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MedStudy

INTERNAL MEDICINE REVIEW

SIXTEENTH EDITION

RE
CURRICULUM

Book 3 of 5

Topics in this volume:

Cardiology

Rheumatology

ERRNVPHGLFRVRUJ
Robert A. Hannaman, MD
Editor in Chief
Disclaimers

NOTICE: Medicine and accepted standards of care are constantly changing. We at MedStudy do
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is referred to solely by its proper name without a following common noun; e.g., "The symptoms are
classic for Crohn's." The AMA Manual of Style, JAMA, and Scientific Style and Format are among the
publications that promote and use the non-possessive form.

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Cardiology

PROCEDURES, LABS, PHYSICAL EXAM ............................................ 5-1 PERIPHERAL AR TERIAL DISEASE ........................................... 5-26
CHEST X-RAYS ..................................................................................... 5-1 CAUSES OF PAD AND INTERMI T TENT
ECH0 ............................... . . ....... . . . . . . ............ . . . .............. . . . ........... . . . . . . . . ...... 5-2 CLAUDICATION .................................................................... 5-26
CARDIAC STRESS TESTS . . . .................... . . . . .............. t......................... 5-2 DIAGNOSIS OF PAD ................................................................. 5-26
Exercise Tolerance Test (Without Imaging) ....................................... 5-2 TREATMENT OF PAD .............................................................. 5-26
Stress Imaging Tests ............................................................................ 5-3 VASOSPASTIC DISEASE .............................................................. 5-27
Cardiac Stress Tests- Picking the Correct Test ................ ,.............. 5-4 CARO TID ARTERY DISEASE ...................................................... 5-27
CARDIOPULMONARY EXERCISE TESTING ..................................5-5 CAROTID ARTERY ATHEROSCLEROSIS............................. 5-27
CARDIAC SCANS I CATHS ............................................... ,................. 5-5 INTERNAL CAROTID ARTERY DISSECTION ..................... 5-28
Contrast Cardiac Catheterization ........................................................ 5-5 CEREBRAL EMBOLIC DISEASE ................................................ 5-28
Cardiac C T ............................................................................. , ............ 5-5 TRANSIEN T ISCHEMIC AT TACK .......................................... 5-28
Cardiac MRJ ........................................................................................ 5-6 AORTIC DISEASE .......................................................................... 5-28
PULMONARY ARTERY CATHETERJZATION .................................. 5-6 AORTIC ANEURYSMS ............................................................. 5-28
CARDIAC BIOPSY ................................................................................ 5-6 Thoracic Aortic Aneurysms .................................................... 5-28
PHYSICAL EXAM ................................................................................. 5-7 Abdominal Aortic Aneurysm .................................................5-29
Pulses ................................................................................................... 5-7 COARC TATION OF THE AORTA ............................................ 5-29
Heart Sounds and Murmurs ................................................................ 5-7 VALV ULAR HEART DISEASE ..................................................... 5-29
Venous Waveforms.............................................................................. 5-9 INFEC TIVE ENDOCARDITIS ................................................. 5-29
HYPERTENSION ...................................................................................... 5-1 0 Overview .................................................................................5-29
CARDIAC MEDICATIONS ..................................................................... 5-10 Antibiotic Prophylaxis ............................................................ 5-30
CARDIAC ISCHEMIA............................................................................. 5-IO RUBELLA ................................................................................... 5-31
ANTI-ANGINAL DRUGS ................................................................... 5-12 RHEUMATIC FEVER ................................................................ 5-31
EVALUATION OF CHRONIC STABLE ANGINA ........................... 5-12 SPECIFIC VALV E LESIONS ..................................................... 5-3 I
Note ...................................................................................................5-12 Aortic Stenosis ........................................................................ 5-31
I. History and Physical Exam: Determine Probabiliry of CAD ...... 5-13 Chronic Aortic Regurgitation.................................................. 5-32
2. Noninvasive Tests for Chronic Stable Angina: Acute Aortic Regurgitation ..................................................... 5-33
Diagnosis and Risk Stratification................................................... 5-13 Mitral Stenosis ........................................................................ 5-33
3. Determination of Further Workup in Chronic Stable Angina ...... 5-13 Chronic Mitral Regurgitation.................................................. 5-36
TREATMENT OF CHRONIC STABLE ANGINA ............................. 5-14 Mitral Valve Prolapse .............................................................. 5-36
CARDIOVASCULAR DISEASE (CVD) PREVEN TION Acute Mitral Regurgitation ..................................................... 5-36
IN WOMEN ........................................................................................ 5-14 Tricuspid Stenosis ................................................................... 5-37
ACUTE CORONARY SYNDROME ....................................................... 5-14 Tricuspid Regurgitation .......................................................... 5-37
CLASSIFICATION OF ACS ................................................................ 5-14 Pulmonic Stenosis ................................................................... 5-37
NOTES................................................................................................... 5-15 Pulmonic Regurgitation .......................................................... 5-37
MARKERS FOR AMI .......................................................................... 5-15 Ebstein Anomaly ..................................................................... 5-37
TREATMENT OF ACS......................................................................... 5-16 VALV E SURGERY ..................................................................... 5-37
Prehospital Management... ................................................................ 5-16 Final Pearls about Murmurs.................................................... 5-38
Evaluation of Patients with Symptoms Suggestive of ACS............. 5-17 ARRHYTHMIAS ............................................................................ 5-38
ACS: GENERAL MEASURES ............................................................ 5-18 MECHANISMS OF ARRHYTHMIAS ..................................... 5-38
ECG, N TG, Morphine, Beta-Blockers, ACE Is, Atropine ................ 5-18 SICK SINUS SYNDROME ........................................................ 5-38
Anticoagulant I Antiplatelet Therapy in ACS ................................... 5-18 HEART BLOCK .......................................................................... 5-38
Fibrinolytic Therapy in ACS............................................................. 5-19 SUPRAV EN TRICULAR TACHYCARDIAS............................ 5-39
Antiarrhythmic Drugs in ACS .......................................................... 5-19 Atrial Flutter ............................................................................ 5-39
ACS: MANAGEMENT OF UA I NSTEMI- Atrial Fibrillation .................................................................... 5-39
THE ACUTE ISCHEMIA PATHWAY .............................................. 5-19 MAT......................................................................................... 5-42
Early Invasive vs. Conservative Therapy ......................................... 5-19 SV T.......................................................................................... 5-42
Early Invasive Therapy in UA I NSTEMI ........................................ 5-19 WPW ....................................................................................... 5-42
Early Conservative Therapy in UA I NSTEMI ................................ 5-20 V EN TRICULAR ARRHYTHMIAS .......................................... 5-43
Long- Term Antiplatelet Therapy after UA I NSTEMI..................... 5-20 PVCs ........................................................................................ 5-43
Cocaine and Methamphetamine Users with ST Elevation .............. 5-20 Ventricular Tachycardia .......................................................... 5-43
ACS: MANAGEMENT W I TH STEMI OR Nonsustained Ventricular Tachycardia ................................... 5-44
NEW LEF T BUNDLE-BRANCH BLOCK ...................................... 5-20 PACEMAKERS........................................................................... 5-44
Note ................................................................................................... 5-20 AN TIARRHYTHMIC THERAPY............................................. 5-45
Immediate Reperfusion Therapies....................................................5-20 Drugs ....................................................................................... 5-45
Additional Recommendations from the 2013 Electrophysiologic Testing ...................................................... 5-46
ACC I AHA STEMI Guidelines .................................................... 5-22 Radiofrequency Ablation ........................................................ 5-46
Complications of Myocardial infarction .......................................... 5-22 SYNCOPE ........................................................................................ 5-47
Implantable Cardioverter-Defibrillators ........................................... 5-23 CARDIOMYOPATHIES ................................................................. 5-48
CORONARY ARTERY DISEASE ........................................................... 5-24 HYPERTROPHIC CARDIOMYOPATHY ................................ 5-48
RISK FACTORS FOR CAD ................................................................. 5-24 Treatment for HCM ................................................................ 5-48
SCREENING ......................................................................................... 5-24 RES TRICTIV E CARDIOMYOPATHY..................................... 5-48
REVASCULARIZATION ..................................................................... 5-24 DILATED AND NONISCHEMIC CARDIOMYOPATHIES ... 5-49
CABG VS. PCI ...................................................................................5-24
Stents ................................................................................................. 5-25
Other .................................................................................................. 5-25
The Electrocardiogram
HEART FAILURE .
...... . . . . ........... . . ... .... ..................... . . ... .................. 5-49 THE I2-LEAD ECG .................................................... . . . . . . .......... . . . . 5-60
OVERVIEW ............ . . . . . . . . . . ... . . .
....... ............ . ......... . .......... ............ 5-49 AXIS DEVIATIONS ............. . ................................. . . . . . . . . .... ..
. ... . . . . . . . 5-60
LOW-OUTPUT HF .. . . . . . . . . . ....... ... .
... ........ . . . . . . . . .... . . . . . . . . . ............... 5-50 R ATES AND INTERVALS .................................................... . ... . . . . . 5-60
NYHA Classification ................. . ........ . . . . . . . . . . . ..... . ................... 5-50 INTERVALS ....... . . . . . . . . . . . . . ................................................ ................ . 5-6 I
ACC I AHA Staging . . . . . . . . . ....... . . . . . . . . .. . .... . .... .. ..
. . . ........ .. .... .. . .... 5-50 P R INTERVAL ............................................................................ 5-6I
Determining Prognosis in HF ... . . ....................... .. . . ...... . . . . . . . . . . . 5-51 QRS DURATION ................................................ . . .. ................. . . . 5-6I
Mechanism of HF .... . .. .. .
. . . . . . . .............. ...................... . . . . . . . . . . . . . . 5-51 QT INTERVAL . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . ..................... ......... 5-6 I
Treatment for HF..................................................................... 5-52 WAVEFORMS AND SEGMENTS ................................................. 5-6 I
Emergency Treatment for Severe Heart Failure . .. .................. 5-54 P WAVE . . . . . . . ................................................................................ 5-6I
HIGH-OUT PUT HF . .. ............... . . . .... . .... . . . . . ...... .. .. ...
. .. ................. 5-54 T WAVE .
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . ................. ......... ... ........ 5-62
RIGHT VENT RICULAR FAILUR.. ........................................5-54 U WAVE....................................................................................... 5-62
PULMONARY EDEMA .. .. ....... .. . . . . . .......... . . . . . . . . . . . . . . . . . . . . . . . . ......... 5-55 S T SEGMENT ............................................................................. 5-62
PERICARDIAL DISEASES . . . . ........ . . . . . . . ... .... ................... ............... 5-55 QRS COMPLEX .................... . . . . . ...................... . . . . . . . ............ . . . . . .. 5-62
NON-CONSTRICTIVE PERICARDITIS ................. . . . . . . . . . ....... 5-55 VENTRICULAR HYPERTROPHY .... . .................. .. ............... .. . .. 5-63 ..

CONSTRICTIVE PERICARDITIS ................ . . . . . . . . . . . . . . . . . . . . . . ...... 5-55 LVH .............................................................................................. 5-63


RECURRENT PERICARDITIS ....... . . . . . . . . ... . .............................. 5-56 RVH ...................................................................... . ....... ........... . ... . 5-63
PERICARDIAL EFFUSION . . . . . . ... . ............................................ 5-56 CONDUCTION DISTURBANCES ............................................... 5-64
CONGENITAL HEART DISEASE ................ .. ....................... . . . . . . . 5-57 AV BLOCKS . . ........ . ................ ..
. ..... . ............... . ..
.. ... . . . . . . . ..... . .... . . . 5-64
ASD .......................................................... . . . . . . . . . . . . . . . . . ................... 5-57 BUND LE-BRANCH BLOCK .................................................... 5-64
Ostium Secundum ASD . . .. . ... . . . . .. . ........ . . . .. . . . . ..... ... .............. . 5-57
.. LBBB .
......... ...... .................................................. .. ............ . . 5-64
.. ..

Ostium Primum ASD .......................................... .. ........... .. ..... 5-57 RBBB ...... . . . . . . . . . . . . . . .......................... .... . . . ................ . . . . ........... . . 5-64
Sinus Venosus ASD ... . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . .......... 5-57 LAFB. .... .. ............................................................... ... ............ .. 5-65
PDA .
............ . . . . . . . . . . . . . ...................... ......................... .. ................. . 5-57
. LPFB ...................................................... . . . . ........... . ................ . 5-65
PULMONARY STENOSIS . . . . . . . . . . . . . . . ............. . . . . . . . . . . . . . . . . . . . ......... 5-57 Bifascicular Block .................. . . . . . . ...... . . . . ........... .. . ... .. . . . . . . ....... . 5-65
VSD . . . . . . . ............. ... . . ..................................................................... 5-58 WIDEQRS ......................................... ............. . ........................... 5-65
COARCTATION OF THE AORTA ...... .. ......... . . . . . . . . . . . . . . . . . . . . . ...... 5-58 ARRHYTHMIAS ........ . . . . . .. . . . . . . . . . . . . ..... . . .... . . . . . . . . . . . . . . ........ . ............... 5-65
ANOMALOUS CORONARY ARTERY ........ . ...... . ..... . . . . . . . . . ..... 5-58 ECTOPIC vs. PACEMAKER . . . . . . . . . . . .......... . . . . . . . . . ..... ... ... . . . . . ....... 5-65
SUDDEN DEATH IN EXERCISING YOUNG PEOPLE ........ 5-58 ATRIAL ARRHYTHMIAS ....................... ... . . ............................. 5-66
OTHER ......... . .
......... ................. .. ............... . ................. . ............... 5-58 VENT RICULAR ECTOPIC BEATS AND HEART BLOCK .. 5-66
PULMONARY HEART DISEASE . . ....... . . . . . . ..... . .............. . . . . . ......... 5-58 MYOCARDIAL INFARCTION . . . . . . . . . . ............... . . . . . . . .......... . . . . . . . . ... 5-66
COPD AND S LEEP AP NEA. ..... .. .......................... . ......... . ... . .... .5-58 COMMON FINDINGS .
.................... ................................. . . . . . .... 5-66
EISENMENGER SYND R OME .................................. . .
.... ......... 5-58 LOCATION OF Ml vs. ECG CHANGES .................................. 5-66
CHRONIC THROMBOEMBOLIC OBSTRUCTION.. ... . . . . . .... 5-58 NOTES .......... . . . . . . . . . . .......... . . .. .
. .. . ..... ...................... . . . . . . ......... . . . . . . .. 5-67
PULMONARY ARTERIAL HYPERTENSION ........................ 5-59 REMEMBER . . . .............................................................................. 5-67
P REGNANCY AND THE HEART.. ........ . ...... .. ......... . . ...... .
. .. .. . . ..... 5-59 ANALYSIS .... . . . . . . . . . . . . . . . . . . ........... .. ................................ . . . . ............ . . . . 5-67
FOR FURTHER READING ............................................................ 5-81
PROCEDURES, LABS, PHYSICAL EXAM 5-1

upper lobe pulmonary veins), Kerley B lines, and pleural


PROCEDURES, LABS, PHYSICAL EXAM
effusions (usually right> left).

CHEST X-RAYS An anomalous pulmonary vein that drains into the


inferior vena cava can create a "scimitar sign" on chest
Know all the following chest x-ray findings!
x-ray. This is a curvilinear opacity in the right lower
Chest x-ray is an effective means of quickly determining lung field due to associated lung hypoplasia.
significant increases in both overall heart size and
Aortic abnormalities that you may see include tortuosity
(sometimes) heart chamber sizes. A cardiothoracic ratio
and calcification. An aortic aneurysm is sometimes easily
> 50% indicates an enlarged cardiac silhouette, sug
visible on the lateral film. An aortic dissection can show
gesting either cardiomegaly or a pericardia! effusion.
up as mediastinal widening on the PA projection.
This is the ratio comparing the most rightward and
leftward borders of the heart seen on a posteroanterior Pericardia! effusion is suggested by a "water bottle" or
(PA) chest x-ray, divided by the transverse chest diam a "water balloon" shape to the heart, sometimes with sig
eter (measured from the inside rib margin at the widest nificant enlargement of the cardiac silhouette (Image 5-3).
point above the costophrenic angles on the same x-ray). Shunt vascularity (enlarged, sharply defined pulmonary
This ratio is valid only for an upright, nonrotated film vasculature) is visible with significant ventricular
on full inspiration (diaphragm fully contracted) with septal defect (VSD), atrial septal defect (ASD), or other
a well-visualized cardiac outline and when there is no left-to-right shunts.
abdominal compression on the diaphragm, such as that
caused by ascites or pregnancy. Areas of calcifications on chest x-ray:

On the PA film, the left ventricle causes the bulge in the Aortic: Think dissection if you see a separation

left-lower side of the cardiac shadow; the right atrium between calcification and the aortic border, especially

(RA) causes the outline on the right; and the area of the if the mediastinum appears wide.

cardiac "waistline"-between the aortic knob and the Myocardial: typically from an apical aneurysm.
left ventricle (LV)-is formed by the main pulmonary Valvular: commonly aortic.
artery and the left atrial (LA) appendage (Image 5-1). Annular (ring-shaped): mitral annular calcification;

On the lateral view, any increase in the mass of the left if it is a perfect ring then a prosthetic valve is likely

ventricle extends the cardiac shadow posteriorly and (especially if surgical clips are also present).

lower-closer to the diaphragm. Any increase in the P ericardia!: Think constrictive pericarditis; or
mass of the right ventricle fills in the lower part of the think TB if the clinical history suggests significant
anterior clear space behind the sternum (Image 5-2). exposure (Image 5-4).
Coarctation of the aorta (COA) is indicated by absence
of a normal aortic arch. Instead, look for the "3" sign,
which is created by a prominent, left subclavian artery,
the coarctation, and poststenotic dilation of the descend
ing aorta. The barium swallow can show a "reversed 3,"
due to the impressions of the arterial structures on the
esophagus. Adults also show intercostal rib notching due
to collateral flow through tortuous intercostal arteries.

Heart failure (HF) is indicated by cardiomegaly,


pulmonary vascular redistribution (with visibly thickened

Image 5-1: Normal posteroanterior chest x-ray Image 5-2: Norma/lateral chest x-ray

2014 MedStudy
5-2 PROCEDURES, LABS, PHYSICAL EXAM

intracardiac shunts. Doppler echocardiography measures


the velocity and direction of the blood flow. Doppler
echo determines mean gradients, peak velocities, and
valve area.

So, Doppler is useful in determining the severity of


valvular stenosis or regurgitation, as well as in evalu
ating left ventricular diastolic function, left ventricular
outflow tract gradients, and intracardiac shunts. It is also
helpful in estimating pulmonary artery (PA) pressure.
To estimate pressure by using peak Doppler velocity
measured on echo: P ressure gradient (mmHg) = 4 x V2
Image 5-3: "Water bottle" heart Image 5-4: Pericardia/ (measured velocity). For example, if the velocity across
calcification
the tricuspid valve is 5 m/sec, then the PA pressure =
4 x ( 5 x 5) + right atrial pressure. So, if the right atrial
Know that a single lead in the apex of the right ventricle
pressure in this example is 10 mmHg, then the PA
(RV) indicates the presence of an electronic ventricu
pressure= 110 mmHg (which is extremely high).
lar pacemaker or implanted defibrillator-with the
defibrillator lead being larger and wider than that of a
pacemaker, 2 leads indicate an atrioventricular (AV ) CARDIAC STRESS TESTS
sequential (dual-chamber) pacemaker, and 3 leads
indicate a biventricular pacemaker. If there is no atrial
Overview
lead, the patient likely has chronic atrial fibrillation. The increased demand for myocardial oxygen with
exercise is the key factor in the use of exercise testing
as a diagnostic tool for coronary artery disease ([CAD];
ECHO
a.k.a. coronary heart disease). Stress tests have an integral
Echocardiography is an ultrasound modality used to role in both the detection of CAD (diagnostic tool) and
image the heart. It utilizes M-mode, 2D, and 3D for in stratification of risk (prognostic tool). To appropriately
structural imaging and Doppler for assessing blood flow utilize stress tests, a patient's pretest probability of CAD
rate and direction. must be taken into account. (A positive test in a low-risk

Best use of echo is for the following scenarios: patient is more likely to be a false positive, and a negative
test in a high-risk patient is more likely to be a false nega
Left ventricular structure and systolic function tive.) Diagnostic testing is most valuable when pretest
Right ventricular structure and systolic function probability for CAD is intermediate.
Valvular heart disease
There are 2 general types of cardiac stress tests done:

Congenital heart disease


Myocardial infarction (including post-MI I) Exercise tolerance test ([ETT]; basic treadmill or
stationary bicycle testing without imaging)
complications)
Cardiomyopathy (both loss of ejection fraction 2) Stress imaging testing-"stress" is induced with:
and hypertrophy of myocardium) exercise (treadmi11 or bicycle), or
Pericardia! disease pharmacologic stress (either dobutamine or a
Cardiac masses (tumor, thrombus, and vegetation) vasodilator)

Diseases of the aorta and pulmonary artery The associated imaging is done with:

Estimation of pulmonary pressure Echocardiography (a.k.a. "stress echo")


Diastolic function Myocardial perfusion imaging (MPI)
Cardiac sources of emboli
Exercise Tolerance Test (Without Imaging)
Transesophageal echocardiogram (TEE) is an echo
performed with an esophageal probe. It offers Exercise tolerance test (ETT), using either a treadmill
higher-resolution images compared to transthoracic or stationary bicycle, is the cornerstone of diagnostic
imaging and is especially useful for evaluating: testing for ischemia and functional capacity and for
determining prognosis (including post-MI).
Valvular structure and function
Left atrium (including left atrial appendage) Despite an overall low sensitivity and specificity (men:
Cardiac masses sensitivity= 68%, specificity= 77%; women: sensitivity
61%, specificity = 70%), the sensitivity and specific
Intracardiac shunts
=

ity increase with higher pretest probability of CAD. ETT


Endocarditis
has a number of advantages, including: the ability to test

Aortic dissection
functional capacity, safety, widespread availability, and

A bubble study (performed by injecting hand-agitated relatively low cost.


saline and air into the venous system) is used to evaluate

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PROCEDURES, LABS, PHYSICAL EXAM 5-3

Technical difficulties in monitoring ECG/BP


Patient requests to stop
Quiz Serious arrhythmia (e.g., sustained ventricular
tachycardia)
On a lateral view CXR, extension of the heart
border posteriorly and inferiorly indicates Achieving target heart rate alone is not a reason to
enlargement of which ventricle? discontinue the ETT, and the individual should be
encouraged to go as long as tolerated until required to
On a lateral view CXR, extension of the
stop for some reason (e.g., dyspnea, fatigue, exhaustion,

cardiac shadow of the lower part of the anterior


or one of the absolute indications for termination).
clear space behind the sternum indicates
enlargement of which ventricle? Excellent exercise tolerance (> I 0 METS) is associated
with a good prognosis independent of the degree of
What conditions is a TEE useful for evaluating?
coronary artery disease.
What are absolute indications for terminating
Absolute contraindications to ETT:
an ETT?
Acute MI within 2 days
When are stress imaging studies done instead
of an ETT? Unstable angina not previously stabilized by
medical therapy
Uncontrolled arrhythmias causing symptoms or
The patient typically exercises on a treadmill using

hemodynamic compromise
standard exercise protocols, such as the Bruce protocol
(see Table 5-6 on page 5-12). The level of maximal
Symptomatic severe aortic stenosis
exercise achieved on the ETT is measured in metabolic Uncontrolled symptomatic heart failure
equivalents (METS).
Acute pulmonary embolus or infarction
ETT should not be performed in 2 groups: Acute myocarditis or pericarditis
Acute aortic dissection
I) Patients unable to exercise sufficiently (must achieve
85% of age-predicted maximum heart rate)
Stress Imaging Tests
2) Patients with baseline ECG abnormalities that can
Overview
interfere with interpretation of the stress test (e.g., left
ventricular hypertrophy [LYH], left bundle-branch The stress imaging studies are the stress echo and
block [LBBB], Wolff-Parkinson-White [WPW], myocardial perfusion imaging (MPI). The choice of
ventricular pacing, and resting ST depression), or which one to use is often based on operator experience
taking digoxin at the facility.

Know the following information related to ETTs: Stress imaging studies are used as the initial diagnostic
method when a patient is not a candidate for ETT due to
Definition of a positive ETT: flat or down-sloping
inability to exercise adequately or when there are ECG
ST-segment depression > I mm and 80 ms after the
changes at rest that can interfere with interpretation of
J-point in 3 consecutive beats.
the ETT. They also are preferred in patients with prior
Unlike ST elevation, ST depression does not correlate revascularization.
with the anatomic location of myocardial ischemia.
Stress imaging studies have greater sensitivity and
Isolated ST depression in inferior leads is far less
specificity than the regular ETT. They are used when
specific than ST depression in lateral leads (V4-V6).
measurement of ejection fraction or myocardial
ST elevation during an ETT in 3 contiguous leads viability is desired in addition to identifying coronary
without Q waves of prior MI is an unusual finding that artery disease.
is suggestive of marked ischemia (can be seen also with
coronary artery spasm).
Stressing the Heart for Imaging Studies
Absolute indications for termination of an ETT:
The "stress" portion of these tests can be performed with
ST elevation > I mm in leads without Q waves from exercise or pharmacologic agents.
prior MI and excluding aVR, aYL, and VI
With exercise, imaging studies are done just like an
Decrease in systolic BP > I 0 mmHg when ETT and require the same ability to meet 85% of age
accompanied by any other evidence of predicted maximum heart rate. Exercise is preferable
ischemia or hypoperfusion because it provides additional functional and prognostic

Moderate-to-severe angina information. Exercise is not used in patients with pace

CNS symptoms (ataxia, dizziness, near syncope) makers or left bundle-branch block (LBBB) because
Signs of poor perfusion (cyanosis/pallor) it can cause false-positive left ventricular anteroseptal

Sustained 2nd or 3rd degree AV block perfusion defects. The pharmacologic agents used for
cardiac imaging studies are dobutamine or vasodilators.

2014 MedStudy
5-4 PROCEDURES, LABS, PHYSICAL EXAM

Dobutamine is both inotropic+ chronotropic and causes dilation and decline in global left ventricular systolic
the heart to act similarly as it would with exercise. As function with stress (suggestive of multivessel disease).
with exercise, a target heart rate must be achieved with Stress echo is less expensive than MPI.
dobutamine. Also, as with exercise, dobutamine is not
Vasodilators are not used for stress echo.
used in patients with pacemakers. Dobutamine stress
echo is fine for LBBB (but not dobutamine MPI with
LBBB). Dobutamine is the agent used for patients who Myocardial P erfusion Imaging

not only are unable to exercise but who also have a con Myocardial perfusion imaging (MPI) uses radioisotopes
traindication to vasodilators (e.g., bronchospasm, severe with single-photon emission computed tomography
carotid artery stenosis). (SPECT). The most commonly used agents are
Vasodilation: Adenosine, dipyridamole, and regad technetium-99m (99mTc)-labeled substances (commonly
enoson are the main coronary vasodilators used in the sestamibi or tetrofosmin). Thallium-201 (21TI) is Jess
pharmacologic MPI stress tests. Vasodilators do not commonly used.
stress the heart by increasing heart rate as is done with These tracers distribute in heart tissue in proportion to
exercise or dobutamine. These vasodilators work in this blood flow; this distribution is recorded by a gamma
setting by dilating and increasing blood flow in normal camera. Perfusion is compared visually between the
cardiac vessels while doing little to change the flow in resting and stressed states. Preserved myocardial perfu
stenotic vessels. The dilated normal vessels steal flow sion at rest but decreased during stress is suggestive of
from the stenotic vessels, causing perfusion defects in ischemia ("reversible defect"), while matched reduction
scans (and ST segment changes in ECGs). Vasodilators in perfusion between the rest and stress images is sug
are not used in patients with history of bronchospasm. gestive of a myocardial infarction ("fixed defect"). Other
Regadenoson is a more selective A2A receptor activator, high-risk markers include transient ischemic LV dilation
has less bronchospasm effect, and allows for a faster (TID), reduced post-stress LV ejection fraction, and
stress test. Even so, for the Boards and per current increased lung or right ventricular uptake, all of which
guidelines, dobutamine is still the pharmacologic agent are suggestive of multivessel disease.
of choice for patients with a history of bronchospasm. MPI is often done with ECG-synchronized "gated"
technique, where multiple images are combined and
Stress Echo and Stress MPIIndications smoothed for better resolution. This allows for assess
ment of wall motion and ventricular size and function
Unlike ETT, exercise stress echo and stress MPI can be
(estimates ejection fraction).
used in patients:
Again, target heart rate must be achieved with exercise
with resting ECG ST changes,
or dobutamine for an adequate test; however, achieve

with WPW syndrome, or ment of target heart rate is not needed with vasodilator
on digoxin therapy. stress. So, dobutamine is used only in cases where the
vasodilator is contraindicated (as it would be in patients
Note that it is a common misconception that these patients
with bronchospasm-see above).
require chemical stress, but this is definitely not true! If
they can exercise, these patients have a class I indication Other imaging modalities that can be used for MPI
for a stress echo with exercise or MPI with exercise (i.e., (other than SPECT imaging) include cardiac positron
these patients need the imaging, not the chemical stress). emission tomography (PET) and cardiac MRl, both of
which are also used to assess for myocardial ischemia
Note: MPI with vasodilators (but not exercise or dobu
and viability.
tamine!) is the test of choice for patients with paced
ventricular rhythm. Myocardial perfusion imaging (MPI) is more expensive
than stress echo, and it involves radiation exposure.

Stress Echo

The stress echo is a widely used test for myocardial Cardiac Stress Tests -
ischemia by the detection of stress-induced wall motion Picking the Correct Test
abnormalities. Stress echo is less sensitive but more spe To determine the correct stress test, go through the
cific than MPI for the detection of coronary artery disease. following scenarios. These are summarized in Table 5-1.
Use exercise or, if unable to exercise, use dobutamine to An exercise stress test (i.e., ETT, exercise echo, exercise
achieve target heart rate. Then take echo images to evaluate MPI) is always preferred if the patient has no limitations
changes in wall motion, systolic wall thickening, and sys to exercise (exceptions are LBBB or paced rhythm).
tolic ejection fraction with stress. Abnormal wall motion or If the resting ECG is normal, proceed with ETT
failure of the wall to thicken (contract) appropriately sug no imaging is needed. If the resting ECG is abnormal
gests ischemia of that region of the myocardium. (with exception of LBBB and paced rhythm), perform
In addition to new regional wall motion abnormalities, exercise testing with echo or MPI.
criteria for abnormal stress echo are left ventricular cavity

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PROCEDURES, LABS, PHYSICAL EXAM 5-5

response to intervention. CPX is well established for


evaluating patients with systolic heart failure (HF),
undergoing a pretransplant assessment, and for patients
with unexplained exertional dyspnea.
When are exercise stress echo and MPI
indicated instead of ETT?
CARDIAC SCANS I CATHS
Which stress imaging tests are used in patients
with LBBB? With paced ventricular rhythm?
Contrast Cardiac Catheterization

Which patients may benefit from CPX?


Coronary angiography is the gold standard for
the diagnosis of coronary artery disease (CAD);
ventriculograms and aortic root angiography can be
A pharmacologic stress test is done if the patient cannot
done at the same time as the coronary angiogram.
do more than moderate exercise, is unable to increase
the heart rate (e.g., pacemaker) or has LBBB. Not only can contrast cardiac catheterization assess
coronary anatomy through contrast ventriculography, it
Follow these indications when choosing the proper agent:
also can assess ejection fraction, wall motion abnormali
If the patient simply is unable to walk and has no ties, ventricular dilatation, degree of mitral regurgitation,
other issues, use pharmacologic stress test. and the presence of a ventricular aneurysm. Cardiac
If the patient has bronchospasm or severe carotid catheterization is an invasive procedure with - I% risk
artery stenosis, use dobutamine. of serious complications (death, M I, stroke, arrhythmia,
If the patient has severe HTN or prior ventricular renal failure, bleeding).
tachycardia (VT), use a vasodilator (adenosine, These studies all involve arterial access, radiation, and
dipyridamole, or regadenoson), not dobutamine. contrast exposure.
If the patient has a paced ventricular rhythm, use a
vasodilator with MPI; again, not dobutamine. Cardiac CT

One more time: Do not use adenosine or dipyridamole Cardiac CT is a newer, noninvasive modality for imaging
in someone with asthma or severe carotid stenosis and the heart. Cardiac CT includes:
do not use dobutamine in someone with a history of VT,
Coronary computed tomographic angiography (CTA)
uncontrolled HTN, or a paced ventricular rhythm.
Coronary artery calcium (CAC) scoring
Assessment of ventricular structure and systolic
CARDIOPULMONARY EXERCISE TESTING function

Cardiopulmonary exercise testing (CPX) is a CTA requires IV contrast (check Cr!); also, the heart rate
special exercise test that measures ventilation and must be < 60 bpm and regular, and patients must be able to
concentrations of oxygen and carbon dioxide during hold their breath.
progressive exercise (stationary bicycle/treadmill) and
CTA is a reasonable diagnostic test for symptomatic
is the gold standard aerobic exercise test. CPX provides
patients who are at intermediate risk for CAD after initial
the most accurate and reproducible measurement of
risk stratification, including patients with equivocal stress
cardiorespiratory fitness, severity of impairment, and
test results. It should not be used in asymptom

Table 5-1: Determining Best Cardiac Stress Test atic patients or in symptomatic patients with very
low or high probability for CAD. The negative
ECG Findings Able to Exercise? predictive value of CTA is very high; that is, a
negative CTA is very helpful in excluding sig
Able NotAble
nificant coronary artery disease. Usefulness is
Resting ECG ETT* Dobutamine echo reduced in patients with pronounced coronary
normal Dobutamine MPI calcification.
Vasodilator MPT
CTA is an excellent test for evaluation of patients
> I mm resting ST Exercise echo* Dobutamine echo with congenital coronary anomalies.
depression, WPW, Exercise MPI* Dobutamine MPI
CAC (coronary artery calcium) scanning detects
LVH, digoxin Vasodilator MPI
atherosclerosis and, unlike CTA, does not
LBBB N/A Vasodilator MPI* require IV contrast. CAC is used for further risk
Dobutamine echo stratification in asymptomatic, intermediate-risk
patients. A CAC score of zero is considered low
Pacemaker N/A Vasodilator MPI
risk for CAD, and > 400 indicates an elevated
* preferred. Vasodilators= adenosine, dipyridamole, regadenoson.
=
(
- 3-fold) risk for CAD.
Vasodilator used if patient has previous V-tach or severe HTN.
Vasodilator not used if patient has asthma or severe carotid stenosis;
instead, use dobutamine.

2014 MedStudy
5-6 PROCEDURES, LABS, PHYSICAL EXAM

A noncontrasted chest CT (which differs from a for the tests that differentiate between these disorders
dedicated cardiac CT) is highly effective in assessing for (page 5-55).
pericardia! thickening if constriction is a concern. 3) If the cardiac output and PCWP are decreased and
Keep in mind that all forms of cardiac CT involve the RA pressure is elevated in the setting of an acute
radiation exposure. inferior Ml, the cause is RV infarction with secondary
right-sided failure. The RV has decompensated and is
unable to fill the left side of the heart. Treatment is to
Cardiac MRI
give fluid until the blood pressure returns to normal.
Static and dynamic cardiac MRI (CMRI) allows high This sounds like stressing an already stressed RV
resolution imaging of ventricular function, valvular and it is-but there is a net positive effect when BP
motion, and myocardial perfusion. and, hence, coronary artery blood flow are returned
CMRI is useful to assess cardiac structure and function, to normal and heart rate is reduced. Think of this in
valvular heart disease, coronary takeoff, the great a hypotensive patient with an inferior infarction and
vessels, pericardia! disease, cardiac masses, myocarditis, raised jugular venous pressure (JVP). Do not give
and infiltrative diseases. preload-reducing agents such as nitroglycerin because
cardiac output depends on adequate preload in the
CMRI also can be used to assess for myocardial setting of an RV infarct.
ischemia and post-MI tissue viability.
4) If the cardiac output is low, PCWP high, and RA
Cardiac MRI involves the use of gadolinium, which pressure high, the patient has biventricular failure
should be avoided in patients with advanced renal failure with cardiogenic shock. Treatment is to give diuretics,
due to the risk of nephrogenic systemic fibrosis. preload and afterload reducers, and inotropes. In a
typical case, a patient gets nitroprusside, nitroglycerin,
milrinone, or dobutamine.
PULMONARY ARTERY CATHE TERIZATION
5) Mitral stenosis (or LV failure) with 2 RV failure.
Pulmonary artery catheterization (PAC) can be used to
assess right and left filling pressures, cardiac output, RV 6) Pulmonary hypertension.
and PA pressures, and systemic and pulmonary vascular Also know that septic shock is mainly due to a low
resistance. This is useful to determine a patient's systemic vascular resistance. These patients have low
volume status, causes of shock, and existence of BP, systemic vascular resistance (SVR), and PCWP
pericardia! disease. and a high CO.
The pulmonary capillary wedge pressure (PCWP) is
the dampened L A pressure that reflects left ventricular CARDIAC BIOPSY
end-diastolic pressure (LVEDP) in most cases. This
reflects LVED volume. Know this entire topic! Endomyocardial biopsy is used to evaluate the cause of
a cardiomyopathy or myocarditis in patients where the
Normal pressures (mmHg): diagnosis is uncertain and would change management,
RA < 7, RV 30/7, PCWP < 12.
= or if the patient is not responding to therapy. Monitoring
Jugular venous distension in the upright patient indi cardiac transplant rejection is the major indication for
cates an elevated R A pressure> 7 em H20 (5 mmHg). endomyocardial biopsy. It also can be considered in
PCWP increases with LV systolic and diastolic failure, patients with rapidly progressive heart failure or wors
mitral stenosis, aortic and mitral insufficiency, tampo ening ventricular dysfunction that persists despite
nade, and constrictive pericarditis. Consider LV failure appropriate medical therapy, and in patients suspected
if the PCWP is> 15-18; PCWP 15-25 causes dyspnea of having myocarditis (particularly giant cell myocar
on exertion (DOE); and PCWP 25-35 causes dyspnea ditis) or a myocardial infiltrative process (particularly
at rest, orthopnea, and interstitial edema. Pressure> 35 amyloidosis).
(acutely) causes frank pulmonary edema.
Table 5-2: Pulmonary Artery Catheterization Scenanos
Note: The RA pressure and PCWP also increase with
RA PA PCWP BP
decreased compliance of the ventricle (as in LVH and
Press Press
right ventricular hypertrophy [RVH]).
A few PAC scenarios are shown in Table 5-2: 0--5 (13-28)/ 3-11 110/70
(normal) (3-13)
1) Normal: Notice in the examples that the diastolic
2 18 32/18 19 70/50
PA pressure is typically very close to PCWP (usual
difference < 5) except in #6, in which there is 3 15 21/11 10 70/50
pulmonary hypertension!
4 18 30/20 20 70/50
2) Diastolic pressure in all 4 chambers is equalized
in both pericardia! tamponade and constrictive 5 18 90/32 30 110/70
pericarditis. See the Pericardia! Diseases discussion 6 18 90/32 10 110/70

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PROCEDURES. LABS, PHYSICAL EXAM 5-7

Pulsus parvus et tardus (parvus-low amplitude,


tardus-slow upswing) = aortic stenosis.

B rachiofemoral delay, the femoral pulse occurring after


the brachial pulse, is present in coarctation of the aorta.
When is PCWP increased?
Pulse asymmetry occurs in aortic dissection, with good
When is diastolic pressure equal in all
upper-extremity pulses and diminished or absent lower

4 chambers?
extremity pulses, or the asymmetry occurs between the
Name 1 indication for doing endomy ocardial left and right extremities.
biopsy.
Peripheral arterial disease ([PAD]; previously called
True or false? Pulsus paradoxus can be seen in peripheral vascular disease [PVD]) can cause decreased
cardiac tamponade. or absent peripheral pulses; a bruit may be heard over the
more proximal artery (such as the femoral artery) as well.
What is pulsus bisferiens? What does it
indicate?

What does pulsus alternans indicate? Heart Sounds and Murmurs

True or false? Sustained handgrip increases the Heart sounds and murmurs: Again, know this topic!
murmur of mitral valve prolapse, but decreases Know the differentiating maneuvers in Table 5-3 and
the murmur of HCM. the heart sounds tables in the Valvular Heart Disease dis
cussion (Table 5-I 0 and Table 5-11 on page 5-34 and
page 5-35). Learn these topics so you can determine
The sensitivity of endomyocardial biopsy in many
how one abnormal finding (e.g., a particular heart sound)
conditions that affect the heart focally is relatively
suggests certain findings on ECG and chest x-ray.
low, so a "negative" biopsy is not as helpful as a
"positive" one.
Murmurs

PHYSICAL EXAM All valve murmurs increase in intensity when blood


flow increases across the valve. Standing and the strain
Note phase of Valsalva decrease right and left cardiac fill
Know this physical exam topic perfectly! You should ing and cause the sound of most murmurs to decrease,
know normal findings as well! Consider this whole topic but these actions increase the intensity of the murmurs
highlighted! of mitral valve prolapse (MVP) and hypertrophic car
diomyopathy (HCM). Squatting and lying down (or
passive straight-leg raises if already supine) increase
Pulses cardiac volume. This increased volume and afterload
Pulsus paradox us (decreased pulse amplitude with also increases intensity of all murmurs except, again,
inspiration seen as absence of Korotkoff sounds during MVP (page 5-36) and and HCM (page 5-48).
inspiration) can be observed clinically by auscultating
Sustained handgrip (20-30 seconds) boosts systemic
the BP and listening for an exaggeration of the normal
vascular resistance and left ventricular volume, and
inspiratory decrease in systolic BP (> 10 mmHg). therefore decreases the murmurs of HCM and aortic
It is present with:
stenosis (AS). It prolongs the murmur of MVP due to
cardiac tamponade (especially), earlier prolapse of the valve; thus, it helps differenti
constrictive pericarditis, ate between HCM and MVP. Typically, use handgrip

asthma, and to differentiate between AS (murmur decreases) and


MVP (murmur increases in duration).
tension pneumothorax.
Right-sided murmurs and heart sounds are louder
Note: Korotkoff sounds are those heard during blood
during inspiration and any maneuvers that increase
pressure determination with a cuff.
venous return, such as passive leg raising and
The paradox is that, when severe, you can hear a abdominal compression. Left-sided murmurs and heart
heartbeat but not feel a pulse during inspiration. sounds are louder during expiration. The only semi
exception to this rule is a right-sided ejection click due
Pulsus bisferiens (bifid with 2 systolic peaks per cardiac
to pulmonic stenosis; this disappears with inspiration.
cycle) is seen with aortic regurgitation (with or without
(On a chest x-ray, pulmonic stenosis can appear as an
stenosis!) and hypertrophic cardiomyopathy (HCM,
enlarged pulmonary artery.)
page 5-48).

Pulsus altemans (varying pulse pressure with a


Heart Sounds
regular pulse rate) is seen with severely depressed
systolic function of any cause that leads to decreased 51 is caused by the closing of the mitral and tricus
stroke volume. pid valves. S1 intensity is decreased when there is

2014 MedStudy
5-8 PROCEDURES, LABS, PHYSICAL EXAM

a prolonged PR interval, mitral regurgitation, acute stenosis, acute pulmonary embolism, ectopic or pace
aortic regurgitation (increased LV pressures cause early maker beats originating in the left ventricle, or right
valve closure), or with a severely calcified mitral valve. bundle-branch block (RBBB)-all of which cause
delayed or prolonged contraction of the right ventricle.
sl intensity is increased (i.e., the mitral valve slams
A widely split S2 can also be caused by early closure
shut) by a short PR interval, mitral stenosis, or
of the aortic valve, as in mitral regurgitation. Pulmonic
hyperdynamic ventricular function.
stenosis is especially likely if the patient has an ejec
52 is caused by the closing of the aortic (A2) and tion click that disappears with inspiration.
pulmonic (P2) valves at the end of systole. P2 usually
You hear a fixed split S2 when there is an atrial septal
occurs just after A2; this physiologic split is increased
defect. The patient presents with a fixed, split-second
with inspiration, because the increased volume of blood
heart sound, a systolic ejection murmur (SEM), and has
in the right ventricle prolongs RV systole and delays
pulmonary vascular congestion on the chest x-ray. You
closure of the pulmonic valve. It generally disappears
can also hear a fixed split S2 with RV failure when the
on expiration.
stroke volume is unable to increase with inspiration.
A persistently (or widely) split S2 can vary with
A delay of aortic closure (A2) causes a paradoxically
respiration but does not disappear on expiration.
split S2> with P2 occurring before A2. In this case you
A widely split S2 that varies with inspiration (but
hear increased splitting with expiration instead of
never completely disappears) can be due to pulmonic

Table 5-3: Maneuvers to Differentiate Murmurs

Maneuver Result

Passive straight-leg raise (to 45 degrees, listen after 15 sec) Increases venous return

Valsalva (hold for 20 sec, listen just before end) Decreases venous return

Standing (squat for> 30 sec then quickly stand; listen during Decreases venous return
first 15 sec after standing)

Transient arterial occlusion (bp cuff on both arms, inflated Increases systemic vascular resistance
> 20 mm above systolic pressure)

Handgrip (isomeric; listen at end of 1 min max grip) Increases systemic vascular resistance

Squatting Increases venous return and increases systemic vascular


resistance, but preload effect is stronger than afterload effect

Maneuvers for increasing/decreasing specific systolic murmurs

For HCM use Result

Standing (from squat) 95o get increased murtnur

Valsalva (if cannot do squat-to-stand) 65% get increased murmur

Passive straight-leg raise 85% get decreased murmur

Handgrip 85% get decreased murmur

ForMVP use Result

Standing and Valsalva Click-murmur moves earlier

Transient arterial occlusion In 80%, click-murmur moves later

Handgrip In 70%, click-murmur moves later

For VSD use Result

Standing and Valsalva Murmur decreased

Transient arterial occlusion 80% get increased murmur

Handgrip 70% get increased murmur

For AS use Result

Transient arterial occlusion Murmur decreased

Handgrip Murmur decreased

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PROCEDURES, LABS, PHYSICAL EXAM 5-9

with concentric hypertrophy. You do not hear an S4


during atrial fibrillation because the sound requires
atrial contraction. S4 also is not audible in mitral steno
sis, where there is obstruction of the ventricular inflow.
When is a persistently split S2 heard?

