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 Table of Contents  
REVIEW ARTICLE
Year : 2011  |  Volume : 1  |  Issue : 1  |  Page : 5-12

Anaesthetic management of patients with peripartum cardiomyopathy


Department of Anaesthesiology, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication25-Aug-2011

Correspondence Address:
Anjan Trikha
Room Number 5020, Department of Anaesthesiology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4472.84249

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  Abstract 

Peripartum cardiomyopathy (PPCM) is a disease affecting the parturient during late pregnancy or immediately after delivery. This unique disorder not just endangers the life of mother and progeny but is also a financial burden to the health system due to its potential to cause prolonged and persistent cardiac function insufficiency in the mother. The hallmark of the disease is onset of decreased cardiac ejection fraction either in the late pregnancy or early puerperium. Over the last few decades, the disease has been extensively researched and investigated to formulate diagnostic guidelines and therapeutic approaches. Many theories regarding its pathophysiology have also been proposed. The clinical presentation and the basic and intensive interventional strategies of the disease are more or less similar to that of dilated cardiomyopathy due to any other cause; however, at all points of time the pregnant or lactating state of mother and the subsequent effect of the medication and therapeutic interventions on the fetus or neonate needs to be considered. Apart from intensive care management, these patients may also require anaesthetic intervention for management of painless labor and/or either vaginal or operative delivery. Favorable maternal and fetal outcome require that the basic hemodynamic goals be always kept in mind while choosing the techniques and drugs to provide anaesthesia to the patients with PPCM. Literature search of the anaesthetic management of patients with diagnosis of PPCM undergoing operative delivery reveals both general and regional anaesthesia being used with comparable outcomes.

Keywords: Anaesthesia, cardiomyopathy, heart failure, peripartum, pregnancy


How to cite this article:
Ramachandran R, Rewari V, Trikha A. Anaesthetic management of patients with peripartum cardiomyopathy. J Obstet Anaesth Crit Care 2011;1:5-12

How to cite this URL:
Ramachandran R, Rewari V, Trikha A. Anaesthetic management of patients with peripartum cardiomyopathy. J Obstet Anaesth Crit Care [serial online] 2011 [cited 2019 Dec 9];1:5-12. Available from: http://www.joacc.com/text.asp?2011/1/1/5/84249


  Introduction Top


Peripartum cardiomyopathy (PPCM) was first reported in the year 1849. [1] Till the middle of 20 th century it was known as postpartal cardiomyopathy [2],[3] as most of the cases reported had symptomatic onset in the postpartum period only. Demakis et al.[1],[4] were probably the first to realize this as more of a peripartum disease rather than a postpartum one, hence the term peripartum cardiomyopathy was considered more acceptable. The first case series of patients with PPCM was published in the year 1971 [4] by Demakis et al. They described the data about 27 patients who presented in the late pregnancy or early puerperium with heart failure. The authors themselves devised a diagnostic criteria that included development of cardiac failure in the last month of pregnancy or within 5 months of delivery, absence of a determinable aetiology for the cardiac failure and absence of demonstrable heart disease before the last month of pregnancy. [2] Over the years, the diagnostic criteria have remained almost the same with the addition of echocardiography findings as another parameter. [5] As more and more research is being conducted, a lot more is now known about the pathophysiology, epidemiology, diagnosis and clinical outcome of the disease. At the same time, the unique anaesthetic challenge that these patients pose for management of their pregnancy was also recognized. This review will undertake a comprehensive look on the above and give a detailed account of the treatment modalities available for this disease in present times.


