Ebook Harrison''s manual of medicine (16th edition): Part 2

SECTION 8
CARDIOVASCULAR DISEASES

117
PHYSICAL EXAMINATION OF THE HEART
General examination of a pt with suspected heart disease should include vital
signs (respiratory rate, pulse, blood pressure), skin color, clubbing, edema, evidence of decreased perfusion (cool and sweaty skin), and hypertensive changes
in optic fundi. Important findings on cardiovascular examination include:
CAROTID ARTERY PULSE (Fig. 117-1)

• Pulsus parvus: Weak upstroke due to decreased stroke volume (hypovole-

mia, LV failure, aortic or mitral stenosis).
• Pulsus tardus: Delayed upstroke (aortic stenosis).
• Bounding (hyperkinetic) pulse: Hyperkinetic circulation, aortic regurgitation, patent ductus arteriosus, marked vasodilatation.
• Pulsus bisferiens: Double systolic pulsation in aortic regurgitation, hypertrophic cardiomyopathy.
• Pulsus alternans: Regular alteration in pulse pressure amplitude (severe LV
dysfunction).
• Pulsus paradoxus: Exaggerated inspiratory fall (Ͼ10 mmHg) in systolic bp
(pericardial tamponade, severe obstructive lung disease).
JUGULAR VENOUS PULSATION (JVP) Jugular venous distention
develops in right-sided heart failure, constrictive pericarditis, pericardial tamponade, obstruction of superior vena cava. JVP normally falls with inspiration
but may rise (Kussmaul’s sign) in constrictive pericarditis. Abnormalities in
examination include:

• Large “a” wave: Tricuspid stenosis (TS), pulmonic stenosis, AV dissociation (right atrium contracts against closed tricuspid valve).
• Large “v” wave: Tricuspid regurgitation, atrial septal defect.
• Steep “y” descent: Constrictive pericarditis.
• Slow “y” descent: Tricuspid stenosis.
PRECORDIAL PALPATION Cardiac apical impulse is normally localized in the fifth intercostal space, midclavicular line (Fig. 117-2). Abnormalities

A. Hypokinetic Pulse B. Parvus et Tardus Pulse

D. Bisferiens Pulse

C. Hyperkinetic Pulse

E. Dicrotic Pulse + Alternans

S

D

FIGURE 117-1 Carotid artery pulse patterns.

593
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594

SECTION 8 Cardiovascular Diseases

A

B

ECG

ECG

AOP

CP
OS

S4
S1

ES SC

S3

Apex

LSB

E
RF

W

a

a

O

ACG

S1

S2

JVP

A2 P2

c

v
x

y

FIGURE 117-2 A. Schematic representation of electrocardiogram, aortic pressure pulse (AOP),
phonocardiogram recorded at the apex, and apex cardiogram (ACG). On the phonocardiogram,
S1, S2, S3, and S4 represent the first through fourth heart sounds; OS represents the opening snap
of the mitral valve, which occurs coincident with the O point of the apex cardiogram. S3 occurs
coincident with the termination of the rapid-filling wave (RFW) of the ACG, while S4 occurs
coincident with the a wave of the ACG. B. Simultaneous recording of electrocardiogram, indirect
carotid pulse (CP), phonocardiogram along the left sternal border (LSB), and indirect jugular
venous pulse (JVP). ES, ejection sound; SC, systolic click.

include:

• Forceful apical thrust: Left ventricular hypertrophy.
• Lateral and downward displacement of apex impulse: Left ventricular dil-

atation.
• Prominent presystolic impulse: Hypertension, aortic stenosis, hypertrophic

cardiomyopathy.
• Double systolic apical impulse: Hypertrophic cardiomyopathy.
• Sustained “lift” at lower left sternal border: Right ventricular hypertrophy.
• Dyskinetic (outward bulge) impulse: Ventricular aneurysm, large dyskinetic
area post MI, cardiomyopathy.

AUSCULTATION
HEART SOUNDS (Fig. 117-2) S1 Loud: Mitral stenosis, short PR interval, hyperkinetic heart, thin chest wall. Soft: Long PR interval, heart failure,
mitral regurgitation, thick chest wall, pulmonary emphysema.
S2 Normally A2 precedes P2 and splitting increases with inspiration; abnormalities include:

• Widened splitting: Right bundle branch block, pulmonic stenosis, mitral regurgitation.
• Fixed splitting (no respiratory change in splitting): Atrial septal defect.
• Narrow splitting: Pulmonary hypertension.
• Paradoxical splitting (splitting narrows with inspiration): Aortic stenosis,
left bundle branch block, CHF.
• Loud A2: Systemic hypertension.
• Soft A2: Aortic stenosis (AS).
• Loud P2: Pulmonary arterial hypertension.
• Soft P2: Pulmonic stenosis (PS).


CHAPTER 117 Physical Examination of the Heart

595

S3 Low-pitched, heard best with bell of stethoscope at apex, following S2;
normal in children; after age 30– 35, indicates LV failure or volume overload.
S4 Low-pitched, heard best with bell at apex, preceding S1; reflects atrial
contraction into a noncompliant ventricle; found in AS, hypertension, hypertrophic cardiomyopathy, and CAD.

Opening Snap (OS) High-pitched; follows S2 (by 0.06– 0.12 s), heard at
lower left sternal border and apex in mitral stenosis (MS); the more severe the
MS, the shorter the S2 – OS interval.
Ejection Clicks High-pitched sounds following S1; observed in dilatation
of aortic root or pulmonary artery, congenital AS (loudest at apex) or PS (upper
left sternal border); the latter decreases with inspiration.
Midsystolic Clicks At lower left sternal border and apex, often followed
by late systolic murmur in mitral valve prolapse.
HEART MURMURS (Table 117-1, Fig. 117-3)
Systolic Murmurs
May be “crescendo-decrescendo” ejection type, pansystolic, or late systolic;
right-sided murmurs (e.g., tricuspid regurgitation) typically increase with inspiration.
Diastolic Murmurs

• Early diastolic murmurs: Begin immediately after S2, are high-pitched, and

are usually caused by aortic or pulmonary regurgitation.
• Mid-to-late diastolic murmurs: Low-pitched, heard best with bell of stethoscope; observed in MS or TS; less commonly due to atrial myxoma.
• Continuous murmurs: Present in systole and diastole (envelops S2); found
in patent ductus arteriosus and sometimes in coarctation of aorta; less common
Table 117-1
Heart Murmurs
SYSTOLIC MURMURS