What causes a paradoxically split S2? Venous Waveforms

When is an S3 important? Venous waveforms: Jugular venous pressure and


waveforms are typically examined on the right side of
When are large v waves seen on the left side?
the neck (Figure 5-l ). [Know these!] See Table 5-4.
Right side?
Large, right-sided v waves are seen in ventricular
When is rapid x and y descent seen?

septal rupture and tricuspid regurgitation.


When are large, right-sided a waves seen?
With severe mitral regurgitation, there are

When are large, left-sided a waves seen? tall, left-sided v waves from the regurgitation
during systole. Note that left-sided waves are not seen
When are "cannon" a waves seen?
on the NP but on Swan-Ganz monitoring.
When does a slow y descent occur?
Rapid x andy descents are seen with constrictive

pericarditis, whereas only a rapid x descent is seen in


inspiration. This delay is commonly caused by LBBB tamponade (loss of they descent).
and ectopic or pacemaker beats originating in the right Large, right-sided a waves are seen in tricuspid
ventricle. Advanced HCM is another cause. stenosis (TS), severe pulmonic stenosis, and severe
53 just follows S2 and indicates the end of rapid noncompliant RVH.
ventricular filling (sounds like lub-dub-huh); this Large, left-sided a waves are seen with mitral
is the first part of diastole, when the first 70% of stenosis (MS).
ventricular filling occurs as the ventricle relaxes. "Cannon" a waves occur in complete heart block,
The sound is thought to be due to the tensing of the ventricular tachycardia, or asynchronous ventricular
chordae tendineae. You often hear it in normal children pacing and all conditions withAV dissociation (times
and in persons with high cardiac output, such as preg when the atrium is contracting against a closed
nant women, but it is typically an abnormal finding in tricuspid valve).
patients > 40 years of age. In these patients, it can be Slow y descent is from delayed atrial emptying as in
from any condition that increases early LV filling rate tricuspid stenosis.
or volume, such as acute ventricular decompensation
or severe aortic or mitral regurgitation. S3 in a patient Also see Table 5-l 0 on page 5-34 for a review of the
with known left ventricular dysfunction is a poor valve disorders.
prognostic indicator-in general, as well as for surgery.
Both S3 and S4 are best heard in left lateral decubitus
position using the bell.
a
54 is heard just before S 1 at
the end of diastole (sounds
Ventricular Diastole
like huh-lub-dub). The S4
Systole
sound is caused by ven
tricular filling during atrial
contraction, and you hear it
in patients with decreased
ventricular compliance.
Increased stiffness of the
ventricles causes force
ful atrial contraction and
causes S4. You may hear S4
in ischemic heart disease,
aortic stenosis, hypertrophic
cardiomyopathy, dia
betic cardiomyopathy, and
hypertensive heart disease
a wave xdescent v wave y descent
Atrium contracting, Atrium relaxing then Atrium tense and full, Atrium emptying,
tricuspid valve open filling, tricuspid closed tricuspid closed tricuspid open

Figure 5-1: Jugular Venous Pulse

2014 MedStudy
5-10 HYPERTENSION

Table 5-4: Venous Waveforms in a Cltnlcal Setting

Condition Neck Vein Appearance Other Diagnostic Features

Pulmonary HTN Elevated a and v waves Other physical exam findings of pulmonary HTN

Tricuspid regurgitation Large v waves TR murmur, pulsatile liver

Constrictive pericarditis Rapid x andy descents Kussmaul sign, pericardia! knock

Tamponade Rapid x descent Pulsus paradoxus, hypotension

Tricuspid stenosis Slow y descent T S murrnur

Restrictive cardiomyopathy Rapid x andy descents Low-voltage ECG, echo, myocardial biopsy

Tension pneumothorax Distended neck veins Dyspnea, unilateral absent breath sounds, deviated
trachea, chest x-ray

Superior vena cava Unilateral distended neck veins Facial edema and cyanosis, diagnosis of cancer
syndrome

AV dissociation Irregular canrion a waves ECG

RV infarction Elevated a and v wave Acute inferior Ml, Kussmaul sign

ASD Large v waves and rapid Fixed split S2, echo


y descent

HYPERTENSION CARDIAC ISCHEMIA

Suspect secondary causes of hypertension (HTN) OVERVIEW


in patients who develop HTN before age 30 years, who
Angina is chest pain caused by a "supply-demand"
have drug-resistant HTN, or who develop uncontrolled
mismatch between coronary perfusion and cardiac
HTN that was previously well controlled.
workload. It is typically classified as either stable or
Systolic abdominal bruits (without a diastolic bruit) unstable (pain at rest, new onset or increased frequency).
suggest renal vascular hypertension. Bilateral renal
Obstructive atherosclerotic coronary artery lesions
artery stenosis (RAS) can lead to severe exacerbation of
(supply problem) are the most common cause of stable
hypertension and decline in renal function with initiation
angina (Image 5-5). Plaque rupture or erosion with
of angiotensin-converting enzyme (ACE) inhibitors or
superimposed thrombus is the most common underlying
angiotensin II receptor blockers (ARBs). Noninvasive
process triggering acute coronary syndrome (ACS).
tests to diagnose RAS include duplex ultrasonography,
CTA (in individuals with normal renal function), and There are many causes of increased demand (e.g.,
magnetic resonance angiography (MRA). When clinical tachycardia, fever, and thyrotoxicosis) and many
suspicion is high and results of noninvasive tests are other causes of a decreased supply (e.g., hypotension,
inconclusive, catheter angiography is recommended coronary vasospasm, anemia, and hypoxia). Coronary
to diagnose RAS. blood flow can be impaired in conditions such as severe
aortic valve disease with left ventricular hypertrophy
Think of primary hyperaldosteronism in a hypertensive
patient with hypokalemia and low renin.
(LVH), hypertension, idiopathic dilated cardiomyopathy,
and hypertrophic cardiomyopathy, even in the absence
Think of pheochromocytoma in a hypertensive of epicardial CAD.
with recurrent and intermittent episodes of severe
Note: Only 20% of patients actually have classic
hypertension, frequently accompanied by palpitations
-

angina at the moment of ischemic ST changes. Silent


and severe apprehension.
myocardial ischemia is painless but just as harmful as
Much more on hypertension in Nephrology, Book 2. angina-associated ischemia. Silent ischemia is seen
frequently in diabetic patients as well as those with
prior ischemic events. Silent ischemia, myocardial
CARDIAC MEDICATIONS infarctions, and thrombotic strokes tend to occur in a
circadian pattern, with the highest incidence in the early
Refer to Table 5-5 for an overview and comparison of morning hours.
commonly used cardiac medications. Pay attention to
The distinction between stable and unstable angina is
those that prolong survival!
a key factor in determining management/diagnostic
strategies. Short- and long-term risk (death and MI) in
patients with acute coronary syndrome is much higher

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CARDIAC ISCHEMIA 5-11

True or false? A systolic abdominal bruit


without a diastolic bruit suggests renal vascular
hypertension.

What time of day does the highest incidence of


spontaneous ischemic cardiac events occur?

than in patients with stable angina, and therefore patients


with ACS warrant emergent medical attention, inpatient
management, and, much more commonly, revascular
ization. (See Acute Coronary Syndrome on page 5-14.)
Stable angina, on the other hand, is generally evaluated
in the outpatient setting and symptoms are often
managed medically.

The most important, easily determinable prognostic


Image 5-5: Angiogram showing narrowing in coronmy artery.
factor in patients with coronary artery disease is the
degree of LV dysfunction. (If severe, it can be a reflection
of multi-vessel or left main/left main-equivalent disease.)

Table 5-5: Common Card1ac Medications

Medication Negative Negative Negative Vaso- Anti- Prolong Prolong Indications


lnotrope Chrono- Dromo- dilator anginal Survival Survival in
trope trope Post-MI HF

Digoxin N + + N N N Systolic HF,


arrhythmias

Beta-blockers +++ +++ +++ N y y y HTN, angina,


HF, arrhyth-
mias

C arvedi\ol ++ +++ +++ y y y y HTN,gina,


HF, arrhyth-
mias

Nifedipine ++ N N y y N N HTN, angina

Amlodipine + N N y N Y(in DCM) HTN, angina,


DCM

Diltiazem ++ ++ ++ y y N N HTN, angina,


arrhythmias

Verapamil +++ +++ y N N

Nitrates N N N y y N Y(with Angina, HF


hydralazine)

ACEis N N N y N y y HTN,HF

ARBs N N N y N y y HTN,HF
,
Hydralazine N N N y N N Y(with HTN,HF
nitrates)
,...,

Spironolac- N N N N N N y HTN,HF
tone

Eplerenone N N N N N Y(w/HF) Y(pMI} HF postMI

2014 MedStudy
5-12 CARDIAC ISCHEMIA

to work by inhibiting the late sodium current in cardiac


Table 5-6: Bruce Protocol
myocytes, thereby reducing sodium and calcium over
Stage Min %Grade MPH METs load that follows ischemia. This improves myocardial
relaxation and reduces left ventricular diastolic stiffness,
I 1.7 4.7
which in turn enhances myocardial contractility and
2 6 12 2.5 7.0 perfusion.

3 3 .4 10.1 More on anti-anginal drugs:

4 12 16 4.2 12.9 Nitrates, beta-blockers, and calcium channel blockers


all decrease myocardial 02 demand, and all decrease
5 15 18 5.0 15.0
afterload.

The exercise tolerance test is an excellent, objective way Nitrates decrease preload more than afterload and
to determine the severity of angina and to determine also dilate coronary vessels. Acute preload reduction
prognosis. Patients who are able to go to stage 4 of is why nitrates can cause severe decompensation
Bruce protocol (Table 5-6) have a nearly 100% 5-year in patients with an acute right ventricular MI.
survival, while those who cannot get past stage I (Remember, do not give nitrates during acute RV
have only a 50% 5-year survival! Note that coronary infarct.) Patients on nitrates get a sympathetic reflex
angiography is not required for the determination of increase in heart rate (HR). Nitrates are degraded in
either of these prognostic factors! the liver. Tolerance develops rapidly with nitrates
(tachyphylaxis), but you can avoid tolerance by
Spasms of the coronary arteries usually show up as
having a 6-hour "nitrate-free window" once a day;
transient ST-segment elevation if they occur during
i.e., between midnight and 6 a.m. Development of
stress testing.
tolerance is less likely with mononitrates than with
What causes resting ST-segment elevation? Acute Ml, dinitrates.
pericarditis, LV aneurysm, LBBB, ventricular pacing, Beta-blockers decrease myocardial 02 demand by
LVH, and benign early repolarization. decreasing HR, blood pressure (BP), and contractility.
Beta-blockers complement nitrates well because they
Hibernating myocardium is chronically underperfused
decrease the reflex tachycardia.
myocardium. There is no irreversible myocyte injury.
When perfusion is restored to normal, contractility Calcium antagonists: The combined vasodilatory and
should return to normal. antihypertensive effects make them ideal for patients
with angina/ischemia and hypertension. See
Reperfusion injury occurs when a severely ischemic
Table 5-5. Verapamil and diltiazem should be
myocardium is reperfused after I hour, causing used cautiously, if at all, in patients with systolic
further irreversible microvascular damage and damage
heart failure due to the negative inotropic effects.
to the myocardial cells.
Short-acting nifedipine is contraindicated due
Stunned myocardium is also the result of acute ischemia. to steep drops in BP and reflex tachycardia.
From the time perfusion is restored, it can take 7-10 days There is a high probability of coronary thrombus
for the ventricular function to return to normal. formation with unstable angina, so always use either
IV heparin or subcutaneous low-molecular-weight
Treatment of all angina: ModifY risk factors and correct
heparin (LMWH) if there are no contraindications.
aggravating factors such as anemia, hypertension,
smoking, drug abuse, and noncompliance. (Good luck!) The following are now recommended concomitantly
with heparin and for follow-up medical therapy for
unstable angina:
ANTI-ANGINAL DRUGS
Aspirin daily for life
Beta-blockers and nitrates are the staples of medical

treatment, but calcium channel blockers can also Clopidogrel x I month and ideally up to a year
help. Nifedipine and amlodipine decrease angina by (particularly if a stent is placed)
both coronary artery vasodilation and peripheral vaso
dilation (decreases workload). The main anti-anginal EVALUATION OF
effect of diltiazem and verapamil is due to their negative CHRONIC STABLE ANGINA
chronotropic effect.
Note
ASA decreases mortality and MI occurrence in unstable
(and probably stable) angina. Use clopidogrel (Plavix) The following is drawn from the 2012 ACC/AHA
in patients who cannot tolerate or are allergic to ASA or guidelines. First and foremost is the involvement by an
who have an indication to take this in addition to ASA. informed patient: Choices about diagnostic and thera
peutic options should be made through a process of
Ranolazine (Ranexa) may also have a role in some
shared decision making involving the patient and phy
patients with persistent angina on maximal standard
sician, with the physician explaining information about
therapy, or as a substitute for beta-blockers. It is thought
risks, benefits, and costs to the patient.

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CARDIAC ISCHEMIA 5-13

can accelerate atherosclerosis, enhance platelet


aggregation, cause vasospasm, and increase
myocardial oxygen demand.
The following comorbid conditions can precipitate
What does ST-segment elevation suggest on an symptoms in the presence of coronary obstruction or,
exercise ECG stress test? when severe, cause angina in the absence of coronary

What are causes of resting ST-segment obstruction by:


elevation? o Increasing cardiac demand: hyperthyroidism,
cocaine use, severe uncontrolled HTN, significant
Explain the similarities and differences between
valvular disorder, aortic stenosis, or HCM
hibernating myocardium, reperfusion injury, and
o Decreasing myocardial oxygen supply: anemia,
stunned myocardium.
hypoxemia, and increased blood viscosity
What are the main drugs used to treat angina?
From the above, determine if the patient has high,
Which patient might ranolazine (Ranexa)
intermediate, or low probability of CAD. Low
benefit?
probability needs no further testing. Those with
Which anti-anginal drugs decrease myocardial intermediate or high probability of CAD should undergo
oxygen demand? "risk stratification" with further testing (discussed next).

Which anti-anginal drugs decrease afterload?

Which anti-anginal drugs decrease preload? 2. Noninvasive Tests for Chronic Stable
Angina: Diagnosis and Risk Stratification
What anti-anginal drug do you not give to a
patient with RV infarct? Why? ECG: especially for checking ST-T wave changes that
suggest ischemia, Q waves, and LVH. Other findings
Why should you determine the probability of
(e.g., RBBB, LBBB, atrial fibrillation, bifascicular
CAD in a person with intermittent chest pain?
block) are not specific indicators of CAD.
For which patient with chronic stable angina do
Chest x-ray is done only if there are signs of heart
you do an echocardiogram? Why?
failure (HF), valvular disorders, or pericardia! disease.
A patient undergoing a workup for chronic stable
Exercise testing is the most important test in risk
angina is determined to be at high risk for death.
stratification. See Tab l e 5-1 on page 5-5 to review how
What is the next step?
to pick the best stress test for your patient. And remem
ber, for those who can exercise, do exercise testing for
Evaluation of a patient with chest pain is a 3-step process: all with stable angina.
I ) Determine the probability of CAD.
Exercise capacity is one of the stronger indicators
2) Noninvasive testing for diagnosis and risk stratification. of long-term risk. For this reason, it is preferable to
3) Additional workup based on estimated risk. perform exercise stress if the patient is able to achieve
maximal workload. In addition, exercise can provide a
1. History and Physical Exam: higher physiological stress than would be achieved by
Determine Probability of CAD pharmacological testing.

First assess the probability of coronary artery disease Assess LV systolic function (generally with echo)
(CAD). Factors used in the assessment include type of only in patients with prior MI, pathological Q waves,
chest pain (typical, atypical, nonanginal), age, gender, symptoms or signs suggestive of heart failure, arrhyth
risk factors (particularly diabetes mellitus, smoking, and mias, or heart murmur.
hypertension), and ECG abnormalities (Q waves and
If the test results won't change management (severe
ST abnormalities). This step is very important because
comorbid conditions that preclude possibility of revas
it determines pretest probability for the rest of the tests,
cularization or patient does not want revascularization),
which improves the positive and negative predictive
do not order.
values of these tests.

After other causes of chest pain are ruled out, determine


the following:
3. Determination of Further Workup in
Chronic Stable Angina
Typical vs. atypical chest pain is determined by
assessing quality, location, and duration of the chest Based on stress test results, determine the probability
pain. Also, what precipitates or relieves the pain? of death or Ml and stratify patient into a high-risk

Cardiovascular risk factors: especially DM, HTN,


(> 3%/year), intermediate-risk (1-3%/year), or low
smoking, hyperlipidemia, family history of CAD,
(< I %/year). Patients with high risk should
risk group
be referred for coronary angiogram. Patients with low
and postmenopausal status in women. History
or intermediate risk should be treated with medical
of substance abuse must be obtained. Cocaine

2014 MedStudy
5-14 ACUTE CORONARY SYNDROME

therapy to improve symptoms and function, and further Stepwise strategy smoking cessation (ask, advise,
workup can be deferred if symptoms can be controlled assess, assist, arrange, avoid), avoidance of exposure
with medical therapy. to environmental tobacco smoke.

Low-risk patient: low-risk Duke treadmill score (2 5) Weight loss.


indicating good exercise capacity with no signs of Blood pressure management (goal< 140/90):
significant ischemia, normal stress echo, or normal or ACEI/ ARB and/or add thiazide diuretics or calcium
small myocardial perfusion defect. channel blockers if needed to obtain goal BP.
Influenza vaccine annually.
High-risk patient: high-risk Duke treadmill score (:S -I 0),

inducible wall motion abnormalities > 2 segments on Statin in all patients (if no contraindications/
stress echo, stress induced perfusion abnormalities adverse effects).
2 10% of myocardium on MPI, or severely reduced left Antiplatelet therapy: aspirin 75-162 mg/d indefinitely;
ventricle (LV) systolic function. clopidogrel when aspirin is contraindicated.
Beta-blockers: started and continued for 3 years
If a patient has an intermediate-risk treadmill score

in all patients with normal LV function. Continue


(score between -I 0 and +5), stress imaging should be
indefinitely ifLVEF < 40%. Use carvedilol,
considered to further assess risk. Again, stress testing is
metoprolol succinate, or bisoprolol in all patients
not as useful for low-risk (false positives) and high-risk
withLVEF< 40%, unless contraindicated.
patients (false negatives).
ACEis in all patients who also have hypertension,
diabetes mellitus, LVEF < 40%, or chronic kidney
TREATMENT OF CHRONIC disease, unless contraindicated (ARB if ACE!
STABLE ANGINA intolerant).

Objectives of treatment of chronic stable angina include


reduction of premature cardiovascular death, prevention CARDIOVASCULAR DISEASE (CVD}
of complications including MI and heart failure, PREVENTION IN WOMEN
complete or near complete elimination of symptoms,
A 2011 update of the AHA Guidelines for CVD
and improvement of functional capacity and quality
Prevention in Women warns that:
of life.
Hormone therapy should not be used as primary or
Medical therapy to prevent Ml and death:
secondary prevention.
Antiplatelet therapy: aspirin (clopidogrel if aspirin is Antioxidants (i.e., vitamin C, E, beta-carotene) should
contraindicated) not be used as primary or secondary prevention.
High-dose statin Folic acid or vitamin B6 should not be used.
Beta-blockers (if left ventricular ejection fraction Garlic, coenzyme Q10, selenium, or chromium
[LVEF] < 40% or prior MI) should not be used.
ACE inhibitors (ifLVEF< 40%, DM, HTN, Do not use aspirin in healthy women< 65 years of
or CKD) age for primary prevention of MI. (Aspirin is okay
for those 2 65.)
Medical therapy for relief of symptoms:

Beta-blockers as initial therapy.


Prescribe calcium channel blockers or long-acting ACUTE CORONARY SYNDROME
nitrates when beta-blockers cannot be used, or in
combination with beta-blockers when beta-blockers CLASSIFICATION OF ACS
are not sufficient.
This is another area from which many exam questions
Ranolazine in combination with beta-blockers.
are drawn. [Know this well!]
High-risk patients and patients with low or intermediate
Acute coronary syndrome (ACS) is generally caused
risk who remain significantly symptomatic should be
by atherosclerotic plaque rupture, fissuring, erosion,
referred for coronary angiogram to define coronary
or a combination with superimposed intracoronary
anatomy.
thrombosis; results in acute ischemia; and is associated
Compilation of all recommendations: with an increased risk of cardiac death and myocardial
infarction. Acute coronary syndrome is composed of
Diet: Limit saturated fats (to< 7% of total calories),
2 types:
eliminate trans fats, and limit cholesterol intake
(to< 200 mg/d). 1) Unstable angina (UA) or non-ST elevation
Physical activity: 30-60 minld of moderate-intensity 2) ST elevation
aerobic activity for 5-7 d/wk.
UA/non-ST elevation ACS includes unstable angina
(UA) or non-ST elevation Mis (NSTEMis). You will
see these terms combined as UA/NSTEMI.

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ACUTE CORONARY SYNDROME 5-15

Inferior vs. anterior MI: Inferior Mis are associated with


more stable arrhythmias, such as junctional escape and
... uiz Mobitz I, instead of the poorer prognosis with Mobitz
2 and bundle-branch blocks (BBBs), which are more
Would you recommend aspirin in a healthy often seen in anterior Mls. Even when Mobitz 2 or com
woman < 65 years old for primary prevention plete heart block is seen in an inferior MI, it is usually
ofMI? temporary. Also, the amount of infarcted myocardium is
typically larger with anterior Mls. Unfortunately, septal
What are the 2 major categories of ACS?
rupture can occur in either type. (See Complications of
Name 1 group of patients that is more likely to Myocardial Infarction on page 5-22.)
present with Ml without chest pain.

How are troponin I and T used? How long do


MARKERS FOR AMI

they stay elevated after an Ml?


Serum markers that increase in response to acute
myocardial necrosis include troponins, creatine kinase
ST elevation ACS is ST elevation Mls (STEMis).
myocardial bands (CKMBs), and myoglobin (Table 5-7).
R arely, ACS can be due to occlusion by coronary
[Know all of the following!]
emboli, congenital abnormalities, coronary spasm, and
a wide variety of systemic inflammatory diseases. Assays to detect components of cardiac muscle,
troponin I and troponin T (cTni and cTnT), are now the
Terms "Q wave" and "non-Q wave MI" are no longer
gold standard for the detection of myocardial necro
used.
sis. The level of either of these also has been shown to
Patients with NSTEMis have a smaller size of infarcted have prognostic implications in the setting of an acute
area and decreased early mortality compared to those MI. The 2 troponin assays are equally useful, and local
with STEMis, but a higher risk for persistent angina, preferences dictate which one is used.
reinfarction, and death within several months! This is
Troponins first become elevated at 4 hours following
due to the diffuse coronary disease more commonly
an MI and peak at about 44 hours after the event. They
seen in NSTEMI patients.
can remain elevated for 10-14 days after an MI, which
So, although NSTEMis have a lower early mortality, can muddy the picture in those suspected of having a
they have a higher 6-month mortality compared to recurrent MI-use myoglobin and/or CKMB instead
STEMis. Also, know that patients with NSTEMis are (see below). On the other hand, because they do stay
more likely than those with STEMis to have had a elevated so long, troponins are beneficial in the workup
prior Ml or angina! of those who present more than 24-48 hours after onset
Differential diagnosis of prolonged chest pain of symptoms.
includes: ACS (MI), aortic dissection, peri Be aware that troponins can also be elevated in chronic
carditis, esophageal or biliary tract problems, renal failure, myopericarditis, HF, sepsis, pulmonary
pneumothorax, pulmonary embolism, pleuritic pain embolism, and cardiac trauma. In addition, troponins can
related to pneumonia, musculoskeletal inflammation, be elevated with RV strain causing microvascular dys
and psychogenic causes. function. Although troponins are sensitive markers for
acute myocardial infarctions (AMI), they are not highly
specific; therefore, they are good for excluding AMI but
NOTES
not as good for confirming one. Sensitive but not specific.
15% of acute myocardial infarctions (AMls) are
CK and its isozyme CKMB have been the traditional
asymptomatic.
markers of choice for myocardial necrosis. CK is a
MI without chest pain or with atypical chest pain is more nonspecific marker of muscle injury (both skeletal and
common in the following:

Elderly (about 2/3 of these patients> 75 years of age) Table 5-7: Acute Myocardial lnfarct1on Markers

Diabetics
Marker Initial Peak Return to

Women Elevation Elevation Normal


Those with prior CAD
Myoglobin 1-4hr 6-7hr 24 hr
Mitral regurgitation due to papillary muscle dysfunction
Troponin I 4hr 44hr 10-14d
is seen more commonly with inferior Mls.
(rule of
Ventricular septal defect (VSD) from septal rupture is 4s!)
seen more commonly with anterior and inferior Mls.
CKMB 3-12 hr 24 hr 2-3 d
Arrhythmias in the first 48 hours after Mls are due to
acute ischemia (or are reperfusion-related) and do not CKMB 2-6 hr 18 hr 2d

imply a need for long-term antiarrhythmic therapy. isoform

2014 MedStudy
5-16 ACUTE CORONARY SYNDROME

myocardial), while CKMB is specific to myocardium. TREATMENT OF ACS


These become detectable at 3-12 hours following an Ml
event and peak at 24 hours. CKMB typically returns to
Overview
normal range after 48-72 hours, earlier than the troponins. In general, the sequence to addressing acute coronary
syndrome is to first take proper care of the patient prior
Both CK and CKMB can be elevated due to non-MI
to arrival in the emergency department. Once the patient
causes, such as in rhabdomyolysis. The CKMB:total CK
arrives, do an assessment, do an ECG, and draw labs.
ratio can be useful to distinguish between cardiac and
Based on these results, determine if the patient with sug
noncardiac sources of CK elevation-although this is not
gestive symptoms is actually having an ACS.
fully reliable in very severe cases of muscle injury.
Figure 5-2 diagrams this process of determining if the
Myoglobin is a very sensitive, but nonspecific, test for
patient has ACS.
acute myocardial necrosis. It rises very rapidly, so a
negative myoglobin in the first few hours is useful in Figure 5-3 diagrams the process of managing UA/
ruling out an infarction (high negative predictive value). NSTEMI ACS vs. ST-elevated ACS.
Because it is excreted quickly in the urine, myoglobin is
lf the patient has definite ACS, pursue I of the following
also the quickest to return to normal-within 24 hours
protocols:
so it can be potentially useful to help evaluate recurrent
chest pain soon after an Ml, when troponins and CKMB Acute Ischemia Treatment Pathway-UA/NSTEMI
are still elevated. Because of its low specificity, it is not (Figure 5-4)
frequently used in clinical practice. Acute MI Treatment Pathway with STEMI or New
LBBB (Figure 5-5 on page 5-21)
The most sensitive and specific markers now used are a
combination of troponin I or T and CKMB. Now, let's go through these steps in more depth.
With both the troponins and CKs, the overall trend is
important and gives added information beyond a single Prehospital Management
elevated value ("trending enzymes"). An individual
2013 ACC/AHA guidelines for chest pain:
whose enzymes continue to rise is a very different
patient from someone whose enzymes peaked earlier in Call 911 and transport to hospital by ambulance
the day, even in the absence of symptoms! (rather than friends/relatives): EMS can diagnose
STEMI earlier with prehospital ECG and prefer
entially transport to PCI -capable hospital (shorter
reperfusion times and lower mortality), and can treat
cardiac arrest en route.
Give nonenteric coated ASA ( 162-325 mg) as bite
Possible ACS with
nondiagnostic ECG and and chew xI.
normal initial serum markers Nitroglycerin (tablets or spray): If the drug is avail
able, give only 1 dose, then:
Observe; o Unimproved or worsening-give no more; call 911.
follow up at 4-8 hrs;
o Improved--can repeat to max of 3 doses (at
recheck ECG &
cardiac markers 3-5-minute intervals).

... ...
No recurrent pain
and negative f/u
Recurrent pain;
+flu studies
I Definite ACS

12 hours
studies x
I
+
No ST elevation but
1
Stress study to provoke ischemia; ST elevation
+ ST and/or T wave changes,
consider evaluation of LV function or new LBBB
or
if ischemia is present --, Positive
+ ongoing pain, or
(these tests done before
+ cardiac markers, or
discharge or as outpatient)
+ hemodynamic abnormalities
Negative Diagnosis of
UA/NSTEMI ACS
. I .
D1agnos1s of Evaluate for

r
Probable diagnosis is confirmed UA/NSTEMI ACS reperfusion
con ed therapy

J
nonischemic discomfort;
pt at low risk for ACS +

'
Admit to hospital and Admit to hospital and Follow guidelines
manage with the manage using the for STEMI or
Arrange for
Acute Ischemia Pathway Acute Ischemia Pathway new LBBB
outpatient follow-up (see Figure 5-5) (see Figure 5-5) (see Figure 5-6)

Figure 5-2: Diagnostic Pathway for Possible ACS Figure 5-3: lnittal Tx Pathway for Definite ACS

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ACUTE CORONARY SYNDROME 5-17

High-risk features include all of the following:

Quiz


Ongoing chest pain for longer than 20 minutes
Reversible ST-segment changes of at least 0.5 mm
Elevated cardiac enzymes
What are the prehospital guidelines for
chest pain? Signs of LV dysfunction

What are the major things you should do in early What happens next depends on the ECG:
risk stratification of a patient who presents with
If the ECG is abnormal: Follow guidelines
ACS in the emergency department?
(see below).
Based on early risk stratification of ACS, to what If the ECG is nondiagnostic: Repeat the ECG q
3 groups can a patient be assigned? 15-30 minutes or do continuous monitoring.

Note: An acute MI involving the left circumflex can still


o Note: If the patient has taken a phosphodiesterase-S
present as a nondiagnostic (or normal) 12-lead ECG;
inhibitor (e.g., sildenafil or vardenafil) within
consider obtaining V7-V91eads.
24 hours (48 hours for tadalafil), do not give
nitroglycerin due to the risk of severe hypotension! Based on this early assessment, assign patients to 1 of
the following 3 groups in the ACC/ AHA protocol:
ECG in the field by EMS.
Be prepared to recognize and manage ventricular 1) Noncardiac chest pain or chronic stable angina: Treat
arrhythmias. accordingly.
2) Possible ACS with nondiagnostic ECG and normal
Evaluation of Patients with initial serum markers (Figure 5-2): Observe at least
Symptoms Suggestive of ACS 12 hours following symptom onset. If there is no
recurrence of symptoms, a 2nd set of markers is nega
Early evaluation: For patients who present to the
tive, and an ECG is unchanged, perform further risk
emergency department with symptoms suggestive of
stratification with an appropriate stress test. Patients
ACS, immediately (within 10 minutes) get an ECG,
who have a negative or low-risk stress test can be
draw blood for cardiac markers, give aspirin if not con
discharged to home and followed as outpatients
traindicated, and conduct a directed history and physical
(green box in Figure 5-2). If the observed patients
examination.
have recurrent symptoms, subsequent positive cardiac

Acute ischemia pathway (UA or NSTEMI):


Give aspirin, 02 prn, beta-blocker, nitrate prn.
Give UFH, enoxaparin, or bivalirudin. Fondaparinux okay if no invasive tx.
Give clopidogrel or prasugrel if ASA-intolerant. Prasugrel not for conservative tx.
Abciximab (GP lib/lila) only if immediate PCI.
NO FIBRINOLYTICS!
Monitor for rhythm and ischemia.

I
1

I I I I
Early invasive Early conservative
therapy therapy

I
l l
Recurrent symptoms , Patient stabilizes;

ischemia , heart failure , do stress test or


serious arrhythmia evaluate LV fn

12-24 hour EF < 40% I Evaluate LV I EF 40%


angiography 1 function
I
-

l
Immediate
angiography Not low risk I Stress test
I
Low Risk

I l
Follow on
medical Tx

Figure 5-4: Acute Ischemia Treatment Pathway- UAor NSTEMI

2014 MedStudy
5-18 ACUTE CORONARY SYNDROME

markers, ECG changes, or a positive stress study, Anticoagulant I Antiplatelet Therapy in ACS
admit and manage according to the acute ischemia
Overview
pathway (Figure 5-4).
Intense antiplatelet and parenteral anticoagulant
3) Defmitive ACS: immediately determine whether there
therapy with multiple agents is a major treatment
is ST-segment elevation or new LBBB (Figure 5-3):
recommendation for ACS.
Patients without ST-segment elevation or new LBBB
should be admitted and treated according to the acute
ischemia protocol. Parenteral Anticoagulants
Patients with ST-segment elevation or new LBBB The parenteral anticoagulants are unfractionated heparin
should be considered for emergent reperfusion (UFH), enoxaparin, fondaparinux, and bivalirudin.
therapy. One of these agents is recommended for most patients
with ACS:
We will discuss each of these scenarios shortly, but
first let's talk about general measures considered for all UFH is preferred if coronary artery bypass graft
patients with ACS. (CABG) is anticipated within 24 hours (or coronary
angiography, although this is not as absolute).
Enoxaparin is commonly used; however, keep in
ACS: GENERAL MEASURES

mind that the dose should be adjusted in the patient


ECG, NTG, Morphine, Beta-Blockers, ACEis, with renal impairment.
Atropine Fondaparinux can be considered if the patient has
increased risk of bleeding, especially if a conservative
General anti-ischemic measures for all patients with
(noninvasive) strategy is chosen for the patient. It is
ACS include:
not used if percutaneous coronary intervention (PCI)
Continuous ECG monitoring is expected (due to increased risk of catheter throm
Aspirin bosis and increased coronary complications). If it
Sublingual nitroglycerin (NTG) spray x 3 pm for pain is in use, and invasive angiography/PCI is planned,
and I V NTG for continued ischemia or hypertension switch to another agent, such as UFH or bivalirudin.
Morphine if pain is not relieved by NTG
Oral beta-blocker and an ACEI if the patient is still Antiplatelet Therapy
hypertensive or has evidence of LV dysfunction (EF Aspirin
<40%)
Administer aspmn at a dose of 162 or 325 mg
Supplemental oxygen should be administered to patients
immediately to all patients with ACS, and continue
with UA/NSTEMI with an arterial saturation < 90%,
indefinitely unless there are contraindications.
respiratory distress, or other high-risk features for
hypoxemia. (Pulse oximetry is useful for continuous
measurement of s.02.) It is reasonable to consider sup Thienopyridines- Platelet P2Y12 Receptor
plemental oxygen during the first 6 hours of any ACS; Blockade
however, supplemental oxygen can increase coronary
Thienopyridines include clopidogrel (Plavix), and
vascular resistance!
prasugrel (Effient). Their effect is additive to aspirin.
Note: Beta-blockers reduce myocardial 02 consumption. These drugs block the ADP receptor P2Y12 on platelets.
Also, by blocking the often-excessive sympathetic Ticlopidine is no longer routinely used due to its side
activity, they reduce the load on the heart and decrease effect profile.
the likelihood of arrhythmias. Oral use is preferred.
Interaction between proton pump inhibitors (PPis) and
Contraindications to beta-blockers include bradycar thienopyridines was thought to be a problem, but latest
dia, hypotension, 2"d or 3rct degree AV block, pulmonary studies do not prove a cause and effect relationship.
edema, and asthma. Caution should be used in giving PPis are not contraindicated with thienopyridines, but
beta-blockers to patients with signs of acute heart fail consider the risks/benefits if using concomitantly.
ure. (See Beta-Blockers on page 5-52).
Clopidogrel requires a liver enzyme (CYP2C19) to
Non-dihydropyridine calcium channel blockers become active. Overall, 2-14% are poor metabolizers:
( verapamil or diltiazem) can be given if beta-blockers 2-5% of African-Americans and Caucasians and up to
are contraindicated and the patient continues to have 20% of Asians. There are genetic tests that can check
ischemia and hypertension but no LV dysfunction. for this issue. In 20 l 0, clopidogrel (Piavix) received
an FDA boxed warning about poor metabolizers and the
Atropine is indicated for the temporary management of
tests available, but genetic testing is not recommended
acute sinus bradycardia with signs of low cardiac output
in any current guideline.
while preparing for temporary pacing. Bradycardia
associated with MI (usually inferior Ml) may be Prasugrel is a thienopyridine that has a faster onset of
temporary, and atropine alone may be sufficient. action and is effective in clopidogrel-resistant patients. It
has significantly more antiplatelet activity and therefore

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ACUTE CORONARY SYNDROME 5-19

ACS: MANAGEMENT OF UA I NSTEMI


-THE ACUTE ISCHEMIA PATHWAY

Early Invasive vs. Conservative Therapy


What anti-ischemic measures are done initially Note: The 2012 update of the ACC/AHA UA/NSTEMI
for all patients with ACS? treatment guidelines have 2 areas of focus (Figure 5-4
Which patients should receive a platelet GP lib/ on page 5-17):
lila inhibitor?
I) Antithrombotic therapy with multiple agents
Of those with ACS, what group gets considered 2) Aggressive use of early cardiac catheterization in those
for fibrinolytic therapy and what group definitely with moderate-to-high risk
does not?

Under what conditions is angiography/PCI Regarding UA/NSTEMI treatment:


considered for those with UA!NSTEMI?
Use antiplatelet therapy, such as clopidogrel,
prasugrel, or ticagrelor for at least I year after receiv
lower cardiovascular events-but also higher rates of ing a drug-eluting (DES) or bare-metal stent (BMS)
significant bleeding and is contraindicated in the elderly. and at least I month without a stent (for up to a year).

Clopidogrel and prasugrel can be used interchangeably Note: If a patient needs surgery, do not stop
for all proven ACS scenarios except if CABG IS clopidogrel, prasugrel, or ticagrelor until at least
imminent (operative bleeding complications). 6 months and preferably 1 year after DES placement.
Similarly, do not stop these agents until at least
30 days after BMS placement. Withholding
Nonthienopyridines- Platelet P2Y12 Receptor
clopidogrel, prasugrel, or ticagrelor and performing
Blockade
surgery prior to these time frames has an increased
Ticagrelor (Brilinta), a nonthienopyridine, is a recently risk of death and in-stent thrombosis.
approved reversible oral antagonist of the platelet Intense lipid and BP control is recommended.
P2Y12 receptor with a rapid onset of action. Similarly Stop all nonsteroidal antiinflammatory drugs
to prasugrel, it is more effective than clopidogrel with (NSAIDs)-except ASA-during hospitalization.
no difference in overall bleeding. It can be used as an
alternative to clopidogrel/prasugrel. Okay, you have determined the patient is having ACS
and have initiated treatment according to the general
measures on the prvious page. You've drawn labs and
Glycoprotein lib/lila Inhibitors
done the ECG, which reveals no acute ST changes.
Glycoprotein (GP) Ilblllla inhibitors act on the final The labs come back, and you determine that the patient
common pathway of platelet aggregation-where fibrin has NSTEMI (cardiac markers abnormal) or UA
binds platelets together by connecting to the GP lib/Ilia (markers normal).
receptor. The most studied drug is abciximab. Others You have 2 options:
are eptifibatide, tirofiban, and lamifiban. Only the IV
forms are effective. GP lib/lila inhibitors are considered I) Early invasive therapy (angiography)
for high-risk ACS patients (elevated troponin, hemo 2) Early conservative therapy
dynamic instability, dynamic ECG changes); however,
since introduction of dual oral antiplatelet therapy they Early Invasive Therapy in UA I NSTEMI
are used less commonly.
Urgent invasive therapy for UA/NSTEMI indications:

HF or hemodynamic instability
Fibrinolytic Therapy in ACS

Recurrent or refractory angina


Do not give fibrinolytic therapy to patients with UN
Life-threatening arrhythmias
NSTEMI because it increases mortality. Do give fibrino
lytic therapy to those ACS patients with STEMI or new Invasive therapy for UA/NSTEMI within 24-48 hours
LBBB if immediate PCI is not available and if there are indications:
no contraindications (discussed later).
Elevated cTnl or cTnT
Dynamic ST changes
Antiarrhythmic Drugs in ACS Diabetes
Give lidocaine only if the patient has ventricular fibril GFR < 60 mL!min
lation/tachycardia. Prophylactic lidocaine is harmful. EF < 40%
Lidocaine has an increased half-life in patients with Early post-MI angina
heart failure (HF) and those on propranolol. Amiodarone
PCI within the previous 6 months
is the current drug of choice for ventricular tachycardia
Prior Ml
and ventricular fibrillation.

2014 MedStudy
5-20 ACUTE CORONARY SYNDROME

Prior CABG Bare-metal stent (BMS):


Intermediate/high-risk patients (either by clinical
ASA 162325 mg/d x 1 month, then 75162 mg/d
judgment or using a scoring system such as the TIMI for life
risk score)
Clopidogrel, prasugrel, or ticagrelor x 1 month to
All UA/NSTEMI patients selected for early mvas1ve 1 year
therapy get the following medical therapy:
Drug-eluting stent (DES):
Parenteral anticoagulant:
ASA 162325 mg/d for 3-6 months, then
o UFH, enoxaparin, or bivalirudin. Do not give 75162 mg/d for life.
fondaparinux due to increased rate of catheter
Clopidogrel, prasugrel, or ticagrelor for at least
thrombus formation.
1 year. Consider continuing for longer than a year.
Antiplatelet therapy:
o ASA plus either clopidogrel, prasugrel, or ticagrelor
Cocaine and Methamphetamine Users
(dual therapy). Note: Do not use prasugrel for
with ST Elevation
patients with prior history of stroke/transient isch
emic attack ([TIA]; use clopidogrel in these cases). Give nitroglycerin, calcium channel blockers, and

o GP lib/lila inhibitor can be given if the patient is benzodiazepines (not beta-blockers):

high risk. If ST-segments are elevated and there is no immediate


improvement with treatment, proceed with coronary
Remember: UA/NSTEMI patients do not receive
angiogram or fibrinolytics if cath lab is not available.
fb
i rinolytic therapy.
If chest pain resolves with treatment, troponin is not
elevated, and there are no ST-T abnormalities, patient
Early Conservative Therapy in UA I NSTEMI does not need stress test.
Patients with UA/NSTEMI who respond to intense Avoid beta-blockers.
medical therapy, have none of the high-risk features
listed under invasive therapy above, and do well on post ACS: MANAGEMENT WITH STEMI OR
ACS stress testing are at low risk for immediate and
NEW LEFT BUNDLE-BRANCH BLOCK
1-year mortality-and can be followed without invasive
evaluation. Note

Conservative therapy for UA/NSTEMI patients: The management of acute coronary syndrome (ACS)
for those with ST elevation MI (STEMI) is the same as
Parenteral anticoagulant:
for those with a new left bundle-branch block (LBBB)
o UFH, enoxaparin, or fondaparinux for 48 hours.
(Figure 5-5). Also know that STEMI includes those with
Fondaparinux is especially useful if there is risk
a posterior infarct (ST depression in V 1, V2 and tall Rs
of bleeding.
in V1, V2). General measures are discussed above.
Antiplatelet therapy:
The following are additions to the general measures for
o ASA with either clopidogrel or ticagrelor. Always
all ACS patients discussed on page 5-18.
give dual antiplatelet therapy.
o Prasugrel or lib/Ilia inhibitors are not given for STEMI (or new LBBB) patients get the following
conservative therapy. medical therapy:

This is basically the same anticoagulant/antiplatelet Parenteral anticoagulant:

treatment as those getting UA/NSTEMI early invasive o UFH, enoxaparin, or bivalirudin. Give UFH or
therapy, except that lib/Ilia inhibitors and prasugrel are bivalirudin if going to cath lab within 24 hours
not used and fondaparinux is now a reasonable option. (which ideally should be nearly everybody).
Antiplatelet therapy:
Again, remember that UA/NSTEMI patients do not
receive fb
i rinolytic therapy. o ASA plus clopidogrel, prasugrel, or ticagrelor
(in emergency department)
o IIb!IIIa inhibitors as early as possible when
Long-Term Antiplatelet Therapy after
patients are going to the cath lab for PCI
UA/ NSTEMI

Without a stent: Immediate Reperfusion Therapies

ASA 75162 mg/d for life Overview


Clopidogrel or ticagrelor x I month to 1 year Consider emergent reperfusion (primary PCI or
fibrinolytic therapy) in all patients who present within
12 hours of the onset of symptoms with a STEMI or a
new (or presumed new) LBBB.

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


ACUTE CORONARY SYNDROME 5-21

uiz
What are the reperfusion therapies you give
to (or consider for) those with STEMI or new
LBBB? Who gets what?

In what conditions has PCI been shown to be


better than fibrinolytic therapy?

