Right Heart Catheterization—Background, Physiological Basics, and Clinical Implications
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Surgical Advances in Heart and Lung Transplantation
Anesthesiology Clin N Am 22 (2004) 789–807 Surgical advances in heart and lung transplantation Eric E. Roselli, MD*, Nicholas G. Smedira, MD Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, Desk F25, 9500 Euclid Avenue, Cleveland, OH 44195, USA The first heart transplants were performed in dogs by Alexis Carrel and Charles Guthrie in 1905, but it was not until the 1950s that attempts at human orthotopic heart transplant were reported. Several obstacles, including a clear definition of brain death, adequate organ preservation, control of rejection, and an easily reproducible method of implantation, slowed progress. Eventually, the first successful human to human orthotopic heart transplant was performed by Christian Barnard in South Africa in 1967 [1]. Poor healing of bronchial anastomoses hindered early progress in lung transplantation, first reported in 1963 [2]. The first successful transplant of heart and both lungs was accomplished at Stanford University School of Medicine (Stanford, CA) in 1981 [3]. The introduction of cyclosporine to immunosuppres- sion protocols, with lower doses of steroids, led to the first successful isolated lung transplant, performed at Toronto General Hospital in 1983 [4]. Since these early successes at thoracic transplantation, great progress has been made in the care of patients with end-stage heart and lung disease. Although only minor changes have occurred in surgical technique for heart and lung transplantation, the greatest changes have been in liberalizing donor criteria to expand the donor pool. This article focuses on more recent surgical advances in donor selection and management, procurement and implantation, and the impact these advances have had on patient outcome. -
Differential Diagnosis of Pulmonic Stenosis by Means of Intracardiac Phonocardiography
Differential Diagnosis of Pulmonic Stenosis by Means of Intracardiac Phonocardiography Tadashi KAMBE, M.D., Tadayuki KATO, M.D., Norio HIBI, M.D., Yoichi FUKUI, M.D., Takemi ARAKAWA, M.D., Kinya NISHIMURA,M.D., Hiroshi TATEMATSU,M.D., Arata MIWA, M.D., Hisao TADA, M.D., and Nobuo SAKAMOTO,M.D. SUMMARY The purpose of the present paper is to describe the origin of the systolic murmur in pulmonic stenosis and to discuss the diagnostic pos- sibilities of intracardiac phonocardiography. Right heart catheterization was carried out with the aid of a double- lumen A.E.L. phonocatheter on 48 pulmonic stenosis patients with or without associated heart lesions. The diagnosis was confirmed by heart catheterization and angiocardiography in all cases and in 38 of them, by surgical intervention. Simultaneous phonocardiograms were recorded with intracardiac pressure tracings. In valvular pulmonic stenosis, the maximum ejection systolic murmur was localized in the pulmonary artery above the pulmonic valve and well transmitted to both right and left pulmonary arteries, the superior vena cava, and right and left atria. The maximal intensity of the ejection systolic murmur in infundibular stenosis was found in the outflow tract of right ventricle. The contractility of the infundibulum greatly contributes to the formation of the ejection systolic murmur in the outflow tract of right ventricle. In tetralogy of Fallot, the major systolic murmur is caused by the pulmonic stenosis, whereas the high ventricular septal defect is not responsible for it. In pulmonary branch stenosis, the sys- tolic murmur was recorded distally to the site of stenosis. Intracardiac phonocardiography has proved useful for the dif- ferential diagnosis of various types of pulmonic stenosis. -
