CORE TOPICS INContents Contributors Preface 1_Who needs cardiothoracic critical care?_3 MLBIESMAVE AND D. SCHMIDLIN, 2_ Scoring systems and prognosis _7 ‘A.HARKER AND S.A.M NASHE 3__Admission to critical care: The cardiology patient _13 SPHOOLEAND Pal scHORELD ly ehicaeke a i u 5 PARAMESHWAR 5_Admission to critical care: The respiratory patient _29 ‘S.KAUL AND L. HOWARD 6 Resuscitation after cardiac surgery 38 MACKAY 7Z_Transport of the cardiac critical care patient _45 SHIRLEY ‘ s 8_Managing the airway 55 ‘A-PEALGE AND 5, NeCORKELL 9 Tracheostomy 65 LLVARIEY AND P. FALTER 10 Venous access 70 ARROWS MINH skim wem ai Material chroniony prL_Invasive haemodynamic monitoring 80 EAWHITRAND A. KLEIN 12__ Pulmonary artery catheter_86 Sueeaeetee 13__Minimally invasive methods of cardiac output and haemodynamic monitoring 97 ML THAVASOTHEY 14_Echocardiography and ultrasound 103 "ST RUNNELS, K, VALCHANOV AND RHA 15 Central nervous system monitoring 109 MLLEEMANS AND GR. WalLey 16_Point of care testing 119 (CHARLES WILLMOTT AND LE, ARROWSMITHT SECHION 3 System Management in Cardiothoracic Critical Care 2.1 CARDIOVASCULAR SYSTEM IN CARDIOTHORACIC CRITICAL CARE 19 Rhythms 139 20 Basic haemodynamic support _148 ‘-SROOMUEAD 21_Mechanical circulatory support _159 ‘STSUI AND J. PARAMES! 22 Systemic hypertension 169 RLEENECK 23_ Pulmonary hypertension _176 26 Weaning from mechanical ventilation 198, ALLEN AND B, McCRATTAN 27_Acute lung injury 205 28 Extracorporeal membrane oxygenation 213 R.TIRUVOIVATI AND G.1, PEEK Material chroniony pr autorskim wer3.3_RENAL SYSTEM IM CARDIOTHORACIC CRITICAL CARE 29 Renal protection and cardiac surgery 225 ‘SL WERE AND 4 VIVIST 30 Renal replacement therapy 232 ; : 3.4 HAEMATOIGY AND TRANSIUSION IN CARDIOTHORACIC CRITICAL CARE ene: 32 Blood conservation strategies 249 aa Sa 33 Haematological diseases _255 P.KESTEVEN AND UL. POWELL 34_Heparin-induced thrombocytopenia _264 T, STRANG AND A. KOSTER 3.5. GASTROINTESTINAL SYSTEM IN CARDIOTHORACIC CRITICAL CARE is aan 3 es is 36_Gastrointestinal catastrophe _279 E.CAMERON AND PJ. ROBERTS 37 Liver failure 284 ‘ALROSCOE AND |, WILUAMS 38_Abdominal hypertension and abdon ‘MLN.G. MALBRAIN AND M. CHEATHAM inal compartment syndrome _291 2.6 IMMUNE SYSTEM AND INFECTION IN CARDIOTHORACIC CRITICAL CARE 39_‘The role of the immune system in critical illness _303 HE GALLEY 40. Sepsis and the systemic inflammatory response syndrome 312 1H. GERLACH AND S, TOUSSAINT 41_Infection conwol 320 G.M.JOVNT AND C0. COMFRSALL 42. Infective endocarditis 328 J. BYGOTT AND JE. FOWERAKER 2.7_ENDOCRINE SYSTEM IM CARDIOTHORACIC CRITICAL CARE 43 Endocrine function 339 F. GIBSON AND A. KLLIN Material vii hroniory prawem autorskin3.5_NEUROLOGICAL SYSTEM IN CARDIOTHORACIC CRITICAL CARE 44 Sedation and analgesia 347 M. DURAND AND ©. ARVIEUX 45 Neurological complications 354 J. STEARNS AND G.W. HOGUE 46. Psychiatric illness duri ©. WEINER? 1g and after discharge from critical care 364 SECTION 4 Procedure-Specific Care in Cardiothoracic Critical Care 47 Routine management after cardiac surgery 373 Nit, DRURY AND S.AM, NASHEE 48 Management after coronary artery bypass grafting surgery 375 N. DRURY, $.A.\1, NASHEE AND N. BRETTENFELDT 49 Management after valve surgery 378 N. DRURY, §.4.\l. NASHEE AND N. BRETTENFELDT 50 Management after aortic surgery 382 IN. DRURY, 8.4.4. NASHEE AND N. BREFTENFELDT 51 Management after thoracic surgery 386 K, VALCHANOV AND 5. GHOSH 52. Lung volume reduction surgery 392 R.A. SAYEED AND T.K, WADDELL 53. Chronic thromboembolic pulmonary hypertension and pulmonary endarterectomy 397 B. THOMSON AND D.P. JENKINS 54 Oesophagectomy 404 B, DELVAUX, M, DE KOCK AND P.F. LATERRE 55 Management after heart transplant 408 J. GOOT AND K. DHITAL 56 Management after lung transplant 414 1. SPENCER. C. LRONARD AND N. YONAN 57. Prolonged critical care stay after cardiac surgery 419 J. MOORE AND J. EDDLESTON 58 Palliative care 427 S.J. HARPER AND L, CHAPMAN SECTION 5 Discharge and Follow-up From Cardiothoracic Critical Care 59 Discharge 435 D, DRAMEEY AND A, KLEIN 60 Outreach ~ Critical care without walls 441 P, HOLDER AND BH. CUTHBERSTON ol Follow-up 444 J. GRIFFITHS AND S.J. BRETT viiiSECTION 6 Structure and Organisation in Cardiothoracic Critical Care 62. Cardiothoracic critical care nursing 455 AMM. INGLE, M. SCREATON AND J. OSGATHORPE 63 Physiotherapy 458 A. BRICE, D. DYKES AND A. HARVEY 64 Clinical pharmacy 465 L BARLOW, 65. Evidence-based design of the cardiothoracic critical care 470 DIK. HAMILTON AND RS, ULRICH 66 Clinical information systems _477 RBOSMAN 67 Resource management _482 D.GHING 68_Education and training in cardiothoracic critical care in the United Kingdom _487 IEREMY CORDINGLEY AND CHARLES GILLDE SECTION 7 Ethics, Legal Issues and Research in Cardiothoracic Critical Care 69 Patient's perspective 495 WL McBRIDE 20 Ethical management 500 wScort 71 Medicolegalissues 504 ‘A.F. MERRY AND D. SIDPROTHAM 72 Research 512 ‘A.P. MBRRY AND D. SIDEROTHAM Appendix _Works Cited 519 IndexContributors S.J. Allen, Mp, ecaRest Consultant, Cardiothoracic Anaesthesia and Intensive Care Royal Victoria Hospital, Belfast, UK LE, Arrowsmith, Mp, ricp, Rca, Consultant, Cardiothoracic Anaesthesia and Intensive Care Papworth Hospital, Cambridge, UK C.C. Arviews, mo Professor, Head of Department Anaesthesiology and Intensive Care University Hospital of Brest, France GAR, Bailey, recs Consultant Cardiothoracic Anaesthesia Guys and St.Thomas’ Hospiaals, London, UK A.P. Barker, MSc, M8ChB, MRCS Specialist Registrar, Cardiothorucie Surgery Papworth Hospital, Cambridge, UK L. Barrow, npharm (148), RSe (Deakin), MREhaemS Pharmacist, Critical Care Papworth Hospital, Cambridge, UK RJ. Bosman, Mp Consultant, Critical Gare Institution Onze Lieve Viouwe Gasthuis, Amsterdam, the Netherlands DEP. Bramley, Mins, FANzca Staff Specialist, Anaesthesia Western Health Melbourne, Australia N. Breitenfeldt, php, arcs Department of Surgery Royal Devon & Fxeter Hospital, Devon, UK S.J. Brett, MD, PRCA Consultant and Honorary Senior Lecturer in Intensive Care Hammersmith Hospital, London, Imperial College, London, UK A. Brice, nse, mcsP Senior Phy Royal Brompton and Hatefield NHS Trust London, UK josherapise C.J. Broomhead, se, mas, eRCA Consultant, Anaesthesia Barts and the London NHS Trust, London, UK W. Buhre, wp Consuteant, Anaesthesia University Medical Centre, Utrecht, The Netherlands. LM, Bygott, nsted8ci, Mm, BS, MPNTM, FRACGE, MRCPath Specialist Registrar Microbiology, Addenbrooke's Hospital, Cambridge, UK Cameron Mp, MA, MB, BChi«, MRCP Consultant, Gastreenterolosy Addenbrooke's Hospital. Cambridge, UK L. Chapman, mucr Consultant, Palliaive d Medicine Marie Curie Palliative Care Institute, Liverpool, UKM.L. Cheatham, 140, FACS, PCOM Director, Surgical Ineensive Care Units Orlando Regional Medical Center, Orlando, Florida, USA D. Cheng, Mp, se, FRCPC, FCAES Professor & Chait/Chief, Anesthesia & Perioperative Medicine University of Western Ontario, Ontario, Canada D. Collins, sxce, FCARCS!, HIFICM Consultant, Anaesthesia and Ci Vincent's University Hospital, Dublin, Ireland itical Care J. Cordingley, c#ts, FKeA, MD Consultant, Anaesthesia & Critical Care Royal Brompton Hospital, London, UK AN.G. Curry, aa, miiichie, FRCA SPR Anaesthetics & bntensive Care Southampton General Hospital, UK Brian Cuthbertson, sachs, PRCA, MD Senior Lecturer, Health Service Unit University of Aberdeen, UK AJ. Dawson, wachs, FANZcA Specialist Anaesthetist Auckland City Hospital, Auckland, New Zealand M, De Kock Professor, Anaesthesia and Critical Care Cliniques Universitaires St Luc, Brussels, Belgium B, Delvaux, mn Fellow, Anaesthesia and Critical Care Cliniques Universitaires St Luc, Brussels, Belgium K. Dhital, 3s, 5x not, FRCS-CP, PhO Consultant, Cardiothoracic Surgery Papworth Hospital, Cambridge, UK N.E. Drury, Bu(Hons), kes Cantiothonacic Surgery Papworth Hospital, Cambridge, UK M. Durand, ao Anesthesiologist and Head of Cardiovascular Intensive Cae Unit University Hospital of Grenoble, Grenoble, France conTRiBUTORS D. Dykes, Bs¢ (Hons), Clinical Specialis in Candiorespiratory Physiotherapy St Richards Hospital, Chichester, UK J. Faldleston, rca Consultant, Critical Care Manchester Royal Infirmary, Manchester, UK F. Falter, mo Consultant, Anaesthesia and Intensive Care Papworth Hospital, Cambridge, UK R. Feneck, so ‘onsultant, Anaesthesia St. Thomas’ Hospital, Lendon, UK J.E, Foweraker, ma, MB, Chir, PhD, FRCPath Fonsuleant, Microbiology Papworth Hospital, Cambridge, UK M. Furlanut, wo Professor, Director of the lastitute of Clinical Pharmacology & Toxicology Department of Experimental and Clinical Pathology and Medicine, University of Udine, Italy S.P. Fyn, ub Consultant, Cardiology Papworth Hospital, Cambridge, UK H. Galley, om Senior Lecturer in Anaesthesia & Intensive Care School of Medicine, University of Aberdeen, UK S. Ghosh, ssc, aps, FRARCS. Consultant, Anaesthesia Papworth Hospital, Cambrid UK M. Georgieva Resideni, Dept. of Anesthesia and Critical Care Medicine Hadassah Hebrew University Medical School, Jerusalem, Israel H. Gerlach Constiltant, Anesthesiology and Intensive Care Medicine Virchow Clinic, Humboldt University, Berlin Sermany F.M. Gibson, 4, rea, Praxcs(\) Consultant, Anaesthesia and Critical Care Royal Victoria Hospital, BelCcoNTRIsuTORS R, Gill, Rca Consultant, Anaesthesia and Intensive Care Southampton General Hospital, Southampton, UK ©. Gillbe, rnea, sanchn Consultant, Critical Care & Anaesthesia Royal Brompton Hospital, London, UK J. Gooi, anns, raacs Consultant, Cardiothoracic Surgery Alfred Hospital, Melboume, Australia C.D. Gomersall, mv Consultant, Anaesthesia and Intensive Care The Chinese University of Hong Kong, Sha Tin, Hong Kong, LA. Gri Honorary Research Associate, Nuffield Department of Anaesthetics John Radcliffe Hospital, Oxford, UK hs, DIC, PRES, MRCP, MA, MNS R. Hall, FRca Consultant, Anaesthesia and Intensive Care Papworth Hospital, Cambridge, UK D.K. Hamilton Bares, ss Associate Professor of Architecture Texas A&M University, College Station, Texas, USA J. Harper, Mp, ex, PRCA Consultant, Intensive Care Royal Liverpool University Hospital, Liverpool, UK A. Harvey, 8c, Hons, MSe, MCSP Lectarer Practitioner Physiotherapist Royal Brompton Hospital/Brunel University, London, UK P.G, Hébert, Mo, aise Professor af Medicine, Surgery, Anesthesiology and Epidemiology University of Ottawa; Critical Care Physician, The Ouawa Hospital, Senior Scientist, Ottawa Health Research Institute (HRD). Ottowa, Ontario, Canada M. Hiesmayr, mo Professor, Cardiothoracic Anaesthesia & Intensive Care Medical University Vienna, Austria xi CW, Hogue, so Staff. Anesthesiology and Critical C The John Hopkins University Hospital, Baltimore, Maryland, USA P, Holder, wa, cat, »RcA Specialist Registrar, Critical Care Aberdeen Royal Infirmary, Aberdeen, UK §.P. Hoole, 8M, sch, Ma, MRCP Specialist Registrar, Cantiology Papworth Hospital, Cambridge, UK LS.G.E. Howard, a, ma, Bchir, DPhil, sence Consultant, Pulmonary Medicine Hammersmith Hospital, London, UK A.M. Ingle, now, nit, nse Assistant Dinector of Nursing Papworth Hospital, Cambridge, UK D.P. Jenkins, ns, ws (Lond), FRCS ( Res (ct) Consuluans, Cardioshoncte Surgery Papworth Hospital, Cambridge, UK ). G.Joynt, mv Professor, Anaesthesia and intensive Care The Chinese University of Hong Kong, Sha'Tin, Hong Kong S. Kaul, 8c, 48, ChB, MRCP, AFRCS Specialist Registrar, Respiratory and Intensive Care Medicine London Deanery, London, UK P, Kesteven, mp, ns, FRAGr, FRCP, PREF, PRD Consultant, Haematolegy Freeman Hospital, Newcastle, UK A.A. Klein, sans, FRCA Consultant, Anaesthesia and Intensive Care Papworth Hospital, Cambridge, UK A. Koster, Mo Vice Chait, Department of Anesthesia German Heart Centre, Berlin, Germany PLE, Laterre, MD Conauleant, Critical Care iques Universitaires St Luc, Brussels, BelgiumM. Lemans, Feca Specialist Registrar, Anaesthesia Guys and St. Thomas’ Hospital, London, UK C.Leonard, rncr Consultant, Respiratory and Transplant Medicine Wythershawe Hospital, Manchester, UK |, MBBS, BAe, Sci, FANZCA Consultant, Cardiothoracic Anaesthesia The Alfred Hospital, Melbourne, Australia J. Mackay, mace, FReA Consultant, Cardiothoracic Anaesthesia Papworth Hospital, Cambridge. UK M.L.N.G. Malbrain, sp, pho Director, Critical Care Ziekenhuis Netwerk Antwerpen, Stuivenberg, Hospital, Antwerp, Belgium, WIT. McBride, nsc, MD, FRCA, FFARCS(1) Consultant, Cardiac Anaesthesia Royal Victoria Hospital, Relfast, UK: 8. McCorkell, rca Consultant, Anaesthesia Guy's and St. Thomas’ Hospital, London, UK B. McGratian, FRc Clinical Fellow, Cardiothoracic Anaesthesia Royal Victoria Hospital, Belfast, UK A.B, Merry, MBChB, FANZCA, FFPMANZCA, FRCA Professor and Head of Department of Anaesthesiology University of Auckland, Auckland City Hospital, New Zealand J. Moore, Fea, MRcP Specialist Registrar, Critical Manchester Royal Infirmary, Manchester, UK care 8. Mordzynski, Mo Resident, Departmen of Anesthesia and Critical Cate Medicine Hadassah Hebrew University Medical School, Jerusalem, israel ©. Moro, so Gonsulwant, Anaesthesia Centre Hospitalier Louis Pasteur Bagnols sur Céze, France conTRiBUTORS S.A.M. Nashef, sn, che, Consultant, Cantiothoracic Surgery Papworth Hospital, Cambridge, UK J. Osgathorp, 1, 25 Hons Senior Nurse, Critical Care Papworth Hospital, Cambridge, UK J. Parameshwar, Mo, ence Consultant, Transplant Cardiology Papworth Hospital, Cambridge, UK A. Pearce, mca Consultant, Anaesthesia Guy's and St'Thomas’ Hospital, London, UK H. Powell, mtb, 39, #8CA Consultant, Cantiothoracic Anaesthesia and Critical Care Freeman Hospital, Newcastle, UK Z. Ricci, Mp Staff Cardiothoracic and Paediatric Anesthesiology Bambino Gesu Hospital, Rome, Italy ©. Ronco ww Head, Department of Nephrology, Dialysis sand Transplantation 5, Bortolo Hospital, Vicenza, Italy F. Pea, mp Institute of Clinical Pharmacology & Toxicology Department of Experimental and Clinical holegy of Udine, Udine, Italy GI. Peek, Fes, crh Consultant, Cantiothoracic Surgery & ECMO nnfield Hospital, Leices S. Rex, Mp Unrecht, The Netherlands LS. Ring, miss, Mace Specialist Registrar, Candielogy Papworth Hospital, Cambridge, UK P. Roberts, mp, rec ronsultary nical Divecior, Gastroenterology Hinchingbrooke Hospital, Huntingdon, UK A. Roscoe, FRC Consultant, Cantiothoracic Anaesthesia & Intensive Care Wythenshawe Hospital, Manchester, UK xiliCcoNTRIsuTORS T. Ryan, sirce, FAR Consultant, Anaesthes Dublin, Ireland a & Intensive Care S-7. Runnels, Mo Assistant Professor, Anesthesia University of Utah Medical Center, Salt Lake City, Utah, USA D. Schmidlin wp, waa, Director, ICU Klinik am Park, Hirslanden Grou Swiverland Zirich, PM. Schofield, an, rece Consultant, Cardiology Papworth Hospital, Cambri