roja said:
Well, an EF of 15% is pretty much a kiss of death in terms of mortality. What I meant by clinical outcome numbers was, does the use of BNP significantly alter clinical outcome from the ED?
Its sort of frustrating that in the era of, "evidence based medicine," it is impossible to separate data from ego. When I sat (not too long ago) in the morning report room as a third year medical student, I endured listening to cardiologist after cardiologist bash EM physicians over the improper ordering and administration of BNP. Depending upon an individual clinician's specialty and scope of practice, BNP was viewed simultaneously as, "costly," "useless," "wonderful," and "of questionable value."
Because it is a relatively new modality receiving a great deal of press, its probably equally important to take a step back from the literature and relate the use of BNP to human physiology. From what I understand (and please correct me when I go too far off of the beaten path), BNP is an endogenous hormone that counterregulates the catecholamine and RAA cascade. Natural opposition to catecholaminergic cascade is beneficial in CHF because the patient is already in extremis. Continued hypoxemia and increasing myocardial oxygen demand further stimulates the release of catecholamines and can potentiate cardiovascular collapse and dysrhythmia. The administration of loop diuretics often activates the RAA via volume depletion and can have unintended effects. Nesiritide's intrinsic natriuretic properties work even in patients with less than optimal renal function and do not cause compensatory activation of the RAA axis. Proponents of BNP argue that cost effectivness of their drug is actualized through the potential decrease in hospital length of stay and admission. Medicare patients afflicted with CHF are over age 65 and are very likely to return to the ED within 30 days. Theoretically, adequate treatment/diuresis with nesiritide lowers the "CHF recidivism" rate and therefore reduces costs. I understand that medicare will only pay for ONE CHF exacerbation within a 30 day period.
From my interaction with attendings and sub-par understanding of the literature, it appears that BNP values have a role in the exclusion of CHF. BNP is quite sensitive above the upper limits of normal (admittedly a controversial discussion) and can assist the emergency clinician with excluding CHF in the elderly patient presenting with dyspnea. Whatever your kidney function is, a BNP value of several thousand usually indicates systolic dysfunction. Similarly, a BNP less than 100 can help to move CHF farther down the differential list. Obtaining a BNP just because someone presents with SOB is probably not the best decision. What does one do with a "moderately" elevated value found in a patient with a past medical significant for MI and CRF ?
This discussion is just plain cool because it highlights just how much the emergency physician can, "fix." I recall my paramedic days when aggressive diuresis and preload reduction could make someone "turn the corner" and stave off an intubation. Recent studies now support the use of aggressive nitroglycerin dosing and diuresis. When I encountered my first patients on the medicine wards, I was surprised at the complete lack of consensus and understanding with regard to patients in CHF. Doses of tridil infusions varied immensely, as did the dosing of PO and IV lasix. Just as the heart failure discussion has moved in the direction of expensive endogenous hormones, it has recently doubled-back into the terrain of good old oxygen. While the debate over administration of nesiritide rages on, what about the use of CPAP as a temporizing measure prior to NTI or OTI ? CPAP is inexpensive, easy to administer, and has the potential to decrease BOTH ICU admission AND endotracheal intubation.
Though this BNP learning curve is rather steep, I hope most emergency clinicians can agree that patients who are in CHF and volume overloaded will benefit from:
-aggressive nitroglycerin dosing
-adequate doses of diuretics
-decrease of myocardial oxygen demand and reduction of RAA/catecholamine cascade
Whether this is achieved through more conventional treatments or via newer modalities like nesiritide infusion is better left to residents and attendings with much more experience in the realm of CHF than myself. In the meantime, I'll continue enjoying the discussion and watching my free CD's from W. Frank Peacock, MD and the Cleveland Clinic.