Signal Processing Techniques for Phonocardiogram De-Noising and Analysis
-3C).1 CBME CeaEe for Bionedio¡l Bnginocdng Adelaide Univenity Signal Processing Techniques for Phonocardiogram De-noising and Analysis by Sheila R. Messer 8.S., Urriversity of the Pacific, Stockton, California, IJSA Thesis submitted for the degree of Master of Engineering Science ADELAIDE U N IVERSITY AUSTRALIA Adelaide University Adelaide, South Australia Department of Electrical and Electronic Faculty of Engineering, Computer and Mathematical Sciences July 2001 Contents Abstract vi Declaration vll Acknowledgement vul Publications lx List of Figures IX List of Tables xlx Glossary xxii I Introduction I 1.1 Introduction 2 t.2 Brief Description of the Heart 4 1.3 Heart Sounds 7 1.3.1 The First Heart Sound 8 1.3.2 The Second Heart Sound . 8 1.3.3 The Third and Fourth Heart Sounds I I.4 Electrical Activity of the Heart I 1.5 Literature Review 11 1.5.1 Time-Flequency and Time-Scale Decomposition Based De-noising 11 I CO]VTE]VTS I.5.2 Other De-noising Methods t4 1.5.3 Time-Flequency and Time-Scale Analysis . 15 t.5.4 Classification and Feature Extraction 18 1.6 Scope of Thesis and Justification of Research 23 2 Equipment and Data Acquisition 26 2.1 Introduction 26 2.2 History of Phonocardiography and Auscultation 26 2.2.L Limitations of the Hurnan Ear 26 2.2.2 Development of the Art of Auscultation and the Stethoscope 28 2.2.2.L From the Acoustic Stethoscope to the Electronic Stethoscope 29 2.2.3 The Introduction of Phonocardiography 30 2.2.4 Some Modern Phonocardiography Systems .32 2.3 Signal (ECG/PCG) Acquisition Process .34 2.3.1 Overview of the PCG-ECG System .34 2.3.2 Recording the PCG 34 2.3.2.I Pick-up devices 34 2.3.2.2 Areas of the Chest for PCG Recordings 37 2.3.2.2.I Left Ventricle Area (LVA) 37 2.3.2.2.2 Right Ventricular Area (RVA) 38 oaooe r^fr /T ce a.!,a.2.{ !v¡u Ãurlo¡^+-;^l ¡rr!o^-^^ \!/ ^^\r¡ r/ 2.3.2.2.4 Right Atrial Area (RAA) 38 2.3.2.2.5 Aortic Area (AA) 38 2.3.2.2.6 Pulmonary Area (PA) 39 ll CO]VTE]VTS 2.3.2.3 The Recording Process . -
PDI 07 Pediatric Heart Surgery Volume
AHRQ QI, Pediatric Quality Indicators #7, Technical Specifications, Pediatric Heart Surgery Volume www.qualityindicators.ahrq.gov Pediatric Heart Surgery Volume Pediatric Quality Indicators #7 Technical Specifications Provider-Level Indicator AHRQ Quality Indicators, Version 4.4, March 2012 Numerator Discharges under age 18 with ICD-9-CM procedure codes for either congenital heart disease (1P) or non-specific heart surgery (2P) with ICD-9-CM diagnosis of congenital heart disease (2D) in any field. ICD-9-CM Congenital heart disease procedure codes (1P)1,2: 3500 CLOSED VALVOTOMY NOS 3551 PROS REP ATRIAL DEF-OPN 3501 CLOSED AORTIC VALVOTOMY 3552 PROS REPAIR ATRIA DEF-CL 3502 CLOSED MITRAL VALVOTOMY 3553 PROS REP VENTRIC DEF-OPN 3503 CLOSED PULMON VALVOTOMY 3554 PROS REP ENDOCAR CUSHION 3504 CLOSED TRICUSP VALVOTOMY 3560 GRFT REPAIR HRT SEPT NOS 3505 ENDOVAS REPL AORTC VALVE 3561 GRAFT REPAIR ATRIAL DEF 3506 TRNSAPCL REP AORTC VALVE 3562 GRAFT REPAIR VENTRIC DEF 3507 ENDOVAS REPL PULM VALVE 3563 GRFT REP ENDOCAR CUSHION 3508 TRNSAPCL REPL PULM VALVE 3570 HEART SEPTA REPAIR NOS 3510 OPEN VALVULOPLASTY NOS 3571 ATRIA SEPTA DEF REP NEC 3511 OPN AORTIC VALVULOPLASTY 3572 VENTR SEPTA DEF REP NEC 3512 OPN MITRAL VALVULOPLASTY 3573 ENDOCAR CUSHION REP NEC 3513 OPN PULMON VALVULOPLASTY 3581 TOT REPAIR TETRAL FALLOT 3514 OPN TRICUS VALVULOPLASTY 3582 TOTAL REPAIR OF TAPVC 3520 OPN/OTH REP HRT VLV NOS 3583 TOT REP TRUNCUS ARTERIOS 3521 OPN/OTH REP AORT VLV-TIS 3584 TOT COR TRANSPOS GRT VES 3522 OPN/OTH REP AORTIC VALVE 3591 INTERAT VEN RETRN TRANSP -