In what conditions has PCI been shown to be


Image 5-6: Angiogram of a blocked coronary arte1y before and after
especially indicated?
stent placement
What are the absolute and relative
Primary PCI is particularly beneficial in patients with
contraindications to fibrinolytic therapy?
highest risk for mortality (e.g., cardiogenic shock) or
acute severe HF following a STEMI or new LBBB MI.
Primary PCI
In the patient who presents with completed STEM!
Primary percutaneous coronary intervention (PCI)
(beyond 12 hours of the onset of symptoms), coronary
is urgent reperfusion therapy typically using a stent
angiogram is indicated if the patient continues to have
(bare-metal or drug-eluting). BMSs should be used in
chest pain or is in heart failure, left ventricular ejection
patients with high bleeding risk, inability to comply with
fraction (LVEF) is moderately to severely reduced, there
I year of dual antiplatelet therapy, or anticipated inva
is electrical instability (ventricular tachycardia [VT]
sive or surgical procedures in the next year (Image 5-6).
or ventricular fibrillation [VF]), or post Ml stress test
Primary PCI has been shown to be superior to fibrinolytic shows significant ischemia.
therapy when used in patients with STEM!, MI with new
LBBB, and new true posterior MI. Outcomes are also Fibrinolytic Therapy
better than fibrinolytic therapy as long as an experienced
practitioner performs the procedure without signifi If reperfusion therapy is indicated and primary PCI is
cant delay, particularly within 12 hours of the onset of not available at the first hospital, or FMC-to-device time
symptoms-and within 90 minutes of the arrival of the at a PCI-capable hospital exceeds 120 minutes, initiate
patient in the emergency department. (Door-to-balloon fibrinolytic therapy in STEM! patients in the absence of
time is a commonly measured metric for quality of contraindications.
care in STEM!.) Patients with STEM! who present Many studies show that the sooner the patient receives
to a hospital without PCI capabilities should be trans fibrinolytic therapy, the greater the benefit in reduction
ferred to a PCI-capable hospital with a goal of no more of mortality, with the most benefit in the first 4 hours and
than 120 minutes from first medical contact (FMC) to the greatest of all in the first hour. Patients with new bun
stent placement. dle-branch block benefit the most, followed by anterior
Ml, then inferior MI. Start fibrinolytic therapy within
30 minutes of arrival in the emergency department.
Note: Fibrinolytics are used for patients at facilities that
STEMI or new LBBB Ml: do not have the capabilities for urgent PCI. Following
Give aspirin, 02 prn, beta-blocker, nitrate prn. treatment with fibrinolytic therapy, high-risk STEMI
Give UFH, enoxaparin, or bivalirudin.
Give clopidogrel, prasugrel, or ticagrelor.
patients (recurrent ischemia, cardiogenic shock, severe
Abciximab (GP lib/lila) only if immediate PC I. HF, or other high-risk features) should be transferred to
Monitor for rhythm and ischemia. a PC! center to undergo coronary angiography and PCI
immediately-without waiting to determine whether

I
reperfusion has occurred.
Percutaneous coronary intervention (PCI)
I Fibrinolytic agents include the recombinant, tissue-type
plasminogen activators (e.g., rt-PA, TNK), anistreplase,
streptokinase, and urokinase.
Fibrinolytic therapy if not contraindicated
Contraindications to fibrinolytic therapy can be either
and if PCI not immediately available
absolute or relative contraindications.

PCI should be done Absolute contraindications:


within 12 hrs of chest pain onset and
within 90 min of arrival to emergency department
Previous hemorrhagic stroke at any time; other
cerebrovascular events within I year
F igure 5-5: Acute Ml Treatment Pathway with Intracranial neoplasm
STEMI or New LBBB Active internal bleeding
Suspected aortic dissection

2014 MedStudy
5-22 ACUTE CORONARY SYNDROME

Relative contraindications: Complications of Myocardial Infarction

Persistent BP > 180/110 Left Ventricular Dysfunction


Remote nonhemorrhagic CVA (> I year) Left ventricular dysfunction after an MI is predictive

Current use of anticoagulants with INR > 2-3; of a poor prognosis. Pump failure is now the
bleeding diathesis primary cause of in-hospital death from ST eleva
Recent (2-4 weeks) major trauma or surgical tion MI (STEMI). Patients in cardiogenic shock have
procedure historically had mortality rates of > 85%, but studies
Noncompressible vascular puncture using PCI or emergent CABG have demonstrated an
Previous exposure to streptokinase/anistreplase improvement in these dismal outcomes.

Pregnancy
Active peptic ulcer Right Ventricular Infarction Complications

Of the patients with STEMI!new LBBB initially eval Right ventricular infarction (RVI) frequently
uated for fibrinolytic therapy, almost 2/3 do not get accompanies an inferior Ml and is almost always due
fibrinolytic therapy for the reasons listed above or to occlusion of the proximal right coronary artery.
because of advanced age. The risk of intracranial hemor Inferior MI complicated by RVI has a significantly
rhage increases with age, to as much as 1% in patients worse prognosis than inferior MI alone.
> 75, but age by itself is no longer a contraindication. ST-segment elevation in right-sided chest leads (e.g.,
Many of these patients are still good candidates for V3R- V7R) is an indication of infarction of the right
primary PCI. ventricle. If a patient with inferior MI presents with
hypotension, suspect RVI.

Additional Recommendations from the Suspect RVI in all cases of inferior Ml, which is
2013 ACC I AHA STEM! Guidelines typified by the clinical triad of hypotension, clear
lung fields, and elevated jugular venous pressure. A
Stop all NSAIDs (except ASA), including COX-2s!
Kussmaul sign is frequently present.
Start oral beta-blocker within 24 hours if no signs of
HF, evidence of low-output state, increased risk for If you perform right heart catheterization, an elevated
cardiogenic shock, PR interval > 0.24 seconds, 2"ct RA pressure of 2: 10 mmHg with decreased pulmonary
or 3'ct degree heart block, active asthma, or reactive capillary wedge pressure (PCWP) and CO are quite
airway disease. specific for right ventricular MI.
Do not give fibrinolytic therapy if immediate PC! is Management of RVI is frequently diametrically
anticipated. ln addition, there is no role for partial- or opposed to that of LV infarction. Avoid nitrates and
low-dose fibrinolytic therapy. preload reducing agents. Fluid support is essential.
Give clopidogrel or ticagrelor (no PCI) + ASA Inotropic support, typically with dobutamine, may
(I year). be necessary.
Place patient on a high-dose statin.
ACEis within 24 hours to all with anterior STEM!, Arrhythmias and Blocks
HF, EF :S 40% (unless contraindicated). Use an
A variety of tachyarrhythmias can occur with myocardial
angiotensin receptor blocker if ACE! intolerant.
infarction/ischemia.
An aldosterone antagonist (e.g., spironolactone,
eplerenone) should be given to those with no Atrial fibrillation (A-fib) with hemodynamic instability
contraindications who are already receiving an ACEI requires emergent treatment with direct current (DC)
and beta-blocker, have an EF :S 40%, and have either synchronized cardioversion. If patients do not require
symptomatic heart failure or diabetes mellitus. cardioversion, control the ventricular rate in these
patients with beta-blockers, diltiazem, or digoxin.
IV nitroglycerin in the first 24 hours for ongoing chest
pain or hypertension. Treat ventricular fibrillation (VF) and pulseless
Blood sugars must be maintained at < 180 using ventricular tachycardia (VT) with defibrillation (DC
insulin-based regimens for diabetics while avoiding unsynchronized cardioversion).
hypoglycemia.
For sustained VT with a pulse accompanied by
Influenza vaccine yearly. hemodynamic instability, treat with DC synchronized
cardioversion.
If urgent CABG is planned, aspmn should be with
held, and clopidogrel, prasugrel, and/or ticagrelor For episodes of sustained VT not associated with
should be stopped 24 hours before urgent on-pump hemodynamic instability:
CABG. Short-acting intravenous GP lib/Ilia recep
Amiodarone is the drug of choice. It can be given as
tor antagonists (eptifibatide, tirofiban) should be
a continuous infusion or as boluses every l 0-15 min
discontinued at least 2-4 hours before urgent CABG;
utes. Lidocaine can be an effective alternative agent,
abciximab should be discontinued at least 12 hours before
and procainamide is also an option.
urgent CABG.

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


ACUTE CORONARY SYNDROME 5-23

Mechanical Complications after STEM I

Rupture of a papillary muscle, if it occurs, usually


does so 3-7 days after an inferior MI. The patient rap
idly develops shock and acute pulmonary edema. You
How does management of RVI differ from
may (or may not) hear a short, early systolic murmur.

LV infarction?
Echocardiography is indicated in any hemodynami
Which patients with VT after an Ml get DC cally unstable MI patient and is the diagnostic modality
cardioversion? of choice for all of these conditions. The treatment is
urgent cardiothoracic surgery.
What are the medical options for
hemodynamically stable Ml patients with VT? Ventricular septal defect, if it occurs, generally does so
3-7 days after an anteroseptal MI. Incidence is about
When do the major mechanical complications
tend to occur after an Ml? How do they present?
0.3% of Mls (before reperfusion therapy era, incidence
was 1-3%). Again, the patient rapidly develops shock.
What is the best initial test to diagnose such a
A loud, holosystolic murmur is heard widely over the

G
complication?
precordium. Samples from a right heart catheter dem
When should a patient with STEM I be referred onstrate an oxygen saturation step-up from the right

R
for consideration for an lCD? atrium to the pulmonary artery of at least 10%. Confirm
the diagnosis by echocardiography. Once again, the

V
Correct any hypokalemia or hypomagnesemia. mortality rate is very high, and the only treatment is
Routine prophylactic use of lidocaine to prevent VT urgent cardiothoracic surgery.

is no longer recommended. F ree-wall rupture of the LV commonly occurs 3-7 days


after a large, anterior MI, most frequently in elderly

ti e
For patients who develop ventricular tachycardia
or ventricular fibrillation after the first 48 hours, the hypertensive women. Sudden syncope is typical. The

short-term and long-term mortality rates are increased. neck veins are grossly engorged from tamponade; pulsus
Such patients should be considered for electrophysiologic paradoxus, tachycardia, and hypotension make up the

n
study and an implantable cardioverter-defibrillator (lCD). triad. Hemodynamic collapse occurs quickly. There
have been a few heroic saves with immediate surgery,
Note that patients with isolated, premature ventricular

U
but rapid death is the usual outcome.
contractions, or runs of nonsustained (< 30 seconds)
VT, do not need antiarrhythmic therapy on a routine The 2013 ACC/AHA STEMI guidelines recommend

-
basis. Beta-blockers are effective for ventricular ectopic diagnosis of mechanical complications after STEMI
activity and preventing arrhythmias. with transthoracic echocardiography. Arterial pressure
monitoring with an indwelling arterial line is appropriate

9
Bradycardia and AV block are more common with
in some patients, particularly those requiring mechanical
inferior Mls than anterior Mls because of the increased
ventilation. Intraaortic balloon counterpulsation is indi

ri 9
vagal tone and AV nodal ischemia associated with an
cated in patients in cardiogenic shock after STEMI who
inferior infarct. Remember: Prognosis is related to the
do not quickly stabilize with pharmacological therapy
size of the infarct, not the presence of AV block itself.
or with a mechanical complication as a bridge to urgent
The block is often transient and does not require a
revascularization and/or surgery.

h
permanent pacemaker.

ta
AV block accompanying an anterior MI implies
Implantable Cardioverter-Defibrillators
destruction of a large amount of myocardium in the
interventricular septum, is associated with a high Implantable cardioverter-defibrillator (ICD) therapy
mortality, and frequently requires permanent pacing if is indicated before discharge in patients who develop
the patient survives. sustained ventricular tachycardia/ventricular fibrilla
tion more than 48 hours after STEMI, provided the
Indications for temporary pacing at the time of an
arrhythmia is not due to transient or reversible ischemia,
MI include:
reinfarction, or metabolic abnormalities.
Symptomatic bradyarrhythmias unresponsive to
Studies have shown that ICDs prolong survival in

medical treatment
post-MI patients with LVEF < 30-35%, depending on
Asystole or sinus arrest NYHA classification. LVEF is typically reevaluated after
Complete (3rd degree) AV block 40 days following revascularization to allow stunned or
Mobitz type 2 second-degree AV block hibernating myocardium to recover. An ICD is particu
larly indicated if there are baseline episodes of ventricular
tachycardia.

2014 MedStudy
5-24 CORONARY ARTERY DISEASE

Patients in the above 4 groups should receive a statin


CORONARY ARTERY DISEASE
medication.

NOTE Lipids can be falsely low for up to 2 months after a


myocardial infarction or cardiac surgery.
We'll talk about the risk factors for coronary artery
disease(CAD), screening, and revascularization options. Statins enhance plaque stabilization and can
independently improve long-term prognosis.

RISK FACTORS FOR CAD ACCIAHA guidelines and drug treatment are covered in
Endocrinology, Book 4, under Lipoproteins.
The primary risk factors for CAD:
Additional factors to consider:
Age
Advise no smoking.
Male gender
Give antihypertensive medications to treat to goal BP.
Family history of early CAD(females< 65,
males< 55) Coronary artery calcium scores and other serum

G
markers, such as high-sensitivity CRP, can be used
Smoking
in some patient populations to add to the total risk
Hypertension

R
assessment for coronary artery disease.
DM
Do not forget to ask about substance abuse,
Elevated LDL level
particularly cocaine.

V
Aerobic exercise and elevated HDL are inversely linked

d
to CAD. HDL is increased by exercise, estrogens, REVASCULARIZATION
niacin, and small amounts of EtOH. HDL is decreased
The revascularization options are:

ti e
by smoking and androgens. However, pharmacologic
treatment of low HDL is no longer recommended by Coronary artery bypass graft(CABG)
national guidelines. Percutaneous coronary intervention(PC!) with either
stents or angioplasty

n
SCREENING
CABGvs. PCI

U
Check a "fasting lipid panel" at least every 5 years in
The 2012 ACC/AHA guidelines recommend
healthy persons, starting at age 20 . The "fasting lipid
revascularization under the following circumstances:

-
panel" includes total cholesterol, LDL, HDL, and
triglycerides. Much more on lipids in Endocrinology, CABG to improve survival for all patients with
Book 4! significant, left main CAD(> 50% diameter stenosis).

9
LDL is usually a calculated value: CABG to improve survival in patients with significant
(> 70% diameter) stenoses in 3 major coronary arter

9
LDL =total cholesterol- HDL- l/5 of triglycerides
ies or in the proximal LAD artery plus I other major

r
The 20 13 ACC/AHA Guideline on the Treatment coronary artery(e.g., proximal circumflex).

i
of Blood Cholesterol to Reduce Atherosclerotic CABG is reasonable to improve survival in patients

h
Cardiovascular Risk in Adults states that all patients with significant(> 70% diameter) stenoses in 2 major
with CAD should receive a high-intensity statin, regard coronary arteries with severe or extensive myocar

ta
less of lipid levels. (A high-intensity statin is defined dial ischemia(i.e., high-risk criteria on stress testing,
as one that lowers LDL cholesterol by at least 50% on abnormal intracoronary hemodynamic evaluation,
average. Currently, that includes atorvastatin 40-80 mg or > 20% perfusion defect by myocardial perfusion
and rosuvastatin 20-40 mg. A moderate-intensity statin stress imaging) or target vessels supplying a large
is one that lowers LDL cholesterol by 30 to< 50%. That area of viable myocardium.
includes all other available statins plus the lower doses CABG is reasonable to improve survival in patients
of atorvastatin and rosuvastatin.) with mild-to-moderate left ventricle(LV) systolic
The 2013 ACC/AHA guidelines identify 4 statin benefit dysfunction(EF 35-50%) and significant(> 70%
groups: diameter stenosis) multivessel CAD or proximal
LAD coronary artery stenosis, when viable myo
I) Patients with clinical atherosclerotic cardiovascular cardium is present in the region of intended
disease(ASC VD)-such as CAD or stroke revascularization.
2) Patients with LDL 190 mg/dL CABG is recommended to improve survival in
3) Patients ages 40-75 with OM and LDL 70-189 mg/dL patients with complex 3-vessel CAD with suitable
anatomy and in those with multivessel CAD and dia
4) Patients without clinical ASCYD or DM who are ages
betes mellitus, particularly if a left internal mammary
40-75 with LDL 70-189 mg/dL and an estimated
artery graft can be anastomosed to the LAD artery.
10-year ASCYD risk of 7.5% or higher

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


CORONARY ARTERY DISEASE 5-25

patient populations and coronary lesions that benefit


from CABG vs. PCI, particularly in the drug-eluting
stent era. This is a "moving target" because left main
disease can be stented as well now with good results in
What are the primary risk factors for CAD? certain patient groups.

What increases HDL? Again: Survival does not improve after bypass unless
the patient has:
Which patient groups definitely should
get CABG? 3-vessel disease with significant LV dysfunction, or

Which patient groups could get either PCI left main or left main-equivalent disease, or
or CABG? diabetes.

In 3-vessel disease, what is the benefit of


CABG-survival, symptoms, or both? Stents

Stents are the mainstay ofPCI. These are placed in the area

G
With saphenous vein bypass, what percentage
of veins is occluded in 10 years? of blockage and then expanded, thereby opening the lumen
to normal size. Stents do not cause as much dissection of

R
Name 2 drugs used with DESs.
the plaque and are not susceptible to elastic recoil-both of

which can occur with angioplasty alone. Stents also have a

V
PCI or CABG to improve symptoms is beneficial lower restenosis rate than plain angioplasty. The in-stent
in patients with l or more significant (> 70% restenosis is almost always due to neointimal hyperplasia,

d
diameter) coronary artery stenoses amenable to but stents also carry a risk of in-stent thrombosis, particu
revascularization and unacceptable angina despite larly during the early period after placement. This is why

ti e
optimal medical therapy. antiplatelet therapy is so important after stent placement,
PCI or CABG to improve survival for survivors of and a bare metal stent requires dual antiplatelet therapy
sudden cardiac arrest with presumed ischemia-medi for a minimum of30 days to prevent in-stent thrombosis.

n
ated ventricular tachycardia caused by significant
Drug-eluting stents (DESs) are made with a metallic
(> 70% diameter) stenosis in a major coronary artery.
stent backbone supporting a polymer covering that con
PCI is reasonable as an alternative to CABG in

U

tains a slow-release drug. These drugs have properties
selected stable patients with significant (> 50% that decrease the neointimal hyperplasia that is the cause
diameter stenosis) unprotected left main CAD with of most restenoses. Commonly used DESs contain med

-
anatomy associated with a low risk ofPCI complica ications such as sirolimus, paclitaxel, and everolimus.
tions and a good, long-term outcome, and clinical With these agents, the restenosis rate drops dramati
characteristics predicting a significantly increased

9
cally (to 5%) compared to bare-metal stents ([BMSs];
surgical morbidity/mortality. 25%), although there is a slight increase in late stent

9
CABG improves symptoms and survival in: thrombosis (0.4%). As opposed to BMSs, DESs require

ir
prolonged obligatory dual-antiplatelet therapy due to the
Left main, left main-equivalent (2-vessel disease with
delay in neointimalization: minimum I year as opposed

I vessel being proximal LAD), or 3-major coronary


to30 days with a BMS. There are growing concerns over

h
artery disease
late stent thrombosis with DES, particularly after anti
Multivessel CAD or proximal LAD disease with LV platelet agent withdrawal. Also, rare local and systemic

a
dysfunction and viable myocardium hypersensitivity reactions have been reported and can

t
Complex 3-vessel CAD contribute to late stent thrombosis risk. Thus, prolonged
Multivessel CAD with DM antiplatelet therapy may be needed > I year.

With saphenous vein bypass, there is a 50% chance


of occlusion in I 0 years (about 5% per year), but with Other
internal mammary grafts, 90% are open at 10 years! Balloon angioplasty stretches the plaque and vessel wall
Think: the word " VEINS" has 5 letters and so 50% open to enlarge the lumen. There is a 30-50% chance of reste
at I 0 yrs; "LIM-ARTERY" has 9 letters so 90% open at nosis within 6 months. Balloon angioplasty is currently
I 0 years! Internal mammary grafts are the standard of used for vessels too small to allow coronary stenting. It
care for surgical revascularization of the LAD. Chance is also used to predilate vessels before stent placement.
of MI is the same after bypass.
Rotational ablation atherectomy (catheter with
CABG vs. PCI: In most of the recent trials, patients diamond-grinding chips in it) has a role for heavily
have the same survival results, but the need for revas calcified lesions.
cularization is greater in the PCI group. In these trials,
survival has been better for diabetics who get an inter
nal mammary-LAD bypass than for those with a PCI.
Studies are continually trying to tease out specific

2014 MedStudy
5-26 PERIPHERAL ARTERIAL DISEASE

Magnetic resonance angiography (MRA) of the


P ERIPHERAL ARTERIAL DISEASE
extremities (with gadolinium enhancement) is useful
to diagnose anatomic location and degree of stenosis of
CAUSES OF PAD AND
PAD. Computed tomographic angiography (CTA) can be
INTERMITTENT CLAUDICATION considered as a substitute if there are contraindications
P eripheral arterial disease (PAD), previously called to MRA.
peripheral vascular disease (P V D), has many causes, Contrast angiography provides detailed information
including the following: about arterial anatomy and is recommended for
Arteriosclerosis (arteriosclerosis obliterans-most evaluation of patients with lower extremity PAD when
common cause in middle-aged and older); 2 major risk revascularization is contemplated.
factors for arteriosclerotic PAD are diabetes (5x greater Thromboembolism is the usual problem with aneurysms
chance) and smoking. Other modifiable risk factors of limb arteries. Aneurysm of the popliteal artery can be
include hyperhomocysteinemia, hyperlipidemia, and diagnosed by U/S or CT scan. In patients with femoral
hypertension. Note: Patients with arteriosclerotic PAD

G
or popliteal aneurysms, U/S (or computed tomography
are at increased risk of MI and stroke. or magnetic resonance) imaging is recommended to
Arteritis (connective tissue disease, Takayasu exclude contralateral femoral or popliteal aneurysms

R
arteritis). and abdominal aortic aneurysms (AAAs).
Trauma (jackhammer hands).

V
Buerger disease (especially smoking males< 30 years
TREATMENT OF PAD

old}-also called thromboangiitis obliterans. It

d
involves medium and small arteries and often affects Recommendations:
arteries of the wrists (positive Allen test) and hands.

ti e
Statin in all patients.
Entrapment-think especially of thoracic outlet Keep BP < 140/90 or< 130/80 with DM or CKD;
syndrome and popliteal artery entrapment. Suspect beta-blockers are effective and not contraindicated.
popliteal artery entrapment in young men with
Proper foot care.

intermittent claudication of calf or foot arch with


Smoking: Counsel to stop smoking, offer behavioral
walking-but not running!
and pharmacologic Rx (varenicline, bupropion, and

U
It is important to differentiate vascular claudication from nicotine replacement therapy); ask smokers/former
lumbar spinal stenosis, and know that the latter causes smokers about tobacco use at every visit.

-
a pseudoclaudication. L umbar spinal stenosis is relieved Antiplatelet therapy with aspirin 75-325 mg or clopi
only by sitting down (flexing the spine), but not by dogrel 75 mg daily is indicated as well to decrease
standing still. It is exacerbated by anything that extends cardiovascular events (warfarin gives no benefit!).

9
the spine, such as standing or walking (especially down Exercise 30-45 minutes at least 3 days/week.
hill). Vascular claudication is relieved by sitting down

9
Cilostazol (Pletal) 100 mg bid, a phosphodiesterase
or standing still. Neither disease causes nocturnal leg
inhibitor that increases the cAMP in platelets and

r
cramps. When the distance to onset of claudication or

i
blood vessels-resulting in a reversible inhibition
severity abruptly changes, thrombosis in situ or an
of platelet aggregation-has been shown to improve
embolic event should be considered.

h
symptoms and increase walking distance. Use only if
LV function is normal because patients with class III

ta
DIAGNOSIS OF PAD or IV heart failure have increased mortality with any
phosphodiesterase inhibitor.
The resting ankle brachial index (ABI) should be used to
P entoxitylline (Trental) effect is marginal and not
establish the lower extremity PAD diagnosis in patients
well established.
with suspected lower extremity PAD; i.e., those with 1
or more of the following: exertional leg symptoms, non If PAD is due to Buerger disease, stop tobacco use.
healing wounds, age 2: 65, or 2: 50 years if history of If Takayasu arteritis is present, treat the disease
smoking/diabetes. with steroids.

ABI classification: noncompressible > 1.40, normal Other treatment: Many forms of PAD can now be
1.00-1.40, borderline 0.91--0.99, and abnormal (i.e., effectively treated with percutaneous intervention (angio
PAD)< 0.90. plasty and stents}-with low restenosis rates. Surgical
bypass can also effectively relieve symptoms and isch
Continuous-wave Doppler ultrasound is useful to diagnose
emia. In general, proximal (iliac and femoropopliteal)
anatomic location and degree of stenosis of PAD.
stenosis and short-segment occlusions are best treated
Exercise tolerance tests (ETTs) are recommended to endovascularly (e.g., focal aortoiliac occlusive disease),
objectively measure functional limitation of claudica with long lesions and occlusions best treated surgically.
tion and response to therapy. ETTs with pre-exercise and
With acute peripheral arterial occlusion, heparin protects
post-exercise ABI values provide diagnostic data useful
the collateral circulation during evaluation by preventing
in differentiating arterial claudication from nonarterial
claudication ("pseudoclaudication").

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


VASOSPASTIC DISEASE 5-27

What are the causes of arteriosclerotic PAD?

What is Buerger disease?

What is the difference between claudication and


pseudoclaudication?

What is the first test to establish the diagnosis of


lower extremity PAD? What result is considered
abnormal?

What antiplatelet therapy is recommended for


patients with PAD?

G
Image 5-7: Thromboangiitis obliterans or Buerger disease
What is primary Raynaud syndrome? How is it symptoms on patients toes
treated?

R
In asymptomatic patients with known or suspected
Atherosclerotic disease of the carotid artery
carotid stenosis, ultrasound is recommended as the initial

provides more risk for which of these: Ml,

V
diagnostic test to detect hemodynamically significant
stroke, or TIA?
carotid stenosis.

d
When is carotid endarterectomy indicated?
Ultrasound is also recommended to detect carotid stenosis
in symptomatic patients (i.e., who develop focal neuro

ti e
thrombus formation around the new clot. Many arterial logical symptoms in left or right internal carotid artery
emboli to the lower extremities come from the heart, territories). Magnetic resonance angiography (MRA) or
but atheromatous emboli from a diseased aorta can also computed tomography angiography (CTA) is indicated
occur, which can cause renal failure and ischemia of the

n
to detect carotid stenosis when ultrasound cannot be
toes (Image 5-7). Embolectomy/thrombectomy is the obtained or yields equivocaVnondiagnostic results.
treatment of choice.

U
Patients who experience nondisabling ischemic stroke or
TIA symptoms within 6 months (symptomatic patients)

-
VASOSPASTIC DISEASE should undergo carotid endarterectomy (CEA) if: 1) the
diameter of the lumen of the ipsilateral internal carotid
Vasospastic disorders: Primary Raynaud phenomenon artery is reduced(> 70% by noninvasive imaging or

9
(Raynaud disease) is constriction of small arteries and > 50% by catheter angiography); and 2) the anticipated
rate of perioperative stroke/mortality is 6%. Carotid

ri 9
arterioles when cold, leading to acrocyanosis. It is some <

times associated with livedo reticularis. It involves small artery stenting is indicated as an alternative to CEA for
arteries and arterioles in the digits and skin (Image 5-8). these same patients. It has the same indications as CEA
but stenting has a higher 30 day postsurgical mortality,
Treatment: calcium channel blockers (CCBs), biofeed

h
so it typically is used for a subset of these patients with
back, and nitroglycerin if CCBs are ineffective.
a lesion not suitable for surgery, restenosis after previous

ta
Prinzmetal angina is a coronary artery vasospastic CEA, or radiation stenosis.
disease that can lead to transient, dramatic ST elevation
Medical therapy for atherosclerotic carotid disease
mainly at rest and occasionally with exercise. T hink of
includes: aspirin, clopidogrel, or low-dose aspirin
this diagnosis in a younger individual with transient ST
+extended release dipyridamole; treat blood pressure to
elevation during an episode of pain but normal coro
goal < 140/90; statins for all; and smokers should quit!
nary arteries on cath. Treatment includes nitrates and
especially calcium channel blockers.

CAROTID ARTERY DISEASE

CAROTID ARTERY ATHEROSCLEROSIS


Atherosclerosis within the carotid artery occurs most
frequently within the common carotid bifurcation and
proximal internal carotid artery. Patients with athero
sclerotic carotid artery disease are at a higher risk of
having an MI than of having a transient ischemic attack
(TIA) or stroke!

Image 5-8: Acute Raynaud phenomenon

2014 MedStudy
5-28 CEREBRAL EMBOLIC DISEASE

INTERNAL CAROTID ARTERY


AORTIC DISEASE
DISSECTION
Suspect spontaneous dissection of the internal carotid AORTIC ANEURYSMS
artery (cervical area) in a patient with unilateral head Overview
ache associated with either TIAs or a dilated pupil. It
can also present with only a history of unilateral neck The causes of aortic aneurysms can be broadly
pain in a hypertensive patient. Look for cholesterol categorized as degenerative diseases, inherited or
emboli on the funduscopic exam. Spontaneous dissec developmental diseases, infections, vasculitis, and
tion of the internal carotid artery typically resolves with trauma. With aortic aneurysms, rupture is the biggest
no treatment, with excellent recovery. Occasionally, threat. Atheroembolism is another complication of
anticoagulation or a stent is needed. abdominal aortic aneurysm. Signs of atheroembolism, in
decreasing order, are: livedo reticularis, then blue toes,
then ischemic ulceration. (Remember, though, that most

CEREBRAL EMBOLIC DISEASE emboli to the lower extremities originate in the heart!)

G
Hypertension from progressive renal insufficiency can
OVERVIEW occur if abdominal aneurysms are not treated.

R
The causes of cerebral embolic events of cardiac origin
(and the approximate % of events they cause): Thoracic Aortic Aneurysms

V
Atrial fibrillation (45%) Thoracic aortic aneurysms tend to dissect as well as
rupture. Aortic dissection is an intimal tear in the aorta,

d
Acute MI (15%)
resulting in a dissecting hematoma, which can cause severe
Ventricular aneurysm (10%)
pain and occlusion of the aorta and involved vessels.

ti e
Mechanical valve prosthesis (10%)
Systemic hypertension, cystic medial necrosis, bicuspid

Valvular heart diseases, including endocarditis ( 10%) aortic valve, coarctation of the aorta, and 3rd trimester of
Other cardiac abnormalities (1 0%) pregnancy are predisposing factors. Aortic dissection is a

n
major cause of death in those with Marfan syndrome.
"Other" includes patent foramen ovale, which allows an
intermittent right-to-left shunt and "paradoxical" emboli, Cystic medial necrosis is the most common pathology in

U
and dilated cardiomyopathy, which allows formation of ascending aortic aneurysms, whereas atherosclerosis is
a mural thrombus. most frequently associated with aneurysms of the aortic

-
arch and descending thoracic aorta. The average growth
Noncardiac cause of embolic cerebral events is
rate of thoracic aneurysms is 0.1-0.2 em per year.
atherosclerosis, both aortic and carotid (discussed above).
The DeBakey classification of aortic dissection lists

9
Nonembolic causes of cerebral ischemic attacks or
3 types:
strokes are thrombosis, systemic hypoperfusion, and

9
blood disorders (especially clotting disorders). Type 1: Involves the ascending aorta, aortic arch, and

r
descending aorta

i
TRANSIENT ISCHEMIC ATTACK Type II: Proximal in the ascending aorta alone

h
The definition of transient ischemic attack (TIA) Type Ill: Involves the descending aorta alone, commonly
has changed and is no longer related to duration of just after the subclavian artery

ta
symptoms. TIA is now defined as any period of CNS The Stanford classification lists 2 types:
ischemia without infarction. Ischemic stroke is defined
as ischemia with infarction. The CNS includes the brain,
Type A: Any dissection involving the ascending aorta
spinal cord, and retina. More on TIA under Dizziness, Type B: Limited to the descending aorta only
Causes of Vertigo in Neurology, Book 5.
Stanford Type A combines DeBakey I and II; this makes
Medical treatment of TIA: If there is a history of TIA sense because all type A aortic dissections are managed
but no history of cardioembolic stroke, no significant similarly. Hence, the Stanford classification is more
lesion is found, and the patient does not have atrial fibril commonly used now.
lation, it is probable that the cause is atherosclerosis;
Proximal dissection can cause aortic regurgitation,
therefore, the patient should be placed on antiplatelet
hemopericardium with tamponade, and MI due to
therapy: ASA + dipyridamole, ASA alone, or clopidogrel
involvement of a coronary artery (usually the right coro
alone. Ticlopidine is similar to clopidogrel but is not a
nary artery). Dissections typically present with severe
I 51 line drug because of severe neutropenia that occurs in
anterior chest pain and/or severe interscapular pain.
1%! Unlike with coronary artery disease, the combination
of ASA + clopidogrel has not been shown to be beneficial Diagnosis [Know]: CT and MRI are the diagnostic
over either agent alone for stroke or TIA prevention. procedures of choice for possible aortic dissection.
Transesophageal echo is a reasonable alternative if the
patient is too unstable to go to radiology.

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VALVULAR HEART DISEASE 5-29

stress test if the patient has 2': 2 CAD risk factors (listed

. Jrl.... on page 5-24 ). Use perioperative beta-blockers in


Q..,_.-quiZ
.

patients with CAD undergoing surgical repair of AAA.

Open or endovascular repair of infrarenal AAAs and/


How might spontaneous dissection of the
or common iliac aneurysms are options in good surgi

internal carotid artery present clinically? What is


cal candidates; however, endovascular repair requires
its prognosis?
periodic long-term surveillance imaging to monitor
What are the procedures of choice for endoleak, shrinkage/stability of excluded aneurysm sac,
diagnosing a dissecting aortic aneurysm? and to determine need for further intervention.

At what size is surgery indicated for a thoracic


aortic aneurysm? COARCTATION OF THE AORTA
At what size is surgery indicated for an Coarctation of the aorta (COA) is a congenital problem
abdominal aortic aneurysm? that causes persistent hypertension, sometimes even after

G
Which Streptococcus, if found as a cause of surgical correction. Cardiac output responds normally to
endocarditis, warrants a colonoscopy? exercise. Blood pressure is higher in the upper extremi

R
ties than in the lower. People with COA have a high risk
of developing subsequent aortic disease, including aneu
Treatment: Decrease elevated blood pressure
rysms and dissection, even after correction of the lesion.

V
immediately with beta-blockers and nitroprusside. There
is preliminary evidence that Marfan's-related aneurysms
A bicuspid aortic valve is often seen ( 50%) in COA
patients. See more on COA on page 5-58.

d
should be treated with an angiotensin-converting enzyme
inhibitor (ACEI) or angiotensin II receptor blocker

ti e
(ARB) to block TGF-signaling. Ascending aortic dissec
tions are at greater risk for complications, so they always
VALVULAR HEART DISEASE
require surgery. Descending aortic dissections are
INFECTIVE END OCARDITIS
mainly treated medically unless evidence of end-organ

n
damage develops (renal insufficiency, GI ischemia, limb Overview
compromise), which suggests continuing dissection and

U
[Know this section well.]
the need for emergent surgery.
More on causes and treatments of infective endocarditis
Thoracic aortic aneurysm: Surgery is indicated at 5.5 em

-
(IE) is discussed in Infectious Disease, Book 1. For
in the ascending aorta (5 em ifMarfan's) and 6 em in the
treatment purposes, endocarditis is classified as:
descending aorta.
Native valve

Also, surgery is indicated if the aneurysm is small but


Prosthetic valve
enlarging rapidly (> I 0 mm in a year), associated with

ri 9
symptoms, compressing surrounding structures, or is of IV drug related
traumatic origin. Culture negative

These can have acute or subacute presentations.

h
Abdominal Aortic Aneurysm
Streptococcus, Enterococcus, and S. epidermidis are
Screening is covered in General Internal Medicine, the usual causes of the subacute form, while S. aureus,

ta
Book 5, under Preventive Medicine, Screening Exams. group B Streptococcus, and gram-negative organisms
cause acute endocarditis.
Abdominal aortic aneurysms (AAAs) are more common
in men. They tend to rupture rather than dissect. Treat S. aureus causes 80-90% of staphylococcal IE and is the
BP and lipids as for patients with CAD, and advise to most common cause of acute IE. Recent data from the
stop smoking (and recommend smoking cessation International Collaboration on Endocarditis (ICE) sug
interventions). gest that S. aureus has become the leading cause of IE
worldwide in injection drug users and prosthetic valves
If asymptomatic, aneurysms 4--5.4 em should be
and most often presents as an acute disease.
monitored with ultrasound or CT every 6--12 months.
Aneurysms > 5.5 em or symptomatic (abdominal/back Strep accounts for 60-80% of all endocarditis cases.
pain + pulsatile mass + hypotension) should undergo Viridans streptococci are responsible for 30-65% of
surgical repair. AAAs that expand > 0.5 em in 6 months native valve endocarditis in adults. S. bovis is often
should undergo surgical repair as well. Put the patient on associated with a GI malignancy in the elderly as well
beta-blockers during the observation period. as polyps and diverticulosis--order colonoscopy in all
patients with S. bovis endocarditis.
Know that acute MI and other CAD-related problems
are the cause of70% of perioperative mortality for AAA Enterococcal endocarditis is found in older men with
repair. Surgical risk is decreased if the patient does not genitourinary disease or after instrumentation or surgery.
have CAD, so perform a CAD screening with a nuclear

2014 MedStudy
5-30 VALVULAR HEART DISEASE

S. aureus (coagulase-positive), S. epi dermidis Endocarditis occurring within 2 months of prosthetic


(coagulase-negative), and gram-negative endocarditis valve placement means the valve was seeded when the
are seen in IV drug abusers and patients with prosthetic valve was implanted. It is harder to treat (especially if
heart valves. Other risk factors for these types of IE S. epidermidis); if there is no response to I round of
include dialysis, Type 1 diabetes, bum victims, H IV, cer adequate antibiotics, replace the valve.
tain chronic dermatologic conditions, and patients with
If it has been > 2 months since the prosthetic valve
recent surgical incisions (including median sternotomy
placement, antibiotic treatment is generally sufficient.
for valve replacement).
The valve must also be replaced if there is evidence of
Right-sided endocarditis and the resulting septic valve ring infection or myocardial penetration or unsta
pulmonary emboli can show up as right ventricle (RV ) ble prosthesis. These can appear as a new heart block or
enlargement and multiple lung infiltrates on chest x-ray. a new BBB.
Onset of heart failure is a bad sign. When there is right
S urgery is indicated in endocarditis for refractory
sided endocarditis, it is almost always due to IV drug
heart failure, usually from acute valve regurgitation,
abuse (IVDA); however, IVDA-associated left-sided

G
extension of the infection to the myocardium (or peri
endocarditis occurs even more commonly! (Left-sided
valvular abscess), failure of medical therapy, or large
endocarditis has a higher incidence, and it has many
vegetations with systemic emboli or recurrent emboli on

R
more causes.)
adequate therapy.
Occasionally, endocarditis presents only with signs of
For treatment of infective endocarditis, see Infectious

V
embolic events, such as black toes or septic emboli to
Disease, Book I .
other organs. It can also present as an illness of smol

d
dering, nonspecific symptoms (weight loss, fevers,
chills, night sweats, etc.), or heart failure due to valvular Antibiotic Prophylaxis

ti e
insufficiency. Overview
Classic physical exam findings include new regurgitant Know the following from the ACC/AH A 2008 Focused
heart murmurs, Osler nodes (tender nodules on the pads Update on Infective Endocarditis.

n
of the digits), Janeway lesions (nontender erythematous/
S ignificant changes to the bacterial endocarditis
hemorrhagic macular/nodular lesions on the palms or
prophylaxis prevention guidelines were made because it

U
soles), splinter hemorrhages (Image 5-9), and Roth spots.
has become clear that infective endocarditis is more likely
Blood cultures are positive in right- and left-sided to occur from bacteremia caused by brushing teeth than

-
endocarditis with equal frequency (95%). This is from medical procedures. It appears that medical proce
because there is a constant level of bacteremia in endo dures cause little if any infective endocarditis.
carditis; whereas with most other bacterial causes of

9
fever, the bacteremia precedes the temperature spike.
Indications for Prophylaxis

9
Diagnosis of endocarditis is by the Duke criteria; echo,
Prophylaxis is no longer indicated for GI/GU surgeries.

r
including TEE, is frequently used to help make the
Prophylaxis prior to dental procedures is now indi

i
diagnosis. Diagnosis is covered in Infectious Disease,
cated only for patients with specific highest-risk-for-TE
Book 1.

h
cardiac conditions:

Prosthetic valves

ta
Previous episode of endocarditis
Congenital heart disease (CHD)
o Unrepaired cyanotic CHD
o Repaired CHD within 6 months of procedure
o Repaired CHD with residual defects
Cardiac transplant patients with valve lesions

Prophylaxis is no longer indicated for bicuspid aortic


valve, any ASD or V SD (unless unrepaired and cya
notic, or repaired with residual defect), native valvular
stenosis or regurgitation, mitral valve prolapse (with
or without murmur), coronary artery bypass graft
(CABG), or H CM (unless repair occurs within 6 months
of procedure).

Image 5-9: Splinter hemorrhage onfingernail in endocarditis

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VALVULAR HEART DISEASE 5-31

Rheumatic fever occurs more frequently in overcrowded


areas. It is the most common cause of mitral stenosis and
tricuspid stenosis (Table 5-9 on page 5-32). Symptoms
of valvular dysfunction generally occur, on average, 20
Which type of ASD requires antibiotic years following acute rheumatic fever infection.
prophylaxis before a dental procedure? Which
of these require antibiotic prophylaxis: previous
SPECIFIC VALVE LESIONS
CABG? VSD? Mitral valve prolapse without
murmur? Mitral valve prolapse with murmur? Note
Prosthetic valve? Are your answers based on
Refer to Table 5-10 and Table 5-11 on page 5-34 and
the ACC/AHA 2008 guideline update?
page 5-35 as you study these valve lesions.
Following acute rheumatic fever, how many
years on average does it take for valvular
dysfunction to occur?
Aortic Stenosis

G
Aortic stenosis (AS) is generally due to age-related,
What common clinical symptoms do patients
with aortic valve stenosis present with?
calcific valve degeneration. Congenital bicuspid aortic
valves usually start getting calcified and stenotic

R
between ages 40 and 70 years, while the normal trileaf
Antibiotic Selection for Prophylaxis let aortic valves become stenotic at > 75 years old. A

V
[Know the following:] bicuspid aortic valve is the most common congenital
valve disorder (1-2%). Less frequently, rheumatic heart

d
Dental procedures: All dental procedures that involve
disease also can cause AS, generally in the setting of
manipulation of gingival tissue or the periapical region
mitral valve disease.

ti e
of teeth or perforation of the oral mucosa require
prophylaxis in high-risk patients. See Table 5-8. Presenting signs and symptoms include the classic triad
of heart failure, angina, and syncope with exercise.
GU/GI procedures: Prophylaxis is not indicated in these

n
high-risk patients for any GI or GU procedures. Bedside physical exam with significant AS: The carotid
pulse has a decreased amplitude and slowed upstroke
Respiratory tract procedures, or skin or musculoskeletal
(parvus et tardus), and the heart has a sustained apical

U
tissue infection: The high-risk patient should receive pro
impulse. Associated heart sounds include:
phylaxis that covers staphylococci and beta-hemolytic

-
streptococci. A mid-to-late peaking, diamond-shaped systolic
ejection murmur at the right upper sternal border
(RUSB) or suprasternal notch, which radiates to

9
RUBELLA the neck
Rubella during pregnancy is a common cause of patent An S4 gallop

ri 9

ductus arteriosus (PDA), supravalvular aortic stenosis, Often a decreased or absent 2"d heart sound due to
branch pulmonary artery stenosis ("peripheral PS"), and decreased mobility of the aortic valve leaflets
other congenital cardiac defects. A paradoxical S2 split with severe AS

h
Occasionally, an AS murmur is transmitted to the apex,
RHEUMATIC FEVER where it can be confused with the systolic murmur of

ta
Rheumatic fever is common mitral regurgitation (the Gallavardin effect).
outside of the U.S., with
Table 5-8: Endocarditis Prophylaxis- Dental Procedures
more than 470,000 cases
worldwide. In the U.S., the Situation Antibiotic Regimen
latest incidence is about
-,0ra1 prophY1 axts
< Amoxtoillin
2-14 cases/100,000. In , ">,iili;Jiil
patients with pharyngitis, Unable to take oral medications Ampicillin or 2 gmiM/IV
always swab throats for a Cefazolin* or ceftriaxone 1 gm IM/IV
strep screen. Joint affliction .
'15-
Allergic to penicillinc!l! Clda,mycin or
in rheumatic fever is distin-
guished from rheumatoid Cephalexin* or
Azithn:>tllycin or clarithromycf
arthritis by the lack of typi - ' '

cal joint deformities and a Both allergic to penicillin and Clindamycin or


negative rheumatoid factor. unable to take oral meds Cefazolin* or ceftriaxone
The associated carditis ,,..,. ' :' - ,!?' ' '
j
typically has no symptoms
*Note: Cephalosporins should not be use q, if the PCN allergy is ap ' immediate-type
hypersensitivity reaqtion.
referable to the heart! .. "'" ' ,, "'
Note: Antibiotics (PO or parenteral) are'gi'ven 30 to 60 minuts before the procedure,
' t.;
, . """"""""' "--'

2014 MedStudy
5-32 VALVULAR HEART DISEASE

Table 5-9: Mod1fied Jones Criteria Results with surgical treatment are much better, so refer

for the D1agnosis of Rheumatic Fever for valve replacement early for all symptomatic patients.
It is also indicated for patients with severe asymptomatic
Major Minor AS who develop left ventricle (LV) dysfunction or who
need CABG.
Carditis Previous rheumatic fever
Percutaneous methods of valve replacement (known as
Polyarthritis Arthralgias "transcatheter" valve placement) are currently available
Chorea Fever for symptomatic patients who are high-risk surgical
candidates.
Erythema marginatum Acute phase reactants
(high sed rate or WBC) Caution must be used with vasodilators in the treatment
of ventricular failure due to AS. Aortic stenosis has the
Subcutaneous nodules ECG changes: prolonged PR worst prognosis of all valvular lesions, and medical
interval therapy alone is not effective.

