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重症患者左心功能紊乱

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重症患者左心功能紊乱 DOI 10.1378/chest.09-1996 2010;138;198-207Chest Dellsperger Anand Chockalingam, Ankit Mehra, Smrita Dorairajan and Kevin C. Critically Ill Acute Left Ventricular Dysfunction in the http://chestjournal.chestpubs.org/content/138/1/198.full.html services ...
重症患者左心功能紊乱
DOI 10.1378/chest.09-1996 2010;138;198-207Chest Dellsperger Anand Chockalingam, Ankit Mehra, Smrita Dorairajan and Kevin C. Critically Ill Acute Left Ventricular Dysfunction in the http://chestjournal.chestpubs.org/content/138/1/198.full.html services can be found online on the World Wide Web at: The online version of this article, along with updated information and ISSN:0012-3692 )http://chestjournal.chestpubs.org/site/misc/reprints.xhtml( written permission of the copyright holder. this article or PDF may be reproduced or distributed without the prior Dundee Road, Northbrook, IL 60062. All rights reserved. No part of Copyright2010by the American College of Chest Physicians, 3300 Physicians. It has been published monthly since 1935. is the official journal of the American College of ChestChest © 2010 American College of Chest Physicians by guest on September 8, 2011chestjournal.chestpubs.orgDownloaded from Postgraduate Education Corner CONTEMPORARY REVIEWS IN CRITICAL CARE MEDICINE CHEST 198 Postgraduate Education Corner Acute left ventricular (LV) dysfunction occurs in about one-third of critically ill hospitalized patients. 1 - 4 The increasing incidence of LV dysfunc- tion in ICUs is likely related to both changing patient characteristics (advancing age, increased comorbidi- ties) and practice patterns (widespread troponin, cre- atine kinase-MB, and brain natriuretic peptide [BNP] testing, as well as more frequent performance of bedside echocardiography). 3 , 5 - 8 A determination as to whether the LV dysfunction is the cause, effect, or a coincidental fi nding has to be made and revisited periodically. Acute medical or surgical plans, ongoing management targets, outcome expectations, and prognosis must be reconciled. Recognizing that all the individual causes and complexities cannot be cap- tured here, we will summarize the most important causes of LV dysfunction in the critically ill ( Table 1 ) and present a unifi ed management approach from the cardiac standpoint. Diagnosis of LV Dysfunction Angina, dyspnea, pulmonary crackles, murmurs, tachyarrhythmias, biomarker elevations, or ischemic ECG changes suggest cardiac pathology in hospital- ized patients. Because of variability in patient charac- teristics and study design, predictive values of each cardiac test remain unclear. Several studies suggest routine troponin screening in ICUs may be sensitive in detecting early cardiac involvement among the critically ill. 9 , 10 Supporting this, 15% to 30% of critically ill noncardiac patients develop troponin elevations and this corresponds with poorer outcomes. Overall Acute Left Ventricular Dysfunction in the Critically Ill Anand Chockalingam , MD ; Ankit Mehra , MD ; Smrita Dorairajan , MD ; and Kevin C. Dellsperger , MD, PhD Manuscript received August 22 , 2009 ; revision accepted December 7 , 2009 . Affi liations: From the Division of Cardiovascular Medicine, Department of Internal Medicine (Drs Chockalingam, Mehra, Dorairajan, and Dellsperger), University of Missouri School of Medicine; and the Cardiology Section (Dr Chockalingam), Harry S. Truman VA Medical Center, Columbia, MO. Funding�Support: This study was funded by Veterans Adminis- tration Research award [VISN 15] to Dr Chockalingam. Correspondence to: Anand Chockalingam, MD, Division of Cardiology, University of Missouri–Columbia, 5 Hospital Dr, CE306, Columbia, MO 65212; e-mail: chockalingama@health. missouri.edu © 2010 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians ( www . chestpubs . org � site � misc � reprints . xhtml ). DOI: 10.1378/chest.09-1996 Acute left ventricular (LV) dysfunction is common in the critical care setting and more frequently affects the elderly and patients with comorbidities. Because of increased mortality and the poten- tial for signifi cant improvement with early revascularization, the practitioner must fi rst consider acute coronary syndrome. However, variants of stress (takotsubo) cardiomyopathy may be more prevalent in ICU settings than previously recognized. Early diagnosis is important to direct treat- ment of complications of stress cardiomyopathy, such as dynamic LV outfl ow tract obstruction, heart failure, and arrhythmias. Global LV dysfunction occurs in the critically ill because of the cardio-depressant effect of infl ammatory mediators and endotoxins in septic shock as well as direct cate cholamine toxicity. Tachycardia, hypertension, and severe metabolic