Blueprints medicine
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Vincent B. Young
•
William A. Kormos
•
Allan H. Goroll
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BLUEPRINTS
MEDICINE
--------------------------------------------------------------------------------------
Third Edition
Vincent B. Young, MD, PhD
Assistant Professor
Departments of Internal Medicine, Microbiology & Molecular Genetics
National Food Safety and Toxicology Center
Michigan State University College of Human Medicine
East Lansing, Michigan
William A. Kormos, MD, MPH
Instructor in Medicine and Medical Education
Harvard Medical School
Massachusetts General Hospital
Boston, Massachusetts
Faculty Advisor
Allan H. Goroll, MD
Associate Professor of Medicine
Harvard Medical School
Associate Physician
Massachusetts General Hospital
Boston, Massachusetts
fl)
Blackwell
Publishing
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© 20U4 by Blackwell Publishing
Blackwell Publishing, Inc. , 350 Main Street, Malden, Massachusetts 02148-5018, USA
Blackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UK
Blackwell Science Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia
All rights reserved. No part of this publication may be reproduced in any form or by any
electronic or mechanical means, including information storage and retrieval systems, without
permission in writing from the publisher, except by a reviewer who may quote brief
passages in a review.
03 04 05 06 5 4 3 2 ]
ISBN: 1-4051-0335-3
Library of Congress Cataloging-in-Publication Data
Young, Vincent B.
Blueprints medicine / Vincent B. Young, William A. Kormos,
Allan H. Gorol1.-3rd ed.
p.; cm.-(Blueprints)
Rev. ed. of: Blueprints in medicine. 2nd ed. c2001.
Includes index.
ISBN 1-4051-0335-3
I. Internal medicine-Outlines, syllabi, etc.
[DNLM:
I. Internal Medicine-Examination Questions.
2004] 1. Kormos, William A. II. Goroll, Allan H.
Blueprints in medicine. IV. Title. V. Series.
WB 18.2 Y 78b
III. Young, Vincent B.
RC59.Y68 2004
616'.0076-dc21
2003001502
A catalogue record for this title is available from the British Library
Acquisitions: Nancy Anastasi Duffy
Development: Julia Casson
Production: Debra Lally
Cover design: Dick Hannus
Interior design: Mary McKeon
Typesetter: SNP Best-set Typesetter Ltd., Hong Kong
Printed and bound by Capital City Press in Berlin, VT
For further information on Blackwell Publishing, visit our website:
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Notice: The indications and dosages of all drugs in this book have been recommended in the medical litera
ture and conform to the practices of the general community. The medications described do not necessarily have
speCific approval by the Food and Drug Administration for use in the diseases and dosages for which they are
recommended. The package insert for each drug should be consulted for use and dosage as approved by the
FDA. Because standards for usage change, it is advisable to keep abreast of revised recommendations, particu
larly those concerning new drugs.
>
Reviewers ..................................................................... viii
Preface
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.ix
Acknowledgments ...............................................................x
Abbreviations ................................................................. .xi
Cardiovascular
Part I
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1
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.3
1
Chest Pain
2
Shock
3
Coronary Artery Disease
4
Myocardial Infarction
5
Heart Failure ..............................................................20
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6
. 9
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15
.
27
6
Bradyarrhythmias ..
7
Tachyarrhythmias ........................................................ 31
8
Hypertension ............................................................ 37
9
Valvular Heart Disease
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Cardiovascular Disease
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Syncope
Part II
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61
12
Dyspnea
13
Cough
14
Chronic Obstructive Pulmonary Disease .....................................64
15
Asthma ..................................................................68
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16
Pulmonary Embolism ..................................................... 73
17
Interstitial Lung Disease
18
Pleural Effusions
19
Lung Cancer . .. .
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Part (((
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Renal ....
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Acid-Base Disturbances .
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Fluid and Electrolytes ... .
22
Acute Renal Failure .
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Chronic Renal Failure ..
24
Glomerular Disease
25
Nephrolithiasis . ..
26
Hematuria
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91
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95
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1 09
112
< not for sale!
> < He �nH npo�� !
>
Part IV Infectious Diseases
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27
Fever and Rash .
28
Pneumonia .
29
Sexually Transmitted Diseases
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Part V Gastrointestinal
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Abdominal Pain
Diarrhea
39
Peptic Ulcer Disease and Gastritis
40
Inflammatory Bowel Disease
41
Hepatitis
42
Cirrhosis
43
Cholestatic Liver Disease
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44
Pancreatitis
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Colorectal Cancer .
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199
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.
Weight Loss
47
Hyperthyroidism
48
Hypothyroidism
49
Diabetes Mellitus
50
Hypercalcemia
51
Diseases of the Adrenal Gland
52
Pituitary Disease
53
Nutritional Disorders
54
Hyperlipidemia
.
.
.
.
.
.
Part VII Rheumatology
.
.
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..
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.
.201
203
206
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209
214
217
221
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189
192
195
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46
176
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152
163
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149
158
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136
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133
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127
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121
. 140
145
.
.
117
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.
HIV Part II: Prophylaxis and Treatment of Opportunistic
Part VI Endocrine
.
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36
.
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Meningitis
.
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HIV Part I: Initial Care of the HIV-Infected Patient
.
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35
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34
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Infective Endocarditis
.
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33
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Gastroenteritis
.
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Infections in HIV
.
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32
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Urinary Tract Infections
.
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.
Tuberculosis
.
.
.
31
.
.
.
30
.
.
. 225
.
230
233
55
Acute Monoarticular Arthritis ........................................ ......235
56
Low Back Pain
57
Rheumatoid Arthritis
58
Seronegative Spondyloarthropathies
.
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59
Connective Tissue Diseases
60
Vasculitis
61
Amyloidosis
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238
. 241
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244
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247
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251
.254
< not for sale!
> < He �nH npo�� !
