Hypertension Blog

>маси и столове assessing a patient’s risk of developing hypertension, consider his race, sex, and age. African-Americans have a greater risk of hypertension than whites. Men have a greater risk of hypertension from early to middle adulthood, but women have greater risk after middle age. Also, the risk of hypertension increases with age. Older African-American women have the greatest risk of developing the condition.

A patient’s educational level and socioeconomic status and the part of the country where he lives or used to live are also risk factors for hypertension. Less educated people, people from lower socioeconomic groups, and people from the southeastern United States have an increased risk of developing it. Obesity, a modifiable risk factor for hypertension, doubles a patient’s risk of developing the disease. As you interview the patient, note whether he’s obese.

Stress also increases a patient’s risk. As you know, stress elevates a person’s circulating catecholamine level. And catecholamines work directly on the sympathetic nervous system to increase heart rate and blood pressure. Therefore, be sure to note the patient’s responses to daily stress. Ask him what type of job he has and whether or not he finds it stressful. Also, ask him whether he uses moderate exercise to reduce tension.

Ask your patient if he drinks alcohol. If he does, ask how much he drinks in an average day. Alcohol abuse can increase his risk of hypertension. Alcohol also interferes with the action of many antihypertensive drugs.

Ask your patient if he smokes. Tobacco has vasoconstrictive effects, thereby increasing a smoker’s blood pressure. Smoking also adds greatly to his risk of developing cardiovascular disease.

Increased systolic blood pressure used to be considered a normal part of aging. An old rule stated that 100 mm Hg plus the patient’s age was tolerable. Isolated systolic hypertension wasn’t a treated condition. However, the results of the Systolic Hypertension in the Elderly Program (SHEP) study changed this way of thinking.

The SHEP study, a double-blind clinical trial, used low doses of chlorthalidone and atenolol to treat systolic hypertension. The participants’ blood pressures were then monitored for 4 to 5 years, after which the researchers found a 36% decrease in cerebrovascular accidents, a 25% decrease in coronary artery disease, and a 54% decrease in left ventricular heart failure in the patients who received the chlorthalidone and atenolol. Similar studies in Sweden and the United Kingdom later confirmed these findings.

Currently, the Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure stresses the importance of systolic blood pressure in evaluating hypertension. Particularly for middle-aged and older patients, systolic hypertension increases the risk of cardiovascular disease, even when diastolic blood pressure is normal.

Alcohol and Cocaine

Both alcohol and cocaine cause hypertension. Excessive ingestion of alcohol can cause a patient to exacerbate his preexisting hypertension, or it can induce hypertension. And cocaine produces devastating effects on blood pressure by increasing the release of norepinephrine, a powerful vasopressor produced by the body in response to hypotension and stress. This can result in acute hypertension, tachycardia, tremor, and seizures as well as coronary artery vasoconstriction from a CVA or Ml.

Poisons

Many poisons can elevate blood pressure and cause hypertension. Some common poisons include cyanide, phencyclidine, and black widow spider venom. Treatment varies depending on the poison, and it usually relieves the poison-induced hypertension.

Pregnancy

Pregnancy-induced hypertension can threaten the lives of both the mother and infant. It causes elevated blood pressure, proteinuria, and edema and may lead to abnormalities in the mother’s coagulation system and liver function. The only treatment for pregnancy-induced hypertension is delivery of the infant.

Stress

For some patients, even mild stress can cause a rise in blood pressure. In response to a stressful event, the patient perceives a stressor, and his body initiates a fight-or-flight reaction. Physical signs and symptoms of stress-induced hypertension include decreased gastrointestinal motility, pupil dilation, and increased perspiration, all of which result from sympathetic nervous system stimulation that causes increased blood pressure and increased heart and respiratory rates.

With the white-coat phenomenon, a patient has elevated blood pressure readings in his physician’s office or the hospital but normal readings elsewhere. To determine if a patient has true hypertension, a physician may order repeated measurements over time or ambulatory measurements.

In postoperative patients, stress-related hypertension commonly results from sympathetic stimulation caused by pain, bladder distention, hypothermia, or respiratory compromise.