Ejection-type

Holosystolic
Late-systolic

Aortic outflow tract

Aortic valve stenosis
Hypertrophic obstructive cardiomyopathy
Aortic flow murmur
Pulmonary outflow tract
Pulmonic valve stenosis
Pulmonic flow murmur
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
Mitral or tricuspid valve prolapse

DIASTOLIC MURMURS

Early diastolic
Mid-to-late diastolic
Continuous

Aortic valve regurgitation
Pulmonic valve regurgitation
Mitral or tricuspid stenosis
Flow murmur across mitral or tricuspid valves
Patent ductus arteriosus
Coronary AV fistula
Ruptured sinus of Valsalva aneurysm


596

SECTION 8 Cardiovascular Diseases

A

B

ECG

ECG
LVP

LVP

AOP

LAP
HSM
S1

EDM
S2

S1

ECG

A2

ECG
LVP
AOP

LVP
LAP

MSM
S1

PSM
A2

MDM
S1

S2

FIGURE 117-3 A. Schematic representation of ECG, aortic pressure (AOP), left ventricular
pressure (LVP), and left atrial pressure (LAP). The hatched areas indicated a transvalvular
pressure difference during systole. HSM, holosystolic murmur; MSM, midsystolic murmur.
B. Graphic representation of ECG, aortic pressure (AOP), left ventricular pressure (LVP),
and left atrial pressure (LAP) with hatched areas indicating transvalvular diastolic pressure
difference. EDM, early diastolic murmur; PSM, presystolic murmur; MDM, middiastolic
murmur.

causes are systemic or coronary AV fistula, aortopulmonary septal defect, ruptured aneurysm of sinus of Valsalva.

For a more detailed discussion, see O’Rourke RA, Braunwald E: Physical
Examination of the Cardiovascular System, Chap. 209, p. 1304, in
HPIM-16.

118
ELECTROCARDIOGRAPHY AND

ECHOCARDIOGRAPHY
STANDARD APPROACH TO THE ECG
Normally, standardization is 1.0 mV per 10 mm, and paper speed is 25 mm/s
(each horizontal small box ϭ 0.04 s).
HEART RATE Beats/min ϭ 300 divided by the number of large boxes
(each 5 mm apart) between consecutive QRS complexes. For faster heart rates,
divide 1500 by number of small boxes (1 mm apart) between each QRS.


CHAPTER 118 Electrocardiography and Echocardiography

N

DE
VI
AT
Ϫ60°
ϪIII

N

EXT
RE
ME

Ϫ90°
ϪaVF

LEFT
AX

IS

IO

Ϫ120°
ϪII

AX
I

Ϫ30°
ϩaVL

Ϫ150°
ϩaVR

0°
ϩI

180°
ϪI

IS

AL

AX

ϩ120°
ϩIII

IS

D

IA
TI

ON

ϩ60°
ϩII

ϩ90°
ϩaVF

RM

HT

EV

NO

RIG

ϩ30°
ϪaVR

ϩ150°

ϪaVL

AX

S

DE

IO
AT
VI

597

FIGURE 118-1 Electrocardiographic lead systems: The hexaxial frontal plane reference system to estimate electrical axis. Determine leads in which QRS deflections are maximum and
minimum. For example, a maximum positive QRS in I which is isoelectric in aVF is oriented to
0Њ. Normal axis ranges from Ϫ30Њ to ϩ90Њ. An axis Ͼ ϩ 90Њ is right axis deviation and Ͻ Ϫ30Њ
is left axis deviation.

I

II

III

aVR aVL aVF

V1

V2

V3

V4

V5

V6

RBBB

LBBB

LAH
RBBB
ϩ
LAH
RBBB
ϩ
LPH
FIGURE 118-2 Intraventricular conduction abnormalities. Illustrated are right bundle branch
block (RBBB); left bundle branch block (LBBB); left anterior hemiblock (LAH); right bundle
branch block with left anterior hemiblock (RBBB ϩ LAH); and right bundle branch block with
left posterior hemiblock (RBBB ϩ LPH). (Reproduced from RJ Myerburg: HPIM-12.)


Early

Early

ECG sequence with inferior Q wave infarction
III
II
I
aVR

ECG sequence with anterior Q wave infarction
aVR
III
II
I

aVL

aVL

aVF

aVF

V2

V2

V4

V4

FIGURE 118-3 Sequence of depolarization and repolarization changes with (A) acute anterior and (B) acute inferior wall Qwave infarctions. With anterior infarcts, ST elevation in leads I, aVL, and the precordial leads may be accompanied by reciprocal
ST depressions in leads II, III, and aVF. Conversely, acute inferior (or posterior) infarcts may be associated with reciprocal ST

depressions in leads V1 to V3. (After AL Goldberger, E Goldberger: Clinical Electrocardiography: A Simplified Approach, 6th
ed. St. Louis, Mosby-Year Book, 1999.)

Evolving

B

Evolving

A

V6

V6


CHAPTER 118 Electrocardiography and Echocardiography

I

II

III aVR aVL aVF

V1

V2

V3

V4

V5

599

V6

11/29

12/5

aVF

V2
2

2

1

3

1

FIGURE 118-4 Acute inferior wall myocardial infarction. The ECG of 11/29 shows minor
nonspecific ST-segment and T-wave changes. On 12/5 an acute myocardial infarction occurred.
There are pathologic Q waves (1), ST-segment elevation (2), and terminal T-wave inversion (3)
in leads II, III, and aVF indicating the location of the infarct on the inferior wall. Reciprocal
changes in aVL (small arrow). Increasing R-wave voltage with ST depression and increased

voltage of the T wave in V2 are characteristic of true posterior wall extension of the inferior
infarction. (Reproduced from RJ Myerburg: HPIM-12.)

