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Papilledema is optic disc swelling that is caused by increased intracranial pressure. The swelling is usually bilateral and can occur over a period of hours to weeks. Papilledema occurs in approximately 50% of those with a brain tumour. more...

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As the optic nerve sheath is continuous with the subarachnoid space of the brain (and is regarded as an extension of the central nervous system), increased pressure is transmitted through to the optic nerve. The brain itself, is relatively spared from pathological consequences of high pressure. However, the anterior end of the optic nerve stops abruptly at the eye. Hence the pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve at its head. The fibers of the retinal ganglion cells of the optic disc become engorged and bulge anteriorly. Persistent and extensive optic nerve head swelling, or optic disc edema, can lead to loss of these fibers and permanent visual impairment.

Checking the eyes for signs of papilledema should be carried out whenever there is a clinical suspicion of raised intracranial pressure. Because of the (rare) possibility of a brain tumor or pseudotumor cerebri, both of which can increase intracranial pressure, this examination has become common for patients suffering from headaches. There are 10 hallmarks of papilledema:

  • blurring of the disc margins
  • filling in of the optic disc cup
  • anterior bulging of the nerve head
  • edema of the nerve fiber layer
  • retinal or choroidal folds
  • congestion of retinal veins
  • peripapillary hemorrhages
  • hyperemia of the optic nerve head
  • nerve fiber layer infarcts
  • hard exudates of the optic disc


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Loosening the grip of hypertension
From Nursing, 12/1/04 by Woods, Anne

Find out how to assess patients for this deadly, often silent disease and what to teach them about protecting their health, based on the latest guidelines.

AN ESTIMATED 50 million Americans have hypertension, but 30% don't know it. And of those who've been diagnosed with hypertension, less than half have their blood pressure (BP) under control. Without treatment, many of these people will face devastating complications down the road, including myocardial infarction (MI), stroke, kidney failure, and blindness.

Because hypertension may not produce signs or symptoms initially, a patient may not learn about his hypertension until it's picked up on a routine assessment. But many people rarely see a primary care provider and remain unaware of the danger. With that in mind, consider every patient assessment an opportunity to ferret out hypertension.

The latest guidelines from the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) provide a detailed blueprint for you to follow. In this article, I'll use the JNC 7 guideline to help you understand how you can help patients. Let's start with a brief review of how and why hypertension develops.

What's new in the numbers

The JNC 7 guideline defines normal BP as systolic BP less than 120 mm Hg and diastolic BP less than 80 mm Hg. It defines hypertension as systolic BP of 140 mm Hg or more and diastolic BP of 90 mm Hg or more.

What's new in the numbers? The guideline now identifies a BP of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic as prehypertensive, a new category. This is significant because people with prehypertension in the 130-to-139 mm Hg systolic and 80-to-89 mm Hg diastolic range face twice the risk of hypertension as people whose BP is normal. The numbers help predict long-term consequences: The higher a persons BP and the longer he has hypertension, the higher his risk of complications, such as MI, heart failure, stroke, and chronic kidney disease.

Class distinctions

Hypertension falls into two classes: primary (also called essential) and secondary.

Most people with hypertension-90% to 95%-have primary hypertension. Although the causes of primary hypertension aren't well understood, we know that these three factors contribute to it:

* hyperactivity of the sympathetic nervous system. Normally, baroreceptors in the large blood vessels sense any drop in BP or blood volume and signal the brain to alert the adrenal glands to pump out more norepinephrine and epinephrine. These neurotransmitters then bind with the alpha^sub 1^-receptors in the blood vessels and beta^sub 1^-receptors in the heart to constrict the peripheral blood vessels and increase heart rate. This response helps the body maintain adequate cardiac output and BP Norepinephrine and epinephrine also bind with beta^sub 2^-receptors in the bronchial smooth muscle, resulting in bronchodilation. Once the circulating blood volume and BP return to normal, the response downregulates. However, in someone with a hyperactive sympathetic nervous system, the system never "turns off," and BP remains persistently high.