Sleep Apnea

Sleep apnea can contribute to the development of hypertension. During apnea, the tongue and soft palate relax and fall back, obstructing the airway either partially or completely. As a result, the patient can’t breathe. His oxygen levels fall, and carbon dioxide levels rise, resulting in acidosis and vasoconstriction of the pulmonary arterioles. Eventually, the patient partially awakens, gasps, and reopens his airway. Episodes of apnea may last from 15 to 90 seconds and occur repeatedly during the night.

Diseases Causing Vasculitis

Scleroderma, polyarteritis nodosa, lupus erythematosus, rheumatoid arthritis, and nonspecific arthritis may cause vasculitis in some patients. About one-half of these patients subsequently develop hypertension because of the effect the diseases have on the arterioles and major arteries.

Only 5% or fewer hypertensive patients have secondary hypertension. If a patient over age 50 suddenly develops hypertension, especially if it’s severe, suspect a secondary cause, such as a disease that increases cardiac output (CO) or peripheral vascular resistance. After the cause has been identified and treated, generally with surgery or drug therapy, the patient’s blood pressure should return to normal.

To identify the cause of secondary hypertension, a physician will order a basic workup that evaluates a patient’s cardiac system. Abnormalities in these systems commonly cause hypertension in young hypertensive patients, severely hypertensive patients, and hypertensive patients who don’t respond to standard antihypertensive therapy.

Cardiovascular Disorders

Coarctation of the aorta, a localized narrowing or constriction of the lumen of the aorta, is a vascular defect that commonly causes hypertension. Generally, the disorder is diagnosed in children.

Coarctation may occur anywhere along the aorta, but it most commonly occurs just beyond the origin of the left subclavian artery. When the condition is severe, the constriction of the lumen produces absent or markedly diminished femoral pulses as well as bruits heard throughout the posterior thorax.

Coarctation of the aorta can be detected by carefully timing the appearance of the patient’s femoral pulse with his radial or brachial pulse to determine if a substantial delay exists between pulses. If so, the patient’s blood pressure should be taken in both arms and his legs. The blood pressure of a patient with coarctation of the aorta will be elevated in the arms and reduced in the legs.

Surgical repair is usually required to correct coarctation of the aorta. Following surgical repair, only 5% to 10% of patients still have hypertension.

Subclavian artery stenosis also causes hypertension. If a patient has subclavian artery stenosis, his pulse in one arm will be absent or significantly diminished, and his blood pressure in that arm will be significantly lower than in his other arm.

Renal Disorders

Renovascular stenosis is the most common cause of hypertension that can be reversed by surgery or percutaneous trans luminal angioplasty. Stenosis of one or both renal arteries can produce severe hypertension and a loss of kidney function. Arterial fibromuscular dysplasia, fibrosis of the muscular layer of the artery wall, is the most common cause of renovascular hypertension in patients under age 40; atherosclerosis is the most common cause of renovascular hypertension in older patients.

Systolic bruits in the upper abdominal quadrants may indicate renovascular stenosis or renal arteriovenous malformation. If the bruit is continuous and extends into diastole, the stenosis is severe.

Hypertension can also result from renal parenchymatous disease, a consequence of acute and chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, collagen vascular disorder, intercapillary glomerulosclerosis, and interstitial nephritis. Many hypertensive patients with renal parenchymatous disease develop chronic renal failure. Generally, the treatment of choice for their condition is a diuretic and a diet limiting them to a daily intake of 2 grams of sodium and 40 to 50 grams of protein. Eventually, these patients may also need dialysis.

Though rare, renin-producing tumors also cause hypertension. These tumors, includingWilms’ tumor found in infants and children, arise from either the cortex or pelvis of the kidney and may be benign or malignant. The malignant form is more common, and the treatment is usually radical nephrectomy and, possibly, radiation therapy.

