Shock

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

all patients

1st line – supportive management of airway

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1st line –

supportive management of airway

Get senior help immediately if you suspect airway compromise.[26]

Use simple airway measures while waiting for help.[26]

Airway opening manoeuvres
- Use head-tilt chin-lift if there is no risk of cervical spine injury.
- Use jaw thrust if risk of cervical spine injury.
Airways suction
- Generally used to clear the airway if there is excess respiratory or gastric secretions.
Consider inserting an oropharyngeal or nasopharyngeal airway in deeply unconscious patients (Glasgow Coma Scale [GCS] ≤8).

Consider early intubation and ventilation for severe shock if there is respiratory distress, severe hypoxaemia, pronounced acidosis, or significantly reduced consciousness (GCS ≤8).[18][34]

Practical tip

Seek senior critical care input at an early stage in profoundly shocked patients, particularly those with severe acidosis or an impaired level of consciousness.

Consider preloading the circulation with intravenous fluids and ensure that a vasopressor can be urgently administered if a patient is undergoing intubation. Induction in severe shock has a significant chance of precipitating profound circulatory collapse through the myocardial depressant effects and vasodilating properties of many induction agents.[18][34]

Plus – supportive management of breathing

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Plus –

supportive management of breathing

Treatment recommended for ALL patients in selected patient group

Monitor controlled oxygen therapy. An upper SpO₂ limit of 96% is reasonable when administering supplemental oxygen to most patients with acute illness who are not at risk of hypercapnia.

Evidence suggests that liberal use of supplemental oxygen (target SpO₂ >96%) in acutely ill adults is associated with higher mortality than more conservative oxygen therapy.[27]
A lower target SpO₂ of 88% to 92% is appropriate if the patient is at risk of hypercapnic respiratory failure.[28]

Evidence: Target oxygen saturation in acutely ill adults

Too much supplemental oxygen increases mortality.

Evidence from a large systematic review and meta-analysis supports conservative/controlled oxygen therapy versus liberal oxygen therapy in acutely ill adults who are not at risk of hypercapnia.

Guidelines differ in their recommendations on target oxygen saturation in acutely unwell adults who are receiving supplemental oxygen.
- The 2017 British Thoracic Society (BTS) guideline recommends a target SpO₂ range of 94% to 98% for patients not at risk of hypercapnia, whereas the 2022 Thoracic Society of Australia and New Zealand (TSANZ) guideline recommends 92% to 96%.[28][120]
- The Global Initiative For Asthma (GINA) guidelines recommend a target SpO₂ range of 93% to 96% in the context of a severe exacerbation of asthma.[178]
A systematic review including a meta-analysis of data from 25 randomised controlled trials, published in 2018, found that in adults with acute illness, liberal oxygen therapy (broadly equivalent to a target saturation >96%) is associated with higher mortality than conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[27] In-hospital mortality was 11 per 1000 higher for the liberal oxygen therapy group versus the conservative therapy group (95% CI, 2-22 per 1000 more). Mortality at 30 days was also higher in the group who had received liberal oxygen (relative risk 1.14, 95% CI 1.01 to 1.29). The trials included adults with sepsis, critical illness, stroke, trauma, myocardial infarction, or cardiac arrest, and patients who had emergency surgery. Studies that were limited to people with chronic respiratory illness or psychiatric illness, or patients on extracorporeal life support, receiving hyperbaric oxygen therapy, or having elective surgery, were all excluded from the review.
An upper SpO₂ limit of 96% is therefore reasonable when administering supplemental oxygen to patients with acute illness who are not at risk of hypercapnia. However, a higher target may be appropriate for some specific conditions (e.g., pneumothorax, carbon monoxide poisoning, cluster headache, and sickle cell crisis).[122]
In 2019 the BTS reviewed its guidance in response to this systematic review and meta-analysis and decided an interim update was not required.[123]
- The committee noted that the systematic review supported the use of controlled oxygen therapy to a target.
- While the systematic review showed an association between higher oxygen saturations and higher mortality, the BTS committee felt the review was not definitive on what the optimal target range should be. The suggested range of 94% to 96% in the review was based on the lower 95% confidence interval and the median baseline SpO₂ from the liberal oxygen groups, along with the earlier 2015 TSANZ guideline recommendation.
Subsequently, experience during the COVID-19 pandemic has also made clinicians more aware of the feasibility of permissive hypoxaemia.[124]
Management of oxygen therapy in patients in intensive care is specialised and informed by further evidence (not covered in this summary) that is more specific to this setting.[125][126][127]