* hyperactivity of the reninangiotensin-aldosterone system. The kidneys respond to a drop in BP or blood volume by secreting renin, a precursor to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE); angiotensin II binds to angiotensin receptors in vascular smooth muscle, blood vessels, the kidneys, adrenal glands, heart, liver, and brain, causing vasoconstriction. High angiotensin II levels trigger the adrenals to release aldosterone, which affects the kidneys, resulting in sodium and water retention to maintain normal BP and cardiac output. But if the system doesn't down-regulate, the person develops hypertension.

* endothelial dysfunction. Damage to the endothelium, the inner layer of blood vessels, prevents blood vessels from dilating. Persistent vasoconstriction eventually leads to target-organ damage such as heart failure and chronic kidney disease. Elevated low-density lipoprotein (LDL) cholesterol levels, an associated disorder, alter the permeability of vascular endothelial cell membranes, which allows monocytes to adhere to the endothelial cell membranes and migrate under the surface. There, the monocytes accumulate lipids and become foam cells, which eventually form the fatty streaks of atherosclerosis. If the endothelium becomes distorted and breaks, platelets are attracted to the damaged areas.

Over time, an abundance of the vasoconstrictors norepinephrine and angiotensin II leads to hypertrophy of vascular smooth muscle and vascular remodeling. Although nitric oxide, secreted by the endothelial cells, is a potent vasodilator that normally inhibits platelet aggregation and monocyte adherence, hypertension and other factors (such as nicotine use and excessive insulin levels) inhibit its release. That prevents blood vessel dilation, and the damage continues, eventually affecting target organs.

Secondary hypertension, which may be severe and difficult to control, results from another problem or condition, such as high-dose estrogen use, polycystic kidney disease, renal artery stenosis, primary hyperaldosteronism, Cushing's syndrome, pheochromocytoma, pregnancy, hyperthyroidism, or neurologic disorders that raise intracranial pressure. Symptoms and treatments vary, depending on the primary disease.

Measuring BP accurately

Knowing how to measure BP accurately is crucial to diagnosing hypertension. Here are some tips:

* For 30 minutes before his BP is taken, the patient should avoid smoking or drinking beverages containing caffeine. Nicotine and caffeine can cause temporary fluctuations in BP.

* Have the patient rest quietly for at least 5 minutes before you take his BP to prevent a falsely high reading. Have him sit in a chair with his feet on the floor and his arm supported at heart level.

* Apply the BP cuff to the patient's bare arm. The height of the cuff bladder should be about 40% of the upper arm circumference, and the length of the cuff bladder should encircle at least 80% of the upper arm. Apply the cuff evenly and snugly, with the lower edge of the cuff 1 inch (2.5 cm) above the point at which you'll place the bell of the stethoscope.

* Palpate the patient's radial pulse and inflate the cuff until you no longer feel a pulse. Read this pressure on the manometer, deflate the cuff, and wait 15 to 30 seconds. Place the bell of your stethoscope lightly over the brachial artery. Inflate the cuff to 30 mm Hg over the initial pressure, then slowly deflate the cuff (about 2 to 3 mm Hg/second).

* If the patient's BP is elevated, wait at least 2 minutes, then take it again. Be sure to check the BP in his other arm too.

Examining your patient

As you take the patients history, assess for major risk factors for hypertension and cardiovascular disease, including:

* family history of hypertension or heart disease

* tobacco use

* body mass index of 30 kg/m^sup 2^ or more

* physical inactivity

* dyslipidemia

* diabetes

* albumin in the urine

* age over 55 for men, over 65 for women (or postmenopausal).

Find out if the patient is taking any prescription or over-the-counter medications that could raise BP, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and oral contraceptives. And don't forget to ask about herbal supplements.

During the physical exam, palpate his thyroid gland to see if it's enlarged. Listen to his lungs for adventitious breath sounds and check his abdomen for bruits, which can indicate renal artery stenosis or aneurysm. Also examine his arms and legs for hair distribution, color, quality of pulses, and edema.

Auscultate the carotid arteries for a bruit and assess for hepatojugular reflux. Also listen to the heart for murmurs and extra heart sounds. If your patient has heart failure, you may hear an S^sub 3^ heart sound. An S^sub 4^ heart sound may indicate hypertension. The patient should also have a funduscopic eye exam for evidence of hypertension, such as arteriovenous nicking, retinal hemorrhages, and papilledema.