When the Heart Kills the Liver: Acute Liver Failure in Congestive Heart Failure
December 14, 2009 Eu Ro PE an JouR nal oF MED I cal RE sEaRcH 541 Eur J Med Res (2009) 14: 541-546 © I. Holzapfel Publishers 2009 WHEn tHE HEaRt KIlls tHE lIvER: acutE lIvER FaIluRE In congEstIvE HEaRt FaIluRE F. H. saner1, M. Heuer1, M. Meyer1, a. canbay2, g. c. sotiropoulos1, a. Radtke1, J. treckmann1, s. Beckebaum1, c. Dohna-schwake2, s. W. oldedamink3, 4, a. Paul1 1Department of general-, visceral- and transplant surgery, university Hospital Essen, germany, 2Department of Pediatric Medicine, university Hospital Essen, germany, 3Department of surgery, university of Maastricht, netherlands, 4Department of surgery, university college london Hospital, ucl, uK Abstract gestive heart failure may be absent [5, 18]. Both, congestive heart failure as a cause of acute liver fail- chronic and acute congestive heart failure can lead to ure is rarely documented with only a few cases. hepatic dysfunction [10, 17]. although there is no although the pathophysiology is poorly under- classic pattern of abnormalities, a cholestatic bio- stood, there is rising evidence, that low cardiac output chemical profile is common, with a mild elevation in with consecutive reduction in hepatic blood flow is a total bilirubin (usually 3 g/dl), a mild elevation in al- main causing factor, rather than hypotension. In the kaline phosphatase and only occasional elevations in setting of acute liver failure due to congestive heart transaminases. another common observation is an in- failure, clinical signs of the latter can be absent, which crease in InR. the presumed causes of hepatic dys- requires an appropriate diagnostic approach. function in congestive heart failure are hepatic con- as a reference center for acute liver failure and liver gestion from venous outflow obstruction and result- transplantation we recorded from May 2003 to De- ing hypertension and decreased oxygen delivery from cember 2007 202 admissions with the primary diag- an impaired cardiac output [10]. -
Thickness After Heart Transplantation Acute Cellular Rejection and Left
Downloaded from heart.bmj.com on 19 November 2006 Intragraft interleukin 2 mRNA expression during acute cellular rejection and left ventricular total wall thickness after heart transplantation H A de Groot-Kruseman, C C Baan, E M Hagman, W M Mol, H G Niesters, A P Maat, P E Zondervan, W Weimar and A H Balk Heart 2002;87;363-367 doi:10.1136/heart.87.4.363 Updated information and services can be found at: http://heart.bmj.com/cgi/content/full/87/4/363 These include: References This article cites 27 articles, 5 of which can be accessed free at: http://heart.bmj.com/cgi/content/full/87/4/363#BIBL 1 online articles that cite this article can be accessed at: http://heart.bmj.com/cgi/content/full/87/4/363#otherarticles Rapid responses You can respond to this article at: http://heart.bmj.com/cgi/eletter-submit/87/4/363 Email alerting Receive free email alerts when new articles cite this article - sign up in the box at the service top right corner of the article Topic collections Articles on similar topics can be found in the following collections Other Cardiovascular Medicine (2051 articles) Transplantation (283 articles) Molecular Medicine (1113 articles) Other immunology (943 articles) Notes To order reprints of this article go to: http://www.bmjjournals.com/cgi/reprintform To subscribe to Heart go to: http://www.bmjjournals.com/subscriptions/ Downloaded from heart.bmj.com on 19 November 2006 363 BASIC RESEARCH Intragraft interleukin 2 mRNA expression during acute cellular rejection and left ventricular total wall thickness after heart transplantation H A de Groot-Kruseman, C C Baan, E M Hagman, W M Mol, H G Niesters, A P Maat, P E Zondervan, W Weimar, A H Balk ............................................................................................................................ -
