Pregnancy induces profound physiological changes, most notably within the cardiovascular system, hence making meticulous maternal haemodynamic management a paramount concern for anaesthesiologists. During pregnancy, generalized vasodilation lowers one’s systemic vascular resistance (SVR) and increases cardiac output (CO); cardiac remodelling occurs simultaneously and extends up to 6 months post-partum. Concomitantly, blood volume expands by 10–50%, producing dilutional anaemia, which mitigates post-partum haemorrhage. Non-invasive haemodynamic monitoring enables both the early detection and tailored management of hypertensive disorders. In the first trimester, SVR >1340–1400 dynes cm−5 coupled with low CO predicts pre-eclampsia with an accuracy rate of 86%. Hypertensive disorders complicate 2–8% of pregnancies and account for 16% of maternal deaths. Chronic or gestational hypertension may progress to pre-eclampsia, which presents two haemodynamic phenotypes: early onset (low CO, high SVR, frequent intra-uterine growth restriction) and late onset (high CO, low SVR). These profiles direct the therapy required: α-methyldopa ± calcium antagonists for the former and labetalol with fluid restriction for the latter, while nitric oxide donors are currently under validation. Complications include HELLP syndrome (characterised by LDH ≥600 IU L−1 and thrombocytopenia) and eclampsia, both demanding magnesium sulphate, strict BP control, and multidisciplinary care. Peripartum cardiomyopathy (PPCM) is defined when the left ventricular ejection fraction (LVEF) <45% between late gestation and the post-partum months. Multimodality imaging underpins diagnosis, while management follows the BOARD scheme (bromocriptine with anticoagulation, oxygen, relaxants, diuretics) and the adjusted heart-failure therapy for pregnancy and lactation according to the guidelines. Maternal sepsis (most often arising from pyelonephritis, chorioamnionitis, or endometritis) is difficult to recognise because conventional SIRS or qSOFA criteria lack obstetric specificity. A sepsis score ≥6 in obstetrics indicates a high risk for admission to an ICU. Management adheres to the “1-hour” bundle: lactate measurement, blood cultures, broad-spectrum antibiotics, balanced crystalloid resuscitation, and vasopressor initiation; norepinephrine is first-line, with vasopressin or dobutamine as adjuncts. Resuscitation targets a mean arterial pressure ≥65 mmHg and employs dynamic indices of fluid responsiveness (pulse-pressure variation, inferior vena cava collapsibility, passive leg raising) to avoid both fluid overload and hypoperfusion. An in-depth understanding of normal and pathological haemodynamics, coupled with serial non-invasive monitoring, underpins a timely diagnosis, phenotype-specific therapy, and improved maternal-fetal outcomes throughout pregnancy, delivery, and the puerperium.

The Anaesthetist’s Point of View

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发表日期：

2026年

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MariaGrazia Frigo,
Alberto Laffi

摘要

Pregnancy induces profound physiological changes, most notably within the cardiovascular system, hence making meticulous maternal haemodynamic management a paramount concern for anaesthesiologists. During pregnancy, generalized vasodilation lowers one’s systemic vascular resistance (SVR) and increases cardiac output (CO); cardiac remodelling occurs simultaneously and extends up to 6 months post-partum. Concomitantly, blood volume expands by 10–50%, producing dilutional anaemia, which mitigates post-partum haemorrhage. Non-invasive haemodynamic monitoring enables both the early detection and tailored management of hypertensive disorders. In the first trimester, SVR >1340–1400 dynes cm−5 coupled with low CO predicts pre-eclampsia with an accuracy rate of 86%. Hypertensive disorders complicate 2–8% of pregnancies and account for 16% of maternal deaths. Chronic or gestational hypertension may progress to pre-eclampsia, which presents two haemodynamic phenotypes: early onset (low CO, high SVR, frequent intra-uterine growth restriction) and late onset (high CO, low SVR). These profiles direct the therapy required: α-methyldopa ± calcium antagonists for the former and labetalol with fluid restriction for the latter, while nitric oxide donors are currently under validation. Complications include HELLP syndrome (characterised by LDH ≥600 IU L−1 and thrombocytopenia) and eclampsia, both demanding magnesium sulphate, strict BP control, and multidisciplinary care. Peripartum cardiomyopathy (PPCM) is defined when the left ventricular ejection fraction (LVEF) <45% between late gestation and the post-partum months. Multimodality imaging underpins diagnosis, while management follows the BOARD scheme (bromocriptine with anticoagulation, oxygen, relaxants, diuretics) and the adjusted heart-failure therapy for pregnancy and lactation according to the guidelines. Maternal sepsis (most often arising from pyelonephritis, chorioamnionitis, or endometritis) is difficult to recognise because conventional SIRS or qSOFA criteria lack obstetric specificity. A sepsis score ≥6 in obstetrics indicates a high risk for admission to an ICU. Management adheres to the “1-hour” bundle: lactate measurement, blood cultures, broad-spectrum antibiotics, balanced crystalloid resuscitation, and vasopressor initiation; norepinephrine is first-line, with vasopressin or dobutamine as adjuncts. Resuscitation targets a mean arterial pressure ≥65 mmHg and employs dynamic indices of fluid responsiveness (pulse-pressure variation, inferior vena cava collapsibility, passive leg raising) to avoid both fluid overload and hypoperfusion. An in-depth understanding of normal and pathological haemodynamics, coupled with serial non-invasive monitoring, underpins a timely diagnosis, phenotype-specific therapy, and improved maternal-fetal outcomes throughout pregnancy, delivery, and the puerperium.