By interfering with calcium ion influx across the cell membrane, calcium channel blockers inhibit calcium-dependent contraction of vascular smooth muscle. This decreases total peripheral vascular resistance and after load, which reduces blood pressure.Calcium channel blockers include diltiazem hydrochloride, felodipine, nicardipine, nifedipine, and verapamil.

Indications and Contraindications

Physicians commonly prescribe these drugs to treat patients with angina pectoris. However, several oral forms are used to treat vasospasm and mild to moderate hypertension. Parenteral forms are used to treat hypertension, atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia. But sustained-release nifedipine is only used to treat hypertension.

Use calcium channel blockers cautiously in patients with heart failure, hypotension, hepatic injury, and renal disease. Do not administer a calcium channel blocker to patients with sick sinus syndrome, second-degree or third-degree heart block, hypotension, acute MI, or pulmonary congestion. Do not administer verapamil to patients with cardiogenic shock or severe heart failure, and administer it cautiously to patients taking beta-blockers.

Adverse Effects and Interactions

The most serious adverse effects of calcium channel blockers include cardiovascular changes such as hypotension, arrhythmias, and worsened eart failure. Other common effects include headache, dizziness, flushing, weakness, and persistent peripheral edema. Your patient may also experience nausea, vomiting, diarrhoea, muscle fatigue, cramps, worsened angina, skin eruptions, photosensitivity, pruritus, nasal congestion, and mood changes.

Calcium channel blockers can interact with beta-blockers, causing heart block and heart failure. When diltiazem is taken with cimetidine, its effect increases. And when it’s administered with cimetidine or ranitidine, felodipine levels increase. Nicardipine increases the effects of digitalis glycosides, neuromuscular blockers, and theophylline. And when nifedipine is administered in combination with theophylline, beta­blockers, other antihypertensives, or digitalis glycosides, it increases their effects.

Quinidine decreases the effects of nifedipine. The hypotensive effects of verapamil increase when the drug is given with prazosin and quinidine. Verapamil also decreases the effects of lithium and increases the blood levels of digoxin, theophylline, cyclosporine, and carbamazepine. Verapamil is incompatible with albumin, amphotericin B, ampicillin, dobutamine, hydralazine, mezlocillin, nafcillin, oxacillin, and sodium bicarbonate.

Direct vasodilators act on arteries and veins. They dilate arteriolar smooth muscle by direct relaxation, reducing systolic and diastolic blood pressure while increasing heart rate and CO.Direct vasodilators include diazoxide, hydralazine hydrochloride, minoxidil, and nitroprusside.

Indications and Contraindications

A physician prescribes diazoxide and nitroprusside to treat patients in hypertensive crisis when an urgent decrease in diastolic blood pressure is needed. Oral hydralazine is used to treat patients with primary hypertension; parenteral hydralazine is used in patients with severe primary hypertension and heart failure. Minoxidil is prescribed when severe hypertension is unresponsive to other therapy.

Don’t administer hydralazine to patients with CAD or rheumatic heart disease. Do not use minoxidil in patients with acute MI, dissecting aortic aneurysm, or pheochromocytoma. And do not administer nitroprusside to patients with compensatory hypertension.

Don’t use diazoxide in patients with hypersensitivity to thiazides or sulfonamide or in patients whose hypertension is caused by coarctation of the aorta, dissecting aortic aneurysm, atrioventricular shunt, or pheochromocytoma. And use it cautiously in patients with tachycardia, fluid and electrolyte imbalances, or impaired cerebral or cardiac circulation.

Adverse Effects and Interactions

Direct vasodilators commonly produce adverse effects related to reflex activation of the sympathetic nervous system, such as palpitations, angina, tachycardia, ECG changes, edema, rash, breast tenderness, fatigue, and headache. Severe pericardial effusions can develop. And alkaline phosphatase, BUN, and creatinine levels may increase.

Diazoxide commonly causes headache, anorexia, nausea, and diaphoresis. It can also cause excessive hypotension, and in diabetic patients, it may cause hyperglycemia. If more serious effects occur, such as rash, urticaria, polyneuritis, GI hemorrhage, anemia, and pancytopenia, diazoxide should be discontinued.

Hydralazine commonly causes headache, diarrhea, constipation, dizziness, orthostatic hypotension, facial flushing, shortness of breath, nasal congestion, urinary hesitancy, edema, tremors, and muscle cramps. It may also cause impotence.

Minoxidil commonly produces hair growth on the face, arms, and back. It also causes reflex tachycardia and fluid retention. When minoxidil is taken with guanethidine, orthostatic hypotension can occur.

