Systemic Hypertension
Essentials of Diagnosis
- Prehypertension: systolic pressure of 120–139 mm Hg or diastolic pressure of 80–90 mm Hg.
- Stage 1 hypertension: systolic pressure of 140–159 mm Hg or diastolic pressure of 90–99 mm Hg.
- Stage 2 hypertension: systolic pressure of 160 mm Hg or diastolic pressure of 100 mm Hg.
- Measure on three separate occasions.
- In diabetic patients, diastolic pressure > 80 mm Hg, systolic pressure > 130 mm Hg, or both, on three separate occasions.
General Considerations
Hypertension is a major modifiable risk factor for cardiovascular disease that can, if untreated, result in serious morbidity and mortality from cardiac, cerebrovascular, vascular, and renal disease. In excess of 62 million persons in the United States are estimated to have hypertension, and only about 70% of these individuals are aware of their diagnosis. Of those, only a third are at their therapeutic goal. The potential for death and disability is therefore quite high and represents a serious public health issue. Once the diagnosis of hypertension is made and therapy instituted, elevated blood pressure can be lowered, reducing the risk of cardiovascular disease in most patients. Major antihypertensive trials, in large populations, have conclusively demonstrated that there is a direct continuous relationship between the level of blood pressure and cardiovascular morbidity and mortality. These studies have shown that treating all levels of hypertension significantly decreases fatal and nonfatal stroke, coronary events, heart failure, and chronic kidney disease and renal failure. The wide array of antihypertensive agents is very effective in reducing blood pressure. Despite similar blood pressure and overall mortality reductions, the reductions in incidence of stroke, coronary ischemic events, heart failure, and renal failure are not the same for all classes of antihypertensive agents. The reasons for these differences have not been totally explained and are the topic of much speculation.
A growing body of direct and inferential evidence suggests that reduction of blood pressure should not be the only goal of antihypertensive therapy. Therapy should also be directed toward controlling all of the patient’s modifiable cardiovascular risk factors, including dyslipidemia, smoking, obesity, physical inactivity, microalbuminuria, and diabetes mellitus.
Pathophysiology & Etiology
Until recently, high blood pressure was synonymous with hypertension; now, however, data suggest that there is considerably more to hypertension than increased blood pressure. Several metabolic and functional abnormalities have even been observed in the children of hypertensive patients prior to blood pressure elevation that are similar to, but of a lesser magnitude than, those found in their parents. Hypertension is also associated with insulin resistance and glucose intolerance. Insulin levels are consistently higher in hypertensive patients than in normotensive persons. Hyperinsulinemia is worsened by thiazide diuretics, especially in the presence of -blocker therapy. Hyperinsulinemia produces a proliferation of vascular smooth muscle and fibrous tissue and adversely affects the serum lipid profile.
Renin and angiotensin levels are also important factors in determining both the response to therapy and the prognosis. Hypertensive patients with high renin levels have a greater incidence of myocardial infarction than do similar patients with lower levels. Normotensive young adults with a family history of hypertension have been found to have thicker left ventricular (LV) walls and alterations of LV diastolic filling in comparison with control subjects. Although not frankly abnormal, these latter two findings are similar to but less severe than those observed in hypertensive patients. Renal reserve also appears diminished in the children of hypertensive parents. LV hypertrophy, a direct result of hypertension, is twice as prevalent in patients with prehypertension than in normotensive persons, demonstrating target organ effects of blood pressures that were previously thought to be normal. Hypertension, therefore, is a multisystem disorder with involvement of the cardiovascular, neuroendocrine, and renal systems with a strong genetic component.
Natural History
Blood pressure gradually increases throughout childhood and adolescence. The best predictor of the level of future blood pressure is the relative level of blood pressure of a child in relation to his or her peers. During childhood and adolescence, body weight is a major determinant of blood pressure, with heavier children having higher blood pressures. High blood pressure is uncommon under the age of 20; if present, it is usually associated with renal insufficiency, renal artery stenosis, or coarctation of the aorta. The initial presentation of high blood pressure usually occurs in the third to the sixth decade, and blood pressure may fluctuate significantly during the early course of the disease. The prevalence of hypertension increases with age and is greater in men than women. In the elderly population, the gender distribution reverses, and more women than men have high blood pressure. More than 50% of the US population age 60–69 years and 75% of those 70 years or older have hypertension.
