In one line
Maternal collapse is the acute loss of circulation, consciousness or both in a pregnant or recently delivered woman, and after 20 weeks its management diverges from standard adult life support in two specific ways: the uterus must be displaced off the great vessels by continuous manual left displacement throughout chest compressions, and if there is no return of spontaneous circulation a resuscitative hysterotomy (peri-mortem caesarean) is performed where she lies — the decision taken by four minutes, aiming to deliver by five — primarily to save the mother, not the fetus.
Mechanism & pathophysiology
The whole of this topic falls out of one anatomical fact: from about 20 weeks the gravid uterus is large enough to compress the inferior vena cava and the aorta when the woman is supine. Caval compression cuts venous return; with a beating heart in shock this drops cardiac output by up to a third, and in cardiac arrest it is catastrophic. Closed-chest compression generates forward flow only by squeezing blood that is already in the thorax. If venous return is throttled by an obstructed cava, the right heart is poorly filled between compressions, so even technically perfect CPR produces a fraction of the stroke volume it would in a non-pregnant adult. Aortic compression compounds the problem by raising afterload against an already failing output. The supine pregnant woman in arrest is therefore being resuscitated against a mechanical obstruction that no drug or shock can overcome.
This is why uterine displacement is not an optional refinement but part of generating any output at all. Tilting the whole woman to the left was the historical solution, but lateral tilt steeply degrades the quality of chest compressions — the force vector is lost, the sternum is harder to reach, and depth falls — so the modern instruction is to keep her flat and have an assistant manually displace the uterus up and to the left (a two-handed cephalad-and-leftward lift from the patient's right side, or a one-handed push from her left), continuously, for the entire arrest. Delivering the fetus and emptying the uterus carries the same logic to its conclusion and abolishes aortocaval compression instantly and permanently: venous return is restored, the diaphragm drops, functional residual capacity and chest compliance improve, and roughly a litre of blood is autotransfused from the uteroplacental bed back into the maternal circulation. Resuscitative hysterotomy is, mechanistically, a resuscitation manoeuvre — it converts an unresuscitatable physiology into a resuscitatable one. Any fetal benefit is secondary.
Pregnancy also lowers the threshold at which hypoxia becomes lethal and shortens the time available. Oxygen consumption is ~20% higher and functional residual capacity ~20% lower, so the apnoeic reserve is small and desaturation is fast; the airway is oedematous, friable and prone to aspiration from a relaxed lower oesophageal sphincter and delayed gastric emptying. The dilutional anaemia and the hypercoagulable, high-output cardiovascular state mean that haemorrhage and thromboembolism — the things most likely to kill her — do so quickly. The clock that governs the four-minute rule is set by the brain: irreversible neuronal injury begins within minutes of arrest, and the fetus, dependent on already-marginal uteroplacental flow, is hypoxic from the moment maternal output fails.
The same physiology explains why the drugs of advanced life support do less in the supine pregnant woman than in a non-pregnant adult. Adrenaline and the rest are delivered to the central circulation only if compressions move blood from the periphery and the venous reservoir into the thorax; if the cava is clamped by the uterus, a drug given into a peripheral or even a femoral line may simply pool below the obstruction. This is the mechanistic reason that upper-limb venous and intraosseous access is preferred (a drug given below the diaphragm has to cross the compressed cava to reach the heart) and the deeper reason that no pharmacological or electrical intervention can substitute for mechanically relieving the obstruction. The uterus is the problem; emptying it is the treatment. It is worth being concrete about the autotransfusion: the term-pregnant uterus and its placental bed hold of the order of 500 mL to a litre of blood, and at delivery a substantial fraction of that volume returns to the maternal circulation — a meaningful preload bolus delivered exactly when the failing right heart needs filling. Mechanistically, then, resuscitative hysterotomy simultaneously removes an obstruction to venous return, restores chest compliance and diaphragmatic excursion, lowers afterload, and autotransfuses volume; no single drug does any one of those things as completely, and none does all four.
