Shock
A systematic surgical approach to shock: classification, pathophysiology, differential diagnosis, diagnosis, investigations, management, complications, and high-yield summary.
Shock: Definition, Epidemiology, Aetiology, Classification and Pathophysiology
Shock is acute circulatory failure causing inadequate tissue oxygen delivery and/or impaired cellular oxygen utilisation, leading to cellular hypoxia, anaerobic metabolism, lactate generation, organ dysfunction, and death if not reversed.
Do not define shock as "low blood pressure." Hypotension is common, but it is late in some patients and absent in compensated shock.
Core Concept
Shock = oxygen delivery is not meeting oxygen demand at tissue level. Blood pressure is only one visible marker. A young bleeding patient can maintain BP through vasoconstriction until they suddenly collapse.
Oxygen delivery depends on:
| Variable | Formula idea | Why it matters |
|---|---|---|
| Cardiac output | HR x stroke volume | Pump failure, volume loss, or obstruction reduces forward flow |
| Arterial oxygen content | Hb-bound oxygen + dissolved oxygen | Anaemia, hypoxaemia, and CO poisoning reduce usable oxygen |
| Microcirculatory flow | Capillary perfusion | Sepsis can have normal/high CO but maldistributed flow |
| Cellular utilisation | Mitochondrial oxygen use | Sepsis and toxins impair extraction and utilisation |
So the treatment question is: which part of oxygen delivery is broken?
Shock is common in acute surgical care because surgery sits at the intersection of:
- Bleeding - trauma, ruptured AAA, GI bleeding, post-operative haemorrhage
- Sepsis - perforated viscus, peritonitis, biliary sepsis, necrotising fasciitis, anastomotic leak
- Fluid loss - vomiting, diarrhoea, bowel obstruction, pancreatitis, burns, high-output stoma
- Cardiac events - peri-operative MI, arrhythmia, pulmonary embolism
- Obstruction - tension pneumothorax, cardiac tamponade, massive PE, abdominal compartment syndrome
For HK surgical exams, shock is high yield because the first answer is rarely "send more tests." The first answer is ABCDE, oxygen, access, monitoring, resuscitation, and treat the cause.
| Type | Primary problem | Cardiac output | SVR | Typical surgical examples |
|---|---|---|---|---|
| Hypovolaemic | Too little circulating volume/preload | Low | High | Haemorrhage, dehydration, bowel obstruction, pancreatitis third-spacing |
| Cardiogenic | Pump failure | Low | High | MI, arrhythmia, myocarditis, acute valvular failure |
| Obstructive | Mechanical block to filling or outflow | Low | High | Tension pneumothorax, tamponade, massive PE, abdominal compartment syndrome |
| Distributive | Vasodilatation and maldistributed flow | Normal/high early, low late | Low | Sepsis, anaphylaxis, neurogenic shock |
Why This Classification Matters
The wrong fluid strategy can harm. Hypovolaemic shock needs volume and haemorrhage control. Cardiogenic shock may drown with blind fluids. Obstructive shock needs mechanical relief. Septic shock needs infection control, fluids, and vasopressors.
D. Pathophysiology From First Principles
All shock types converge on:
- Reduced effective tissue perfusion
- Reduced oxygen delivery or extraction
- Anaerobic glycolysis
- Lactate accumulation
- ATP depletion
- Na+/K+ pump failure
- Cellular swelling, acidosis, membrane injury
- Organ dysfunction
The earliest organs to show dysfunction are often:
- Brain - agitation, confusion, reduced consciousness
- Kidney - oliguria
- Skin - cool peripheries, delayed capillary refill, mottling
- Gut/liver - ileus, transaminitis, bacterial translocation
| Phase | Physiology | Bedside picture |
|---|---|---|
| Compensated shock | Sympathetic tone, RAAS, ADH maintain BP | Tachycardia, cool peripheries, thirst, oliguria, narrow pulse pressure |
| Decompensated shock | Compensation fails; CO and BP fall | Hypotension, altered mental state, rising lactate, anuria |
| Irreversible shock | Cellular injury and microthrombosis persist despite correction | Multi-organ failure, DIC, severe acidosis |
Hypotension is therefore not the start of shock; it is the point where compensation is failing.
E. Aetiology by Shock Type
Hypovolaemic shock means inadequate preload.
Causes:
| Cause | Mechanism |
|---|---|
| Haemorrhage | Loss of red cells and plasma -> reduced venous return, reduced oxygen-carrying capacity |
| Vomiting / NG aspirate | Water, chloride, hydrogen ion loss -> hypovolaemia plus metabolic alkalosis |
| Diarrhoea / high-output stoma | Water, sodium, potassium, bicarbonate loss -> hypovolaemia plus acidosis |
| Bowel obstruction | Vomiting plus fluid sequestration in bowel lumen and bowel wall |
| Acute pancreatitis | Retroperitoneal inflammation -> massive third-spacing |
| Burns | Capillary leak and evaporative loss |
Pathophysiology:
Volume loss -> reduced venous return -> reduced end-diastolic volume -> reduced stroke volume -> reduced cardiac output -> compensatory tachycardia and vasoconstriction.