G
To make the diagnosis: requires 2 major criteria or
1 major and 2 minor criteria and evidence of a preceding
Chronic Aortic Regurgitation
group A strep infection (positive strep test or rising or

R
elevated[> 250 Todd units] ASO titers). Chronic aortic regurgitation (AR) occurs as a result
of valve deformity (e.g., bicuspid valve, rheumatic

V
fever, endocarditis, or degenerative valve disease) or
The systolic ejection murmur of AS is louder with
an abnormal aortic root (e.g., dilation seen in Marfan
squatting, whereas the murmur of hypertrophic cardio

d
syndrome, senile aortic disease, giant cell arteritis,
myopathy (HCM) decreases.
relapsing polychondritis, or syphilis).

ti e
An ejection click sounds like a guitar string being
Chronic AR causes LV volume overload, which
plucked immediately after S1 This ejection click is clas
eventually causes LV dilation and a drop in LV systolic
sic and common in bicuspid aortic valve patients but is
function.
not heard with age-related calcific AS. Ejection clicks

n
can also be heard in patients with pulmonic stenosis. Bedside physical exam with chronic AR: Chronic aortic
regurgitation has several classic physical findings:
With aortic stenosis, a systolic thrill can sometimes

U
be felt over the upper precordium and the suprasternal A decrescendo diastolic high-pitched blowing
notch. This thrill is a palpable sensation similar to murmur caused by the regurgitation through the

-
feeling the purring of a cat. valve. This murmur is loudest at the left sternal
border (3rd space) if due to the aortic leaflet, and at
Doppler echo is very accurate in detecting severe AS.
the right sternal border (RSB) if due to aortic root

9
A left heart cath is typically used in the determination disease (because the root is closer to the RSB). The
of AS if there is a discrepancy between clinical and high-pitched blowing sound of this murmur indi

9
echo findings--or to detect concomitant coronary artery cates a high flow, whereas mitral stenosis, which

r
disease. also causes a diastolic murmur, causes a low-flow

i
diastolic "rumble."
Patients with AS have a high rate of coronary artery

h
disease (CAD): 113 in those 40-60 years of age and Occasionally, you hear an Austin Flint murmur,

2/3 in those> 60. which does sound similar to the low-flow rumble of

ta
mitral stenosis. It is thought to be due to the high
AS severity by valve area: pressure regurgitant jet striking the anterior mitral
Mild= 1.9-1.5 cm2 leaflet and impeding mitral valve inflow by causing
Moderate= 1.5-1 cm2 early closure. This murmur is not associated with a
presystolic accentuation as seen in MS.
Severe= :S 1 cm2
A wide and bounding "Corrigan" pulse 2 to
Mean gradients are also frequently used: elevated systolic and low diastolic components of
Mild= 25 mmHg
< BP that causes "water-hammer" arterial pulses.

Moderate= 25-40 mmHg There are many other exam findings associated with

Severe > 40 mmHg


=
chronic AR that have eponyms and are all related to
pulsations; e.g., Becker sign= visible pulsations of
Without surgical intervention, median survival depends the retinal arteries; de Musset sign = bobbing of the
on clinical presentation, given by the mnemonic SASH: head with the pulse; Muller sign = bobbing of uvula
Survival in AS: during systole.

o Angina= 5 years Chest x-ray shows an enlarged left ventricle and


o Syncope= 3 years may show dilation of the ascending aorta. Aortic
o Heart failure = 2 years angiography can be performed at the time of cardiac

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


VALVULAR HEART DISEASE 5-33

When should valve replacement occur for aortic


valve stenosis?

Name 2 conditions that cause chronic aortic


regurgitation.

What is the usual treatment for acute aortic


regurgitation?

When the mitral stenosis is more severe, is the


STOS interval smaller or larger?

Which type of murmur occurs in mitral stenosis?

G
Which mitral lesion is associated with
hemoptysis?

R
cath and is the gold standard to diagnose AR-although

V
it is more frequently diagnosed with echo.

d
Patients with chronic AR should be monitored
Image 5-10. Mitral stenosis with enlarged left atrium
with echocardiograms to follow chamber size and

ti e
LV function.
Mitral Stenosis
Treat chronic and severe AR with vasodilators. Routine
Mitral stenosis (MS) is relatively rare in the U.S. It is
use of vasodilator therapy is no longer recommended
almost always due to rheumatic fever. Other causes are

n
for non-severe AR. ACE Is/ARBs are typically used,
SLE, rheumatoid arthritis, and severe valve calcification.
along with diuretics to treat symptoms. Valve surgery
Atrial fibrillation is common. MS can cause heart failure
is indicated if the patient is symptomatic or when

U
(HF), but sometimes 2 pulmonary hypertension is the
echocardiogram shows LV end-systolic dimension
main physical finding.
55 mm, LV end-diastolic dimension > 75 mm, or E F

-
>

<55% (remember AR: the 55155 rule!). Bedside physical exam with MS: Patients have a
diastolic murmur with a diastolic opening snap (OS)
Intraaortic balloon pump placement is contraindicated
caused by the tensing of the chordae tendineae and ste

9
in patients with aortic regurgitation.
notic leaflets. The time interval between the second heart
sound (S2) and the OS or the S2-0S interval is inversely

ri 9
Acute Aortic Regurgitation related to the severity of the MS: the more severe the
Native acute AR is normally caused by a flail leaflet MS, the higher the left atrial (LA) pressure, and thus the
due to: earlier the mitral valve is forced open in diastole, the

h
smaller the S2-0S interval.
Endocarditis
As mentioned in heart sounds, the S 1 is accentuated and

ta
Type A aortic dissection
can also have a snapping quality. The diastolic murmur
o Trauma
is often described as a "rumble," which suggests low
Prosthetic valve acute AR can be caused by: flow, in contrast to the high-pitched, high-flow diastolic
murmur heard in aortic regurgitation.
o Tissue valve leaflet rupture
o Mechanical valve closure problem (e.g., thrombosis) The chest x-ray shows the following triad:
o Paravalvular regurgitation due to infection 1) Prominent pulmonary artery revascularization
Patients with acute AR present with severe pulmonary 2) An enlarged left atrium (see straightening of left atrial
edema and low cardiac output. Because the cardiac border in Image 5-10 on page 5-33)
output and BP are low, there is no bounding arterial 3) Normal-sized LV
pulse. The diastolic murmur is short because it ends
when the ventricular pressure rises to the level of the The ECG also shows the enlarged left atrium. Do an
low aortic pressure. The LV in these patients does not echo to confirm the diagnosis. Hemoptysis can occur in
have time to compensate for the LV volume overload. patients with MS; it is due to rupture of the pulmonary
bronchial vessels distended by pulmonary venous
Patients with significant acute AR and heart failure
hypertension.
without a reversible cause almost always need
immediate surgery.

2014 MedStudy
5-34 VALVULAR HEART DISEASE

Table 5-10: Heart Defects and Associated Sounds (1 of 2)

Valve Defect Murmurs Clicks Change in Heart Pulse Waveforms;


Sounds a/vWaves

Aortic stenosis S: Ejection Absent 82 (occ); S4; Slowed carotid


click if congeni Paradoxically split S2 upstroke
tal or bicuspid

Acute aortic D: Short diastolic murmur s3 if severe Thready


regurgitation

Chronic aortic S: Occasional early systole SEM. s3 if severe "Corrigan pulse";


regurgitation D: l ) High pitched, decrescendo "Water-ha.mmer pulse"
early to holodiastolic (regUrgitation
through the valve) 2) AustinFlint:
low, rumbling diastolic (regurgitant
stream striking the anterior mitral
.leaflets)

Mitral stenosis D: Diastolic rumble D: Opening S 1 is enhanced, some Large left a waves and
snap (only times "snapping." May y descent
diastolic click!) be silent if severely
calcified

MVP with S: MVP: Mid- s3 if severe;


murmur; chronic CMR: Pansystolic constant s4
mitral regurgita- mul;ll1ur
tion (CMR)

Acute mitral S: Pansystolic decrescendo at apex s3 if severe Large left


regurgitation vwaves

Tricuspid D: Diastolic at LSB Giant right


stenosis a waves

Tricuspid D: Systolic at LLSB Large right


regurgitation v waves

'
Pulmonic Persistently/wl4ely split Large right (jugular)
stenosis s2 a wave

VSD S: Holosystolic at LLSB

ASD-ostium S: SEM at LSB (increased flow Fixed-split S2


secundum aq()s,s pulmonic valve)

ASD-ostium S: SEM at LSB (increased flow Fixed-split S2


primum across pulmonic valve); also often
associated TR or MR murmur

Coarctation of
the aorta

HCM S: Harsh midsystolic murmur Brisk carotid upstroke


that is BIFID in 2/3

PDA So.,t, Q: Continuous "machinery"


..

murmur at LUSB

Note that S4 is also heard in ischemic heart disease, diabetic cardiomyopathy, and hypertensive heart disease with concentric
hypertrophy.
Note: Right-sided murmurs sound louder on Inspiration; lEft on Expiration; all right-sided valve problems can rarely be caused
by carcinoid.
Cannon a waves occur in complete heart block and with ventricular pacing.

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VALVULAR HEART DISEASE 5-35

Table 5-11: Heart Defects and Associated Sounds (2 of 2)

Murmur Louder with: CXR Other: Valve Defect

Squatting*, expiration LVE Sustained apical impulse; etio: bicuspid valve Aortic stenosis

after PVCs classic triad is LVF, angina, and


syncope with exercise

Squatting*, expiration LAE Etio: virtually always rheumatic fever Mitral stenosis
SSx: hemoptysis. Secondary pulmonary HTN

Squatting*, expiration LVE Etio: congenital, endocarditis, or dilated


aortic root from: Marfan, VSD, arteritis, regurgitation
polychondritis, syphilis

Squatting*, expiration Normal Cardiogenic shock and pul edema Acute aortic
Consider aortic dissection regurgitation

Standing or Valsalva: LAE Etio of MVP: congenital; ischemia MVP with murmur;
longer-moves earlier chronic mitral
into systole; sustained regurgitation (CMR)
handgrip, expiration

Squatting*, expiration Normal Etio: endocarditis, Ml with papillary muscle Acute mitral
ischemia or rupture, chordae tendineae rupture; regurgitation
SSx: pul edema

Inspiration RVH; enlarged Etio: virtually always congenital-rarely caused by Pulmonic stenosis
pulmonary artery rheumatic fever and carcinoid; congenital type
usually does not progress

Squatting*, inspiration RAE TS is rare; Etio: usually rheumatic fever but also Tricuspid stenosis
congenital and carcinoid synd. with carcinoid, pt.
usually also has TR SSx: venous congestion

Squatting*, inspiration RVE Etio: usually dilation from pul HTN; Tricuspid regurgitation
other: rheumatic fever, endocarditis (IVDA),
carcinoid. L iver pulsations, ND

Handgrip RVE+LVE Consider in new MI with new systolic murmur VSD

RVE; ECG: RAD, RBBB ASD -ostium


shunt vascularity secundum

RVE ECG: LAD , RBBB ASD---ostium primum

Rib notching, Coarctation of the aorta


loss of aortic
notch

Standing, Valsalva. LVE Apical impulse may have double- or HCM


Note: Sustained handgrip triple-taps
decreases murmur.

Calcification of PDA
ductus arteriosis

*Squatting or lying down; or raising legs if already supine.


... Persistently/widely split S2 (still varies with inspiration but never goes away) occurs with pulmonic stenosis, PE, RBBB , LV
ectopic beats.
... Fixed split S2 (A2-P2 interval remains the same throughout breathing cycle) from ASD .
... Paradoxically split S2 (P2 before A2) is caused by severe HCM, LBBB , RV ectopic beats, AS, and PDA.

2014 MedStudy
5-36 VALVULAR HEART DISEASE

Pregnancy: The increased blood volume in pregnancy MVP. Most MVPs are considered a normal variant; in
can cause a precipitous exacerbation of MS. The initial these, the chordae tendineae are weakened, causing a
presentation of MS in a pregnant patient may be new billowing of the otherwise normal mitral valve leaflets.
onset atrial fibrillation and pulmonary edema. Heart On the other hand, myxomatous changes in the mitral
rate and volume control (beta-blockers and diuretics) valve leaflets (determined by echo) invariably progress
are an essential part of treatment. If anticoagulation is to mitral regurgitation. Many symptoms (dyspnea, panic
necessary, never give warfarin in the I 51 trimester; it is attacks, chest pain, etc.), previously attributed to MVP,
teratogenic. Give adjusted-dose heparin instead. have been shown to occur with no greater frequency
than in otherwise healthy people.
All nonpregnant patients with MS-caused atrial
fibrillation should be anticoagulated with warfarin. Bedside physical exam with MVP: These patients
have a midsystolic click (followed by a mid-to-late
Do percutaneous valvotomy in patients with
systolic murmur [click-murmur syndrome] if there is
symptomatic MS or asymptomatic MS with pulmo
associated MR).
nary hypertension (pulmonary artery systolic pressure
> 50 mmHg at rest or > 60 mmHg with exercise). The murmur of MVP is like the murmur in hypertrophic
Surgical mitral valve replacement is less desirable but cardiomyopathy (HCM) in that decreased preload
frequently is a necessary alternative if valvular anatomy increases the intensity of the murmur. The click and
is not favorable for percutaneous valvotomy (especially murmur become louder and move earlier into systole
if there is severe calcification of the valve) or significant with standing or Valsalva, both of which decrease pre
(more than mild) mitral regurgitation is present. load and, hence, LV volume. (An earlier click means a
longer murmur.) This gives the clue for how you can
tell the difference between an ejection click (aortic or
Chronic Mitral Regurgitation
pulmonary stenosis) and the midsystolic click-an
Chronic mitral regurgitation (MR) can be due to ejection click is fixed, whereas the midsystolic click
rheumatic heart disease, mitral valve prolapse (below), varies in timing with changes in the patient's position.
annulus dilation from left ventricular dilation, prior Stand the patient up, and the midsystolic click sounds
episode of endocarditis, and/or ischemic effects on just like an ejection click. Squatting or supine position
the papillary muscle (from coronary artery disease or increases LV size and causes the click to occur later,
Ml). Chronic MR presents differently from acute MR. thereby shortening the murmur. Dynamic auscultation is
Because the heart has an enlarged left atrium in the required to diagnose MVP clinically.
chronic form, there is less back pressure to the flow
across the incompetent mitral valve, resulting in a
Acute Mitral Regurgitation
constant intensity, holosystolic murmur instead of decre
scendo (as in acute MR). Atrial fibrillation frequently Acute mitral regurgitation (AMR) commonly presents
develops. In both severe chronic and acute MR, the S1 with acute-onset pulmonary edema.
is soft or absent and S2 is widely split. (The aortic valves
Causes of native valve AMR include:
close early because of decreased volume ejected from
the left ventricle.) An S3 is common in severe MR. Flail leaflet (due to endocarditis, MVP, or trauma)
Papillary muscle ischemia or rupture (MI, trauma)
The left ventricular ejection fraction (LV EF) in MR is

frequently normal or above normal, because LV outflow Chordae tendineae rupture (endocarditis, acute

now has 2 routes of exit during systole (forward through rheumatic fever, trauma, spontaneous)

the aorta and backward through the regurgitant mitral Causes of prosthetic valve AMR include:
valve). Significant MR should be treated with diuretics
Tissue valve leaflet rupture
and afterload reducing agents (ACEis/ARBs). Do

surgery if the patient is symptomatic or if asymptomatic Mechanical valve closure problem (e.g., thrombosis)
with: Paravalvular regurgitation due to infection

LVEF < 65%, and/or Bedside physical exam with AMR: Decrescendo systolic
LV enlargement with left ventricular end-systolic murmur at the apex. Echocardiogram shows a hyperac
diameter> 40 mm, or tive LV with normal-to-high ejection fraction and a
pulmonary hypertension. normal-sized left atrium. There are large, left-sided v

waves on wedge pressure tracing.


Repair (if possible) is preferable to replacement.
Treat with afterload reduction and diurese. Unlike severe
Percutaneous valve repair is now available.
AR, intraaortic balloon pump can be helpful for patients in
heart failure from AMR. Urgent surgery is often required.
Mitral Valve Prolapse

Mitral valve prolapse (MVP) is the most common


valvular problem seen in practice (up to 2.4%) and is
more common in women. There are different causes of

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VALVULAR HEART DISEASE 5-37

Bedside physical exam with TR: Patients have a


holosystolic murmur along the lower left sternal border
(increases with inspiration) that does not radiate to the
axilla. Severe TR can cause a parasternal heave, liver
What should you consider in a pregnant pulsations, venous distention, ascites, and lower extrem
woman with new onset of atrial fibrillation and ity edema (signs of RV failure). There are large, jugular
pulmonary edema? v waves, reflecting the backflow through the tricuspid
valve during ventricular contraction.
Describe the murmur sometimes heard with
MVP. Does that murmur's intensity decrease Diagnose with echo. Treat the underlying disease.
or increase with standing? With Valsalva Antibiotic treatment is usually sufficient for endocarditis;
maneuver? the valve rarely needs to be removed, unless the cause is

Carcinoid usually results in what type of tricuspid


Candida. Surgery also can be indicated in circumstances
of severe destruction of the valve.
murmur?

On physical exam, in patients with tricuspid


regurgitation, what large waves are noted on the Pulmonic Stenosis
jugular waveform? Pulmonic stenosis is virtually always congenital, and it
True or false? Pulmonic stenosis is virtually typically does not progress! It is a fairly common con
always acquired. genital valve anomaly in adults. Rarely is it caused by
rheumatic heart disease or carcinoid. It may cause RV
Ebstein anomaly is occasionally associated with
hypertrophy. Although it generally is not seen along with

which structural and electrical abnormalities?


other abnormalities, it does occur in Noonan syndrome,
in which the patient has low-set ears and hairline.
Tricuspid Stenosis
Bedside physical exam with severe pulmonic stenosis:
Tricuspid stenosis (TS) is rare. Causes are rheumatic Patients have an ejection click and a prominent jug
fever (usual), congenital, carcinoid syndrome, and endo ular a wave, which is caused by backflow during
carditis. If the cause is carcinoid, the TS is generally atrial contraction against an inadequately emptied
found in association with tricuspid regurgitation (TR). right ventricle.
Note: Carcinoid can affect either right-sided heart valve
If needed, open the stenotic pulmonic valve with balloon
and typically implies a hepatic tumor if valvular involve
valvuloplasty.
ment is present. (The pulmonary vascular bed is generally
quite effective in removing the active 5-HIAA products
that lead to valve damage.) Patients have systemic venous Pulmonic Regurgitation
congestion without pulmonary venous congestion or
Pulmonic regurgitation is typically secondary to
pulmonary hypertension.
pulmonary hypertension (e.g., primary, cor pulmonale,
Bedside physical exam with TS: Patients have a diastolic mitral stenosis), but it may be due to a primary valve
murmur along the left sternal border, which increases lesion (congenital, rheumatic heart disease, endocarditis,
with inspiration (as do all right-sided murmurs). They carcinoid). Pulmonary artery pressure is > 60 mmHg in
have a giant a wave, caused by backflow during atrial patients with secondary pulmonic regurgitation.
contraction against a stenotic tricuspid valve. There may
be ascites and lower-extremity edema.
Ebstein Anomaly
The ECG shows the tall, peaked P waves in II and
With Ebstein anomaly, the tricuspid septal leaflet is
VI (evidence of the right atrial hypertrophy) but no
positioned lower in the ventricle than normal (apically
indications of right ventricular hypertrophy (RVH).
displaced)-so the RA appears huge and the RV small.
Chest x-ray shows an enlarged right atrium.
Tricuspid regurgitation (TR) murmur is common. It is
Treat the underlying disease and perform surgery. occasionally seen with atrial septal defect (ASD) and
with WPW syndrome.

Tricuspid Regurgitation
Tricuspid regurgitation (TR) often is a functional result VALVE SURGERY
of RV dilation, which can be caused by end-stage left In general, valve surgery is indicated for any valve
ventricular failure, pulmonary embolism, or other problem if the patient is symptomatic at rest or with low
causes of pulmonary hypertension. TR can also be levels of exertion. Even though there is high mortality,
caused by rheumatic heart disease, endocarditis, valve surgery is better than no surgery in patients with
carcinoid, and congenital disease-Ebstein anomaly. severe valve disease and ventricular failure (since the
Endocarditis affecting the tricuspid valve is typically natural history in these cases is 100% early mortality).
seen in drug abusers, and it is often caused by staph; also
consider Candida.

2014 MedStudy
5-38 ARRHYTHMIAS

Bioprosthetic valves are less durable (especially in 3rd intercostal space, with patient leaning forward
young patients and those on hemodialysis) but do not and exhaling; also, low-pitched late-diastolic rumble
require anticoagulation. These are indicated in patients (A ustin Flint)
with a life expectancy of < 5-10 years and those with Mitral stenosis: hemoptysis, opening snap, low-
contraindications to anticoagulation (chronic bleeding pitched diastolic murmur at the apex
problems, ulcers). They also are often given to women
of childbearing age to avoid having to use anticoagulants Valsalva (one last time): decreases the murmur of aortic

during pregnancy. stenosis (A S), increases the murmur of hypertrophic


cardiomyopathy, and increases the murmur of mitral
Mechanical valves are used for all others and do require valve prolapse.
anticoagulation, but they are very durable-typically
lifelong in most cases.

Balloon valvuloplasty is the procedure of choice in ARRHYTHMIAS


pulmonic valve stenosis and frequently mitral stenosis
but not aortic stenosis due to a very high short-term MECHANISMS OF ARRHYTHMIAS
restenosis rate (6-12 months). The 3 usual mechanisms of abnormal rhythms are
For mitral regurgitation (MR), if surgery is required, reentry, triggered activity, and automaticity. The reentry
do valve reconstruction whenever possible because is the most common mechanism of arrhythmias, espe
it has better outcomes and about half the morbidity of cially AV node reentrant tachycardia (AVNRT), atrial
MV replacement. Reconstruction is valve repair and/ flutter, and most ventricular tachycardias. AVNRT is the
or annuloplasty with an annuloplasty ring, and is espe most common type of reentrant tachycardia-hence it
cially likely to be done with MVP, ruptured chordae, also is the most common supraventricular tachycardia
flail leaflets, endocarditis, and annular dilation. Valve (SV T). Be able to diagnose all rhythms at a glance (see
replacement is usually necessary in MR that is due to ECGs on page 5-60).
rheumatic fever.

Newer "edge-to-edge" percutaneous MV repair, where SICK SINUS SYNDROME


a device (a clip) is placed across the two leaflets in their
Sick sinus syndrome causes any one (or combination) of
mid-part, creating a double-orifice mitral valve, is now
sinoatrial node problems, including sinus bradycardia,
being performed; this procedure is ordinarily reserved
sinus pauses/sinus arrest, and tachy-brady syndrome
for patients who are high risk for traditional repair.
(typically baseline sinus bradycardia or sinus pauses
Similarly, percutaneous aortic valve replacement is now
with intermittent episodes of rapidly conducting atrial
available for patients who are at high risk for surgery.
fibrillation/atrial flutter). These patients generally do not
The major determinants in prognosis after valve surgery need electrophysiologic testing. Because prognosis is
include ejection fraction, degree of symptoms, and type good, there are only 2 indications for treatment with a
of valve surgery (valve repair is better than replace pacemaker:
ment). Echocardiography is best for checking for
1) Symptomatic patient
prosthetic valvular function. A transesophageal echocar
diogram (TEE) is especially useful for checking mitral 2) Patient with tachy-brady syndrome where treatment
valve prosthesis. Fluoroscopy is also a useful tool for of tachyarrhythmias might precipitate or worsen
documenting leaflet motion with mechanical valves if bradycardia
valve dysfunction is suspected.

When anticoagulating mechanical valves, keep the INR HEART BLOCK


2.0-3.0 for the aortic valve and 2.5-3.5 for the mitral 151 degree heart block: PR interval > 200 ms. Can
valve. A mechanical mitral valve has a higher risk for be caused by medications and generally requires no
a thrombus formation compared to an aortic (hence the treatment.
higher INR requirement). Therefore, if holding warfarin
2"d degree heart block (Mobitz 1, Wenckebach):
for a procedure or surgery, then bridging anticoagula
gradual prolongation of PR interval until QRS drops;
tion with unfractionated heparin is recommended for
return PR interval shorter than last conducted PR
mechanical mitral valves.
interval. I t can occur during periods of high vagal tone
during sleep (obstructive sleep apnea) or in endurance
Final Pearls about Murmurs athletes. It generally does not require treatment unless it
is causing symptoms.
[Know:]

A ortic stenosis: suprasternal notch thrill with systolic


2nd degree heart block (Mobitz 2): abrupt loss of P wave
conduction to the ventricle with no evidence of grad
murmur, paradoxically split s2
ual prolongation. Generally, it indicates higher grade
Chronic aortic regurgitation: early diastolic, blowing,
AV block, and associated symptoms can necessitate
decrescendo murmur heard best at left sternal border,
pacemaker placement.

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ARRHYTHMIAS 5-39

The normal AV block is 2:1 with a ventricular rate


of half the atrial rate. If it is 2: 3: 1, the cause is either
medications or can suggest advanced AV conduction
system disease. Systemic embolization (most notably
What are the major prognostic factors after TINstroke) can occur due to atrial flutter or atrial
valve surgery? fibrillation; thus, anticoagulation needs to be considered
in both disorders.
Describe the abnormal heart sounds found in
AS, chronic AR, and MS. Vagal maneuvers or adenosine cannot terminate atrial
flutter; however, they can slow the ventricular rate and
What is the treatment sequence for atrial flutter?
allow better diagnosis. Rule out pulmonary emboli
What procedure can cure the most common (often multiple) and thyroid disease-especially if there
types of atrial flutter with 85-95% success rate? is no heart or lung history.

The most effective treatment for atrial flutter is


3rd degree heart block (complete heart block): None of
synchronized DC (direct current) cardioversion. Always
the P waves are conducted to the ventricles, and there
shock if the patient is hemodynamically compromised.
is often a regular junction (40-60 bpm) or ventricular
(20-40 bpm) escape rhythm. Do not continue DC cardioversion if the patient
repeatedly reverts back to atrial flutter.
Permanent pacing is indicated if there is a Mobitz 2 or
complete heart block-especially if symptomatic. See Antiarrhythmic drugs can be used for nonemergent
Arrhythmias and Blocks, starting on page 5-22, for cardioversion. I V ibutilide is most effective and can be
more detailed pacing criteria post-MI. considered a I st line pharmacologic cardioversion for
atrial flutter; however, be aware that it can cause QT
To differentiate between AV node block vs. infranodal
prolongation (8%) and torsades de pointes. Make sure
block: AV node block typically has narrow QRS com
potassium and magnesium levels are normal prior to
plexes, has escape focus rate > 40 bpm (typically
administering ibutilide to minimize risks of torsades.
40-60 bpm), and is responsive to atropine. Infranodal
block (involving the His-Purkinje system) is mostly Procainamide, flecainide, and propafenone can be used
associated with widening of the QRS complex. as well. See Antiarrhythmic Therapy on page 5-45.

In patients with atrial flutter and preexcitation syndrome

SUPRAVENTRICULAR TACHYCARDIAS (WPW), avoid digoxin, calcium channel blockers, and


beta-blockers. See WPW, page 5-42.
Atrial Flutter
Radiofrequency ablation is a treatment modality that can
Typical (Type I) atrial flutter, the common cure the most common types of atrial flutter (success
form, has a characteristic atrial rate of 300 bpm rate 85-95%), and it is used for persistent or recurrent
(240-340)---commonly with a 2:1 AV block. Pay close atrial flutter, although recent studies have suggested it is
attention for atrial flutter when any ECG is shown with a reasonable I st line approach in some circumstances.
a heart rate of 150 bpm; atrial flutter waves at 300 bpm
Anticoagulate patients with atrial flutter, as you would
with 2:1 AV block gives a heart rate of 150 bpm.
for atrial fibrillation (see next). Indeed, up to 60% of
Atrial flutter can be: patients with atrial flutter have had atrial fibrillation in
typical counterclockwise rotation around the right the preceding year.
atrium, characterized by negative sawtooth flutter
waves in II, III, and a VF (with positive deflection Atrial Fibrillation
in V1);or
Overview
clockwise, characterized by positive flutter waves in
ECG leads II, III, and a VF (with prominent negative Atrial fibrillation (A-fib) is the most common sustained
deflection in V 1). arrhythmia. Ventricular rhythm is irregularly irregular
with ventricular rate generally in the range of 120-180
These 2 atrial flutter types share the same right atrial
bpm in the absence of drug therapy. Many patients with
reentrant circuit around the cava-tricuspid isthmus
atrial fibrillation have structural heart disease, and it is
(circuit running between the inferior vena cava and the
commonly associated with hypertension, heart failure,
tricuspid valve).
valvular heart disease, coronary artery disease, chronic
Atrial flutter is generally an indication of disease, lung disease, and obstructive sleep apnea.
most often either organic heart disease or pulmonary
A-fib can be classified as first detected (only I diagnosed
disease. Flutter is a relatively unstable rhythm and often
episode), paroxysmal (2: 2 episodes, self-terminating, each
spontaneously converts to either atrial fibrillation or a
lasts :S 7 days, most 24 hours), persistent (2: 2 episodes,
<
normal sinus rhythm.
each lasts > 7 days), and permanent (> 6-12 months).

The symptoms of A-fib vary widely between patients.

2014 MedStudy

------ -- ---
5-40 ARRHYTHMIAS

Some patients are asymptomatic and others have severe, A-Fib Rhythm Control: Pharmacologic
functionally disabling symptoms. Complications are Cardioversion
embolic events-mainly stroke, and tachycardia-induced
When attempting pham1acologic cardioversion, use
cardiomyopathy.
these guidelines-again, use is based on duration of
With new-onset A-fib or in A-fib not responsive to the symptoms.
usual treatment, consider hyperthyroidism, untreated or
For A-fib> 7 days:
undertreated obstructive sleep apnea, hypomagnesemia,
o I st line: dofetilide
alcoholism/cocaine abuse, excessive caffeine (energy
beverages), and nicotine as possible causes. o 2nd line: amiodarone or ibutilide
For A-fib< 7 days:

Treatment of Atrial Fibrillation o 1st line: dofetilide, ftecainide, ibutilide, or


propafenone (previously, dronedarone*)
Rhythm Control vs. Rate Control
o 2nd line: amiodarone (Exception: If< 48 hours and
You have 2 choices for the treatment of A-fib: poor cardiac function, amiodarone is 1st line.)

1) Rhythm control (restoration and maintenance of sinus *Do not prescribe dronedarone to patients with class
rhythm) I V heart failure or those who have had decompensated
heart failure in the past month, especially if LVEF
2) Rate control (control of ventricular response)
< 35%, because it causes increased mortality in these
There are no significant differences in mortality or patients. In addition, dronedarone should not be
morbidity between the 2 treatments. Rate control is the used in patients who have had pulmonary toxicity on
common strategy for asymptomatic or minimally symp amiodarone or elevated LFTs.
tomatic patients, while rhythm control is often selected
for significantly symptomatic and younger patients.
Maintenance Drugs for Rhythm Control
For patients with hemodynamic instability, ongoing
myocardial ischemia, symptomatic hypotension, angina Pharmacological therapy can be useful in patients with
or heart failure, emergent/urgent direct-current (DC) recurrent paroxysmal or permanent A-fib to maintain
cardioversion is recommended. sinus rhythm. Before initiating antiarrhythmic drug
therapy, treatment of precipitating or reversible causes
of A-fib is recommended. Deciding which drug to use is
A-Fib Rhythm Control: DC Cardioversion
based on the presence of structural heart disease (safety)
DC cardioversion is the most effective method to and, to a lesser degree, on efficacy. Catheter ablation is
restore sinus rhythm. Pharmacologic rates of successful useful in maintaining sinus rhythm for selected patients
cardioversion are lower and depend on the antiarrhyth with significantly symptomatic, paroxysmal A-fib who
mic drug used and clinical scenario. If possible, DC have failed treatment with an antiarrhythmic drug and
cardioversion should be carried out under sedation, with have a normal or mildly dilated left atrium, normal or
appropriate cardiac and hemodynamic monitoring. mildly reduced LV systolic function, and no severe
pulmonary disease. Catheter ablation is less useful
Emergent/Urgent DC cardioversion is recommended for
(however, can be considered) in treatment of patients
patients with hemodynamic instability (angina pectoris,
with symptomatic persistent A-fib.
MI, shock, or pulmonary edema), ongoing myocardial
ischemia, symptomatic hypotension, angina or heart Selection of antiarrhythmic drugs:
failure, and WPW syndrome with rapid ventricular rate.
No or minimal heart disease: ftecainide, propafe
Important points regarding DC cardioversion: none, sotalol, and dronedarone; if ineffective, then
amiodarone, dofetilide, or catheter ablation.
With slow A-fib, consider inserting a temporary
pacemaker before DC cardioversion because the Heart failure (EF < 35%): amiodarone or dofetilide
patient could have sinus nodal disease and may (definitely not dronedarone!); if ineffective, then
have asystole after cardioversion. catheter ablation.

TEE-guided cardioversion is done frequently, Coronary artery disease: dofetilide or sotalol; if


especially if the time of onset of the A-fib is ineffective, then amiodarone or catheter ablation.
unclear. It is fast and cost-effective. Hypertension:
Just as with atrial flutter, do not continue DC o Left ventricular hypertrophy (LVH) present: Use
cardioversion if the patient repeatedly goes right amiodarone; if ineffective, then catheter ablation.
back into A-fib shortly after being shocked. o LVH not present: Use ftecainide, propafenone,
or sotalol. If these fail, then go to amiodarone,
Note: In what other scenarios do you not shock a
dofetilide, or catheter ablation.
patient with an abnormal tachycardic atrial rhythm (but
stable hemodynamically)? Digitalis intoxication and
hypokalemia.

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ARRHYTHMIAS 5-41

blockers (verapamil, diltiazem) should be used with cau


tion to slow the ventricular response in patients with
hypotension or heart failure because of negative inotro
pic effects.
In what circumstance is immediate DC
I V digoxin or amiodarone is used to control the heart

cardioversion indicated for A-fib?


rate acutely in patients with A-fib and HF who do not
What can happen after DC cardioversion to the have an accessory pathway.
patient who has A-fib with a slow rate? What
lf exertional symptoms related to A-fib are present, assess
intervention prevents this complication?
heart rate control during exercise, adjusting pharmaco
According to the 2013 guidelines, what HR is logical treatment to keep the rate in physiological range.
an acceptable target for patients with A-fib and
Digoxin is useful to control the heart rate at rest in
stable ventricular function? For others, how is
patients with A-fib with HF, LV dysfunction, or for
strict control of heart rate defined?
sedentary individuals.
For patients undergoing cardiac surgery,
Radiofrequency ablation of the AV node with subsequent
what medication should be used to prevent
permanent pacing is a treatment for patients with refrac
postoperative A-fib?
tory A-fib and for those who cannot tolerate the meds
needed for rate or rhythm control. This strategy provides
Use of classIC agents for atrial fibrillation: definitive rate control but does not cure the underly
The unopposed use of class IC agents (e.g., no ing atrial fibrillation-hence, patients still require
concomitant AV nodal blocking agents) can organize anticoagulation.
atrial fibrillation into atrial flutter conducting to the In many patients, A-fib originates as abnormal impulses
ventricles much more rapidly. This rapid conduction arising in the pulmonary veins. Radiofrequency ablation,
could degenerate into ventricular tachycardia ( VT) or or isolation of the pulmonary veins, is becoming increas
ventricular fibrillation ( VF). To avoid this potentially ingly popular in treating recurrent, drug refractory,
fatal event, always use class TC agents with AV nodal symptomatic A-fib, although it is not yet established as
agents such as beta-blockers, non-dihydropyridine Ist line therapy.
calcium channel blockers, or digoxin.

Reminders for rhythm control of atrial fibrillation: Postoperative A-Fib

I) Dofetilide and sotalol require hospital monitoring to For patients undergoing cardiac surgery, give an oral
initiate therapy. beta-blocker to prevent postoperative A-fib (unless
2) Dronedarone cannot be used in the New York Heart contraindicated). For those who develop postoperative
Association (NYHA) class I V heart failure (HF) or A-fib, achieve rate control with AV nodal blocking drugs
if HF exacerbation in past 4 weeks. (beta-blockers, calcium channel blockers, or digoxin).
Routine postoperative amiodarone is not indicated for
A-Fib Rate Control the prevention of atrial fibrillation.

The 2013 update to the ACC/AHA Practice Guideline:


Anticoagulation for Atrial Fibrillation
Management of Patients with Atrial Fibrillation states
that a resting heart rate < II 0 bpm is acceptable and is Before and After Cardioversion
as good as strict control if stable ventricular function
If it has been< 48 hours since the onset of A-fib, cardia
(LVEF > 40%) and there are no or acceptable symp
vert most patients without any preceding anticoagulation.
toms related to the arrhythmia; though uncontrolled
tachycardia may, over time, be associated with a revers If it has been > 48 hours since the onset of A-fib (or
ible decline in ventricular performance. Strict control of duration of A-fib is unknown) and the patient is stable,
heart rate is considered 80 bpm at rest or 11 0 bpm during you must achieve adequate anticoagulation x3 weeks
a 6-minute walk. before you attempt cardioversion. As an alternative to
preceding anticoagulation, it is reasonable to perform
Use beta-blockers (atenolol, metoprolol) or calcium
TEE, and if there is no identifiable thrombus, perform
channel blockers (verapamil, diltiazem) for rate con
a cardioversion.
trol at rest and with exercise. Digoxin can have a
synergistic effect for rate control when combined with After cardioversion: Treat with low-molecular-weight or
these medications. unfractionated heparin until INR = 2-3 on warfarin. As
an alternative to heparin/warfarin, one of the novel oral
A-fib with HF: acute setting and no preexcitation-I V
anticoagulants (NOACs) can be considered.
beta-blockers (esmolol, metoprolol, or propranolol) to
slow ventricular rate or amiodarone to slow ventricular
rate and possibly restore sinus rhythm. Calcium channel

2014 MedStudy
5-42 ARRHYTHMIAS

Chronic Anticoagulation If no P wave is seen (buried in QRS) or is seen at the


end of the QRS (very short R-P interval), the patient has
Antithrombotic therapy to prevent thromboembolism is
AV node reentrant tachycardia (AVNRT). Representing
recommended for all patients with A-fib (irrespective of
60-70% of regular S VT, AVNRT is the most common
rate or rhythm control strategy), except for those with
reentrant tachycardia.
lone A-fib (age < 60 years without heart disease and
without risk factors) or contraindications. The selection If a P wave is somewhere in ST-segment (short R-P
of the antithrombotic agent should be based upon the interval) AV reentrant tachycardia ([AVRT]; 20-30%
absolute risk of stroke. Patients with rheumatic mitral of regular S VT) should be considered.
stenosis and prior thromboembolism are at highest risk.
If a P wave is seen after a T wave (long R-P interval),
For patients with non-valvular A-fib (without rheumatic
atrial tachycardia (10% regular S VT) is most likely
mitral stenosis or prosthetic valves), the CHADS2
the diagnosis. In acute management of narrow QRS
scoring system is often used for risk stratification:
complex, regular tachycardia treatment options include
CHF during last year or EF < 35% (any history): beta-blockers, adenosine, calcium channel blockers, or
I point carotid sinus massage.
HTN (prior history): I point Most S VTs are due to a reentrant mechanism. Again,
Age 2: 75: I point the most common S VT is AVNRT. Rate is typically
OM: 1 point 150-250 bpm (although it can be slower or faster).
Prior Stroke, TIA, or embolic event: 2 points Radiofrequency ablation is highly successful and
can be considered equally with medical therapy as
Meds based on CHADS2: I st line long-term therapy. Situations where ablation
0 points = ASA alone is preferred include hemodynamic instability, severe
I point= oral anticoagulation or ASA symptoms, failed medical therapy, public safety
(pilots and bus drivers), and clear patient preference.
2 points or more = oral anticoagulation
If medical therapy is chosen, beta-blockers, calcium
Oral anticoagulation can be achieved with vitamin K channel blockers, or digoxin are I st line options,
antagonists or new anticoagulant agents (dabigatran, followed by antiarrhythmic drugs (typically flecainide
rivaroxaban, and apixaban). New agents do not require or propafenone if there is no structural heart disease).
monitoring (INR); however, they cannot be used
in patients with prosthetic valves, rheumatic mitral
WPW
stenosis, renal insufficiency, and advanced liver disease.
Wolff-Parkinson-White ([WPW]; preexcitation
Dabigatran is useful as an alternative to warfarin for
syndrome): P R interval is < 0.12 seconds due to a
prevention of stroke and systemic thromboembolism
delta wave and symptoms of tachycardia. Total QRS is
in patients with A-fib and risk factors for stroke or
> 0.12 seconds because of the fusion between the
systemic embolization who do not have a prosthetic
impulse that uses the normal conduction system
heart valve, significant valve disease, severe renal failure
and that which uses the abnormal (accessory) path
(Cr clearance I 5 mL/min) or advanced liver disease
way, which bypasses the AV node. This bypass tract
(impaired baseline clotting function).
(accessory pathway, AP) conducts faster than the AV
node; therefore, a portion of the electrical current
MAT reaches the ventricle sooner (the delta wave on the
ECG) and preexcites the ventricle-hence the alterna
Multifocal atrial tachycardia (MAT) is mainly
tive name, "preexcitation syndrome." Occasionally, the
diagnosed by ECG criteria of atrial rate > I 00 beats/
accessory pathway is concealed, and the delta wave
minute with P waves of at least 3 distinct morphologies.
is not visible. An unusual cause of WPW can involve
MAT is usually seen in patients with pulmonary disease Ebstein anomaly of the tricuspid valve.
and may be a result of theophylline use. MAT can also
Spectrum of arrhythmias related to WPW includes
be caused by very low K+ and Mg+2.
orthodromic AVRT (narrow QRS complex regular
Therapy is directed at underlying illness. If medications tachycardia, which uses the AV node antegrade and
are deemed necessary, calcium channel blockers or AP retrograde), antidromic AVRT (wide QRS complex
amiodarone might be useful. Digoxin is of no use in regular tachycardia, which uses the AP antegrade and
MAT! It can actually worsen it, in addition to causing AV node retrograde), and atrial fibrillation (irregularly
digoxin-toxic arrhythmias. irregular wide QRS complex tachycardia using
antegrade AP conduction).
SVT Treatment of accessory pathways: Many patients have
Supraventricular tachycardia (S VT) refers to narrow completely asymptomatic AP and no dysrhythmias.
QRS complex tachycardias originating above the Patients with AP and symptoms of tachycardia (called
ventricles. The key step in assessment is recognition of WPW syndrome) can be treated with vagal maneuvers,
P wave and position of P wave in comparison to QRS. adenosine, or calcium channel blockers-same as any

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ARRHYTHMIAS 5-43

Ventricular Tachycardia
ECG Findings
Ventricular tachycardia (VT) is defined as 3 or more
How is the CHADS2 score calculated? At what sequential QRS complexes of ventricular origin at a rate
CHADS2 score should you treat with warfarin/ of 100 bpm or faster. Based on duration and association
NOACs (unless contraindicated)? with symptoms, VT can be defined as nonsustained
(asymptomatic with duration of less than 30 seconds)
In what patient group is MAT found?
or sustained (symptomatic or duration of more than

What is the treatment for acute A-fib in WPW? 30 seconds). VT can be monomorphic and polymorphic.

On an ECG, PVCs are often followed by what Monomorphic VT is generally regular in rate and
type of pause? appearance. It needs to be differentiated from SVT with
aberrant conduction, bundle-branch block, pacing, and
Ventricular tachycardia (VT) is defined as ::: 3
QRS changes due to severe hyperkalemia. The majority
sequential PVCs occurring at what bpm?
of patients with monomorphic VT have structural heart
List the ECG criteria consistent with VT. disease (particularly ischemic heart disease). Idiopathic
VT occurs in otherwise structurally normal hearts and
SVT! (In these cases, the impulses are moving down has much better prognosis. The most common idiopathic
the normal conduction system and returning via the VT is right ventricular outflow tract (RVOT) VT.
accessory pathway to complete the circuit.) But never
ECG criteria indicative of VT [Know!]:
treat acute A-fib in WPW with digoxin, verapamil,
or beta-blockers. Although verapamil and digoxin AV dissociation
increase the refractory period in the AV node, they can Fusion and capture beats
preferentially enhance conduction down the accessory Northwest axis
pathway and precipitate ventricular fibrillation (V-fib ). Positive or negative concordance in precordial leads
Instead, treat acute A-fib in WPW with IV Absence of rS complex in all precordial leads
procainamide, ibutilide, or amiodarone. Shock if there If rS is present, r to S time > I 00 msec
are any signs of hemodynamic deterioration in any QRS width of > 140 msec with a RBBB
WPW tachyarrhythmia; especially watch those with
QRS width > 160 msec with a L BBB
ventricular rate > 285 bpm because they are at greatest
risk of V-fib. If a patient with a history of structural heart disease
develops wide QRS complex regular tachycardia, VT is
WPW syndrome is associated with a low but definitive
significantly more likely than SVT.
risk of sudden death, and therefore radiofrequency
ablation is the preferred long-term treatment option! VT also can be bidirectional, with the complexes
alternating in direction; this is usually due to digitalis
intoxication but also can be seen post-MI and in a rela
VENTRICULAR ARRHYTHMIAS tively rare genetic condition called catecholaminergic
PVCs polymorphic ventricular tachycardia (CPVT).