WEE. Scott, us, chs, PRCA, DECOC Consultant, Anaesthesia Derby Hospitals NHS Foundation Trust, Derk uk N.J. Screaton, Bs, HCH, MRCP, FRCR Consultant, Cardiothoracic Radiology Papworth Hospital, Cambridge, UK M, Screaton, non, Se Senior Nurse Practice Development, Critical Care Papworth Hospital, Cambridge, UK PJ. Shirley, sunche, #RCA, FING, RCSEA, EDIC Consultant, Intensive Care Medicine and Anesthesia Royal London Hospital, London, UK D.A. Sidebotham, mach, FANZzcA Consultant, Anaesthesia andl Invensive Care Auckland City Hospital, Auckland, New Zealand L. Spencer, scr Specialist Registrar, Thoracic Medicine and Transplantation Wythenshawe Hospital, Manchester, UK R, Sayeed ma pho Mace FRcs (C-Th) Consultant, Cardiothoracic Surgery John Radeliffe Hospital, Oxford, UK E.P. Smith, 8S, MBChB, MRCP, FRR Consultant, Radiology University Hospital of South Manchester, Wythenshawe, Manchester, UK LD. Stearns, Mp Department of Anes The lohn Hopkins University Hospital, Baltimore, Maryland, USA hesiology arud Critical Core M. Thavasothy, FRcA, MD Consultant, Anaesthesia Royal London and St Bartholomew's Hospitals, London, UK A.A. Tinmouth, B. Thomson, mp, Consultant, Cardiothoracic Surgery Prince Charles Hospital, Brisbane, Australia R. Tiruvoipati, res CESAR Trial Fellow, Cardiothoracic Surgery University of Leicester, Leicester, UK S.SL Tsui, enc, m4, MD, PRCS(C-Th) Consultant, Cardiothoucte Surgery, Director of Transplantation Papworth Hospital, Cambridge, UK T, Strang, erca Consultant, Cantiothoracic Anaesthesia Wythenshawe Hospital, Manchester, UK 8. Toussaint, so Consultant Anesthesiology and Intensive Care Medicine Virchow Clinic, Humboldt University, Berlin, Germany A. Turgeon, “up, ercre Staff, Anaesthesiology and Critical Care Medicine Ottawa Health Research Institute, Ottawa Hospital, Ottawa, Canada RS. Ulrich, Po Professor, Architecture Texas A&M University, College Station, Texas, USA K, Valchanoy, mp, exc Consultant, Anaesthesia and Intensive Care Papworth Hospital, Cambridge, UK J. Varley, ap, Fnca Specialist Registrar, Anaesthesia East Anglican Deanery, UKA. Vuylsteke, Mp, FCA Consultant, Caniiothoracic Anaesthesia and Intensive Care Lead Consultant Critical Care, Papworth Hospital, Cambridge, UK TK. Waddell mp, use, rhb, FRESC, Associate Professor, Division of Thoracic Surgery University of Toronto, Toronto General Hospital, Toronto, Ontario, Canada S.T. Webb, stn, neh, nao, Pres Specialist Registrar, Anaesthesia & Intensive Care Medicine Royal Victoria Hospital, Belfast, UK GR. Weinert, up, wrt Associate Professor of Medicine, Division of Pulmonary, Allergy and Critical Care University of Minnesota Medical School, Minneapolis, Minnesota, USA Y.G. Weiss, sp, Foo Senior Lecturer in Anesthesia aed Critical Care Medicine Hadassah Hebrew University Medical School, Jerusalem, Israel, Adjunct Assistant Professor in Anesthesia and Critical Care Medicine University of Pennsylvania Medical School, Philadelphia, Pennsylvania, USA conTRiBUTORS PA. White, Msc Phb, DIC, MIPEM Consultant, Clinical Scierist, Head of Clinical Engineering Addenbrooke's Hospital, Cambridge, UK J.M. Williams, exca Consultant, Candiothoracic Anaesthesia & Intensive Care Glenfield Hospital, Leicester, UK C.I.A. Willmott, uncns, Fanzca Pellow, Anaesthesia and Critical Care Princess Alexandra Hospital, Brisbane, Australia N. Yonan, an, enes(crb) nsultant, Cantiosheracie Surgery Honorary Senior Lecturer Wythenshawe Hospital, Manchester University, Manchester, UK R. Zarychanski, Mp, FRCPC Staff, Haematology and Critical Care Ottawa Health Research Institute, Ottawa Hospital, Ota | Ontario, CanadaPreface In the corner, a patient isrecovering well aftera heart operation. Evenso, the lights of five infusion pumps are blinking regularly, the ventilator is sighing, the electrocardiograph, several pressures, temperature and oxygen saturation are continuously displayed and massive amounts of data are being generated and recorded, and this is when things are going well! Elsewhere, another patient may be on an intra- aortic balloon pump, athird may beon haemofiltra- tion, a fourth may be on a ventricular assist device and occasionally, behind drawn curtains, a mad- eyed surgeon may be performing open heartsurgery on the unit due to unexpected complications ‘The cardiothoracic critical care area can be a frightening place indeed. Managing the critically ill cardiothoracic patient is no different from any other patient. The ciples of good clinical practice apply here as they do elsewhere. Knowingthehistory helps. Clini- cal examination, as in every field of medicine, yields valuable information, However, critical care provides additional, hard clinical data like no other area of medical prac- tice. Continuous and regular monitoring of physio- logical and haematological parameters makes most diagnoses easy «9 make. If here is still doubt about the status of the patient, further information is easy to obtain, whether by pulmonary artery flota- tion catheter, transoesophageal echocardiography or computed tomography. This is one area where most decisions are made on the basis of sound evi- dence rather ona clinical hunch. All thats required is some basic knowledge, a degree of thoroughness and sound judgment. ‘This book aims to guide caregivers from all disci- plines in themanagement of cardiothoracic patients during their time in the critical care environment. ‘Thework is not exhaustive nor, we hope, exhausting, {tis written by experts in their fields and its primary aims are to explain and demystify the approach to various areas of cai thoracic critical care. We truly believe the topicof cardiothoracic critical care can be accessible and easy to learn. We hope, with this book, to have made it more so. ‘Thanks also to Graham Hilton for photographs, including the cover. Andrew Klein Alain Viylsieke Samer Nashef EditorsForeword Cardiac intensive care is a peculiarity in the United Kingdom. In many hospitals, it is the only single specialty critical care area. We should not be too surprised at this; cardiac disease is common and its frequency has spawned many new and innova. tive treatments. Changes in the organization of our hospitals may mean more patients with cardiac dis- ease are treated in specialist centers and even fewer seen in general intensive care units, thus reducing the skill base and so comfort of many intensivists in managing these patients. Patients do not just present with heart disease, they also require surgery for other problemsand familiarity with car sup. port is essential for all who work in general units. ‘Thisis not an in-depth tome, butrather a practical text full of the kind of tricks of the trade that makea skilled cardiac intensivist, One potential problem of a single specialty unitisa tendency to “forget” about the other systems; these are all addressed herein, along with other essential elements such as ethics and the run) ng of a successful unit This is a welcome text targeting a multi disciplinary audience. It will be useful for those approaching an attachment to a cardiac unit as well as for those of us outside who want to update our selves on the latest treatments available. Anna M. Batchelor, ‘MBChB, FRCA Consultant, Anaesthesia and Intensive Care Royal Victoria Infirmary Newcastle President of the Intensive Cave Society xviiMaterial chroniony prawem autorskimAbbreviations ABG ACE ACEI ACLS. ACS. act ACTA ACTH acy ADP AED AEP AIDS ALL ALS ANH AP APACHE Angiotensin Arterial blood gas Angiotensin-converting enzyme Angiotensin-converting enzyme inhibitor Advanced cardiac life support Abdominal compartment syndrome Activated coagulation time Association of Cardiothoracic Anaesthetists Adrenocorticotrophic hormone Assist-control vent Activity of daily living Adenosine diphosphate Automatic external defibrillator Auditory evoked potential Atrial fibrillation Acquired immunodeficiency syndzome Acute lung injury Advanced life support Acute normovolaemic haemodilution Anteroposterior Acute Physiology and Chronic Health Evaluation APC apt ARDS. ARE ASV Ass AT ATG ATN auc av B BAEP BiPAP Bis BiVAD BLS BMI BMR BPE bpm BUN Activated protein C Activated partial thromboplastin time Acute respiratory distress syndrome Acute renal failure Adaptive support ventilation Area under the systolic fraction Antithrombin Antithymocyte globulin Acute tubular necrosis Area under the curve Brainstem auditory evoked potentials, Bi-level positive airway pressure, bilevel pressure assist spectral (index) Biventricularassist device Rasicllife support Body mass index Basal metabolic rate Bronchopleural fistula Beats per minute Blood urea nitrogenc CABG CAM.ICU cAMP CBF cco ccr coc cr cl cl cls ML MRO: cMv CNS co CoA (CoBatniGe corp cox cpar CPB CPOE cre CPR cR CRBSI CSE cr crePH cvA cv Coronary artery bypass graft Confusion assessment method for the intensive care unit iclicadenosine monophosphate Cerebral blood flow Continuous measurements of cardiac output c Centers for Disease Control and Prevention (USA) Cystic fibrosis Cardiac index Confidence interval Clinical information system Chronic myelomonocytic leukaemia Cerebral metabolic rate (for oxygen) tical care practitioner Controlled mechanical ventilation Cytomegalovirus Central nervous system Cardiac output Coarctation of the aorta ‘Competency based training for intensive care medicine Chronic obstructive pulmonary disease Cyclo-oxygenase Continuous positive airway pressure Cardiopulmonary bypass (Computer aided physician order entry Cerebral perfusion pressure Cardiopulmonary resuscitation ‘Computed radiography Catheter-related bloodstream infection Cerebrospinal fluid ‘Computed tomogram/tomography Chronic thromboembolic pulmonary hypertension Cerebrovascular accident Central venous pressure cWH cvvuD CVVHDF cx CYP3A4 D pe DDAVP DHA DIC DLco DNAR DR pst pvr EAA EBM Ect ECMO ecr EDIC EDTA EDV EEG EF EHR eV EMR EPAP EPO Continuous venovenous haemofilua Continuous venovenous haemodialysis Continuous venovenous haemodiafiltration Circumflex artery (coronary artery) cytochrome microsomal system Isoform 3Aa Direct current Desmopressin (I-desamino-8 vasopressin) Deep hypothermic circulatory arrest Disseminated intravascular arginine coagulation Transfer coefficient for carbon monoxide Do not attempt resuscitation Direct radiography Down-slope time Deep venous thrombosis Excitatory amino acid Evidence-based medicine Electrocardiograph Extracorporeal membrane oxygenation Fearin clotting time Furopean Diploma in Intensive Care Ethylenediamine tetra-acetic acid End-diastolic volume Electroencephalograph Ejection fraction Flectronichealth record External jugular vein Electronic medical record expiratory positive airway pressure ErythropoietinG-CSF HADS Hb HBOC Hb-s CSW HDU HE HEFL HEV HPOV HPV HEPPV FuroQol five-dimension Erythrocyte sedimentation rate End-tidal Extravascular lung water Farly waming scores Forced expiratory volume in 1 second Film to focus distance Fresh-frozen plasma Filtration gradient Fraction of inspired oxygen Functional residual capacity y-Aminobutyric acid Clasgow Coma Scale Global end-diastolic volume Glomerular filtration rate Gastrointestinal Granulocytes colony stimulating factor Glyceryl vinitrate Hospital anxiety and depression scale Haemoglobin Haemoglobin-based oxygen carriers Haemoglobin S Health care support worker High-dependency unit Haemofiltration High-frequency flow interruption High-frequency jet ventilation High-frequency oscillatory ventilation High-frequency percussive ventilation HEV Hr HLA HMT HP HPA HR HRQOL 1 TARP, 1AH IAP, IBTICM ICA ICAM icp 1cp Icu IE TEN Ig mp uy 1 IMV INR IpaP IPD Ie ippy TRY ISHLT Ist i rev rrp Irv ABBREVIATIONS high-frequency ventilation Heparin-induced thrombocytopenia Human leukocyte antibody Heparin management test Haemoperfusion Human platelet antigen Heart rate Health-related quality of life Intra-aortic balloon pump. Intra-abdomninal hypertension Intra-abdominal pressure Intercollegiate Board for Training in Intensive Cate Medicine Internal carotid artery Intercellular adhesion molecule implantable cardiac defibrillator Intracranial pressure Intensive care unit Infective endocarditis, Interferon Immunoglobulin Intermittent haemodialysis nternal jugular vein Interleukin Intermittent mandatory venti International Normalized Ratio inspiratory positive airway pressure Intermittent peritoneal dialysis Idiopathic pulmonary fibrosis, Intermittent positive.pressure ventilation Inverse ratio ventilation International Society of Heart and Jung Transplantation International Sensitivity Index Information technology intrathoracic blood volume Idiopathic thrombocytopenic purpura Intrathoracic thermal volumetu Vv we LAP LcP LDH LIMA LMWH LMS. Los LPs. Lsv Iv LvaD LvEDP. LVEDV LVRS M MAP MCA MCAEP McP MDE MDD MDT. MEP MET MHC. MI xxl Intensive therapy unit Intravenous Inferior vena cava Clearance Membrane coefficient Karnofsky performance status Left anterior descending (coronary amtery) Left atrial pressure Liverpool Care Pathway for Dying Patients Lactate dehydrogenase Left internal mammary artery Low-molecular-weight heparin Left main stem (coronary artery) Length ofstay Lipopolysaccharide Jong saphenous vein Left ventricle/ventricular Left ventricular assist device Left ventricular end-diastolic ressure Left ventricular end-diastolic volume Lung volume reduction surgery Mean arterial pressure Middle cerebral artery Midcortical auditory evoked potentials. Monocyte chemotactic protein Major depressive episode Major depressive disorder Multidisciplinary tan Motor evoked potential Medical emergency team. Major histocompatibility complex Myocardial infarction MIDCAB MMV MOD MOF MPAP MRI MRSA MIT Mu NEEP NExB NHP NIRS. NIV NK NMDA NSAID NSE NYHA P PA PAC PACS Pacor Pacs PADP PAE PAH PAMP Pao: PAP Pc Minimally invasive direct coronary artery bypass Mandatory minute ventilation Malti-organ dysfunction Malti-organ (system) failure Mean pulmonary artery pressure Magnetic resonance imaging Methicillin-resistant Staphylococcus aureus Mean transit time Million units Negative end-expiratory pressure Transcription factor nuclear factor kB Nottingham Health Profile Near-infrared spectroscopy Noninvasive ventilation Natural killer (cells) N-methyl-p-aspartate Nonsteroidal anti-inflammatory drug Neuron-specific enolase New York Heart Association Pulmonary artery Pulmonary artery catheter Picture Archiving and Communication system Carbon dioxide abv Jar pressure Picture archiving and communication system Pulmonary arterial diastolic pressure Platelet activated factor Pulmonary arterial hypertension Pathogen-associated molecular patierns Oxygen alveolar pressure Pulmonary artery pressure Personal computer Pericardial collectionPowe PCA, pa Pcp Pov PD PDE, PDMS