Anesthesia forCardiac SurgeryThird Edition

James A. DiNardo, MDClinical Co-Director of Cardiac AnesthesiaDepartment of AnesthesiaChildren’s Hospital Bostan300 Longwood AvenueBoston, MA, 02115USA

David A. Zvara, MDJay J. Jacoby Professor and ChairDepartment of AnesthesiologyThe Ohio State University410 West 10th AvenueColumbus, Ohio, 43210USA

Anesthesia for Cardiac Surgery

Dedication

To my wife Denée for her love, support and wisdom.To my daughter Isabel and her limitless potential.To my mother Josephine Ann who taught me the value of honesty and perseverance.

James A. DiNardo

Tomywife, Bharathi, and daughters, Alexandra, Jessica, Gracie andOlivia: each of you have inspiredme in ways that youwill never know. I love you and dedicate this book to you and your life’s dreams.

Go confidently in the direction of your dreams. Live the life you have imagined. (Henry David Thoreau)

David A. Zvara

Anesthesia forCardiac SurgeryThird Edition

James A. DiNardo, MDClinical Co-Director of Cardiac AnesthesiaDepartment of AnesthesiaChildren’s Hospital Bostan300 Longwood AvenueBoston, MA, 02115USA

David A. Zvara, MDJay J. Jacoby Professor and ChairDepartment of AnesthesiologyThe Ohio State University410 West 10th AvenueColumbus, Ohio, 43210USA

© 1990 and 1997 James A. DiNardo© 2008 James A. DiNardo and David A. ZvaraPublished by Blackwell PublishingBlackwell Publishing, Inc., 350 Main Street, Malden, Massachusetts 02148-5020, USABlackwell Publishing Ltd, 9600 Garsington Road, Oxford OX4 2DQ, UKBlackwell Publishing Asia Pty Ltd, 550 Swanston Street, Carlton, Victoria 3053, Australia

The right of the Author to be identified as the Author of this Work has been asserted inaccordance with the Copyright, Designs and Patents Act 1988.

All rights reserved. No part of this publication may be reproduced, stored in a retrievalsystem, or transmitted, in any form or by any means, electronic, mechanical,photocopying, recording or otherwise, except as permitted by the UK Copyright, Designsand Patents Act 1988, without the prior permission of the publisher.

First published 1990Second edition 1997Third edition 2008

1 2008

Library of Congress Cataloging-in-Publication Data

DiNardo, James A.Anesthesia for cardiac surgery/James A. DiNardo, David A. Zvara. – 3rd ed.

p. ; cm.Includes bibliographical references and index.ISBN 978-1-4051-5363-8 (alk. paper)1. Anesthesia in cardiology. 2. Heart–Surgery. I. Zvara, David A. II. Title.

[DNLM: 1. Cardiac Surgical Procedures. 2. Anesthesia. WG 169 D583a 2007]

RD87.3.H43D5 2007617.9’67412–dc22

2007001204

ISBN: 978-1-4051-5363-8

A catalogue record for this title is available from the British Library

Set in 9/12pt Meridien byNewgen Imaging Systems (P) Ltd, Chennai, IndiaPrinted and bound in Singapore by Fabulous Printers Pte Ltd

Commissioning Editor: Stuart TaylorEditorial Assistant: Jennifer SewardDevelopment Editors: Adam Gilbert and Victoria PittmanProduction Controller: Debbie Wyer

For further information on Blackwell Publishing, visit our website:http://www.blackwellpublishing.com

The publisher’s policy is to use permanent paper from mills that operate a sustainableforestry policy, and which has been manufactured from pulp processed using acid-free andelementary chlorine-free practices. Furthermore, the publisher ensures that the text paperand cover board used have met acceptable environmental accreditation standards.

Blackwell Publishing makes no representation, express or implied, that the drug dosages inthis book are correct. Readers must therefore always check that any product mentioned inthis publication is used in accordance with the prescribing information prepared by themanufacturers. The author and the publishers do not accept responsibility or legal liabilityfor any errors in the text or for the misuse or misapplication of material in this book.

Contents

Preface, vii

1 Introduction, 1

2 Myocardial Physiology and the Interpretation ofCardiac Catheterization Data, 20

3 Monitoring, 42

4 Anesthesia for Myocardial Revascularization, 90

5 Anesthesia for Valvular Heart Disease, 129

6 Congenital Heart Disease, 167

7 Anesthesia for Heart, Heart-Lung, and Lung Transplantation, 252

8 Pericardial Disease, 289

9 Anesthesia for Surgery of the Thoracic Aorta, 304

10 Management of Cardiopulmonary Bypass, 323

11 Mechanical Circulatory Support, 375

12 Myocardial Preservation during Cardiopulmonary Bypass, 409

13 Special Considerations during Cardiac Surgery, 425

Index, 439

v

Preface

Anesthesia for Cardiac Surgery originally published in1989, and revised in 1998, was written with theintention of filling the perceived void in cardiacanesthesia reference material between definitive,heavily referenced texts and outline-based hand-books. The updated 3rd Edition strives to do thesame. This book is intended to provide practi-cal recommendations based on sound principlesof physiology. The text provides a comprehensiveoverview of the contemporary practice of cardiacanesthesia. There is a place for this work as a compo-nent of a core curriculum in cardiac anesthesiologytraining as well as in the library of the busy, practic-ing clinician. We hope this work helps you in caringfor your patients.

JADDAZ

Acknowledgements

The authors would like to acknowledge Adela S.F.Larimore at the Wake Forest University School ofMedicine, Department of Anesthesiology for hereditorial support in the preparation of this textbook.Without her assistance this work would not bepossible.

vii

C H A P T E R 1

Introduction

A complete evaluation of the patient’s medicalhistory, physical examination, and review of per-tinent laboratory and supportive tests is necessaryprior to any elective cardiac surgical procedure. Theintention of the preoperative evaluation is sever-alfold: define the status of the patient’s medicalcondition, identify areas of uncertainty that requirefurther evaluation, consultation or testing, devisea strategy to improve or stabilize ongoing medi-cal conditions prior to surgery, determine a prog-nostic risk classification, and provide informationto formulate an intraoperative and postoperativeplan. The anesthesiologist must clearly understandthe intended surgical procedure. This chapter willpresent a systems review of the common and sig-nificant features found preoperatively in the cardiacsurgical patient. There will be a special emphasis onthe methodology, limitations, and accuracy of thetests used most commonly in evaluation of cardiacsurgical patients.

Cardiovascular evaluation

A directed history and physical examination areessential before any cardiac surgical procedure.The information obtained, in the context ofthe anticipated surgical procedure, will deter-mine the requirement for subsequent evaluation,consultation or testing.

History and physical examinationThere are no controlled trials evaluating the effec-tiveness of the history and physical; however,

conditions discovered in the process help definethe anesthetic plan and are often associated withstrong prognostic value. For example, a history ofmyocardial infarction, unstable angina, congestiveheart failure, dyspnea, obstructive sleep apnea, andany number of other conditions may directly affectthe course of the preoperative evaluation, operativeoutcome, and patient satisfaction. There are manyalgorithms for quantifying patient risk, includingthe American Society of Anesthesiologists Physi-cal Status Classification. The Revised Cardiac RiskIndex is a clinically useful example of a preopera-tive scoring system to define perioperative cardiacrisk (Table 1.1).

In most cardiac surgical procedures, the preanes-thetic evaluation should take place prior to theday of surgery. This will allow time for additionaltesting, collection, and review of pertinent pastmedical records, and appropriate patient counsel-ing. The examination can be obtained on the dayof surgery for procedures with relatively low sur-gical invasiveness. The history provides insight intothe severity of the pathologic condition. For exam-ple, a history consistent with heart failure is mostalarming and requires careful deliberation beforeproceeding (Table 1.2). In evaluating a patient withangina, it is essential to determine if the symp-toms represent unstable angina (Table 1.3). TheCanadian Cardiovascular Society Classification ofAngina defines anginal symptoms (Table 1.4).

At a minimum, the physical examination mustinclude the vital signs and an evaluation of

1

2 Chapter 1

Table 1.1 The Revised Cardiac Risk Index.

Ischemic heart disease: Includes a history of myocardialinfarction, Q waves on the ECG, a positive stress test,angina, or nitroglycerine use

Congestive heart failure (CHF): Includes a history of CHF,pulmonary edema, paroxysmal nocturnal dyspnea, rales,S3 gallop, elevated β-naturetic peptide, or imaging studyconsistent with CHF

Cerebrovascular disease: Includes a history of transientischemic attack or stroke

Diabetes mellitus treated with insulin:

Renal dysfunction (serum creatinine >2)

High-risk surgery: Includes any intraperitoneal,intrathoracic or suprainguinal vascular procedures

CABG, coronary artery bypass surgery; ECG, electrocardio-gram.0–2 risk factors = low risk.3 or more risk factors = high risk.

the airway, lungs and heart. Auscultation of thechest may reveal wheezing, rales, or diminishedbreath sounds. Auscultation of the heart is critical inuncovering new murmurs, S4 gallops, and rhythmabnormalities. In patients older than 40 years, newheart murmurs are found in upwards of 4% ofpatients. Further screening with echocardiographyreveals significant valvular pathology in 75% ofthese patients. Arterial hypertension is commonin the cardiac surgical patient; however, there islittle evidence for an association between admis-sion arterial pressures less than 180mmHg systolicor 110mmHg diastolic and perioperative compli-cations. In patients with blood pressures abovethis level, there is increased perioperative ischemia,arrhythmias, and cardiovascular lability.Once the history and physical examination are

complete, attention turns to what additional eval-uation, consultation or studies are indicated priorto the operative procedure. The decision regard-ing which test to order should be based uponan analysis of value of the information obtained,resource utilization and timeliness in regards tothe scheduled procedure. Several common tests arereviewed below.