RHYTHM Sinus rhythm is present if every P wave is followed by a QRS,
PR interval Ն 0.12 s, every QRS is preceded by a P wave, and the P wave is
upright in leads I, II, and III. Arrhythmias are discussed in Chap. 125.
MEAN AXIS If QRS is primarily positive in limb leads I and II, then axis
is normal. Otherwise, find limb lead in which QRS is most isoelectric (R ϭ S).
The mean axis is perpendicular to that lead (Fig. 118-1). If the QRS complex
is positive in that perpendicular lead, then mean axis is in the direction of that
lead; if negative, then mean axis points directly away from that lead.
Left-axis deviation (more negative than Ϫ30Њ) occurs in diffuse left ventricular disease, inferior MI; also in left anterior hemiblock (small R, deep S in
leads II, III, and aVF).
Right-axis deviation (Ͼ90Њ) occurs in right ventricular hypertrophy (R Ͼ S
in V1) and left posterior hemiblock (small Q and tall R in leads II, III, and aVF).
Mild right-axis deviation is seen in thin, healthy individuals (up to 110Њ).
INTERVALS (Normal values in parentheses) PR (0.12– 0.20 s)

• Short: (1) preexcitation syndrome (look for slurred QRS upstroke due to

“delta” wave), (2) nodal rhythm (inverted P in aVF).
• Long: first-degree AV block (Chap. 125).
Table 118-1
Leads with Abnormal Q Waves in MI
Leads with Abnormal Q Waves

Site of Infarction

V1 – V2
V3 – V4

I, aVL, V5 – V6
II, III, aVF
V1 – V2 (tall R, not deep Q)

Anteroseptal
Apical
Anterolateral
Inferior
True posterior


600

SECTION 8 Cardiovascular Diseases

Table 118-2
Differential Diagnosis of Q Waves (with Selected Examples)
Physiologic or positional factors
1. Normal variant “septal” Q waves
2. Normal variant Q waves in V1 to V2, aVL, III, and aVF
3. Left pneumothorax or dextrocardia
Myocardial injury or infiltration
1. Acute processes: myocardial ischemia or infarction, myocarditis, hyperkalemia
2. Chronic processes: myocardial infarction, idiopathic cardiomyopathy, myocarditis, amyloid, tumor, sarcoid, scleroderma
Ventricular hypertrophy/enlargement
1. Left ventricular (poor R-wave progression)a
2. Right ventricular (reversed R-wave progression)
3. Hypertrophic cardiomyopathy
Conduction abnormalities
1. Left bundle branch block

2. Wolff-Parkinson-White patterns
a

Small or absent R waves in the right to midprecordial leads.
Source: After AL Goldberger: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby-Year Book, 1991.

QRS (0.06– 0.10 s) Widened: (1) ventricular premature beats, (2) bundle
branch blocks: right (RsRЈ in V1, deep S in V6) and left [RRЈ in V6 (Fig. 1182)], (3) toxic levels of certain drugs (e.g., quinidine), (4) severe hypokalemia.
QT (Յ0.43 s; Ͻ50% of RR interval) Prolonged: congenital, hypokalemia,
hypocalcemia, drugs (quinidine, procainamide, tricyclics).
HYPERTROPHY

• Right atrium: P wave Ն 2.5 mm in lead II.
• Left atrium: P biphasic (positive, then negative) in V1, with terminal negative

force wider than 0.04 s.
Table 118-3

Clinical Uses of Echocardiography
2-D echo
Cardiac chambers:
size, hypertrophy,
wall motion abnormalities
Valves: morphology and motion
Pericardium: effusion, tamponade
Aorta: Aneurysm, dissection
Assess intracardiac masses
Doppler echocardiography
Valvular stenosis and regurgitation
Intracardiac shunts

Diastolic filling/dysfunction
Approximate intracardiac pressures

Transesophageal echocardiography
Superior to 2-D echo to identify:
Infective endocarditis
Cardiac source of embolism
Prosthetic valve dysfunction
Aortic dissection
Stress echocardiography
Assess myocardial ischemia and
viability


CHAPTER 118 Electrocardiography and Echocardiography

601

FIGURE 118-5 Two-dimensional echocardiographic still-frame images from a normal patient
with a normal heart. Upper: Parasternal long axis view during systole and diastole (left) and
systole (right). During systole, there is thickening of the myocardium and reduction in the size
of the left ventricle (LV). The valve leaflets ate thin and open widely. Lower: Parasternal short
axis view during diastole (left) and systole (right) demonstrating a decrease in the left ventricular
cavity size during systole as well as an increase in wall thickening. LA, left atrium; RV, right
ventricle; Ao, aorta. (Reproduced from RJ Myerburg in HPIM-12.)

• Right ventricle: R Ͼ S in V1 and R in V1 Ͼ 5 mm; deep S in V6; right-axis
deviation.
• Left ventricle: S in V1 plus R in V5 or V6 Ն 35 mm or R in aVL Ͼ 11 mm.
INFARCTION (Figs. 118-3 and 118-4) Q-wave MI: Pathologic Q waves

(Ն0.04 s and Ն25% of total QRS height) in leads shown in Table 118-1; acute
non-Q-wave MI shows ST-T changes in these leads without Q wave development. A number of conditions (other than acute MI) can cause Q waves (Table
118-2).
ST-T WAVES

• ST elevation: Acute MI, coronary spasm, pericarditis (concave upward) (see
Fig 121-1 and Table 121-2), LV aneurysm.
• ST depression: Digitalis effect, strain (due to ventricular hypertrophy), ischemia, or nontransmural MI.
• Tall peaked T: Hyperkalemia; acute MI (“hyperacute T”).
• Inverted T: Non-Q-wave MI, ventricular “strain” pattern, drug effect (e.g.,
digitalis), hypokalemia, hypocalcemia, increased intracranial pressure (e.g., subarachnoid bleed).


602

SECTION 8 Cardiovascular Diseases

A

C

2
1

AR

0 m/s
1

AS

2
3
Vmax ϭ 3.8 m/s

4
B

D

2
1

MS

0 m/s
1

MR

2
3
FIGURE 118-6 Schematic presentation of normal Doppler flow across the aortic (A) and mitral
valves (B). Abnormal continuous wave Doppler profiles are depicted in C. Aortic stenosis (AS)
[peak transaortic gradient ϭ 4 ϫ Vmax2 ϭ 4 ϫ (3.8)2 ϭ 58 mmHg] and regurgitation (AR). D.
Mitral stenosis (MS) and regurgitation (MR).

