The Most Common Inpatient Problems in Internal Medicine pdf

Loss of atrial systole may have pronouncedconsequences in patients with decreased ventricu-lar compliance i.e., left ventricular hypertrophy,hypertrophic cardiomyopathy or mitral stenosi

1600 John F Kennedy Blvd, Suite 1800

Philadelphia, Pennsylvania 19103–2899

The Most Common Inpatient Problems in Internal Medicine

ISBN-13: 978-1-4160-3203-8 ISBN-10: 1-4160-3203-7 Copyright# 2007, Elsevier Inc All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photoco- pying, recording, or any information storage and retrieval system, without permission in writing from the publisher Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (þ1) 215 239 3804, fax: (þ1) 215 239

3805, e-mail: healthpermissions@elsevier.com You may also complete your request on-line via the Elsevier homepage ( http://www.elsevier com ), by selecting ‘Customer Support’ and then ‘Obtaining Permissions’.

Notice Knowledge and best practice in this field of Internal Medicine are constantly changing As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product

to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindica- tions It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses,

to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions To the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material con- tained in this book.

The Publisher International Standard Book Number 1-4160-3203-7

Editor: Rolla Couchman

Developmental Editor: Adrianne Brigido

Design Direction: Gene Harris

Printed in the United States of America.

Last digit is the print number: 9 8 7 6 5 4 3 2 1

We learned a tremendous amount aboutinpatient medicine during our internship andresidency We are indebted to the many talentedcolleagues, residents, chief residents, fellows,and staff physicians with whom we worked dur-ing those formative years We especially thank

Dr Joel Katz, the Program Director for theInternal Medicine training program at Brighamand Women’s Hospital who constantly strives toimprove the residency program and who haskindly agreed to write a foreword for this book

We also thank Dr Marshall Wolf, a masterclinician-educator, for believing in us and grant-ing us the privilege of training at one of the besthospitals in the country We thank Rolla

Couchman and Dylan Parker, our contacts atElsevier, for their expertise, guidance, profes-sionalism, and patience as we worked towardmeeting deadlines Without them, this bookwould still be a figment of our imagination andnot this work of which we are both very proud.John Sun would like to thank Dr DavidKatzka and Dr Anil Rustgi for their outstandingteaching and mentorship He also thanks hisparents, his brother, Alan, and his extendedfamily for their encouragement Most impor-tantly, he thanks his wife, Yumee, for her manyyears of dedication, love, and support

Hylton Joffe would like to thank Dr SamuelGoldhaber, Dr Arthur Sasahara, and Dr RobertUtiger—phenomenal role models as physicians,mentors, and human beings He also thanks hisparents, his sister, Karen, and his brother-in-law,Daniel, for their encouragement and love Most

of all, he thanks his wife, Sarah, for her unselfish,unwavering, and unconditional love and support

v

According to the eminent medical educator,

Dr Marshall Wolf, the fundamental skillrequired to master the Art of Medicine is theability to accurately make critical—oftenlife-sustaining—decisions in the face ofincomplete data Every trainee and practicingphysician will encounter common medicalconditions with a high degree of regularity,and needs an approach to clinical decision-making that is reflexive and yet retains thenuanced recognition of the subtleties affectingthe individual patient Skilled providers musthave, at the same time, a command of

practical, evidence-based management

strategies as well as an appreciation of theguideposts requiring individual variations Thelatter skill comes only from experience Theformer is the goal of this clear and

subtlety, they have captured the key aspects

of modern therapeutics in chapters addressingthe most frequent and, therefore, mostimportant acute medical problems The text

is organized for clarity, simplicity, and

accessibility—critical commodities to thebusy, and often over-stretched, physician-in-training I predict with confidence thatthis volume will play a vital role in teaching

vii

and learning medicine Future generations ofstudents and teachers, and ultimately thepatients they serve, will benefit from thisimportant contribution.

Joel T Katz, MD

DirectorInternal Medicine Residency ProgramBrigham and Women’s HospitalMember, Academy of Teaching ScholarsAssistant Professor of MedicineHarvard Medical SchoolBoston, Massachusetts

Are you a medical student, intern, or residentwho is (or will be) caring for patients on themedical ward? Do you find it challenging tolocate practical and pertinent information aboutmany of the common inpatient medical condi-tions? If your answers to these questions are

‘‘yes,’’ then this book is for you!

Not too long ago, we were trying to learn thebasic principles for the day-to-day care of medi-cal inpatients We found that review articles andbook chapters provided an overview of medicaltopics but often lacked specific informationdirectly applicable to patient care Frequently,

we also had difficulty determining the relevance

of findings from original journal articles, cially when there were prior conflicting studies

espe-As a result, we learned a vast amount of practicalinpatient medicine from our co-interns,

residents, fellows, and staff physicians Theseteachers explained how to choose a dose

of intravenous furosemide for our patientwith decompensated heart failure or how tocalculate the dose of subcutaneous insulin for apatient with resolving diabetic ketoacidosis.Basic concepts such as these have often beenfrustratingly difficult to acquire from othersources Until now

Our book, The Most Common InpatientProblems in Internal Medicine, provides practicaland pertinent information for the most commonmedical problems encountered on the hospitalward The chapters cover basic principles thatevery house officer should know, emphasizing

‘‘bread-and-butter’’ medicine You will find ful information about common disorders you seeeveryday, including heart failure, pancreatitis,hyperkalemia, acute exacerbation of chronicobstructive pulmonary disease, asthma, acute

use-ix

renal failure, hyponatremia, and unstable angina.After reading this book, you will have a solidfoundation upon which to build your knowledge

as you advance in your career

You will find answers to the following types

of questions:

 What rate and type of intravenous fluid should

I administer to my patient with acute, tomatic hyponatremia?

symp- Does my patient have iron deficiency anemia

or anemia of chronic disease?

 How do I teach my patient with chronicobstructive pulmonary disease to use a spacerfor delivery of her inhaled glucocorticoids?

 How do I differentiate aspiration pneumoniafrom chemical pneumonitis and do thesepatients require antibiotics?

 How can I determine whether my patient’s renalfailure is acute or chronic when prior serumcreatinine measurements are unavailable?

