HISTORY 42-year-old white man.

CHIEF COMPLAINT: Hypertension discovered in routine insurance

examination.

PRESENT ILLNESS: At age 22 a “slight” elevation in blood pressure was

noted on a military discharge physical examination. Since then he has gained

30 pounds, continued to smoke one package of cigarettes a day and has no

regular program of exercise. In the past he has noted mild dyspnea on exertion

and occasional headaches in the evening.

There is no history of heart murmur, renal disease, diabetes, or chest pain.

Proceed

36-1

PRESENT ILLNESS (continued): He has had no history of weakness,

polyuria, syncope, paroxysmal sweating, palpitations or abdominal pain. He

takes no drugs. His cholesterol has never been measured.

FAMILY HISTORY: An older brother has hypertension. His father also had

hypertension and died suddenly of a “heart attack.”

Question: Based on this history, what is your initial diagnostic impression?

36-2

Answer: The patient probably has primary (essential) hypertension.

In well over 90% of patients, hypertension is primary. This patient has no

historical clues to a secondary cause. With a positive family history, primary

hypertension is even more likely. Secondary causes of hypertension should

still be considered. In most cases, they may be excluded by the history,

physical examination and simple laboratory tests.

Question: What are the major causes of secondary hypertension?

36-3

Answer: The major causes of secondary hypertension include:

I. Adrenal

– Pheochromocytoma

– Hyperaldosteronism

– Cushing’s syndrome

II. Renal

– Parenchymal disease

– Vascular (e.g., arterial stenosis)

– Obstructive uropathy

III. Exogenous

– Drugs (e.g., NSAIDS, steroids, birth control pills)

IV. Coarctation of the aorta

Question: Has the history excluded any of these diagnoses?

36-4

Answer: Most of the causes of secondary hypertension have been virtually

excluded by the history.

Pheochromocytoma is usually associated with “spells.” A convenient mnemonic

is the 6 “P’s”–pheochromocytoma, paroxysms, perspiration, postural

hypotension, palpitations and pain (headaches). Obesity is uncommon, weight

gain is rare. Hyperaldosteronism is frequently associated with polyuria and

weakness. Cushing’s syndrome is primarily excluded by physical examination

and laboratory tests.

Proceed

36-5

There is no history to suggest glomerulonephritis, urinary infections or

obstructive uropathy. Physical examination is also important to detect some

causes of renal hypertension.

There is no history of drug use. If the patient were a woman, she should be

closely questioned about birth control pills.

Coarctation is best excluded by physical examination. In addition, there is no

history of murmur.

Question: How do you interpret the patient’s complaint of headache?

36-6

Answer: It is not uncommon for patients with hypertension to complain

of headache, tinnitus and nosebleeds, but these symptoms are not of

diagnostic value, as they are no more frequent in hypertensive patients than in

the general population.

The headache associated with severe hypertension is classically occipital in

location and is present upon awakening in the morning.

Questions: 1. What risk factors for coronary artery disease have been identified

by the history?

2. How do you interpret the patient’s dyspnea?

36-7

Answers: 1. Hypertension, smoking, and a positive family history are all risk factors for

coronary artery disease in this patient.

2. His exertional dyspnea may reflect his weight gain, smoking, poor physical

fitness and/or left ventricular dysfunction.

PHYSICAL SIGNS

a. GENERAL APPEARANCE - Normal appearing, moderately obese man.

Question: How is this patient’s general appearance helpful in excluding

secondary causes of hypertension?

36-8

Answer: The general appearance makes Cushing’s syndrome unlikely (no

“buffalo hump,” centripetal obesity, striae, or change in hair pattern). Rarely,

pheochromocytoma may be associated with neurofibromatosis, and coarctation

of the aorta with Turner’s syndrome.

Proceed

36-9

PHYSICAL SIGNS (continued)

b. JUGULAR VENOUS PULSE - The CVP is estimated to be 5 cm H2O.

Question: How do you interpret the jugular venous pulse?

