 mg IM	Adrenaline IV infusion; fluids; glucagon if on β-blockers	Any delay to adrenaline
Peri-operative / spinal hypotension	Metaraminol 0.5–2 mg IV bolus	Noradrenaline infusion once CVC placed; phenylephrine if bradycardic	—
Bradycardic shock	Atropine → isoprenaline infusion	Temporary transvenous pacing	Phenylephrine, metaraminol (worsen bradycardia)
LVOTO / HOCM	Phenylephrine + fluid bolus	Esmolol infusion (rate control)	Inotropes, vasodilators, tachycardia-promoting agents
Adrenal crisis	Hydrocortisone 100 mg IV + saline	Noradrenaline if MAP not restored	Delaying hydrocortisone for investigations

Fluid Responsiveness

See Fluid Responsiveness

Steroids

Corticosteroids should not be used routinely for patients with septic shock
- the weight of evidence does not support a benefit in terms of patient-orientated outcomes
- ACTH stimulation tests are not useful in this patients
- hydrocortisone 200 mg IV daily is an option for septic shock patients who are refractory to vasopressors (e.g. adults requiring IV noradrenaline at 20-30 micrograms/h) and no other cause found; despite an absence of convincing supportive evidence of benefit
Corticosteroids should be used in patients who have shock and a specific indication for corticosteroid therapy
- e.g. anaphylaxis, known steroid dependence (e.g. for chronic immunosuppression), known hypoadrenalism, other steroid-responsive conditions like asthma or rheumatoid arthritis

Fluid Replacement in Dehydrated Patients

Fluid replacement in dehydrated patients

Resuscitate intravascular volume until perfusion is normalised as above with 20 mL/kg boluses of crystalloid (normal saline preferred)

Calculate fluid losses (generally at least 10% of body weight if patient is dehydrated and hypotensive, i.e. 70kg patient is depleted of 7L of fluid)

Subtract from this defecit the amount of fluid already given for resuscitation (e.g. if 2L given during resuscitation, a 70kg patient still requires 5L of fluid)

Replace this amount over the next 24 hours together with maintenance fluid and ongoing losses

Use 4:2:1 rule, or add 60mL to their weight for hourly fluid requirement ⇒ 110mL/hr ≈ 2.5L/day

Total fluid to be replaced is 7.5 L

Replace half in first 8 hours and remainder in next 16 hours

3.75L over 8 hours ≈ 450 mL/h

3.75L over 16 hours ≈ 230 mL/h

Monitor adequacy of replacement by perfusion and vital signs, urine output and electrolyte changes

Appendix

Drug	Alpha-1	Beta-1	Beta-2	Dopamine	Effect on SVR	Effect on HR	Effect on CO	Effect on BP
Phenylephrine	+++	0	0	0	↑↑	↓ / ↔	↓	↑↑
Metaraminol	+++	+ (indirect)	0	0	↑↑	↔ / ↑	↔ / ↑	↑↑
Vasopressin (V1 agonist)	0	0	0	0	↑↑	↔	↓	↑
Noradrenaline	+++	++	0	0	↑↑	↑	↔ / ↑	↑↑
Adrenaline (Low dose)	+	+++	++	0	↓	↑	↑	↔ / ↑
Adrenaline (High dose)	++	+++	++	0	↔ / ↑	↑	↑	↑↑
Dopamine (Low dose)*	0	+	0	++	↔	↑	↑	↑
Dopamine (Moderate dose)*	+	++	0	++	↑	↑	↑	↑↑
Dopamine (High dose)*	++	++	0	++	↑↑	↑	↔ / ↑	↑↑
Dobutamine	0 / +	+++	++	0	↓	↑	↑↑	↓ / ↔ / ↑
Isoprenaline	0	+++	+++	0	↓	↑↑	↑↑	↓ / ↔
Milrinone (PDE inhibitor)	0	0	0	0	↓	↔ / ↑	↑↑	↓ / ↔ / ↑

Sources

Youtube Videos
- Strong Medicine
LITFL:
Deranged Physiology
- Definition and classification of shock
- Approach to the undifferentiated shock patient
UpToDate: Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock
Undifferentiated Shock — ICU One Pager
Vasopressors — ICU One Pager
Fluid Responsiveness - could this hemodynamically unstable patient respond to IV fluids? — ICU One Pager
Thiele H, Hassager C. Cardiogenic Shock. New England Journal of Medicine. 2025;394(1):62-77. doi:10.1056/NEJMra2312086

Footnotes

Dexamethasone does not interfere with the cortisol level allowing one to perform an ACTH stimulation test later if indicated
Rossaint R, Afshari A, Bouillon B, et al. The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition. Critical Care. 2023;27:80. doi:10.1186/s13054-023-04327-7
National Blood Authority. Patient blood management guideline for adults with critical bleeding (v2.0, September 2025)
CRASH-2 trial collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2). Lancet. 2010;376(9734):23-32. doi:10.1016/S0140-6736(10)60835-5
Roberts I, Prieto-Merino D, Manno D. Mechanism of action of tranexamic acid in bleeding trauma patients: an exploratory analysis of data from the CRASH-2 trial. Critical Care. 2014;18:685. doi:10.1186/s13054-014-0685-8
Queensland Spinal Cord Injuries Service. Spinal and neurogenic shock