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This is a clinician-written, evidence-based guide aligned to the MCC Examination Objectives. It is structured by clinical presentation — the way the MCCQE tests and the way patients actually present. Management reflects current Canadian guidelines (CMA, CFPC, CPS). Always cross-reference with institutional protocols and clinical judgment.
Key points
- Shock = inadequate tissue perfusion, NOT just low BP. Signs: tachycardia, altered mental status, cool/mottled extremities, oliguria, elevated lactate
- Four types: hypovolaemic (haemorrhage, dehydration), cardiogenic (MI, HF), distributive (sepsis, anaphylaxis, neurogenic), obstructive (PE, tamponade, tension pneumo)
- Septic shock is the most common type in the ICU. Surviving Sepsis: 30 mL/kg crystalloid within 3h + norepinephrine first-line vasopressor + early antibiotics (within 1h)
- Bedside POCUS (RUSH exam) is the fastest way to differentiate shock types: IVC size/collapse, cardiac function, lung sliding, free fluid
- Cardiogenic shock: avoid excessive fluids — inotropes (dobutamine) + vasopressors (norepinephrine) + treat underlying cause. Obstructive shock: treat the obstruction (needle decompression, pericardiocentesis, thrombolysis)
Approach to the Presentation
Shock is defined as a state of circulatory failure leading to inadequate tissue oxygen delivery. It is a clinical diagnosis based on signs of hypoperfusion, NOT solely on a BP number — a patient can be in compensated shock with a "normal" BP due to tachycardia and vasoconstriction. The approach involves: (1) Recognise shock early (tachycardia, AMS, mottling, oliguria, lactate >2 mmol/L); (2) Begin resuscitation immediately while simultaneously determining the type; (3) Bedside assessment with POCUS (RUSH protocol) to rapidly classify; (4) Targeted treatment based on type. The mortality of untreated shock rises ~7% per hour of delayed treatment.
Differential Diagnosis — Types of Shock
| diagnosis | likelihood | key features | distinguishing test |
|---|---|---|---|
| Septic Shock (distributive) | must-not-miss | Fever (or hypothermia), suspected infection source, warm extremities initially ("warm shock"), tachycardia, hypotension refractory to fluids, elevated lactate, elevated WBC or bandaemia | qSOFA >=2, blood cultures x2, lactate >2 mmol/L, source identification. POCUS: hyperdynamic LV, dilated IVC with poor collapse |
| Hypovolaemic Shock — Haemorrhagic | must-not-miss | Trauma, GI bleeding, ruptured AAA, ruptured ectopic. Cool/clammy, tachycardia, flat neck veins, decreased urine output. Class I-IV based on estimated blood loss | Clinical + CBC (may be initially normal in acute haemorrhage). FAST exam for free fluid. Source identification |
| Cardiogenic Shock | must-not-miss | Acute MI (especially large anterior), acute decompensated HF, massive MR (papillary rupture), myocarditis. Cool extremities, elevated JVP, pulmonary oedema, S3 gallop | ECG + troponin + BNP. POCUS: poor LV function, dilated IVC, B-lines (pulmonary oedema). Swan-Ganz: CI <2.2, PCWP >18 |
| Obstructive — Tension Pneumothorax | must-not-miss | Trauma or mechanical ventilation + sudden hypotension + tracheal deviation + absent breath sounds + hyperresonance. JVD (unless hypovolaemic) | CLINICAL DIAGNOSIS — immediate needle decompression. POCUS: absent lung sliding |
| Obstructive — Cardiac Tamponade | must-not-miss | Beck triad (hypotension, JVD, muffled sounds), pulsus paradoxus, tachycardia. Trauma, malignancy, pericarditis, post-procedure | POCUS: pericardial effusion + RA/RV diastolic collapse. Immediate pericardiocentesis |
