Pocket Cardiology, 2nd Edition

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Echocardiography
Nuclear Cardiology
Coronary CT Angiography
Cardiac MRI
Coronary Angiography

ACLS
 CONTRIBUTING AUTHORS

Deepak S. Atri, MD
Cardiology Fellow, Brigham and Women’s Hospital
Electrocardiography, Dyslipidemia, CV Risk Reduction in Diabetes, Evaluation of Chest Pain, Stable Ischemic Heart
Disease, Acute Coronary Syndromes, Cardiac Risk Assessment for Noncardiac Surgery
Ron Blankstein, MD, MPH
Associate Director, Cardiovascular Imaging Program
Director, Cardiac Computed Tomography
Co-Director, Cardiovascular Imaging Training Program
Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Professor of Medicine and Radiology, Harvard Medical School
Exercise Electrocardiography, Echocardiography, Nuclear Imaging, Cardiac Computed Tomography, Cardiac MRI,
Noninvasive Evaluation of CAD
Erin A. Bohula, MD, DPhil
Investigator, TIMI Study Group
Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Assistant Professor of Medicine, Harvard Medical School
Overview of Shock, PA Catheter Monitoring, Vasoactive Drugs Used in Shock, Cardiogenic and Mixed Shock,
Mechanical Circulatory Support, Hypovolemic/Hemorrhagic Shock, Distributive Shock and Sepsis, Cardiac Arrest
Care, Respiratory Failure, Mechanical Ventilation, ARDS, Acid-Base Disturbances, Renal Failure, Toxins, ICU
Bundle and Nutrition
Marc P. Bonaca, MD, MPH
William R. Hiatt Endowed Chair in Cardiovascular Research
Director of Vascular Research
Professor of Medicine, University of Colorado School of Medicine
Aortic Aneurysms, Acute Aortic Syndromes, Peripheral Artery Disease, Renovascular Disease, Cerebrovascular
Disease, Venous Thromboembolism, Pulmonary Hypertension, Hypertension
Rhanderson Cardoso, MD
Cardiovascular Imaging Fellow, Brigham and Women’s Hospital
Exercise Electrocardiography, Echocardiography, Nuclear Imaging, Cardiac Computed Tomography, Cardiac MRI,
Noninvasive Evaluation of CAD
Akshay S. Desai, MD, MPH
Medical Director, Cardiomyopathy and Heart Failure Program
Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Heart Failure Fundamentals, HF with Reduced EF, HF with Preserved EF, Acute Decompensated Heart Failure,
Dilated Cardiomyopathies, Myocarditis, Hypertrophic Cardiomyopathy, Restrictive and Infiltrative
Cardiomyopathies, Other Cardiomyopathies, Permanent VAD & Cardiac Transplant, Cardio-Oncology,
Cardiopulmonary Exercise Testing
Michael J. Landzberg, MD
Boston Adult Congenital Heart Group, Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Acyanotic Defects, Cyanotic Defects, Stenotic Lesions, Pregnancy & CV Disease
Mathew S. Lopes, MD
Cardiology and Critical Care Fellow, Brigham and Women’s Hospital
Overview of Shock, PA Catheter Monitoring, Vasoactive Drugs Used in Shock, Cardiogenic and Mixed Shock,
Mechanical Circulatory Support, Hypovolemic/Hemorrhagic Shock, Distributive Shock and Sepsis, Cardiac Arrest
 Care, Respiratory Failure, Mechanical Ventilation, ARDS, Acid–Base Disturbances, Renal Failure, Toxins, ICU
Bundle and Nutrition
Victor Nauffal, MD, MSc
Cardiology Fellow, Brigham and Women’s Hospital
Supraventricular Tachycardias, Atrial Fibrillation, VT vs. SVT with Aberrancy, Ventricular Tachycardia, Bradycardia &