Neurologic Disorders

A patient who has sustained a spinal cord injury above the T7 level is at risk for hypertension because of autonomic hyperreflexia, a potentially life-threatening complication resulting from the sympathetic neurons’ loss of control over their sympathetic outflow. Stimulation of nerves below the injury, such as from fecal impaction, urine retention, or tactile stimulation, can cause reflex sympathetic activity along the spinal cord resulting in hypertension, bradycardia, severe headache, sweating, blurred vision, a flushed feeling, and nasal congestion. Any quadriplegic who complains of a headache should have his blood pressure promptly checked to determine if hypertension exists as a possible result of autonomic hyperreflexia.

When a patient with a spinal cord injury develops hypertension, his systolic blood pressure may rise to 300 mm Hg, and if the condition is left untreated, he may have a CVA or die. Treatment of autonomic hyperreflexia consists of immediately removing the source of the nerve stimulation, such as bladder distention. If the patient’s hypertension persists, his physician may prescribe antihypertensive drugs.

Patients with brain injuries are also at risk for hypertension. When a patient’s brain is injured, his intracranial pressure increases, and the blood volume and flow to his brain becomes passively controlled by the pressure in his systemic circulation. So a patient who sustains a brain injury has an elevated blood pressure because of the autoregulatory and compensatory mechanisms within the brain trying to maintain optimal cerebral perfusion pressure.

Diuretics promote renal excretion of water and electrolytes by increasing the glomerular filtration rate. They can also decrease sodium reabsorption and increase the rate of sodium excretion .

Diuretics are divided into several classes: loop, potassium sparing, thiazide, and thiazide-like. Each of these classes has a single mechanism of action. Combination diuretics contain two different classes of diuretic .

Potassium Sparing Diuretics

Potassium sparing diuretics have weaker diuretic and antihypertensive effects than loop diuretics. However, by acting on the distal tubule to inhibit the reabsorption of sodium and water, these drugs increase potassium retention. The potassium sparing diuretics include amiloride, spironolactone, and triamterene.

Indications and Contraindications

Physicians prescribe potassium sparing diuretics to treat patients with hypertension or with edema from heart failure. These drugs are also used in combination with other classes of diuretics to maintain a patient’s serum potassium levels.

Potassium sparing diuretics shouldn’t be used to treat patients with anuria, hyperkalemia, or impaired renal function. Amiloride should be used cautiously in those with dehydration, diabetes, or acidosis. And spironolactone should be given cautiously to patients with hepatic disease. Use triamterene cautiously in patients with heart failure, renal disease, and cirrhosis. When administering any potassium sparing diuretics, monitor your patient’s serum chemistry levels for early indications of electrolyte imbalance and increasing renal or hepatic failure.

Diuretics Side Effects

These drugs produce fewer side effects than other diuretics. However, a patient taking a potassium sparing diuretic has a greater risk of hyperkalemia, especially if he’s also taking potassium supplements.

Dose-related adverse effects include megaloblastic anemia, arrhythmias, headache, dizziness, and orthostatic hypotension. Spironolactone may cause amenorrhea, a deeper voice, gynecomastia, hirsutism, irregular menses, and postmenopausal bleeding. Triamterene may cause a bluish discoloration of the urine.

Your patient may experience hyperkalemia if he takes one of these drugs with another potassium sparing diuretic, an ACE inhibitor, or a salt substitute. If given with lithium, a potassium sparing diuretic may provoke lithium toxicity. Nephrotoxicity may increase if a patient takes triamterene with indomethacin. Also, aspirin decreases the effects of spironolactone.

The effects of cerebrovascular disease on your patient and his family can be devastating. A tremendous amount of education and support is needed for optimum recovery.

During the acute phase of a CVA, orient the patient and his family to the unit, to the procedures being performed and the equipment used, and to the treatment plan. Explain the need for rehabilitative therapy after the acute phase has passed.

Once the patient’s condition has stabilized and the amount of cerebral tissue damage has been determined, explain the disease, his deficits, and the planned rehabilitation. If necessary, ensure that each rehabilitation team member explains his or her specialty so that the patient and his family fully understand the rehabilitation process.

Teach the patient the signs and symptoms of a CVA and stress the importance of seeking treatment immediately if any of the following occur:

• sudden onset of weakness, numbness, or paralysis of the face, arm, or leg, usually on one side of the body
• sudden blurring or loss of vision in one or both eyes
• loss of speech or trouble talking or understanding speech
• sudden severe headache
• unexplained dizziness or loss of balance, especially if combined with other signs and symptoms.