>
<
Part VIII Hematology/Oncology
62
Anemia
63
Hemolytic Anemia
64
Adenopathy
.
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257
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259
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.
Leukemia and Lymphoma
69
Acute Complications of Cancer Therapy
70
Paraneoplastic Disorders
.
.
.
Prostate Cancer
.
.
.
68
Index
.
.
Bleeding Disorders
Ques tions
.
.
Breast Cancer
Ans wers
.
>
.
65
.
.
9T �pOHT. py
.
66
67
.
MYC�
CKaM H �e�aBID-KoHBepCHH
264
267
269
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280
284
287
290
.
.306
.319
vii
James Fletcher
Class of 2003
Eastern Virginia Medical School
Norfolk, Virginia
Danny Liaw, MD
Intern, Department of Medicine
Beth Israel Deaconess Medical Center
Boston, Massachusetts
Nancy Pandhi, MD
Resident, Shenandoah Valley Family Practice Residency
Front Royal, Virginia
Diane Rychlik, MD
Class of 2002
Spartan Health Sciences University School of Medicine
Vieux Fort, St. Lucia
Edward O. Senu-Oke, MD
Resident, Eastern Virginia Medical School
Norfolk, Virginia
Jason Sluzevich, MD
Resident, Department of Dermatology
University Hospital
Cincinnati, Ohio
viii
n 1997, the first five books in the Blueprints series were published as board review for medical
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"
5-ASA
5-aminosalicylic acid
EBV
ABGs
arterial blood gases
ECG
electrocardiography
ACE
angiotensin-converting enzyme
EF
ejection fraction
ACTH
adrenocorticotropic hormone
EGD
esophagogastroduodenoscopy
ADH
antidiuretic hormone
EMG
electromyography
AI
aortic insufficiency
ERCP
endoscopic retrograde
AIDS
acquired immunodeficiency syndrome
ALL
acute lymphocytic leukemia
ESR
erythrocyte sedimentation rate
ALT
alanine transaminase
FEV
forced expiratory volume
E pstein-Barr virus
cholangiopancreatography
AMS
acute myelogenous leukemia
FNA
fine needle aspiration
ANA
antinuclear antibody
FTA-ABS
fluorescent treponemal antibody
ARDS
adult respiratory distress syndrome
ASD
arterial septal defect
FVC
forced vital capacity
absorption
ASO
anti-streptolysin 0
GFR
glomerular filtration rate
AST
aspartate transaminase
GH
growth hormone
AV
atreoventricular
GI
gastrointestinal
BE
barium enema
GU
genitourinary
BP
blood pressure
HAV
hepatitis A virus
BUN
blood urea nitrogen
HbA1C
glycosylated hemoglobin
CAD
coronary artery disease
HIV
human immunodeficiency virus
CALLA
common acute lymphoblastic
HLA
human leukocyte antigen
leukemia antigen
HR
heart rate
CBC
complete blood count
HS
hereditary spherocytosis
CHF
congestive heart failure
Ig
immunoglobulin
CK
creatine kinase
1M
intramuscular
CLL
chronic lymphocytic leukemia
INH
isoniazid
CML
chronic myelogenous leukemia
INR
international normalized ratio
CMV
cytomegalovirus
JVP
jugular venous pressure
CNS
central nervous system
KUB
kidneys/ureter/bladder
COPD
chronic obstructive pulmonary
LDH
lactate dehydrogenase
disease
LES
lower esophageal sphincter
CPK
creatine phosphokinase
LFTs
liver function tests
CSF
cerebrospinal fluid
LP
lumbar pressure
CT
computed tomography
LV
left ventricular
CVA
cerebrovascular accident
LVH
left ventricular hypertrophy
CXR
chest x-ray
Lytes
electrolytes
DIC
disseminated intravascular
MCHC
mean corpuscular hemoglobin
coagulation
concentration
DKA
diabetic ketoacidosis
MCV
mean corpuscular volume
DM
diabetes mellitus
MEN
multiple endocrine neoplasia
DTRs
deep tendon reflexes
MHC
major histocompatibility complex
DVT
deep venous thrombosis
MI
myocardial infarction
< not for sale !
> < He �nH npo�� ! >
MR
magnetic resonance (imaging)
N HL
non-Hodgkin's l ymphoma
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SIADH
>
syndrome of inappropriate secretion
of ADH
NPO
nil per os (nothing by mouth)
SLE
NSAID
nonsteroidal anti-inflammatory drug
STD
sexually transmitted disease
PA
posteroanterior
SVT
supraventricular tachycardia
systemic lupus erythematosus
PBS
peripheral blood smear
TFTs
thyroid function tests
PCP
pneumocystis carinii pneumonia
TIA
transient ischemic attack
PE
physical exam
TIBC
total iron-binding capacity
PFTs
pulmonary function tests
TIPS
transj ugular intrahepatic
PMI
point of maximal intensity
PMN
polymorphonuclear leukocyte
portosystemic shunt
PT
prothrombin time
tPA
tissue plasminogen activator
PTCA
percutaneous transluminal coronary
TPO
thyroid peroxidase
TMP-SMZ trimethoprim-sulfamethoxazole
angioplasty
TSH
thyroid-stimulating hormone
PTH
parathyroid hormone
TIP
thrombotic thromboc ytopenic
PTI
partial thromboplastin time
PUD
peptic ulcer disease
UA
urinalysis
RBC
red blood cell
UGI
upper GI
RPR
rapid plasma reagin
URI
upper respiratory infection
RR
respiratory rate
US
ultrasound
RS
Reed-Sternberg (cell)
VORL
Venereal Disease Research
RV
right ventricular
RVH
right ventricular h ypertrophy
VS
vital signs
SBFT
small bowel fOllow-through
VT
ventricular tachycardia
SGOT
serum glutamic-oxaloacetic
WBC
white blood cell
transaminase
WPW
Wolff-Parkinson-White (syndrome)
purpura
Laboratory
Cardiovascular
In diagnosing the patient with chest pain, it often
helps to categorize the pain by its pathophysiology.