AV Block, Syncope, Antiarrhythmic Drugs, Electrophysiology Study, Permanent Pacemaker, Implantable
Cardioverter-Defibrillator, Cardiac Implantable Electronic Device Infection
Michelle L. O’Donoghue, MD, MPH
Senior Investigator, TIMI Study Group
Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Electrocardiography, Dyslipidemia, CV Risk Reduction in Diabetes, Evaluation of Chest Pain, Stable Ischemic Heart
Disease, Acute Coronary Syndromes, Cardiac Risk Assessment for Noncardiac Surgery
Patrick T. O’Gara, MD
Watkins Family Distinguished Chair in Cardiology, Brigham and Women’s Hospital
Professor of Medicine, Harvard Medical School
Aortic Stenosis, Aortic Regurgitation, Mitral Regurgitation, Mitral Stenosis, Tricuspid Regurgitation, Prosthetic Heart
Valves, Endocarditis, Pericardial Disease
Siddharth M. Patel, MD
Cardiology Fellow, Brigham and Women’s Hospital
Aortic Stenosis, Aortic Regurgitation, Mitral Regurgitation, Mitral Stenosis, Tricuspid Regurgitation, Prosthetic Heart
Valves, Endocarditis, Pericardial Disease
Marc S. Sabatine, MD, MPH
Chair, TIMI Study Group
Lewis Dexter, MD, Distinguished Chair in Cardiovascular Medicine, Brigham and Women’s Hospital
Professor of Medicine, Harvard Medical School
Keri M. Shafer, MD
Boston Adult Congenital Heart Group, Division of Cardiovascular Medicine, Brigham and Women’s Hospital;
Department of Cardiology, Boston Children’s Hospital
Assistant Professor of Medicine, Harvard Medical School
Acyanotic Defects, Cyanotic Defects, Stenotic Lesions, Pregnancy & CV Disease
Pinak B. Shah, MD
Director of Cardiac Catheterization Lab
Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Coronary Angiography & Percutaneous Coronary Intervention, Coronary Artery Bypass Grafting, and the
interventional sections of Mechanical Circulatory Support, Aortic Stenosis, Aortic Regurgitation, Mitral
Regurgitation, Mitral Stenosis, Prosthetic Heart Valves, Venous Thromboembolism
Hasan K. Siddiqi, MD, MSCR
Heart Failure/Transplant Fellow, Center for Advanced Heart Disease, Brigham and Women’s Hospital
Heart Failure Fundamentals, HF with Reduced EF, HF with Preserved EF, Acute Decompensated Heart Failure,
Dilated Cardiomyopathies, Myocarditis, Hypertrophic Cardiomyopathy, Restrictive and Infiltrative
Cardiomyopathies, Other Cardiomyopathies, Permanent VAD & Cardiac Transplant, Cardio-Oncology,
Cardiopulmonary Exercise Testing
Usha B. Tedrow, MD, MS
Director, Clinical Cardiac Electrophysiology Fellowship
Clinical Director, Ventricular Arrhythmia Program
Physician, Division of Cardiovascular Medicine, Brigham and Women’s Hospital
Associate Professor of Medicine, Harvard Medical School
Supraventricular Tachycardias, Atrial Fibrillation, VT vs. SVT with Aberrancy, Ventricular Tachycardia, Bradycardia &
AV Block, Syncope, Antiarrhythmic Drugs, Electrophysiology Study, Permanent Pacemaker, Implantable
Cardioverter-Defibrillator, Cardiac Implantable Electronic Device Infection
Ryan A. Watson, MD
Interventional & Structural Fellow, Brigham and Women’s Hospital
Coronary Angiography & Percutaneous Coronary Intervention, Coronary Artery Bypass Grafting, and the
interventional sections of Mechanical Circulatory Support, Aortic Stenosis, Aortic Regurgitation, Mitral
Regurgitation, Mitral Stenosis, Prosthetic Heart Valves, Venous Thromboembolism
 PREFACE

