Postpartum Presentations: When Risk Arises After Delivery – Shortness of Breath

Published on June 30, 2025

Download the article PDF: Postpartum Presentations When Risk Arises After Delivery Shortness Of Breath

Urgent Message: Shortness of breath presentations for postpartum patients in urgent care should prompt consideration of venous thromboembolism or peripartum cardiomyopathy, or more benign conditions like deconditioning, bronchitis, or anxiety.

Alexa Bailey, DO; Lauren Kostandaras, DO; Hannah Poorman, BS; Michael Weinstock, MD; Catherine Neal, DO.

Key Words: Shortness Of Breath, Postpartum, Venous Thromboembolism, VTE, Deep Vein Thrombosis, DVT, Pulmonary Embolism, PE, Peripartum Cardiomyopathy

Editor’s Note: The patient case scenario is hypothetical.

Abstract

Background: The postpartum period introduces a broader range of possible diagnoses for shortness of breath complaints seen in urgent care (UC).

Aim: The aim of this review is to enhance clinician familiarity with the diagnosis and management of both common and life-threatening postpartum conditions that may present with shortness of breath in the UC setting.

Conclusion: In addition to the common etiologies of shortness of breath, it is important for UC clinicians to consider other entities in postpartum patients that are summarized in this review, such as venous thromboembolism and peripartum cardiomyopathy.

Background

The postpartum period is variably defined and ranges from 6 weeks to 6 months after delivery.[1]^,[2] However, the majority of physiologic change and risk is limited to the first 6 weeks postpartum.² Women experience a variety of symptoms and physiologic changes in the weeks after childbirth. Differentiating expected postpartum signs and symptoms from pathologic conditions can be challenging for patients (especially first-time mothers) and clinicians alike.[3] However, understanding the conditions for which women are at risk after delivery is a critical first step for clinicians who evaluate postpartum patients.

Given that postpartum symptomology may be related to anything from benign physiologic changes to life threatening conditions, it is important for UC clinicians to appropriately balance reassurance and vigilance. Assessment begins with a detailed history and focused physical exam. Vigilance should be exercised while considering and evaluating for serious pathologies. Reassurance becomes clinically indicated only after these have been excluded.[4]

Hypothetical Clinical Scenario

A 36-year-old G2P2 (2 pregnancies, 2 live births) woman presented to UC with her husband 6 days after giving birth to a healthy infant by cesarean delivery (C-section) without complication. She presented with a chief complaint of 2 days of difficulty catching her breath and feet swelling, not associated with increased exertion. She noted having to take breaks and sit down after performing simple tasks like changing her baby’s diaper and preparing a bottle for feeding due to shortness of breath.

On exam, her heart rate was elevated to 115 beats per minute, but vital signs were otherwise normal. She was sitting upright on the table. Her abdomen was soft, non-tender, and her incision was intact, dry, and without surrounding erythema. Her uterus was firm, nontender, and palpable just below the umbilicus. Her neurologic exam was unremarkable, and specifically her extraocular movements and the remainder of the cranial nerve exam were normal. Her visual fields were intact bilaterally to confrontation. Her patellar reflexes were brisk and symmetric, but there was no inducible ankle clonus.

Her cardiopulmonary exam revealed reduced bilateral breath sounds, and bibasilar rales were present. S1 and S2 were rhythmic, and the rate was tachycardic. Both lower extremities were symmetrical in size and non-erythematous but had 2+ pitting edema.

Shortness of Breath

Within the first 24 hours after delivery, the mother’s heart rate begins to decrease, and temperature may be slightly elevated. Deconditioning related to the process of labor may occur immediately after delivery, but shortness of breath that was not present during pregnancy or that worsens after childbirth should prompt immediate medical attention.[5] There are several diagnoses specific to the postpartum period that should be considered when a postpartum patient presents to UC with shortness of breath.