| Obstructive — Massive PE | must-not-miss | Acute dyspnoea + hypotension + tachycardia + JVD. Risk factors for VTE. Acute RV failure | POCUS: RV dilation, D-shaped septum, McConnell sign. CTPA if stable enough. Systemic tPA if too unstable for CT |
| Anaphylactic Shock (distributive) | must-not-miss | Exposure to allergen (drug, food, insect sting) + rapid onset of urticaria/angioedema + bronchospasm + hypotension. Warm, flushed | Clinical diagnosis. Tryptase level (if measured within 1-2h). Treatment precedes diagnosis: IM epinephrine (adrenaline) 0.3-0.5 mg |
| Hypovolaemic Shock — Non-haemorrhagic | common | Dehydration, vomiting, diarrhoea, burns, diabetic emergencies (DKA/HHS). Dry mucous membranes, decreased skin turgor, tachycardia | Clinical assessment, BMP (elevated BUN:Cr ratio, electrolyte abnormalities). POCUS: collapsed IVC |
| Neurogenic Shock (distributive) | less common | Spinal cord injury (above T6) + hypotension + BRADYCARDIA (unlike other shock types which cause tachycardia) + warm, dry extremities below the lesion | Clinical in context of spinal cord injury. Differentiate from haemorrhagic shock in trauma (neuro shock = bradycardia, haemorrhagic = tachycardia) |
| Adrenal Crisis | less common | Known adrenal insufficiency or chronic steroid use + acute stress (illness, surgery) + hypotension refractory to fluids + hypoglycaemia + hyperkalaemia + hyponatraemia | Random cortisol (low). Treat empirically: IV hydrocortisone 100 mg bolus + aggressive IV fluids |
Red Flags & Key Assessment
Symptoms
Altered mental status / confusion (cerebral hypoperfusion)
Oliguria / anuria (<0.5 mL/kg/h) (renal hypoperfusion)
Mottled, cool extremities (peripheral vasoconstriction — hypovolaemic/cardiogenic)
Warm, flushed extremities in early phase (distributive — septic, anaphylactic)
Massive haematemesis, rectal bleeding, or trauma (haemorrhagic source)
Signs
Tachycardia (compensatory in all EXCEPT neurogenic shock which causes bradycardia)
Hypotension (SBP <90 or MAP <65 — but shock can exist with "normal" BP in compensation)
Elevated lactate >2 mmol/L (tissue hypoperfusion, anaerobic metabolism)
JVP assessment: flat = hypovolaemic, elevated = cardiogenic/obstructive
Capillary refill >3 seconds (peripheral hypoperfusion)
Approach to Investigation
First-line
Bedside POCUS (RUSH exam)Rapid Ultrasound in Shock and Hypotension. Assess: (1) Pump — LV function, RV size; (2) Tank — IVC size/collapsibility (flat IVC = hypovolaemic, plethoric = cardiogenic/obstructive), free peritoneal/pericardial fluid; (3) Pipes — aorta (AAA), DVT. Also: lung sliding (pneumothorax), B-lines (pulmonary oedema)
Lactate (venous or arterial)>2 mmol/L = tissue hypoperfusion. >4 mmol/L = severe. Serial lactate to monitor resuscitation response. Lactate clearance >10% in 6h associated with improved mortality
Blood cultures (x2 sets)BEFORE antibiotics if possible (but do NOT delay antibiotics >1h to obtain cultures)
CBC, BMP, liver enzymes, coagulation, troponinBaseline organ function assessment. Troponin if cardiogenic suspected. Coagulation for DIC screening in sepsis
ECGAcute MI (cardiogenic), RV strain (PE), low voltage/alternans (tamponade)
Blood gas (ABG or VBG)Assess pH, pCO2, bicarbonate, base deficit. Metabolic acidosis with elevated lactate = shock
Second-line
CXRPneumothorax, pulmonary oedema, widened mediastinum, pneumonia
CTPAIf PE suspected and patient stable enough for transport
CT abdomenIf intra-abdominal source suspected (ruptured AAA, intra-abdominal sepsis, mesenteric ischaemia)
Specialist
Pulmonary artery catheter (Swan-Ganz)Rarely used now — POCUS has largely replaced it. Still useful in complex cases where fluid responsiveness is unclear. Cardiogenic: CI <2.2, PCWP >18. Septic: CI >2.5, PCWP <18, low SVR
