Case Files Cardiology.pdf

Eugene C. Toy, MdVice Chair of Academic Affairs and Clerkship DirectorDirector of Division of General Obstetrics-GynecologyDepartment of Obstetrics and GynecologyThe Methodist HospitalHouston, TexasClinical Professor and Clerkship DirectorDepartment of Obstetrics and GynecologyUniversity of Texas Medical School at HoustonHouston, TexasAssociate Clinical ProfessorWeill Cornell College of MedicineNew York, New York

Michael d . Faulx, MdAssistant Professor of MedicineCase Western Reserve University Lerner College of Medicine Cleveland, OhioAssociate Program DirectorInternal Medicine ResidencyCleveland ClinicCleveland, OhioStaff Cardiologist, Section of Clinical CardiologyMiller Family Heart and Vascular InstituteCleveland ClinicCleveland, Ohio

New York Chicago San Francisco Athens London Madrid Mexico City Milan New Delhi Singapore Sydney Toronto

CASE FILESCardiology

00_Toy-Cardiology_FM_p00i-xiv.indd 1 11/10/14 6:01 PM

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To the amazing members o our Cambodia medical mission team o 2014, who sacrif cially shared their talents and compassion to help hundreds o villagers in the

province o Kratie, Kingdom o Cambodia.

To my daughter A llison, our team leader, who is already showing wisdom at such a young age and is my hero.

To my wi e Terri, who served as team administrator and team mom, and is an organizational genius.

To our super nurses, Erin, Natalie, and Elizabeth, who went above and beyond each day, tending to the medical and spiritual needs o our patients.

To Amy, who organized and updated our pharmacy, keeping hundreds o dispenses straight.

To Khai and Meredith, our gi ted counselors, who shared the love o God each day;

And f nally to Archie and his amily, his leaders, his interpreters, and his church, who blazed the trail, ministered to us, and who continue Gods work in the lovely Kingdom

o Cambodia.

ECT

To my lovely wi e Ashley and my sons, Jackson and Gregory, or making it so easy to f nd balance and happiness in my li e. You are the reason I cant wait to get home every

evening.

To the medical students, residents, and ellows at Case Western Reserve University Lerner College o Medicine and Cleveland Clinic, or making it so easy to f nd balance and happiness in my career. You are the reason I cant wait to

get to work every morning.

MDF

d ed ic at io n


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c o n t en t s

Contributors / viiAcknowledgments / xiIntroduction / xiii

Section IHow to Approach the Cardiology Patient ................................................................ 1P r 1. c r v l r H ry Phy l ex ...................................... 2P r 2. a ppr h h el r r gr (ec G) ................................................ 22P r 3. c r v l r Pr v r Pr r ................................................. 40

Section IIClinical Cases .......................................................................................................... 57t h r y c s r ............................................................................................. 59c 15. c r ry V l r d ...................................................... 59c 610. s r r l H r d ............................................................... 125c 1115. Rhy h d r r .......................................................................... 177c 1620. P p d r r ............................................................................. 237c 2125. c l c pl .............................................................. 287c 2630. o h r c r d ................................................................. 335

Section IIIListing of Cases ..................................................................................................... 399L g y c n r ....................................................................................... 401L g y d r r (a lph l) ....................................................................... 402

Index / 403


vii

c o n t Ribu t o Rs

Mosi Bennett, Md , PhdAdvanced Heart Failure and Transplant CardiologistMinneapolis Heart Institute at Abbott Northwestern HospitalMinneapolis, Minnesota Acute decompensated heart ailure

E mon Cronin, Md , MRCPIStaff Physician, Cardiology and Cardiac ElectrophysiologyHartford HospitalHartford, ConnecticutAtrial f brillationSudden cardiac death

Mohame Elshazly, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioAcute type A aortic dissection

Michael d . Faulx, MdAssistant Professor of MedicineCase Western Reserve UniversityLerner College of MedicineCleveland, OhioAssociate Program DirectorInternal Medicine ResidencyCleveland ClinicCleveland, OhioStaff Cardiologist, Section of ClinicalCardiologyMiller Family Heart and Vascular InstituteCleveland ClinicCleveland, OhioAdult congenital heart diseaseHow to approach the cardiology patientCardiogenic shockApproach to the patient with chronic dyspneaCardiac risk assessment prior to noncardiac surgery

A am Gol berg, MdFellow, Cardiac Electrophysiology and Pacing Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioBradycardiaAV nodal reentrant tachycardia


viii c o n t Rib u t o Rs

Justin Gro in, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioCardiomyopathiesHypertension

Serge C. Harb, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland ClinicCleveland, OhioAcute pericarditis

Nael Hawwa, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland ClinicCleveland, OhioPulmonary hypertension

Michael Hoosien, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioChronic stable coronary artery diseasePreventive cardiology

Michael Johnson, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioIn ective endocarditis

Jason Lappe, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioWide complex tachycardia

Si harth Mahure, MdResearch FellowNYU Hospital for Joint DiseasesDepartment of Orthopaedic SurgeryShoulder & Elbow DivisionNew York, New YorkPeripheral arterial disease


c o n t Rib u t o Rs ix

Christopher May, MdAdvanced Cardiovascular Imaging FellowMiller Family Heart and Vascular InstituteCleveland Clinic Cleveland, OhioAnterior STEMINSTEMI

Kenneth A. Mayuga, Md , FACC, FACPClinical Instructor of MedicineCleveland Clinic Cleveland, OhioAssociate Staff, Section of Cardiac Electrophysiology and PacingMiller Family Heart and Vascular InstituteCleveland ClinicCleveland, OhioSyncope

Shruti Patel, MdResident, Nassau University Medical Center Department of Internal MedicineEast Meadow, New YorkHypertrophic cardiomyopathy

Liane Porepa, Md , FRCPC, FACCAdvanced Heart Failure CardiologistDirector, Heart Failure ProgramSouthlake Regional Health CentreNewmarket, Ontario, CanadaAdvanced heart ailure and transplantation

Grant Ree , MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland ClinicCleveland, OhioSevere aortic stenosisChest pain, undi erentiated

Brett Sperry, MdFellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioAcute RV ailure complicating MIChronic heart ailure


x c o n t Rib u t o Rs

Newton Wiggins, MdChief Fellow, Cardiovascular Medicine Miller Family Heart and Vascular Institute Cleveland Clinic Cleveland, OhioAcute aortic valve regurgitationChronic aortic valve regurgitation

Allison L. ToySenior Nursing StudentScott & White Nursing SchoolUniversity of Mary Hardin-BaylorBelton, TexasPrimary Manuscript Reviewer


xi

a c kn o w Led Gmen t s

The curriculum that evolved into the ideas for this series was inspired by Philbert Yau and Chuck Rosipal, two talented and forthright students, who have since graduated from medical school. It has been a tremendous joy to work with my excellent coauthor, Dr. Michael Faulx, who exemplifies the qualities of the ideal physiciancaring, empathetic, and brilliant educator who can make complex topics understandable; he also has the unique ability to bridge the disciplines of internal medicine and cardiology, no easy feat!

Michael D. Faulx would like to acknowledge Dr. Eugene Toy for his vision for and commitment to this wonderful book series. He would also like to acknowledge Catherine Johnson and Cindy Yoo for their helpful editorial suggestions and Anu-priya Tyagi for her tireless attention to detail. He lastly wish to acknowledge the Cleveland Clinic Department of Medical Art and Photography, particularly Joe Pangrace, Jeff Loerch, and Ken Celebucki for their outstanding medical illustrations.

I am greatly indebted to my editor, Catherine Johnson, whose exuberance, experi-ence, and vision helped to shape this series. I appreciate McGraw-Hills belief in the concept of teaching through clinical cases. I am also grateful to Catherine Saggese for her excellent production expertise, and Cindy Yoo for her wonderful editing. I cherish the ever-organized and precise Anupriya Tyagi who has nurtured this book from manuscript to print. It has been a privilege and honor to work with my daugh-ter Allison, a senior nursing student, who was the principal manuscript reviewer. I appreciate Linda Bergstrom for her sage advice and passion. At Methodist, I appre-ciate Drs. Judy Paukert, Marc Boom, and Alan Kaplan for their support. Without my dear colleagues, Drs. Konrad Harms, Priti Schachel, Gizelle Brooks Carter, and Russell Edwards, this book could not have been written. Most of all, I appreciate my ever-loving wife Terri, and our four wonderful children, Andy and his wife Anna, Michael, Allison, and Christina, for their patience and understanding.

