[HSF] RV failure management strategies

[Salerno, Tomas]

Prevention is the key word for the development of RV failure during surgery. All myocardial protective strategies do not afford full protection to the RV (and neither to the LV), which is subjected to warmer temperatures of the environment and poor deliver of cardioplegia. And most surgeons, who rely on cold cardioplegia, do not even measure myocardial temperatures!   Continuous perfusion (beating heart surgery, as I have described) avoids this problem all together.
 
RV failure in the face of AVR should be suspicious of occlusion (for a variety of reasons) of the RCA, and in previous reports, we recommended bypassing that artery should the situation occur for unexplained reasons.
 
Nothing worse that a poorly protected RV in face of pulmonary hypertension. Treatment after the injury has occurred usually results in poor outcome.  

________________________________

From: openheart-l-bounces at lists.hsforum.com on behalf of Tea Acuff
Sent: Thu 11/30/2006 10:24 PM
To: OpenHeart-L at lists.hsforum.com
Subject: Re: [HSF] RV failure management strategies



It seems to me that proper treatment of RV failure likely depends on its etiology and is largely unrelated to RV effects itself. I am of the belief that acute ischemic RV failure is a contradiction for almost any indication of LV revascularization. The treatment is volume to the LV which is in turn deadly to the ischemic LV. I used the Amed device, which unfortunately got pushed into the Embolex venture for economic and ultimately fatal device reasons, for about 50 OPCABs and was impressed in its small size and 50-60cc internal volume in supporting CO in the contorted RV even when the LV was not working. RVs unlike LVs do seem to have the capacity to recover if LV filling can be maintained in the ischemic/ failing R ventricle. Fontan physiology seems to suggest the same argument. I don't know if models of primary RV failure exist as isolated RV and even RV valvular problems are rare. Almost all surgical treatments of the LV temporarily worsen the resistance to flow faced by
 the RV except if the LV can be markedly improved. In other words I think the question itself is largely misstated. Kind of like asking how can one get better pacing when the patients is in electromechanical dissociation (to use old descriptives.) 
This kind of BS reasoning is one looking for counter arguments (and better understanding).
Tea


----- Original Message ----
From: prasannasimha <prasannasimha at gmail.com>
To: "OpenHeart-L at lists.hsforum.com" <OpenHeart-L at lists.hsforum.com>; ccm <ccm-l at ccm-l.org>
Sent: Thursday, November 30, 2006 8:40:26 PM
Subject: [HSF] RV failure management strategies


Can the list members enumerate their management strategies for RV failure.
This is for two reasons. _ one for th3e Wiki and presently
I have  a patient who was in low output  and taken for a semi emergency
MVR with maze with TV plasty. Patient had RV dysfunction and congestive
hepatopathy. Had a difficult wean - LV good but RV function was pretty
poor. Patient is in coagulopathy which seems to have decreased .No
mechanical problem on epicardial echo.
Patient has an open chest and has adequate CI (PA cath with CCO) has a
high PVR and low SVR and is requiring multiple inotropes (Dopa = Dobut
+Adrenaline + Norad +Milrinone and Vasopressin on one hand and multiple
vasodilators on the other (getting constrictors via the central lumen of
the IABP and dilators via the PA catheter) . I put the IABP as the
patient has OK CI but low pressures due to a vasoplegic state and was
worried that the coronary flow may not be adequate creating a vicious
spiral 9and is helping in maintaining pressures).
Funny thing is patient has bilateral dilated and fixed pupils but has
actually woken up once !! (On an infusion of morphine + Ketamine)
Prasanna
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