Inflammation of serous surfaces leads to pleuritic
pain, characterized by increased pain with inspiration
or cough. This pain may also be aggravated by move
ment or position. Pleuritic pain can be seen in pul
monary etiologies, pericarditis, and musculoskeletal
disorders. Visceral pain, such as in myocardial
ischemia and esophageal disease, often produces dull,
aching, tight, or sometimes burning pain that is
poorly localized.
The most important decision for the physician
is to distinguish life-threatening causes, such as
myocardial ischemia, pulmonary embolus, and aortic
dissection, from non-life-threatening causes. The key
to identifying the etiology of the pain lies in the
patient's history.
CLINICAL MANIFESTATION S
----------------------------------------------
History
The following diseases often present with the sharp
pleuritic type of pain. Pneumothorax has an acute
onset and is pleuritic and associated with dyspnea.
This occurs mostly in young patients (spontaneous)
or those with underlying lung disease (secondary to
blebs) . Pulmonary embolism is similar to pneumoth
orax with pleurisy and dyspnea. Risk factors should
be taken into account (see Chapter 1 6) . The pain in
pericarditis is pleuritic and positional, typically
relieved by sitting forward. Substernal pain in peri
carditis may radiate to the shoulder/trapezius (due to
diaphragmatic/phrenic nerve irritation).
In contrast, other diseases may produce a more
visceral type of pain, aching and poorly localized.
Patients with myocardial ischemia often present with
a
sensation of squeezing or pressure and possibly
• RIS K FACTO RS
with a burning sensation. Located substernally, the
In evaluating patients with chest pain, certain risk pain classically radiates to the ulnar aspect of the left
factors may increase the suspicion for coronary artery arm but may also go to the jaw, shoulders, epigas
trium, or back. Brought on by exertion or emotional
disease. Risk factors for CAD include:
stress, it usually lasts only minutes. Worrisome
• Diabetes mellitus
features include prolonged pain (>30 minutes) with
• Smoking
myocardial infarction and rest pain with unstable
• Hypertension
angina. Aortic dissection presents with abrupt pain
• Hyperlipidemia
that is most intense at onset, which distinguishes this
• Family history of CAD
"must not miss" diagnosis. Pain is often tearing and
radiates
to the back. In gastrointestinal disease (such
Patients with chest pain and many cardiovascular risk
as
refl
u
x
and esophageal spasm), symptoms may be
factors require further workup for CAD, even if
relieved
with
antacids, are r elated to food intake, and
the story is atypical. CAD is uncommon (but not
are
worsened
in the supine position. Esophageal
unheard of) before age 40, and men are at greater
spasm
may
share
many similar qualities with angina.
risk than women until about age 65. Cocaine abuse
Finally,
other
conditions
may have a component of
is an important consideration, especially in younger
both
types
of
pain.
In
musculoskeletal
disorders, pain
patients with no other cardiac risk factors.
< not for sale!
4
•
> < He �nH npo�� ! >
Blueprints
Medicine
is more easily localized and worsens with movement
or palpation. Pain ranges from darting, lasting
seconds, to a prolonged dull ache that lasts for days.
In herpes zoster, because pain may precede rash by
several days, a burning sensation in a dermatomal dis
tribution is a key feature. With anxiety, pain is often
atypical and prolonged. and workup reveals no other
cause.
Physical Exam i n ation
Remember that a patient with ischemic heart disease
may present (and often does) with a completely
normal physical examination. However, some physi
cal findings may lead to the correct diagnosis.
•
•
•
•
Unequal blood pressures between arms is an
important feature for aortic dissection. Tachypnea
is seen in pulmonary cases such as pneumothorax
or pulmonary embolism.
Reproduction of the chest pain by palpation is a
key feature of musculoskeletal causes. This is not
the case in angina, pulmonary embolus, aortic dis
section, or true pleuritic disease.
Cardiac findings to look for include a fourth heart
sound (ischemia), an apical holosystolic murmur
(ischemic mitral regurgitation), a blowing diastolic
murmur (aortic regurgitation as a result of aortic
dissection involving the valve root), and a pericar
dial rub (pericarditis).
Pulmonary findings of a pneumothorax include
hyperresonance to percussion, decreased fremitus,
and tracheal deviation to the opposite side. A
pleural rub may indicate pulmonary infarction or
pneumonia.
• DIAG NOSTIC EVALUATIO N
----------------------------------------------
The initial history and physical examination should
guide the diagnostic workup. If the chest pain
appears cardiac in nature, an electrocardiogram
should be obtained. Furthermore, in those patients
with a high probability of underlying CAD (older
patients, smokers, etc.), an ECG should be checked
even if the story is atypical. Some helpful findings are
listed in Table 1 - 1 .
In patients with pleuritic pain and dyspnea as
predominant symptoms, a chest x-ray should be the
initial step to rule out pneumothorax, pulmonary
infiltrates, and rib fractures. A widened mediastinum
on chest x-ray may be seen with aortic dissection.
TABLE 1-1
Electrocardiogram
•
Q waves in two or more leads; Previous myocardial
infarction
•
ST depression > 1 mm; Ischemia
•
ST elevation; Acute myocardial infarction or
pericarditis (the latter often has involvement of all
leads and associated PR depression)
•
Left bundle branch block: Suggests underlying heart
disease (ischemic, hypertensive)
•
Right bundle branch block; May be indicative of right
heart strain (as in pUlmonary embolus)
•
T-wave inversions and nonspecific ST changes; Seen
in both healthy individuals and in many diseases
(therefore, not useful)
Note: A normal
ECG does not rule
out ischemia or serious disease,
especially when recorded in the absence of pain. Right bundle branch
block and early repolarization may be seen in young, healthy, normal
individuals.
