Dental Management of Patients with Hypertension
J. Bruce Bavitz, DMD, FACD
Department of Surgical Specialties, University of Nebraska Medical Center, College of Dentistry, 40th and Holdrege, Lincoln, NE 68583-0757, USA
Surprisingly, there is little if any data to indicate that treating a patient with hypertension alone increases the risk for adverseoutcomes or complications. Most dentists, however, realize that hypertension often leads to cardiovascular disease, renal disease, and strokes, which are conditions that increase the risk for complications, both during and after dental care. Oral and systemic side eﬀects may also arise from the medicines used to treat hypertensive patients. This article reviews the current thought on the pathogenesis,diagnosis, and treatment of hypertension, and provides guidance on how best to treat patients with this common medical problem.
Physiology Blood pressure (BP) is determined by how much blood the heart pumps (ie, cardiac output) and by the resistance to blood ﬂow in the vascular system. Cardiac output in turn is determined by how often the pump contracts (ie, heart rate) and by the amount ofblood ejected during each beat (ie, stroke volume). High blood pressure, therefore, results from either narrow inﬂexible arteries, an elevated heart rate, increased blood volume, more forceful contractions, or any combination of the above. BP is never constant; it peaks right after the ventricles contract (systole) and reaches its low point as the ventricles ﬁll (diastole). Mean arterial pressure(MAP) is calculated by multiplying the diastolic BP by two, adding the systolic BP, and dividing by three. Diastolic BP is multiplied by two as, on average, the heart spends roughly twice the amount of time in diastole as in systole. The long-term regulation of BP is controlled predominantly by the kidneys through their variable release of the enzyme renin. Renin goes on to
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cleave angiotensinogen to angiotensin 1, which is converted by angiotensin converting enzyme (ACE) to angiotensin 2. Angiotensin 2 causes vasoconstriction (ie, elevated vascular resistance) and stimulates the release of aldosterone, anenzyme that increases sodium resorption in the kidney. Increased sodium resorption raises blood volume, again elevating the BP. In response to fear (such as impending extraction), exercise, and other environmental stimuli, the autonomic nervous system (ANS) activates its ‘‘ﬁght or ﬂight’’ response and can, within seconds, raise the blood pressure. The sympathetic arm of the ANS releases norepinephrine,which acts on the beta-1 receptors of the heart to increase the rate and force of contractions. This is the positive chronotropic and inotropic eﬀect. Norepinephrine release also triggers the alpha-1 receptors on the vasculature to initiate vasoconstriction, again raising pressure. In summary, over a given day or week, MAP readings are primarily under control of the kidneys, while fear and stresscan provoke the ANS to quickly and dramatically raise values. Interestingly, some patients respond to severe psychologic stress (such as a dental injection) by ﬁrst activating the sympathetic arm of the ANS, but then have an exaggerated parasympathetic response. The acetylcholine transmitter of the parasympathetic system causes the heart to slow, leading to a dramatic fall in BP and a resultantsyncopal event, such as fainting. These patients usually regain consciousness after being placed in a supine position.
Diagnosis Many common medical conditions now have guidelines to aid in their diagnosis and treatment. These guidelines are typically formulated by recognized experts from multiple disciplines. In 2003, the National High Blood Pressure Education Program promulgated their latest...