HYPERTENSION

• Overview
• Table: Classification and Follow-up of Blood Pressure Measurement for Adults
• Epidemiology
• Etiology and Pathogenesis
• Clinical Presentation
• Diagnosis
• Medical Management and Treatment
• Figure: Stepped-Care Algorithm for the Treatment of Hypertension
• Table: Drugs Used in the Treatment of Hypertension
• Dental Considerations
• Reference List

Synonyms
High blood pressure

Overview
Hypertension is defined as a persistent elevation in blood pressure that is considered to be higher than normal. More specifically, the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure defines hypertension as a systolic blood pressure greater than or equal to 140 mm Hg or a diastolic blood pressure greater than or equal to 90 mm Hg as recorded during two or more readings on two or more occasions (office visits).

Classification and Follow-up of Blood Pressure Measurement for Adults Aged 18 Years or Older*

Adapted from: The Fifth Report of the Joint National Committee on Detection, Education, and Treatment of High Blood Pressure (JNC-V), Arch Intern Med 1993;153-54.

Epidemiology
It is estimated that at least 58 million Americans have, or are receiving treatment for, systemic hypertension. Primary (or essential) hypertension has no clearly identifiable etiology, and accounts for 90-95% of cases. An estimated 10-15% of white adults and 20-30% of black adults in the USA currently have primary hypertension. Between 70-90% of affected individuals have mild (stage 1 or early stage 2) primary hypertension. The age of onset of primary hypertension usually ranges between ages 25 and 55. There is no clearly defined sex predominance for the disease.

Etiology and Pathogenesis
Hypertension is classified by etiology as being either primary (essential, idiopathic) or secondary. As previously stated, primary hypertension accounts for 90-95% of cases of hypertension, while the remaining 5-10% of cases are the result of secondary hypertension.

Primary hypertension has no clearly defined etiology. Current evidence suggests the disease is caused by varying combinations of many potential interacting factors. Patients with primary hypertension do not appear to share any one, or a specific combination of, suspected etiologic factors. Some of the potential etiologic factors for primary hypertension include:

• Sympathic nervous system dysfunction and/or hyperactivity: An exaggerated response to external stimuli, or insensitivity of the baroreflexes may result in tachycardia, increased cardiac output and blood pressure.
• Renin-angiotensin system defects: Defects or abnormalities in the juxtaglomerular cell's response to various stimuli may cause excessive and/or inappropriate renin secretion and, therefore, result in elevated blood pressure.
• Sodium transport defects: An inability of the kidneys to excrete a normal sodium load results in an increased plasma volume.
• Intracellular sodium and calcium defects: Elevated intracellular sodium and calcium levels in blood cells (as a result of abnormalities in sodium/potassium exchange or other sodium transport mechanisms) may possibly explain an increase in vascular smooth muscle tone seen in hypertension.
• Other factors have been implicated as either predisposing or contributing to the development of primary hypertension. These include obesity, excessive alcohol use, cigarette smoking, excessive salt intake, stress, and physical inactivity.

No clearly established genetic pattern has been established for primary hypertension. However, blood pressure levels appear to have strong familial tendencies. Children with one (and to a greater degree two) hypertensive parent(s) tend to have higher blood pressures and are perceived to be at an increased risk to develop hypertension.

Etiologies of secondary hypertension include: renal vascular disease (atherosclerotic, thrombotic, embolic stenosis or obstruction, fibromuscular hyperplasia, etc.), parenchymal renal disease (diabetic nephropathy, connective tissue disease (systemic lupus erythematosus, scleroderma), glomerulonephritis, chronic pyelonephritis, interstitial nephritis, polycystic kidney, neoplastic renal disease, etc.), primary hyperaldosteronism, Cushing's syndrome, pheochromocytoma, hyperthyroidism, hyperparathyroidism, coarctation of the aorta, toxemia of pregnancy (preeclampsia and eclampsia), and drug use (oral contraceptives, estrogens, NSAID's, amphetamines, sympathomimetics, monoamine oxidase inhibitors, lithium, etc.).