Occlusion of the right coronary artery by an aortic dissection may
present with inferior ST elevation. This is a vital distinction to make.
Chest x-ray findings seen in pulmonary embolism
can be found in Chapter 1 6.
In the case of suspected musculoskeletal pain in
the low-risk patient, a trial of nonsteroidal anti
inflammatory drugs is appropriate. Pericarditis will
also respond to this treatment.
Other important diagnostic tests include the aor
togram, by which patients with worrisome histories
for aortic dissection should be further evaluated
regardless of chest x-ray or ECG results. Trans
esophageal echocardiogram is a minimally invasive
method of making the diagnosis. The VIQ scan is
used in patients with pleuritic pain and normal chest
x-ray who may need further workup. A normal V/Q
scan rules out the diagnosis of pulmonary embolus,
whereas a high-probability scan confirms the diag
nosis when accompanied by a high clinical suspicion.
This is further detailed in Chapter 16. The exercise
stress test may be the appropriate next step in
patients with a chronic stable pattern of pain (see
Chapter 3).
In chest pain of esophageal origin, pain induced
by esophageal reflux may be confirmed by 24-hour
esophageal pH monitoring, or by an empiric trial of
antacids or H2 blockers. The Bernstein test (acid
instillation into the esophagus, reproducing pain) is
not commonly used today.
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Ch apter 1 / Chest Pain
KEY POINTS
_
1. Patients with h i stories suggestive of serious
�
causes o f chest pain (ischemia, dissection,
embolus) deserve further eval uation even if
physical examination, chest x-ray, and ECG results
are normal.
2. Certain ch est pai n syndromes h ave very typical
patterns, such as the acute tearing pain of aortic
dissection, the dermatomal distribution of herpes
zoster, or the positional pleuritic pain of pericardi
tis (relieved when the patient sits forward) .
•
3. Risk factors are i mportant to determine the prob
ability of CAD in a patient with chest pain. These
include age, sex, diabetes mellitus, h ypertension,
hyperlipidemia, smoking, and family hi story.
4. The ECG is a key test in patients with a su spected
cardi ac origin of chest pain. Th e findings of Q
waves, ST elevation, or ST depression al l signi fy
cardiac isch emia. A notable exception is pericardi
ti s, which has diffuse ST elevation, often with
associ ated PR depression.
5
Shock is a term used to describe decreased perfusion
and oxygen delivery to the body. Shock presents
with a decrease in blood pressure and may result
from either a decrease in cardiac output (CO) or a
decrease in systemic vascular resistance (SVR) . This
is best defined by the following equation:
Blood Pressure
=
CO
x
SVR
The three main syndromes leading to shock (i.e.,
hypovolemia, cardiogenic, and sepsis) are defined by
their effect on the CO or SVR. An additional clini
cal feature is the volume status, best assessed at the
bedside by the jugular venous pressure (JVP) and in
the intensive care unit by the pulmonary capillary
wedge pressure (PCWP). The syndromes and their
features are defined in Table 2-l.
The low CO seen in cardiogenic shock may also
be seen in syndromes resulting in right heart failure
(such as massive pulmonary embolism), decreased
venous filling of the heart (tension pneumothorax),
and obstruction of outflow ( cardiac tamponade) . The
low vascular resistance that occurs in sepsis may be
mimicked by adrenal crisis (insufficiency) or ana
phylaxis. CO varies in these conditions, depending
on severity and volume status.
Although often defined as a systolic blood pres
sure less than 90 or a mean arterial pressure less than
60, shock is truly defined by its effect on other organ
systems. Failure of other organs is evidence of
insufficient blood pressure regardless of the actual
value. Manifestations of inadequate perfusion
include:
•
•
•
Renal dysfunction ( decreased or no urine output)
Central nervous system dysfunction (worsening
mental status)
Tissue hypoxia (lactic acidosis)
• C LINICAL MANIF ESTATIO N S
-------------------------------------------
H istory
History is usually not helpful because the patient
often has a clouded sensorium as a result of decreased
perfusion. However, the following findings may be
helpful:
•
•
•
Recent use or discontinuation of corticosteroids
(adrenal crisis)
Ingestion of certain foods or drugs or the occur
rence of bee sting ( anaphylaxis)
History of chest pain (pleuritic: pulmonary
embolism or tension pneumothorax; nonpleuritic:
ischemia)
Physical Exam i n ation
Vital signs are essential to evaluating the patient with
shock. Tachycardia is almost always present; failure
to increase the heart rate in the presence of hypoten
sion suggests a primary cardiac conduction distur
bance (see Chapter 7) . Pulsus paradoxus is seen in
TABLE 2-1
Definitions of Shock Syndromes
CO
SVR
JVP/PCWP
Hypovolemia
Decrease
Increase
Decrease
Cardiogenic
Decrease
Increase
Increase
Sepsis
Increase
Decrease
Decrease
co, cardiac output; SVR, systemic vascular resistance; JVp, jugular
venous pressure;
PCWp, pulmonary capillary wedge
pressure.
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Chapter 2 / Shock
cardiac tamponade; this is defined as a decrease
in systolic blood pressure of greater than 1 0 mm Hg
with inspiration.
JVP provides a rough bedside estimate of central
venous pressure. Shock from cardiopulmonary causes
(see later) will present with increased JVP. Systemic
causes of shock are caused by either systemic vasodi
lation or decreased volume; JVP is decreased or
undetectable in these patients.
Absence of breath sounds on one side and tracheal
deviation to the opposite side are findings of a
tension pneumothorax. Pulmonary examination may
also reveal rales in cardiogenic shock or wheezing in
anaphylaxis.