To my parents, Matt and Lee Sabatine, to their namesake

grandchildren Matteo and Natalie, and to my wife Jennifer

With this second edition of Pocket Cardiology, we now offer a greatly expanded handbook to those taking care of
patients with complex cardiovascular disease. We start with an overview of the broad array of cardiovascular
evaluation tools, from the electrocardiogram to cardiac MRI. We then cover the major areas of cardiovascular care
with comprehensive sections on preventive cardiology, coronary disease, heart failure, critical care, valvular and
pericardial heart disease, vascular disease, arrhythmias, and adult congenial heart disease.
We have incorporated key references to the most recent high-tier reviews and important studies published right up
to the time Pocket Cardiology went to press. This edition builds on the work of the contributors to the first edition of
Pocket Cardiology as well as portions from several sections from the seventh edition of Pocket Medicine. We
welcome any suggestions for further improvement.
Of course, cardiology is far too vast a field to ever summarize in a textbook of any size. Long monographs have
been devoted to many of the topics discussed herein. Pocket Cardiology is meant only as a starting point to guide
one during the initial phases of diagnosis and management until one has time to consult more definitive resources.
Although the recommendations herein are as evidence-based as possible, medicine is both a science and an art. As
always, sound clinical judgment must be applied to every scenario.
I am grateful for the support of the house officers, fellows, and attendings at Brigham and Women’s Hospital. It is
a privilege to work with such a knowledgeable, dedicated, and compassionate group of physicians. I am grateful to
the many outstanding clinical cardiology mentors and role models I have had at both Brigham and Women’s Hospital
and the Massachusetts General Hospital, including Roman DeSanctis, Bill Dec, Mike Fifer, Eric Isselbacher, Jim
Kirshenbaum, Pat O’Gara, and the late Peter Yurchak.
This edition would not have been possible without the help of Kate Brennan, my academic coordinator. She
shepherded this project from start to finish, with an incredible eye to detail to ensure that each page of this book was
the very best it could be.
Lastly, special thanks to my parents for their perpetual encouragement and love and, of course, to my wife,
Jennifer Tseng, who, despite being a surgeon, is my closest advisor, my best friend, and the love of my life.
I hope the information contained within Pocket Cardiology proves useful in your quest to deliver the best possible
care to your cardiology patients.

MARC S. SABATINE, MD, MPH

 ELECTROCARDIOGRAPHY

Approach (a systematic approach is vital)

• Rate (? tachy or brady)
• Rhythm (? P waves, ? relationship between P and QRS, ? regular)
• Intervals (PR, QRS, QT) and axis (? LAD or RAD)
• Chamber abnormality (? LAA and/or RAA, ? LVH and/or RVH)
• QRST changes (? Q waves, poor R-wave progression V1–V6, ST ↑/↓ or T wave Δs)
Figure 1-1 QRS axis

Left axis deviation (LAD)

• Definition: axis beyond −30° (S > R in lead II)
• Etiologies: LVH, LBBB, inferior MI, WPW
• Left anterior fascicular block (LAFB): vide infra
Right axis deviation (RAD)
• Definition: axis beyond +90° (S > R in lead I)
• Etiologies: RVH, PE, COPD (usually not >+110°), septal defects, lateral MI, WPW,
limb lead reversal
• Left posterior fascicular block (LPFB): vide infra

Fascicular Blocks (Pathophysiology of Heart Disease, 7th ed, 2021)

Left anterior fascicular block (LAFB) Left posterior fascicular block (LPFB)
1. LAD (−45 to −90°) 1. RAD (90–180°)
2. qR in aVL 2. rS in I & aVL and qR in III & aVF
3. QRS <120 msec 3. QRS <120 msec
 4. No other cause of LAD (eg, IMI) 4. No other cause of RAD

Bundle Branch Blocks (Circ 2009;119:e235)

