Perioperative Critical Care Cardiology - part 1 ppsx

Preface to the 2nd editionPerioperative critical care cardiology PCCC includes the cardiovascularmanagement of patients with any underlying diseases or imposed conditionswhether natural

Perioperative Critical Care Cardiology

JOHNL ATLEE ANTONINOGULLO

Department of Anesthesiology Department of Anaesthesia andUniversity of Wisconsin (Madison) Intensive Care

Medical College of Wisconsin (Milwaukee) Policlinic University Hospital

GIANFRANCOSINAGRA JEAN-LOUISVINCENT

Cardiovascular Department Department of Intensive Care Ospedali Riuniti and University Erasme University Hospital

of Trieste, Italy Brussels, Belgium

Library of Congress Control Number: 2006937626

ISBN-10 88-470-0557-4 Springer Milan Berlin Heidelberg New York

ISBN-13 978-88-470-0557-0 Springer Milan Berlin Heidelberg New York

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Preface to the 2nd edition

Perioperative critical care cardiology (PCCC) includes the cardiovascularmanagement of patients with any underlying diseases or imposed conditions(whether natural or iatrogenic) that involve or affect the heart–including,acute or chronic mechanical heart failure (HF) This can result from ischemicheart disease, diabetes mellitus, uncontrolled hypertension, arrhythmias thatcompromise heart function, circulatory shock, or dilated or obstructive car-diomyopathy Patients needing therapy for HF are especially challenging toclinicians involved their perioperative care

While PCCC has traditionally been within the context of anesthesia andsurgery, we now must consider the implications of other therapeutic interven-tions outside of surgery in critically ill patients Thus, we may becomeinvolved in any stage of their care, including specialized diagnostics, nonsur-gical interventions, both during and after such intervention, all of which occuroutside of traditional OR settings Interventions can include percutaneouscoronary angioplasty; aortic, endovascular or intracranial aneurysm repair;specialized imaging (magnetic resonance imaging and the like); radiationoncology; etc Any of these “non-OR” interventions performed in a critically illpatient require the same level of care provided to surgical patients, including:1) preprocedural patient evaluation and risk stratification; 2) periproceduralcare; 3) post-procedural care (post-anesthetic care unit) and 4) any neededcritical care (intensive care unit) for whatever reason Also, as perioperativephysicians, we must be able to anticipate and plan for any needed therapy thatmay improve our patient’s well-being or physical status

Professor Gullo generously provided me with the opportunity to organizethe topics for this 2nd edition of Perioperative Critical Care cardiology I gavethis serious thought at the time of A.P.I.C.E 20, and we agreed there to theTable of Contents I hope this volume adequately addresses the “idealls” setforth above

The first chapter addresses sudden death (SD) in HF, including strategiesfor stratifying risk and therapy An important conclusion is that despiteadvances in therapy for improving the prognosis for these patients, SDremains a leading cause for death As the authors suggest, new, non-pharmaco-logic strategies (discussed in more detail later in this book) may offer some

hope However, most, today, are ill-affordable to most of the world Our besthope for now may be high-risk behavior modification, including more healthydiets and exercise Next, two chapters address 1) the etiology and pathophysi-ology of HF, and 2) cardiac protection for non-cardiac surgery The first ofthese is required reading for anyone who treats patients with or at risk for HF.The second addresses drug-protection against myocardial ischemia, arrhyth-mias and HF in noncardiac surgical patients Prof Gombotz and colleaguesdeal with anesthetic preconditioning as protection in a later chapter (CH 14)

on prevention and management of cardiac dysfunction during and after diac surgery Chapters 4-6 address hypertensive crises, atrial fibrillation anddiabetes mellitus in patients with HF, and bedside monitoring for circulatoryfailure CH 6 is especially interesting in that it discusses the merits and disad-vantages of available, relatively noninvasive strategies for bedside hemody-namic monitoring, a field of technology that is rapidly evolving CH 7 by Prof.Auler et al on perioperative cardiac risk stratification was a “must” for thiswork, and is up to date and current with the available literature CH 8 by Prof.Vincent and Holsten addresses invasive and noninvasive monitoring inpatients with acute HF; including, an analysis of the advantages and disadvan-tages of pulmonary artery catheter (PAC) monitoring A relatively noninvasivealternative is needed Two chapters follow, one on electrocardiography in heartfailure and another on pacemaker and internal cardioverter-defibrillator ther-apies in HF, interposed between which is an extremely relevant chapter on themanagement of patients with acute HF In addition to monitoring and drugsfor management of acute HF, this latter chapter also addresses devices as ther-apy for acute HF Next, Prof Weil and colleagues provide us with a up-to-datereview of recent advances in cardiopulmonary resuscitation, a topic notaddressed in the first edition of this work The management of circulatoryshock is discussed by Prof Vincent and Rapotec in the following chapter Itdescribes four types of circulatory shock (hypovolemic, distributive, cardio-genic and obstructive), which dictates the diagnosis and management of each.Prevention and management of cardiac dysfunction after cardiac surgery fol-lows (Prof Gombotz and colleagues), and this in turn by a chapter on differen-tial monitoring and therapy for systemic or pulmonary arterial hypertension.The last chapter, based on a registry of data in Trieste, Italy, reviews the natur-