Use non-invasive ventilation (NIV) if necessary unless contraindicated. Beware that use of NIV in shocked patients can worsen hypotension. Therefore, monitor blood pressure closely.[37][109]

NIV is contraindicated in the following:[37]
- If pneumothorax is suspected
- Confusion/agitation (especially if Glasgow Coma Scale ≤8)
- Severe hypoxaemia
- Copious respiratory secretions
- Recent facial or upper airway surgery or in the presence of facial abnormalities such as burns or trauma
- Fixed obstruction of upper airway
- Vomiting.
Consider continuous positive airway pressure (CPAP) in the following:[37]
- Hypoxaemia requiring high respiratory rate, effort, and fraction of inspired oxygen (FiO ₂)
- Left heart failure with severe dyspnoea and acidaemia at acute presentation or as an adjunct to medical therapy to improve hypoxaemia if the patient's condition has failed to respond.[29]
  Evidence: Use of CPAP in cardiogenic shock reduces mortality
  Several studies show that CPAP is effective in patients with cardiogenic shock with acute heart failure as it rapidly improves gas exchange and cardiac haemodynamics, and can decrease intubation rates and in-hospital mortality.
  - One study randomised 40 patients to either face mask CPAP (10 cm H₂O) or standard medical therapy, and showed improvement in gas exchange, decrease in respiratory work, and reduced need for intubation for those patients with CPAP.[128] Another study randomised 55 patients to CPAP or high-flow oxygen therapy, and showed significant decrease in the intubation rates in the CPAP group compared with controls (28% vs 60%, respectively).[129]
  - A further comparison of the efficacy of CPAP (10 cm H₂O) with that of conventional treatment was made in a study of 39 patients with cardiogenic pulmonary oedema and found a significant and rapid improvement in arterial oxygen tension and a significant decrease in arterial carbon dioxide tension in patients treated with CPAP compared with those treated conventionally. Whereas no patient required endotracheal intubation in the CPAP group, 35% of the patients in the oxygen group were intubated within 3 hours of study entry. Although the final death rate was similar in both groups, patients receiving CPAP showed a significant reduction in intensive care unit length of stay.[130]

Consider bilevel positive airway pressure (BiPAP) if the patient has hypercapnic (type II) respiratory failure (PaCO ₂ >6 kPa or 45 mmHg and acidotic [pH <7.35 or free hydrogen ion {H+} >45 nanomol/L]), with targeted oxygen therapy if respiratory acidosis persists for more than 30 minutes after initiation of standard medical management.

Practical tip

Assess whether the patient needs intubation and invasive ventilation more than NIV. Do not hesitate to involve senior support.[37]

Escalate to critical care in any of the following:[37]

Impending respiratory arrest
NIV failing to augment chest wall movement or augment partial pressure of carbon dioxide (pCO₂)
Inability to maintain target oxygen saturations on NIV
Need for intravenous sedation or presence of adverse features requiring closer monitoring.

Plus – treat underlying cause

cardiogenic shock suspected or confirmed

Consider – intravenous fluids

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Consider –

intravenous fluids

Additional treatment recommended for SOME patients in selected patient group

Ensure early intravenous access in all patients.[31]

Use 2 wide-bore cannula, especially in patients who are actively bleeding.
Consider intraosseous access if intravenous access is challenging.

Practical tip

The intraosseous route can be used to administer most drugs and fluids, including blood products. However, they will not flow freely and drugs will need to be given by syringe, and blood/fluids need to be given through a pressure bag.

Give careful fluid resuscitation for patients with cardiogenic shock as too much fluid may lead to onset or worsening of acute pulmonary oedema.