If the physician prescribes an antihypertensive, anticoagulation, or anti platelet aggregation drug, teach your patient the name of the drug, its dosage, and its therapeutic and adverse effects. If he must take an anticoagulant, also teach him the signs and symptoms of bleeding that he should report .

If the physician has prescribed warfarin, tell your patient which drugs interact with it. Instruct him to maintain a diet that provides moderate amounts of vitamin K. Explain that extreme variations in vitamin K intake can cause wide fluctuations in the anticoagulant level. Tell the patient to avoid trauma and to wear a medical alert tag or bracelet at all times. Inform him that he’ll need frequent blood tests for his physician to adjust the warfarin dose.

Depending on the amount of cerebral damage, your patient may be transferred to a rehabilitation facility or a skilled nursing facility for further treatment. If he requires a wheelchair or walker, tell him that a home care nurse or other health provider should visit his home to identify physical barriers that would limit their use.

Explain that the home care nurse will monitor his vital signs, check his compliance with antihypertensive drug therapy, and assess his response to the drug. She’ll evaluate his bowel and bladder function and provide retraining, if necessary. She’ll also assess his response to rehabilitation, determining which assistive devices might be useful to him.

Systolic hypertension is more common in elderly patients. Elevated systolic blood pressure readings are usually caused by increased CO, systemic vascular resistance, or both. The main vascular cause of systolic hypertension is rigidity of the aorta, which develops from arteriosclerosis and increases total peripheral vascular resistance. Normally, the elastic aorta stretches as blood is pumped from the heart, but with decreased elasticity and compliance, systolic pressure increases significantly.

Aging also causes hyaline degeneration of the tunica media of arterioles, reducing lumen size. Further, decreased baroreceptor sensitivity may contribute to increased sympathetic nervous system activity and elevated levels of norepinephrine.

About 45% of the elderly in the United States have systolic blood pressures of 160 mm Hg or higher and diastolic pressures of less than 90 mm Hg-a condition known as isolated systolic hypertension. Generally, this condition reflects a disease process resulting in lost elasticity of the aorta and its large branches. Other than advanced age, this condition is the greatest risk factor of endocrine disease in elderly patients.

Endocrine Disorders

Pheochromocytoma, an abnormal growth of new tissue on the adrenal medulla, produces excessive catecholamines, causing hypertension. These tumors occur most commonly in patients ages 40 to 60, and about 90% of them are benign.

A patient with pheochromocytoma may experience severe headaches, profuse sweating, palpitations, and pronounced pallor caused by a sudden release of catecholamines resulting in a hypertensive crisis. These attacks can be triggered by physical activity, postural changes, emotional distress, hypoglycemia, and surgical trauma. An attack may also be provoked when the tumor is palpated.

If left untreated, a patient with pheochromocytoma can develop diabetes, cardiomyopathy, and hypertension, any of which can result in death. The usual treatment is surgical removal of the tumor, which relieves hypertension in about 75% of patients. The remaining 25% can usually manage their hypertension with antihypertensive drug therapy.

Caused by excessive aldosterone secretion of the adrenal gland, primary hyperaldosteronism is another endocrine disorder that causes hypertension. This condition is more common in women ages 20 to 50. Suspect it in hypertensive patients who have hypokalemia and don’t take diuretics.

The three causes of primary hyperaldosteronism are unilateral adrenocortical adenoma, adenomatous hyperplasia, and adrenocortical carcinoma. Unilateral adrenocortical adenoma alone causes 80% to 85% of the cases of primary hyperaldosteronism.

Physicians typically treat primary hyperaldosteronism by surgically removing the tumor. Unfortunately, surgery generally doesn’t cure hypertension resulting from adenomatous hyperplasia.

