(BQ) Part 2 book “Herzog’s CCU book” has contents: Acute aortic syndrome, pathway for the management of pericardial disease, infective endocarditis, percutaneous therapy for valvular heart disease, contemporary surgical approach to valvular disease, mechanical ventilation in the cardiac care unit,… and other contents.
914 915 Acute Aortic Syndrome INTRODUCTION Acute aortic syndrome (AAS) represents a spectrum of life-threatening conditions with similar clinical presentation and the need for urgent management It includes classic acute aortic dissection (CAAD), intramural hematoma (IMH), and penetrating aortic ulcer (PAU) Although not included in the original definition of AAS, traumatic aortic rupture (TAR) and aortic aneurysm rupture have also been considered to be part of the AAS spectrum AAS is characterized by disruption of the media layer of the aorta and typically presents with acute chest pain The term “acute aortic syndrome” was first coined in 2001 by the Spanish cardiologists Vilacosta and San Román, who described AAS as a spectrum of interlinked lesions1 with the intent to increase awareness and to speed up diagnosis and appropriate treatment (Figure 32.1) 916 FIGURE 32.1 Acute aortic syndrome The acute aortic syndrome triad first described by Vilacosta and San Román Arrows signify possible progression of aortic lesions (penetrating aortic ulcer to IMH, penetrating aortic ulcer to classic dissection, IMH to classic dissection) IMH, intramural hematoma Although the incidence of AAS is lower than that of acute coronary syndrome (ACS), AAS carries a higher mortality, and is therefore a critical component of the differential diagnosis of chest pain in the Cardiac Care Unit (CCU) Overall incidence of AASs is to cases per 100,000 individuals Because AAS is rare, the International Registry of Acute Aortic Dissection (IRAD) was created in 1996 as a way to combine data acquired from multiple top institutions in Europe, North America, and Asia.2 The 2010 intersocietal guidelines for the diagnosis and management of patients with thoracic aortic disease proposed a standard approach to the diagnosis and treatment of AAS.3 Although clinical history and physical examination are important, imaging is essential in the diagnosis of AAS Transesophageal echocardiography (TEE), computed tomography (CT), and magnetic resonance imaging (MRI) are the preferred imaging modalities and angiography is rarely needed CLASSIFICATION OF ACUTE AORTIC SYNDROMES Historically, CAAD was the first recognized form of AAS The 917 classification schemes used for the classic aortic dissection were subsequently extended to include IMH and PAU AASs are classified on the basis of the location and extent of involvement of the aorta Two systems have been proposed, the DeBakey and the Stanford systems (Figure 32.2) The DeBakey system, which was proposed in 1965 by the Lebanese-American surgeon Michael Ellis DeBakey, divided aortic dissection into three types based on the anatomic location Type I originates in the ascending aorta and propagates beyond the aortic arch, type II is limited to the ascending aorta only, and type III is limited to the descending aorta.4 FIGURE 32.2 DeBakey and Stanford classifications Left: DeBakey classification of aortic dissection Type I includes the ascending and descending aorta, type II includes the ascending aorta only, and type III includes the descending thoracic aorta only (DeBakey ME, Henly WS, Cooley DA, et al Surgical management of dissecting aneurysms of the aorta J Thorac Cardiovasc Surg 1965;49:130-149.) Right: Stanford classification Type A aortic dissection involves the ascending thoracic aorta, and type B involves the descending thoracic aorta only All three AAS conditions; CAAD, IMH, and PAU use the Stanford classification CAAD, classic acute aortic