If the patient is newly diagnosed with hypertension, hell need routine studies to establish a baseline and pinpoint any target-organ damage related to hypertension. Expect the health care provider to order an electrocardiogram, hematocrit level, urinalysis, serum potassium level, serum calcium level, blood urea nitrogen and creatinine levels, fasting blood glucose level, and cholesterol profile, including triglycerides.

Taking aim at the target

To reduce complications related to cardiovascular disease (CVD), the JNC 7 guideline recommends a target BP of less than 140/90. Patients with diabetes or renal disease need to go even lower: less than 130/80.

The treatment needed to reach the target BP depends on where the patient's numbers fall in the JNC 7 classification system (see How to Classify and Treat Hypertension) and any concurrent health problems, such as diabetes.

Lifestyle alternatives

The backbone of treatment for all patients with prehypertension or hypertension is lifestyle modification, including the following recommendations.

* Lose excess weight. Being overweight can raise BP and lipid levels and increase the patient's risk of diabetes and coronary artery disease (CAD). Maintaining a normal body mass index (18.5 to 24.9 kg/m^sup 2^) is associated with reduced BP: For every 22 pounds (10 kg) of weight lost, the BP will drop 5 to 20 mm Hg. Educate your patient about the benefits of a reduced-calorie, low-fat, low-cholesterol diet. He should limit his total fat intake to 25% to 35% of calories, with saturated fat accounting for less than 7% of total fat intake.

* Cut back on salt. Too much sodium in the diet can increase BP, especially in patients who are African-American or elderly and in those with diabetes. Advise the patient to consume less than 2.4 grams of sodium per day by ignoring his saltshaker and carefully reading food labels for sodium content. A low-sodium diet can reduce BP by 2 to 8 mm Hg.

* Exercise regularly. Engaging in aerobic physical activity, even brisk walking, for at least 30 minutes per day most days of the week, will help the patient control his weight and may also decrease his BP by 4 to 9 mm Hg.

* Limit alcohol intake. Imbibing a bit too much may contribute to hypertension by increasing caloric intake without adding nutritional value. Alcohol also decreases glucose levels in patients with diabetes and increases lipoprotein levels associated with CVD. A normal-weight man should drink no more than 1 ounce of ethanol per day. That translates to 24 ounces of beer, 10 ounces of wine, or 3 ounces of 80-proof whiskey. Women and lighter-weight men should restrict their intake to half that amount.

* Adopt the DASH eating plan to decrease cholesterol intake. The DASH (Dietary Approaches to Stop Hypertension) eating plan is rich in fruits, vegetables, and low-fat dairy products. It can help the patient reduce BP by 8 to 14 mm Hg.

* Stop smoking. Smoking tobacco is one of the leading risk factors for CAD. It's also highly addictive, so your patient may need help. Encourage him to start and stick with a smoking cessation program, which may include medications, counseling, and support groups. Because many patients who stop smoking gain weight, make sure that weight management and exercise are part of the program. If he decides to use a nicotine patch, warn him that some medications taken concurrently could raise his BE Teach him to inform his health care provider about all medications and over-the-counter products he takes and tell him to check with his provider before taking any new medication or product.

Drug therapy: The right balance

If lifestyle modifications don't get his BP under control, your patient will need drug therapy. For best results, most patients need two or more drugs that tackle hypertension via different mechanisms.

Thiazide diuretics are usually the first line of therapy. There are exceptions, of course. For example, patients with diabetes and hypertension should take an ACE inhibitor instead of a thiazide diuretic as a first-line drug; an angiotensin receptor blocker (ARB) can be used as an alternative to an ACE inhibitor. Both classes of drugs help maintain renal function in patients with diabetes.

Besides diabetes, other health problems can influence the prescribed drug regimen.

* If the patient has a history of stable angina, a beta-blocker is the recommended first-line drug; a long-acting calcium channel blocker can be used as an alternative.

* A patient with acute coronary syndrome may respond well to a beta-blocker combined with an ACE inhibitor.

* For patients who've had an MI, an ACE inhibitor, a beta-blocker, and an aldosterone antagonist have proven beneficial when combined with intensive lipid management and aspirin therapy.

* A patient with symptomatic heart failure should be treated with an ACE inhibitor or an ARB, a beta-blocker, and an aldosterone antagonist, along with a loop diuretic.