INDICATIONS FOR ECHOCARDIOGRAPHY
(Table 118-3 and Fig. 118-5)
VALVULAR STENOSIS Both native and artificial valvular stenosis can

be evaluated, and severity can be determined by Doppler [peak gradient ϭ 4 ϫ
(peak velocity)2].
VALVULAR REGURGITATION Structural lesions (e.g., flail leaflet,
vegetation) resulting in regurgitation may be identified. Echo can demonstrate
whether ventricular function is normal; Doppler (Fig. 118-6) can identify and
estimate severity of regurgitation through each valve.
VENTRICULAR PERFORMANCE Global and regional wall motion
abnormalities of both ventricles can be assessed; ventricular hypertrophy/infiltration may be visualized; evidence of pulmonary hypertension may be obtained.
CARDIAC SOURCE OF EMBOLISM May visualize atrial or ventricular thrombus, intracardiac tumors, and valvular vegetations. Yield of identifying cardiac source of embolism is low in absence of cardiac history or physical
findings. Transesophageal echocardiography is more sensitive than standard
transthoracic study for this purpose.
ENDOCARDITIS Vegetation visualized in more than half of pts (transesophageal echo has much higher sensitivity), but management is generally


CHAPTER 119 Valvular Heart Disease

603

based on clinical findings, not echo. Complications of endocarditis (e.g., valvular regurgitation) may be evaluated.
CONGENITAL HEART DISEASE Echo, Doppler, and contrast echo
(rapid IV injection of saline) are noninvasive procedures of choice in identifying
congenital lesions.
AORTIC ROOT Aneurysm and dissection of the aorta may be evaluated
and complications (aortic regurgitation, tamponade) assessed (Chap. 127).
HYPERTROPHIC CARDIOMYOPATHY, MITRAL VALVE PROLAPSE, PERICARDIAC EFFUSION Echo is the diagnostic technique of
choice for identifying these conditions.

For a more detailed discussion, see Goldberger AL: Electrocardiography,
Chap. 210, p. 1311; Nishimura RA, Gibbons RJ, Glockner JF, Tajik AJ:
Noninvasive Cardiac Imaging: Echocardiography, Nuclear Cardiology,

and MRI/CT Imaging, Chap. 211, p. 1320, in HPIM-16.

119
VALVULAR HEART DISEASE
MITRAL STENOSIS (MS)
ETIOLOGY Most commonly rheumatic, although history of acute rheumatic fever is now uncommon; congenital MS is an uncommon cause, observed
primarily in infants.
HISTORY Symptoms most commonly begin in the fourth decade, but
MS often causes severe disability by age 20 in economically deprived areas.
Principal symptoms are dyspnea and pulmonary edema precipitated by exertion,
excitement, fever, anemia, paroxysmal tachycardia, pregnancy, sexual intercourse, etc.
PHYSICAL EXAMINATION Right ventricular lift; palpable S1; opening snap (OS) follows A2 by 0.06 to 0.12 s; OS– A2 interval inversely proportional to severity of obstruction. Diastolic rumbling murmur with presystolic
accentuation in sinus rhythm. Duration of murmur correlates with severity of
obstruction.
COMPLICATIONS Hemoptysis, pulmonary embolism, pulmonary infection, systemic embolization; endocarditis is uncommon in pure MS.
LABORATORY ECG Typically shows atrial fibrillation (AF) or left
atrial (LA) enlargement when sinus rhythm is present. Right-axis deviation and
RV hypertrophy in the presence of pulmonary hypertension.
CXR Shows LA and RV enlargement and Kerley B lines.
ECHOCARDIOGRAM Most useful noninvasive test; shows inadequate
separation, calcification and thickening of valve leaflets, and LA enlargement.


604

SECTION 8 Cardiovascular Diseases

Doppler echocardiogram allows estimation of transvalvular gradient and mitral
valve area (Chap. 118).

TREATMENT

See Fig. 119-1.

Pts should receive prophylaxis for rheumatic fever (penicillin) and infective
endocarditis (Chap. 85). In the presence of dyspnea, medical therapy for heart
failure; digitalis, beta blockers, or rate-limiting calcium channel antagonists
(i.e., verapamil or diltiazem) to slow ventricular rate in AF; diuretics and
sodium restriction. Warfarin (with target INR 2.0– 3.0) for pts with AF and/
or history of systemic and pulmonic emboli. Mitral valvotomy in the presence
of symptoms and mitral orifice Յ ϳ1.7 cm2. In uncomplicated MS, percutaneous balloon valvuloplasty is the procedure of choice; if not feasible, then
open surgical valvotomy.

MITRAL REGURGITATION (MR)
ETIOLOGY Rheumatic heart disease in ϳ33%. Other causes: mitral
valve prolapse, ischemic heart disease with papillary muscle dysfunction, LV
dilatation of any cause, mitral annular calcification, hypertrophic cardiomyopathy, infective endocarditis, congenital.
CLINICAL MANIFESTATIONS Fatigue, weakness, and exertional
dyspnea. Physical examination: sharp upstroke of arterial pulse, LV lift, S1 diminished: wide splitting of S2; S3; loud holosystolic murmur and often a brief
early-mid-diastolic murmur.

Mitral Stenosis

Rheumatic fever prophylaxis until ϳ age 35
(Benzathine penicillin G 1.2 M units IM q month
or penicillin V 125–250 mg PO bid)
Endocarditis prophylaxis (Chap. 85)

? atrial
fibrillation

(AF)

yes

Control ventricular rate
(beta blockers, digoxin,
verapamil, or diltiazem)
Anticoagulation
(heparin, warfarin)

no
Valve surgery
or balloon
valvuloplasty

yes

? severe
symptoms

? AF poorly
tolerated or
recent onset

no
yes
Control mild
symptoms
with low-dose
diuretic

FIGURE 119-1 Management of mitral stenosis.

Chemical/electrical
cardioversion
(ideally Ն 3 weeks
of anticoagulation)


CHAPTER 119 Valvular Heart Disease

605

ECHOCARDIOGRAM Enlarged LA, hyperdynamic LV; Doppler echocardiogram helpful in diagnosing and assessing severity of MR.

TREATMENT

See Fig. 119-2.

For severe/decompensated MR, treat as for heart failure (Chap. 126), including diuretics and digoxin. Afterload reduction (ACE inhibitors, hydralazine,
or IV nitroprusside) decreases the degree of regurgitation, increases forward
cardiac output, and improves symptomatology. Endocarditis prophylaxis is
indicated, as is anticoagulation in the presence of atrial fibrillation. Surgical
treatment, either valve repair or replacement, is indicated in the presence of
symptoms or evidence of progressive LV dysfunction (LVEF Ͻ 60% or endsystolic LV diameter by echo Ͼ45 mm). Operation should be carried out
before development of severe chronic heart failure.

MITRAL VALVE PROLAPSE (MVP)
ETIOLOGY Most commonly idiopathic; ?familial; may accompany
rheumatic fever, ischemic heart disease, atrial septal defect, the Marfan syndrome.

