Hypertension (Case 7)

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Hypertension (Case 7)

Elie R. Chemaly MD, MSc and Michael Kim MD

Case: A 59-year-old African-American woman is referred by her primary physician. She has had a history of severe hypertension for 38 years. She complains of dizziness, occipital headaches with blurred vision, and palpitations correlated with high BP sometimes reaching 200 mm Hg systolic and 120 mm Hg diastolic. She also has claudication of the legs and thighs upon walking four street blocks. She has a history of thyroid disease and is presently hypothyroid. Her medications on presentation were valsartan/hydrochlorothiazide 320 mg/25 mg (one tablet daily in the morning), clonidine 0.3 mg (one tablet daily in the evening), verapamil SR 240 mg (one tablet twice a day), and levothyroxine 0.1 mg (one tablet daily). Although she takes her medications each day as directed, she confides to you that she is concerned that they are becoming increasingly difficult for her to afford on a limited budget. She has an extensive family history of hypertension, and her father died at the age of 57 years in his sleep. On examination she weighs 68 kg, her pulse is 60 bpm, and her BP is 148/88 mm Hg. Her examination is remarkable for bilateral femoral bruits.

Differential Diagnosis

Essential hypertension


Sleep apnea

Renovascular disease

Primary aldosteronism

Primary mineralocorticoid excess, other than primary aldosteronism

Alcohol and substance abuse


Cushing syndrome (glucocorticoid excess)

Iatrogenic hypertension

Primary (parenchymal) renal disease

Other endocrine disorders: hypothyroidism, hyperthyroidism, hyperparathyroidism, acromegaly


Speaking Intelligently



Clinical Thinking

• The definition of hypertension is an operational definition, which means that a BP is considered to be in the hypertensive range when it requires treatment to lower it, not just when it is above the number considered to be normal, and such treatment is required when the benefit of therapy outweighs the risk of therapy. This explains the changes in the definition of hypertension over the course of the years, motivated by treatment availability and data on treatment benefit and treatment targets.

• The seventh report of the Joint National Committee (JNC 7), published in 2003, has issued those definitions.1 Based upon the average of two or more BP readings at each of two or more visits after an initial screen, the following classification is used:

Normal blood pressure: systolic less than 120 mm Hg and diastolic less than 80 mm Hg

Prehypertension: systolic 120 to 139 mm Hg or diastolic 80 to 89 mm Hg


Stage 1: systolic 140 to 159 mm Hg or diastolic 90 to 99 mm Hg

Stage 2: systolic ≥160 mm Hg or diastolic ≥100 mm Hg

• It is not the same thing to have hypertension and to have a BP that is not normal. The normal BP definition comes from studies recognizing a continuous rise in the risk of hypertension complications starting at a BP over 110/75 mm Hg (mainly cardiovascular morbidity and mortality).

• These definitions apply to adults on no antihypertensive medications and who are not acutely ill. If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension. The systolic pressure is the greater predictor of risk in patients over the age of 50 to 60 years. Also, systolic blood pressure (SBP) is measured more reliably than diastolic blood pressure (DBP) and classifies most patients. Isolated systolic hypertension is common in elderly patients; younger hypertensive patients tend to have elevations of both SBP and DBP. An isolated elevation of the DBP is much less common.

• I need to know if the patient, especially in the acute setting, is presenting with malignant hypertension, hypertensive emergency, or hypertensive urgency.

• If the patient is already receiving antihypertensive therapy, the diagnosis of hypertension is made. I need to assess the particular therapeutic goal for the BP of this patient, since BP treatment goals vary from patient to patient (see JNC 7 report1) and the appropriateness of the treatment.

• The decision to search for a secondary cause of hypertension and/or poor BP control is made on a case-by-case basis.


The history should search for precipitating or aggravating factors as well as an identifiable cause (secondary hypertension), establish the course of the disease, assess the extent of target organ damage, and look for other risk factors for cardiovascular disease.

• Duration and course of the disease

• Prior treatment, response, tolerance, and compliance. Noncompliance with treatment is an important cause of poor BP control.

• Medications, diet, and social history: Drugs that may aggravate or cause hypertension include sympathomimetics, steroids, NSAIDs, and estrogens; psychiatric medications causing a serotonin syndrome; cocaine and alcohol abuse. Withdrawal syndromes and rebound effects also need to be considered: alcohol, benzodiazepines, β-blockers, and clonidine.

• Family history

• Comorbidities, especially diabetes; diseases that can be secondary causes of hypertension (e.g., kidney disease); other cardiovascular risk factors (e.g., tobacco).

• Symptoms of sleep apnea: early-morning headaches, daytime somnolence, snoring, erratic sleep.

• Symptoms of severe hypertension, end-organ damage, or volume overload: epistaxis, headache, visual disturbances, neurologic deficits, dyspnea, chest pain, syncope, claudication.

• Symptoms suggestive of a secondary cause: headaches, sweating, tremor, tachycardia/palpitations, muscle weakness, and skin symptoms.

