INTRODUCTION

Peripartum cardiomyopathy (PPCM) is a rare but potentially life-threatening form of heart failure that develops in the last month of pregnancy or within the first five months postpartum in women without prior known heart disease or other identifiable causes of cardiac dysfunction. The incidence of PPCM exhibits significant geographic variation, ranging from approximately 1 in 1,000 to 1 in 4,000 live births in Western countries (including Europe and the United States), with higher rates reported in certain regions of Asia and Africa, potentially reaching 1 in 300–1,000 live births in high-prevalence areas such as parts of Nigeria or Haiti.[1,2] Maternal mortality associated with PPCM has improved in high-resource settings but remains elevated globally, ranging from 4–10% at six months in Europe and Asia-Pacific regions to higher rates in low-resource settings, influenced by access to advanced heart failure therapies and timely diagnosis.[3,4] The condition contributes substantially to maternal and fetal morbidity and mortality, particularly when compounded by additional risk factors such as morbid obesity and hypertensive disorders of pregnancy.[5]

The differential diagnosis of cardiomyopathy during pregnancy encompasses several distinct entities, including peripartum cardiomyopathy (PPCM), non-ischaemic dilated cardiomyopathy (NICDM), ischaemic dilated cardiomyopathy (IDCM), and acute decompensated heart failure (ADHF). PPCM is defined by the European Society of Cardiology as heart failure secondary to left ventricular (LV) systolic dysfunction (LV ejection fraction <45%) occurring toward the end of pregnancy or in the months following delivery, with no other identifiable cause and exclusion of pre-existing cardiac disease.[6] The echocardiographic hallmarks include reduced LV ejection fraction and often LV dilatation. In contrast, NICDM and IDCM typically have an onset unrelated to pregnancy and may involve different aetiologies (e.g. genetic, toxic, or ischaemic), whereas ADHF represents acute exacerbation in patients with pre-existing chronic heart failure. Accurate differentiation is critical, as it informs therapeutic strategies and long-term prognosis.[7,8]

The association between hypertensive disorders of pregnancy and PPCM has been the focus of intensive research over the past decade. Severe preeclampsia confers the highest risk for PPCM development, with adjusted odds ratios reported as high as 13–21 (95% CI varying by cohort), followed by superimposed preeclampsia (OR ~5–6), chronic hypertension (OR ~4–5), preeclampsia (OR ~4–5), and gestational hypertension (OR ~3–5).[9,10] A fundamental distinction lies in LV remodeling patterns: patients with PPCM accompanied by preeclampsia often exhibit concentric remodeling, associated with relatively preserved or more rapid recovery of LV function and better prognosis, compared to eccentric remodeling in PPCM without preeclampsia, which correlates with poorer response to standard heart failure therapies.[11,12] This pathophysiological divergence may explain differential responses to conventional agents such as angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), or beta-blockers, with patients displaying concentric remodeling potentially deriving less benefit from these therapies in the acute phase.[13]

Morbid obesity during pregnancy introduces additional perioperative complexities, with a globally rising prevalence that poses specific challenges in anaesthetic and intensive care management. Patients with morbid obesity (BMI ≥40 kg/m²) face elevated risks of cardiorespiratory complications, including difficult airway management, impaired respiratory function, and increased thromboembolic events.[14] Pregnancy outcomes are adversely affected, with higher rates of maternal and foetal complications and prolonged intensive care unit stays. Anesthetic management requires comprehensive preoperative evaluation, weight-adjusted dosing of anesthetic agents, and vigilant cardiorespiratory monitoring throughout the perioperative period.[15]

Pickwickian syndrome, also known as obesity hypoventilation syndrome (OHS), represents a severe complication of morbid obesity characterized by chronic alveolar hypoventilation, daytime hypercapnia (PaCO₂ >45 mmHg), and sleep-disordered breathing, with a prevalence of 8–20% among morbidly obese individuals.[16,17] Untreated OHS can progress to pulmonary hypertension and right heart failure (cor pulmonale). Diagnosis necessitates a thorough history, physical examination, and polysomnography to distinguish it from isolated obstructive sleep apnoea. Early identification and appropriate management, including noninvasive ventilation, are essential to prevent progression to severe pulmonary hypertension and subsequent heart failure.[16]