Normal Initial depol. is left-to-right across septum (r in V1 & q
in V6; nb, absent in LBBB) followed by LV & RV free
wall, with LV dominating (nb, RV depol. later and
visible in RBBB)
LBBB 1. QRS ≥120 msec (110–119 = incomplete)
2. Broad, slurred, monophasic R in I, aVL, V5–V6 (±
RS in V5–V6 if cardiomegaly)
3. Absence of Q in I, V5 and V6 (may have narrow q
in aVL)
4. Displacement of ST & Tw opposite major QRS
deflection
5. ± PRWP, LAD, Qw’s in inferior leads
LBBB pattern commonly seen with RV pacing
RBBB 1. QRS 120 msec (110–119 = incomplete)
2. rSR′ in R-precordial leads (V1, V2)
3. Wide S wave in I and V6
4. ± ST↓ or TWI in R-precordial leads
Does not cause right axis deviation
IVCD QRS ≥110 msec w/o criteria for RBBB/LBBB or w/ features of both
Bifascicular block: RBBB + LAFB/LPFB. Trifascicular block: bifascicular block + 1° AVB (nb, misnomer as 1° AVB
involves AV node but no fascicle per se).
Prolonged QT interval (NEJM 2008;358:169; www.torsades.org)
• QT measured from beginning of QRS complex to end of T wave (measure longest QT)
• QT varies w/ HR → corrected w/ Bazett’s formula: (RR in sec, can be
estimated by 60/HR), overcorrects at high HR and undercorrects at low HR (normal
QTc < 440 msec ♂ and < 460 msec ♀)
• Fridericia’s formula preferred at very high or low
• QT prolongation associated with ↑ risk TdP (espec >500 msec); perform
baseline/serial ECGs if using QT prolonging meds, no established guidelines for
stopping Rx if QT prolongs
• Etiologies:
Antiarrhythmics: class Ia (procainamide, disopyramide), class III (amiodarone,
sotalol, dofetilide)
Psych drugs: antipsychotics (phenothiazines, haloperidol, atypicals), Li, ? SSRI,
TCA
Antimicrobials: macrolides, quinolones, azoles, pentamidine, atovaquone,
atazanavir
Other: antiemetics (droperidol, 5-HT3 antagonists), alfuzosin, methadone,
ranolazine
Electrolyte disturbances: hypoCa (nb, hyperCa a/w ↓ QT), ± hypoK, ? hypoMg
Autonomic dysfxn: ICH (deep TWI), stroke, carotid endarterectomy, neck
dissection
Congenital (long QT syndrome): K, Na, & Ca channelopathies (Circ 2013;127:126)
Misc: CAD, CMP, bradycardia, high-grade AVB, hypothyroidism, hypothermia, BBB
Atrial Abnormalities
ECG P- Left Atrial Abnormality (LAA) Right Atrial Abnormality (RAA)
wave
Criteria

Left ventricular hypertrophy (LVH) (Circ 2009;119:e251)

• Etiologies: HTN, AS/AI, HCMP, coarctation of aorta
• Criteria (all w/ Se <50%, Sp >85%; accuracy affected by age, sex, race, BMI)
Romhilt–Estes point-score system (4 points 5 probable; 5 points 5 diagnostic):
Criteria Points
Voltage (any of the following): R or S in limb leads ≥20 mm; S in V1 or V2 3
≥30 mm; R in V5 or V6 ≥30 mm

ST-T displacement opposite to QRS deflection (either):

• Pt not on digoxin 3
• Pt on digoxin 1
Left atrial enlargement 3
Left axis deviation 2
 QRS duration ≥90 msec 1
Delayed intrinsicoid deflection (QRS onset to R peak) in V5 or V6 >50 msec 1