 My patient with suspected pulmonary lism has a normal first-generation lung com-puted tomography (CT) scan—what should I

embo-do next?

Each chapter is divided into sections that coverthe epidemiology, pathophysiology, signs andsymptoms, laboratory abnormalities, diagnosis, andmanagement of the disorder under discussion A

‘‘Key Points’’ box at the beginning of each chapterhighlights some important take-home messages.Tables and figures clarify important and complexconcepts Each chapter ends with a list of refer-ences, which can also be used by those who wish tofurther their knowledge in specific areas

We hope that you will enjoy reading thisbook as much as we enjoyed writing it

Best of luck in your career!

About the Authors

Dr John C Sun received his medical education

at Temple University where he was elected tothe Alpha Omega Alpha Honor Society duringhis junior year Dr Sun received the GoldenStethoscope Award for outstanding teachingduring his internal medicine training at Brighamand Women’s Hospital and Harvard MedicalSchool After residency, Dr Sun completed aGastroenterology fellowship at the University ofPennsylvania, where he served on the Gastroen-terology Education Committee He is currently agastroenterologist at Kaiser Permanente, SanFrancisco, and participates in medical studentteaching at the University of California, SanFrancisco He lives in San Francisco with hiswife, Yumee, and son, Ethan

Dr Hylton V Joffe received his medicaleducation at the University of Arizona where hewas elected to the Alpha Omega Alpha HonorSociety during his junior year Dr Joffe receivedrecognition from the internship class for excel-lence in teaching during his internal medicinetraining at Brigham and Women’s Hospital andHarvard Medical School After residency, Dr.Joffe completed an Endocrinology fellowship atBrigham and Women’s Hospital and receivedformal training in Clinical Investigation throughthe Scholars in Clinical Science Program atHarvard Medical School He is currently aMedical Officer in the Division of Metabolismand Endocrinology Products at the U.S Foodand Drug Administration as well as a member ofthe Division of Endocrinology and Metabolism

at the Johns Hopkins University School of icine Dr Joffe lives in Washington, DC, with hiswife, Sarah

Med-xi

C H A P T E R 1 Atrial Fibrillation

K E Y P O I N T S

1 Atrial fibrillation is an irregular

supraventricular arrhythmia that maycause thromboembolism, hypotension,and cardiac ischemia or infarction

2 Risk factors for thromboembolisminclude increasing age, prior history ofthromboembolic events, hypertension,heart failure, and diabetes mellitus

3 Evaluation of a patient with atrial lation includes a history and physicalexamination to assess the timing andduration of symptoms, potential triggers

fibril-or reversible causes, and presence ofcomplications

4 Basic laboratory testing, thyroid functiontests, electrocardiogram, echocardiogra-phy, and chest x-ray should be performed

5 Rate-control or rhythm-control strategieshave similar thromboembolism rates.Both require anticoagulation to decreasethe risk of embolic events

6 Most patients should be treated usingrate-control Rhythm control should bereserved for patients who prefer rhythm-control, have continued symptomsdespite adequate rate control, or fail toachieve rate control

7 Acute rate control may be achieved withintravenous metoprolol, verapamil, ordiltiazem (see text for dosing) Digoxinshould not be used

8 Beta-blockers, calcium channel blockers(verapamil, diltiazem), or digoxin may beused for chronic rate control

3

Beta-blockers and calcium channel

blockers will provide rate control at restand with exercise Digoxin provides ratecontrol at rest, but not with exercise

D E F I N I T I O N

Atrial fibrillation (Afib) is an irregularlyirregular supraventricular tachyarrhythmiathat results in loss of coordinated atrialsystole The American College of Cardiology/American Heart Association/European Society

of Cardiology (ACC/AHA/ESC) PracticeGuidelines define the following categories foratrial fibrillation that lasts for longer than

30 seconds, and is not due to a reversible cause:

 Recurrent: Two or more episodes of Afib

 Paroxysmal: Recurrent Afib that nates spontaneously (usually within 7 days)

termi- Persistent: Afib that is sustained (does notspontaneously resolve) for longer than 7days

 Permanent: Afib that lasts longer than

1 year

 Lone Afib: Occurs in a patient:

○ Younger than 60 years of age

○ Without evidence of cardiac or pulmonarydisease

EPIDEMIOLOGY

The prevalence of Afib increases with age, from

<1% in patients under age 60, to >6% in patientsabove age 80 Afib is also more common in malesthan in females, and in Caucasians than in AfricanAmericans The incidence for Afib is under0.1% annually for persons under age 40, rising to

1.5% to 2% annually in persons over age 80 In

a large study of almost 2 million members of ahealth maintenance organization (HMO), theoverall prevalence of Afib was 1%, but rangedfrom 0.1% in patients under age 55 to 9% inpatients over age 80 The prevalence of Afib alsoincreases with the severity of heart failure.The ischemic stroke risk for persons withnonvalvular Afib ranges from 2 to 7 times that ofpersons without Afib For persons with rheumaticheart disease and Afib, the stroke risk is evenhigher, up to 17 times that of persons withoutAfib For untreated patients, the stroke riskincreases with age, from 1.5% annually in patientsbetween the ages of 50 and 59, to 23.5% inpatients between the ages of 80 and 89

PATHOGENESIS

Potential Mechanisms

Afib is thought to be due to either enhancedautomaticity of atrial foci or the presence ofreentry circuits

 Foci of enhanced automaticity:

○ Are usually located in the superior monary veins

pul-○ May also be located in the right atrium,superior vena cava, or coronary sinus

○ May be an important pathophysiologicmechanism in paroxysmal Afib

increasing the sinus node recovery time Inaddition, prolonged duration of Afib may result

in an increased recovery time for atrial tility after cardioversion

contrac-Afib is often initiated by other lar arrhythmias or atrial premature beats Atrio-ventricular (AV) nodal reentry and atrioventricularreentry tachycardias may also result in Afib

con- There is an inverse relationship betweenthe atrial and ventricular rates Higheratrial rates are associated with lowerventricular rates, and lower atrial rates areassociated with higher ventricular rates