CASE DESCRIPTION

A 32-year-old primigravida woman (Mrs. D, medical record number 002334225) at 29 weeks and 1 day of 002334225 was admitted to the Medical Adult Intensive Care Unit (MAICU) of Dr. Hasan Sadikin Central General Hospital on 4 January 2025 with progressive dyspnoea that had begun at approximately 16 weeks of gestation. Initially exertional, the dyspnoea worsened over months to occur at rest and became orthopnea-dependent, preventing supine positioning for the past month. She also reported paroxysmal nocturnal dyspnoea and cough. The patient had been previously managed at two referring hospitals with diuretics, antenatal corticosteroids, and electrolyte supplementation but required escalation of care due to persistent respiratory failure and limited facilities at peripheral centres.

Her medical history was notable for chronic hypertension diagnosed during early pregnancy, which was treated with oral antihypertensives for 2.5 months prior to admission. She had no history of diabetes mellitus or other comorbidities. Anthropometric evaluation revealed morbid obesity with a pre-pregnancy weight of 130 kg, current weight of 147 kg, height of 162 cm, and a body mass index of 49.5 kg/m². On initial examination in the MAICU, the patient was conscious (Glasgow Coma Scale E4M6V5) but tachypneic (respiratory rate 24 breaths/min) and tachycardic (heart rate 105 beats/min) with a blood pressure of 134/65 mmHg. Oxygen saturation was 97% on high-flow nasal cannula (HFNC) at 60 L/min and FiO₂ 80%. Bilateral fine basal crepitations consistent with pulmonary oedema were observed. Urine output responded briskly to diuretic therapy (2000 mL in 5 h post-furosemide). Laboratory investigations revealed mild anaemia and leukocytosis that subsequently resolved, as well as persistent electrolyte derangements, including hyponatraemia, hypokalaemia, hypochloremia, and hypocalcaemia (Table 1).

Table 1. Serial Laboratory Parameters

Arterial blood gas analyses repeatedly showed chronic respiratory acidosis with compensatory metabolic alkalosis and elevated pCO₂, consistent with obesity hypoventilation syndrome (Pickwickian syndrome) (Table 2).

Table 2. Serial Arterial Blood Gas Analysis

Noted: Serial ABG revealed chronic respiratory acidosis with severe hypercapnia (pCO₂ 63–83 mmHg) and compensatory metabolic alkalosis (HCO₃ 36–53 mmol/L, BE +11 to +27), consistent with obesity hypoventilation syndrome.

Transthoracic echocardiography performed at the referring hospital (2 January 2025) and subsequent bedside studies confirmed severe left ventricular systolic dysfunction (LVEF 35–42%) with left ventricular dilatation, mild regional wall motion abnormalities, and trivial-to-moderate mitral regurgitation without left ventricular hypertrophy. Haemodynamic assessment revealed a low cardiac index (1.75 L/min/m²) and mild pericardial effusion without tamponade physiology (Table 3). Chest radiography performed on admission revealed cardiomegaly with pulmonary congestion, which progressively improved. The working diagnoses included acute decompensated heart failure secondary to non-ischaemic dilated cardiomyopathy versus ischaemic cardiomyopathy in the setting of gestational hypertension, morbid obesity, obesity hypoventilation syndrome (Pickwickian syndrome), and electrolyte imbalances.

Table 3. Echocardiographic and Hemodynamic Findings

After a multidisciplinary discussion on 7 January 2025 involving the cardiology, anaesthesiology, and perinatology teams, preterm caesarean delivery under general anaesthesia was planned for maternal stabilisation. Preoperative optimisation included fluid restriction, aggressive diuresis, electrolyte correction, head-up positioning, and continuous fetal monitoring. A caesarean section was performed on 8 January 2025 under carefully titrated general anaesthesia (propofol induction, rocuronium, post-delivery fentanyl) with invasive arterial monitoring and advanced haemodynamic assessment (MostCare). The intraoperative course was stable, with a blood loss of 400 mL and a urine output of 70 mL (Table 4).

