Shock

A systematic surgical approach to shock: classification, pathophysiology, differential diagnosis, diagnosis, investigations, management, complications, and high-yield summary.

Exam domain	One-glance essentials
Definition / diagnosis	*Shock is circulatory failure causing inadequate tissue perfusion and cellular hypoxia* ^[1] Oxygen delivery = cardiac output × arterial oxygen content; cardiac output = heart rate × stroke volume ^[1] Hypotension is not required early; rising lactate, oliguria, confusion and poor capillary refill may precede it ^[1]
Epidemiology / risks	Haemorrhage, gastrointestinal loss, burns, pancreatitis and dehydration predispose to hypovolaemic shock ^[1] MI, arrhythmia, myocarditis and acute valve disease predispose to cardiogenic shock ^[1] Surgery risks sepsis, tension pneumothorax, tamponade, pulmonary embolism and anaphylaxis ^[1]
Core mechanism	Hypovolaemic: low preload and cardiac output with compensatory vasoconstriction ^[1] Cardiogenic: pump failure with low output and high filling pressures; obstructive: impaired cardiac inflow or outflow ^[1] Distributive: pathological vasodilation and maldistributed or increased vascular permeability ^[1]
Clinical picture	Early features: tachycardia, cool peripheries, delayed capillary refill, oliguria, anxiety or confusion ^[1] Warm, flushed skin suggests early distributive shock; late sepsis may become cold and clammy ^[1] Pulmonary oedema suggests cardiogenic shock; unilateral absent breath sounds or raised JVP suggests obstructive shock ^[1]
Investigations	*Use echocardiography as first-line imaging when shock type is unclear* ^[1] Check serial lactate, ABG, glucose, FBC, renal function, electrolytes, coagulation, cultures when infection is possible, ECG and troponin ^[1] *Use capillary refill, mottling, skin temperature and dynamic fluid-response tests*; arterial monitoring is indicated in persistent shock or vasopressor use ^[1]
Management	Start ABCDE, oxygen if hypoxaemic, monitoring, two large-bore IVs or IO access, bloods and urgent senior/ICU review ^[1] Give crystalloid for likely hypovolaemia or fluid responsiveness; reassess dynamically and avoid blind boluses in cardiogenic shock ^[1] *Norepinephrine is usual first-line vasopressor for vasodilatory shock*; treat the cause concurrently ^[1] Decompress tension pneumothorax, drain tamponade, and urgently reperfuse or remove massive PE obstruction ^[1]
Complications	Persistent hypoperfusion causes AKI, myocardial injury, hepatic injury, bowel ischaemia and delirium ^[1] Severe shock may cause ARDS, DIC, multiorgan failure and death ^[1] Haemorrhagic shock is worsened by the hypothermia–acidosis–coagulopathy cycle ^[1]
Prevention / follow-up	Identify and control bleeding, infection and mechanical obstruction early; reassess perfusion after every intervention ^[1] Use dynamic assessment to reduce unnecessary fluid loading and prevent pulmonary oedema ^[1] Provide frequent urine-output, capillary-refill, lactate and organ-function surveillance in at-risk patients ^[1]
Exam traps	Normal blood pressure does not exclude shock; hypotension can be a late sign ^[1] Do not label every hypotensive surgical patient dehydrated: fluids can worsen cardiogenic shock and delay decompression ^[1] Warm skin does not exclude sepsis, and cold skin does not distinguish hypovolaemic, cardiogenic or obstructive shock ^[1] Vasopressors support perfusion but do not replace haemorrhage control, source control or relief of obstruction ^[1]

References

^[1] Lecture slides: ESICM guidelines on circulatory shock and hemodynamic monitoring 2025.

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.

Shock

A. Definition - What Shock Actually Means

B. Epidemiology and Surgical Relevance

C. Classification of Shock - The Four Big Buckets

D. Pathophysiology From First Principles

1. The Final Common Pathway

2. Compensated vs Decompensated Shock

E. Aetiology by Shock Type

1. Hypovolaemic Shock

2. Cardiogenic Shock

3. Obstructive Shock

4. Distributive Shock

F. Hong Kong-Relevant Causes to Keep in Mind

Active Recall - Shock Etiology

A. First Principle: Shock Is a Syndrome, Not a Diagnosis

B. Rapid Bedside Pattern Recognition

C. Differential by Shock Category

1. Hypovolaemic Shock

2. Cardiogenic Shock

3. Obstructive Shock

4. Distributive Shock

D. Mermaid Diagram - Undifferentiated Shock DDx

Active Recall - Shock Differential Diagnosis

A. Diagnostic Concept

B. Bedside Diagnostic Algorithm

C. Clinical Criteria - What You Need to See

D. Phenotyping at the Bedside

E. Shock Index

F. Diagnostic Endpoints After Initial Treatment

Active Recall - Shock Diagnosis

A. Bedside and Monitoring Investigations

B. Core Blood Tests

C. Microbiology When Sepsis Is Possible

D. Imaging by Shock Phenotype

E. Dynamic Fluid Responsiveness Tests

F. Interpreting Lactate Correctly

Active Recall - Shock Investigations

A. Principles

B. Management Algorithm

C. Universal First 10 Minutes

D. Fluids, Blood, and Vasopressors

1. Fluids

2. Blood Products in Haemorrhagic Shock

3. Vasopressors

E. Cause-Specific Management

1. Hypovolaemic Shock

2. Distributive Shock

3. Cardiogenic Shock

4. Obstructive Shock

F. Monitoring During Resuscitation

Active Recall - Management of Shock

A. Multi-Organ Dysfunction Syndrome

B. Reperfusion Injury

C. Complications by Shock Type

1. Hypovolaemic / Haemorrhagic Shock

2. Cardiogenic Shock

3. Obstructive Shock

4. Septic / Distributive Shock

D. Iatrogenic Complications

Active Recall - Shock Complications

Active Recall - Shock Summary

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