Shock Basics
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Direct answer
A normal blood pressure has never excluded shock — compensated hypovolaemia can hold a respectable cuff reading while tissue perfusion is already failing. Shock is inadequate cellular oxygen delivery: the classification worth reciting is hypovolaemic (haemorrhagic or fluid-depleted), cardiogenic (pump failure after infarction or arrhythmia), obstructive (tension pneumothorax, cardiac tamponade, massive pulmonary embolism) and distributive (septic, anaphylactic, neurogenic — the vasodilated states). Haemorrhagic shock is graded in ATLS classes I to IV by volume lost: class II (750-1500 mL, 15-30 per cent) shows tachycardia above 100 with a narrowed pulse pressure, while hypotension and confusion appear only in class III. Treatment is restore volume, control the cause, and watch urine output — 0.5 mL/kg/hour — as the bedside proof that perfusion has returned.
What you must remember
- Definition: circulatory insufficiency such that oxygen delivery fails to meet cellular demand, producing anaerobic metabolism and lactic acidosis — a perfusion state, not a pressure reading.
- Haemorrhagic classes (ATLS): class I up to 750 mL — essentially no findings; class II 750-1500 mL — heart rate over 100, narrowed pulse pressure, normal blood pressure; class III 1500-2000 mL — hypotension, tachypnoea, confusion; class IV over 2000 mL — lethargy, marked tachycardia, collapsing pressure. Roughly 30 per cent blood loss is the threshold where compensation fails in adults.
- Early signs are subtle: tachycardia, cool pale skin, delayed capillary refill, narrowed pulse pressure and anxiety appear before the systolic pressure falls — pulse pressure is the most sensitive early vital sign.
- Stages of shock: compensated (barely visible), progressive (falling pressure, oliguria, metabolic acidosis), irreversible (cellular death despite resuscitation) — the classical triad of exam terminology.
- Each type, one intervention: haemorrhagic — volume plus surgical haemostasis; cardiogenic — inotropes and cause-specific care; obstructive — needle decompression or pericardiocentesis; anaphylactic — intramuscular adrenaline 0.5 mg of 1:1000 promptly; neurogenic — vasopressors for lost vascular tone.
- Resuscitation targets: mean arterial pressure at least 65 mmHg, urine output 0.5 mL/kg/hour, falling serum lactate, warm pink peripheries and a correcting base deficit.
- Fluid logic: warmed crystalloid (normal saline or Ringer lactate) first; blood products early in class III and IV haemorrhage; permissive hypotension until surgical control in penetrating trauma, per current trauma teaching.
Two patients, one algorithm
Run the primary survey on a road-traffic victim who is anxious, pale, heart rate 118, blood pressure 104/68, respiratory rate 26. The cuff looks reassuring until you compute the pulse pressure of 36 and note the cool knees — class II haemorrhagic shock, most likely from a splenic injury or a femoral fracture, each femur holding up to 1.5 litres in its thigh compartment. Management: two large-bore intravenous cannulae, warmed crystalloid bolus, activate the blood bank, and hunt the bleeding source with focused assessment by sonography or CT if stable — because class II shock that answers fluids and then relapses is the signature of ongoing bleeding that only a surgeon stops. Contrast a ward patient hours after a routine procedure: fever, warm flushed peripheries, wide pulse pressure, heart rate 120, blood pressure 88/50. Warm shock in a febrile patient is distributive until excluded — sepsis with vasodilation, not volume depletion — and giving litres of fluid without antibiotics misses the cause entirely. The same numbers (tachycardia, hypotension) point in opposite physiological directions, and the skin tells you which: cold and pale means pump the volume; warm and wide means find the cause and use vasopressors.
How the exam frames it
BDS and viva questions concentrate on three things: the classification with one example each, the ATLS class table (examiners repeatedly ask which class first shows hypotension — class III), and the endpoints of resuscitation with urine output as the quotable number. The classic long answer is a haemorrhagic shock case — describe recognition, resuscitation, monitoring and definitive haemostasis in order. A frequently mishandled viva question is anaphylactic shock in the dental chair after a drug or latex exposure: the expected sequence is stop the trigger, IM adrenaline into the anterolateral thigh, oxygen, supine positioning with legs raised, fluids and antihistamine-steroid backup — adrenaline first, everything else later.
Frequently asked questions
Which vital sign falls first in class II haemorrhagic shock?
The pulse pressure narrows while systolic pressure is still maintained; heart rate above 100 with a narrowed pulse pressure is the earliest reliable bedside clue.
In which ATLS class does hypotension first appear?
Class III, representing 1500-2000 mL (30-40 per cent) blood loss, accompanied by tachypnoea, confusion and marked tachycardia.
How does septic shock differ physiologically from haemorrhagic shock?
Septic shock is distributive — vasodilation with maldistribution despite adequate or high cardiac output, giving warm peripheries and a wide pulse pressure, versus the cold, vasoconstricted peripheries of volume loss.
What is the first-line treatment of anaphylactic shock in the dental clinic?
Intramuscular adrenaline 0.5 mg (0.5 mL of 1:1000) into the anterolateral thigh, repeated every 5 minutes as needed, with the supine-legs-raised position, high-flow oxygen and intravenous fluids.
Why is urine output used to monitor resuscitation?
At 0.5 mL/kg/hour or better, the kidneys — the most sensitive visceral flowmeter — confirm that renal perfusion, and by proxy organ perfusion, has been restored.