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Cardiovascular Pharmacology Concepts

Richard E. Klabunde, PhD

Clinical Disorders:

Therapeutic Classes:

Mechanism Classes:


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Vasoconstrictor Drugs

Therapeutic Use and Rationale

As the name implies, vasoconstrictor drugs contract the smooth muscle in blood vessels, which causes the vessels to constrict. Constriction of arterial (resistance) vessels increases systemic vascular resistance, which leads to an increase in arterial blood pressure because mean arterial pressure is determined by the product of systemic vascular resistance and cardiac output.. Constriction of venous (capacitance) vessels increases venous blood pressure and increases cardiac preload and cardiac output by the Frank-Starling mechanism, which increases arterial pressure. Because vasoconstrictor drugs increase arterial pressure, they comprise a functional group of drugs known as pressor drugs.

Hypotension, which is a systolic pressure of less than 90 mmHg or a diastolic pressure less than 60 mmHg, needs to be aggressively treated because blood flow to critical organs, particularly the brain, heart and kidneys may become compromised to an extent that organ failure and death occur. Although vasoconstrictors can elevate arterial pressure, there is a drawback to their use. Unless cardiac output is increased at the same time systemic vascular resistance is increased, blood flow to some organs may actually decrease. The reason for this is that if the vascular resistance of an organ increases, for example, by 30% and mean arterial pressure increases by 30%, the organ blood flow will not change. If on the other hand, resistance is increased in some organs by 50%, and in others by only 10%, yet the arterial pressure is increased by 30%, blood flow will be increased to those organs that had the smaller increase in resistance because arterial pressure increased more than their resistance. This is precisely how pressor drugs can have a benefit in treating hypotension. Although blood flow may be reduced in some organs (e.g., to the splanchnic and muscle circulations), blood flow to critical organs (e.g., brain, heart and kidneys) may actually increase. Part of this benefit may be lost if systemic vascular resistance is increased too much with a pressor drug, especially if the hypotension is caused by cardiogenic shock, because the increase in ventricular afterload will reduce cardiac output. For a greater understanding of the hemodynamics associated with regional vasoconstriction, the reader is encouraged to read about the significance of the parallel arrangement of vascular beds in the body.

Drug Classes, General Mechanisms of Action, and Contraindications

There are two general functional classes of vasoconstrictors based on their mechanism of action that are used in the treatment of hypotension. The first class is sympathomimetic drugs that have alpha-adrenoceptor agonist (α-agonist) properties. Although many sympathomimetics possess other mechanisms that contribute to their pressor effects (e.g., β1-adrenoceptor agonist activity), a common property of several of these these drugs is that they bind to α1-adrenoceptors on vascular smooth muscle thereby promoting smooth muscle contraction. A second class of vasoconstrictor (non-sympathomimetic) that has been utilized increasingly in recent years is vasopressin analogs. These drugs are a synthetic form of the naturally occurring hormone (vasopressin or antidiuretic hormone) that is released by the posterior pituitary. These drugs possess both both vasoconstrictor and antidiuretic properties, both of which contribute to elevating arterial pressure.

Alpha1-agonists produce systemic vasoconstriction, which increases the work of the heart. If the coronary circulation is impaired, as in patients with coronary artery disease, the resulting decrease in myocardial oxygen supply/demand ratio can precipitate angina. Likewise, AVP can produce a powerful vasoconstrictor response, and therefore should be administered cautiously to patients with coronary artery disease because it constricts coronary arteries (thereby reducing oxygen delivery) and increases myocardial oxygen demand by increasing afterload on the heart.

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Revised 03/15/07

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.