She was diagnosed with atrial septal defect 8 years ago and had a corrective surgery done at that time. She was free of symptoms till one year ago. No co-morbidities.
Examination revealed a cachectic female lying comfortably on the bed. Vitals were normal except for a bradycardic pulse with an irregularly irregular pulse and low BP ( 97/50 )
Cardiac examination revealed multiple valvular heart lesions. There were presence of a Grade 3 pansystolic murmur heard best at the apical region radiating to axilla as well as a pansystolic murmur at the tricuspid region( pulsatile liver was also present). An early diastolic murmur was also heard at the left sternal edge on sitting position and in expiration.
Patient also had signs suggestive of congestive cardiac failure as evidenced by a displaced apex beat, raised JVP, hepatomegaly, bibasal crepitations ,scleral jaundice and pedal oedema. CXR showed cardiomegaly.
ECG tracing revealed atrial fibrillation with right bundle branch block. Liver function test indicated unconjugated hyperbilirubinaemia with evidence of hepatocyte injury. A previous ECHO done last year showed ejection fraction of 55 %.
She was started on IV Frusemide to initiate diuresis. She was also given IV dopamine infusion, T.Spironolactone and put on fluid restriction of 800 cc per day.
Any comments?
Is this management optimal for this patient?
According to history given, this case would be decompensated heart failure due to multiple valvular lesions. From physical examination most probably could be mitral regurgitation, tricuspid regurgitation and aortic regurgitation. In the acute management of IV Furosemide i don't really agree in giving furosemide to initiate diuresis that fast. This is because patient is haemodynamically unstable and we could actually say that this patient acute heart failure is due to increase left ventricular filling pressure and reduce cardiac output. Giving dopamine which is an inotrope can increase cardiac output which could improve his haemodynamics. However, by giving furosemide which causes reduce in the amount of fluids would probably cause the condition to worsen due to sudden loss of fluid which leads to hypotension. Inotrope itself can already help in reducing left ventricular filling pressure and relieve the shortness of breath. eg : dobutamine or dopamine. Perhaps a much more suitable in acute setting would be inotropes with vasodilators.
ReplyDeleteHello hello, according to my understanding of this situation, the hypotension could be due to the decrease cardiac output of a failing heart. Therefore to help the heart to return to its normal functioning level therefore diuresis is indicated to reduce the cardiac strain. I understand that Dopmaine would be successful in bring the Blood Pressure back up. But on the other hand would further strain the already failing heart thus causing more harm than good towards this patients heart.
ReplyDeleteTherefore in my opinion, a higher/stronger dose of furesemide (80mg STAT to BD) should be given on admission to try and reduce the access fluid as soon as possible, and then see how the things from there move on. You may never know, once a significant amount of fluid is reduced resulting in reduced cardiac strain, the heart itself might be able to stabilize the blood pressure.This is just my 2cents, please feel free to comment. =D
I see this 63 year old woman as someone who had a congenital heart disease - atrial septal defect - which was uncorrected till age 55 years. By this time, I suspect she had already developed significant cardiomegaly and pulmonary hypertension. The mitral regurgitation and tricuspid regurgitation seen now are most likely related to LV and RV dilatation respectively and may not be due to intrinsic valvular disease. The early diastolic murmur could be due to pulmonary regurgitation secondary to pulmonary hypertension. I see that she had a BP of 97/50mm Hg when she presented with CCF. I would give frusemide, but cautiously, in low doses. Normally if the BP is below 90mm Hg systolic, one will not give diuretics because of fear of reducing blood pressure too much. She needed inotropes because her myocardium was too weak or because the significant pulmonary hypertension reduced inflow of blood into the left ventricle and reduced cardiac output.
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