Heart and Soul: Cardiomyopathy in the Pregnant Patient
- Hanna Thompson
- Sep 11
- 8 min read

You and your partner are working a hot summer day, and it’s already proven to be busy with multiple calls. When you finally get back to base, you grab a freeze pop and are restocking when you get another request. Dispatch tells you this is for a 36-year-old female with breathing difficulty.
When you arrive on scene you find a 36-year-old female sitting on the couch in the living room. She is pale, sweaty, lethargic, and appears to be in obvious respiratory distress. You also see that she is pregnant. She tells you, in broken sentences, that she has been feeling short of breath today and it’s getting worse. She denies any medical history, doesn’t take any medications, and doesn’t have any known allergies.
She proceeds to tell you that she is currently 35 weeks and 5 days gestation with her third pregnancy. She has had prenatal care and takes prenatal vitamins every day. She did not have any complications with her previous pregnancies, and they were both delivered vaginally. She says that, as far as she knows, everything with this pregnancy has been normal too. She denies any membrane rupture, feeling contractions, or vaginal bleeding or discharge.
While you were obtaining this information, your partner was placing the cardiac monitor and doing additional assessment. B/P 187/96, HR 119, sinus tachycardia with an occasional PVC, RR 32, labored and shallow, lungs are diminished in the bases and crackles in the apexes, O2 saturation on room air, 88%, JVD, abdomen is gravid, non-tender, lower extremities are edematous, upper extremities are normal, and CMS is appropriate. Blood glucose is 77.

With this information, what are your thoughts? What are your priorities? Where are you going to transport her to?
Pregnancy Induced Cardiomyopathy
You might be thinking, oh boy Hanna where do you come up with this stuff? This isn’t a case that I just dreamt up, I’ve taken care of patients presenting like this with pregnancy induced cardiomyopathy. These patients are extremely sick with complicated presentations that can result in mortality for the mother and the infant if we don’t intervene quickly and efficiently.
Approximately 1 in 1,000 to 1 in 4,000 pregnant women develop pregnancy induced cardiomyopathy, which can present about one month before delivery of the infant, up to five months post-partum (As a little side note, if the patient develops cardiomyopathy after the infant is delivered it is known as Postpartum Cardiomyopathy). Women of African American decent are at an increased risk of having cardiomyopathy during or after pregnancy. Also, smoking, obesity, multiple parity, and hypertension or history of pre-eclampsia/eclampsia increase the prevalence of pregnancy induced cardiomyopathy.
The exact pathophysiology isn’t known either, however there have been many possibilities proposed. One thought is that it could be due to increased blood volume and cardiac output in late pregnancy. In addition, some researchers think it could be caused by myocarditis, but there are numerous cases where the patients will test negative for any viruses that would cause myocarditis or don’t present with myocarditis.
Another thought is the possibility of hormone changes and imbalances, creating issues with the patients’ vasculature. More specifically, Prolactin levels increase in the later months of pregnancy and normally this is a good thing. What scientists have found in mice models with pregnancy induced cardiomyopathy is a lack of an enzyme called STAT3. This enzyme is responsible for protecting the myocytes from oxidative stress. So, what happens is there is a buildup of stress causing Prolactin to break down into smaller enzymes and create little fragments that will damage the endothelial lining of the blood vessels and damage the myocytes, causing cells to self-destruct or apoptosis. This leads to weakening of the vasculature and heart muscles, creating cardiomyopathy.
Other ideas include the possibility of the female having inflammation or an autoimmune response. It has been found that patients with pregnancy induced cardiomyopathy have increased inflammatory markers, cytokines TNF-alpha and interlukin-6. The autoimmune response idea is for those who have Post Partum Cardiomyopathy. The thought is that there is immunosuppression during pregnancy increasing the chance that the patient will be exposed to antigens from the fetus. Once the infant is born the patient’s immune system returns to normal and attacks cardiac cells causing cardiomyopathy.
Diagnosis
It’s interesting because in order to be diagnosed with pregnancy induced cardiomyopathy, other differential diagnosis need to be ruled out. When caring for the patient presenting like the ones above, you must consider other causes like normal hemodynamic alternations during pregnancy, pulmonary embolism, amniotic fluid embolism, pre-eclampsia, pulmonary edema secondary to prolonged tocolytic use, and cardiac dysrhythmias. Pregancy induced cardiomyopathy is a dilated cardiomyopathy, meaning the left ventricle is dilated out and hypodynamic. This can be seen on the ultrasound below.

