Maternal critical care: part II

Abstract

Learning objectivesBy reading this article you should be able to;•Apply the principles of care of the pregnant or recently pregnant woman in critical care.•Describe the pregnancy-specific conditions in patients presenting to critical care.•Consider the pitfalls in managing the obstetric patient with pregnancy-related conditions.Key points•Multiple comorbidities in pregnant women can be more challenging to manage in critical illness.•Close working between the critical care, other specialist, and maternity teams is essential.•Maternal admissions to critical care result most frequently from major obstetric haemorrhage, sepsis, and pre-eclampsia.•Non-obstetric causes of deterioration should always be considered. By reading this article you should be able to;•Apply the principles of care of the pregnant or recently pregnant woman in critical care.•Describe the pregnancy-specific conditions in patients presenting to critical care.•Consider the pitfalls in managing the obstetric patient with pregnancy-related conditions. •Multiple comorbidities in pregnant women can be more challenging to manage in critical illness.•Close working between the critical care, other specialist, and maternity teams is essential.•Maternal admissions to critical care result most frequently from major obstetric haemorrhage, sepsis, and pre-eclampsia.•Non-obstetric causes of deterioration should always be considered. Pregnancy is becoming more complex to manage because of the increasing prevalence of multiple morbidities and advanced maternal age. In Part I of this article we covered the general principles of management.1Banerjee A. Cantellow S. Maternal critical care.BJA Educ. 2021; https://doi.org/10.1016/j.bjae.2020.12.003Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar In Part II we discuss pregnancy-specific conditions and pitfalls in the setting of critical care. The commonest reasons for admission to critical care in pregnant women are massive or major obstetric haemorrhage (MOH), sepsis, and pre-eclampsia (PET).2Jardine J, NMPA Project Team. England Wales and Scotland in 2015/16: A Report from the Nafional Maternity and Perinatal Audit. Maternity admissionsto intensive care in England, Wales and Scotland.Google Scholar Women who have undergone fertility treatment are generally more likely to be admitted to ICU. MOH, sepsis, and PET have been covered separately in previous articles in this journal. Here we emphasise their management in the context of critical illness. Challenges arise because of alterations in maternal physiology. Critical care specialists should be involved early in the management of pregnant and peripartum women, whose condition may deteriorate rapidly. For these patients, especially in the context of changing physiology, the emphasis should be on making, not simply excluding a diagnosis. Many medical disorders can mimic obstetric disorders. Expediting delivery alters the progression of obstetric but not medical disorders. Uterine blood flow at term is 600–900 ml min−1. Uncontrolled bleeding from the uteroplacental bed is the commonest cause of maternal death worldwide and it is the most frequent obstetric reason for admission to critical care. It is postpartum haemorrhage (PPH) and not antepartum haemorrhage that is associated with the vast majority of maternal morbidity. Most PPH cases referred to critical care are primary (occurring within the first 24 h after delivery). Emergency Caesarean section, prolonged labour, multiple pregnancy, polyhydramnios, macrosomia, obesity, intrapartum sepsis, and uterine inversion are all associated with an increased risk. Secondary PPH is defined as excessive vaginal bleeding in the period from 24 h after delivery to 12 weeks postpartum. The commonest cause of secondary PPH is endometritis or retained products of conception. Blood loss of ≤500 ml after a vaginal delivery or ≤1000 ml after Caesarean section is considered normal. There is no universally agreed definition of MOH and while a loss of ≥1500 ml is commonly suggested for convenience, women of low weight and stature will have reduced reserve. Activation of the MOH protocol ensures the urgent availability of the requisite clinical