Physical Examination

Proper measurement of BP: Away from stressors, with an appropriate cuff size, use Korotkoff phase V for auscultatory DBP. Korotkoff phase V is when the sounds disappear; one can use phase IV when they muffle if they do not disappear until a BP of 0 mm Hg. SBP, measured by auscultation, can and should also be measured through the radial pulse: when the cuff is inflated above the SBP, the radial pulse disappears. This maneuver allows the assessment of auscultatory gap (a stiff artery that does not oscillate and leads to an auscultatory underestimation of SBP) and pseudo-hypertension (a stiff artery not compressed by the cuff; SBP is overestimated). In selected settings, BP should be measured in both arms (especially in the younger patient to assess for coarctation of the aorta). Measurements should be repeated at different visits, unless BP is markedly elevated, before treatment.

Vital signs, in particular heart rate in relationship to BP and treatments already taken. It may be important, especially in the acute setting, to know if the patient is febrile or hypoxic. Mental status is an important vital sign in the acute setting (hypertensive emergencies and urgencies).

General appearance: body fat, skin (cutaneous manifestations of endocrinopathies causing secondary hypertension).

Funduscopic examination to evaluate retinal complications.

Thyroid examination.

Cardiac auscultation (for murmurs and abnormal sounds: An S4 gallop may indicate the stiff left ventricle of hypertensive heart disease).

Vascular auscultation (carotid bruits, renal bruits, pulses): to assess atherosclerotic status and the presence of renal artery stenosis; the relationship between carotid artery disease, its treatment, and hypertension is not well understood.

Abdominal examination, especially of the aorta and the kidneys.

Neurologic examination, if applicable.

Tests for Consideration

ECG, mainly to assess for complications (atrial fibrillation, myocardial ischemia, LVH). Tachycardia (or atrial fibrillation) in the setting of hypertension may point to a secondary cause as well.


Glucose finger-stick to rule out hypoglycemia, pulse oximetry, arterial blood gas to rule out hypercapnia or hypoxia (in acute settings).


Metabolic panel: serum creatinine and electrolytes, especially potassium and glucose. The kidney is a key organ in the pathology of hypertension (see causes and complications), renal function and electrolytes are affected by antihypertensive therapy, and some metabolic abnormalities are a clue to a secondary cause. Examples include hypokalemia (in mineralocorticoid excess) and new-onset diabetes in the setting of several causes of secondary hypertension (e.g., Cushing).


Complete blood count including hemoglobin and hematocrit.
These abnormalities can be a clue to many life-threatening illnesses, some related to the hypertension. Besides, anemia can cause hyperdynamic circulation and polycythemia can cause hyperviscosity, and, in acute settings, thrombocytopenia can point to a microangiopathic condition associated with hypertension.


Urinalysis and microalbumin/creatinine ratio in urine.


Thyroid profile and other endocrine studies as indicated in the search for a secondary cause. Hypothyroidism is common in older women, has atypical presentations, and may worsen atherosclerosis and obesity; it is listed as a secondary cause of hypertension.


Lipid profile to assess cardiovascular risk.


Toxicology screen, especially when substance abuse is suspected.


• Laboratory and imaging workup for secondary causes (see individual paragraphs).


Sleep studies if applicable.


Ambulatory BP monitoring, when white coat hypertension or masked hypertension is suspected, to diagnose paroxysmal hypertension (i.e., pheochromocytoma), and to assess resistance to treatment.


Echocardiography to assess LVH (end-organ damage) and if cardiac dysfunction is suspected.



→ Echocardiography to assess LVH or if heart failure symptoms are present. Not routinely done on all hypertensive patients.


→ Renal artery imaging as needed for suspicion of renovascular hypertension (see Renovascular Disease under Clinical Entities).


→ Adrenal imaging as needed for primary aldosteronism, pheochromocytoma, or Cushing syndrome (see specific Clinical Entities). Pituitary imaging may also be needed. When searching for an endocrine cause of the hypertension, imaging should always be guided by hormonal assessment.


→ Peripheral vascular imaging (carotid arteries especially) in selected cases.


→ Brain imaging when a central nervous system cause of the hypertension is suspected (especially pituitary tumors for endocrine hypertension) or when stroke or brain hemorrhage is suspected as a complication.


Clinical Entities Medical Knowledge
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Essential Hypertension (90% of Patients)

Essential hypertension accounts for 90% of the cases of hypertension. The pathogenesis of essential hypertension is poorly understood. In fact, it does not appear to be one disease so that, among the multiple processes involved in the development of hypertension, one particular process may dominate the pathophysiology in a particular patient or group of patients. Among the important factors involved in essential hypertension are increased activity of the sympathetic nervous system, increased activity of the renin-angiotensin-aldosterone system, increased sodium retention (concepts of low-renin hypertension and impaired pressure natriuresis), low nephron mass, increased stiffness of the aorta and central arteries (thought to explain isolated systolic hypertension in the elderly), genetic factors, diet (high sodium and probably also low potassium intake), and psychosocial factors (especially the white coat form of hypertension).

Hypertension (whether essential or secondary) can lead to multiple complications, and the treatment of hypertension (a disease that is generally asymptomatic) is directed toward the prevention of those complications: cardiovascular disease (ischemic stroke, ischemic heart disease, aortic dissection—all manifestations of atherosclerosis), left ventricular hypertrophy, heart failure, atrial fibrillation, intracerebral hemorrhage, hypertensive nephropathy (different types exist), and hypertensive retinopathy.