Nitroprusside causes headache, dizziness, nausea, vomiting, abdominal pain, and thiocyanate or cyanide toxicity . Severe hypotension occurs when nitroprusside is administered with ganglionic blockers, volatile liquid anesthetics, halothane, enflurane, and circulatory depressants. Nitroprusside is incompatible with any drug in syringe or solution.

When diazoxide is administered with a thiazide diuretic, another antihypertensive drug, warfarin, guanethidine, or a sympathomimetic, its effects increase. It’s incompatible with other drugs in a syringe or solution. Hyperglycemia and hyperuricemia can result when diazoxide is combined with thiazides and other diuretics. The effects of both diazoxide and sulfonylureas decrease when the drugs are given together.

When hydralazine is used with epinephrine or norepinephrine, tachycardia and angina increase. Hydralazine increases the effects of beta-blockers. And it is incompatible with aminophylline, ampicillin, edetate calcium disodium, chlorothiazide, ethacrynic acid, hydrocortisone, mephentermine, methohexital sodium, nitroglycerin, phenobarbital, verapamil, fructose 10%, dextrose 10%, and lactated Ringer’s solution.

If your patient has hypertensive retinopathy, a physician may prescribe an antihypertensive drug to regulate his diastolic blood pressure-typically, a beta-blocker or diuretic. If other drugs or disorders contraindicate these antihypertensive drugs. the physician will prescribe another one, such as an ACE inhibitor. Controlling the patient’s blood pressure may reduce or eliminate the signs and symptoms of retinopathy. However, if he has experienced optic nerve ischemia, he may have a permanent loss of vision.

Complementary Therapies

Stress reduction and management help reduce blood pressure. Therefore, you should urge your patient to identify the stressors in his life and help him develop and implement methods to cope with them.

Relaxation techniques-exercises that reduce stress by decreasing sympathetic nervous system activity-can reduce blood pressure. In combination with drug therapy, these techniques have even been effectively used for patients with severe hypertension. Relaxation techniques include yoga, meditation, physical relaxation, and physical exercise.

Psychotherapy has also been used successfully as a method of lowering blood pressure. It helps patients deal with anxiety and constructively handle hostile and aggressive impulses. Counseling can also help increase patient compliance with the prescribed drug regimen.

Another therapy, biofeedback, uses specialized equipment to give the patient feedback about his bodily processes. The patient learns to achieve relaxation by self-regulating the autonomic nervous system. Biofeedback can decrease blood pressure; however, the long-term effects of biofeed­back and its success in controlling hypertension aren’t known.

Normally, hypertensive patients have a systolic blood pressure of 140 mm Hg or higher or a diastolic pressure of 90 mm Hg or higher on at least two separate occasions. However, even in healthy people, blood pressure fluctuates depending on the time of day and the activities they’ve been performing, so assessing hypertension requires several blood pressure measurements.Obtain at least one reading in both arms with the patient sitting, lying, and standing. A difference of 5 to 10 mm Hg between the arms is normal, but if the difference is more than 10 mm Hg, the patient may have arterial compression or obstruction on the side with the lower pressure.

If a hypertensive patient’s diastolic pressure increases when he stands up from a supine position, he may have primary hypertension. However, if his diastolic pressure decreases when he stands (and he’s not taking an antihypertensive drug), he may have secondary hypertension.

Take at least two measurements separated by at least 2 minutes. If the readings from the same arm vary by more than 5 mm Hg, recheck your technique and take additional readings until you obtain two that are similar. In particular, confirm a high reading with at least two subsequent readings. This helps to rule out white-coat syndrome­elevated blood pressure in response to the stress of having a health care professional take the reading. White-coat syndrome occurs about 20% of the time. Several other factors also can influence the accuracy of blood pressure readings.

Placing the cuff improperly or using a wrong­sized cuff may result in inaccurate readings. For example, using a regular adult cuff on an obese patient may give an incorrectly high reading .

You can use either a mercury or aneroid manometer. But remember that aneroid manometers require monthly calibration to ensure their accuracy.

Patient Preparation

To prepare the patient for blood pressure measurement, make sure you have him remain seated quietly, in a comfortable environment, for at least 5 minutes. Free his arm from clothing by either roIling up the sleeve or having him remove his long-sleeved shirt and offering him a patient gown, if necessary. Then place the arm in a comfortable position. Make sure his arm doesn’t have an AV fistula for dialysis, scarring from brachial artery cut­downs, or lymphedema, which may follow axillary node dissection and radiation therapy.