Isolated systolic hypertension is a specific form of hypertension most commonly found in elderly individuals (especially in the seventh decade of life). It is defined as a systolic blood pressure of 140 mm Hg or more and a diastolic blood pressure of less than 90 mm Hg. The most common etiology of isolated systolic hypertension is decreased aortic distensibility (elasticity) secondary to aortic arteriosclerosis.

Complications of untreated hypertension are numerous. The degree of damage to susceptible "target" organs is closely related to both the duration and severity of the hypertension. These complications include:

• Cardiovascular disease: Hypertension is the most important etiologic factor for cardiovascular disease in the USA. Also, cardiovascular and atherosclerotic complications are the major cause of morbidity and mortality in patients with primary hypertension. In adults, systolic blood pressure elevations are usually considered to be more a determinant of cardiovascular risk than are diastolic blood pressure elevations. Hypertension accelerates the development and progression of atherosclerosis (leading to peripheral and coronary vascular insufficiency), and subsequently increases the patient's risk for myocardial infarction. Hypertension also causes left ventricular hypertrophy, which may result in congestive heart failure, ventricular arrhythmias, myocardial ischemia, and sudden death. Hypertension is a major etiology for both dissecting and atherosclerotic aortic aneurysms, and also acts as an exacerbating factor in the progression of these conditions. Retinal vascular narrowing, hemorrhages, exudates, and papilledema are also consequences of hypertension.
• Cerebrovascular disease: Hypertension increases the risk of cerebral vascular insufficiency, and is a also major cause of stroke (cerebrovascular accident), especially those resulting from intercerebral hemorrhage, cerebral infarction, or subarachnoid hemorrhage.
• Renal disease: Untreated hypertension may lead to nephrosclerosis and accounts for 40% of cases of chronic renal failure (end-stage renal disease). Hypertension may also accelerate the progression of other forms of renal disease such as diabetic nephropathy.

Clinical Presentation
Mild to moderate primary hypertension is usually asymptomatic and can remain so for many years. Some of the "early" symptoms of primary hypertension that patients may eventually experience include headaches (especially early morning, pulsating, suboccipital headaches), visual disturbances, ringing in the ears, dizziness, coldness or tingling of the extremities, and fatigue. Symptoms of severe or later stage hypertension are related to the potential cardiovascular, cerebrovascular, and renal complications of the disease.

Diagnosis
Most clinicians will perform the following in their diagnostic examination of a patient with suspected primary hypertension: a complete medical history, blood pressure measurement, ocular fundus and retinal examination, auscultation of the heart and arteries, examination of all major peripheral pulses, a complete blood count, complete urinalysis, serum creatinine, serum uric acid, electrolytes (especially potassium and calcium), blood urea nitrogen, blood glucose, a lipid panel (total cholesterol, VLDL, HDL, LDL cholesterol, and triglycerides), and an electrocardiogram. Optional or ancillary tests may include an echocardiogram, chest x-ray, plasma renin activity, plasma and urinary catecholamines and steroids (vanillymandelic acid, 17-hydroxy ketosteroids, metanephrine), renal imaging studies (sonography or angiography), and a thyroid panel.

Medical Management and Treatment
The goal of the treatment of hypertension should be to lower the patient's blood pressure to normal levels with minimal side effects. It may not be possible in all cases to reduce a patient's blood pressure to what would be considered an optimum level; it may be necessary to reduce it to a level that is as low as can be achieved using an acceptably tolerated therapeutic regimen.

Treatment of primary hypertension is most frequently accomplished pharmacologically (Table 1), although nonpharmacologic therapy may be considered for use for the management of patients categorized as having "high normal" or possibly Stage 1 hypertension. Nonpharmacologic therapy approaches for primary hypertension include weight reduction and cessation of smoking (where applicable), reduced alcohol consumption (to less than 1 oz or less per day), a regular exercise program (30 minutes at least 3 times per week), and modification of sodium intake to 2-2.5 grams per day. If the patient's blood pressure does not return to normal within 3 to 6 months after the start of nonpharmacologic therapy, then initiation of pharmacologic treatment is warranted.

The "stepped care" approach for the pharmacologic management of primary hypertension (Figure 1) has been advocated for over 20 years. Approximately 80% of patients who are compliant with their medications will obtain adequate blood pressure control using this treatment strategy.