Cardiogenic shock means the pump cannot generate forward flow despite adequate or high filling pressure.
Causes:
- Acute myocardial infarction
- Severe bradyarrhythmia or tachyarrhythmia
- Acute myocarditis
- Decompensated heart failure
- Acute severe mitral regurgitation
- Ventricular septal rupture
- Severe aortic stenosis
- Stress cardiomyopathy
Pathophysiology:
Myocardial contractility falls -> LV stroke volume falls -> pulmonary venous pressure rises -> pulmonary oedema -> hypoxaemia -> further myocardial hypoxia -> worsening pump failure.
Obstructive shock means the heart may be intrinsically capable, but mechanical obstruction prevents filling or ejection.
| Cause | Mechanism |
|---|---|
| Tension pneumothorax | Raised intrathoracic pressure compresses vena cava and heart -> reduced venous return |
| Cardiac tamponade | Pericardial pressure restricts diastolic filling |
| Massive PE | RV outflow obstruction -> RV failure -> reduced LV preload |
| Abdominal compartment syndrome | Raised intra-abdominal pressure reduces venous return and renal perfusion |
The treatment is mechanical: decompress chest, drain pericardium, reperfuse PE, decompress abdomen.
Distributive shock means vascular tone and microcirculatory distribution are abnormal.
| Cause | Mechanism |
|---|---|
| Septic shock | Cytokine-mediated vasodilatation, capillary leak, myocardial depression, mitochondrial dysfunction |
| Anaphylactic shock | IgE-mediated mast cell degranulation -> vasodilatation, capillary leak, bronchospasm |
| Neurogenic shock | Loss of sympathetic tone after spinal cord injury -> vasodilatation and bradycardia |
| Adrenal crisis | Cortisol deficiency -> vasopressor-resistant vasodilatation and hypoglycaemia |
Distributive shock can look deceptively "warm" early because the skin is flushed and pulse pressure is wide. Later, as myocardial depression and hypovolaemia develop, it may become cold.
In Hong Kong surgical practice, local relevance is mostly about case mix and antimicrobial resistance:
- Biliary sepsis is common in an older population with gallstones, CBD stones, cholangitis, and recurrent pyogenic cholangitis.
- Intra-abdominal sepsis from perforated viscus, appendicitis, diverticulitis, strangulated hernia, and anastomotic leak is high yield for surgery.
- Urosepsis from obstructing stones or retention is common in surgical/urology settings.
- Local antimicrobial guidance emphasises AMR awareness; Hong Kong IMPACT notes MRSA, ESBL-producing Enterobacterales, CRE/CPE, carbapenem-resistant Acinetobacter, and VRE as important local multidrug-resistant organisms [3].
- HA/CHP antimicrobial stewardship programmes, including SmartASP, aim to reduce inappropriate broad-spectrum antibiotic use while preserving early adequate treatment in severe infection [3].
Local Practical Point
In Hong Kong, empiric antibiotics for septic shock should not be copied blindly from overseas tables. Use local cluster/HA antibiograms, IMPACT guidance, recent cultures, travel/residence history, prior ESBL/CRE/MRSA/VRE colonisation, and discuss early with microbiology/ID for severe or resistant-risk cases.
High Yield Summary
Shock = acute circulatory failure causing tissue hypoxia, not simply low blood pressure.
Four types: hypovolaemic, cardiogenic, obstructive, distributive.
Final pathway: inadequate oxygen delivery/use -> anaerobic metabolism -> lactate -> ATP failure -> organ dysfunction.
Compensation: tachycardia, vasoconstriction, RAAS/ADH, oliguria. Hypotension is late in young/fit patients.
Hypovolaemic shock: low preload; causes include bleeding, vomiting, diarrhoea, bowel obstruction, pancreatitis, burns.
Cardiogenic shock: pump failure; causes include MI, arrhythmia, myocarditis, acute valve failure.
Obstructive shock: mechanical block; tension pneumothorax, tamponade, massive PE, abdominal compartment syndrome.
Distributive shock: low SVR/maldistribution; sepsis, anaphylaxis, neurogenic shock, adrenal crisis.
Local HK relevance: biliary sepsis, intra-abdominal sepsis, urosepsis, and AMR risk including MRSA, ESBL-E, CRE/CPE, CRAB, and VRE.
Active Recall - Shock Etiology
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[2] Lecture slides: Surviving Sepsis Campaign international guidelines for management of sepsis and septic shock 2026.
[3] Lecture slides: Hong Kong IMPACT antimicrobial guideline / CHP antimicrobial resistance materials.
