Introduction

As many as 50 million Americans have elevated blood pressure. The prevalence of high blood pressure increases with age, is greater for blacks than whites, and is greater for both races in the less educated and lower socioeconomic groups. Nonfatal and fatal cardiovascular diseases including coronary heart disease, stroke, and renal disease. Mortality increases progressively with higher levels of both systolic and diastolic blood pressures. Since hypertension is mostly asymptomatic and occurs in 20 to 40 percent of the population, it is essential the General Medical Officer (GMO) is knowledgeable on how to diagnose and treat this medical condition.

Therapeutic management relates to the severity of the blood pressure:

Hypertension should not be diagnosed on the basis of a single measurement. Initially elevated readings should be confirmed on at least two subsequent visits (unless severely elevated) over 1 to several weeks and should reflect the patient's usual levels. The following techniques are recommended:

• The patient should be seated, arm exposed, supported, and at heart level. No smoking, caffeine, or excessive exercise 30 minutes before measurement.

• Measurement should be made 5 minutes after restful adjustment to the surroundings.

• The appropriate sized cuff should be used (bladder should be at least 80 percent of the circumference of the upper arm).

• Both systolic and diastolic measurements should be made; the disappearance of sound used for the latter.

• Two or more measurements should be averaged.

The clinical evaluation of patients with confirmed hypertension should help answer the following questions:

• Does the patient have primary or secondary hypertension?

• Is target-organ disease present?

• Are cardiovascular risk factors present in addition to high blood pressure?

History, Physical Exam and Diagnostic Testing

The following is the suggested history, physical evaluation, and diagnostic testing that should be performed and recorded on the SF 600. (It is understood that not all testing modalities may be available.)

Medical History

• Note the duration of elevated blood pressure, if known.

• Note any symptoms from the elevated blood pressure.

• Note medications used to control blood pressure with any coexistent side effects, if present.

• Note any of the following risk factors:

• Smoking, diabetes, elevated lipids, alcohol use.

• Exercise history, family history of HTN.

• Rule out secondary causes with significant historical negatives:

  • Renal: history of renal trauma, infections, calculus, hematuria, proteinuria, and toxemia.

  • Pheochromocytoma: history of paroxysms of headache, hyperhidrosis, HTN pallor, and/or palpitations.

  • Cushings Syndrome: central adiposity, muscle weakness, purplish striae, amenorrhea, easy bruising, and diabetes.

  • Hyperparathyroidism: history of calcium nephrolithiasis, proximal. muscle weakness, psychiatric disturbances, abdominal symptoms.

  • Hyperthyroidism: rule out this condition. (not usually associated with HTN)

• Family history of polycystic kidney disease, collagen vascular disease, thyroid disease, parathyroid disease, and HTN.

• Medication history: include anabolic steroids, cocaine, decongestants, alcohol, licorice, tobacco, birth control pills, nonsteroidal anti-inflammatory drugs (NSAIDs), appetite suppressants, and tricyclic antidepressants.

Physical Examination

• Record height and weight.

• Note body habitus (hypercortisolism).

• Verify the blood pressure in the contralateral arm.

• Fundoscopy - grade hypertensive retinopathy, if present.

• Neck - listen for carotid bruits, look for distended neck veins.

• Heart - increase rate, size, (laterally displaced point of maximal intensity (PMI)), clicks, murmurs, heaves, and gallops.

• Lungs - rales (congestive heart failure (CHF), wheezes (avoid beta-blockers).

• Abdomen - auscultate for renal artery bruits (over flanks or to the right or left of midline just above umbilicus), masses, enlarged kidneys, aortic dilatation, decreased femoral pulses.

• Extremities - for edema, decreased peripheral pulses.

• Neurologic - for paresthesias, weakness (Diabetes mellitus, hyperthyroidism, previous cerebrovascular accident (CVA)).

Laboratory Evaluation

• Urinalysis - for protein, blood, and glucose. Microscopic for red blood cell (RBC) casts seen with glomerulonephritis.

• Hematocrit - increased in polycythemia vera, pheochromocytoma, obstructive sleep apnea, decreased in renal insufficiency.

• Blood sugar - diabetes, Cushings, pheochromocytoma, hyperaldosteronism.

• Potassium - decreased in mineralocorticoid induced HTN.

• Blood urea nitrogen (BUN) and creatinine - for renal failure.

