Cardiac Surgery: A Complete Guide PDF

Shahzad G. Raja Editor Cardiac Surgery A Complete Guide 123 Cardiac Surgery Shahzad G. Raja Editor Cardiac Surgery A Complete Guide Editor Shahzad G. Raja Harefield Hospital Royal Brompton & Harefield NHS Trust London UK ISBN 978-3-030-24173-5    ISBN 978-...

Shahzad G. Raja Editor Cardiac Surgery A Complete Guide 123 Cardiac Surgery Shahzad G. Raja Editor Cardiac Surgery A Complete Guide Editor Shahzad G. Raja Harefield Hospital Royal Brompton & Harefield NHS Trust London UK ISBN 978-3-030-24173-5    ISBN 978-3-030-24174-2 (eBook) https://doi.org/10.1007/978-3-030-24174-2 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. 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This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Dedicated to my parents for their love, endless support, encouragement and sacrifices. Preface Cardiac Surgery: A Complete Guide provides a succinct and solid overview of the specialty of cardiac surgery. The book predominantly aimed at trainees as well as practicing surgeons pres- ents in a clear and accessible way the most up-to-date knowledge of the entire specialty of cardiac surgery. With an emphasis on key concepts, high-yield information, and international best practice, it concisely covers the breadth of material needed for certification and practice of cardiac surgery. Thanks to the reader-friendly design, featuring an abundance of illustra- tions, intraoperative photographs, tables as well as information boxes, the book enables the readers to visually grasp and retain difficult concepts. Evidence-based approaches to the man- agement of a range of cardiac surgical conditions will help readers overcome tough clinical challenges and improve patient outcomes. Cardiac Surgery: A Complete Guide brings together experts from around the world to dis- cuss the full scope of cardiac surgery. It provides essential, up-to-date, need-to-know informa- tion about the latest surgical perspectives and approaches to treatment including innovations in minimally invasive surgery and percutaneous devices. Drawing together current knowledge and evidence and examining all aspects of cardiac surgery in one succinct volume, Cardiac Surgery: A Complete Guide is the ideal resource for the trainees as well as practicing surgeons enabling them to effectively apply the latest techniques and evidence-based approaches in their day-to-day practice. A key feature of the book is the section on Review Questions that contains Single Best Answer Questions that will prove to be an invaluable resource for residents preparing for their certification examinations. The breadth of topics covered and detailed answers expand the versatility of this book to a larger audience including doctors preparing for postgraduate exams and other allied healthcare professionals who will be examined in cardiac surgery. The questions are in line with the most recent developments in clinical guidelines and have been written in accordance with the recent changes in certification examinations. They are designed to provide a comprehensive coverage of the cardiac surgery curriculum and are simi- lar to those that have or will feature in certification examinations. The answers provide detailed explanations as to how the correct answer is reached, followed by a clear discussion of how the incorrect answers are ruled out and supplementary information about other important aspects of each question. The answers are designed to allow the reader to further enhance their clinical knowledge, understanding, and single best answer technique, thus making this book an excel- lent aid for exam preparation. I would like to thank all the contributors who have produced excellent chapters and made this collaborative venture worthwhile. Last but not least, my special thanks to the Springer Nature team—Grant Weston, Leo Johnson, Rajeswari Balachandran, and Swathi Chandersekar—for managing the project with courtesy and patience. London, UK Shahzad G. Raja 2020 vii Contents Part I Perioperative Care and Cardiopulmonary Bypass 1  Cardiac Catheterization    3 Konstantinos Kalogeras and Vasileios F. Panoulas 2 Fractional Flow Reserve   15 Vasileios F. Panoulas 3  Echocardiography   23 Shelley Rahman Haley 4 Cardiac Computed Tomography and Magnetic Resonance Imaging    41 Tarun K. Mittal 5 Assessment of Myocardial Viability    55 Chandra Katikireddy, Nareg Minaskeian, Amir Najafi, and Arang Samim 6 Blood Conservation Strategies in Cardiac Surgery   63 David Royston 7 Inotropes, Vasopressors and Vasodilators   69 Nandor Marczin, Paola Carmona, Steffen Rex, and Eric E. C. de Waal 8 Cardiac Pacing in Adults   81 Daniel Keene, S. M. Afzal Sohaib, and Tom Wong 9 Adult Cardiopulmonary Bypass   93 Demetrios Stefanou and Ioannis Dimarakis 10 Myocardial Protection in Adults 101 Francesco Nicolini and Tiziano Gherli 11 Heparin-Induced Thrombocytopenia 109 Benilde Cosmi 12 Tissue Sealants in Cardiac Surgery 119 Louis P. Perrault and Fatima Zohra Moukhariq Part II Coronary Artery Disease 13 Conduits for Coronary Artery Bypass Surgery 131 Cristiano Spadaccio and Mario F. L. Gaudino 14 Endoscopic Saphenous Vein and Radial Artery Harvesting 139 Fabrizio Rosati and Gianluigi Bisleri 15 Conventional Coronary Artery Bypass Grafting 149 Kirthi Ravichandren and Faisal G. Bakaeen ix x Contents 16 Off-Pump Coronary Artery Bypass Grafting  157 Shahzad G. Raja and Umberto Benedetto 17 Minimally Invasive Coronary Artery Bypass Grafting 167 Ming Hao Guo, Janet M. C. Ngu, and Marc Ruel 18 Totally Endoscopic Coronary Artery Bypass Grafting 175 Brody Wehman and Eric J. Lehr 19 Redo Coronary Artery Bypass Grafting 185 Hitoshi Yaku, Sachiko Yamazaki, and Satoshi Numata 20 Hybrid Coronary Revascularization 193 Elbert E. Williams, Gianluca Torregrossa, and John D. Puskas 21 Bilateral Internal Mammary Artery Grafting 199 Shahzad G. Raja and David Taggart 22 Total and Multiple Arterial Revascularization 207 James Tatoulis 23 Anastomotic Devices for Coronary Artery Surgery 219 Nirav C. Patel and Jonathan M. Hemli 24 Post-infarction Ventricular Septal Defect 229 Joseph Nader, Pierre Voisine, and Mario Sénéchal 25 Ischemic Mitral Regurgitation 237 Michael Salna and Jack H. Boyd 26 Post-infarction Ventricular Aneurysms 243 Manish K. Soni and Shahzad G. Raja 27 Coronary Endarterectomy 253 Nikolaos A. Papakonstantinou 28 Transmyocardial Laser Revascularization 261 Justin G. Miller and Keith A. Horvath 29 Gene Therapy for Coronary Artery Disease 269 Vivekkumar B. Patel, Christopher T. Ryan, Ronald G. Crystal, and Todd K. Rosengart 30 Combined Carotid and Coronary Artery Disease 277 Salah E. Altarabsheh, Carolyn Chang, Yakov E. Elgudin, and Salil V. Deo 31 Coronary Artery Aneurysms and Fistulas 281 Aimee Wehber, Kevin Oguayo, Joseph Pendley, Jonathan J. Allred, J. Christopher Scott, and William Jeremy Mahlow Part III Valvular Heart Disease 32 Mechanical Prosthetic Valves 291 Matthew C. Henn and Marc R. Moon 33 Stented Bioprosthetic Valves  299 Giuseppe Santarpino and Shahzad G. Raja 34 Bentall and Mini-Bentall Procedure 307 Adam Chakos and Tristan D. Yan Contents xi 35 Aortic Valve-Sparing Root Replacement  315 Mateo Marin-Cuartas and Michael A. Borger 36 Aortic Valve Repair 325 Igo B. Ribeiro and Munir Boodhwani 37 The Small Aortic Root  345 John R. Doty 38 The Ross Procedure  351 Ismail Bouhout and Ismail El-Hamamsy 39 Bicuspid Aortic Valve and Aortopathy 359 Sri Harsha Patlolla and Hartzell V. Schaff 40 Mitral Valve Replacement  373 David Blitzer, Jeremy J. Song, and Damien J. LaPar 41 Techniques for Mitral Valve Repair  381 Bassman Tappuni, Hoda Javadikasgari, Bajwa Gurjyot, and Rakesh M. Suri 42 Mitral Valve Repair in Rheumatic Mitral Disease 389 Taweesak Chotivatanapong 43 Native Valve Endocarditis  397 Kareem Bedeir and Basel Ramlawi 44 Prosthetic Valve Endocarditis  405 Bobby Yanagawa, Maral Ouzounian, and David A. Latter 45 Tricuspid Valve Surgery 415 Christoph T. Starck and Volkmar Falk 46 Minimally Invasive Aortic Valve Surgery 421 Mattia Glauber and Antonio Miceli 47 Minimally Invasive Mitral Valve Surgery 429 Mateo Marin-Cuartas and Piroze M. Davierwala 48 Transcatheter Aortic Valve Therapies 437 Mohanad Hamandi and Michael J. Mack 49 Transcatheter Pulmonary Valve Replacement 447 Hussam S. Suradi and Ziyad M. Hijazi 50 Transcatheter Mitral Valve Therapies  455 Adolfo Ferrero Guadagnoli, Maurizio Taramasso, and Francesco Maisano 51 Carcinoid Heart Disease 463 Anita Nguyen, Hartzell V. Schaff, and Heidi M. Connolly Part IV Thoracic Aorta 52 Acute Type A Aortic Dissection 475 Alice Le Huu, Umang M. Parikh, and Joseph S. Coselli 53 Acute Type B Aortic Dissection 487 Ashraf A. Sabe and G. Chad Hughes 54 Chronic Type B Aortic Dissection 497 Konstantinos Spanos and Tilo Kölbel xii 55 Aortic Intramural Hematoma and Penetrating Aortic Ulcer 507 Abe DeAnda Jr. and Christine Shokrzadeh 56 Descending Thoracic and Thoracoabdominal Aortic Aneurysms  515 Konstadinos A. Plestis, Oleg I. Orlov, Vishal N. Shah, Robert J. Meisner, Cinthia P. Orlov, and Serge Sicouri 57 Aortic Arch Aneurysms  529 