  Definition and Diagnostic Criteria Top


One of the most recent definitions of PPCM has been provided by the Heart Failure Association of the European Society of Cardiology Working Group on PPCM which describes it as "an idiopathic cardiomyopathy presenting with heart failure secondary to left ventricular systolic dysfunction towards the end of pregnancy or in the months following delivery, where no other cause of heart failure is found. It is a diagnosis of exclusion. The left ventricle may not be dilated but the ejection fraction is nearly always reduced below 45%." [6]

Earlier, in the year 1997, the National Heart, Lung and Blood Institute and the Office of Rare Diseases of the National Institutes of Health had convened a Workshop on Peripartum Cardiomyopathy to foster a multidisciplinary review and defined the diagnostic criteria [5] based on the work by Demakis et al.[2] [Table 1]. This definition was being followed comprehensively till now, but the European Society definition claims to be more simplified and capable of preventing underdiagnosis of the disease.
Table 1: Criteria for diagnosis of peripartum cardiomyopathy*

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  Epidemiology Top


Actual incidence of PPCM has not been clearly evaluated in the Indian subcontinent. Pandit et al. report it as 1 in 1374 live births from a tertiary referral hospital from South India, [7] Hasan et al. state this as 1 in 837 in their analysis from Pakistan, [8] while Chee et al. report the incidence as 34 per 1,00,000 live births in a hospital from Malaysia. [9] The incidence of the disease world over has also a wide range with the occurrence of the disease in 1 in 2000-4000 live births in the Unites States, 1 in 1000 live births in South Africa and the highest being reported from Haiti (1 in 300). [10] Many risk factors have been implicated in the development of this disease condition which include advanced maternal age, multiparity, Afro-American race, twin pregnancy, pre-eclampsia and gestational hypertension and diabetes. Use of tocolytics, high sodium salt, deficiency of certain micronutrients and smoking during pregnancy have also been implicated. [9]


  Pathophysiology Top


Several mechanisms have been postulated to explain the pathogenesis of PPCM although no single factor has ever been implicated in all the cases. The disease is now known to have a multifactorial pathogenesis.

Myocarditis has been shown to be associated with PPCM although the incidence spans a wide range (8.8-78%) [11],[12] in different studies. Bultmann et al.[13] took endomyocardial biopsy from 26 patients with PPCM and analyzed the specimens for detection of viral genomes by polymerase chain reaction. The specimens of eight patients (31%) showed presence of various viral genomes (parvovirus B19, human herpes virus 6, Epstein-Barr virus and human cytomegalovirus). They postulated that changes in immune function during pregnancy may have exacerbated de novo infection or reactivated latent virus in the pregnant females leading to viral myocarditis followed by cardiomyopathy. Activation of autoimmune response has been cited as another causative factor with compelling evidence supporting it. Sera from PPCM patients contain high titres of autoantibodies against normal human cardiac tissue proteins that are not present in the sera of patients with idiopathic cardiomyopathy. [14] Antibodies against fetal cells (which may escape into maternal circulation) and various proteins, such as actin and myosin, released from uterus during delivery have been demonstrated in patients with PPCM. These autoantibodies may cross-react with maternal myocardial proteins and lead to PPCM. [15] In addition, the peripheral blood from PPCM patients demonstrate an abnormal cytokine profile, decreased levels regulatory T cells and a significant reduction in the plasma levels of progesterone, estradiol and relaxin when compared with other normal pregnant non-PPCM patients. [16] Another hypothesis postulated is that PPCM may be an abnormal cardiac response to hemodynamic changes associated with pregnancy. A reversible decrease in left ventricle systolic function has been demonstrated in normal pregnant patients in the second and third trimester. [17] A magnified decrease in left ventricle function in association with increase in cardiac output and decrease in systemic vascular resistance which occurs in late pregnancy can explain features of PPCM. [15] However, scientific evidence to confirm this hypothesis is lacking. Other probable mechanisms proposed are an accelerated myocyte death (apoptosis), increase in proinflammatory cytokines, excessive prolactin production and coronary microangiopathy. [15] A few reports of familial association of the disease have also appeared which may warrant further evaluation for a probable genetic cause of the disease. [18],[19]