These patients may need additional specialised monitoring of their cardiac function, cardiac output, and preload to determine fluid requirements.[2][14]

Give fluid resuscitation in all patients apart from those with evidence of cardiogenic pulmonary oedema. This is crucial for stabilisation of a patient with shock.[1][3]

Give a fluid challenge.[2][3][30]
- Use crystalloids, starting with a bolus of 500 mL given over less than 15 minutes.[30]
  - Adjust according to patient’s characteristics such as age, size, and comorbidities.
  - In a patient with known cardiac failure, use smaller volumes (e.g., 250 mL).[26]
- Do not give clear fluids to patients with hypovolaemic shock secondary to acute blood loss especially in trauma unless blood products are not immediately available.[31][39]
  - These patients will need urgent identification and cessation of the source of bleeding and may need a blood transfusion or immediate transfer to theatre (e.g., in ruptured abdominal aortic aneurysm or major trauma).
Repeat fluid challenges depending on clinical need.[30]
- Following initial fluid resuscitation, additional fluids should be guided by frequent reassessment of haemodynamic status.[1]
- Examine for hypovolaemia/fluid overload and assess the patient’s response to fluids. Possible outcomes include:
  - A sustained increase in blood pressure: proceed cautiously with fluids, then reassess in 15 to 30 minutes
  - An increase and then a decrease in blood pressure: give another fluid bolus and reassess as the patient appears fluid responsive
  - No change in blood pressure: means that the patient is not fluid responsive, hypovolaemia is not the cause for the low blood pressure, or the patient has had adequate fluid replacement.

Practical tip

Fluid titration is essential in all patients (especially those with raised intravascular filling pressures or pulmonary oedema) as both hypovolaemia and hypervolaemia can be harmful.[2]

Check local protocols for specific recommendations on fluid choice. There is debate, based on conflicting evidence, on whether there is a benefit in using normal saline or balanced crystalloid in critically ill patients.

Practical tip

Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis.

Also note that use of lactate-containing fluid in a patient with impaired liver metabolism may lead to a spuriously elevated lactate level, so results need to be interpreted with other markers of volume status.

Evidence: Choice of fluids

Evidence from two large randomised controlled trials (RCTs) suggest there is no difference between normal saline and a balanced crystalloid for critically ill patients in mortality at 90 days, although results from two meta-analyses including these RCTs point to a possible small benefit of balanced solutions compared with normal saline.

There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann’s solution [also known as Ringer’s lactate] or Plasma-Lyte®). Clinical practice varies widely, so you should check local protocols.

In 2021-2022, two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte®) versus normal saline. The Plasma-Lyte 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[132][133]
- In the PLUS study, 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
- In BaSICS, almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
- Both found no difference in 90-day mortality overall or in prespecified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
- In BaSICS, for patients with traumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.

A meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[134]
A subsequent individual patient data meta-analysis included 6 RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (OR 0.96, 95% CI 0.91 to 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[135]
- A prespecified subgroup analysis of patients with traumatic brain injury (N=1961) found that balanced solutions increased the risk of in-hospital mortality compared with normal saline (OR 1.42, 95% CI 1.10 to 1.82).

Previous evidence has been mixed.
- A 2015 double-blind, cluster randomised, double-crossover trial conducted in four ICUs in New Zealand (N=2278), the 0.9% Saline vs Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, acute kidney injury, or use of renal-replacement therapy.[136]
- However, a 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4%, respectively (OR 0.91, 95% CI 0.84 to 0.99).[136]
A 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[138]
- The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
- There was no difference in in-hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).

