So this brings us to the question of which IV vasoactive therapy to choose. I feel that nesiritide, a recombinant form of human B-type natriuretic peptide, has been a valuable addition to our armamentarium of IV vasoactives in the ED.
<ss="Pharmacologic Actions of Endogenous hBNP">
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As we saw earlier, the natriuretic peptides are natural counter-regulatory hormones that help to compensate for the vasoconstrictive effects of elevated RAAS and SNS activity.
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B-type natriuretic peptide, in particular, has several biologic effects that are beneficial for patients with heart failure. Endogenous human BNP increases excretion of sodium and fluids and, at the same time, increases vasodilation of veins, arteries, and coronary arteries, thus improving the cardiac performance of patients with decompensated heart failure. Endogenous hBNP also suppresses vasoconstrictive and antinatriuretic neurohormones, in addition to relaxing the heart through its lusitropic effect.
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Endogenous hBNP has antifibrotic and antiproliferative effects, which help to prevent ventricular remodeling. However, in acute heart failure, the body cannot produce enough endogenous hBNP to overcome the negative effects of the antinatriuretic and vasoconstrictive neurohormones.
<ss="Nesiritide: Recombinant Human BNP">
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Nesiritide is the recombinant form of endogenously produced human BNP (hBNP). The structure of nesiritide is identical to that of the naturally occurring B-natriuretic peptide.
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Although CHF patients have elevated circulating BNP levels, the counter-regulatory effects of endogenous BNP are not fully manifested because of loss of sensitivity to BNP due to a variety of factors. Administration of exogenous BNP (ie, nesiritide) increases circulating BNP levels by several fold, allowing the relative resistance to the effects of endogenous BNP to be overcome.
<ss="Nesiritide Safety Profile">
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The most serious side effect of nesiritide is hypotension, but as you can see here, the incidence of symptomatic hypotension was relatively low in the pivotal VMAC trial, at 4% for nesiritide and 5% for nitroglycerin. If hypotension does occur, the nesiritide dose should be reduced or discontinued, and blood pressure should be monitored closely. Nesiritide should be avoided in patients with cardiogenic shock, systolic blood pressure ^<90 mm Hg, or in patients with low cardiac filling pressures.
<ss="Nesiritide Is Not Proarrhythmic">
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An important point is that, unlike inotropes, nesiritide is not proarrhythmic. In this study, nesiritide either decreased or had a neutral effect on heart rate and ectopy (as measured by premature ventricular beats and hourly repetitive beats) over a 24-hour period of Holter monitoring. Of significant note is that this study used higher-than-standard doses of nesiritide.
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Welcome to our program on Acute Heart Failure: The Emergency Department and the Economics of Care. This is a CME-accredited program that focuses on optimizing treatment strategies in the Emergency Department in order to improve outcomes and reduce overall costs to the hospital.
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When you think about the overall hospital costs of a 5-day admission for an acute condition that often requires ICU care and invasive procedures, you don't necessarily think about the Emergency Department. After all, the patient is usually only in the ED for a few short hours, compared to the several days they will spend as an inpatient. But when it comes to treating acute heart failure, we are beginning to learn that what occurs during those critical initial hours in the Emergency Department has a direct and significant impact on overall treatment outcomes, including the length of stay as an inpatient, the utilization of expensive resources, and the likelihood of readmission to the hospital within the near term.
