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Year : 2020  |  Volume : 9  |  Issue : 4  |  Page : 238-241

Anaesthetic management of a parturient patient with peripartum cardiomyopathy

1 Department of Anaesthesia, Institute of Pregnant Women, Tirupati, Andhra Pradesh, India
2 Department of Anaesthesia, Sri Venkateswara Medical College, Tirupati, Andhra Pradesh, India
3 Department of Obstetrics, Sri Venkateswara Medical College, Tirupati, Andhra Pradesh, India

Date of Submission19-Apr-2019
Date of Decision23-Oct-2019
Date of Acceptance12-Mar-2020
Date of Web Publication5-Jan-2021

Correspondence Address:
K G Sree Hari
Assistant Professor, Department of Anaesthesia, Institute of Pregnant Women, Sri Venkateswara Medical College, Tirupati, Chittor, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JCSR.JCSR_47_19

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Peripartum cardiomyopathy (PPCM) is a rare life-threatening clinical entity of unknown aetiology. The hallmark of the disease is the onset of decreased left ventricular ejection fraction either in late pregnancy or puerperium. 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. Apart from intensive care management, these patients also require anaesthetic intervention for the management of painless labour for either vaginal or operative delivery. Favourable maternal and foetal outcomes require haemodynamic goals to be always kept in mind while choosing the technique and drugs to provide anaesthesia to the patients with PPCM. We report the case of a patient with PPCM requiring emergency lower segment caesarean section who was managed with titrated epidural anaesthesia.

Keywords: Epidural anaesthesia, ionotropes, peripartum cardiomyopathy, pregnancy

How to cite this article:
Sree Hari K G, Radha J, Mydhili K, Meghana A, Sunitha K. Anaesthetic management of a parturient patient with peripartum cardiomyopathy. J Clin Sci Res 2020;9:238-41

How to cite this URL:
Sree Hari K G, Radha J, Mydhili K, Meghana A, Sunitha K. Anaesthetic management of a parturient patient with peripartum cardiomyopathy. J Clin Sci Res [serial online] 2020 [cited 2021 Jan 28];9:238-41. Available from: https://www.jcsr.co.in/text.asp?2020/9/4/238/306193

  Introduction Top

Peripartum cardiomyopathy (PPCM) was first reported in the year 1849. The first case series of patients with PPCM was published in 1971.[1] The criteria for the diagnosis of PPCM[2] include: (i) development of heart failure in the last month of pregnancy or within 5 months after delivery; (ii) absence of any identifiable cause for heart failure; (iii) absence of recognisable heart disease before the last month of pregnancy; (iv) left ventricular (LV) systolic function demonstrated by LV ejection fraction (EF) <45%; fractional shortening <30% or both with or without LV end-diastolic dimension <2.7 cm/m2 body surface area. Potential risk factors are as follows: advanced maternal age, multiparity, multiple gestation, Afro-American race, pre-eclampsia, gestational hypertension and diabetes mellitus.[3]

The disease is known to have multifactorial pathogenesis[4],[5],[6] Symptoms of PPCM include palpitations and fatigue; shortness of breath (paroxysmal nocturnal dyspnoea, orthopnoea and oedema) should raise the doubt of PPCM, especially when the prenatal history has been otherwise uneventful.[7] Clinical signs depend on the severity of disease. Echocardiography is helpful in establishing the diagnosis of PPCM. Goals of anaesthetic management include improving oxygenation and maintaining cardiac output so as to improve maternal and foetal outcomes, among others.[8]

  Case Report Top

A 23-year-old parturient gravida 2, para1, with one live birth at 34 weeks of twin gestation reported to our institute with complaints of history of occasional dry cough, progressive breathlessness for 1 week, orthopnoea and paroxysmal nocturnal dyspnoea for 1 day. There was no history of previous heart diseases and no similar complaints during the previous pregnancy.

On examination, the patient was conscious and oriented. Pallor and generalised oedema were present. Pulse was 110/min and blood pressure was 150/90 mmHg in the sitting position. On cardiovascular system examination severe mitral regurgitation, moderarately severe tricuspid regurgitation,. Rest of the physical examination was unremarkable.