Mahnoor Imran, Mohammad A. Zafar, Tamta Chkhikvadze, Bulat A. Ziganshin, and John A. Elefteriades 58 Hybrid Aortic Arch Repair  545 Oliver J. Liakopoulos, Julia Merkle, and Thorsten Claus W. Wahlers 59 Endovascular Stent Grafting of Thoracic Aorta  553 David Tobey, Allan Capote, Rodney White, and Ali Khoynezhad 60 Neuroprotective Strategies During Aortic Surgery 561 Jee Young Kim, Helen A. Lindsay, and George Djaiani 61 Sinus of Valsalva Aneurysms 567 Manish K. Soni and Shahzad G. Raja 62 Elephant Trunk Procedures 573 Suyog A. Mokashi and Lars G. Svensson 63 Porcelain Ascending Aorta 579 Yigal Abramowitz and Raj R. Makkar 64 Cardiovascular Manifestations of Marfan and Loeys-Dietz Syndrome  587 Florian S. Schoenhoff and Thierry P. Carrel Part V Mechanical Circulatory Support and Transplantation 65 Pharmacologic Support of the Failing Heart 597 Haifa Lyster and Georgios Karagiannis 66 Cardiac Resynchronization Therapy for Heart Failure  607 Mumin R. Noor, Rebecca E. Lane, and Owais Dar 67 Intra-aortic Balloon Pump 613 Nnamdi Nwaejike and Mani A. Daneshmand 68 Extracorporeal Life Support in the Adult  623 Adeel Abbasi and Corey E. Ventetuolo 69 Temporary Circulatory Support Devices 631 Gerin R. Stevens and Brian Lima 70 Heart Transplantation  639 Aravinda Page and Yasir Abu-Omar 71 Heart-Lung Transplantation 645 Don Hayes Jr., Michael S. Mulvihill, and David McGiffin 72 Immunosuppression in Cardiac Transplantation  655 Yu Xie, Kevin W. Lor, and Jon A. Kobashigawa 73 Complications of Heart Transplantation  665 Mayooran Shanmuganathan and Owais Dar   xiii Part VI Miscellaneous Cardiovascular Disorders 74 Cardiac Tumors 673 Maria Romero and Renu Virmani 75 Concomitant Coronary Artery Disease and Lung Cancer 691 Wilhelm P. Mistiaen 76 Trauma to the Heart and Great Vessels  697 Ankur Bakshi, Matthew J. Wall Jr., and Ravi K. Ghanta 77 Pericardial Diseases  703 Rolando Calderon-Rojas and Hartzell V. Schaff 78 Pulmonary Thromboendarterectomy 717 Michael M. Madani and Jill R. Higgins 79 Surgical Management of Atrial Fibrillation 727 Kareem Bedeir and Basel Ramlawi 80 Hypertrophic Cardiomyopathy 735 Hao Cui and Hartzell V. Schaff 81 Left Ventricular Volume Reduction 749 Antonio M. Calafiore, Massimiliano Foschi, Antonio Totaro, Piero Pelini, and Michele Di Mauro 82 Renal Failure After Cardiac Surgery 755 Marc Vives and Juan Bustamante-Munguira 83 Bleeding and Re-exploration After Cardiac Surgery  763 Xun Zhou, Cecillia Lui, and Glenn J. R. Whitman 84 Sternal Wound Infections 769 Tomas Gudbjartsson 85 Atrioventricular Disruption 777 Sheena Garg and Shahzad G. Raja Part VII Paediatric and Congenital Heart Disease 86 Pediatric Cardiopulmonary Bypass and Hypothermic Circulatory Arrest  783 Craig M. McRobb, Scott Lawson, Cory Ellis, and Brian Mejak 87 Myocardial Protection in Children 791 Abdullah Doğan and Rıza Türköz 88 Pediatric Extracorporeal Membrane Oxygenation and Mechanical Circulatory Assist Devices  797 Akif Ündar, Shigang Wang, Madison Force, and Morgan K. Moroi 89 Palliative Operations for Congenital Heart Disease  813 Masakazu Nakao and Roberto M. Di Donato 90 Coronary Anomalies in Children 821 Phan-Kiet Tran and Victor T. Tsang 91 Congenital Valvar and Supravalvar Aortic Stenosis 829 Viktor Hraska and Joseph R. Block xiv Contents 92 Atrial Septal Defects 839 Iman Naimi and Jason F. Deen 93 Isolated Ventricular Septal Defect 849 Sian Chivers and Attilio A. Lotto 94 Patent Ductus Arteriosus 865 Robroy H. MacIver 95 Aortopulmonary Window  869 G. Deepak Gowda and B. C. Hamsini 96 Coarctation of the Aorta 875 Shafi Mussa and David R. Anderson 97 Pulmonary Valve Stenosis  885 Fazal W. Khan and M. Sertaç Çiçek 98 Truncus Arteriosus 891 Sandeep Sainathan, Ken-Michael Bayle, Christopher J. Knott-Craig, and Umar S. Boston 99 Transposition of the Great Arteries 897 Erik L. Frandsen and Matthew D. Files 100 Congenitally Corrected Transposition of the Great Arteries 905 Michel N. Ilbawi, Chawki El-Zein, and Luca Vricella 101 Tetralogy of Fallot 917 Damien J. LaPar and Emile A. Bacha 102 Hypoplastic Left Heart Syndrome 923 David J. Barron 103 Congenital Aortic Arch Interruption and Hypoplasia  933 Serban C. Stoica 104 Pulmonary Atresia with Intact Septum  941 Imran Saeed 105 Complete Atrioventricular Septal Defect 949 Tom R. Karl, Nelson Alphonso, John S. K. Murala, and Kanchana Singappulli 106 Double Outlet Right Ventricle 961 Ravi S. Samraj, Ross M. Ungerleider, and Inder Mehta 107 Neonatal Ebstein’s Anomaly  971 Umar S. Boston, Ken Bayle, T. K. Susheel Kumar, and Christopher J. Knott-Craig 108 Vascular Rings and Pulmonary Artery Sling 981 Carl L. Backer 109 Congenital Left Ventricular Outflow Tract Obstruction 993 Imran Saeed 110 Pediatric Heart Transplantation 1001 James K. Kirklin Review Questions  1011 Answers 1033 Index 1061  Part I Perioperative Care and Cardiopulmonary Bypass  Cardiac Catheterization 1 Konstantinos Kalogeras and Vasileios F. Panoulas further developed by Kurt Amplatz and Melvin Judkins in High Yield Facts 1967 (Fig. 1.1). The coronary arteries soon became the Selective coronary angiography was first described most frequently examined vessels, using mainly pre-shaped by Mason Sones in 1958. femoral catheters by Judkins, but also those by Bourassa, The main goals of invasive coronary angiography Schoonmaker, King, El Gamal and many others. After the are to confirm the presence and nature of coronary establishment of coronary angiography, a new era began in artery disease, to assess the location and extent of September 1977 when the first coronary angioplasty was luminal stenosis and finally, to decide upon the opti- achieved by Andreas Gruentzig. mal therapeutic approach. Coronary angiography is a relatively safe procedure in experienced hands with a mortality rate of Invasive Diagnostic Coronary Angiography 1/1000. Ongoing infections, acute kidney injury or failure, Coronary angiography is an integral part of the workup of severe anemia, active bleeding, previous allergic patients with heart disease and a key element in the evaluation reaction to contrast and severe electrolyte imbal- of patients with coronary artery disease (CAD). The main ance are considered relative contraindications. History of Cardiac Catheterization Although the first cardiac catheterization in animals was per- formed by the French physiologist Claude Bernard in 1840s, it was not before 1929 when the first right heart catheteriza- tion was done in human by the German doctor Werner Forssmann on himself. Selective coronary angiography was first described by Mason Sones in 1958, while special cath- eters for coronaries engagement and contrast injection were K. Kalogeras Royal Brompton and Harefield NHS Foundation Trust, Harefield, UK V. F. Panoulas (*) Royal Brompton and Harefield NHS Foundation Trust, Harefield, UK Fig. 1.1 Melvin Paul Judkins (1922–1985) with his pre-shaped coro- nary catheters for femoral access (Reprinted from “The PCR-EAPCI National Heart and Lung Institute, Imperial College London, Textbook”, chapter: A history of cardiac catheterization, Authors: London, UK Michel E. Bertrand, Bernhard Meier ) e-mail: [email protected] © Springer Nature Switzerland AG 2020 3 S. G. Raja (ed.), Cardiac Surgery, https://doi.org/10.1007/978-3-030-24174-2_1 4 K. Kalogeras and V. F. Panoulas goals of invasive coronary angiography are to confirm the of kidney or liver injury. Bleeding history and evidence of presence and nature of CAD, to assess the location and extent elevated international normalized ratio (INR) or activated of luminal stenosis and finally, to decide upon the optimal partial thromboplastin time (aPTT) are elements of great therapeutic approach. Today, the simple coronary angiography importance to ensure patient safety. In patients who are anti- has been further enriched by functional evaluation by means coagulated (warfarin, novel oral anticoagulants) and man- of intracoronary pressure measurements and anatomical eval- aged with transradial approach, there is increased confidence uation using advanced intracoronary imaging modalities. to do diagnostic angiography without treatment interruption Although coronary angiography is a relatively safe procedure [9, 10]. However, elective percutaneous interventions, in experienced hands (mortality rate of 1/1000), it can rarely including pressure wire measurements, should not be per- be potentially harmful [4, 5]. formed in anticoagulated patients as the risk of bleeding complications rises. A transthoracic echocardiogram prior to any coro- Indications nary catheterization is essential to identify regional wall motion abnormalities, valvular disease or left ventricular A coronary angiogram is indicated as an elective procedure thrombus, information that will guide the decision making during coronary angiography. For any patient in whom a diagnosis of CAD is suspected There is evidence to support the pre-hydration before or made on clinical grounds or based on additional non-­ administration of contrast medium, particularly in patients at invasive stress tests for the purpose of confirming the risk of contrast