CONFIRMING DIAGNOSIS Arterial digital subtraction angiography with assays of venous renin is the definitive diagnostic procedure. When stenosis is significant, transluminal angioplasty can be done during the same procedure.
❑ Gadolinium enhanced magnetic resonance angiography can identify turbulent blood flow indicative of renal stenosis.
❑ Duplex Doppler ultrasonography scans the renal artery and will reveal stenosis but results vary.
❑ Oral captopril renography is the simplest, noninvasive test for detection of renovascular hypertension but has a relatively high false-positive rate.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Pregnancy-induced hypertension:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
The following findings suggest preeclampsia:
❑ elevated blood pressure readings: 140 systolic, measured on two occasions, 6 hours apart; 90 diastolic, measured on two occasions, 6 hours apart
❑ proteinuria: at least 300 mg/24 hours.
The following findings suggest severe preeclampsia:
❑ higher blood pressure readings: 160/110 mm Hg or higher on two occasions, 6 hours apart, on bed rest
❑ increased proteinuria: 5 g/24 hours or more
❑ presence of pulmonary edema
❑ ultrasound: may reveal oligohydraminos
❑ oliguria: urine output less than or equal to 400 ml/24 hours.
Seizures strongly suggest eclampsia. Rarely, ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.
Real-time ultrasonography, stress and nonstress tests, and biophysical profiles evaluate fetal status. In the stress test, oxytocin stimulates contractions; fetal heart tones are then monitored electronically. In the nonstress test, fetal heart tones are monitored electronically during periods of fetal activity, without oxytocin stimulation. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.
Ultrasonography aids evaluation of fetal health by assessing fetal breathing movements, gross body movements, fetal tone, reactive fetal heart rate, and qualitative amniotic fluid volume.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Pulmonary hypertension:
Diagnosis
(Professional Guide to Diseases (Eighth Edition))
Characteristic diagnostic findings include:
❑ Auscultation reveals abnormalities associated with the underlying disorder.
❑ Arterial blood gas (ABG) analysis indicates hypoxemia (decreased partial pressure of arterial oxygen).
❑ Electrocardiography shows right axis deviation and tall or peaked P waves in inferior leads in the patient with right ventricular hypertrophy.
❑ Cardiac catheterization reveals pulmonary systolic pressure above 30 mm Hg as well as increased pulmonary artery wedge pressure (PAWP) if the underlying cause is left atrial myxoma, mitral stenosis, or left-sided heart failure (otherwise normal).
❑ Pulmonary angiography detects filling defects in pulmonary vasculature such as those that develop in patients with pulmonary emboli.
❑ Pulmonary function tests may show decreased flow rates and increased residual volume in underlying obstructive disease and decreased total lung capacity in underlying restrictive disease.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Blood pressure increase [Hypertension]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If you detect sharply elevated blood pressure, quickly rule out possible life-threatening causes. (See Managing elevated blood pressure.)
After ruling out life-threatening causes, complete a more leisurely history and physical examination. Determine if the patient has a history of cardiovascular or cerebrovascular disease, diabetes, or renal disease. Ask about a family history of high blood pressure—a likely finding in patients with essential hypertension, pheochromocytoma, or polycystic kidney disease. Then ask about its onset. Did high blood pressure appear abruptly? Ask the patient’s age. Sudden onset of high blood pressure in middle-aged or elderly patients suggests renovascular stenosis. Although essential hypertension may begin in childhood, it typically isn’t diagnosed until near age 35. Pheochromocytoma and primary aldosteronism usually occur between ages 40 and 60. If you suspect either, check for orthostatic hypotension. Take the patient’s blood pressure with him supine, sitting, and then standing. Normally, systolic pressure falls and diastolic pressure rises on standing; in orthostatic hypotension, both pressures fall.
Note headache, palpitations, blurred vision, and sweating. Ask about wine-colored urine and decreased urine output; these signs suggest glomerulonephritis, which can cause elevated blood pressure.