dissection; IMH, intramural hematoma; PAU, penetrating aortic ulcer (Daily PO, Trueblood HW, Stinson EB, et al Management of acute aortic dissections Ann Thorac Surg 1970;10[3]:237-247.) The Stanford system, which was created by researchers at Stanford University in 1970, divides aortic dissections into two types Type A includes any dissection that involves the ascending aorta, whereas type B dissections are limited to the descending thoracic aorta.5 The Stanford classification appears to have wider acceptance and is now used for all 918 three AAS types: CAAD, IMH, and PAU INTRAMURAL HEMATOMA IMH is defined by crescentic or circumferential thickening of the media layer of the aortic wall IMH is likely due to a ruptured vasa vasorum resulting in intramural bleeding but without a detectable intimal tear It was first described in 1920 by the German pathologist Ernst Kruckenberg, who is also well known for his description of the so-called Kruckenberg tumors (transperitoneal ovarian metastases from stomach and colon cancers) On TEE, CT, or MRI, IMH is typically visualized as a crescentic or concentric thickening of the aortic wall > mm (Figure 32.3) The natural history of IMH often includes progression to CAAD, which accounts for its high morbidity and mortality 919 FIGURE 32.3 Intramural hematoma: CT CT of the chest shows the descending thoracic aorta The crescentic-shaped lesion on the patient’s left signifies an IMH (dashed arrows) CT, computed tomography; IMH, intramural hematoma Etiology and Pathophysiology IMH may account for up to 6% to 30% of all AAS, with a higher reported prevalence among the Korean and Japanese populations as compared with Western subjects.6 It is unclear whether this is a true discrepancy in prevalence versus a reflection of differing classification, evaluation, or treatment practices Often, IMH is diagnosed as such even though very small intimal tears indicative of limited aortic dissection may be present but missed by modern imaging modalities This may overestimate the true 920 prevalence of IMH as opposed to CAAD The characteristic feature of IMH is its location in the portion of the media closer to the adventitia, as opposed to CAAD which is typically located in the media closer to the intima Although the most cited hypothesis of the pathophysiologic mechanism of IMH is rupture of the vasa vasorum, there is very little corroborating clinical or experimental evidence Owing to the low incidence of IMH and the close association with CAAD, a definitive etiology still remains unclear.7 Clinical Manifestations According to the IRAD experience, IMH typically presents with the symptoms of severe chest and back pain, similar to CAAD However, IMH is less likely to present with manifestations of severe aortic regurgitation and pulse deficits.6 IMH is rarely stable It may either progress to CAAD or regress spontaneously, and therefore serial imaging is crucial Stanford type B lesions in the descending aorta are more common than type A lesions in the ascending aorta (60% vs 35% of all IMH, respectively) Cardiogenic shock may be present in 14% of patients, more typically with type A IMH.8 Pericardial effusion and tamponade may also be present, which are also more common in type A IMH When compared with CAAD, type A IMH has a significantly higher risk of rupture (26% vs 8%, respectively).9 A widened mediastinum may be present on chest X-ray; however, this is neither sensitive nor specific to IMH Diagnosis As with all types of AAS, rapid diagnosis is paramount in IMH TEE, CT, and MRI are the preferred diagnostic tools CT is often chosen because of widespread availability, rapid acquisition, and its ability to diagnose other causes of acute chest pain such as trauma and pulmonary embolism Classically, absence of an intimal flap or tear differentiates IMH from CAAD