Table 4. Intraoperative Hemodynamic Parameters

Noted: Intraoperative haemodynamics remained stable under general anaesthesia and low-dose dobutamine: BP 99–128/62–82 mmHg, HR 118–130 bpm, CO 3.9–6.4 L/min, SVV 6–8%, SpO₂ 90–94% (FiO₂ 60–80%), peak pressure 22–25 cmH₂O, EtCO₂ 44–47 mmHg; reflecting a controlled low-output state without significant instability.

Postoperatively, the patient required prolonged mechanical ventilation (6 days) with gradual weaning from pressure support to CPAP, followed by HFNC and eventual nasal cannula oxygen therapy. Inotropic support (dobutamine) was weaned on postoperative day 8. Strict negative fluid balance (500–1000 mL/day, occasionally up to 3400 mL/day) was maintained using loop diuretics. Thromboprophylaxis was intensified due to obesity and postoperative immobility. Left common femoral vein deep vein thrombosis was diagnosed and managed with therapeutic-dose low-molecular-weight heparin. Persistent electrolyte disturbances and postoperative delirium secondary to prolonged hypoxia were successfully treated. By postoperative day 19 (27 January 2025), the patient was haemodynamically stable without vasoactive support, maintained oxygen saturation on a 4 L/min nasal cannula, achieved normalised sodium (133 mmol/L), and tolerated oral feeding. She was transferred to the regular ward for continued heart failure therapy, multidisciplinary follow-up (cardiology, obstetrics, and endocrinology), and gradual cardiac rehabilitation. The newborn was cared for in the neonatal intensive care unit, and an uncomplicated course was reported.

DISCUSSION

The present case exemplifies the complex interplay of morbid obesity, gestational hypertension, obesity hypoventilation syndrome (OHS), and acute decompensated heart failure secondary to non-ischaemic dilated cardiomyopathy (NICDM), unmasked or exacerbated by pregnancy, culminating in preterm delivery at 29 weeks gestation. This scenario highlights the challenges in cardio-obstetric intensive care, where physiological adaptations of pregnancy impose substantial hemodynamic stress on a compromised myocardium, compounded by obesity-related respiratory and metabolic burdens.[17] The patient’s progressive dyspnea since mid-pregnancy, orthopnea, paroxysmal nocturnal dyspnea, and chronic respiratory acidosis with compensatory metabolic alkalosis (pCO₂ consistently >70 mmHg) reflect the synergistic effects of low cardiac index (1.75 L/min/m²), pulmonary congestion, and alveolar hypoventilation characteristic of OHS in the setting of extreme obesity (BMI 49.5 kg/m²).[18]

Figure 1 Serial arterial blood gas trends showing chronic hypercapnia and compensatory metabolic alkalosis

Differential diagnosis in this peripartum presentation required careful exclusion of peripartum cardiomyopathy (PPCM), which shares echocardiographic features such as left ventricular dilatation and reduced ejection fraction (<45%) but is defined by onset in the last month of pregnancy or within five months postpartum without identifiable prior heart disease.[19,20] In contrast, the patient’s symptoms commenced at approximately 16 weeks gestation, predating the classic PPCM temporal window, and echocardiography revealed no concentric remodeling typically associated with preeclampsia-related PPCM, favoring preexisting NICDM exacerbated by gestational hemodynamic load rather than de novo pregnancy-associated cardiomyopathy.[21,22] Gestational hypertension without proteinuria or end-organ damage further distinguished this case from preeclampsia, where severe forms confer markedly elevated odds ratios for PPCM development (up to 13–21).[9,10] The absence of significant left ventricular hypertrophy or ischemic changes on serial echocardiography supported NICDM over hypertensive or ischemic dilated cardiomyopathy.[23]

Figure 2 Serial Transthoracic Echocardiography Images Atau Schematic Comparison Of Eccentric Vs Concentric LV Remodeling In PPCM With/Without Preeclampsia