Obtain a drug history, including past and present prescription and over-the-counter drugs (especially decongestants) as well as herbal preparations. If the patient is already taking an antihypertensive, determine how well he complies with the regimen. Ask about his perception of elevated blood pressure. How serious does he believe it is? Does he expect drug therapy to help? Explore psychosocial or environmental factors that may impact blood pressure control.
Follow up the history with a thorough physical examination. Using a funduscope, check for intraocular hemorrhage, exudate, and papilledema, which characterize severe hypertension. Perform a thorough cardiovascular assessment. Check for carotid bruits and jugular vein distention. Assess skin color, temperature, and turgor. Palpate peripheral pulses. Auscultate for abnormal heart sounds (gallops, louder second sound, murmurs), rate (bradycardia, tachycardia), or rhythm. Then auscultate for abnormal breath sounds (crackles, wheezing), rate (bradypnea, tachypnea), or rhythm.
Palpate the abdomen for tenderness, masses, or liver enlargement. Auscultate for abdominal bruits. Renal artery stenosis produces bruits over the upper abdomen or in the costovertebral angles. Easily palpable, enlarged kidneys and a large, tender liver suggest polycystic kidney disease. Obtain a urine specimen to check for microscopic hematuria.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Hypertension:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Assessment for comorbid conditions. The patient’s past medical history should include an assessment for previous blood pressure readings. Any history of secondary disease or comorbid conditions should be documented: age more than 60 years, obesity, ischemic heart disease (IHD), cerebrovascular disease, peripheral vascular disease, retinopathy, nephropathy, dyslipidemia, diabetes mellitus, and menopausal status in women. A family history of these problems should also be documented, with particular emphasis on premature IHD in women aged less than 65 years, and in men aged less than age 55 years.
B. Medication history. The medication history should document the use of prescription, over-the-counter, and herbal preparations that may have hypertensive side effects.
C. Social history or habits. In addition, determine the use of tobacco, alcohol, or street drugs. The social history should also address leisure time physical activity and relevant psychosocial factors, which could affect ongoing HTN management.
D. Dietary history. Explore the ingestion of salt and saturated fats. Note recent weight changes, which can have significant effects on blood pressure.
Physical examination
A. Blood pressure measurement. Use a standardized technique (2,3) when measuring blood pressure to avoid spuriously high or low values. Patients should be seated in a chair, upright with back support, feet flat on the floor, arms bared, and supported at heart level. The patient should be resting at least 5 minutes before blood pressure measurements are taken. Stimulants such as nicotine and caffeine should be avoided at least 30 minutes prior to measurement. Appropriate cuff size is very important; the bladder within the cuff should circle at least 80% of the arm. Initial blood pressure measurements should include both arms; the arm with the higher reading should be used thereafter. It is recommended that two or more readings, separated by 2 minutes, be averaged. If the first two readings differ by more than 5 mm Hg, then additional readings should be obtained and averaged.
B. Additional physical examination. Height and weight should be measured. In a focused physical examination, pay particular attention to the fundi (for hemorrhages or vascular changes), the carotid arteries (for bruits), the heart (for murmurs), the abdomen (for bruits), and the extremities (for pulses, bruits, edema).
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Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Hypertension:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Essential hypertension
❑ White coat hypertension
❑ Renal artery stenosis
❑ Drug-induced hypertension
❑ Atherosclerotic vascular noncompliance
❑ Pheochromocytoma
❑ Cushing syndrome
❑ Hyperaldosteronism
❑ Aortic coarctation
❑ Acute renal artery obstruction
❑ Toxemia
Diagnostic Approach
The level of blood pressure associated with 50% increase in cardiovascular mortality: men younger than 45 years old, 130/90; men older than 45 years, 140/95; women, 160/95. An ankle-brachial systolic blood pressure ratio of less than 0.9 predicts a fourfold increase in cardiovascular mortality.