Mitral Regurgitation (MR)

• Afterload reduction;
e.g. IV nitroprusside
(Chap. 123)
• Diuretics if needed
for LV failure

yes

? acute
severe
MR
no
yes
? atrial
fibrillation

• Control ventricular
rate (e.g., beta
blockers, digoxin)
• Anticoagulation
(heparin, warfarin)
If AF poorly tolerated:
• Chemical/electrical
cardioversion
(ideally Ն 3 weeks
of anticoagulation)
no

Surgical
reconstruction
or replacement

yes ? surgical
candidate

yes
? symptoms*
no

no

Chronic management
of asymptomatic patient:
• endocarditis prophylaxis
• serial assessment of LV
function by echo

• Oral afterload reduction
(ACEI or hydralazine)
• Diuretics and/or digoxin
for CHF symptoms

yes

? LV
Progressive
enlargement or

ESD Ͼ 45 mm

no

FIGURE 119-2 Management of advanced mitral regurgitation. *Including class II; ACEI, angiotensin-converting enzyme inhibitors; ESD, end-systolic diameter.


606

SECTION 8 Cardiovascular Diseases

PATHOLOGY Redundant mitral valve tissue with myxedematous degeneration and elongated chordae tendineae.
CLINICAL MANIFESTATIONS More common in females. Most pts
are asymptomatic and remain so. Most common symptoms are atypical chest
pain and a variety of supraventricular and ventricular arrhythmias. Most important complication is severe MR resulting in LV failure. Rarely, systemic
emboli from platelet-fibrin deposits on valve. Sudden death is a very rare complication.
PHYSICAL EXAMINATION Mid or late systolic click(s) followed by
late systolic murmur; exaggeration by Valsalva maneuver, reduced by squatting
and isometric exercise (Chap. 117).
ECHOCARDIOGRAM Shows posterior displacement of one or both mitral leaflets late in systole.

TREATMENT
Asymptomatic pts should be reassured, but if systolic murmur and/or typical
echocardiographic findings with thickened leaflets are present, or significant
MR, prophylaxis for infective endocarditis is indicated. Valve repair or replacement for pts with severe mitral regurgitation; aspirin or anticoagulants
for pts with history of TIA or embolization.

AORTIC STENOSIS (AS)
ETIOLOGY Often congenital; rheumatic AS is usually associated with
rheumatic mitral valve disease. Idiopathic, calcific AS is a degenerative disorder

common in the elderly and usually mild.
SYMPTOMS Dyspnea, angina, and syncope are cardinal symptoms; they
occur late, after years of obstruction.
PHYSICAL EXAMINATION Weak and delayed arterial pulses with carotid thrill. Double apical impulse; A2 soft or absent; S4 common. Diamondshaped systolic murmur Ն grade 3/6, often with systolic thrill.
LABORATORY ECG and CXR
useful for predicting gradient.

Often show LV hypertrophy, but not

ECHOCARDIOGRAM Shows thickening of LV wall, calcification and
thickening of aortic valve cusps. Dilatation and reduced contraction of LV indicate poor prognosis. Doppler useful for estimating gradient and calculating
valve area.

TREATMENT

See Fig. 119-3.

Avoid strenuous activity in severe AS, even in asymptomatic phase. Treat
heart failure in standard fashion (Chap. 126), but avoid afterload reduction.
Statin therapy may slow progression of leaflet calcification. Valve replacement is indicated in adults with symptoms resulting from AS and hemodynamic evidence of severe obstruction. Operation should be carried out before
frank failure has developed.

AORTIC REGURGITATION (AR)
ETIOLOGY Rheumatic etiology is common, especially if rheumatic mitral disease present; may also be due to infective endocarditis, syphilis, aortic


CHAPTER 119 Valvular Heart Disease

607

AS without
symptoms present
on physical
examination

Mild-to-moderate
AS and symptoms
present on physical
examination

Severe
AS and symptoms
present on physical
examination

Perform Doppler
echocardiography

Search for other
causes of
symptoms

Perform coronary
arteriography
and AVR

If
echocardiography
shows mild-tomoderate AS,
monitor patient

for development
of symptoms

If symptoms
develop,
repeat
echocardiography

If AS
becomes
severe,
perform
coronary
arteriography
and AVR

If patient
remains
asymptomatic
but findings
on examination
change,
repeat
echocardiography

If echocardiography
shows severe AS,
perform exercise
testing

If results
are normal,
monitor
patient
closely

If results
are abnormal,
perform coronary
arteriography
and AVR

If AS
remains mild
to moderate,
continue
follow up

FIGURE 119-3 Algorithm for the management of aortic stenosis (AS). AVR, aortic valve
replacement. (From BA Carabello: N Engl J Med 346:677, 2002.)

dissection, or aortic dilatation due to cystic medial necrosis; three-fourths of pts
are males.
CLINICAL MANIFESTATIONS Exertional dyspnea and awareness of
heartbeat, angina pectoris, and signs of LV failure. Wide pulse pressure, waterhammer pulse, capillary pulsations (Quincke’s sign), A2 soft or absent, S3
common. Blowing, decrescendo diastolic murmur along left sternal border
(along right sternal border with aortic dilatation). May be accompanied by systolic murmur of augmented blood flow.
LABORATORY ECG and CXR

LV enlargement.

ECHOCARDIOGRAM Increased excursion of posterior LV wall, LA
enlargement, LV enlargement, high-frequency diastolic fluttering of mitral
valve. Doppler studies useful in detection and quantification of AR.


608

SECTION 8 Cardiovascular Diseases

TREATMENT
Standard therapy for LV failure (Chap. 126). Vasodilators (long-acting nifedipine or ACE inhibitors) may delay need for operation. Surgical valve replacement should be carried out in pts with severe AR when symptoms develop or in asymptomatic pts with LV dysfunction (LV ejection fraction
Ͻ 55%, LV end-systolic volume Ͼ 55 mL/m2, or end-systolic diameter Ͼ 55
mm) by echocardiography.

TRICUSPID STENOSIS (TS)
ETIOLOGY Usually rheumatic; most common in females; almost invariably associated with MS.
CLINICAL MANIFESTATIONS Hepatomegaly, ascites, edema, jaundice, jugular venous distention with slow y descent (Chap. 117). Diastolic rumbling murmur along left sternal border increased by inspiration with loud presystolic component. Right atrial and superior vena caval enlargement on chest
x-ray.

TREATMENT
In severe TS, surgical relief is indicated, with valvular repair or replacement.

TRICUSPID REGURGITATION (TR)
ETIOLOGY Usually functional and secondary to marked RV dilatation
of any cause and often associated with pulmonary hypertension.
CLINICAL MANIFESTATIONS Severe RV failure, with edema, hepatomegaly, and prominent v waves in jugular venous pulse with rapid y descent
(Chap. 117). Systolic murmur along lower left sternal edge is increased by
inspiration.