and support staff, appropriate initial blood products, and established lines of communication with laboratory staff. It is essential to be familiar with local systems and guidelines. While PPH can be extremely brisk, it can also be insidious manifesting only as a trickle of ongoing vaginal loss. Quantifying losses is problematic and a lag between actual and calculated losses can cause delay in activating the MOH protocol and transferring to the operating theatre for evaluation and intervention. An obstetric shock index (HR/systolic BP) >1 has been shown to be associated with PPH and the need for intensive resuscitation and blood transfusion.3Borovac-Pinheiro A. Pacagnella R.C. Cecatti J.G. et al.Postpartum hemorrhage: new insights for definition and diagnosis.Am J Obstet Gynecol. 2018; 219: 162-168Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar,4Kohn J.R. Dildy G.A. Eppes C.S. Shock index and delta-shock index are superior to existing maternal early warning criteria to identify postpartum hemorrhage and need for intervention.J Matern Fetal Neonatal Med. 2019; 32: 1238-1244Crossref PubMed Scopus (15) Google Scholar The usual cause of MOH is uterine atony, but other causes must also be ruled out systematically (Table 1). Usually women with PPH will be referred to critical care after resuscitative efforts and a plan for haemostasis has been initiated in the maternity unit. Once an MOH is declared, urgent obstetric and anaesthetic assessment, i.v. access, volume replacement, and emptying the bladder are undertaken. Bimanual uterine compression may temporise losses. Uterine atony must be immediately corrected with uterotonic drugs given in sequence (Table 2). Tranexamic acid should also be given. Transfusion should be via an appropriate warmer in appropriate ratios of packed red cells to clotting components: point of care thromboelastometry is invaluable. Transfusion targets are the same as in non-pregnant individuals, as is the need to ensure normothermia, and correct hypocalcaemia and acidaemia.Table 1Causes for obstetric haemorrhage—‘the 4 Ts’ToneUterine atonyTraumaHaematomaLacerationInversion, uterine rupture, or bothTissueRetained tissueInvasive placentaThrombinCoagulopathy Open table in a new tab Table 2Uterotonic drugs used in PPH. aSyntometrine is ergometrine 500 μg with oxytocin 5 UDrug classExampleMode of actionImportant considerationsOxytocinSyntocinona5 U i.v. or i.m.Myometrial contractionOnset within 1 min i.v. (4 min i.m.). May be repeated to total 10 U followed by infusion (e.g. 40 U over 4 h)Causes transient hypotension, arrhythmias, and nausea. Structurally similar to antidiuretic hormone: causes water retention and hyponatraemiaErgot alkaloidsErgometrinea250–500 μg i.m.I.V. injection slowly with cautionVasoconstriction and myometrial contractionHighly emetogenic—give antiemetic.Causes hypertension (can be severe), coronary vasospasm, and pulmonary hypertension. Avoid in PET, hypertension, coronary disease, aortopathies, aneurysmsProstaglandin analogues1. Carboprost (e.g. Hemabate) 250 μg i.m.Prostaglandin F2α agonist: myometrial contractionMay only be given i.m. Dose of 250 μg may be repeated eight times at 15 min intervals.Prostaglandin analogues can cause bronchospasm but may be given in asthma with atonic bleeding because of threat to life. Cause severe diarrhoea, hyperthermia, rash, dizziness2. Misoprostol600 μg per rectumProstaglandin E1 agonist: myometrial contraction and cervical relaxationSee note above regarding unwanted effects in prostaglandin analogues Open table in a new tab Uterine-preserving interventions include arterial ligation, B-Lynch compression sutures, uterine packing and uterine balloon tamponade. Timely hysterectomy should be performed if necessary to save life. Where MOH is anticipated (morbidly adherent placenta) prophylactic bilateral placement of arterial balloon catheters before Caesarean section may be uterus-preserving. In cases of unanticipated MOH, the role of interventional radiology services is less well-defined: they should be accessed in accordance with the locally agreed policy. In some cases, it may be difficult for resuscitative efforts to keep pace with losses, requiring temporising measures such as