Cardiovascular drugs: implications for dental practice part 1 - cardiotonics, diuretics, and vasodilators

Abstract

Appropriate preoperative assessment of dental patients should always include analysis of their medications. Cardiovascular diseases are the most common group of medical disorders that dentists encounter, and the number of drugs prescribed for managing these conditions is staggering. This justifiably raises concern and probable confusion regarding side effects and possible drug interactions with medications the dentist may deem necessary for dental care. This continuing education article is the first in a series that will address essential pharmacology of medications commonly prescribed for chronic medical care. A reasonable understanding of these agents will allow the dentist to better appreciate the medical status of their patients and avoid adverse interactions with drugs they might administer or prescribe.

Figure 1

Influences provided by vasodilators. Cardiac output is the principal determinant of systolic pressure while arterial resistance determines diastolic pressure. Venous dilation reduces venous return and subsequent cardiac output, while arterial dilation reduces arterial resistance. This accounts for the value of vasodilation in managing hypertension. In contrast, benefits for managing coronary artery disease (CAD) and congestive heart failure (CHF) relate to reducing stresses on the heart—preload and afterload. Preload (venous return) is a stress factor during diastole, and afterload (arterial resistance) stresses the heart during systole.

Figure 2

Renin angiotensin pathway. Angiotensinogen is a protein synthesized in the liver and released into the blood stream. Renin, an enzyme released by the juxtaglomerular cells, converts angiotensinogen to the inactive precursor, angiotensin I. Angiotensin-converting enzyme (ACE), found primarily on vascular endothelium, converts angiotensin I to the active molecule, angiotensin II. Angiotensin II is a potent vasoconstrictor, and also stimulates aldosterone release from the adrenal cortex. This increases sodium and water reabsorption in the kidney. ACE inhibitors limit the conversion of angiotensin I to angiotensin II and therefore act as vasodilators and also diminish sodium and water retention. These same effects can be produced by angiotensin-receptor blockers (ARBs) that act as antagonists at angiotensin II receptors on target tissues.