Differential Diagnosis of Shock
Shock means life-threatening circulatory failure with inadequate cellular oxygen use. The differential diagnosis is the search for why oxygen delivery has failed:
- Is there not enough volume? -> hypovolaemic shock
- Is the pump failing? -> cardiogenic shock
- Is the circulation blocked? -> obstructive shock
- Is vascular tone lost or maldistributed? -> distributive shock
The dangerous trap is to label every hypotensive surgical patient as "dehydrated". A cardiogenic shock patient given litres of fluid may drown; a tension pneumothorax patient given fluids without decompression may arrest; a septic shock patient given no antibiotics may die despite good fluids. Current shock guidance therefore emphasises early phenotyping, bedside perfusion assessment, and echocardiography when the type of shock is unclear [1].
| Pattern | Think | Why |
|---|---|---|
| Cold, clammy, flat neck veins | Hypovolaemia | Low preload -> sympathetic vasoconstriction |
| Cold, clammy, raised JVP, crepitations | Cardiogenic shock | Pump failure -> pulmonary congestion + low output |
| Raised JVP + clear lungs + sudden collapse | Obstructive shock | Venous return or ventricular filling blocked |
| Warm peripheries early, bounding pulse, fever | Septic distributive shock | Vasodilatation and maldistributed flow |
| Urticaria, wheeze, facial swelling | Anaphylaxis | Mast-cell mediator release -> vasodilatation + bronchospasm |
| Bradycardia with hypotension after spinal injury | Neurogenic shock | Loss of sympathetic tone, unopposed vagal tone |
High Yield Bedside Rule
JVP and lungs help separate low preload from pump/obstructive problems. Flat JVP suggests volume loss; raised JVP suggests pump failure or obstruction. Always interpret with the whole patient, because ventilated patients and tamponade can confuse the exam.
C. Differential by Shock Category
| Cause | Clues | Pathophysiology |
|---|---|---|
| Haemorrhage | Trauma, GI bleed, post-op drain blood, ruptured AAA, ectopic pregnancy | Loss of RBC mass and plasma -> reduced preload and oxygen-carrying capacity |
| Dehydration | Poor intake, vomiting, diarrhoea, fever | Water and sodium loss -> reduced extracellular and intravascular volume |
| Third-spacing | Pancreatitis, peritonitis, bowel obstruction, burns | Capillary leak traps protein-rich fluid outside the vascular space |
| High-output stoma/fistula | Ileostomy or enterocutaneous fistula output | Sodium-rich GI fluid loss -> hypovolaemia, electrolyte derangement |
| Cause | Clues | Pathophysiology |
|---|---|---|
| Acute MI | Chest pain, ECG changes, troponin rise | Myocardial necrosis -> poor contractility -> low CO |
| Arrhythmia | AF with fast ventricular response, VT, complete heart block | Too fast or too slow -> poor filling/ejection |
| Acute valvular failure | New murmur, pulmonary oedema | Regurgitant flow or outflow obstruction prevents forward flow |
| Myocarditis/cardiomyopathy | Viral prodrome, young patient, dilated LV | Inflamed or failing myocardium cannot generate pressure |
| Cause | Clues | Pathophysiology |
|---|---|---|
| Tension pneumothorax | Unilateral absent breath sounds, tracheal deviation, hypoxia, distended neck veins | Intrathoracic pressure compresses vena cava and heart |
| Cardiac tamponade | Beck's triad: hypotension, raised JVP, muffled heart sounds | Pericardial pressure prevents diastolic filling |
| Massive pulmonary embolism | Sudden dyspnoea, pleuritic pain, hypoxia, RV strain | Pulmonary vascular obstruction -> acute RV failure |
| Abdominal compartment syndrome | Tense abdomen, ventilatory difficulty, oliguria | High intra-abdominal pressure reduces venous return and renal perfusion |
| Cause | Clues | Pathophysiology |
|---|---|---|
| Sepsis | Infection source, fever/hypothermia, high lactate, organ dysfunction | NO-mediated vasodilatation, capillary leak, mitochondrial dysfunction |
| Anaphylaxis | Allergen exposure, urticaria, angioedema, wheeze | Histamine/leukotrienes -> vasodilatation + permeability + bronchospasm |
| Neurogenic shock | Spinal trauma, hypotension with bradycardia | Loss of sympathetic vascular tone |
| Adrenal crisis | Steroid withdrawal, Addison's, hyperkalaemia, hypoglycaemia | Cortisol deficiency -> poor catecholamine responsiveness |
High Yield Summary
Shock DDx starts with physiology: volume, pump, obstruction, or tone.
Hypovolaemic: flat JVP, cold clammy skin, dry mucosa, bleeding/GI loss/third-spacing.
Cardiogenic: cold clammy skin plus raised JVP, pulmonary oedema, ECG/troponin/echo abnormalities.
Obstructive: raised JVP with a mechanical block: tension pneumothorax, tamponade, massive PE, abdominal compartment syndrome.