car-al history of dilated cardiomyopathy

Again, I express my appreciation to Prof Gullo for recruiting me to nize the topics for this edition of PCCC, and to my co-editors Profs A Gullo,

orga-G Sinagra, and J-L Vincent for their valauable contributions and support inthis collegial, international effort

Milwaukee, November 2006 John L Atlee, MS (Pharmacology)

MD, FACA, FACC, FAMA

Preface to the 1st edition

The peri-operative period represents a crucial phase not only for the patient, butalso for the surgical and anaesthesiological team which must coordinate harmo-niously to ensure the patient’s rapid functional recovery Therefore, an interdisci-plinary approach to peri-operative care is essential, both in terms of clinicalcompetency and of instrumental monitoring Obviously, patient monitoring andall diagnostic and treatment procedures must be modulated in relation to theactual situation Above all, the pre-operative evaluation of the patient’s healthconditions and surgical needs has to follow standardized protocols It is impor-tant to determine the functional state of the patient and, in particular, the func-tional reserves of the cardiovascular system

Determining the surgical indications and carrying out the intervention bothdepend on the rigorous control of the patient’s homeostasis throughout the peri-operative phase Anesthesiological protocols are by now codified and familiar toall experienced operators On this basis, I wished to offer votaries of this field, inparticular anesthesiologists, surgeons, cardiologists, internists and intensive carephysicians, an update on the more relevant problems that arise during peri-oper-ative care The focus of this volume is on surgery patients (including thoseundergoing non-cardiac interventions) whose clinical conditions require specialstrategies for the prevention and eventual treatment of critical conditions.Considering the innumerable pathophysiological and clinical situations thatmay develop in the peri-operative period, continuous education is essential It isparticularly opportune to stress the importance of first-hand experience and theability to interpret the multiplicity of the hemodynamic complications that canoccur in the delicate phase of the peri-operative period

Sure progress has come from the availability of sophisticated means of dynamic monitoring, particularly the noninvasive techniques such as trans-esophageal echocardiography (TEE) and intra-esophageal echo Doppler ultra-sound In addition to methods for monitoring blood pressure, it is now routine toperform bedside monitoring of cardiac volumes, myocardial contractility, andorgan perfusion based on entidal CO2levels These methods are now common-place in modern clinical practice

hemo-In this context, the management of arrhythmias assumes an important role.The correct and timely diagnosis of arrhythmias and the appropriate use of the

different anti-arrhythmic drugs depend on an accurate knowledge of currentmedical practices Therefore, the chapter on temporary pacing for the treatment

of dangerous arrhythmias is extremely important basically for the trainingprocess

The contributions on monitoring for myocardial ischaemia in the tive period and on the principal trials of novel clinical approaches to acutemyocardial infarction are germane to this volume Another interesting contribu-tion focuses on dilated cardiomyopathy and on the different therapeutic optionsfor this disorder In addition, two chapters are dedicated to the care of patientsundergoing surgical intervention for myocardial revascularization Thesepatients require different strategies of intervention to improve ventricular failureand to treat secondary complications due to cardiac dysfunction Finally, this vol-ume could not fail to include a chapter on cardiogenic pulmonary edema that

peri-opera-often characterizes the clinical iter of patients with cardiac insufficiency.