 Increased parasympathetic and decreasedsympathetic tone decrease conductionacross the AV node Decreased parasympa-thetic tone and increased sympathetic toneincrease conduction across the AV node.Hemodynamic Effects

Afib results in the loss of atrial systole (causingdecreased ventricular filling) and the potentialfor a rapid ventricular response Both have thepotential to lower cardiac output

Loss of atrial systole may have pronouncedconsequences in patients with decreased ventricu-lar compliance (i.e., left ventricular hypertrophy,hypertrophic cardiomyopathy) or mitral stenosis.Rapid ventricular response to Afib may result

in decreased cardiac output due to lack of cular filling time compounded by loss of atrioven-tricular synchrony and suboptimal contractility

Over time, atrial and ventricular tachycardiaresult in atrial and dilated ventricular cardio-myopathy, respectively Atrial cardiomyopathyleads to decreased myocyte contractility andpropensity for the development of sustainedAfib Ventricular cardiomyopathy may lead tosigns and symptoms of heart failure Both arepotentially reversible with control of Afib.Embolic Complications

Thrombus formation tends to occur in the leftatrial appendage, accessible to examination bytransesophageal echocardiography Although theprecise mechanism of thrombus formationremains unclear, a combination of decreasedblood flow through the atrial appendage andregional coagulopathy likely play a role

Risk factors for stroke in patients with Afibinclude:

 Hypertension: Patients with hypertensionand Afib have lower flow rates through theleft atrial appendage and higher associatedthrombus formation

 Increasing age: Older patients with Afib tend

to have left atrial enlargement and lower leftatrial appendage flow rates, resulting in ahigher risk of thrombus formation

 Left ventricular systolic dysfunction: Heartfailure is associated with a higher stroke risk

in patients with Afib

Risk Factors and Potential Causes

Patients without Cardiac Disease

Metabolic factors (such as obesity and

hyperthyroidism) and drugs (such as adenosine,theophylline, and alcohol) may cause Afib.Noncardiac (particularly thoracic) surgery mayinduce Afib Pulmonary embolism, chronicobstructive pulmonary disease, and obstructivesleep apnea are associated with Afib, as well.Obstructive sleep apnea does not initiate Afib

but has been found to increase the risk of Afibrecurrence.

Autonomic dysfunction may be associated withAfib Vagally mediated Afib tends to occur duringperiods of heightened parasympathetic tone, such

as mealtimes, or during sleep Adrenergicallymediated Afib usually happens during the day, withexercise, or during emotional or physical stress.Patients with Cardiac Disease

Hypertension, coronary artery disease, and lar heart disease are the most common cardiacdisorders associated with Afib, and are found inroughly 21%, 17%, and 15% of patients with Afib,respectively Afib is an unusual presentation ofcardiac ischemia or infarction, with the latteroccurring in 5.5% of patients seen in an emergencydepartment For valvular heart disease, mitralvalve disorders have a higher association with Afibthan do aortic valve disorders

valvu-Other cardiac diseases associated with Afibinclude hypertrophic cardiomyopathy, heartfailure, pericarditis, myocarditis, presence ofother supraventricular arrhythmias, cor pulmo-nale, cardiac surgery, and transplantation.CLINICAL FEATURES AND EVALUATIONPatients most commonly complain of palpita-tions, lightheadedness, fatigue, chest pain, ordyspnea However, many episodes of Afib areasymptomatic The physical examination mayreveal an irregularly irregular pulse, varyingintensity of the first heart sound, or murmursassociated with valvular disease

The ACC/AHA/ESC Practice Guidelinespresent a coherent plan for the evaluation of thepatient with Afib, described in the following text:

History and Physical Examination

The history should attempt to determine:

 Time of initial diagnosis or onset of symptoms

 Presence of other symptoms due to AfibParticular attention should be placed ondetermining if any of the risk factors or potentialcauses described in the prior section apply to thepatient

 Alcohol and medication use should be mined Precipitation of Afib with alcoholintake may also suggest vagal-mediated Afib,particularly if it also occurs at night or duringmeals

deter- Findings of heat intolerance, modest weightloss, changes in hair or skin texture, or hyper-reflexia should suggest hyperthyroidism.However, many patients may have subclinicalthyroid disease

 Dyspnea, history of tobacco use, tion, wheezing, or decreased breath soundsmay be consistent with chronic obstructivepulmonary disease Pleuritic chest pain, dys-pnea with lower extremity swelling, and arecent history of prolonged immobilizationsuggest a pulmonary embolus

hyperinfla- Evidence of cardiac disease, including tension, heart failure, history of supraventri-cular arrhythmias, or valvular disease should

hyper-be sought

Laboratory and Other Tests

A 12-lead electrocardiogram (EKG) should beobtained to ascertain the diagnosis of Afib AnEKG may also reveal evidence of cardiac ischemia,prior myocardial infarction, presence of otherarrhythmias, and left ventricular hypertrophy

A chest x-ray should be obtained to evaluatethe pulmonary parenchyma, vasculature, andcardiac silhouette.

Transthoracic echocardiography (TTE) should

be performed TTE can assess atrial size, cular size and function, and evaluate for valvularheart disease, pulmonary hypertension, and peri-cardial disease Although TTE may show leftatrial thrombus formation, it is not the diagnostictest of choice A transesophageal echocardiogram(TEE) should be performed to definitively assessfor the presence of left atrial thrombi

ventri-Thyroid function tests should be obtained toassess for hyperthyroidism

Further Testing

Holter Monitor and Exercise Tests

Holter monitoring may be helpful to establishthe diagnosis in patients with signs and symp-toms consistent with Afib, but in whom a routineEKG is unrevealing (i.e., paroxysmal Afib).Exercise testing may reveal associated cardiacischemia in patients with Afib In addition, bothHolter monitoring and exercise testing may beused to determine whether a patient’s ratecontrol is sufficient

Transesophageal Echocardiography (TEE)

The major role of TEE is to assess for left atrial

or left atrial appendage thrombus This may beuseful to determine whether there is an atrialthrombus in patients with ischemic stroke, orprior to cardioversion In patients with Afib forlonger than 48 hours, use of TEE to exclude anatrial thrombus prior to cardioversion resulted insimilar thromboembolism rates (<1%) comparedwith traditional anticoagulation strategies, whichuse 3 to 4 weeks of anticoagulation prior tocardioversion

Electrophysiological Study (EP Study)

EP studies may be utilized in patients who arecandidates for catheter ablation, AV conductionmodification, or pacemaker placement aspotential treatments for Afib

TREATMENT

Overview

The major issues in the management of Afib are:

 Should a rate-control or rhythm-controlstrategy be used?