Eugene C. Toy and Michael D. Faulx


xiii

in t Ro d u c t io n

Mastering the cognitive knowledge within a field such as cardiology is a formidable task. It is even more difficult to draw on that knowledge, procure and filter through the clinical and laboratory data, develop a differential diagnosis, and, finally, to make a rational treatment plan. To gain these skills, the student learns best at the bedside, guided and instructed by experienced teachers, and inspired toward self-directed, diligent reading. Clearly, there is no replacement for education at the bed-side. Unfortunately, clinical situations rarely encompass the breadth of the specialty. Perhaps the best alternative is a carefully crafted patient case designed to stimulate the clinical approach and the decision-making process. In an attempt to achieve that goal, we have constructed a collection of clinical vignettes to teach diagnostic or therapeutic approaches relevant to cardiology.

In this age of technology and high-definition imaging, we would like to reinforce the importance of the history and physical examination. We urge that students diligently read through this area in Section I of the book, and practice their skills. We likewise urge our peer colleagues to spend time demonstrating to students and trainees how to properly perform the physical exam maneuvers. We hope that our cases will stimulate excitement for the clinical care of patients.

Most importantly, the explanations for the cases emphasize the mechanisms and underlying principles, rather than merely rote questions and answers. This book is organized for versatility: it allows the student in a rush to go quickly through the scenarios and check the corresponding answers, and it allows the student who wants thought-provoking explanations to obtain them. The answers are arranged from simple to complex: the bare answers, an analysis of the case, an approach to the per-tinent topic, a comprehension test at the end, clinical pearls for emphasis, and a list of literature sources for further reading. The clinical vignettes are purposely placed in random order to simulate the way that real patients present to the practitioner. A listing of cases is included in Section III to aid the student who desires to test his/her knowledge of a certain area, or to review a topic, including basic definitions. Finally, we intentionally did not use a multiple-choice question format in the case scenarios, because clues (or distractions) are not available in the real world.


SECTION I: HOw TO Appr OACH THE CAr d IOl Og y pATIENT 1

SECTION I

How to Approach the Cardiology Patient

Part 1 A oach to the patient (Histo an ph sica )

Part 2 A oach to the E ect oca io am (ECg )

Part 3 p ovi e s an p oce u es

01_Toy-Cardiology_Sec-I_p001-0056.indd 1 11/7/14 7:11 PM

2 CASE FIl ES: CAr d IOl Og y

Part 1. Cardiovascular History and Physical Examination

There are four main components of cardiovascular history and physical examination:

A. Taking a cardiovascular history

B. Performing the cardiovascular examination

C. Interpreting heart sounds

D. Evaluating cardiac murmurs

Despite the proliferation of medical technology over the past several decades, there remains no single imaging study or laboratory assay more valuable to patient care than a proper history and physical examination (H&P). A thoughtful H&P will provide you with the correct diagnosis for most patients presenting with cardiovas-cular disease complaints. The act of performing the H&P also affords the caregiver an opportunity to forge a therapeutic relationship with the patient. The attention paid to a frightened patient by a thoughtful practitioner during the H&P, however brief, can have both diagnostic and therapeutic benefits. Finally, in this current era of cost-conscious medical care, there are few tools as cost-effective as a good H&P.

CLINICAL PEARL C The most im o tant too in the assessment o the atient ith ca iovas-

cu a isease is a e - e o me histo an h sica examination.

A. TAKING A CARDIOVASCULAR HISTORYPrior to entering into a discussion of the cardiovascular history, there are a few gen-eral rules of history taking that merit a review. The first is to establish a meaningful rapport with the patient. As the provider, you should be the adaptable member of this relationship as you will need to alter your history-taking approach from one patient to the next to account for differences in individual language comprehen-sion, cultural background, and level of education. The use of medical or technical jargon during the history should be avoided. Similarly, common colloquial medical terms should be carefully scrutinized as they often mean different things to different patients. For example, a patient may tell you that she has had five heart attacks in the past 2 years, but a careful review of her records reveals no evidence of myocar-dial infarction but rather five emergency department visits for chest pain and severe hypertension in the setting of medication noncompliance.

Another important skill in history taking is the ability to adjust ones interview style to best suit the patient and setting. It is generally advisable to begin the inter-view with open-ended questions (eg, What brings you to the emergency depart-ment today, Mr. Smith?) to allow patients to guide you through their histories. However, there are certainly patients who do not provide much open-ended infor-mation (eg, My wife made me come.), in which case direct initial questions may



Table I-1 A GENERAL APPROACH TO CARDIAC HISTORY TAKINGSymptom Feature Examplesd esc i tion Subjective cha acte (sha , u , bu nin , etc)?

l ocation ( oca , i use, e t, i ht, etc)?

Associate items r a iation o ain?Accom an in s m toms?

Seve it Nume ica sca e ( ain 110 o 10 sca e)?w ith activit (CCS o NyHA c ass 14)?

Timin Onset d u ation F equenc Tem o

w hen i s m tom sta t?Ho on i s m tom ast?Ho o ten oes s m tom occu ?A e s m toms becomin mo e o ess seve e?

In uences T i e s r e ieve s

Exe tion, eatin , bo osition, etc?r est, me ications, h sica mani u ation, etc?

Im ai ment l imitations at o k, ith Ad l s, socia i e, etc?

Note: Each atient s m tom shou be assesse o seve a ke eatu es as esc ibe above. CCS; Cana ian Ca io-vascu a Societ . NyHA; Ne yo k Hea t Association.

have a higher yield (eg, Have you been having any chest pain, Mr. Smith?) . It is helpful to repeat the history back to the patient to ensure that the patient agrees with the history as you understand it. This approach tends to give patients a greater sense of involvement in the evaluation process and also an opportunity to edit the history before you proceed with the physical examination.

Finally, it is important to be consistent and thorough in your approach to each element of the cardiovascular history (Table I-1). Every symptom should be assessed for its subjective description and overall level of severity. The timeframe for each symptom, including time of onset, duration, frequency, and pattern of evolution should be ascertained. Whenever possible, one should quantify symptom severity (eg, On a scale of 1 to 10 how severe was your chest pain? or How many yards can you walk before you develop calf pain?). It is also important to know whether the symptom has any clear triggers or relieving factors. Understanding how symp-toms impact the patients quality of life is also instructive (eg, We have discussed a number of symptoms, Mr. Jones; which one worries you the most?). You will occasionally find that the presenting complaint is not the patients major concern. For example, Mr. Jones may have visited the office today because his wife is worried about his newly swollen ankles, but the most concerning issue to Mr. Smith may be his worsening erectile dysfunction and the tension it is causing in his marriage.

CLINICAL PEARL C Be consistent in ou a oach to each e ement o the histo an acqui e

as much objective in o mation as ossib e.



Chest PainChest pain is the most common complaint presented by patients to cardiologists. The differential diagnosis for chest pain is quite broad and includes both cardiac and noncardiac conditions. A full review of the approach to chest pain is beyond the scope of this introductory chapter, but the topic of chest pain is covered as a case file later in this book. In a patient complaining of chest pain, the principal concern is whether the patient is experiencing angina, or chest pain secondary to myocardial ischemia. Chest pain can be classified as typical for angina, atypical for angina, or noncardiac, on the basis of its description, triggers, and response to intervention (Table I-2).

Typical angina pectoris is relatively easy to recognize; unfortunately, many patients with myocardial ischemia lack typical symptoms of angina, especially women and patients with diabetes mellitus. Angina is typically described as diffuse and pres-surelike and localizes to the retrosternal area. Dullness and burning are common descriptors of anginal chest pain, and the inability to adequately describe ones chest pain is also suggestive of angina. The act of balling the fist and holding it against the chest while trying to describe chest pain, called Levines sign, is actually fairly specific for angina. Pain radiating from the chest to the neck, jaw, or arms is sugges-tive of angina. Angina typically lasts between 5 and 30 minutes; chest pain lasting for mere seconds or for hours or days without resolution is practically never angina. Angina is usually triggered by physical activity or emotional distress and resolves with rest, relaxation, or sublingual nitroglycerin. Typical chest pain occurring 2030 minutes after a meal is also consistent with postprandial angina, although this often is mislabeled as esophageal reflux or dyspepsia. Chest pain provoked or worsened by manual palpation is unlikely to be angina.