Target an initial mean arterial pressure (MAP) of 65 mmHg if the cause of shock is unknown.[1][2]

This target may change depending on the cause of shock and the patient’s normal blood pressure.[1][2]
- Aim for a higher MAP in patients with a history of hypertension, and in those who show clinical improvement with higher blood pressure.[2]
- Adjust the target MAP for all patients with cardiogenic shock. No clinical studies have investigated the optimal blood pressure level, and current guidelines no longer recommend a target blood pressure.[2]

Consider – loop diuretic

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Consider –

loop diuretic

Additional treatment recommended for SOME patients in selected patient group

Use a loop diuretic if there is pulmonary oedema and fluid overload.[3][29]

Intravenous furosemide is the most commonly used first-line diuretic.
If the patient is already on oral furosemide (or has used diuretics previously), a higher intravenous starting dose may be required. In these cases, the initial intravenous dose should be at least equal to the pre-existing oral furosemide dose used at home. The dose should be titrated gradually according to response, renal function, and blood pressure.
Combination therapy requires careful monitoring of serum electrolytes and renal function.[3]

Evidence: Loop diuretics are widely used but may cause adverse outcomes

There is a lack of high-quality data that supports the safety and efficacy of loop diuretics in cardiogenic shock. Despite this they are still widely used and recommended in major guidelines.[3][29]

Intravenous furosemide in patients with cardiogenic shock typically results in a prompt diuretic effect (within 30 minutes) that peaks at 1.5 hours. This leads to a decrease in ventricular filling pressures and improvement in symptoms in most patients. Two large randomised controlled trials showed this effect and that treatment based primarily on loop diuretics was associated with rapid and substantial improvement of dyspnoea.[139][140]
However, administration of loop diuretics activates the renin-angiotensin-aldosterone system and the sympathetic nervous system, both of which play a fundamental role in heart failure progression.[141][142][143]
Loop diuretics also significantly decrease glomerular filtration rate in some patients with heart failure, presumably due to renin-angiotensin-aldosterone system and sympathetic nervous system activation with related changes in renal blood flow and glomerular filtration pressure.[144]
Clinically, observational studies suggest an association between diuretic use and worsening outcomes in patients.[145][146] In a retrospective study of 6797 patients, use of a diuretic was associated with a 37% increase in the risk of arrhythmic death after controlling for multiple other measures of disease severity.[147]
Several other studies have identified an association between higher doses of diuretics and adverse outcomes in patients.[148][149]

Primary options

furosemide: 20-50 mg intravenously initially, increase by 20 mg every 2 hours if required according to response, maximum 1500 mg/day

Consider – vasodilator

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Consider –

vasodilator

Additional treatment recommended for SOME patients in selected patient group

If the patient has pulmonary oedema and systolic blood pressure >90 mmHg, consider a vasodilator (e.g., glyceryl trinitrate, nesiritide) and ensure the patient is transferred to a critical care environment so that blood pressure can be continuously monitored.[3][150]

Both intravenous glyceryl trinitrate and nesiritide lower left ventricular filling pressure and provide symptomatic improvement.[151]
Glyceryl trinitrate is the preferred drug.
- Nesiritide is used less commonly, as there is some concern about worsening renal function and increased mortality.[152][153][154] Nesiritide is not available in the UK.

Primary options

glyceryl trinitrate: 10 micrograms/minute intravenous infusion initially, increase gradually according to response, maximum 400 micrograms/minute

Consider – vasoactive drug

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Consider –

vasoactive drug

Additional treatment recommended for SOME patients in selected patient group

Manage patients who require a vasoactive drug (vasopressor/inotrope) in a critical care setting.

Insert an arterial line and central venous catheter (CVC) in patients with shock that is not responsive to initial therapy and/or requires infusion of a vasoactive drug.[2]

This allows continuous accurate blood pressure monitoring, and regular blood gas analysis.
Give all vasoactive drugs through a CVC (with the exception of metaraminol and adrenaline [epinephrine], which can be given both peripherally and through a CVC) to minimise the risk of extravasation and subsequent tissue necrosis.
- Adrenaline can be given as a bolus via peripheral access while preparing a noradrenaline (norepinephrine) infusion or obtaining central or arterial access. Ideally this should be through a large-bore cannula in the antecubital fossa. However, an adrenaline infusion should always be given via a CVC.