PE PEA PEEP PEG PHT PICC PMN Po: Poc PPE PPH ppv PRBC PRvc Psv Pr Pre PIT rsp PVAD PVR Pvco; @& a QoL Pulmonary artery wedge pressure Patient-contiolled analgesia Percutaneous coronary intervention Pneumocystis carinié Polymerase chain reaction Pressure-controlled ventilation Peritoneal dialys is Phosphodiesterase Patient data management system Pulmonary embolus/embolism Pulmonary endarterectomy Positive ends piratory pressure Percutaneous endoscopic gastroscopy Pulmonary hypertension Peripherally inserted central catheter Polynuclear neutrophils partial pressure of oxygen Point of care Personal protective equipment Primary pulmonary hypertension Pulse pressure variation Packed red blood cells, Pressure-regulated volume-controlled ventilation Pressure-support ventilation Prothrombin time Proximal tubular pressure Partial thromboplastin time Post-traumatic stress disorder Pulmonary thermal volume paracorporeal ventricular assist device Pulmonary vascular resistance pulmonary venous CO; Filtration flow Blood flow Dialysis flow Quality of life RA RATG RBC RCA RFID RY RRT RSIP RV RVAD s SAH SAM spr sc Sevox SCUP spp SP36 si SINV SIRS Sio2 SNP SOFA spv SSEP SSRIs sts sv svc Svoz SVR ABBREVIATIONS Right atrium/atrial Rabbit antithymocyte globulin Red blood cell Right coronary artery Radiofrequency identification Right internal jugular Renal replacement therapy Risk score for transport patient ight ventricle/ventricular right ventricular assist device Subarachnoid haemorrhage Systolic anterior motion (of the anterior mitral leaflet) Spontaneous breathing trial Subcutaneous Membrane sieving coefficient Central venous oxygen saturation Slow continuous ultrafiltration Selective decontamination of digestive tract Short Form Heath Survey Systéme Internationale Ssnchronized mandatory ventilation Systemic inflammatory response to sepsis Jugular venous oxygen saturation Sodium nitroprusside Sequential Organ Failure Assessment Systolic pressure variation Somatosensory evoked potenti Selective serotonin reuptake inhibitors Society of Thoracic Surgeons (cisk scoring) Stroke volume Superior vena cava Mixed venous oxygen saturation Systemic vascular resistance xailiSVT swe TAH TAT Te rcp TEG TFPI TLR TMP TNF TOE TPN TRALI TREM-1 TRIM xxiv Supraventricular tachycardia Standard Wire Gauge ‘Total artificial heart ‘Thrombin-antithtombin complex Lymphocytes T cytotoxic Transcranial Doppler Thromboelastogram/ thromboclastography ‘Tissue factor pathway inhibitor Lymphocytes T helpers ‘Voll-ike receptor Transmembrane pressure Tumor necrosis factor ‘Transoesophageal echocardiography Total parenteral nutrition ‘Transfusion-related acute lung injury Triggering receptor expressed myeloid cells ‘Transfusion-related immunomodulation TRS TSH Tre UF ut VAD vAU VAS vATS Veo: ve VILI vor vIQ vWE wee Toronto Risk Score Thyroid-stimulating hormone Transthoracic echocardiography Ultrafiltration Urinary tract infection Ventricular assist device Ventilator-associated lung injury Visual analog scale Video-assisted thoracoscopy total volume of CO> exhaled over a defined period Ventricular fibrillation Ventilator-induced lung injury (Oxygen consumption Ventilation-perfusion Ventricular tachycardia von Willebrand factor White cell countPICSOJONY P2-OSOJOW — QeOSO{0W SECTION 1 Admission to critical care Who needs cardiothoracic critical care? 1M, HIESMAYE AND D. SCHIDLIN Scoring systems and prognosis |A, BARKER AND S.A.M. NASHEF Admission to critical care - the cardiology patient Sf HODLE AND RM, SCHOFIELD ‘Admission to critical care ~ heart failure J. PARAMESIWAR Admission to critical care - the respiratory patient S. KAUL AND L. HOWARD Resuscitation after cardiac surgery JH. MACKAY Transport of the cardiac critical care patient fe SHIRLEYPLOSOIOW’ PROSOFEWY QEESE|OW Toso Prine: ve To Come sraai7o1erscot — CUINBBE Keine Ioouary9, 2008 4 em autorskim Material chroniory prP2OsojovY QC OsojOW chapter 1 Who needs cardiothoracic critical care? What is critical care? Critical Care Units (oF intensive care units {ICU} ean be defined as "specialised sections of a hospi tal containing the equipment, medical and aus: ing staff and monitoring devices necessary to pro: vide continuous and closely monitored health care to critically ill patients" Such paticats may be at high risk of acquiring a life-threatening condition co requirea high level of nursing and medical care to maintain physiologicequilibrium. Critical care is a complex and diverse network that interacts with all areas of the hospital. level of care Critical care areas have traditionally been divided into Intensive Therapy Units, where the highest level of care is given to the sickest patients, and high-dependency units or step-down units, where an intermediate level of care between the ICU and the ward is provided. Another classification divides patients according the level of care required, a the bedside is the primary critical care provider. The complexity of the care and moni The nu toring of mostcritical care patients and the machin: ery requited to treat them means that the majority require one nurse per patient, and this is the stan: dard in level 3 cate in some countries such ay the United Kingdom, Patients who require lessintensive monitoring and treatment may require less nursing time, and level 2 care may be provided by one nurse for oxo or more patients Regardless of the level of care, specialized doc tors provide medical supervision, These phy are usually iniensivists who work together with sur- eons, physicians, microbiologists and other medi cal disciplines. The multidisciplinary team includes physiotherapists, pharmacists, dieticians and other support staff as well Cardiothoracic critical care provision All patents are admit to erties cate environ ter cardiac surgery whether cardiopulmo. nary bypass was used or not. Many recover quickly if the postoperati ated, This rapid change in status (from highest level of intensive care to lowdependency cardiac moni period is uncomp| toring over a few hours) has moulded the cur- rent cardiothoracic critical care environment, This allows patients to progress from level 3 to level L care ready for discharge to the ward in less than 24 hours, ‘Some patients need critical care longer. This may be because of the complexity of surgery, because comorbidities dictate a more prolonged recovery, or because of the development of postoperative complications. Transplantation and other invasive treatment forsevere heart failure often requires pro- longed critical care. Medical patients with unstable cardiac conditions and all patients with respiratory or renal disease may also need a prolonged stay ‘The oumber of such patien care planning difficuly bur up 1 10% of patients s varies, making critical 3PROSO}OVY —_QCOSO]ONY THOS Care required D Cae can be provided on a normal ward within an-acute hospital 1 Patients whese condition is at rik of deterioating or who ate recovering from a serious illness, whose care may be pravided on ‘an acute ward wih additioral support 2 Patients who require detailed observation or Intervention, including support fara single falling organ system of postoperative care, induding these “stepping down” trom higher levels cf cave 3 Patients requting advanced respatory support Crsupport at atleast two organ systems. Adopted tram comprerensie crtval Cor, London, Deparment of Heath Proportion of patients Duration of artificial ventilation(h) Figure 1.1. Propartion of ectubated patients ater cardiac suger, (The proportion of intubated and surviving patients 's displayed versus duration since aémssion in tical care. ach line represents one individual critical care nit. The light grey area inicates the total variability and the derk ‘rey area the makr-steam behaviour the arow indicates the range of time until 50% of patients have been extubated. (Hom Lassrigg etal. Intensive Care Wedicine 2002.) Proportion of patients on & 2 o% Wo mm Duration of critical care stay (h) Figure 1.2 Proportion of patients stayingin crticl care after cardiac surgery. The propastion of surviving patients in itcal cates displayed versus duration since admission in itcal cate tach line fepresents one individual critical care ‘unit, the light grey area indicates the total variability and the dak grey area the mainstream behaviour. The arow Indicates the duration ange untl 50% of patients have been discharged from cital care. (From Lassnigg eta Intensive Care Medicine 2002.) undergoing cardiac surgery are admitted for lon- get than 7 days, ‘The service should be flexible; a prolonged stay is not always expected. Managers and intensivists often struggle to deter minethe number of critical bedsneeded in an insti tution, taking into account elective admissions from theatre and emergency admissions from within the hospital and from other institutions. In_an ideal world, there would always be reasonable spare capacity, but in reality few spare beds can be pro: vided, and bed occupancy is often more than 90% ‘This allows for rapid turnover, but places strain on the critical care staff and environment expensive, and typically consumes 15-2596 of the total budget of a tertiary care centre. Use and availability is therefore sub: ject to control owing to financial restiictions, which often dictate the number of available beds and sat Critical care provisionP2OsojovY QC OsojOW CHAPTER | WHO NERDS CARDIOTHORACIC CRITICAL CARE? Discharge ‘hi dein that inienivaeanut lenpir gassed and reduced monitoring is safe, is straightforward after uncomplicated recovery from surgery. How ever, readiness for discharge after complex surgery anor dificult to deter or prol Hare aged cr mine, and careful consideration by the multidisci: plinary team is necessary. Adequate planning and support is required, and follow-up by critical care staff may be benef ial. Some patients may expe rience long-term complications or psychological effects, and follow-up should allow assessment and treatment of such sequelae. Shortage of beds due to unespected emergency admissions or pressure of elective operating work may necessitate early discharge of some patients. ‘This is associated with increased readmission rates and possibly morbidity and moctality ‘cumstances, careful discharge planning and follow upcare arrangements may help to reduce these risks. n such cin Intensive care without walls Sick patients are not always located in esitical care areas. Thismay be because ofan unexpected deterio: ration in their condition, a postoperative complica: tion, orafier premature discharge to the ward when lose monitoring isstil required. Lower staffing ev: els on wards and lack of experience managing very sick patients has led to the development of critical carecutreach services, Theseusually consist of aurs {Ing and medical staff from the IC, who may advise, assist and above all educate ward staff. The effect of such services on morbidity, mortality, readmission to critical care and incidence of cardiac arrest is cur rently the subject of intense scrutiny. When does a patient receive cardiothoracic intensive care? After cardiac surgery All cardiac sive postope urgery patients need a period of inten: rive care because of the nature oftheir surgery and the relatively high incklence of com plications sueh as bleeding and respiratory failure Immediately after surgery, many patients havea rel atively unstable phase during which a aumber of interventionsmnaybeindicated without delay w pre vent further deterioration and apoor outcome. The risk of such complications i related to the patient’ premorbid condition and the success ofthe surgical proceduue After thoracic surgery The majerity of thoracic surgical patientsare looked after in the postsurgical recovery unit for a shor. period before discharge to the ward, Afier more extensive surgery such as pneumonectomy or 38 a result of complications of surgery or theie pre morbid condition, patientsmay require critical care. this may occasionally be prolonged oF unexpec ted Nonsurgical cardiothoracic admissions CARDIAC FAILURE Medical and surgical management of cardiac fail apidly evolving, and recent data suggests that morality is reducing as a result. Patients in severe heart failure need monitoring and treatment in a critical care environment, and some may require transfer oa specialized unit where mechanical sup port or transplantation can be offer for intensive management of heart failure can be expected to increase in the funuce. sd, Admissions LUNSIABLE CARDIAC CONDITIONS The medical management of patients with unsta ble angina or after myocardial infarction may also require intensive monitoring and support, Admis: sion may be prolonged, and surgical treat may be indicated after a period of treatment and further investigation, Depending on the provi sion of services, nsfer to surgical units may bePROSEIOKY —PRESOFOW QCOsE;0v" SECTION 1: Advis to critical ane RESPIRATORY FAILURE Intensive management of respiratory failure is a common indication for critical care, Intervention may range from noninvasive support to tracheal intubation and invasive ve ilation; prolonged care is often needed. Some patients may require more spe {ion suchas extracorporeal oxy- genation in dedicated units. Long-term ventilatory alized interver support may also be necessary in some instances, and this isusually offered in regional centes SPECIALIZED WORK Some units (usually regional or national ceferral centres) admit patients for highly specialized crit ical care. This can be for the teatment of com plex medical conditions such as cystic fibrosis or pulmonary hypertension, or after super-specialist surgery (eg, heart and lung transplantation, pul monary endarerectomy, ventricular assist device implantation) Readmission Readmission to critical care after cardiac surgery is needed in 3~4% of patients; he commonest causes are renal, respiratory and cardiac complications. Readmission is associated with greatly increased morbidity and mortality, and because ofthis, strin- gent efforts are made to reduce iis incidence, Key points © Thete is wide variability in the level of care requited after caidiothoracke surgery. ‘The number of cadiothoracicerkical care beds needed in a hospital is not easily predicted and the service should be flexible to match the elective and emergency workload. ‘* Readmission is a predictor of poor outcome, and may be reduced by careful discharge planning and REFERENCES 1 Lasoniga, A, M.J. Hiesmeyer, P. Bauer, ot a. Effect of centre-, patient- and procedure-related factors in intensive care resource ulization after ‘cardiac surgery. Intensive Care Medicine, 28 (2002), 1453-61, 2 Comprehensive Critical Care: Review of Critical Cave Sewices, (London: Depariment of Health, May 