Clues to secondary hypertension include onset at a young age (,35), abrupt onset of hypertension, blood pressure difficult to control requiring high dosages of two or more drugs, and very high or labile blood pressure. Hypertension with relative tachycardia may be a clue to sympathetic effect or diastolic dysfunction. Headaches with severe hypertension are occipital and worse in the morning.
Hypertensive end organ damage must be searched for when the diastolic BP is greater than 130 mm Hg and the patient exhibits confusion, dyspnea, restlessness, or blurred vision. Perform fundoscopy looking for papilledema or retinal hemorrhages, and cardiopulmonary exam for third heart sound or bibasilar rales. Clues to hypertension-associated left ventricular hypertrophy include a fourth heart sound, an apical impulse greater than two intercostal spaces, a holosystolic sustained apical impulse diameter, and a hypertensive response to exercise ( .210 systolic). Cotton wool spots, which are caused by anoxic edema with axon degeneration, are seen in advanced hypertension (also in diabetes, dysproteinemia, and fat emboli).
Grading hypertensive retinopathy provides a marker of end-organ damage, which is tied to prognosis:
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Source: Field Guide to Bedside Diagnosis, 2007
Hypertension:
Diagnosis
(Handbook of Diseases)
Serial blood pressure measurements that are greater than 120/80 mm Hg but less than 140/90 mm Hg indicate prehypertension; measurements that are greater than 140/90 mm Hg confirm hypertension. Moderate (stage 1) and severe (stage 2) stages are based on systolic and diastolic levels. Auscultation may reveal bruits over the abdominal aorta and the carotid, renal, and femoral arteries; ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema.
The patient history and the following additional tests may show predisposing factors and help identify an underlying cause such as kidney disease:
❑ Urinalysis — The presence of protein, red blood cells, and white blood cells may indicate glomerulonephritis.
❑ Excretory urography — Renal atrophy indicates chronic kidney disease; one kidney that is more than ⅝"(1.5 cm) shorter than the other suggests unilateral kidney disease.
❑ Serum potassium — Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).
❑ Blood urea nitrogen (BUN) and serum creatinine levels — A BUN level that’s normal or elevated to more than 20 mg/dl and a serum creatinine level that’s normal or elevated to more than 1.5 mg/dl suggest kidney disease.
Other tests help detect cardiovascular damage and other complications:
❑ Electrocardiography may show left ventricular hypertrophy or ischemia.
❑ Chest X-ray may show cardiomegaly.
❑ Echocardiography may show left ventricular hypertrophy.
❑ Oral captopril challenge tests for renovascular hypertension. This functional diagnostic test depends on the abrupt inhibition of circulating angiotensin II by angiotensin-converting enzyme (ACE) inhibitors, removing the major support for perfusion through a stenotic kidney. The acutely ischemic kidney immediately releases more renin and undergoes a marked decrease in glomerular filtration rate and renal blood flow.
❑ Renal arteriography may show renal artery stenosis.
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Source: Handbook of Diseases, 2003
Hypertension, pregnancy-induced:
Diagnosis
(Handbook of Diseases)
The following findings suggest mild preeclampsia:
❑ elevated blood pressure readings — 140 mm Hg systolic or a rise of 30 mm Hg or more above the patient’s normal systolic pressure measured on two occasions, 6 hours apart; 90 mm Hg diastolic or a rise of 15 mm Hg or more above the patient’s normal diastolic pressure measured on two occasions, 6 hours apart
❑ proteinuria — greater than 500 mg/24 hours.
The following findings suggest severe preeclampsia:
❑ much higher blood pressure readings — 160/110 mm Hg or higher on two occasions, 6 hours apart, while on bed rest
❑ increased proteinuria — 5 g or more/24 hours
❑ oliguria — urine output less than or equal to 400 ml/24 hours
❑ deep tendon reflexes — possibly hyperactive as central nervous system (CNS) irritability increases.
