All systems for categorizing high BP are somewhat arbitrary, but the current consensus is that normal BPs are < 120 mm Hg systolic and < 80 mm Hg diastolic. Borderline high BPs (prehypertension) are between 120 and 139 mm Hg systolic and 80 to 89 mm Hg diastolic. Patients with BP readings between 140/90 and 160/100 mm Hg are said to have stage 1 HTN.

Stage 2 HTN is a pressure from 160/100 to 179/109 mm Hg. Stage 3 HTN begins at 180/110 mm Hg and has no upper limit. At each stage of HTN, from prehypertensive levels through the three stages of HTN, the risks of strokes, heart attacks, and kidney failure increase. See: table

Hypertension in children has been defined as BP above the 95th percentile for age, height, and weight. As many as 28% of children have secondary HTN compared to 1% to 5% in adults.

Etiology

Hypertension results from many different conditions, some curable and others treatable. Curable forms of HTN (secondary HTN), which are relatively rare, may be caused by coarctation of the aorta, pheochromocytoma, renal artery stenosis, primary aldosteronism, and Cushing's syndrome. Excess alcohol consumption (more than two drinks daily) is a common cause of high BP; abstinence or drinking in moderation effectively lowers BP in these cases. Aortic valve stenosis, pregnancy, obesity, and the use of certain drugs (such as cocaine, amphetamines, steroids, or erythropoietin) also may lead to hypertension. Usually, however, the cause is unknown; then high BP is categorized as primary, essential, or idiopathic. Primary hypertension may result from the body's resistance to the action of insulin, hyperactivity of the sympathetic nervous system, hyperactivity of the renin-angiotensin-aldosterone system, or endothelial dysfunction.

Symptoms

Hypertension is usually a silent (asymptomatic) disease in the first few decades of its course. Because most patients are symptom-free until complications arise, they may have difficulty taking seriously a condition from which they perceive no immediate danger. Occasionally, patients with HTN report headache. When complications result from high BPs, patients mention symptoms referable to the affected organs.

Treatment

If HTN is newly diagnosed, routine studies should be done on the patient to establish a baseline for treatment. In addition to a thorough patient history, assessment for risk factors, and physical examination, these studies include an ECG, urinalysis, serum potassium and calcium levels, blood urea nitrogen, fasting glucose level, and cholesterol profile, including triglycerides. The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC) guidelines to reduce cardiovascular disease complications recommends a target blood pressure of less than 140/90; 130/80 for patients with diabetes mellitus or renal disease. Because HTN has been identified as a growing concern among children, the JNC recommends regular BP checks beginning at age 3. Lifestyle modifications that lower BP include dietary sodium restriction to about 2 g/day, made possible by avoiding salted food such as ham, potato chips, and processed foods and by not adding salt to food at the table; maintaining a healthy weight (a body mass index above 24.9 can elevate BP); eating lower-calorie foods; restricting total cholesterol and saturated fat intake; quitting smoking; limiting alcohol intake (to about one drink daily); and participating in a program of regular exercise. When lifestyle modifications fail over the course of several months to control BP naturally, medications should be used. Drug therapy for stage 1 HTN includes low-dose thiazide diuretics for most patients, although angiotensin converting enzyme (ACE) inhibitors, beta blockers, calcium channel blockers or a combination of these may be prescribed. For stage 2 HTN, two-drug combinations are prescribed for most patients, usually a thiazide-type diuretic along with a beta blocker, ACE inhibitors, angiotensin receptor blockers, alpha blockers, or centrally active alpha blocking agents. If a woman develops HTN during pregnancy, treatment should be with methyldopa, a beta blocker, or a vasodilator, as these drugs provide the least risk to the fetus. See: table pregnancy-induced hypertension

Patient care

Blood pressure should be checked at every health care visit, and patients should be informed of their BP reading and its meaning. Positive lifestyle changes should be encouraged. Adherence to medical regimens is also emphasized, and patients are advised to inform their health care providers of any side effects of therapy that they experience because these can often be managed with dosage adjustment or a change in medication. The technique of home BP monitoring is taught to receptive patients. Pressures should be measured and recorded for both arms, unless there is a medical prohibition for one arm, indicating which arm was used for each reading.

Symptoms

Symptoms usually include shortness of breath, esp. during exercise.

Treatment

The disease, when identified, may be treated with surgical removal of blood clots.

CAUTION!

CAUTION!

Etiology

The cause of PIH is unknown, but there are several major contributing theories: vasoconstriction and vasospasm, and a possible imbalance between prostaglandins, prostacyclin, and thromboxane A². The incidence is higher among adolescent and older primigravidas, diabetics, and women with pre-exisitng vascular problems or multiple pregnancies. Geographical, ethnic, racial, familial, low socioeconomic, nutritional, and immunological factors may contribute to PIH. Characteristic complaints include sudden weight gain, severe frontal headaches, and visual disturbances. Indications of increasing severity include complaints of epigastric or abdominal pain; generalized, presacral, and facial edema; oliguria; and hyperreflexia.

The treatment consists of bedrest, a high-protein diet, and medications including mild sedatives, antihypertensives, and intravenous anticoagulants if indicated. Complications are HELLP syndrome (hemolysis, elevated liver enzymes and low platelets) and eclampsia (the convulsive form of PIH).

Patient care

To enable the woman to actively participate in her health maintenance, reduce the potential for development of PIH, and facilitate early diagnosis and treatment, the health care provider should emphasize the importance of regular prenatal visits and good prenatal nutrition. Signs to report promptly are identified with the patient: sudden weight gain, swelling of the hands and face, headache, pitting edema of the ankles and legs, and reduced urine output.