induced nephropathy (CIN). However, the diagnosis as well as for defining the optimal therapeutic modalities of fluid administration remain uncertain. strategy. Patient’s hydration status should be assessed prior to the pro- As part of the preoperative work-up in patients planned cedure, while the aim is to have the patient euvolemic or for a major non-cardiac or valvular cardiac surgery. even slightly hypervolemic before the angiogram. For most patients 1000 ml of 0.9% saline infused over 6 h is consid- On an emergency basis, all patients presenting with acute ered sufficient. Although not proven, it is considered reason- ST-elevation myocardial infarction (STEMI) should undergo able to routinely pre-hydrate all patients regardless of renal a coronary angiogram and a percutaneous coronary interven- function [13, 14]. tion (PCI) within 90 min from presentation. On a semi-urgent basis, coronary angiography is indi- cated for all patients presenting with non ST elevation acute Technical Aspects of the Procedure coronary syndromes (NSTEACS) including unstable angina or non-STEMI (NSTEMI) within a timeframe, defined by Access risk stratification scores. This can be gained through femoral, radial, ulnar, brachial or Ongoing infections, acute kidney injury or failure, severe in rare circumstances, axillary/subclavian artery approach. anemia, active bleeding, previous allergic reaction to con- However, transradial approach has mostly replaced the other trast and severe electrolyte imbalance are considered relative techniques, becoming the most popular approach, due to the contraindications. However, each patient should be evalu- better hemostasis control, faster patient mobilization and ated separately and analyzed on a risk-benefit basis. increased patient comfort, while data suggest that it is asso- ciated with reduced vascular and bleeding complications alongside reduced mortality, particularly in emergency cases Pre-procedure Preparation [15, 16]. The Seldinger technique used for access is shown in Fig. 1.2. Subsequently, all catheters can be introduced Following history and clinical examination, a written through the sheath and over a J guidewire to the aortic root, informed consent should be obtained in every patient follow- to avoid dissecting the vasculature. Problems that can be ing a clear and full description of the indication(s), the pro- encountered in advancing the guidewire include severe arte- cedure and the treatment options. A routine recent set of rial tortuosity, stenosis, occlusion or dissection. Such diffi- blood samples (within a week), is required to ensure patient culties can be overcome only by understanding the anatomy safety. From the hematology profile, hemoglobin, white cell using peripheral contrast injections and the appropriate use and platelets count are important to ensure there is no of kit (e.g., hydrophilic wires (e.g., Terumo®) or insertion of recent or occult blood loss, no underlying infection or throm- long sheaths (45 cm), use of guide rather than diagnostic bocytopenia. With regards to biochemistry tests, creatinine, catheters, use of stiff wires (Amplatz super stiff)), ensuring urea and liver profile are equally important to ensure absence optimal catheter and/or wire manipulation at all times. 1 Cardiac Catheterization 5 Fig. 1.2 Vascular access for percutaneous insertion of a sheath (a) Vessel punctured with the needle until blood back flows. (b) A flexible J-tip guidewire advanced through the needle into the vessel lumen. (c) The needle a b c removed, and the wire is left in place. The hole around the wire can be enlarged with a scalpel. (d) Sheath and dilator placed over the guidewire. (e) Sheath and dilator advanced, over the guidewire, into the vessel. (f) Dilator and guidewire removed, while sheath is left in the vessel d e f JR 3.5 JR 4 JR 5 JR 6 JL 3.5 JL 4 JL 45 JL 5 JL 6 AL I AL II AL III AR Mox ARI AR II AR III MPA 1 155° 145° MPA 2(1) MPA 2 MPB 1 MPB 2 SK PIG PIG PIG PIG LCB SON I SON II SON III CAS I CAS II CAS III Fig. 1.3 Different catheters available for diagnostic coronary angiog- J. Peace, Chrysafios Girasis, Christoph K. Naber, Christos V. Bourantas, raphy (Reprinted from “The PCR-EAPCI Textbook”, chapter: Invasive Patrick W. Serruys ) diagnostic coronary angiography, Authors: Guy R. Heyndrickx, Aaron Pharmacology  atheter Selection and Manipulation C Intra-arterial administration of verapamil or nitrates via the Improvements in catheter technology have allowed the grad- radial sheath is used to limit the occurrence of vascular ual decrease of diagnostic catheters’ size from 8 Fr during the spasm, an issue not encountered with transfemoral access. early years of coronary angiography to 6 Fr and even 5 or 4 Fr Vascular spasm, as well as patient anxiety can be effectively size catheters. The Judkins left and right (JL/JR) pre-­shaped addressed with the use of sedation prior to coronary angio- catheters are the most commonly used catheters in the world gram. With regards to anticoagulation, for routine transradial for engaging the left and the right coronary arteries, respec- diagnostic coronary angiography, an intravenous bolus of tively. Other pre-shaped catheters (e.g., Amplatz) can be used 2500–5000 units of unfractionated heparin is adequate for for injecting both coronary vessels (Fig. 1.3). While initially optimal short-term anticoagulation to avoid radial artery the same type of preformed catheters were used for the radial occlusion. Finally, it is general practice to administer nitrates approach, more dedicated catheters are now available for (sublingual, intravenous or intracoronary) before starting the radial procedures such as the Kimny (Boston Scientific®), coronary angiographic injections to obtain maximal coro- Optitorque Tiger, Jacky and Sarah (Terumo®), Sones (Cordis®) nary dilatation and prevent potential arterial spasm at the and PaPa (Medtronic®) catheters which allow for engagement time of catheter manipulation. of both coronary ostia without need for exchanging catheters. 6 K. Kalogeras and V. F. Panoulas Angiographic Views (also termed spider), LAO cranial, PA cranial and RAO Angiographic views are labelled according to the position of cranial. the C-arm image receptor (the flat portion of the C-arm posi- The right coronary artery (RCA) is intubated in the LAO tioned over the patient) in relation to the patient. In the left projection (Fig. 1.6). One of the easy ways to recognize the anterior oblique (LAO) and right anterior oblique the type of view is the presence (in all cranial vies) or absence X-ray machine is positioned on the left or right side of the (in all caudal views) of the diaphragm. Furthermore to iden- patient respectively, while in the cranial (CRAN) and caudal tify whether the projection is LAO or RAO one has to locate (CAUD) views the machine is positioned cranially or cau- the spine which should be seen at the contralateral site of the dally respectively. When the receptor is in the midline then image in relation to the projection—i.e., on the right of the the term postero-anterior (PA) is used. image in an LAO view. Left coronary angiography can be performed by using a In 10%–15% of cases an abnormal origin of the RCA wide range of catheters, depending on the approach used complicates the search for the right coronary ostium. A mul- (radial, femoral, other) and other anatomic variables includ- tipurpose, a 3DRC or Williams, an Amplatz right or Amplatz ing aortic root size, coronary ostia location (high, low, ante- left catheter can be used in these circumstances. For the RCA rior, posterior) and coronary artery take off (superior, three views, the LAO, RAO and LAO cranial (20/20) or PA horizontal, inferior, Shepherds crook). Before engaging and cranial (showing the bifurcation-crux to PDA and PL) are making injections to the left main or any vessel it is ­important usually sufficient to identify all stenoses. On rare occasions, to recognize that blood is coming freely from the catheter the left circumflex artery (LCx) can be seen originating from ensuring that the catheter has been purged of air and that a the right coronary sinus (Fig. 1.7). satisfactory arterial pressure trace is obtained. Any reduction Left ventricular angiography used to be an essential part in arterial pressure or change in the morphology of the arte- of invasive coronary angiogram with pigtail catheters being rial waveform (ventricularization—low diastolic values), the first choice. After entering the left ventricle cavity, a cor- should alert the operator that the catheter is obstructing flow, rect measurement of the left ventricular end diastolic pres- due to either the presence of a true ostial stenosis, or deep sure is the first and most important measurement to evaluate catheter engagement (Fig. 1.4). Although individual prefer- global LV function, while during catheter withdrawal, the ences between operators exist as to which angiographic pressure gradient across the aortic valve should be measured. views and in what order to be obtained, paired orthogonal Apart