Palpate for the brachial pulse to make sure it’s present. Before applying the cuff, make sure the brachial artery, located at the crease of the antecubital fossa, is positioned at heart level. If the patient is sitting, a table that reaches just above his waist is usually sufficient. If the patient is standing, support his arm at midchest level. The reading can be falsely elevated if he expends effort keeping his arm up.

Nursing Considerations

If using a mercury manometer, position the gauge vertically with the meniscus at eye level. If using a calibrated aneroid manometer, turn the gauge so that it faces you. Place the cuff on the patient’s arm by centering the inflatable bladder over the brachial artery. Securely fasten the lower border of the cuff about 2.5 cm above the antecubital crease.

Falsely low blood pressure readings commonly occur when the cuff isn’t inflated high enough. To prevent this, first estimate the patient’s systolic blood pressure. Then add 30 mm Hg to this estimated pressure. This number will be the target for subsequent inflations; using it should prevent errors caused by an auscultatory gap. After obtaining the target number, deflate the cuff completely and wait a few minutes before taking an actual measurement .

To obtain the patient’s blood pressure measurement, place the bell of the stethoscope lightly over his brachial artery. The full rim should be in contact with his arm to create an air seal. Remember, the bell of the stethoscope will allow you to hear low-pitched Korotkoff sounds better than the diaphragm will.

Inflate the bladder quickly to the target level. Then deflate it at a rate of 3 mm Hg per second. As the pressure decreases, note the patient’s systolic pressure as the level at which you hear the sounds of at least two consecutive beats.

While continuing to release the pressure in the bladder, listen for the Korotkoff sounds to become muffled and then disappear. Note this level as the patient’s diastolic pressure. Usually, the points where the sounds are muffled and where the sounds disappear differ by only a few mm Hg. However, if the difference is more than 10 mm Hg, record both numbers along with the systolic pressure-for example, you might record a patient’s blood pressure as 160/90/72.

After the sounds have disappeared, continue listening while the pressure decreases another 10 to 20 mm Hg. Then rapidly deflate the cuff to zero.

If the sounds are difficult to hear, have your patient raise his arm and then open and close his hand five to ten times. Quickly inflate the cuff with his arm raised, then lower it and take a reading. This maneuver should help intensify the Korotkoff sounds.

You may also measure blood pressure in a patient’s leg, particularly if you’re trying to detec coarctation of the aorta. Wrap a thigh cuff around his thigh and place the stethoscope bell in the popliteal space. Then obtain the blood pressure measurement just as you would in the arm. If the systolic pressure in the leg is more than 20 mm Hg lower than the brachial systolic pressure, the patient probably has an arterial occlusion.

Another simple technique-the cold pressor test-can be used to enhance blood pressure measurement and help identify the severity of hypertension.

Recognizing Korotkoff Sounds

To accurately assess your patient’s systolic and diastolic blood pressure readings, you need to recognize the variations in the sounds you hear. After you inflate the blood pressure cuff and begin releasing air from it, you’ll hear the first of the five Korotkoff sounds described below. In this example, the blood pressure reading is 140/90 mm Hg.

Phase 1 (systolic blood pressure) A sharp thump, and then tapping.

Phase 2 A murmuring or swishing sound

Phase 3 The murmuring disappears, and sounds increase in intensity and clarity.

Phase 4 (first diastolic blood pressure) A softer blowing sound that fades.

Phase 5 (second diastolic blood pressure) The sounds disappear

Most aortic aneurysms are found during a routine physical examination or chest X-ray. A physician may also use ultrasound, CT, MRI, and aortoiliac angiography to diagnose the condition.If the patient has an aortic aneurysm, a chest X-ray may show a widening of the mecamylamine silhouette and aortic arch. If the aneurysm is in the abdominal aorta, an abdominal X-ray may show calcification in the aorta’s wall. If the patient reports thoracic pain, the physician also may use an ECG to rule out an MI.

If the physician suspects an aortic aneurysm, he may order ultrasonography to confirm the aneurysm and detect thrombus formation. He may order a CT scan to determine the anterior-to­posterior and crosssectional diameters of the aneurysm. A CT scan also helps to detect a thrombus in the pouch of the aneurysm. The physician may use an MRI to help diagnose these aortic conditions. And he may use aortoiliac angiography, an invasive procedure for locating the aneurysm’s exact position, to help determine whether other arteries that receive blood from the aorta are affected by the condition.

Hypertensive retinopathy results from chronic primary hypertension, malignant hypertension, or eclampsia. If untreated, it can lead to retinal detachment. Plus, retinal vessel damage suggests that the patient has suffered damage to other organs, as well.

Pathophysiology

With retinopathy, retinal changes are categorized according to the severity of the vessel damage. Retinal arteriolar narrowing and increased dias­tolic blood pressure are directly related.