It makes sense to rule out other disease processes because the patient can present with a multitude of signs and symptoms. Breathing can be labored with severe hypoxia and shortness of breath. Pulmonary edema can be present, including coughing up pink frothy sputum. Other signs of fluid overload like pitting edema in the extremities will present along with third shifting outside of the vasculature. She can present with hypertension and cardiac arrythmias, with chest pain or pressure, and if not addressed quickly can lead to cardiogenic shock and cardiac arrest.
Once other causes of the above signs and symptoms are ruled out, a diagnosis of pregnancy induced cardiomyopathy can be considered if specific conditions are present.
In 2019 the European Society of Cardiology determined that there needed to be 3 criteria to diagnose a patient with pregnancy induced cardiomyopathy:
· Development of heart failure toward the end of pregnancy or in the postpartum period.
· Absence of another identifiable cause of heart failure.
· Left ventricular systolic dysfunction with a left ventricle ejection fraction <45%.
Then in the year 2000 the National Heart Lung and Blood Institute and The Office of Rare Diseases follow suit with 4 criteria for diagnosis:
Cardiac failure in the last month of pregnancy or within 5 months of delivery.
Absence of a determinable etiology for the cardiac failure.
Absence of demonstrable structural cardiac disease before the last month of pregnancy.
Echocardiographic evidence of diminished left ventricular systolic function.
Treatment & Transport
Prioritization of oxygenation is key, not only for your patient but for the fetus as well. You can always start with high flow with a non-rebreather mask, but if the patient is fluid overloaded with pulmonary edema the use of CPAP or BiPap would be much more beneficial. Depending on how lethargic she is or if she’s severely altered, you will need to consider establishing an airway. For BLS providers, NPAs with assisting ventilations with a BVM would be a good choice. If she doesn’t have a gag reflex, you can utilize an OPA and/or a supraglottic airway until you are able to intercept with ALS or get her to definitive care.
If you’re planning to perform RSI, it’s important to choose your induction and paralytic medications thoughtfully. One interesting consideration with Succinylcholine is its altered behavior in pregnant patients. By the third trimester, plasma volume increases by about 40% to 50%, which leads to a dilutional decrease in plasma pseudocholinesterase levels. Since this enzyme is responsible for breaking down Succinylcholine, reduced levels mean the drug isn’t metabolized as quickly. As a result, more Succinylcholine remains active in the bloodstream for longer, increasing the duration of paralysis.
Etomidate, Fentanyl, and Rocuronium are great choices for intubation, they are safe for use in pregnancy. If in your guideline, Propofol would be a good choice for induction and continued sedation too. Ketamine wouldn’t be the best choice in this case. Ketamine could have the potential to increase uterine tone and cause fetal distress.
Continuous cardiac monitoring will be important. I would also recommend placing D-Fib pads. She may go into a dysrhythmia, ventricular tachycardia or atrial fibrillation with rapid ventricular response being the most common. You should also obtain a 12 lead EKG, there could be ST segment changes, and if you’re lucky enough to have an ultrasound, obtaining cardiac images would be beneficial too.
Ensure to have IV access, however, do not give any fluids, she is already fluid overloaded. Any additional fluid boluses will only worsen any pulmonary edema and oxygenation status.
Medical management will include the administration of vasodilators. Nitrates will decrease afterload on the heart, preserving uteroplacental circulation. Starting a Nitro infusion at 100mcg/min would be a good place to start and titrate from there. Hydralazine is another good choice, if you carry it. This medication will also reduce afterload. Dosing for Hydralazine is normally 5mg-10mg IV bolus initially and can be repeated as needed up to 40mg. Lasix is recommended for true fluid overload elimination because it has been proven to be safe to administer during pregnancy. It is recommended to start at a lower dose of 40mg IV and giving additional doses if needed, but not to exceed 160mg.
Heparin should be considered if there is potential of thrombus forming in the left ventricle secondary to low ejection fraction. One article suggests that the patient should receive 5,000 units SQ twice a day. Another article stated one dose of 5,000 units SQ followed by an infusion of 20,000-40,000 units over 24 hours. Inotropes may be needed to maintain adequate perfusion if the patient develops cardiogenic shock, including Dobutamine starting at 5mcg/kg/min. Another option is a Milrinone infusion of 0.5mcg/kg/min.