Large epidemiologic and intervention trials have clearly defined the risks of elevations of blood pressure and the benefits of treatment. Evidence of target organ damage has been demonstrated at lower levels of blood pressure than was previously known. As a result, the definition of hypertension has been revised. The new definition includes a new classification of prehypertension, which is thought to identify individuals at increased risk for hypertension and therefore require closer follow-up. Everyone should be screened for the presence of high blood pressure; testing should be done routinely in the physician’s office or at one of the larger community screening activities.
These activities are typically targeted at those at greater risk for high blood pressure: older individuals, individuals with previously high-normal blood pressures (prehypertension), blacks, sedentary individuals, and those with a family history of hypertension.
Ethnic and Socioeconomic Factors
Blacks have both an earlier onset and a greater prevalence of high blood pressure than do whites, Asians, and Native Americans at all ages. Over the age of 50 years, hypertension is prevalent in more than 40% of black males, compared with approximately 27% in white males. Severe high blood pressure (diastolic blood pressure at least 115 mm Hg) is five times more common in black men than in white men and seven times more common in black women than in white women. Blacks therefore tend to have more serious complications, especially strokes, from high blood pressure. Other factors also affect the prevalence of high blood pressure. Among all ethnic groups, less-educated individuals have a greater prevalence of high blood pressure than do more highly educated individuals, especially in lower socioeconomic groups.
The level of blood pressure elevation is directly related to total cardiovascular risk, and the presence of other cardiovascular disease risk factors, especially diabetes or dyslipidemia, is synergistic with high blood pressure.
Clinical Findings
Blood pressure is a continuous variable with a reasonably normal, or bell-shaped-curve, distribution across the general population. The higher the blood pressure, the greater the risk of a cardiovascular event; conversely, the lower the blood pressure, the lower the cardiovascular risk. It is important to stress that isolated systolic hypertension, a systolic pressure of greater than 140 mm Hg with a diastolic pressure of less than 90 mm Hg, is abnormal and requires attention.
The diagnosis of hypertension should not be based on measurements taken at a single office visit. Elevated readings should be confirmed at a second or third visit to establish the diagnosis, and any factors that might elevate blood pressure should be excluded. The patient should refrain from smoking for at least 30 minutes prior to blood pressure measurement. The blood pressure should be measured, with a cuff of the appropriate size, after at least 5 minutes of rest in a seated or supine position. The cuff should cover approximately one-third of the length of the upper arm and should completely or almost completely encircle the arm. Too small a cuff may overestimate the true blood pressure because it may only partially compress the artery, requiring a higher pressure for total occlusion. The measurements should be made twice in both arms, for a total of four measures. The average of the two measurements in the arm with the higher values is used as the baseline value of blood pressure. Systolic blood pressure is indicated by the phase 1 Korotkoff sound (onset) and diastolic pressure by phase 5, or disappearance, in adults. In children, phase 4, or muffling, has been suggested as the best indicator of diastolic pressure.
The blood pressure obtained in the physician’s office, however, does not always accurately represent that experienced by the patient during routine daily living. About 20–30% of patients with mildly elevated office blood pressure may have a hyperadrenergic response to having their blood pressure measured. This hyperreactivity is called white-coat, pseudo-, or office hypertension and may be related to anxiety from merely being in the physician’s office or clinic. If the blood pressure is measured in a non-threatening situation by a friend or relative or with an automated device, the blood pressure in these individuals may be normal. Blood pressure hyperreactivity should be suspected in patients who have persistently elevated blood pressure in the office and normal pressure measurements out of the office or in patients who have hypotensive symptoms but remain hypertensive in the office despite therapy. It has not been clearly established whether the blood pressure in these individuals is truly normal or whether they have an early or different form of hypertension. Several studies have found alterations in cardiac structure and function that are somewhere between those found in normotensive subjects and those found in hypertensive patients. No large outcome studies are available.
