It should also be recalled that heart rate—especially influenced by antidysrhythmic medications—is also a property of hemodynamics. Drugs that affect afterload either enhance vasoconstriction or vasodilation. Vasodilators are intravenous medications that are ordered to decrease afterload on the heart by dilating arteries. The consequence of these drugs is decreased workload on the heart without decreasing contractility.
Morphine and hydralazine are administered by slow IV pushes; nitroprusside is administered by intravenous infusion with calculated doses that are titrated to blood pressure.
Nitroglycerin can be administered by a variety of routes with intravenous infusion the most easily regulated, but other routes may be sublingual, oral, or topical. Two types of side effects can be seen with hydralazine.
One is genetically based and is an immunologic response to the drug. The others are side effects typical of a vasodilator. The likelihood of the lupus-like syndrome is increased in the slow acetylator population. The tachycardia can be blocked by co-administration of beta blockers. Water and salt retention occurs as a result of the fall in blood pressure.
This problem can be alleviated by diuretics. It is also light sensitive and solutions must be protected from light. The body can buffer some of this cyanide with thiosulfate, cysteine or cystine. However, large blood concentrations or prolonged infusions of nitroprusside can overwhelm the ability to buffer the cyanide and increase the risk of cyanide poisoning.
Nesiritide is human B-type natriuretic peptide hBNP , a hormone produced by the heart ventricles. BNP is a different molecular entity than atrial natriuretic peptide ANP which is produced in heart atria. As a natural consequence of heart failure, circulating levels of endogenous BNP are elevated.
Nesiritide usage further increase these levels. Nesiritide stimulates soluble guanylate cyclase and increases vascular levels of cyclic GMP. This results in a dilation of arterial and venous smooth muscle. Hence, nesiritide is considered a balanced vasodilator. This results in a decrease in total peripheral vascular resistance, mean arterial blood pressure, pulmonary arterial blood pressure and right atrial blood pressure.
As a result, cardiac output and stroke volume are increased without an increase in heart rate. Natriuresis and diuresis also occur.
Unlike the nitrates, tolerance does not develop with this drug. Nesiritide is given by intravenous administration. It is recommended for use in decompensated congestive heart failure to produce a rapid decrease in peripheral vascular resistance and blood pressure.
This decreases pulmonary arterial blood pressure and improves the symptoms of heart failure. Recent clinical trials have suggested that Nesiritide may not be as efficacious as previously thought following the initial approval of the drug.
The major side effect associated with nesiritide is prolonged hypotension. Clinical trials have shown bisoprolol, bucindolol carvedilol and metoprolol to be effective in treating heart failure.
Cardiac glycosides are one of the oldest groups of drugs used in cardiovascular therapeutics. There is evidence of use in Egyptian and Roman times. Two active principals, digoxin and digitoxin, are now used in cardiovascular therapeutics. The uses of these drugs are in heart failure and supraventricular tachyarrhythmias.
These agents have a limited therapeutic index. Mechanism of Positive Inotropic Action. At one time cardiac glycosides were considered the mainstays of heart failure therapy.
However, with the evolution of therapeutic approaches and understanding of the disease state the status of the cardiac glycosides and usage has been altered. These drugs are now added to therapeutic regimes if necessary to provide inotropic support in patients who do not adequately respond to ACEI, AT1 blockers or beta blockers. In addition, cardiac glycosides can be used in heart failure patients who have atrial fibrillation see below for reasons.
Antiarrhythmic Actions. In addition, cardiac glycosides act at sites extrinsic to the heart to affect cardiac conduction. This is the same reflex arc that is activated when blood pressure is elevated. Therefore, there is an increase in neural traffic from the baroreceptors and carotid arch to CNS cardiovascular centers. This results in an enhanced level of vagal outflow from the CNS to the myocardium.
It also improves survival, but is associated with a relatively high frequency of side effects necessitating discontinuation of one or both agents.
The drugs are not approved by the Food and Drug Administration for the treatment of heart failure. Flosequinan, a new orally administered, long-acting, balanced arteriovenous dilator, improves exercise tolerance and symptoms. However, preliminary analysis of data from a large, multicenter trial revealed increased mortality and hospitalization for worsening CHF.
The drug has recently been withdrawn from the market.
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