2000).PEOSOION FOSO/OW Qe-OSO{owW Tso chapter 2 Scoring systems and prognosis Grystal balls Knowing the likelihood of survival ater cardiac Sane a asc ge ci i BY utcto we can compare with actual outcome and thus gain some insight into the overall perorance of the cardiac surgical unit, Knowledge of who is titely 19 develop major morbidly also has an impact on the use of valuable esources and may allow for sensible planning of operating ist ta addition, some believe that being able to pre ict mova with sore cette may help clin idans to determine when further efforts are file Unfortunately, the perfect predicor- a crystal bal to foresee the furure ~ hes not yet been fll developed Risk models or scoring systems Scoting systems allow reasonable prediction of out come after casdiaewugery. Many models have been devised work out the likelihood of survival. and thee and othes have aloo been show o pretia mnajor morbidity, Jongerm survival and resource use with some accuraey, Moddls can be broadly divided ito two groupe «+ preapoative mode's, applied before the operation, with no knowledge of intraoperative events and + potopentive model, applied immediatdy ater the apetion on admission id the Gidea eae unit, takingsome account of what the operation dia to the patient Preoperative models These are most useful for + establishing the risk of sargery asan adjunct to surgical decision making (determining the indication o operate on the basis of Fiskto-benefit assessment); + providing the patient with information, which ishelpful in obtaining consent: + helping to measute the performance ofthe service by comparing actual and predicted ‘autcomes;and + comparing the performance of different institutions, surgeons and anaesthetists by correcting for rsk when outcomes are assessed Preoperative models take no account of what hap- pens in the oper useful in predicting which of a number of pos: i theatre and are therefore less operative patients with complications are likely 10 emerge intact from the critical cise nit There are probably more risk models in cardiac surgery than in any other branch of medicine. Most rely on a combination of risk factors, eaci of which is given a numerical “weight.” Weights are added, muhiplied or otherwise mathematically processed to come up with a percentage figure to predic: mor tality or survival. In additive models, the weights given to the risk factors are simply summed to give the predicted risk. They are easy to use and can be calculated mentally or “on the back ofan envelope” They are less accurate than more sophisticated sys tems and have a tendency to overscore slightly inPxosojovy QC OsojOW SECTION 1: Admission to critical care low-risk patients and to underscore considerably in very high-tiskpatients. Examples of such models are Parsonnet and the additive BuroSCORE. for cardiac surgery overall. Other models deal specifically with cardiac surgical subsets, like coronary surgery and valve surgery. Sophisticated models use Bayesian analysis logistic regression or even computer neural networks. They do not allow easy bedside calcul tion (unless you are Binstein) and need the help ofa computer. They are. however, more stable than additive models across the tisk range and slightly more accurate in exact risk prediction. Examples of such models are the Society of Thoracic Surgeons (S18) model and the logistic EumSCORE for over all candiac surgery. Preoperative model risk foctors Not surprbingly, the usual suspects are common to-all models (age, gender and left ventricular [IV] function). Other risk factors feature in some mod- cls but not in others, such as hypertension and diabetes. Models also ite they deal with all ead lepending on whether surgeries ora specific subs set, such as coronary surgery. AGE Theres an incwased tisk above the age of 60 years GENDER Females have a higher operative mortality than ma naller coronary artery size, although the reason for the difference is un les, possibly because of s known LEFT VENTRICULAR FUNCTION As estimated by echocardiography or angiography, LY function is a good measure of cardiae stats, but determination can be operator dependent tis df ficult produce an accurateand reproducible per centage ejection fraction. Generally, LV function is classified as “good,” “moderate” or “poor TYPE oF SURGERY General cardiac tisk models take into account patients that undergo different surgeries ~ the risk for coronary artery bypass graft (CABG) surgery is less an for valve surgery, which in turn islessthan that for surgery of the thoracic aosta. Combined procedures like CABG with valve carry a higher tisk than single procedures, EXTENT OF CAROIAC DISEASE ‘The severity of coronary disease is subjective and therefore not included in risk scores, although left main stem disease may be associated with more risk, Objective measures of cardiac disease include recent myocardial infarction (MI), unstable angina or mechanical complications of MI such as acute rupture of the mitral valve or ventricular septum, EPEAT OPERATION. Previous cardiac surgery (oF previous sternotomy) increases difficulty of access and prolongs opera- five time. These patients therefore carry aninereased tisk of bleeding as well as possibly having more advanced disease than those undergoing theie fist cardiac procedure. UNG DISEASE The presence of chronic pulmonary disease such 26 chronic obstructive pulmonary disease (COPD) has a large impact on how a patient is managed in anaesthet surgery, patients with concurrent lung disease are morelikely to require extended ventilation, develop and ventilatory terms. After cardiac chest infections or require support such as contin: uous positive airway pressure (CPAP) ventilation, Lung function is difficult to quantify with a sin- gle test and severity based partly on subjective judgments, However, chronic pulmonary disease is taken into account in the EuroSCORE and STS. Parsonnet includes smoking but not the presence of COPD particularly,Q€.0s0,0 urran EuroSCORE Parsonnet sts Patient-related factors Age (ys) Age (y15) ae (8) Gender Gender Gender Exttacardiae arteriopathy Obesity ace Newolgkal dysfunction Hypertension Body mass index Chronic pulmonary disease smoking Smoking Creatinine >200 mol/L Diabetes Diabetes itil preoperative state Dyslipdaemia Dyslipidaemia Previous cardiac surgery Dialyss Geeatinine Active endocartitis (atastophic state Renal failure ‘ther rare creuristance (eg, Dalyst paraplega, pacemaker dependency) —_Hypertensicn Caréiac-telated factors Unstable angina Pulmonaty hypertension Recent Ml Lv funtion Operation-related factors Emegency Post ant septal rupture Other than isoloted CABG Surgery thoracic aorta W function Preoperative IABP tmergency Type of procedure (ther than isolated CABG Cetebiovascular accident Endocarditis Chronic puimonayy disease Immunosuppression Exracardic arteriopathy Reoperation LW function Recent Congestive cardiac faire Previous percutaneous coronary intervention New York Heart Association casstication Preoperative ino\ropes/venticular assist device (ABP Emergency Type of procedure Surgery on thoracic aorta -Abbreviatns: 486, coronary arty bypass aaftna ABP to-aotcboloon pump LY, kt veoticuye My myocar indaraion; PC, percutaneous coronary interventionPxosojovy QC OsojOW SECTION 1: Admission to critical care RENAL DISEASE Renal dyst dialys the nction, as evidenced by dependence on increases mortality by as much as 40%, but pectrum of renal failures wide and difficult © quantify. Creatinine levels are easy to measure, but are not always an accurate measure of true kidney function, EuroSCORE uses grossly deranged serum creatinine (>200 pmol/L) as a measure of signif. Fant renal impairment, Other scores use dialysis dependence. The best measure is probably creati nine dearance. OTHER RISK FACTORS Theseinclude peripheralvascular disease, neurolog ical dysfunction, degree of urgency, diabetes, hyper- tension an addition, sarious scoring systems give weight to the type of operation pertormed. degree of pulmonary hypertension, In Postoperative models Such models benefit from information that is only available after the completion of the operation, such as the physiological parameters on admission to critical care. Many have been devised for critically ill patientsoutside the cardiac surgical spedalty, but have been used and validated in catdiac surgery. The most well-known models arethe Acute Physiol: ‘ogy and Chronic Health Evaluation (APACHE) and the Sequential Organ Failure Assessment (SOFA), The APACHE score is used on admission to critical care to assess the risk of in-hospital death, whereas the SOFA was developed to quanuify the severity of 1silInes api using the degree of organ dysfunc tion at any one time Postoperative model risk factors Postoperative risk scores look at each organ system 9 ‘of function. Basically, the more organ dysfunction, the poorer the prognosis atically and score according to d angement 0 RESPIRATORY Oxygenation and the requirement of respiratory support (ventilation) are measured to determine respiratory function cagcutaTory Most scores taken postoperatively use mean arte rial pressure as an easily measured and monitored parameter, However, wheteas APACHE concentrates tan derangement of normal physiology, SOFA con centrates on the need for (and level of) inotropic support euRoLoGicat ‘Trends are more useful thana shap-shot ata partic ular point in time, but the Glasgow Coma Seale is casily measured and provides an easily reproducible measure of neurological status. RENAL As in score used preoperatively, the mainstay of renal fanctionis serum creatinine level, Easily mea sured with a relatively inexpensive test this variable can be used to monitor changes in renal function and to compare current with preoperative function, GASTROINTESTINAL /HEPAnIC Both APACHE and SOFA use bilirubin levels as a measure of liver function. APACHE is used more widely in general critical care nits and includes many moze variables, such as amylase, albumin (as 2 rough measure of nutritional stats) and other liver junction ests The APACHEscore also contains ratiables to measure metabolic function and sep- fic status. These criteria are less relevant in cardiac surgery, Thoracic surgery Risk modeling is not as developed in thors gery, although recently some attempts have been made to produce models for predicting mortalityPEOSOIORY PLOSOJOW —_QEOSO|OW TOO Printer Ye to Come CHAPYER > SCORING SYSTEMS AND PROGNOSIS operative caidi mre Organ system SOFA APACHE Respiratory ‘Oxygenation (Pan: /Fin2) Respiratory fale nowwentiated Respiratory support ace with Fi, 1.0 Pac, Coagulation raematological wee wee Haematocrit Platelet count Prothrombin be Greuatory ean arteral pressure ‘Mean arterial pressure Dopamine dose Heat rate ventricuar response ‘Adkenaline dose Central Venous Pressure Norepinphrne dose Evidence of acute Mt Dobutamine use ahythnia Serum lactate Arterial pH Newological ‘Glasgow Cana Scale Glasgow Coma Scale Renal Geatinine Creatinine Lime ouput/24 he Unne oviput/24 hr Blond urea nitrogen Gastointstinal /hepatle flirubin amylase Albumin Bitubin Allaine phosphatase Liver enzymes nergy by skin testing septic Cerebrospinal tid posibve culture Blood culture posite Fungal culture postive Redal temperature metabolic alcum level Glucose Sodium Potassium Bicarbonate Serum osmoleity -Abbrevioins: APACHE Acute Physiology and Conc Health Eralvaton; Fa, tection of inspired oxygen: A, myocard ifotin Paco, paral pressure of carbon daxide in arena oad, Pao, paral pressure af axigen i rts blsod, SOFA, Sequential ogon Fee assesmenty WEC white cell ou nPRESKIORY —PRESOFOW — QcOsO,0v" SECTION 1: Admission to critical care ater lng esccion. The mostimportant risk factors associated with a poor outcome are age (older peo- pledotess ell) andhow much functioning remains long after he resection (the more, the beter) Key points ‘© Many madels help to predict the outcome of 200 mol/L. Haemofiltration immediately after contrast admin- istration teduces plasimaconast load, although the u clearance is modest (20% of total). The expense and complexity of haemofiltration has prevented widespread elective use, and iti generally reserved for patients who are already receiving long-term renal support Emergency admissions Admission of cardiology patients tothe critical care area is more likely to be in an emergent or urgent Zoiiie Tea ciate pedicel ead as early PCI after acute myocarcil infarction (Ml) becomes more commen, Such patients may need criial care admission because of postinfarct or polipeScedunl Zintie fun, wide mie! to require invasive monitoring, inotropicand IAB? support, and ventilatory or renal support ‘Although these are discussed in more specific etait ly n subsequent chapters, broad principles are outlined hereafter, Invasive monitoring Many acutely ill cardiac patients need inowopic drugs and other supportive measures. Although inotropes can be administered outside the critical ernie Catdiogeric shock and pulmorary edema Uncontroled acute myocardial ischaernia/efiactory angina/acute coronary syndrome. Prolonged cardiac arest Athythoa stern, Infective endocardis, Coronary artery rupture /pesforation Conttast-nduced nephropathy. Failed PC Abbreviation: PO, percutaneous cronay intervention,PEOSOIORY PLOSOJOW —_QEOSO|OW _TLOSO Printer Ye to Come care setting, titration of treatment to the therapeu: tic response is best undertaken in conjunction with invasive haemodynamic monitoring, For this rea son, the critical care unit is the optimal environ: iment to cate for patients tequiting inotropic drugs. Insertion of a pulmonary artery flotation catheter {PAC} may be necessary to help guide the titration of vasoactive drugs and the administration of intra venous fluid. 11s particularly helpfulin guiding the ‘management of patients with shock of any cause and those with acute heart failure Pulmonary artery ‘wedge pressure provides a direct measurement of LV filling pressure, and is elevated (>18 em H0) in cardiogenic shock. This. in conjunction with 2 low cardiac index (Cl < 2.0 Lmin-'m”) and a high systemic vascular resistance (> 1200 dynes scm”) conficms the diagnosis of acute cardiac failure. 