Venous Thromboembolism

Epidemiology and Pathophysiology

In the postpartum period, the risk of venous thromboembolism (VTE) is increased 400-500% above baseline.[6] The hypercoagulability that occurs during pregnancy isn’t well understood but is hypothesized to occur due to increased production of thrombin and other pro-coagulant factors that would serve to mitigate the severity of postpartum hemorrhage.[7] It’s estimated that 9.3% of all maternal deaths are caused by VTE.⁶

The epidemiology of deep vein thrombosis (DVT) is somewhat different in pregnant and postpartum patients as well. Peripartum DVTs occur more commonly in the proximal leg veins such as femoral, iliac, or popliteal veins; compared to distal leg veins such as peroneal, posterior tibial, anterior tibial veins in nonpregnant patients.⁶ Peripartum VTE presents as DVT in 75-80% of cases, however, in up to a  quarter of cases, the initial presentation is that of pulmonary embolism.⁶ Additional risk factors for postpartum VTE include: prior history of VTE or thrombophilia; delivery by C-section; postpartum endometritis; hypertension; heart disease; autoimmune diseases; obesity; sickle cell disease; preeclampsia; and multiple gestation.⁶

History

The symptoms of DVT and pulmonary embolism (PE) are the same in pregnancy and the postpartum period as would be expected in non-pregnant patients, which include, but are not limited to: unilateral leg swelling; shortness of breath; tachycardia; and fever.⁶ However, there are features of pregnancy that can make these symptoms less apparent to patients. For example, some degree of leg swelling/edema is common in normal pregnancy and the postpartum period.  Large differences in degree of leg swelling and/or calf or thigh pain complaints, however, should raise suspicion for DVT.

Similarly, physiologic changes in late pregnancy and the early postpartum period can create symptoms of breathing difficulty for patients. The enlarged uterus limits diaphragmatic excursion. However, considering PE in this period is important if the patient’s shortness of breath rapidly increases or is associated with chest pain, syncope or near-syncope, or hemoptysis.

Exam

Accurate vital signs are critical in the assessment of postpartum patients in whom VTE is being considered. Tachycardia, tachypnea, hypoxemia, and/or hypotension may be present in patients with PE. Fever may also be present in patients with VTE.⁶ In assessing for DVT, inspect the lower extremities for symmetry. A >2 cm discrepancy in calf diameter is considered abnormal.⁶ Additionally, palpate the lower extremities for tenderness, pitting edema, and/or palpable cords.⁶

While PE can cause suggestive changes in vital signs discussed above, it can also present with normal or near-normal vital signs. Examination of the heart and lungs is most commonly normal, although wheezing may be present.

Testing

For postpartum patients (ie, young women recovering from delivery and caring for a newborn), the use of evidence-based decision support tools is critical to minimize unnecessary testing without exposing patients to excessive risk of missed serious diagnoses.[8]

In patients in whom there is a moderate/high clinical suspicion of DVT based on a Wells Criteria for DVT (Table 1),[9] a venous duplex ultrasound of the affected leg should be promptly obtained.⁶ A D-dimer should only be used to rule-out a DVT if the patient has a low Wells score.  An ultrasound can be repeated in 1-2 weeks if symptoms persist.

Clinical Characteristic	Score
Active cancer (patient treated for cancer within 6 months or currently receiving palliative treatment)	1
Paralysis, paresis, or recent immobilization of lower extremities	1
Major surgery within 12 weeks requiring general or regional anesthesia (vaginal delivery with epidural or cesarean delivery)	1
Localized tenderness along the distribution of the deep venous system	1
Leg swelling	1
Calf swelling > 3 cm compared to other lower extremity	1
Collateral superficial veins (pregnancy can result in varicose veins, which are not considered collateral superficial veins)	1
Alternative diagnosis at least as likely as deep-vein thrombosis	-2

The Pulmonary Embolism Rule-Out Criteria (PERC) has gained popularity as a clinical decision instrument for PE risk stratification in recent years. However, PERC has not been validated in pregnant or postpartum patients.[10] The Well’s Criteria for Pulmonary Embolism is useful in determining likelihood of PE (Table 2).