ElectrocardiogramA preoperative electrocardiogram (ECG) should beobtained in all cardiac surgical patients. There is noconsensus on the minimum patient age for obtain-ing an ECG, although ECG abnormalities are morefrequent in older patients and those with multiplecardiac risk factors. The ECG should be examinedfor rate and rhythm, axis, evidence of left and rightventricular (RV) hypertrophy, atrial enlargement,conduction defects (both AV nodal and bundlebranch block (BBB)), ischemia or infarction, andmetabolic and drug effects.

Rate and rhythm abnormalitiesThere are a large number of rate and rhythm abnor-malitieswhichmay be present in the cardiac surgicalpatient. Tachycardia may be a sign of anxiety, drugeffect (i.e. sympathomimetics, β-adrenergic ago-nists, and cocaine intoxication), metabolic disorder(hypothyroidism), fever, sepsis or other condi-tions. Bradycardia is typically due to medications(β-adrenergic blocking agents), although a slowheart rate may by indicative of other pathol-ogy (hypothyroidism, drug effect, hypothermia,conduction defects). Arrhythmias are potentiallymore serious and require immediate evaluation.Electrolyte abnormalities are common in cardiacsurgical patients and may lead to premature ven-tricular contractions (PVCs). The actively ischemicpatientmay present with ventricular irritability, fre-quent ormultifocal PVCs, or ventricular tachycardia(VT). Atrial fibrillation is frequently observed inthe elderly cardiac surgical patient. The diagnosisof new atrial fibrillation requires evaluation prior tosurgery if time and the clinical condition permit.

AxisAxis refers to the direction of depolarization inthe heart. The mean QRS vector (direction ofdepolarization) is normally downward and to thepatient’s left (0–90◦). This axis will be displacedwith physical relocation of the heart (i.e. extrinsiccardiac compression from a mass effect), hypertro-phy (axis moves toward hypertrophy), or infarction(axis moves away from infarction). In the normalcondition, the QRS is positive in lead I and aVF.

Introduction 3

Table 1.2 American College of Cardiology/American Heart Association Classification of chronic heart failure.

Stage Description

A. High risk for developing heart failure Hypertension, diabetes mellitus, coronary artery disease, family history ofcardiomyopathy

B. Asymptomatic heart failure Previous myocardial infarction left ventricular dysfunction, valvular heartdisease

C. Symptomatic heart failure Structural heart disease, dyspnea and fatigue, impaired exercise tolerance

D. Refractory end-stage heart failure Marked symptoms at rest despite maximal medical therapy

Stage A includes patients at risk of developing heart failure but have no structural heart disease at present. A highdegree of awareness is important in this group

Stage B includes patients with known structural heart disease but no symptoms. Therapeutic intervention withangiotensin converting enzyme inhibitors or adrenergic beta-blocking agents may be indicated for long-term chronictreatment in this group

Stage C includes patients with structural heart disease and symptomatic heart failure. Operative risk is increased in thisgroup. Medical therapy may include diuretics, digoxin, and aldosterone antagonists in addition to ACE inhibitors andbeta-blockers depending upon the severity of symptoms. Cardiac resynchronization therapy also may be considered inselected patients

Stage D includes patients with severe refractory heart failure. These patients frequently present for heart transplantationor bridging therapy with ventricular assist devices. Acute decompensation is managed with inotropes and vasodilatortherapy

ACE, angiotensin-converting enzyme.

Table 1.3 The principal presentations ofunstable angina. Rest angina Angina occurring at rest and usually prolonged greater

than 20 minutes

New onset angina Angina of at least CCSC III severity with onset within2 months of initial presentation

Increasing angina Previously diagnosed angina that is distinctly morefrequent, longer in duration or lower in threshold(i.e. increased by at least one CCSC class within2 months of initial presentation to at least CCSC IIIseverity)

CCSC, Canadian Cardiovascular Society Classification.

Left atrial enlargementIn adults, left atrial enlargement (LAE) may befound in association with mitral stenosis, aorticstenosis, systemic hypertension, and mitral regur-gitation. In mitral stenosis, LAE occurs secondary tothe increased impedance to atrial emptying across

the stenotic mitral valve. In aortic stenosis andsystemic hypertension, an elevated left ventricu-lar (LV) end-diastolic pressure results in left atrialhypertrophy. In mitral regurgitation, LAE occursbecause of the large volumes of blood regurgitatedin the left atrium during systole.

4 Chapter 1

Table 1.4 The Canadian Cardiovascular Society Classification System of angina pectoris.

Class I: Ordinary physical activity, such as walking and climbing stairs does not cause angina. Angina occurswith strenuous, rapid, or prolonged exertion

Class II: Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walkinguphill, walking or stair climbing after meals, in the cold or wind, under emotional stress or only during thefew hours after awakening. Angina occurs on walking more than two blocks on the level and climbing morethan one flight of ordinary stairs at a normal pace and under normal conditions

Class III: Marked limitations of ordinary physical activity. Angina occurs on walking one or two blocks on thelevel ground and climbing one flight of stairs in normal conditions and at a normal pace

Class IV: Inability to carry on any physical activity without anginal discomfort. Symptoms may be present at rest

Right atrial enlargementRight atrial enlargement (AAE) may be seen withRV hypertrophy secondary to pulmonary outflowobstruction or pulmonary hypertension. RAE alsomay be observed in patients with tricuspid stenosis,tricuspid atresia, or Epstein’s abnormality.

Left ventricular hypertrophyIn adults, left ventricular hypertrophy (LVH) com-monly occurs in LV pressure overload lesions suchas aortic stenosis and severe systemic hypertension.In children, LVHmay be present with coarctation ofthe aorta and congenital aortic stenosis.

Right ventricular hypertrophyRight ventricular hypertrophy (RVH) is a commonfinding in patients with congenital heart diseaseand may be seen in pulmonic stenosis, tetralogyof Fallot and transposition of the great arteries.In adults, RVH frequently results from pulmonaryhypertension.

Conduction defectsSimilar to rate and rhythm abnormalities, there area wide variety of conduction defects which maybe observed in the cardiac surgical patient. Atrio-ventricular (AV) block may be innocuous (1st and2nd degree type 1) or clinically significant requir-ing immediate evaluation of pacemaker placement(2nd degree type 2 and 3rd degree). BBB delaydepolarization in the effected ventricle andmay leadto ineffective ventricular contraction.

Ischemia and infarctionNew findings of active ischemia require immedi-ate attention. In the patient with known coro-nary artery disease (CAD) and unstable angina,ST segment abnormalities may be observed.In patients with diabetes, there may be episodes ofsilent ischemia during which the heart is ischemic,but due to autonomic dysfunction and a dimin-ished ability to perceive nociceptive signals, thepatient does not experience pain. The presence ofQ waves indicates an old transmural myocardialinfarction. Determining the timing of the Q wavefinding may be clinically relevant. For example,a Q wave not seen on an ECG 6months priorto the evaluation suggests a myocardial infarctionsometime during this recent interval. Periopera-tive cardiac morbidities are related to timing ofsurgery after a myocardial infarction, and there-fore this information requires attention and clinicalresolution.

Metabolic and drug effectsElevated serum potassium will flatten the P wave,widen the QRS complex, and elevate the T wave.Low serum potassium will flatten of invert theTwave. A Uwavemay appear.With elevated serumcalcium the QT interval shortens; whereas withhypocalcemia, the QT interval is prolonged. Digi-talis toxicity will cause a gradual down sloping ofthe ST segment. There may also be atrial and junc-tional premature beats, atrial tachycardia, sinus, andAV nodal blocks.

Introduction 5

It must be emphasized that a normal ECG doesnot preclude the presence of significant cardiac dis-ease in the adult, child, or infant. The ECG is normalin 25–50% of adults with chronic stable angina.Likewise, the ECG may be normal in children withLV pressure overload (aortic stenosis) and volumeoverload (patent ductus arteriosus or ventricularseptal defect) lesions.

Chest radiographObtaining a Chest radiograph (CXR) should bebased upon the necessity for the planned clini-cal procedure (i.e. a lateral chest film is essen-tial in a repeat sternotomy), or in assessing thepatient’s clinical condition. Clinical characteristicssuggesting a benefit to obtaining a CXR includea history of smoking, recent respiratory infection,chronic obstructive pulmonary disease (COPD), orcardiac disease. The posterior–anterior and lateralCXR provide a wealth of information including anassessment of pulmonary condition and maybe car-diovascular status. For example, radiographic evi-dence of pulmonary vascular congestion suggestspoor systolic function. For patients with valvu-lar heart disease, a normal CXR is more usefulthan an abnormal radiograph in assessing ventricu-lar function. The presence of a cardio-to-thoracicratio less than 50% is a sensitive indicator of anejection fraction greater than 50% and of a car-diac index greater than 2.5 L/min/m2. On the otherhand, a cardio-to-thoracic ratio greater than 50% isnot a specific indicator of ventricular function. Forpatients with CAD, an abnormal CXR is more usefulthan a normal radiograph in assessing ventricu-lar function. Cardiomegaly is a sensitive indicatorof a reduced ejection fraction, whereas a normal-sized heart may be associated with both normal andreduced ejection fractions.As with the ECG, efforts should be made to corre-

late radiographic findings with the clinical history.LAE is expected inmitral stenosis and regurgitation.Enlargement of the pulmonary artery and right ven-tricle occurs with disease progression. Eccentric LVhypertrophy results from mitral and aortic regur-gitation. Aortic stenosis results in concentric LVhypertrophy. In infants and children with increasedpulmonary blood flow (as with a large ventricular

septal or atrial septal defect), the pulmonary arteryand pulmonary vasculature is prominent. In con-trast, patients with reduced pulmonary blood flow(as with tetralogy of Fallot or pulmonary atre-sia) may manifest a small pulmonary artery anddiminished vascularity. Some congenital lesions areassociated with classic radiographic cardiac silhou-ettes: the boot-shaped heart of tetralogy of Fallot,the “figure 8” heart of total anomalous pulmonaryvenous return, and the “egg-on-its-side”-shapedheart seen in D-transposition of the great arteries.