  Clinical Features and Diagnosis Top


Clinical features of PPCM are similar to those seen in any cardiac failure. Women in either third trimester of the pregnancy or early peurperium presenting with palpitations, fatigue, shortness of breath, cough and paroxysmal nocturnal dyspnea or orthopnea should raise the doubt of PPCM, especially when the prenatal history has been otherwise uneventful. [10] Other additional features such as abdominal discomfort, dizziness, precordial pain and postural hypotension may also be seen. Majority of patients become symptomatic in the postpartum period. [20],[21] In a prospective follow-up study of 56 patients, Mishra et al. found that 62.5% of the patients presented in the postpartum period, [20] while a similar follow-up study of 33 patients from a hospital in Turkey found the postpartum manifestation of disease in 72.7% of the patients. [22] Clinical signs of PPCM include pedal edema, pulmonary rales, raised jugular venous pressure, hepatomegaly, new regurgitant murmurs and gallop rhythm depending on the severity of disease. Diagnosis of PPCM can be confounded by the presence of some of the mild form of these symptoms in an otherwise healthy parturient also, especially in the late pregnancy or early peurperium. The diagnosis is essentially by exclusion of other causes. Once heart failure has been confirmed in a pregnant patient, it is imperative to rule out other causes of heart failure such as valvular lesions, congenital heart diseases, hypertensive or ischemic heart disease, severe anemia and thyrotoxicosis. The presenting symptom in most of the patients is dyspnea on exertion (NYHA-III or IV) although patients may present with complex arrhythmias [23] or with signs and symptoms of peripheral or pulmonary embolic episodes [24] or even cardiac arrest. Routine blood investigations are required to rule out anemia, electrolyte dysfunction and kidney, liver, or thyroid abnormality. Chest x-ray may reveal radiological signs of heart failure such as cardiomegaly, pulmonary congestion and pleural effusion. Multiple ECG changes have been described in patients with PPCM. In a study undertaken in South Africa involving 97 patients diagnosed with PPCM, 96% had ST-T wave abnormality and 66% of the patients had changes suggestive of left ventricular hypertrophy. [25] Duran et al. identified QRS time of equal to or more than 120 ms in the ECG of patients with PPCM as a predictor for mortality, indicating a potential impact of QRS time on the mortality of patients with PPCM. [22] Echocardiography needs to be done in all the patients suspected with PPCM to clinch the diagnosis. Typical findings include a dilated left ventricle, increase in end-diastolic left ventricular diameter and an ejection fraction less than 45%. Presence of left ventricle clot should also be ruled out by echocardiography. A left ventricular end-diastolic diameter of more than 55 mm or an ejection fraction of less than 27% in echocardiography predicts poor long-term prognosis in these patients. [22] Cardiac magnetic resonance imaging provides more accurate measurement of cardiac dimensions and functions and can also be used to guide the site of myocardial biopsy if required. [26]


  Management Top


The goals of medical management in a patient diagnosed with PPCM should include measures to improve oxygenation and maintain cardiac output so as to improve both maternal and fetal outcome. Interventions are required to decrease both preload and afterload as well as to improve cardiac contractility.

