Normally, the kidneys excrete creatinine-a waste product of muscle metabolism. Usually, serum creatinine levels range from 0.8 to 1.2 mg/dl in men and from 0.6 to 0.9 mg/dl in women. But when reduced blood flow through the glomeruli hinders renal excretion, serum creatinine levels are elevated.

The kidneys also filter and excrete the nitrogen fraction of urea-a waste product of protein metabolism. Normal BUN levels range from 8 to 26 mg/dl.

Test Implications

Elevated BUN levels alone don’t indicate renal dysfunction because infection, trauma, GI bleeding, diet, and dehydration can also increase BUN levels. But when a patient has elevated BUN and serum creatinine levels, he probably has reduced glomerular blood flow and kidney dysfunction.

If a patient is taking a diuretic or an ACE inhibitor to treat his hypertension, closely monitor his BUN and creatinine test results. Diuretics generally increase water and sodium excretion, which lowers circulating intravascular volume. As circulating volume decreases, so does renal blood flow, causing a rise in BUN and creatinine levels.

Other drugs can also influence a patient’s test results. For example, aminoglycosides can increase creatinine levels. Drugs such as allopurinol, furosemide, and indomethacin can increase BUN levels. And chloramphenicol can decrease BUN levels.

Changes in the patient’s protein intake and overhydration and underhydration can also affect the test results

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To avert this, one can definitely start with the positive lifestyle regime and also take plaque breaking medicines like EDTA Cardio Renew. This type of chelation therapy is said to be very effective for re-establishing the arterial blood flow. It literally detoxifies the arteries by expelling the excess minerals, calcium, and heavy metals out of them by chelation. Obviously when the blockages are removed, the blood flow reaches to vital organs without fail and they function efficiently.

The oral chelation therapy is effective not only against the plaque building within the arteries but also effective against certain diseases like Alzheimer’s disease, accelerated aging, diabetes and its complications, chronic fatigue syndrome, glaucoma, Raynaud’s disease, scleroderma, senile dementia, stroke, hair fall, and heart failure. There are many other conditions for which your doctor may like to prescribe you the easy oral chelation therapy.

For those who fret the long term extensive cardiac treatments and surgeries pertaining to them, oral chelation therapy is a blessing for sure. They can embark on healthy diet and exercise regime while continuing the therapy under an expert, and get rid of all their problems with this single-therapy regime!

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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.

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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.

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If your hypertensive patient has experienced an ischemic or hemorrhagic eVA, the physician may prescribe an antihypertensive drug to lower his blood pressure. However, if elevated Iep results from a hemorrhagic eVA, his blood pressure shouldn’t be reduced too quickly or too much.

The physician may prescribe heparin I.V. to treat TlAs and ischemic eVAs, but not to treat hemorrhagic eVAs because it increases the risk of bleeding. If heparin is administered for a TIA or an ischemic eVA, titrate the drug to maintain the PTT at about twice the normal level. Once your patient’s PTT has reached this therapeutic level, the physician may prescribe warfarin, which is taken orally. Typically, heparin therapy continues until the warfarin brings the prothrombin time to a therapeutic level.

If the patient has experienced an ischemic eVA, the physician may prescribe recombinant t-PA to disintegrate the thrombus or embolus that’s causing the occlusion .

A physician also may prescribe a drug that prevents platelet aggregation, such as aspirin, dipyridamole, or ticlopidine hydrochloride, to prevent thrombus and embolus formation and to treat an ischemic CVA.

After the patient has been stabilized, the physician may use drug therapy to minimize disability. Typically, he’ll prescribe mannitol I.V. to reduce cerebral edema. This drug draws fluid out of the extravascular space and into the vascular system.

If the patient has a large hematoma displacing a considerable amount of surrounding tissue or if drug therapy fails to lower his elevated ICP, he may require a craniotomy to remove the hematoma and relieve pressure.

A surgeon may perform an endarterectomy to reduce the risk of future TIAs or a CVA. This procedure removes atherosclerotic plaque that’s obstructing blood flow to the brain. Commonly, endarterectomies are performed on the common carotid bifurcation and the arch of the aorta.

If the surgeon can’t remove the obstruction causing an ischemic CVA, he may perform an extracranial-intracranial bypass. This procedure involves bypassing the intracranial artery just beyond the obstruction with an extracranial artery, thus restoring blood flow.

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Initially, your patient may complain of a severe, generalized headache and restlessness. This may progress to nausea and projectile vomiting. His neurologic signs and symptoms may include confusion, drowsiness, stupor, and generalized tonic­clonic or focal seizures. Because the encephalopathy results from emergency hypertension, he also may exhibit signs of impaired cardiovascular and renal function, such as myocardial ischemia and a decreased glomerular filtration rate.

Retinal damage also can result from hypertensive encephalopathy. An ophthalmic examination may reveal retinal hemorrhages, exudates, and papilledema-a condition known as grade I.V. hypertensive retinopathy.

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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.

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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.

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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.

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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.

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