TREATMENT
Intensive diuretic therapy when right-sided heart failure signs are present. In
severe cases (in absence of severe pulmonary hypertension), surgical treatment consists of tricuspid annuloplasty or valve replacement.

For a more detailed discussion, see Braunwald E: Valvular Heart Disease,
Chap. 219, p. 1390, in HPIM-16.


CHAPTER 120 Cardiomyopathies and Myocarditis

609

120
CARDIOMYOPATHIES AND MYOCARDITIS
Table 120-1 summarizes distinguishing features of the cardiomyopathies.

DILATED CARDIOMYOPATHY (CMP)
Symmetrically dilated left ventricle (LV), with poor systolic contractile function; right ventricle (RV) commonly involved.
ETIOLOGY Previous myocarditis or “idiopathic” most common; also
toxins (ethanol, doxorubicin), connective tissue disorders, muscular dystrophies,
“peripartum.” Severe coronary disease/infarctions or chronic aortic/mitral regurgitation may behave similarly.
SYMPTOMS Congestive heart failure (Chap. 126); tachyarrhythmias and
peripheral emboli from LV mural thrombus occur.
PHYSICAL EXAMINATION Jugular venous distention (JVD), rales,
diffuse and dyskinetic LV apex, S3, hepatomegaly, peripheral edema; murmurs
of mitral and tricuspid regurgitation are common.
LABORATORY ECG
normalities common.

Left bundle branch block and ST-T-wave ab-

CXR Cardiomegaly, pulmonary vascular redistribution, pulmonary effusions common.
Echocardiogram LV and RV enlargement with globally impaired contraction. Regional wall motion abnormalities suggest coronary artery disease
rather than primary cardiomyopathy.
Brain Natriuretic Peptide (BNP) Level elevated in heart failure/cardiomyopathy but not in patients with dyspnea due to lung disease.

TREATMENT
Standard therapy of CHF (Chap. 126); vasodilator therapy with ACE inhibitor
(preferred), angiotensin receptor blocker or hydralazine-nitrate combination
shown to improve longevity. Add beta blocker in most pts (Chap. 126). Add
spironolactone for patients with advanced heart failure. Chronic anticoagulation with warfarin, recommended for very low ejection fraction (Ͻ25%), if
no contraindications. Antiarrhythmic drugs (Chap. 125), e.g., amiodarone,
indicated only for symptomatic or sustained arrhythmias as they may cause
proarrhythmic side effects; implanted internal defibrillator is often a better
alternative. Consider biventricular pacing for persistently symptomatic patients with widened (Ն130 ms) QRS complex. Possible trial of immunosuppressive drugs, if active myocarditis present on RV biopsy (controversial as
long-term efficacy has not been demonstrated). In selected pts, consider cardiac transplantation.

RESTRICTIVE CARDIOMYOPATHY
Increased myocardial “stiffness” impairs ventricular relaxation; diastolic ventricular pressures are elevated. Etiologies include infiltrative disease (amyloid,
sarcoid, hemochromatosis, eosinophilic disorders), myocardial fibrosis, Fabry’s
disease, and fibroelastosis.
SYMPTOMS Are of CHF, although right-sided heart failure often predominates, with peripheral edema and ascites.


Left ventricular dilatation and dysfunction

Left ventricular dilatation and dysfunction (RVG)
Left ventricular dilatation and dysfunction
Elevated left- and often right-sided filling pressures
Diminished cardiac output

Echocardiogram

Radionuclide studies

Note: RVG, radionuclide ventriculogram; 201Tl, thallium 201.
Source: J Wynne, E Braunwald, Table 221-3 in HPIM-16.

Cardiac catheterization

Electrocardiogram

Moderate to marked cardiac silhouette
enlargement
Pulmonary venous hypertension
ST-segment and T-wave abnormalities

Chest roentgenogram

Dilated

Laboratory Evaluation of the Cardiomyopathies

Table 120-1

Increased left ventricular wall thickness
Normal or mildly reduced systolic function
Normal or mildly reduced systolic function (RVG)
Normal or mildly reduced systolic function
Elevated left- and right-sided filling

pressures

Low voltage,
conduction defects

Mild cardiac silhouette enlargement

Restrictive

ST-segment and T-wave abnormalities
Left ventricular hypertrophy
Abnormal Q waves
Asymmetric septal hypertrophy (ASH)
Systolic anterior motion (SAM) of the
mitral valve
Vigorous systolic function (RVG)
Perfusion defect (201Tl)
Vigorous systolic function
Dynamic left ventricular outflow obstruction
Elevated left- and right-sided filling
pressures

Mild to moderate cardiac silhouette enlargement

Hypertrophic


CHAPTER 120 Cardiomyopathies and Myocarditis

611

PHYSICAL EXAMINATION Signs of right-sided heart failure: JVD,
hepatomegaly, peripheral edema, murmur of tricuspid regurgitation. Left-sided
signs may also be present.
LABORATORY ECG
T-wave abnormalities.

Low limb lead voltage, sinus tachycardia, ST-

CXR Mild LV enlargement.
Echocardiogram Bilateral atrial enlargement; increased ventricular thickness (“speckled pattern”) in infiltrative disease, especially amyloidosis. Systolic
function is usually normal but may be mildly reduced.
Cardiac Catheterization Increased LV and RV diastolic pressures with
“dip and plateau” pattern; RV biopsy useful in detecting infiltrative disease
(rectal or fat pad biopsy useful in diagnosis of amyloidosis).
Note: Must distinguish restrictive cardiomyopathy from constrictive pericarditis, which is surgically correctable. Thickening of pericardium in pericarditis usually apparent in CT or MRI.

TREATMENT
Salt restriction and diuretics ameliorate pulmonary and systemic congestion;
digitalis is not indicated unless systolic function impaired or atrial arrhythmias
present. Note: Increased sensitivity to digitalis in amyloidosis. Anticoagulation often indicated, particularly in pts with eosinophilic endomyocarditis. For
specific therapy of hemochromatosis and sarcoidosis, see Chaps. 336 and 309,
respectively, in HPIM-16.