Distributive: low SVR; sepsis is most common in wards/ICU, anaphylaxis and neurogenic shock are time-critical mimics.
Mixed shock is common: septic patient with cardiomyopathy, trauma patient with tension pneumothorax and bleeding, pancreatitis patient with third-spacing and sepsis.
Active Recall - Shock Differential Diagnosis
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
Diagnosis of Shock
Shock is diagnosed clinically when there is circulatory failure causing inadequate tissue perfusion. Hypotension helps, but it is not required early; current shock monitoring guidance emphasises perfusion markers and early haemodynamic phenotyping [1].
The key diagnostic move is:
Recognise hypoperfusion first, then phenotype the shock type while resuscitation begins.
Classic threshold:
- SBP < 90 mmHg, or
- MAP < 65 mmHg, or
- A fall in SBP > 40 mmHg from baseline
But compensated shock may have normal BP. A young trauma patient can lose a large blood volume before becoming hypotensive because catecholamines maintain vascular tone.
| Domain | Finding | Why it matters |
|---|---|---|
| Circulation | Tachycardia, hypotension, narrow pulse pressure | Compensation and then decompensation |
| Skin | Cool clammy skin, mottling, delayed capillary refill | Peripheral vasoconstriction and poor microcirculatory flow |
| Kidneys | Oliguria < 0.5 mL/kg/hr | Reduced renal perfusion pressure |
| Brain | Agitation, confusion, drowsiness | Poor cerebral perfusion or inflammatory encephalopathy |
| Metabolism | Lactate rise, base deficit, acidosis | Anaerobic metabolism and oxygen debt |
Blood Pressure Trap
A normal BP does not exclude shock. BP = cardiac output x systemic vascular resistance. Early shock may preserve BP by raising SVR. Look for perfusion: mentation, urine output, capillary refill, lactate, and skin.
| Clue | Suggests | Mechanism |
|---|---|---|
| Flat neck veins, dry mucosa, bleeding, collapsible IVC | Hypovolaemic | Too little preload |
| Raised JVP, crepitations, S3, chest pain, poor LV function | Cardiogenic | Pump failure |
| Raised JVP with clear lungs, muffled heart sounds, pulsus paradoxus | Tamponade | External compression blocks filling |
| Sudden dyspnoea, hypoxia, RV strain, pleuritic pain | Massive PE | RV afterload crisis |
| Fever or hypothermia, warm peripheries early, bounding pulse | Septic distributive | Vasodilatation and capillary leak |
| Wheeze, urticaria, angioedema, sudden collapse | Anaphylactic distributive | Mast-cell mediator vasodilatation and bronchospasm |
| Bradycardia with hypotension after spinal injury | Neurogenic distributive | Loss of sympathetic tone |
Shock index = heart rate / systolic BP
- Normal: about 0.5-0.7
-
0.9 suggests significant circulatory stress
- Useful in trauma and occult bleeding
Why it works: tachycardia rises and SBP falls as compensatory reserve is consumed.
Diagnosis is dynamic. The response to treatment gives information:
| Response | Interpretation |
|---|---|
| Improves after fluid bolus | Fluid responsive: hypovolaemia or early distributive shock likely |
| No improvement and lungs become wet | Cardiogenic shock or fluid intolerance |
| No improvement with raised JVP and clear lungs | Obstructive shock until proven otherwise |
| BP improves with noradrenaline but lactate persists | Vasoplegia improved, but tissue perfusion/source/pump may remain unresolved |
Active Recall - Shock Diagnosis
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
Investigations for Shock
Investigations in shock have three jobs:
- Confirm tissue hypoperfusion
- Identify the shock phenotype
- Find the treatable cause
Do not wait for all results before resuscitating. In shock, treatment and investigation run in parallel.
| Investigation | What it tells you | Why it matters |
|---|---|---|
| Continuous ECG | Arrhythmia, ischaemia, rate problem | Cardiogenic shock may be rhythm-driven; shock itself causes myocardial strain |
| Pulse oximetry | Oxygenation trend | Hypoxaemia worsens oxygen delivery and anaerobic metabolism |
| Non-invasive BP then arterial line if persistent shock | Perfusion pressure | ESICM recommends arterial pressure monitoring when shock is not responsive to initial therapy or vasopressors are needed [1] |
| Temperature | Sepsis, hypothermia in trauma | Hypothermia worsens coagulopathy and oxygen delivery |
| Urinary catheter | Hourly urine output | Target at least 0.5 mL/kg/hr in adults; oliguria is renal hypoperfusion until proven otherwise |
| Capillary refill time, mottling, skin temperature | Microcirculatory perfusion | ESICM specifically highlights capillary refill assessment, complemented by skin temperature and mottling [1] |
Why Urine Output Is So Useful
The kidney is a high-flow organ that autoregulates until perfusion pressure falls too low. When renal blood flow drops, RAAS and ADH conserve salt and water, so urine output falls early. Oliguria is not "just renal"; it is a whole-body perfusion warning.