Angina severity is commonly graded using the Canadian Cardiovascular Soci-ety (CCS) classification system (Table I-3). Class 3 or 4 angina is considered to be severe. Recent-onset (within 2 weeks) severe angina is referred to as unstable angina and generally requires hospitalization and immediate medical attention.

Table I-2 CHARACTERIZATION OF CHEST PAIN AS TYPICAL FOR ANGINA, ATYPICAL FOR ANGINA, OR NONANGINAL ACCORDING TO KEY CLINICAL FEATURESFeatures Aggravating Factors Alleviating Factorsd i use subste na iscom o td u , essu e ike qua it r a iation to neck o ja 530-minute u ation

ph sica exe tionEmotiona ist esspost an ia state*

r est o e axationNit o ce in

Typical chest ain A three o the above

Atypical chest ain An two o the above

Non-anginal chest ain One or none o the above*Chest ain that consistent be ins a oximate 30 minutes a te mea s is su estive o ost an ia an ina.



Table I-3 CLASSIFICATION OF ANGINA AND DYSPNEA SEVERITYClass CCS Angina NYHA Dyspnea1 O ina h sica activit oes not cause an ina;

an ina occu s on ith st enuous, a i , o o on e h sica activit at o k o u in ec eation

No imitation o h sica activit ; h sica activit oes not cause s nea, ati ue, o a itations

2 S i ht imitation o h sica activit ; an ina occu s ith a kin > 2 b ocks o c imbin > 1 FoS ith usua ace an ci cumstances or occu s ith ess istance i un e st ess ( a i ace, stee inc ine, a te mea s, emotiona u set, ea mo nin )

S i ht imitation o h sica activit ; com o tab e at est but ext ao ina h sica activit causes s nea, ati ue, o a itations

3 Ma ke imitation o h sica activit ; an ina occu s ith a kin 12 b ocks o < 1 FoS at usua ace an ci cumstances

3A. l imite activit ; com o tab e at est but o ina activit causes s nea, ati ue, o a itations3B. Si ni icant imitation; com o t-ab e at est but ess than o ina activit causes s nea, ati ue, o a itations

4 Inabi it to e o m an h sica activit ithout an ina; an ina ma be esent at est

Inabi it to e o m an h sica activit ithout s nea, ati ue, o a itations; s m toms ma occu at est

Abbreviations: CCS, Cana ian Ca iovascu a Societ ; NyHA, Ne yo k Hea t Association; FoS, f i ht o stai s.

Angina present for more than 2 weeks that is clearly triggered by predictable physi-cal activity is termed stable angina and is often managed in the outpatient setting.

Another common type of chest pain encountered in patients with heart disease is inflammatory chest pain, which can accompany conditions such as pericarditis, myocarditis, or acute pulmonary thromboembolism. Unlike angina, inflammatory chest pain is typically sharp and focal. It is commonly pleuritic, becoming more severe during inspiration or laying supine and improving with expiration or lean-ing forward. Pleuritic chest pain that can be reproduced by manual palpation of the chest wall is most likely related to costochondritis. Pulmonary infections such as pneumonia can also produce pleuritic chest pain, although there are often other symptoms that support the diagnosis such as fevers or productive cough. Pulmo-nary thromboembolic disease can also cause pleuritic plain and should be considered early in the differential diagnosis of any patient with pain and risk factors for venous thromboembolic disease. The combination of severe, tearing, or ripping chest and/or back pain and hypertension raises the concern for an acute aortic syndrome such as aortic dissection. The evaluation and differential diagnosis of the patient present-ing with chest pain is separately discussed later in this book.

CLINICAL PEARL C women an iabetic atients a e mo e ike to ex e ience at ica s m -

toms u in e iso es o m oca ia ischemia.



Shortness of BreathShortness of breath (dyspnea) is another common symptom that can be the present-ing complaint for many cardiac diagnoses, including heart failure, valvular heart dis-ease, atrial fibrillation, and even myocardial ischemia. As with angina, we quantify shortness of breath using a four-point scale developed by the New York Heart Asso-ciation (NYHA; Table I-3). Shortness of breath accompanied by difficulty breathing while supine (orthopnea) or paroxysmal nocturnal dyspnea (PND) is strongly sug-gestive of increased left atrial pressure, a common feature of heart failure or left-sided valvular heart disease. Associated symptoms such as exercise tolerance and fatigue are also suggestive of shortness of breath due to cardiovascular causes. Heart failure is also frequently accompanied by central volume overload; this may be heralded by symptoms such as leg swelling (edema), weight gain, or tighter-fitting clothes. Excessive somnolence, profound weakness, and a subjective decrease in urine output that accompanies shortness of breath may be features of advanced heart failure with low cardiac output. It should be noted that symptoms attributable to heart failure can be present in the setting of normal left ventricular systolic function. The dif-ferential diagnosis of dyspnea is enormous and includes a wide range of cardiac and noncardiac diagnoses. The evaluation and differential diagnosis of the patient pre-senting with shortness of breath is separately discussed later in this book.

Dizziness and SyncopeLoss of consciousness (syncope) and dizziness are also common cardiovascular com-plaints with a broad differential diagnosis. These complaints are common in patients presenting with rhythm disorders (both tachy- and bradyarrhythmias) and structural heart disease, particularly conditions that limit ventricular outflow such as aortic or mitral valve stenosis, or hypertrophic cardiomyopathy with dynamic obstruction of the left ventricular outflow tract. Syncope that occurs during or just after physical exertion suggests the presence of reduced outflow. Syncope that is accompanied by palpitations suggests the presence of a tachyarrhythmia. Syncope accompanied by lightheadedness and nausea and followed by diaphoresis suggests a neurocardiogenic cause such as vasovagal syncope. Ominous syncope features include abrupt onset without warning, prolonged unconsciousness, and injury as a result of syncope; these features suggest a high-risk cause for syncope such as a malignant arrhythmia.

CLINICAL PEARL C A e is an im o tant o nostic acto in atients esentin ith s n-

co e. patients a e 60 ea s o ten have s nco e ue to oten-tia an e ous ca iac causes.

Adjunctive HistoryA complete cardiac H&P should include a thorough noncardiac review of sys-tems. This is important because cardiovascular diseases can have extracardiac



manifestations and noncardiac illnesses can have cardiovascular implications. For example, erectile dysfunction in an otherwise asymptomatic patient might suggest the presence of occult vascular disease. Alternatively, a history of rash with swol-len and painful joints can indicate the presence of rheumatoid arthritis, a diagnosis associated with an increased risk for many cardiovascular problems including coro-nary artery disease, pericarditis, and pulmonary arterial hypertension. Some noncar-diac conditions are highly prevalent among patients with heart disease, particularly obstructive sleep apnea (OSA). Untreated severe OSA can have a major impact on a patients general health and quality of life, and for this reason it is important to inquire about the signs and symptoms of OSA during the H&P, including daytime sleepiness, snoring, witnessed apneas, and cognitive impairment.

Another important and often overlooked feature of the H&P involves a thor-ough review of the patients medication list for potential drug-drug or drug-food interactions and adverse drug reactions (ADRs). In some cases the patients present-ing complaints may be related to the adverse effects of their prescribed medications. Although some cardiovascular medications have well-described side effects or inter-action potential (Table I-4), one must maintain a high index of suspicion for ADRs related to any agent, particularly when a patient has symptoms that are not readily explainable despite extensive evaluation or bear some temporal relationship to a

Table I-4 COMMONLY PRESCRIBED CARDIAC MEDICATIONS AND THEIR POTENTIAL ADVERSE EFFECTSDrug Class Examples Common Adverse EffectsACE inhibito s l isino i , ami i Non o uctive cou h

A oste one ece to b ocke s

S i ono actone g necomastia

Anticoa u ants wa a in, abi at an, iva oxaban, a ixaban

B ee in , co sensation ( a a in)

Anti ate et a ents As i in, c o i o e , asu e , tica e o

B ee in , s nea (tica e o )

Beta b ocke s Ca ve i o , meto o o , ateno o , o ano o

Fati ue, e ecti e s unction, sho tness o b eath*

Ca cium channe b ocke s

Am o i ine, i tiazem, ve a ami l e e ema, consti ation

HMg -CoA e uctase inhibito s

r osuvastatin, ato vastatin, avastatin, simvastatin

Musc e ain an eakness

H a azine H a azine Ab omina ain, u us ike s m toms ( a e)

Nicotinic aci Niacin, Nias an Facia ushin

Nit o ce in Sub in ua , isoso bi e init ate an mononit ate

Hea ache

Abbreviations: ACE, an iotensin-conve tin enz me; HMg -CoA, 3-h ox -3-meth - uta -coenz me A.*Sho tness o b eath is mo e ike to occu in atients takin non-1-se ective a ents (ca ve i o , o ano o ) ho have a histo o eactive ai a isease o b onchos asm.



recent hospital discharge, office visit, or other encounter where medications may have been introduced or changed. In keeping with this theme, it is also important to inquire about the use of over-the-counter and alternative medical agents.