Premature ventricular contractions (PVCs) often have Polymorphic VT generally has irregular ventricular
a compensatory pause; that is, they do not reset the rate and displays polymorphic QRS morphology. QRS
sinoatrial node, and the time between the sinus beats that complexes appear to twist around an isoelectric axis.
are on either side of the PVC= 2 basic RR intervals. Duration of polymorphic VT is typically brief; however,
it can be sustained and can degenerate into V-fib. It can
Asymptomatic, simple PVCs do not need to be treated
occur in patients with prolonged QT interval (torsades
if LV function is normal. If you do attempt treatment
de pointes) or in patients with normal QT interval (typi
(beta-blockers are I 51 line), the PVCs should decrease
cally in the setting of ischemia/M1).
by 80% for the treatment to be considered successful
otherwise, stop treatment. (Most patients have spontane
ous resolution, or decrease anyway.) Simple PVCs occur Treatment

beyond the T wave, are uniform, and have constant cou For sustained monomorphic VT, do the following:
pling (reentrant).
Stable: Give IV amiodarone.
Complex PVCs (pairs, triplets) also do not need to be Hemodynamically compromised: Shock.
treated if the patient is asymptomatic and has no heart
Unstable and refractory to electrical cardioversion:
disease!
Give IV amiodarone/procainamide.
If a patient has had an MI and has an ejection fraction of VT specifically with acute MI: Most use amiodarone
< 40%, frequent PVCs (> 10/hour) indicate a high risk of first. IV lidocaine can be useful.
sudden cardiac death-especially if they are sequential.

2014 MedStudy
5-44 ARRHYTHMIAS

For sustained polymorphic VT, do the same as Haloperidol and tricyclic antidepressants
monomorphic, except: Antibiotics (macrolides)
IV beta-blockers if ischemia is suspected or cannot be Antihistamines (astemizole and terfenadine)
excluded Antifungal agents (ketoconazole)
IV amiodarone, as long as there is no prolonged QT
You also can see TdP in association with very low K+

Urgent cath if ischemia is suspected or Mg+2. Bradycardia can promote TdP in patients with
Assess for torsades de pointes (see below) prolonged QT.

Never use verapamil with any wide complex Treat torsades de pointes with:
tachycardias in the emergency setting. (30% of those
DC cardioversion for sustained episode.
with ventricular tachycardia rapidly deteriorate!)
Magnesium sulfate 2--4 grams IV over 1 0-15
RVOT VT can be terminated acutely with adenosine, minutes.
and beta-blockers/calcium channel blockers (CCBs) Correction of hypokalemia.
can be used for long-term management. Remember, you
Correction of bradycardia (isoproterenol or pacing).
generally do not want to use CCBs for wide-complex
Never treat with Class Ia or Class III antiarrhythmic
tachycardias.

drugs (AADs).

Implantable Cardioverter-Defibrillators To prevent recurrence of TdP: 1) discontinue any


offending medications, 2) prevent bradycardia with
Implantable cardioverter-defibrillators (ICDs) can be used
isoproterenol or overdrive pacing, 3) supplement
for secondary (after event occurs) or primary prevention.
potassium and magnesium.
The following are Class I indications for ICDs from the
2008 ACC/AHA device therapy guidelines and 2012 Nonsustained Ventricular Tachycardia
focused update:
Nonsustained ventricular tachycardia (NSVT) is defined
Patients who are survivors of cardiac arrest due to VF
as asymptomatic VT (> 3 sequential PVCs with HR

or who have hemodynamically unstable sustained


> 100 bpm) lasting for< 30 seconds.
VT after evaluation has excluded any completely
reversible causes NSVT can indicate increased risk for death in
patients with heart disease, particularly ischemic
Patients with structural heart disease and spontaneous
cardiomyopathy. NSVT patients are at risk of sustained
sustained VT (> 30 sec), whether hemodynamically
VT and sudden death when:
stable or unstable
Patients with syncope of undetermined origin with they have ischemic cardiomyopathy (LVEF< 40%), or
clinically relevant, hemodynamically significant sustained sustained VT can be induced at electrophysiologic
VT or VF induced at electrophysiological study testing (EPT).
Patients with LVEF::; 35% due to prior MI who
These patients benefit from lCD implantation.

are at least 40 days post-MI and are in the NYHA


functional Class II or III; also, LVEF< 30% and in Patients with NSVT without structural heart disease
the NYHA functional Class I have good prognosis, and they do not require further
Patients with nonischemic dilated cardiomyopathy management.
(DCM) who have an LVEF::; 35% and who are in the
NYHA functional Class II or III
PACEMAKERS
Patients with nonsustained VT due to prior MI,
Permanent pacing is indicated for patients with
LVEF::; 40%, and inducible VF or sustained VT at
symptomatic bradycardia, sinus node dysfunction (sick
electrophysiological study
sinus syndrome), and AV conduction problems. In the
absence of symptoms, permanent pacing should be
Torsades de Pointes
strongly considered for patients with complete heart
Know this topic! Torsades de pointes (TdP) is a common block and advanced (i.e., not Wenckebach) type 2 second
type of polymorphic VT. It is associated with prolonged degree AV block (particularly associated with wide QRS).
QT interval (congenital or acquired). Acquired forms are
The most common pacemaker (Table 5-12) is DOD,
most often drug induced.
which stands for dual-chamber paced, dual-chamber
Drugs that commonly cause TdP are: sensed, and dual response to sensing: triggered and

Class Ia antiarrhythmic drugs (quinidine, inhibited. Most clinicians use DDD, unless the patient is
procainamide, disopyramide) in chronic, slow atrial fibrillation. The DDD is the most
physiologic and provides better exercise tolerance.
Class III antiarrhythmics (sotalol, dofetilide, and
amiodarone)

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ARRHYTHMIAS 5-45

Mexiletine is effective in most patients who respond


to lidocaine.
Digoxin works by inhibiting membrane ATPase.
It increases contractility and slows AV conduction
With what type of tachycardia should you never and HR.
use verapamil? Quinidine increases digitalis levels.
ICDs are recommended for primary prevention
Class 1: Sodium channel blockers that slow electrical

in what situations with ischemic and


conduction in the heart.
nonischemic cardiomyopathy patients?
Ia: Quinidine, procainamide, disopyramide-slow
Which antiarrhythmic drugs prolong the
conduction velocity, prolongs action potential duration,

QT interval?
and can prolong QT interval.
What is the treatment for torsades de pointes?
lb: Lidocaine, tocainide, mexiletine, phenytoin-shorten
Under what conditions is permanent pacing action potential duration slightly with no significant QT
recommended? prolongation.

How long do you have to wait for an lc: Flecainide and propafenone-slow conduction veloc
antiarrhythmic to reach steady-state ity without effect on potential duration or QT interval.
therapeutic levels?
Class II: Beta-blockers-decrease heart rate and blood
pressure by blocking impulses that can cause irregular
"Pacemaker syndrome" (associated lightheadedness and/ heart rhythm and decreasing hormonal effects (e.g.,
or syncope) can occur with single-chamber ventricular adrenaline) on the heart.
pacing and is commonly cured by dual-chamber (DDD)
pacers, which restore the atrial "kick." Class Ill: Amiodarone, sotalol, and the newer agents,
dofetilide (oral Tikosyn) and dronedarone (Multaq}
"Pacemaker-mediated tachycardia" can occur when prolong the action potential by potassium channel
paced ventricular complexes are sensed by the atrial lead blockade. These agents can cause QT prolongation.
and then trigger subsequent ventricular paced beats; this Note: See side effects on dronedarone below.
cycle can continue indefinitely.
Class IV: Calcium channel blockers, especially vera
pamil and diltiazem, slow inward current. They decrease
ANTIARRHYTHMIC THERAPY heart rate and blood pressure like class II.

Drugs
Adenosine and Digoxin
Overview
Digoxin is not in the above classes of antiarrhythmics,
With antiarrhythmic drugs (AADs), always wait 4--5
but it has antiarrhythmic effects and occasionally is used
half-lives before determining whether a drug is effective.
for this. Remember that digoxin is usually reserved for
Notes: treating severe heart failure.
All AADs have a proarrhythmic potential. Adenosine is also not in the above groups. Adenosine
Per the CAST study, there is evidence that Ic slows conduction in the AV node and is used for
anti-arrhythmic drugs decrease survival in patients conversion of S VT (AV node reentry) to normal sinus
with ventricular arrhythmias that occur post-MI. The rhythm. It also induces coronary artery vasodilation and
only drug that shows a benefit is a beta-blocker after a is used in cardiac perfusion imaging. It depresses LV
Q wave (ST elevation) infarction. function, but it has such a short half-life, it can even be
used in patients with decreased LV function.

Table 5-12: Permanent Pacemakers

The North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology
Group (NBG) Code

First letter= chamber(s) paced-VIAID (ventricle, atrium, or dual [V +A])

Second letter= chamber(s) sensed-V/A/D/0 (ventricle, atrium, dual [V +A], or none)

Third letter= mode(s) of response---T


- /1/D/0 (triggered, inhibited, dual[!+ I], or none)

Fourth letter= programmability-P/M/C/R/0 (programmable rate and output, multiprogrammable, communicating,


rate-modulated, or none)

Fifth letter= arrhythmia control-P/S/D/0 (pacing, shock, dual[P + S], or none)

2014 MedStudy
5-46 ARRHYTHMIAS

Notes on Verapamil Class Ill: All of them can cause prolonged QT, QRS,
Avoid verapamil with: and torsades de pointes.

Atrial fibrillation or atrial flutter occurring in WPW Amiodarone is the most effective, but also, due to
the extremely high iodine content, it is the most
Wide-complex tachycardias
toxic antiarrhythmic drug. It causes corneal deposits
Beta-blockers-relative contraindication because they
in 98% of patients!-also, hyper/hypothyroidism,
are both negative chronotropes and negative inotropes
pulmonary fibrosis, gray skin, and sun sensitivity
Patients with asymptomatic hypertrophic
but not hematologic changes. Pulmonary fibrosis
cardiomyopathy (HCM)
from amiodarone can be severe and is fatal 10%
Patients with obstructive HCM in the setting of of the time. It ordinarily occurs in the first year of
systemic hypotension or severe dyspnea at rest treatment. It tends to occur only in older patients

Okay to use verapamil: (> 40 years old), and in those with low CO dif
fusing capacity. (Pulmonary fibrosis is unlikely to
To control the ventricular response to A-fib or atrial develop on a maintenance dosage of< 200 mg/day.)
flutter in an otherwise healthy heart Amiodarone also causes a less common acute form
MAT of pulmonary toxicity. Again, amiodarone: hepatic
SVT (2"d choice after adenosine) toxicity; extremely long half-life (40-55 days);
Symptomatic treatment in HCM (but look above hyper/hypothyroidism; gray skin.
regarding avoiding verapamil in HCM) Dronedarone: July 2011-dronedarone showed
Severe, concentric LVH 2x increased mortality in patients with permanent
Hypertension A-fib and class III and IV heart failure. Current
recommendation is to not prescribe dronedarone to
patients with permanent A-fib.
Major Side Effects of AADs
Dofetilide: works by blocking the cardiac ion
[Know!] All AADs are, by their nature, arrhythmogenic.
channel carrying the delayed rectifier potassium
Especially remember the following:
current (IKr) . It is used to treat highly symptomatic
Class Ia: A-fib and can be used in patients with CAD and
HF. Dofetilide must be started as an inpatient by
Quinidine: prolongs the QRS complex and the QT
approved prescribers and is renally-dosed. It can
interval--occasionally leading to torsades de pointes,
cause significant Q T prolongation requiring dose
diarrhea, and (rarely) autoimmune thrombocytopenic
reduction or discontinuation. Do not use dofetilide
purpura. Also "cinchonism": hearing loss, tinnitus,
with the following medications: cimetidine, vera
and psychosis.
pamil, ketoconazole, trimethoprim, prochlorperazine,
Procainamide: Prolongs QT and QRS but also
megestrol, or any form of hydrochlorothiazide; these
causes blood dyscrasias, such as agranulocytosis,
agents can increase the activity of the CYP3A4 liver
neutropenia, and thrombocytopenia, in - 0.5%.
enzyme and increase dofetilide levels.
It also causes drug-induced lupus and must be used
with caution in HF patients because it has a mild Digitalis toxicity is more likely to occur in elderly
myocardial depressive effect. patients and in those with low K+, low Mg+2, or low
Disopyramide: prolonged QT, QRS, and torsades de p02 (low, low, low), and impaired renal function. The
pointes. It is also anticholinergic and vagolytic, so toxic levels of digoxin are determined by changes in the
it causes urinary retention, constipation, dry mouth, ECG, not by blood levels. Most common ECG changes
and negative inotropic effects. Because quinidine are bradycardia and prolonged PR interval.
and disopyramide prolong both the QRS and QT
intervals, avoid them in patients with 2nd or 3'd degree Electrophysiologic Testing
heart block. Disopyramide has a negative inotropic
effect, so avoid in patients with HF. Electrophysiologic (EP) studies are most commonly
used to identity and characterize SVTs and VTs, often as
Class lb: a precursor to radiofrequency ablation.
Lidocaine: seizures.
Tocainide is now used less often because of an Radiofrequency Ablation
association with aplastic anemia.
Radiofrequency ablation is the treatment of choice for
Class II: Beta-blockers commonly cause decreased libido WPW syndrome.
and impotence. They must be tapered slowly; stopping a
It is also used for the following if the patient prefers it to
beta-blocker abruptly can precipitate angina.
standard drug therapy or the condition is not responsive
to meds:

AVNRT
Atrial tachycardia

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SYNCOPE 5-47

MI within 3 months and TIA/CVA within 3 months.


Q.. trk... Relative contraindications to CSM include previous
u--'-!uiz VTNF or carotid bruit.

Arrhythmia: Bradycardia, SVT, or VT.


When is it okay to use verapamil; when is it
not okay? Orthostatic hypotension: Syncope due to orthostatic
hypotension 2 autonomic dysfunction causes symptoms
Which antiarrhythmic drug can cause lupus?
with no increase in the patient's heart rate with standing
Name the side effects associated with or during the vertical phase of tilt-table testing.
amiodarone.
Typically, try nonpharmacologic therapy first (e.g.,
What determines a toxic level of digoxin? support hose and increased salt); but treatment can
For what conditions is the treatment of choice also include midodrine (ProAmatine). Midodrine is a
radiofrequency ablation, guided by EP studies? prodrug for desglymidodrine, an alpha agonist that stim
ulates the alpha-adrenergic receptors of both arteriolar
What is the most common cause of syncope?
and venous vessels. Fludrocortisone, a mineralocorticoid

Explain how you approach the diagnostic agonist that promotes retention of sodium and water,
workup in a patient with probable also can be used but can cause supine hypertension.
neurocardiogenic (vasovagal) syncope.
Organic heart disease: Anatomic causes include
What are the tests used to work up high-risk depressed EF (causing VTNF), AS, HCM, atrial
patients with syncope? myxoma, PE, pulmonary hypertension (HTN), and
ischemia.
Atrial flutter Medications: Check the patient's history for new
Idiopathic VT medications. Common medications associated with
syncope include cardiovascular, neurologic, antipar
It has also been used to treat atrial fibrillation by ablating
kinsonian, and antidepressants. A classic cause of
a focal source of A-fib or by destroying the AV node and
drug-related syncope includes medications for BPH
placing a ventricular pacemaker.
(prazosin, terazosin, and tamsulosin).

A thorough history, physical exam, supine and upright


SYNCOPE blood pressure, and ECG are an essential part of the ini
tial evaluation followed by additional testing in selected
Syncope is sudden transient loss of consciousness subgroups (carotid sinus massage, echocardiogram). If
with associated loss of postural tone and spontaneous the diagnosis is certain, treatment is initiated. If the diag
recovery. It is important to differentiate syncope from nosis remains uncertain, stratify the patient to determine
other types of loss of consciousness. Classifications of whether the patient is at increased risk of death (typically
syncope: patients with severe structural heart disease, clinical, or
ECG features suggesting arrhythmic syncope).
Neurally mediated (reflex) syncope symptoms include
dizziness, lightheadedness, and fatigue, with prodro High-risk patients should be admitted for further
mal features such as diaphoresis, pallor, palpitations, workup, which can include coronary angiogram and EP
nausea, hyperventilation, and yawning. Myoclonic study. Low-risk patients, particularly with only I episode
jerks can occur when the patient is unconscious, and of syncope, usually do not require further evaluation.
it needs to be distinguished from seizure activity. If the history is typical, and this is the first episode in
Several subtypes: a young patient with no suspected heart disease, the
Vasovagal syncope, as in the common faint, is the patient can be reassured and sent home.
most common cause of syncope. It is triggered by Initial measures aimed at reducing events include
intense emotion, pain, prolonged standing, alcohol, avoidance of precipitating factors and also avoiding
or heat exposure. Vasovagal episodes are typically volume depletion. Patients should also be taught to sit or
preceded by a prodrome that includes nausea, vomit lie down at the onset of symptoms and to initiate physi
ing, flushing, hot flashes, and diaphoresis. Extremely cal isometric maneuvers (leg crossing and hand grip).
elderly patients may not have a classic prodrome. Value of pharmacologic agents (beta-blockers, fludro
Situational reflex syncope is triggered by cough, cortisone, midodrine) is less certain. Frequent episodes,
micturition, etc. These triggers provoke reflex despite initial management, require evaluation with con
vasodilation and bradycardia leading to syncope. tinuous ambulatory electrocardiography (patients with
Carotid sinus hypersensitivity may be responsible for severe cardioinhibitory response during syncope could
up to 40% of falls in the elderly and is diagnosed with benefit from pacemaker placement). Patients in high
a pause > 3 seconds during carotid sinus massage risk occupations should be investigated with the first
(CSM). Absolute contraindications to CSM include episode of syncope.

2014 MedStudy
5-48 CARDIOMYOPATHIES

Approximately 1/4 of patients with HCM have a resting


CARDIOMYOPATHIES
gradient (greater than 30 mmHg).

There are 3 main types of nonischemic cardiomyopathy: A majority of patients with HCM have normal life
hypertrophic, restrictive, and dilated. expectancy with little or no disability; however, subgroups
of patients are at risk for complications, including sudden
death, progressive heart failure, and atrial fibrillation.
HYPERTROPHIC CARDIOMYOPATHY
Risk factors for sudden death in HCM (and possible role
Hypertrophic cardiomyopathy (HCM) is the most
for ICDs):
common of the genetic cardiovascular diseases
(autosomal dominant pattern of inheritance; Septal thickness > 30 mm
[Image 5-11]). It is characterized by a thickened but not Personal history of syncope
dilated left ventricle in the absence of other cardiac or Family history of sudden death in I st degree
systemic conditions (HTN, aortic valve stenosis). HCM family member
is the most common cause of sudden death in young age
NSVT on Holter monitor
(age < 35), including competitive athletes.
Failure to augment systolic BP on exercise tolerance
Patients with HCM typically present with heart failure, testing (< 10 mmHg increase at peak exercise)
chest pain (typical or atypical), or syncope. They can
be asymptomatic and recognized because of abnormal Treatment for HCM
physical exam (murmur).
Treatment for HCM:
Bedside with HCM: The patient typically has a harsh,
crescendo-decrescendo systolic murmur, typically in
Beta-blockers (obstructive and nonobstructive
HCM) and verapamil (obstructive HCM) improve
the left yct space, which increases with Valsalva and
diastolic filling by slowing heart rate.
decreases with sustained handgrip. There is a carotid
pulse that has a brisk upstroke, but, because outflow Disopyramide with beta-blockers for obstructive
obstruction occurs late in systole, it is bifid in 2/3 of HCM when other drugs fail to achieve
HCM patients. The briskness of the upstroke further symptom control.
distinguishes it from aortic stenosis. Palpation at the apex IV phenylephrine (or other pure vasoconstrictor) is
can surprise you with a double- or triple-tap impulse. recommended for treating acute hypotension in HCM
A mitral regurgitation murmur can also be heard from patients who do not respond to IV fluids.
systolic anterior motion (SAM) of the mitral valve due lCD placement is recommended for HCM patients
to a suction-like effect of the outflow obstruction. with prior documented cardiac arrest, ventricular
fibrillation, or hemodynamically significant VT.
The ECG with HCM is abnormal in more than 90%
lCD is also reasonable to place if sudden cardiac
of patients. Most common abnormalities include LVH,
death (SCD) in 2: 1 first-degree relative(s), LV
ST-T changes with sometimes marked T wave inversion
wall thickness 2: 30 mm, or 2: 1 recent unexplained
in the lateral precordial leads, and Q waves in inferior
syncopal episode(s).
and lateral leads.
Septal reduction therapy via intracoronary injection
Diagnosis is commonly made with echocardiogram,
of ethanol to cause a controlled septal infarction can
although recently cardiac MRI has emerged as a new
reduce the obstruction in eligible patients with severe
diagnostic modality. There is no single classic mor
drug refractory symptoms and left ventricular outflow
phologic form, and virtually all possible patterns of
tract (LVOT) obstruction. Diuretics with beta-blockers
hypertrophy have been described. Some patients have
to reduce filling pressures in hypertrophic cardiomy
dynamic obstruction related to SAM of the mitral valve.
opathy (HCM) patients with severe heart failure, and
then only with extreme caution!
Septal myectomy is preferred treatment for patients
with severe drug refractory heart failure (HF)
symptoms (NYHA III and IV).

RESTRICTIVE CARDIOMYOPATHY
Restrictive cardiomyopathy must be differentiated from
constrictive pericarditis (page 5-55) because the signs
and symptoms can be similar. Although constrictive
pericarditis is often quickly treated with good results,
restrictive cardiomyopathy is not reversible.

Arrhythmias, such as atrial fibrillation, occur early in


the course of these diseases. Constrictive pericarditis is
a pericardia! problem; restrictive cardiomyopathy is a
myocardial problem.
image 5-11: Hypertrophic cardiomyopathy

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HEART FAILURE 5-49

Catecholamines
Organic solvents ("glue sniffers" heart)
Quiz

L ate hemochromatosis

What are the risk factors for sudden death in Think Chagas disease in patients from Central and South
patients with HCM? American countries.

What are the 3 main medications used in the In contrast, nonischemic cardiomyopathies include
treatment of HCM? cardiomyopathies due to volume or pressure overload,
such as hypertension or valvular heart disease.
What are some causes of restrictive
cardiomyopathy? In pregnant women, a peripartum cardiomyopathy can
occur anytime from the beginning of the last trimester
List some of the etiologies of DCM.
through the first 6 months postpartum.

In the 2013 ACC/AHA, what are the newly


Heart failure due to dilated cardiomyopathy is treated
defined 2 major subdivisions of heart failure?
similarly to other causes of HF (see below).

Causes of restrictive cardiomyopathy include amyloi


dosis, sarcoidosis, hemochromatosis, and lipid storage HEART FAILURE
diseases. On 20 echocardiogram, the myocardium may
be thickened with a granularity, which suggests an OVERVIEW
infiltrative process.
Heart failure (HF ) is defined as a complex clinical
Thoracotomy is occasionally done to ensure that you do syndrome resulting from any structural or functional
not miss a treatable constrictive pericarditis; these are cardiac disorder that impairs the ability of the ventricle
treated with pericardiectomy. to fill with or eject blood. Left ventricular ejection frac
Treat mild-to-moderate restrictive cardiomyopathy with tion (LVEF ) is considered important in classification of
diuretics. patients with HF.

The lifetime risk of developing HF is 20% for

DILATED AND NONISCHEMIC Americans :::0: 40 years of age. African-American males


have the highest risk for HF, and the highest 5-year mor
CARDIOMYOPATHIES
tality rate (Atherosclerosis Risk in Communities [ARIC]
Patients with dilated cardiomyopathy (DCM) have Study-ongoing).
ventricular dilation and depressed myocardial contractility
The 2013 ACC/AHA definitions:
in the absence of abnormal loading conditions such as
hypertension or valvular disease. African-Americans have Heart failure with reduced ejection fraction (HF rEF):
nearly a 3-fold risk for developing DCM when compared EF :::; 40%, systolic HF
to Caucasians. Heart failure with preserved ejection fraction
(HFpEF): EF :::0: 50%, diastolic HF
The prognosis of patients with symptomatic HF and
DCM is poor, with 50% mortality at 5 years. Cardiac output is well maintained in mild HF, usually
Etiologies of DCM: at the expense of increased left ventricular end-diastolic
volume (LVEDV) and increased heart rate.
Familial cardiomyopathies (e.g., noncompaction)
Numerous adaptations occur in response to heart
Idiopathic (probably viral-most common)
failure in the peripheral circulation, kidney, skeletal
Obesity
muscle, and other organs. The changes contribute to the
Diabetes
overall clinical manifestations and ultimately become

Hyperthyroidism maladaptive.
Acromegaly
In response to exercise, LVEDV and plasma
Alcohol
norepinephrine rise more than in controls, but the

Cocaine resulting cardiac output increase does not rise in


Cancer chemotherapy (especially anthracyclines) proportion to 02 consumption-so the patient has
Ephedra dyspnea on exertion and is easily fatigued. The
Cobalt adrenergic system and the renin-angiotensin-aldosterone
Anabolic steroids system play a major role in progression of heart failure
and maladaptive mechanisms.
Chloroquine
Clozapine
Amphetamines
Methylphenidate

2014 MedStudy
5-50 HEART FAILURE

LOW-OUTPUT HF Stage C HF patients have structural heart disease


with prior or current symptoms of heart failure. These
NYHA Classification
are patients with structural heart disease as described
NYHA (New York Heart Association) classification above in Stage B, and who additionally have signs and
of heart failure (classes and definitions) is a functional symptoms of HF (e.g., dyspnea, fatigue, and decreased
classification based on how much the patient is limited exercise tolerance).
during physical activity. In clinical use, it is being
Goals for Stage C therapy are control symptoms, patient
superseded by the ACC/AHA classification (next).
education, improved health-related quality of life, and
NYHA classification:
prevention of hospitalization and mortality.
Class 1: Cardiac disease but no limitation in physical
Stage C drugs are:
activity.
loop diuretics for all volume overload NYHA
Class II: Slight limitation of normal physical activity
II-IV patients, hydralazine/isosorbide dinitrate
(fatigue, palpitations, dyspnea, and/or angina).
for symptomatic African-American NYHA III-IV
Class III: Marked limitation of physical activity. Slight patients, aldosterone antagonist for NYHA II-IV
activity causes symptoms. patients (Cr > 30 mL/min and K < 5 mEq/dL), and

Class IV: Symptoms may be present at rest. Unable to statins and beta-blockers as used in Stage B (i.e., if

carry on any physical activity without discomfort. MilACS), and ACEis/ARBs as used in Stage A.

Use lCD and/or cardiac resynchronization therapy


ACC I AHA Staging (CRT) if indicated, and revascularization or vascular
surgery as appropriate.
The 2013 ACCIAHA staging system for HF shows heart
failure as more of a progressive disorder and has goals Stage D HF patients have marked symptoms at rest
of therapy for each stage (A through D). Know the defi and frequent hospitalizations despite maximal medical
nition, goal of therapy, and medications for each stage therapy.
of HF. Goals for Stage D therapy are to control symptoms,
Stage A HF patients are at high risk for heart failure but improve health-related quality of life, reduce hospital
have no structural heart disease/symptoms of HF and readmissions, and establish patient's end-of-life goals.
include those with hypertension (HTN), atherosclerotic Stage D drugs are the same as those for Stage C.
disease, diabetes, obesity, and metabolic syndrome.
Options for Stage D patients also include consideration
Stage A also includes any asymptomatic patient using
of "extraordinary measures," including heart transplant,
cardiotoxins (such as anthracycline) or with a family
chronic inotropes, temporary or permanent mechanical
history of cardiomyopathy.
circulatory support (ventricular assist devices), and
So yes, you read this right: Just having HTN means you experimental surgery or experimental drugs; and palliative
have Stage A heart failure! care, hospice, and lCD deactivation.
Goals for Stage A therapy are to treat the disorder Until definitive therapy (coronary revascularization,
(HTN, lipid disorder) and control/avoid other condi mechanical circulatory support, or heart transplantation)
tions that can lead to or contribute to HF, such as obesity, is performed or acute precipitating problem resolves,
diabetes mellitus, tobacco use, and known cardiotoxic patients with cardiogenic shock should receive tempo
agents (excess alcohol/illicit drug use). Regular physical rary IV inotropic support to maintain systemic perfusion
activity to improve functional status is recommended in and preserve end-organ performance.
all HF patients.
The most common causes of HF with reduced EF
Stage A drugs include ACEis/ARBs/statins in appropriate (HFrEF) are:
patients.
coronary artery disease (40%-although recent data
Stage 8 HF patients have structural heart disease but pushes this to near 60% of etiologies),
without signs or symptoms of heart failure. This stage dilated cardiomyopathy (30%),
includes patients who have a history of a previous MI
valvular disease (15%), and
and those with LV remodeling from left ventricular
hypertension (10%).
hypertrophy (LVH) or low LVEF, and those with

asymptomatic valvular heart disease. HF is the most common diagnosis in hospitalized elderly

Goals of Stage B therapy are to prevent HF symptoms patients. Only 50% of patients with HF die from actual
pump failure; - 40% die from arrhythmias!
and prevent further cardiac remodeling.

Stage B drugs are: ACEis/ ARBs, beta-blockers, and


statins if history of Mil ACS. Use lCD if indicated, and
revascularization or vascular surgery as appropriate.

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HEART FAILURE 5-51

,.------ LV dysfunction
Define Stage A through Stage D heart failure
(ACC/AHA classification). What are the goals of
therapy for each of these stages?
!
Deer BP/Decr Renal perfusion

What is the sequence of drugs used to treat HF


based on ACC/AHA stages? Na and H,O retention
l
!ncr sympathetic tone
+- !ncr renin-angiotensin
What are the most common causes of Vasoconstriction I ncr vasopressin

low-output HF?
Adapted from Califf . NEJM 330(24): 1724-30
What factors are associated with poor prognosis
in HF?
Figure 5-6: Sptral of Worsentng HF
What is the sequence of events that
worsens HF?
Let's see if we have all of that: Low CO --> low renal
perfusion --> high renin --> high angiotensin I high
Determining Prognosis in HF
angiotensin II --> high aldosterone --> retentton of
In severe HF, a worse prognosis is associated with: Na + --> retention of water --> high filling pressure -->
Lower ejection fraction exacerbation of HF (Figure 5-6). The increased heart

Low sodium rate in HF is due to both an increased sympathetic tone


and an increased level of catecholamines in an attempt
CKD
to compensate for reduced stroke volume. The higher
Anemia
the catecholamine pool, the worse the prognosis.
Elevated troponin
ADH is released from the hypothalamus but has
High brain natriuretic peptide (BNP)
a minor effect.
Increased width ofQRS
Persistent sinus tachycardia Atrial (or A-type) natriuretic peptide (ANP) and bra n
_
natriuretic peptide ([BNP]; also called B-type natnurettc
Poor functional capacity (NYHA III and I V)
peptide) are released from the heart myocytes; the release
High norepinephrine and catecholamine levels
is stimulated by stretching of the atrium (ANP and BNP)
Exercise training in patients with stable chronic HF is and the ventricle (BNP). ANP and BNP increase excre
associated with an II% reduction in combined all-cause tion of sodium and water, cause vasodilation, and inhibit
death or hospitalization (2009 HF-ACTlON Trial). the effects of aldosterone. These peptides are released in
an attempt to offset the effects of renin angiotensin and
The Seattle Heart Failure Model and/or The Heart
ADH but cannot antagonize them adequately.
Failure Survival Score can provide a reasonable
"ballpark" estimate of HF prognosis based on standard In severe heart failure, the BNP increases
clinical data. 20-100-fold. High levels of these peptides (especially
BNP) actually correlate directly with a poor prognosis in
HF. BNP is also elevated in restrictive cardiomyopathy
Mechanism of HF
but not constrictive pericarditis and is used to differentiate
Heart failure with reduced ejection fraction (HFrEF) between these disorders.
results in decreased cardiac output. This in tum causes
About 50% of HFs are caused by diastolic dysfunction
an increased A-a 02 difference and decreased renal
perfusion. The decreased cardiac output can be due to
(more recently termed "heart failure wit preserved E ";
HFpEF) rather than systolic dysfunctton. Myo ardtl
systolic dysfunction, diastolic dysfunction, or both. Note
ischemia, severe concentric LYH, HCM, and dtabettc
that diastolic dysfunction can occur with normal cardiac
cardiomyopathy cause diastolic dysfunction, at least
output (see below). After a certain point, decreased car
initially. With diastolic dysfunction, the CO is often
diac output from any type of HF causes decreased renal
normal; HF develops from increased filling ressure
perfusion. This stimulates the release of renin, which
_ (from decreased relaxation due to increased sttffne s).
allows the conversion of angiotensinogen to angiO
So the problem is not that the ventricle is not squeezmg
tensin I. Angiotensin I is converted to angiotensin II _
enough, but rather that it is not relaxing enough. Thts ts
in the lungs. Angiotensin II then stimulates the secre
reflected in elevated left and right end-diastolic pressure
tion of aldosterone, which then causes retention of Na+
(LVEDP and RVEDP), tachycardia, and an S4.
and water, causing a greatly increased filling pressure
(moving the Starling curve to the right).

2014 MedStudy
5-52 HEART FAILURE

Treatment for HF Eprosartan (Teveten)

General Measures
L osartan (Cozaar)
Telmisartan (Micardis)
See above for treatment according to ACC/AHA stage.
*Randomized controlled trial data show mortality
We will now discuss the individual drugs and how they
benefit in heart failure.
affect/improve survival in heart failure.

(Note: In our discussion, the term class refers to NYHA


Beta-Blockers
classification; the term stage refers to the ACC/AHA
classification.) Beta-blockers are now part of standard heart failure
treatment. In HF, the sympathetic nervous system is
Current pharmacologic management of low-output
overstimulated. This raises norepinephrine levels, which
heart failure is aimed at reducing ventricular preload
can cause cardiac remodeling, lead to arrhythmias, and
and afterload as well as diminishing, inhibiting, and/or
increase mortality risk. Mortality is clearly improved by
antagonizing neurohormonal vasoconstrictor activation,
carvedilol (
65% relative risk reduction), metoprolol
rather than directly increasing cardiac contractility as in
succinate, and bisoprolol ( 35%).
They are indicated in
the past.
patients with HFrEF and current or prior symptoms to
The optimal treatment of heart failure aggressively reduce morbidity and mortality.
addresses the major risk factors including hypertension,
Previously, it was taught that starting these drugs while
diabetes, obesity, metabolic syndrome, hyperlipidemia,
patients are decompensated is contraindicated. Current
and coronary artery disease (CAD). Therapies that
guidelines recommend initiation of beta blockade at any
promote regression ofLV H or reverse remodeling of the
stage of heart failure, once adequate diuresis has been
dilated heart should be used; these include inhibitors of
achieved and intravenous diuretics have been discontin
catecholamines and the renin-angiotensin-aldosterone
ued. Carvedilol (Coreg) is a nonselective beta-blocker
pathway.
that also has some alpha-blocker effect. Use in conjunction
with ACE inhibitors in Class I-IV heart failure.
ACE Inhibitors and ARBs

Angiotensin-converting enzyme inhibitors ([ACEis]; Diuretics


captopril, enalapril, lisinopril, benazepril, fosino
Give diuretics if needed for volume control (i.e.,
pril, quinapril, ramipril) are 1st line therapy. They are
decrease edema and pulmonary congestion) during
indicated in patients with HFrEF and current or prior
Stage C therapy. Remember: Therapy now begins with
symptoms to reduce morbidity and mortality. They
ACEIs/ ARBs and beta-blockers before patients even
decrease systemic vascular resistance, pulmonary
have symptoms.
capillary wedge pressure, right atrial pressure, and
end-diastolic and end-systolic dimensions; and they Diuretics are effective in both heart failure with
improve cardiac performance, as evidenced by increased reduced or preserved EF for symptom control (volume
cardiac output and stroke volume, and by improved overload). All but the aldosterone antagonist diuret
fractional shortening, as determined by echocardiogra ics have no mortality benefit, unlike ACEis/ ARBs and
phy. Hence, they decrease tachycardia due to HF. ACEis beta-blockers.
block formation of angiotensin II. They also decrease Treat heart failure (HF) patients admitted with signifi
the incidence of ventricular arrhythmia and prolong cant fluid overload promptly with IV loop diuretics. In
survival. In addition, they reverse the remodeling in the those already receiving outpatient loop diuretics, the
myocytes, which causes progression of heart failure. initial IV dose should be > their chronic oral daily dose
Angiotensin II receptor blockers (ARBs) block the effect and be given as either intermittent boluses or continu
of angiotensin II at the cell wall. ARBs are given in place ous infusion. Adjust diuretic dose for symptom relief, to
of ACEis (if ACEI intolerant) and are equally effective reduce volume, and avoid hypotension.
(commonly grouped as "ACEVARB"). If a loop diuretic given twice daily in doses equivalent
ARBs cause less cough than ACEis and are often given to furosemide 100-200 mg/d is inadequate, a thiazide
when patients develop refractory cough on ACEis. Cough diuretic or metolazone can be added, which results in a
is caused by excessive bradykinin. synergistic effect. This combination can result in severe
hypokalemia, so close monitoring is necessary.
Monitor patients on ACEis/ARBs for renal impairment
and hyperkalemia. Aldosterone antagonists (aka mineralocorticoid
antagonists) reduce morbidity and prolong survival in
Commonly used ARBs:
NYHA II-IV and with reduced EF < 35%:
Candesartan (Atacand)*
Spironolactone showed a 30% decrease in mortality

Valsartan (Diovan)* at 24 months when given to patients with Class IV


Irbesartan (Avapro) HF or Class III having had Class IV in the previous
Olmesartan (Benicar) 6 months ( 1999 RALES trial).

2014 MedStudy-Piease Report Copyright Infringements to copyright@medstudy.com


HEART FAILURE 5-53

the baroreceptors and dampen the renin-angiotensin


effects; it has very little inotropic effect. It also is used
to control the ventricular rate in a patient with HF and
atrial fibrillation. Digoxin has no mortality benefit. See
When are beta-blockers started in the treatment Table 5-13 for Drugs that Increase Digoxin Level.
ofHF?

With what type of HF do aldosterone antagonists Nitrates


prolong survival?
Nitrates are occasionally used next (good venodilator,
True or false? Digoxin can be beneficial in moderate arterial dilator}-remember the nightly 6-hour
HFrEF patients to decrease hospitalizations nitrate-free window to prevent tolerance (discussed
forHF. under Anti-Anginal Drugs on page 5-12).
In what population is hydralazine + isosorbide With ventricular failure, patients can have increased
dinitrate beneficial? systemic (peripheral) vascular resistance (SVR) with a
Which patients with chronic HF should receive
normal or low BP, and they still benefit from an arteriolar
anticoagulation?
vasodilator.

Eplerenone showed a 15% decrease in mortality at Hydralazine and lsosorbide Dinitrate


16 months in patients with recent Ml and EF Hydralazine is an afterload reducer (arterial vasodilator);
< 40% and evidence of HF or diabetes mellitus it also increases heart rate. Hydralazine is fre
(2003 EPHESUS trial). Monitor patients closely quently used with nitrates to get the added benefit of
for hyperkalemia. decreased preload.
NYHA II patients should have prior HF
The combination of hydralazine and isosorbide
hospitalization and elevated plasma natriuretic
dinitrate is recommended to reduce morbidity and
peptides before being placed on aldosterone
mortality in African-Americans with NYHA III-IV
antagonists.
HFrEF, as adjunctive therapy to ACEis (or ARBs) and
More notes on diuretics: beta-blockers (2004 A-HeFT). The combination can
also be helpful in patients with current or prior symp
Thiazides mainly block Na+ and Cl- resorption in the
tomatic HFrEF who cannot be given ACEIs/ARBs
distal convoluted tubule and, to a minor extent, block
(drug intolerance, hypotension, renal insufficiency).
Na+ resorption in the proximal tubule. Examples are
hydrochlorothiazide and metolazone (Zaroxolyn).
Spironolactone competitively inhibits aldosterone Anticoagulation
(so, is K+ sparing) and is being used increasingly in For patients with chronic HF and permanent, persistent,
the management of chronic heart failure. Eplerenone or paroxysmal atrial fibrillation plus an additional risk
is similar to spironolactone but more selective for the factor for cardioembolic stroke (Hx HTN, DM, previous
mineralocorticoid receptor. stroke/TIA, or age 2': 75) give individualized anticoagu
Furosemide (Lasix), bumetanide (Bumex), lation (warfarin, dabigatran, apixaban, or rivaroxaban).
torsemide (Demadex), and ethacrynic acid are
the loop diuretics. They block Na+ resorption in the
ascending limb of the loop of Henle. Bumetanide
may also have some action on the proximal tubule. Table 5-13: Drugs that Increase D1goxm Level
lndapamide (Lozol, Lozide) has an unknown
Alprazolam
mechanism of action. It has an antihypertensive effect
occurring far below the antidiuretic effect. Probably Amiodarone
has renal and extrarenal effects.
Abx: Macrolides and tetracycline
Triamterene has an unknown mechanism of action.
CyclospMin
With azotemia, do not use spironolactone or triamterene
because these can cause hyperkalemia; thiazides are not Diphenoxylate or propantheline (decrease bowel motility)
effective, but furosemide usually is. Much more on this ..
Indomethacin
in Nephrology, Book 2.
Itraconazole (antifungal)

Digoxin Omeprazole

Digoxin can be beneficial in HF with reduced EF to Propafenone (class Ic antiarrhythmic)


decrease hospitalizations for HF. It is started after
Quinin
the above therapies are established and the patient
is still symptomatic. In HF, digoxin appears to reset Spironolactone

2014 MedStudy
5-54 HEART FAILURE

Clinical practice guidelines also recommend anti Milrinone (Primacor) is an inotropic/vasodilator agent
coagulation in heart failure patients with a cardioembolic with phosphodiesterase inhibitor activity (peak III
source (history of systemic or pulmonary embolism, cAMP-an isoenzyme of cAMP). It is also indicated
or a mobile left ventricular thrombus). In the absence for short-term I V treatment of HF. It does not cause
of above mentioned indications, anticoagulation is not thrombocytopenia (unlike amrinone), and it is not
recommended in patients with HFrEF. associated with tachycardia.

Decompensated HF patients admitted to hospital should Rarely used: Prazosin and minoxidil are also afterload
receive VTE prophylaxis. reducers but are associated with rapid development of
tolerance and fluid retention. Nitroprusside is not used
much now because of tolerance and toxicity problems.
Other Therapy

The 2013 ACC/AHA guideline update for the Mechanical circulatory support (MCS) is beneficial in
Management of Heart Failure recommends implantable selected patients with Stage D HFrEF in whom defini
cardioverter-defibrillator (lCD) for primary prevention tive management (cardiac transplantation) or cardiac
recovery is anticipated or planned. Nondurable MCS
of sudden cardiac death and to reduce total mortality
(percutaneous and extracorporeal ventricular assist
in patients with HF (nonischemic dilated cardiomyopa
devices) are reasonable as a "bridge" to recovery/deci
thy or ischemic heart disease) who are at least 40 days
sion in carefully selected HFrEF patients who have
post-MI and who have an EF :S 35% and NYHA III
acute, profound hemodynamic compromise. Durable
III symptoms on optimal medical therapy, or who are
MCS can be used to prolong survival for carefully
post-MI with EF :S 30% and NYHA I symptoms on
selected HFrEF patients.
optimal medical therapy. ICD candidates must also
have an expected survival > 1 year. See Implantable Revascularization (CABG or PCI) is indicated for
Cardioverter-Defibrillators on page 5-44 for Class I patients on optimal medical therapy with angina and
indications for ICD therapy. suitable anatomy, especially left main stenosis (> 50%)
or left main equivalent disease. For end-stage HF,
Ventricular dyssynchrony is caused by electrical
cardiac transplant is the best option. There is a 65%
disturbances that cause the heart to pump blood in an
inefficient way. It is suggested by severe HF (NYHA III! 5-year survival and a 55% 10-year survival!
I V), severely decreased ejection fraction (LVEF :S 35%), Harmful for HFrEF patients:
and QRS exhibiting LBBB configuration with QRS
Definitely avoid or withdraw most antiarrhythmics,
duration 2: 120 ms.
calcium blockers (except amlodipine), NSAIDs, and
Cardiac resynchronization therapy (CRT) involves thiazolidinediones.
pacing the right and left ventricles and is recommended Long-term use of positive inotropic drugs is
for patients with EF :S 35%, sinus rhythm, LBBB with potentially harmful, except as palliation for patients
a QRS duration of 2: 150 ms, and is NYHA II/III, or with end-stage disease (Stage D) who cannot be
patients who are ambulatory with NYHA IV symptoms stabilized with optimal medical therapy.
despite optimal medical therapy. (Per 2012 ACC/AHA
update of device therapy guidelines.)
HIGH-OUTPUT HF
"High-output" ventricular failure is seen with
Emergency Treatment for Severe Heart Failure
peripheral shunting (large AV fistulas, severe hepatic
[Know:] With severe ventricular failure, patients may hemangiomatosis, and Paget disease!) and low-systemic
require short-term treatment with inotropes (dopamine, vascular resistance, as seen in gram-negative sepsis. You
dobutamine, and milrinone). can also see it in patients with hyperthyroidism, beri
beri, carcinoid, or anemia. Remember, though, these
Dobutamine is another inotropic agent that can be
patients often have a normal cardiac output at the time of
used for severe ventricular failure. It does not have the
diagnosis-because of the worsening ventricular failure!
vasoconstrictor activity of dopamine and actually has
some vasodilatory effects.