manual pressure on the aorta or aortic cross-clamp. Resuscitative endovascular balloon occlusion of the aorta (REBOA) does not require radiological expertise, has an established role in major trauma, and may have an emerging role in MOH.5Osborn L.A. Brenner M.L. Prater S.J. Moore L.J. Resuscitative endovascular balloon occlusion of the aorta: current evidence.Open Access Emerg Med. 2019; 11: 29-38Crossref PubMed Scopus (32) Google Scholar There are no universally agreed criteria for when critical care admission is necessary, but it includes massive transfusion with metabolic insult and organ impairment. Before admission to critical care, it is important to ascertain which procedures have been performed and if the uterus is still in situ. A plan of action in the context of recurrent bleeding must be agreed (e.g. return to theatre, transfer to interventional radiology suite). Uterotonic drugs must be immediately available (Table 2).6Vallera C. Choi L.O. Cha C.M. Hong R.W. Uterotonic medications: oxytocin, methylergonovine, carboprost, misoprostol.Anesthesiol Clin. 2017; 35: 207-219Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar It is important to discuss the ongoing need for uterotonics with the obstetricians on an individualised case-by-case basis. Contact the obstetric team if there is evidence of uterine tenderness, offensive vaginal discharge, passage of large clots, or continuous bleeding. Early clinical assessment and an ultrasound scan are warranted to exclude retained products of conception. Occasionally, there may be an intrauterine balloon tamponade system in place (e.g. Bakri). It is important to ensure that the uterus is well contracted around the balloon—an increasing symphysis-fundal height and new blood loss into the drains indicates fresh bleeding and should prompt immediate attendance by the obstetric team. The critical care management of MOH is otherwise as for any major haemorrhage/transfusion: correction of coagulopathy, monitoring for rebleeding and transfusion reactions, establishing normothermia, and ensuring the resolution of metabolic endpoints such as serum lactate. An analgesia plan will also be required before ‘waking and weaning’ from mechanical ventilation. Complications of PPH include Sheehan's syndrome (pituitary necrosis).7Matsuzaki S. Endo M. Ueda Y. et al.A case of acute Sheehan's syndrome and literature review: a rare but life-threatening complication of postpartum hemorrhage.BMC Pregnancy Childbirth. 2017; 17: 188Crossref PubMed Scopus (22) Google Scholar Hypoperfusion of other organ systems may result in brain injury, type II myocardial infarction, ischaemic hepatitis, and acute kidney injury (AKI). The physiology of normal pregnancy and response to labour may mask the presence of sepsis. Intrapartum, women may be tachypnoeic with increases in temperature, white cell count, and lactate even in the absence of infection. Assessment by the multidisciplinary team (MDT) with close attention to physiological trends and a high index of suspicion. Delirium is an ominous sign in maternal sepsis; it is seen infrequently in the labour suite and may be misdiagnosed as puerperal psychosis. The Sepsis-3 definition of sepsis makes reference to the Sequential Organ Failure Assessment score (SOFA), which is not formally validated in pregnancy. The WHO in 2017 adopted the following definition of maternal sepsis:‘Maternal sepsis is a life-threatening condition defined as organ dysfunction resulting from infection during pregnancy, childbirth, post-abortion, or postpartum period.’8World Health OrganizationStatement on maternal sepsis. World Health Organisation, Geneva2017Google Scholar The maternal sepsis bundle should be initiated without delay (refer to Inpatient Maternal Sepsis Tool, UK Sepsis Trust).9The UK Sepsis Trust. Inpatient Maternal Sepsis Tool. Available from: https://sepsistrust.org/wp-content/uploads/2018/06/Inpatient-maternal-NICE-Final-1107-2.pdf (accessed 11th January 2021).Google Scholar Fluid resuscitation of 30 ml kg−1 may be deemed excessive, especially peripartum, as the maternal circulation is vulnerable to fluid overload. Reassessment after each 500 ml is prudent. Special care should be applied in the context of comorbid