Management Principles
Surviving Sepsis Campaign 2021 + CAEP Shock Management1
Universal initial steps (all shock)
- ABCs: secure airway if needed, high-flow O2, 2 large-bore IVs
- IV crystalloid bolus: 500 mL-1 L normal saline or Ringer lactate, reassess after each bolus
- Continuous monitoring: telemetry, SpO2, foley catheter for urine output, arterial line if vasopressors needed
- Bedside POCUS to classify shock type within minutes
- Lactate measurement — serial monitoring to guide resuscitation
2
Septic shock
- IV crystalloid 30 mL/kg within first 3 hours (reassess fluid responsiveness frequently — avoid overresuscitation)
- Broad-spectrum IV antibiotics within 1 hour of recognition (every hour of delay increases mortality ~7%)
- Norepinephrine first-line vasopressor (target MAP >=65 mmHg)
- Add vasopressin as second agent if norepinephrine insufficient
- IV hydrocortisone 200 mg/day if shock refractory to fluids + vasopressors (>4h)
- Source control: drain abscesses, debride necrotic tissue, remove infected devices
3
Hypovolaemic shock
- Crystalloid resuscitation for non-haemorrhagic (NS or RL)
- Haemorrhagic: massive transfusion protocol (1:1:1 PRBC:FFP:platelets), permissive hypotension (SBP 80-90) until surgical control achieved
- Identify and control bleeding source: surgery, endoscopy, interventional radiology
- Tranexamic acid (TXA) within 3h if traumatic haemorrhage (CRASH-2)
4
Cardiogenic shock
- AVOID large-volume fluid boluses (worsen pulmonary oedema)
- Norepinephrine first-line vasopressor (over dopamine — SOAP II trial)
- Dobutamine or milrinone for inotropic support
- Treat underlying cause: emergent PCI for MI, valve surgery for acute MR/VSD
- Mechanical support: IABP, Impella, ECMO in refractory cases
5
Obstructive shock
- Tension pneumothorax: immediate needle decompression then chest tube
- Cardiac tamponade: emergent pericardiocentesis (or thoracotomy if traumatic/clotted)
- Massive PE: systemic thrombolysis (alteplase) if hemodynamically unstable
6
Anaphylactic shock
- IM epinephrine (adrenaline) 0.5 mg (1:1000) into lateral thigh — FIRST-LINE, repeat q5-15 min
- IV crystalloid bolus (1-2 L), trendelenburg position
- Adjuncts: nebulised salbutamol (bronchospasm), IV diphenhydramine, IV methylprednisolone
- Observe >=4-6h after resolution (risk of biphasic reaction)
MCCQE1 Exam Tips
- 1Shock is a clinical diagnosis based on hypoperfusion signs (tachycardia, AMS, oliguria, mottled skin, lactate >2), NOT just a BP number. Compensated shock can have "normal" BP
- 2POCUS (RUSH exam) is the single fastest bedside tool to classify shock type — know the IVC assessment: flat IVC = needs fluid, plethoric IVC = cardiogenic/obstructive
- 3Septic shock: antibiotics within 1 hour + 30 mL/kg crystalloid + norepinephrine if MAP <65 after fluids. Every hour of antibiotic delay increases mortality
- 4Neurogenic shock is the exception: BRADYCARDIA + hypotension (loss of sympathetic tone). All other shock types cause tachycardia
- 5Cardiogenic shock: do NOT give large fluid boluses — it worsens pulmonary oedema. Use inotropes + vasopressors + treat cause
- 6Tension pneumothorax: clinical diagnosis. Needle decompression BEFORE imaging. Do not delay for CXR
- 7Anaphylaxis: IM epinephrine is the answer, always. Not IV antihistamines, not steroids — IM epinephrine FIRST
- 8Adrenal crisis: suspect in any patient on chronic steroids who presents with refractory hypotension. Empiric IV hydrocortisone 100 mg while awaiting cortisol level
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