•
7
The diagnosis of adrenal ins uffic iency is suggested
by:
•
•
•
•
•
Hyponatremia
Hyperkalemia
Hypoglycemia
Eosinophilia
Mild hypercalcemia
Adrenal insufficiency is then confirmed by a sub
optimal response t o corticotropin (ACTH) (see
later). However, the emergent nature of adrenal crisis
requires treatment with intravenous steroids (lOOmg
hydrocortisone IV) while waiting for the test results
to return .
Patients with possible sepsis should have blood
cultures drawn and empiric antibiotic therapy
• DIF F E RE NTIAL DIAGNOSIS
directed at the most likely pathogens.
Shock from cardiopulmonary causes (increased
JVP) requires specific treatment aimed at the under
Cardiac
lying pathology. [n cardiogenic shock, intravenous
• Low output heart failure
fluids are likely to be more harmful; they may be
• Cardiac tamponade
temporizing measures in pulmonary embolism or
Pulmonary
tamponade. An ECC should be obtained t o look for
• Tension pneumothorax
an acute myocardial infarction.
• Massive pulmonary embolism
Along with the clinical examination and empiric
treatment, the chest x-ray is a useful first test
Systemic
in hypotension with increased JVP. A chest film
• Sepsis
may show bilateral alveolar infiltrates (pulmonary
• Hypovolemia
edema), an enlarged cardiac silhouette (tamponade
• Adrenal crisis
or cardiomyopathy) , or a pneumothorax with medi
• Anaphylaxis
astinal shift to the opposite side. Chest x-ray is often
normal in pulmonary embolism, but certain findings
may be present (see Chapter 16).
• DIAGN OSTIC EVALUATION A N D
An ECC may show acute myocardial ischemia,
TREATMENT
with either ST segment elevation or depression.
The hypotension present in shock is easily diagnosed, Old Q waves may suggest past myocardial injury
and efforts are directed at discerning the correct eti and a predisposition to cardiogenic shock. In pul
ology of shock. This always begins with treating the monary embolism, the ECC may show evidence
hypotension itself The initial approach is based on of right heart strain, such as right bundle branch
the volume status, often using the JVP as a guide. For block.
Although a chest x-ray can confirm the diagnosis
patients with shock due to systemic etiology (with
decreased JVP), treatment should begin with intra of tension pneumothorax, the emergent nature of the
venous fluids (normal saline or Ringer's lactate) problem may demand immediate treatment. [n
while evaluating the cause of the hypotension. The a patient at risk for pneumothorax with typical
patient should be examined for possible causes of findings (absent breath sounds, tracheal deviation,
hypovolemia, including blood loss, dehydration, and increased JVP) , decompression of the affected side
third-spacing of fluid (as in pancreatitis) . An acute must be accomplished immediately. Insertion of a
onset after ingestion of a food (especially nuts) or chest tube is the optimal treatment, but if one is not
drug suggests an anaphylactic reaction, and 0.3 mg readily available, a large-gauge needle should be
epinephrine subcutaneously should be given inserted in the midclavicular second intercostal space
of the affected side.
immediately.
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8
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Blueprints
Medicine
In the patient with hypotension and increased
JVP, an echm:ardiugram may help determine the
underlying cause. For example, echocardiographic
findings seen in pericardial tamponade include mod
erate to large pericardial effusion and diastolic col
lapse of the right atrium or ventricle. In addition, the
echocardiogram may reveal diffuse hypokinesis (car
diogenic shock), right-sided heart failure (pulmonary
embolism), or valvular or septal wall rupture. Inva
sive monitoring may be necessary to evaluate and
treat the patient with shock. [n the patient whose eti
ology is unclear or in whom treatment is ineffective,
a Swan-G3\1Z (pulmonary artery) catheter should be
placed. This can be used to obtain a PCWP, which is
a proxy for left atrial filling pressures. The PCWP is
elevated only in cardiac etiologies of shock. In cardiac
tamponade, equalization of pressures may occur; that
is, the right atrial pressure is equal to the right ven
tricular diastolic pressure and the left atrial pressure.
CO may also be measured with a pulmonary
artery catheter; the output is then divided by the
patient's body size to yield a cardiac index . Normal
values for cardiac index are 2.2 to 4 Llmin/m2 . CO
is decreased in cardiopulmonary etiologies and
increased in early (warm) sepsis. In late sepsis, CO
may decline (cold sepsis) .
The ACTH st imulation test involve� measure
ment of a basal cortisol level (preferably at its
morning peak, 8 to 9 A.M.), followed by a cortisol
measurement 1 hour after administration of ACTH .
Basal or poststimulation values greater than 20/-lg/dL
rule out adrenal insufficiency. However, because
stress increases cortisol levels, some authorities have
recommended increasing this cutoff to 25/-lg/dL in
the acutely ill patient.
In the patient who is not improved after initial
treatment, vasupressors may be needed. The choice
of drug depends on the pathophysiology and the
severity of the patient's condition. Dobutamine is a
selective �l-receptor agonist that increases cardiac
contractility. It is useful in cardiogenic shock to
increase cardiac output and decrease SVR. However,
it must be used with caution when blood pressure is
below 90, since it may cause a further drop in BP
when started. Norepinephrine has effects on b oth (X
and �I-receptors. It can be useful in septic shock and
cardiogenit shock. Phenylephrine is a pure (Xr
receptor agonist and m ay be appropriate in early
(warm) sepsis when SVR is low but CO is high. The
effects of dopamine are dose dependent. At low
doses (0.5-2.0/J.g/kg/min), it dilates renal and mesen
teric arteries, and at intermediate doses (2.0-6.0/J.g/
kg/min) , dopamine acts similarly to dobutamine. At
the highest doses, it becomes a vasoconstrictor with
norepinephrine-like effects.
;�_
KEY POINTS
.-
1. Shock, manifested by decreased blood pressure,
is the result of decreased cardiac output or
decreased systemic vascular resistance.
2. Shock due to cardiopulmonary etiologies results
from decreased CO and presents with increased
jugular venous pressure. Hypovolemia may also
decrease CO, but the JVP is undetectable.