1.0 SECOND

S1 S2

JUGULAR

VENOUS

PULSE

ECG

PHONO

LOWER LEFT

STERNAL EDGE

36-10

Answer: The CVP and jugular venous pulse are normal.

c. ARTERIAL PULSE - (BP = 170/110 mm Hg, right arm, lying)

Questions:

1. How do you interpret the blood pressure and arterial pulse?

2. What additional information concerning the blood pressure and arterial

pulses is required?

CAROTID

ECG

PHONO

LOWER LEFT

STERNAL EDGE S2

S1

36-11

Answers: 1. There is systolic and diastolic hypertension. The carotid pulse contour

is normal.

2. The blood pressure should be recorded in both arms lying and standing. It

should also be recorded in the legs, and the upper and lower extremity

pulses should be simultaneously palpated.

The blood pressure measured in the left arm, lying, was also

170/110 mm Hg. It did not change upon standing. Postural hypotension

may be seen in renovascular disease and pheochromocytoma, and its

absence is a significant negative finding.

The blood pressure is normally higher in the legs. In this patient, the

pressure measured with an appropriate size thigh cuff was 190/112 mm Hg.

In addition, simultaneous palpation of the upper extremity and femoral

pulses demonstrated no femoral decrease or delay. These observations

exclude coarctation of the aorta.

Proceed

36-12

d. PRECORDIAL MOVEMENT

Question: How do you interpret the apical impulse?

5th ICS

MIDCLAVICULAR

LINE

APEXCARDIOGRAM

ECG

36-13

Answer: The left ventricular impulse is sustained, but not displaced. There

is an abnormally prominent atrial filling wave (arrow). The sustained impulse is

consistent with ventricular hypertrophy from chronic hypertension. The

palpable presystolic impulse reflects enhanced left atrial contraction against a

poorly compliant left ventricle.

Proceed

36-14

e. CARDIAC AUSCULTATION

Question: How do you interpret the acoustic events at the apex?

PHONO-APEX

LOW FREQUENCY

APEXOCARDIOGRAM

36-15

36-16

Answer: The first and second heart sounds are normal. A fourth heart

sound is present (arrow). It is the acoustic equivalent of the palpable presystolic

movement of the apex impulse (broken arrow).

e. CARDIAC AUSCULTATION (continued)

Question: How do you interpret the acoustic events at the upper left

sternal edge?

UPPER LEFT STERNAL EDGE

ECG

EXPIRATION INSPIRATION

1

2L

1 1 2

A2 P2 A2

P2 .06 sec

Answer: There is a normal inspiratory splitting of the second sounds of .04

seconds. The aortic component is increased in intensity due to the high aortic

closing pressure. The increase in A2 is also well heard at the upper right

sternal edge.

Palpation of the abdomen revealed no masses, and on auscultation no bruits

were heard.

Question: What is the significance of these latter observations?

36-17

Answer: Palpation and auscultation of the abdomen are important in the

search for secondary causes of hypertension. Polycystic kidneys, if present

are frequently palpable. Abdominal and/or flank bruits suggest renal artery

stenosis. An enlarged urinary bladder may be seen with obstructive uropathy.

These findings are not present in this patient.

f. PULMONARY AUSCULTATION

Question: How do you interpret the acoustic events in the pulmonary lung

fields?

Proceed

36-18

36-19

g. FUNDOSCOPIC EXAMINATION - LEFT EYE

Question: How do you interpret these funduscopic findings?

Answer: In all lung fields, there are normal vesicular breath sounds.

Answer: The fundus shows a normal optic disk and mild hypertensive

vascular changes with a diminished arteriovenous (AV) ratio of 1/2

(normal = 4/5) and focal arteriolar spasm (arrow). The latter may imply rapidly

progressive and/or secondary forms of hypertension. Although significant

AV nicking (broken arrow) and increased arteriolar light reflex (white arrow)

are also present, the latter changes are arteriolar-sclerotic (reflecting chronicity

of the disease) and are not directly related to the degree of hypertension

or prognosis.

