01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Tissue oxygen delivery depends on cardiac output and arterial oxygen content. Shock develops when delivery or distribution fails to meet metabolic needs, and can arise from insufficient circulating volume, vasodilatation, pump failure or mechanical obstruction. The useful diagnostic question is which mechanism is dominant now, because an intervention that helps one mechanism can worsen another.
Clinical assessment must continue during resuscitation. A modest pressure increase after fluid does not prove that more fluid is beneficial; it may be transient while haemorrhage continues. Conversely, warm skin does not exclude dangerous distributive shock. Combine the clinical trend with biochemical evidence and the likely cause.
Key points
- Shock is inadequate tissue perfusion; a preserved blood pressure does not exclude it.
- Distinguish hypovolaemic, distributive, cardiogenic and obstructive mechanisms, recognising that several may coexist.
- Use history, peripheral perfusion, jugular venous pressure, lungs and focused ultrasound to direct treatment.
- For suspected sepsis needing fluids, start 250 mL isotonic crystalloid over 10–15 minutes and reassess each bolus.
- In hospital traumatic active bleeding, activate haemorrhage control and blood-component resuscitation rather than repeated crystalloid.
- Escalate persistent shock early; a higher pressure alone does not establish restored organ perfusion.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Volume loss
Blood loss, dehydration and fluid sequestration reduce venous return; the immediate treatment depends on whether the missing circulating volume is blood or non-blood fluid.
Pump and vascular failure
Myocardial dysfunction, systemic vasodilatation and mechanical obstruction can each reduce effective circulation, and frequently overlap in critically ill patients.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Reduced oxygen delivery
A fall in cardiac output or haemoglobin reduces oxygen delivery, while regional maldistribution can impair tissues despite an apparently adequate global pressure.
- 2Compensatory responses
Sympathetic activation initially increases heart rate and peripheral resistance; these responses can preserve pressure while concealing progressive depletion of circulating volume.
- 3Organ injury
Persistent perfusion failure promotes cellular dysfunction and organ injury, while inflammation and capillary leak can further reduce effective circulating volume and worsen shock.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Recent haemorrhage, gastrointestinal loss or major fluid redistribution suggests reduced preload. Look for cool peripheries, narrow pulse pressure and compensatory tachycardia, while remembering beta-blockade may blunt the pulse response.
Infection, anaphylaxis or neurogenic causes may produce low vascular tone and relatively warm peripheries. A later cold pattern does not invalidate an initial distributive mechanism.
Chest discomfort, pulmonary congestion, elevated venous pressure or new severe cardiac dysfunction raises concern that additional fluid may worsen oxygenation without increasing useful forward flow.
Abrupt hypoxaemia or collapse with raised venous pressure suggests pulmonary embolism, tamponade or tension pneumothorax. Mechanical relief or reperfusion may be the decisive treatment.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Lactate and serial blood gasesFirst step - Why
- Estimate physiological disturbance and follow the treatment response.
- Interpretation and limitations
- Lactate elevation can reflect hypoperfusion but also adrenergic stimulation or impaired clearance. Interpret its trajectory with perfusion rather than treating a single value as a diagnosis.
- 02
ECG and focused cardiac ultrasound - Why
- Look for a pump, rhythm or obstructive explanation.
- Interpretation and limitations
- ECG may reveal infarction or arrhythmia; ultrasound estimates ventricular function and pericardial fluid. Findings are operator-dependent and should not delay urgent treatment.
- 03
Blood count, renal function and coagulation - Why
- Identify consequences and prepare for definitive management.
- Interpretation and limitations
- Early haemoglobin can remain normal during acute bleeding. Renal injury, thrombocytopenia or coagulopathy may indicate severity without establishing the cause of shock.
- 04
Cause-directed cultures and imaging - Why
- Find the lesion or infection that needs control.
- Interpretation and limitations
- Obtain cultures before antibiotics when this causes no significant delay. Choose CT only if safe enough for transport; suspected tension physiology needs treatment before imaging.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Isolated low blood pressure
An asymptomatic low reading may reflect the usual baseline or measurement error, but this interpretation requires reassuring perfusion and a consistent clinical assessment.
Vasovagal episode
Transient bradycardia and hypotension after a trigger can resolve quickly with positioning, but persistent hypoperfusion requires investigation for more dangerous causes.