Electrocardiogram (ECG) showed no specific changes; two-dimensional echocardiography revealed global hypokinesia; left ventricular EF was 34%, moderate LV systolic dysfunction, severe mitral regurgitation (4+), moderate tricuspid regurgitation/pulmonary arterial hypertension and mild aortic and pulmonary regurgitation.

The patient was kept on tablet digoxin 0.25 mg once daily for 5/7 days, tablet torsemide 10 mg once daily, tablet isolazine (20/37.5 mg) thrice daily and tablet carvedilol 3.125 twice daily. Ultrasonography revealed twin gestation with the first foetus in a transverse lie and second foetus breech.

After clinical, biochemical, and echocardiograhic findings, the patient was diagnosed to have PPCM, mild pre-eclampsia, moderate anaemia and twin pregnancy (first foetus in a transverse lie) at 34 weeks of gestation. After 2 days of medical management, in the view of the above complications, the patient was planned for the emergency caesarean section.

To avoid the risk of aspiration, failed intubation and to avoid haemodynamic perturbations during general anaesthesia, we planned to do emergency caesarean under titrated epidural anaesthesia to avoid sudden haemodynamic variations associated with subarachnoid block. About 200 mL of lactated Ringer's solution was infused before epidural catheter insertion.

Intravenous access was secured with an 18G intravenous cannula and standard monitoring (non-invasive blood pressure, SPO2 and ECG Lead II and V) was connected. Baseline vitals were heart rate – 80/min, blood pressure – 130/80 mmHg and arterial oxygen saturation measured by pulse oximetry (SpO2) 98% on room air.

Under strict aseptic precautions, intravenous access was secured with triple lumen 15 cms/7F central venous catheter in the right internal jugular vein. Under strict aseptic precautions, the patient in the sitting position using 18G Tuohy needle (loss of resistance to air) epidural catheter was inserted at L2/L3 interspace and fixed at 10 cm. Epidural test dose 2 mL of 2% lignocaine without adrenaline was given. This was followed by 18 mL of 2% lignocaine and 25 μg fentanyl in small increments of 5 mL until sensory level achieved was up to T6 dermatome. She was delivered of female twins with APGAR scores at 0 and 5 min recorded as 8–10.

Oxytocin 15 U in 500 mL of normal saline was given slowly. Autotransfusion after delivery was countered by 20 mg of intravenous frusemide. The patient was haemodynamically stable throughout the procedure.

The patient was shifted to the intensive care unit for further management. Epidural analgesia (0.1% bupivacaine with 1 μg/mL fentanyl) in the post-operative period was continued for 3 days. In the 1st post-operative day, the patient complained of sudden breathlessness; on examination, she developed hypotension (systolic blood pressure <90 mm of Hg) and acute pulmonary oedema. Dobutamine (10 μg/kg/min) was started and furosemide 20 mg was given intravenously. The patient's hemodynamics were stabilised on post-operative day 3, and injection dobutamine was tapered and discontinued.

  Discussion Top

We report a patient with PPCM requiring emergency lower segment caesarean section who was managed with titrated epidural anaesthesia. PPCM is a diagnosis of exclusion, the treatment of PPCM is similar to other types of congestive heart failure. The main stay of therapy is a combination of digoxin, hydralazine, nitrates (decrease afterload) and loop diuretics. [2,7-10]

Calcium channel blockers, except amlodipine, have a negative inotropic effect and should be avoided. Amlodipine may be used if PPCM is associated with pre-eclampsia to control blood pressure. Angiotensin-converting enzyme 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 foetal toxicity associated with them.[9],[10],[11] 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 LV 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.

Anticoagulation is recommended in patients with PPCM, especially if left ventricular EF is <35% and there are other associated risk factors such as atrial fibrillation; the presence of mural thrombus on echo cardiography and history suggestive of previous thromboembolic episodes.

Dobutamine, dopamine, milrinone and levosimendan can be used to provide inotropic support to failing heart; these ionotropes along with nitroglycerine can be used in the pregnancy if the condition existing valid their use.[12] Any technique/drugs resulting in sudden fall in systemic vascular resistance should be avoided, and careful titration of anaesthetic drugs (intravenous and local anaesthetics) is important.