B. PERFORMING THE CARDIOVASCULAR EXAMINATIONThe physical examination of the cardiac patient, particularly cardiac auscultation, has intimidated medical students and residents alike since the invention of the stethoscope by Dr. Ren Laennec in 1816. The process of examination and cardiac auscultation can be challenging, but the experience need not be stressful if one has a solid understanding of cardiovascular physiology, a good stethoscope, a quiet examination area, patience, and a bit of curiosity. Like most things in life, good examination skills develop with practice over time. You should also appreciate the limitations of the physical examination; even the most experienced cardiologist will miss a soft diastolic murmur in a tachycardic, morbidly obese patient on mechanical ventilation in a noisy intensive care unit. Whenever possible, it is useful to com-pare your examination findings to the findings of dynamic cardiac studies such as echocardiograms and magnetic resonance images (MRIs). Did you miss the murmur of the severe, posteriorly directed mitral regurgitation that was seen by echocardiog-raphy? Go back and listen to the patient again, armed with the knowledge of the imaging study. You will probably hear the murmur and be able to recognize it when you admit your next patient with severe mitral regurgitation.

Nonauscultory ExaminationThe cardiovascular examination should begin with a general inspection of the patient and the patients chest. You should note any obvious abnormalities, as these may provide you with diagnostic clues. Does the patient have any scars indicative of prior cardiac surgery? Is there an implanted cardiac device? Are there any chest wall deformities that might indicate a congenital disorder such as Marfan syndrome (pectus excavatum or carinatum) or Turner syndrome (shield-shaped chest)?

Blood pressure measurements should be obtained from both arms and compared; differences in systolic and diastolic blood pressures of greater than 10 or 5 mmHg, respectively, are considered abnormal and may warrant further investigation for dis-orders such as aortic dissection or subclavian stenosis. If one suspects the diagnosis of aortic coarctation, then bilateral lower extremity blood pressure measurements should also be obtained.

Jugular Veins Examination of the right internal jugular vein allows for estimation of a patients central volume status and provides clues for the diagnosis of right-sided heart disease and pericardial disease. The right internal jugular vein is best examined with the patient seated at a 45 angle. It is noteworthy that, in patients with marked central volume overload, the top of the venous column of blood (meniscus) may not be visible until the patient is seated upright at 90. Similarly, patients with low filling pressures may not exhibit a visible meniscus until they are nearly flat (180).

To estimate the right atrial pressure, the examiner measures the distance between the sternal angle (angle of Louis) and the meniscus of the jugular pressure wave



(Figure I-1). The jugular venous pulsation may be distinguished from the carotid pulse by applying gentle tension to the overlying skin with your finger; this should obliterate the venous pulse, whereas the arterial pulse should remain visible. The center of the right atrium is approximately 5 cm below the angle of Louis, so the measured distance (in centimeters) between the angle of Louis and the meniscus plus 5 cm approximates right atrial pressure. Normal jugular venous pressure is 8 cm or less. Recall that 1 cm H2O is equivalent to 0.735 mmHg.

Increased jugular venous pressure is indicative of high right atrial pressure, and this finding can suggest several cardiac diagnoses, including left or right ventricular failure, tricuspid valve disease, and pericardial disease. During inspiration the nor-mal right heart will dilate in response to negative intrathoracic pressure and accom-modate more venous flow, resulting in a decrease of the jugular venous pulse (JVP). A paradoxical increase in the JVP during inspiration is called Kussmauls sign, and this finding is indicative of abnormal right ventricular filling. Kussmauls sign can be seen with pericardial disease (constriction and tamponade), restrictive cardiomy-opathies, and advanced right ventricular systolic failure. The response of the jugular venous pulse to prolonged abdominal palpation, termed hepatojugular reflux or the abdominojugular test, can also be a useful examination tool. With this maneuver, the JVP is observed during and after at least 10 seconds of sustained firm palpa-tion over the right upper quadrant or midepigastrium. This maneuver will increase venous return to the heart. A normal heart can quickly accommodate the extra pre-load, and the JVP will increase momentarily before returning to normal. Conversely, a patient with a sustained increase in JVP of >4 cm or an abrupt decrease in JVP of >4 cm on release of abdominal pressure is considered to have an abnormal response. Abnormal abdominojugular testing correlates with increased pulmonary capillary wedge pressure and is typically seen in patients with left ventricular failure.

Figure I-1 Estimation o the ju u a venous essu e.

45

5 cm

Right a trium

Meniscus

Angle of Louis



The normal jugular vein has two visible waves, the A and V waves (Figure I-2). A third small c wave is measurable invasively but is practically never seen on physi-cal examination. The c wave is essentially a ripple in the jugular waveform caused by the upward motion of the tricuspid valve during early right ventricular systole. The A and V waves are followed by negative pressure deflections, called the x and y descents, respectively. The A wave occurs just before the first heart sound (S1) and is caused by atrial contraction. If the patient has a fourth heart sound, the A wave will occur simultaneously with the S4. The x descent occurs during atrial relaxation after closure of the tricuspid valve. The V wave is the result of right atrial filling dur-ing ventricular systole and is normally smaller and broader than the A wave. The V wave is followed by the y descent, which is caused by emptying of the right atrium after opening of the tricuspid valve in early diastole.

Abnormalities of the right internal jugular venous waveforms are directly related to right-heart pathology. Consistently large A waves are present in disorders that result in right atrial pressure overload such as tricuspid stenosis or pulmonary hyper-tension. Intermittently large A waves, called cannon A waves, can be seen during arrhythmias when the right atrium contracts while the tricuspid valve is closed. Complete absence of the A wave occurs when there is no atrial contraction such as in atrial fibrillation. Large V waves indicate volume overload of the right atrium during ventricular systole; this most commonly occurs with tricuspid regurgitation but can also be seen in patients with atrial septal defects. The x and y descents are often affected by pericardial diseases. In pericardial tamponade one typically sees a prominent x descent because the contracting right ventricle occupies less space within the fluid-engorged pericardial sac during systole, reducing the pericardial pressure around the adjacent right atrium and allowing it to expand in size. During diastole, pericardial pressure is highest as the ventricles expand and passive flow between the right atrium and ventricle practically stops, producing an absent or significantly blunted y descent. In pericardial constriction, hemodynamic changes occur more as the result of tethering of the cardiac chambers to the noncompliant pericardium. The x descent is steep because the right atrium is pulled toward the contracting right ventricle during systole, expanding its size. The y descent is also prominent because the resting early diastolic pressure in the right ventricle is typi-cally much lower than the resting right atrial pressure, resulting in rapid early dia-stolic filling. The y descent abruptly ends by middiastole in constrictive pericarditis as the pressure hits a plateau (square-root sign) because the thickened pericardium limits full expansion of the right ventricle.

AC

X

S1 S2

V

Y

Figure I-2 The no ma cent a venous ave o m.



CLINICAL PEARL C Examination o the inte na ju u a vein usin ob ique i umination b a

en i ht can o ten make the ju u a venous u se easie to see.

Arterial Pulse The normal arterial pulse has an initial brisk upstroke followed by a systolic peak that corresponds to early ventricular ejection (Figure I-3). This is fol-lowed by a decline in systolic pressure as the elastic aortic walls expand to accom-modate the systolic pressure wave. Aortic valve closure produces the incisura, a small wave that appears at the end of the systolic pressure tracing in central aortic tracings but appears later in peripheral arterial tracings as the wave is transmit-ted down the arterial tree. Following systolic ejection, arterial runoff results in a decrease in atrial pressure during early diastole while pressure recovery due to the elastic recoil of the artery produces a plateau phase in the pressure tracing in late diastole.