Mild to moderate symptoms may be managed with rest, salt restriction and diuretic therapy. Oxygen may be instituted via face mask, or continuous positive airway pressure may be applied up to a level which does not further jeopardize the cardiac output. Salt restriction helps in preventing further water retention, while diuretics help in decreasing pulmonary congestion. Fluid restriction may not be warranted in patients with mild to moderate heart failure. [27] Hydralazine and nitrates decrease the afterload and are the mainstay of treatment in pregnant patients with heart failure. Calcium channel blockers, except amlodepine, have a negative inotropic effect and should be avoided. Amlodepine may be used if PPCM is associated with pre-eclampsia to control blood pressure. ACE inhibitors, both direct acting or receptor blockers, although the first line of drug for patients in heart failure due to any cause, are however, contraindicated in pregnant females due to the risk of fetal toxicity associated with them. [28] They, however, should be used in all symptomatic patients in the postpartum period and are safe for the breastfed infant. Beta-blockers such as metoprolol decrease the heart rate, improve left ventricular diastolic function and protect against arrhythmias but are only used as a second line of treatment as their prolonged usage in the prenatal period is associated with low-birth weight of the baby. However, their use is considered safe during lactation. Digoxin may be indicated in certain patients for its inotropic effect. Although it is a safe drug to be used during pregnancy and puerperium, its plasma level needs to be strictly maintained in the therapeutic range with close monitoring. [29] Anticoagulation is recommended in patients with PPCM, especially if the ejection fraction is less than 35% and there are other associated risk factors such as severely dilated ventricles, atrial fibrillation and presence of mural thrombus on echocardiography or history suggestive of previous thromboembolic episodes. The risk of venous thromboembolism is per se increased in pregnant patients and associated heart disease and bed rest (if advised for heart failure) may further increase the risk of development of this complication. [30] Warfarin is teratogenic in early pregnancy and can cause fetal warfarin syndrome, while intake in the second and third trimester may lead to fetal cerebral hemorrhage, microcephaly, blindness, deafness and growth retardation. Unfractionated heparin on the other hand has low bioavailability in pregnant patients and is associated with thrombocytopenia. Thus, low-molecular-weight heparins are preferred in pregnancy as they do not cross the placenta, have a lower risk of osteoporosis and thrombocytopenia and their bioavailability is more predictable. [31] In the postpartum period, thromboprophylaxis may be continued with warfarin if required as it appears in the breast milk in very insignificant quantities.

If the patient presents with acute failure, it is important to undertake urgent steps to achieve above goals. Such a patient would usually be managed best in an intensive care unit. The patient is nursed in a propped up position with continuous hemodynamic and oxygenation monitoring which may warrant central venous and arterial cannulation. Pulmonary artery wedge catheter may also be required in patients on high dose of multiple cardiac drug infusions. Noninvasive ventilation with suitable positive end expiratory pressure may be instituted if oxygen by simple face mask fails to improve SpO 2 more than 95%. In case invasive ventilation is required, standard precautions regarding potential for aspiration in a pregnant patient should be taken. Loop diuretics may be more amenable in a patient in acute failure for their efficacy. Nitroglycerine should be given via intravenous infusion to decrease afterload if the systolic blood pressure is more than 110 mm Hg. Nitroprusside, however, may be relatively contraindicated in pregnant patients due to risk of thiocyanate and cyanide accumulation in the fetus. Nitroglycerin (NTG) should be titrated to effect starting from a dose of 10-20 μg/min up to a maximum of 200 μg/min. Dobutamine, dopamine and milrinone can be used to provide inotropic support to the failing heart. These inotropes along with nitroglycerine can be used in pregnancy if conditions exist to warrant their use. [32] Levosimendan is another novel cardiotropic agent that improves cardiac output by increasing the response of myofilaments to intracellular calcium unlike the above mentioned traditional inotropes that do so by increasing the intracellular calcium itself. Levosimendan has been proven to be effective in improving the cardiac output and decreasing mortality [33],[34] in patients with severely low output cardiac failure; however, its safety and efficacy in PPCM have not been evaluated by randomized controlled studies although reports of its successful use in this condition are there in the literature. [35],[36] Levosimendan is used as an intravenous infusion at the rate of 0.1-0.2 μg/kg/min in cardiac failure with or without a loading dose of 3-12 μg/kg over 10 minutes. [37] Hemodynamically unstable pregnant patients who are on multiple drugs should also undergo intensive fetal monitoring and continuous evaluation by obstetricians to prevent fetal loss.