Often, IMH can be identified even on non–contrast-enhanced CT On contrast CT scans, a crescentic or circular area of high attenuation that does not enhance with contrast is present Similar findings are seen on MRI, which has the advantage of not requiring iodinated contrast On TEE, IMH is diagnosed if there is regional thickening of the aortic wall > mm in a crescentic or circumferential pattern without an intimal flap or tear (Figure 32.4A, B) Limitations of TEE in diagnosing IMH 921 arise from the TEE’s inability to visualize all portions of the aorta including the area around the origin of the brachiocephalic artery and all but the most proximal portions of the abdominal aorta TEE is very useful in diagnosing complications of IMH, such as pericardial effusion or aortic regurgitation FIGURE 32.4 Intramural hematoma: TEE Two-dimensional (2D) TEE of the ascending thoracic aorta in the long-axis (A) and short-axis (B) views Yellow arrows point to a crescentic thickening of the anterior portion of the ascending thoracic aortic wall, consistent with a type A IMH IMH, intramural hematoma; TEE, transesophageal echocardiography Small intimal tears may be missed by any modern imaging technique, challenging the diagnosis of classic IMH Management and Prognosis The prognosis of IMH is somewhat better than that of CAAD As in all AAS, the main determinant of prognosis is its aortic location According to the IRAD registry, the mortality of type A IMH is approximately 27%, compared with 4% in type B IMH Invasively managed patients with type A IMH typically fare better than medically managed patients Invasive options include open surgical repair and percutaneous thoracic endovascular aortic repair Medical management typically consists of heart rate (HR), blood pressure, and pain control Surgical mortality for IMH is similar to that for other forms of AAS Type B IMH is often managed medically Approximately 50% of type B patients may improve with medical management alone, 15% will remain 922 stable, and 35% may progress to aneurysm formation, CAAD, or focal aortic rupture (pseudoaneurysm).10 Intramural Hematoma in Pregnancy Although there are no specific guidelines in pregnancy for patients with IMH, pregnancy is considered a risk factor for the development of aortic pathology, especially in Marfan syndrome As with other forms of AAS, expedited delivery via caesarian section is considered reasonable for pregnant patients with acute IMH, if possible CLASSIC ACUTE AORTIC DISSECTION CAAD is the most common form of AAS.2 It occurs in approximately 66% to 75% of all AAS The overall incidence of CAAD is low, estimated at 0.5 to 4.0 cases per 100,000 per year, and is thought to affect men more than women in a 2:1 ratio Risk factors for CAAD include connective tissue disorders such as Marfan (fibrillin gene), Loeys–Dietz (transforming growth factor β receptor and genes), Ehlers–Danlos type (collagen gene), and Turner syndrome (X monosomy), as well as the aortopathy associated with bicuspid aortic valve (NOTCH1 gene) In addition, hypertension is a significant risk factor and is more prevalent among older patients Last, aortic instrumentation or surgery, as well as cardiac catheterization, are rare but reported causes of aortic dissection CAAD was first described in 1555 by Andreas Vesalius (1514–1564) who reported traumatic abdominal aortic aneurysm in a man who fell off a horse.11 Intimal tear, the hallmark of CAAD, was first described by Daniel Sennert (1572–1637), a German anatomist and published in 1650 posthumously.12 A very famous description of CAAD was by the British royal physician Frank Nichols (1699–1778) who provided the first unmistakable account of CAAD (deemed a “Transverse fissure of the aortic trunk”) in his autopsy of King George II, who died in 1760 while straining in the