Stress testingPatients presenting for cardiac surgery frequentlyundergo stress testing to establish the diagnosis ofCAD, assess the severity of known CAD, establishthe viability of regions of myocardium, or eval-uate anti-anginal therapy. Stress testing may useexercise or pharmacological agents. Pharmacolog-ical agents are useful for patients with physicaldisabilities that preclude effective exercise. It alsois useful for patients who cannot reach an optimalexercise heart rate secondary to their medicationregimen (i.e. patients on beta-blockers).

Pharmacological stress testingPharmacologic stress testing uses dipyridamole,adenosine, or dobutamine. Pharmacologic stresstesting can be performed in conjunctionwith myocardial perfusion scintigraphy orechocardiography.

Adenosine and dipyridamole are potent coro-nary vasodilators that increase myocardial bloodflow three to fivefold independent of myocardialwork. Adenosine is a direct vascular smooth musclerelaxant via A2-receptors; whereas, dipyridamoleincreases adenosine levels by inhibiting adenosinedeaminase. Dobutamine increases myocardial workthrough increases in heart rate and contractility viaβ1-receptors. The increased work produces propor-tional increases in myocardial blood flow. In thissense, dobutamine stress testing is similar to exercisestress testing.

The hyperemic response to adenosine and dipyri-damole produce increased myocardial blood flowin regions supplied by normal coronary arteries.In regions of myocardium supplied by steal prone

6 Chapter 1

anatomy or diseased coronary arteries, myocardialblood flow increases will be attenuated or decreasedbelow resting levels.Dipyridamole is infused at 0.56–0.84mg/kg for

4minutes, followed by injection of the radiophar-maceutical for myocardial perfusion scintigraphy3minutes later. If infusion produces headache,flushing, gastrointestinal (GI) distress, ectopy,angina, or ECG evidence of ischemia, the effectcan be terminated with aminophylline 75–150mgintravenously (IV). Adenosine is infused at140μg/kg/min for 6minutes with injection ofthe radiopharmaceutical for myocardial perfu-sion scintigraphy 3minutes later. Side effectsare similar to dipyridamole and are termi-nated by stopping the infusion (the half-life ofadenosine is 40 seconds). Dobutamine is infused at5μg/kg/min for 3minutes and then is increased to10μg/kg/min for 3minutes. The dose is increasedby 5μg/kg/min every 3minutes until a maximumof 40μg/kg/min is reached or until significantincreases in heart rate and blood pressure occur.Injection of the radiopharmaceutical for myocar-dial perfusion scintigraphy takes place 1minuteafter the desired dose is reached, and the infusionis continued for 1–2minutes after injection. Sideeffects of dobutamine (headache, flushing, GI dis-tress, ectopy, angina, or ECG evidence of ischemia)can be terminated by discontinuing the infusion(the half-life of dobutamine is 2minutes).

Exercise stress testingExercise stress testing increases in myocardialoxygen consumption to detect limitations in coro-nary blood flow. Exercise increases cardiac out-put through increases in heart rate and inotropy.Despite vasodilatation in skeletal muscle, exercisetypically increases arterial blood pressure as well.As a result, exercise is accompanied by increases inthe three major determinants of myocardial oxygenconsumption: heart rate, wall tension, and contrac-tility. Tomeet the demands of exercise, the coronaryvascular bed dilates. The ability of the coronarycirculation to increase blood flow tomatch exercise-induced increases in demand is compromised in thedistribution of stenosed coronary arteries becausevasodilatory reserve is exhausted in these beds.

All exercise tests increase metabolic rate andoxygen consumption (VO2). Isometric exercisemay be used to increase the workload, but morecommonly, dynamic exercise using either a tread-mill or a bicycle is used. VO2max is the maximalamount of oxygen a person can use while per-forming dynamic exercise. VO2max is influencedby age, gender, exercise habits, and cardiovascu-lar status. Exercise protocols are compared by usingmetabolic equivalents (METs). One MET is equal toa VO2 of 3.5mL oxygen(O2)/kg/min and representsresting oxygen uptake. Different exercise protocolsare compared by comparing the number of METsconsumed at various stages.

The Bruce treadmill protocol is the most com-monly used protocol for exercise stress testing.This protocol uses seven 3-minute stages. Eachprogressive stage involves an increase in boththe grade and the speed of the treadmill. Dur-ing stage 1 the treadmill speed is 1.7miles/h ona 10% grade (5 METs); during stage 5 the tread-mill speed is 5miles/h on an 18% grade (16 METs).The patient progressively moves through thestages until either exhausted, a target heart rateachieved without ischemia, or the detection ofischemic changes on the ECG. Exercise stress test-ing can be performed in conjunction with tradi-tional ECG analysis, myocardial perfusion scintig-raphy, or echocardiography. The details of stressmyocardial perfusion scintigraphy, stress radionu-cleotide angiography, and stress echocardiographyare discussed below.

The following factors must be considered ininterpretation of an ECG exercise stress test:• Angina. Ischemia may present as the patient’stypical angina pattern; however, angina is not auniversal manifestation of ischemia in all patients.Ischemic pain induced by exercise is stronglypredictive of CAD.• VO2max. If patients with CAD reach 13 METs,their prognosis is good regardless of other fac-tors; patients with an exercise capacity of less than5 METs have a poor prognosis.• Dysrhythmias. For patients with CAD, ventricu-lar dysrhythmias may be precipitated or aggravatedby exercise testing. The appearance of reproduciblesustained (>30 seconds) or symptomatic ventricular

Introduction 7

tachycardia (VT) is predictive of multivessel diseaseand poor prognosis.• ST segment changes. ST segment depression is themost common manifestation of exercise-inducedmyocardial ischemia. The standard criterion for anabnormal response is horizontal or down sloping(>1mm) depression 80ms after the J point. Downsloping segments carry a worse prognosis than hor-izontal segments. The degree of ST segment depres-sion (>2mm), the time of appearance (startingwith<6 METs), the duration of depression (persisting>5minutes into recovery), and the number ofECG leads involved (>5 leads) are all predictive ofmultivessel CAD and adverse prognosis.• Blood pressure changes. Failure to increase systolicarterial blood pressure to greater than 120mmHg,or a sustained decrease in systolic blood pressurewith progressive exercise, is indicative of cardiacfailure in the face of increasing demand. This findingsuggests severe multivessel or left main CAD.

Comparison of stress test methodsThe sensitivity of detection of CAD with exer-cise myocardial perfusion scintigraphy or exerciseechocardiography is superior to that of exerciseECG testing. The superiority of these two modal-ities over ECG testing in detecting CAD is great-est for patients with single vessel CAD. Whencomparing myocardial perfusion scintigraphy tostress echocardiography, the data suggest a trendtoward greater sensitivity with myocardial per-fusion scintigraphy, particularly for patients withsingle-vessel disease. Moderate to large perfusiondefects by either stress echocardiography or thal-lium imaging predicts postoperative myocardialinfarction or death in patients scheduled for elec-tive noncardiac surgery. Negative tests assure theclinician of a small likelihood of subsequent adverseoutcome (negative predictive value = 99%). Unfor-tunately, however, the positive predictive value(i.e. the chance that a patient with a positive testwill have an adverse cardiovascular event) is poorranging from 4% to 20%. In a meta-analysis com-paring the two techniques, stress echocardiographyis slightly superior to thallium imaging in predictingpostoperative cardiac events. The choice of whichtechnique should be made based upon institutional

expertise and patient-specific attribute. In eithercase, angiography should be considered in patientswith moderately large defects.

Limitations of exercise ECG testing are the inabil-ity to accurately localize and assess the extentof ischemia. Furthermore, no direct informationregarding left ventricle function is available. Stressmyocardial perfusion scintigraphy, radionuclideangiography, and echocardiography provide thisinformation. On the other hand, these methods aremore expensive and technically more demandingthan exercise ECG testing.

Myocardial perfusion scintigraphyMyocardial perfusion scintigraphy assesses myocar-dial blood flow, myocardial viability, the numberand extent of myocardial perfusion defects, tran-sient stress-induced LV dilatation, and allows forrisk stratification. Myocardial perfusion scintigra-phy is performed most commonly in conjunc-tion with stress testing. Stress testing can beaccomplished with exercise or pharmacologicallywith dipyridamole, adenosine, or dobutamine.Withthis technology, it is possible to determine whichregions of myocardium are perfused normally,which are ischemic, which are stunned or hibernat-ing, and which are infarcted. The technique is basedon the use of radiopharmaceuticals that accumulatein the myocardium proportional to regional bloodflow. Single-positron emission computed tomogra-phy (SPECT) or planar imaging is used to imageregional myocardial perfusion in multiple viewsand at variousmeasurement intervals. Patients withsmall fixed perfusion defects have reduced periop-erative risk profiles, whereas patients with multiplelarger defects are at higher risk.