Use a vasopressor (e.g., noradrenaline) if there is hypotension or continuing reduced tissue hypoperfusion despite intravenous fluids.[1]

Vasopressors are particularly useful in high cardiac output, low peripheral resistance states.
Give them only after adequate fluid resuscitation. Use of vasopressors when the patient is fluid-deplete can worsen tissue perfusion.
Vasopressors cause vasoconstriction that aims to reverse the mismatch between vessel tone and intravascular volume.
They increase the risk of tissue ischaemia and necrosis in a dose-dependent manner. Other adverse effects include decreased cardiac output, increased risk of tachycardia and arrhythmias, and increased cardiac work.[158][159][160]

Use an inotrope (e.g., dobutamine) if there is impaired cardiac function and a low/inadequate cardiac output and signs of tissue hypoperfusion persist after preload optimisation.[2]

Do not use for isolated impaired cardiac function without a low/inadequate cardiac output.
Do not use in patients with haemorrhagic shock.
Inotropes increase cardiac output by increasing both stroke volume and heart rate. This increases mean arterial pressure and maintains perfusion to vital organs and tissues.
Adverse effects include arrhythmias, tachycardia, hypertension/hypotension, and anginal chest pain.[161]

Consult a specialist for guidance on suitable vasopressor/inotrope regimens.

haemorrhagic shock suspected or confirmed

Plus – activate major haemorrhage protocol

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Plus –

activate major haemorrhage protocol

Treatment recommended for ALL patients in selected patient group

Ensure early intravenous access in all patients.[31]

Use 2 wide-bore cannula, especially in patients who are actively bleeding.
Consider intraosseous access if intravenous access is challenging.

Practical tip

Activate local major haemorrhage protocol for all patients with haemorrhagic shock.

Use blood products (red blood cells and fresh frozen plasma [FFP]).[31][39][94]

Look up your local major haemorrhage protocol as the ratio of these vary.
UK National Institute for Health and Care Excellence guidelines and British Society of Haematology (BSH) guidelines suggest using a 1:1 ratio of red blood cells to FFP in trauma and at least a 1:2 ratio in non-trauma patients .[31][94]
BSH guidelines also recommend further blood products in the following circumstances:
- Give platelets if platelets <75 x 10⁹/L (or <100 x 10⁹/L in brain and spine injuries)
- Give cryoprecipitate or fibrinogen concentrate if fibrinogen <1.5 g/L (<150 mg/dL) (<2 g/L [<200 mg/dL] if obstetric)
- Give FFP if prothrombin time and/or activated partial thromboplastin time >1.5 times normal.

Target a haemoglobin (Hb) level of 7-9 g/dL (70-90 g/L).[18][39]

Consider a target Hb of 8-10 g/dL (80-100 g/L) in patients with ischaemic heart disease.

Reverse anticoagulation if a patient is taking an anticoagulant.

Give a prothrombin complex concentrate to reverse warfarin.
Give idarucizumab to reverse dabigatran.[156]
Give andexanet alfa (recombinant coagulation factor Xa) to reverse apixaban and rivaroxaban.[157] Andexanet alfa is not available in the UK.
There is no licensed reversal agent for edoxaban as yet.

Give intravenous tranexamic acid in trauma patients with major trauma and active or suspected active bleeding. Treatment should commence within 3 hours of injury. Use may be considered in non-traumatic haemorrhage also.[31][94]

Practical tip

Do not be falsely reassured by a normal haemoglobin in an early blood sample. Vasoconstriction in acute blood loss delays a fall in haemoglobin and may mask the severity of haemorrhagic shock.

Primary options

Reversal of warfarin

prothrombin complex concentrate: consult local protocols for guidance on dose

Reversal of dabigatran

idarucizumab: 5 g intravenously as a single dose, followed by 5 g if required

Major trauma and active or suspected active bleeding

tranexamic acid: 1 g intravenously as a loading dose, followed by 1 g by intravenous infusion over 8 hours

Consider – intravenous fluids (if blood products unavailable)

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Consider –

intravenous fluids (if blood products unavailable)

Additional treatment recommended for SOME patients in selected patient group

If blood products are not immediately available, give early clear fluids until blood products are available. This is crucial for stabilisation of a patient with shock.[1][94]