lavatory Successful surgical repair of descending aortic dissection was not reported until 1955, by Michael Debakey (1908–2008) and his colleagues, and ascending dissection until 1962 by Frank Spencer and Hu Blake.13,14 Etiology and Pathophysiology 923 TR See Tricuspid regurgitation Trabecular ventricular septal defect, 453 Trans fat, 708 Transcatheter aortic valve replacement (TAVR) aortic regurgitation, 387, 393 aortic stenosis, 387, 390–391, 391f, 450 caval-aortic, 424 conduction system disease, 424 coronary ostia occlusion, 424 echocardiography and fluoroscopy, 423f Edwards S3 and Sapien XT valves, 423, 424 intraprocedural complications, 424 leaflet thrombosis, 424 life expectancy, 422 myocardial infarction, 424 paravalvular leak, 424 patient selection, 422 risk assessment, 422 stroke, 424 survival, 421, 424 transfemoral, 424 valve-in-valve TAVR, 423 Transcatheter mitral valve replacement (TMVR), 427–428 Transcatheter pulmonary valve replacement, 428 Transcatheter tricuspid valve intervention, 428 Transcutaneous pacing, 74, 234, 234f Transeptal puncture, 184 Transesophageal echocardiography (TEE) acute coronary syndrome, 40 aortic stenosis, 387, 387f atrial fibrillation, 254 cardiopulmonary bypass, 71 hypertrophic cardiomyopathy, 156 infective endocarditis, 414, 415f mitral regurgitation bileaflet mitral valve endocarditis, 402f eccentric paravalvular, 404f myxomatous mitral valve, 403f prosthetic valve endocarditis, 404f mitral valve stenosis, 397, 398f, 400 pericardial effusion and tamponade, 374 sedatives and analgesic medications, 495 tricuspid regurgitation, 409f Transthoracic echocardiography (TTE) 1940 acute decompensated HCM, 156 atrial septal defect, 452 classic acute aortic dissection, 366 coarctation, 455 hypertrophic cardiomyopathy, 151, 151f infective endocarditis, 414, 415f mitral regurgitation bileaflet mitral valve endocarditis, 402f papillary muscle rupture, 403f mitral valve stenosis, 399, 400 myocardial rupture, 125, 125f pericardial effusion and tamponade, 373 ventricular septal defect, 453 Transvenous pacing wires, 74 Traumatic aortic rupture (TAR) in acute aortic syndrome, 372 clinical manifestations, 368 diagnosis, 368–369, 369f etiology and pathophysiology, 368 management and prognosis, 369 pregnancy, 369 Traumatic tricuspid valve rupture, 444 Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-TIMI (TRITON-TIMI), 14, 28 Tricuspid annular (TA) dilatation, 407 Tricuspid regurgitation (TR) clinical findings, 444 clinical presentation, 407 diagnosis, 407–408 etiology and pathophysiology, 407, 407t, 408f, 409f medical therapy, 408 morphology, 444 pregnancy, 412 surgical therapy, 408–409, 412 transcatheter tricuspid valve intervention, 428 tricuspid valve surgery, 444 Tricuspid ring annuloplasty, 441 Tricuspid stenosis (TS), 409, 410f Tricuspid valve (TV) endocarditis, 407 Triglycerides, 680 Trileaflet aortic valve (TAV), 387 Triple lumen catheter, 543f, 543t, 544, 573 Triple rule out protocol, 48 Troponins 1941 myocardial damage, 41 STEMI, True left ventricular aneurysm See Left ventricular aneurysm (LVA) Trypanosoma cruzi, 200 TTE See Transthoracic echocardiography TTM See Targeted temperature management Tubular necrosis, acute, 510 Tubular obstruction, 506 Turbulent flow, 433 U Ultrafiltration, 104 Ultrasound, 620–621, 621f See also Point-of-care ultrasound; Abdominal ultrasonography arterial line placement, 569–570 central venous catheters, 550–552 kidney failure, 513 Unfractionated heparin (UFH) availability, 483t acute coronary syndrome, 90 modern anticoagulation therapy, 346 non–ST-elevation myocardial infarction, 28 percutaneous coronary intervention, 62 United Kingdom National Cardiac Arrest Audit database, 320 United States Food and Drug Administration (US FDA), 345 UNload the Left ventricle in patients with ADvanced heart failure (UNLOAD) trial, 206 Unstable angina (UA), 82 Upper limit of normal (ULN), 675 U.S Clinical Practice Guidelines for Treating Tobacco Use and Dependence, 685 U.S Department of Health and Human Services, 688 US Food and Drug Administration, 322 Uvulopalatopharyngoplasty (UPPP), 220, 224 V VA See Ventricular arrhythmia VAD See Ventricular assist device VA-ECMO See Venoarterial extracorporeal membrane oxygenation Vagal atrioventricular block, 230, 230f Vagal maneuvers atrial tachycardia, 247 AVNRT, 243 VALIANT trial, 85 Valsartan 1942 dosage, 209t elimination, 209t Valve sparing procedures, 437 Valvular disease, acute coronary syndromes, myocarditis and peripartum/postpartum cardiomyopathy (VAMP), 102 Valvular heart disease evaluation, 431 heart surgery, 431 HFrEF, 110 pathophysiology, 431 percutaneous intervention, 431–432 signs and symptoms, 431 Vancomycin, 71 Varenicline, 688–689 Vascular function, 718 Vascular site hemostasis, 58–59 Vascular ultrasound, 620–621, 621f Vasoconstrictors, 194 Vasodilator Heart Failure Trial (V-HeFT), 210 Vasodilators intestinal ischemia, 533 nesiritide, 207 nitroglycerin, 207 nitroprusside, 207 Vasoplegia, 194 Vasopressin, 323 Vasopressors acute heart failure, 104 pulmonary embolism, 484 Vasovagal syncope, 292 Venoarterial extracorporeal membrane oxygenation (VA-ECMO), 143, 144, 186 Venous thromboembolism (VTE) deep vein thrombosis See Deep vein thrombosis incidence, 477 new oral anticoagulants, 91 pathogenesis, 477 pulmonary embolism See Pulmonary embolism Veno-venous extracorporeal membrane oxygenation (VV-ECMO), 186 Ventilator-associated pneumonia (VAP), 473 Ventricular arrhythmia (VA) abnormal automaticity, 273 after STEMI, 18 antiarrhythmic medications, 283 basic definitions, 273, 274t, 283 1943 cardiac magnetic resonance hypertrophic cardiomyopathy, 171–173 ischemic cardiomyopathy, 170–171 nonischemic cardiomyopathy, 171 causes, 283 durable left ventricular assist device, 188–189 heart transplantation, 195 and myocardial scarring, 133 nonsustained ventricular tachycardia, 273 obstructive sleep apnea, 216 premature ventricular complexes, 273, 274f reentry, 273 symptoms, 283 triggered activity, 273 types, 283 ventricular fibrillation, 278 ventricular tachycardia See Ventricular tachycardia Ventricular assist device (VAD) cardiogenic shock, 144 heart failure, 460 HFrEF, 113 Ventricular fibrillation (VF), 278, 284 Ventricular intrinsic preference (VIP), 302 Ventricular pace suppression (VPS), 302 Ventricular septal defect (VSD), 167, 453, 453f Ventricular septal rupture (VSR) clinical presentation, 126 incidence, 126 pathophysiology, 126, 126f treatment, 126–127, 127f, 128f Ventricular tachycardia (VT) adult congenital heart disease, 458–459 arrhythmogenic right ventricular cardiomyopathy, 280 atrioventricular dissociation, 275, 276f Brugada syndrome, 280 cardiac sarcoidosis, 281 catecholaminergic polymorphic, 280 catheter ablation, 284 commotio cordis, 281 dilated cardiomyopathy, 279–280 drug-induced, 281 fascicular, 279 focal, 279 hypertrophic cardiomyopathy, 280 1944 ischemic heart disease, 279 long QT syndrome, 280 mitral valve prolapse, 281 pacing and electric shock, 284 pulseless sustained, 275 supraventricular tachycardia vs., 275, 275t sustained monomorphic, 276, 277f, 277t sustained polymorphic, 276, 278, 278f tetralogy of Fallot, 281 types and etiologies, 275, 275t Ventriculophasic sinus arrhythmia, 227 Verapamil acute decompensated HCM, 156 antiarrhythmic drug therapy, 340 nonobstructive HCM, 154 obstructive HCM, 154 Vernakalant, 339–340 Virchow triad, 477 Visual Analog Scale (VAS), 488 Vital exhaustion, 734 Vitamin K antagonists (VKAs), 351, 354t, 355–356 deep vein thrombosis, 483 intracranial hemorrhage, 525, 526t VO2 max, 724 Volutrauma, 469 VSR See Ventricular septal rupture VT See Ventricular tachycardia VTE See Venous thromboembolism