...Though not very frequently. A lot of the doctors look upon it as "expensive nitroglycerin," so refuse to use it (COSTS $570 per bag). Have only seen it a few times since introduced.
According to the information sheet provided to us from the drug rep, Natrecor is indicated for the intraveous treatment of patients with acutely decompensated congestive heart failure who have dyspnea at rest or with minimal activity. It reduces PCWP and dyspnea. Natrecor should be avoided in patients with cardiogenic shock or in patients with a systolic BP < 90, or pts known to have low cardiac filling pressures.
This is a quote from a pertinent article, More Than a Pump: The Endocrine Functions of the Heart:
The heart is an endocrine organ. Two of the hormones it produces are atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). BNP was first discovered in animal brain tissue, a fact that accounts for its name, even though the peptide is generated by the heart. ANP is made in several body sites but is present in greatest abundance in the granules of myocytes in the atria of the heart. BNP is present in ventricular muscle tissue. ANP and BNP are made up of chains of 28 and 32 amino acids, respectively, that bind to receptor sites. Receptor sites for these hormones are present in all tissue types but are most prevalent in the heart, blood vessels, adrenal glands, kidneys, lungs, and central nervous system.1
Atrial Natriuretic Peptide
When natriuretic hormones bind to receptors in the microvasculature of the kidney, urinary output is increased because sodium transport in the collecting ducts of the kidney is inhibited.2 ANP also blocks sodium reabsorption induced by angiotensin. Natriuretic peptides are considered counterbalances to neurohormones such as angiotensin, epinephrine, and endothelin.3 The renin-angiotensin-aldosterone cascade is blunted by the release of ANP, which diminishes the secretion of both renin and aldosterone.4
In the cardiovascular system, ANP decreases heart rate and preload and promotes venodilatation and arterial relaxation. When activated in arteries and veins, ANP causes pronounced vasodilatation by promoting guanylyl cyclase activity. Guanylyl cyclase then triggers the production of cyclic guanosine monophosphate, which leads to smooth muscle relaxation.5 The dilatation that occurs shifts fluids from the heart into the vessels. ANP appears to decrease heart rate by augmenting the action of the vagus nerve.
Natriuretic peptides also apparently inhibit ventricular hypertrophy, decreasing the production of cardiac fibroblasts and smooth muscle cells in cases of cardiac wall stress. Natriuretic peptides have an antiproliferative effect on ventricular remodeling.3"
SOOO... The hormone BNP in Natrecor counteracts aldosterone and the body.... Effect is diruesis and natraesis (release of sodium from the body), resulting in lower BP. Due to this antagonist effect on aldosterone, natrecor may affect renal function in susceptible individuals. In pts with severe heart failure whose renal function may depend on the activity of the renin-angiotensisn-aldosterone system, treatment with Natrecor may be associated with azotemia. BNP also binds to cyclic GMP receptors in vascular smooth muscle cells, acting as a second messenger to dilate veins and arteries (hence, like nitroglycerin). In one test, Natrecor was more effective in lowering PCWP than nitroglycerin. Natrecor, as per the above article, also inhibits ventricular hypertrophy, helping to prevent ventricular remoldeling (similar to an ACE).
Natrecor may cause hypotension. Therefore, blood pressure should be monitored closely during infusion. Symptomatic hypotension occurs in 4% of patients and asymptomatic hypotension rate is 8%.
Natrecor may affect renal function in susceptibel patients--increased risk of elevated creatinine. Other listed side effects are ventricular tachycardia (3%), non-sustained v-tach (3%), headache (8%), abdominal pain (1%), and nausea (4%).
Recommended starting dose is a bolus of 2 mcg/kg over 60 seconds, followed by a continuous infusion of 0.01mcg/kg/minute.
Natrecor is INCOMPATIBLE with heparin, insulin, ethacrynate sodium, bumetanide, enalaprilat, hydralazine, and furosemide, and the preservative sodium metabisulfite. Natrecor binds to heparin and therefore could bind to the heparin lining of a heparin-coated catheter, decreasing the amount of Natrecor delivered to the patient for some period of time. Therefore, Natrecor must not be administered through a central heparin-coated catheter.
Hope this helps
. In answer to your question on safety, we only administer this medication in our ICU unit (2:1 pt ratios) or cardiac stepdown (4:1). These patients require constant EKG monitoring and q15 minute BP's (at least to start...). So, any higher patient ratios than this (IMHO) is UNSAFE.