abnormalities can independently cause global LV dysfunction, which typically improves with addressing the precipi- tating factor. Routine troponin testing may help early detection of cardiac injury and biomarkers could have prognostic value independent of prior cardiac disease. Echocardiography is ideally suited to quantify LV dysfunction and determine its most likely cause. LV dysfunction suggests a worse prognosis, but with appropriate therapy outcomes can be optimized. CHEST 2010; 138( 1 ): 198 – 207 Abbreviations : ACS 5 acute cardiac syndrome ; BNP 5 brain natriuretic peptide ; LV 5 left ventricular ; NT-proBNP 5 N-terminal- pro-B-type natriuretic peptide ; RWMA 5 regional wall motion abnormalities © 2010 American College of Chest Physicians by guest on September 8, 2011chestjournal.chestpubs.orgDownloaded from CHEST / 138 / 1 / JULY, 2010 199www.chestpubs.org mortality in one study was 27% (58 of 217 patients), but patients with troponin elevation had a much higher mortality (51%) compared with those without (16%). 10 Although routine troponin testing may help identify LV dysfunction early, there is currently no evidence that this improves outcomes in critical care patients. Signifi cant elevation in plasma levels of N-terminal- pro-B-type natriuretic peptide concentrations (NT-proBNP) and BNP are typically diagnostic of car- diac pathology as cause for dyspnea and heart fail ure. In critically ill patients with shock, however, BNP tends to be elevated and is thus not reliable for diagnosing heart failure. 11 , 12 Because BNP is higher in sepsis non- survivors (943 pg�mL vs 378 pg�mL in survivors), some believe it may play a prognostic role. 13 Transthoracic echocardiography, being portable, noninvasive, and easily repeatable, is ideal to evaluate LV dysfunction in critical care settings. 3 , 5 In addition, right ventricular function, pulmonary pressures, valve disease, and pericardial pathology, along with hemo- dynamic parameters, such as central volume status and cardiac output, can be quantifi ed and serially monitored. 6 About 8% to 20% of critically ill patients manifest LV dysfunction, although one serial echo- Table 1 —Causes of Acute Left Ventricular Dysfunction in the Critical Care Setting Myocardial infarction Typical acute coronary syndromes Signifi cant myocardial involvement Mechanical complications, such as ventricular septal rupture and papillary muscle rupture Paradoxical venous thromboembolism Coronary emboli—left atrial myxoma, LV or atrial thrombus Coronary thrombosis—antiphospholipid antibody syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura Aortic dissection—with right coronary occlusion Stress cardiomyopathy Apical ballooning 6 LV outfl ow obstruction Basal cardiomyopathy (apex-sparing) Focal cardiomyopathy (noncoronary distribution) Global hypokinesis Tachyarrhythmias Hypertensive emergency Sepsis Metabolic and multiorgan insults Post cardiac arrest and resuscitation Myocardial injury with minor troponin elevations (including supply-demand mismatch) Myopericarditis—viral, autoimmune, giant cell Trauma—chest contusion, prolonged resuscitation, bleeding Congestive heart failure—decompensated, with anemia, shunts Pulmonary embolism—with right ventricle strain Sepsis—hypotension, catecholamine drips Extracardiac stressors—hypertensive crisis, thyrotoxicosis, cocaine, hypothermia, drowning Prolonged surgery—hypotension, blood loss LV 5 left ventricular. cardiographic study suggests a higher incidence, up to 30%. 2 Importantly, presence, extent, and location of regional wall motion abnormalities as well as LV dimensions and shape help determine the most likely cause for LV dysfunction and guide further manage- ment in most instances. Cardiac catheterization provides defi nitive assess- ment of coronary disease. CT scan angiography and cardiac MRI may be valuable in specifi c situations but are limited in ICU settings. 14 Table 2 summarizes key diagnostic advantages and limitations with var- ious cardiac tests in the critical care setting. Acute Coronary Syndromes Diagnosis Plaque rupture resulting in total occlusion of a major coronary artery results in chest pain with ECG evidence of ST elevation. This is associated with a siz- able territory of myocardium in jeopardy. This war- rants emergent coronary angiography and revascular- ization. Chest pain with diaphoresis and dyspnea may be reported but classic symptoms may be masked in many ICU patients because of sedation or altered mental status. 3 , 5 Hemodynamic changes, such as hypo- tension, low cardiac output, reduced mixed venous saturation, and increasing pulmonary wedge pressures may trigger performing a 12-lead ECG in the sedated or unconscious patient. Increasing ventricular ectopy, ST segment changes, or new bundle branch blocks on telemetry may also be the initial evidence for cardiac ischemia. 