| Test | Expected abnormality | Interpretation |
|---|---|---|
| ABG/VBG with lactate | Metabolic acidosis, raised lactate | Lactate reflects anaerobic metabolism, adrenergic drive, impaired clearance, or all three |
| FBC | Anaemia, leukocytosis, leukopenia, thrombocytopenia | Anaemia worsens oxygen delivery; leukocyte patterns suggest infection or marrow stress |
| U&E / creatinine | AKI, hyperkalaemia, sodium disorders | Renal hypoperfusion and electrolyte danger |
| LFT | Shock liver pattern, biliary source | Hepatic hypoperfusion gives marked transaminase rise |
| Coagulation profile | Prolonged PT/APTT, low fibrinogen | Trauma, DIC, liver dysfunction, massive transfusion effect |
| Group and screen / crossmatch | Prepares blood products | Mandatory if bleeding is possible |
| Troponin | MI or demand injury | Distinguishes primary cardiogenic shock from secondary myocardial strain |
| Glucose | Hypoglycaemia or stress hyperglycaemia | Both can worsen neurological state |
| CRP / procalcitonin | Infection support, trend only | Never use as sole sepsis rule-in/rule-out |
- Blood cultures before antibiotics if this does not delay treatment
- Urine microscopy/culture
- Sputum or tracheal aspirate if respiratory source suspected
- Wound, drain, bile, pus, or intra-abdominal fluid cultures where relevant
Hong Kong relevance:
- Local prescribing should consider IMPACT guidance and local resistance patterns [3]
- Hong Kong commonly deals with MRSA, ESBL-producing Enterobacterales, CRE/CPE, carbapenem-resistant Acinetobacter, and VRE resurgence [3]
- In severe sepsis or septic shock, early microbiology and early de-escalation are both important: broad enough at the start, narrow once cultures return
| Suspected cause | First imaging / test | Key finding |
|---|---|---|
| Free intra-abdominal blood | FAST ultrasound, CT if stable | Free fluid, solid organ injury |
| AAA rupture | Bedside US, CT angiogram if stable | Aneurysm with leak/retroperitoneal haematoma |
| Cardiogenic shock | ECG + bedside echo | LV/RV failure, mechanical complication, tamponade mimic |
| Pulmonary embolism | Echo if unstable, CTPA if stable | RV strain, clot burden |
| Tension pneumothorax | Clinical diagnosis; CXR after decompression | Hyperinflated hemithorax, mediastinal shift |
| Sepsis source | CXR, CT abdomen/pelvis, US biliary/KUB as indicated | Pneumonia, abscess, perforation, cholangitis, pyelonephritis |
| Bowel ischaemia | CT angiography | Mesenteric vessel occlusion, pneumatosis, portal venous gas |
Bedside Echocardiography
Echo is the single most useful bedside imaging tool in undifferentiated shock. ESICM suggests echocardiography as first-line imaging to assess shock type [1].
| Echo finding | Think |
|---|---|
| Poor LV contraction | Cardiogenic shock |
| Dilated RV with septal flattening | Massive PE, pulmonary hypertension, RV infarct |
| Small hyperdynamic ventricles | Hypovolaemia, early distributive shock |
| Pericardial effusion with chamber collapse | Tamponade |
| Plethoric IVC | Raised right-sided pressure, tamponade, PE, overload |
| Collapsible IVC | Low filling pressure, but interpret with ventilation and context |
Static Numbers Are Not Enough
CVP, one BP reading, or one lactate value can mislead. Modern shock assessment favours dynamic response: passive leg raise, stroke volume change, pulse pressure variation in selected ventilated patients, capillary refill trend, lactate trend, and bedside echo.
| Test | How it works | Useful when |
|---|---|---|
| Passive leg raise | Temporarily transfers venous blood from legs/abdomen to thorax | Reversible "self-bolus"; useful before giving more fluid |
| Mini-fluid challenge | Small bolus with stroke volume assessment | Tests response while limiting overload |
| Pulse pressure variation / stroke volume variation | Uses heart-lung interaction during ventilation | Only valid in controlled ventilation, regular rhythm, adequate tidal volume |
| End-expiratory occlusion test | Increases venous return transiently on ventilator | ICU setting |
ESICM recommends dynamic variables over static preload markers when applicable [1].
Raised lactate in shock usually means tissue hypoxia, but not always.
Mechanisms:
- Low oxygen delivery -> anaerobic glycolysis
- Catecholamine-driven glycolysis in sepsis
- Liver hypoperfusion -> reduced clearance
- Seizures, beta-agonists, metformin, severe liver disease
Use lactate as:
- A severity marker
- A resuscitation trend
- A clue to occult hypoperfusion
Do not use lactate as:
- A substitute for examining perfusion
- Proof that every patient needs more fluid
Active Recall - Shock Investigations
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[3] Lecture slides: CHP/HA IMPACT antimicrobial guideline and Hong Kong AMR materials.
