Does pulmonary hypertension with unrelated pericardial effusions buffer, to any degree, tamponade pressures on the RA and its resultant pathology? Is the decreased forward flow with PHT a similar trade off with the tamponade effects of PE to some degree? Can the addition of ACEi/b, treating increased downstream pressures, affect up stream pressures enough that the pressure drop could lead to more significant deleterious PE tamponade effects in dogs with increased LA pressures treated for CHF and unrelated PE? Similarly with PDEi’s used to treat pre capillary PHT and unrelated PE?
Comments
Hi!
This is an academic question and – as far as I know – there are no studies addressing any of these questions. First of all, Doppler-derived gradients of TI or PI give you a rough estimate about pressures, but not about pulmonary vascular resistance which also influences trans pulmonary flow (not only pressures).
Theoretically, any disease causing increased RA pressures will theoretically decrease the risk of tamponade. If you add drugs which are supposed to decrease vascular resistance in a case with decreased forward output (e.g. Mitral valve Disease, DCM, also precapillary PHT), forward flow will increase and pressures will not really drop. This has been shown for instance in MVD dogs and amlodipine (decrease in volume overload, no decrease in blood pressure) and very likely also applies to PHT in case it is pre-capillary (increase in left heart size, relatively minimal disease in measurable TI gradients). I think the effect of ACE in dogs is rather minimal, if given as single medication and I do not think it really influences central venous pressures.
Also, I have never seen a dog with congestive PE and pericardial tamponade. In my experience, tamponade is usually combined with inflammatory, neoplastic or idiopathic PE.
Hope this helps
Best wishes,
Peter
Thanks! I have a Dog with a heart base mass and PE with only mild diastolic RA collapse.. I suspect the mild PHT noted is a left sided cause. LA pressures are high with a restrictive MV inflow pattern , LV systolic function decreased ( all possibly related to neoplasia) being managed with Pimo and a low dose furosemide( CHF). Clinically doing well now but was going to add on ACEi at standard dose as per Dr.L. I understand the issues with lasix and PE but was wondering about ACE i in a situation like this one in terms of tweaking meds. Wasn’t sure if mild PHT could/was having a positive affect on the PE and ACEi could affect that to any degree. Regardless, I guess centesis would always be an immediate at least temporary resolution should a clinically sig.PE develop. Just wondering how these heart issues and drugs used would all interact together..