Typical clinical features — especially seizures — with typical findings for severe preeclampsia strongly suggest eclampsia. An ophthalmoscopic examination may reveal vascular spasm, papilledema, retinal edema or detachment, and arteriovenous nicking or hemorrhage.
Real-time ultrasonography and stress and nonstress tests evaluate fetal well-being. In the stress test, oxytocin stimulates contractions; fetal heart tones are then monitored electronically.
In the nonstress test, fetal heart tones are monitored electronically during periods of fetal activity without oxytocin stimulation. Electronic monitoring reveals stable or increased fetal heart tones during periods of fetal activity.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Pulmonary hypertension:
Diagnosis
(Handbook of Diseases)
Characteristic diagnostic findings in patients with pulmonary hypertension include the following:
❑ auscultation: abnormalities associated with the underlying disorder
❑ arterial blood gas (ABG) analysis: hypoxemia (decreased partial pressure of oxygen)
❑ electrocardiography: in right ventricular hypertrophy, shows right-axis deviation and tall or peaked P waves in inferior leads
❑ cardiac catheterization: increased PAP — pulmonary systolic pressure above 30 mm Hg; pulmonary artery wedge pressure (PAWP) increased if the underlying cause is left-sided myxoma, mitral stenosis, or left-side failure — otherwise normal
❑ pulmonary angiography: detects filling defects in pulmonary vasculature, such as those that develop in patients with pulmonary emboli
❑ pulmonary function tests: in underlying obstructive disease, may show decreased flow rates and increased residual volume; in underlying restrictive disease, total lung capacity may decrease.
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Source: Handbook of Diseases, 2003
Pulse pressure, widened:
History
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Obtain the patient’s history, including a family medical history. Obtain a drug history. Has he experienced chest pain, shortness of breath, weakness, fatigue, or syncope? Ask the patient whether he recently had a fever. Ask about prolonged exposure to hot weather, excessive exercise, anxiety, or anemia.
Physical examination
Assess the patient for signs and symptoms of heart failure, such as crackles, dyspnea, and jugular vein distention. Check for changes in skin temperature and color and strength of peripheral pulses. Evaluate the patient’s LOC. Auscultate the heart for the presence of a murmur, and check for peripheral edema.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Pulse pressure, widened:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Obtain the patient’s medical, family, and drug histories. If you don’t suspect increased ICP, ask about such associated symptoms as chest pain, shortness of breath, weakness, fatigue, or syncope.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Hypertension:
Clinical Features and Diagnosis
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
Transient Hypertension
Frequentcauses are stress related (e.g., anxiety, pain, and burns). BP becomesnormal with relief of stress.Another cause is increase in intravascularvolume with excessive use of saline, blood, or plasma. When intravascularvolume normalizes, BP returns to normal.Finally, immobilization with placementin traction may cause increased BP, which resolves when immobilizationis no longer necessary. Sustained Hypertension
Birth–1 Yr
Renal Artery Thrombosis after Umbilical Artery Catheterization
BP shouldbe monitored in infants with umbilical artery catheter; they shouldcontinue to be monitored after catheter has been removed.Unilateral or bilateral enlarged kidneysand hematuria are clues to this diagnosis, which is usually confirmedby abdominal U/S with Doppler methods.If thrombosis involves aorta, femoralpulses may not be palpable and blood flow to lower extremities maybe compromised. Coarctation of Aorta
Usuallyinvolves thoracic aorta, although it can involve abdominal aorta.Increased BP occurs at least in rightupper arm with decreased BP and diminished or absent pulses in lowerextremities.2-D echocardiography, MRI, or aorticangiography can confirm diagnosis.After surgical repair, transient increasein BP may occur within 1–2 days. Sustained increase inBP may be observed during week after repair, and often a few weeksto a few months thereafter.Mechanism for persistent hypertensionin some patients after successful repair of coarctation may be relatedto overactivity of renin-angiotensin-aldosterone system. Congenital Renal Disease