Mechanical assist devices and extracorporeal membrane oxygenators have been used in these patients if medical therapy fails to improve cardiac status. These devices can be used as bridging therapy as in most of the patients partial or complete recovery can be expected within a year of delivery. [38] Up to 11% of patients will eventually require cardiac transplantation. [6]


  Anaesthetic Management Top


It was not until 1985 when the first report of a patient undergoing caesarean section under anaesthesia with PPCM was reported. [39] A literature review done with PPCM and anaesthesia as key words on Pubmed revealed 41 results in English language. A further search on Google revealed another five articles. A total of 46 articles were analyzed, out of which there were six review articles and two reports describing management of patients with familial dilated cardiomyopathy during pregnancy. The 38 case reports were further sieved for postnatal and prenatal diagnosis. Out of these 38 reports, 22 described patients who were diagnosed as PPCM after delivery of the child, either operative or vaginal. The rest of the 16 reports describe 17 patients who had prenatal diagnosis of PPCM and underwent LSCS under anaesthesia. In the latter group of patients, anaesthetic management included general anaesthesia, regional anaesthesia, or both. The data have been tabulated [Table 2] and [Figure 1] for further elucidation.
Table 2: Salient features in anaesthetic management for caesarean section of patients with preoperative diagnosis of peripartum cardiomyopathy

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Figure 1: Flow Chart depicting the type of anaesthesia used in various case reports describing patients with peripartum cardiomyopathy undergoing caesarean section. GA: General Anaesthesia, EA: Epidural Anaesthesia, CSE: Combined Spinal Epidural, SA: Spinal Anaesthesia

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Patients with prenatal diagnosis of PPCM need to be treated by a multidisciplinary approach with cardiologists, anaesthetists, intensivists and neonatologists being actively involved in the obstetric management. Issues such as whether the pregnancy should be allowed to reach term and the mode of delivery need to be addressed by the team with a tailored approach according to the patient's medical status on a periodical basis. In general, unless there is deterioration in the maternal or fetal well-being, there is no need for urgent or emergent delivery and the pregnancy is allowed to progress to term. The patient may be allowed to deliver the baby vaginally or operatively according to obstetric parameters or patient's wish. The vaginal delivery needs to be done with continuous hemodynamic monitoring and even invasive monitoring has been advocated according to patient's profile. [6] Pain and anxiety associated with labor can increase sympathetic nervous system activity with a resultant increase in cardiac output and peripheral vascular resistance leading to an increase in cardiac afterload. This sympathetic activity also decreases uteroplacental outflow, thus jeopardizing an already compromised fetus. Effective labor analgesia decreases sympathetic outflow and decreases plasma catecholamine levels in the mother. [40] Multiple modalities of labor analgesia can be provided to these patients to prevent increase in cardiac afterload associated with labor pains, but regional anaesthesia (RA) remains the method of choice as the sympathectomy associated with it causes a decrease in cardiac preload and afterload which is beneficial in patients with PPCM. [6],[10],[41] RA, however, may be contraindicated in an anticoagulated patient.

The second stage of labor during vaginal delivery needs to be curtailed by application of forceps or vacuum to expedite the delivery of the baby. It is important to prevent any fluid overload during labor and delivery.

As outlined in the flow chart, multiple modes of anaesthesia have been described in the literature for operative delivery of patients with PPCM. The hemodynamic goals of anaesthesia, however, are common to all approaches. These are to reduce cardiac preload and afterload and to prevent any decrease in the already compromised cardiac contractility. Any technique or drugs resulting in sudden fall in systemic vascular resistance should be avoided. and careful titration of both intravenous and local anaesthetic drugs is important. Wherever possible, it is important to institute invasive monitoring including blood pressure and central venous pressure before commencement of anaesthesia. Perioperative use of pulmonary artery catheter and transesophageal echocardiography has been described in patients with severely depressed cardiac function [42],[43] [Table 2]. In general, RA has been used in patients undergoing nonemergent caesarean section with relatively stable hemodynamics, while moderately symptomatic patients or parturients undergoing emergency surgery have received general anaesthesia (GA). General anaesthesia will have to be given rapidly in a pregnant female to avoid risk of aspiration which may be detrimental in a patient with heart failure at the same time complications of GA such as failed intubation may be avoided by choosing continuous epidural anaesthesia (CEA) as anaesthetic technique. Infiltration anaesthesia has also been described in a patient for caesarean section although the patient died eventually in the postoperative period. [44]