Management of Shock
Shock management has two simultaneous tracks:
- Generic resuscitation - keep the patient alive now.
- Cause-specific reversal - stop the physiology causing shock.
Generic resuscitation without cause control is temporary. Cause control without resuscitation may be too slow.
The ward-round sentence is:
ABCDE, oxygenate, monitor, get access, send bloods, give targeted fluids/blood/vasopressors, use bedside echo, and reverse the cause.
| Step | Action | Why |
|---|---|---|
| Call for help | Senior surgeon, anaesthetist, ICU, ED, blood bank as needed | Shock deteriorates faster than one person can manage |
| Airway | Assess patency, GCS, aspiration risk | Shock reduces consciousness and airway reflexes |
| Breathing | High-flow oxygen if hypoxaemic; ventilate if tiring | Oxygen delivery = cardiac output x arterial oxygen content |
| Circulation access | Two large-bore IV cannulae; IO if no access | Treatment cannot happen without access |
| Monitoring | ECG, NIBP, SpO2, temperature, urine catheter | Shock treatment is titrated to response |
| Bloods | Lactate/VBG, FBC, UEC, LFT, coag, glucose, group and crossmatch, cultures if sepsis | Identifies anaemia, AKI, acidosis, coagulopathy, infection |
First Principle
Do not wait for a named diagnosis before treating shock. Restore oxygen delivery while you identify the cause.
D. Fluids, Blood, and Vasopressors
Use IV fluid when the physiology is low preload or likely fluid responsive.
| Situation | Fluid approach |
|---|---|
| Dehydration, GI loss, burns, pancreatitis | Balanced crystalloid bolus, reassess |
| Septic shock | At least 30 mL/kg crystalloid in first 3 hours if hypoperfusion; balanced crystalloid preferred where suitable [2] |
| Cardiogenic shock with pulmonary oedema | Avoid blind boluses; small test bolus only if RV infarct or underfilled |
| Obstructive shock | Small bolus may temporise preload, but definitive treatment is relieving obstruction |
| Haemorrhagic shock | Crystalloid only as bridge; blood products are definitive volume and oxygen-carrying replacement |
Haemorrhage is loss of:
- Volume
- Red cells
- Clotting factors
- Platelets
- Calcium and temperature homeostasis
So treatment must replace all of them.
Principles:
- Control bleeding early
- Activate massive haemorrhage protocol
- Give balanced blood products rather than litres of crystalloid
- Keep warm
- Correct hypocalcaemia
- Check coagulation and fibrinogen
Trauma haemorrhage:
- Avoid excessive crystalloid because it causes dilutional coagulopathy, hypothermia, acidosis, and clot disruption
- Permissive hypotension may be appropriate before haemostasis if no traumatic brain injury
- In suspected significant traumatic brain injury, avoid hypotension because cerebral perfusion depends on MAP
Vasopressors are for vascular tone failure or persistent hypotension after appropriate preload correction.
| Drug | Main receptor action | Use |
|---|---|---|
| Norepinephrine | Alpha-1 vasoconstriction plus beta-1 support | First-line in septic/distributive shock and useful in cardiogenic shock with hypotension [2] |
| Vasopressin | V1 vasoconstriction independent of adrenergic receptors | Add-on in septic shock with escalating norepinephrine requirement [2] |
| Epinephrine | Beta-1/beta-2 at lower dose, alpha at higher dose | Add-on refractory septic shock; useful when bradycardic or low cardiac output [2] |
| Dobutamine | Beta-1 inotropy | Cardiogenic shock or septic myocardial dysfunction with persistent hypoperfusion despite adequate MAP |
Vasopressors Do Not Replace Volume
Norepinephrine squeezes the vascular tree. If the tank is empty from bleeding or dehydration, squeezing alone does not restore oxygen-carrying capacity or venous return. Conversely, if the patient is vasoplegic and already fluid replete, more fluid just causes oedema.
E. Cause-Specific Management
Non-haemorrhagic
- Give balanced crystalloid bolus
- Replace ongoing measured losses
- Treat cause: stop vomiting, manage diarrhoea, replace stoma/NG losses, treat burns/pancreatitis
- Monitor urine output and electrolytes
Haemorrhagic
- Control bleeding: direct pressure, tourniquet, pelvic binder, endoscopy, IR embolisation, operation
- Group and crossmatch
- Activate massive haemorrhage protocol
- Warm patient and fluids
- Correct coagulopathy, platelets, fibrinogen, calcium
Septic shock
- Cultures before antibiotics if this does not delay treatment
- Broad-spectrum antibiotics
- Source control
- Crystalloid resuscitation if hypoperfused
- Norepinephrine to MAP 65 mmHg if persistent hypotension
- ICU early
Anaphylaxis
- IM adrenaline immediately
- Airway support
- High-flow oxygen
- IV fluids
- Antihistamine and steroid as adjuncts
- Remove trigger
Neurogenic shock
- Immobilise spine
- Fluids cautiously
- Vasopressor with alpha activity
- Treat bradycardia
- Maintain spinal cord perfusion
Core rule: do not flood a failing pump.