The initial testing for PE includes D-dimer and/or computed tomography pulmonary angiography (CTPA), and lung scintigraphy/ventilation-perfusion (V/Q) scanning. A V/Q scan is a diagnostic tool for PE, however, it has fallen out of favor due to increasing numbers of nondiagnostic and inconclusive results.[11] It is an option for pregnant patients due to the decreased risk of radiation but has been shown less safe in comparison to CTPA when the patient is at high risk for PE.¹¹

	No	Yes
Clinical signs and symptoms of DVT	0	3
PE number-one diagnosis OR equally likely	0	3
Heart rate > 100	0	1.5
Immobilization at least 3 days OR surgery in previous 4 weeks	0	1.5
Previous, objectively diagnosed PE or DVT	0	1.5
Hemoptysis	0	1
Malignancy with treatment within 6 months or palliative	0	1

Based on the Wells Criteria for Pulmonary Embolism, a score of 4 or less suggests “PE unlikely,” and it is appropriate to rely on a negative D-dimer to rule out PE.¹² A Wells PE score of 5 or higher suggests “PE likely” and a negative D-dimer should not be relied upon to exclude PE. For such patients, an immediate CTPA is indicated.¹²

The Pregnancy-Adapted Geneva Score (Table 3) has been proposed as a version of the original Geneva score to identify pregnant women with a low, intermediate, or high clinical pretest probability of PE.[13]

	Score
Age 40 years or older	+1
Surgery (under general anesthesia) or lower limb fracture in the past month	+2
Previous DVT or PE	+3
Unilateral lower limb pain	+3
Hemoptysis	+2
Pain on lower limb palpation and unilateral edema	+4
Heart rate >110 bpm	+5

Initial Management

Most cases of VTE in postpartum patients will be treated with therapeutic anticoagulation. Heparin is safe in breastfeeding and the postpartum period; a VTE diagnosed in pregnancy or postpartum is treated with unfractionated heparin or low molecular weight heparin.[14]

Currently, direct oral anticoagulants (DOACs) are not recommended in pregnant or breastfeeding patients due to the limited evidence of safety.¹⁴ A case study conducted at Ritsumeikan University followed two breastfeeding patients on rivaroxaban.¹⁴ There were no pharmacokinetic concerns in the patient or the infant, suggesting that rivaroxaban could be safe anticoagulation for breastfeeding patients, but more research is needed.¹⁴ If a postpartum patient is not breastfeeding, DOAC therapy would be acceptable.¹⁴

Indications for Referral to Emergency Department

If the patient’s history and physical exam classify them as being high-risk for PE by the Wells Criteria or intermediate-high risk by the Pregnancy-Adapted Geneva Score, they would require a CTPA. If this is unattainable at the facility, the patient should be sent to the emergency department (ED) for emergent testing.

Peripartum Cardiomyopathy

Epidemiology and Pathophysiology

Peripartum cardiomyopathy (PPCM, also called pregnancy-associated cardiomyopathy) is a rare cause of heart failure (HF) that affects females late in pregnancy or in the early puerperium.[15] A large prospective international registry of 411 females from 43 countries has demonstrated that PPCM occurs globally, affecting females from all ethnicities on all continents.¹⁵ A higher incidence of PPCM is observed in Zaria, Nigeria, and Haiti, whereas a lower incidence of PPCM is seen in Sweden, Denmark, and Japan. The United States incidence of PPCM is roughly 1:1000 to 1:4000.[16] A genetic predisposition may contribute to geographical variability. The higher prevalence in Haiti supports the notion that females in the African diaspora have a higher risk of developing PPCM.[17]

The mean age at PPCM presentation is 31 years, and the mean parity is 3.¹⁵ Additional risk factors increase the risk of PPCM: age greater than 30 years; African ancestry; pregnancy with multiple gestation; prior or concurrent preeclampsia; eclampsia; postpartum hypertension; maternal cocaine use; long-term (>4 weeks) of oral tocolytic therapy with beta adrenergic agonists such as terbutaline; and parity ≥4.[18]^{,[19],[20],[21],[22],[23]}

Whereas no single unifying cause for PPCM has been identified, several contributing pathogenic factors have been identified. Experimental research suggests that in the setting of pregnancy-related maternal cardiovascular changes, these multiple factors result in a common final pathway with enhanced oxidative stress, cleavage of prolactin to an angiostatic N-terminal 16 kDA prolactin fragment, and impaired vascular endothelial growth factor signaling because of upregulated soluble fms-like tyrosine kinase.^{15,[24],[25],[26]}