• Total cholesterol, triglycerides, high density lipoprotein (HDL) for coexistent CAD risk.

• Calcium - for hyperparathyroidism.

• Uric acid - increased with renal disease and HTN.

• Chest x-ray (CXR) - cardiomegaly, left ventricular hypertrophy (LVH), CHF, rib notching seen in coarctation of the aorta.

• Electrocardiogram (ECG) - LVH and left atrial enlargement (LAE) of HTN, and/or previous myocardial infarction (MI).

End Organ Damage

Use your history and physical examination and screening tests to determine if end organ disease is present.

Cardiac:

• Coronary artery disease (chest pain, ECG).

• Left ventricular hypertrophy (strain on ECG).

• Left ventricular dysfunction (cardiac failure).

CVA - transient ischemic attack or stroke.

Vascular - absence of pulses, claudication, aneurysm.

Renal.

• Serum creatinine 130 umol/L.

• Proteinuria (1 + or greater).

• Microalbuminuria.

Retinopathy - hemorrhages or exudates, with or without papilledema.

Treatment

The goal is to achieve and maintain blood pressure below 140/90 mmHg.

Treatment includes pharmacologic and nonpharmacologic therapy.

• Nonpharmacologic therapy - includes weight reduction, sodium restriction (4 to 6 gm salt/day), alcohol in moderation only, tobacco avoidance, regular aerobic exercise, and decreased dietary fat.

• Pharmacologic therapy - In general, Beta-blockers and diuretics are preferred for initial pharmacologic therapy because a reduction in morbidity and mortality has been demonstrated. Angiotension converting enzyme (ACE) inhibitors, calcium channel antagonists, alpha-1 receptor blockers. The alpha-beta blockers have not been tested or shown to reduce morbidity and mortality.

If initial mono-drug therapy produces an inadequate response, increase the drug dosage, substitute another drug, or add a second drug from a different class. If the response is still not adequate consider adding a second drug or diuretic, if not already prescribed.

Special considerations in each drug class include the following:

• Initial treatment of choice for black hypertensive.

• Use judiciously in the elderly (hypovolemia causes hip fractures).

• Effect is antagonized by NSAIDS.

• Cause hypokalemia, sexual dysfunction, hyperuricemia, hyperglycemia, insulin resistance, and hypercalcemia.

• Don't use if the patient has asthma, chronic obstructive pulmonary disease (COPD), CHF, or greater than a first degree heart block.

• Use cautiously if patient on a calcium channel antagonist.

• May exacerbate symptoms of peripheral vascular disease.

• May cause fatigue, sexual dysfunction, insomnia, etc.

• Use with caution if the patient has CHF.

• Causes headaches, edema, and constipation.

• Works well in hypertensive blacks.

• Causes a dry, nonproductive cough, hyperkalemia, and angioedema.

• Can cause renal failure if the patient has bilateral renal artery stenosis.

• Contraindicated in pregnancy.

• Causes drowsiness, sedation, dry mouth, fatigue, and sexual dysfunction.

• Causes rebound hypertension with abrupt cessation.

The typical dose range for some commonly used antihypertensive medications are included in the following table:

Hypertensive emergencies or urgencies can be stabilized with:

Oral drugs.

Parenteral drugs

• Sodium nitroprusside 0.25-10 ug/kg/min.

• Hydralazine 10-20 mg.

• Nitroglycerine 5-100 ug/min.

Final notes

Avoid over aggressive treatment. Elevated blood pressure (without progressive end-organ damage) demands treatment but rarely requires emergent therapy.

References

1. The 6^th Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997; 157:2413-2444.

2. Collins R, Peto R, MacMahon S et. al. Blood Pressure, Stroke, and Coronary Disease. Part Il: Short Terrn Reductions in Blood Pressure. Lancet 1990; 335:827.

3. Croog SH, Levine S, Testa MA et. al. The Effects of Antihypertensive Therapy on the Quality of Life. NEJM, 1986;314:1657.

4. Fletcher AK, Bulpitt CJ. How Far Should Blood Pressure Be Lowered NEJM, 1992;326:251.

5. Houston MC. New Insights and New Approaches for the Treatment of Essential/ Hypertension. Am Heart J.1989;117:911. 6. MacMahon SW, Peto R, Cutler J et al. Blood Pressure, Stroke, and Coronary Heart Disease. Lancet 1990,335:765