Management depends on cause:
- Acute MI -> urgent PCI/revascularisation
- Arrhythmia -> cardioversion/pacing/antiarrhythmic
- Valvular catastrophe -> echo and surgical/cardiology intervention
- Myocarditis/cardiomyopathy -> ICU, inotrope, mechanical support if needed
Support:
- Oxygen/ventilation
- Norepinephrine if hypotensive
- Dobutamine if low output with adequate pressure
- Diuretics if pulmonary oedema
- Mechanical circulatory support in selected refractory cases
Obstructive shock improves only when obstruction is relieved.
| Cause | Definitive action |
|---|---|
| Tension pneumothorax | Immediate needle decompression, then chest drain |
| Cardiac tamponade | Pericardiocentesis or surgical drainage |
| Massive PE | Anticoagulation plus thrombolysis/embolectomy if unstable |
| Abdominal compartment syndrome | Decompression |
| Target | Practical endpoint |
|---|---|
| Perfusion | Improved mentation, warm skin, capillary refill improving |
| Blood pressure | MAP about 65 mmHg for most shock states, individualised |
| Renal perfusion | Urine output at least 0.5 mL/kg/hr |
| Metabolism | Falling lactate, improving pH/base deficit |
| Lung safety | No new pulmonary oedema or worsening oxygenation |
| Cause control | Bleeding stopped, source controlled, obstruction relieved, pump treated |
Use dynamic reassessment:
- Passive leg raise response
- Stroke volume/cardiac output change if monitored
- Pulse pressure variation where valid
- Echo assessment of ventricular function and IVC context
High Yield Summary
Shock management = resuscitate + reverse cause.
Universal first steps: ABCDE, oxygen, monitoring, 2 large-bore IV/IO access, lactate/VBG, bloods, group and crossmatch, catheter, senior help.
Hypovolaemic shock: Give fluid if non-haemorrhagic; give blood products and haemorrhage control if bleeding.
Distributive shock: Septic = antibiotics + source control + fluids + norepinephrine. Anaphylaxis = IM adrenaline. Neurogenic = spinal immobilisation + vasopressor + bradycardia treatment.
Cardiogenic shock: Do not blindly give large fluids. Diagnose with ECG/troponin/echo. Treat MI, arrhythmia, valve disease, or myocarditis. Use norepinephrine +/- dobutamine if needed.
Obstructive shock: Relieve the obstruction: chest drain, pericardiocentesis, PE reperfusion, decompression.
Monitoring: Capillary refill, skin temperature/mottling, urine output, lactate trend, echo, dynamic fluid responsiveness, and arterial line if persistent shock or vasopressors.
Active Recall - Management of Shock
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[2] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
[4] Lecture slides: Trauma haemorrhage and fluid replacement guideline update 2025.
Complications of Shock
Shock complications are the predictable result of sustained tissue hypoxia, reperfusion injury, inflammation, and iatrogenic treatment harms. The longer the patient remains under-perfused, the more organs cross from reversible dysfunction into structural injury [1].
| Organ | Complication | Pathophysiological basis |
|---|---|---|
| Kidney | AKI / ATN | Renal medulla is hypoxia-prone. Low perfusion first causes pre-renal azotaemia; prolonged ischaemia causes tubular epithelial injury and ATN |
| Lung | ARDS | Endothelial leak and neutrophil activation flood alveoli with protein-rich fluid -> stiff hypoxaemic lungs |
| Brain | Delirium, coma, hypoxic-ischaemic injury | Low cerebral oxygen delivery plus inflammatory encephalopathy |
| Heart | Arrhythmias, myocardial stunning | Acidosis, catecholamines, electrolyte disturbance, and coronary hypoperfusion |
| Liver | Ischaemic hepatitis | Centrilobular hepatocytes have low oxygen reserve; AST/ALT can rise dramatically |
| Gut | Ileus, mucosal ischaemia, bacterial translocation | Splanchnic vasoconstriction sacrifices gut perfusion; barrier failure feeds sepsis |
| Haematological | DIC, coagulopathy | Tissue factor activation, endothelial injury, consumption of platelets and clotting factors |
When flow is restored after ischaemia:
- Oxygen returns to damaged mitochondria
- Reactive oxygen species form
- Calcium floods cells
- Neutrophils adhere to endothelium
- Capillary leak worsens
This is why a patient can look worse temporarily after circulation is restored: lactate may lag, pulmonary oedema may emerge, and inflammatory injury can continue.