The management adhered to contemporary cardio-obstetric principles, emphasising multidisciplinary decision-making for timely delivery to halt maternal deterioration. Preoperative optimization with high-flow nasal cannula (HFNC), fluid restriction, aggressive diuresis, and electrolyte correction mitigated pulmonary edema and hypoventilation, while invasive hemodynamic monitoring (MostCare) and low-dose dobutamine facilitated safe general anesthesia for cesarean section, avoiding neuraxial techniques in the context of anticipated difficult airway and hemodynamic instability.[24,25] Postoperative prolonged mechanical ventilation with gradual weaning, persistent negative fluid balance (up to 3400 mL/day), and intensified thromboprophylaxis addressed the heightened risks of respiratory failure, venous thromboembolism, and delirium secondary to chronic hypercapnia in OHS.[26,27] Successful extubation on day 6 and inotrope discontinuation by day 8, culminating in ward transfer on day 19 with normalized sodium and oxygen requirement of 4 L/min, underscore the efficacy of targeted decongestion and ventilatory support in reversing acute decompensation.[28,29]

Figure 3 Timeline Of Clinical Course Atau Graphical Abstract Of Daily Fluid Balance, Ventilator Settings, Inotrope Weaning, And Key Milestones (Day 1–19)

Morbid obesity profoundly amplified perioperative complexity, manifesting as obesity hypoventilation syndrome with daytime hypercapnia, reduced functional residual capacity, and increased work of breathing, predisposing to atelectasis and prolonged ventilation.[30,31] The observed deep vein thrombosis and postoperative delirium align with established complications in this population, where prevalence of OHS approaches 8–20% and untreated progression risks pulmonary hypertension and cor pulmonale.[32,33] Anesthetic conduct—titrated general anesthesia with volume-controlled ventilation, weight-adjusted rocuronium, and post-delivery fentanyl—reflected evidence-based adaptations for difficult airway and altered pharmacokinetics in extreme obesity.[34,35]

Figure 4 Pathophysiology Schematic Of Obesity Hypoventilation Syndrome Atau Chest X-Ray Progression From Admission To Day 15

This case illustrates that while PPCM remains a critical differential in peripartum heart failure, early-onset symptoms in the presence of morbid obesity and gestational hypertension more commonly represent unmasking of underlying dilated cardiomyopathy or acute decompensation driven by obesity-related cardiorespiratory strain.[36] Prompt recognition, multidisciplinary intervention, and delivery for maternal stabilization yielded favorable maternal recovery despite initial severity, emphasizing the imperative of cardio-obstetric collaboration in high-risk pregnancies.[37] Long-term follow-up with guideline-directed medical therapy for heart failure (including sacubitril/valsartan, beta-blockers, mineralocorticoid antagonists, and SGLT2 inhibitors when postpartum and breastfeeding status permit), aggressive weight management, and contraception counseling is essential to mitigate recurrence risk in subsequent pregnancies and progression to chronic cardiomyopathy.[38-42]

CONCLUSION

Acute decompensated heart failure due to non-ischaemic dilated cardiomyopathy, aggravated by morbid obesity (BMI 49.5 kg/m²), obesity hypoventilation syndrome, and gestational hypertension at 29 weeks gestation, was successfully managed with multidisciplinary intervention: preterm caesarean section under general anaesthesia, advanced monitoring, aggressive decongestion, and stepwise ventilatory weaning, achieving full maternal recovery by postoperative day 19. This underscores the critical value of integrated cardio-obstetric critical care in high-risk peripartum decompensation amid rising maternal obesity and multi-morbidity.

DECLARATIONS

None

CONSENT FOR PUBLICATION

The Authors agree to be published in the Journal of Society Medicine.

FUNDING

None

COMPETING INTERESTS

The authors declare no conflicts of interest in this case report.

AUTHORS’ CONTRIBUTIONS

All authors made substantial contributions to the case report. AD was responsible for patient management, data collection, and initial drafting of the manuscript. All authors reviewed and approved the final version of the manuscript, ensuring its accuracy and integrity, and are accountable for all aspects of the work.

ACKNOWLEDGMENTS

None

REFERENCE

1. Metgud SC, Patil A, Renuka PM. Epidemiology, risk factors, and pregnancy outcomes in peripartum cardiomyopathy. J Sci Soc. 2025;52(1):43-48.

2. Jackson AM, Macartney M, Brooksbank K, et al. A 20-year population study of peripartum cardiomyopathy. Eur Heart J. 2023;44(48):5128-5141.