History

PPCM is less commonly seen before 36 weeks of gestation and affects patients most often during the first month postpartum.¹⁵ Most patients with PPCM are diagnosed early after delivery during a readmission. Pregnant females with other types of cardiac disease (e.g., ischemic, valvular, or myopathic) may present earlier in the antepartum period coincident with increases in the hemodynamic burden imposed by the gravid state during the second trimester, though they may also present during the third trimester or postpartum.[27]

Presentation of PPCM is variable and similar to other forms of systolic heart failure (HF) due to cardiomyopathy.¹⁴ The most common symptoms seen are dyspnea, cough, orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, and hemoptysis.¹⁴

Exam

A thorough cardiopulmonary exam and close assessment of vital signs should be performed. Physical signs of PPCM can include an elevated jugular venous pressure, a displaced apical impulse, a third heart sound, a murmur of mitral regurgitation, and peripheral edema.[28] Signs and symptoms of systemic or pulmonary thromboembolism may be present.

Testing/Diagnostic Criteria

The diagnosis of PPCM is based upon 3 clinical criteria: development of HF toward the end of pregnancy or in the months following delivery, absence of another identifiable cause of HF, and left ventricular (LV) systolic dysfunction with an LV ejection fraction (LVEF) generally <45%.¹⁴ An electrocardiogram (ECG) should be performed in all patients with suspected PPCM to detect other conditions in the differential diagnosis such as myocardial infarction and pulmonary embolism. ECG abnormalities may be found in up to 50% of patients with PPCM, but a normal ECG does not exclude PPCM.[29] ECG findings in patients with PPCM are nonspecific and include sinus tachycardia and nonspecific ST- and T-wave abnormalities.

The ECG generally reveals a global reduction in LV systolic function with LVEF nearly always <45%.¹⁴ Other possible echocardiographic findings include left atrial enlargement, LV or left atrial thrombus, dilated right ventricle, right ventricular hypokinesis, mitral and tricuspid regurgitation, and rarely small pericardial effusion.[30]

Plasma B-type natriuretic peptide (BNP) measurement is suggested in the evaluation of patients with suspected HF, especially when the diagnosis is uncertain. Females with PPCM typically have elevated BNP levels that are higher than those seen in healthy females during pregnancy or postpartum.[31] A chest radiograph is not necessary to make the diagnosis of HF or PPCM.

Initial Management

UC providers can initiate supplemental oxygen and assisted ventilation as needed. Treatment of PPCM is generally similar to treatment for other types of HF with reduced ejection fraction. However, several medications used in nonpregnant patients are not safe or do not have sufficient safety data in pregnancy or breastfeeding to support their use. For women with PPCM who have delivered and are not breastfeeding, acute and chronic HF are managed using standard therapy, and patients should be referred to a cardio-obstetrics team.[32]

Indications for Referral to Emergency Department

If PPCM is suspected, UC providers should have a low threshold for ED referral for several reasons. One, since the clinical criteria for diagnosing PPCM includes measurement of a LVEF, a rapid ECG needs to be performed. Two, excluding other causes of HF may be necessary, especially if the diagnosis of PPCM is not certain. This work-up may include tests such as CTPA, coronary angiography, or cardiac MRI. Thus, quick referral to the ED is indicated. Additionally, if the patient presents during pregnancy, referral to a cardio-obstetrics team and careful labor and delivery planning may be required.

Other Causes of Shortness of Breath

In addition to the causes of shortness of breath unique to the postpartum period, patients may also experience shortness of breath from asthma, pneumonia, bronchitis, anxiety, deconditioning, obesity, or infections. The list of differential diagnoses for postpartum shortness of breath presentations, therefore, should also include any etiology that might otherwise explain the shortness of breath in addition to the postpartum specific diagnoses discussed in this review.

Clinical Scenario Conclusion

In UC, the patient underwent an ECG and a chest x-ray. A 12-lead ECG revealed normal sinus rhythm, right bundle branch block, a prominent R wave in lead V1, and sinus tachycardia. Anteroposterior chest x-ray showed bilateral pleural effusions.