In light of this brief preface, I have valid motives to retain that this volumewill arouse interest in both researchers and experts of this subject It will also beinformative for young physicians who are completing their training

I wish to thank all the authors for their valuable contributions and for helping

to bring this initiative to a fulfillment I particularly thank my friends and leagues J.L Atlee and J.-L Vincent, with whose efforts this volume became possi-ble

col-Trieste, November 2000

Antonino Gullo University Medical School

Trieste, Italy

Table of Contents

1 Sudden Death in Heart Failure: Risk Stratification and Treatment Strategies

M Zecchin, G Vitrella, G Sinagra 1

2 Etiology and Pathophysiology of Heart Failure

5 Heart Failure, Atrial Fibrillation, and Diabetes Mellitus

A Aleksova, A Perkan, G Sinagra 77

6 Circulatory Failure: Bedside Functional Hemodynamic Monitoring

C Sorbara, S Romagnoli, A Rossi, S.M Romano 89

7 Perioperative Cardiac Risk Stratification

F.R.B.G Galas, L.A Hajjar, J.O.C Auler jr. 109

8 Hemodynamic Monitoring in Patients with Acute Heart Failure

J.-L Vincent, R Holsten 135

9 Electrocardiography of Heart Failure: Features and Arrhythmias

J.L Atlee 145

10 Management of Patients with Acute Heart Failure

W.G Toller, G Gemes, H Metzler 159

11 Pacemaker and Internal Cardioverter-Defibrillator Therapies

J.L Atlee 175

12 Updates on Cardiac Arrest and Cardiopulmonary Resuscitation

G Ristagno, A Gullo, W.Tang, M.H Weil 195

13 Circulatory Shock: Hypovolemic, Distributive, Cardiogenic, Obstructive

J.-L.Vincent, A Rapotec 211

14 Prevention and Management of Cardiac Dysfunction during and afterCardiac Surgery

W Moosbauer, A Hofer, H Gombotz 225

15 Management of Systemic and Pulmonary Hypertension

P Giomarelli, S Scolletta, B Biagioli 243

16 Recent Advances in the Natural History of Dilated Cardiomyopathy:

A Review of the Heart Muscle Disease Registry of Trieste

M Moretti, A Di Lenarda, G Sinagra 267

Subject Index 279

A ALEKSOVA, 77

J L ATLEE, 61, 145, 175J.O.C AULER JR., 109

G VITRELLA, 1

M H WEIL, 195

M ZECCHIN, 1

List of Contributors

1 Sudden Death in Heart Failure: Risk Stratification and

Treatment Strategies

M ZECCHIN, G VITRELLA ANDG SINAGRA

Definitions and Epidemiology

Attempting a careful evaluation of the incidence of sudden death (SD) incongestive heart failure is inevitably a complex and imprecise task In partic-ular, this is due to the difficulties in defining and understanding the baselinemechanisms underlying SD “Sudden” death is commonly regarded as a syn-onym of “cardiac arrest due to ventricular fibrillation,” which is in turn con-sidered to be a merely arrhythmic phenomenon occurring during apparentwellbeing, and without any precipitating cause other than an extrasystole or

a sustained ventricular tachycardia Cardiac arrest may also be the terminalevent during refractory pulmonary edema and/or cardiogenic shock in apatient with end-stage heart failure, a pulmonary embolism in a patient withsevere biventricular dysfunction, bradyarrhythmia due to advanced atri-oventricular (AV) block, electrical asystole, ventricular fibrillation secondary

to myocardial ischemia or infarction, or secondary to a noncardiac eventsuch as a cerebrovascular accident or a ruptured aortic aneurysm Pratt et al.[1] analyzed a population of 834 patients with an automatic implantable car-dioverter defibrillator (ICD) implanted for ventricular tachycardia or sus-tained ventricular tachycardia During follow-up 109 patients died (17 died

“suddenly”) Autopsy findings revealed a nonarrhythmic cause (pulmonaryembolism, ruptured aortic aneurysm, stroke, acute myocardial infarction) in7/17 patients Postmortem analysis of the ICD memory revealed ventriculartachyarrhythmias preceding death in only 7/17 patients Both cardiac andnoncardiac events may cause SD, which may be indistinguishable fromarrhythmic death

Cardiovascular Department,“Ospedali Riuniti” and University of Trieste, Trieste, Italy

Before large pharmacologic trials in heart failure were published, the minal mechanisms of death were never thoroughly evaluated Hinkle andThaler [2] provided a first classification: death was to be considered arrhyth-mic when pulselessness preceded cardiocirculatory collapse, and due topump failure when cardiocirculatory collapse preceded pulselessness Thisclassification tends to overestimate the incidence of SD due to the aforemen-tioned causes Furthermore, it was not able to distinguish between the vari-ous mechanisms of SD.