Techniques of RA used include combined spinal epidural (CSE) in six patients, [43],[45],[46],[47],[48],[49] continuous spinal anaesthesia (CSA) in two patients, [42],[46] and CEA in two patients. [50],[51] RA provides many advantages for patients with PPCM. Sympathetic blockade associated with RA is beneficial in a decompensated heart as it decreases both preload and afterload. Use of a catheter gives freedom of titrability of the local anaesthetic drug both in epidural and intrathecal space. Thus, the level of motor and sensory block can be gradually increased so as not to cause sudden hypotension which can lead to sudden decompensation in these patients. Schnaider et al. describe CSE in a morbidly obese patient with an ejection fraction of 20% who underwent caesarean section successfully under RA and had an uneventful perioperative course. [47] They preferred CSE over CEA as it has lower failure rate, better patient satisfaction and pain scores and superior hemodynamic profile than the CEA. Velickovic et al. advocate CSA for its more rapid and effective titrability. [42],[46] They inserted a 19-G flexible single orifice catheter in the intrathecal space and gave small boluses of bupivacaine with fentanyl in dextrose to achieve the desired level of anaesthesia. [42] The catheter was left in situ for several hours postoperatively for management of postoperative pain and possible postdural puncture headache. George et al. have described the management of a patient with PPCM with CEA using bupivacaine with fentanyl in which the level of anaesthesia was slowly allowed to develop over 6 hours. [51] They enumerate many advantages of CEA which include avoidance of cardio-depressant general anaesthetic drugs, easy and slow titrability and improvement in cardiac function due to decrease in cardiac preload and afterload.

GA has been described in six patients. [43],[52],[53],[54],[55],[56] The choice of anaesthetic technique is the anaesthetist's prerogative and if the goals of hemodynamic management are adhered to, the outcome can be expected to be favorable of the anaesthetic technique used. For any urgent or emergent lower segment caesarean section (LSCS), GA is preferred. GA is also preferred in patients with borderline cardiac decompensation as an already dyspneic patient may not be amenable to the procedure of RA. In such a patient, even minor degrees of sympathetic blockade associated with RA may lead to fulminant cardiac failure. Another contraindication to RA is the anticoagulated patient. McCarroll et al. describe the caesarean section in a patient with PPCM under GA with use of remifentanil and propofol. [56] Remifentanil was chosen for its efficacy in controlling intraoperative stress response and rapid recovery independent of duration of infusion. They feel that the hemodynamic responses of the patient during a general anaesthetic technique using appropriate agents are more predictable than those seen with RA. Similarly, Zangrillo et al. believe that potential benefits of cardiovascular effects of RA may not be greater than the risks of maternal hypotension and low cardiac output in such a patient. [54] Excessive reduction of preload may worsen cardiac output, while the decrease in after load can actually jeopardize coronary perfusion in some patients. Opioid-based anaesthesia provides good hemodynamic control and obtundation of response to endotracheal intubation but may require postoperative ventilatory support for both mother and neonate. Thus, it is obvious that favorable maternal and fetal outcome is not dependent on anaesthetic technique, but strict hemodynamic control and meticulous cardiovascular monitoring with close coordination between various involved specialists. Use of other nonanaesthetic drugs intraoperatively should be done with caution. Ergometrine should preferably be avoided and oxytocin should be given as an infusion or slowly titrated to response. Autotransfusion after delivery can be countered by a small dose of furosemide just before delivery of the baby.


  Conclusion Top


PPCM is a disease associated with high morbidity and mortality and can lead to maternal and fetal loss and persistent decrease in quality of life in mother. Early diagnosis, continued monitoring and prolonged therapy may be beneficial in a good amount of patients. Principles of therapy remain more or less same as that in heart failure due to any cause, but careful selection of drugs is important with due consideration to the pregnant or lactating mother. The anaesthetists may be involved in the intensive care management of an acutely decompensating patient or anaesthetic management of labor and operative or nonoperative delivery. In all the situations, careful and intense hemodynamic monitoring and slow and judicious titration of anaesthetic drugs is important to provide good maternal and fetal outcome.

 
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