The Artificial Heart: Costs, Risks, and Benefits
The Artificial Heart: Costs, Risks, and Benefits May 1982 NTIS order #PB82-239971 THE IMPLICATIONS OF COST-EFFECTIVENESS ANALYSIS OF MEDICAL TECHNOLOGY MAY 1982 BACKGROUND PAPER #2: CASE STUDIES OF MEDICAL TECHNOLOGIES CASE STUDY #9: THE ARTIFICIAL HEART: COST, RISKS, AND BENEFITS Deborah P. Lubeck, Ph. D. and John P. Bunker, M.D. Division of Health Services Research, Stanford University Stanford, Calif. Contributors: Dennis Davidson, M. D.; Eugene Dong, M. D.; Michael Eliastam, M. D.; Dennis Florig, M. A.; Seth Foldy, M. D.; Margaret Marnell, R. N., M. A.; Nancy Pfund, M. A.; Thomas Preston, M. D.; and Alice Whittemore, Ph.D. OTA Background Papers are documents containing information that supplements formal OTA assessments or is an outcome of internal exploratory planning and evalua- tion. The material is usually not of immediate policy interest such as is contained in an OTA Report or Technical Memorandum, nor does it present options for Con- gress to consider. -I \lt. r,,, ,.~’ . - > ‘w, . ,+”b Office of Technology Assessment ./, -. Washington, D C 20510 4,, P ---Y J, ,,, ,,,, ,,, ,. Library of Congress Catalog Card Number 80-600161 For sale by the Superintendent of Documents, U.S. Government Printing Office, Washington, D.C. 20402 Foreword This case study is one of 17 studies comprising Background Paper #2 for OTA’S assessment, The Implications of Cost-Effectiveness Analysis of Medical Technology. That assessment analyzes the feasibility, implications, and value of using cost-effec- tiveness and cost-benefit analysis (CEA/CBA) in health -
Shock and Hemodynamic Monitoring
Shock and Hemodynamic Monitoring Matthew Bank, MD, FACS Assistant Professor Hofstra North Shore‐LIJ School of Medicine Director, Surgical Intensive Care Unit North Shore University Hospital I do not have any financial conflicts of interest to disclose for this presentation Shock • Multiple different strategies for classifying shock, but all forms of shock result in impaired oxygen delivery secondary to either one or both: – reduced cardiac output (cardiogenic, septic) OR – loss of effective intravascular volume (hypovolemic, neurogenic, anaphylactic, septic). Septic Shock –Gram Negative • Gram negative septic shock: —Very studied well studied in animal models —Lipopolysaccharide (LPS) in bacterial cell wall binds to LPS binding protein. —LPS‐LBP complex then binds to cell surface CD14 receptors on monocytes and macrophages. —The LPS‐LBP‐CD14 complex then activates cells via Toll‐like receptor‐4 (TLR4). —TLR4 then “activates” cells which produce a cytokine “cascade” of proinflamatory mediators. Septic Shock –Gram Negative • Tumor Necrosis Factor (TNF) – First cytokine produced in response to gram negative sepsis – Principal mediator for acute response to gram negative bacteria – Major source of TNF is from activated macrophages – High levels of TNF predict mortality and can cause apoptosis. Septic Shock –Gram Negative • Interleukin‐1 (IL‐1) – Levels of IL‐1 increase soon after TNF production in gram negative sepsis (second cytokine to be elevated) – IL‐1 produced by macrophages, neutrophils and endothelial cells – IL‐1 increases levels of next proinflammatory cytokines in cascade, IL‐2 and IL‐12. – IL‐1 does NOT cause apoptosis Septic Shock –Gram Negative • Interleukin‐10 – Anti‐inflammatory cytokine – Inhibits production of IL‐12 – Inhibits T‐cell activation Septic Shock –Gram Positive • Gram positive sepsis – Gram positive cell wall components are also known to be involved in septic response – Peptidoglycans – Teichoic Acid – Likely act in a similar manner as LPS, but less potent on a weight bases. -