Grade I retinal changes may occur when a patient has mildly elevated diastolic blood pressure, about 90 mm Hg. These retinal changes include vascular spasm and arteriolar constriction.

Grade II retinal changes occur when a patient has sustained elevated diastolic blood pressure of more than 100 mm Hg. These retinal changes include localized and generalized arteriole nar­rowing at arteriovenous junctions.

If the patient’s hypertension is left untreated and his diastolic blood pressure remains above 100 mm Hg, he may experience grade III retinal changes. Occlusion of the retinal arterioles may cause superficial, flame-shaped hemorrhages and small, white areas of retinal ischemia called soft exudate or cotton wool spots. Hard, yellow ­white exudate may produce a star-shaped figure around the macula.

Further untreated hypertension can lead to grade IV retinal changes. The occluded arterioles cause the optic disk to become congested and edematous, leading to papilledema (swelling of the optic nerve head). Papilledema causes the optic disc margins to become blurred and indistinct. Without treatment, this condition can lead to blindness.

In helping a hypertensive patient control his weight, your primary responsibilities include educating him about his prescribed diet and monitoring his weight reduction. You’ll also need to regularly measure his blood pressure.Review the elements of the weight-reduction diet with your patient. If appropriate, obtain a referral for a dietitian to assist him and his family with planning appropriate meals. Provide him with suggestions to help him comply with the prescribed diet, keeping in mind his food preferences and ethnic background. Also, recommend alternative food choices for patients with poor dentition, food intolerances, and limited physical mobility. And stress the importance of reducing weight to reduce blood pressure.

When teaching your patient, tell him to eat regularly planned meals and to not skip meals. Teach him to measure his foods to determine the correct portions. Also, tell him to avoid foods that are high in fat and sugars and to reduce the amount of fat he uses in cooking. Suggest baking, broiling, or steaming food as a way to eliminate all fried foods from his diet. Also, recommend he reduce fat by removing the skin on poultry before cooking and have him increase his daily intake of fruits and vegetables. And warn your patient to avoid fad and crash diets, which reduce weight only temporarily. Monitor the success of your patient’s weight reduction by recording weekly weights. Don’t measure daily weights because they reflect the body’s fluid status and don’t usually indicate total body weight reduction.

Use ongoing blood pressure measurement to evaluate his body’s response to weight reduction. Blood pressure readings don’t immediately show dramatic decrease. However, some reduction in blood pressure may occur with a weight loss of as little as 10 pounds. Reinforce the success of weight and blood pressure reductions with your patient to encourage ongoing compliance with the prescribed regimen.

During treatment and then every hour thereafter, assess your patient’s organ functions until his blood pressure stabilizes. Once his blood pressure is stable, continue your assessments every 4 hours. Immediately report any changes to the physician.Assess your patient’s cardiovascular system for signs and symptoms of heart failure, including increased heart rate, arrhythmias, chest pain, shortness of breath, jugular vein distention, edema, crackles, murmurs, and heart sounds. Listen for carotid and abdominal bruits . Also, palpate peripheral pulses to determine whether they are of equal strength.

Monitor your patient’s neurologic status by determining his level of consciousness, pupil size, reaction to light, limb movement, and reactions to physical stimuli. To determine if his retinal function is impaired, ask him if he has experienced blurred vision, loss of vision, and any other vision changes.

Assess your patient’s renal status by measuring fluid intake and output hourly. Oliguria is the first sign of renal impairment, so immediately report urine output of less than 30 ml per hour for 2 consecutive hours. Obtain a urinalysis for proteinuria and hematuria. Also, obtain laboratory studies to detect rising BUN and creatinine levels.

When administering a parenteral drug to initially reduce your patient’s blood pressure, be sure to titrate the dosage based on the prescribed target pressure. Following the physician’s guidelines, decrease the dosage or discontinue the drug if the patient’s blood pressure drops below the target level.

While you titrate the dosage, monitor your patient’s blood pressure and MAP every 1 to 5 minutes, using an intra-arterial line. Intra-arterial pressure monitoring reflects systemic vascular resistance, not just blood flow.

When using intra-arterial blood pressure monitoring, remember to immobilize the insertion site and keep it visible. If the line is ejected or the tubing becomes detached, the patient can quickly lose a great deal of blood.

Familiarize yourself with the tubing and stop­cock positions. Set the alarm parameters 10 to 20 mm Hg above and below the patient’s baseline blood pressure and leave the alarm on at all times.