3. Unilateral absence of breath sounds, increased
JVp, and tracheal deviation suggest tension pneu
mothorax. lmmediate decompression is required.
4.
Hyponatremia and hyperkalemia in the patient
with hypotension may suggest adrenal crisis.
Treatment with intravenous hydrocortisone is
indicated. Diagnosis may be confirmed by an
ACTH stimulation test.
�
E PIDEMIO LOGY
Coronary artery disease is the leading cause of death
in people over the age of 45 in the United States. An
estimated 5 million people in the United States have
CAD. Many more have conditions that predispose to
its development. CAD is responsible for an estimated
500,000 deaths each year, but overall the death rate
has been declining over the past 20 to 30 years. T his
is believed to be due to improvements in the m an
agement of CAD, including prevention of CAD
progression, treatment of myocardial ischemia, and
management of acute myocardial infarction. This
chapter details the diagnosis of CAD and the man
agement of stable angina. Treatment of the acute
coronary syndromes is described in Chapter 4.
• ETIOLOGY A N D PATHOGEN ESIS
The formation of an atherosclerotic plaque within a
coronary artery proceeds through a number of stages.
In the first stage, formation of a "fatty streak"-a
longitudinal accumulation of lipid with surround
ing smooth muscle proliferation-occurs. This can
happen quite early in life (during the second decade) .
In the second stage, low-density lipoprotein (L DL)
enters the endothelium in the area of the fatty streak
The LDL becomes oxidized, attracting macrophages
that ingest the LDL These macrophages ("foam
cells") release factors that recruit more macrophages,
fibroblasts, and other inflammatory cells. In the final
stage, proliferating smooth muscle cells, connective
tissue (produced by infiltrating fib roblasts), and lipids
(cholesterol, cholesterol esters, triglycerides, and
phospholipids) become incorporated into the matur
ing plaque. At this point, the formation of a "fibrous
cap" results in narrowing of the artery lumen . Areas
of cell necrosis and calcification within the plaque
may occur.
Myocardial ischemia occurs in the setting of coro
nary artery atherosclerosis. The narrowing of the
coronary artery lumen by an atherosclerotic lesion
reduces blood flow to the distal myocardium. As
the lesion continues to grow, oxygen supply be
comes increasingly limited, and under conditions of
increased demand (e.g., exerCise, emotional stress)
myocardial ischemia occurs. At this stage, the cross
sectional area of artery is generally less than 30% of
normaL
Progressive luminal compromise can lead to the
expansion of collateral circulation, alternate distal
vessels that can increase blood supply to the com
promised area. In some cases, complete occlusion of
the diseased artery can result in little or no myocar
dial damage due to extensive distal collateralization .
RISK FACTO RS
Standard risk factors for CAD are described in
Chapter 1 . Diabetes mellitus and patient age are two
of the strongest risk factors. In aJdition, an elevated
homocysteine level or an elevated C-reactive protein
level appears to confer additional risk for future
cardiac events.
CLINICA L MANIF ESTATIO N S
----------------------------------------------
H i story
The typical manifestation uf symptomatic CAD is
angina pectoris, characterized as a substernal pres-
< not for sale ! > < He �nH npo�� ! >
10
•
Blueprints Medicine
sure, heaviness, burning, squeezing, or choking. The
discomfort is rarely well localized or described as
sharp pain. Radiation to the J·aw shoulder back or
arms can occur.
In so-called stable angina pectoris, attacks are
brought on by exertion or emotional stress. The pain
will increases over several minutes and is relieved by
rest in several minutes. Unstable angina pectoris is
defined as angina that occurs at rest or as a signifi
cant change in the pattern of existing chronic angina
(see Chapter 4) . Angina is classified by the amount
of exertion needed to reproduce symptoms: class
I (strenuous activity), class II (walking several
blocks or up incline), class III (mild activity, such as
walking short distances), and class IV (any activity or
at rest).
It is important to note that not all patients will
describe typical anginal pain during periods of
myocardial ischemia. Patients with atypical angina
may manifest with isolated symptoms such as jaw
pain or dyspnea. This is particularly true in pa
tients with underlying diabetes. Patients with silent
ischemia can be completely asymptomatic. In some
patients with angina who have underlying compro
mise of ventricular function or severe widespread
ischemia, angina can be accompanied by symptoms
of heart failure (dyspnea, orthopnea) .
,
"
• DIF F ERENTIAL DIAG NOSIS
----------------------------------------------
The differential diagnosis of chest pain is discussed
in Chapter 1. The probability that a patient with
chest pain has significant coronary artery disease is
estimated by considering the following::
•
•
•
•
Characteristics of pain
Patient age and gender
Patient risk factors (especially diabetes)
Electrocardiogram
• DIAGN OSTIC EVALUATION
----------------------------------------------
The resting electrocardiogram is normal in about
half of patients with angina pectoris. Some may have
evidence of old myocardial infarction (0 waves,
inverted T waves) . The typical ECG change seen
during actual ischemia is ST-segment depression,
defined as a depression of the ST segment from base
line greater than 1 mm in at least two contiguous
leads.
The suspected diagnosis of CAD can be confirmed
with an exercise stress test. During a stress test, the
patient exercises on a treadmill or bicycle ergometer.
The workload is increased in a standardized progres
sive manner, and symptoms, vital signs, and ECG are
monitored. Exercise is continued to achieve 85%
Physica l Exam i n ation
maximal heart rate (maximal heart rate 220 beats
CAD patients often have a normal physical exami per minute minus patient age) . Reasons for stopping
nation, particularly if they are not symptomatic the test include moderate to severe chest pain or
at the time of examination. They may have findings dyspnea, dizziness, greater than 2 mm ST-segment
of predisposing conditions or from atherosclerosis depression, fall in systolic blood pressure of more
than 1 0 mm Hg when associated with ischemia, or
outside of the coronary arteries:
sustained ventricular tachycardia. Development of
• Retinal
vascular changes (e.g., arteriovenous diagnostic ST-segment depression (> 1 mm down
nicking and/or "copper wire" changes due to sloping or horizontal) is considered to be a positive
hypertension)
test (Figure 3- 1 ) .