1 enables the severity of cardiovascular compromise to be assessed along with response to therapy by monitoring trends and changes in cardiac indices. Insertion of a PACs not without riskand therefore should he performed by experienced phy: the critical care unit Supporting the failing heart In pati gests that adrenaline should be the first choice inotrope, although it can increase the ischaemic 18 with cardiogenic shock, evidence sug. burden of the LY. Other inotropic agents and their cardiovascular effects are outlined in Table 3:3. In patients with refractory LY failure and catdio- genic shock, mechanical circulatory support with an IABP may be beneficial as a bridge to surgery for haemodynanically correctable lesions. Inflation of the [ABP in early diastole is thought to augment coronary blood flow (although this theory is con tuoversial). Balloon deflation. during, isovolaemic contraction in early systole reduces afterload, LV wallstress, LVwork and myocardial oxygen demand, It can improve the CI by 20-25% and improve myocardial energy efficiency by 15%. Patients with An TABP should be cared for on the critical care unit by appropriately trained staff familiar with trigger- ing and augmentation settings of the pump console and arterial line care t0 minimize the risks of this Intewention. In severe oF refractory heart fuilure, pharmacological treatment and an IABP may not be sufficient to improve cardiac output and tissue perfusion. Worsening organ function may neces- sitate consideration of more invasive mechanical support modalities. In such cases, specialist refer: ral to and support from heart failure units should be sought; such patients may benefit from transfer to a critical care are ability of advanced mechanical support with ven tricular assist devices or extracorporeal membrane unit where there is avail Systemic vascular Blood cardiac Inotope resistance pressure output ‘Adrenergic agonists Dobutamine tt tt tt t tt Dopamine t tt tt + tt Isoprenaline tt i: i - 1 Adrenaline if + +t tt > Novepinephiine => = = tt ttt Phosphodiestorase inhibitor Enoximone 1 ~ - - ttPROSO}OVY _QCOSO]OY TOS SECTION 1: Admission to critical care ‘oxygenation. This type of trearment may beusedasa bridge to recovery, transplantation or, on occasion, asa permanent solution, Noninvasive ventilation ‘Continuous positive airway pressure or other forms of noninvasive ventilation (NIV) are useful in teat ing acute pulmonary oedema, It reduces the need for endotracheal intubation and may also reduce mortality. Invasive ventilation Some patients do not respond to or are noi suitable for NIV and need endotracheal intubation and pos: itive pressure ventilation, This may enable higher ventilatory pressures and Fio; to be administered. Sedative drugs are required and detrimental haemo: dynamic changes often ensue. Vasodilatation is common, leading w reduced mean arterial pres- sure and tissue perfusion. In addition, the increase In intrathoracic pressure may reduce venous return, further compromising cardiac output, Positive pres sure ventilation of patients with interatrial shunts, can exacerbatea right-to-left shunt by elevating ight, arial pressure, which may lead to further deteriora- tion in arterial oxygenation, Renal failure therapy Cardiogenic shock and decompensated acite heart iahiis art aseaciaed wah ohgicia aiid sane al filure. Teatment of such patients is problematic: ‘As well as fluid accumulation, serum hydrogen ion concentration tses, Aciosisis negatively inotropic and failure to correct i raphdly is asocited with increased mortality. As fluid accumulates, heartfil- ‘ure worsens, leading o further deterioration renal function and acidosis - a vicious circle that can bbe broken by continuous venovenous haemof tion (CVVH), either alone or with dialysis; CWVH rapidly corrects acidosis without the risk of sodium or fluid overload. It enables contiolled plasma vol- ume and solute depletion, without the profound 6 cree er Ens: me eae eae eatet Cem Reduction of myocardial oedema, Reduction in lft ventricular end-diastolic pressure —> ‘optimizaton o the saring featarship — increased myocardial pevformance. Removal of circulating myocardial depressant factrs hypotension seen with intermittent haemodialy- sis and can be safely administered to critically ill patients Specific scenarios ‘The following means all) situations in which cardiology patients are admited urgently to the critical care unit, with salient aspects of their management. cxamples of some (but by no Catheter laboratory complications Im the contest of PCL the guidewire may cause coronary artery perforation and deploying a bal loon or sent may cause coronary artery rupture “These are rare complications of PCI, but both may 30 min- utes), oliguria (urine outpat 85 mmHg Stable or improxing renal functon EHiminaion of peripheral and pulmonary vedema liproving ot normal iver function and coagulation parametets Adequate oxygenation Central venous tight atrial pressure <8 rami Pulmonary capilary wedge pressure <16 mmHg Cardiac index >2 L «min Mixed venous oxygen saturation >60% A secondaty goals systemic vasculrresstance 800-1,200 dynes « sec -cm® (helps to guide therapy) Mechanical ventilation with endotracheal intubation If noninyasive venti emia, endotracheal intubation is indicated. Respi ratory muscle fatigue often results from hypoxaemia and low CO. ion docs not reverse hypox brug therapy ANTICOAGULATION ‘The tole of anticoagulation is well established in acute coronary syndromes and atrial brillation, Patients with 2 history of an embolic event or evi dence of ventricular thrombus on echocardiogra: phy should alo receive anticoagulation. A large, placebo-controlled trial of daily 40 mg enoxaparin in acutely il patients, including those with heart failure, showed less venous thrombosis but no dif. ference in overall outcome. Pulmonary emboli are also commonly associated with severe heart failure and it seems reasonable to anticoagulate patients who are confined to bed in the intensive care needed as concomitant liver dysfunc tion may lead to & prolonged prothrombin time. unit. Car In patients with a creatinine clearance below 30 mL/min, low-molecular-weight heparin in thera: peutic doses should be used cautiously, probably with monitoring of facior Xa level Lor o1ueerics The reduction of elevated filling pressures is the mos effetive way to relieve symptoms of heart fal ure, Patients with acute decompensation of chronic heart failure are likely to be on diuretic therapy when admitted. Data are lacking on the relative efficacy and tolerability of different diuretics. In this setting, 2 loop diuretic is administered intra venously with dose titration to produce optimal urine output A loading dose followed by intra venous infusion has been shown to be more effec- tive than bolus dosing alone. A large bolus of diuretic may also lead to reflex vasoconstriction and pethaps a higher risk of ototoxicity. An intra venous infusion of furosemide at 5-10 mg/h issutti- cient in most patients once steps have been taken to increase the CO. Fluid restriction (usuallyto 1.5 L/d) is an important adjunct to diuretic therapy in severely Muid-overloaded patients. Using a ‘fluid challenge’in such patients with obvious peripheral oedema is irrational; inadequate urine output in these patients is invariably related to a low CO and tueating this often requires inouopic therapy. Once filling pressures have been reduced to normal, the dose of diuretic should be reduced promptly; the dose required to maintain eavolaemia is usually less than that required to achieve it, 2BPROSO}ONY ACOSO] THOS SECTION 1: Admission to critical care THAZiDES ‘The combination ofa thiazide (metolazone is com- monly used) with a loop diuretic can produce dramatic diuresis in patienis with chronic heart failure and is of use in the acute sewing, Heart failure patients are often hyponatraemic in the Intensive care unit and care needsto be taken not to exacerbate this with combination diuretic ther- apy. Thlazides act on the proximal wubule and deliver more sodium to the loop of Henle, where furosemide and other loop diuretis act, ALDOSTERONE ANTAGONISTS ‘Once diuresis is induced, itis important to moni- tor serum potassium, as hypokalaemia may predis- ose to arthyth diluted potassium chloride as an intravenous infu- sion to maintain K* levels, However, intravenous K* supplements have been shown to induce aldos- terone release from the suprarenal gland. Aldos- terone acts on the myocardium inducing remod- elling which isassociated with adverse outcomes in chronic heart failure, It seems rational, therefore, to combine loop diuretics with an aldosterone antag. ‘nist like spironolactone provided the serum K* is <5 mmoljl. and serum creatinine <200 jrmol/L In patients who have been intolerant of spironolac tone in the past (usually owing to gynaecomastia), epleronone (a selective aldosterone antagonist) isa suitable alternative. It is common practice to use vasoDILAToRS In the absence of severe hypotension, vasodila tors are indicated in most patients with acute heart failure, Decreasing preload relieves conges- tion and decreasing afterload is usually beneficial most patients with heart failure are vasocon stricted, When administering vasodilators or posi- LUve Inotropic drugs, the followingequation isuseful in manipulating the circulation MAP — CVP = CO = SVR ‘where MAP is the mean arterial pressure. 4 eee moe ieee Drug Dose Glyceryl tinitate Start at 20 g/min, increase upto 200 g/min Isosorbide dintrate Start att mg/ty, increase up 020:mg/h Sodium nitropmusside 0.2-5.0 a/kg/min Nestiide Bolus 2 j9/kg, infusion (0.01-0.03 as/kg/min Nitrates In low doses, nitrates are venodilators; high doses may also cause arterial dilatation, They are partic- ularly useful in acute coronary syndromes associ ated with hear failure. Oral nitrates in combination with hydralazine have been shown to be beneficial in chronic heart failure and at least two random- ized controlled trials have shown that intravenous nitraies in combination with furosemide are supe rior t furosemide alone. Tolerance to nitrates can develop within 24 hours of commencing an infu Sodium nitroprusside A powerful arterial dilator, sodium nitroprusside (SNP) can increase CO by lowe patients whose heart failure is not associated with hypotension. Prolonged administration of SNP may be toxic due to its metabolites. There are few con: tolled trials of SNP in heart failure and, because many patientsare admitted w the intensive careunit with hypotension, itis rarely used, ing afterload in Nesiritide ‘This drug (recombinant brain natriuretic peptide) is licensed in the United States for the treatment of acute heart failure. It relaxes smooth muscle, lead- ing to arterial and venous dilatation. 1t leads to 1 in CO without ditect positive inowopicPROsojOvY —_QEOSO|OW 1.050, ffect Compared with nitroglycerin, nesisitide pro duced fasier relief of dyspnoea and a more pro: nounced decrease in pulmonary capillary wedge pressure, and the benefit wassustained for24 hours. Although the drug has naiuretic and diuretic fects, up to 50% of patients with advanced heart failure have been reported to be resistant 10 its natriuretic effects, There is no conclusive evidence that nesiziide improves kidney function and ihere has been recent concern that it actually may worsen it, Clinical studies have not confirmed better clini: «al outcomes and at present the sole of nesirtide in the management of heart failure! Hydralazine Acombination of hydralazine and nitrates hasbeen shown 10 be beneficial in patients with chronic heart failure. in patients who. cannot tolerate an angiotensin-converting enzyme (ACE) because of hyperkalaemia or worseningrenal function, itistea sonable to use this combination, ANGIOTENSIN-CONVERTING ENIYME INHIBITORS ‘The first drug class shown to improve outcome in severe chronic heart failure, ACE inhibitors are the comerstone of ouspatient heart failure treatment. They haveno role ia theearly stabilization of unsta: ble heart fale patients, but should be introduced as soon as the patient is haemodynamically stable and has acceptable perfusion and renal function. ACE inhibitors decrease renal vascular resistance, increase renal blood flow and promote sodium and water CO, they may. ration rate. Ifpatients with acute decompensation of chronic heart failure are admitted to the critical care unit, it may be necessary to discontinue them temporarily xxcretion, However, inpatients with avery low nificantly decrease glomerular fi rBLOcKERS The role of -blockers in the management of chronic heart failure is well estab wed, based ADMISSION TO CRFFICAL CARH: HRART FAILURE fon several large trials involving many thousand patients. In volume-overloaded patients, 6-blockers are likely to increase the severity of heart failure and are usually avoided. There is no consensus on the management of a p jent receiving p-blockers for cheonic heartfailure admitted to hospitalwith acute decompensation, Most require at least a decrease in the dose of the drug but in patients requiring (f- agonist) inowopic therapy, It Is logical wo discon- tinue f-blockers altogether. INOTROPIC AGENTS Inovopic agents are indicated In the presence of tissue hypoperfusion (often manifested by wore ‘ening renal function) or fluid retention (periph: eral or pulmonary oedema) refractory to treat vent with diuretics and vasodilators, A common clini cal scenatio is a volume-overlaaded patient with hypotension, hyponatraemia and a rising serum urea and creatinine on intravenous diuretic ther apy. Continuing such therap likely to exacerbate the metabolic abnormalities and unlikely to induce a significant dinvesis. 