Cushing’s syndrome, another cause of hypertension, results from either prolonged treatment with large doses of glucocorticoids or excess cortisol production by the adrenal cortex, which is most commonly caused by a pituitary tumor. In either case, hypertension results from the mineralocorticoid effects of the hyperfunctioning adrenal tissue. When a pituitary tumor causes Cushing’s syndrome, the usual treatment consists of surgical removal. Hypertension can also be caused by acromegaly-a chronic metabolic condition resulting from excessive production of growth hormone in the anterior pituitary. The condition is characterized by enlargement and elongation of the bones of the face, jaw, and extremities. Although one­third of patients with acromegaly have hypertension, it’s usually not severe, and the treatment of acromegaly-surgery, radiation, and drugs-usually alleviates the hypertension.

Hypertension is sometimes called the “silent killer” because many people don’t know they have it. If left untreated, chronic systolic and diastolic hypertension damages the walls of systemic blood vessels and organs such as the heart, brain, kidneys, and retina. Eventually, this organ damage can result in coronary artery disease (CAD), CVA, renal failure, and blindness .

Coronary Artery Disease

Hypertension is the main risk factor for developing CAD from atherosclerosis. With hypertension, atherosclerotic plaque forms in the inner lining of the artery at an accelerated rate. As the artery narrows, more force is needed to pump blood through it, creating an even further elevation in blood pressure.

Cerebrovascular Accident

Hypertension is also a serious risk factor of CVA. In fact, hypertension is a leading cause of transient ischemic attacks and CVAs resulting from cerebral thrombosis, intracerebral hemorrhage, and emboli.

Cerebral arterial hemorrhage can occur when progressive atherosclerotic changes take place and blood pressure increases in the affected vessels. Eventually, smooth blood vessel tissue is replaced with fibrous tissue, causing vessel walls to become thicker and more rigid. But the vessels also weaken because of intense constriction of the cerebral arterioles and arteries, resulting in the development of microaneurysms that tend to rupture easily.

Renal Disease

Hypertension also leads to end-stage renal disease. During the early stage of hypertension, the capillary basement membrane of the glomeruli becomes thickened by atherosclerosis. Hypertension then causes a gradual destruction of the glomeruli, tubules, and nephrons. At first, a patient’s glomerular filtration rate may remain normal, but scarring eventually occurs, causing renal failure. Although most hypertensive patients have some degree of renal dysfunction, African-American hypertensive patients have the greatest risk of developing end-stage renal disease.

Retinopathy

Hypertension can also cause retinopathy. The resulting retinal changes are categorized in four stages of increasingly severe vessel damage.

Usually, the early stages go undetected because the patient has no significant signs or symptoms to report and no apparent reason to seek medical attention. However, if his hypertension is left untreated and his condition progresses into the later stages of retinopathy, he may develop retinal lesions, which can cause blurred vision, or papilledema and retinal hemorrhaging, which can result in blindness.

Diagnostic testing for heart failure includes chest X-ray, ECG, echocardiography, and pulmonary artery catheterization.In a patient with heart failure, a chest X-ray reveals an enlarged heart, indicating hypertrophy or dilation. If the patient is in the early stages of heart failure, the chest X-ray may show congested pulmonary veins in the upper lobes. If he is in the late stages, the X-ray may show interstitial pulmonary edema and pulmonary effusion. If the patient has biventricular failure, the chest X-ray may show a pleural effusion.

A physician uses an ECG to detect left ventricular hypertrophy. An ECG also detects signs of arrhythmias, such as irregular QRS complexes and F waves, and signs of myocardial ischemia, such as T-wave inversion and ST-segment elevation.

Used to measure the size of the heart chambers, echocardiography may reveal an enlarged right or left atrium. This test also is used to assess ventricular function and to detect ventricular hypertrophy. With normal ventricular function, echocardiography shows concentric contractility, a lack of abnormal wall movement, and a left ventricular ejection fraction of 55% to 60%. With left ventricular hypertrophy, it displays a ventricular wall thickness that exceeds 1.2 cm during diastole.

Pulmonary artery catheters are used to measure cardiac pressures. In right ventricular heart failure, the patient’s right atrial pressure may be elevated. In left ventricular heart failure, his pulmonary artery pressure and pulmonary artery wedge pressure are elevated, and CO is reduced.