Arterial pulses should be assessed for their contour, intensity, and timing relative to apical systolic ejection. Pulses with two palpable systolic peaks (bisferiens) can be due to dynamic left ventricular outflow obstruction or the combination of aortic valve stenosis and severe regurgitation; the latter is typically associated with a wid-ened pulse pressure. In contrast, low-volume pulses with palpable peaks in systole and early diastole are common in low-cardiac-output states and are referred to as dicrotic pulses. A weak pulse (parvus) with a delayed peak (tardus) is the hallmark of severe aortic stenosis. A palpable low-frequency vibration over a peripheral artery (thrill) is indicative of peripheral arterial stenosis.

Peripheral pulses can also vary with the respiratory cycle. A small (


ventricular systolic failure or as a consequence of frequent ectopic ventricular beats (ventricular bigeminy).

Precordial Palpation Palpation of the chest can provide useful diagnostic informa-tion. The patient should be examined in the supine and left lateral decubitus posi-tions, and palpation should be performed over the LV apex and across the upper and lower portions of the sternum with the hand covering the left and right parasternal areas. Normal palpation is straightforward; the examiner will feel nothing other than the LV apical impulse, which should feel like a gentle tap against the finger in the 5th intercostal space near the midclavicular line during early systole. The apical impulse should be approximately 2 cm in diameter and brief. Abnormalities of apical palpation are described in Table I-5. Please note that the apical impulse and point of maximal impulse (PMI) are not synonyms, although the apical impulse is the PMI in normal patients.

Palpable impulses adjacent to the sternum are abnormal and should be noted. Impulses felt at the lower sternal border are usually caused by anterior motion of the right ventricle. A sustained lower apical impulse during systole can be seen with RV pressure overload in conditions such as pulmonic stenosis or pulmonary hyper-tension. Rarely, severe mitral regurgitation can produce a vigorous systolic pulse at the lower sternal border due to displacement of the right ventricle by an enlarged left atrium; posterior displacement of the left atrium is hindered by the spine. A dynamic, sometimes visible lower apical impulse during diastole can be seen with atrial septal defects or severe pulmonic regurgitation. Upper sternal border impulses are usually caused by enlargement of the great arteries. Pulmonary artery enlarge-ment or increased pulmonary artery flow can produce a left upper sternal border pulsation, whereas palpable pulses at the right upper sternal border are usually due to aortic enlargement.

Table I-5 ABNORMALITIES OF THE APICAL IMPULSEApical Impulse Abnormality Causesw i e (>3 cm) o i use l e t vent icu a en a ement

l ate a is ace l e t vent icu a en a ement

Faint o non a ab e pe ica ia e usion o const iction; mo bi obesit ; COpd

d namic an b ie Acute mit a e u itation

d namic an sustaine l e t vent icu a h e t o h

Faint an sustaine Seve e ao tic stenosis; e t vent icu a s sto ic s unction

d oub e H e t o hic ca iom o ath ( ith namic l VOT obst uction

p es sto ic ( a ab e A ave)* Ao tic stenosis; h e t o hic ca iom o ath ; acute mit a e u itation

Abbreviations: COpd , ch onic obst uctive u mona isease; l VOT, e t vent icu a outf o t act.*p es sto ic a ica im u ses a e best a eciate b obse vin o movement o a stethosco e that is i ht a ie to the chest a u in auscu tation.



CLINICAL PEARL C Consi e the ia nosis o e ica ia tam ona e o atients ith h o-

tension an tach ca ia ho o not have a a ab e a ica im u se.

Cardiac AuscultationTo understand what you are hearing during cardiac auscultation, it is imperative that you understand what the valves and chambers are doing throughout the car-diac cycle and that you can readily identify systole and diastole (Figure I-4). Systole occurs between the first and second heart sounds and generally has a fixed dura-tion. Systole includes an early period of isovolumic contraction of both ventricles

Figure I-4 The no ma ca iac c c e. Cent a a te ia , venous, an vent icu a essu es a e sho n in conjunction ith the ECg an hono a hic in in s [AV; at iovent icu a va ves (t icus i an mit a )]. Semi una e e s to the u monic an ao tic va ves. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography 2013. All rights reserved.)

Semilunarclose

Centra l a rte ria l pressureSemilunaropen

Ventricula r pressure

AVopen

AVclose

S4Late dias tole Sys tole Early dias tole

S1 S2 S3

Atria l pressure



followed by the opening of the semilunar valves (aortic and pulmonic valves) and ventricular ejection. The atria are filling during systole.

Diastole occurs between the second and first heart sounds, and its duration var-ies with heart rate; at normal heart rates [under 100 beats per minute (


1 234

5

Figure I-5 Anatomic ocation o the ca iac soun s on the ante io chest a : 1ao tic va ve, 2n inte costa s ace, i ht ste na bo e ; 2 u monic va ve, 2n inte costa s ace, e t ste na bo e ; 3E bs oint, 3 inte costa s ace, e t ste na bo e ; 4t icus i a ea, 4th inte costa s ace, e t ste na bo e ; 5mit a a ea, 5th inte costa s ace, mi c avicu a ine (a ex). (Reprinted with permis-sion, Cleveland Clinic Center for Medical Art & Photography 2013. All rights reserved.)

Table I-6 TYPES AND CAUSES OF SECOND HEART SOUND (S2) SPLITTING

Normal ExaggeratedFixed

ParadoxicalVariable WideExpiration

Inspiration

Physiology Ne ative int atho acic essu e

r V vo ume ove oa

Inc ease pVr , e a e r V activation

Inc ease r V o

d e a e ao tic va ve c osu e

Causes No ma b eathin

pu monic e u itation, r V ai u e

pu mona h e tension,*r BBB, u monic stenosis

ASd Seve e AS, l BBB

Abbreviations: AS, ao tic stenosis; ASd , at ia se ta e ect; l BBB, e t bun e b anch b ock; pVr , u mona vascu a esistance; r BBB, i ht bun e b anch b ock; r V, i ht vent ic e. A2 an p2 e esent the ao tic an u monic va ve cont ibutions to S2, es ective .*The intensit o p2 is a so inc ease .

A2 A2 A2p2 p2 p2p2

p2



The fourth heart sound (S4) occurs in late systole just before S1. It is also a low-pitched sound best heard with the bell of the stethoscope. S4 is caused by turbulent filling of the ventricle in late diastole during atrial contraction; patients in atrial fibrillation cannot have an S2. The presence of S4 correlates with increased left ventricular stiffness and is commonly seen in conditions such as systemic hyperten-sion, severe aortic stenosis, hypertrophic cardiomyopathy, and myocardial ischemia.

Some abnormal heart sounds are fairly specific indicators of certain cardiac diag-noses. The opening snap (OS) is a brief, high-pitched sound heard in early diastole in patients with stenosis of the mitral or (less commonly) tricuspid valve. Patients with left atrial myxomas can present with a middiastolic tumor plop that can be distinguished from the opening snap by its very low pitch, best heard with the bell of the stethoscope. The OS associated with mitral stenosis is heard best at the lower left sternal border and radiates to the base of the heart. The presence of an OS implies that the mitral valve remains somewhat pliable; in advanced stenosis of a heavily calcified mitral valve, the OS typically disappears. The time interval between S2 and the OS, which represents the period of isovolumic relaxation, is inversely pro-portional to the severity of mitral stenosis, although any process that increases LA pressure can affect the S2-OS interval. The OS can be distinguished from a split S2 by having the patient stand during auscultation; the S2-OS should widen as preload decreases, but a split S2 should not change in duration. Clicks are also heard during cardiac auscultation. Early systolic or ejection clicks occur just after S1 and reflect abnormal semilunar valve opening or robust early systolic flow across a semilunar valve. Causes of ejection clicks include bicuspid aortic valve, congenital pulmonic valve disease, or dilatation of the aortic root or pulmonary artery. Midsystolic clicks are most commonly caused by mitral valve prolapse. Mitral valve clicks are affected by left ventricular loading conditions; decreasing preload by standing or performing the Valsalva maneuver will produce an earlier click, while increased preload from squatting or leg elevation will result in a later click.

Pericardial friction rubs can be heard in patients with active pericardial inflam-mation. The classic rub has three components heard in late diastole, systole, and early diastole. Friction rubs have a characteristically squeaky sound that is best heard with the patient leaning forward during inspiration. Friction rubs are notori-ously transient accumulation of a pericardial effusion.

CLINICAL PEARL C I ou ant to kno hat a e ica ia iction ub soun s ike, sim o to

a ca iotho acic osto e ative unit an ask e mission to examine atients ho have un e one ca iac su e ithin the evious 48 hou s; vi tua a o these atients have osto e ative e ica itis, an thei iction ubs a e t ica ou . Ext a c e it: A so have a eek at thei ECg s.