VV-ECMO See Veno-venous extracorporeal membrane oxygenation W Wall Motion Score Index (WMSI), 32 Warfarin acute coronary syndrome, 91, 97 availability, 483t intracranial hemorrhage, 525, 526t modern anticoagulation therapy, 345, 354t, 355–356 Watchman LAA closure, 256, 257f Weaning, mechanical ventilator, 473 Weight loss and weight management, 715 Wells score, 480–481, 480t Wet signs, 100 White blood cell (WBC), 683 Wilkins Score/Mitral Valvuloplasty Score, 400t 1945 Windsock shape, LAA morphology, 256f Winged peripheral IV catheter system, 541f Wisconsin Sleep Cohort, 216 WiSE-CRT system, 303, 304f Women’s heart disease See Coronary microvascular dysfunction Women’s Ischemia Syndrome Evaluation, 694 1946 目录 Halftitle Page Title Page Copyright Page Dedication Contributors Preface Acknowledgments Contents Section I: ACUTE CORONARY SYNDROME Pathway for the Management of Acute Coronary Syndrome: Eyal Herzog, Jacqueline E Tamis-Holland, Emad F Aziz ST-Segment Elevation Myocardial Infarction: Chirag Bavishi, Eyal Herzog, Jacqueline E Tamis-Holland PATIENT AND FAMILY INFORMATION FOR: STELEVATION MYOCARDIAL INFARCTION Non–ST-Elevation Acute Coronary Syndromes: Ronen Jaffe, Eyal Herzog, Moshe Flugelman PATIENT AND FAMILY INFORMATION FOR: NON– ST-ELEVATION ACUTE CORONARY SYNDROMES Echocardiography in Acute Coronary Syndrome: Eyal Herzog, Indra Warren PATIENT AND FAMILY INFORMATION FOR: ECHOCARDIOGRAPHY IN ACUTE CORONARY SYNDROME Use of Radionuclide Imaging in Acute Coronary Syndrome: Edgar Argulian, Ernest G DePuey, Seth Uretsky PATIENT AND FAMILY INFORMATION FOR: USE OF RADIONUCLIDE IMAGING IN ACUTE CORONARY SYNDROME Computed Tomographic Angiography in Acute Cardiac Care: Ronen Rubinshtein, Harvey Hecht PATIENT AND FAMILY INFORMATION FOR: 1947 28 30 31 40 42 57 91 96 113 117 131 137 151 153 COMPUTED TOMOGRAPHIC ANGIOGRAPHY IN ACUTE CARDIAC CARE Coronary Angiography and Percutaneous Coronary Intervention: Arpit Shah, Angela Palazzo PATIENT AND FAMILY INFORMATION FOR: CORONARY ANGIOGRAPHY AND PERCUTANEOUS CORONARY INTERVENTION Coronary Artery Bypass Surgery: Jonathan Price, Sandhya K Balaram PATIENT AND FAMILY INFORMATION FOR: CORONARY ARTERY BYPASS SURGERY Medications Used in the Management of Acute Coronary Syndrome: Basheer Karkabi, Eyal Herzog, Jacob Goldstein PATIENT AND FAMILY INFORMATION FOR: MEDICATIONS USED IN THE MANAGEMENT OF ACS Section II: HEART FAILURE 10 Pathway for the Management of Acute Heart Failure: Edgar Argulian, Marrick L Kukin, Emad F Aziz, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: THE MANAGEMENT OF ACUTE HEART FAILURE 11 Heart Failure with Reduced Ejection Fraction: Yaron Hellman PATIENT AND FAMILY INFORMATION FOR: HEART FAILURE WITH REDUCED EJECTION FRACTION 12 Heart Failure with Preserved Ejection Fraction: Manpreet Sabharwal, Eyal Herzog, Edgar Argulian PATIENT AND FAMILY INFORMATION FOR: HEART FAILURE WITH PRESERVED EJECTION FRACTION 13 Mechanical Complications of Myocardial Infarction: Eyal Herzog, Indra Warren PATIENT AND FAMILY INFORMATION FOR: MECHANICAL COMPLICATIONS OF MYOCARDIAL INFARCTION 14 Cardiogenic Shock Complicating Acute Myocardial Infarction: Andrew Higgins, May Bakir, Venu Menon PATIENT AND FAMILY INFORMATION FOR: CARDIOGENIC SHOCK COMPLICATING ACUTE 1948 162 163 199 205 230 233 268 279 281 297 301 316 323 334 337 376 381 396 MYOCARDIAL INFARCTION 15 Hypertrophic Cardiomyopathy: Richard Ro, Patricia Chavez, Bette Kim PATIENT AND FAMILY INFORMATION FOR: HYPERTROPHIC CARDIOMYOPATHY 16 Cardiac Magnetic Resonance Imaging in the Cardiac Care Unit: Nina Kukar, Gina LaRocca, Ziad Sergie, Javier Sanz PATIENT AND FAMILY INFORMATION FOR: CARDIAC MAGNETIC RESONANCE IMAGING 17 Mechanical Circulatory Support in the Cardiac Care Unit : Noah Moss, Sean P Pinney PATIENT AND FAMILY INFORMATION FOR: MECHANICAL CIRCULATORY SUPPORT 18 