Cardiomyopathy :: Postpartum Cardiopulmonary a dangerous compl-A nightmare for all of us,. Comes suddenly like a thunder or atonic PPH.

PQ.1 . What is the definition of Peripartum cardiomyopathy-Ans;-Postpartum cardiomyopathy, also known as peripartum cardiomyopathy (PPCM), is defined as new onset of heart failure between the last month of pregnancy and 5 months post delivery with no determinable cause. First described in a case series in 1937. Postpartum cardiomyopathy is a rare cause of heart failure.

Q.2: How severe is this uncommon compl  ? Ans:-Postpartum cardiomyopathy is a
dreaded complication of pregnancy  and if left untreated there  will be 100% mortality. May be we have missed some cases in our lifetime and written as amniotic Fluid embolism or Pulm embolism in death certificate

Q,. 3. What are the symptoms?? Ans . Such features are exhibited clinically by unexplained tachycardia, breathless, low O2 saturation, and basal crepitations (all were present in this case)   
. Q. 4. Time of onset of PPCM Ans:-Most patients present soon after delivery especially in the first week postpartum. The symptoms as mentioned earlier are suggestive of heart failure, for example, orthopnea and paroxysmal nocturnal dyspnea.  In antenatal period (not in this case) these symptoms are usually attributed to normal pregnancy and that is why a diagnosis of postpartum cardiomyopathy can be easily missed.

Q.5: What are the signs?? Ans:- There will be sudden  onset of tachycardia, elevated jugular venous pressure, bilateral pulmonary crackles due to pulmonary edema, third heart sound (S3) and displaced apical pulse. Severe cases may present with acute respiratory failure( as was typical in this case)  or cardiogenic shock and a need for close monitoring in the intensive care unit. 

Q.6:-What are the risk Factors??

·         1) Advanced maternal age (more cases reported in both extremes of age) 

·        2)  High parity (71% of women diagnosed with PPCM had three or more prior pregnancies) 3) ·         Twin pregnancy (more endemic in women with twin pregnancies)

·          4) Use of tocolytic therapy (greater than 4 weeks can cause silent ischemia)-a great warning to all of us.

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5)        Poverty 6)      Hypertension 7) such cardiomyopathy is more prevalent in association with mild PIH. & 8) in cases with increased liquor  for reasons not clear to us 9) PGF2alpha

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Q. 7:-What about ECG?? ECG may show non-specific changes like sinus tachycardia, interventricular delay and sometimes, LBBB pattern and Echocardiography suffices to differentiate it from other causes and usually shows left ventricle dilatation of variable degrees, left ventricle systolic dysfunction, right ventricular and bi-atrial enlargement, mitral and tricuspid regurgitation, and pulmonary hypertension..

Q. 8: What about Echo?  Echocardiography criteria to diagnose PPCM includes ejection fraction less than 45%,(this was however present in this case) , end-diastolic diameter greater than 2.7 cm/m2 and/or M-mode fractional shortening less than 30%.

 used to diagnose when an accurate estimation of the ejection fraction (EF) is required.

Q. 9 . What should be the ideal Treatment??

Treatment is usually supportive and directed toward the management of the heart failure symptoms. Standard heart failure therapy is used to optimize the patient's volume status. Beta-blockers and ACEIs are the most commonly used drugs and have shown to lower the mortality. The caveat is ACEI is contraindicated in pregnant patients. Diuretics are often used to ease symptoms related to heart failure(this life saving agent was very rightly used in this case) . Novel anti-heart failure medications, such as sacubitril/valsartan have been reported to improve heart failure symptoms in pregnancy-related cardiomyopathy but the decision to prescribe such modern agents are best left to Internist/In charge of ICU..

 Q. 8. What is the presumed etiology?? Ans:-Recent data suggest that an increase in oxidative stress during the peripartum period increases the formation of abnormal 16-kDa prolactin which induces toxic effects on cardiac myocyte. Bromocriptine, a dopamine receptor agonist with prolactin-blocking properties, decreases the effect of 16-kDa prolactin on cardiac myocyte and has been associated with better outcomes in small studies. Cardiac resynchronization therapy has also shown to improve ejection fraction and outcomes when medical therapy alone is ineffective.