Through history-taking and physical exam, the clinician determined her Wells score for PE was  6. Her Pregnancy-Adapted Geneva Score was 7, classifying her as intermediate risk for having PE. As her Wells score was 6, a negative D-dimer cannot exclude PE, so the urgent care provider did not draw a D-dimer. In the presence of the patient’s findings, the provider decided to transfer the patient to the ED to be evaluated for pulmonary embolism and undergo immediate CTPA. The patient was placed on supplemental oxygen, with vital sign monitoring, and the urgent care provider called for ambulance transport to the ED.

Extensive laboratory tests were ordered as part of her initial workup in the ED. Her test results were as follows:

• Arterial blood gas:
  • pH: 7.40 (7.35-7.45)
  • PCO2: 26.5 (35-45 mmHg)
  • PO2: 49.8 (75-100 mmHg)
  • SO2: 84.1 (94-100%)
• CRP: 23.28 mg/L (<0.3mg/L)
• White blood cell count: 22.81 K/μL (4.5-11 K/ μL)
• Hemoglobin: 12.1 g/dL (12-15g/dL)
• Platelets: 652 K/μL (150-450 K/μL)
• Troponin: 0.354 ng/mL (<0.04 ng/mL)

The CTPA revealed a central filling defect, indicative of a PE, and the patient was started on IV heparin for 24 hours. She was discharged home on enoxaparin as she was breastfeeding.

Takeaways for Urgent Care Providers

• If an urgent care provider has concern for a peripartum VTE or cardiomyopathy, the patient should be immediately referred to the ED for further evaluation and treatment.
• Vital signs in a pregnant/postpartum patient can fluctuate compared to non-pregnant patients due to the physiologic demands of a growing fetus.
• The risk of VTE in the postpartum period is significantly increased above baseline, with a notable portion of maternal deaths attributed to VTE. Risk factors include cesarean delivery, obesity, hypertension, preeclampsia, and prior VTE.
• Symptoms of VTE overlap with normal postpartum changes, such as leg swelling or shortness of breath. Red flag signs include asymmetric leg swelling (>2 cm calf difference), significant leg pain, sudden-onset shortness of breath, chest pain, or syncope. Accurate assessment of vital signs is critical noting any signs of tachycardia, tachypnea, and/or fever.
• For suspected DVT using the Wells criteria as a diagnostic tool, venous duplex ultrasound is first-line for diagnosis. A low Wells score for DVT and a negative D-dimer may eliminate the need for an ultrasound.
• In the case of suspected PE, a Wells score >5 or Pregnancy-Adapted Geneva score >10 requires an urgent CTPA.
• Heparin is typically first-line for anti-coagulation, as DOACs are avoided in pregnancy and breastfeeding.
• PPCM is defined as the development of systolic HF toward the end of pregnancy or in the months following pregnancy, with LVEF generally less than 45% in the absence of another identifiable cause of HF.
• The clinical presentation of PPCM is variable and similar to new onset systolic HF due to cardiomyopathy in the non-pregnant person. Common findings include dyspnea, lower extremity edema, increased jugular venous pressure, and crackles on lung exam.
• An ECG and B-type natriuretic peptide are performed in most patients with suspected PPCM.

Manuscript submitted December 3, 2024; accepted May 21, 2025.