ter-When evaluating studies that have assessed the incidence of SD, it is ofthe first importance to take account of the definition of SD used, and, in par-ticular, the time from symptom onset to SD Classification was not always thesame in all studies In the SOLVD [3] study 23% of deaths were considered

“arrhythmic, without worsening heart failure”; in VHeFT I [4] 43.8% ofdeaths were “sudden, witnessed as instantaneous, or considered instanta-neous on a clinical basis when unwitnessed.” In VHeFT II [5], an incidence of36.5% of SD was found, with a similar definition of SD In STAT-CHF [6]death was considered “sudden” in 49% and 52% of cases, respectively in theamiodarone and placebo groups, but individual cases were evaluated by aclinical events committee, not by the investigators In conclusion, accurateevaluation of the epidemiology of SD must take into account the differentdefinitions among studies, even if very similar populations were being ana-lyzed [7]

Whether novel therapeutic interventions, improved diagnostic niques, and increasing attention given to the problem in recent years havemodified (and if so to what extent) the incidence of SD in addition to theimprovement in the prognosis in patients with heart failure remains to beestablished A study by Stevenson et al [8] showed a reduction in the inci-dence of SD in patients with heart failure from diverse causes, from 20%(1986–1988) to 8% (1991–1993) Although a reduction in global mortalityhas been observed in patients with dilated cardiomyopathy, a reduction in

tech-SD remains to be established [9], even though it was found to be lower thanexpected in more recent trials In the CAT [10] trial, expected mortality inthe control group according to the literature [11] was 12% However, none of

109 study patients suffered SD A 2% annual incidence of SD was observed[12] in patients with dilated cardiomyopathy receiving optimized medicaltreatment In more recent studies evaluating the use ofβ-blockers in patientswith heart failure from different causes [13–15], the incidence of SD variedfrom 1.7% to 6.4% during follow-up (from 10 months to 1.3 years)

Lastly, the reduction in mortality in patients with heart failure mayincrease the number of patients at risk of SD This may in part explain a per-sistently elevated risk of SD in paucisymptomatic patients with a long histo-

ry of disease and persistent severe left ventricular dilatation and tion, in whom SD is the first cause of mortality [12]

Understanding the mechanisms underlying SD is the first step toward itsprevention Different etiologies and degrees of severity of heart failure mayresult in a wide variety of arrhythmias In ischemic heart failure, cardiacarrest is frequently caused by tachyarrhythmias (ventricular tachycardia/fib-rillation), while hypokinetic deaths (AV block, pulmonary embolism, pulse-less electrical activity) cause only 5% of total deaths [16] Conversely, inpatients with advanced stages of dilated cardiomyopathy, nontachyarrhyth-mic SD is more common [17]

Ventricular arrhythmias may have various origins In ischemic patientssustained VT are generally caused by reentry mechanisms, with an anatomicsubstrate of scarred myocardium (post myocardial infarction) and slow elec-trical conduction, which is necessary to initiate and maintain the arrhythmia[18] Ventricular fibrillation may be primary (in around 10% of cases) or sec-ondary to degeneration of sustained ventricular tachycardia [19] In patientswith heart failure from coronary artery disease, SD is in more than 50% ofcases caused by an ischemic episode (myocardial infarction or transientmyocardial ischemia), which very often goes unrecognized [20]

In patients with nonischemic dilated cardiomyopathy, monomorphic tricular tachycardias are quite rare Since the distribution of fibrosis ishomogeneous, a slow conduction pathway may be recognizable in only 14%

ven-of cases [21]

In failing hearts, a suppression of potassium channels and consequentinduction of early afterdepolarizations are observed Early afterdepolariza-tions are thought to be the basis of triggered activity [22, 23], which isknown to be the most frequent mechanism causing ventricular tach-yarrhythmias in nonischemic dilated cardiomyopathy [24]

An additional subgroup of arrhythmias in patients with heart failure,especially in severe left ventricular dilation and dysfunction, are branch-to-branch tachyarrhythmias These arrhythmias represent up to 20% of inducedarrhythmias in nonischemic dilated cardiomyopathy They may be found inpatients with infra-His conduction abnormalities They are characterized by

a macro-reentry, which generally involves the right bundle branch as theorthodromic pathway and the left bundle branch as the antidromic pathway.This causes VT which are morphologically similar to left bundle branchblock It is important to recognize them, as their treatment is relatively sim-ple: ablation of the right bundle branch prevents the arrhythmia from occur-ring and perpetuating [25]

3

Sudden Death in Heart Failure: Risk Stratification and Treatment Strategies