Sokolow–Lyon: S in V1 + R in V5 or V6 ≥35 mm or R in aVL ≥11 mm

Cornell: R in aVL + S in V3 >28 mm in men or >20 mm in women
If LAD/LAFB, S in III + max (R+S) in precordium ≥30 mm
Right ventricular hypertrophy (RVH) (Circ 2009;119:e251)
• Etiologies: cor pulmonale, congenital (tetralogy, TGA, PS, ASD, VSD), MS, TR
• Criteria (all tend to be insensitive, but highly specific, except in COPD)
R > S in V1or R in V1≥7 mm, S in V5 or V6 ≥7 mm, drop in R/S ratio across
precordium
RAD ≥+110° (LVH + RAD or prominent S in V5 or V6 → biventricular hypertrophy)
Ddx of dominant R wave in V1 or V2
• Ventricular enlargement: RVH (RAD, RAA, deep S waves in I, V5, V6); HCMP
• Myocardial injury: posterior MI (anterior Rw = posterior Qw; often w/ inferior or lateral
MI)
• Abnormal depolarization: RBBB (QRS >120 msec, rSR′); WPW (↓ PR, δ wave, ↑ QRS)
• Other: dextroversion; Duchenne muscular dystrophy; lead misplacement; nl variant
Poor R-wave progression (PRWP) (AHJ 2004;148:80)
• Definition: loss of anterior forces w/o frank Q waves (V1–V3); R wave in V3 ≤3 mm
• Possible etiologies (nonspecific):
old anteroseptal MI (usually w/ R wave V3 ≤1.5 mm, ± persistent ST ↑ or TWI V2 &
V3)
cardiomyopathy
LVH (delayed RWP with prominent left precordial voltage), RVH, COPD (which may
also have RAA, RAD, limb lead QRS amplitude ≤5, SISIISIII w/ R/S ratio <1 in
those leads)
LAFB/LBBB; WPW; clockwise rotation of the heart; lead misplacement; PTX, prior
cardiac surgery.
Pathologic Q waves
• Definition: ≥30 msec (≥20 msec V2–V3) or >25% height of R wave in that QRS
complex
• Small (septal) q waves in I, aVL, V5 & V6 are nl, as can be isolated Qw in III, aVR, V1
• “Pseudoinfarct” pattern may be seen in LBBB, infiltrative dis., HCM, COPD, PTX,
WPW
• In WPW, Qw pattern may help localize site of accessory pathway (Bundle of Kent)
ST elevation (STE) (NEJM 2003;349:2128; Circ 2009;119:e241 & e262)
• Acute MI (upward convexity ± TWI) or prior MI with persistent STE
• Coronary spasm (Prinzmetal’s angina): transient STE in a coronary distribution
• Pericarditis (qv): diffuse, upward concavity STE; a/w PR ↓; Tw usually upright,
absence of Qw
• HCM, Takotsubo CMP, LV aneurysm, cardiac contusion, myocarditis
• Pulmonary embolism: occ. STE V1–V3; classically a/w TWI V1–V4, RAD, RBBB,
S1Q3T3
• Repolarization abnormalities
LBBB (↑ QRS duration, STE discordant from QRS complex). Dx of STEMI in setting
of LBBB challenging but possible (see “ACS”).
LVH (↑ QRS amplitude, a/w J-point elevation)
Brugada pattern (qv)
rSR′, downsloping STE V1–V2
Na+ channelopathy associated with SCD
Hyperkalemia (see below)
Hypothermia: Osborn waves
⊕ deflection at J point, typically in R-precordial leads proportional to degree of
hypothermia

• aVR: STE >1 mm a/w ↑ mortality in STEMI; STE aVR > V1 a/w left main disease
May also represent diffuse ischemia, such as w/ multivessel disease & noncardiac
HoTN
STE >1 mm aVR w/ STD in ≥8 leads suggests left main or mutivessel CAD
• Early repolarization: most often seen in V2–V5 in young adults (JACC 2015;66:470)
1–4 mm elevation of peak of notch or start of slurred downstroke of R wave (ie, J
point); ± up concavity of ST & large Tw (∴ ratio of STE/T wave <25%; may
disappear w/ exercise)
? early repolarization in inferior leads may be associated with ↑ risk of VF (NEJM
2009;361:2529; Circ 2011;124:2208)