PET. Vasopressor therapy may be needed concurrently with resuscitation with i.v. fluids. Noradrenaline (norepinephrine) is the first-line agent. A target MAP of ≥65 mmHg applies to non-pregnant patients, but is nevertheless a reasonable starting point. Empiric antimicrobial therapy (to be given within 1 h on suspicion of sepsis) should be guided by local hospital policy and microbiological advice. Sepsis may be attributable to obstetric or non-obstetric causes.10Nesrine T.A. El Refai M.D. Gomaa H.M. Patil V. Update in obstetric maternal sepsis.2019Google Scholar Obstetric infections are usually polymicrobial and initial antimicrobial therapy must cover both Group A Streptococcus and E. coli (the organisms most commonly associated with maternal mortality). In a recent meta-analysis, i.v. immunoglobulin, used as an adjunct to clindamycin for the treatment of streptococcal toxic shock, was found to be beneficial.11Parks T. Wilson C. Curtis N. Norrby-Teglund A. Sriskandan S. Polyspecific intravenous immunoglobulin in clindamycin-treated patients with streptococcal toxic shock syndrome: a systematic review and meta-analysis.Clin Infect Dis. 2018; 67: 1434-1436Crossref PubMed Scopus (46) Google Scholar Source control is paramount. Obstetric sites of infection include retained products of conception, chorioamnionitis, endometritis, pelvic abscess, and wound infection. Chorioamnionitis should be suspected if there is foul-smelling liquor, pyrexia, maternal and fetal tachycardia. The risk is increased in the presence of prolonged rupture of membranes. Chorioamnionitis is the only definite indication for delivery in maternal sepsis; otherwise, delivery should be guided by obstetric indications. Non-obstetric infection may arise from any site, with pneumonia and pyelonephritis being common. A viral or fungal aetiology should be considered especially if the patient is immuno-naive (e.g. herpes simplex virus [HSV]) or immunocompromised. COVID-19 and the other newly-identified associated diseases of the 21st century may pose serious health risks to obstetric patients as seen in the current pandemic.12Rasmussen S.A. Smulian J.C. Lednicky J.A. Wen T.S. Jamieson D.J. Coronavirus disease 2019 (COVID-19) and pregnancy: what obstetricians need to know.Am J Obstet Gynecol. 2020; 222: 415-426Abstract Full Text Full Text PDF PubMed Scopus (567) Google Scholar Diseases that may masquerade as infection are important to consider in the context of deterioration without an identifiable cause. These include haemophagocytic lymphohistiocytosis, thrombotic microangiopathy, malignancy, and autoimmune diseases. PET affects 5–7% of pregnancies and is one of a heterogeneous group of hypertensive disorders in pregnancy that include chronic essential hypertension, gestational hypertension, and superimposed PET on chronic hypertension. It is defined as new-onset hypertension after 20 weeks' gestation associated with proteinuria, evidence of end-organ involvement, or utero-placental dysfunction.13National Institute of Clinical Excellence QualityStandard 135.October 2016https://www.nice.org.uk/guidance/qs135/chapter/Quality-statement-5-Corticosteroids-for-women-between-240-and-336-weeks-of-pregnancyGoogle Scholar The diagnosis of hypertension is made by recording a BP of ≥140/90 mmHg on two separate occasions, at least 4 h apart. A protein-creatinine ratio of ≥30 mg mmol−1 is used as a surrogate for 24-h urine collection. While there are a range of differential diagnoses, it is safest to assume that new-onset hypertension in pregnancy with proteinuria on urinalysis could be attributable to PET in the first instance. The early diagnosis and management of PET includes MDT input; midwives, obstetricians, maternal fetal specialists, obstetric physicians, neonatologists, anaesthetists, and critical care. The National Institute of Health and Care Excellence (NICE) Guideline on Hypertension in Pregnancy provides comprehensive guidance on the clinical criteria for the choice of the critical care level bed required for mild, moderate, and severe PET. Once diagnosed, it is recognised that PET can rapidly progress from a ‘mild’ condition to one with severe end-organ involvement compromising the physiology of both