• Fourth heart sound (hypertension)
The sensitivity o f exercise testing in detecting sig
• Arterial bruits (peripheral atherosclerosis)
nificant CAD (>709h stenosis of at least one artery)
• Absent or diminished peripheral pulses (peripheral
is 50% to 66%. The test is more sensitive for three
atherosclerosis)
vessel disease. The specificity of the test ranges from
• Xanthomas (hyperlipidemia)
77% to 90%. Left bundle branch block, left ventric
ular
hyp ertrophy, preexcitation (Wolff-Parkinson
Examination during an anginal attack can reveal a
W
hite)
syndrome, and digoxin use are associated
fourth heart sound (due to decreased compliance of
with
false
positive ST depressions. Patients with
the ischemic myocardium) or signs of left ventricu
these
conditions
should have imaging studies (see
lar failure (third heart sound, single Sz, rales, elevated
below)
done
along
with the exercise test. The exer
jugular venous pressure) . The examination should
cise
test
also
offers
prognostic information; in
also look for Ilndings that would prohibit safe exer
patients
who
complete
an exercise study (>1 0
cise testing (e.g., critical aortic stenosis).
minutes) without chest pain or ST depressions,
=
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>
Chapter 3 / Coronary Artery Disease
11
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Figure 3-1 The resting ECG (a) and the peak exercise ECG (b) of a patient with a positive exercise test. Note the ST depression in
the inferior and anterior chest leads. (This patient proved to have left main coronary artery disease.)
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annual mortality from CAD is very low (less than 1 %
annually).
The sensitivity and specificity of exercise testing
can be improved by the use of radiolabeled tracers
(e.g., thallium-20l, sestamibi) to determine regional
myocardial perfusion (Figure 3-2) . Images are
recorded immediately after exercise, and then after a
several-hour rest period, to identify ischemic areas
that have decreased blood flow after exercise but
normal or increased flow after rest. Infarcted areas of
myocardium lack perfusion at both time points. This
technique is semiquantitative, estimating the amount
of ischemic or infarcted myocardium by the size of
the defect seen on the images.
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Figure 3-2
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Thallium-201 myocard ial perfusion scans. On the exercise scan there is a large area of very reduced uptake in the
i nferior wall of the left ventricle (arrow), with normal redistribution of the thallium on the rest scan indicating an area of ischemia.
Only the left ventricular wall is demonstrated because there is too l i ttle uptake of thallium by the normal right ventricle.
Patients who are unable to exercise because of
orthopedic problems or severe deconditioning
can have stress testing with the administration of
dipyridamole or adenosine. These agents act as
vasodilators of normal but not atherosclerotic
coronary vessels and thus can cause shunting of
blood flow away from diseased vessels, resulting
in ischemia. They may cause bronchospasm, and
should be used with caution in patients with
chronic obstructive pulmonary disease (COPD) or
asthma. Dobutamine stress echocardiography,
which looks for wall motion abnormalities
with increasing myocardial demand, has similar
test characteristics to the pharmacologic imaging
studies.
The gold standard to diagnose coronary artery
disease remains coronary angiography (Figure 3-3).
Angiography is indicated when noninvasive testing is
inconclusive, or when clinical parameters suggest
severe (i.e., three-vessel) coronary artery disease. The
parameters include: severe (class III or IV) angina
despite medical therapy, angina associated with CHF,
ejection fraction less than 3 5%, or large perfusion
defect on stress testing.
• TREATM ENT
The initial treatment of angina pectoris is usually
medical. The goals of treatment are to (1) prevent
myocardial infarction and death from CAD and (2)
decrease angina and improve quality of life. The
American Heart Association suggests the following
mnemonic for the important elements in treatment
of stable angina:
A: Aspirin and antianginals
B: Beta blocker and blood pressure
C: Cholesterol and cigarettes
0: Diet and diabetes
E: Education and exercise
Prevention of Myoca rd ial Infarction a n d
Death from Coronary Artery Disease
Aspirin (75-325 mg daily) limits platelet aggregation
by inhibiting platelet thromboxane Az. Multiple
studies have demonstrated that aspirin reduces the
risk of subsequent Ml as primary prevention, in
patients with CAD, and for postmyocardial infarc
tion. Patients who are allergic to aspirin should be
placed on clopidogrel, which prevents ADP
mediated platelet aggregation.
Older studies of lipid lowering agents suggested
that every 1 % reduction in cholesterol level de
creased the relative risk of coronary events by 2%.
Newer studies of HMG-CoA reductase inhibitors
(see Chapter 54) demonstrate convincing benefit
(25% to 35% relative risk reductions) in patients with
established CAD, even when cholesterol levels are
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Antia n g i n a l Treatment
a
b
Figure 3-3
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Coronary arteriog raphy in a patient with CAD. (a)
Left coronary artery injection showing a moderate stenosis
between the arrows in the mid left anterior descending artery.
(b) Right coronary artery injection showing tight stenosis
(arrow) of the mid right coronary artery.
"normal." Patients with CAD should aim for an L DL
level of less than 1 00 mg/dL .
Finally, there are some studies that suggest
higher-risk patients with CAD benefit from angio
tensin-converting enzyme inhibitors or angiotensin
II receptor blockers, even when blood pressure
is optimal (SP goal is <130/85). The role of
these agents in all patients with stable angina is
unclear.
