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SN6 SHORT NOTE 5M

Write a short note on shock — types, pathophysiology, clinical features and management.

General Medicine · Final Professional

Definition

Shock is a state of acute circulatory failure resulting in inadequate tissue perfusion and cellular oxygen delivery, leading to cellular hypoxia, anaerobic metabolism, lactate accumulation and, if uncorrected, multi-organ failure and death. Hypotension is a late and unreliable sign — shock may be present with a normal blood pressure, particularly in young patients and in the compensated stage.

Classification

TypeMechanismCardiac OutputPreload (JVP/CVP)SVRExtremities
HypovolaemicLoss of circulating volume — haemorrhage, burns, vomiting, diarrhoea, third spacingLowLowHighCold
CardiogenicPump failure — MI, arrhythmia, myocarditis, valve ruptureLowHighHighCold
ObstructiveMechanical obstruction — tension pneumothorax, cardiac tamponade, massive pulmonary embolismLowHighHighCold
DistributiveVasodilatation and maldistribution — sepsis, anaphylaxis, neurogenic, adrenal crisisHigh (early)LowLowWarm (early)

Pathophysiology & Stages

1. Compensated (pre-shock): baroreceptor-mediated sympathetic activation with tachycardia, vasoconstriction and increased contractility; the renin-angiotensin-aldosterone system and ADH conserve salt and water. Blood pressure is maintained; the clues are tachycardia, narrowed pulse pressure, cool peripheries, anxiety and reduced urine output.

2. Decompensated: compensation fails; hypotension appears, tissue perfusion falls, anaerobic metabolism produces lactic acidosis, capillary leak and microvascular thrombosis develop.

3. Irreversible: cellular death, multi-organ failure, and unresponsiveness to therapy.

Clinical Features

  • General: tachycardia, narrow pulse pressure, hypotension (late), tachypnoea, cool clammy peripheries with prolonged capillary refill (> 2 seconds) — or warm flushed peripheries in early septic and anaphylactic shock.
  • Neurological: anxiety and restlessness progressing to confusion, drowsiness and coma.
  • Renal: oliguria (< 0.5 mL/kg/hour) — a sensitive early marker of perfusion.
  • Specific pointers: raised JVP with muffled heart sounds and pulsus paradoxus in tamponade; tracheal deviation with absent breath sounds in tension pneumothorax; urticaria and stridor in anaphylaxis; fever with a focus in sepsis; and warm peripheries with bradycardia in neurogenic shock.

Investigations

Do not delay resuscitation for investigations. In parallel: CBC, urea and electrolytes, serum lactate (a key marker of tissue hypoperfusion and of response to treatment), arterial blood gas, blood glucose, coagulation profile and blood grouping and cross-match; blood cultures before antibiotics in sepsis; cardiac troponin and ECG; chest X-ray; bedside echocardiography (invaluable for distinguishing cardiogenic, obstructive and hypovolaemic states); ultrasound (FAST scan in trauma); and CT pulmonary angiography where embolism is suspected.

Management

Immediate — the same for all types:

  • Airway, breathing, circulation; high-flow oxygen; secure two large-bore intravenous cannulae; continuous monitoring of ECG, blood pressure, saturation and urine output via a catheter.
  • Identify and treat the cause simultaneously — this is what distinguishes management between types.

Type-specific:

  • Hypovolaemic: rapid balanced crystalloid boluses with reassessment after each; blood products for haemorrhage, with early activation of a massive transfusion protocol and control of bleeding (surgery, endoscopy, interventional radiology). Permissive hypotension may be appropriate in uncontrolled traumatic haemorrhage.
  • Septic: early broad-spectrum antibiotics after cultures, source control, fluid resuscitation, and noradrenaline as the first-line vasopressor if hypotension persists; consider hydrocortisone in refractory shock. Lactate clearance guides response.
  • Cardiogenic: cautious or no fluid; inotropes (dobutamine) and vasopressors as needed; urgent revascularisation for myocardial infarction; treat arrhythmia; mechanical support (intra-aortic balloon pump, ECMO) in selected cases.
  • Obstructive: immediate needle decompression and chest drain for tension pneumothorax; pericardiocentesis for tamponade; thrombolysis or embolectomy for massive pulmonary embolism.
  • Anaphylactic: intramuscular adrenaline immediately, repeated as required; remove the trigger; fluids, oxygen, antihistamines and corticosteroids as adjuncts.

Monitoring response: improving mental state, warm peripheries with capillary refill under 2 seconds, urine output above 0.5 mL/kg/hour, falling lactate, and restored blood pressure. These are better targets than blood pressure alone.

DANGER / REMEMBER

Fluid is not the answer in every shock. Giving aggressive fluid to a patient in cardiogenic shock worsens pulmonary oedema and can be fatal. Distinguish the type before loading fluid — the JVP and bedside echocardiogram are the fastest way to do so. Likewise, in tension pneumothorax and tamponade, fluid buys only minutes; the obstruction must be relieved mechanically.

All questions in Fluids & Electrolytes

  1. Q1Discuss the causes, clinical approach, investigations and management of a patient presenting with generalised oedema (anasarca). ★
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  3. SN1Write a short note on hyperkalaemia.
  4. SN2Write a short note on hypokalaemia.
  5. SN3Write a short note on hyponatraemia.
  6. SN4Write a short note on hypercalcaemia.
  7. SN5Write a short note on hypocalcaemia.
  8. SN6Write a short note on shock — types, pathophysiology, clinical features and management.
  9. SN7Write a short note on nutritional support and refeeding syndrome.

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