Shock Physiology
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Direct answer
Shock is inadequate tissue perfusion for metabolic need, whatever the blood pressure number. It evolves in stages: an initial compensated (nonprogressive) phase where baroreceptor reflexes, venous capacitance mobilisation (especially splanchnic), tachycardia, peripheral vasoconstriction, ADH and the renin-angiotensin-aldosterone axis, and transcapillary refill defend the circulation; a progressive phase where positive feedbacks take over — myocardial depression, increased capillary permeability with sludging, tissue hypoxia and lactic acidosis, vasomotor failure, disseminated intravascular coagulation and bacterial translocation; and an irreversible phase where ATP depletion and lysosomal rupture make death inevitable despite transfusion. The physiologic classification is hypovolaemic, cardiogenic, and distributive (septic, anaphylactic, neurogenic), with obstructive (tension pneumothorax, tamponade) often added.
What you must remember
- Compensated mechanisms: fast baroreceptor-mediated sympathetic drive (heart rate, contractility, venoconstriction), then RAAS and ADH volume retention; transcapillary refill draws interstitial fluid into vessels after haemorrhage (up to 1 L per hour early); the splanchnic venous bed is the body's autotransfusion reservoir.
- Haemorrhage grading (ATLS convention): class I up to 15% loss (minimal changes), class II 15-30% (tachycardia, narrowed pulse pressure — the earliest reliable sign), class III 30-40% (hypotension, tachypnoea, confusion), class IV over 40% (life-threatening).
- Early versus late signs: pulse pressure narrows before systolic pressure falls; tachycardia precedes hypotension; a "normal" blood pressure on a young patient with tachycardia and narrow pulse pressure is compensated class II — not reassurance.
- Progressive-stage vicious cycles: cardiac depression from acidosis and myocardial depressant factor, microvascular permeability and sludging, vasomotor centre failure after prolonged severe hypotension, DIC consuming clotting factors, and gut bacterial translocation fuelling sepsis.
- Shock types by physiology: hypovolaemic and cardiogenic share cold clammy skin with high systemic resistance (cold shock); distributive shocks run low resistance — septic shock classically warm and vasodilated early with high cardiac output; neurogenic shock is hypotension with bradycardia (sympathetic chain interrupted, no reflex tachycardia — the differentiating exam point); anaphylactic adds bronchospasm and urticaria.
- Sepsis physiology: nitric oxide-mediated vasoplegia, capillary leak and mitochondrial dysfunction; early goal-directed resuscitation with crystalloid (about 30 mL/kg), lactate clearance as the perfusion gauge, vasopressors (noradrenaline first-line) after volume.
- Irreversibility markers: refractory acidosis with deep lactate rise, coagulopathy, and the failure to respond to adequate volume — cellular ATP depletion, lysosomal rupture and myocardial depressant factor make transfusion futile.
How to work through a shocked patient
A young man arrives after a road traffic accident: pulse 118, blood pressure 104/72 (pulse pressure 32), anxious, pale, cold. That pulse pressure is the tell — about 20-25% volume loss, class II, compensated. Resuscitate with two large-bore cannulas, crystalloid and blood, and re-assess perfusion (mental state, urine output above 0.5 mL/kg/h, lactate), not just the pressure cuff. If he instead arrives drowsy at 78/40 with 130 beats per minute, he is class III-IV and needs blood products urgently, with trauma-panel activation.
Contrast the pathways: a post-myocardial infarction patient with cold extremities, distended neck veins and hypotension has a pump problem — fluids can worsen him, and the answer is inotropy, rhythm correction and revascularisation. The septic patient in the emergency department with fever, warm extremities and hypotension is vasodilated and volume-relative: crystalloid, then noradrenaline for vasoplegia, with cultures and antibiotics within the hour. The spinal injury patient hypotensive but bradycardic breaks the haemorrhage script — no sympathetic vasoconstriction, so no tachycardia; treat with volume and vasopressors rather than reflex fluid loading for bleeding that does not exist. One algorithm, four physiologies: identify the deranged variable — volume, pump, tone, or obstruction — and correct that variable.
Where students slip
The commonest error is equating shock with hypotension: compensation maintains pressure until 30% loss or more, so the earliest exam-answerable signs are tachycardia and a narrowed pulse pressure with cold skin; waiting for the pressure to drop is waiting for decompensation. The second is misreading neurogenic shock: students reach for more fluids when the missing element is sympathetic tone, and the bradycardia (unopposed vagal action on the heart) actively contradicts the haemorrhage reflex pattern. In viva, expect the classic progression question — what makes progressive shock progressive — and answer with the positive feedbacks (cardiac depression, vasomotor failure, sludging and DIC), because naming mechanisms, not adjectives, is what scores.
Frequently asked questions
What are the earliest clinical signs of compensated haemorrhagic shock?
Tachycardia with a narrowed pulse pressure and cold clammy skin; systolic pressure is defended until roughly 30% volume loss, so a normal cuff reading does not exclude significant haemorrhage.
Why does neurogenic shock cause bradycardia with hypotension?
Spinal sympathetic interruption removes vasomotor tone (vasodilation, hypotension) and cardiac accelerator drive, leaving unopposed vagal influence — bradycardia instead of the compensatory tachycardia of haemorrhage.
What is transcapillary refill in haemorrhage?
Fall in capillary hydrostatic pressure after vasoconstriction draws interstitial fluid into the circulation, an internal autotransfusion of up to a litre in the first hours, diluting proteins and haematocrit in the process.
Which positive feedbacks drive progressive shock?
Myocardial depression from acidosis, increased capillary permeability and sludging, failure of the vasomotor centre, disseminated intravascular coagulation, and bacterial translocation from the ischaemic gut.
Why is septic shock warm and vasodilated early?
Endotoxin-driven nitric oxide and inflammatory mediators relax vascular smooth muscle, dropping systemic vascular resistance while cardiac output rises compensatory — until hypovolaemia from capillary leak and myocardial depression convert it to cold shock.