The radiopharmaceuticals currently in use arethallium-201 and technetium-99m methoxyiso-butyl isonitrile (Sestamibi). Thallium has biologicproperties similar to potassium and thus is trans-ported across the myocardial cell membrane bythe sodium–potassium adenosine triphosphatase(ATPase) pump proportional to regional myocar-dial blood flow. Sestamibi is not dependent onATP to enter myocardial cells because it is highlylipophilic but its distribution in myocardial tissue isproportional to blood flow.

8 Chapter 1

ThalliumThallium-201 is injected at the peak level of a mul-tistage exercise or pharmacological stress test. Scin-tillation imaging begins 6–8minutes after injection(early views) and is repeated again 2–4hours afterinjection (delayed or redistribution views). Identi-cal views must be used so the early and delayedimages can be compared. During stress, myocardialblood flow and thallium-201 uptake will increase inareas of the myocardium supplied by normal coro-nary arteries. Subsequently, thallium redistributesto other tissues, thus clearing from the myocardiumslowly. Areas of myocardium supplied by diseasedarteries are prone to ischemia during stress andhave a reduced ability to increase myocardial bloodflow and thallium-201 uptake. These areas willdemonstrate a perfusion defect when comparedwith normal regions in the early views. In thedelayed views, late accumulation or flat washoutof thallium-201 from the ischemic areas comparedwith the nonischemic areas results in equalizationof thallium-201 activity in the two areas. Thesereversible perfusion defects are typical of areas ofmyocardium that suffer transient, stress-inducedischemia. Nonreversible perfusion defects are presentin both the early stress and delayed redistributionimages. These defects are believed to represent areasof nonviable myocardium resulting from old infarc-tions. Reverse redistribution is the phenomenon inwhich early images are normal or show a defect andthe delayed images show a defect or a more severedefect. This is seen frequently in patients who haverecently undergone thrombolytic therapy or angio-plasty and may result from higher-than-normalblood flow to the residual viable myocardium in thepartially infarcted zone.Modified thallium scintigraphy protocols are use-

ful in detecting areas hibernating myocardium.Hibernating myocardium exhibits persistentischemic dysfunction secondary to a chronic reduc-tion in coronary blood flow, but the tissue remainsviable. Hibernating myocardium has been shownto exhibit functional improvement after surgicalrevascularization or angioplasty and restoration ofcoronary blood flow. Stunned myocardium, in con-trast, has undergone a period of transient hypop-erfusion with subsequent reperfusion. As a result,

these regions exhibit transient postischemic dys-function in the setting of normal coronary bloodflow. Stunned myocardium is detected by identify-ing regions of dysfunctional myocardium in whichno perfusion defect exists.Some regions of myocardium that do not

exhibit redistribution at 2.5–4.0 hours exhibit redis-tribution in late images at 18–24hours. Thislate redistribution represents areas of hibernatingmyocardium. Another approach to detecting hiber-nating myocardium is reinjection of thallium at restafter acquisition of the 2.5–4.0-hour stress images.Persistent defects that show enhanced uptake afterreinjection represent areas of viable myocardium.Finally, serial rest thallium imaging has proved use-ful in detecting hibernating myocardium. Imagesare obtained at rest after injection of thalliumand then are repeated 3hours later. Regionsof myocardium that exhibit rest redistributionrepresent areas of viable myocardium.Increased lung uptake of thallium is related to

exercise-induced LV dysfunction and suggests mul-tivessel CAD. Because increased lung uptake ofthallium is due to an elevated left atrial pressure(LAP), other factors besides extensive CAD andexercise-induced LV dysfunction (such as mitralstenosis, mitral regurgitation, and nonischemic car-diomyopathy) must be considered when few or nomyocardial perfusion defects are detected. TransientLV dilation after exercise or pharmacologic stressalso suggests severe myocardial ischemia.

SestamibiSestamibi, unlike thallium, does not redistribute.As a result, the distribution of myocardial bloodflow at the time of injection remains fixed overthe course of several hours. This necessitates twoseparate injections: one at rest and one at peakstress. The two studies must be performed so thatthe myocardial activity from the first study decaysenough not to interfere with the activity from thesecond study. A small dose is administered at restwith imaging approximately 45–60minutes later.Several hours later, a larger dose is administeredat peak stress, with imaging 15–30minutes later.Reversible and fixed defects are detected by com-paring the rest and stress images. As with thallium,

Introduction 9

late imaging after Sestamibi stress imaging may behelpful in detecting hibernating myocardium.Sestamibi allows high-count-density images to be

recorded, providing better resolution than thallium.In addition, use of Sestamibi allows performance offirst pass radionuclide angiography (see below) tobe performed in conjunctionwithmyocardial perfu-sion scintigraphy. Use of simultaneous radionuclideangiography and perfusion scintigraphy has proveduseful in enhanced detection of viable myocardium.Viable myocardium will exhibit preserved regionalperfusion in conjunction with preserved regionalwall motion.

Radionuclide angiographyRadionuclide angiography allows assessment ofRV and LV performance. Two types of cardiacradionuclide imaging exist: first-pass radionuclideangiography (FPRNA) and equilibrium radionu-clide angiography (ERNA), also known as radionu-clide ventriculography or gated blood pool imaging.ERNA is also known as multiple-gated acquisition(MUGA) ormultiple-gated equilibrium scintigraphy(MGES).FPRNA involves injection of a radionuclide bolus

(normally technetium-99m) into the central circu-lation via the external jugular or antecubital vein.Subsequent imaging with a scintillation camera in afixed position provides a temporal pictorial presen-tation of the cardiac chambers as the radiolabeledbolus makes its way through the heart. First-passstudies may be gated or ungated. Gated studiesinvolve synchronization of the presented imageswith the patient’s ECG such that systole and dias-tole are identified. Ungated studies simply present aseries of images over time.ERNA involves use of technetium-99m-labeled

red cells, which are allowed to distribute uniformlyin the blood volume. Radiolabeling of red cells isaccomplished by initially injecting the patient withstannous pyrophosphate, which creates a stannous-hemoglobin complex over the course of 30minutes.Subsequent injection of a technetium-99m bolusresults in binding of technetium-99m to thestannous-hemoglobin complex, thus labeling thered cells.

After equilibrium of the labeled red cells in thecardiac blood pool, gated imaging with a scintil-lation camera is performed. A computer dividesthe cardiac cycle into a predetermined number offrames (16–64). Each frame represents a specifictime interval relative to the ECG R wave. Datacollected from each time interval over the courseof several hundred cardiac cycles are then addedtogether with the other images from the same timeinterval. The result is a sequence of 16–64 images,each representing a specific phase of the cardiaccycle. The images can be displayed in an endlessloop format or individually. The procedure canthen be repeated with the camera in a differentposition.

Below is a summary of the relative advantagesand disadvantages of first-pass and equilibrationstudies. Both types of studies currently are used foradults, infants, and children.• With both FPRNA and ERNA studies, the num-ber of radioactive counts during end systole andend diastole can be used to determine strokevolume, ejection fraction, and cardiac output.• Both types of studies allow reliable quantificationof LV volume using count-proportional methodsthat do not require assumptions to be made aboutLV geometry.• Although both studies allow determination of RVand LV ejection fractions, determination of RV ejec-tion fraction is more accurate with a first-pass studybecause the right atrium overlaps the right ventriclein equilibrium studies.• First-pass studies allow detection and quantifica-tion of both right-to-left and left-to-right intracar-diac shunts, whereas shunt detection is not possiblewith equilibration studies.• First-pass studies allow sequential analysis ofright atrial (RA), RV, left atrial (LA), and LV size,whereas equilibration studies do not. Abnormalitiesin the progression of the radioactive tracer throughthe heart and great vessels assist in the diagnosis ofcongenital abnormalities.• Equilibration studies provide better analysis ofregional wall motion abnormalities than first-passstudies due to higher resolution.• Both types of studies can be used with exer-cise. First-pass studies can be performed rapidly

10 Chapter 1

but do not allow assessment of ventricular wallmotion at different exercise levels, nor do they allowassessment of wall motion from different angles.• Mitral or aortic regurgitation is detectable withboth first-pass and equilibration studies by analysisof the stroke volume ratio. This method tends tooverestimate regurgitant fraction and is not reliablefor detection of minor degrees of regurgitation.