3. Okeke TC, Ezenyeaku C, Ikeako LC. Peripartum cardiomyopathy. Ann Med Health Sci Res. 2013;3(3):313-319.

4. Nugrahani AD, Maulana S, Tjandraprawira KD, et al. Analysis of clinical profiles and echocardiographic cardiac outcomes in peripartum cardiomyopathy (PPCM) vs PPCM with co-existing hypertensive pregnancy disorder (HPD-PPCM) patients: a systematic review. J Cardiothorac Vasc Anesth. 2024 [in press].

5. Fahreza L, Winato BM, Nugrahani AD, Arianto S. Peripartum cardiomyopathy vs peripartum cardiomyopathy with preeclampsia: from biomolecular approach to management. J Biomedika Kesehat. 2024;7(3):351-361.

6. Kaw R, Dupuy-McCauley K, Wong J. Screening and perioperative management of obesity hypoventilation syndrome. J Clin Med. 2024;13(17):5000.

7. Ramadhan AR, Betcy B, Aurora RG, Prasenohadi P, Alatas MF. Obesity hypoventilation syndrome (Pickwickian syndrome): a literature review. Respir Sci. 2024;5(1):48-61.

8. Kharawala A, Nagraj S, Setia G, Reynolds D, Thachil R. Cardiac critical care of the cardio-obstetric patient. J Intensive Care Med. 2025 [Epub ahead of print].

9. Xu C, Yang F, Wang Q, Gao W. Comparison of high flow nasal therapy with non-invasive ventilation and conventional oxygen therapy for acute hypercapnic respiratory failure: a meta-analysis of randomized controlled trials. Int J Chron Obstruct Pulmon Dis. 2023;18:2221-2233.

10. Yan L, Lu Y, Deng M, et al. Efficacy of high-flow nasal cannula in patients with acute heart failure: a systematic review and meta-analysis. BMC Pulm Med. 2023;23(1):476.

11. Luebcke CD, Smith BE, Abrahamson K. An integrated review of obstetric admissions in the intensive care unit. Dimens Crit Care Nurs. 2022;41(3):132-143.

12. Abie A, Mehari MG, Dagnew TE, et al. Obstetric admission and maternal mortality in the intensive care unit in Africa: a systematic review and meta-analysis. PLoS One. 2025;20(4):e0320254.

13. Sanfilippo F, Noto A, Ajello V, et al. The use of pulmonary artery catheters and echocardiography in the cardiac surgery setting: a nationwide Italian survey. J Cardiothorac Vasc Anesth. 2024;38(9):1941-1950.

14. Dodiyi-Manuel ST, Ezennaka RC. Current management of peripartum cardiomyopathy: a review. Niger J Med. 2015;24(4):363-369.

15. Kamajaya IGNAT, Ariyana MBD. Updated study of peripartum cardiomyopathy and preeclampsia. Maj Obstet Ginekol. 2022;30(2):101-107.

16. Tsabedze N, Ramsay M, Krause A, et al. The genetic basis for adult-onset idiopathic dilated cardiomyopathy in people of African descent. Heart Fail Rev. 2023;28(4):879-892.

17. Luciani M, Del Monte F. Insights from second-line treatments for idiopathic dilated cardiomyopathy. J Cardiovasc Dev Dis. 2017;4(3):12.

18. Perone F, Dentamaro I, La Mura L, et al. Current insights and novel cardiovascular magnetic resonance-based techniques in the prognosis of non-ischemic dilated cardiomyopathy. J Clin Med. 2024;13(4):1017.

19. Sabina M, Barakat Z, Feliciano A, Lamb A, Alsamman MM. Unlocking the potential of acetazolamide: a literature review of an adjunctive approach in heart failure management. J Clin Med. 2024;13(1):288.

20. Braunthal S, Brateanu A. Hypertension in pregnancy: pathophysiology and treatment. SAGE Open Med. 2019;7:2050312119843700.

21. Townsend R, O’Brien P, Khalil A. Current best practice in the management of hypertensive disorders in pregnancy. Integr Blood Press Control. 2016;9:79-94.

22. Anthony J, Damasceno A, Ojjii D. Hypertensive disorders of pregnancy: what the physician needs to know. Cardiovasc J Afr. 2016;27(2):104-110.