1 is essential 10 improve the patient’shaemodynamic state with intravenous inotropictherapy until some form of definitive thes apy oF long erm palliation can be considered. It rust be remembered that inotrmpic agents in heart failure are like whipping an exhausted horse: they give short-term beneficial haemodynamic effects at the expense of accelerating the undeslying problem, This may be due t the increase in myocardial oxy gen consamption that results from inotropic ther apy. There i also a risk of inducing life-threatening, arshythmia, Rational se of inoteopic theropy in a critically ill populaion requires some form of haemodynamic monitoring; at the very least the CVP, arterial blood pressure, andl CO need to be assessed while on therapy Inotropic therapy Despite the desensitization of P-receptor path= ways in the failing human heart, most patients Bra osojery _Qcosojow 1-080 SECTION 1: Admission to critical care Pen eer orug solus Dose Dopamine No io a/gimn Dobutamine No 2220 na/ka/min Fpinephuine No 085-050 n/kg/min Norepneptrne No 082-020 a/ka/min Enoximone 025-075 mg/g 125-75 u9/ko/nin ainone 25-75 ng/kg 0375-0750 w9/lg/min Levosmerdan 12-24 ng/kg 005-0.20 g/kg/min ‘with advanced heat failure sill show a substantial response to adrenergic agents. The lowest effective dose should be used; patients receiving p-blockers may require higher doses. Very few trials have been conducted in patients with advanced heart fature and thete ino evidence of the agent over any other. ipetiority af one: Dopamine Avery sinall dose of the drug (<2 pg/ke/min) is said toact predominantly on peripheral dopaminer- gic receptors leading to vasodilatation. An increase in renal blood flow may lead to diuresis. Higher doses certainly increase CO; above 5 jug/ky/t dopamine also has a-adrenergic effects, increas- ing peripheral vascular resistance and blood pressure. Dobutamine Dobutamine acts through simulation of 8-1 and 8-2 recepiors in a 3:1 ratio and is. positively Inotropic and chronotropic, There may be a sec ondary decreave in sympathetic tone, decreasing, peripheral vaseular resistance; at low doses it may also induce mild arterial vasodilatation, High doses oF dobutamine (>10 y1g/kg/min) cause vasocon- striction, butthe exact effect at any given dose varies 26 by patient. Heart sate Increases as atrioventricular conduction is facilitated. The commonly used dose range is 2t0 10 jg/kg/min, Epinephrine ‘This drug has a high affinity for Bt, 8-2 and e-receptors and is generally infused at a rate of 0.05 to 0.50 ug/ky/min, Use of epinephrine ust ally requires invasive arterial pressure and CO monitoring. Norepinephrine This drug is used to increase SVR because of its affinity for «receptors. The lowest dose required to increase the SVR (and hence the blood pressure), and to maintain perfusion of vital organs should be used. Septic shock is a common indication for its use; the occasional patient after acute MI presents with low SVR owing to cytokine release and benefits from norepinephrine. Itis essential t9 monitor CO and the SVR when using thisagent. Inthe absence of appropriate monitoring, a common error is to use a-dose that maintains a “normal” blood pressure at the expense of adequate flow. A sise in the SVR in this situation is usually associated with a drop in the CO. In young patients, MAP of 65 mmHg may be adequate to maintain renal and systemic perfusion,PROsojOvY —_QEOSO|OW 1.050, ‘Type II phosphodiesterase inhibitors Phosphodiesterase (PDE) inhi breakdown of cyclic adenosine monophosphate: enoximone and milrinone are the two agents used in clinical practice. They cause marked peripheral tors. block the therefore, vasodilatationand have inotropic effec they are useful in patients with advanced heart fail ure who have an elevated SVR but remain hypoten: sive because ofa very low CO. Because of their pow erful vasodil ing is recommended whenever they are used, Both agents have a long elimination half-life and tend to accumula ifthe patient ts ollguric. Because thele Site of action is distal to the f-adrenergic receptor, PDE inhibitors maintain their effect in patientswho have been treated with f-blocking drugs. In patients With atrial fibrillation, they may increase ventricular ng effect, haemodynamic monitor rate less than dobutamine, Levosimendan This drug has two main mechanisms of action calcium ion sensitization of the contractile pro ‘eins (Positive inoopic effect) and smooth mus dle potassium ion channel opening (peripheral sasodilating effect) There is also a suggestion that levosimendan has a POE inhibiting effect tna ‘enous infusions oflevesimendan areusually main. tained for24 hours, but the haemodynamic eifects persist, probably because of the long half-life of its metabolite, Levosimendan infusions in patients with heart failure have been associated with a dase dependent increase in stoke volume and CO, 2 decline in the pulmonary capillary wedge pressure a decrease in SVR and pulmonary vascular resis tance.aslight decrease in blood pressure and a slight increase in heart rate toms of dyspnoea and fatigue has been shown in tials comparing levosimendan with dobutamine The haemodynamic effects were seen even in the presence of blocker therapy. Tachycardia and hypotension are side effecs associated with the An improvement in symp: use of levosimendan and it is: not recommended in paticnts with a systolic blood pressure below 85 mmHg, Ultrafiltration Patients with gress Muid retention and hypona- a difficalt clinical problem. Diures icsoften worsen hyponatraemiaand sometimes fea tures of the cardiorenal syndrome become appar ent. Inowopic drugs may help in this situation, but if therapy needs 1 be prolonged, the sisk of arthythmia needs to be considered. Continuous venovenous haemofiltration (CVVH) is effective in removing fluid and the sate of fluid removal can be tailored to the patients needs: CVVH may also remove cytokines with myocardial depressant prop- erties (¢.g. tumour necrosis factor) because macro: molecules up to 20,000 D can pass through the tultafilration membrane. IF necescary, large vol umes of fluid can be removed in a relatively short time to ready the patient for a definitive proce: dure heart transplantation, mechanical circulatory support). Although CVVH usually requites large-bore cen: tral venous access, there are devices that allow ultrafiltration via cannulaein peripheral arm veins, Although the maximum rate of fluid removal is less than that attainable by central CVVH, an ade- quate rate is achieved for the most common clinical situations. Compared with high-dove diuretic therapy, ultra filtrationhas been reportedto induce lessneurohor- monal activation and vasoconstriction. It is under- Utilized in the management of fluid-overloaded patients with advenced heart faite. Intro-aortic balloon pump Intra-aonic balloon pump (IABP) use may reduce afteload, thereby decreasing left ventscilar stroke work and myocardial oxygen consumption, 2s well a8 augmenting disstolic blood flow in the coronary and systemic circulation, Functions! mitral regur- gitaion, a common problem in a patient with a 7PROsojOvY —_QEOSO|OW 1.050, SECTION 1: Advis to critical ane dilated left ventricle, decreases with the use of the TABP. The IABP is extremely useful in critically ill patients with heart failure who can be stabilized until definitive therapy can be carried out. It is underused in patients with advanced heart failure in the intensive care unit. In patients requiring sup port beyond that provided by IABP, consideration should be given to the use of a ventricular assist device, Conclusion Advanced heart failure in patients on critical care units carries a high mortality. Optimal management requites close cooperation between a cardiologist ‘with an interest inv heat failure, an intensive care physician and cardiac surgeon. With appropriate therapy, many critically ill patients can be resusci- tated and returned to a productivelife.In the United Kingdom, there is often a reluctance to admit these patients (o critical care units; this is not in the best interests of the patients concerned. Key points © Heart failure, most commonly secondary to coronary attery disease, caries a poor overall prognosis, © Adinission to citial care is usually due to pulmenary oedema or cardiogenic shock, # Aggressive diuresis is indicated, end renal replacement therapy may be necessary to temove an adequate amount o fluid © Inowopes are often started to enance CO, but may lead to other complications; therapy should be closely monitored, + Anintra-aortc balloon pump may improve the clinical picture greatly, FURTHER READING ACCIAHA guidelines for the evaluation and management of chronic heart failure in the adult. Am Coll Cardio! 2005;46:1116-1143, Updates available via www. acccorg Binanay C, Califf EM, Hasselblad V, et al. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness, the ESCAPE ual. JAMA 2005,294:1625-1033. Nohtia A, Lewis E, Stevenson LW. Medical management of advanced heart failure, JAMA 2002;287:628-640, Steime AB, Stevenson LW, Chelimsky-Fallick C, et al, Sustained hemodynamic efficacy of therapy tailored to reduce filling pressures in survivors with advanced heart failure, Circulation 1997:96 1165-1172, The European Society of Cardiology. Executive summary of the guidelines on thed testment of acute heart failure, Eur Heart J 2005;26:381-416, Ic Force on Acute Heart Failure of the ignosis andPROSOIOWY QCOSOIONY TOS Chapter 5 Admission to critical care: The respiratory patient Introduction Acute respiratory failure is a common reason for admission to critical care. This chapter focuses on acute respiratory failure as a consequence of pri mary lung or chest wall assessment and specific medical management of these conditions. Acute conditions, such as asthma ase, examining the and community-acquired pneumonia, have clear itera for referral to cstical care; however, admis: sion of patients limited by chronic respiratory dis wot be straightforward Primary respiratory conditions in those with previously normal lungs Clinical assessment of community acquired pew complications and comorbidities, including para pneumonic effuslon ot empyema, which should be drtined, Detailed microbiological investigations should be performed, including blood and spu tumytracheal aspirate for culture and tivities (preferably before starting antibioic teatment) and urine for both pneumococcal and legionella antigen. In addition, sputum should be exam: ined by Gram stain and direct immunofluores: cence for viral pathogens. Additional investigations for severe community acquited pneumonia indude paired viral and atypical serology. The incidence of Staphylococcus aureus and Legionella pneumophila is increased in severe pncumonia, and a history of influenza symptoms and foreign travel should be sought Empirical intravenous antibiotic therapy with a broad-spectrum f-lactamase~stable antibiotic (eg. co-amoxiclav) or a second- or third-generation cephalosporin should be initiaved, combined with an intravenous macrolide, Where legionella infec tion is suspected, rifampicin may be added and where aspiration isthoughtto have occurred, amtibi otic cover should be broadened to cover anaerobic organisms. Oxygen therapyshould maintain satura tions beeen 92% and 98%. In refractory bypox: aemia, a trial of continuous positive airway pres sure (CPAP) or noninvasive ventilation (NIV) can be considered, but this should be instiusted in a critical care environment where the patient can be intubated swiftly in the event of failure, ‘Nosocomial pneumonia Nosocomial pneumonia can be classified in terms of severity and-managed in the same way as community-acquired pneumonia, although empir- ical antibiotic therapy should be adjusted to eflet the likely different microbiological aetiology. In severe nosocomial pneumonia, a standard regimen should include tteatment of methiclln-resistant S aureus (e. vancomycin) and gram-negative organisms such as pseuddomonas and enterobacter (cg ciprofloxacin or ceftazidime) Underlying comorbidities, such as malnutition (Chapter 35), diabetes (Chapeer 43), oF hsonic 2»PEOSOIOY PLOSOJOW —_QEOSO|OW TOO SECTION 1: Admission to critical care heart disease (Chapter 3), need to be managed con currently, Pulmonary infiltrates in the immunocompromised host ‘The development of pulmonary infiltrates isa fre- quent, lifethreatening complication in immuno- compromised patients, requiting early diagnosis and teatment. Infection should always be sus pected and treated empirically. The cause is often related tothe patient’sunderlyingdiagnosis, current immunosuppressive regimen, curation ofimmuno. suppression, and prior therapies. More often than not, the diagnosis isuunknown atthe time of referral to theintensive care unit Achieving a diagnosis is central to the man- agement of these patients. New infiltrates may represent a complication or progression of the underlying lung disease, such as the accelerated phase of idiopathic pulmonary fibrosis, Immuno suppressants themselves may be associated with new infiltrates, for exam, sirolimus induced pull monary hypersensitivity, Noninfecti mn ince Pulmonary oedema (cardiogenic/noncaidiogenic) Acie lung injury/acute iespiatoy distress syndrome Idiopathic intesttial pneumonias ‘Acute nterstial pneumonia Gyptogenic organizing pneumonia ‘Aicelerated idiopathic pulmonary fibrosis Acie eosinophilic pneumonia Hypersensitiviy pneumnitis (dsugindured, EAA) Ditfuse alveolar haemorhage Abhievition EAA, exrnsicollorgealveois are di erse and responsible for between 25% and 50% of infiltrates in these patients. The i cal appearance is rarely helpful in identifying a spe fic cause. Standard chest radiographs should be regarded es a screcning test and the carly use of com tial clini puted tomography (CI) scans is recommended, Type of immunosuppression common associated conditions Infectious agent affecting the lung Neulophitmedatedimmunity — Neutopenia Chemotherapy and cytotaxc agents Bone martow transplantation omicosteraids Diabetes Teel medated immunity Coiosteroids Antibody deficiency Splenectomy Congenital detisency mmunosuppressive agents, 4 ‘sed in heart/lung transplantation (cjlosparine, tacrolims) Myeloma, ymphom, CLL Staphylococcus Gram-negative hactetia Fungal infections Fungal infections ycohacterial species Nocardio. Vinuses (HSV, VZV, CMM, adenovius, PSY, influenza, parainuenze) Pheumocystis sirveci Encapsulated bacteria ‘Mycoplasma Abbrev: CU, crane Iymphocytic kukaerna; CY, ytomegalarius; HY, bumar immunodeficiency vies HS herpes Simplex vis; 8S, respiratory syretol nus, V2, vaiel zaster vis 30PROSO}OVY _QCOSO]OY TOS Rout ADMISSION CRITICAL CARE! THE RESPIRATORY PATIENT Culture and sensitivities Gultue and sensitivities (including fungal Mycobacteriat opportunistic organisms e.g PCR (HSV, V2v, CY) FF (influenza, parainfluenza, RSY, adenovins) Bacteriology and mycology iam stain ‘Auramine sain jor AFB legionefo, Nocarda)) Virology PCR (sv, EV, Oxy) cytology Grocott stain (for Pneumocystis raved) Differential cell count Abbreviotns: AS, at-fas boil BAL, brenchoalveokr lavage flac CV, cytomeyaloveus SY, herpes simplex vis, PCR olynerase chan seacion; v2, vaniel zoster viv with some aetiologies having characteristic pat terns, for example, angjoinvasive aspergillosis and cryptogenic oiganizing pneumonia, Furthermore, CT may help in planning bronchoscopic lavage or biopsy, whether transbronchial or surgical, Bron: choscopy is often the next investigation of choice. IF the patient is highly oxygen dependent, inva sive or noninvasive ventilation may be required during or after the procedure, With experience, use of sedation may be minimized. Bronchoscopic lavage is commonly favoured for reasons of sim: plicity and safety, but transbronchial biopsy may Increase the diagnostic yield. However, there may be an increased risk of bleeding owing to coagy: lopathy, thrombocytopenia or pulmonary hyper tension. Once intubated, the risk of pneumothorax with tansbronchial biopsy increases to atleast 5%, ‘The differential cell count in bronchoalveolar lavage may help in the diagnosis of noninfectious causes, such as hypersensitivity or eosinophilic pneumonia, Nasopharyngeal aspirate may often yield a vitological diagnosis when bronchoscopy cannot be undertaken, Blind empirical therapy usually includes coverage against Gram-negative and Gram-positive organisms. Additional empiri cal therapy is guided by likely immune deficit. 