ST depression (STD)
• Myocardial ischemia (± Tw abnormalities) or acute posterior STEMI (V1–V3)
• Digitalis effect (downsloping ST ± Tw abnormalities, does not correlate w/ dig levels)
• Hypokalemia (± U wave)
• Repolarization abnormality in a/w LBBB or LVH (usually in leads V5, V6, I, aVL)
Cannot reliably interpret STD as a sign of ischemia in setting of LBBB or PPM unless
possibly if concordant w/ direction of QRS or discordant but ≥5 mm
T-wave inversion (TWI; generally ≥1 mm; deep if ≥5 mm) (Circ 2009;119:e241)
• Ischemia or infarct; Wellens’ sign (deep, symmetric precordial TWI) → proximal LCA
lesion
(Wellens’ sign, from The Washington Manual Cardiology Subspecialty Consult, 3rd ed., 2014)

• DeWinter’s sign (upsloping STD V2-V6 w/ hyperacute Tw suggests proximal LAD

occlusion).
• Myopericarditis; CMP (Takotsubo, ARVC, apical HCM); MVP; PE (espec. if TWI V1–
V4)
• Repolarization abnormality in association with LVH/RVH (“strain pattern”), BBB
• Post-tachycardia or postpacing (“T-wave memory”)
• Electrolyte, digoxin, PaO2, PaCO2, pH, or core temperature disturbances
• Intracranial bleed (“cerebral T waves,” usually asymmetric w/ ↑ QT)
• Normal variant in children (V1–V4) and leads in which QRS complex predominantly ⊝
• Isolated TWI in lead III normal
True posterior MI (posterior STE appearing as anterior STD)
• STD ± ↑ R wave in leads V1–V4 may correspond to acute posterior “ST-elevation” MI
• ✓ Posterior ECG leads; manage as a STEMI with rapid reperfusion
Anterior leads w/ ST Placement of posterior ECG
depression leads Posterior leads s/ STE
(Modified from A Visual Guide to ECG Interpretation, 2nd Ed, 2017)

Low voltage
• Can be seen in limb leads, precordial leads or both
• Defined as QRS amplitude (R + S) <5 mm in limb leads and <10 mm in precordial
leads (variably as either the average of the leads or required to be in all of the leads)
• Etiologies: COPD (precordial leads only), pericardial effusion, myxedema, obesity,
pleural effusion, restrictive or infiltrative CMP, diffuse CAD
Electrolyte Abnormalities
↑K Tented Tw, ↓ QT
Small Pw, ↑ PR, AVB
Wide QRS → sinusoidal pattern
STE (typically V1–V2)

↓K Flattened Tw
U waves (⊕ deflection after T)
ST depression
Ectopy; ↑ QT & TdP
↑ Ca ↓ QT, flattened Tw & Pw
J-point elevation

↓ Ca ↑ QT; Tw Δs

(Marriott’s Practical Electrocardiography, 13th ed, 2021)