Selection and Care of the Heart Transplant Patient: Eric Adler, Johanna Contreras, Sean P Pinney PATIENT AND FAMILY INFORMATION FOR: SELECTION AND CARE OF THE HEART TRANSPLANT PATIENT 19 Medications Used in the Management of Heart Failure: Yaron Hellman, Ashish Correa, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: MEDICATIONS USED IN THE MANAGEMENT OF HEART FAILURE 20 Pathway for the Management of Sleep Apnea in the Cardiac Patient: Allison Selby, Eyal Herzog, Edgar Argulian, Emad F Aziz PATIENT AND FAMILY INFORMATION FOR: THE MANAGEMENT OF SLEEP APNEA IN THE CARDIAC PATIENT Section III: ARRHYTHMIA IN THE CCU 21 Bradycardia and Heart Block: Asaf Danon, Seyed Hamed Hosseini Dehkordi, Eyal Herzog, Arie Militianu, Jorge E Schliamser PATIENT AND FAMILY INFORMATION FOR: BRADYCARDIA AND HEART BLOCK 22 Supraventricular Arrhythmias: Todd Kobrinski, Emad F Aziz PATIENT AND FAMILY INFORMATION FOR: 1949 400 426 431 489 492 519 522 551 554 578 585 606 608 610 637 640 SUPRAVENTRICULAR ARRHYTHMIAS 23 Fundamentals of Atrial Fibrillation and Atrial Flutter: Olga Reynbakh, Joshua Aziz, Eyal Herzog, Emad F Aziz PATIENT AND FAMILY INFORMATION FOR: ATRIAL FIBRILLATION AND ATRIAL FLUTTER 24 Pathway for the Management of Atrial Fibrillation and Atrial Flutter: Eyal Herzog, Edgar Argulian, Steven Levy, Emad F Aziz 25 Ventricular Arrhythmia: Ankit Chothani, Shawn Lee, Ashish Correa, Davendra Mehta PATIENT AND FAMILY INFORMATION FOR: VENTRICULAR ARRHYTHMIAS 26 The Approach to the Patient with Syncope: Emad F Aziz, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: THE APPROACH TO THE PATIENT WITH SYNCOPE 27 Basic Approach to Pacemaker and ICD Interrogation: Emad F Aziz, Nektarios Souvaliotis 28 Strategies for the Prevention of Sudden Cardiac Death: Emad F Aziz, Eyal Herzog 29 Cardiopulmonary Resuscitation and Cardiocerebral Resuscitation Using Therapeutic Hypothermia: Eyal Herzog, Lee Herzog, Emad F Aziz 30 Principles of Antiarrhythmic Drug Therapy: Emad F Aziz, Joshua Aziz, May Bakir PATIENT AND FAMILY INFORMATION FOR: PRINCIPLES OF ANTIARRHYTHMIC DRUG THERAPY 31 Modern Anticoagulation Therapy: Steven B Levy, Kimberly M Sarosky, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: MODERN ANTICOAGULATION THERAPY Section IV: AORTIC, PERICARDIAL, AND VALVULAR DISEASE IN THE CCU 32 Acute Aortic Syndrome: Alan F Vainrib, Muhamed Saric PATIENT AND FAMILY INFORMATION FOR: ACUTE AORTIC SYNDROME 1950 669 699 701 715 737 741 757 762 794 816 850 877 881 910 914 916 938 AORTIC SYNDROME 938 33 Pericardial Effusion and Tamponade: Edgar Argulian, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: PERICARDIAL EFFUSION AND TAMPONADE 34 Pathway for the Management of Pericardial Disease: Eyal Herzog, Dan G Halpern, Emad F Aziz, Edgar Argulian 35 Aortic Valvular Disease in the Cardiac Care Unit: Gustavo S Guandalini, Alan F Vainrib, Muhamed Saric PATIENT AND FAMILY INFORMATION FOR: AORTIC VALVULAR DISEASE IN THE CARDIAC CARE UNIT 36 Mitral Valve Disease in the Cardiac Care Unit: Ahmadreza Moradi, Karan Sud, Jacqueline Danik PATIENT AND FAMILY INFORMATION FOR: MITRAL VALVE DISEASE IN THE CARDIAC CARE UNIT 37 Tricuspid and Pulmonic Valvular Disease in the Cardiac Care Unit: Avinoam Shiran PATIENT AND FAMILY INFORMATION FOR: TRICUSPID AND PULMONIC VALVULAR DISEASE IN THE CARDIAC CARE UNIT 38 Infective Endocarditis: Ankit Chothani, Eyal Herzog, Edgar Argulian PATIENT AND FAMILY INFORMATION FOR: INFECTIVE ENDOCARDITIS 39 Percutaneous Therapy for Valvular Heart Disease: Chetan Huded, Samir Kapadia PATIENT AND FAMILY INFORMATION: PERCUTANEOUS THERAPY FOR VALVULAR HEART DISEASE 40 Contemporary Surgical Approach to Valvular Disease : Joanna Chikwe, Henry Tannous PATIENT AND FAMILY INFORMATION FOR: CONTEMPORARY SURGICAL APPROACH TO VALVULAR DISEASE 41 The Care of the Adult Patient With Congenital Heart