Clinical overview
Shock is inadequate effective tissue perfusion and oxygen use. Hypotension is common but not required; a pregnant patient can maintain blood pressure through tachycardia and vasoconstriction until reserve is nearly exhausted. The registrar must recognise shock before collapse, identify the dominant mechanism and resuscitate while definitive treatment is mobilised.
The four classical mechanisms are hypovolaemic, distributive, cardiogenic and obstructive. Obstetric patients often have mixtures: placental abruption produces blood loss and DIC; sepsis causes vasodilatation, capillary leak and sometimes myocardial depression; pre-eclampsia can combine high afterload, pulmonary oedema and intravascular–interstitial mismatch; amniotic-fluid embolism can cause acute right-heart failure followed by left-heart dysfunction and coagulopathy. “Mixed shock” should prompt a prioritised plan, not diagnostic paralysis.
Core knowledge
Oxygen supply and cellular distress
Oxygen delivery depends on cardiac output and arterial oxygen content. Cardiac output depends on heart rate and stroke volume; stroke volume depends on preload, contractility and afterload. Arterial oxygen content depends mostly on haemoglobin and saturation. Shock can therefore arise from insufficient volume, abnormal vascular tone, pump failure, mechanical obstruction, severe anaemia/hypoxaemia or failure of tissue extraction.
Compensatory responses preserve pressure and flow to heart and brain by increasing heart rate and vascular tone. Skin and renal perfusion fall first. Look for cool peripheries, delayed capillary refill and oliguria, but remember that early distributive shock may be warm with a bounding pulse. Lactate rises when production exceeds clearance; this may reflect hypoperfusion, adrenergic drive, seizures, liver dysfunction or drugs. A normal lactate does not exclude shock, and a raised lactate does not specify its cause.
Figure M6.1 — The shock engine links cardiac output and arterial oxygen content to six routes of oxygen-delivery failure, while showing how tachycardia and vasoconstriction can preserve pressure until skin, renal and ultimately organ perfusion deteriorate.
Phenotypes
| Phenotype | Mechanism | Typical obstetric causes | Useful bedside pattern |
|---|---|---|---|
| Hypovolaemic | Reduced preload and output | PPH, APH/abruption, ruptured ectopic/uterus, surgical bleeding, dehydration | Bleeding or losses, narrow pulse pressure, cool skin, small hyperdynamic LV; signs may be late |
| Distributive | Low vascular tone with maldistributed flow | Maternal sepsis, anaphylaxis, high neuraxial block | Warm early phase, low diastolic pressure, hyperdynamic LV; may become cold/mixed |
| Cardiogenic | Pump failure | PPCM, valve disease, ischaemia/SCAD, arrhythmia, myocarditis, severe hypertension | Congestion, B-lines, impaired LV or RV, raised venous pressure, poor response to fluid |
| Obstructive | Mechanical block to filling/outflow | Massive PE, tamponade, tension pneumothorax, severe aortocaval compression, AFE | Shock with RV strain/raised venous pressure, absent lung sliding or pericardial features according to cause |
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