17 therapy based on CT imaging and available cultures has failed, then surgical lung biopsy may be con sidered, Ultimately, intubation in the immunocom- promised patient carries a grave prognosis and NIV should be attempted in suitable patients, Pulmonary infiltrates in the immunocompetent host New pulmonary infiltrates in the immunocompe- tent hort have a broad differential diagnosis and are similar to those in the immunosuppressed, although opportunistic infection is far less likely Clinical history taking and examination, coupled with standardimagingannd haematological and bio chemical analyses identifies most causes, the com- monest beinginfection and cardiogenic pulmonary oedema. Where standard therapy has failed and the patient is deteriorating, CT imaging and bron choscopy may be required. Table 5.2 lists some of the more common forms of noniniectious pulmonary infiltrate. Some condi- tions are exquisitely steroid responsive (e.g. chronic obstructive pulmonary disease [COPD], hypersen- sitivity pneumonitis). Heavy immunosuppression maybe beneficialin certain cases and interventions, such as plasma exchange may also be considered 31PROSO}OVY _QCOSO]OY TOS SECTION 1: Admission to critical care ‘Consequently, carly lung biopsy can be helpful in managing these conditions, particularly in cases of partial response to steroids, Pulmonary embolism Pulmonary embolism (PE) can be classified as follows: + massive PE in association with hypotension; + submassive PE in association with right ventricular hypokinesia on echocardiography: and + nonmassive PE in the absence of the above features Emergency imaging in the form of CI‘ pul monary angiography or transthoracic echocardiog- rophy is advocated when massive PE is suspected, In massive PE, CT pulmonary angiography reli ably demonstrates proximal thrombus. Both sight ventricular dysfunction on echocardiography and an elevated serum troponin T predict & higher mortality ‘Thrombolysis given peripherally) isthefirstline treatment and may be instituted on clinical grounds. in the peti-artest situation, Where thrombolysis is contraindicated or hes failed, surgical embolec- tomy, clot lysis by direct fragmentation or high: pressure jetlysis may beconsidered. Ideally, throm. bol ting. Intubation and ventilation should be avoided because of theincteasein pulmonary vascular tess tance associated with positive pressure ventilation and the added risk of hypotension produced by induction agents. There is considerable disagree- ment about the role of thrombolysis in submassive PE, Ithas been shown to improve the clinical course (by reducing the rate of rescue thrombolysis) when compared with intravenous unfractionated heparin, but no change in mortality has been reported and itcarsies an increased risk of haemorthage. should be instituted in a critical care set- Mechanical respiratory failuie Acute ventilatory flute owing to extrapulmonary causes may result de nove, from conditions such 2s Guillain-Barré syndrome, ar decompensation of preexisting conditions that may or may not have been diagnosed previously. dently sary and may he extremely effective in addition 10 supportive care, Additional processes that con. tribute to respiratory decompensation include the following 1g a cause is vital; specific weatments LUPPER-AIRWAY COMPROMISE Weaknessofthe facial, oropharyngeal and laryngeal muscles can result in swallowing dysfunction and Table 5.4 Comin Acute Neuronal Guillain-8ar syndrome Diphihesia Tick paralysis Paliomyettis Neuromuscular junction Botulism Myasthenia gravis Musde 32 Detmatomyosits/palymyosits Chronic Motor neurone disease IMyasthesia gravis Lamvert-faton synckome Desmatomyoss/polymyosiis Duchenne muscular dystrophy Chest wall dsorders (e9, thoraceplasy, kyphoscolioss)PROSO}OVY _QCOSO]OY TOS interfere with secretion clearance and increase the risk of aspiration pneumonia. Furthermore, weak ness of those muscles may result in upper airway ‘obstruction, particalarly in the supine position INSPIRATORY MUSCLE WEAKNESS ‘This results in poor lung expansion and atelecta sis, leading to ventilation/perfusion mismatch, and consequent hypoxzemia, [EXPIRATORY- MUSCLE WEAKNESS ‘This prevents adequate cough and secretion clear ance, again increasing the rsk of pneumonia. Additional pathology includes: + primary respiratory tract infection, + pulmonary embolus owing to immobility in chronic disease; + cowxistent asthma: and + pulmonary oedema owing to cardiomyopathy. Guillain-Barré syndrome is the commonest neu: ological cause of respiratory failure requiring mechanical ventilation. It is an acute, autoim. ‘mune polyradiculoneuropathy. Most commonly it presents as an ascending paralysis spreading to the ‘upper limbs and the face, Bulbar palsy may also be present. Baily recogniti venous immunoglobulin or plasmapheresis within the frst 2 weeks of presentation and adequate sup- portive care results in near full functional recov: cry in most patients, However, iis associated with an appreciable mortality, mainly owing to pul monary and autonomic complications. About 30% of patients requite ventilatory assistance largely coving to diaphragmatic failure. Close clinical supervision in combination with bedside respiratory function tests is required. Serial measurements (3 times a day) of vital capacity and maximal inspiratory and expiratory pressures should be performed; arterial blood gases may not demonstrate hypoxaemia and hypercapniauntil Inte inthe disease process. During the night, ventila ‘ory function is more dependenton the diaphragm ni, treatment with intra ADMISSION TO CRITICAL CARE: THE RESPIRATORY PATIENT eer rn care unit Physiological features Clinical features ular dysturtion ‘MIP = 30.em H,0 or MEP = 49cm H:0 ‘Autonomic nsabilty Ve = 26 mi/kg Bilateral facial palsy Fall of 309% over 24 hows in YC. MIP or MEP Rapid disease progression Pan: <9 kPa or increasing Pao, Abreviotons: MER maximum exptatry pressure MIP ‘maximum insprotory presser; Fcc, pot presare of carton dixie in areal Hood, Poo, portilpresure of ‘oxygen in artenl bod, vital capacity and continuous oxygen saturation should be moni tored during sleep; transcutaneous CO; monitoring may be useful. 1 is important to note that endotra- cheal intubation in these patients can tigger auto- nomic instability. The consequences of respiratory arrest can therefore be devastating and early intuba Lion and assisted ventilation is preferred. At present, there is no evidence supporting the use of CPAP or NIV in patients with respiratory decompensation due to Guillain-Barré syndrome. Other causes of acute respiratory muscle weak: hess require mechanical ventilation less frequently than Guillain-Barcé syndrome, Specific treatments include plasma exchange and acetylcholinesterase inhibitors in myasthenia gravis or immunosuppres- sion in polymyositis. A detailed diagnostic strategy is therefore warranted, but is beyond the scope of this chapter Infection is often the triggering event for the first presentation of respiratory failure in the chronic neuromuscular disorders. Unlike the mote rapidly progressive conditions, it is reasonable to con sider NIV as an initial form of ventilatory support, and this may be required long term. If invasive ventilation is necessary, then early extubation 33PROsojOvY —_QEOSO|OW 1.050 SECTION 1: Admission to critical care facilitated by NIV or tracheostomy should be con sidered, Respiratory conditions in those with previously abnormal lungs Asthma A significant proportion of asthma deaths occur during hospitalization, Exacerbations of asthma are reversible; therefore, ensuring institution of correct treatment, adequate monitoring and appropriate ciitcal care admission isa priority Patients meeting the criteria for acute life ning or near-fatal asthma should be admit ted to intensive care and maximal therapy admin. istered. As part of their assessment, additional reversible causes mast be excluded, such as pew threat mothorax and lobar collapse owing to mucus plug: ging or pneumonia ‘Oxygen, nebulized bronchodilators and steroid therapy are required. Acterial blood gases should be sampled to assess Paco» and pH. Although high: flow oxygen is associated with higher levelsof Paco, Moderate asthma ‘ne of more ofthe following + Na features of acue severe asthma * PEFR >50-75th best or presicied Severe asthma and lower peak expiratory flow in patients with acute asthma, this should not prevent the admin- ‘stration of maximal oxygen therapy in patients who are persistently hypoxaemic. Oxygen delivered via reservoir bag mask worsening bronchospasm. Ideally, oxygen should be delivered warm and humidified. There is cur rently no good evidence for use of Helios in acute dy and cold, potentially asthma, Nebulized bronchodilators and -agonists should be driven by oxygen and may be adminis- tered continuously. If there is no response, intra- venous f-agonists can be considered, although evidence for this is limited, Intravenous magne. sium sulphate (1.2-2.0 g) is effective and should be administered over 20 minutes; more rapid infu- sion can cause flushing, hypotension and flaccid paralysis. If repeat boluses are required, aclmission to critical careis necessary and continuous infusion may be more appropriate, Intravenous. amino: phylline is rarely administered owing to its side ffect profile and paucity of evidence in its favour ‘One of more ofthe following *# Cannot complete sentences * Pulse > 110 beats/min + Respiratory rate > 25 breaths/min PEFR 33-5014 predicted or usual best life-threatening asthma (ne or mare ofthe following: + Silent chest, feeble effet + Cyenosis/ Spor < 92% * radycarda, hypotension + Exhaustion, confusion, cama * Namal Paco, * PEFR <33H) predicted or usual Dest Raised Pac Abbrevotions: Pow, parts pressive of ca Spa, Soturation ef perpherd angen. a4 Near-fatal asthma ‘One of mare ofthe following and/or requiring mechanical ventilation with increased ventiPROSOIORY PRESOFOWY _QEOSEOW —TLOSO Ik has a narrow therapeutic range and regular monitoring of theophylline and potassium levels is also required, Other agents such as ketamine and halogenated inhalational anaesthetic agents may be necess in refractory bronchospasm. Steroids can usually be given enterally (pred: nisolone 40-50 mg) and intravenous hydrocorti: sone (100 mg 4 times a day) is res erved for patients ‘unable 10 swallow or absorb tab! Hypovelaemia iscommon and fluid resuscitation, is required. 1f intubation and invasive ventilation are necessary, the high pressures required for lation coupled with often severe gas rapping and intrinsic positive end-expiratory pressure lead 10 4 ‘marked reduction in preload to the left ventricle: systemic hypotension and loss of cardiac output er# igno role for NIV in asthma outside of crt. ical care. Low-level CPAP offsets intrinsic positive end-expiratory pressure and may be started after critical care admission Aniibiotics should only be administered if there is objective evidence of infeciion, such as consolida tion on chest radiographs orhigh C-reactive protein levels "Pscudo-asthma! may occur in acute hypewen tilation, vocal cond dysfunction and thoracoab: dominal asynchrony. I is often extremely diff ‘ult to differentiate these from true asthma in. an emergency setting, In this instance, ifthe patient is intubated, then their airway pressures should be dacumented immediately after incubation. This can be useful when treating subsequent exacerba Ghronic obstructive pulmonary disease Exacerbations of COPD account for about 10% of all emergency medical ade quarter present with acidosis. There isa high (7.4%) inpatient mortaliy, In addition, comorbidities often coexist, including heart disease (40%), dia betes (1096), stroke (5%) sions and around a nnd) other chest dis ADUISSION TO CRITICAL CARE: THE RESPIRATORY PATIENT case (1196). Differential or concomitant diagnoses include the following, © Prewmnonia, * Preumothorax: Often this may be difficult © detect on plain radiographs owing to bullae or anterior or posterior pneumothoraces. CT may be required, + Pulmonary embolism: In uncomplicated ‘exacerbation, the incidence of PE Is lows however, up to 50% of patients with COPD have pe artery thrombosis, st mortem evidence of pulmonary + Pulmonary oedema: The features of oedema on, radiograph are often atypical in COPD and old radiographs may be helpful * Lang cancer, © Aspiraion Hypoxiemia should be prevented, while mini mizing acidosis and hypercapaia. Lung function must be optimized while the precipitating cause of the exacerbation is treated, Many paients have an uncomplicated admission responding w the standard regimen of controlled oxygen therapy, bronchodilators (8-agpnists and anticholinesgics) steroids (prednisolone 30 mg for 7-14 days) and antibiotic therapy. Antiobiotic therapy should be instituted in the presence of increased production ‘of purulent sputum anel can usually be given orally Targeted therapy may often be guided by present or past sputum culture results Many patients at risk of hypercapnic respira tory failure are hypoxaemic between exacerbations and do not require high target saturations dur ing an exacerbation. Oxygen therapy may worsen ventilation-perfusion mismatch, cause absorption atelectasis, decrease haemoglobin buffering of CO: by the Haldane effect and reduce the hypoxic ven- Lilatory response. These factors lead to an increase in Paco: via a decrease in effective alveolar venti buffering if patient is found not be hypercapnic, then their saturations may be kept abowe 929, However either until Paco, is known lation and C 35PROsojOvY —_QEOSO|OW 1.050 SECTION 1: Admission to critical care rif they are hypercapnic, their saturations should be kept within the range of 88-9296 or even lower Twenty percent of patients remain acidotic (pH = 7.35) despite optimal medical therapy and these patients are potemtial candidates for NIV. It should be considered before intravenous aminophylline sion, and doxapram. These agents may be used in con: junction with NIV, however, or as a ceiling of ther apy if NIVis not tolerated and invasive ventilation is notindicated, A decision regarding invasive ventilation should be made before commencing NIV, Where possible, decisions should be made in consultation with the patient, relatives, nursing staff, admisting medical team members and critical care eam. This should not be basedl on age or forced expiratory volt 1 second (FEV!) alone because itis a poor predic. tor of physical capacity. Furthermore, it should not be based on a personal