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY
(HOCM)
Marked LV hypertrophy; often asymmetric, without underlying cause. Systolic
function is normal; increased LV stiffness results in elevated diastolic filling
pressures.
SYMPTOMS Secondary to elevated diastolic pressure, dynamic LV outflow obstruction, and arrhythmias; dyspnea on exertion, angina, and presyncope;

sudden death may occur.
PHYSICAL EXAMINATION Brisk carotid upstroke with pulsus bisferiens; S4, harsh systolic murmur along left sternal border, blowing murmur of
mitral regurgitation at apex; murmur changes with Valsalva and other maneuvers (Chap. 117).
LABORATORY ECG LV hypertrophy with prominent “septal” Q
waves in leads I, aVL, V5 – 6. Periods of atrial fibrillation or ventricular tachycardia are often detected by Holter monitor.
Echocardiogram LV hypertrophy, often with asymmetric septal hypertrophy (ASH) and Ն1.3 ϫ thickness of LV posterior wall; LV contractile function
excellent with small end-systolic volume. If LV outflow tract obstruction is
present, systolic anterior motion (SAM) of mitral valve and midsystolic partial
closure of aortic valve are present. Doppler shows early systolic accelerated
blood flow through LV outflow tract.

TREATMENT
Strenuous exercise should be avoided. Beta blockers, verapamil, diltiazem, or
disopyramide used individually to reduce symptoms. Digoxin, other ino-


612

SECTION 8 Cardiovascular Diseases

tropes, diuretics, and vasodilators are generally contraindicated. Endocarditis
antibiotic prophylaxis (Chap. 85) is necessary when outflow obstruction or
mitral regurgitation is present. Antiarrhythmic agents, especially amiodarone,
may suppress atrial and ventricular arrhythmias. In selected pts, LV outflow
gradient can be reduced by dual-chamber permanent pacemaker or controlled
septal infarction by ethanol injection into the septal artery. Consider implantable automatic defibrillator for pts with high-risk profile, e.g., history of syncope or sudden cardiac death, ventricular tachycardia, marked LVH (Ͼ3 cm),
family history of sudden death. Surgical myectomy may be useful in pts refractory to medical therapy.

MYOCARDITIS
Inflammation of the myocardium most commonly due to acute viral infection;

may progress to chronic dilated cardiomyopathy. Myocarditis may develop in
pts with HIV infection or Lyme disease.
HISTORY Fever, fatigue, palpitations; if LV dysfunction is present, then
symptoms of CHF are present. Viral myocarditis may be preceded by URI.
PHYSICAL EXAMINATION Fever, tachycardia, soft S1; S3 common.
LABORATORY CK-MB isoenzyme and cardiac troponins may be elevated in absence of MI. Convalescent antiviral antibody titers may rise.
ECG Transient ST-T-wave abnormalities.
CXR Cardiomegaly
Echocardiogram Depressed LV function; pericardial effusion present if
accompanying pericarditis present.

TREATMENT
Rest; treat as CHF (Chap. 126); immunosuppressive therapy (steroids and
azathioprine) may be considered if RV biopsy shows active inflammation, but
long-term efficacy has not been demonstrated.

For a more detailed discussion, see Wynne J, Braunwald E: Cardiomyopathy and Myocarditis, Chap. 221, p. 1408, in HPIM-16.

121
PERICARDIAL DISEASE
ACUTE PERICARDITIS
CAUSES See Table 121-1
HISTORY Chest pain, which may be intense, mimicking acute MI, but characteristically sharp, pleuritic, and positional (relieved by leaning forward); fever
and palpitations are common.


CHAPTER 121 Pericardial Disease

613

Table 121-1
Most Common Causes of Pericarditis
Idiopathic
Infections (particularly viral)
Acute myocardial infarction
Metastatic neoplasm
Radiation therapy for tumor (up to 20 years earlier)
Chronic renal failure
Connective tissue disease (rheumatoid arthritis, SLE)
Drug reaction (e.g., procainamide, hydralazine)
“Autoimmune” following heart surgery or myocardial infarction (several weeks/
months later)
PHYSICAL EXAMINATION Rapid or irregular pulse, coarse pericardial friction rub, which may vary in intensity and is loudest with pt sitting
forward.
LABORATORY ECG (See Table 121-2 and Fig. 121-1) Diffuse ST
elevation (concave upward) usually present in all leads except aVR and V1; PRsegment depression may be present; days later (unlike acute MI), ST returns to
baseline and T-wave inversion develops. Atrial premature beats and atrial fibrillation may appear. Differentiate from ECG of early repolarization variant
(ERV) (ST-T ratio Ͻ0.25 in ERV, but Ͼ0.25 in pericarditis).
CXR Increased size of cardiac silhouette if large (Ͼ250 mL) pericardial
effusion is present, with “water bottle” configuration.
Echocardiogram Most sensitive test for detection of pericardial effusion,
which commonly accompanies acute pericarditis.

TREATMENT
Aspirin 650– 975 mg qid or NSAIDs (e.g., indomethacin 25– 75 mg qid); for
severe, refractory pain, prednisone 40– 80 mg/d is used and tapered over
Table 121-2
ECG in Acute Pericarditis vs. Acute (Q-Wave) MI
ST-Segment Elevation

Evolution of ST and T
Waves

PR-Segment
Depression

All leads involved
except aVR and V1

ST remains elevated
for several days;
after ST returns to
baseline, T waves
invert

Yes, in
majority

ST elevation over
infarcted region
only; reciprocal ST
depression in
opposite leads

T waves invert
within hours, while
ST still elevated;
followed by Q
wave development

No

ECG Lead Involvement

PERICARDITIS

Concave
upward

ACUTE MI

Convex
upward


aVL

aVF

II

III

V5

V6

V3

V4

V2

V1

FIGURE 121-1 Electrocardiogram in acute pericarditis. Note diffuse ST-segment elevation and PR-segment depression.

aVR

I

PR

ST


CHAPTER 121 Pericardial Disease

615

several weeks or months. Intractable, prolonged pain or frequently recurrent
episodes may require pericardiectomy. Anticoagulants are relatively contraindicated in acute pericarditis because of risk of pericardial hemorrhage.

CARDIAC TAMPONADE
Life-threatening emergency resulting from accumulation of pericardial fluid under pressure; impaired filling of cardiac chambers and decreased cardiac output.
ETIOLOGY Previous pericarditis (most commonly metastatic tumor,
uremia, acute MI, viral or idiopathic pericarditis), cardiac trauma, or myocardial
perforation during catheter or pacemaker placement.
HISTORY Hypotension may develop suddenly; subacute symptoms include dyspnea, weakness, confusion.
PHYSICAL EXAMINATION Tachycardia, hypotension, pulsus paradoxus (inspiratory fall in systolic blood pressure Ͼ10 mmHg), jugular venous

distention with preserved x descent, but loss of y descent; heart sounds distant.
If tamponade develops subacutely, peripheral edema, hepatomegaly, and ascites
are frequently present.
LABORATORY ECG Low limb lead voltage; large effusions may
cause electrical alternans (alternating size of QRS complex due to swinging of
heart).
CXR Enlarged cardiac silhouette if large (Ͼ250 mL) effusion present.
Echocardiogram Swinging motion of heart within large effusion; prominent respiratory alteration of RV dimension with RA and RV collapse during
diastole.
Cardiac Catheterization Confirms diagnosis; shows equalization of diastolic pressures in all four chambers; pericardial ϭ RA pressure.