 What is the best method to decrease therisk of thromboembolism?

 How should patients with recent onset ofAfib be managed?

 Which patients should be considered forurgent cardioversion?

Rate or Rhythm Control?

Theoretically, maintenance of normal sinusrhythm should be the optimal strategy, shoulddecrease the risk of thromboembolism, andshould result in better overall outcomes How-ever, two major studies, the Atrial FibrillationFollow-Up Investigation of Rhythm Manage-ment (AFFIRM) and Rate Control versus Elec-trical Cardioversion for Persistent Atrial

Fibrillation (RACE) trials, demonstrated thatthere is no significant difference in the embolicrisk between a rate-control and a rhythm-controlstrategy This is likely due to:

 Recurrence of Afib in patients aftercardioversion, with most episodes beingasymptomatic

 Presence of other risk factors for boembolism, such as atherosclerosis orheart failure

Therefore, anticoagulation should be usedregardless of whether a rate-control or rhythm-control strategy is chosen.

In addition, there was a trend to increasedmortality for the rhythm-control arm of theAFFIRM trial, which is likely due to medication-related adverse events The RACE trial alsoshowed a trend toward higher nonfatal adverseoutcomes in the rhythm-control arm

The results of these studies suggest that there

is no significant benefit to a rhythm-controlstrategy in terms of need for anticoagulation oroverall outcomes Thus, the American Academy

of Family Physicians/American College of sicians (AAFP/ACP) guidelines (2003) recom-mend that a rate-control strategy with

Phy-anticoagulation be used for most patients Arhythm control strategy should be reserved for:

 Patients who continue to have angina, heartfailure, dyspnea, or other symptoms despiteachieving good rate control (see followingtext for parameters of adequate ratecontrol)

 Patients who fail to achieve good ratecontrol

 Patients who prefer a rhythm-controlstrategy

A limitation of the already cited studies isthat the average patient age was over 68 yearsold These results may not be generalizable toyoung, otherwise healthy patients As a result,some experts may attempt cardioversion inyounger patients with a reversible cause of Afib(such as pericarditis, hyperthyroidism, or pul-monary embolism), and without hypertension,heart disease, or left atrial enlargement (leftatrial size should be<4.5 cm)

rhythm-control strategy Both methods requireanticoagulation to decrease the risk of throm-boembolism We will describe pharmacologicmethods for rate control here A discussion ofnonpharmacologic approaches to rate control isbeyond the scope of this chapter.

Targets for rate control differ among ent patient populations For example, a seden-tary patient with heart failure may require onlycontrol of ventricular rate at rest, whereas anactive, younger patient may require adequatecontrol of ventricular rate during exercise.The AFFIRM trial used the following criteria todefine successful rate control:

differ- Resting average heart rate<80 bpm

 Either one of the following:

○ Maximum heart rate during a 6-minutewalk<100 bpm, or

○ Average heart rate<100 bpm during24-hour Holter monitor, and heart rate

<110% of maximum predicted heart ratefor patient’s age at all times

The ACC/AHA/ESC guidelines state thatventricular rate should be maintained between

60 and 80 bpm at rest, and between 90 and

115 bpm with moderate exercise Practicallyspeaking, the goal is to achieve symptom controlduring a patient’s routine daily activities.Medications used to achieve rate control fallinto three groups:

 Beta-blocking agents, such as metoprolol oratenolol

○ Control ventricular rate at rest and ing exercise

dur-○ Beneficial in patients with Afib and heartfailure, myocardial ischemia, or infarction

○ Should be used with caution in patientswith pulmonary disease such as asthma

 Calcium channel blockers, such as mil and diltiazem

○ Control ventricular rate at rest and ing exercise

dur-○ Use with caution in patients with heartfailure or second- or third-degree AVblock

○ Verapamil increases the serum digoxin level

 Digoxin:

○ Controls ventricular rate at rest Lacksefficacy for control of ventricular rateduring exercise

○ Should not be used as first-line therapyfor rate control except in patients withAfib and heart failure

○ Has a slow onset of action and should not

be used for acute rate control

Overall, the most effective regimen appears to

be combination therapy with beta-blockers anddigoxin For monotherapy, beta-blockers are moreeffective than calcium channel blockers, anddigoxin is the least effective None of the threemedications should be used in patients withWolff-Parkinson-White syndrome

Acute Therapy

Both beta-blockers and calcium channel blockersmay be used for acute therapy of rapid ventri-cular rate Digoxin should not be used, because

it has an onset of action up to 60 minutes fromtime of infusion

 Metoprolol:

○ Give 2.5–5 mg IV over 2 min

○ May repeat every 5 min, as needed

○ Maximum IV dose is 15 mg

 Verapamil:

○ Give 5–10 mg IV over 2 min

○ May repeat every 15 min, as needed

○ Once rate control is achieved, may givecontinuous infusion of 0.125 mg/min tomaintain rate control

 Diltiazem:

○ For initial dose, give 0.25 mg/kg bodyweight IV over 2 min.