At each prenatal visit, the pregnant woman's BP is monitored. The patient also is assessed for albuminuria; weekly weight gain of more than 3 lb (1.36 kg) in the second trimester or more than 1 lb (0.45 kg) in the third trimester; and generalized edema, esp. of the face and hands, and pitting edema of the ankles and legs. Protein intake is monitored to ensure adequate maternal serum protein levels, normal oncotic pressure, limitation of edema formation, and normal fetal development.

As preeclampsia progresses, the woman may complain of headaches, blurred vision or other visual disturbances, epigastric pain or heartburn, chest pressure, irritability, emotional tension, and decreased fetal activity. The patient is assessed for hyperreflexia of the deep tendon reflexes and clonus, and, if preeclampsia worsens, for oliguria. The goals of treatment are to stop progress of the condition and to ensure survival of the fetus and the mother's health.

Hospitalization may be necessary if the patient exhibits signs of moderate to severe preeclampsia and has failed to respond to home management. Intravenous magnesium sulfate may be given, first as a bolus and continued as a maintenance dose, until the severity of the disease decreases. If magnesium sulfate is used, the patient must be assessed frequently for the presence of deep tendon reflexes, respirations over 12 per minute, hourly urine output, and signs and symptoms of magnesium toxicity. Calcium gluconate, if needed, is the antidote for magnesium sulfate.

The clinical status of mother and fetus is continually evaluated; maternal vital signs and fetal heart rate are monitored. The patient is assessed for impending labor, and fetal and maternal responses to labor contractions are evaluated. The obstetrician is notified of any change in the patient's or the fetus' condition. Emergency care is provided during convulsions; prescribed medications are administered as directed, and patient and fetal response are evaluated. Careful monitoring of the administration of magnesium sulfate, intake and output, and the woman's response to the medication are necessary. Health care providers should be esp. alert for signs of toxicity, e.g., an absence of patellar reflexes (hyporeflexia), flushing, and muscle flaccidity.

Psychological support and assistance to develop effective coping strategies are provided to both patient and family, who are to be prepared for possible premature delivery. Cesarean birth or oxytocin induction may be required. Although infants of mothers with PIH are usually small for gestational age, they sometimes fare better than other premature infants of similar weight because they have developed adaptive ventilatory and other responses to intrauterine stress.

Etiology

The cause of PIH is unknown, but there are several major contributing theories: vasoconstriction and vasospasm, and a possible imbalance between prostaglandins, prostacyclin, and thromboxane A². The incidence is higher among adolescent and older primigravidas, diabetics, and women with pre-exisitng vascular problems or multiple pregnancies. Geographical, ethnic, racial, familial, low socioeconomic, nutritional, and immunological factors may contribute to PIH. Characteristic complaints include sudden weight gain, severe frontal headaches, and visual disturbances. Indications of increasing severity include complaints of epigastric or abdominal pain; generalized, presacral, and facial edema; oliguria; and hyperreflexia.

The treatment consists of bedrest, a high-protein diet, and medications including mild sedatives, antihypertensives, and intravenous anticoagulants if indicated. Complications are HELLP syndrome (hemolysis, elevated liver enzymes and low platelets) and eclampsia (the convulsive form of PIH).

Patient care

To enable the woman to actively participate in her health maintenance, reduce the potential for development of PIH, and facilitate early diagnosis and treatment, the health care provider should emphasize the importance of regular prenatal visits and good prenatal nutrition. Signs to report promptly are identified with the patient: sudden weight gain, swelling of the hands and face, headache, pitting edema of the ankles and legs, and reduced urine output.

At each prenatal visit, the pregnant woman's BP is monitored. The patient also is assessed for albuminuria; weekly weight gain of more than 3 lb (1.36 kg) in the second trimester or more than 1 lb (0.45 kg) in the third trimester; and generalized edema, esp. of the face and hands, and pitting edema of the ankles and legs. Protein intake is monitored to ensure adequate maternal serum protein levels, normal oncotic pressure, limitation of edema formation, and normal fetal development.

As preeclampsia progresses, the woman may complain of headaches, blurred vision or other visual disturbances, epigastric pain or heartburn, chest pressure, irritability, emotional tension, and decreased fetal activity. The patient is assessed for hyperreflexia of the deep tendon reflexes and clonus, and, if preeclampsia worsens, for oliguria. The goals of treatment are to stop progress of the condition and to ensure survival of the fetus and the mother's health.

Hospitalization may be necessary if the patient exhibits signs of moderate to severe preeclampsia and has failed to respond to home management. Intravenous magnesium sulfate may be given, first as a bolus and continued as a maintenance dose, until the severity of the disease decreases. If magnesium sulfate is used, the patient must be assessed frequently for the presence of deep tendon reflexes, respirations over 12 per minute, hourly urine output, and signs and symptoms of magnesium toxicity. Calcium gluconate, if needed, is the antidote for magnesium sulfate.

The clinical status of mother and fetus is continually evaluated; maternal vital signs and fetal heart rate are monitored. The patient is assessed for impending labor, and fetal and maternal responses to labor contractions are evaluated. The obstetrician is notified of any change in the patient's or the fetus' condition. Emergency care is provided during convulsions; prescribed medications are administered as directed, and patient and fetal response are evaluated. Careful monitoring of the administration of magnesium sulfate, intake and output, and the woman's response to the medication are necessary. Health care providers should be esp. alert for signs of toxicity, e.g., an absence of patellar reflexes (hyporeflexia), flushing, and muscle flaccidity.

Psychological support and assistance to develop effective coping strategies are provided to both patient and family, who are to be prepared for possible premature delivery. Cesarean birth or oxytocin induction may be required. Although infants of mothers with PIH are usually small for gestational age, they sometimes fare better than other premature infants of similar weight because they have developed adaptive ventilatory and other responses to intrauterine stress.