D. EVALUATING CARDIAC MURMURSBlood flow within the heart is generally laminar and quiet. Murmurs are produced by turbulent flow between cardiac chambers or across cardiac valves and in most cases indicate some sort of pathology. Murmurs can be caused by valve stenosis,



valve regurgitation, or abnormalities within the cardiac chambers due to some form of obstruction (hypertrophic cardiomyopathy) or shunt [atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA)].

Murmurs are classified principally by the phase of the cardiac cycle during which they occur (systolic, diastolic, or continuous) and can be further subcategorized by their timing within each phase (late systolic, holodiastolic, midpeaking systolic). The shape or contour of the murmur is commonly described and refers to the pat-tern of the murmurs intensity (crescendo, decrescendo, crescendo-decrescendo, or diamond-shaped or plateau). The subjective description a murmurs sound is also helpful (low-pitched/rumbling versus high-pitched/musical). The location of the murmur on the chest wall is also important in identifying the source of the mur-mur (Figure I-5). In certain circumstances it is helpful to have the patient perform maneuvers during auscultation in order to alter loading conditions. For example, right-sided murmurs typically vary much more in response to the respiratory cycle or Valsalva maneuver than left-sided murmurs. Although aortic stenosis and hyper-trophic cardiomyopathy (HCM) both produce harsh systolic murmurs at the right upper sternal border, the murmur of HCM is dynamic and will soften with handgrip and become louder with the Valsalva maneuver.

Systolic murmur intensity is graded using a six-point scale (Table I-7). Grade 1 systolic murmurs are barely audible with a stethoscope and are most commonly due to increased transvalvular flow rather than actual valve pathology. Conversely, grade 6 murmurs are loud enough to be heard with the stethoscope off the chest wall, and in some cases they are audible without a stethoscope. A systolic murmur that is grade 4 or louder is associated with a palpable thrill. Diastolic murmurs are usually graded on a four-point scale (Table I-7). Diastolic murmurs are always abnormal and warrant investigation.

Systolic MurmursMost murmurs during systole arise from stenosis of the semilunar valves (aortic and pulmonic) or regurgitation of the atrioventricular valves (AV valves; mitral and tricuspid) (Figure I-6). Systolic murmurs also occur as the result of ventricular septal

Table I-7 GRADING CARDIAC MURMURSSystolic Murmurs Diastolic Murmurs

Grade Description Grade Description1 Ba e au ib e in quiet oom 1 Ba e au ib e

2 So t but au ib e ith ambient noise 2 Au ib e but so t

3 C ea au ib e ithout th i 3 r ea i au ib e

4 l ou ith th i 4 l ou , th i ike

5 Ve ou ith th i

6 Ve ou ith th i ; mu mu is au ib e ith stethosco e o chest o ithout stethosco e at a


Centra l a rte ria l pressure

Atria l pressure


S1 S2 S1 S2Sys tole Dias tole Sys tole Dias tole

Figure I-6 Common causes o s sto ic mu mu s. Cent a hemo namic ave o ms a e sho n in conjunction ith hono a hic in in s inc u in the sha e o the mu mu . The ca iac c c e on the e t e icts at iovent icu a (AV; t icu si o mit a ) va ve e u itation. The ca iac c c e on the i ht e icts semi una ( u monic o ao tic) va ve stenosis. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography 2013. All rights reserved.)

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defects and dynamic obstruction of the left ventricular outflow tract in patients with HCM. The duration of the murmur in systole is important in the identification of systolic murmurs.

Holosystolic murmurs begin early in systole and tend to last for the duration of systole. AV valve regurgitation and ventricular septal defects are the main causes of holosystolic murmurs. Regurgitant AV valves tend to produce decrescendo, high-pitched murmurs, whereas murmurs due to VSD tend to be plateau-shaped. The pitch can vary greatly with the size of the defect and the systolic pressure gradient between the ventricles.

Midsystolic murmurs are most commonly caused by stenosis of the semilunar valves or dynamic left ventricular outflow tract (LVOT) obstruction. These mur-murs are usually diamond-shaped and tend to have lower pitch than holosystolic murmurs. Soft midsystolic murmurs are often called innocent (innocuous) mur-murs and are usually due to increased flow across a normal pulmonic valve. The murmur of aortic stenosis is harsh, and with severe stenosis, the murmur can obscure the second heart sound and radiate to the carotid arteries. The murmur of HCM with LVOT obstruction can be similar to that of aortic stenosis, but the diagnosis can nonetheless be made reliably by physical examination. HCM causes dynamic obstruction, so maneuvers that reduce left ventricular preload and/or afterload (Valsalva, use of amylnitrite) will increase murmur intensity, whereas maneuvers that increase ventricular preload and/or afterload (handgrip, squatting) soften the murmur. Aortic stenosis causes fixed obstruction, and thus the murmur remains unchanged during these same maneuvers. The murmur of HCM generally originates along the left lower sternal border and rarely radiates to the carotids, whereas aortic stenosis murmurs are loudest at the base of the heart and commonly project to the carotids.

Late systolic murmurs (murmurs that begin after midsystole) are uncommon and are best heard at the left ventricular apex. They can be due to mitral regurgita-tion caused by prolapse, and in this circumstance they may follow the midsystolic click. Late systolic murmurs can also be heard in patients with advanced ischemic heart disease, possibly as a result of mitral valve dysfunction caused by papillary muscle ischemia.

Pansystolic murmurs are typically caused by ventricular septal defects (VSDs). VSD murmurs often have a rectangular profile and an associated thrill, but their loudness and contour are heavily influenced by the pressure difference between the ventricles and the size of the defect.

CLINICAL PEARL C Be si e han i is a ast an eas maneuve to he istin uish bet een

the mu mu s o h e t o hic ca iom o ath an ao tic stenosis. Han - i i inc ease a te oa , e ucin the namic l VOT a ient an so tenin the mu mu . Ao tic stenosis is ixe an i not chan e ith han i .



Diastolic MurmursDiastolic murmurs are typically caused by stenosis of the atrioventricular (AV) valves or regurgitation of the semilunar valves (Figure I-7).

Early diastolic murmurs begin immediately after S2 and are caused by regurgita-tion of the semilunar valves. These murmurs are typically decrescendo in contour and high-pitched; they are best heard with the diaphragm of the stethoscope. The murmur of aortic regurgitation can be faint and difficult to hear. Maneuvers that increase afterload such as grip will increase the severity of aortic regurgitation and produce a louder murmur.

Middiastolic murmurs are most often caused by stenosis of the AV valves. These diastolic filling murmurs are low pitched or rumbling and typically loud. They tend to have a decrescendo-crescendo contour and are best heard with the bell of the stethoscope. The severity of AV valve stenosis is reflected more by the duration of the murmur than the murmurs loudness, which is proportional to transvalvular flow. A classic example of a middiastolic murmur is the murmur of mitral stenosis. The murmur of mitral stenosis begins with the opening snap (OS) and it is most clearly heard at the left ventricular apex. As the severity of mitral stenosis increases, the OS occurs earlier in diastole and the length of the murmur increases. At the same time there is a decrease in cardiac output that results in a decrease in murmur intensity.

Severe, acute aortic regurgitation can sometimes result in a middiastolic murmur due to diastolic mitral regurgitation. Diastolic mitral regurgitation occurs when left ventricular diastolic pressure exceeds left atrial pressure due to high-volume regur-gitation, resulting in reversal of flow from the left ventricle to the left atrium. In chronic severe aortic regurgitation, this same phenomenon can occur in late systole as the left ventricle dilates in response to chronic volume overload. The late systolic murmur of diastolic mitral regurgitation caused by severe chronic aortic regurgita-tion is commonly referred to as the Austin-Flint murmur.

Late diastolic or presystolic murmurs begin just after atrial contraction and are caused by stenosis of the AV valves. These murmurs are low-pitched and rum-bling but tend to have a crescendo contour and peak just before S1, which is usu-ally increased in intensity. These murmurs cannot be heard in patients with atrial fibrillation.

Continuous MurmursContinuous murmurs are caused by abnormal flow throughout the cardiac cycle and are typically due to abnormal arteriovenous communications within the chest such as a patent ductus arteriosus, acquired or congenital arteriovenous fistulae, or anom-alies of the coronary arteries. These murmurs tend to be loudest in systole, peaking in intensity with the second heart sound but with an audible component throughout diastole as well.