from pressure evaluation, left ventriculography offers views are generally required for a correct diagnosis and ade- a lot of information regarding the regional wall motion func- quate treatment guidance (Fig. 1.5a, b). Most commonly tion of the left ventricle. Usually, it is obtained in two orthog- used views include: RAO caudal, PA caudal, LAO caudal onal views, RAO (30°) and LAO (40°–60°). Fig. 1.4 Waveform of pressure ventricularization during coronary ostia engagement due to forward blood flow obstruction 1 Cardiac Catheterization 7 RAO CAUDAL PA CAUDAL LAO CAUDAL a LAD RAO 20° Caudal 20° LMT LAD LAD LMT OM Septal OM Diag LMT LCx LCx Septal Perforators LCx Obtuse Marginal LAO 50 Caudal 30 RAO CRANIAL PA CRANIAL LAO CRANIAL b Fig. 1.5 (a) Angiographic caudal views of the left coronary artery system. (b) Angiographic cranial views of the left coronary artery system. LMT left main stem, LAD left anterior descending, LCX left Circumflex, OM oblique marginal, Diag diagonal a b Fig. 1.6 Angiographic views of the right coronary artery (RCA). (a) Left anterior oblique view (LAO). (b) Right anterior oblique. (RCA right coronary artery, PDA posterior descending artery, PL posterolateral branch, RV right ventricle branch) 8 K. Kalogeras and V. F. Panoulas Post-procedure Care  oronary Angiogram Analysis C The conventional angiographic classification is based on  heath Removal and Closure Devices S visual estimation of the diameter reduction of the stenosis Standard manual compression after sheath removal is usu- compared to a normal segment. The severity classification ally enough to acquire haemostasis after transfemoral ranges from low grade stenosis (10% tion of the European Society of Cardiology (ESC). Eur Heart J. 2018;39:119–77. rise) compared to mixed venous SaO2. Mixed venous SaO2 7. Neumann FJ, Sousa-Uva M, Ahlsson A, Alfonso F, Banning AP, is calculated as (3xSVC + IVC)/4. The degree of the Benedetto U, et al. 2018 ESC/EACTS Guidelines on myocardial shunting can then be calculated using the ratio of pulmonary revascularization. Eur Heart J. 2018; https://doi.org/10.1093/eur- flow (Qp) to systemic flow (Qs) as shown below. heartj/ehy394. [Epub ahead of print]. 8. Maluenda G, Lemesle G, Collins SD, Ben-Dor I, Syed AI, Qp / Qs  SAO 2  SMVO 2 / SPVO2  SPAO 2 Torguson R, et al. The clinical significance of hematocrit values before and after percutaneous coronary intervention. Am Heart J. where: SAO2 is arterial (aortic) saturation, SMVO2 is mixed 2009;158:1024–30. venous saturation, SPVO2 is pulmonary vein saturation, and 9. Karjalainen PP, Vikman S, Niemela M, Porela P, Ylitalo A, Vaittinen MA, et al. Safety of percutaneous coronary intervention SPAO2 is pulmonary artery saturation. during uninterrupted oral anticoagulant treatment. Eur Heart J. Finally, the calculation of systemic and pulmonary vascu- 2008;29:1001–10. lar resistance can be estimated from CO using the Ohm’s law 10. Ziakas AG, Koskinas KC, Gavrilidis S, Giannoglou GD, (Resistance = Pressure/Flow): Hadjimiltiades S, Gourassas I, et al. Radial versus femoral access for orally anticoagulated patients. Catheter Cardiovasc Interv. SVR  80   mean arterial pressure  RA  / CO 2010;76:493–9. 11. Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette PVR  80   mean PA PCWP  / CO D. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med. 1970;283:447–51. 12. Mueller C, Buerkle G, Buettner HJ, Petersen J, Perruchoud AP, Eriksson U, et al. Prevention of contrast media-associated Conclusion nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. The standard coronary angiography, despite its invasive 2002;162:329–36. 13. Barrett BJ, Parfrey PS. Clinical practice. Preventing nephropathy character and the drawback of relying on a limited number of induced by contrast medium. N Engl J Med. 2006;354:379–86. subjectively selected 2D acquisitions, remains the gold stan- 14. Briguori C, Visconti G, Focaccio A, Airoldi F, Valgimigli M, dard method for the evaluation of patients with coronary Sangiorgi GM, et al. Renal insufficiency after contrast media artery disease. However, several softwares have been devel- administration trial II (REMEDIAL II): RenalGuard System in high-risk patients for contrast-induced acute kidney injury. oped that permit online co-registration of intravascular imag- Circulation. 2011;124:1260–9. ing, hemodynamic indices and angiographic data. These 15. Jolly SS, Yusuf S, Cairns J, Niemela K, Xavier D, Widimsky systems provide representation of coronary angiography, P, et al. Radial versus femoral access for coronary angiogra- combined with details about lesion morphology and plaque phy and intervention in patients with acute coronary syndromes (RIVAL): a randomised, parallel group, multicentre trial. Lancet. composition, as given by intravascular imaging modalities 2011;377:1409–20. such as intravascular ultrasound and optical computed 16. Jolly SS, Amlani S, Hamon M, Yusuf S, Mehta SR. Radial ver- tomography [32, 33]. While these approaches have still sus femoral access for coronary angiography or intervention and application mainly in the field of research, the role of stan- the impact on major bleeding and ischemic events: a system- atic review and meta-analysis of randomized trials. Am Heart J. dard coronary angiography and right heart catheterization in 2009;157:132–40. everyday clinical practice remains fundamental. 17. Heyndrickx GR, Peace AJ, Girasis C, Naber CK, Bourantas CV, Serruys PW. Invasive diagnostic coronary angiography. The PCREAPCI Textbook. Available at https://www.pcronline.com/ eurointervention/textbook/pcr-textbook/. References 18. Saleem T, Baril DT. Vascular access closure devices. Copyright © 2018: Treasure Island (FL): StatPearls Publishing LLC; 2019. 1. Bertrand ME, Meier B. A history of cardiac catheterization. The 19. Robertson L, Andras A, Colgan F, Jackson R. Vascular closure PCR-EAPCI Textbook. Available at https://www.pcronline.com/ devices for femoral arterial puncture site haemostasis. Cochrane eurointervention/textbook/pcr-textbook/. Database Syst Rev. 2016;3:CD009541. 2. Judkins MP. Selective coronary arteriography. I. A percutaneous 20. Kelly AE, Gensini GG. Coronary arteriography and left-heart stud- transfemoral technic. Radiology. 1967;89:815–24. ies. Heart Lung. 1975;4:85–98. 1 Cardiac Catheterization 13 21. Ryan TJ, Faxon DP, Gunnar RM, Kennedy JW, King SB 3rd, Loop 27. O'Quin R, Marini JJ. Pulmonary artery occlusion pressure: clinical FD, et al. Guidelines for percutaneous transluminal coronary angio- physiology, measurement, and interpretation. Am Rev Respir Dis. plasty. A report of the American college of cardiology/American 1983;128:319–26. heart association task force on assessment of diagnostic and thera- 28. Nemens EJ, Woods SL. Normal fluctuations in pulmonary artery peutic cardiovascular procedures (subcommittee on percutaneous and pulmonary capillary wedge pressures in acutely ill patients. transluminal coronary angioplasty). Circulation. 1988;78:486–502. Heart Lung. 1982;11:393–8. 22. Leaman DM, Brower RW, Meester GT, Serruys P, van den Brand 29. Snyder RW 2nd, Glamann DB, Lange RA, Willard JE, Landau C, M. Coronary artery atherosclerosis: severity of the disease, sever- Negus BH, et al. Predictive value of prominent pulmonary arterial ity of angina pectoris and compromised left ventricular function. wedge V waves in assessing the presence and severity of mitral Circulation. 1981;63:285–99. regurgitation. Am J Cardiol. 1994;73:568–70. 23. Sianos G, Morel MA, Kappetein AP, Morice MC, Colombo A, 30. Yelderman ML, Ramsay MA, Quinn MD, Paulsen AW, McKown Dawkins K, et al. The SYNTAX Score: an angiographic tool grad- RC, Gillman PH. Continuous thermodilution cardiac output ing the complexity of coronary artery disease. EuroIntervention. measurement in intensive care unit patients. J Cardiothorac Vasc 2005;1:219–27. Anesth. 1992;6:270–4. 24. Farooq V, van Klaveren D, Steyerberg EW, Meliga E, Vergouwe Y, 31. Flamm MD, Cohn KE, Hancock EW. Measurement of systemic Chieffo A, et al. Anatomical and clinical characteristics to guide cardiac output at rest and exercise in patients with atrial septal decision making between coronary artery bypass surgery and percu- defect. Am J Cardiol. 1969;23:258–65. taneous coronary intervention for individual patients: development 32. Carlier S, Didday R, Slots T, Kayaert P, Sonck J, El-Mourad M, and validation of SYNTAX score II. Lancet. 2013;381:639–50. et al. A new method for real-time co-registration of 3D coronary 25. Kearney TJ, Shabot MM. Pulmonary artery rupture associated with angiography and intravascular ultrasound or optical coherence the Swan-Ganz catheter. Chest. 1995;108:1349–52. tomography. Cardiovasc Revasc Med. 2014;15:226–32. 26. Sharkey SW. Beyond the wedge: clinical physiology and the Swan-­ 33. Tu S, Holm NR, Koning G, Huang Z, Reiber JH. Fusion of 3D Ganz catheter. Am J Med. 1987;83:111–22. QCA and IVUS/OCT. Int J Cardiovasc Imaging. 2011;27:197–207.  