○ After 15 min, repeat with 0.35 mg/kg bodyweight given over 2 min, if necessary

○ In patients who respond to either 1 or 2 IVbolus doses, start maintenance infusion of

5 to 15 mg IV per hour

Chronic Therapy

Long-term ventricular rate control may beachieved with oral doses of beta-blockers,calcium channel blockers, digoxin, or a combi-nation of the previously mentioned drugs:

 Metoprolol: 25–100 mg orally twice a day

 Atenolol: 25–100 mg orally daily

 Verapamil: 40–120 mg orally three times aday

 Diltiazem: 30–90 mg orally four times a day

 Digoxin: 0.25 mg orally every 2 hr up to 1.5 mgtotal loading dose, then 0.125–0.375 mg orallydaily Digoxin levels should be monitored atabout 1 week when steady levels are achieved,

or when digoxin toxicity is suspected

In patients with rapid ventricular rate despitetreatment with these medications, amiodaronemay be used for rate control:

 Amiodarone: 800 mg orally daily for 1 week,followed by 600 mg daily for 1 week, then

400 mg daily for 4–6 weeks

 Amiodarone: 200 mg orally daily as tenance may then be continued after theloading regimen is completed

main-Due to the significant side effects, one should be initiated after consultation with acardiologist

amiodar-Rhythm Control

Results from the AFFIRM and RACE trials show

no significant difference in rates of embolic eventsbetween rate and rhythm control strategies There

may be a trend toward decreased overall mortality

in patients treated with rate-control Therefore,rhythm control is reserved for patients who:

 Fail an adequate trial of rate control:

○ Patients who have continued symptomsdespite good rate control

○ Patients who continue to have rapidventricular response despite use of maxi-mal pharmacologic rate control

○ Patients who fail rate control may need to bemaintained on anti-arrhythmic medications

○ Patients who fail rate may also be sidered for nonpharmacologic treatment

con-of Afib, including catheter ablation

 Prefer a rhythm control strategy

○ Routine use of anti-arrhythmic tions not recommended by the AAFP/ACP guidelines

medica-○ Anticoagulation is recommended

○ If rhythm control is unsuccessful in thesepatients, rate-control is recommended

 Have an initial episode of Afib

○ Routine use of anti-arrhythmic tions not recommended by the AAFP/ACP guidelines

medica-○ Anticoagulation is recommended

○ If rhythm control is unsuccessful,

initiation of rate-control is recommended

 Have Afib associated with symptoms andsigns of hypotension, heart failure, myocar-dial ischemia, or infarction despite maximalrate control

○ In the acute setting, these patients should

be considered for emergent cardioversion

Methods of Cardioversion

Either electrical or pharmacologic sion may be used Electrical cardioversion isaccomplished using a synchronized direct cur-rent delivered via electrodes on the patient’sthorax Pharmacologic cardioversion is achieved

using antiarrhythmic medications Both ods require appropriate anticoagulation orTEE, discussed in the section on prevention ofthromboembolism Although a detailed analysis

meth-of cardioversion is beyond the scope meth-of thischapter (the reader is referred to the ACC/AHA/ESC guidelines listed in the followingtext), a brief discussion follows Cardioversionshould be performed by an experiencedcardiologist

Electrical Cardioversion

Electrical cardioversion is more effective thanpharmacologic cardioversion, and is usually themethod of choice The patient is asked to fastovernight and is given conscious sedation prior

to the procedure Subsequently, electrode pads

or paddles are placed either in the anterior–posterior (sternum anteriorly and left subscapu-lar position posteriorly) or anterior–lateral (rightsubclavicular anteriorly and ventricular apexlaterally) positions Some data suggest that theanterior–posterior configuration may result in ahigher success rate compared to the anterior–lateral configuration

For monophasic waveform, an initial energysetting of 200 J, synchronized with the QRScomplex should be used The energy may beincreased by 100 J for additional shocks, to amaximum of 400 J A minimum of 1 minuteshould elapse between successive shocks tominimize myocardial damage The success rate forelectrical cardioversion is between 70% and 90%.The major risks associated with electricalcardioversion are thromboembolism, myocardialdamage, and arrhythmias Embolic events occur

in 1% to 7% of patients; this risk may bedecreased with appropriate anticoagulation prior

to cardioversion The risk of myocardial damage

is usually not clinically significant Benignarrhythmias, including premature beats, brady-cardia, and short sinus pauses may commonlyoccur after cardioversion Patients with abnormal

potassium or digitalis levels are at risk for thedevelopment of ventricular tachycardia or fibril-lation; potassium and digoxin levels should bedetermined prior to cardioversion Sinus nodedysfunction may be present in patients withchronic Afib These patients often have normalventricular rates without the use of pharmacolo-gic rate control Prophylactic pacemaker use may

be considered in these patients prior to version

The ACC/AHA/ESC guidelines state thatdofetilide, flecainide, propafenone, ibutilide, andamiodarone are efficacious in patients with Afib

of less than 7 days’ duration, while dofetilide,ibutilide and amiodarone may be useful inpatients with Afib of longer than 7 days’ duration

Prevention of Thromboembolism

As has been stated, the stroke risk for patientswith Afib is two to seven times that of age-adjusted controls and is higher in older patients.Use of aspirin or warfarin with a target Interna-tional Normalized Ratio (INR) of at least 2.0 to3.0 lowers the risk of thromboembolic events inpatients with Afib Risk factors for thromboem-bolism include a history of thromboembolism,hypertension, increasing age, diabetes mellitus,

coronary artery disease, hyperthyroidism, andfemale sex.

Chronic Prevention

Patients should be risk-stratified to determineappropriate therapy to prevent thromboembolism.The ACC/AHA/ESC guidelines recommend:

 Aspirin 325 mg orally daily for

○ patients under age 60 with heart diseasebut without risk factors of heart failure,hypertension, or left ventricular ejectionfraction less than 35%

○ Patients older than 60 without risk factors

○ Patients under age 60 without heartdisease or risk factors for thromboembo-lism may be treated with aspirin 325 mgorally daily, or no therapy

 Warfarin therapy should be offered, in theabsence of contraindications, for patientswho do not fall into these categories.Specifically,

○ Target INR 2.0–3.0 for patients with:

▪ Age >60 with diabetes mellitus or onary artery disease; Additional low-dose aspirin therapy optional

cor-▪ Age >75, particularly females

▪ Heart failure with left ventricular tion fraction less than 35%

ejec-▪ Hypertension or thyrotoxicosis

○ Target INR 2.5–3.5 for patients with:

▪ Rheumatic heart disease or mitralstenosis

▪ Prosthetic heart valves

▪ Prior thromboembolism

▪ Persistent atrial thrombus on TEEThe CHADS2 scoring system is another riskstratification method The CHADS2 values areassigned as follows:

 Congestive heart failure—1 point

 Hypertension—1 point

 Age>75—1 point

 Diabetes mellitus—1 point

 Secondary prevention for prior history ofthromboembolism—2 points

Therapy should be administered as follows:

 CHADS2 score of 0—low risk of boembolism Aspirin therapy may be used

throm-if no contraindications exist

 CHADS2 score>3—high risk of boembolism Warfarin therapy should beused if no contraindications exist

throm- CHADS2 score of 2 in a patient with priorhistory of thromboembolism—high risk ofthromboembolism Warfarin therapy should

be used if no contraindications exist

 CHADS2 score of 1 to 2—intermediate risk

of thromboembolism Determination ofaspirin or warfarin therapy should beguided by other clinical factors and patientpreference

Anticoagulation and Cardioversion

Patients with Afib of less than 48 hours’ durationand no risk factors for thromboembolism (seepreceding text) do not need 3 to 4 weeks of antic-oagulation prior to cardioversion However, thesepatients should receive heparin (unfractionated orlow molecular weight) before and during cardio-version, and anticoagulation (usually with war-farin) for at least 4 weeks after cardioversion.Afib of less than 48 hours’ duration in apatient with significant risk factors for throm-boembolism, including prior thromboembolicevent, valvular heart disease, or heart failure,should receive 3 to 4 weeks of warfarin therapyprior to cardioversion These patients should bemaintained on warfarin for at least 4 weeks aftercardioversion

Afib of unknown or greater than 48 hours’duration may be managed with either:

 Prolonged anticoagulation:

○ Patient is given 3–4 weeks of warfarintherapy, with a target INR of 2.5 (goal2.0–3.0) prior to cardioversion.

○ Lower risk of thromboembolic events isseen with an INR> 2.5 on the day ofcardioversion

○ Anticoagulation should be maintained for

at least 4 weeks after cardioversion

○ Anticoagulation should be maintained for aminimum of 4 weeks after cardioversion.REFERENCES

Guidelines

1 Fuster V, Ryden LE, Asinger RW, et al ACC/AHA/ESC guidelines for the management ofpatients with atrial fibrillation J Am CollCardiol 2001;38:1231–1266

2 Snow V, Weiss KB, LeFevre M, et al.Management of newly detected atrial

fibrillation: A clinical practice guideline fromthe American Academy of Family Physiciansand the American College of Physicians.Ann Int Med 2003;139:1009–1017

3 Singer DE, Albers GW, Dalen JE, et al.Antithrombotic therapy in atrial fibrillation:The Seventh ACCP Conference on

Antithrombotic and Thrombolytic Therapy.Chest 2004;126:429S–456S

Review Articles

1 Page RL Clinical practice Newly

diagnosed atrial fibrillation N Engl J Med.2004;351:2408–2416

2 Falk RH Atrial fibrillation N Engl J Med.2001;344:1067–1078

Rate Control versus Rhythm Control

1 Van Gelder IC, Hagens VE, Bosker HA, et al

A comparison of rate control and rhythmcontrol in patients with recurrent

persistent atrial fibrillation N Engl J Med.2002;347:1834–1840

2 Wyse DG, Waldo AL, DiMarco JP

A comparison of rate control and rhythmcontrol in patients with atrial fibrillation

N Engl J Med 2002;347:1825–1833

Cardioversion and Anticoagulation

1 Gage BF, Waterman AD, Shannon W, et al.Validation of clinical classification schemes forpredicting stroke: Results from the NationalRegistry of Atrial Fibrillation JAMA

2001;285:2864–2870

2 Go AS, Hylek EM, Chang Y, et al

Anticoagulation therapy for stroke prevention

in atrial fibrillation: How well do randomizedtrials translate into clinical practice? JAMA2003;290:2685–2692

3 Klein AL, Grimm RA, Murray RD, et al.Use of transesophageal echocardiography toguide cardioversion in patients with atrialfibrillation N Engl J Med 2001;344:1411–1420

4 Weigner MJ, Caulfield TA, Danias PG, et al.Risk for clinical thromboembolism associatedwith conversion to sinus rhythm in patientswith atrial fibrillation lasting less than 48hours Ann Int Med 1997;126:615–620

C H A P T E R 2 Heart Failure

K E Y P O I N T S

1 Systolic heart failure (HF) is caused byimpaired ventricular ejection of blood.Diastolic HF results from impairedrelaxation and filling of the left ventricleduring diastole

2 Symptomatic HF has a 1-year mortality

of almost 50%

3 The most common cause of HF is leftventricular systolic dysfunction, whichtypically results from coronary arterydisease

4 Symptoms of HF include dyspnea,orthopnea, paroxysmal nocturnal dys-pnea, fatigue, exercise intolerance,peripheral edema, and weight gain

5 Signs of HF include jugular venousdistension, extra heart sounds (S3in left-sided HF and S4in patients with in-creased resistance to ventricular filling),pulmonary crackles, wheezing, pleuraleffusion, and pitting edema

6 Initial testing should include electrolyteswith blood urea nitrogen and creatinine,complete blood count, PA and lateralchest x-ray, electrocardiogram, andechocardiography Cardiac catheteriza-tion is usually performed when noobvious cause for the HF is found orwhen myocardial ischemia is suspected

7 Chest x-ray findings of HF may beobscured or distorted if there is

underlying lung disease, and findingsmay be absent in patients with

chronic HF

23

8 HF is an unlikely cause of dyspnea inthe emergency room when an untreatedpatient has normal levels of B-typenatriuretic peptide.