Give a fluid challenge.[2][3][30]
- Use crystalloids, starting with a bolus of 500 mL given over less than 15 minutes.[30][47]
  - Adjust according to patient’s characteristics such as age, size and comorbidities.
  - In a patient with known cardiac failure, use smaller volumes (e.g., 250 mL).[26]
- Do not give clear fluids in hypovolaemic shock due to acute blood loss especially in trauma unless blood products are not immediately available.[31][39]
  - These patients need urgent identification and cessation of the source of bleeding and may need a blood transfusion or immediate transfer to theatre (e.g., in ruptured abdominal aortic aneurysm or major trauma.)
Repeat fluid challenges depending on clinical need, in boluses of 250-500 mL.[30]
- Following initial fluid resuscitation, additional fluids should be guided by frequent reassessment of haemodynamic status.[1]
- Examine for signs of hypovolaemia/fluid overload and assess the patient’s response to administration of fluids. Possible outcomes include:
  - A sustained increase in blood pressure: proceed cautiously with fluids, then reassess in 15 to 30 minutes
  - An increase and then a decrease in blood pressure: give another fluid bolus and reassess as patient appears fluid responsive
  - No change in blood pressure: means that either the patient is not fluid responsive, hypovolaemia is not the cause for the low blood pressure, or the patient has had adequate fluid replacement.

Practical tip

Titration of fluids is important as both hypovolaemia and hypervolaemia can be harmful. This applies even in patients responding well to fluids, especially if there is elevated intravascular filling pressures or pulmonary oedema.[2]

Practical tip

Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis.

Evidence: Choice of fluids

There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann's solution [also known as Ringer's lactate] or Plasma-Lyte®). Clinical practice varies widely, so you should check local protocols.

In 2021-2022, two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte®) versus normal saline. The Plasma-Lyte 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[132][133]
- In the PLUS study, 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
- In BaSICS, almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
- Both found no difference in 90-day mortality overall or in prespecified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
- In BaSICS, for patients withtraumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.

A meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[134]
A subsequent individual patient data meta-analysis included 6 RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (OR 0.96, 95% CI 0.91 to 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[135]
- A prespecified subgroup analysis of patients with traumatic brain injury (N=1961) found that balanced solutions increased the risk of in-hospital mortality compared with normal saline (OR 1.42, 95% CI 1.10 to 1.82).

Previous evidence has been mixed.
- A 2015 double-blind, cluster randomised, double-crossover trial conducted in four ICUs in New Zealand (N=2278), the 0.9% Saline vs Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, acute kidney injury, or use of renal-replacement therapy.[136]
- However, a 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4%, respectively (OR 0.91, 95% CI 0.84 to 0.99).[137]
A 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[138]
- The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
- There was no difference in in-hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).

Target an initial mean arterial pressure (MAP) of 65 mmHg if the cause of shock is unknown.[1][2]

This target may change depending on the cause of shock and the patient’s normal blood pressure.[1][2]
- Aim for a higher MAP in patients with a history of hypertension, and in those who show clinical improvement with higher blood pressure.[2]
- Tolerate a lower MAP in patients with uncontrolled bleeding until the source of bleeding is controlled unless they have a traumatic brain injury or spinal injury.[2][31]

Practical tip

Targeting a higher blood pressure in patients with uncontrolled bleeding can potentially increase bleeding, promote coagulopathy by diluting clotting factors, and cool the patient.[2][31]

Consider – vasopressor

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Consider –

vasopressor

Additional treatment recommended for SOME patients in selected patient group

Manage patients who require a vasopressor in a critical care setting.

Insert an arterial line and central venous catheter (CVC) in patients with shock that is not responsive to initial therapy and/or requires infusion of a vasopressor.[2]

This allows continuous accurate blood pressure monitoring, and regular blood gas analysis.
Give all vasopressors through a CVC (with the exception of metaraminol and adrenaline [epinephrine], which can be given both peripherally and through a CVC) to minimise the risk of extravasation and subsequent tissue necrosis.
- Adrenaline can be given as a bolus via peripheral access while preparing a noradrenaline (norepinephrine) infusion or obtaining central or arterial access. Ideally this should be through a large-bore cannula in the antecubital fossa. However, an adrenaline infusion should always be given via a CVC.