* A patient with chronic kidney disease will benefit from an ACE inhibitor or ARB; these drugs have been shown to slow the progression of renal disease. But keep a close eye on the creatinine level: If it rises more than 35% or if the patient develops hyperkalemia, notify the health care provider.

A patient's ethnic group can also affect medication choices. For example, an African-American patient may not respond well to monotherapy with an ACE inhibitor, an ARB, or a beta-blocker. A diuretic or calcium channel blocker may be more effective, especially if given in combination.

Antihypertensive therapy is especially important in the elderly: Besides controlling BP, it may also slow the progression of dementia. Because the elderly are especially vulnerable to adverse drug effects, the prescriber will start with a reduced dosage and slowly increase it as tolerated until the patients BP is under control.

Special considerations for women and children

Women who develop hypertension during pregnancy should be treated with methyldopa, a beta-blocker, or a vasodilator because these drugs are safer for the fetus. Pregnant women or women likely to become pregnant should avoid ACE inhibitors and ARBs because of the potential for birth defects.

In some women, oral contraceptives may increase BP, but hormone replacement therapy for menopause hasn't been shown to increase BP

Unfortunately, high BP is a growing problem in children. In May, guidelines from the National High Blood Pressure Education Program called for regular BP checks for children beginning at age 3. Under the new guidelines, BP readings once considered high normal are now considered prehypertensive.

If a child's BP is high, the health care provider should thoroughly investigate the cause. If she can find no specific cause for hypertension, she'll prescribe diet and lifestyle modifications, possibly with drug therapy. Drug therapy is similar for adults and children; ACE inhibitors and ARBs should be avoided in pregnant or sexually active girls.

Putting drugs to work

Now let's look at how drugs in each class work.

The mainstay of therapy for hypertension, thiazide diuretics such as hydrochlorothiazide work on the kidneys to rid the body of excess water. Other classes of diuretics are loop diuretics (such as furosemide) and potassium-sparing diuretics (such as amiloride).

In general, diuretics can raise plasma triglyceride and LDL cholesterol levels, so make sure your patient's lipid levels are being monitored and treated. Thiazide diuretics can also increase blood glucose levels, so use caution if your patient has diabetes. They can be quite useful in elderly patients, however, because they reduce bone breakdown in osteoporosis. Avoid giving a potassium-sparing diuretic to a patient on an ACE inhibitor because of the potential for hyperkalemia.

Aldosterone antagonists (such as spironolactone) block the effects of aldosterone on the kidneys, which allows the kidneys to get rid of extra sodium and water.

Three classes of beta-blockers are available: cardioselective, nonselective, and combined alpha-beta-blockers.

Cardioselective beta-blockers (such as atenolol) primarily work by blocking the beta-receptors in the heart. This decreases myocardial workload and reduces ventricular remodeling from endothelial dysfunction.

Nonselective beta-blockers (such as propranolol) block the beta-receptors in the heart, blood vessels, and lungs. This causes blood vessels to dilate, reducing myocardial workload. One problem with nonselective beta-blockers is that they block the beta-receptors responsible for bronchodilation in the lungs, so patients with preexisting reactive airway disease or chronic obstructive pulmonary disease may develop bronchospasms. In these patients, a cardioselective beta-blocker would be a better choice, but the patient should still be closely monitored for problems. Nonselective beta-blockers also depress the tachycardia associated with hypoglycemia, so using a cardioselective beta-blocker in patients with diabetes is a better option.

Alpha-beta-blockers combine nonselective beta-blocking effects with blocking of the alpha-receptors on the vascular smooth muscle, which results in vasodilation. Alpha-beta-blockers don't reduce the heart rate as much as cardioselective or nonselective beta-blockers.

Beta-blockers have been found to increase serum triglyceride levels and decrease high-density lipoprotein (HDL) cholesterol levels. They also can worsen depression and cause impotence.

Calcium channel blockers decrease heart rate and contractility and help prevent vasospasm by blocking slow-moving calcium channels in the heart and vascular smooth muscle. Nondihydropyridines (such as diltiazem) decrease heart rate and contractility; dihydropyridines (such as amlodipine) dilate blood vessels. Calcium channel blockers are effective in ischemic heart disease, but use caution in a patient with heart failure because his myocardial contractility is already compromised.