There are several systems for grading hypertensive funduscopic findings. One

such system follows. The increasingly severe changes to be described are

directly related to prognosis. This patient has grade II hypertensive retinopathy

by this classification.

Proceed

36-20

36-21

KEITH-WAGNER-BARKER GRADING SYSTEM

FOR HYPERTENSIVE RETINOPATHY

GRADE I Arteriolar Narrowing

GRADE II More Pronounced Generalized Narrowing

Plus Focal Areas of Narrowing

GRADE III Increased Severity of Grade II Changes

Plus Hemorrhages and Exudates

GRADE IV All of the Above Plus Papilledema

Proceed

36-22

g. FUNDOSCOPIC EXAMINATION (continued) - LEFT EYE

Question: How do you interpret this fundus from another patient?

36-23

Answer: The fundus is normal.

g. FUNDOSCOPIC EXAMINATION (continued) - LEFT EYE

Question: How do you interpret this fundus from still another patient?

36-24

Answer: This fundus shows papilledema (arrow), generalized and focal

arteriolar spasm (broken arrow), flame-shaped hemorrhages (white arrow) and

cotton-wool exudates (red arrow) - Grade IV hypertensive retinopathy.

ELECTROCARDIOGRAM

Question: How do you interpret this ECG?

III II aVR

V6 V5 V4 V3 V2 V1

aVF aVL I

V2 - 6 1/2 Standard

Answer: There is normal sinus rhythm and left ventricular hypertrophy as

evidenced by an increased QRS voltage, intrinsicoid delay and ST-T

wave changes.

CHEST X RAYS

Question: How do you interpret these chest X rays?

LATERAL PA

36-25

Answer: The pulmonary vasculature is normal. On the PA film there is a

prominent aortic knob (arrow). The cardiothoracic ratio is normal. In contrast to

ventricular dilation, it is common for concentric ventricular hypertrophy to occur

without an increase in cardiothoracic ratio.

In the lateral film, the inferoposterior prominence of the cardiac silhouette

(arrow) suggests some degree of left ventricular enlargement.

Question: Based in the history, physical examination, ECG and X rays,

what is your diagnostic impression?

36-26

Answer: This patient has significant hypertension with resulting left

ventricular hypertrophy and funduscopic changes. In patients with less

significant hypertension, the average of three blood pressure determinations

taken on separate occasions is necessary to establish the diagnosis.

In men between the ages of 35 and 50, with a positive family history and with

no evidence to suggest a secondary cause, hypertension is almost always

primary. It is, nonetheless, necessary for the physician to consider secondary

causes of hypertension, even though patients with potentially curable causes

make up less than 1% of all hypertension.

Question: What routine laboratory work should be obtained in this patient?

36-27

Answer: Routine tests that are recommended for hypertensive patients

include a urinalysis, BUN or creatinine and serum potassium. These tests are

obtained to screen for renal disease and hyperaldosteronism. In this patient,

they were normal.

In addition, risk factors for coronary artery disease should be determined. This

patient’s total cholesterol was elevated and his high density lipoprotein (HDL)

cholesterol was low, indicating an increased risk for coronary artery disease.

His triglycerides and fasting blood glucose were normal.

Question: Are additional laboratory tests indicated to rule out secondary

causes of hypertension and further evaluate this patient?

36-28

Answer: In this patient expensive screening tests for rare, curable

secondary causes of hypertension are unwarranted, as the history, physical

examination and simple laboratory tests have indicated that their presence is

unlikely. Thyroid studies might be helpful to rule out hyperthyroidism.

Echocardiography may be indicated in selected patients to define the anatomy

and function of the left ventricle.

Question: What are your therapeutic recommendations for this patient?

36-29

Answers: The goal of therapy should be to achieve blood pressure control

with the simplest, least costly program with the fewest side effects. The

therapeutic steps to be taken include:

1. Patient Education: He should be informed of the risk of his disease, the

benefits of therapy, and the likely need for lifelong serial blood pressure

assessment and treatment. Most patients can be instructed in how to take

their own blood pressure.