Hypertension may occur with renal dysplasia,hydronephrosis, nephrotic syndrome, and polycystic kidney disease.See Chap. 1, Abdominal Masses; Chap. 28, Hematuria; and Chap. 50, Proteinuria. Renal Artery Stenosis
Stenosisof main or segmental renal artery caused by intrinsic or extrinsicrenal disease may result in severe hypertension.Causes of intrinsic disease includemedial fibromuscular dysplasia (neurofibromatosis, idiopathic),intimal fibroplasia (neurofibromatosis), arteritis (Kawasaki disease,Takayasu disease, moyamoya, radiation), trauma (blunt, surgical),atherosclerosis (familial dyslipoproteinemia), posttransplantation(surgical, immune), aneurysm, embolism, and specific syndromes (Williams,Turner).Causes of extrinsic disease includetumor (Wilms, pheochromocytoma, neuroblastoma, lymphoma), fibrousbands (congenital, postsurgical), and perirenal hematoma (trauma).Renal arteriography remains gold standardfor visualization of lesions. Other useful tests include abdominalU/S with Doppler methods, captopril renography, and CTfor detection of mass lesions. Bronchopulmonary Dysplasia
Infants with bronchopulmonary dysplasia maydevelop hypertension, even after discharge from nursery. See Chap. 10, Cough; Chap. 56, Respiratory Distress and Apnea;and Chap. 75, Wheezing. Patent Ductus Arteriosus
Common in neonates, especially in preterminfants. Diastolic pressure is typically low or normal, and pulsepressure is increased. Increase in systolic BP is presumably dueto larger LV stroke volume. See Chap.7, Cardiac Failure, and Chap. 27, Heart Murmurs (Asymptomatic). Intraventricular Hemorrhage
Common occurrence in preterm infants, especiallythose <32 wks' gestation. The more severe the hemorrhage(grades III and IV), the more likely that increased intracranialpressure will occur with an associated increase in BP. 1–10 Yrs
Renal Disease
Hypertension may occur with glomerulonephritis,pyelonephritis, hydronephrosis, hemolytic-uremic syndrome, and refluxnephropathy. See Chap. 1, AbdominalMasses; Chap.15, Dysuria; Chap.28, Hematuria; and Chap.50, Proteinuria. Coarctation of Aorta
See previous section Coarctation of Aorta. Renal Artery Stenosis
See previous section Renal Artery Stenosis. Glucocorticoid Excess
Most commoncause is use of corticosteroids or adrenocorticotropic hormone (ACTH)for underlying medical disorder.Less common cause is Cushing syndrome,which is usually due to adrenal hyperplasia or adrenal tumor thatresults in excess production of glucocorticoids and androgens. Usualcause of Cushing disease is pituitary adenoma producing excessiveamount of ACTH.Produces increased weight gain, hypertension,and slow linear growth. See Chap.44, Obesity. Sex Hormones
Oral contraceptives may produce hypertension.So may anabolic steroids that contain testosterone. Catecholamine Excess
Major catecholaminesare dopamine, norepinephrine, and epinephrine.Tumors that secrete excess catecholaminesinclude neuroblastoma and pheochromocytoma. Neuroblastoma
Malignanttumor that may arise from adrenal medulla or other sympathetic nervous tissue.Abdominal mass is common finding. Thereis usually increase in 24-hr urinary excretion of catecholamines.Abdominal U/S and CT can usuallylocate the tumor. See Chap. 1,Abdominal Masses. Pheochromocytoma
Peak incidenceof pheochromocytoma is in older children and adolescents. It maybe associated with neurofibromatosis and multiple endocrine neoplasiasyndromes.Clinical manifestations include paroxysmalhypertension, palpitations, headache, nausea, vomiting, and emotionallability.Increased concentration of catecholaminesand their metabolites (vanillymandelic acid is major metaboliteof epinephrine and norepinephrine) may be found in blood or 24-hrurine collectionIf suspected by biochemical tests,abdominal U/S, CT, or MRI can usually locate tumor in adrenalgland or along sympathetic chain. Another useful test is scintigraphywith metaiodobenzyl guanidine (MIBG) labeled with 123I.This compound concentrates in tissues that actively synthesize catecholaminesand can locate small tumors that may be otherwise difficult to detect. Mineralocorticoid Excess
Rare inchildhood.Plasma aldosterone concentration isincreased in true aldosterone excess, whereas in apparent mineralocorticoidexcess, features of aldosterone excess occur without increase inplasma aldosterone concentration.Causes of mineralocorticoid excessproducing hypertension are listed in Table32.3. '>
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Blood pressure, increased [Hypertension]:
History and physical examination
(Nursing: Interpreting Signs and Symptoms)
If you detect sharply elevated blood pressure, quickly rule out possible life-threatening causes. (See Managing elevated blood pressure, page 84.)