mother and fetus. Early-onset PET often causes severe morbidity to mother and fetus.14National Institute of Clinical ExcellenceHypertension in pregnancy: diagnosis and management.June 2019https://www.nice.org.uk/guidance/ng133Google Scholar A diagnosis of ‘PET with severe features’ is made if the patient has a systolic BP (SBP) ≥160 mmHg or any of the following features: cerebral involvement (e.g. headache, visual disturbance, or altered mental state), an otherwise unexplained severe right upper quadrant pain, serum transaminases more than twice the normal limit, platelets less than 100×109 L−1, progressive renal insufficiency, or pulmonary oedema. The treatment of PET is delivery of the placenta. It should be noted that PET is frequently diagnosed after birth and can persist and worsen initially before resolving. While risk to the mother takes precedence, those with mild disease are frequently monitored, allowing the pregnancy to continue with the intention of improving fetal outcome. Women with PET frequently labour quickly and Caesarean section is not always necessary, but in the presence of severe disease, birth must be expedited once supportive measures have been instituted. Supportive measures include control of hypertension, reducing the risk of eclampsia, and correction of coagulopathy. At all times, attention must also be given to preventing fluid overload. In the context of PET, a BP of 160/110 mmHg is an obstetric emergency. The goal of treatment is to aim for a SBP of <140 mmHg: it is systolic pressure that is associated with adverse endpoints such as intracerebral haemorrhage. SBP≥180 mmHg is an indication for urgent treatment with boluses of an i.v. drug followed by an infusion, or oral nifedipine modified release (MR) (see Table 3).15Lisonkova S. Joseph K.S. Incidence of preeclampsia: risk factors and outcomes associated with early- versus late-onset disease.Am J Obstet Gynecol. 2013; 209: 544.e1-544.e12Abstract Full Text Full Text PDF PubMed Scopus (455) Google Scholar,16Duley L. Meher S. Jones L. Drugs for treatment of very high blood pressure during pregnancy.Cochrane Database Syst Rev. 2013; 2013 (CD001449)Google Scholar Improvement of symptoms such as headache may be seen as BP improves. Infusion of an antihypertensive agent is usually considered an indication for invasive monitoring of arterial BP. A central venous catheter is not required initially and should not delay therapy. Once BP control has been achieved the woman can be weaned from i.v. to enteric therapies in a controlled manner: significant hypertension may persist for some time. All women with PET should be under close monitoring postpartum because of the risk of worsening BP control: a physiological increase in BP occurs 3–5 days postpartum because of volume expansion and fluid shift.Table 3Commonly used antihypertensive agents in PETDrugRouteAdverse effect/interactionsEntericI.V. bolusI.V. infusionHydralazineYYMaternal hypotension and tachycardia.Adequate hydration before administration is importantLabetalolYYYNausea (4.1%)Dizziness (4.1%)Nifedipine MRYHeadache (5.4%), maternal tachycardia (4.1%), dizziness (2.7%) Open table in a new tab Women are highly vulnerable to fluid overload in the peripartum period even in the absence of PET. In PET, pulmonary oedema occurs in 9.5% of women with severe disease.17Shekhar S. Sharma C. Thakur S. Verma S. Oral nifedipine or intravenous labetalol for hypertensive emergency in pregnancy: a randomized controlled trial.Obstet Gynecol. 2013; 122: 1057-1063Crossref PubMed Scopus (34) Google Scholar In contrast with sepsis, the capillary leak is subject to an increased driving pressure (i.e. hypertension is present). The increased afterload and reduced vascular compliance result in ventricular remodelling and diastolic dysfunction. As a default, it is important to restrict fluids in severe disease, even at the expense of kidney function (which may also be adversely affected by the PET itself). Reducing the fluid volume in which drugs are diluted through the use of concentrated formulations can be helpful, as can the use of concentrated feeds. Assessing fluid requirements in PET is notoriously difficult, especially as the intensivist will often become