23. Loh CJL, Qi Y, Sultana R, Tan CW, Sng BL, Yahaya Z. Hemodynamic changes of women with preeclampsia undergoing spinal anesthesia for emergency cesarean section: a prospective observational study. Bali J Anaesthesiol. 2024;8:164-168.

24. Abate S, Mergia G, Basu B. Maternal and neonatal outcomes of preeclamptic and normotensive women who underwent cesarean section under spinal anesthesia: systematic review and meta-analysis. Int J Surg Open. 2021;26:6-16.

25. Akter R, Abdullah-Hel-Baki M, Neher J, et al. The efficacy of spinal anesthesia during emergency cesarean section for severe preeclampsia and eclampsia patients. Saudi J Med Pharm Sci. 2023;9(1):6-12.

26. Manuaba IBGRS, Widana IW. Anesthesia management in cesarean section with severe preeclampsia and non-reactive nonstress test. Int J Res Med Sci. 2024;12(6):2104-2105.

27. Ramos Mayordomo P, Capilla Díez M, Ticona Espinoza DA, et al. Thrombotic microangiopathy (TMA) associated with pregnancy: role of the clinical laboratory in differential diagnosis. Clin Chem Lab Med. 2024 [in press].

28. Kalicka M, Bielak A, Gryta J, et al. How maternal obesity affects pregnancy? Literature review. Qual Sport. 2023;10:11-17.

29. Carrasco Catena A, Ruiz Sacedón N, Ortiz Murillo E, Balanzá Chancosa R. Pregnant women with morbid obesity: pregnancy and perinatal outcomes. Adv Obes Weight Manag Control. 2018;8(5):00257.

30. Kammies JD, De Waard L, Muller CJB, Hall DR. Delivery outcomes in women with morbid obesity, where induction of labour was planned to prevent post-term complications. J Obstet Gynaecol. 2022;42(8):3450-3455.

31. Eissa GA, Khurmi RA, Holbah TJ, et al. The effect of sleeve gastrectomy on pregnancy complications: a cross-sectional study in Saudi Arabia. Cureus. 2023;15(6):e40157.

32. Li J, Chen AE, Ye R. Comparison of three neuraxial anesthesia approaches in parturient women with obesity and pregnancy-induced hypertension who underwent cesarean section. J Int Med Res. 2021;49(12):3000605211066433.

33. Ismail N, Ismail MF. Maternal obesity and obstetric anesthesia: a comprehensive review of challenges and clinical strategies. Asian J Med Health. 2025;23(3):105-111.

34. Machado LS. Cesarean section in morbidly obese parturients: practical implications and complications. N Am J Med Sci. 2012;4(1):13-18.

35. Bisri DY, Maharani MI, Bisri T. Anesthesia for craniotomy tumor removal patient with morbid obesity. J Law Sust Develop. 2024;12(1):e1816.

36. Agha M, Agha RA, Sandell J. Interventions to reduce and prevent obesity in pre-conceptual and pregnant women: a systematic review and meta-analysis. PLoS One. 2014;9(5):e95132.

37. Moxth LC, Sauls R, Ruiz M, Stem M, Gonzalvo J, Gray HL. Effects of bariatric surgeries on male and female fertility: a systematic review. J Reprod Infertil. 2020;21(2):71-86.

38. Fadl AA, Shahatah MA, Asiri AY, et al. Obesity hypoventilation syndrome: a comprehensive review. Int J Med Res Health Sci. 2024;13(5):112-125.

39. Shah NM, Shrimanker S, Kaltsakas G. Defining obesity hypoventilation syndrome. Breathe (Sheff). 2021;17(3):210089.

40. Mishra P, Gupta S, Devmurari P, Raj N, Priya Natarajan N, Kumar A. Obesity-related breathing disorders: diagnosis and treatment of hypoventilation syndrome. Health Leadersh Qual Life. 2025;4:612.

41. Guan L, Wu W, Huo Y, et al. Efficacy of bilevel positive airway pressure and continuous positive airway pressure therapy in patients with obesity hypoventilation syndrome: protocol for systematic review and meta-analysis. BMJ Open. 2018;8(5):e020832.

42. De Jong A, Chanques G, Jaber S. Mechanical ventilation in obese ICU patients: from intubation to extubation. Crit Care. 2017;21(1):63.