9 Angiotensin-converting enzyme (ACE)inhibitors improve mortality, symptoms,left ventricular ejection fraction, andexercise tolerance and reduce hospitali-zations ACE inhibitors should beinitiated early during the treatment of

HF before excessive diuresis hasoccurred

10 Patients who develop a cough orangioedema with ACE inhibitor therapyshould be switched to an angiotensinreceptor blocker (ARB)

11 Patients who develop significant renalinsufficiency or hyperkalemia with ACEinhibitor or ARB therapy should beswitched to combination hydralazineand isosorbide dinitrate

12 Some beta-blockers such as carvediloland bisoprolol improve morbidityand mortality in patients with HF, butshould be initiated only after thepatient’s condition has stabilized andthe volume status has been

normalized

13 Digoxin reduces hospitalization ratesand improves symptoms and quality oflife but does not lower mortality inpatients with HF

14 Mineralocorticoid receptor antagonistshave shown promise in HF when usedwith ACE inhibitors but their concomi-tant use may be limited by hyperkalemia

15 Clinical trials testing medications fordiastolic HF are limited ACE inhibitorsand ARBs may improve exercisecapacity and reduce the risk of hospita-lization Diuretics are appropriate forvolume management but should be used

with caution because these patients aresensitive to excessive preload reduction.

16 Upon discharge, patients should beeducated about dietary salt and fluidrestriction and should weigh themselvesdaily on the same scale Early identifi-cation and treatment of HF can reducethe likelihood of hospitalization

D E F I N I T I O N S

Heart failure (HF): Clinical syndrome ized by signs and symptoms of volume over-load and reduced organ perfusion

character-Systolic heart failure:HF caused by impairedventricular ejection of blood

Diastolic heart failure:HF resulting fromimpaired relaxation and filling of the leftventricle during diastole Diastolic HF canoccur in patients with normal systolic

function or can coexist with systolic HF.Since the normal lower limit of the ejectionfraction is arbitrary, distinguishing betweendiastolic HF and systolic HF is sometimes dif-ficult At many medical facilities, an ejectionfraction below 50% is considered abnormal

EPIDEMIOLOGY

HF affects nearly 5 million Americans andaccounts for at least 20% of hospital admissionsamong people over 65 years of age Symptomatic

HF has a 1-year mortality of almost 50%, ferring a worse prognosis than most cancers

con-As many as one-half of the patients with HF havenormal or only minimally reduced systolicfunction, and are diagnosed with diastolic HF

Systolic Heart Failure

When the myocardium is weakened, the bodyattempts to maintain perfusion to vital organs byimproving cardiac output and using systemicvasoconstriction to redistribute blood flow.Reduced renal perfusion leads to activation ofthe renin–angiotensin–aldosterone system, whichcauses extracellular volume expansion that raisesend-diastolic volume and improves strokevolume via the Frank-Starling mechanism (thislaw states that increases in end-diastolic volumelead to increases in contractility and strokevolume) Catecholamines improve cardiac output

by increasing heart rate and contractility Thesecompensatory neurohormonal mechanisms areinitially beneficial but become deleterious overtime The systemic vasoconstriction increases theworkload of the heart, which can lead to furthermyocardial deterioration The raised diastolicpressures are transmitted to the pulmonary andsystemic veins, and can cause pulmonary con-gestion and peripheral edema Catecholamineactivation may worsen coronary ischemia orinduce cardiac arrhythmias Activation of therenin–angiotensin system causes sodium andwater retention and may promote further cardi-ovascular injury, including left ventricular hyper-trophy and remodeling

Diastolic Heart Failure

Diastolic HF occurs when there is reduced cardial relaxation (e.g., from ischemia, myocytehypertrophy, aging), increased passive stiffness ofthe ventricle (e.g., from infiltrative diseases such

myo-as hemochromatosis and amyloidosis), or limitedventricle mobility (e.g., from pericardial

tamponade or extrinsic compression by tumor)

In patients with left ventricular hypertrophy,ischemia may contribute to diastolic HF evenwhen there are no significant coronary stenoses,

because the elevated diastolic pressures mayimpair blood flow through capillaries and smallresistance vessels.

Causes and Precipitants

The most common cause of HF is left ventricularsystolic dysfunction, which typically results fromcoronary artery disease (Box 2-1) These patientsmay have a history of myocardial infarction or mayhave viable but underperfused myocardium Inpatients with a history of HF, a frequent precipitant

is dietary or fluid indiscretion or medication compliance Tachyarrhythmias (most commonlyatrial fibrillation) may reduce cardiac output bylimiting the duration of ventricular filling, increas-ing myocardial oxygen demands, and eliminating

non-‘‘atrial kick.’’ Atrial kick refers to atrial contraction,which promotes ventricular filling during diastole.Loss of atrial kick may precipitate HF in patientswith stiffened ventricles from diastolic dysfunction.Myocardial infarction or ischemia can cause ven-tricular stiffening (diastolic dysfunction), reducedmuscle mass for pumping blood, valvular leakagefrom papillary muscle dysfunction, and increasedoxygen demand from pain and tachycardia, all ofwhich may precipitate or contribute to HF.Systemic infections or hyperthyroidism increasethe metabolic rate, which increases the workload

on the heart Newly prescribed medications maycause salt retention, myocardial depression, orarrhythmias (Table 2-1)

SYMPTOMS

1 Dyspnea, orthopnea (dyspnea upon lyingsupine), and paroxysmal nocturnal dyspneaare common symptoms of pulmonary con-gestion Patients with paroxysmal nocturnaldyspnea describe wakening from sleepwith shortness of breath The presence and

severity of orthopnea can be assessed by ing (a) ‘‘With how many pillows do yousleep?’’ and (b) ‘‘With how many pillows didyou sleep weeks/months ago?’’ If there is anincrease in the number of pillows, ask whatsymptoms prompted the change Whenorthopnea is severe, patients may be unable

ask-to sleep in bed and may choose ask-to sleep in arecliner or chair

2 Fatigue, exercise intolerance, and mentalobtundation are symptoms of poor cardiacoutput

3 Peripheral edema suggests right-sided HF

4 Weight gain results from fluid retention

Box 2-1 Common Precipitants of Heart Failure

Table 2-1 Potentially Dangerous Medications in Patients with Heart Failure (HF)

Medication Precaution

Time to Onset of HF Recommendation

weeks

Use lowest dose possible Monitor for heart failure symptoms Nonsteroidal anti-

Avoid all class I anti-arrhythmics

Consider amiodarone or dofetilide if symptomatic or non-device-managed arrhythmias

Avoid in class III or IV heart failure and in patients with a history of hospitalizations for heart failure

Continued

Table 2-1 Potentially Dangerous Medications in Patients with Heart Failure (HF)—cont’d

Medication Precaution

Time to Onset of HF Recommendation

ino-trope and chromoino-trope

Hypokalemia promotes arrhythmias Adapted from Amabile CM and Spencer AP Keeping your patient with heart failure safe: A review of potentially dangerous medications, Arch Int Med 2004;164:709–720.