Stopping bleeding is the main priority in haemorrhagic shock, but a vasopressor may be needed if there is continued evidence of tissue hypoperfusion despite optimisation of preload.[1][2]

Vasopressors are particularly useful in high cardiac output, low peripheral resistance states.
Give them only after adequate fluid resuscitation. Use of vasopressors when the patient is fluid-deplete can worsen tissue perfusion.
Vasopressors cause vasoconstriction and increase systemic vascular resistance, which aims to reverse the mismatch between vessel tone and intravascular volume.
They increase the risk of tissue ischaemia and necrosis in a dose-dependent manner. Other adverse effects include decreased cardiac output, increased risk of tachycardia and arrhythmias, and increased cardiac work.[158][159][160]

Consult a specialist for guidance on suitable vasopressor regimens.

obstructive OR distributive OR hypovolaemic non-haemorrhagic shock suspected or confirmed

Plus – intravenous fluids

Back

Plus –

intravenous fluids

Treatment recommended for ALL patients in selected patient group

Ensure early intravenous access in all patients.[29]

Use 2 wide-bore cannula especially in patients who are actively bleeding.
Consider intraosseous access if intravenous access is challenging.

Practical tip

Give fluid resuscitation in all patients apart from those with shock secondary to acute blood loss or evidence of pulmonary oedema.This is crucial for stabilisation of a patient with shock.[1][3]

Give a fluid challenge.[2][3][30]
- Use crystalloids, starting with a bolus of 500 mL given over less than 15 minutes.[30]
  - Adjust according to patient’s characteristics such as age, size, and comorbidities.
  - In a patient with known cardiac failure, use smaller volumes (e.g., 250 mL).[26]
Repeat fluid challenges depending on clinical need in boluses of 250-500 mL.[30]
- Following initial fluid resuscitation, additional fluids should be guided by frequent reassessment of haemodynamic status.[1]
- Examine for signs of hypovolaemia/fluid overload and assess the patient’s response to administration of fluids. Possible outcomes include:
  - A sustained increase in blood pressure: proceed cautiously with fluids, then reassess in 15 to 30 minutes
  - An increase and then a decrease in blood pressure: give another fluid bolus and reassess as patient appears fluid responsive
  - No change in blood pressure: means that either the patient is not fluid responsive, hypovolaemia is not the cause for the low blood pressure, or the patient has had adequate fluid replacement.

Practical tip

Titration of fluids is important as both hypovolaemia and hypervolaemia can be harmful. This applies even in patients responding well to administration of fluids, especially in the presence of elevated intravascular filling pressures or pulmonary oedema.[2]

Practical tip

Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis.

Evidence: Choice of fluids

In 2021-2022, two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte®) versus normal saline. The Plasma-Lyte 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[132][133]
- In the PLUS study, 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
- In BaSICS, almost half the patients (48.4%) were admitted to ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
- Both found no difference in 90-day mortality overall or in prespecified subgroups for patients with acute kidney injury (AKI), sepsis, or post-surgery. They also found no difference in the risk of AKI.
- In BaSICS, for patients with traumatic brain injury, there was a small decrease in 90-day mortality with normal saline - however, the overall number of patients was small (<5% of total included in the study) so there is some uncertainty about this result. Patients with traumatic brain injury were excluded from PLUS as the authors felt these patients should be receiving saline or a solution of similar tonicity.

A meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[134]
A subsequent individual patient data meta-analysis included 6 RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (OR 0.96, 95% CI 0.91 to 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[135]
- A prespecified subgroup analysis of patients with traumatic brain injury (N=1961) found that balanced solutions increased the risk of in-hospital mortality compared with normal saline (OR 1.42, 95% CI 1.10 to 1.82).

Previous evidence has been mixed.
- A 2015 double-blind, cluster randomised, double-crossover trial conducted in four ICUs in New Zealand (N=2278), the 0.9% Saline vs Plasma-Lyte for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, acute kidney injury, or use of renal-replacement therapy.[136]
- However, a 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4%, respectively (OR 0.91, 95% CI 0.84 to 0.99).[137]
A 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[138]
- The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
- There was no difference in in-hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).

