why does pleural effusion occur in Congestive Cardiac Failure?

Question

why must the Left lung be affected first (the effusion starts from the left lung) then the Right??

Answer 1

There was a debate on the above and a lot of answers were delivered on the above subject " you are correct".
Some called it BEWARE OF THE LEFT PLEURAL EFFUSION others used a conservative approach.
This will give you an insight view of one of the respondents:
Heart failure (CHF) is the first cause of pleural effusion in the western world. Mrs Dempsey’s pre-test probability of CHF calculated with the Boston criteria is very high. Coronary heart disease is the first cause of CHF in the western world and, despite the absence of ECG findings or chest pain, should not be excluded. The presence of a holosystolic murmur could suggest a mitral rigurgitation or an interventricular septal defect due to a silent ischemic injury, even though the absence of a third heart sound seems unlikely in this clinical presentation. An infective endocarditis is unlikely, because of the normal WBC and the absence of renal failure, spleen enlargment or systemic findings. It is not known, however, if the patient had fever. The rupture of a tendinae chordae would be also possible, but the insidious onset of breathlessness argues against this possibility. A dilatative cardiomyopathy, either primitive, ischemic, valvular or due to hypertension cannot be excluded and the worsening of the mitral regurgitation could have led to this clinical presentation.

The predominance of the effusion on the left lung is strange, because more tipically, when the effusion due to CHF is in both lungs, it is of the same size or bigger on the right side. Constrictive pericarditis (as restrictive cardiomyopathy) could be an interesting hypothesis due to the presence of a raised central venous pressure, a tricuspid murmur and dispnoea on exertion. It’s not known if she had a history of TBC exposure, even though there’s not anemia, lymphocytosis, cough, weight loss or systemic illness. A neoplastic constrictive pericarditis in another interesting option and pleural effusion could be a consequence of this as well as a concomitant process. The primitive and secondary lung cancer rarely cause such a cardiac failure unless there are cardiac metastases or there’s an involvment of pulmonary arteries. I would consider in particular lymphoma, lung cancer (even though there’s not smoking history), breast, ovarian, renal cancer and melanoma. Nonetheless weight loss, anorexia or other systemic symptoms are not known and the plasma viscosity and WBC are normal. However, a cardio-pulmonary neoplastic syndrome should not be excluded and the greatest effusion on the left could also suggest a retraction of the lung induced by cancer. The association between hypertension and constrictive pericarditis has been moreover described. Some connective tissue disorders as some vasculitis can present with a pleuro-pericardial involvment, but the apparent lack of systemic finding, the normal WBC and plasma viscosity make this diagnoses unlikely. Furthermore these elements, as the absence of the cough, argue against a parapneumonic effusion. Pulmonary embolism looks like an attractive hypothesis, mainly multiple micro-embolization altough there are any risk factor known for deep venous thrombosis. The bilateral ankle oedema could suggest thrombosis of the inferior vena cava. Systemic hypertension and orthopnoea lower the probability of pulmonary embolism as well as the absence of chest pain or cough, but do not rule out it.

In conclusion, CHF remains the leading hypothesis and the cause of this syndrome needs to be rapidly discovered. Even constrictive pericarditis, particulary neoplastic, and pulmonary embolism should be carefully considered. With regard to the concomitant hypertension, I would keep in mind other less probable etiologies, such as renal artery stenosis, a carcinoid syndrome or an atrial septal defect.

I would continue the diuretic therapy, increasing the dose (intravenous) and monitoring the patient for two-three days. I think that we still don’t need to make a thoracentesis, unless the patient develops rest dispnoea. I would not give her an ACE inhibitor before a renal artery stenosis has been excluded. I would make thoracentesis if there has been any improvement after two days.

I would ask echocardiography at this instant and the next steps are largely dependent on his results.

I would dose glicemia, lipids, amilase, lipase, DE-dimers, serum globulins level and ask for an abdominal-pelvic ecography. I would ask more about her past history and make an accurate objective examination.

If these investigations would not be available, the dosage of BNP could be an idea, but the pre-test probability of CHF is very high and only a very low level of BNP could significantly lower this value. I would esplain to Mrs Dempsey that her dispnoea is due to an overload of fluids in her lungs an that this condition can be due to many causes, most of which are resolvable. I would also tell her that in the next days it could be necessary to make a thoracentesis in order to discover the cause of her illness and give her relief.

Answer 2

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Answer 3

Yrs, in congestive cardic failure, and many other conditions in which the pumping of the heart (strenght) may be affected...
It can appear with irritations of the pleura (the cover of the lungs) with nrken ribs, chemotherapy, cancer, lots of things,,,
The treatment is given according to the cause and nature of the effusion..(if too big, needle aspiration and analysis of a sample is a solution)

Answer 4

closest to heart.basically the heart if filling up hence congestive and not able to pump off fluids/waste and essentially the person drowns lasix can help but if ur old once u lose it its gone, sorry if blunt