---

1. [1]. National Research Council (US) Committee on Population. Measuring the Risks and Causes of Premature Death: Summary of Workshops. National Academies Press (US); 2015. Accessed February 1, 2025. https://www.ncbi.nlm.nih.gov/books/NBK310595/
2. [2]. Romano M, Cacciatore A, Giordano R, La Rosa B. Postpartum period: three distinct but continuous phases. J Prenat Med. 2010;4(2):22-25.
3. [3]. Cooklin AR, Amir LH, Jarman J, Cullinane M, Donath SM; CASTLE Study Team. Maternal Physical Health Symptoms in the First 8 Weeks Postpartum Among Primiparous Australian Women. Birth. 2015;42(3):254-260. doi:10.1111/birt.12168
4. [4]. Blenning CE, Paladine H. An approach to the postpartum office visit. Am Fam Physician. 2005;72(12):2491-2496.
5. [5]. Lorenz TK, Ramsdell EL, Brock RL. Communication changes the effects of sexual pain on sexual frequency in the pregnancy to postpartum transition. Journal of Psychosomatic Obstetrics & Gynecology. 2020;43(2):91-98. doi:10.1080/0167482X.2020.1826429
6. [6]. ACOG Practice Bulletin No. 196: Thromboembolism in pregnancy. Obstet Gynecol. 2018;132(1):e1-e17. doi:10.1097/AOG.0000000000002706. Erratum in: Obstet Gynecol. 2018;132(4):1068. doi:10.1097/AOG.0000000000002923.
7. [7]. Bagot CN, Leishman E, Onyiaodike CC, Jordan F, Freeman DJ. Normal pregnancy is associated with an increase in thrombin generation from the very early stages of the first trimester. Thromb Res. 2017;157:49-54. doi:10.1016/j.thromres.2017.06.027
8. [8]. Weinstock MB, Heitsch VM, Probst MA. Balancing the legal risk to the clinician with the medical interests of the patient. Emerg Med Clin North Am. 2024;43(1):9-18. doi:10.1016/j.emc.2024.05.021
9. [9]. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon C, Dreyer J, Kovacs G, Mitchell M, Lewandowski B, Kovacs MJ. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl J Med. 2003 Sep 25;349(13):1227-35. doi: 10.1056/NEJMoa023153. PMID: 14507948.
10. [10]. Makowska A, Treumann T, Venturini S, Christ M. Pulmonary embolism in pregnancy: a review for clinical practitioners. J Clin Med. 2024;13(10):2863. doi:10.3390/jcm13102863
11. [11]. Thomas SE, Weinberg I, Schainfeld RM, Rosenfield K, Parmar GM. Diagnosis of pulmonary embolism: a review of evidence-based approaches. J Clin Med. 2024;13(13):3722. doi:10.3390/jcm13133722
12. [12]. Silveira PC, Ip IK, Goldhaber SZ, Piazza G, Benson CB, Khorasani R. Performance of Wells score for deep vein thrombosis in the inpatient setting. JAMA Intern Med. 2015;175(7):1112-1117. doi:10.1001/jamainternmed.2015.1687
13. [13]. Robert-Ebadi H, Elias A, Sanchez O, et al. Assessing the clinical probability of pulmonary embolism during pregnancy: the pregnancy-adapted Geneva (PAG) score. J Thromb Haemost. 2021;19(12):3044-3050. doi:10.1111/jth.15521
14. [14]. Yamashita Y, Hira D, Morita M, et al. Potential treatment option of rivaroxaban for breastfeeding women: a case series. Thromb Research. 2024;237:141-144. doi:10.1016/j.thromres.2024.04.003
15. [15]. Sliwa K, Hilfiker-Kleiner D, Petrie MC, et al; Heart Failure Association of the European Society of Cardiology Working Group on Peripartum Cardiomyopathy. 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(8):767-778. doi:10.1093/eurjhf/hfq120
16. [16]. Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, Ansari A, Baughman KL. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA. 2000 Mar 1;283(9):1183-8. doi: 10.1001/jama.283.9.1183. PMID: 10703781.
17. [17]. Karaye KM, Ishaq NA, Sai’du H, et al; Peripartum Cardiomyopathy in Nigeria (PEACE) Registry Investigators. Disparities in clinical features and outcomes of peripartum cardiomyopathy in high versus low prevalent regions in Nigeria. ESC Heart Fail. 2021;8(4):3257-3267. doi:10.1002/ehf2.13463