Fractional Flow Reserve 2 Vasileios F. Panoulas emia as demonstrated in prior non-invasive testing. However, High Yield Facts commonly the lesions encountered in coronary angiograms Visual angiographic stenosis assessment is a poor are intermediate (Fig. 2.1), with luminal stenosis in the range predictor of the functional significance of a of 40–80% diameter reduction [1, 2]. In this subtype of stenosis. lesions coronary artery physiologic data, usually coronary Sensor tipped angioplasty guidewires have been artery pressure and flow, can aid decision on the need for developed and are used to measure pressure and revascularization, particularly in individuals without prior flow across a coronary stenosis in the catheteriza- non-invasive stress test. Furthermore, visual estimation of tion laboratory. stenosis severity has been shown to be highly variable A normal fractional flow reserve (FFR) value is 1, between different operators (inter-observer) but also in while a positive test is considered when the FFR repeated assessments (intra-observer). Visual angio- 40 mm Aortic stenosis Aortic valve and root Choice between Assessment of Valve Pathology dimensions, prostheses; valve or root myocardial thickness, replacement; moderate-­ Aortic Stenosis diastolic function severe left ventricular hypertrophy may cause myocardial protection The appearance of the valve is considered first—the mor- issues; diastolic phology and motion of the leaflets, any degenerative changes dysfunction may prolong and the degree of calcification, which is categorized qualita- ITU stay if filling is very impaired especially if tively as mild, moderate or severe. Color flow Doppler is there is perioperative used to assess turbulence through the valve and then pulse atrial dysrhythmia and continuous wave Doppler is used to measure the velocity Aortic Aortic root Choice of operative of blood flow in the left ventricular outflow tract (LVOT) and regurgitation dimensions, valve strategy—valve through the valve respectively. The pressure drop or “gradi- morphology, replacement or repair, ventricular function root replacement, ent” across a narrowed valve is calculated using a simplified valve-sparing root Bernoulli equation, where pressure drop (gradient) ΔP = 4V2 surgery? (V is the maximum velocity of blood flow through the valve) Endocarditis Evidence of Informs operative (Table 3.2). In cases where the LVEF and flow rate are nor- complications e.g. planning regarding likely fistulae and abscess length and complexity of mal, a velocity of 4 m/s across the aortic valve (gradient of formation surgery 64 mmHg) is indicative of severe aortic stenosis (AS). The ITU intensive therapy unit, LVEF left ventricular ejection fraction, RV shape of the CW Doppler waveform is also a clue to sever- right ventricular ity—as AS advances from “just-about-severe” to “critical” a This is NOT comprehensive the shape of the trace changes from being asymmetrical with a faster upstroke to becoming symmetrical or “dagger-­ Flow-corrected EOA = Subaortic CSA ´ VTI1 / VTI 2 shaped” (Fig. 3.9) However, in many cases, the LVEF and flow rate are reduced and in these cases it can be much more The calculation uses the square of the radius of the LVOT, difficult to appreciate the degree of valve stenosis. Other use- which relies on accurate measurement of the LVOT diame- ful measures are the effective orifice area (EOA) and the ter. Any error in this measurement is compounded by the dimensionless velocity index (Table 3.3). Calculation of squaring operation and hence is a significant source of error EOA is done using the continuity equation, shown below, in the calculation of EOA. The dimensionless velocity index where CSA is the cross-sectional area of the LVOT, VTI1 is is the ratio of maximum flow velocity in the LVOT to maxi- the subaortic velocity-time integral and VTI2 is the transaor- mum flow velocity through the stenotic valve. It eliminates tic velocity-time integral. error due to inaccurate measurement of the LVOT diameter. 3 Echocardiography 31 Fig. 3.9 The symmetrical “dagger-shaped” CW Doppler trace seen in very severe aortic stenosis Table 3.3 Criteria for assessing severity of aortic stenosis may be used to calculate EROA and regurgitant volume. Criterion Mild Moderate Severe The most commonly-­quoted parameter is the pressure half- Vmax (m/s) 2.5–3.0 3.0–4.0 >4.0 time, measured from the CW Doppler trace. This can be Peak gradient (mmHg) 64 misleading in advanced disease, because the pressure half- Mean gradient (mmHg) 40 time is shortened in the presence of raised end-diastolic Effective orifice area (cm2) >1.2 0.8–1.2 0.5 0.25–0.5 40 mmHg 5 μg/kg/min). It has been demon- inhibitors and calcium sensitizers (levosimendan). strated to increase cardiac output in patients with septic 7 Inotropes, Vasopressors and Vasodilators 75 shock. This effect appears to be due to increased stroke vol- As they are metabolised in the liver and excreted by the ume as it has minimal effect on SVR. While dopamine kidney, liver and renal dysfunction will lead to accumulation increases urine output in different settings, the promise of of these agents in the circulation with potentially disastrous prevention of renal failure in critically ill patients has not consequences. Therefore, SVR should also be tightly moni- realised. To the contrary, the use of dopamine as a first-line tored and controlled and plasma levels of milrinone moni- vasopressor increased mortality in patients with cardiogenic tored if its prolonged use is warranted by the clinical scenario. shock when compared to noradrenaline in a large interna- Such vigilance with the use of this class of drugs cannot be tional multicenter trial. This recognition has led to a dra- overemphasized as it has been suggested that the use of mil- matic reduction in the use of dopamine in patients with rinone in cardiac surgery was associated with an increase in perioperative cardiac failure. mortality. Dobutamine Dobutamine is a synthetic catecholamine possessing the Levosimendan same basic structure of dopamine with a bulky ring substitu- tion on the terminal amino group. Due to its attractive com- The main mechanisms of action of levosimendan include bination of haemodynamic properties including strong increasing the sensitivity of cardiac troponin C to calcium as positive inotropy with mild chronotropy and overall periph- a “calcium-sensitizer” and opening of K+-ATP channels in eral effect of an increase in blood flow to skeletal muscle and smooth muscle cells and mitochondria [19, 20]. This mecha- splanchnic circulation, dobutamine has become the standard nism of action conveys positive inotropy plus vasodilation inotrope in perioperative medicine. While it is believed to be (“inodilator”) and cardioprotection with anti-stunning and a pulmonary vasodilator, the decrease in PVR generally anti-inflammatory effects. In contrast to other inotropes, results from increases in cardiac output due to an enhanced levosimendan does not raise intracellular calcium-levels contractility. High doses can cause severe tachycardia thus, myocardial oxygen consumption is not increased and and might even result in pulmonary vasoconstriction, therefore, it does not produce adverse events with tachyar- depending upon the baseline tone. rhythmias. Moreover, levosimendan improves microcircula- tion and renal function. While recent large RCTs (LICORN, CHEETAH, and Phosphodiesterase-Type III Inhibitors LEVO-CTS) demonstrated that levosimendan was safe and well tolerated in patients with low LV ejection fraction Selective phosphodiesterase-type III inhibitors (enoximone, undergoing cardiac surgery with CPB, they failed to show milrinone) increase intracellular levels of the second mes- improvement in major clinical outcomes for regulatory senger cyclic adenosine monophosphate. The degree of this approval [21, 22]. However, subsequent consensus state- response depends on the expression and activity of this ments and meta-analyses still advocate physiological and enzyme in the myocardium and vasculature and on the clinical benefits in reducing low output syndrome following ­stimulation level of the adenylate cyclase by endogenous and surgery, especially in the CABG population with severe ven- exogenous agonists. In particular these drugs cause a posi- tricular dysfunction (LVEF 200 ms as a result of delayed conduction through the AV node. It is not a common indication for pacing but is not benign 320 ms Second degree AV block (Mobitz type I): Here there is progressive prolongation of the PR interval until there is failure to conduct an atrial beat and a ventricular beat is dropped. 120 ms 280 ms 320 ms Pause Second degree AV block (Mobitz type II): Here there are regularly dropped ventricular beats. There is no change in the PR interval prior to transient failure of conduction. This is a definite indication for pacing as this has a high likelihood of progression to complete heart block (CHB). P P QRS Complete heart block: Here there is no coordinated conduction from the atria to the ventricles. There is complete atrio— ventricular dissociation and often a wide QRS results as the ventricular complex is idioventricular in origin. Definite indication for pacing. 