The best way to evaluate a patient with suspected white-coat hypertension is to use an automated ambulatory blood pressure device that measures the blood pressure periodically throughout the day and night. The patient quickly becomes accustomed to the small, light-weight, portable device, and a representative series of recordings can be obtained. The accuracy of these devices allows separation of those patients with true elevations of blood pressure from those who are hyperreactors. The devices are also useful in evaluating patients with episodic hypertension and those with borderline blood pressure elevations who already have evidence of involvement of the heart, kidneys, or vasculature. Automated blood pressure monitoring can be used to evaluate the duration and effectiveness of antihypertensive medication; correlate blood pressure with damage to the heart, kidneys, or blood vessels; and determine the prognosis. Its value in routine evaluation of hypertensive patients has not been clearly established, however.
Initial Evaluation
The initial evaluation should be focused on excluding secondary or reversible causes of hypertension and looking for the presence and severity of organ damage caused by hypertension. A reversible cause for high blood pressure is found in less than 5% of adult patients. The causes of secondary hypertension include renovascular, chronic kidney disease, coarctation of the aorta, pheochromocytoma, obstructive uropathy, primary hyperaldosteronism, Cushing syndrome, obstructive sleep apnea, and thyroid or parathyroid disease. Signs of a secondary cause are frequently present and should be looked for in the patient’s history, the screening physical examination, blood chemistries, and urinalysis. A more exhaustive evaluation for a secondary cause is needed for patients whose blood pressure is difficult to control medically, who have malignant hypertension, or who have a sudden onset of high blood pressure.
Most patients with mild-to-moderate hypertension are asymptomatic. A careful history should be obtained, including first-degree relatives (siblings, parents, children, aunts, uncles) with high blood pressure, stroke, coronary artery disease, or diabetes; any knowledge or personal history of high blood pressure; smoking; alcohol consumption; and history of headache, sweats, palpitations, and pallor. Alcohol consumption can cause acute elevations of blood pressure; long-term consumption can cause sustained elevations. A complete evaluation of all prescription and nonprescription medications the patient is taking should be done to exclude any possible contribution to the elevation or any interaction that might limit a given drug’s antihypertensive effects. In particular, the clinician should ask about use of estrogens, nonsteroidal antiinflammatory agents, and decongestants. Approximately 5% of women taking oral contraceptives have elevations of blood pressure; these usually resolve when the medication is discontinued. This side effect of oral contraceptives is more common in women over the age of 35 and in the presence of obesity; the use of low-dose estrogen oral contraceptives greatly reduces the incidence. Nonsteroidal antiinflammatory agents may cause hypertension or antagonize the antihypertensive effects of medications, especially angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). Any previous antihypertensive medication use should be documented as well as the blood pressure response and side effects.
Physical Examination
The physical findings suggestive of secondary or potentially reversible high blood pressure include abdominal or flank bruits suggestive of renovascular hypertension; absent or diminished femoral pulses suggestive of aortic coarctation; and flank or abdominal masses suggestive of polycystic renal disease or abdominal aortic aneurysm. Careful evaluation for target organ damage from hypertension should include funduscopic examination for arteriovenous nicking, arteriolar narrowing, hemorrhages, exudates, or papilledema; and cardiac examination for signs of heart failure (S3 or a laterally displaced LV apical impulse), LV hypertrophy (S4 or a sustained LV apical impulse). The patient should also be examined for any neurologic deficit compatible with stroke.
Diagnostic Studies
Clinical laboratory tests should be performed to screen for occult renal or cardiac disease that might contribute to the elevation of blood pressure and to assess overall cardiovascular risk. The complete blood count might demonstrate the presence of anemia, suggesting chronic renal disease. Urinalysis is a good screening tool for occult renal disease, diabetes, renal protein loss, or abnormal sediment. All hypertensive diabetic patients and patients with moderate to severe hypertension should be tested for microalbuminuria. Levels of serum electrolytes; blood urea nitrogen; creatinine; fasting blood glucose; hemoglobin A1c; total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol; triglycerides; calcium; uric acid; and magnesium provide information on other potential cardiovascular risk factors and also establish a baseline for the effects of drug therapy.
Electrocardiography
Although not a particularly sensitive tool, an electrocardiogram (ECG) should be obtained to look for LV hypertrophy, which, if present, is an independent risk factor for cardiovascular morbidity and mortality. In hypertensive patients, this is a significant predictor of poor cardiovascular outcomes.
Chest Radiography
Chest radiography is not a routine part of the screening process for the uncomplicated cases of hypertension.