involved when other problems are present, such as PET combined with sepsis and AKI. A thorough assessment must be made at the bedside, taking into account symptoms, trends, and changing physiology. Adjuncts such as focussed echocardiography have a role. Table 4 describes the therapeutic options available for life-threatening emergencies of PET.Table 4PET emergencies—therapeutic options and considerationsInitial managementClinical tipsPulmonary oedemaConventional supportive management including oxygen, diuretics and where necessary CPAPOnce stabilised expedite deliveryNeuraxial anaesthesia preferable where possibleMost cases of PET pulmonary oedema are postpartumDifferential diagnoses:1. Acute coronary syndrome (e.g. related to spontaneous coronary artery dissection)2. Peripartum cardiomyopathy3. Overzealous fluid administration (common)4. Tocolytic use5. Lung injury (e.g. transfusion/infection/ARDS)Hypertensive encephalopathy:•Cerebral oedema•Intracranial haemorrhageSupportive management and urgent optimisation of BP controlMagnesium infusion as eclampsia prophylaxis in all symptomatic PETCortical blindness is managed by controlling and optimising the BPDifferential diagnoses: metabolic abnormalities, drugs, infection, and cerebral venous sinus thrombosisEclampsiaA 4 g loading dose of magnesium sulphate (MgSO4) followed by an infusion 1–2 g i.v.aaAKI: halve the infusion dose.Give additional bolus of MgSO4 should the woman have a fit while on MgSO4. If refractory to MgS04 give antiepileptic drugs (e.g. benzodiazepines, levetiracetam)1% Risk of recurrence of eclampsia in a future pregnancySubcapsular liver ruptureStabilise and contact nearest liver unitSubsequent pregnancies are infrequently complicated by HELLP (2–19%) Open table in a new tab Once pulmonary oedema is established, efforts to reduce both preload and afterload while paying attention to factors that exacerbate cardiac ischaemia are equally important. In this respect nitrate infusions, opioids (e.g. diamorphine), furosemide, and CPAP all have a role. If the patient deteriorates to require tracheal intubation and artificial ventilation, it is vital that BP is controlled and that the pressor response to direct laryngoscopy is attenuated. While invasive ventilation may ameliorate pulmonary oedema, the intensivist should be mindful that the brain is also vulnerable (see posterior reversible encephalopathy syndrome [PRES] below). Magnesium sulphate infusions reduce the risk of eclampsia and should be instituted in the presence of PET with severe features. While magnesium is a neuromuscular blocking agent, it does not reduce blood pressure significantly in PET: conventional antihypertensive drugs will be required. Thrombocytopenia may occur even in the absence of the haemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. Correction of platelets to above 50×109 L−1 is important before delivery (>80×109 L−1 if a neuraxial technique is being considered). NSAIDs should be avoided in women with PET and thrombocytopenia or AKI. The overall mortality from subcapsular haematoma, liver infarction, and liver rupture is up to 50% in those with PET or HELLP. The incidence of liver rupture in pregnancy is estimated as one per 67,000 deliveries and one per 2000 patients with PET or HELLP. The current theories suggest that subsequent vascular injury from endothelial damage leads to formation of microvascular thrombi and necrosis that result in rupture.18Sibai B.M. Ramadan M.K. Usta I. Salama M. Mercer B.M. Friedman S.A. Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome).Am J Obstet Gynecol. 1993; 169: 1000-1006Abstract Full Text PDF PubMed Scopus (871) Google Scholar The identification of a triad, epigastric/right upper quadrant pain, hypotension without evidence of a cause for bleeding, and clinical confirmation of a hypertensive disorder, should steer to a high index of suspicion to consider these life-threatening conditions.19Escobar Vidarte M.F. Montes D. Pérez A. Loaiza-Osorio S. José Nieto Calvache A. Hepatic rupture associated with preeclampsia, report of three cases and literature review.J Matern Fetal Neonatal Med. 2019; 32: 2767-2773Crossref PubMed Scopus (13) Google Scholar Management with an MDT approach