EchocardiographyTransthoracic and transesophageal echocardiogra-phy has revolutionized the noninvasive structuraland functional assessment of acquired and con-genital heart disease. Transthoracic echocardiogra-phy (TTE) and transesophageal echocardiography(TEE) often play a major role in the evaluationof cardiac surgical patients. Routine use of two-dimensional imaging, color flow Doppler, contin-uous wave Doppler, pulsed wave Doppler, andM-mode imaging allows the following:• Assessment of cardiac anatomy. Delineation of themost complex congenital heart lesions is feasi-ble. In many instances, information acquired froma comprehensive echocardiographic examinationis all that is necessary to undertake a surgicalrepair.• Assessment of ventricular function. A comprehen-sive assessment of RV and LV diastolic and systolicfunction is feasible.• Assessment of valvular abnormalities. Assessmentof the functional status of all four cardiac valvesis possible. In addition, quantification of valvularstenosis and insufficiency is accurate and reliable.Assessment of prosthetic valves also is feasible.• Characterization of cardiomyopathies. Hypertrophic,dilated, and restrictive cardiomyopathies can beidentified.• Assessment of the pericardium. Pericardial effusions,cardiac tamponade, and constrictive pericarditis arereliably identified.• Assessment of cardiac and extracardiac masses. Vege-tations, foreign bodies, thrombi, and metastatic andprimary cardiac tumors can be identified.• Contrast echocardiography. Contrast solutions con-taining microbubbles enhance the image allowingassessment of myocardial perfusion, intracardiac

shunts, enhancement of Doppler signals, andimproved assessment of regional and global LVfunction.• Stress echocardiography. Stress echocardiography isbased on the concept that exercise or pharmacolog-ically induced wall motion abnormalities developearly in the course of ischemia. Stress-inducedwall motion abnormalities occur soon after perfu-sion defects are detected by radionuclide imagingbecause, in the ischemic cascade, hypoperfusionprecedes wall motion abnormalities. Comparisonof resting and stress images allows resting abnor-malities to be distinguished from stress-inducedabnormalities. Resting abnormalities indicate priorinfarction, hibernating or stunned myocardium;whereas, stress-induced abnormalities are spe-cific for ischemia. Furthermore, dobutamine stressechocardiography may be useful in determin-ing myocardial viability. Regions that are hypo-kinetic, akinetic, or dyskinetic at rest and improvewith dobutamine administration probably containareas of stunned or hibernating myocardium. Suchareas demonstrate functional improvement aftermyocardial revascularization.

Computerized tomography and magneticresonance imagingAdvances in imaging techniques have played amajor role in defining anatomy in cardiac surgi-cal patients. Computerized tomography (CT) andmagnetic resonance imaging (MRI) now allow theclinician detailed anatomy, three-dimensional ren-dering, and functional assessment of myocardialperformance and blood flow (Fig. 1.1). It is likelythat new advances in imaging techniques will con-tinue to improve the quality and the anatomic detailafforded by these techniques. Molecular imaging,i.e. imaging of cellular function, is a developing areain cardiac imaging. The applications of these newtechnologies remain to be seen.

Cardiac catheterizationCardiac catheterization remains the gold standardfor evaluation of acquired and congenital heartdisease. Cardiac catheterization is covered in detailin Chapter 2.

Introduction 11

Fig. 1.1 Three dimension reconstruction of the heartand aorta

Respiratory evaluation

A preoperative assessment of pulmonary function(other than CXR) is required in all cardiac surgi-cal patients. The evaluation must include a historyof known pulmonary disease, current respiratorysymptoms, and a physical examination. Evalua-tion may include consultation with specialists andspecific pulmonary testing (pulmonary functiontesting, spirometry, pulse oximetry, arterial bloodgas analysis). The history should determine theextent and length of tobacco use, the presence ofCOPD, asthma, recurrent or acute pulmonary infec-tions, and the presence of dyspnea. Physical exam-ination should focus on the detection of wheezes,flattened diaphragms, air trapping, consolidations,and clubbing of the nails. A CXR is indicated innearly all cardiac surgical patients. Pulmonary func-tion tests (PFTs) play a limited role in preoperativeassessment. If there is confusion about whetherintrinsic pulmonary disease exists, its cause, andits appropriate treatment, then pulmonary func-tion testing may help guide the clinician. Spirom-etry measures lung volumes, capacities, and flow.Spirometry of expiratory flow rates allowsmeasure-ment of the forced expiratory volume in 1 second

(FEV1), the forced vital capacity (FVC), and theforced mid-expiratory flow (FEF 25–75%). Arterialblood gases should be obtained for patients inwhomcarbon dioxide (CO2) retention is suspected and forthose with severe pulmonary dysfunction as deter-mined by history, physical examination, PFTs, orcardiac catheterization.

Pulmonary assessment and congenitalheart diseaseLesions that produce excessive pulmonary bloodflow (large ventricular septal defect, truncus arte-riosus, dextrotransposition of the great arteries,and patent ductus arteriosus) are associated withpulmonary dysfunction. Occasionally, large airwaycompression occurs in response to enlargementof the pulmonary arteries. More commonly, how-ever, these lesions produce pulmonary vascularchanges that affect pulmonary function. The pul-monary vascular smooth muscle hypertrophy thataccompanies increased pulmonary blood flow pro-duces peripheral airway obstruction and reducedexpiratory flow rates characteristic of obstructivelung disease. In addition, smooth muscle hypertro-phy in respiratory bronchioles and alveolar ductsin patients with increased pulmonary blood flowcontributes to this obstructive pathology. Thesechanges predispose the patient to atelectasis andpneumonia. Children with Down syndrome havea more extensive degree of pulmonary vascularand parenchymal lung disease than other childrenwith similar heart lesions. This predisposes patientswith Down syndrome to greater postoperativerespiratory morbidity and mortality.

Patients with lesions that reduce pulmonaryblood flow (pulmonary atresia or stenosis, tetralogyof Fallot) also have characteristic pulmonary func-tion changes. These patients have normal lung com-pliance as compared with the decreased complianceseen in patients with increased pulmonary bloodflow. However, the large dead space to tidal volumeratio in these patients greatly reduces ventilationefficiency, and large tidal volumes are required tomaintain normal alveolar ventilation. Finally, 3–6%of patients with tetralogy of Fallot will have anabsent pulmonary valve and aneurysmal dilata-tion of the pulmonary arteries. This aneurysmal

12 Chapter 1

dilatation produces bronchial compression andrespiratory distress at birth.

Pulmonary assessment and acquiredheart diseasePulmonary dysfunction ranks among the highestpredictors of postoperative pulmonary complica-tions. Pulmonary dysfunction is defined as a pro-ductive cough, wheeze, or dyspnea. Pulmonaryfunction testing consistent with pulmonary dys-function shows a FEV1 < 70% of predictedor FEV1/FVC < 65% of predicted, plus eithervital capacity (VC) < 3.0 L or maximum volun-tary ventilation (MVV ) < 80 L/min. For patientsundergoing valvular surgery, the presence of pul-monary dysfunction is associated with up to a2.5-fold increase in perioperative mortality and a2.5-fold increase in postoperative respiratory com-plications. For patients undergoing only coronaryrevascularization, pulmonary dysfunction is lesspredictive of postoperative morbidity andmortality.

Pulmonary assessment and tobacco useChronic tobacco use has several physiologic effectsthat may complicate anesthetic management.Smoking accelerates the development of atheroscle-rosis. Further, smoking reduces coronary blood flowby increasing blood viscosity, platelet aggregation,and coronary vascular resistance. Nicotine, throughactivation of the sympathetic nervous system andelevated catecholamine levels, increases myocardialoxygen consumption by increasing heart rate, bloodpressure andmyocardial contractility. Furthermore,the increased carboxyhemoglobin level, which mayexceed 10% in smokers, reduces systemic andmyocardial oxygen delivery. This is particularlydetrimental to the patient with CAD due to the highextraction of oxygen that normally occurs in themyocardium. The threshold for exercise-inducedangina is reduced by carboxyhemoglobin levels aslow as 4.5%. Short-term abstinence (12–48hours)is sufficient to reduce carboxyhemoglobin and nico-tine levels and improve the work capacity of themyocardium.There is an increased incidence of postoperative

respiratory morbidity in patients who smoke. These

complications include respiratory failure, unantic-ipated intensive unit admission, pneumonia, air-way events during induction of anesthesia (cough,laryngospasm), and increased need for postopera-tive respiratory therapy. Smoking increases mucussecretion, impairs tracheobronchial clearance, andcauses small airway narrowing. For patients under-going coronary revascularization, abstinence fromsmoking for 2months may reduce the incidenceof postoperative respiratory complications. Absti-nence for less than 2months is ineffective inreducing the incidence of postoperative respiratorycomplications. Similar studies of patients under-going other surgical procedures have confirmedthe necessity of a 4–6-week abstinence period.Typically, tobacco-using patients presenting for car-diac surgery will not have had the recommendedabstinence period required to reduce complications.Acute cessation of smoking during the perioperativeperiod is not associated with elevated risk. Thereis no added cardiovascular risk for patients usingnicotine replacement therapy (NRT).

Pulmonary assessment and asthmaAsthma is characterized by paroxysmal or persis-tent symptoms of wheezing, chest tightness, dys-pnea, sputum production, and cough with airflowlimitation. There is hyper-responsiveness to endo-genous or exogenous stimuli. Preoperative evalua-tion of asthma confirms the diagnosis and evaluatesthe adequacy of treatment. Adequate control isdemonstrated when the patient reports normalphysical activity, mild and infrequent exacerba-tions, no missed school or work days, and lessthan four doses of β2-agonist therapy per week.Long-term treatment is largely preventive in nature.First-line pharmacologic treatment often incorpo-rates inhaled corticosteroids (ICSs). Beclometha-sone significantly improves FEV1, peak expiratoryflow, and reduces β-agonist use and exacerba-tions. Leukotriene receptor antagonists (LTRAs) aresometimes used as first-line therapy; however, theirrole is less clearly established when compared tothe ICS agents. Long-acting β2-agonists are safe andeffective medications for improving asthma controlin older children and adults when ICSs therapy doesnot adequately control the disease. Theophylline is

Introduction 13

less effective than ICSs and LTRAs in improvingasthma control.For patients in whom bronchospasm is well con-

trolled preoperatively, it is essential to continuetherapy during the perioperative period. Beta-2-agonist metered-dose inhaler or nebulizer therapycan be continued until arrival in the operating roomand can be restarted soon after emergence fromanesthesia. Metered-dose inhalation therapy can bedelivered via the endotracheal tube. For patients noton bronchodilator therapy who present for surgerywith bronchospasm, a trial of bronchodilators withmeasurement of PFTs before and after therapy isoften helpful. An increase in the FEV1 of 15% ormore after inhalation of a nebulized bronchodilatorsuggests a reversible component of bronchospasm.Surgery should be delayed until the asthma is con-trolled. If this is not possible, acute therapy withsteroids and β2-agonists is indicated. Therapy forthe cardiac surgical patient should be initiated witha β2-selective metered-dose inhaler or nebulizedsolution.