Ensure you are monitoring the fetal heart rate at a minimum of every 15 minutes. You can do this with a doppler or an ultrasound. Fetal heart rate will let you know if you are providing enough oxygenation to your patient and is the best indicator of fetal well-being. A normal fetal heart rate is between 120 and 160 beats per minute.
Other transport considerations include choosing a destination facility. This may be complicated by where you are and what is available to you. Ideally, she needs to go to a facility that has maternal/fetal resources, NICU capabilities, and specialty cardiology services. Another consideration is choosing a facility that will be able to provide invasive cardiac support such as ECMO cannulation. If she progresses into cardiogenic shock and/or cardiac arrest, ECMO could bridge her to other therapies or even transplant.
Advocacy & Resources
It is important to note that maternal morbidity and mortality in the United States is the highest compared to other developed nations or nations that are considered wealthy. There are many reasons for this including loss of OB services in rural areas, loss of providers, and reimbursement issues. Morbidity and mortality for cardiovascular conditions during pregnancy is on the rise and in 2022 it was estimated that approximately 600 women died. For this reason, it is imperative that we continue to advocate for our patients and ensure that they receive the care they need and get to the most appropriate facility.
The non-profit organization Let’s Talk about PPCM is a great resource. They focus on pregnancy induced cardiomyopathy awareness including advocation of timely diagnosis and intervention by providers, women empowerment, education, and support for patients and family members. More specifically, they are educating women on how to ask for appropriate testing including EKG, BNP and Troponin I labs, and being referred to cardiology, if they are having chest pain or shortness of breath or feeling lethargic during or following pregnancy. You can visit them on social media or their website: https://letstalkppcm.org/
Case Conclusion
You and your partner were able to start CPAP on the patient and that improved her oxygenation status, and her breathing improved along with her lung sounds. During transport you monitored her and started a Nitro infusion. You also monitored the fetal heart rate, and it stayed between 135 and 140. She was much improved when you arrived at the hospital with perinatal and cardiac ICU services and her prognosis is good. Congratulations on a job well done!
“The moral responsibility of the healer is to step inside the patients' experiences and accompany them through the worst moments with empathy and expertise” -Dr. Paul Farmer
References
Archanna Radakrishnan, Dokko, J., Pastena, P., & Kalogeropoulos, A. P. (2024). Thromboembolism in peripartum cardiomyopathy: a systematic review. Journal of Thoracic Disease, 16(1), 645–660. https://doi.org/10.21037/jtd-23-945
Cardiomyopathy - Pregnancy and Cardiomyopathy | NHLBI, NIH. (2025, February 4). Www.nhlbi.nih.gov. https://www.nhlbi.nih.gov/health/cardiomyopathy/pregnancy
Haghighi, Mohammad, et al. “The Utero-Tonic Effects of Low Dose Intravenous Ketamine in Cesarean Section under Spinal Anesthesia; a Randomized Double-Blind Clinical Trial.” PubMed, vol. 14, no. 2, 1 Jan. 2023, pp. 218–225, https://doi.org/10.22088/cjim.14.2.218. Accessed 8 May 2025.
Hodgson, N. R., Lindor, R. A., Monas, J., Heller, K., Kishi, P., Thomas, A., Petrie, C., Querin, L. B., Andrej Urumov, & Majdalany, D. S. (2025). Pregnancy-Related Heart Disease in the Emergency Department. Journal of Personalized Medicine, 15(4), 148–148. https://doi.org/10.3390/jpm15040148
LetsTalkPPCM. (2025). LetsTalkPPCM. LetsTalkPPCM. https://letstalkppcm.org/
Napoli, N. (2025). Maternal Deaths From Cardiovascular Causes On the Rise in U.S. - American College of Cardiology. American College of Cardiology. https://www.acc.org/About-ACC/Press-Releases/2025/03/25/10/19/Maternal-Deaths-From-CV-Causes-On-the-Rise-in-US
Rodriguez Ziccardi, M., & Siddique, M. S. (2020). Peripartum Cardiomyopathy. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482185/