ECHOCARDIOGRAPHY

General principles
• Technique: based on emission and detection of sound waves with frequencies
between 1.5 and 7.5 MHz. Higher frequencies lead to smaller wavelength, higher
spatial resolution, but decreased depth of penetration.
• Major advantages: safe, portable, low cost, noninvasive, high temporal resolution
• Limitations: acquisition operator dependent, limited tissue characterization, limited
windows in Pts who are obese, have lung disease, or chest wall deformities
Types of echo imaging (see Photo Inserts)
• M-mode: U/S waves emitted/received along a single line. Image reports depth (y-axis)
vs. time (x-axis). High sampling rate allows for excellent temporal resolution.
Therefore, useful for rapidly moving structures, such as valves.
• 2D: U/S waves emitted/received along a range of lines (sector) in a single plane.
Useful for assessing cardiac morphology and function.
• 3D: U/S waves emitted/received along a range of lines (sector) in a pyramidal scan
volume. Allows for better assessment of volume and mass and simultaneous
assessment of function in different regions. Limited spatial and temporal resolution
compared with 2D.
• Doppler imaging: Based on the change in U/S frequency when reflected by moving
targets, such as blood (red blood cells) or tissue (myocardium).
Continuous wave (CW): measures highest velocity along a single line. Separate
crystals for continuous transmission and receiving U/S waves. Cannot localize
peak velocity.
Pulsed wave (PW): same crystals transmit and detect U/S wave after a delay
matched to area of interest. Due to time delay needed for U/S detection, this
technique can only detect velocities up to a certain limit, called the Nyquist limit.
Color: Velocities and direction of blood flow are encoded with color in a 2D or 3D
image. Velocities toward the transducer are represented in shades of red and
velocities away from the transducer are displayed in shades of blue.
Main indications
• Structure: evaluate chamber sizes, wall thickness, valve structure (including
vegetations), anatomy (eg, congenital heart disease), cardiac masses, including
thrombus, and pericardial effusions
• Function: evaluate valvular hemodynamics and ventricular function (systolic and
diastolic)
Standard echo view
• Specific transducer positions on the chest wall to produce standard echo views
• Main TTE views obtained from the left parasternal (long axis and short axis), apical
(4Ch, 3Ch, 2Ch), and subcostal positions (see Photo Inserts)
• Additional views can be obtained for specific indications (eg, suprasternal to evaluate
the aorta or right parasternal for aortic valve gradients).
LV systolic function
• Methods for assessing LVEF can be divided in linear, 2D, and 3D
• Linear (eg, Teichholz and Quinone): simple mathematical calculation based on mid-
cavity diameter of LV in systole and diastole and assumption that LV is a prolate
ellipsoid. Should be avoided due to extensive volumetric assumptions.
• 2D: Simpson’s method is most widely used for LVEF assessment. Endocardial
border is traced in A4C and A2C views. Model of disks that are summated to create
end-systolic and diastolic volumes. Foreshortening of the LV apex can significantly
impair LVEF assessment.
• 3D: no volumetric assumptions; instead uses semiautomated identification of
endocardial borders. Limited by low temporal and spatial resolution compared with
2D.
• Both 2D and 3D methods are highly dependent on image quality
• Assessment of regional wall motion abnormalities is done by a comprehensive
evaluation using multiple different planes (eg, anterior wall on short axis & 2Ch)
• Clear endocardial visualization is essential to global & regional assessment of LV
function. Looking for LV wall thickening in systole, not just movement in space.
Contrast agents indicated when ≥2 segments are not well visualized.
• Stress echocardiography: Pt exercises (treadmill or bicycle) or is given dobutamine.
Look for development of new or worsening regional wall motion abnormalities at or
immediately after peak exercise.
LV diastolic function
• Assessment primarily focused on evaluation of left-sided filling pressures. With
impaired relaxation, higher diastolic pressures are needed to fill the LV. Also see
“HFpEF.”
• Parameters for assessment of diastolic function and filling pressures
Mitral annular velocities (e′): determined by LV relaxation and less by filling pressure.
Assess by using tissue Doppler. Normal values: septal ≥7 cm/s; lateral ≥10 cm/s.
Mitral E velocity: reflects gradient between LA and LV pressure in early diastole
E/e′: as diastolic function worsens and filling pressure increases, e′ will ↓ and E will
↑.
E/e′ ≥14 used as a marker of elevated left-sided filling pressures.
E/A ratio: classified into four general patterns
Diastolic Dysfunction
Pattern E/A e′ (cm/s) E/e′
Normal 1–2 ≥10 <8
Impaired relaxation <0.8–1 <8 Variable
Pseudonormal 1–1.5 <8 >14 indicates
elevated left-sided
Restrictive >1.5–2.0 <8 (usually ≤5) filling pressures
Left atrial enlargement: a marker of chronically elevated left atrial pressure
TR velocity: a measurement of ≥2.8 m/s suggests elevated left atrial pressure
RV evaluation
• Anatomy: inlet, body, and outlet
• Dimensions and function evaluated best in A4C view
• On visual assessment, normal RV size should be <2/3 of the LV and should not form
part of the ventricular apex
• Quantitative parameters for RV function:
Tricuspid annular plane systolic excursion (TAPSE): measured using M-mode to
quantify amount of systolic longitudinal displacement of lateral tricuspid annulus
toward the apex; normal ≥17 mm