84 D. Keene et al. Table 8.2 Guideline recommendations for pacing high risk of sudden cardiac death. These devices can also ECG findings and symptoms provide pacing function whether required for bradycardia Guideline Atrio-ventricular reasons or to try and improve cardiac function. recommendation Sinus node disease block Class I (Must) Documented Complete Heart Block symptomatic sinus Mobitz type II (even if bradycardia asymptomatic) Basic Principles of Pacing Symptomatic Mobitz type I Pacing systems consist of a generator (battery) and up to Class II (Should/ Documented Bi/Trifasicular block three leads, with the number of leads often used to describe Could) bradycardia in a and symptoms symptomatic patient but reported consistent the type of pacemaker (single chamber (1), dual chamber (2), no symptoms during with complete heart or biventricular pacemaker (3)) (Fig. 8.2). The system is documented bradycardia block designed to detect the underlying heart rhythm (sense) and (Rarely) symptomatic deliver a stimulus to capture the myocardium if required first degree AV block (pace). In an ICD the generator includes components to Class III Asymptomatic patient Asymptomatic first (Should Not) with documented degree AV block or allow defibrillation and leads include coils to facilitate this. bradycardia Mobitz type I A single chamber permanent pacemaker (PPM) will usu- Asymptomatic Bi/ ally only pace the ventricle and is often used in patients with Trifasicular block permanent AF. A dual chamber PPM will pace the right Reversible causes: drugs/Lyme disease / metabolic/electrolyte imbalance atrium and right ventricle (Fig. 8.3). A biventricular pace- maker (CRT) will pace the right atrium, the right ventricle, and the left ventricle (via the coronary sinus). Causes of cardiac conduction disease briefly include intrinsic and extrinsic causes. Intrinsic causes are mostly commonly idiopathic and degenerative (calcification), but Commonly Used Terms also include ischemic heart disease (30%), or infiltrative con- ditions. Extrinsic causes include rate limiting drugs, Threshold increased vagal tone, infections (Lyme disease) and meta- bolic derangements. Conduction disease may either be due This is the minimum electrical stimulus needed to consis- to failure to generate an impulse (problems with the sino-­ tently stimulate the heart to provide cardiac contraction. It atrial node) or failure to propagate an impulse (problems must be large enough (voltage) for a long enough (pulse with the AV node). width) period to cause depolarisation of the myocardium. Bradycardia can lead to presyncope, syncope and injury. The output delivered by a pacing device must have an ade- Sinus node disease is considered benign and pacing is indi- quate safety margin, usually twice the threshold. cated to improve symptoms not prognosis. High grade AV block (complete heart block (CHB) or Mobitz type II block) can be fatal and irrespective of symptoms pacing is indicated Sensitivity. The danger of AV block is due to progression to CHB with an unstable escape rhythm. Bundle branch block does In order for a pacemaker to know whether it needs to deliver not cause bradycardia per se but can lead to dyssynchronous a pacing stimulus (i.e., if an intrinsic heart beat is missing) cardiac activation. In patients with left ventricular impair- the pacemaker must be able to “see” the hearts intrinsic elec- ment and left bundle branch block (LBBB), positioning a trical signals. “Sensing” is the ability of the pacemaker to pacing lead via the coronary sinus (so it activates the heart at detect cardiac electrical signals (measured in millivolts). Any a site on the left ventricle) can in part correct this (cardiac electrical activity below the set value for the sensitivity is resynchronisation therapy (CRT)) and improves patient ignored. This helps to prevent sensing of T waves or far field symptoms and prognosis [4, 5]. signals from the chamber not being paced which would oth- Defibrillators are implanted to reduce the risk of sudden erwise inhibit pacing (Fig. 8.4). cardiac death in those with a prior history of ventricular arrhythmia associated with haemodynamic compromise (secondary prevention) and those at high risk of ventricular Implantation Techniques arrhythmias (primary prevention). High risk patients include those with LV impairment (EF < 35%) or alterna- Pacemakers and ICDs are usually implanted under local tively those with a diagnosis of an inherited disease (cardio- anaesthesia. Depending on procedure type, implantation myopathy or channelopathy) which may put a patient at a typically takes 45–120 min. Pacemakers are typically 8 Cardiac Pacing in Adults 85 Single chamber device: single lead Dual chamber device: leads Triple chamber (commonly commonly placed in right ventricle. commonly placed in right known as biventricular pacing Occasionally single lead placed in atrium and right ventricle. or cardiac resynchronization right atrium. therapy): leads placed in right atrium and then the right ventricle and coronary sinus to activate the left ventricle. Fig. 8.2 Types of pacemaker Fig. 8.3 A dual chamber pacemaker implanted on the left side of the chest wall through a 4–5 cm are used to deliver the leads to their appropriate position. incision made horizontally approximately 2 cm infraclavicu- Leads are fixed to the myocardium using either an active fix larly. Dissection down to the pre-pectoral plane is performed screw or tines (small hooks) that passively grip the lead to and within this plane a pocket fashioned for the device. the heart muscle. Once the leads are in situ the electrical Venous access is then obtained via a cephalic vein following (sensing and capture) parameters are checked. The leads are cut down and venotomy or puncture of the axillary or subcla- secured in place to muscle with sutures prior to connecting to vian vein. Sheaths positioned using a Seldinger technique the generator and closing the wound [6, 7]. 86 D. Keene et al. Fig. 8.4 Pacemaker sensitivity 5.0mV 2.5mV 1.25mV Time Sensitivity can be explained with this image. At a sensitivity level of 5.0mV no cardiac signals are seen. At a sensitivity level of 2.5mV only the QRS electrogram signal is seen. At a sensitivity of 1.25mV the P wave, QRS and perhaps T wave would be sensed. This would mean for a ventricular lead this amount of sensitivity is too great. A pacemaker interprets all signals as QRSs if it is a ventricular lead or as P waves if an atrial lead. If programmed with a sensitivity of 1.25mV and this was a ventricular lead — the pacemaker might think there were three QRSs when in fact there is only one. The lower the programmed number the greater sensitivity and more electrical signals will be seen. Long term lead complications: Over time leads can  ommon Complications and Problems C become damaged, eventually leading to the leads failing to with Devices capture, or in the case of ICD leads where noise is inappro- priately detected as VT/VF, inappropriate shocks. This is Venous thrombosis occurs peri-procedurally in 1/50 cases usually manifested early on as falls in the impedance when affecting the ipsilateral arm. This may cause swelling in the the insulation is damaged or rises in the impedance when the arm, but it usually settles in a few days and is rarely a serious lead is beginning to fracture. problem. Pacemaker infection: 1% of patients will develop an infection post implant. This almost always requires removal Novel Device Approaches of the whole system to reduce the risk of endocarditis. Pneumothorax: 1% of patients during pacemaker His Bundle Pacing implantation will suffer a pneumothorax when venous access for the leads is attempted. This is more common with subcla- Pacing the His bundle has recently emerged as a method for vian access. Management is guided by the size of the pneu- delivering more physiological pacing. This approach has mothorax and the clinical status. been demonstrated to be safe and feasible even in patients Pericardial effusion/tamponade: Positioning pacing with distal infra-hisian block and can also reverse bundle leads can lead to the development of a pericardial effusion. branch block [9, 10]. Large randomised controlled trial This can be asymptomatic, and no intervention is required as (RCT) data is awaited to demonstrate its superiority over the perforation spontaneously repairs itself. However, for both RV pacing or even biventricular pacing. 