Target an initial mean arterial pressure (MAP) of 65 mmHg if the cause of shock is unknown.[1][2]

This target may change depending on the cause of shock and the patient’s normal blood pressure.[1][2]
- Aim for a higher MAP in septic patients, patients with a history of hypertension, and in those who show clinical improvement with higher blood pressure.[2]

Consider – vasoactive drug

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Consider –

vasoactive drug

Additional treatment recommended for SOME patients in selected patient group

Manage patients who require a vasoactive drug (vasopressor/inotrope) in a critical care setting.

Insert an arterial line and central venous catheter (CVC) in patients with shock that is not responsive to initial therapy and/or requires infusion of a vasoactive drug.[2]

This allows continuous accurate blood pressure monitoring and regular blood gas analysis.
Give all vasoactive drugs through a CVC (with the exception of metaraminol and adrenaline [epinephrine], which can be given both peripherally and through a CVC) to minimise the risk of extravasation and subsequent tissue necrosis.
- Adrenaline can be given as a bolus via peripheral access while preparing a noradrenaline (norepinephrine) infusion or obtaining central or arterial access. Ideally this should be through a large-bore cannula in the antecubital fossa. However, an adrenaline infusion should always be given via a CVC.

Use a vasopressor (e.g., noradrenaline) if there is hypotension or continuing reduced tissue hypoperfusion despite intravenous fluids.[1]

They are particularly useful in high cardiac output, low peripheral resistance states.
Give them only after adequate fluid resuscitation. Use of vasopressors when the patient is fluid-deplete can worsen tissue perfusion.
Vasopressors cause vasoconstriction and increase systemic vascular resistance, which aims to reverse the mismatch between vessel tone and intravascular volume.
They increase the risk of tissue ischaemia and necrosis in a dose-dependent manner. Other adverse effects include decreased cardiac output, increased risk of tachycardia and arrhythmias, and increased cardiac work.[158][159][160]

Use an inotrope (e.g., dobutamine) if there is impaired cardiac function and a low/inadequate cardiac output and signs of tissue hypoperfusion persist after preload optimisation.[2]

Do not use for isolated impaired cardiac function without a low/inadequate cardiac output.
Do not use in patients with haemorrhagic shock.
Inotropes increase cardiac output by increasing both stroke volume and heart rate. This increases MAP and maintains perfusion to vital organs and tissues.
Adverse effects include arrhythmias, tachycardia, hypertension/hypotension, and anginal chest pain.[161]

Consult a specialist for guidance on suitable vasopressor/inotrope regimens.

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Shock

Treatment algorithm

all patients

supportive management of airway

Practical tip

supportive management of breathing

Evidence: Target oxygen saturation in acutely ill adults

Evidence: Use of CPAP in cardiogenic shock reduces mortality

Practical tip

treat underlying cause

cardiogenic shock suspected or confirmed

intravenous fluids

Practical tip

Practical tip

Practical tip

Evidence: Choice of fluids

loop diuretic

Evidence: Loop diuretics are widely used but may cause adverse outcomes

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

vasodilator

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

vasoactive drug

haemorrhagic shock suspected or confirmed

activate major haemorrhage protocol

Practical tip

Practical tip

Primary options

Reversal of warfarin

Reversal of dabigatran

Major trauma and active or suspected active bleeding

These drug options and doses relate to a patient with no comorbidities.

Primary options

Reversal of warfarin

Reversal of dabigatran

Major trauma and active or suspected active bleeding

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

Reversal of warfarin

Reversal of dabigatran

Major trauma and active or suspected active bleeding

intravenous fluids (if blood products unavailable)

Practical tip

Practical tip

Evidence: Choice of fluids

Practical tip

vasopressor

obstructive OR distributive OR hypovolaemic non-haemorrhagic shock suspected or confirmed

intravenous fluids

Practical tip

Practical tip

Practical tip

Evidence: Choice of fluids

vasoactive drug