Assessment
Collapse is a presentation, not a diagnosis, and the resuscitation and the search for the cause run in parallel from the first second. Confirm arrest the standard way — unresponsive, not breathing normally, no central pulse within ten seconds — and call the obstetric arrest team immediately; the response must bring obstetrics, anaesthesia, a scalpel and a neonatal team to the bedside, because the definitive treatment may be surgical and cannot wait for transfer.
The causes are the universal reversible causes of arrest plus a set specific to pregnancy. Work the 4 Hs and 4 Ts and overlay the obstetric list:
- Hypovolaemia — almost always haemorrhage in this population: antepartum (abruption, praevia, uterine rupture, accreta spectrum) or postpartum (atony, trauma, retained tissue, coagulopathy). Concealed abruption and intra-abdominal bleeding after caesarean can present as collapse with a deceptively soft abdomen. This is the commonest correctable cause and the first to exclude. See Postpartum haemorrhage for the haemorrhage drills.
- Hypoxia — failed or difficult intubation, aspiration, high neuraxial block paralysing the diaphragm, severe asthma, pulmonary oedema (commonly from pre-eclampsia or cardiac disease).
- Hyperkalaemia / metabolic — and, in pregnancy specifically, hypoglycaemia (insulin-treated diabetes) and hypocalcaemia/hypermagnesaemia from magnesium sulphate toxicity in an eclamptic woman with renal impairment, which can itself arrest the heart.
- Hypothermia — uncommon but relevant in trauma and prolonged field resuscitation.
- Thromboembolism — pulmonary embolism, the leading cause of direct maternal death in many high-income settings; also myocardial infarction and aortic dissection, both rising with maternal age.
- Toxins — local-anaesthetic systemic toxicity (LAST) from epidural or paracervical block, magnesium toxicity, illicit drugs, and iatrogenic overdose.
- Tamponade — pericardial, or after cardiac surgery/trauma.
- Tension pneumothorax.
To these add the causes that are only obstetric: eclampsia and intracranial haemorrhage (the hypertensive woman who fits and does not recover, or who collapses with a thunderclap headache — a ruptured aneurysm or hypertensive bleed); amniotic-fluid embolism (sudden collapse around the time of delivery with hypoxia, hypotension and disseminated intravascular coagulation, often heralded by a seizure or sense of impending doom); high or total spinal block; anaphylaxis (antibiotics, oxytocin, latex, suxamethonium); and sepsis, which in South Africa frequently means a background of HIV with opportunistic infection, pneumonia, or genital-tract and post-abortal sepsis. The mnemonic matters less than the discipline of running the whole list while compressions continue, because the treatable causes — haemorrhage, hypoxia, magnesium and local-anaesthetic toxicity, hypoglycaemia, tension pneumothorax — are precisely the ones a structured search will catch.
Reading the cause from the pattern of collapse separates the candidates who manage from those who merely list. A sudden collapse at delivery or in the minutes after, with hypoxia, hypotension and bleeding from every puncture site, is amniotic-fluid embolism until proven otherwise — a clinical diagnosis with no confirmatory test, in which the coagulopathy is profound and the treatment is supportive resuscitation plus aggressive correction of DIC. Collapse shortly after a regional block points to a high or total spinal (ascending block, bradycardia, apnoea, loss of consciousness) or to local-anaesthetic systemic toxicity (perioral tingling and agitation progressing to seizures and a refractory, often broad-complex, cardiac arrest); the two are distinguished by the timing and the prodrome, and LAST has a specific antidote. Collapse in a woman on a magnesium infusion, particularly with reduced urine output, is magnesium toxicity until the level is known — loss of reflexes precedes respiratory and then cardiac arrest. Collapse after a seizure that does not resolve is eclampsia complicated by, or mimicking, intracranial haemorrhage. And collapse with chest pain, breathlessness or after a long immobilisation or caesarean raises pulmonary embolism and, with increasing maternal age, myocardial infarction and aortic dissection. The history that produces the collapse is therefore as diagnostic as the examination.