Acute Kidney Injury in Cardiogenic Shock: an Updated Narrative Review
Journal of Cardiovascular Development and Disease Review Acute Kidney Injury in Cardiogenic Shock: An Updated Narrative Review Sohrab Singh 1 , Ardaas Kanwar 2, Pranathi R. Sundaragiri 3, Wisit Cheungpasitporn 4 , Alexander G. Truesdell 5, Syed Tanveer Rab 6, Mandeep Singh 7 and Saraschandra Vallabhajosyula 8,* 1 Department of Medicine, The Brooklyn Hospital, Brooklyn, NY 11201, USA; [email protected] 2 Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA; [email protected] 3 Section of Primary Care Internal Medicine, Wake Forest Baptist Health, High Point, NC 27262, USA; [email protected] 4 Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 5 Virginia Heart/Inova Heart and Vascular Institute, Falls Church, VA 22042, USA; [email protected] 6 Section of Interventional Cardiology, Division of Cardiovascular Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; [email protected] 7 Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, USA; [email protected] 8 Section of Cardiovascular Medicine, Department of Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27262, USA * Correspondence: [email protected] Abstract: Acute myocardial infarction with cardiogenic shock (AMI-CS) is associated with high mortality and morbidity despite advancements in cardiovascular care. AMI-CS is associated with multiorgan failure of non-cardiac organ systems. Acute kidney injury (AKI) is frequently seen in patients with AMI-CS and is associated with worse mortality and outcomes compared to those without. The pathogenesis of AMI-CS associated with AKI may involve more factors than previously Citation: Singh, S.; Kanwar, A.; understood. -
Cardiac Amyloidosis and Surgery. What Do We Know About Rare
Cardiac amyloidosis and surgery. What do we know about rare diseases? Carlos Mestres1 and Mathias van Hemelrijck2 1University Hospital Zurich 2UniversitatsSpital Zurich May 3, 2021 Commentary to JOCS-2020-RA-1888 JOCS-2020-RA-1888 Cardiac amyloidosis in non-transplant cardiac surgery Cardiac amyloidosis and surgery. What do we know about rare diseases? Running Title: Cardiac amyloidosis and cardiac surgery Carlos { A. Mestres MD PhD FETCS1, 2, Mathias Van Hemelrijck MD1 1 - Clinic of Cardiac Surgery, University Hospital Zurich,¨ Zurich¨ (Switzerland) 2 - Department of Cardiothoracic Surgery, The University of the Free State, Bloemfontein, (South Africa) Word count (All): 1173 Word count (Text): 774 Key words : Cardiac amyloidosis, cardiac surgery, rare disease Correspondence: Carlos A. Mestres, MD, PhD, FETCS Clinic for Cardiac Surgery University Hospital Zurich,¨ R¨amistrasse 100 CH 8091 Zurich¨ (Switzerland) Email: [email protected] Rare diseases are serious, chronic and potentialy lethal. The European Union (EU) definition of a rare disease is one that affects fewer than 5 in 10,000 people (1). In the EU, these rare diseases are estimated to affect up to 8% of the roughly 500 million population (2). In the United States, a rare disease is defined as a condition affecting fewer than 200,000 people in the US (3). This a definition created by Congress in the Orphan Drug Act of 1983 (4). Therefore, the estimates for the US are that 25-30 million people are affected by a rare disease. There are more than 6000 rare diseases and 80% are genetic disorders diagnosed during childhood. Despite all community efforts, there are still a lack of an universal definition of rare diseases. -