Beta-adrenergic blocking agents (propranolol, meto
prolol, atenolol, etc.) reduce myocardial workload by
limiting adrenergic increases (from stress or exercise)
in heart rate and contractility. Although the data
suggesting that beta blockers decrease the risk of MI
or death in stable angina are limited (or nonexistent),
many physicians extrapolate the benefits from post
MI patients or elderly patients with hypertension.
Furthermore, beta blockers are clearly effective at
reducing anginal symptoms. Contraindications to
beta blockers include severe bradycardia, high-degree
AV block, and decompensated CHF. Dose should be
titrated to a goal heart rate of 50 to 60 beats per
minute. Side effects include fatigue, impotence,
bradycardia, and the development or worsening of
heart failure.
Calcium channel blockers decrease myocardial
contractility and increase coronary blood flow.
They are equivalent antianginals compared with
beta blockers. However, studies have demonstrated
increased cardiac risk with short-acting dihydropyri
dine calcium channel blockers (nifedipine). There
fore, only long-acting dihydropyridines (nifedipine
X L, amlodipine) or nondihydropyridines (verapamil,
diltiazem) are recommended. Contraindications are
the same as for beta blockers, and side effects include
peripheral edema and constipation.
Nitrates (nitroglycerin, isosorbide mononitrate or
dinitrate) are endothelium-independent vasodilators
that lead to venous pooling (decreased preload), arte
rial dilation (decreased afterload), and coronary
vasodilation, increasing myocardial blood flow. They
are used in sublingual form for relief of acute
ischemia and also in long-acting forms (via transder
mal patches or slow-release oral formulations) for
limiting frequency and severity of attacks. Side
effects (most prominent with sublingual adminis
tration) are hypotension, lightheadedness, and
headache. Constant use results in nitrate tolerance,
which is prevented by an adequate (8 hour) nitrate
free interval.
Some patients with CAD will benefit from sur
gical revascularization with coronary artery bypass
grafting (CASG). Each patient must be assessed
individually, hut general situations where surgical
therapy is superior to medical therapy include:
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Left main coronary disease or left main equivalent
(proximal left anterior descending [LAD] stenosis
plus proximal left circumflex artery stenosisJ
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Blueprints Medicine
Three-vessel disease, especially with decreased
ejection fraction
Severe proximal LAD stenosis after surviving
ventricular tachycardia/fibrillation or with "myo
cardium at risk" on noninvasive testing
Percutaneous transluminal coronary angioplasty
(PTCA) can be used to relieve symptoms in patients
who fail medical therapy but who do not have sig
nificant enough disease to require CABG. The
routine use of coronary stents has led to decreased
risk of restenosis in the treated vessel. PTCA has
not demonstrated a benefit in preventing mortality
when compared with medical treatment, but clearly
is effective at decreasing angina.
KEY POINTS
1. The risk for underlying CAD is determined by
patient age, gender, cardiac risk factors, and
characteristics of chest pain.
2. Exercise testing can give both diagnostic and
prognostic information. Sensitivity can be
increased with imaging studies.
3. Aspirin and HMG-CoA reductase inhibitors
decrease mortality from CAD.
4. Beta blockers are the first-line antianginal drugs.
Calcium channel blockers and nitrates may be
used as well.
5. Stenosis of the left main coronary artery or equiv
alent lesions (proximal lesions in LAD and left cir
cumflex artery) requires CABG for survival benefit.
• E PIDEMIOLOGY
Acute myocardial infarction (AMI) is a common
manifestation of coronary artery disease. Each year,
approximately one million people suffer an AMI in
the United States. Many patients with AMI die sud
denly before hospitalization. In patients admitted to
the hospital, 30-day mortality is about 5% to 1 0%.
• ETIOLOGY/PATHOG E NESIS
Most myocardial infarctions occur in the setting of
underlying CAD. The formation of an atherosclerotic
plaque within a coronary artery is a multistep process
(see Chapter 3).
Spontaneous fissuring and rupture of a coronary
atherosclerotic plaque may occur, exposing a highly
thrombogenic surface. Platelet aggregation and fibrin
formation follow, and the patient clinically presents
with an acute coronary syndrome. The specific clin
ical manifestation depends on the extent. of the
thrombus. If the thrombus causes complete occlusion
of the coronary artery, the result is often an ST-ele
vation myocardial infarction. When untreated, this
leads to necrosis of the myocardium previously sup
plied by the occluded vessel. Necrosis may occur
throughout the entire thickness of the affected
myocardium, resulting in a so-called transmural or
Q-wave infarction.
If the thrombotic occlusion is transient, with spon
taneous lysis before the occurrence of full-thickness
myocardial death, a non ST-elevation myocardial
infarction (NSTEMI) may occur. This has previously
been associated with a non-Q-wave or subendocar-
dial infarction. It can also occur in the setting of com
plete vessel occlusion when extensive distal collater
alization is present. Unstable angina (UA) is a closely
related condition, with transient thrombus and
occlusion, but markers of infarction are not present
(see "Diagnostic Evaluation") .
Although rupture of an atherosclerotic plaque
with thrombus formation is responsible for most
AMIs, there are other mechanisms by which coro
nary blood flow or oxygen supply or both can
be acutely compromised, leading to myocardial
ischemia and infarction:
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"Demand ischemia" (tachycardia, hypotension
and/or severe hypoxia in setting of existing fixed
CAD)
Coronary artery dissection (often in the setting of
a dissecting aortic aneurysm)
Coronary vasospasm (either idiopathic or drug
induced, e.g., cocaine)
In situ thrombus formation (in the setting of a
hypercbagulable state)
Coronary embolism
Vasculitis (e.g., Kawasaki's disease)
Carbon monoxide poisoning
Early death (within the first month) from AMI can
be due to a number of complications:
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Arrhythmias (ventricular fibrillation/tachycardia,
complete heart block)
Heart failure (cardiogenic shock)
Ventricular rupture (peak incidence within 3 to 5
days of AMI)
Other mechanical complications (ventricular
septal defect, mitral papillary rupture)