To ensure accurate readings, level the transducer’s air reference point at the phlebostatic axis-an imaginary line between the fourth intercostal space and the anteroposterior chest wall. And compare the arterial line pressure with the cuff pressure at least once per shift.

If direct blood pressure monitoring isn’t available, use an automated blood pressure monitoring machine. Monitor blood pressure and MAP every 15 to 30 minutes after your patient’s blood pressure stabilizes.

To prevent orthostatic hypotension, a common adverse effect of antihypertensive drugs, keep your patient on bed rest and help him change positions slowly. When his blood pressure stabilizes, administer an oral antihypertensive drug, as ordered, and monitor his blood pressure every 1 to 2 hours.

To relieve your patient’s anxiety, explain all procedures, monitoring equipment, and unfamiliar sounds. Also, explain why he must remain in the ICU. Don’t overwhelm him with too much information, but try to allay his fears by discussing his concerns and by making him as comfortable as possible.

Determine the extent of your patient’s pain and the severity of his headaches. Provide analgesics and anxiolytics, as prescribed, and monitor their effectiveness. Maintain a quiet environment and, if possible, place your patient in a private room. Reassure him that efforts are being made to reduce his blood pressure.

What to Tell The Home Care Nurse?

When your patient is discharged after treatment for emergency hypertension, give this information to his home care nurse:

• systolic and diastolic blood pressures at the time of discharge
• blood pressure abnormalities to report to the patient’s physician
• time of the last dose of each drug given in the hospital
• physical assessment findings upon discharge, including cardiovascular, neurologic, retinal, and renal findings
• a list of patient-education topics covered in the hospital and a note indicating which points may need reinforcement
• observations of interactions between the patient and his family
• an assessment of the patient’s ability to handle stress and a list of coping mechanisms that worked and didn’t work during his hospitalization.

You can measure a patient’s blood pressure directly or indirectly. To measure it directly, you’ll need an arterial catheter attached to a pressure measuring monitor. To measure it indirectly, you’ll need a blood pressure cuff, a stethoscope, and a sphygmomanometer, such as a mercury gravity or aneroid type.When performed correctly, indirect measurements are within 5 mm Hg of direct measurements. To measure blood pressure indirectly, first place an appropriate-sized blood pressure cuff on the patient’s arm. Then, place the bell of the stethoscope over the artery distal to the cuff. Next, inflate the cuff 30 mm Hg beyond the patient’s systolic pressure, at which point blood flow in the artery stops. Then, lower the cuff pressure and auscultate for Korotkoff sounds.

Korotkoff sounds

During auscultation, you’ll hear five Korotkoff sounds or phases. Phase 1 is characterized by a faint, clear, rhythmic tapping gradually increasing in intensity. The first sharp thump you hear is the systolic blood pressure, and this sound is produced by blood rushing into the collapsed artery as the pressure in the cuff decreases. The force of the blood determines the intensity of the sound.

Phase 2 begins when murmuring or swishing sounds are produced by blood flowing through the narrowed artery under the pressure cuff and into a wider artery distal to it. The difference in artery widths creates currents that cause the blood and vessel walls to vibrate. These sounds may temporarily disappear, particularly in hypertensive patients, and this silence is called the auscultatory gap. If you don’t detect the auscultatory gap, you may underestimate the patient’s systolic blood pressure or overestimate his diastolic pressure.

Phase 3 begins when the murmur of phase 2 disappears and the sounds begin to increase in intensity and clarity. In phase 3, the compressed vessel opens during systole but closes during diastole.

Phase 4 occurs when the sounds become muffled and less intense. This phase is referred to as the first diastolic pressure.

Finally, the sounds disappear completely in phase 5, also called the second diastolic pressure. During this phase, the vessel is completely open, and blood flows freely through the artery. At this point, you can palpate a strong radial pulse

Capillaries

Capillaries are the smallest and most numerous vessels in the arterial circulatory system. The walls of the capillaries consist of a fine, transparent, endothelial layer of tissue similar to the inner layer of the arteries. Capillaries have no elastic or muscular tissues, so nutrients and metabolic end products can pass through their thin walls.

Capillaries are interposed between arterioles and venules, creating networks. These networks permeate all tissues, supplying blood and nutrients. The more active the function of an organ or tissue, the greater the network of capillaries with­in it. These networks are typically large in bones and ligaments, smaller in glands and mucous membranes, and nearly absent in tendons.

Capillary networks contain specialized channels called metarterioles and rings of smooth muscle called precapillary sphincters. These sphincters contract and relax, regulating the flow of blood through the capillaries. Blood enters the capillary network as arterial blood, and after the exchange of nutrients and metabolic end products takes place, it exits as venous blood returning to the heart through the venous system .