Whenever possible, it is important to institute invasive monitoring including blood pressure and central venous pressure before the commencement of anaesthesia. Haemodynamically, unstable pregnant patients who are on multiple drugs require continuous haemodynamic and oxygenation monitoring with intensive foetal monitoring. To avoid stress of laryngoscopy and intubation and rapid sequence induction on a patient with compromised cardiac function and to avoid the use of cardiac depressant drugs such as thiopentone and propofol/inhalational agents during general anaesthesia, we planned for titrated epidural anaesthesia.

Regional (epidural) anaesthesia remains the method of choice, as the sympathectomy associated with it causes a decrease in cardiac preload and afterload which is beneficial in patient with PPCM. Regional anaesthesia, however, is contraindicated in patients with anticoagulants. Effective (labour/postoperative) analgesia decreases the sympathetic out flow and decreases the plasma catecholamine levels in mother.[9],[10]

Post-operative period is crucial in PPCM, as the reabsorption of the third space fluid after 24–48 h of lower segment caesarean section may increase the pre-load causing congestive cardiac failure and avoid post-operative pain which is associated with haemodynamic variation.

PPCM disease is associated with high morbidity and mortality and can lead to maternal and foetal loss and persistent decrease in quality of life in mothers. Early diagnosis continued monitoring and prolonged therapy may be beneficial in these patients.

Principles of therapy remain the more or less the same as that in congestive heart failure due to any cause, but careful selection of drugs is important with due consideration to pregnant or lactating mother. The anaesthetist may be involved in the intensive care management of an acutely decompensating or anaesthetic management of labour and operative/non-operative delivery.

In all the situations, careful and intense haemodynamic monitoring and slow and judicious titration of anaesthetic drugs are important to provide good maternal and foetal outcomes.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Demakis JG, Rahimtoola SH, Sutton GC, Meadows WR, Szanto PB, Tobin JR, et al. Natural course of peripartum cardiomyopathy. Circulation 1971;44:1053-61.  Back to cited text no. 1
Sliwa K, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: A position statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy. Eur J Heart Fail 2010;12:767-78.  Back to cited text no. 2
Chee KH, Azman W. Prevalence and outcome of peripartum cardiomyopathy in Malaysia. Int J Clin Pract 2009;63:722-5.  Back to cited text no. 3
Bültmann BD, Klingel K, Näbauer M, Wallwiener D, Kandolf R. High prevalence of viral genomes and inflammation in peripartum cardiomyopathy. Am J Obstet Gynecol 2005;193:363-5.  Back to cited text no. 4
Ansari AA, Fett JD, Carraway RE, Mayne AE, Onlamoon N, Sundstrom JB. Autoimmune mechanisms as the basis for human peripartum cardiomyopathy. Clin Rev Allergy Immunol 2002;23:301-24.  Back to cited text no. 5
Geva T, Mauer MB, Striker L, Kirshon B, Pivarnik JM. Effects of physiologic load of pregnancy on left ventricular contractility and remodeling. Am Heart J 1997;133:53-9.  Back to cited text no. 6
Pyatt JR, Dubey G. Peripartum cardiomyopathy: Current understanding, comprehensive management review and new developments. Postgrad Med J 2011;87:34-9.  Back to cited text no. 7
Stoelting RK, Dierdorf SF. Cardiomyopathy. In: Stoelting RK, editors. Anaesthesia and Coexisting Disease. 3rd ed. New York: Churchill Livingstone; 1993. p. 97.  Back to cited text no. 8
Ray P, Murphy GJ, Shutt LE. Recognition and management of maternal cardiac disease in pregnancy. Br J Anaesth 2004;93:428-39.  Back to cited text no. 9
Cruz MO, Briller J, Hibbard JU. Update on peripartum cardiomyopathy. Obstet Gynecol Clin North Am 2010;37:283-303.  Back to cited text no. 10
Mastrobattista JM. Angiotensin converting enzyme inhibitors in pregnancy. Semin Perinatol 1997;21:124-34.  Back to cited text no. 11
Mebazaa A, Nieminen MS, Packer M, Cohen-Solal A, Kleber FX, Pocock SJ, et al. Levosimendan vs dobutamine for patients with acute decompensated heart failure: The SURVIVE Randomized Trial. JAMA 2007;297:1883-91.  Back to cited text no. 12


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