Primary metabolic disturbance
Hypoglycaemia and drug effects can impair consciousness without shock; they may also coexist with circulatory failure and should be tested promptly.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Initial mechanismLinking bedside findings to resuscitationFirst stepA hypotensive adult has not yet had the principal cause of shock established.+
- 1Support oxygenation, obtain large-bore access and ask about bleeding, infection, allergy, cardiac symptoms and recent procedures while a colleague starts monitoring.
- 2Examine the lungs, neck veins and peripheral perfusion before selecting fluid; treat an immediately reversible obstruction or uncontrolled external haemorrhage when identified.
- 3DefinitiveReassess after every intervention and organise the definitive destination, such as theatre, interventional radiology, coronary intervention or critical care, while stabilisation continues.
02Sepsis branchMeasured fluid and antimicrobial treatmentSuspected infection accompanies high-risk physiological deterioration, and clinical assessment supports intravenous resuscitation.+
- 1Take appropriate blood samples and give indicated broad-spectrum IV antibiotics within one hour of the initial high-risk NEWS2 assessment, selecting agents for the suspected source and patient factors.
- 2Give 250 mL balanced isotonic crystalloid over ten to fifteen minutes, using 0.9% saline if balanced fluid is unavailable; reassess and repeat only if needed.
- 3Count all previous boluses toward the initial 1,000 mL total. If improvement is insufficient, obtain senior advice and discuss vasopressors with critical care rather than automatically continuing fluid.
03Congestion or obstructionWhen further fluid is unlikely to solve shockHypoperfusion persists with pulmonary oedema, marked venous congestion or evidence of a mechanical obstruction.+
- 1Stop reflexive volume loading and obtain urgent skilled cardiac and respiratory assessment, using focused imaging when it can clarify treatment promptly.
- 2Arrange cause-specific intervention, such as coronary reperfusion, decompression or treatment of high-risk pulmonary embolism, while expert circulatory support is prepared.
- 3Check both perfusion and oxygenation after support changes; an intervention that increases pressure but worsens pulmonary flooding requires immediate reassessment.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Isotonic crystalloid for suspected sepsis
Give 250 mL IV over 10–15 minutes initially; reassess after each bolus and repeat if needed up to 1,000 mL total including earlier fluids, then seek senior advice if improvement remains insufficient.Assess for contraindications and overload before and after each bolus. This sepsis-specific regimen is different from general non-haemorrhagic fluid resuscitation and active traumatic bleeding management.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Acute kidney injury
Renal hypoperfusion can progress to intrinsic injury, reducing fluid and electrolyte tolerance even after the original circulatory problem begins to improve.
Myocardial and cerebral injury
Inadequate coronary or cerebral perfusion can produce arrhythmia, ischaemia and altered consciousness, creating additional threats during the initial shock state.
Treatment-related congestion
Excessive volume administration can worsen pulmonary oedema and tissue swelling, especially when cardiac dysfunction or capillary leak limits the benefit of further fluid.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record response in mental state, capillary refill, pulse and pressure alongside the time and volume of every administered bolus.
- Measure urine output where clinically indicated; persistent oliguria may reflect ongoing hypoperfusion or established kidney injury requiring reassessment.
- Repeat lactate and acid–base assessment according to severity, looking for improvement and investigating a persistently adverse trajectory.
- Check for pulmonary crackles, increasing oxygen requirement and venous congestion that indicate reduced fluid tolerance during treatment.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Mixed shock mechanisms
A patient with sepsis can also have ventricular dysfunction or bleeding. Revisit the working mechanism when treatment produces less benefit than expected.
Pressure and flow
Vasoconstriction can maintain arterial pressure while tissue flow falls; therefore normal pressure cannot substitute for examination of organ perfusion.
Peripheral vasopressors
When central access is unavailable, critical care may start a vasopressor through an appropriate visible peripheral line using specified concentration, dose and extravasation monitoring.
Goals of treatment
Discuss escalation in the context of the illness, previous function and recorded preferences, while delivering immediately necessary care within the agreed treatment goals.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not use a normal first haemoglobin result to dismiss clinically important acute haemorrhage.
- 02
Do not assume every cold hypotensive patient has dehydration that will respond to unlimited fluid.
- 03
Do not postpone source control because blood pressure temporarily improves with resuscitation measures.
- 04
Do not label a falling lactate as complete recovery when consciousness, urine output or respiratory support requirements worsen.