Late Atrioventricular Block and Permanent Pacemaker Implantation After Heart Transplantation
572 Türk Kardiyol Dern Arş - Arch Turk Soc Cardiol 2009;37(8):572-574 Late atrioventricular block and permanent pacemaker implantation after heart transplantation Kalp nakli sonrası geç dönemde atriyoventriküler blok ve kalıcı kalp pili uygulaması Mustafa Akçakoyun, M.D., Ahmet Duran Demir, M.D., Mehmet Ali Özatık, M.D.,1 Şeref Küçüker, M.D.1 Departments of Cardiology and 1Cardiovascular Surgery, Türkiye Yüksek İhtisas Heart-Education and Research Hospital, Ankara The need for permanent pacemaker implantation due Kalp nakli sonrasında geç dönemde atriyoventrikü- to late atrioventricular (AV) block after heart transplan- ler (AV) blok nedeniyle kalıcı kalp pili uygulaması tation is rare. A 59-year-old male patient underwent nadirdir. Elli dokuz yaşında erkek hastaya kalp nakli heart transplantation. He presented with syncope eight yapıldı. Ameliyattan sekiz ay sonra hastada bayılma months after transplantation. Ambulatory 24-hour Holter yakınmaları ortaya çıktı. Ambulatuvar 24 saatlik Holter monitoring showed predominant sinus rhythm with a takibinde, ortalama 74 atım/dk kalp hızı ile esas olarak mean heart rate of 74 bpm, intermittent second-degree sinüs ritminde olan hastada geçici ikinci derece AV AV block, and high-degree AV block with pauses of up blok ve 10.6 saniyeye kadar varabilen ileri derecede to 10.6 seconds. Percutaneous transvenous endomyo- AV blok atakları izlendi. Perkütan transvenöz endo- cardial biopsy yielded a histologic diagnosis of grade IA miyokardiyal biyopsi materyalinin histolojik inceleme- rejection according to the ISHLT (International Society sinde, ISHLT (International Society of Heart and Lung of Heart and Lung Transplantation) scoring system. A Transplantation) sınıflamasına göre derece IA doku permanent pacemaker with DDD-R mode was implant- reddi saptandı. -
Heart Valve Disease: Mitral and Tricuspid Valves
Heart Valve Disease: Mitral and Tricuspid Valves Heart anatomy The heart has two sides, separated by an inner wall called the septum. The right side of the heart pumps blood to the lungs to pick up oxygen. The left side of the heart receives the oxygen- rich blood from the lungs and pumps it to the body. The heart has four chambers and four valves that regulate blood flow. The upper chambers are called the left and right atria, and the lower chambers are called the left and right ventricles. The mitral valve is located on the left side of the heart, between the left atrium and the left ventricle. This valve has two leaflets that allow blood to flow from the lungs to the heart. The tricuspid valve is located on the right side of the heart, between the right atrium and the right ventricle. This valve has three leaflets and its function is to Cardiac Surgery-MATRIx Program -1- prevent blood from leaking back into the right atrium. What is heart valve disease? In heart valve disease, one or more of the valves in your heart does not open or close properly. Heart valve problems may include: • Regurgitation (also called insufficiency)- In this condition, the valve leaflets don't close properly, causing blood to leak backward in your heart. • Stenosis- In valve stenosis, your valve leaflets become thick or stiff, and do not open wide enough. This reduces blood flow through the valve. Blausen.com staff-Own work, CC BY 3.0 Mitral valve disease The most common problems affecting the mitral valve are the inability for the valve to completely open (stenosis) or close (regurgitation).