Dopamine: RIGHT VENTRICULAR FAILURE

At < 2 J.lg/kg/min dopamine stimulates the "The most common cause of right heart failure is left
dopaminergic receptors and causes mesenteric heart failure!" is what you heard on rounds. And, indeed,
dilation. right ventricular failure (RVF) is mainly caused by pul
monary hypertension (1 or 2)-typically secondary
At 2-5 J.lg/kg/min, it has a predominantly beta
to left ventricular failure (LVF). RVF is also seen with
agonist effect (positive inotropy) and increases renal
large RV infarctions and cor pulmonale. Remember: If
perfusion.
the patient has signs of RVF (ND and liver congestion),
At> I 0 J.lg/kg/min, it mainly has an alpha-agonist
but pressures are the same in all chambers in diastole,
effect and causes vasoconstriction. Generally never
think external compression (constriction or effusion).
use> 10 J.lg/kg/min!

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PERICARDIAL DISEASES 5-55

Renal failure (uremic)


Cancer
Postradiation
Hypothyroidism
CRT is indicated for which HF patients?
MI (Dressler syndrome)
Know all drugs used for emergency treatment of Open heart surgery (postpericardiotomy syndrome)
severe HF!
Certain drugs, especially procainamide and
What does dopamine do at low doses hydralazine
(< 2 IJg/kg/min)? At doses of 2-5 IJg/kg/min?
Suspect TB as the cause if the patient is at high risk, or if
True or false? MCS is beneficial in selected the symptoms of pericarditis do not resolve after 2 weeks
patients with stageD HFrEF in whom definitive of treatment.
management (cardiac transplantation) or
Both Dressler syndrome and postpericardiotomy
cardiac recovery is anticipated or planned.
syndrome are autoimmune processes that occur several
With what diseases does high-output heart weeks after the precipitating event. Even if the history is
failure occur? very suggestive, you must consider the following entities
What is the treatment for acute pulmonary and exclude them to make the diagnosis: MI, pulmonary
edema? embolus, and endocarditis. Other causes include uremia
and connective tissue disease.
What are some causes of non-constrictive
pericarditis? What ECG changes can you see? Patients with pericarditis commonly present with very
severe chest pain, sometimes pleuritic, which (classically)
improves when leaning forward. The pain is retro-sternal
Orthopnea: As LVF progresses, orthopnea usually
and left precordial, and referred to the neck, arms, or left
worsens, but it may then actually improve temporarily as
shoulder. Typically, the patient has some fever and tachy
RV function worsens due to the pulmonary hypertension.
cardia. A pericardia! friction rub, which does not always
Paroxysmal nocturnal dyspnea does not improve with occur and can be evanescent, is diagnostic for pericarditis.
sitting up, as orthopnea does.
The ECG may show diffuse concave-up ST elevation (vs.
localized, concave-down ST elevation in an acute MI)
PULMONARY EDEMA and, occasionally, depressed PR segments, especially in

Immediate treatment for acute pulmonary edema: lead II. ECG changes occur in 4 stages:

Patient should be sitting with legs dangling, if Stage I: diffuseST elevation segments with upward

possible, to decrease venous return. concavity with PR depression


Stage 2: normalization ofST segments after
Give I 00% 02, morphine (to decrease anxiety and

decrease vasoconstriction). several days

Give furosemide (causes venodilation even before Stage 3: inverted T waves


the diuresis). Stage 4: weeks or months after onset of acute

IV nitroglycerin or nitroprusside can be used if pericarditis, ECG returns to normal

systolic BP is > I 00. Pericarditis can cause transient increases in troponin


Strongly consider the use of dobutamine if systolic (secondary to associated myocarditis). Treat pericarditis
BP< 90. by stopping any possible causative drugs and giving
Aminophylline is rarely used to increase respiratory NSAIDs. Do not treat idiopathic pericarditis with steroids
muscle function. because there can be a relapse when they are stopped.
Treatment with colchicine has been shown to reduce
recurrence.
PERICARDIAL DISEASES

NON-CONSTRICTIVE PERICARDITIS CONSTRICTIVE PERICARDITIS

90% of non-constrictive pericarditis is idiopathic and It occurs when resorption of pericardia! effusion is
probably viral in origin; often, there is a preceding URI or followed by obliteration of the pericardia! cavity with
gastroenteritis. scarring. Constrictive pericarditis must be differentiated
from restrictive cardiomyopathy (page 5-48) because
Causes of non-constrictive pericarditis:
the signs and symptoms can be similar.
Idiopathic (90%), probably viral
(Again: Although constrictive pericarditis is often

Tuberculosis quickly treated with good results, restrictive cardio


Connective tissue diseases myopathy is not reversible.)
Sepsis

2014 MedStudy
5-56 PERICARDIAL DISEASES

Constrictive pericarditis may follow: component ofHF, and BNP levels are markedly elevated
(e.g., 8x max normal). With constrictive pericarditis,
Viral or idiopathic pericarditis
there is little or no actual HF, and BNP levels are
Traumatic hemopericardium
typically just above normal.
Tuberculosis
Cardiac surgery
Mediastinal irradiation
RECURRENT PERICARDITIS
Purulent infection Recurrent pericarditis is a condition in which the only
Histoplasmosis disabling problem is the associated chest pain. It does
not progress to constrictive pericarditis. It is only rarely
Rheumatoid arthritis
associated with arrhythmias. Treat with NS AIDs,
SLE
colchicine, and glucocorticoids. Pericardiectomy often
Neoplastic disease (especially breast cancer, lung
does not have good results and is tried only after medical

cancer, and lymphoma)


treatment options have been exhausted.
Chronic renal failure with uremia treated by chronic
dialysis
PERICARDIAL EFFUSION
In constrictive pericarditis, ventricular filling is normal
during early diastole but reduces abruptly when the Pericardia! effusion is generally diagnosed with an

elastic limit of the pericardium is reached. echocardiogram, but CT and MRI are the most accurate,
especially if the resultant tamponade is due to localized
Constrictive pericarditis is characterized by rapid, early, pockets of effusion. Surgical drainage is preferable in
diastolic filling of the LV, causing a loud presystolic traumatic hemopericardium, post-surgical effusion, and
knock just after S2. Pulsus paradoxus can occur but is when bacteria or TB is suspected as the cause of tampon
usually mild. ade. On the other hand, pericardiocentesis rarely helps
There are 2 clinical hallmarks of constrictive pericarditis: in diagnosis but is often used to treat viral, idiopathic,
neoplastic, hypothyroid, and renal failure-related tam
Kussmaul sign: When, because the heart is encased
ponade. Pericardia! window biopsy can help diagnose
in a "shell," the negative pressure during inspiration
TB. Sometimes, you need an endomyocardial biopsy
is transferred to the venous inflow tract, resulting
to differentiate constrictive vs. restrictive etiology. If
in a lack of the normal decrease in jugular venous
pericardiocentesis fluid is diagnostic in acute pericardia!
distention (ND) during inspiration. When severe,
effusion in an otherwise normal person, it is normally
ND can increase even during inspiration.
due to a neoplasm! (Read the previous sentence again
Large, right-sided x andy descents. This is seen as a
it's a little tricky.)

brisk collapse of the jugular veins during diastole.


Tamponade [Know!] is a critical cardiovascular
Constrictive pericarditis can cause calcification of compromise caused by a pericardia! effusion. There
the pericardium (-50%). You can see this best on the is obstruction to the inflow of blood to the ventricles.
lateral chest x-ray because it is typically found over the The most common causes are trauma, cancer, uremia,
right ventricle, but you also can see it on the PA view and acute pericarditis. When there is rupture of the free
and on CT. A lateral chest x-ray that shows calcification wall of the heart, as in trauma or post-MI, tamponade
over the right ventricle is pathognomic for constrictive develops quickly; otherwise, it generally develops
pericarditis. slowly.
CT and MRI are best for measuring thickness of
The 3 hallmarks of acute tamponade:
pericardium, but echo is also used. A pericardia! thick
ness of > 5 mm is suggestive of, but not sufficient for, I) Hypotension and muffled heart sounds
diagnosis. The pericardium can be of normal thickness
2) Pulsus paradoxus (systolic BP drops> I 0 mmHg during
in -20-25% of cases of constrictive pericarditis.
inspiration)
In both tamponade and constrictive pericarditis, 3) Jugular venous distention with no collapse during
cardiac cath shows the same pressure during diastole diastole (i.e., an attenuatedy descent)
in all 4 chambers. You can often make the differentia
Tamponade causes soft, distant heart sounds. Compare
tion between tamponade and constrictive pericarditis at
and know the difference between this and constrictive
the bedside using these hallmark signs (see tamponade
pericarditis (above).
below). Constrictive pericarditis must be treated with an
open thoracotomy and pericardiectomy. Unfortunately,
this resolves the problem only 50% of the time!

Brain natriuretic peptide (BNP) plasma levels are being


used to differentiate between constrictive pericarditis
and restrictive cardiomyopathy. BNP increases with
heart failure. With restrictive cardiomyopathy, there is a

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CONGENITAL HEART DISEASE 5-57

Standard treatment had been open surgical closure, but


now most secundum ASDs are closed percutaneously. If
there is a> 2:1 left-to-right (pulmonary/systemic) shunt,
a surgical closure is done, even if the patient is asymp
What are the 2 clinical hallmarks of constrictive tomatic. In this case, the ASD would eventually cause an
pericarditis? increase in pulmonary vascular resistance and associated
complications.
When is the measured diastolic pressure of all
4 chambers equal? Generally, severe, fixed pulmonary hypertension IS

considered a contraindication to surgical repair of


How is BNP used to differentiate constrictive
the ASD.
pericarditis from restrictive cardiomyopathy?

What treatments can be helpful in recurrent


pericarditis? Ostium Primum ASD

Name the 3 hallmarks of cardiac tamponade. This form of ASD is seen most commonly in Down
syndrome. Patients with ostium primum atrial septal
What is the most common congenital
defect may have a loud pansystolic murmur 2 to mitral

abnormality found initially in adults?


and/or tricuspid regurgitation. The regurgitation is due to
True or false? Ostium secundum ASD often has the ostium being low on the septum, interfering with the
right axis deviation and/or RBBB on EGG. function of the AV valves or left mitral valve. ECG has
left axis and RBBB.
When should surgery be performed for a
secundum ASD? Surgery for any type of ASD essentially cures the
problem. Functional Class III/IV patients can revert to
What type of cyanosis would you expect to see
in someone with a PDA?
functional Class I with excellent survival! Eisenmenger
syndrome is a contraindication to ASD surgery.
What is the most common congenital defect
in children?
Sinus Venosus ASD
Sinus venosus ASD is associated with anomalous
CONGENITAL HEART DISEASE pulmonary venous return because it occurs high on the
septum. It is a cause of 10% of ASDs.
NOTE
Most adult patients with congenital heart disease are
PDA
asymptomatic! Know that the magnitude of any shunt does
not depend on the total blood flow rate, but is commonlyly Adult patients with patent ductus arteriosus (PDA)
a constant ratio of pulmonic to systemic flow (Qp/Qs). are usually asymptomatic; females > males. PDAs are
typically discovered early by detection of the distinct
murmur. Endarteritis can occur in PDA.
ASD
PDA causes a continuous, "machinery" murmur at
Ostium Secundum ASD the LUSB. As pulmonary pressures rise, the murmur
Secundum atrial septal defect comprises 70% of all atrial becomes less continuous. Differential cyanosis
septal defects (ASD). It is the most common form of (e.g., clubbed toes, normal fingers) with pulmonary
congenital heart disease found initially in adults (F> M), hypertension is possible.
excluding a bicuspid aortic valve. With a large secun Chest x-ray shows calcification of the ductus arteriosus
dum ASD, there is a systolic ejection murmur at the left in adults.
sternal border (2 to increased flow across the pulmonic
valve), occasionally a diastolic murmur (from increased If the patient develops pulmonary hypertension, consider

flow across the tricuspid valve), and a fixed split S2. The Eisenmenger syndrome (see page 5-58).
left-to-right shunt causes diastolic overloading of the Surgical or percutaneous closure in symptomatic patients
right ventricle and increased pulmonary blood flow with has excellent results. Elderly patients also benefit
inspiration and expiration. from surgery.
ECG shows right axis deviation and/or right
bundle-branch block (RBBB). Chest x-ray shows an PULMONARY STENOSIS
enlarged RV with shunt vasculature. Notice all of the
right-sided stuff with ASD-makes sense because ASD Balloon valvuloplasty is the procedure of choice for

causes a volume load on the right side of the heart. treating pulmonary stenosis. It has favorable long-term

Patients can develop 2 atrial fibrillation. clinical and hemodynamic results.

2014 MedStudy
5-58 PULMONARY HEART DISEASE

VSD Etiologies of sudden death in exercising young people:

Ventricular septal defects (VSDs) are the most common HCM (36%)
congenital defect in children. They are uncommon in Coronary anomalies (17%)
adults because most have either closed spontaneously Possible HCM (8.2%)
or have been surgically closed in childhood. 80% of Myocarditis (5.9%)
small VSDs close spontaneously in the first I 0 years
Arrhythmogenic RV cardiomyopathy (4.3%)
of life. Large VSDs usually require surgery (although
Ion channelopathies including long QT syndrome
even I 0% of these eventually close spontaneously).

([LQTS]; 3.6%)
A loud holosystolic murmur is heard at the left lower
sternal border.
OTHER
Marfan syndrome causes decreased strength of the aorta
COARCTATION OF THE AORTA
(with aortic regurgitation and dissection) and mitral
Know that a bicuspid aortic valve occurs in 50% of regurgitation. Rubella causes congenital pulmonic steno
patients with coarctation of the aorta (COA)! Other sis, PDA, and multiple pulmonary artery stenoses. Cystic
associated anomalies include mitral valve problems, fibrosis can eventually cause pulmonary hypertension.
left ventricular myocardium problems, and membranes
in the left atrium. Notice that all of the heart problems
'
associated with coarctation of the aorta are left-sided! PULMONARY HEART DISEASE
The classic physical findings are either a delayed fem
oral/brachial pulse (feeling the brachial and femoral COPD AND SLEEP APNEA
pulses, there is a distinct delay in femoral pulse) or an
The most common causes of pulmonary heart disease
absent femoral pulse. Patients can have upper-body
are COPD and sleep apnea syndrome. These two are
hypertension and can get hypertensive aneurysmal
covered extensively in Pulmonary Medicine, Book 2, so
dilatation and rupture of the circle of Willis. Look
we will cover the other causes here.
for rib notching on chest x-ray due to the collateral
vessels getting very large and eroding the ribs. Turner
syndrome is associated with coarctation of the aorta EISENMENGER SYNDROME
and a bicuspid aortic valve.
Eisenmenger syndrome occurs in patients with a
large, intracardiac shunt when the pulmonary vascular
ANOMALOUS CORONARY ARTERY resistance becomes greater than systemic vascular
resistance-so, the shunt becomes right-to-left instead
Pre-mortem detection is extremely difficult and requires
of the more normal left-to-right. It is a result of severe
a high index of suspicion. This can present as exertional
pulmonary hypertension, which can develop early (or
chest pain or exertional syncope in a young, otherwise
late) in patients with large, cardiac, left-to-right shunts
healthy individual. Syncope after exercise can occur
of virtually any type: VSDs, PDAs, and ASDs. Cyanosis
in "normal" people, but syncope during exercise is
is common. Heart-lung transplant is the only effective
never normal.
treatment for Eisenmenger syndrome.
With anomalous coronary artery, there is an abnormal
course of I of the 2 coronary arteries between the
2 great vessels, the pulmonary artery and aorta. At rest, CHRONIC THROMBOEMBOLIC
there is plenty of room for the vessel to pass without OBSTRUCTION
compromise; however, in extreme exercise, the cardiac
Chronic thromboembolic obstruction mainly occurs
output can increase 4-8-fold. This expands the elastic
as a result of impaired fibrinolytic resolution of acute
pulmonary artery and aorta, resulting in compression
thromboembolism, leading to organization, incomplete
of the coronary artery as it courses between the great
recanalization, and chronic obstruction of the pulmonary
vessels. This compression creates coronary ischemia
vascular bed. Most patients treated for acute pulmonary
and arrhythmias.
thromboembolism do not develop chronic pulmonary
hypertension. Chronic thromboembolic obstruction
SUDDEN DEATH IN EXERCISING is also the result of other causes of secondary pulmo
nary hypertension such as large left-to-right shunts and
YOUNG PEOPLE
chronic LVF.
The most common cause of death in exerctsmg
Progression of this disease probably results from the
young people is HCM (36%). Next most common are
pulmonary arteriolar changes (instead of more PEs);
coronary anomalies (17%)-although this is a more
these are similar to the changes that develop with
likely cause in the 30-40-year-old group.
large septal defects. The resultant increased pulmonary
Also consider primary pulmonary hypertension as the vascular resistance causes RVF. Surgical removal of
cause in young women. the thromboembolic material results in significant

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PREGNANCY AND THE HEART 5-59

Warfarin is contraindicated in pregnancy due to its


teratogenic effects. It is absolutely contraindicated in
the I st trimester; although, to be safe, most physicians
do not give it at all during pregnancy. Heparin, LMWH,
What are the 2 most common causes of sudden digoxin, quinidine, propranolol, calcium channel
death in an exercising young person? What third blockers, and DC cardioversion are not contraindicated.
cause do you consider in young women? Although heparin is not contraindicated, it does cause
increased morbidity and mortality in mother and child.
What is the only effective treatment for
Eisenmenger syndrome? A maternal rubella infection during pregnancy is
a common cause of supravalvular aortic stenosis,
What are the 2 cardiac-related absolute
contraindications to pregnancy?
pulmonic stenosis, and other congenital cardiac defects.

True or false? Warfarin is not contraindicated


HCM among asymptomatic women is not a

in pregnancy. contraindication for pregnancy. In women with HCM


who are asymptomatic or whose symptoms are controlled
Know how to very quickly determine the axis
with beta-blockers, the beta-blockers should be

of an ECG. Brand Figure 5-7 into your brain!


continued during pregnancy with increased surveillance
for fetal bradycardia, cretinism, or intrauterine growth
improvement. Vena cava filters may be used in patients retardation. In women with HCM and resting or
with deep vein thrombosis (DVT). Anticoagulate. provocable LVOT obstruction (2: 50 mmHg) and/or
cardiac symptoms not controlled by medical therapy
alone, pregnancy is associated with increased risk; refer
PULMONARY ARTERIAL HYPERTENSION
these patients to a high-risk obstetrician.
Note that the terms for this disease are changing.
Most pregnant women experience some pedal edema.
Previously it was called idiopathic pulmonary
F low murmurs and S3 gallops are also common, and the
hypertension (IPH), and before that, primary pulmonary
jugular venous pressure increases. Remember to rule out
hypertension. The World Health O rganization has
both mitral stenosis and secundum ASD in the pregnant
reorganized causes of pulmonary hypertension into
patient presenting with new-onset atrial fibrillation and
5 groups of which !PH is now part of Group 1:
pulmonary edema.
Pulmonary arterial hypertension (PAH).

PAH includes the "sporadic idiopathic pulmonary


hypertension" that commonly occurs in young women,
is refractory, and results in death within 5-10 years.
Treatment: Calcium channel blockers (in patients who
are "reactive" to vasodilator testing) and sildenafil
(Viagra, Revatio) are helpful. Endothelin antagonists
and prostacyclins can also be of use. Heart-lung
transplant is occasionally used.

It is important to differentiate between 1 o and 2 because


surgery may help 2 PAR. A heart catheterization
rules out secondary causes such as right-to-left shunt
and chronic LVF. A perfusion lung scan rules out PE.
Pulmonary capillary wedge pressure (PCWP) is, of
course, increased only in the pulmonary hypertension
caused by, or concurrent with, LVF.

PREGNANCY AND THE HEART

Pregnancy: Absolute contraindications to pregnancy


include PAH and Eisenmenger syndrome (particularly
deadly if cyanosis is present); both are discussed
above. In secundum ASD, aortic stenosis, and dilated
cardiomyopathy, the patient must be closely watched. In
aortic stenosis and dilated cardiomyopathy, patients are
typically kept at bed rest. Secundum ASD patients are
normally not at risk for cardiac decompensation, unless
they develop atrial fibrillation.

2014 MedStudy
5-60 THE 12-LEAD ECG THE ELECTROCARDIOGRAM

THE ELECTROCARDIOGRAM

THE 12-LEAD ECG

F irst, we will briefly go over the basics of ECGs. Refer


to Figure 5-7 as we go through this.

A lead tracing is positive if the wave of depolarization


spreads toward the positive pole of that lead, and it is I &aVL:
Lateral Leads
negative if it spreads away from the positive pole. The
tracing is zero if the wave spreads at a 90 angle to it. For
instance, if II is zero, look for the maximum projection
to be at aVL (either + or -).
THE FRONTAL
With the 12-lead ECG, the wave of depolarization is
LEADS
recorded on both the frontal and horizontal planes and
gives a 3-dimensional representation of the heart. The
projection of the electrical activity of the heart onto
the frontal plane is recorded by the frontal leads I, II, II, III, aVF: Inferior Leads
III, aVR, aVL , and aVF. On the horizontal plane, it is
recorded via electrodes placed in the V l -6 position. Figure 5-7: Axis Determination Diagram
Occasionally, a V3R and V4R (placed same as V3
and V4, except on the right side of the chest) are used
posterior hemiblock(LPHB), RVH, and acute or chronic
to better monitor the right side of the heart (e.g., right
RV overload syndromes such as pulmonary hypertension!
sided ischemia). Depolarization moving toward the lead
embolism, and pulmonic stenosis. If an adult is
causes a positive deflection (P wave and QRS), as does
incidentally found to have RAD, do further workup.
repolarization moving away from the lead (T wave).

The frontal leads give inferior-superior-left-right


information. For example, II, III, and aVF cover the RATES AND INTERVALS
inferior area. ST variations/Q waves occur in these leads
with inferior ischemia and infarction.
The ECG is recorded on paper with a 1 mm2 graph, with
The horizontal leads relay anterior-posterior-lateral a thicker line every 5 mm. Because the paper moves
information. Think of VI as looking at the right side of at 25 mrn!s, each thicker line is 115 of a second-or
the heart while V6 looks at the left side. The QRS in VI 0.2 sec(200 ms), and each mm represents 0.04 sec(40 ms).
is positive when the right ventricle(RV) is depolarizing The interval covering 5 thicker lines (or "big squares")
(and negative when the LV is depolarizing), whereas the is 1 second.
QRS in V6 is positive when the LV is depolarizing.
There are a couple of quick ways to determine the heart
rate. I'll discuss the RR interval, but any prominent
I wave of the standard QRS may be used to determine the
AXIS DEVIATIONS interval. Using a calculator, a quick and accurate method
for determining heart rate is 1,500/RR interval in mm.
The normal mean QRS axis is between -30 and +100. So, if the beat interval is 28 mm, the rate is 1,500/28 =
> +100 is right axis deviation (RAD), whereas< -30 54 bpm. A less accurate, but easier, method is to divide
is left axis deviation (LAD). A quick, fairly accurate 300 by the number of "big squares" in the RR inter
method to determine this is to just look at I and aVF. val. If the beat interval is 28 mm, this is not quite 6 big
If both are prominent, you can quickly tell in which squares. You divide 300 by 6 and get 50, but you know
quadrant the mean vector lies. Visualize the following: the heart rate is actually a little faster because the inter
Both (+) = normal val is not quite 6 big squares. A derivative of this is the
method taught in Dubin's book, Rapid Interpretation
I(+) and aVF (-)=check for LAD
of EKG s, in which you memorize 2 sets of triplicates:
Both(-) extreme right or left axis
300-150-100 and 75-60-50. These match to the heart
=

I(-) and aVF (+)=check for RAD rates corresponding to RR intervals of 1, 2, 3, 4, 5, and
Left axis deviation(LAD) is usually due to left anterior 6 big squares.
hemiblock and, therefore, is a marker for CAD-as are Normal rate is 60-100 bpm. Sinus tachycardia is defined
all fascicular blocks. as a sinus rhythm of > 100 bpm; sinus bradycardia is
Right axis deviation (RAD) is often a normal finding < 60 bpm. So, an RR interval < 3 big squares indicates
in children and young adults. Other causes include left tachycardia; > 5 big squares indicates bradycardia.

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THE ELECTROCARDIOGRAM INTERVALS 5-61

Hypothermia
Type la and III antiarrhythmics (Ia = quinidine,
procainamide; III= amiodarone, sotalol)

More recently discovered causes of prolonged QTc are:


What are the causes of left axis deviation?
Non-sedating antihistamines such as astemizole and
What are the causes of right axis deviation?

terfenadine (since pulled from the market}-their QT


Does RAD always warrant additional workup prolongation tendency can be increased by erythro
in an adult? mycins, some "azoles" such as ketoconazole, and
Name the causes of prolonged QT intervals. hepatic dysfunction.
Yes, all of them that are listed in the text! Drugs such as methadone, phenothiazines,
amiodarone, sotalol.
What are the P wave findings for RAH?
For LAH? Liquid protein diet.

Short QTc can be caused by hypercalcemia and digitalis.


INTERVALS

PRINT ERVAL WAVEFORM S AND SEGMENTS


The PR interval indicates the time between atrial and
ventricular depolarization. Normal duration is 3- 5 small
PWAVE
squares (120-200 ms). Longer than 200 ms (1 big The P wave results from the depolarization of the atrium.
square) is the definition of I 0 AV block. The normal P wave is <2 mm in height and < 120 ms

Shorter than 120 ms (3 small squares) may indicate (3 small squares) in duration, and the normal axis is-50

WPW (delta wave), junctional rhythm (with retrograde to +60 degrees. (Where else have you seen 120 ms? The
normal PR interval is 120-200 ms.) See Figure 5 -8.
P wave-see next), or left atrial overload (widened P
wave-see next). Most information from the P wave can be derived from
II, a VR, and Vl. As the wave of depolarization spreads
from the SA node high in the right atrium and through
QRS DURATION
the right and then left atrial myocardium, the mean
QRS duration is normally < 100 ms (i.e., 1 /2 a big vector is downward and to the patient's left-so the
square). QRS > 120 ms may be caused by bundle-branch normal P wave is positive in II and negative in aYR.
block, ventricular beat/rhythm/ventricular pacemaker,
A retrograde P wave is negative in II and positive in
drugs such as tricyclics, and WPW. I00-120 ms is often
a VR-indicating an ectopic focus originating in the
due to an incomplete 888.
inferior part of the atrium or at the AV junction, result
ing in a wave of depolarization traveling toward a VR
QT INTERVAL (picture this!). A retrograde P wave from the AV junction
often causes a tracing with a short PR interval.
The QT interval corrected for rate is normally
340-4 70 ms depending on gender and age. QTc = QTI Because atrial depolarization traverses from the patient's
(RR)05; that is, the QT interval (in ms or sec) divided right to left, the left/initial side of the P wave represents
by a conversion factor that, although dimensionless, is the right atrium, while the right/terminal side of the
derived from the square root of the beat interval in sec P wave represents the left atrium (mid-P wave is both).
onds. Again: The RR interval in this calculation must be
in seconds. (Consider the difference in dividing by the
square root of0 .7 vs. the square root of700 !) When scan

E1G
ning ECGs, a rule of thumb is: The QT interval normally
Normal LAH RAH
is40% of the RR interval-- do the calculation for QTc if
it appears shorter or longer.
RA LA RA LA RA LA

vI\
With prolonged QT"' there is a tendency to develop
torsades de pointes. II tfT: ----' 1\r-
II'"""
-
1-
Prolonged QTc has many causes:

If1'--
Tricyclic overdose
Hypocalcemia
Vl r h
-
\___.f- --'
f- f-
IV
-

Hypomagnesemia
Hypokalemia
Starvation
CNS insult F i gure 5-8: P Wave in Atnal Enlargement

2014 MedStudy
5-62 WAVEFORMS AND SEGMENTS THE ELECTROCARDIOGRAM

The normal P wave is positive in lead II and positive or Metabolic abnormality


biphasic in V1; when biphasic, the P wave is positive on Intracerebral hemorrhage
the left side and a little negative on the right side. This is
because the wave of depolarization through the atrium is
UWAVE
toward V1 in the right atrium (left side of P wave) and
somewhat away from V1 in the left atrium (right side of The U wave occurs just after the T wave. It is commonly
P wave). small and is best seen in V2-3. If seen, it is usually a
< 1 mm, rounded deflection in the same direction as the
With right atrial preponderance, (enlargement,
T wave. If the U wave is prominent, there is an increased
hypertrophy, overload), the right atrial (initial) portion of
tendency for torsades de pointes. Prominent U waves
the P wave is widened, and therefore overlaps onto the
are present with hypokalemia, bradycardia, digitalis,
left atrial portion of the P wave. The P wave width stays
and amiodarone.
normal (< I20 ms), but look for an increased P wave
amplitude in II (also III and aVF, but just look at II) and Negative U waves are considered significant-even
in VI (the positive portion). Actually, the P wave being if the rest of the ECG is normal! Causes are ischemia,
"peaked" in II is more important than it being tall. HTN, AV valve disease, and RVH. Negative U waves
occur in up to 60% of patients with an anterior MI, up
Decreased P wave amplitude is seen in severe
to 30% of patients with an inferior MI, and up to 30% of
hyperkalemia.
angina patients.
With left atrial overload, the right side of the P wave is
enlarged, resulting in a wide P wave with a shortened
ST SEGMENT
or absent PR interval (i.e., < 120 ms). Other typical
findings are a widened notched P wave in II and an There are 3 main causes of ST-segment elevation: acute
enlargement of the negative portion of the P wave in V1. MI, Prinzmetal angina, and pericarditis. It may also
The most sensitive ECG finding for left atrial enlarge be present with early repolarization variant, intracere
ment is a negative P wave in VI, with a duration of bral hemorrhage, hypertrophic cardiomyopathy, LVH,
> 40 ms (1 small square). On the other hand, the most LBBB , cocaine abuse, myocarditis, and hypothermia.
specific ECG finding is a notched P wave (usually in II)
ST-segment depression occurs with:
with an interpeak distance of> 40 ms.
Subendocardial ischemia (especially if downsloping
COPD: B ecause of the hyperexpanded lungs, the heart
or flat), such as seen in classic angina.
assumes a more vertical position, and there is resultant
ST depression in V1-2 with an acute posterior MI.
RAD of the P wave. A +90 P wave axis is highly sug
R eciprocal depression in V1-2 with some inferior
gestive of COPD. The pulmonary hypertension may

wall Mls-especially those with lateral or posterior


result in right atrial preponderance with associated
extension. There may also be reciprocal ST depres
P wave changes (see previous discussion).
sion in inferior leads with some anterior/septal Mis.
LVH with LV strain (ST depression with flipped T
TWAVE waves in precordial leads).
The T wave is ordinarily in the same direction as the Isolated RV infarction, when there is ST elevation in
QRS, indicating that repolarization is actually occurring Vl and ST depression in V2.
in the opposite direction of depolarization. RVH that may cause RAD and ST-segment
depression preceding a flipped T wave in VI.
Peaked T waves are sometimes associated with the
following: Digitalis toxicity.
Hypokalemia.
Hyperkalemia
Hyperacute MI
QRS COMPLEX
Intracerebral hemorrhage
In septal leads (V1-2) in evolving post-MI In QRS complex, depolarization of the ventricles
occurs simultaneously after the depolarization of the
Focal-flipped T waves may accompany: interventricular septum. The normal mean vector of
Ischemia depolarization of the interventricular septum points
V1-2 with RBBB , RVH, and RV HTN from the patient's left to the right across the septum. You
see this as a small initial deflection, which is positive in
VI-2 with LVH
V1 (R wave) and negative in V6 (Q wave) (Figure 5-9).
L ateral leads (I, aVL , V6) with LBBB
The precordial leads with LVH with "strain" The left ventricle is normally much more massive than
the right ventricle; therefore, the mean QRS vector
Diffuse flipped T waves may accompany: (reflecting depolarization of the ventricles) is strongly to
Pericarditis the patient's left. You see a large negative deflection in
VI and positive deflection in V6. On the frontal plane,
Diffuse ischemia ; post-resuscitation

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THE ELECTROCARDIOGRAM VENTRICULAR HYPERTROPHY 5-63

E& Normal LVH RVH

~
~ 1-s
When are peaked T waves seen? VI
Sand Q
When are focal-flipped T waves seen? variable

U waves indicate a predisposition to what


serious condition?

L+
R
What is the significance of a negative U wave?

What are the common causes of U waves?

j:

Name the 3 main causes of ST-segment


elevation. V6

G
What are the causes of ST-segment
depression?

R
Figure 5-9: Ventricular Hypertrophy
What are the ECG criteria for LVH? RVH?

V
In LBBB, the left side of the septum depends on
what to depolarize? to check the PR interval-you might be looking at a
delta wave in WPW!

d
as mentioned above, the mean vector is between -30 Although the specificity of the various ECG criteria

e
and +I 00 degrees. for LVH is quite high at 95%, the sensitivity is low

t
and varies from 25% for the above criteria to 50% for
The normal duration of the QRS is< 100 ms.

i
a complicated point system. Note that if the prevalence
QRS changes seen with ventricular hypertrophy and of LVH in a population is 5%, there are many more

n
conduction disturbances are discussed next. false negatives and many more false positives than true
positives, making this fairly useless as a screening test.

U
(Go and work this out using the Bayesian 4-square!
VENTRICULAR HYPERTROPHY Population I 0,000; sensitivity = 25%; specificity =

95%; find all the other numbers. Answer: TP 125, FP

-
=

LVH = 475, FN = 375, TN= 9,025; PPV = 2 1% [not good!];


LVH (left ventricular hypertrophy) causes a prolongation NPV = 96%. Statistics are covered in General Internal

9
of activation of the myocardium. It is thought that rela Medicine, Book 5.)
tive coronary insufficiency (increased muscle mass > When there is left axis deviation, the ECG criteria for

ri 9
increase in size of the capillary bed) may be a factor LVH change! Use: SIII> 15 mm (Rosenbaum).
in this prolonged activation. Another factor may be
A left ventricular "strain" pattern may be present with
the overgrowth of the muscle mass relative to the
LVH. LV strain is precordial ST-segment depression and
Purkinje system.

h
flipped T waves seen in a patient with ECG criteria for
This prolongation of activation, in addition to moving LVH.

ta
the mean QRS axis more posterior, superior, and to the
left, also results in a reversal of repolarization, which
now proceeds from the endocardium to epicardium, RVH
and is reflected by a flipped T wave in the septal leads Because RVH (right ventricular hypertrophy) is such an
(VI-2). abnormal condition, with the mass of the right ventricle

LVH causes an exaggeration of the negative deflection increasing to the point of shifting the mean QRS vector

in VI and the positive deflection in V6. There are sev to a right axis, the specificity for RVH is very high when
eral accepted ECG criteria for LVH, including: SV 1 + ECG criteria are met-although, as with LVH criteria,
(RV5 or RV6) > 35 mm or (RV5 or RV6)> 25-35 mm. the sensitivity is low.
This is read "the S in Vl +the R in V5 is> 35 mm," etc. ECG criteria for RVH are right axis deviation and,
(Figure 5-9). again, because of repolarization changes, ST-segment
The diagnosis of LVH is strengthened by an intrinsicoid depression and a flipped T wave in VI, sometimes in
deflection of > 50 ms ( 1.25 small squares). This is the V2. The ST-segment depression and flipped T wave
time from the beginning of the QRS complex to the generally indicate RV stress/hypertension (Fig ure 5-9).

peak of the R wave. For greater ease of use, intrinsicoid Pulmonary embolism (PE): Note that with acute,
deflection is often called the "R peak time." Note: When severe pulmonary embolism (acute cor pulmonale),
you notice an obvious intrinsicoid deflection, make sure ECG changes are reflective of acute RV strain with RV
and RA dilation +/- ischemia. There is often a R BBB,

2014 MedStudy
5-64 CONDUCTION DISTURBANCES THE ELECTROCARDIOGRAM

sometimes RAD, and usually clockwise rotation. LBBB


Because these are all nonspecific findings, and because
Left bundle-branch block (LBBB): The QRS is
of the changing nature of this event, the most important
prolonged with a duration of 120--180 ms (3-4.5 small
factors that increase sensitivity of the ECG in the setting
squares). Because the left ventricle depolarization is now
of possible PE is a prior ECG tracing for comparison
transmyocardial, it is depolarized over a longer period,
and serial tracings after admission. S l Q3T3 pattern
resulting in an RR' (notched or slurred) in the lateral
(S wave in lead I, Q wave in lead III, and an inverted
T wave in lead III) is an indication of RV strain and is a leads (I, aVL, and V6), and there is a corresponding SS'
specific, but not sensitive, indication for acute PE. (also called QS) in VI. 112 of patients have a normal
axis, l/2 have LAD (-30 to -90).
The T wave vector and sometimes the ST segment are
CONDUCTION DISTURBANCES opposite in direction to the mean QRS vector in LBBB.
Therefore, as illustrated in Figure 5-l 0, you see nega
AVBLOCKS tive T waves following the positive RR' in I, a VL, and

G
Atrioventricular (AV) blocks are due to conduction V6-and positive T waves following the negative QRS
disturbances at the AV node. Know the 3 degrees and in Vl-3.

R
their patterns. Important note: In LBBB, the left side of the septum
151 degree AV block prolongs the PR interval by depends on myocardial conduction to depolarize; hence,

V
> 200 ms ( l big square). conduction is slow over the left side and depolariza
tion progresses from right to left, causing an rS or QS
251 degree AV block results in 2 main patterns:

d
in V l . This right-to-left depolarization of the septum
Mobitz I, Wenckebach phenomenon: progressive pro overcomes the expression of any septal Q waves with an

ti e
longation of the PR interval until there is a dropped MI-including the inferior leads. So, just as new septal
QRS (ventricular beat). Q waves do not appear in a patient with LBBB and an
Mobitz 2: Normal PR intervals, but periodically there acute MI, MI-related septal Q waves disappear if LBBB
is a dropped QRS. 2: l AV block is 2 P waves for each develops because of the MI. Therefore, LBBB makes

n
QRS, 3: l is# of P waves for each QRS, etc. Mobitz it impossible to use the ECG as an evaluation tool in a
2 almost always has a wide QRS complex (if narrow, patient you suspect of having an MI.

U
typically Mobitz 1). Criteria for LBBB:
3rd degree AV block: No depolarizations are conducted

-
QRS 120--180 ms (3-4.5 small squares).
=

through the AV node. The P wave and QRS have inde The left ventricle is depolarized, later resulting in an
pendent regular rhythms (AV dissociation). If the QRS RR' (slurred or notched) in V6 and an SS' (QS) in VI.

9
complex has a normal width (< I00 ms), there is a junc The T wave is often opposite the mean QRS vector in
tional ectopic pacemaker. Junctional pacing rate is 40--60
anteroseptal and lateral leads.

9
bpm, whereas ventricular pacing is 20-40 bpm. Note:

ir
The AV node has no pacemaker activity. Junctional Incomplete LBBB fulfills the above criteria, except QRS
pacing originates from the myocardial tissue at the AV < 120 ms.
junction. (It may be near the AV node, but it is not a part

h
of the AV node!) RBBB

a
Right bundle-branch block (RBBB): The direction

t
BUNDLE-BRANCH BLOCK of septal depolarization is normal-left to right, but
Overview
Just a little after the AV node, the fast conduction Normal RBBB LBBB
pathway, known as the bundle of His, splits in two. These
E

f. t \"(:
2 fast conduction pathways travel down the interven
tricular septum, and one then goes to the right ventricle, VI
while the other one-functionally if not anatomically
splits again and proceeds to the anterior and posterior
( )
sections of the left ventricle. If conduction in one of these
pathways is blocked, the depolarization downstream to

j:_ ~
+
that pathway is delayed because the myocardial tissue
in that area can then be depolarized only via the depo
V6
larization wave from much more slowly conducting
adjacent myocardial tissue. Refer to Figure 5-10.

F i gure 5-10: Bundle-Branch Block

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THE ELECTROCARDIOGRAM ARRHYTHMIAS 5-65

LPFB

Left posterior fascicular block (LPFB) or left posterior


hemiblock (LPHB): This problem is rare, and the ECG
pattern is rather nonspecific because you can also see
What do you see on an ECG in LBBB? RBBB?
it in patients with RVH, lateral infarction, and emphy

What is so serious about a recent Ml and the sema. You can be sure that it is a LPFB only if it is a
development of a bifascicular block? recent change-all else being the same. The septal
depolarization is left to right but directed superiorly,
What is the difference between an ectopic beat
causing a small Q wave in the inferior leads. Because
and an escape beat?
final depolarization in the heart is in the inferior and
posterior walls with the vector pointing inferior and to
the right ventricle is depolarized over a longer period, the right, there are large R waves in the inferior leads (II,
resulting in an RR' or RSR' ("rabbit ears") in V1 and an III, aVF) and large abnormal S waves in the lateral limb
S wave in V6. Visualize how the RSR' in V l is formed: leads (I, aVL). This also results in a mean QRS axis of

G
m
The initial R wave is due to normal left-to-right septal +80 to + 140. The T wave is normal. (")
depolarization, the S is depolarization of the left ventri G)
til
Criteria for LPFB:

R
cle, and the final R' is due to the delayed depolarization
of the right ventricle. In V6, the S wave is due to delayed Small Q and large R (qR) waves in II, III, and aVF
depolarization of the right ventricle. Small R wave in I, followed by a large S wave in I,

aVL
The T wave is usually negative in VI, sometimes in V2.

d
Rightward axis ( +80 to +140)
Criteria for RBBB:

ti e
QRS > 120 ms (3 small squares). Bifascicular Block
Depolarization of the right ventricle is delayed, result
Bifascicular block has 3 presentations:

ing in an RSR' ("rabbit ears") or RR' in V l and often


I) Complete LBBB

n
a slurred S wave in V5-6.
Flipped T waves in VI, sometimes V2. 2) RBBB + LAFB
3) RBBB + LPFB

U
Incomplete RBBB fulfills the above criteria, except QRS
< 120 ms. The last is the least common. Anterior MI and calcific

-
aortic stenosis are associated with bifascicular block.
LAFB Remember that acute MI + a new bifascicular block
indicate a high risk for progression to complete heart

9
Left anterior fascicular block (LAFB) or left anterior
block.
hemiblock (LAHB). QRS duration is 100-120 ms.

ri 9
Septal activation is in a left-to-right (normal) and infe
rior direction. This inferior septal depolarization is WIDEQRS
sometimes reflected in a Q wave in the lateral leads (I
Wide-complex QRS may be caused by BBB, ventricular
and aVL). Because the last part of the heart to depolar origin of the complex, and/or aberrant conduction.

h
ize is the left posterobasal to anterolateral wall, the mean
More on this is discussed next and under the previous
frontal QRS vector has a left-facing axis (-45 to 0).

ta
Arrhythmia topic on page 5-38.
This also causes lead I to record a large R wave and the
inferior leads to record a large S wave. Left axis devia
tion (LAD) more negative than -45 with a normal QRS
duration is nearly always due to LAFB. Actually, LAFB ARRHYTHMIAS
is the component that causes the LAD in 1/2 of patients
with LBBB. ECTOPIC vs. PACEMAKER

Criteria for LAFB: An ectopic beat occurs from an ectopic (abnormal) focus
earlier than the expected next beat. It may originate in
Left axis deviation (LAD) -45 to -90, with a large
the atria, AV junction, or the ventricle.

S wave in the inferior leads (II, III, and aVF) and a


dominant R wave in I Throughout the heart are foci of cells with pacemaker
capability, which can take over if there is a delay in
Absence of other causes of LAD (incomplete or
depolarization, such as when the SA node ceases to
complete LBBB)
function normally or there is a severe conduction
Poor R wave progression across the precordium
disturbance. Atrial, non-SA node pacemaker activity
has an inherent rate of 60-80 bpm. AV junction (not
AV node!) pacemaker rate is 40-60 bpm. Ventricular
pacemaker rate is 20-40 bpm (idioventricular rhythm).

2014 MedStudy
5-66 MYOCARDIAL INFARCTION THE ELECTROCARDIOGRAM

Note that ectopic beats are different from escape/ VENTRICULAR ECTOPIC BEATS
pacemaker beats. Ectopic beats are early. Escape beats
AND HEART BLOCK
are at the rate of inherent pacemaker activity.
Premature ventricular contraction (PVC):

TheQRS complex occurs earlier than expected


ATRIAL ARRHYTHMIAS

(premature), is wider than normal, and has a higher


Atrial fibrillation: amplitude than normal.
No P waves: "irregularly irregular" rhythm P wave is obscured in theQRS complex.
Clinically: varying pulse pressure and no a waves T wave is inverted.
The next RR interval is longer than normal. This is
Atrial fibrillation is the result of multiple ectopic foci
called a full compensatory pause. The SA node is not
firing continuously or disorganized atrial activity. It is
reset by the ventricular depolarization-hence, the
thought to be due to a micro-reentry mechanism. No
P waves march out normally.
P waves are seen, although there is loud, chaotic atrial

G
"noise" throughout the tracing. A ventricular escape beat may occur if the sinus pause
is long enough, and no atrial or junctional pacemakers
Atrial flutter ( Type 1):
kick in.

R
High atrial rate: characteristic rate 300 bpm
Complete (3rd degree) heart block has an atrial beat
(range 240-340), typically with a 2:1 AV block
marching independently of a junctional or ventricular

V
Sawtooth formation
escape beat. Remember junctional = narrow, 40--60 bpm.