2. Diet: He should restrict salt, alcohol, cholesterol and saturated fat intake

and lose weight.

Proceed

36-30

36-31

Answers (continued):

3. Habits: He should stop smoking. After his blood pressure is controlled and

an exercise test is performed, he should consider a graded

exercise program.

4. Drug therapy: His initial therapy might include a beta-adrenergic blocker or

a low dose thiazide diuretic. Angiotensin converting enzyme (ACE)

inhibitors and calcium channel blocking agents may also be considered for

initial drug therapy in certain patients depending on age, race, associated

medical conditions and social background. If concomitant non-

pharmacologic therapy is successful in lowering the blood pressure,

medication may be reduced or eliminated.

Question: What is the mechanism of antihypertensive action of

thiazide diuretics?

Answer: The initial antihypertensive effect of thiazide diuretics relates to a

decrease in intravascular volume and, thereby, cardiac output. With continued

use, however, the cardiac output returns to control levels despite a continuing

antihypertensive effect. This long term antihypertensive action of thiazides is

related to their natriuretic effect and resultant decrease in arteriolar smooth

muscle sodium content and tone.

Proceed

36-32

The patient was initially treated with 25 mg of hydrochlorothiazide each

morning. The dose was increased to 50 mg due to an inadequate therapeutic

response. This therapy, coupled with his weight loss and sodium restriction,

resulted in an average blood pressure of 130/80 mm Hg sitting and standing.

Repeat laboratory studies revealed the potassium to be normal and the BUN,

fasting blood glucose, serum triglycerides and uric acid to be mildly elevated.

Question: What changes in his regimen are indicated?

36-33

Answer: Mild increases in BUN, triglycerides, glucose and uric acid are

common with high-dose thiazide therapy. Mild changes are not an indication to

modify treatment. Mild decreases in potassium are similarly not a cause for

concern in the patient without heart disease. With heart disease or with severe

hypokalemia, potassium supplementation with potassium chloride may be

indicated. Alternatively, a potassium sparing diuretic may be used.

Question: How should the patient be treated if there is an inadequate

response to high-dose diuretic therapy?

36-34

Answer: A second drug such as an ACE-Inhibitor may be added. ACE-

inhibitors or Angiotensin Receptor Blockers (ARBs) are indicated in

hypertensive patients with elevated serum glucose levels.

Other antihypertensive drugs include beta-blockers, vasodilators and CNS

active agents. These are outlined in the next slide.

Proceed

36-35

36-36

Proceed for Summary

VASODILATORS

ACE Inhibitors

Angiotensin-II Antagonists

Calcium Channel Blockers

Alpha 1 ( Beta) Blockers

Hydralazine / Minoxidil

CNS ACTIVE AGENTS

Clonidine

SUMMARY

Primary hypertension affects a very significant percent of the adult population.

It is often associated with a positive family history. In those who experience a

recent significant increase in blood pressure or refractory hypertension,

secondary causes should be sought.

The majority of patients with primary hypertension are asymptomatic. Hence,

detection is difficult, and the patient must be educated regarding the need for

long-term treatment. An initial observation of hypertension should be confirmed

by at least two additional determinations at least a week apart.

There are several variations of primary hypertension including labile, “white

coat,” isolated systolic hypertension and pre-hypertension. Labile hypertension

is a blood pressure that is quite variable from day-to-day. White coat

hypertension is hypertension only in the clinician’s office. Isolated systolic

hypertension is common in the elderly and is a systolic pressure of > 139

mmHg in the presence of a diastolic pressure of < 90 mmHg. Pre-hypertension

is a blood pressure of 120-139 / 80-89 mmHg. These patients should be

followed closely, as they are at higher risk for developing sustained

hypertension.

Proceed 36-37

SUMMARY (continued)

The need for medical treatment is determined not only by the level of blood

pressure, but also by risk factors such as age, sex, family history, smoking,

dyslipidemia and diabetes, as well as the presence or absence of damage to

the vessels of the heart, brain, kidney and eye (target organs). Anti-

hypertensive treatment should be initiated immediately not only in patients with

blood pressures of 170/90 mm Hg or more, but also in patients with lesser

degrees of hypertension who are diabetic or have evidence of target organ

damage.