Renal function

Patients presenting for cardiac surgery may pos-sess varying degrees of renal dysfunction rangingfrommild elevations in creatinine to dialysis depen-dence. Assessing renal function preoperatively isvitally important in the cardiac surgical patient.Renal dysfunction after cardiac surgery is associ-ated with increased mortality, morbidity, resourceutilization and intensive care unit stay. Dependingon the definition of acute renal failure (ARF), any-where from 5% to 30% of patients demonstraterenal dysfunction after cardiac procedures. Renaldysfunction requiring dialysis is associated with a50–80% increased risk of death. ARF is among thestrongest predictors for death with an odds ratioof 7.9 (95% confidence interval 6–10) in cardiacsurgical patients. Identification of high-risk can-didates remains important for appropriate patientconsent, risk-benefit analysis, and hospital resourceutilization planning (Table 1.5).The dialysis-dependent patient will require dial-

ysis preoperatively. If dialysis is unobtainablepreoperatively, it can be managed intraoperatively.

Table 1.5 Risk factors for acute renal failure aftercardiac surgery.

Female genderCongestive heart failureLV ejection fraction <35%Preoperative use of an intraaortic balloon pumpChronic obstructive pulmonary diseasePrevious cardiac surgeryEmergency surgeryValve or valve + CABG surgeryElevated preoperative creatinine

CABG, coronary artery bypass graft.

Dialysis will correct or improve the abnormalities inpotassium, phosphate, sodium, chloride, and mag-nesium. In addition, the platelet dysfunction thataccompanies uremia will be improved. L-deamino-8-D-arginine vasopressin (DDAVP) administrationmay improve uremia-induced platelet dysfunctionand should be considered if clinically significantpost-dialysis platelet dysfunction exists. Dialysiswill not favorably affect the anemia, renovascu-lar hypertension, or immune-system compromiseassociated with chronic renal failure.

For nondialysis-dependent patients, preoperativehydration is necessary to prevent prerenal azotemiafrom complicating the underlying renal dysfunc-tion. This is particularly important after proceduressuch as cardiac catheterization with arteriography.Creatinine clearance falls after contrast arterio-graphy; in patients with preexisting azotemia, thisreduction is much more likely to result in ARF.Hydration ameliorates contrast-induced renal dys-function. Treatmentwith acetylcysteine and sodiumbicarbonate reduce post-contrast ARF.

Patients with renal transplants occasionallypresent for cardiac surgical procedures. The extra-renal component of renal blood flow autoregula-tion is absent in the denervated kidney. Therefore,preoperative hydration and maintenance of sys-temic perfusion pressure are particularly importantto maintain renal perfusion. Sterile technique ismandatory in these immunocompromised patients.

Renal dysfunction often results in electrolyteimbalance. Potassium regulation is often difficultin the cardiac surgical patient. Hyperkalemia

14 Chapter 1

(>5.5mEq/L) is uncommon in patientswith normalrenal function; however, it may occur with injudi-cious potassium administration. Themajor causes ofhyperkalemia result from diminished renal excre-tion of potassium secondary to reduced glomerularfiltration rate (acute oliguric renal failure, chronicrenal failure). Reduced tubular secretion may leadto hyperkalemia as seen in Addison’s disease,potassium-sparing diuretics and angiotensin con-verting enzyme inhibitors. Other causes includetranscellular shifts of potassium as seen in acido-sis, trauma, burns, beta-blockade, rhabdomyolysis,hemolysis, diabetic hyperglycemia, and depolar-izing muscle paralysis with succinylcholine. Theclinical manifestations relate to alterations in car-diac excitability. Peaked T waves will appear with apotassium level of 6.5mEq/L. At levels of 7–8mEq/Lthe PR interval will prolong and the QRS complexwill widen. At 8–10mEq/L sine waves appear andcardiac standstill is imminent. Treatment is multi-modal and includes glucose, insulin, bicarbonateand β-agonists (shifting potassium to the intracel-lular compartment), diuretics, exchange resins anddialysis (enhancing potassiumelimination), and cal-cium (no change in serum potassium concentra-tion, but calcium counteracts the cardiac conductioneffects of hyperkalemia).Hypokalemia (<3.5mEq/L) is not uncommon in

the cardiac surgical patient. The most common eti-ology is chronic diuretic therapy, but other causessuch as GI loss (nasogastric suction, diarrhea, vom-iting), mineralocorticoid excess, acute leukemia,alkalosis, barium ingestion, insulin therapy, vita-min B12 therapy, thyrotoxicosis and inadequateintake must be considered. The clinical manifesta-tions of hypokalemia are observed in skeletal mus-cle, heart, kidneys, and the GI tract. Neuromuscularweakness is observed with levels of 2.0–2.5mEq/L.Hypokalemia leads to a sagging of the ST segment,depression of the T wave, and the appearance of aU wave on the ECG. In patients treated with digi-talis, hypokalemia may precipitate serious arrhyth-mias. Treatment of hypokalemia involves eitheroral or parenteral replacement. A deficit in serumpotassium reflects a substantial total body deficit.A decrease in plasma potassium concentration of1mEq/Lwith a normal acid-base balance represents

approximately 300mEq of total body potassiumdeficiency. In preparing the cardiac surgical patientfor surgery, it is reasonable to maintain serumpotassium higher than 3.5mEq/L for patients ondigitalis, those at high risk for myocardial ischemiaand those who have suffered acute reductions inserum potassium. Potassium replacement is notwithout risk (iatrogenic hyperkalemia). In gen-eral, potassium replacement should not exceed10–20mEq/h or 200mEq/day. Serum potassiummust be closely monitored during the replacementtherapy.

Endocrine evaluation

A careful evaluation for endocrine abnormalitiesshould be sought in the history and physical exami-nation. Diabetes mellitus (DM) and hypothyroidismdeserve special consideration.

Diabetes mellitusDiabetes mellitus is a risk factor for developmentof CAD; therefore, perioperative management ofDM is a common problem facing those who anes-thetize patients for cardiac surgery. Patients withinsulin-dependent diabetes have reduced or absentinsulin production due to destruction of pancre-atic beta cells. Patients with noninsulin-dependentdiabetes have normal or excessive production ofinsulin but suffer from insulin resistance. Thisresistance may be due to a reduction in insulinreceptors, a defect in the second messenger onceinsulin binds to receptors, or both. Patients withnoninsulin-dependent diabetes may be managedwith diet, oral hypoglycemic agents (agents thatincrease pancreatic insulin production), or exoge-nous insulin. Patients with insulin-dependent dia-betes must receive exogenous insulin.Cardiopulmonary bypass (CPB) is associated with

changes in glucose and insulin homeostasis in bothdiabetic and nondiabetic patients. During normoth-ermic CPB, elevations in glucagon, cortisol, growthhormone, and catecholamine levels produce hyper-glycemia through increased hepatic glucose produc-tion, reduced peripheral use of glucose, and reduced

Introduction 15

insulin production. During hypothermic CPB, hep-atic glucose production is reduced and insulin pro-duction remains low such that blood glucose lev-els remain relatively constant. Rewarming on CPBis associated with increases in glucagon, cortisol,growth hormone, and catecholamine levels and isaccompanied by enhanced hepatic production ofglucose, enhanced insulin production, and insulinresistance. The transfusion of blood preserved withacid-citrate-dextrose, the use of glucose solutions inthe CPB prime, and the use of β-adrenergic agentsfor inotropic support, further increase exogenousinsulin requirements. For nondiabetic patients,these hormonally mediated changes usually resultin mild hyperglycemia. For diabetic patients, thesechanges may produce significant hyperglycemiaand ketoacidosis.Management of perioperative glucose is directly

related to perioperative outcome. Uncontrolled, orpoorly controlled, perioperative glucose is associ-atedwith increasedmortality, wound infection, andintensive care unit length of stay. This relationshipis true in cardiac and noncardiac surgical patientsadmitted to an intensive care unit setting. The ideallevel of glucose is unknown; however, if a targetof 130mg/dL can be achieved, this is associatedwith improved clinical outcome. Administration ofexogenous insulin should be administered early inthe perioperative period to achieve this goal. Theclinician must remember that achieving this goalmay be impossible in some patients. Insulin resis-tance and the physiologic conditions encouraginghyperglycemia may be too great in some patients.Similarly, the clinician must exercise caution whenadministering insulin. Serum glucose levels shouldbe checked as frequently as every 15–30minutesperioperatively while insulin therapy is utilized.Unrecognized hypoglycemia can adversely affectpatient outcome.Because of the varying insulin requirements dur-

ing cardiac surgery and the unreliable absorptionof subcutaneously administered insulin in patientsundergoing large changes in body temperatureand peripheral perfusion, insulin is best deliveredIV for patients undergoing cardiac surgery. Thegoal of therapy should be maintenance of normo-glycemia during the pre-CPB, CPB, and post-CPB

Table 1.6 Recommendations for insulin administration.