Disease 1951 942 959 961 981 1003 1006 1027 1030 1042 1044 1062 1065 1089 1093 1138 Chakravarti, Dan G Halpern Section V: INTENSIVE CRITICAL CARE 42 Mechanical Ventilation in the Cardiac Care Unit: Janet M Shapiro, Vishal P Patel PATIENT AND FAMILY INFORMATION FOR: MECHANICAL VENTILATION 43 Pulmonary Embolism and Deep Vein Thrombosis: Matthew Durst, Hooman Poor PATIENT AND FAMILY INFORMATION FOR: PULMONARY EMBOLISM AND DEEP VEIN THROMBOSIS 44 Sedation and Analgesia in the Cardiac Care Unit: Louis Brusco, Diana Anca PATIENT AND FAMILY INFORMATION FOR: SEDATION AND ANALGESIA IN THE CARDIAC CARE UNIT 45 Renal Failure in the Cardiac Care Unit: Karim El Hachem, James Jones, Ira Meisels PATIENT AND FAMILY INFORMATION FOR: RENAL FAILURE IN THE CARDIAC CARE UNIT 46 Acute Neurologic Emergencies in the Cardiac Care Unit: Elissa K Fory, Stephan A Mayer PATIENT AND FAMILY INFORMATION FOR: STROKES 47 Gastrointestinal Emergencies in the Cardiac Care Unit: Pavan K Mankal, Carly E Glick, Donald P Kotler PATIENT AND FAMILY INFORMATION FOR: GASTROINTESTINAL EMERGENCIES IN THE CARDIAC CARE UNIT 48 Line Access in the CCU: Ismini Kourouni, Gopal Narayanswami, Joseph P Mathew PATIENT AND FAMILY INFORMATION FOR: LINE ACCESS IN THE CCU 49 Invasive Hemodynamic Assessment in the CCU: Gopal Narayanswami, Gabriela Bambrick-Santoyo, Joseph P Mathew PATIENT AND FAMILY INFORMATION FOR: INVASIVE HEMODYNAMIC ASSESSMENT IN THE 1952 1173 1175 1201 1206 1229 1231 1260 1273 1293 1299 1334 1338 1364 1367 1450 1456 1491 INVASIVE HEMODYNAMIC ASSESSMENT IN THE CCU 50 Noninvasive Hemodynamic Assessment in the CCU: Yuvrajsinh J Parmar, Itzhak Kronzon 51 Noncardiac Point-of-Care Ultrasound in the CCU: Ismini Kourouni, Gopal Narayanswami, Joseph P Mathew 52 End-of-Life Care in the CCU: Janet M Shapiro PATIENT AND FAMILY INFORMATION FOR: ENDOF-LIFE CARE IN THE CCU Section VI: RISK FACTORS: FROM THE ACUTE SETTING TO CHRONIC MANAGEMENT 53 Hypertension in the Cardiac Care Unit: Ashish Correa, Petra Zubin Maslov, Emad F Aziz, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: HYPERTENSION IN THE CARDIAC CARE UNIT 54 Diabetes Mellitus in the Cardiac Care Unit: Rodolfo J Galindo, Mario Rodriguez Rivera, Seyed Hamed Hosseini Dehkordi, Eyal Herzog, Jeanine Albu PATIENT AND FAMILY INFORMATION FOR: DIABETES MELLITUS IN THE CARDIAC CARE UNIT 55 Lipid Management in the Cardiac Care Unit: Barak Zafrir PATIENT AND FAMILY INFORMATION FOR: LIPID MANAGEMENT IN THE CARDIAC CARE UNIT 56 Smoking Cessation in the Cardiac Patient: Mary O’Sullivan, Diandra Fortune PATIENT AND FAMILY INFORMATION FOR: SMOKING CESSATION FOR THE CARDIAC PATIENT 57 Women’s Heart Disease in the Cardiac Care Setting: May Bakir, Eyal Herzog PATIENT AND FAMILY INFORMATION FOR: WOMEN’S HEART DISEASE IN THE CARDIAC CARE SETTING 58 Lifestyle Management after the Diagnosis of Heart Disease: Alan Rozanski, Randy Cohen 59 Nutrition and Weight Management in Cardiac Patients: Randy Cohen, Alan Rozanski 1953 1491 1495 1521 1573 1589 1594 1596 1624 1635 1679 1687 1707 1714 1740 1745 1755 1757 1772 Cohen, Alan Rozanski 61 Applying Psychological Principles for the Lifestyle Management of Cardiac Patients: Alan Rozanski, Randy Cohen Index 1823 1851 1954 ... aorta Ann Surg 1955;1 42: 586-610; discussion 611-6 12 14 Spencer FC, Blake H A report of the successful surgical treatment of aortic 935 15 16 17 18 19 20 21 22 23 24 25 26 27 regurgitation from... an autopsy study Am J Forensic Med Pathol 20 06 ;27 :29 2 -29 5 29 Smith RS, Chang FC Traumatic rupture of the aorta: still a lethal injury Am J Surg 1986;1 52: 660-663 937 Patient and Family Information... Surg 20 14 ;26 : 123 -131 Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K Clinical features and long-term outcome of type A and type B intramural hematoma of the aorta J Thorac Cardiovasc Surg 20 04; 127 : 421 - 427