Whole number ratio of flutter waves toQRS

d
Ventricular = wide, 20-40 bpm. Medication and certain

complexes
illnesses can affect these rates.

ti e
Atrial flutter is due to a wave of depolarization repeatedly Study tip: Now is a good time to review ventricular
going around and around the atrium-usually with an tachycardias vs. aberrant conduction. See the discussion
anatomic obstacle, such as an AV valve, in the pathway. on page 5-43.
This results in the "sawtooth"-appearing P wave with

n
an atrial rate of 300 bpm (but it varies between 240
and 340 bpm). There is commonly a 2:1 or 3:1 AV MYOCARDIAL INFARCTION

U
block with a resulting ventricular rate of 150 or 1 00,
respectively. COMMON FINDINGS

-
There is also a Type II atrial flutter with a much higher
[Know this section!] Common findings in myocar
atrial rate: 340-440 bpm.
dial infarction: Within the first minute or so of acute

9
Wandering pacemaker is exactly what the name ischemia, the T waves flip. After 1-2 minutes, they
implies. The pacing impulse migrates from one atrial become positive and peaked (hyperacute). Then injury

9
pacemaker focus to another. It is a benign condition to the cells occurs, causing the S T segment to elevate.

r
seen mostly in young people-especially athletes. The Q waves are associated with cell death. These associa

i
varying focus is reflected by varying shapes of the tions of ECG changes with the actual pathophysiologic
P wave. processes are somewhat artificial, but clinically useful.

h
Multifocal atrial tachycardia (MAT) is similar to Again:

ta
wandering pacemaker, except that MAT occurs at
a higher rate with more chaotic switching between 1) T wave changes (ischemia), then
pacemakers. MAT is associated with COPD, hypoxia, 2) S T-segment changes (injury), and then
digitalis, theophylline, severe hypokalemia, and 3) Development ofQ waves (cell death)
hypomagnesemia. Atrial rate is 100-130 bpm. The
rhythm is "irregularly irregular."
LOCATION OF Ml vs. ECG CHANGES
Sinus pauses result in a long TP interval. An
Left ventricle:
ectopic escape beat (different P wave) may pre
cede the resumption of the rhythm. If an atrial Septal MI = changes in V1-2
pacemaker takes over the rhythm, the rate is usu Anterior MI =V3-4
ally 60-80 bpm. If a junctional pacemaker focus Anteroseptal MI = V1-4
takes over the rhythm, this is termed a "junctional
Lateral MI=I, aVL, V5, V6
(escape) rhythm." With a junctional rhythm, there
Anterolateral=I, aVL, V3-6 (if V1-6=extensive
is a change in the P wave-it may not be visible
anterolateral MI)
or it may be a retrograde P wave very close to the
Inferior MI II, III, aVF
QRS (short PR interval). Junctional rate is normally
=

40-60 bpm. Apical MI =II, III, aVL and any of V1-4

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THE ELECTROCARDIOGRAM REMEMBER ... 5-67

REMEMBER ...

These ECG changes [Know!]:

o What are the ECG findings with A-fib? o Diffuse, inverted T waves: ischemia, pericardi
tis, drugs, metabolic abnormality, and CNS insult
o What are the ECG findings with MAT?
(intracerebral hemorrhage).
o What are the ECG findings with a PVC?
o Prolonged QT: drug effect (quinidine, sotalol,
o Describe the sequence of ECG changes with dofetilide), hypocalcemia, hypomagnesemia, and
the different phases of an MI. CNS insult. This is a precursor to torsades de pointes.

o What ECG changes occur with a septal Ml? o Peaked T waves: hyperkalemia. (If severe, ECG looks
Anterior? Lateral? Know all these! like a sine wave.)
o Large U waves are associated with hypokalemia,
o What conditions can cause diffuse inverted
bradycardia, and digitalis toxicity.

G
T waves? m
o A low-voltage ECG tracing is associated with pericar 0
G')
o What conditions can cause a prolonged QT? dia! effusion, hypothyroidism, obesity, and COPD. (/)

R
o What type of Ml is AV node dysfunction o AV node dysfunction is associated with an inferior MI
associated with? What about bifascicular block? and with digitalis and verapamil toxicity.

V
o What conditions cause resting ST elevation? Bifascicular block, in contrast, is associated more
with anteroseptal MI and calcific aortic stenosis.

d
What causes ST-segment elevation during a stress
o Posterior MI =tall R in Vl -2; ST depression in Vl -2
test? Stress-induced coronary artery spasms.

ti e
o High lateral MI = I, a VL
What causes resting ST elevation?
Right ventricle: o Acute MI
o RV infarction is best determined by placement of the o Post-MI wall motion abnormalities in the

n
right precordial leads. ST elevation in V4R to V6R infarcted areas
is fairly sensitive and specific for RV infarction o Spontaneous spasm of the coronary artery

U
( 90% each). It is diagnostic of RV infarction if the o Pericarditis
ST elevation is greater in V4R than in Vl -3.

-
o With the standard ECG, suspect an RV infarction if,
with an inferior infarction, there is also ST-segment ANALYSIS
elevation in V1-2. Also be suspicious in the instance

9
where you see ST-segment elevation in VI, along Analyzing the ECG:
with ST-segment depression in V2!

ri 9
First, check the rate and rhythm. Next, check the
intervals-especially the PR, QRS, and QT. Then, check
NOTES waveforms.

With acute inferior MI, there may be reciprocal ST The ECGs on the following pages give you a little practice.

h
depression in septal leads (Vl -2). With an anterior/septal
Figure 5-11 provides a memory aid for ECG
MI, there may be reciprocal ST depression in the

ta
interpretation. This memory aid is copied below each
inferior leads.
ECG on the following pages.
The trick for reading the ECG with a suspected acute
Table 5-14 and Table 5-15 summarize the information in
posterior MI is to hold the ECG upside-down and back
the ECG section of the text.
wards, while holding it up to a light to see the tracing.
Study Vl-2. A posterior MI assumes the morphology of Study tip: To the top left of each ECG is the presenting
other Mls with this trick. (R waves look like Q waves information. The bottom-left notes are the main find
and ST depression appears to be ST elevation.) ings. So do not look at the bottom information until you
have done your reading of the ECG!
Posterior MI is often associated with inferior- and
lateral-wall Mis. So, if you see either of these, look
closely for signs of a posterior MI.

Signs of acute infarct and ischemia signs may be


obscured by LBBB, WPW, HCM, and ventricular
pacemakers.

2014 MedStudy
5-68 ECG INTERPRETATION

Rate
QTc
=

=
I ,500/#mm or 300/#large squares
QT/j(R-R)
E18
Waveforms:
Rate ------
Pwave -------
QRS voltage
Rhythm
___
_______

QRS axis/shape ___

Rwaves ------

G
Intervals: PR -------
ST segment
QRS
_______
____

Twaves

R
QTc ____
-------

u waves ------

V
Figure 5-11: Memory Aid for ECG Interpretation

d
ti e
Un
-
Table 5-14: ECG Summary Table (1 of 2)

Normal Abnormal Common Causes

9
Heart Rate 1 )HR <60bpm
;; - },

ir 9
> 100bpm Sinus tach, A -fb
i with rapid V response, V-tach, SVT

= 1 50bpm Rule out atrial flutter with 2:1 AV Block.

h
Heart Rhythm 2) Rhythm NSR Many Multiple (see text)

a
Intervals l2200 ms < 120 ms Shorter than 120 ms (3 all squares) may indiate:

t
and iv(delta wave)
Durations Junctional rhythm (with'retrograde P wave)
Left atrial overload

l st degree AVblock

wPW if the PR intlfval is shortened


Wntficular ectopy or pacaker
ABerrant conduction (BBB,r
Drugs; tricyclic overdose,(a1so causes long QT)i'\
"' , ' ; m-::s& -"-

340-450 ms > 450 ms Hypocalcemia lengthens ST segment


(men) (men) Hypokalemia (often w/large U waves)
340-470 ms > 470 ms Type Ia (quinidine) and III (amiodarone) antiarrhythmics
(women) (women) Tricyclic overdose (also causes long QRS)
Intracranialbleed (also causes inverted Ts)

, Hypercalemia
Digitalis effects (which also o;ften causes a scooping of the
"
ST segt!lent) )r('

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ECG INTERPRETATION 5-69

Table 5-15: ECG Summary Table (2 of 2)

Waves and Abnormal Common Causes


Segments
6)P wave > 2 mm,> 120 ms Tall, peaked P waves in II suggest right atrial overload
Biphasic in VI and broad and notched in II suggest left atrial overload

Decreased Severe hyperkalemia

7) Q waves In ant or inf leads Acute: More severe MI

8)QRS High LVH (SVI + RV5> 35 or RV6> 25-35)


voltage
Low 1) Pericardia! effusion 2) Tamponade 3) Emphysema 4) Obesity 5)Amyloid

9) QRS axis Right:>+110 Right axis may be seen in:


Left: <-30 I) Normal in children and young adults 2) LPFP (+80 to+ 140)
3) RVH 4) RV overload (pul HTN, PE)
Left axis may be seen in: LAFB and LBBB

G
m
10) R wave 1) lntrinsicoid deflection> 50 ms with some LVH 0
G')
fl)
2) Delta wave with WPW; V1 shows RR' or RSR' with RBBB

R
3) Large R in I with LBBB and LAFB
4) Large R in inferior leads with LPFB

V
5)R in V1, V2 with posterior MI
6) Six causes of Tall R wave in V1: RVH, RBBB, WPW with delta wave,

d
Posterior Infarct, Duchenne's muscular dystrophy, Dextrocardia

II) S wave 1) S wave in V6 with RBBB

ti e
2) Large S waves in inferior leads with LAFB
3) Large abnormal S waves in lateral leads (1, a VL) with LPFB

12)ST segment Elevation 1) Diffuse: acute pericarditis or myocarditis

n
2) Localized means MI, transmural ischemia, or wall motion disorder:
Area involved: 1) Septal= changes in V1-2

U
2)Anterior MI = V3-4
3)Anteroseptal MI = V1-4

-
4)Anterolateral =I, a VL, V3-6
(if V1-6 also, then= extensive anterolateral MI)
5) Lateral MI =I, a VL, V5, V6

9
6) Inferior MI =II, III, a VF

Depression 1) Subendocardial ischemia (esp if downs! oping or flat) such as seen in classic angina

9
2) ST depression V1-2 with acute posterior MI

ir
3)Reciprocal depression V1-2 with some inferior wall Mls-esp. those w/ lateral
posterior extension; also, conversely, reciprocal ST depression in INFERIOR leads

h
with some ANTERIOR Mls
4)Dig toxicity 5) LVH 6)hypokalemia 7) LV strain (ST depression with flipped precordial

a
T waves) 8)RVH with RAD and ST depression preceding a flipped T wave in Vl

t
1 3) T wave Tall, peaked 1) Hyperacute MI (usually with ST elevation and sometimes Q waves)
T hese are followed in time by a more prolonged T wave inversion
2) Hyperkalemia (early sign-followed in time by widened QRS and
deer. P wave, prolonged QRS, and AV conduction problems)
3) Intracerebral hemorrhage
4) Common in Vl-2 with evolving posterior MI

Inverted 1) Post hyperacute MI (see above) 2) Severe ischemia (may have prolonged QT)
3) Post resuscitation 4) Pericarditis
5) Intracranial bleed can cause deep inverted T waves (along with prolonged QT)
6) In lateral leads (I, aVL, V6) with LBBB
7) In septal leads ( VI-2) with RBBB and LVH
8) ln Vl with some RVH (suggests RV hypertension)

14) U wave > 1 mm, I) Indicates increased susceptibility to torsades de pointes


positive (nl) 2) Drugs: Type Ia (usu w/prolonged QT )
3) Hypokalemia: (usu w/prolonged QT)

Negative l) HTN 2)AV valve disease 3) Major ischemia 4)RVH


5) Up to 60% of patients with an anterior MI
6) Up to 30% of patients with an inferior Ml
7) Up to 30% of angina patients

2014 MedStudy
5-70 ECG INTERPRETATION

Case I: A 57-year-old man


with previous myocardial
infarction and chronic \.
r..
Ill'- I- LJ
hypertension on digoxin, I v I I k

beta blockers, and ACEI.

I I VI
II. \. \. '\ J
II v 2

I
j
' I v -;

G
II I I I
J ! ! I I

R
r- I
I

V
Note I'' degree AV block with P-R

d
of 340 ms. Left ventricular hyper Waveforms:
Rate _____ _ _

trophy. Probable early Pwave

e
_____

QRS voltage
repolarization-the sharp S wave Rhythm
___

t
_____ _

QRS axis/shape
in V4-5 enhances the likehood
__

i
R waves _____

of the ST segment being due to Intervals: PR _____

ST segment ____

repolarization. Possible inferior QRS ____

n
T waves _____
QTc
ischemia.
____

U waves _____

Case 2: A 36-year-old man


with history of cocaine abuse

- U I
I

9
and "slow heart rate" since
lA I V\ It\
his teens. I

i r 9
h
I-I ' r--

ta
lA ' II
n

Ill II
r- H
I

Waveforms:
Rate
Note sinus rhythm with Mobitz type
_ ______

Pwave ____

.,---
2 second-degree 2: I AV block. This QRS voltage ___
Rhythm ______

initially looks like Mobitz 2, but QRS axis/shape __

there is a subtle increase in the PR R waves _____


Intervals: PR _____

interval and this also has a narrow ST segment ____


QRS ____

T waves
QRS complex (Mobitz 2 usually has
_____
QTc ___ _

U waves
a wide complex).
____ _

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ECG INTERPRETATION 5-71

Case 3: A 76-year-old man


with chronic heart failure. I
[/\ u [;;; V\ I
!"' IV II 1 u y[ll

I
lA
!--- t-t- f---

y D 11\:1.7 V\ I'
Iii a VI 3 I U Jv,
II

G
m
0
G")
Ill
I I

R
I i'!
I ., IV
I

Note second-degree Mobitz type I


aVR -aVL
Rate _______

d V Waveforms:
Pwave _____

ti e
I QRS voltage ___
(Wenckebach) 3:2 AV block. The Rhythm ______
. QRS axis/shape __
first P wave is visible, the second is Ill
aVF II Intervals: PR _____
R waves __ ___

just peeking out of the previous T ST segment ____


QRS ____
wave, and the third is fused with the T waves _____

n
QTc ____
previous T wave. Possible COPD. U waves ___ __

Case 4: A 36-year-old man


with history of drug abuse h

- U
9
and "slow heart rate" since f--. v
a m v llf 4
he was young.

ri 9
II
Ill Ill IJ
' +-

h
ta
h

I\..
'" a
IV 6

II II I
Ul 1-\. r._ lv L/

.
Waveforms:
aVK . .VL

.
Rate __ _____

Pwave _____
. QRS voltage
_
__

II\>' '
Rhythm ______
QRS axrs/shape
Ill II
aVF Intervals: PR _____
R waves _____

Note sinus rhythm with complete, ST segment _ ___


QRS ____
T waves
3'd degree AV block. QTc ____
_____

U waves _____

2014 MedStudy
5-72 ECG INTERPRETATION

Case 5: A 54-year-old
woman with history of
chronic smoking. ,_., f'-.
a[R v
41v v

I
rv- - -v

,...... r- h r---1-''-r- r- 1-
a iti

R G !1\ !All' ..1.

Rate ________

d V Waveforms:
Pwave _____

ti e
QRS voltage ___
Rhythm _ __ __ _

QRS axis/shape __

Note sinus rhythm with right axis R waves _____


Intervals: PR - ---
deviation and incomplete RBBB .,--- ST segment ____
QRS ____
T waves _ _ _ __

n
consistent with pulmonary disease QTc ____

U waves
pattern. ____ _

Case 6: A 77-year-old man


with a history of chronic

- U I/ I 1/ lA

9
congestive heart failure. r-'
rn I I I
II il !I

i r 9
1\
1-'
1\
I I 1\. j...l 1-J 1'- [\: (

h
a L 2 5

ta h
I'-
1\
\ f- \ 1--'1\. riJ J ""- r- I'- f- I

Note sinus rhythm with complete


LBBB and left atrial enlargement.
This LBBB is a little atypical, but
Waveforms:
notice the large slurred S in the aVR VL
Rate ________
Pwave _____

anteroseptal leads and the T wave QRS voltage __ _


Rhythm
II\;[
_______
opposite the mean QRS in the QRS axis/shape __

III II
anterolateral leads. Also notice the aVF R waves ___ __
Intervals: PR ::------
terminal portion of the QRS in Vl-3 QRS ____
ST segment ____

T waves _____
is slurred-also consistent with QTc _ _ __
U waves ____ _
LBBB.

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EGG INTERPRETATION 5-73

Case 7: A 67-year-old man


with a history of a cardiac
II
1' - 1-
murmur and prior repair of a
congenital heart defect.

.n 1n IT
/"\ I IN IN Ul '-

I. v 2 v IV

G
m
0
(j')
Ill
+- U\V 1,...[\. 1---UVI'- 11\. U\. \-

R
t-
I

aVR L
Rate ______

d V _
Waveforms:
Pwave _____

ti e
QRS voltage

fl\/
___
Rhythm _ _____

QRS axis/shape __

Ill II
aVF R waves _ ____
Intervals: PR _____

ST segment _ ___

QRS _ ___
T waves

n
_____
QTc ____

U waves _ ____

Note sinus rhythm with RBBB.

Case 8: A 77-year-old man


with a history of myocardial fl

- U
9
infarction and recurrent Il l Ill Ill !'-
h

9
syncope.

i r
h
1T 1'/1 II -
1'- !-J'r 1-- 11 fA-f../ L1--- f--..J l.r- \. lr-
r-

h
1-r

ta
I I
v v
II Ill ' Ill
IU II
II

lFf
Il l
II 10

Note sinus rhythm, I'' degree AV


aVR )\9
., VL
il
Rate ______ _
Waveforms:
P wave
.,.-
----
QRS voltage ___

...._/ Rhythm ------


block, RBBB and left ante- QRS axis/shape __

rior fascicular block (bifascicular Ill II


aVF R waves _____
Intervals: PR _____

block). Note also Q waves from VI ST segment ____


QRS _ ___
to V4 consistent with anteroseptal T waves _____
QTc ____

infarct. U waves _____

2014 MedStudy
5-74 ECG INTERPRETATION

Case 9: A 65-year-old man


with recurrent palpitations.

l'l
1"- tIL r4 r----
f-"" 1/
til 1 1' IU

h
lA n
r\ i-
v r--.A\]\ 1-- Jll/1- lr-' Jl V'
v
I a L
Ill V2 Ir 5

II
i-1 V \1! 1: I"- r-'lr' I-"'

h
lA I! lA A II ll)
\. r-- r- fJ\ \. r-- f- i- , 1-'\. f- 1'--r i- Wl
I I

Waveforms:
Rate __ ______
Pwave _____
QRS voltage ___
Rhythm ______
QRS axis/shape __
Note sinus rhythm with frequent R waves _____
Intervals: PR _____

ventricular premature beats ST segment ____


QRS ____

in bigeminy. Note the full T waves _____


QTc ___ _

compensatory pause after the PVC. U waves _____

Case I 0: A 45-year-old man


with a history of rheumatic
I
fever as a child and cardiac I I
R IV II
murmurs. I

:II
lr-'- I

IV

I
II I
1-'
l v:
Lr-. .II
II !av

li I
A ll

Waveforms:
Rate ________
aVR)f7 Pwave _____

QRS voltage ___


Rhythm ______
QRS axis/shape __
Ill II
aVF R waves _____
Intervals: PR ___ __
ST segment ____

Note atrial fibrillation and flipped Ts QRS ____


T waves _____
QTc ____
in the inferior-lateral leads. U waves ____ _

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ECG INTERPRETATION 5-75

Case II: A 44-year-old


man with a history of
I I
J L HJ' 1!.
2-pack-per-day smoking for
15 years.

I
"'' "'r'-o r-<
41' rm' 1---Jr r""1r- f..-

il II

I I n I I
J I.'(\('.N('-,''-f"..N (\... N '\ IJI, !.[.!' Ul
II V3 6

m
0
(j)
I n n n 1n Ill n In (II
'i I'\I'll I'\/'\/I"V"
I '\ii'Y V rvrv1V vvv v IV'VIY v'lv"

Waveforms:
Rate _______
Pwave _____

QRS voltage _ __
Rhythm ______
QRS axis/shape __

R waves _____
Intervals: PR _____
ST segment ____
Note atrial flutter with 4: I block, QRS ____
Twaves _____
vertical axis, and incomplete QTc _ ___
U waves _____
RBBB.

Case 12: A 34-year-old man 1111


I II II Ir--' - (\ I'
with history of palpitations I
\I ,, lu Ill" w
r
since childhood.

rh A I' II
l!-- J r' I L f.-" r-- r- 1'-
v 6
J
a

I I I I
I I. "' J1 .)\
:ir y Ia,iF lv v
I

IM
I r
1-"r
1- f.- 1'-' r- r- r-
:- r--
r

I
Note sinus rhythm, short P-R
interval, and delta wave consistent
with Wolff-Parkinson-W hite
Waveforms:
Rate _______
syndrome. This is one of those avRFt Pwave c-----
ECGs on which you may mistake QRS voltage _ __
Rhythm ______
the delta wave for prolonged QRS axis/shape __

intrinsicoid deflection (as seen with


Il aVF I Intervals: PR =--
- ---
R waves _____

LBBB and LVH) until you check ST segment ____


QRS ____
T waves _____
the PR interval and find it is short! QTc _ ___
U waves _____

2014 MedStudy
5-76 ECG INTERPRETATION

Case 13: A 74-year-old


woman with recent episodes V\. r--
r-- v rv 1"-- hi'"'- r- t'--\1/\.1
I a rll 1 4
of light headedness and
palpitations.

v I !A.
II' III III U; If-

I
a
,J f.1 J;1 6
I'-' Jl

f--1 I Vfll. A -A lA
1r

Note narrow QRS tachycardia with


retrograde P waves evident in
precordial leads VI and V2
Waveforms:
consistent with AV node Rate _______
oVRL Pwave _____
reentrant tachycardia at a rate of
QRS voltage _ __
Rhythm
approximately 150 bpm. Also
______

QRS axis/shape __
pronounced ST-segment depression Ill aVF II R waves _____
Intervals: PR _____

in the inferio-lateral leads-it is ST segment ____


QRS ____

likely that the rapid rate is a factor T waves _____


QTc _ ___

in the ischemia. U waves _____

Case 14: A 71-year-old


man with history of previ
/l I I IJ\ '\ J 1\! '\ 1\ I I II
ous myocardial infarction IV \ I .I II \
and coronary artery bypass
'
surgery admitted for chest
pains and syncope. A lA A 1\
1\ I'I
_/ I \ II J I,JI\ II II II rJ I \ \
:r \ \1 v IJ' \. \1 \ 011 1\,
IV I IV v v

'
I II\ I 1 \o I 'I '\ I \ I 1\
1"\ r II II I II II\ 1\ \ \ 1\
a 6

y II

1\ 1\
I 111 \ 1/\ II\ 1\ ( \I ( \ I 1\ I I' If\
tl 1\ II \ 1\. II I II J \ I IJ \ II \
IV v
ll
v

Note the wide QRS tachycardia


with negative concordance in Waveforms:
Rate _______
the precordial leads consistent Pwave _____

with ventricular tachycardia. QRS voltage _ __


Rhythm ______

QRS axis/shape __
Negative concordance is the QS
R waves _____
pattern throughout the precordial Intervals: PR _____
ST segment ____
leads; there is no hint of R wave QRS ____

T waves _____

progression. QTc ___ _


U waves ____ _

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ECG INTERPRETATION 5-77

Case 15: A 47 -year-old man


with Type I diabetes and II II
' II
chronic renal insufficiency I Ill A .ft)\ r--- nr -JI l t"'1r- '\._ f.l\ 1\ ) ' \ \)
I I hl I V II V II
admitted with diabetic I
ketoacidosis and serum
potassium of7.
II A II A ,il II
I I III II 1\ /I I I' 1\ jl
r:w1'-'Uv 'V uv h 1'-' 1- V "' I '- v

II II lA !
I"' v II '\ ) 1\ ) II\ 1l ) il
II a F rr V6

m
0
G')
I I lA 1 n II lA \A (/)
I 1\ 'I ) I-
lu' w !V il./lr jV' IV M '\J


Waveforms:
Rate _______
" VR VL Pwave ---
.,--
QRS voltage
/1 Rhythm ______
QRS axis/shape
___

__
fl\
Ill
aVF
II
Rwaves _ _ __
Intervals: PR ____
ST segment ___
Note tall and peaked T waves. QRS ____
Twaves __ __
LVH by voltage criteria consistent QTc ____
U waves _____
with hyperkalemia.

Case 16: A 39-year-old


woman successfully I lA
resuscitated from ventricular
rv-
fibrillation with no evidence
of acute myocardial
infarction.
II
f/
J 1--- t"-it
II aVl 2
II 5

I
.A .A lA .I n
In
I

II I

I I
i'-1\Jr-- II- i-VIf-"i'- ,__ [IV JV

Note prolonged QT of 530 and a


"VR L
Rate _______
Waveforms:
Pwave
QRS voltage
____

___
Rhythm ______
QTc of 640 ms. When measuring QRS axis/shape __

Ill II
the QT interval, you must look at all aVF Rwaves ____
Intervals: PR =--
---
the leads and choose the longest QT ST segment ___
QRS ____
Twaves ____
interval-in this case, use lead V2. QTc ____
U waves _____

2014 MedStudy
5-78 ECG INTERPRETATION

Case 17: A 65-year-old man


admitted for pleuritic chest _I J
! I
pains I week following a
bout of flu-like symptoms.

I I
II
!IL II
a L \12

I th h
r- I. rv '" 'I , I"- 1'- I"'H"

WI-

Waveforms:
Rate ________
ote diffuse ST-segment elevations P w ave ,------

consistent with pericarditis. There is QRS voltage _ __


Rhythm _______

QRS axis/shape __
PR segment depression best seen in
R waves _____
II also often seen with pericarditis. Intervals: PR =------
ST segment ____
Also note the concave up ST QRS ____

T waves _____
segment elevation more consistent QTc ____

U waves ___ __

with pericarditis than MI.

Case 18: A 65-year-old


man admitted with a 2-hour
episode of severe retroster
I ! II I
I I r---
tR v: I"-
nal chest pains and shortness
of breath.

IIJ 1'\
v. 1'- I" \.
'U
'I

Ill I I I II I
r-
;v:
I I IJL
H r--

Ill
I ll I! A
hi' ,._, r-

Waveforms:
Rate ________
P wave ----
.,--
QRS voltage ___
Rhythm ______
Note marked ST-segment QRS axis/shape __

elevation in precordial leads R waves _____


Intervals: PR =------

consistent with acute extensive ST segment ____


QRS ____

anterolateral infarction. Associated T waves _____


QTc ____

U waves
T waves are hyperacute. _____

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ECG INTERPRETATION 5-79

Case 19a: An 80-year-old fl J II


:
I II /\
woman is seen in the -
1-Ji \. ..)'f I

rv i1/I u ' ,\.
- ,.>-.!
r--
r
emergency department 3 f--
hours after waking up with
severe retrosternal pressure
and lightheadedness. I I I !
I N'"'- r-. "-f--A l/1 J, Jl Jl
II a\IL V2 Yl5

:
I I
' It
-;;_;r 1"-' r-----'
b -r 1 1'- -'I I'IV,
HI?J
. I
I
m
h 0
I I (j)
I-' I"--f.- f--
Vol\- i-f--' M- 1'-,..-.' v I (I)

ll
I

Waveforms:
Note ST-segment elevations in the Rate _______
P wave ----
precordial leads consistent with .,-
QRS voltage ___
acute anterolateral STEM I. Even Rhythm _ _____
QRS axis/shape __

though the ST segment is mildly


R waves _____
Intervals: PR
concave up, the lack of an S wave
___ __

ST segment ____
QRS
in V 4-5 makes early repolarization
____

T waves ____
QTc
_

U waves
____

unlikely-as does the presenting ____ _

complaint!

Case 19b: 20 minutes I


following infusion of a lr I I lA " r
- }, '7-
I \I II I
thrombolytic, a repeat """II 1vR
r I n
4
-
I'
ECG is performed. I\/
I I'

H- f-- Jo
.lil J- If\. ( II
I I\/ Iii II i aVI!. V2 \1 U VIi II :1 I
'

I
I /j {\
/'1.. 10. '\ "' LLI 1/ I I I
v 6 I'- I'-
i-1 n v v
y U I IV

lr
H- I/\ (\ II II 'II
'- r-
i' ;-,. r-,,.f [---,/ r- 1'-- /I'- I/ r- 1'- ,/I'-
I
Ill
tt f-
f-- f-- I

Shows accelerated idioventricular Waveforms:


Rate ___ ___

rhythm (reperfusion arrhythmia) or


_

P wave ----
,.-
"slow" ventricular tachycardia at QRS voltage ___
Rhythm _____ _

90 bpm. Note change in QRS QRS axis/shape __


duration and axis shift with R waves _____
Intervals: PR _____

retrograde P waves-showing a ST segment ____


QRS ____

V-A association (i.e., the ventricle is QTc


T waves _____

U waves
____

resetting the atrium!). _____

2014 MedStudy
5-80 ECG INTERPRETATION

Case 19c: 90 minutes after


thrombolysis the patient is il I
I n 1--\ nv
f-1 Il r r
r-

pain free.

h ll\ ! II
1\'- t-
a
f"J 1--"- f.--- ...... j fJ""

II
r.. f- !/' v -
I A''F

f"r t- It- 1-"''t-


r'l-
c

Waveforms:
Rate ________
aVR)fL P wave ___
-,-----
_

QRS voltage _ __
Rhythm _______
QRS axis/shape __
Ill II
aVF R waves _____
Intervals: PR ----
A repeat ECG shows significant ,----- ST segment ____
QRS ____
T waves
resolution of the precordial QTc ____
_____

U waves ___ __
ST-segment elevations.

Case 20: A 65-year-old man


II I
with severe epigastric pains,
nausea, and vomiting of
2-hour duration.

A/ n
f.-- " r--.. '""'-/ r'l r-- Jl

A A I
LJI r-
I I v w v

r- I
ll
I

Waveforms:
Rate ________
P wave -,------
ote acute inferior infarction with QRS voltage _ __
Rhythm ______
reciprocal ST segment changes in QRS axis/shape __
the right precordial leads and R waves _____
Intervals: PR ,-----
complete AV block shown by AV QRS ____
ST segment ____

dissociation with an atrial rate of 75 T waves _____


QTc ____
U waves
and a ventricular rate of 40.
_____

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FOR FURTHER READING 5-81

Reeves RA. The rational clinical examination. Does this


FOR FURTHER READING patient have hypertension? How to measure blood pressure.
JAMA. Apr 19, 1995;273(15):1211-1218.
[Guidelines in blue)
Richard C, Monnet X, et al. Pulmonary artery catheter

PROCEDURES, LABS, PHYSICAL EXAM monitoring in 2011. Current Opinion in Critical Care. June
2011;17(3):296-302.
Badheka AO, Hendel RC. Radionuclide cardiac stress testing.
Current Opinion in Cardiology. Sep20 II;26(5):370-378. Sauve JS, Laupacis A, et al. The rational clinical examination.
Does this patient have a clinically important carotid bruit?
Braunwald E. Heart Disease: A Textbook of Cardiovascular
JAMA. Dec 15, 1993;270(23):2843-2845.
Medicine. P hiladelphia, PA: WB Saunders; 2012.
Sharma K, Kohli P, et al. An update on exercise stress testing.
Chotenimitkhun R, Hundley WG. Pharmacological stress
Curr Probl Cardiol. 2012 May;37(5):177-202.
cardiovascular magnetic resonance. Postgraduate Medicine.
2011;123(3):162-170. Turnbull JM. The rational clinical examination. Is listening
for abdominal bruits useful in the evaluation of hypertension?
Conn RD, O'Keefe JH. Cardiac physical diagnosis in the
JAMA. Oct 25, 1995;274(16):1299-1301.
digital age: an important but increasingly neglected skill
(from stethoscopes to microchips). Am J Cardiol. 2009 Aug Yeinot JP. Endomyocardial biopsy-when and how?

15;I 04(4):590-595. Cardiovascular Pathology. 20(5):291-296.

Cooper LT. Baughman KL, ct al. The role of enclomyocardial


Dvir D, Kornowski R. Real-time 3D imaging in the cardiac
catheterization laboratory. Future Cardiol. 20 I0 Jul;6(4): biopsy in the management of cardiovascular disease: a

463-471. sc ientific statement from the American Heart Association, the


A merican Coll<:: ge o i'Cardiology, and the European Society of
Evans DC, Doraiswamy VA, et ai.Complications associated
Ca rdio logy. Circulation. 2007 Nov 6; 11 6( 1 9 ):2 21 6- 2 233.
with pulmonary artery catheters: a comprehensive clinical re
Douglas PS, Garcia M.l. et al. ACCF/ASE / AHA/ASNC/
view. Scandinavian Journal of Surgery. 2009;98(4):199-208.
HFSA/HRS/SCAIISCCM/SCCT/SCMR 2011 Appropriate
From AM, Maleszewski JJ, et al. Current status of
Use Criteria tor Echocardiography. A Rcport of the American
endomyocardial biopsy. Mayo Clinic Proceedings. Mayo
College of Cardiology Foundation Appropriate Use Criteria
Clinic. Nov 2011;86(11 ):I 095-1102.
Task Force. American Society of' Echocardiography, American

Fuster V, Walsh RA, et al. (eels.) Hurst s The Heart, 131h Ed. fleurt Assoc iation Joumal of' the .1merican Society of'Echo

McGraw-Hill, 2010. ml<liographr: ol'ficial pu blicatio n ot'thc American Society of


Echoardiography. 20 II :24(3 ):229-26 7.
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Surawicz B. Childers R. et al. Pan Ill: intnl,cntricular


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Wagner GS, Macrarlanc P, et al. Part VI: acute ischemia/


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LABS ................................................... ............................................... 6- I INFECTIOUS ARTHRITIDES .......................................................6-28


OVERVIEW .................................................................................. 6-1 SEPTIC ARTHRITIS ..................................................................6-28
ANTINUCLEAR ANTIBODIES .................................................6-1 Overview ................................................................................. 6-28
ANA. .......................................................................................... 6-1 Gonococcal Arthritis ............................................................... 6-29
Specific ANA Te sts ................................................................... 6-1 Nongonococcal Arthritis ......................................................... 6-29
ANCA ............................................................................................ 6-2 A cute Rhe umatic Fe ver .......................................................... 6-29
COMPLEMENT............................................................................ 6-3 WHIPPLE DISEASE ..................................................................6-30
RHEUMATOID FACTOR AND ANTI-CCP ............................... 6-4 TUBERCULOUS ARTHRITIS ..................................................6-30
MAJOR HISTOCOMPATIBILITY COMPLEX: HUMAN VIRAL ARTHRITIS .................................................................... 6-30
LEUKOCYTE ANTIGENS ....................................................... 6-4 LYME ARTHRITIS .....................................................................6-30
HLA-B27 ................................................................................... 6-4 LESS COMMON ARTHROPATHIES ....................................... 6-31
HLA -DR2, 3, 4 .......................................................................... 6-4 A dult-Onse t Still's Disease ..................................................... 6-31
ERYTHROCYTE SEDIME TAT!ON RATE AND He mochromatosis Arthritis ..................................................... 6-32
C-REA CTIVE PROTEIN .......................................................... 6-5 Neuropathic Arth ropathy (Neuropathic Joints) ...................... 6-32
THE JOINT ........................................................................................6-5 Hypertrophic Pulmonary Oste oarth ropath y ...........................6-32
SYNOVIA L FLUID AND CRYSTA L ANA LYSIS ..................... 6-5 Post-Streptococcal Reactive Arthritis ..................................... 6-32
IMAGING STUDIES .................................................................... 6-6 OTHER CONNECTIVE TISSUE DISEASES ...............................6-33
GENETIC COLLA GEN DISORDERS ............................................ 6-6 RAYN A UD PHENOMENON .................................................... 6-33
RHEUMATOID ARTHRITIS ............................................................6-6 MIXED CONNECTIVE TISSUE DISEASE ............................. 6-33
OVERVIEW .................................................................................. 6-6 lgG4 RELATED DISEASES ......................................................6-34
SIGNS I SYMPTOMS OF RA ......................................................6-7 ANTIPHOSPHOLIPID SYNDROME............................................ 6-34
EXTRAARTICULAR MANIFESTATIONS ............................... 6-8 SJOGREN SYNDROME.................................................................6-34
TREATMENT OF RHEUMATOID ARTHRITIS ....................... 6-9 SYSTEMIC SCLEROSIS I SCLERODERMA ..............................6-35
NSAIDs ................................................................................... 6-10 TYPES OF SYSTEMIC SCLEROSIS .......................................6-35
DMARDs ................................................................................ 6-10 Diffuse SSe(- 20%) ...............................................................6-35
Biologic Age nts ....................................................................... 6-12 Limited SSe(- 80%) ............................................................... 6-35
Immunosuppre ssants ...............................................................6-13 Systemic Sclerosis Sine Scleroderma ..................................... 6-36
Misce llaneous .......................................................................... 6-14 MANIFESTATIONS OF SSc ...................................................... 6-36
SYSTEMIC LUPUS ERYTHEMATOSUS .................................... 6-14 SSe: Skin .................................................................................6-36
MANIFESTATIONS OF SYSTEMIC LUPUS .......................... 6-14 SSe: Joints ............................................................................... 6-36
SLE: Joints .............................................................................. 6-14 SSe: Muscle s ........................................................................... 6-36
SLE: Skin and Mucous Me mbrane s ....................................... 6-14 SSe: Lungs .............................................................................. 6-36
SLE: Lung ............................................................................... 6-15 SSe: Kidney .............................................................................6-37
SLE: Heart ...............................................................................6-15 SSe: GI ....................................................................................6-37
SLE: Kidney ............................................................................ 6-15 SSe: Heart ................................................................................6-37
SLE: Blood ..............................................................................6-15 TREATMENT ..............................................................................6-37
SLE: CNS (Ne uropsychiatric Lupus) .....................................6-16 EOSINOPHILIC FASCIITIS ...........................................................6-38
DIAGNOSIS ................................................................................6-16 INFLAMMATORY MYOPATHIES ...............................................6-38
SLE AND PREGNANCY ...........................................................6-16 POLYMYOSITIS AND DERMATOMYOSITIS ......................6-38
PROGNOSIS ............................................................................... 6-17 Polymyositis ............................................................................ 6-38
TREATMENT OF SL............................................................... 6-17 Dermatomyositis .....................................................................6-38
DRUG-INDUCED LUPUS ........................................................ 6-17 Antisynth e tase Syndrome ....................................................... 6-39
SERONEGATIVE SPONDYLOARTHRITIS ................................ 6-17 Diagnosis of PM and DM ....................................................... 6-39
ANKYLOSING SPONDYLITIS ................................................ 6-18 Cancer in PM and DM ............................................................ 6-39
Overview ................................................................................. 6-18 Treatment of PM and DM ....................................................... 6-40
Diagnosis .................................................................................6-18 INCLUSION BODY MYOSITIS ...............................................6-40
Treatment .................................................................................6-19 COLCHICINE MYOPATHY INEUROPATHY ........................6-40
REACTIVE ARTHRITIS ............................................................6-19 DRUG-INDUCED MYOPATHY ...............................................6-40
Overview ................................................................................. 6-19 NONARTICULAR RHEUMATISM .............................................. 6-40
Treatme nt.................................................................................6-20 FIBROMYALGIA .......................................................................6-40
lBO-ASSOCIATED ARTHROPATHY ...................................... 6-20 MYOFA SCIAL PAIN SYNDROME .........................................6-41
PSORIATIC ARTHRITIS ........................................................... 6-20 COMPLEX REGIONA L PAIN SYNDROME ..........................6-41
SUMMARY ................................................................................. 6-21 OTHER CA USES OF NONARTICULAR RHEUMATISM ....6-42
OSTEOARTHRITIS ........................................................................ 6-21 VA SCULITIS ...................................................................................6-42
CRYSTAL DEPOSITION ARTHRITIDES .................................... 6-23 OVERVIEW ................................................................................6-42
GOUT........................................................................................... 6-23 LARGE VESSEL VA SCULITIS ................................................6-42
A cute Treatment ...................................................................... 6-24 Overview .................................................................................6-42
Chronic Treatme nt...................................................................6-25 Giant Cell( Te mporal) Arteritis ...............................................6-43
Gout Pearls ..............................................................................6-26 Polymyalgia Rhe umatica ........................................................6-43
CPPD DEPOSITION DISEASE.................................................6-26 Takayasu Arteritis .................................................................... 6-44
HYDROXYA PATITE ARTHROPATHY ................................... 6-27 Aortitis ....................................................................................6-44
MEDIUM I SMALL ARTERY VASCULITIS ........................... 6-44
Polyatteritis Nodosa ....... . . . . . . . ....... . . . . . .............................. . . . . . . . . 6-44
Eosinophilic Granulomatosis with Polyangiitis
(a.k.a. Churg-Strauss Vasculitis) .... . . . . . . . . . . . . . .................. . . . .... 6-45
Granulomatosis with Polyangiitis ......... . . . . . . . . . . . . . . . . . .. . . . . . .......... 6-45
Microscopic Polyangiitis . . ................... . . . . . . . . . . . . . . . . . . . . . . ............. 6-46
OTHER SMALL-V ESSEL VASCULITIDES . . . . . . . . . . . . . . . ............ 6-46
Hypersensitivity Vasculitis ....... . . . . . . ....................... ........ . . . . ...... 6-46
Henoch-Schiinlein P ur pura (lgA Vasculitis) .. . . . . . ...... . . . . . . . . . . . . . 6-47
Cryoglob ulinemia . . ........... . . . . . . ........ . . . . . .............................. . . . . . . 6-47
ANTI-GLOMERULAR BASEMENT MEMBRANE
DISEASE I GOODPASTURE SYNDROME ......................... 6-48
BEH<;ET DISEASE . . . . . . . . ..... . . . . . . . ....... . . . . . .......................... .. . . . . . ... 6-48
RELAPSING P OLYCHONDRITIS .......................... . . . . . . . . . . . . . . . . . 6-49
RHEUMATOLOGIC ISSUES ASSOCIATED WITH
MALIGNANCY AND DIABETES MELLITUS .... . . . . . . . . ............ 6-49
PAGET DISEASE . . . . ........ ................ .. ............ . . . . . . . ....................... . . . . 6-49
AMYLOIDOSIS . . . . . ..................................... . . . . . . . ..................... ... . . . . . 6-49
OFFICE ORTHOP EDICS .......................... . . . . . . . . . . .. . . . . . . ........... . . .. . . . . 6-50
OSTEOPOROSIS ......... . . . . . . ................... . . ........ . . . . . . . . . . . . . . . . . . .......... 6-50
BURSITIS ...... ................... . . . . . . . . ....... . . . . . . . . . ............ . . . . . . . . ............... 6-50
JOINT PAIN ....... . . . . . . . . . . . .. . . . . . . ........ . . . . . . ................ . . . . . . . . . . . ............. 6-50
Shoulder ....... . . . . . . . . . ................................ ...... . . ................ . . ........ 6-51
Elbow ...... ...................... . . . . . ...................................................... 6-53
Wrist . . . . . . . . . . . ........ . . . ............ . . . . ......... . . . ... .............. ...... ............... 6-54
Hand .................. . . . . . . ........... ............... . . . . . . ..................... . . . . . . . . . . . 6-54
Hip .... . . . .... . . . ....... . . . . . . . . ....... . . . ......... . . . . . . . . ............. . . . . . . . . . ............. 6-54
Knee ................... . . . . . . . . . . . . . . . . . . . . ........... . . . ......... . . . . . . . . ....... . . . . . . . . . ... 6-56
Foot ........... ...................... . . . ..................................... . . . . . . . . ......... 6-57
LOW BACK PAIN . . . . . . . . . . . ...... . . . . . ....... . . . . . . . . . ................................ 6-58
General Approach to Lower Back P ain ............................ ...... 6-58
Muscle Strain ...... . . . . . . . . ...... . . . . ............. . . . . . ....................... . . . . . . . . . 6-58
Disk Herniation ...... . . . . . ........ . . . . ....... . . . . . . . . . . . . . . . . . ........................ 6-58
Spondylolysis and Spondylolisthesis ...................................... 6-58
Spinal Stenosis ......... . . . . ........................ . . . .... ............................ 6-59
FOR FURTHER READING . . ...... . . . . . . . ....... . . . . . . . . ..... .................. . . . . . . . 6-59
LABS 6-1

ANA titers are considered pos1t1ve only if > I:80.