Bloodglucose(mg/dL)

Insulininfusionrate(U/kg/h)

Rate in100 kgpatient(U/h)∗

150–200 0.02 2200–250 0.03 3250–300 0.04 4300–350 0.05 5350–400 0.06 6

∗ The actual rate of administration will vary from patientto patient and should be titrated against measured serumglucose levels and patient response.

periods. On the morning of surgery, the usualinsulin dose is withheld. On arrival in the operatingroom, the patient’s blood glucose is measured. Fortight control, a continuous regular insulin infu-sion can be started and adjusted to maintain bloodglucose between 100 and 150mg/dL during theoperative procedure. Determinations of blood glu-cose are made every 15–30minutes. Table 1.6provides guidelines for insulin administration. Itmust be emphasized that the alterations in glucosehomeostasis and the insulin resistance that accom-pany hypothermic CPB may necessitate alterationin infusion rates, and therefore insulin must betitrated against demonstrated patient response bymeasuring serial serum glucose levels.

Patients taking oral hypoglycemic agents shoulddiscontinue them at least 12hours before surgery.For patients managed with these agents andpatients managed with diet, blood glucose deter-minations should be made every 30–60minutesduring the operative procedure. These patientsfrequently require insulin infusions to maintainglucose homeostasis during surgery.

HypothyroidismHypothyroidism is characterized by a reduction inthe basal metabolic rate. In patients with hypothy-roidism cardiac output may be reduced by up to40% due to reductions in both heart rate and strokevolume. In addition, both hypoxic and hypercapnicventilatory drives are blunted by hypothyroidism.

16 Chapter 1

Furthermore, hypothyroidism may be associatedwith blunting of baroreceptor reflexes, reduced drugmetabolism, renal excretion, reduced bowel motil-ity, hypothermia, hyponatremia from syndrome ofinappropriate antidiuretic hormone (SIADH), andadrenal insufficiency. The hypothyroid patient maynot tolerate usual doses of antianginal drugs such asnitrates and β-adrenergic blocking agents. Hypothy-roid patients on beta-blockers typically require verylow anesthetic drug requirements.Despite these problems, thyroid replacement

for cardiac surgical patients, particularly thosewith ischemic heart disease, is not always desir-able. For hypothyroid patients requiring coronaryrevascularization, thyroid hormone replacementmay precipitate myocardial ischemia, myocar-dial infarction, or adrenal insufficiency. Coronaryrevascularization may be managed successfully inhypothyroid patients with thyroid replacementwithheld until the postoperative period. Mild tomoderate hypothyroid patients undergoing cardiacsurgery have perioperative morbidity and mortalitysimilar to euthyriod patients. Hypothyroid patientsmay experience delayed emergence from anesthe-sia, persistent hypotension, tissue friability, bleed-ing and adrenal insufficiency requiring exogenoussteroids. Hypothyroidism is preferentially treatedwith levothyroxine (T4). In healthy adults withoutCAD, a starting dose of 75–100μg/day is appro-priate. In elderly patients, and those with CAD,the initial dose is 12.5–25.0μg/day and is increasedby 25–50μg every 4–6weeks allowing for a slowincrease in metabolic rate thereby avoiding a mis-match in coronary blood supply and metabolicdemand.

Hematologic evaluation

By the nature of the surgery, and the associatedcardiovascular medications (heparin, clopidogrel),cardiac surgical patients are at higher periopera-tive risk of bleeding. A hemoglobin and hema-tocrit is indicated based on the invasiveness ofthe procedure (i.e. relative risk of blood loss andtransfusion), the history of liver disease, anemia,bleeding, other hematologic disorders or an extreme

in age. Serum chemistry (i.e. potassium, sodium,glucose, renal and liver function studies) are indi-cated in patients anticipating invasive surgery withpossible metabolic alterations, diabetic patients andother patients at specific risk of renal or liver dys-function. Plasma N-terminal pro-brain natureticpeptide (NTproBNP) is secreted by the left ven-tricle in response to wall stress. It is elevated inpatients with LV dysfunction and heart failure. Pre-operative NTproBNP levels greater than 450ng/Lare predictive of cardiac complications with a sen-sitivity of 100% and a specificity of 89%. Hence,an NTproBNP level may assist in preoperative riskassessment and resource management in selectedpatients. A urinalysis is usually not indicated unlessthere are specific urinary findings. A pregnancytest should be considered in all female patientsof childbearing age. Coagulation studies are indi-cated depending on the invasiveness of the proce-dure, a history of renal or liver dysfunction, and inpatients on anticoagulant medications.Medical management of acute coronary syn-

dromes, myocardial infarction, peripheral vasculardisease, atrial fibrillation, and stroke often includesantithromboticmedications such as aspirin, clopido-grel bisulfate, heparin, coumadin, and others. Thesemedications are common in patients presenting forcardiac surgery and may have a major impact onthemanagement and preoperative evaluation of thepatient. Patients may present with a long history ofaspirin or clopidogrel use. In the acute setting, hep-arin or shorter acting IIb/IIIa inhibiting agents suchas integrelin may be in use. These agents are ben-eficial in reducing the incidence of stent occlusion,myocardial infarction, or other thrombotic sequaelaof peripheral vascular disease or hyper-coagulation.A thoughtful plan regarding the continued admin-istration of these medications is required prior tothe operative procedure. In the case of clopido-grel, stable patients presenting for elective surgerymay be advised to stop the medication for 5 daysto reduce the risk of excessive bleeding duringthe operation. All of the agents, including aspirin,are associated with increased blood loss duringsurgery. The relative risk of stopping the agentversus the increased risk of excessive bleeding must

Introduction 17

be weighed in each patient. Consultation withsurgeon and cardiologist are recommended beforediscontinuing antithrombotic therapy.In addition to the medication history, all patients

scheduled for cardiac surgical procedures require acareful bleeding history with emphasis on abnor-mal bleeding occurring after surgical procedures,dental extractions and trauma. Signs of easy bruis-ing should be sought on physical examination.All patients should undergo laboratory screeningfor the presence of abnormalities in hemostasis.A platelet count, partial thromboplastin time (PTT),and prothrombin time (PT) should be obtained.Time permitting, all abnormalities should be eval-uated prior to surgery so that post-CPB hemostasisis not complicated by unknown or unsuspectedmedical conditions.

PT and PTT elevationsElevations in PT and PTT should be investigatedfor factor deficiencies, factor inhibitors, and thepresence of anticoagulants such as warfarin andheparin. It is important that documentation of anormal PTT and PT existing before warfarin orheparin administration is initiated so that othercauses of an elevated PTT and PT are not over-looked. Deficiencies of factors VIII, IX, and XIare most commonly encountered. These deficien-cies and their management are summarized in thefollowing sections.

Factor VIII deficiency (hemophilia A)The half-life of factor VIII in plasma is 8–12hours;normal persons have approximately 1unit offactor VIII activity per 1mLof plasma (100%activity).Patients with severe hemophilia A will have aslittle as 1% factor VIII activity, whereas mildlyaffected patients will have up to 50% activity.Patients present with an elevated PTT and varyingdegrees of clinical bleeding. The diagnosis is madeby a factor assay. Safe conduct of cardiac surgeryrequires 80–100% factor VIII activity during theoperative procedure, with maintenance of activitylevels in the 30–50% range for 7 days postopera-tively. An infusion of 1.0 unit of factor VIII perkilogram of body weight will increase the patient’s

factor VIII activity level by 2%. The 12-hour half-lifeof factor VIII requires that factor VIII be re-infusedevery 12hours during the perioperative period.Factor VIII may be provided with cryoprecipitate,which contains 100units of factor VIII per bag(10–20mL). Factor VIII concentrates that contain1000units of factor VIII in 30–100mL also mayprovide factor VIII.

Factor IX deficiency (hemophilia B)The half-life of factor IX in plasma is 24hours; nor-mal persons have approximately 1unit of factorIX activity per 1mL of plasma (100% activity).Factor IX deficiency is clinically indistinguishablefrom factor VIII deficiency. Diagnosis is made byfactor assay. Safe conduct of cardiac surgery requires60% factor IX activity during the operative pro-cedure, with maintenance of activity levels in the30–50% range for 7 days postoperatively. An infu-sion of 1.0 unit of factor IX per kilogram of bodyweight will increase the patient’s factor IX activ-ity level by 1%. The 24-hour half-life of factor IXrequires that factor IX be re-infused only every24hours during the perioperative period. Freshfrozen plasma (FFP) contains 0.8 units of all ofthe procoagulants per milliliter and generally isused to replace factor IX. A 250-mL bag of FFPwill provide 200 units of factor IX. For patients inwho factor IX replacement with FFP will requireinfusion of prohibitively large volumes, factor IXconcentrates are used.

Factor XI deficiency (Rosenthalsyndrome)The half-life of factor XI in plasma is 60–80hours;normal persons have approximately 1unit offactor XI activity per 1mLof plasma (100%activity).Factor XI deficiency is most common amongpatients of Jewish descent and is associated witha prolonged PTT. Many of these patients haveno symptoms or have a history of bleeding onlywith surgery or major trauma. The diagnosis ismade by factor assay. FFP administration replen-ishes factor XI. It is recommended that 10–20mLof FFP/kg/day be used during the preoperative andpostoperative periods to manage this deficiency.

18 Chapter 1

Platelet dysfunctionThrombocytopenia should be evaluated and treatedas necessary to avoid excessive operative bleeding.A platelet count and platelet function monitoringare important laboratory evaluations. The bleed-ing time is not a reliable predictor of perioperativeor postoperative bleeding. Other measurements ofplatelet dysfunction include thromboelastographyand assays of activated platelet aggregation (aggre-gometry). These evaluations provide informationon the functional integrity of platelet action. In thecase of thromboelastography, clot formation andfibrinolysis are observed. The information gainedprovides insight into both factor content and plateletfunction. The activated platelet aggregation assaysprovide both a total platelet count and a percent-age of active platelets. Platelet dysfunction can resultfrom a variety of causes.