TREATMENT
Immediate pericardiocentesis and IV volume expansion.

CONSTRICTIVE PERICARDITIS
Rigid pericardium leads to impaired cardiac filling, elevation of systemic and
pulmonary venous pressures, and decreased cardiac output. Results from healing
and scar formation in some pts with previous pericarditis. Viral, tuberculosis,
previous cardiac surgery, uremia, neoplastic pericarditis are most common
causes.
HISTORY Gradual onset of dyspnea, fatigue, pedal edema, abdominal
swelling; symptoms of LV failure uncommon.
PHYSICAL EXAMINATION Tachycardia, jugular venous distention
(prominent y descent), which increases further on inspiration (Kussmaul’s sign);
hepatomegaly, ascites, peripheral edema are common; sharp diastolic sound,
“pericardial knock” following S2 sometimes present.
LABORATORY ECG
common.

Low limb lead voltage; atrial arrhythmias are

CXR Rim of pericardial calcification in up to 50% of pts.
Echocardiogram Thickened pericardium, normal ventricular contraction;
abrupt halt in ventricular filling in early diastole.


616

SECTION 8 Cardiovascular Diseases

CT or MRI More precise than echocardiogram in demonstrating thickened
pericardium.
Cardiac Catheterization Equalization of diastolic pressures in all chambers; ventricular pressure tracings show “dip and plateau” appearance. Pts with
constrictive pericarditis should be investigated for tuberculosis (Chap. 102).

TREATMENT
Surgical stripping of the pericardium. Progressive improvement ensues over
several months.

Approach to the Patient
With Asymptomatic Pericardial Effusion of Unknown Cause
If careful history and physical exam do not suggest etiology, the following may
lead to diagnosis:

•
•
•
•
•
•

Skin test and cultures for tuberculosis (Chap. 102)
Serum albumin and urine protein measurement (nephrotic syndrome)
Serum creatinine and BUN (renal failure)
Thyroid function tests (myxedema)
ANA (SLE and other collagen-vascular disease)
Search for a primary tumor (especially lung and breast)

For a more detailed discussion, see Braunwald E: Pericardial Disease,
Chap. 222, p. 1414, in HPIM-16.

122
HYPERTENSION
DEFINITION Chronic elevation in bp Ͼ140/90; etiology unknown in
90– 95% of pts (“essential hypertension”). Always consider a secondary correctable form of hypertension, especially in pts under age 30 or those who
become hypertensive after 55. Isolated systolic hypertension (systolic Ͼ 160,
diastolic Ͻ 90) most common in elderly pts, due to reduced vascular compliance.

SECONDARY HYPERTENSION
RENAL ARTERY STENOSIS Due either to atherosclerosis (older men)
or fibromuscular dysplasia (young women). Presents with sudden onset of hypertension, refractory to usual antihypertensive therapy. Abdominal bruit often
audible; mild hypokalemia due to activation of the renin-angiotensin-aldosterone system may be present.


CHAPTER 122 Hypertension

617

RENAL PARENCHYMAL DISEASE Elevated serum creatinine and/or
abnormal urinalysis, containing protein, cells, or casts.

COARCTATION OF AORTA Presents in children or young adults; constriction is usually present in aorta at origin of left subclavian artery. Exam
shows diminished, delayed femoral pulsations; late systolic murmur loudest
over the midback. CXR shows indentation of the aorta at the level of the coarctation and rib notching (due to development of collateral arterial flow).
PHEOCHROMOCYTOMA A catecholamine-secreting tumor, typically
of the adrenal medulla, that presents as paroxysmal or sustained hypertension
in young to middle-aged pts. Sudden episodes of headache, palpitations, and
profuse diaphoresis are common. Associated findings include chronic weight
loss, orthostatic hypotension, and impaired glucose tolerance. Pheochromocytomas may be localized to the bladder wall and may present with micturitionassociated symptoms of catecholamine excess. Diagnosis is suggested by elevated plasma metanephrine level or urinary catecholamine metabolites in a 24-h
urine collection (see below); the tumor is then localized by CT scan or angiography.
HYPERALDOSTERONISM Due to aldosterone-secreting adenoma or
bilateral adrenal hyperplasia. Should be suspected when hypokalemia is present
in a hypertensive pt off diuretics (Chap. 174).
OTHER CAUSES Oral contraceptive usage, Cushing’s and adrenogenital
syndromes (Chap. 174), thyroid disease (Chap. 173), hyperparathyroidism
(Chap. 179), and acromegaly (Chap. 171).

Approach to the Patient
History
Most pts are asymptomatic. Severe hypertension may lead to headache, epistaxis, or blurred vision.
Clues to Specific Forms of Secondary Hypertension Use of birth control pills or glucocorticoids; paroxysms of headache, sweating, or tachycardia
(pheochromocytoma); history of renal disease or abdominal traumas (renal hypertension).
Physical Examination
Measure bp with appropriate-sized cuff (large cuff for large arm). Measure bp
in both arms as well as a leg (to evaluate for coarctation). Signs of hypertension
include retinal arteriolar changes (narrowing/nicking); left ventricular lift, loud
A2, S4. Clues to secondary forms of hypertension include cushingoid appearance, thyromegaly, abdominal bruit (renal artery stenosis), delayed femoral
pulses (coarctation of aorta).
Laboratory Workup
Screening Tests for Secondary Hypertension Should be carried out on
all pts with documented hypertension: (1) serum creatinine, BUN, and urinalysis

(renal parenchymal disease); (2) serum K measured off diuretics (hypokalemia
prompts workup for hyperaldosteronism or renal artery stenosis); (3) CXR (rib
notching or indentation of distal aortic arch in coarctation of the aorta); (4) ECG
(LV hypertrophy suggests chronicity of hypertension); (5) other useful screening blood tests include CBC, glucose, cholesterol, triglycerides, calcium, uric
acid.
Further Workup Indicated for specific diagnoses if screening tests are
abnormal or bp is refractory to antihypertensive therapy: (1) renal artery ste-