Shock Classification and Haemodynamics
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Direct answer
Shock is acute circulatory failure with inadequate cellular oxygen utilisation, classified physiologically into four categories: hypovolaemic (volume loss), cardiogenic (pump failure), obstructive (mechanical impediment to flow) and distributive (vasoplegia with capillary leak, as in sepsis, anaphylaxis and neurogenic injury). Each carries a signature haemodynamic profile — central venous pressure, cardiac output and systemic vascular resistance — that the bedside examination and echocardiography reproduce, and each has a cause-specific intervention alongside the shared targets of mean arterial pressure 65 mmHg or above, urine output and lactate clearance.
What you must remember
- Hypovolaemic shock: haemorrhage (trauma, gastrointestinal bleeding, ruptured ectopic) or fluid loss (burns, diarrhoea); profile of low central venous pressure, low cardiac output and high systemic resistance with cold, clammy peripheries; treat with bleeding control, crystalloid and blood products — balanced transfusion in massive haemorrhage, with tranexamic acid early in trauma.
- Cardiogenic shock: extensive infarction, myocarditis, arrhythmia or valve failure; high central venous pressure, low cardiac output, high resistance with cool peripheries and pulmonary congestion; treat with revascularisation or cause correction, inotropes such as dobutamine, cautious fluids and mechanical circulatory support.
- Obstructive shock: tension pneumothorax (immediate needle decompression then drain), cardiac tamponade (Beck triad of hypotension, raised venous pressure and muffled sounds with pulsus paradoxus — pericardiocentesis), and massive pulmonary embolism (thrombolysis or embolectomy); the profile mimics cardiogenic shock with high venous pressure but the lesion is mechanical.
- Distributive shock: septic shock is the commonest shock in intensive care — early vasoplegia gives a high cardiac output with low resistance and warm peripheries, though late or cold septic shock with low output occurs; anaphylactic shock needs intramuscular adrenaline 0.5 mg (0.5 mL of 1 in 1000) into the anterolateral thigh, repeated every five minutes; neurogenic shock from spinal injury is warm and hypotensive with bradycardia — the absence of compensatory tachycardia is the clue — treated with vasopressors and careful fluids.
- Monitoring set: lactate and base deficit for severity, hourly urine output, capillary refill, arterial and central lines as needed, and focused echocardiography to separate the categories and guide fluid responsiveness.
- Shared endpoints: mean arterial pressure 65 mmHg or above (higher in chronic hypertension), urine 0.5 mL per kg per hour or better, falling lactate and clearing mentation; permissive hypotension applies only until haemorrhage control in trauma.
- Staging by blood loss: class 1 haemorrhage under 750 mL is compensated, class 2 (750 to 1500 mL) shows tachycardia with narrow pulse pressure, class 3 (1500 to 2000 mL) adds hypotension and class 4 (over 2000 mL) is immediately life-threatening — the classical adult trauma table.
Reading the haemodynamic profile at the bedside
Four patients, four profiles. A trauma victim with a rigid abdomen, pulse 122, pressure 88/56, narrow pulse pressure, cold fingers: A large infarct yesterday, now distended neck veins, crackles and cold peripheries: cardiogenic — high venous pressure, low output, high resistance — needing revascularisation, inotropes, cautious fluids and mechanical support. A uraemic patient with muffled sounds, pulsus paradoxus and falling pressure: tamponade, treated by pericardiocentesis, as are tension pneumothorax (needle decompression, then drain) and massive embolism (thrombolysis) — mechanical problems, mechanical answers. A febrile, warm, vasodilated patient with lactate of 4: distributive — low resistance, high output — where warm skin must not exclude shock, because pressure, lactate and mentation define it. Neurogenic shock completes the set: warm hypotension with bradycardia after cervical injury, treated with vasopressors and careful fluids.
Where students slip
Three distinctions lose the marks. Neurogenic shock is confused with other warm shocks, but bradycardia with hypotension after spinal injury — absent compensatory tachycardia — is close to pathognomonic. Anaphylaxis route errors persist: a ward reaction gets intramuscular adrenaline into the thigh, and intravenous first is the planted wrong option. And in every obstructive stem, tamponade and tension pneumothorax share physiology but demand opposite first procedures — pericardiocentesis against needle decompression.
Frequently asked questions
What are the four physiological categories of shock?
Hypovolaemic, cardiogenic, obstructive and distributive (septic, anaphylactic and neurogenic).
How does distributive (early septic) shock read haemodynamically?
Low systemic vascular resistance with high cardiac output and warm peripheries, central venous pressure normal or low.
Why is neurogenic shock warm and bradycardic?
Sympathetic disruption after spinal injury removes vasoconstrictor tone and cardiac acceleration, leaving vasodilation with an unopposed vagal bradycardia.
What is the dose and route of adrenaline in anaphylactic shock?
0.5 mg intramuscularly (0.5 mL of 1 in 1000) into the anterolateral thigh, repeated every five minutes as needed.
How do obstructive shocks present at the bedside?
Raised neck veins with hypotension and quiet or tracheal-shifted chest — Beck triad in tamponade, tracheal deviation and hyperresonance in tension pneumothorax.
What circulatory endpoints guide therapy?
Mean arterial pressure 65 mmHg or above, urine output at least 0.5 mL per kg per hour, and a falling lactate with improving mentation.