1 , 15 When clinical and ECG fi ndings are equivocal, bedside echocardiography with careful evaluation for regional wall motion abnormalities (RWMA) conforming to typical coronary distributions may help to confi rm acute coronary syndrome (ACS). 3 , 6 , 9 Mechanical complications of ACS, such as mitral regurgitation or ventricular septal defects, may also be detected with echocardiography. 16 ACS Without Critical Coronary Artery Disease Medical, surgical, or trauma intensive care may result in substantial physiologic and mental stress. This may cause alterations in hemodynamics, coagula- bility, and metabolic parameters. Patients with preex- isting signifi cant atherosclerotic stenosis may not be able to increase blood supply commensurate with the increasing demands resulting in supply-demand mis- match. This usually manifests as ACS with ischemic ECG changes and troponin elevations. Although new LV dysfunction is not typical with supply-demand mismatch, it is included in this review because of the relatively higher incidence of supply-demand mis- match in critical care settings. 17 - 19 This may account © 2010 American College of Chest Physicians by guest on September 8, 2011chestjournal.chestpubs.orgDownloaded from 200 Postgraduate Education Corner for troponin elevations seen in about one-fourth of critically ill noncardiac patients ( Table 1 ). 9 , 10 In instances without angiographic culprit lesions, in situ coronary arterial thrombosis due to hyperco- agulable conditions, such as thrombocytosis, dissem- inated intravascular coagulation, thrombocytopenic purpura, and antiphospholipid antibody syndrome, need to be considered. 20 , 21 Rarely embolic coronary occlusion may be due to left-side heart (atrial or ventric- ular) mural thrombi, endocarditis, prosthetic valve thrombi, or cardiac myxoma. 22 Paradoxical emboli and thrombi from intracardiac catheters or guide- wires have to be considered in patients with a patent foramen ovale. 23 Therapy is mainly supportive and aimed at preventing recurrence by addressing pre- cipitation factors. This might involve surgery for car- diac tumors, percutaneous device closure of patent foramen ovale, or anticoagulation for hypercoagu- lable states. Cardiac status may potentially improve with antiplatelet (aspirin, clopidogrel, glycoprotein IIb�IIIa antagonists) and anticoagulant therapy (hep- arin, warfarin). However there are no studies in crit- ical care settings for these therapies because of wide variability in cause for ACS and comorbidities. With the higher bleeding risk in this population, these agents must be used on a case-by-case basis. Stress Cardiomyopathy Defi nition and Epidemiology Originally described in Japan as takotsubo cardio- myopathy, stress cardiomyopathy by defi nition implies completely reversible acute LV dysfunction. 24 - 28 ICU admission because of medical illness, surgical proce- dure, or traumatic injuries could typically be suffi cient stress to cause stress cardiomyopathy. 29 By perform- ing serial echocardiography in consecutive ICU patients, 28% (26 of 92 patients) had stress cardiomy- opathy in one series reported from South Korea. 2 This is much higher than we typically encounter and a more recent larger series in which echocardiograms were obtained routinely in the fi rst 24 h of ICU admission detected LV systolic dysfunction in 132 of 704 (18%) patients. 3 Pathogenesis of Stress Cardiomyopathy Catecholamine excess in circulation has been iden- tifi ed and possibly mediates the acute cardiac dys- function in stress cardiomyopathy. 30 This condition typically affects women (in . 80% of most series) in the 62- to 75-year-old age range. 31 , 32 Severe emotional stress (approximately 27%) or physical illness (approx- imately 38%), such as sepsis, head trauma, and cere- brovascular accident, may precipitate stress cardio- myopathy in about two-thirds of the instances. 32 In about 60% to 80% of those with this condition the mid and distal segments of the LV are akinetic with a hypercontractile base giving the appearance of “apical ballooning.” Stress cardiomyopathy can also affect the base with apical sparing in another 10%. The remainder manifests nonspecifi c regional wall motion abnormalities or global hypokinesia not conforming to any particular coronary territory. 28 , 33 This global hypokinesia variant of stress cardiomyopathy is unlikely Table 2 —Summary of Various Cardiac Tests Available Highlighting Their Key Characteristics in Critical Care Settings Test Key Diagnosis Advantages Limitations ECG ST elevation MI Widely available Stress cardiomyopathy may mimic MI Non-ST elevation MI Inexpensive Arrhythmias Troponin Any myocardial injury High sensitivity and specifi city ( . 