After ruling out life-threatening causes, complete a history and physical examination. Determine if the patient has a history of cardiovascular or cerebrovascular disease, diabetes, or renal disease. Ask about a family history of high blood pressure—a likely finding with essential hypertension, pheochromocytoma, or polycystic kidney disease. Then ask about its onset. Did high blood pressure appear abruptly? Ask the patient's age. The sudden onset of high blood pressure in middle-aged or elderly patients suggests renovascular stenosis. Although essential hypertension may begin in childhood, it typically isn't diagnosed until near age 35. Pheochromocytoma and primary aldosteronism usually occur between ages 40 and 60. If you suspect either, check for orthostatic hypotension. Take the patient's blood pressure with him lying down, sitting, and then standing. Normally, systolic pressure falls and diastolic pressure rises on standing. With orthostatic hypotension, both pressures fall.
Note headache, palpitations, blurred vision, and sweating. Ask about wine-colored urine and decreased urine output; these signs suggest glomerulonephritis, which can cause elevated blood pressure.
Obtain a drug history, including past and present prescriptions, herbal medicines, and over-the-counter drugs (especially decongestants). If the patient is already taking an antihypertensive, determine how well he complies with the regimen. Ask about his perception of elevated blood pressure. How serious does he believe it is? Does he expect drug therapy to help? Explore psychosocial or environmental factors that may impact blood pressure control.
Follow up the history with a thorough physical examination. Using a funduscope, check for intraocular hemorrhage, exudate, and papilledema, which characterize severe hypertension. Perform a thorough cardiovascular assessment. Check for carotid bruits and jugular vein distention. Assess skin color, temperature, and turgor. Palpate peripheral pulses. Auscultate for abnormal heart sounds (such as gallops, louder second sound, or murmurs), rate (for example, bradycardia or tachycardia), or rhythm. Then auscultate for abnormal breath sounds (such as crackles or wheezing), rate (for example, bradypnea or tachypnea), or rhythm.
Palpate the abdomen for tenderness, masses, or liver enlargement. Auscultate for abdominal bruits. Renal artery stenosis produces bruits over the upper abdomen or in the costovertebral angles. Easily palpable, enlarged kidneys and a large, tender liver suggest polycystic kidney disease. Obtain a urine sample to check for microscopic hematuria.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
HYPERTENSION:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Take the blood pressure yourself to be sure the hypertension is real;
24-hour blood pressure monitoring is now available. The workup of
hypertension includes a family history, serial electrolytes, urinalysis and
urine culture, and possibly “hypertensive” IVP and 24-hour urine VMA to
rule out treatable causes of hypertension. A complete hypertensive workup is
not usually performed today unless there is no family history of
hypertension, the hypertension does not respond to treatment, there are
other symptoms suggesting a surgical lesion (e.g., paroxysmal headaches), or
there is sudden onset of hypertension in a known normotensive individual.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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