CLINICAL PEARL C The esence o an o enin snap, a ou S1 an a en th iasto ic mu mu

is in icative o seve e mit a stenosis even hen the mu mu is so t.


Atria l pressure

S1 S2Sys tole Dias tole

S1 S1


Centra l a rte ria l pressure

S2Sys tole Dias tole

Figure I-7 Common causes o iasto ic mu mu s. Cent a hemo namic ave o ms a e sho n in conjunction ith hono a hic in in s inc u in the sha e o the mu mu . The ca iac c c e on the e t e icts semi una ( u monic o ao tic) va ve e u itation. The ca iac c c e on the i ht e icts at iovent icu a (AV; t icus i o mit a ) va ve stenosis. (Reprinted with permission, Cleveland Clinic Center for Medical Art & Photography 2013. All rights reserved.)

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Part 2. Approach to the Electrocardiogram (ECG)

Three major topics are covered as follows:

A. ECG fundamentals

B. Approach to ECG interpretation

C. The ECG in cardiovascular disease

A. ECG FUNDAMENTALSThe 12-lead electrocardiogram (ECG) has endured throughout the years as the car-diologists primary diagnostic tool. Although the ECG certainly has its limitations, the wide availability of bedside electrocardiography combined with its low cost and lack of risk has kept the ECG on the frontlines in the war against cardiovascular disease. Major management decisions in cardiology such as the late-night activation of the cardiac catheterization laboratory or the use of potent fibrinolytic therapy are made based on ones interpretation of the ECG. For this reason it is essential that all physicians who care for patients with or at risk for cardiovascular disease have some basic understanding of electrocardiography and ECG interpretation.

ECG SetupThe ECG is a skin-surface recording of the extracellular electrical potentials pro-duced by deeper cardiac tissues. The 12 individual leads on a standard surface ECG represent the same electrocardiographic events captured over the same period of time but from differing electrical viewpoints determined by the location of the lead and its polarity. The ECG itself can be regarded as a graph with voltage plot-ted on the Y axis (ordinate; vertical axis) and time plotted on the X axis (abscissa; horizontal axis). The appearance of ECG paper is standardized and consists of large 55-mm square boxes that each contain 25 11-mm boxes as shown in Figure I-8. At standard paper speed (25 mm/s) and standard voltage calibration (10 mm/mV), each large box represents 200 ms on the X axis and 0.5 mV on the Y axis, whereas the smaller boxes represent 40 ms and 0.1 mV on the X and Y axes, respectively.

Smallbox

(1 1 mm)

Time (ms)25 mm/s

0.5

200

0.140

V

o

l

t

a

g

e

(

m

V

)

1

0

m

m

/

m

V

La rgebox

(5 5 mm)

Figure I-8 Stan a a ea ance an ca ib ation o ECg a e .



The resting ECG is performed with the patient supine. Adhesive stickers or clips are placed on the patients left arm, right arm, left leg, and right leg, and these are attached to their corresponding wires labeled LA, RA, LL, and RL, respectively. The right leg electrode is inert and can be considered a ground. A second series of stickers are placed across the anterior chest wall starting at the right upper sternal border, and these are attached to their corresponding wires, labeled V1V6. When all wires have been attached to their respective electrodes, the ECG is recorded with the patient remaining motionless and supine. Data acquisition takes approxi-mately 12 seconds, and the machine prints the 12-lead tracing immediately after data acquisition. Most ECG tracings are printed with the six bipolar (limb) leads oriented to the left and the six unipolar (precordial) leads oriented to the right; the waveforms in each lead represent the same 3-second timespan (Figure I-9). Along the bottom of the tracing one may see three rhythm strips, which are standard leads displayed continuously for the full 12 seconds. Leads V1, II, and V5 are typi-cally shown as rhythm strips, but the operator can program the machine to display the ECG data in any number of ways. The voltage calibration and paper speed can be adjusted by the operator as needed; this information is printed along the bottom of the page and graphically displayed (a rectangle 10 mm high and 5 mm wide for standard settings) to the left of each row.

ECG LeadsThere are 12 ECG leads: six limb leads and six precordial leads. The limb leads are so named because each lead has its positive pole on either arm or the left leg. The precordial leads are named for their location across the anterior chest wall.

The issue of lead polarity is important because it relates to perhaps the most important fundamental principle of electrocardiography; a positively charged wave-front moving toward a positive pole produces an upright deflection on the ECG. Similarly, a positively changed wavefront moving away from a positive pole produces a nega-tive ECG deflection. In the normal heart the depolarization wave starts in the sino-atrial node and spreads via the atria to the atrioventricular node, then through the His bundle to the bundle branches and ventricles. The path of normal conduction is therefore from right to left and from base to apex. A lead with its positive pole at the apex (lead II) will have upright atrial and ventricular waveforms because the depolarization wave is moving toward the positive pole. A lead with its positive pole at the right arm (lead aVR) will have inverted waveforms because the wavefront is moving away from the positive pole.

The orientation and polarity of the limb leads are shown in Figure I-10a. The limb leads are oriented across the chest in the frontal plane like the spokes of a wheel. There are three bipolar limb leads, labeled I, II, and III. Lead I represents the potential difference between the left arm (positive pole) and right arm and its posi-tive pole is located at 0. Lead II represents the potential difference between the left leg (positive pole) and the right arm and is located at 60. Lead III represents the potential difference between the left leg (positive pole) and left arm and is located at 120. There are three additional limb leads referred to as augmented leads. The augmented leads represent the potential difference between electrodes on the right arm (aVR), left arm (aVL), and left foot (aVF), and a common reference electrode



(Wilsons central terminal). Wilsons central terminal is created by connecting the remaining limb leads via resistors oriented in series. This results in a zero-potential reference electrode that acts as a negative pole; the positive pole for each of these leads is the named limb electrode. The use of a zero-potential reference electrode produces a smaller potential difference for these leads than their bipolar counter-parts, so the signals are augmented for better detection.

The precordial leads are oriented in the horizontal plane from right to left across the chest (Figure I-10b) and represent the potential difference between the anterior chest wall and Wilsons central terminal. The surface electrodes are the positive poles for these leads, and because of their proximity to the heart, they do not require augmentation.

The Normal ECGThe ECG events that occur during a typical cardiac cycle are shown in Figure I-11. Another important concept in ECG interpretation is the understanding that QRS voltage is proportional to mass. The QRS is the largest complex on the ECG because it represents depolarization of the most massive cardiac structure, the left ventricle. Right ventricular depolarization is also represented by the QRS, but in the normal heart the right ventricle is only one-third the mass of the left ventricle so the size and contour of the QRS complex is dominated by the left ventricle. Other structures such as the His bundle are too small to produce a deflection on the surface ECG (although the His bundle can be visualized on an invasive intracardiac electrogram).

The P wave represents activation of the atria. It begins with firing of the sino-atrial node (SAN), which is located in the right atrium near the insertion of the

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Figure I-9 Stan a a ea ance o a 12- ea e ect oca io am.



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Figure I-10 l ocation o the ositive o es o the imb (a) an eco ia (b) ECg ea s. The o ienta-tion o the imb ea s in the onta ane o ms a 360 axia a a that is use to ca cu ate the Qr S axis.

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Figure I-11 Cont ive ECg t acin ith e initions o ave o ms, com exes, an inte va s.



superior vena cava. The depolarization wave spreads from the right atrium to the left atrium across the interatrial septum via organized tracts of tissue that allow both atria to depolarize nearly simultaneously. The P wave is normally 8000 ms in dura-tion and less than 2.5 mm (0.25 mV) in amplitude. Repolarization of the atria is not seen on the surface ECG because it occurs during ventricular activation and is hidden within the QRS.

The PR interval represents the time from the onset of the P wave to the onset of the QRS complex. This interval includes conduction through the atrioventricular node (AVN). The AVN is too small to produce a deflection on the surface ECG but the health of the AVN is assessed by the duration of the PR interval. The normal PR interval is 120200 ms in duration.

The QRS complex represents ventricular depolarization. The positively changed depolarization wave spreads to the ventricles quickly via the left and right bundle branches before propagating cell to cell through specialized ventricular myocytes from the endocardium to the epicardium. The QRS duration is relatively short in a normal heart (60100 ms). The QRS complex shown in Figure I-12 is a contrived one; the appearance of the QRS varies from lead to lead, and Q waves are not uni-formly present. Small Q waves can be normal variants in most leads except leads V1V3; the normal Q wave is felt to represent left-to-right depolarization of the interventricular septum.