LABS
Titers > I :320 are considered clinically relevant for
autoimmune diseases. Some rheumatologic diseases that
OVERVIEW
are ANA+:
Know everything covered in this topic area about Labs!
o Drug-induced lupus (100%)
If this is your first time through the Rheumatology
o SLE (98-IOO%): Note that ANA-negative lupus is
section, go over this topic several times before you
rare; so ANA is pretty useful for ruling out SLE!
continue. What you learn here will enable you to make
better sense of lab references later in this section. o Mixed connective tissue disease (MCTD; 93-IOO%)
o Limited systemic sclerosis and diffuse systemic
Remember: No single blood test makes any
sclerosis (60-90%)
rheumatologic diagnosis. For example, ANA can be
o Sjogren syndrome (48-70%)
positive in many non-rheumatologic diseases and in
healthy individuals. The key is whether the test results o Polymyositis/dermatomyositis (60%)
match the clinical picture. o Rheumatoid arthritis (RA; 40%)

To interpret a test result, it is important to understand Example of ruling in vs. ruling out: The ANA is positive
the sensitivity and specificity of the test. Sensitivity is in almost all patients with SLE (high sensitivity) but also
the proportion of those with a positive test result among is positive in many other diseases (low specificity). So,
patients with disease; tests that are very sensitive are a negative ANA test is helpful for ruling out SLE, but a
useful for "ruling out" the disease. Specificity is the positive test is poor for ruling it in.
proportion of those with a negative test result among The patterns found with fluorescent staining differ with
patients without disease; tests that are very specific are the various types of ANA patterns. These different ANA
useful for "ruling in" the disease. attack different points in the nucleus, causing various
diseases. We now have tests (below) that identify these

ANTINUCLEAR ANTIBODIES antibodies far more precisely than with fluorescent


staining.
ANA
When the ANA is positive and you suspect a specific
Antinuclear antibodies (ANA) are autoimmune rheumatologic disease, order the more specific antibody
antibodies that attack components of the nucleus. They subtypes (ANA profile). Know which diseases are also
are found in many autoimmune disorders. The most associated with specific subtypes (Table 6-1 on page
common ANA tests: 6-2). Again, the general ANA test is not specific
o Indirect immunofluorescence enough to diagnose any disease, only to rule one out.

o Enzyme-linked immunosorbent assay (ELISA)

Indirect immunofluorescence is more sensitive; ELISA Specific ANA Tests


is less expensive. Anti-clsDNA (in high titer) and anti-Smith (anti-Sm) are

Results are reported as titers (e.g., I:320), with a very specific for SLE. If one or both of these are strongly
particular pattern when positive. positive, the diagnosis of SLE is strongly supported.
However, patients with drug-induced lupus can have
Titers show the dilution at which the antibodies become
antibodies to anti-dsDNA (hence, they are ANA positive
undetectable. It is shown in doublings: I :40, I:80, I:I60,
also).
I :320, I:640, etc.-so, the higher the titer, the more
antibodies in the serum. Anti-U1-RNP is very sensitive for MCTD but not
very specific because it can be seen in SLE and other
Patterns are determined by looking at a specially
connective tissue diseases. In general, absence of the
prepared fluorescent stain slide to ascertain where the
antibody excludes MCTD. Anti-UI-RNP and anti
antibodies attack the nucleus. There are 6 different
dsDNA are often seen together because they bind to
patterns: centromere, rim or peripheral, speckled,
related antigens known as epitopes. An epitope, also
diffuse, homogenous, and nucleolar. While ANA
known as antigenic determinant, is the part of an antigen
patterns may provide some information, they do not
that is recognized by the immune system. The term
identify the specific antibody present, nor are they
epitope is often used interchangeably when describing
specific for any particular disease. The homogenous
an antigenic component of a cell.
and rim patterns can be observed in systemic lupus
erythematosus (SLE). Anti-centromere patterns are The clinical significance of anti-ribosomal P protein
suggestive of anti-centromere antibodies, which are seen antibodies is their specificity for the diagnosis of
with the limited form of systemic sclerosis (formerly SLE. These antibodies have not been found in normal
known as CREST-calcinosis, Raynaud 's, esophageal controls and are rare in patients with other autoimmune
dysmotility, sclerodactyly, telangiectasia). diseases. There are studies suggesting an association
and/or predisposition with CNS and liver disease in

2014 MedStudy
6-2 LABS

Table 6-1: Antinuclear Antibody Disease Assoc1at1ons

Antibody Subclass Associated with:

Specific ANAs Anti-dsDNA Specific for SLE; an indicator of disease activity (as are complement levels)
and identifies SLE eatients with potential fr significant renal dis,ase.
Absent in classic drUg-induced SLE; sometime.s develops in patjnts treated
with TNF inhibitors.

Anti-Sm Specific for SLE.

SSA(Ro) SLE, neonatal SLE; Sjogren's, and sometimes myositis. Usually not found
in scleroderma; passively transferred from mother to baby --+neonatal heart
block. DR3 is associated with SSA.

SSB (La) SLE and Sjogren's; sometimes found in patients with +SSA. Also passively
transferred from mother to baby neonatal heart block.

Anti-Ul-RNP Sensitive for MCTD; also found in SL.e-- usually in association with
" anti-
Sm or anti-dsDNA.

Antihistone Drug-induced lupus and SLE. Mainly used to rule out drug-induced lupus
caused by procainamide, hydralazine, chlorpromazine, and quinidine.

Anti-centromere Limited scleroderma; identifies increased incidence of pulmonary arterial


hypertension and improved survival.
_ __,,..._... .. ; .. . "'

Anti-Scl-70 Progressive systemic sclerosis; identifies increased incidence of interstitial


(Anti-topoisomerase I) lung disease and reduced survival.

, Antisynthetases Anti-Jo-1 = type of anti-synthetase antiboi:ly; associated with myositis;


identifies increased incidence of interstitial lung disease.
Anti- SRP(signal recognition protein) is associated with cardiomyopathy
and refractory to trafi1lent.

lupus patients. Do not confuse anti-ribosomal with specific ANA antibody causing the "speckled" ANA
anti-ribonucleoprotein antibodies (not the same)! pattern found mainly in SLE and Sjogren syndrome.
During the same period, a serum antibody was
Antihistone antibody can be seen both in SLE and
discovered in these patients, which was named anti-SSA
drug-induced lupus. The antihistone antibody test
(or SSA). These 2 antibodies turned out to be the same
is very sensitive (> 95%) for drug-induced lupus
antibody. So, these terms can be used interchangeably
(DIL). Drugs commonly associated with DIL include:
you commonly see them together; e.g., Ro/SSA, SSA
procainamide, hydralazine, chlorpromazine, isoniazid,
(Ro). Similarly, SSB is identical to La and commonly
sulfasalazine, methyldopa, quinidine, minocycline,
seen as La/SSB or SSB (La). The "SS" in SSA and
and anti-TNF agents. The absence of the antihistone
SSB stands for Sjogren syndrome. The most important
antibody effectively rules out DIL in patients taking any
thing to remember about Ro and La is their association
of these agents, with the exception of patients who are
with congenital heart block. Patients with SLE who are
on anti-TNF therapy or minocycline. It is rare to see
pregnant or who plan to become pregnant should be
antihistone antibodies in patients on anti-TNF biologics
tested for Ro and La antibodies.
or minocycline, even though they manifest symptoms
suggestive of DIL. Further information on DIL can be
seen on page 6- I 7. ANCA
Anti-Scl-70 (a.k.a. anti-topoisomerase I) is specific Anti-neutrophil cytoplasmic antibodies (ANCAs) are,
for progressive systemic sclerosis, formerly known as the term indicates, autoimmune antibodies against
as diffuse scleroderma; it is present in - 75% of cases. antigens in the cytoplasm of neutrophils. ANCAs are
Its presence supports a diagnosis of a systemic, diffuse markers for vasculitis, including drug-induced vasculitis
process (not a limited cutaneous one) and is associated (Table 6-2).
with progressive skin involvement, pulmonary fibrosis,
It is thought that the vasculitis may be caused by the
and a higher mortality.
ANCA antibodies, which stimulate the release of lytic
Before going further, let's clarify the terms Ro and enzymes from neutrophils.
La. Anti-Ro (or just "Ro") was the term given for the

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LABS 6-3

rapidly progressive glomerulonephritis (RPGN), anti


GBM disease, and drug-induced ANCA-associated
vasculitis.

The most common causes of anti-MPO+ drug-induced


What two ANA subtypes are specific for a diagnosis

ANCA-associated vasculitis are the anti-thyroid drugs
ofSLE?
propylthiouracil (PTU) and methimazole. Many other
Anti-U1-RNP is a very sensitive indicator for what drugs are much less commonly associated.
rheumatologic disorder?
In summary:
Which antibody is associated with drug-induced
c-ANCA+ plus anti-PR3+: Think GPA.

lupus?
p-ANCA+ plus anti-MPO+: Think MPA, EGPA,
Which drugs are associated with drug-induced Churg-Strauss, pauci-immune RPGN, Anti-GBM, and
lupus? drug-induced.
Which rheumatologic disease is associated The sensitivity and specificity of these antibody tests
with a positive c-ANCA and anti-PR3? are, in general, not high enough for them to be used for
Name 2 diseases that are p-ANCA+ and screening. P retest probability of the disease in question
anti-MPO+. is important and should be considered before ordering
ANCAs.

Two ANCAs are identified by their immunofluorescence


(IF) pattern: COMPLEMENT
I) c-ANCA: Antibodies are diffuse in the cytoplasm. The complement system is comprised of a variety
2) p-ANCA: Antibodies are perinuclear. of small proteins that function to enhance, or
complement, the action of antibodies and phagocytic
cells. Hypocomplementemia is seen in SLE, vasculitis,
These ANCAs can then be subdivided based on
rheumatoid arthritis, and infective endocarditis.
the antigen, or epitope, they are directed against:
anti-proteinase 3 (anti-PRJ; PRJ ANCA) or anti There is more on the complement pathway in Allergy
myeloperoxidase (anti-MPO; MPO ANCA). Laboratories & Immunology, Book 4. But note: Complement
determine these antigens using an enzyme-linked components can be decreased due to a genetic deficiency,
immunosorbent assay (ELISA). This further analysis of consumption during complement activation, or
the ANCA helps you narrow down a diagnosis. underproduction-as in eclampsia or HELLP syndrome
So again, we have 2 ANCAs (c-ANCA and p-ANCA) (hemolysis, elevated liver enzymes, low platelets).

that are further categorized, based on ELISA, into whether


or not antibodies are directed against the PRJ or MPO
antigens. (P roteinase 3 and myeloperoxidase are enzymes
located in neutrophil cytoplasmic alpha granules.)

I) c-ANCA-anti-PR3
2) p-ANCA-anti-MPO Table 6-2: ANCAs

IFANCA ELISA Disease


c-ANCA and anti-PR3 are strongly related while
p-ANCA and anti-MPO are more loosely related.
PR3 antigens usually cause the diffuse pattern seen in
c-ANCA+ IF tests. p-ANCA Anti-MPO+ MPA
EGPA
The combination of c-ANCA+ and anti-PR3+ is very
Churg-Strauss
specific for granulomatosis with polyangiitis (GPA;
Pauci-immune RPGN
previously Wegener granulomatosis). Anti-GBM disease
p-ANCA is less helpful because this IF pattern is Drug-induced; e.g., PTU,
nonspecific. Table 6-2 shows you that many diseases methimazole
are p-ANCA+ (especially in the anti-MPO category).
Further test any p-ANCA+ results with ELISA for
anti-MPO antibodies.

If a patient is anti-MPO+, think vasculitis: microscopic


polyangiitis (MPA), eosinophilic granulomatosis with
polyangiitis (EGPA), Churg-Strauss, pauci-immune

2014 MedStudy
6-4 LABS

Know: MAJOR HISTOCOMPATIBILITY COMP LEX:


C2 or C4--usually a genetic allele deficiency. HUMANLEUKOCYTEANTIGENS
C3 is consumed with any activation of the complement Overview
pathway (classical or alternative).
There are 2 main classes of major histocompatibility complex
C4 is consumed only with activation of the classical
(MHC) human leukocyte antigens (HLA) antigens:
pathway (as with SLE).
CH50 assay measures total hemolytic complement Class I includes the HLA-A, HLA-8, and HLA-C
of the classical pathway and requires all components antigens, which interact with CD8 or T suppressor
(C1-C9) of the classical pathway for a normal result. cells.
Class II includes the HLA-D antigens; e.g., DR2,
The CH50 assay is most useful as a screening tool for DR3, and DR4, which interact with CD4 or T helper
disease states resulting in hypocomplementemia. A cells.
low CH50 should prompt you to order the individual Note: An easy way to remember this relationship
complements listed above to help you in your diagnosis. between MHC and CD T cells is that both form a
For example, patients with recurrent or severe neisserial product of 8-MHCI x CD8= 8, while MHCII x
(meningococcal or gonococcal) infections may have CD4= 8.
terminal complement deficiency (C5-C9). Patients
with SLE may have low C3 and C4; C3 is a more
HLA-827
sensitive index of disease activity in SLE. Therefore,
normalization of individual complement levels and Know when HLA-827 is found:
CH50 can be used to follow disease activity. Reactive arthritis: 60-80%, higher when sacroiliitis
is present.

RHEUMATOID FACTOR AND ANTI-CCP Ankylosing spondylitis (AS): 90%.


Psoriatic arthritis: up to 60% (particularly with
Rheumatoid factor (RF) is an auto-antibody that binds
spinal/axial disease).
to the Fe region of IgG. It is positive in 80-85% of
patients with RA, which makes RF a fairly sensitive Inflammatory bowel disease (IBD) with

test for RA, but it is not specific because a positive associated axial joint arthritis: up to 60%.

RF can be seen in other diseases, including: chronic But there is no HLA-827 association when only

lung disease, chronic infections (e.g., TB, HIV, viral appendicular joint disease is present in IBD patients.

hepatitis), Sjogren's, SLE, infectious endocarditis, and Note that if axial disease is present, HLA-B27 is
hematologic malignancies. typically positive. Keep in mind that 7-8% of the healthy

The anti-citrullinated cyclic peptide (anti-CCP antibody), Caucasian North American population carries this
haplotype; therefore, an individual with HLA-B27 has
however, is highly specific for RA (specificity 97%)
and tends to portend a poorer prognosis. The presence only a I 0-20% risk of developing an HLA-827-related

of both RF and anti-CCP antibodies is associated with disease. Consequently, this test has limited clinical
usefulness if not ordered in the right clinical scenario. A
more aggressive RA and extra-articular manifestations
(e.g., rheumatoid nodule, rheumatoid lung/interstitial negative HLA-B27 test is useful in ruling out ankylosing
spondylitis. See Table 6-3.
lung disease).

HLA-DR2, 3, 4
Table 6-3: lnc1dence of HLA-827 DR2 and DR3 are associated with SLE. DR3
is occasionally found in Sjogren syndrome and
Ankylosing spondylitis 90%
polymyositis. DR4 antigens are associated with severe
Reactive arthritis; typically secondary to 60-80% RA. More in Allergy & Immunology, Book 4.
GU/GI infections
----- Other important general HLA associations to know:
c. jejuni and C. trachomatis arthropathy 50%
1) HLA-85701 is strongly associated with abacavir
50% hypersensitivity reaction (see Infectious Disease,
Book 1).
Healthy Caucasian population 7-8%
2) HLA-851 is associated with Beh;:et disease.
Rheumatoid arthritis, osteoarthritis, 10%
3) HLA-DQ2/DQ8 is associated with celiac disease (see
rubella arthritis
Gastroenterology, Book 1 ).
Although it does not cause reactive arthritis,
Klebsiella pneumoniae has an enzyme (not encoded)
that cross-reacts with the HLA-B27 test.

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THE JOINT 6-5

THE JOINT

S YNO VIAL FLUID AND CRYSTAL

Name 2 diseases that consume complement


ANALYSI S
during a flare.
Synovium and synovial fluid: Type A cells of the
Other than rheumatoid arthritis, a positive RF can synovial membrane are phagocytic, whereas type B
be seen with what other diseases? cells probably synthesize hyaluronic acid. Chondrocytes
What antibody test is more specific than RF for make the cartilage. Cartilage is avascular and depends
rheumatoid arthritis? on the synovial fluid for nutrients. The chondrocytes
can produce only a limited amount of collagen, so only
Compare and contrast "normal," "noninflammatory,"
slight damage is repairable.

"inflammatory," and "septic" joint fluid.


(See Table 6-4.) Joint fluid is categorized based on the inflammatory
response (WBC/mm3). The WBC count in aspirated joint
Describe gout crystals and their birefringence.
fluid decreases rapidly, so analyze it immediately. See

Table 6-4.
ERYTHROCYTE SEDIMENTATION RATE
Also, know that frank blood (hemorrhagic joint) can be
AND C-RE ACTIVE PROTEIN caused by trauma, bleeding diathesis, tumor, and pig
The erythrocyte sedimentation rate (ESR) and mented villonodular synovitis (PVNS).
C-reactive protein (CRP) are the most common acute Look for crystals in inflammatory fluid using the polarizing
phase reactants (APRs; inflammatory markers) used in microscope. Look for monosodium urate crystals (gout)
clinical medicine. They are most helpful in determining and calcium pyrophosphate dihydrate (CPPD) crystals
disease activity and response to therapy. (pseudogout). Both types have 2 colors: blue and yellow;
Unfortunately, they are of limited diagnostic utility. hence, they are termed "birefringent." The crystals are
Although they are sensitive markers of inflammation identified, however, by the color of the crystals that are
in general, they are not specific for any particular parallel to the microscope's color compensator. (Crystals
disease. Diagnostically, they are most helpful in ruling perpendicular to the color compensator are the opposite
out inflammatory disease, especially when the pretest color.) Be concerned only about the crystal color that is
likelihood is low to moderate. Note that an extreme parallel! If the crystals are yellow when parallel to the
elevation of the ESR (> I 00 mm/hr) is almost always a compensator, they are termed "negatively birefringent,"
hallmark of serious underlying disease, most commonly and when they are blue, they are "positively birefringent."
malignancy, infection, or vasculitis. Uric acid (gout) crystals are yellow when parallel to
the compensator (negatively birefringent), and they are
needle-like. (Helpful hint: The double Ls in "yellow" are
parallel to each other.)

Table 6-4: Synov1al Flu1d Analys1s

Joint Fluid WBC (cells/mm3) Other Findings Disease Associations

Normal (}-200 None


RBC Internal derangement

Noninflammatory 200-2,000 None OA, trauma, neuropathic joints, hypertro


RBC phic arthropathy, TB, PVNS; occasionally
SLE, scleroderma, and rheumatic fever.

Inflamatory 2,00(}-50,000 None , RA, gout, pseudogout, SLE, scleroderma,


Intracellular, strongly negatively reactive arthritis,' 'ankylosing spondylitis,
birefringent crystals (yellow) TB or fungal infection
lntraceullar, weakly positively
birefringent crystals (blue)
RBC

Septic 50,000-100,000 None Septic joint (but gonococcal septic joint


Organisms on Gram stain can be 10,000 cells/rnm3)
RA (very inflarnmed), gout,
pseudogout

2014 MedStudy
6-6 GENETIC COLLAGEN DISORDERS

The following are the ones to remember.

Marfan syndrome:

Long limbs (outstretched arm length> height)


Pectus excavatum (sternum dips inward), or pectus
carinatum (sternum protrudes outward)
Aortic aneurysm/dissection
Ectopia lentis (lenses displaced upward)
Heart valve disease

Ehlers-Danlos syndrome: variable skin hyperelasticity


and joint hypermobility. Several classifications:

Classic type (old Types I and II) = includes most

Image 6-1: Birefringent crystals severe form (easily scarred skin and hypermobile
joints)
CPPD (pseudogout) crystals are blue (weakly positive
Hypermobility type (old Type III) = manifestations
birefringent) when parallel to the compensator; they
predominantly joint, not skin
appear as small, rhomboid structures.
Vascular type (old Type IV ) = manifestations
CPPD crystals attract neutrophils and can cause a predominantly skin, not joint, and predilection for
purulent joint similar to gout with high synovial fluid rupture of large vessels
WBC count. To be very certain that the crystals are Several other rarer types
actually causing the inflammatory reaction in the joint,
you must see intracellular crystals, which are crystals Osteogenesis imperfecta (OJ): Defects in procollagen
within the neutrophils, as opposed to crystals just genes cause the variants, but all have:
floating around freely in the joint space. Important: Osteopenia
Crystalline and infectious arthritis can coexist, so it is Multiple bone fractures
important to always send studies for both.
Varying degrees of blue sclera
Again, you cannot simply look at a photo of a crystal and Lucent (brittle) teeth
see whether it is positively or negatively birefringent;
Hearing loss
you must know the direction of the compensator dial.
For instance, in Image 6-1, you see needle-shaped There are 7 types of OJ; Type I is autosomal dominant
crystals (so probably uric acid), but you won't know and the mildest.
they are negatively birefringent unless the compensator Pseudoxanthoma elasticum: autosomal recessive and
is vertical and the vertical crystals are yellow (yellow involves skin (easy bruising), blood vessels, and eyes. The
parallel = gout). main problem is recurrent UGI bleeds as they affect the
elastic media of blood vessels. Classic findings include a
cobblestone appearance of the skin with yellow papules
IMAGING STUDIES
and plaques that resemble "plucked chicken skin" on the
Weight-bearing knee films are the initial diagnostic neck/axillae and angioid streaks on funduscopic exam.
tests of choice for nontraumatic knee disorders (RA or (But this also occurs in Paget disease!)
OA) because weight bearing allows a more realistic
evaluation of the joint space. If necessary, MRI can
visualize all the components, except for normal RHEUMATOID A RTHRITIS
synovium (too thin).
OVERVIEW
The worldwide prevalence of RA is 0.5-1%.
GENETIC COLLAGEN DISORDERS
-

Women outnumber men 3: 1. The typical age of onset


is 40--50 years. Etiology of RA is multifactorial and
The inherited disorders of collagen encompass several
basically unknown. There is a low concordant incidence
different diseases, many of which cause hypermobility
of RA in identical twins, but RA does seem to have some
e.g., Marfan syndrome, Ehlers-Danlos syndrome (EDS),
genetic basis ( - 10% of patients have a 1" degree relative
and homocystinuria. Defects in elastic fiber formation
with RA; higher concordance in identical twins than in
(Marfan syndrome) or in type II collagen (Stickler
fraternal ones).
syndrome) are well defined; different proteins are
responsible for these syndromes. It is now recognized that RA is a heterogeneous disease
with various HLA polymorphisms resulting in anything
from mild joint involvement to severely erosive

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RHEUMATOID ARTHRITIS 6-7

They include:

interleukins(especially IL- l , IL-6, and


IL-17interferons),
B cells forming antibodies(RF and anti-CCP),
Describe pseudogout crystals and their
colony-stimulating factors(CSF),
birefringence.

growth factors, and


Which factors suggest aggressive RA?
tumor necrosis factor (TNF-a; also important when
How long is the typical morning stiffness in RA? considering treatment for RA).
lnOA?

What are the essential diagnostic criteria for RA? SIGNS I SYMPTOMS OF RA
Signs and symptoms of RA include > I hour of morning
joint deformity. These genetic haplotypes have been stiffness/pain that improves with activity, fatigue,
identified, and tests are commercially available to help low-grade fever, anorexia, and weight loss. Remember:
predict which patients will develop aggressive disease Noninflammatory joint diseases, such as OA, cause
and benefit from early pharmacotherapy. < 30 minutes of stiffness, and pain is worse with activity.
As mentioned under Labs, rheumatoid factor (RF) is Buzzwords for both RA and SLE: The arthritis
positive in only 80-85% of patients with RA. It may is symmetric and polyarticular. There is specific
take up to 2 years for patients with RA to become involvement of the hands-especially the MCP and
RF positive. PIP joints (Image 6-2); the DIP joints are spared!
Know that anti-CCP antibody: Boutonniere and swan-neck deformities occur in
advanced disease, although they are nonspecific for RA.
appears earlier than RF,
Symptoms of RA may be intermittent (15-30%) or
has greater specificity for the diagnosis of RA(97%),
progressive. Intermittent disease has remissions lasting
and
up to 1 year and is considered a variant of RA known as
is associated with more aggressive disease and
palindromic rheumatism.
extraarticular involvement.
Know the diagnostic criteria for RA, which changed in
Antibodies play a prominent role in the current 20I 0
2010. A complete list of criteria can be found in the 2010
ACRIEULAR diagnostic criteria for RA. A high titer
ACRIEULAR guidelines on the American College of
of either RF or anti-CCP contributes 3 of the 6 points
Rheumatology website at www.rheumatology.org.
required for the diagnosis.
From this, remember the following essentials-RA can
Poor prognostic indicators of RA include:
be diagnosed when all of the following are present:
presence of HLA-DR4 antigen(HLA-DRB I *040 I),
I 0 joints)

Inflammatory arthritis(from 1 to
high-titer RF or anti-CCP antibodies,
RF and/or anti-CCP
elevated acute phase reactants(ESR and CRP),
Increased ESR or CRP
multiple joint involvement(> 6),
Duration > 6 weeks
constitutional symptoms,
Other causes must be excluded (especially if symptoms
radiographic evidence of erosive disease, and
have been present for< 6 weeks), such as SLE, Sjogren's,
extraarticular disease(e.g., rheumatoid nodules,
overlap syndromes, sarcoidosis, and viral reactive arthritis
vasculitis, lung involvement).
(i.e., hepatitis B and C, parvovirus B 19).
In an affected RA joint, there is inflamed synovium(with
increased type A and B synovial cells). In its chronic
phase, this inflamed membrane of granulation tissue
(pannus) stimulates the release of cytokines, which
leads to cartilage destruction, bone erosion, and an
inflammatory synovial fluid that has decreased viscosity.

Present in the synovium of the rheumatoid joint are


cytokines and chemokines, which are secreted by
activated lymphocytes, macrophages, and fibroblasts;
these probably account for most of the destructive
effects of RA.

Image 6-2: Rheumatoid arthritis ofthe metacarpophalangealjoints,


with an endarteritis-associated ulcer on dorsum

2014 MedStudy
6-8 RHEUMATOID ARTHRITIS

Seronegative RA is diagnosed when patients meet other lumbar spine pain. If you see a patient withRA and spine
criteria but lack both RF and anti-CCP. These patients pain, think about the myriad other potential causes of
tend to have less severe disease than what is seen in spine pain; e.g., compression fractures, infections-not a
antibody-positive patients. flare ofRA.

Hemochromatosis is another disease that commonly


involves the 2"d and 3'd MCP and PIP joints, but EXTRAAR TICULAR MANIFESTATIONS
the arthropathy of hemochromatosis is distinctly
Remember: Extraarticular manifestations of RA are
asymmetric. Also, hemochromatosis has hook-like
more common in the presence of RF and anti-CCP
osteophytes on the MCP joints and chondrocalcinosis
antibodies (seropositiveRA). Know these extraarticular
neither finding is seen in RA. Patients can easily be
manifestations ofRA:
screened for hemochromatosis with iron studies. An
elevated transferrin saturation (Fe/TIBC of> 45%) or Cardiac:
elevated ferritin level suggests the diagnosis. Know Pericarditis (with effusion or thickening)
these clues for differentiating RA and SLE from and myocarditis.
hemochromatosis. Rheumatoid nodules on the valves.
Hoarseness, sore throat, and/or neck pain may indicate
Atherosclerosis-3x increased risk of
involvement of the cricoarytenoid joint in the patient atherosclerotic cardiovascular disease (sudden death
with RA. The temporomandibular joints may also be and MI). Coronary artery disease is the leading cause
affected. of death among patients with RA.
The knee is the most common single joint initially Renal (all very rare):
involved in RA; but, over time, small joints-in a
Drug-related renal disease
symmetric fashion-are more commonly involved. In
fact, the forefoot has proven to be the site of earliest
Amyloid renal disease occurring late inRA
radiographic changes in RA, and the head of the Lungs (males more often):
51h metatarsal bone may be the location of the earliest
Exudative pleural effusion with low glucose
erosion. Carpal tunnel and tarsal tunnel syndromes
(< 30 mg/dL) and pH.
can occur in RA. If a patient with inflammatory knee
Diffuse interstitial fibrosis and intrapulmonary
arthritis presents with a swollen calf, suspect a ruptured

rheumatoid nodules; when caused by mine dust, it is


Baker cyst (popliteal cyst) causing pseudophlebitis.
called Caplan syndrome (mine dust pneumoconiosis).
Occasionally, a Baker cyst can cause extrinsic venous
compression that can simulate a deep vein thrombosis. Vasculitis:
C-spine: Patients with chronic, severe disease may May resemble polyarteritis nodosa and cause nailfold
develop cervical instability at the atlanto-axial infarcts and splinter hemorrhages.
articulation (C l-C2). The rest of the axial skeleton is Necrosis with ulceration may occur, especially over
spared. the malleoli.
While patients can be asymptomatic, suspect cervical (C l Nerves:
C2) involvement when a patient with RA complains of:
Mononeuritis multiplex, which may manifest as foot
recurrent occipital headaches, or wrist drop
limited neck range of motion, or Carpal and tarsal tunnel syndromes

paresthesias of the hands and feet. Cervical myelopathy

If these symptoms are present, order cervical spine Eyes:


x-rays with flexion and extension views. InRA patients Episcleritis
scheduled to undergo endotracheal intubation, an Scleritis
evaluation for cervical instability is mandatory. Acute Sicca/secondary Sjogren syndrome
subluxation, which may occur with extension of the neck
for intubation, can cause spinal cord compression or Skin:
vertebral artery compression leading to quadriparesis or Rheumatoid nodules occur in 25% and indicate
sudden death.Remember: All patients with long-standing potential for more severe disease. These nodules
RA should have flexion and extension neck films before usually appear on extensor surfaces but may also be
surgery to assess for subluxation. found in the lungs and on heart valves.
The thoracic, lumbar, and sacral spine and the Sljoints are
usually spared inRA (in contrast to ankylosing spondylitis
and psoriatic arthritis). Again, RA does not present as

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RHEUMATOID ARTHRITIS 6-9

Trials have shown that 70% of patients with active,


polyarticular, RF-positive disease develop joint damage
or erosions within 2 years of onset. Other trials show
that early treatment with a DMARD may alter the course
What is the pattern of arthritis in RA? of the disease. Trials with combination DMARDs in
early disease also show benefit. NSA!Ds may help with
Which part of the spine is sometimes involved
inflammation and pain, but do not prevent the formation
in RA? Which parts are never involved?
of either erosions or joint deformities. Glucocorticoids,
What is the most common manifestation of RA like DMARDs, can alter the course of disease but are
in the lungs? associated with significant long-term side effects.
What is Felty syndrome? Current treatment paradigms focus on early diagnosis
Name some indicators of active RA. If a patient and early aggressive therapy to allow patients a chance at
has these indicators, when do you start treatment? remission. The goal is to try to initiate DMARD therapy
With what? within 3 months of symptoms and, if needed, to titrate
drugs (add additional DMARDs or biologic agents) to
attain low disease activity or remission. Previously,
Blood and lymphatics:
treatment of RA followed a pyramid regimen consisting
Anemia of chronic disease initially of NSAlDs and glucocorticoidswith DMARDs
Neutropenia (seen in Felty syndrome and large added only as the disease progressed. Now we know
granular lymphocyte [LGL] syndrome) that RA-associated disability can be drastically reduced
Increased risk of lymphoma (particularly in when treated early and aggressively.
longstanding, untreated, active disease) Recognize that glucocorticoid use in RA IS
Felty syndrome consists of the classic triad of controversialinfluenced by the efficacy of the
rheumatoid arthritis, splenomegaly (the spleen biologics and the well-known side effects of systemic
can be "felt-y"), and neutropenia. These patients glucocorticoids. Generally, as the patient improves on
usually have long-standing disease associated with early aggressive therapy, the more toxic drugs, such
high titers of rheumatoid factor and subcutaneous as steroids, are withdrawn, while DMARDs and/or
rheumatoid nodules and suffer increased mortality from biologics are used as maintenance therapy.
infections. Treatment: methotrexate, cyclosporine A,
Now we'll discuss these RA medications in more detail.
corticosteroids, granulocyte colony-stimulating factor
(GCSF), and, if needed, splenectomy. If splenectomy
is ineffective, the prognosis is poor. TNF inhibitors are
currently being evaluated.

Large granular lymphocyte (LGL) syndrome may


be difficult to distinguish from Felty syndrome since
Table 6-5: Drugs Used to Treat RA
it also presents with neutropenia, splenomegaly,
and susceptibility to infections. It differs from Felty Nonsteroidal Nonselective (e.g., ibuprofen,
syndrome in that it is less commonly associated with naprosyn, nonacetylated
RA and rarely may progress to LGL leukemia. In salicylates) and COX-2 inhibitor
contrast to Felty syndrome, these patients do poorly
Nonbiologic Methotrexate, leflunmide,
with splenectomy. Definitive diagnosis can be made by
DMARDs hydroxychloroquine, sulfasalasine
detecting clonal T-cell gene rearrangement, which is not
present in Felty syndrome.
Immunosuppressants Azathioprine, chlorambucil,
corticosteroids, cyclophosphamide,
TREATMENT OF RH EUMATOID ARTHRITIS cyclosporine, mycophenolate
mofetil, tacrolimus
Overview
Biologics TNF inhibitors (monoclonal
Drugs used to treat RA (see Table 6-5) are categorized as
antibodies and soluble receptors),
nonsteroidal antiinflammatory drugs (NSAIDs), which
IL-l and IL-6 antagonists,
help with pain but do not modify the disease course:
anti-B cell antibody, T-cell
Nonbiologic disease-modifying antirheumatic drugs inhibitor
(DMARDs)
Miscellaneous Acetaminophen, colchicine,
Immunosuppressants dapsone, IVIG, plasmapheresis/
Biologics or biologic response modifiers (BRMs) plasma exchange, thalidomide,
Miscellaneous (steroids, minocycline, doxycycline) intraarticular viscosupplementation

2014 MedStudy
6-10 RHEUMATOID ARTHRITIS

NSAIDs DMARDs

NSAIDs are part of the initial treatment. NSAIDs General Characteristics


decrease inflammation and joint swelling but do not alter
Disease-modifYing antirheumatic drugs (DMARDs):
the course of the disease. Again, know that DMARDs
(next) are now given with onset of RA symptoms. Methotrexate (MTX)
NSAIDs are added to help control pain. L eflunomide (LEF)
Hydroxychloroquine (HCQ)
For patients with ASA allergy, use a sodium, magnesium,

or choline salicylate. These nonacetylated salicylates do Sulfasalazine (SSZ)


not cause an ASA allergy reaction and also may have Azathioprine (AZA)
less GI toxicity (but may be less effective). Cyclosporine A (Cyc A)
Cyclophosphamide (Cytoxan)
What about the COX-2 inhibitors? Selective DMARDs are a major component of RA treatment.

G
COX-2 inhibitors, like other NSAIDs, inhibit They have a slow onset of action (several months), so
cyclooxygenase-2 but, unlike other NSAIDs, do not concurrent NSAIDs or low-dose glucocorticoids are
inhibit cyclooxygenase-1. Currently, the only COX-2 required initially. HCQ and SSZ are sometimes used

R
inhibitor available in the U.S. is celecoxib (Celebrex), first in cases of early, mild RA; these drugs are also
which is approved for treatment of RA, OA, ankylosing safe in pregnancy and breastfeeding. DMARDs are

V
spondylitis, and acute pain (and adjunctive for familial started with onset of symptoms. Aggressive treatment
adenomatous polyposis). with MTX, LEF, SSZ or combination DMARDs is

d
The antiinflammatory effects of COX-2 inhibitors are recommended for patients with moderate-to-severe
disease. The following DMARDs are recommended by

ti e
comparable to other NSAIDs, with possibly reduced GI
irritation and ulcer development. the 2012 American College of Rheumatology updated
clinical practice guidelines.
Other benefits of selective COX-2 inhibitors: no effect
on platelet function, so bleeding time is unchanged; less

n
risk of bleeding in anticoagulated patients; less likely Methotrexate

than other NSAIDs to precipitate bronchoconstriction in MTX is an antifolate agent with antiinflammatory

U
patients with aspirin-induced asthma. properties that is very effective in the treatment of
The problem with selective COX-2 inhibitors (and RA. Because it has the most predictable benefit and is

-
NSAIDS in general) is that they increase the risk for usually the best tolerated, the 2012 American College
adverse cardiac events such as myocardial infarction, of Rheumatology updated clinical practice guidelines
recommend MTX as the initial DMARD for patients

9
stroke, heart failure, and sudden cardiac death in some
patient groups. Celecoxib is contraindicated in patients with moderate-to-severe RA without poor prognostic

9
who are in the postoperative recovery phase after features and as the main DMARD when combination
therapy is used in those with poor prognostic features.

r
artery bypass graft. One trial of 4,000 patients showed

i
celecoxib increased risk of death or recurrent MI ( 2x)

Again, most experts are now starting DMARDs with
if taken longer than I month after an MI. Analysis of onset of RA symptoms! Some patients begin to improve

h
2 recent long-term adenoma prevention trials studying within 6 weeks. It is administered orally, subcutaneously,
celecoxib concluded there is an increased risk of serious or intramuscularly I x/week and is often combined with

ta
cardiovascular events that may be dose-dependent. other agents to maximize disease control. Preexisting
liver disease (e.g., HBV, HCV, heavy alcohol use), severe
Patients who are allergic to sulfa appear to have a high
renal disease, and pregnancy are contraindications to
risk of rash with COX-2 inhibitors.
using this drug.

Common side effects and complications of MTX


Know these important drug interactions: NSAIDs and
include:
lithium have common excretory pathways, so check
lithium levels periodically if a patient is receiving both Alopecia
meds. ASA decreases the breakdown of oral hypoglyce GI distress (nausea, vomiting, diarrhea, mucositis)
mics, so decrease dosage of these when given with ASA. Bone marrow suppression even at low doses
All NSAIDs, selective and nonselective, may precipitate (Prescribe folate replacement 1 mg/day for
or worsen heart failure and may raise blood pressure. prevention. Coadministration of sulfa drugs or
antifolate agents can worsen cytopenias, so
follow CBC.)
Increased liver transaminases (AST/ALT)

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RHEUMATOID ARTHRITIS 6-11

Important: Because LEF has an extremely long


half-life and is teratogenic, women planning to conceive
Quiz must discontinue the drug and undergo treatment with
cholestyramine to eliminate the drug.
Which DMARDs are used to treat mild RA and
are relatively safe during pregnancy? Hydroxychloroquine
Which DMARD is recommended by the American

The main side effect to know is retinopathy. The usual
College of Rheumatology as 1st line for all
risk is considered to be 115,000 patients after prolonged
moderate-to-severe cases of RA?
use. If renal dysfunction occurs, the risk of retinopathy
What are methotrexate contraindications? rises greatly. Patients started on HCQ need a baseline
ophthalmologic evaluation to serve as a reference point
Name another DMARD recommended to treat RA
and to rule out existing retinopathy. After 5 years of
in patients who cannot tolerate methotrexate.
continuous HCQ, annual exams are recommended in

G
What follow-up is required in patients treated with average-risk patients. Routine CBC and CMP should be
hydroxychloroquine? obtained every 3-6 months. Also, consider monitoring

R
muscle strength periodically because of the risk of
Other serious, but less common, reactions to be aware myopathy. Know that the use of HCQ in psoriatic
of include: patients may exacerbate psoriasis.

V
increased susceptibility to opportunistic infections,

d
severe hepatotoxicity (follow AST/ALT), Sulfasalazine

nephrotoxicity (follow creatinine), and Also used for inflammatory bowel disease (IBD).

ti e

pneumonitis/pulmonary fibrosis. In RA, the sulfapyridine portion of the molecule


produces effects; in IBD, the 5-amino salicylic acid
The MTX pneumonitis is idiosyncratic (i.e.,
(5-ASA) portion is the effective component. The
non-dose-related). Initial symptom is nonproductive

n
most common side effects are sulfa-allergic reactions,
cough. Radiograph is initially normal but shows alveolar
nausea, vomiting, diarrhea, and crampy abdominal
infiltrates in later stages.
pain. It may cause reversible oligospermia (no effect on

U
MTX-related toxicities are not age-related. Monitor female reproduction), cytopenias, and an elevation in
CMP and CBC every 4 weeks for the first 3 months transaminases (monitor with periodic CBC and LFTs).

-
of therapy, then every 12 weeks thereafter; labs should The 5-ASA component can cause Reye syndrome in
be monitored more frequently if clinically indicated. patients vaccinated with the varicella vaccine (because
Baseline hepatitis B and C serologies and CXR should

9
it's a live virus vaccine). Check G6PD levels in patients
be obtained prior to initiating therapy. Order pulmonary at increased risk for G6PD deficiency (e.g., males of

ri 9
function tests in patients with symptoms of dyspnea or a African or Mediterranean descent).
history of COPD (pay attention to the carbon monoxide
diffusing capacity [DLCO]). Monitoring renal function
DMARDs in Pregnancy
is important because most of MTX is excreted

h
unchanged in the urine. Renal failure from any cause Essentially any DMARD or antirheumatic drug taken
leads to accumulation of the drug and increased toxicity. during pregnancy, especially during the 1" trimester

ta
where organogenesis is predominant, can pose a risk to
the fetus. The general rule is to avoid any and all drugs
Leflunomide
if at all possible. If a medication is required, the minimal
LEF (Arava) is used to treat RA. It is a pyrimidine effective dose to maintain the disease under control is
antagonist and may be used as an initial DMARD in recommended.
patients unable to take MTX.
The following are general recommendations:
Its side effects are very similar to MTX. Minor adverse
Hydroxychloroquine and sulfasalazine are allowed
reactions include diarrhea and respiratory infections.
during pregnancy.
Its major side effect is hepatotoxicity, and it should
Azathioprine, IVIG, cyclosporine A, and
be avoided in those with preexisting liver disease.

cyclophosphamide are relatively contraindicated


Other important side effects include cytopenias, renal
(weigh risks vs. benefit).
dysfunction, interstitial lung disease, peripheral
neuropathy, and opportunistic infections. Methotrexate, leftunomide, and mycophenolate
mofetil are absolute contraindications.
Screen for latent TB before prescribing this drug. CBC,
LFTs, and creatinine need to be monitored frequently,
as with MTX. The drug is contraindicated in pregnancy
and unsafe for lactation.

2014 MedStudy
6-12 RHEUMATOID ARTHRITIS

Biologic Agents Anti-TNF Biologics (TNF Inhibitors)

See Table 6-6 for a synopsis of the biologics currently Infliximab, adalimumab, certolizumab, and golimumab
approved for RA. Biologics are made with animal, are monoclonal antibodies that bind and inactivate
microbial, or human proteins, in contrast to DMARDs, tumor necrosis factor (TNF), an important mediator
which are made from chemicals. The biologics have of the inflammatory response in RA. Etanercept is a
opened a new era in RA treatment in that they are soluble TNF receptor that is linked to IgG 1 and also
highly selective in their targets, yielding better efficacy binds and inactivates TNF. It has been suggested that
with improved safety profiles. They are designed to monoclonal anti-TNF agents may cause greater risk for
inhibit specific components of the immune system infections (e.g., TB, herpes zoster, nonserious infections
that regulate inflammation. They can be broken [NSIEs]) compared to etanercept. The anti-TNF drugs
down into those that inhibit tumor necrosis factor are approved for a variety of indications, including RA,
(anti-TNFs) or those that inactivate other pivotal sites psoriasis, psoriatic arthritis, ankylosing spondylitis, and
related to inflammation. inflammatory bowel disease.

Drug Name Brand Name


Table 6-6: Biologics

Approved Use

RG
Most Common Side Effects

V
TNF-a inhibitors Boxed warnings: Serious infections and TB

d
Infliximab Remicade RA, P,AS, Crohn 's, UC URI, nausea,headache,infusion reactions,
DIL with antinuclear and anti-dsDNA ab

t e
Adalimumab Humira RA, P,AS, Crohn's URI,headache, rash

i
Certolizumab Cimzia RA, Crohn's URI, headache, nausea

n
URI

U
Etanercept EnbreJ RA,P,AS URI, headache, rash, local site reaction,DIL with
antinuclear and anti-dsDNA ab

-
Non-TNF-a inhibitors

IL-l antagonist

9
Anakinra Kineret Refractory RA Boxed warning: Serious infections, do not

9
combine with TNFi
Neutropenia, headache, local site reaction

ir
IL-6 antagonist

h
Tocilizumab Refractory RA Boxed warning: Serious infections and TB

a
URI, increased LFTs, neutropenia, serious GI

t
infections

Anti-CD20

Rituximab Rituxan RA(with MTX) Boxed warning: Fatal infusion reactions,


anti-CD20+ NHL progressive multifocal leukoencephalopathy,
anti-CD20+ CLL severe mucocutaneous reactions
GPA Fever, nausea/diarrhea, cytopenias, peripheral
MFA edema, hypertension or hypotension, rash;
headache, neuropathy

T-cell inhibitor

Abatacept Orencia Refractory RA Boxed warning: COPD exacerbation, avoid


combining with TNFi
Infections, headache

RA = rheumatoid arthritis; P = psoriasis/psoriatic arthritis; AS = ankylosing spondylitis; UC = ulcerative colitis; NHL = non
Hodgkin lymphoma; CLL = chronic lymphocytic leukemia; MTX = methotrexate; GPA= granulomatosis with polyangiitis;
MPA= microscopic polyangiitis

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RHEUMATOID ARTHRITIS 6-13

These potential complications sound terrible (and they


are!), but know that they are not common-the most
common side effect is an increase in NSIEs as upper
respiratory tract infections and urinary tract infections.
What are the categories of biologics used Patients with active infections that have potential to
to treat RA?
progress to serious infections need to discontinue their
What are representative drugs for each category biologic or delay treatment until the infection has
of biologics? resolved. Less common but noteworthy complications
include worsening psoriasis and reactivation of HBV.
Name some serious complications of the
various biologics. [Know:] Because DMARDs and biologics can suppress
the immune system and increase susceptibility to infec
What is the most common side effect
tion, routine vaccinations for influenza and pneumonia
of the non-TNF biologics?
are recommended; patients on biologics, prednisone

G
> 20 mg/day, methotrexate > 25 mg/week, and azathio
[Know:] For RA, these agents are most beneficial when
prine > 3 mglkg/day should avoid live vaccines per ACIP
combined with methotrexate and have been shown to

R
2012 guidelines. The only live vaccines that are relevant
halt and possibly heal erosive damage!
to clinical practice are MMR and shingles vaccines.

V
These agents have been associated with drug-induced
lupus as well as other side effects including: injection
Immunosuppressants

d
site/infusion reactions, infections, increased risk for
skin cancer, cytopenias, CNS demyelination, and Azathioprine

ti e
worsening heart failure. They are not recommended for AZA has shown some benefit for RA, but is much more
patients with NYHA class III/IV heart failure and an commonly used in SLE. Its main side effects include bone
ejection fraction :5 50% because they may worsen CHF marrow suppression, NN, diarrhea, and hepatotoxicity.
symptoms and increase morbidity. Inftiximab has been

n
It is important to understand AZA's metabolism. It is
associated with fatal hepatosplenic T-cell lymphoma.
first metabolized to 6-mercaptopurine (6-MP) by the
liver. AZA and 6-MP are inactive prodrugs. 6-MP can

U
Non-TNF Biologics then be metabolized by 3 different pathways.

-
Interleukin antagonists (anakinra = IL-l; tocili