ThrombocytopeniaThrombocytopenia may due to dilution (i.e. withmassive fluid replacement), increased peripheraldestruction (sepsis, disseminated intravascular coag-ulation, thrombotic thrombocytopenic prupura,prosthetic valve hemolysis or platelet antibodies)or sequestration (splenomegaly, lymphoma). Inthe cardiac surgical patient, dilutional thrombo-cytopenia is common. Thrombocytopenia is alsofrequently the result of platelet destruction from theCPB circuit and from activation of heparin inducedplatelet antibodies.Heparin-induced thrombocytopenia and throm-

bosis (HITT) occurs due to the presence of an anti-heparin-platelet factor 4 antibodies. The conditioncan be terminated by withdrawal of heparin ther-apy. Ideally, heparin therapy should not be restarteduntil in-vitro platelet aggregation in response toheparin no longer occurs. Heparin induced throm-bocytopeniamay re-occur up to 12months after theinitial episode. Patients with HITT requiring CPBbefore the antibody can be cleared present a man-agement problem. These patients may be treatedby a variety of alternate anticoagulation agents.Direct thrombin inhibitors such as danaparoid, lep-irudin, bivalirudin, and argatroban have all beenused with success. Other agents such as tirofibanand epoprostenol have been used in combination

with unfractionated heparin with good result. Inthe preoperative setting, identification of patientswho have experienced HITT is paramount. If HITTis diagnosed, then the surgery should either bedelayed long enough to clear the heparin antibodies(usually 90–100 days), or an alternate anticoagu-lation strategy devised. If heparin re-exposure isconsidered, testing for the presence of HITT anti-bodies, generally by enzyme-linked immunosobentassay (ELISA), is required.

Qualitative platelet defectsAbnormalities in platelet function are observedwithsome medications, renal failure, hepatic failure,paraproteinemias (i.e. multiple myeloma), myelo-proliferative disorders, and hereditary disorders ofplatelet function. In the cardiac surgical patient,medication related dysfunction, uremic dysfunctionare most common.There is an ever growing list of medications

that inhibit platelet function. Some medicationsaltering function and commonly observed in thecardiac surgical patient include aspirin, nonsteroidalanti-inflammatory drugs (NSAIDs), thienopyridineadenosine diphosphate (ADP) receptor antago-nists (clopidogrel, ticlopidine) and GP IIb/IIIaantagonists (abciximab, integrelin, and tirofiban),dextran, dipyridamole, heparin, plasminogen acti-vators, and beta-lactam antibiotics. NSAIDs inhibitplatelet function by blocking platelet synthesis ofprostaglandins and platelet function is normalizedwhen these drugs are cleared from the blood.Aspirin irreversibly acetylates prostaglandin syn-thase (cyclooxygenase) impairing platelet functionfor the life of the platelet (7–10 days). Like aspirin,the effects of clopidogrel are present for the lifeof the platelet. It is recommended that for elec-tive surgery, clopidogrel should be held for 5 daysallowing adequate time to reestablish a normalplatelet response to bleeding. Integrelin inhibitsfibrinogen from binding to the platelet surfaceGP IIb/IIIa receptor. Integrelin should be discon-tinued 12hours before surgery to ensure adequatereturn of platelet function.Renal dysfunction with uremia inhibits platelet

function. The cause of this effect is unknown. Inaddition to the qualitative defect there is often

Introduction 19

thrombocytopenia in these patients. The bleed-ing time is usually prolonged and there is asso-ciated anemia. Bleeding may be treated withplatelet transfusion or administration of DDAVP,or cryoprecipitate. DDAVP and cryoprecipitate raisethe levels of factor VIII (antihemophilic factor/von Willebrand factor). When DDAVP is used,0.3μg/kg is infused IV over 15minutes and thehalf-life of its activity is 8 hours.

Coagulopathy and congenital heartdiseaseCoagulopathies in children with congenital heartdisease are common. The etiology of these coag-ulopathies is multifactorial. Cyanosis has beenimplicated in the genesis of coagulation and fib-rinolytic defects particularly in patients wheresecondary erythrocytosis produces a hematocritgreater than 60%. Thrombocytopenia and qualita-tive platelet defects are common. Defects in bleedingtime, clot retraction, and platelet aggregation toa variety of mediators have all been described.Platelet count and platelet aggregation response toADP are inversely correlated with hematocrit andpositively correlated with arterial oxygen satura-tion. In cyanotic patients, generation of plateletmicroparticles, hypofibrinogenemia, low-grade dis-seminated intravascular coagulation (DIC), defi-ciencies in factors V and VIII, and deficiencies inthe vitamin-K-dependent factors (II, VII, IX, X) haveall been implicated in the genesis of coagulapathy.In patients who are cyanotic and erythrocytotic,the plasma volume and quantity of coagulation fac-tors are reduced, and this may contribute to thedevelopment of a coagulopathy. In some instances,erythrophoresis with whole blood removed andreplaced with fresh frozen plasma or isotonic salinemay be justified.

In addition to the defects induced by cyanosis,defects inherent to normal infants and to childrenwith congenital heart disease are present. Neonatalplatelets are hypo-reactive to thrombin (the mostpotent platelet agonist), epinephrine/ADP, colla-gen, and thromboxane A2. In addition, neonatalfibrinogen is dysfunction as compared to older chil-dren and adults. An acquired deficiency of thelarge von Willebrand multimers has been demon-strated in patients with congenital heart disease.Finally, factors synthesized in the liver may bereduced in both cyanotic and acyanotic patientsin whom severe right heart failure results in pas-sive hepatic congestion and secondary parenchymaldisease.

Suggested reading

Ashley EA, Vagelos RH. Preoperative cardiac evaluation:

mechanisms, assessment, and reduction of risk. Thorac

Surg Clin 2005;15:263–75.Katz RI, Cimino L, Vitkun SA. Preoperative medical con-

sultations: impact on perioperative management and

surgical outcome. Can J Anaesth 2005;52:697–702.Maurer WG, Borkowski RG, Parker BM. Quality

and resource utilization in managing preoperative

evaluation. Anesthesiol Clin North America 2004;22:155–75.

Practice Advisory for Preanesthesia Evaluation. A report

by the Society of Anesthesiologists Task Force

on Preanesthesia Evaluation. Anesthesiology 2002;96:485–96.

Schmiesing CA, Brodsky JB. The preoperative anesthesia

evaluation. Thorac Surg Clin 2005;15:305–15.Thakar CV, Arrigain S, Worley S, Yared JP, Paganini EP.

A clinical score to predict acute renal failure after cardiac

surgery. J Am Soc Nephrol 2005;16:162–8.Wesorick DH, Eagle KA. The preoperative cardiovascular

evaluation of the intermediate-risk patient: new data,

changing strategies. Am J Med 2005;118:1413.e1–9.

C H A P T E R 2

Myocardial Physiology andthe Interpretation ofCardiac Catheterization Data

The ability to interpret cardiac catheterization datais essential to the cardiac anesthesiologist. Catheter-ization data provide information about the extentand distribution of coronary stenosis, the type andextent of valvular lesions, the location and quantifi-cation of intracardiac shunts, congenital lesions, andan assessment of systolic and diastolic function. Thisinformation contributes to a complete preoperativeevaluation and serves as a predictor of postoperativefunctional status.

Right heart catheterization

A fluid-filled catheter capable of making high-fidelity pressure measurements in the right atrium,right ventricle, pulmonary artery, and pulmonaryartery occlusion position is passed antegrade viaa basilic, cephalic, or femoral vein under fluoro-scopic guidance. In addition, the catheter may havethe capability of making thermodilution cardiacoutput and mixed venous oxygen saturation mea-surements. Angiography is performed by recordingseveral cardiac cycles on cine film while radio-graphic contrast material is injected into the rightheart chambers.For infants and children, the femoral vein is the

usual access site; however, right heart catheteri-zation via the umbilical vein may be possible inthe first few days after birth. Catheterization of theright ventricle and pulmonary arteries may be diffi-cult via the umbilical route because umbilical veincatheters tend to pass directly into the left atrium via

the foramen ovale. Right atrial, right ventricular,and pulmonary angiography may be performedon infants and children to delineate congenitallesions.

Left heart catheterization

A fluid-filled catheter capable of making high-fidelity systolic, diastolic, and mean pressure mea-surements and capable of allowing angiographic dyeinjection is used. The catheter may be passed retro-grade via the brachial or femoral artery to the aorticroot under fluoroscopic guidance where pressuresare recorded. In infants and children the femoralartery is the preferred route. The umbilical arteryis small and its course is tortuous; therefore, is notuseful except for pressuremonitoring and angiogra-phy of the descending aorta. Left heart catheteriza-tion can be performed antegrade via the right atriumin patients inwhom the atrial septum can be crossedvia a patent foramen ovale or an atrial septal defect.This is a common approach in infants and children.In patients in whom the retrograde approach tothe left ventricle is undesirable, and where an atrialor ventricular level communication does not exist,the atrial septum can be intentionally punctured togain access to the left atriumusing a Brockenbroughneedle.Pressures in the aorta, left ventricle, and left

atrium are recorded. Aortography may be per-formed by recording on cine film the injection ofradiographic contrast material into the aortic root.

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