is paramount. Options range from a conservative approach to more aggressive interventions and should be individualised. The surgical options depend on the severity of the rupture intervention and include partial resection, embolisation and hepatic artery ligation, packing of the bleeding and liver transplantation. The risk of stroke in women with PET/eclampsia appears highest in the postpartum period. The most common symptoms of stroke include severe headache, impairment of consciousness, and increased systolic BP. Women with severe PET and a high isolated systolic BP should be immediately treated with antihypertensive therapy because of a very high risk for haemorrhagic stroke. PET is also associated with PRES and reversible cerebral vasoconstriction syndrome (RCVS). RCVS can be complicated by seizures, ischaemic and haemorrhagic stroke, including subarachnoid haemorrhage.20Too G. Wen T. Boehme A.K. et al.Timing and risk factors of postpartum stroke.Obstet Gynecol. 2018; 131: 70-78Crossref PubMed Scopus (42) Google Scholar PRES in severe cases can cause seizure, status epilepticus, coma, or all three. There should be a low threshold for CT scanning to exclude a haemorrhagic stroke or an MRI scan to confirm the diagnosis of PRES or RCVS. Respiratory, cardiovascular, haematological, and renal system disorders are common causes for admission to critical care; neurological dysfunction is less frequent. It is important to involve specialist medical teams when organ dysfunction is present. Chronic maternal hypoxia (Spo2<85%) affects fetal growth and well-being. Asthma can worsen during pregnancy; the management is the same as in non-obstetric patients. Decompensation (‘tiring’) should be considered at Paco2≥4.0 given the physiological respiratory alkalosis of pregnancy. Acute respiratory distress syndrome (ARDS) may arise as a result of obstetric causes including MOH, sepsis and amniotic fluid embolism (AFE). There is a variety of non-obstetric causes including viral pneumonitis (e.g. COVID-19, H1N1). Management of mechanical ventilation is outlined in Part I.1 The aetiology of cardiac disease in pregnancy includes PET; dilated cardiomyopathy; obesity cardiomyopathy; peripartum cardiomyopathy (PPCM); myocarditis; hypertrophic obstructive cardiomyopathy; arrhythmogenic right ventricular cardiomyopathy and ventricular dysfunction.21van Hagen I.M. Cornette J. Johnson M.R. Roos-Hesselink J.W. Managing cardiac emergencies in pregnancy.Heart. 2017; 103: 159-173Crossref PubMed Scopus (10) Google Scholar Management of pulmonary oedema is described above. Ischaemic heart disease in pregnancy is likely to become more prevalent because of the increased prevalence of cardiovascular risk factors in women of childbearing age such as obesity, hypertensive disorders, smoking and advanced maternal age.22Cauldwell M. Baris L. Roos-Hesselink J.W. Johnson M.R. Ischaemic heart disease and pregnancy.Heart. 2019; 105: 189-195Crossref PubMed Scopus (13) Google Scholar PPCM is characterised by reduced ejection fraction (<45%), without known pre-existing structural heart disease. PPCM presents in the 3rd trimester or within 5 months of delivery. The incidence is one in 300–3000. Management includes standard treatments for heart failure and anticoagulants to prevent intracardiac mural thrombus. A toxic metabolite of prolactin may drive PPCM and bromocriptine has been used as a treatment in very small studies— its use remains controversial but can be considered on a case-by-case basis.23Koenig T. Bauersachs J. Hilfiker-Kleiner D. Bromocriptine for the treatment of peripartum cardiomyopathy.Card Fail Rev. 2018; 4: 46-49Crossref PubMed Google Scholar Morbidity and mortality are high in obstetric patients with pulmonary arterial hypertension.24Sarkar M.S. Desai P.M. Pulmonary hypertension and cardiac anesthesia: anesthesiologist's perspective.Ann Card Anaesth. 2018; 21: 116-122PubMed Google Scholar In the 3rd trimester and in the initial postpartum period there is a greater risk of venous thromboembolism, refractory right heart failure, and pulmonary hypertensive crisis. Therapeutic options include inhaled iloprost or i.v. prostaglandin. Maternal mortality has improved to 17–33%, and neonatal survival