Wednesday, September 22, 2010
Hospital management of acute decompensated heart failure---odds and ends from the Tutorials in the Tetons 36th Annual Update in Cardiovascular Disease
I know this is a little late to be blogging on a session which was held August 14. This topic was too complex and nuanced to live blog or tweet, and life has been very busy since my return home from this meeting. Besides that I needed time to go and check out some primary sources.
Anyway, on August 14 John O'Connell, MD, executive director of the heart failure program at St. Joseph's Heart and Vascular Institute in Atlanta discussed some recent evidence on acute decompensated heart failure (ADHF).
First an observation of my own. Speakers on this topic are fond of saying that, in contrast to the long term management of heart failure, there's practically no evidence to guide us in the management of ADHF. Although that's not entirely true (see here and here) the recommendations for ADHF in the 2009 Focused Update for the ACCF/AHA heart failure guidelines are based largely on expert opinion (level C). 76% of the recommendations were level C, 19% were level B (single small RCT) and only 5% are considered based on high level evidence (level A).
According to Dr. O'Connell's update there has been little in the way of new evidence to change practice, as most recent trial results in ADHF have been negative or inconclusive.
Here are some highlights:
ASCEND HF, underway now and estimated to be completed at the end of this year, is a large RCT of nesiritide versus placebo, both alongside standard heart failure treatment. Major clinical outcomes will be recorded and it is hoped that this will put to rest the controversy that has surrounded nesiritide the last several years.
In EVEREST (reported in these two papers) several soft short term outcomes but not major clinical outcomes (mortality or heart failure related morbidity) were improved by the vasopressin antagonist tolvaptan. Accordingly, the FDA has approved it only for euvolemic hyponatremia.
The use of loop diuretics, though tried and true in the management of ADHF, is supported mainly by tradition and expert opinion. Two studies reported this year compared dosing strategies (comparative effectiveness studies, get that?!). This study found no difference in short term outcomes between bolus and continuous infusion dosing at equivalent doses of furosemide. DOSE, looking at high dose versus low dose furosemide both in continuous and bolus dosing forms, presented at ACC 2010, found no difference in the primary outcome which was a global clinical assessment. Secondary endpoints in the high dose group (dyspnea, fluid loss and biomarker levels) were improved at 72 hours at the price of more renal deterioration but that was transient. All in all there seems to be little difference in dosing strategies and we may have little to guide us that's any better than Samuel Shem's rule: Lasix dose=age+BUN or the old adage that we give the patient “enough.”
Dr. O'Connell reminded the audience that loop diuretics have some negative consequences. At the same time a brisk diuresis ensues an acute fall in GFR occurs. However, the relationship between diuresis and worsening renal function, as well as the pathophysiology of the cardiorenal syndrome, are complex. One fascinating paper he cited from last year sought to determine the factors causing decreased renal function during diuresis for acute heart failure. Only high CVP readings at the beginning and end of hospital treatment predicted worsening renal function. So venous congestion in the kidney may be more important than decreased cardiac output. To the extent this is true one would expect better renal outcomes with more aggressive fluid removal.
A related issue is the use of ultrafiltration (UF) in the treatment of ADHF. The UNLOAD trial (a comparative effectiveness study conducted before comparative effectiveness research was a catch phrase) showed superiority of ultrafiltration over standard loop diuretic therapy for weight loss, net fluid removal and 90 day readmissions. Why? There are several likely reasons. UF addresses refractoriness to loop diuretics. A diuretic holiday allows reversal of renal epithelial cell changes induced by the loop diuretic. Also, loop diuretics remove approximately one third normal saline, as observation of the common appearance of “lasix urine” will attest. UF on the other hand removes isotonic fluid.
Dr. O'Connell concluded his talk and commented in the Q&A on the vexing problem of readmissions. He expressed some reservations when I asked him specifically about the effects of the hospitalist model. He listed some key objectives to be met in every ADHF admission:
1) Achieve adequate fluid removal---in other words, completely decongest the patient. Many heart failure patients are discharged before this is accomplished.
2) Initiate life prolonging neurohumoral antagonists.
3) Assess the patient for candidacy for evidence based invasive therapies such as device or revascularization therapies.
4) Educate the patient.
5) Arrange for continuity with post hospital care. Initiation of neurohumoral antagonists is not enough. They need to be sequentially added and titrated to evidence based goals in a timely manner, and this is primarily done in the out patient setting.
The hospitalist model, with its fragmentation of care and its agenda to discharge patients more quickly, may be adverse to goals 1, 3 and 5.