18. [18]. Elkayam U, Akhter MW, Singh H, et al. Pregnancy-associated cardiomyopathy: clinical characteristics and a comparison between early and late presentation. Circulation. 2005;111(16):2050-2055. doi:10.1161/01.CIR.0000162478.36652.7E
19. [19]. Veille JC. Peripartum cardiomyopathies: a review. Am J Obstet Gynecol. 1984;148(6):805-818. doi:10.1016/0002-9378(84)90572-6
20. [20]. Bello N, Rendon ISH, Arany Z. The relationship between pre-eclampsia and peripartum cardiomyopathy: a systematic review and meta-analysis. J Am Coll Cardiol. 2013;62(18):1715-1723. doi:10.1016/j.jacc.2013.08.717
21. [21]. Mendelson MA, Chandler J. Postpartum cardiomyopathy associated with maternal cocaine abuse. Am J Cardiol. 1992;70(11):1092-1094. doi:10.1016/0002-9149(92)90369-a
22. [22]. Lampert MB, Hibbard J, Weinert L, Briller J, Lindheimer M, Lang RM. Peripartum heart failure associated with prolonged tocolytic therapy. Am J Obstet Gynecol. 1993;168(2):493-495. doi:10.1016/0002-9378(93)90479-3
23. [23]. Gunderson EP, Croen LA, Chiang V, et al. Epidemiology of peripartum cardiomyopathy: incidence, predictors, and outcomes. Obstet Gynecol. 2011;118(3):583-591. doi:10.1097/AOG.0b013e318229e6de
24. [24]. Lampert MB, Lang RM. Peripartum cardiomyopathy. Am Heart J. 1995 Oct;130(4):860-70. doi: 10.1016/0002-8703(95)90089-6. PMID: 7572598.
25. [25]. Patten IS, et al. Cardiac angiogenic imbalance leads to peripartum cardiomyopathy. Nature. 2012 May 9;485(7398):333-8. doi: 10.1038/nature11040. PMID: 22596155; PMCID: PMC3356917.
26. [26]. Halkein J, et al. MicroRNA-146a is a therapeutic target and biomarker for peripartum cardiomyopathy. J Clin Invest. 2013 May;123(5):2143-54. doi: 10.1172/JCI64365. Epub 2013 Apr 24. PMID: 23619365; PMCID: PMC3638905.
27. [27]. Grewal J, Siu SC, Ross HJ, Mason J, Balint OH, Sermer M, Colman JM, Silversides CK. Pregnancy outcomes in women with dilated cardiomyopathy. J Am Coll Cardiol. 2009 Dec 29;55(1):45-52. doi: 10.1016/j.jacc.2009.08.036. PMID: 20117363.
28. [28]. Desai D, Moodley J, Naidoo D. Peripartum cardiomyopathy: experiences at King Edward VIII Hospital, Durban, South Africa and a review of the literature. Trop Doct. 1995 Jul;25(3):118-23. doi: 10.1177/004947559502500310. PMID: 7660481.
29. [29]. Honigberg MC, et al; IPAC Investigators. Electrocardiographic findings in peripartum cardiomyopathy. Clin Cardiol. 2019 May;42(5):524-529. doi: 10.1002/clc.23171. Epub 2019 Mar 29. PMID: 30843220; PMCID: PMC6522992.
30. [30]. Blauwet LA, Cooper LT. Diagnosis and management of peripartum cardiomyopathy. Heart. 2011 Dec;97(23):1970-81. doi: 10.1136/heartjnl-2011-300349. PMID: 22058286.
31. [31]. Forster O, et al. Reversal of IFN-gamma, oxLDL and prolactin serum levels correlate with clinical improvement in patients with peripartum cardiomyopathy. Eur J Heart Fail. 2008 Sep;10(9):861-8. doi: 10.1016/j.ejheart.2008.07.005. Epub 2008 Sep 2. PMID: 18768352.
32. [32]. Bauersachs J, et al. Pathophysiology, diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy. Eur J Heart Fail. 2019 Jul;21(7):827-843. doi: 10.1002/ejhf.1493. Epub 2019 Jun 27. PMID: 31243866.

Author Affiliations: Alexa Bailey, DO, University of Pikeville. Lauren Kostandaras, DO, Lincoln Memorial University. Hannah Poorman, BS, Lincoln Memorial University. Michael Weinstock, MD, Adena Health System; Wexner Medical Center at The Ohio State University; The Journal of Urgent Care Medicine. Catherine Neal, DO, Adena Regional Medical Center. Authors have no relevant financial relationships with any ineligible companies.

Read More on Postpartum and Shortness of Breath

• Postpartum Presentations: When Risk Arises After Delivery – Vaginal Bleeding and Discharge
• Postpartum Presentations: When Risk Arises After Delivery – Headache
• Shortness of Breath in a Postprocedural Pneumothorax
• Dyspnea in an Asthmatic Patient Following an Influenza Infection: A Case Report