ACE inhibitors (such as enalapril) dilate blood vessels by inhibiting the formation of angiotensin II. Because they preserve renal function, ACE inhibitors are first-line treatment for patients with hypertension and diabetes, heart failure, or impaired renal function.

ACE inhibitors may slightly increase serum potassium levels, so use them cautiously if the patient also is taking a potassium-sparing diuretic or an oral potassium supplement. Also, ACE inhibitors inhibit the degradation of bradykinin, which may cause a dry, hacking cough in some patients. Switching to an ARB, which doesn't affect bradykinin levels, is an acceptable alternative.

Counsel a patient taking an ACE inhibitor to avoid long-term NSAID use because the NSAID will reduce the effectiveness of the ACE inhibitor. NSAIDs inhibit formation of prostaglandin, which is necessary to maintain renal function. In the presence of NSAIDs, the kidneys will retain sodium and water, contributing to hypertension and worsening heart failure.

Some patients taking ACE inhibitors develop angioedema. If this occurs, the drug should be stopped immediately.

ARBs (such as valsartan) block the angiotensin receptors on vascular smooth muscle, which results in vasodilation. They also maintain renal function, making them an effective alternative to ACE inhibitors. Like ACE inhibitors, they can cause angioedema.

Alpha-adrenergic receptor blockers (such as prazosin) dilate peripheral blood vessels by blocking the effects of norepinephrine on the alpha-receptors. These drugs, often used to treat symptoms of benign prostatic hyperplasia, also increase HDL cholesterol and decrease LDL cholesterol. They aren't considered first-line choices for hypertension because they can increase the risk of angina, stroke, and heart failure. But they may be effective as an add-on if the patient has hyperlipidemia or benign prostatic hyperplasia.

Direct arteriole dilators (such as hydralazine) are rarely used anymore because they can cause reflex tachycardia, inotropic stimulation, and fluid retention.

Alpha-receptor agonists (such as clonidine) act on the central nervous system, lowering peripheral vascular resistance. Also used infrequently, these drugs can cause rebound hypertension if withdrawn suddenly. They can also cause sedation, hypotension, dry mouth, and fatigue.

Staying vigilant

By learning how to spot hypertensive patients, you can help them get their BP under control and avoid serious complications down the road.


National Heart, Lung, and Blood Institute-DASH Eating Plan heart/hbp/dash

Blood Pressure Tables for Children and Adolescents hyper tension/child_tbl.htm

National High Blood Pressure Education Program Updates Pediatric Guidelines 484933

Last accessed on November 1, 2004.

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Loosening the grip of hypertension


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Alves, L., et al.: "White Coat Hypertension and Nursing Care," Canadian Journal of Cardiovascular Nursing. 13(3):29-34, Summer 2003.

Bengtson, A., and Drevenhorn, E.: "The Nurse's Role and Skills in Hypertension Care: A Review," Clinical Nurse Specialist. 17(5):260-268, September 2003.

Pepine, C., et al.: "A Calcium Antagonist vs. a Non-Calcium Antagonist Hypertension Treatment Strategy for Patients with Coronary Artery Disease. The International Verapamil-Trandolapril Study (INVEST): A Randomized Controlled Trial," JAMA. 290(21):2805-2816, December 3, 2003.

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md., U.S. Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute, May 2003.

Woodruff, D.: "The Trouble with NSAIDS," Nursing made Incredibly Easy!. 2(1):6-7, January/February 2004.

Woods, A.: "Improving the Odds against Hypertension," Nursing2001. 31(8)36-41, August 2001.

Woods, A.: "Managing Hypertension," Nursing99. 29(3):41-47, March 1999.

Woods, A.: "X Marks the Spot: Understanding Metabolic Syndrome," Nursing made Incredibly Easy! 1(1):19-27, September/October 2003.


Anne Woods is clinical director of journals at Lippincott Williams & Wilkins in Ambler, Pa.; a nurse practitioner at The Wellness Center, Chandler Hall, in Newtown, Pa.; and an adjunct faculty member at Immaculata (Pa.) University. Meet Ms. Woods, who's speaking at the Nursing2005 Symposium in New Orleans, La., March 19 to 22, 2005.

The author has disclosed that she has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

Copyright Springhouse Corporation Dec 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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