Figure 1 - STEPPED-CARE ALGORITHM
FOR THE TREATMENT OF HYPERTENSION

Table 1. Drugs Used in the Treatment of Hypertension

Dental Considerations
Evaluation of a patient with hypertension:

Determine:

• Time of diagnosis of hypertension.
• Present medication(s) and dosage used to control hypertension as well as any recent changes or modifications to antihypertensive medication(s) or dosage.
• The presence of any systemic complications secondary to hypertension including retinopathy, nephropathy, history of cerebrovascular disease, or cardiovascular disease.

Physical and Dental Exam:

• Establish the patient's baseline blood pressure at the first dental appointment. Two to three blood pressure measurements separated by at least five minutes should be taken, and the results averaged to determine the patient's baseline blood pressure. The patient's baseline blood pressure will serve as a point of reference from which to make decisions for the emergency management of the patient should a cardiovascular or adverse reaction develop during dental treatment. The patient's blood pressure should be checked at all subsequent appointments prior to the use of a local anesthesia.

Dental Management Precautions:

• Reduce stress and anxiety during dental treatment: consider the use of N₂O-O₂ inhalation sedation and/or premedication with oral anti-anxiety medications such as benzodiazepines.
• Do not use local anesthetics with vasoconstrictors in patients with uncontrolled or poorly controlled hypertension. This is defined as any patient with a systolic blood pressure greater than or equal to 180 mmHg and/or a diastolic blood pressure greater than or equal to 100 mmHg.
• For patients with controlled hypertension, where the use of local anesthetics with vasoconstrictors is not contraindicated because of potential drug interactions, limit the total dose of vasoconstrictor to maximum of 0.04 mg of epinephrine (2.2 carpules of 2% lidocaine with 1:100,000 epinephrine) or 0.2 mg of levonordefrin (2.2 carpules of 2% carbocaine with 1:20,000 levonordefrin).

  Additional precautions:

  • Avoid the use of epinephrine-impregnated gingival retraction cord.
  • Avoid the use of vasoconstrictors for direct hemostasis to control local bleeding.
  • Avoid the use of a local anesthetic with vasoconstrictors for intraligamentary or infrabony infiltrations.
• Avoid stimulating the gag reflex in patients with a history of hypertension.

Treatment Planning Considerations:

• There are no specific treatment planning modifications or considerations for patients with controlled hypertension. No elective dental procedures should be performed on a patient with severe or uncontrolled hypertension.

Dental Drug Interactions:

• Concurrent use of local anesthetics with vasoconstrictors and non-cardioselective beta-adrenergic blockers can result in an acute elevation of blood pressure and reflex bradycardia. In patients with hypertension, a local anesthetic agent without a vasoconstrictor should be used.
• Use of a local anesthetic with a vasoconstrictor concurrently with reserpine (Serpasil), can result in a possible prolonged and/or increased effect of the vasoconstrictor. In addition, the use of norepinephrine in patients taking methyldopa (Aldomet) and guanethidine (Ismelin) may result in an increased pressor effect of norepinephrine, resulting in hypertension and an increased tendency to develop cardiac arrhythmias (guanethidine). This reaction may also occur when other vasoconstrictors (e.g., epinephrine, levonordefrin) are used concurrently with methyldopa or guanethidine.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the antihypertensive efficacy of diuretics (especially loop diuretics), beta-adrenergic blockers, ACE inhibitors, hydralazine (Apresoline), prazosin (Minipress), and selective alpha₂ agonists (to a lesser degree). The patient's blood pressure should be monitored frequently when NSAID's and these antihypertensives are used concurrently, especially if NSAID therapy is necessary longer than 5 days.
• Beta-adrenergic blockers impair the hepatic metabolism of amide local anesthetics resulting in a possible increased risk of local anesthetic toxicity with high doses. This reaction usually will not have clinical significance given the amounts of local anesthetic typically used for a single dental procedure (e.g., less than 120 mg of lidocaine or equivalent).

Insurance coding: ICD-9-CM
401.1 hypertension

Authored by F. John Firriolo, DDS, PhD

Dr. Firriolo is an Associate Professor in the Division of Oral Diagnosis and Oral Medicine at the University of Louisville, School of Dentistry.

Reference List