95%) Initially, mild elevations are common in MI and stress cardiomyopathy Quantifi es overall muscle damage BNP Not reliable in determining cardiac cause for pulmonary congestion May predict ICU outcomes Not reliable in obese patients Normal values excludes cardiac disease Echocardiogram LVD, MI, valve, and pericardial disease vs possible stress cardiomyopathy Noninvasive, bedside Limited quality images in intubated ICU patients Valuable hemodynamic information Catheterization CAD diagnosis and revascularization Systolic and diastolic LV function measurement Invasive Higher risk due to ICU comorbidities Contrast renal injury Cardiac CT scan Excludes CAD Noninvasive Contrast renal injury. Challenging to perform in critically ill and unstable patients. Cardiac MR scan MI, cardiomyopathies and valve disease by scarring pattern Noninvasive Challenging to perform in critically ill, unstable, and intubated patients Best test for LV regional wall motion abnormalities and RV function measurement BNP 5 brain natriuretic peptide; CAD 5 coronary artery disease; LVD 5 left ventricular dysfunction; MI 5 myocardial infarction; MR 5 magnetic resonance; RV 5 right ventricular. See Table 1 for expansion of other abbreviation. © 2010 American College of Chest Physicians by guest on September 8, 2011chestjournal.chestpubs.orgDownloaded from CHEST / 138 / 1 / JULY, 2010 201www.chestpubs.org to be a separate pathogenic entity from LV dysfunction seen in sepsis. We discuss this with other condi- tions causing global LV dysfunction in the following section to emphasize the underlying reversible pre- cipitating conditions. Diagnosis of Stress Cardiomyopathy Angina, heart failure, arrhythmias, ECG changes (ST elevations or T inversions), and mild troponin elevations are often triggers for performing cardiac catheterization. Typically a culprit coronary artery lesion is not evident. 24 - 26 Left ventriculography dem- onstrates signifi cant reduction in LV function and symmetric akinesia involving the mid and apical seg- ments with relative hypercontractility of the cardiac base ( Fig 1 ). Published guidelines require angiographic proof of absence of coronary artery disease (CAD). 34 In ICU settings, especially where bleeding risk, severe comorbidity, or terminal illness precludes catheteri- zation and revascularization, the following may be useful indicators that the LV dysfunction is due to stress cardiomyopathy and not true ACS: Severe acute LV dysfunction without a signif-1. icant serum troponin and creatine kinase-MB elevation. Symmetrical mid and apical RWMA by echocar-2. diography—akinesia extending equally in the inferior and lateral walls as the anteroseptum. In ACS of the left anterior descending coronary artery, anteroseptal extent of RWMA from the apex is usually greater than the inferior and lat- eral walls. Conversely, ACS of the right coro- nary or left circumfl ex, if left dominant, usually spares the anteroseptum. Repeat echocardiography in a few days to weeks 3. confi rming complete recovery of LV function with normalization of typical apical RWMA (in the absence of lytics and percutaneous coronary intervention). Atypical forms of stress cardiomyopathy with RWMA involving the base, entire LV, or focal LV areas may be more diffi cult to identify. Table 3 summarizes salient features of the most common subgroups of LV dysfunction in critically ill patients. Being noninva- sive and easy to perform, CT angiography can poten- tially replace cardiac catheterization in excluding sig- nifi cant CAD especially when the suspicion for CAD is low. 14 However, excellent quality coronary imaging requires patient cooperation (breath holding) and the ability to tolerate b -adrenergic blockade to slow the resting heart rate. Treatment Options for Stress Cardiomyopathy In ICU settings, identifying and effectively treat- ing the medical or surgical condition that precipi- tated stress cardiomyopathy is essential. Supportive treatment includes addressing heart failure and arrhythmias as well as optimizing hemodynamics and metabolic parameters. The prognosis may not be benign, with one review estimating shock (6.5%), LV thrombus formation (3.8%), congestive heart failure (3.8%), and death (3.2%) in patients with stress cardiomyopathy. 35 There are no randomized data on stress cardiomyopathy to guide therapy, but prophy- lactic anticoagulation with warfarin appears reason- able until LV function recovers. 34 , 35 Because central sympathetic neurohumoral excess occurs in stress cardiomyopathy, 30 we believe b -adrenergic block- ade may be cardioprotective. Because stress car- diomyopathy is a completely reversible condition, if the patient can be suffi ciently supported through the acute phase, long-term cardiac prognosis is gen- erally good. 34 LV Outfl ow Tract Obstruction in Stress Cardiomyopathy About 25% of patients
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