Guyton perspective in managing peripartum cardiomyopathy patient with pulmonary edema: a case report.

BACKGROUND

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related condition characterized by left ventricular dysfunction and heart failure, typically occurring in the peripartum period. Individuals with a history of preeclampsia and hypertension are particularly prone to developing PPCM. Recent research suggests that the condition may be triggered by vascular dysfunction influenced by maternal hormones in the late stages of gestation. The onset of left heart failure results in decreased cardiac output, leading to insufficient perfusion, which in turn, contributes to pulmonary edema and exacerbates tissue hypoxia. This cardiovascular response activates the neurohumoral system, causing peripheral vasoconstriction and elevating both mean capillary filling pressure (MCFP) and central venous pressure (CVP). Early administration of furosemide reduces volume overload due to negative cumulative fluid balance gaining and vasodilation, which increases the velocity of intravascular refilling and causes interstitial edema to resolve. This will decrease interstitial fluid pressure, resulting in decreased mechanical compression to systemic capillary and systemic vein pressure, thus decreasing MCFP and CVP subsequently. Reduced CVP also contributes to increased venous return by decreasing the gradient pressure between MCFP and CVP, resulting in increased cardiac output (CO) and improved tissue oxygenation.

CASE

A 33-year-old Asian woman, para 3 at full term pregnancy, admitted to the intensive care unit (ICU) after c-section and tubectomy due to shortness of breath and palpitation. Based on history taking, physical examination and echocardiography the patient fulfilled the criteria of PPCM which was also complicated by pulmonary edema. Despite impending respiratory failure, the patient rejected intubation and continuous positive airway pressure (CPAP), and was given oxygen supplementation through nasal cannula. Furosemide was given rapidly continued by maintenance dose and CVP was monitored. Antihypertensive drug, anticoagulants, and bromocriptine were also administered. After achieving negative cumulative fluid balance the patient's symptoms resolved and was discharged one week later.

CONCLUSION

There is a correlation between negative cumulative fluid balance and reduced central venous pressure after early furosemide therapy. Suspicion for PPCM should not be lowered in the presence of preeclampsia, it could delay appropriate treatment and increase the mortality.