The ST segment begins with the end of the QRS complex at the J point and ends with the onset of the T wave. The ST segment represents the period of time when

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Figure I-12 d ete mination o the Qr S axis. The o ientation o the ositive o es o ea s I, II, an aVF a e sho n.



the ventricles are fully depolarized, and in a normal heart this segment is isoelectric and level with the PR and TP segments. Myocardial ischemia and metabolic abnor-malities can create electrical currents during this quiet time that can cause the ST segment to deviate.

The T wave represents repolarization of the ventricles. The normal T wave is oriented in the same direction as its preceding QRS complex because repolarization occurs in the opposite direction (negative wavefront moving epicardial to endocar-dial) as depolarization (positive wavefront moving endocardial to epicardial).

The QT interval begins with the onset of the QRS complex and ends with the end of the T wave. The QT interval represents the total time needed for depolariza-tion and repolarization of the ventricles. The QT interval decreases as the heart rate increases and can be corrected (QTc) by the using the Bazett formula: QTc = QT/RR, where RR is the interval between the two R waves on either side of the QT interval measured. A normal QTc is between 350 and 440 ms.

The U wave is a deflection that is sometimes seen on a normal ECG after the T wave. The U wave appearance is similar to that of the T wave, but the U wave is much smaller. The origin of the U wave is unclear but may represent repolarization of the mitral papillary muscles or the Purkinje fibers.

B. APPROACH TO ECG INTERPRETATIONThere is no right or wrong way to read an ECG provided that the readers approach is consistent and complete. Every ECG needs to be assessed for the features described in the paragraphs below; the order of that assessment is up to the individual reader. Clinical information is of major importance for correct ECG interpretation; when-ever possible, one should know the patients age, gender, and presenting complaint. A prior ECG for comparison is also extremely valuable, particularly in patients with chest pain and abnormal ST segments.

RhythmAssess each ECG to determine whether the rhythm is normal. Normal sinus rhythm is defined by the presence of sinus P waves (upright P waves in II, III, and aVF) that precede each QRS complex. The normal sinus rate is 60100 bpm; bradycardia is defined as a heart rate < 60 bpm and tachycardia is defined as a heart rate > 100 bpm.

Heart RateThe heart rate on the ECG can be calculated by noting the time interval between two R adjacent waves (provided that the rhythm is regular). Recall that if the paper speed is standard at 25 mm/s, then the time interval of one large square is 200 ms and the time interval of one small box is 40 ms (Figure I-8). The heart rate can then be determined by the following equation: HR = [1 beat / R-R interval (seconds)] (60 sec / min). If there are three large boxes and two small boxes between two consecu-tive R waves, then the R-R interval is 680 ms or 0.68 second. The heart rate would then be 1/0.68 60/1 = 60/0.68 = 88 bpm. A common quick and dirty method for heart rate estimation is to simply count the number of large boxes between consecu-tive R waves. At standard paper speed the heart rate for R-R intervals of 1, 2, 3, 4, and 5 large boxes is 300, 150, 100, 75, and 60 bpm, respectively. If the rhythm is



irregular or extremely slow, one can refer to the vertical hash marks situated at the bottom of most ECG tracings. These marks are spaced 3 seconds apart, so counting the number of complexes within a 6-second span and multiplying by 10 can give you an estimate of the heart rate. If the hash marks are not there, you can draw your own; 15 large boxes = 3 seconds.

RegularityEach ECG should be assessed for rhythm regularity, and calipers are a useful tool for this purpose. One should assess the regularity of the atrial waveforms (P waves) and ventricular waveforms (QRS complexes) using the rhythm strips at the bottom of the ECG tracing. Are the P-P and R-R intervals regular? Are these intervals the same? With normal conduction the P-P and R-R intervals should match, but in disorders such as atrioventricular (AV) block or ventricular tachycardia, the inter-vals will differ. An atrial rate that is regular and greater than the ventricular rate is referred to as complete heart block. In complete heart block the atrial impulses are not activating the ventricles, forcing the QRS complexes to originate from a lower secondary pacemaker such as the AVN-His bundle junction. A ventricular rate that is regular and greater than the atrial rate is referred to as A-V dissociation. A-V dissociation is a hallmark finding in ventricular tachycardia where the ven-tricular complexes originate from an abnormal area of the ventricle that depolarizes independently.

QRS AxisThe QRS axis is a vector that represents the net direction of ventricular depolariza-tion. Deviation of the QRS axis occurs in a number of cardiovascular disorders, and detection of QRS axis deviation is useful for generating a differential diagnosis. Axis deviation is also a criterion for some ECG diagnoses such as anterior and posterior fascicular blocks.

The limb leads form an axial array in the frontal plane that serves as the template for QRS axis derivation. Inspection of the limb leads will allow the reader to deter-mine the QRS axis. In reality the QRS vector is three-dimensional (3D), but the bedside measurement of a 3D QRS vector using ECG data, although possible via a process called spatial vectorcardiography, is technically cumbersome and impracti-cal in real-world cardiology practice.

The normal QRS vector lies between - 30 and 90in the frontal plane (Figure I-12). Deviation of the axis from - 30 to - 90 is termed left-axis devia-tion, and deviation of the axis between 90 and 180 is termed right-axis deviation. Left- or right-axis deviation can occur as the result of structural heart disease such as left or right ventricular hypertrophy or dilatation. Extreme axis deviation (180 to - 90) is typically seen with conduction from the ventricles such as during ven-tricular tachycardia.

There are numerous techniques available for determining the QRS axis. One commonly used method is to examine the orientation of the QRS complexes in leads I and aVF (see Figure I-12). A positive QRS deflection in lead I tells you that the QRS vector lies between 90 and - 90. A positive QRS deflection in lead aVF tells you that the QRS vector lies between 0 and 180. Thus, if you have an



upright QRS deflection in I and aVF, then the QRS vector must lie in the shared right lower quadrant between 0 and 90, and therefore the axis must be normal. If you have a positive QRS in lead I but a negative QRS in lead aVF, the QRS axis might be normal (0 to - 30) or deviated to the left (- 30 to - 90). In this case one should look at lead II. A positive deflection in lead II tells you that the QRS must lie between - 30and 150. Thus, if you have an upright QRS in leads I and II, then the QRS axis must project to the shared area between 0 and - 30. If the QRS is negative in II, then left axis deviation is present.

IntervalsAssessment of the PR and QTc intervals should be performed on each ECG tracing using calipers. The best lead to use for this assessment is whichever lead gives you the best landmarks for caliper measurement. The PR interval can be shortened (< 140 ms) in conditions such as ventricular preexcitation or lengthened (> 200 ms) by AVN disease. The QTc can be lengthened by myocardial ischemia, hypokalemia, congenital ion channel disorders, and numerous medications (Table I-8). QTc pro-longation is dangerous because it is associated with a form of ventricular tachycardia called torsades de pointes (TdP, commonly referred to simply as torsade). When the QTc is prolonged, there is a longer relative refractory period during which a prema-ture beat may fall and cause early depolarization of myocardium that is not yet ready to be depolarized. These early afterdepolarizations (EADs) can reach a threshold potential and cause TdP (Figure I-13). Torsades de pointes has a characteristic undu-lating appearance from which its name (translated from French as twisting of the points) is derived.

SegmentsPart of the routine assessment of the ECG should include assessment of the segments between the individual waveforms on the ECG (Figure I-14). The segment between the T wave and the P wave of the next cardiac cycle is called the T-P segment. The T-P segment is an electrically silent period and serves as the baseline reference point for comparison with the other baseline segments for deviation. The PR segment is included within the PR interval. During the PR segment the depolarization wave-front is moving through the atrioventricular node, His bundle, and bundle branches. These structures have very little mass, and so their depolarization does not produce a deflection within the PR segment. Additionally the atria have already depolarized and have not yet repolarized (the wave of repolarization is normally buried within the QRS). For these reasons the normal PR segment is isoelectric. However, the PR segment can be elevated or depressed in the setting of atrial ischemia or injury, respectively. Atrial ischemia or infarction can sometimes occur in the setting of myocardial infarction. Pericarditis is also associated with PR segment depression.

The ST segment is the focus of extreme attention in patients presenting with chest pain or who are suspected of

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