1/500 cases a pericardial drain is required. Lead displacement: In 1% of patients leads displace. This usually occurs within the first 6 weeks prior to fibrosis Leadless Pacing occurring around the lead. Lead displacement in a pacing dependent patient may lead to development of presyncope or Leadless pacing systems have been developed which can syncope as the lead may fail to sense missed events or fail to avoid the complications of conventional transvenous system. capture myocardium when pacing is attempted. The Micra (Medtronic) is an example of a, transcatheter, 8 Cardiac Pacing in Adults 87 Fig. 8.5 Deployment of a leadless pacemaker Fig. 8.6 A subcutaneous implantable cardioverter defibrillator (ICD). This image shows the location of the ICD generator. It is often posi- tioned underneath the latissimus dorsi muscle and the lead passed sub- single chamber ventricular pacemaker (Fig. 8.5). The cap- cutaneously utilising 2–3 small skin incisions so that it runs inferior to sule has tines at the end that allow it to attach to right ven- the heart and then superior to the left side of the sternum. These devices tricular endocardium. For now it can only function as a single cannot deliver long-term pacing to patients chamber ventricular pacemaker but this technology is likely to evolve. Perioperative Management of Devices Subcutaneous ICDs Pacemakers and ICD generators have filters to minimise the Subcutaneous ICDs have emerged as an alternative to trans- effect of electrical and magnetic interference. However, if venous defibrillators to avoid complications of transvenous the interference is of a magnitude or frequency which cannot devices. These are particularly useful if there is no addi- be filtered it can potentially cause inhibition of pacing, tional pacing indication. The defibrillator lead is tunnelled induction of a fixed rate pacing, software reset or inappropri- subcutaneously lateral to the sternum and then across to the ate ICD shocks. Electromagnetic interference will usually left axillary region where it is connected to the generator only have a transient effect on device function. Very power- (Fig. 8.6). ful fields (e.g., gamma radiation) may have permanent effects [14–16]. When surgical diathermy/electrocautery is to be used WiSE CRT remote from the implanted device, there is only a low risk of problems. Bipolar diathermy reduces the risk compared to The WiSE CRT system is an endocardial leadless option for unipolar. Other precautions include limiting diathermy use to left ventricular pacing (Fig. 8.7). This can be used where short bursts and placing the return electrode away from the conventional LV pacing cannot be performed via the coro- device so the components are kept away from the diathermy nary sinus. The device requires an extended period of dual circuit [17, 18]. antiplatelets or anticoagulation. Randomized controlled tri- If detectable pacemaker inhibition occurs during dia- als are needed to assess long-term clinical outcomes, and thermy, the surgeon should either discontinue diathermy, use further advances are needed for selecting the optimal endo- shorter bursts or the device should be programmed in an cardial location for pacing. obligatory pacing mode (e.g., VOO). 88 D. Keene et al. Co-Implant Co-Implanted Co-Implant pacemaker or ICD Receiver Electrode paces the RV Length: 9.1mm Diameter: 2.7mm Receiver Electrode Paces the left ventricle Transmitter Synchronizes with RV pacing pulse to transmit ultrasound energy to receiver electrode Transmitter Battery Battery Powers the transmitter Clinical Response Structural Remodeling Electrical Remodeling 85% of patients Absolute increase in LV EF Shortening of intrinsic QRS experienced an improvement by 7%, and relative by at least 20 ms in 55% of in clinical composite score decrease in LV ESV of 15% patients Fig. 8.7 WiSE cardiac resynchronization therapy (CRT) system. The electrode converts the ultrasound energy into an electrical pacing pacing system consists of a receiver electrode and an ultrasound trans- impulse. The effects are shown in the diagram. ESV end systolic vol- mitter which is battery powered. The transmitter detects when standard ume, ICD implantable cardioverter defibrillator. (Reproduced from right ventricle (RV) pacing is delivered from a co-implanted pacemaker. Reddy et al. J Am Coll Cardiol 2017;69:2119–2129. Copyright © The transmitter then transmits ultrasound energy to a receiver electrode, 2017 American College of Cardiology Foundation. Published by which is implanted in the left ventricular endocardium. The receiver Elsevier Inc.) MRI and Pacing  acing in the Peri- and Post-operative P Setting There is potential for MRI-induced cardiac lead heating and movement which may alter pacing properties (inappropriate  eri-operative and Post-operative Pacing P sensing/activation of the device) or even damage the myocar- in Cardiac Surgery dium. This concern has previously limited those patients with a pacemaker from having an MRI. Many modern pace- Epicardial pacing wires are placed during surgery to pro- makers (post 2008) can now safely withstand standard MRI vide pacing for transient bradyarrhythmia post-cardiac sur- scanning movement if a set of specified MRI conditions are gery. These are usually placed on the ventricles and the met. Often the device needs to be reprogrammed prior to the atria. patient undergoing the scan. Most scanning centres insist The wires are embedded in the myocardium and then tun- that there are no redundant pacing leads and that the devices nelled through the body wall to bring the wire to the skin and leads have been manufacturer approved as MRI compat- surface. The leads need to be sufficiently well anchored in ible. That said, there is increasing evidence that even those the myocardium to avoid premature dislodgement whilst with non-MRI-conditional devices can safely undergo MRI allowing removal by gentle traction alone. In the immediate scans. post-operative period patients with pacing need are often left 8 Cardiac Pacing in Adults 89 to pace at 60–80 beats per minute to try and maximise car- dium is not captured. Causes include acute fibrosis around diac output. When weaning from pacing to intrinsic cardiac the pacemaker lead, ischaemia; metabolic imbalance, and rhythm often a period of “back-up” pacing is programmed at drugs including flecainide. ~40 bpm. If further pacing is required, it can be commenced Progressively increasing thresholds is often a sign of safely. impending loss of capture. To avoid this, reversible causes Epicardial wires are subject to an inflammatory reaction should be corrected. Reversing the polarity of the lead or that effects the wire-myocardium interface. This process is switching to a unipolar approach with positioning of a sub- usually accelerated with delivery of higher energy pacing. cutaneous patch could be considered. These are usually tem- Unfortunately, the only remedy for increased resistance porary solutions and alternatives are often required (i.e., (apart from siting a new pacing lead often via a transvenous temporary transvenous pacemaker, or implant of a perma- approach) is the application of increased current or volt- nent system) [21, 22]. age—which further increases the inflammation. Epicardial wires often fail to sense and/or capture within a week. Increases in stimulation threshold typically occur after  ransitioning to Permanent Pacing in the Post-­ T 5 days. Failure to pace has been observed in >60% of atrial operative Period wires after 5 days [21, 22]. The daily checks required are outlined in Table 8.3. Post-operative conduction disorders can affect up to ~25% of patients in some series. Optimal timing for PPM insertion in the post-operative setting has not been clearly defined due to Troubleshooting Temporary Epicardial the relatively poor understanding of the natural history of Systems post-operative conduction disturbances. There is significant variability in how pacemaker dependency is assessed and If pacing is not being delivered as expected, failure to pace defined. Of the 5% of patients who receive permanent pacing and failure to capture should be considered as causes. the long-term pacing dependency rates reported in the cur- Failure to pace occurs when the pacemaker lead does not rent literature vary from 32 to 91%. deliver an electrical output to the myocardium. No pacing The risks and costs of permanent pacemaker implantation spikes are seen on the ECG, and the heart rate is lower than (which may not be necessary) need to be balanced against the pacing rate. Causes include an unstable connection the prospects of a prolonged hospital stay with epicardial between lead and generator; battery depletion, oversensing wires. or cross-talk (where electrical signals are misinterpreted as P Numerous causes contribute to postoperative bradycardia waves or QRS complexes resulting in inhibition of pacing (Table 8.4, Fig. 8.8). delivery). Existing guidelines reflect the lack of evidence and con- Failure to capture occurs when there is electrical output sensus in this area. Guidelines provide a class I indication for from the device and lead (pacing spikes seen) but myocar- PPM implantation in “postoperative atrioventricular block Table 8.3 Daily checks required on epicardial leads Underlying The presence of a stable rhythm This is best done by turning down the pacing rate and watching for the intrinsic rhythm to rhythm will determine the need for appear (or to turn down the pacing output until capture is lost but this may be limited if there is ongoing pacing requirements no underlying rhythm). Sensitivity This is a number (measured in To check sensitivity the pacemaker rate should be programmed below the intrinsic heart rate if mV) representing the minimum present and the sensitivity number then turned down (making the pacemaker more sensitive) current (electrical activity) that until the sense indicator notes each intrinsic depolarisation (in time with the P or R wave on the pacemaker is able to sense the surface ECG). The lower the number The number at which this first occurs is the sensitivity threshold. It is recommended to set the programmed means greater pacing generator at half this threshold, to allow for detection of abnormally small signals, and sensitivity and more electrical for the possibility that progressive lead fibrosis over the course of the day will reduce the signals will be seen current transmitted to the pacemaker. If there is no endogenous rhythm, it is impossible to determine the pacemaker sensitivity, in which case the sensitivity is typically set to 2 mV. Capture This is the minimum energy The capture threshold should not be checked if there is no underlying rhythm for fear of losing threshold output required to stimulate an capture and not being able to regain it. If this is the case, careful continuous attention should action potential in the be paid to the development of occasional missed beats, which will indicate a rise in the capture myocardium threshold and a need to increase the pacing output further or find an alternate means to safely activate the heart. If safe to check the pacing threshold, the pacemaker rate should be set above the patient’s intrinsic rate, so that the chamber of interest is consistently paced. The pacemaker energy output is then reduced until a QRS complex no longer follows each pacing spike. This is the capture threshold. Typically, the output is left at twice the threshold this allows a margin of safety. 90 D. Keene et al. Table 8.4 Causes of postoperative bradycardia Right atrial May cause sinus node dysfunction but usually resolves within 7 days [23, 24]. cannulation for cardiopulmonary bypass Aortic valve Particularly calcific aortic valve stenosis is often associated with underlying conduction disease even if not overtly apparent disease/ on a surface ECG. The aortic valve sits in close proximity to the bundle of His and local damage to this structure may be to Intervention blame for increased conduction disease. Damage may be caused by trauma including laceration of conduction system fibres by sutures used to anchor the valve prosthesis or pressure from residual calcific material and impingement of the prosthetic valve seat on conduction tissue. This could be the mechanism for conduction disease even in sutureless valve surgery [24–26]. Peri-operative Ischemic injury to the conduction tissue can contribute to a transient need for pacing, most likely facilitated by left main or ischemic injury proximal LAD artery disease. There has been no independent association between coronary artery disease and late pacemaker dependency however. Other peri-­ Extended duration of cardioplegia may contribute to the incidence of heart block postoperatively. The longer the duration operative factors the greater the exposure to the high concentration of potassium ions in cardioplegic solution which raises extracellular potassium concentration in the conduction tissue reducing the automaticity of the AV nodal cells and suppressing the excitability and conductivity of the conduction system leading to increased pacing needs immediately post-operatively and in a single study long-term pacemaker dependency. Patient factors Preoperative conduction disease has been shown to predict postoperative pacemaker dependency particularly those with first degree AV block and QRS duration >120 ms. Fig. 8.8 Diagram highlighting pre-operative, Pre-operative Factors peri-operative and post-­ First Degree AV block operative factors that may Bundle Branch Block lead to a patient needing a Aortic Valve Disease pacemaker after cardiac Left main or Left Anterior Descending At risk patient Coronary disease surgery Peri-operative Factors Cardiopulmonary Bypass time Cardioplegia Aortic Valve Replacement Surgery Suture trauma Post-operative heart block Post-operative Factors Duration of heart block Persistent high grade AV block New bundle branch block Pacemaker Recovery of Dependency conduction 8 Cardiac Pacing in Adults 91 that is not expected to resolve”, however there are no recom- Table 8.5 Risks associated with percutaneous extraction mendations regarding identification of the patients at higher Reported frequency risk for delayed or non-resolution of post-operative block Major. If adopting a conservative approach to permanent pace- Death 0.8% maker insertion a waiting period of 5–7 days may be reason- Cardiac tamponade 1.4% Haemothorax 0.4% able. Beyond this, epicardial wires may begin to fail. Pulmonary embolus 0.1% Lead ragment migration 0.1% Total major complications 1.9%  ardiothoracic Surgeon Involvement C Minor in Pacing Procedures Perforation 0.4% Myocardial Avulsion 0.1% There are two procedures, discussed below, where cardiotho- Venous Avulsion 0.1% Other 0.9% racic surgeons work closely with cardiologists in pacing Total minor complications 1.4% procedures. Any complication 3.3% Surgical Lead Implantation The most common approach for lead placement is transve- nous. However, with venous occlusions or multiple leads overcrowding and impeding blood flow alternative solutions are often required. Furthermore, in cardiac resynchronisation therapy, there are occasions where there is unfavourable cor- onary sinus anatomy for positioning the left ventricular lead. In these situations, surgical epicardial pacing lead placement can be considered. If concomitant cardiac surgery is being performed the leads are placed at the end of case. If the leads are affixed to the heart in areas of bare muscle not covered with epicardial fat or scar, contact and electrical conditions are usually very good. Epicardial leads are usually of a sew-on or screw-in type, (commonly bipolar sew-on atrial leads and bipolar screw-in ventricular leads). If left ventricular pacing is required, the lead should be targeted to the lateral or postero- lateral basal left ventricle between the first and second obtuse marginal coronaries. In general, available epicardial lead sys- Fig. 8.9 Radiographic image of an occlusion balloon having been tems demonstrate decreased longevity and worse chronic lead deployed to tamponade a superior vena cava tear. This is done to allow performance compared with endocardial pacing [30, 31]. time for a surgeon to perform emergency surgery to perform emergency surgery and cardiopulmonary bypass Lead Extraction should be aware and available if needed. The risk associ- ated with percutaneous extraction are highlighted in Device infections and in many cases lead failure will neces- Table 8.5. A surgical approach may be required if per- sitate lead extraction. Leads that have been in for >1 year can cutaneous techniques fail. Primary thoracotomy should adhere due to fibrosis within the heart and the vascular tree. also be considered when there is a large lead vegetation A percutaneous extraction is normally attempted first. This (>2.5 cm) or a vegetation associated with the lead and a may involve traction-counter traction approaches using a right-to-left intracardiac shunt. locking stylet and mechanical extraction tool or the use of a Death and major complications often result from vascular laser sheath to free a lead from fibrotic adherence. tears or cardiac perforation. A tear in the SVC can lead to Lead extraction may be performed in either a special- rapid life-threatening haemorrhage and requires immediate ized cardiac catheter laboratory or in cardiac theatres. surgery. Occlusion balloons exist to rapidly stem blood loss Regardless of the venue, equipment, and personnel needed as a bridge to surgical intervention (Fig. 8.9). 92 D. Keene et al. Conclusion 16. Zaremba T, Jakobsen AR, Søgaard M, Thøgersen AM, Riahi S. Radiotherapy in patients with pacemakers and implant- able cardioverter defibrillators: a literature review. Europace. Cardiac pacing and arrhythmia management are of paramount 2016;18:479–91. importance in the peri- and post-operative setting. Whether or 17. Salukhe TV, Dob D, Sutton R. Pacemakers and defibrillators: not arrhythmia is the primary concern, the cardiothoracic sur- anaesthetic implications. Br J Anaesth. 2004;93:95–104. 18. American Society of Anesthesiologists. Practice advisory for the geon needs to be proficient in arrhythmia recognition, tempo- perioperative management of patients with cardiac implantable rary pacing, and basic device troubleshooting of previously electronic devices: pacemakers and implantable cardioverter-­ implanted cardiac devices. At the same time with increasing defibrillators: an updated report by the american society of anes- numbers of implants, close collaboration is required between thesiologists task force on perioperative management of patients with cardiac implantable electronic d