C. Complications by Shock Type
- Pre-renal AKI -> ATN
- Dilutional coagulopathy from excess crystalloid
- Hypothermia from exposure and cold fluids
- Acidosis from hypoperfusion
- Coagulopathy from factor consumption and dilution
- Abdominal compartment syndrome after massive resuscitation
The Trauma Death Spiral
Hypothermia, acidosis, and coagulopathy amplify one another. Cold patients do not clot, acidotic patients do not clot, bleeding patients become colder and more acidotic. This is why haemorrhagic shock management is not just "give fluid"; it is haemorrhage control, warming, blood products, calcium, and correction of coagulopathy [4].
- Pulmonary oedema
- Refractory hypoxaemia
- Ventricular arrhythmias
- Cardiac arrest
- Renal and hepatic congestion from high venous pressures
- Cardiac arrest if tamponade, tension pneumothorax, or massive PE is not relieved
- RV failure after massive PE
- Hypoxic brain injury from pulseless electrical activity
- ARDS
- DIC
- AKI
- Critical illness weakness
- Secondary infections
- Long-term cognitive and functional decline
| Treatment | Possible complication | Prevention |
|---|---|---|
| Large-volume crystalloid | Pulmonary oedema, tissue oedema, abdominal compartment syndrome, hyperchloraemic acidosis with NS | Reassess fluid responsiveness; prefer balanced crystalloids when appropriate |
| Vasopressors | Digital/ischaemic limb injury, arrhythmias, extravasation injury | Use correct concentration, monitor peripheral site, move to central access when ongoing |
| Central venous catheter | Pneumothorax, arterial puncture, CLABSI, thrombosis | Ultrasound guidance, asepsis, daily line review |
| Blood transfusion | TACO, TRALI, hypocalcaemia, hyperkalaemia, transfusion reaction | Monitor, warm blood, check calcium, use protocol |
| Mechanical ventilation | Ventilator-associated pneumonia, barotrauma, haemodynamic compromise | Lung-protective ventilation and daily liberation assessment |
Active Recall - Shock Complications
References
[1] Lecture slides: ESICM circulatory shock and haemodynamic monitoring guideline 2025.
[4] Lecture slides: Trauma haemorrhage and fluid replacement guideline update 2025.
High Yield Summary
Definition: Shock = life-threatening circulatory failure causing inadequate oxygen delivery, cellular hypoxia, anaerobic metabolism, lactate production, organ dysfunction, and death if not reversed [1].
Core equation: Oxygen delivery = cardiac output x arterial oxygen content. Cardiac output = heart rate x stroke volume. Shock is any state where this system fails.
Four major types:
- Hypovolaemic: tank empty. Low preload, low cardiac output, compensatory high SVR.
- Cardiogenic: pump failure. High filling pressures, low cardiac output, pulmonary oedema.
- Obstructive: flow blocked. Tension pneumothorax, tamponade, massive PE.
- Distributive: pipes dilated/leaky. Sepsis, anaphylaxis, neurogenic shock.
Early signs: tachycardia, cool peripheries, delayed capillary refill, oliguria, anxiety/confusion, rising lactate. Hypotension is late.
Bedside classification: cold/clammy suggests hypovolaemic, cardiogenic, or obstructive shock. Warm/flushed early suggests distributive septic shock, but late septic shock can become cold.
Initial approach: ABCDE, high-flow oxygen if hypoxaemic, monitoring, two large-bore IVs or IO, bloods including lactate, bedside glucose, ECG, CXR, POCUS, catheterise for urine output.
Mermaid algorithm mindset: recognise shock -> resuscitate immediately -> identify phenotype -> treat cause in parallel -> reassess response -> escalate monitoring and ICU support.
Fluids: Give crystalloid when fluid responsive or hypovolaemic. After initial resuscitation, use dynamic assessment before more fluid.
Vasopressors: Norepinephrine is the usual first-line vasopressor for vasodilatory shock. Use it early if hypotension persists despite initial fluid or if fluids are unsafe [2].
Cardiogenic shock: avoid blind fluids. Use ECG/troponin/echo, treat ACS/arrhythmia/valve problem, consider norepinephrine plus inotrope, and urgent cardiology/ICU.
Obstructive shock: fluids and pressors buy time only. Definitive treatment is decompression or relief of obstruction: needle/finger thoracostomy, pericardiocentesis, thrombolysis/embolectomy, or operation.
Complications: AKI, ARDS, DIC, bowel ischaemia, hepatic injury, myocardial injury, pressure injury, delirium, ICU-acquired weakness, death.
Active Recall - Shock Summary
References
[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.
[2] Lecture slides: Surviving Sepsis Campaign International Guidelines for Management of Sepsis and Septic Shock 2026.
Fluid Replacement
A practical, pathophysiology-first guide to peri-operative fluid resuscitation, replacement, maintenance fluids, electrolyte correction, and monitoring in general surgery.
Sepsis
Sepsis and septic shock for surgical patients, covering infection-triggered organ dysfunction, source control, investigations, antimicrobial therapy, haemodynamic resuscitation, and complications using current 2026 guidance with Hong Kong relevance.