Therapy in these patients as well as those with milder disease reduces the risk

for subsequent target organ damage, reduces the risk for sudden death from

aortic dissection, and may reduce the mortality from myocardial infarction. The

optimal goal of therapy is BP < 120/80 mm Hg.

Proceed

36-38

SUMMARY (continued)

In most cases, extensive metabolic and renal studies are unwarranted. In

addition, the history, physical examination and simple routine laboratory work

most often identify the very small subset of patients in whom additional studies

are indicated.

Maintenance of ideal weight, salt restriction and medication are the

cornerstones of initial medical therapy. The key to effective treatment,

however, is patient education. The patient should be advised of all correctable

risk factors for atherosclerotic cardiovascular disease and of the extreme

importance of long-term therapy and follow-up.

If hypertension remains undetected and/or untreated, serious disability and/or

death from stroke, renal failure, dissecting aortic aneurysm, congestive heart

failure or myocardial infarction are the usual sequelae. If detected early and

effectively treated, the risk of developing these complications is comparable to

the nonhypertensive patient.

36-39

36-40

PATHOLOGY

A typical autopsy specimen from a patient with untreated hypertension. There

is severe symmetrical thickening of the left ventricular wall measuring

approximately 25 mm (normal = 9-11 mm). The right ventricular wall thickness

is normal.

Proceed for Case Review

LEFT RIGHT

POSTERIOR

ANTERIOR

36-41

To Review This Case of

Moderate Primary Hypertension:

The HISTORY is typical in that the patient is asymptomatic, or has only

mild symptoms, and there are no historical clues to a secondary cause of

hypertension. The family history is positive for hypertension. Additional risk

factors (smoking and positive family history) for the development of

atherosclerotic cardiovascular disease are present.

PHYSICAL SIGNS:

a. The GENERAL APPEARANCE reveals the patient to be overweight,

without evidence of endocrinologic or other causes of hypertension.

b. The JUGULAR VENOUS PULSE is normal in mean pressure and

wave form.

c. The carotid and peripheral ARTERIAL PULSES are normal, and the

blood pressures in both upper and lower extremities reveal systolic and

diastolic hypertension. These findings exclude coarctation of the aorta.

Proceed

d. PRECORDIAL MOVEMENT reveals a nondisplaced, sustained systolic

impulse reflecting the afterloaded, hypertrophied left ventricle, and a

presystolic impulse due to an enhanced atrial contraction against the

thickened ventricle.

e. CARDIAC AUSCULTATION at the base reveals an enhanced A2 due to

augmented aortic root pressure. The second sound splits normally.

At the apex there is a fourth heart sound, the acoustic equivalent of the

palpable apical presystolic movement. The absence of abdominal and flank

bruits is an important negative finding, as they are commonly heard with

renal artery stenosis.

f. PULMONARY AUSCULTATION reveals normal vesicular breath sounds

in all lung fields.

g. FUNDUSCOPIC examination reveals arteriolar narrowing and focal

spasm (Grade II hypertensive retinopathy).

Proceed

36-42

The CHEST X RAYS show a slightly prominent aortic knob and

suggest left ventricular enlargement.

LABORATORY DATA show normal renal function, electrolytes and

uric acid. The results do not suggest a secondary cause of hypertension. The

total cholesterol is elevated with a low HDL cholesterol, indicating an increased

risk for coronary heart disease.

TREATMENT consists of weight reduction, salt restriction and

antihypertensive medication. A majority of hypertensive patients will require

multiple drug therapy. The treatment of his additional risk factors for coronary

artery disease includes the cessation of smoking, weight loss, restriction of

alcohol, cholesterol and saturated fats, and a graded exercise program after a

baseline exercise stress test. Careful follow-up of treatment and continuing

patient education and encouragement are mandatory.

36-43