The goal of the focused physical exam is todetermine volume status and to search forpotential precipitants of the HF

1 Jugular Venous Distension

Jugular venous pressure (JVP), which reflectsright atrial pressure (central venous pressure),

is estimated by examining the internal jugularveins We do not recommend using the externaljugular vein pulsations to estimate central venouspressure, because valves in these veins may lead

to inaccurate readings To assess JVP, turn thepatient’s head slightly away from the side beingexamined and elevate the head of the bed to atleast 30 degrees until the jugular venous pulsa-tions are visible in the lower part of the neck.Several features help differentiate internal jugu-lar pulsations from carotid pulsations The inter-nal jugular vein is not visible (lies deep to thesternocleidomastoid muscles), is rarely palpable,and the level of its pulsations drops withinspiration or as the patient becomes moreupright

The jugular vein pulsations usually have twoelevations and two troughs The first elevation(a wave) corresponds to the slight rise in atrialpressure resulting from atrial contraction.The first descent (x descent) reflects a fall inatrial pressure that starts with atrial relaxation.The second elevation (v wave) corresponds toventricular systole when blood is entering theright atrium from the vena cavae while thetricuspid valve is closed Finally, the seconddescent (y descent) reflects falling right

atrial pressure as the tricuspid valve opensand blood drains from the atrium into theventricle

Once the highest point of internal jugularpulsation has been identified, the vertical dis-tance between this point and the sternal angle

represents the JVP Regardless of the patient’sposition, the sternal angle remains approximately

5 cm above the right atrium Venous pressuregreater than 3 to 4 cm above the sternal notch isconsidered elevated, suggesting right-sided HF,constrictive pericarditis, tricuspid stenosis, orsuperior vena cava syndrome

2 Heart

The heart examination should include ment of the cardiac impulse (lateral displace-ment suggests cardiomegaly), heart rate

assess-(decompensated HF causes tachycardia),rhythm, murmurs (such as aortic stenosis ormitral regurgitation), and extra heart sounds(S3or S4) An S3is a soft, low-frequency soundcaused by vibrations of the ventricular walls,valves, and supporting structures as blooddecelerates in the left ventricle during rapidventricular filling Although an S3is normal insome healthy children and young athletes, thepresence of an S3in older adults suggests anabnormality, such as left HF or mitral regurgita-tion The fourth heart sound (S4) is caused byvibrations in the ventricular walls and supportingstructures as blood from atrial contractiondecelerates in the ventricle An S4occurs whenthere is increased resistance to ventricular filling(diastolic dysfunction) A loud, widely split S2sup-ports the diagnosis of pulmonary hypertension.Muffled heart sounds and a globular heart on chestx-ray suggest a pericardial effusion and shouldprompt assessment for pulsus paradoxus (morethan 10 mmHg fall in systolic blood pressure withinspiration)

3 Lungs

a Crackles

The crackles (‘‘Velcro’’ sound) of HF aredescribed as ‘‘wet’’ as compared to the ‘‘dry’’crackles of pulmonary fibrosis, and are caused by

air moving through fluid-filled airways In mild

HF, crackles will be limited to the lung bases.Atelectasis also causes bibasilar crackles, but thecrackles of atelectasis clear after several repeatedinspirations Crackles will be detected higher inthe chest with worsening severity of HF.Crackles may be absent in patients with chronic

HF even in the setting of elevated pulmonarycapillary wedge pressure Also, crackles may bedifficult to hear in patients with emphysema orother coexisting pulmonary diseases

b Pleural Effusion

Pleural effusions in patients with HF usually donot require thoracentesis, and typically resolvewith diuresis Although effusions are classicallytransudative, diuretic therapy can cause theeffusion to become exudative In this setting, thetraditional Light’s criteria used to differentiatetransudative from exudative pleural effusionsmay be misleading and it may be more appro-priate to use the pleural fluid/serum albumingradient A gradient>1.2 g/dL suggests that theeffusion is likely due to HF

c Wheezing

Some patients with pulmonary edema developwheezing Potential mechanisms include reflexbronchoconstriction from elevation of pulmonary

or bronchial vascular pressure, and decreasedairway size from intraluminal edema andbronchial mucosal swelling

4 Pitting Edema

Right-sided HF reduces venous return to theheart and causes pitting edema of the lowerextremities Because gravity plays an importantrole in the formation of edema, patients who arepredominantly bed-bound may have very littlelower extremity edema even when there isprofound fluid overload In these cases, thepitting edema may be detected at the sacrum or

along the lower back Peripheral edema may beabsent in patients with chronic HF.

5 Cheyne-Stokes Respiration

Cheyne-Stokes respiration is a breathing der of sleep seen in almost one-half of HFpatients with ejection fractions below 40%.Cheyne-Stokes breathing is characterized by

disor-a crescendo–decrescendo disor-alterdisor-ation in tiddisor-alvolume separated by periods of apnea orhypopnea The mechanisms for Cheyne-Stokesrespiration are not fully understood, but mayinclude increased central nervous system sensi-tivity to changes in arterial partial pressures ofoxygen and carbon dioxide Therapeutic optionsinclude medical optimization of HF, nocturnaloxygen therapy, and nasal continuous positiveairway pressure

6 Other Findings

Other findings of right-sided HF include tosplenomegaly, ascites, and imaging evidence ofbowel wall edema (which may affect medicationabsorption) Other findings of left-sided HF andpoor cardiac output include mental obtundation,cool skin, and cachexia

hepa-LABORATORY DATA

Initial laboratory testing should include:

1 Electrolytes, blood urea nitrogen,

creatinine, and complete blood count (with differential if infection is suspected)

2 PA and lateral chest x-ray

Classic chest x-ray findings of HF include:a) Cardiomegaly—defined on chest x-ray as a

‘‘cardiothoracic ratio’’ (horizontal width of the