Echocardiography
This imaging method, which is much more sensitive for the presence of LV hypertrophy, should be done in selected individuals. Although the role of echocardiography as a screening tool has not been established, it is excellent for assessing the degree of LV hypertrophy and systolic functional status in hypertensive patients. Cardiac Doppler allows the assessment of LV diastolic dysfunction, which may be associated with signs and symptoms of heart failure. Borderline hypertensive patients whose echocardiograms show LV hypertrophy should probably be treated.
Organ Involvement
The main organs (target or end organs) that suffer the ravages of high blood pressure are the heart, brain, kidneys, and blood vessels. High blood pressure is an independent risk factor for coronary artery disease, and cardiac involvement is responsible for the largest portion of the increase in morbidity and mortality observed in patients with high blood pressure. Up to one-third of untreated patients with mild-to-moderate elevations of blood pressure have LV hypertrophy. Increasing LV mass is generally associated with increasing blood pressure, although patients vary greatly in the extent of hypertrophy for any given level of blood pressure. Increased LV mass also can be present in the absence of elevated blood pressure, however, and may be related to metabolic differences in hypertensive patients. The prognosis is significantly worse when LV hypertrophy is present with any amount of blood pressure elevation. Effective antihypertensive therapy will cause regression of LV hypertrophy, but it is apparent that simple reduction of blood pressure is not always sufficient to cause regression. The anticipated beneficial effects of LV mass reduction with antihypertensive therapy have yet to be convincingly demonstrated.
Atherosclerotic Complications
The most common causes of death in patients with high blood pressure are complications from atherosclerosis. These are unstable coronary syndromes characterized by angina, acute myocardial infarction, and sudden cardiac death. Large blood pressure reduction trials have shown disappointingly small decrease in the incidence of these atherosclerotic complications. When therapy is directed at reducing both blood pressure and cholesterol, the results are somewhat more encouraging—although not consistent. The addition of any of the “statins” or hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors is particularly effective in reducing acute coronary ischemic events.
Cardiac Dysfunction
Other sequelae of long-standing high blood pressure are systolic and diastolic dysfunction. Reduced systolic function may result from myocardial ischemia, infarction, fibrosis, or cardiomyopathy. Diastolic dysfunction results directly from LV hypertrophy and, even in the absence of systolic dysfunction, can cause symptoms of heart failure. It is estimated that 40–50% of patients admitted to a hospital for heart failure have preserved systolic cardiac function. This is especially prevalent in the older (> 65-years-old) population. Cardiac dysrhythmias and sudden cardiac death are also more prevalent in the presence of LV hypertrophy.
Stroke
Hypertension is the major risk factor for hemorrhagic stroke and, to a lesser extent, cerebral infarction. The level of systolic pressure is more closely related to stroke incidence than is diastolic pressure. The incidence of hemorrhagic stroke, at any raised level of systolic pressure, is significantly higher among blacks than among other groups; when stroke occurs, it also tends to be more extensive. Effective antihypertensive therapy reduces the risk of stroke to almost normotensive levels.
Hypertensive Renal Disease
Renal disease due to hypertension is characterized by nephrosclerosis with chronic renal insufficiency and ultimately renal failure. Microalbuminuria is a marker of asymptomatic renal dysfunction in hypertensive patients with renal dysfunction. The renal complications of high blood pressure can be virtually eliminated by effective antihypertensive therapy. All agents have been shown to be equally effective in their renal protective effects in nondiabetic patients. The combination of hypertension and diabetes mellitus is particularly damaging to the kidneys and causes earlier onset and more rapid progression of renal insufficiency and renal failure if untreated.
Aorta and Peripheral Blood Vessels
The aorta and peripheral blood vessels are involved in the genesis of high blood pressure and in its consequences. High blood pressure is a contributing and exacerbating factor in ascending aortic dissection and contributes to abdominal aortic aneurysm by virtue of the expansile effect of increased distending pressure. Changes in the elastic properties of the peripheral vasculature are manifest early in the course of hypertension as a decrease in arterial compliance that is related to the increase in blood pressure.
Eyes
The eyes suffer vascular damage as a result of untreated hypertension. The characteristic ocular findings of hypertensive retinopathy include arteriolar narrowing, arteriovenous nicking, flame hemorrhages, hard exudates, and papilledema-progressive changes related to increasing severity and duration of hypertension.
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