assessment of quality of, ie, The attitude towards mechanical ventilation and COPD is often nihilistic. However, in-hospital sur vival is better and duration of ventilation shorter in patients ventilated for an exacerbation of COPD than all causes of acute respiratory failure, with a L-year survival of 40-60%. Paradoxically, previ ‘ous mechanical ventilation is associated with an Improved survival, perhaps suggesting more vari able disease. Factors that may influence the deci sion regarding ventilation include body mass index, functional status and the presence of other organ failure ‘Often patients are ‘accepted! for mechanical ven: tlation if there is deemed 1 be some reversible pathology such as pneumonia, Although there is. a component of logic in this, the higher mortal- ity associated with COPD end pneumonia vom pared with an exacerbation of COPD alone draws into question. Furthermore, although COPD itsefis not reversible, the physiology of the this strate, 36 patient improves after weatment of the exacerba ‘The decision @ admit 10 critical care and/or implement invasive mechanical ventilation needs to consider how intensive therapy can patient, whether they have the functional reserve to withstand therapy and whether further treatment could be given safely on the medical wards. Clear efits and risks of critical care management is required. deally,thisshould be done in anticipation of critical care referral before the patient becomes unstable, even inthe outpatient mprove the communication of the bs dinic, where reasonable Interstitial lung disease Underlying causes of deterioration in a patient with 2 background of interstitial lung disease should be sought, such a8 infection. Serial chest radiographs are often helpful in diagnosing new ine tn particular no clear progression of diseas CP pulmonary angiography should be performed jopathic pulmonary fibrosis and asbestosis are at much higher risk of developing carcinoma of the bronchus, which may cause acute deterioration de © bronchial eccha mia, PE, pneumothorax or tion; if no change is noted, then to exclude PE, Patients with i Idiopathic pulmonary fibrosismayenteran accel erated. phase, with rapidly worsening respiratory Gailure and increased alveolar opacification, The histological features show diffuse alveolar damage akin co acute interstitial pneumonia. Patchy disease on CT is associated with 50% momtality and dit fase involvement is nearly always fatal. Often these patients have been immunosuppressed and conse: quently, conventional and opportunistic infection must be excluded, often by bronchoscopy. Lung biopsy is not usually requited in deteriorations of well-documented idiopathic pulmonary fibrosis: however, where diagnostic uncertainty exists, the cause of the deterioration should be sought andPLOSOION’ PROSOFEVY _QEOSE|OW Toso cnaerer biopsies obtained because intense immunosup: pression may be required. Key points ‘¢ Wellevidenced guidelines for management of ‘many respiratory conditions have been preduced ics stientiic societies (British thoracic ‘+ The use of diagnostic tess, n particular CTand bronchoscopy, help to guide therapy in cases where the diflerential diagnosis is bread + Noninvasive ventilation can be used succesfully outside the citical cate setting in coFD. It may ako be usedin other condiions, but usualy within te critical care unit, + Empirical antibiotic therapy should always take in consideration the provenance and immunocompetence ofthe patient. ADUISSION RETICAL CARE: THE RESPIRATORY PATIENT FURTHER READING British Thoracic Society Standaxds of Care ‘Committee, Non-invasive ventilation in acute respiratory failure. Thora: 2002;57:192-211, British Thoracic Society Standards of Care Committee Pulmonary Embolism Development Group. British Thoracic Society guidelines for the management of suspected. acute pulmonary embolism. Thon 2003;58: 470-483 British Thoracic Society; Scottish Intercollegiate Gauideines Network British guideline on the management of asthma, Thonx 2003;58(Suppl ayitesa National Collaborating Centre for Chronic conditions. Chionic obstructive pulmonary disease, National clinical guideline on idelines management of chronic obstructive pulmonary disease in adults in primary and secondary care, Thorax 2004;59(Suppl 1):1=232. 37Pxasojowy — Qcosojow Tso chapter6 Resuscitation after cardiac surgery Introduction Defibrillation, ventilation, pacing and resuscitation are essential components of cardiac surgical care The 2005 European Resuscitation Council Guide lines report the incidence of resuscitation as 0.7% in the first 24 hours, rising to 1.4% within the first 8 days of cardiac surgery. Overall in-hospital cardiac surgical mortality rates (>3.0%), together with the low incidence of do not attempt resus citation (DNAR) orders and the high proportion oF treatable arvests in this population all suggest a higher true incidence of postoperative resuscita tion, The most likely explanation for the discrep- ancy is that many resuscitation interventions are ‘undertaken in house on the cardiac surgical critical care. Aspatients undergoing cardiac surgerybecome older and sicker, the quality of postoperative care and resuscitation will continue to increase in impor lance. Conventional advanced life support (ALS) fauidelines provide a useful framework but require modificatio critical care setting, This chapter highlights some of the key differences. particularly in the cardiac surgical Resuscitation guidelines Adult basic life support Maintaining the crculation has been promoted aheadof airway managementandbreathingin adult brsic life support (BLS) guidelines, The traditional 38 ABC’ (airway, breathing, citculation) in the previ ‘ous BLS algorithm has been replaced by ‘CAB’ (cit ulation. airway. breathing). Thirty chest compres: sions should be given before any attempt to deliver rescue breaths, In situations where BLS is under- taken, the recommended ratio of chest compres sions to ventilations is now 30:2 for both one. and ‘wo-person cardiopulmonary resuscitation (CPR) More chest compressions and fewer interruptions are achieved with this ratio than with 15:2. In the presence of a patent airway, effective chest compres: sions are considered more important than venti lation in the first few minutes of resuscitation. It should be bore in mind that coronary perfusion pressure progressively rises during chest compres sions and rapidly falls with each pause for ven tilation. Rescuers can now be instructed to place ather than waste time using the ‘rib margin’ method. The single BLS algorithm facilitates teaching BLS to lay people and reminds rescuers to consider airway obstruc: tion ~ but it is also a potential flaw. Future adult sidelines should further increase the emphasis on chest compressions in witnessed unexpected sud: den collapse (patients with saturated arterial blood) and reserve initial combined assisted ventilations and chest compressions for unwitnessed arrests or primary respiratory arrest (patients with desatu rated arterial blood). their hands over the centre of the chestPROSO}OVY ACOSO] THOS Adult advanced life support ‘The ALS algorithm for the management of cardiac arrest in adults has shockable and nonshockable limbs, Prompt and effective BLS and early defib: ‘illation for shockable rhythms are the :wo most important interventions after cardiac arrest, There have been fairly radical changes in defibrillation rec: ‘ommendations forshockable thythms. PULSELES VENIRICULAR TACHYCAROIA/ VENTRICULAR FBRILATION ARRESTS Plseless venticula tachycardia (VI) and ventric Alar Mibglation (VF) secount for the majorly of SS) Figure 6.1. New 2005 Advanced life support algorithm for ‘the management of cardhac atest in adults, (Courtesy of the UK Resuscitation Council and repreduced with petmision.) patients who survive cardiac arrestin a general hos pital. Forevery minute thatthe arthythmia persist the chances of successful defibrillation decline by 7-10%6. Specialist cardiothoracic units should be capable of eaily detection, rapid defibrillation and superior outcomes. A single defibillatory shock (£150 J biphasic oF =360 | monophasic is recom- mended instead of three stacked shocks. Inthe set- Lingof thecardiaccritical cave, when extemal cardiac massage maybe injurious, immediate defibrillation should be the firs-line response for all monitored in-hospital VF arrests, First shock efficacy is greater th biphasic chan monophasic waveforms. Dura tionof CPR between shocks hasincreased to 2 min- utes, Contrary to the new guidelines, there is usu ally no need to commence chest compressions after a successful shock in invasively monitored cardiac surgieal patient NON-VENTRICULAR FIBRLLATION/ VENTRICULAR TACHYCARDIA ARRESTS Aheserogencous group ofcondlilons amy present as non-VF/VT cardiac arrest. Outcome is generally poor unless 2 reversible cause can be found and treated effectively. The frequent absence of a read- ily ueatable undeatying cause means that this ype of arrest has a poor prognosis in general hospitals with only 5-105 patents surviving to discharge. In contrast, in the cardiac surgical critical care ~ where bleding, hypovolaemia and tamponade are all readily treatable, and where additional thers peutic options are available - outcomes should be considerably better, Examination of tends in cena venous pressure, pulmonary artery weds ashi al alrway peut all pleas” wach pointersas tothe possible aetiology of ares. Cessa- tlon of drainage from chest drains doesnot exclude haemormageor tamponade becausethe drains my have become blocked. Although echocardiography is often very useful in the cardiac critical care, tran- soesophageal echocardiography (TOE) may miss 39PROSO}OVY ACOSO] THOS SECTION 1: Admission to critical care Tren ae and asyst Hypoxia Tension pneumothorax Hypovolaemia_ Tamponade itypetalaemia thromboembolic ttypothermia Therapeutic substances in overdose Toxic substances localized collectionsand delay reoperation, Patients with clinical signs suggestive of tamponade should be reopened, even if the TOF is inconclusive ‘When faced with an arrest of this type, Its essen: tialto confirm that VF is not being missed and that leads or pads are correctly attached: ‘treat bradycardias with epicardial pacing if possible; + exclude underlying VF in the presence of fixed-rate pacing and *# consider chest reopening if closed chest CPR is unsuccessful ‘Symptomatic bradycardia is extremely common in the cardiac surgical critical care unit. The ALS guide- lines cecommend atropine as first-line teatment In the cardiac surgical critical care, where tachyear dia is equally undesirable, pacing (when possible) is the preferred option. If pacing is not an option (eg, no wires in situ oF failure to capture), isopro- terenol or dopamine areoften used before atropine is considered. Management of asystole that fails to respond to pacing is an indication for prompt chest reopening. Drugs in advanced cardiac life support Although the use of vasopressors at cardiac arrests seems intuitive and has become standard prac: tice, proof of efficacy has been more dificult to achieve. Epinephrine (1 mg)is recommended every 40 3 minutes to improve coronary and cerebral perf sion. The American Heart Association hassugeested that vasopressin may be used as an alternative to epinephrine. I studies, however, have failed to demonstrate that either vasopressin or high-dose epinephrine (5 mg) offer any additional benefit On the cardiac surgical critical care, it may be entirely appropriate to modify the recommended pharmacological management of a monitored cat: diac arrest. An a-agonist or smaller initial dosages of epinephrine (0.1-0.5 mg) may be administered ‘o minimize the risk of hypertension and tachycar- dia afver successful resuscitation, For patients wi VE/VE arrests it is standard practice to attempt at least two shocks before giving epinephrine, The administration of amiodarone after three unsuc- cessfll shocks increases likelihood of survival to hospital admission, but not survival to discharge A bolus of 300 mgof amiodarone is recommended for VE/VT arrests that persist after three shocks. & further dose of 150 mg may be given for recur rent of refractory VE/VI, followed by an infusion 0f 900 mg over 24 hours, Lidocaine can be given for VE/VP if the patient has received amiodarone, but the evidence supporting its efficacy is weak, Con ider giving magnesium if there is clinical suspicion of hypomagnesaemia. Administration of bicarbon- ate should be considered if arterial or mixed venous pHis 7.1 or less Chest opening Afier surgery via sternotomy, chest reopening is an additional diagnostic and therapeutic option in the eardive surgical eriial care. In addition, chest reopening allows internal cardiac massage, which is considerably more effective than external chest compressions, Bleeding, tamponade, graft occlu a and graft avulsion are conditions likely to be remedied by this approach. Patients most likely to benefit from chest reopen- ing are those with a surgically remediable lesion, those who arsest within 24 hours of surgery andPROSO}OVY ACOSO] THOS those in whom the chest is reopened within 10 minutes of arrest. Delayed reopening or the find: ing of a problem that is not amenable to surgery (eg, global cardiac dysfunction) is associated with 4 poor prognosis. Chest reopening should not be manoeuvre after a prolonged resuscitation sequence. used as a ‘lastditeh Cardiopulmonary bypass The rinstitution of cardiopulmonary bypass (CPB) after emergency chest reopening may allow the resuscitation of a patient who would otherwise de. Hypothermic CPB restores organ perfusion, decom: presses the heart and allows the surgeon to consider all possible options in a more controlled setting Valve replacement, the tepair of bleeding cannula tion sites, graftrevision and additional grafting may he undertaken with often surprisingly successful clinical outcomes. Whenever possible, the patient should betransferred tothe operatingtheatre before the emergency reinstitution of CPB. late resuscitation on critical care Patients with greater preoperative surgical risk adverse intraoperative events and poor physiolog. ical state atthe time of critical care admission are Jess likely o survive to hospital discharge. Similaty, refractory mukisysiem organ failure and recurrent nosocomial infection while on the entical care unit have been shown to be important determinants of mortality. For some patients, there comes a point vwhen aggressive resuscitation is inappropriate and 36 ieulation All cardiac arrests Pulse tate <4 or >140 ‘Neurology Unexplained fallin GCS >2 points Renal Urine output <0.5 mL/ka/hr for 2 consecutive hours Oximetry Spo» <<9040 regardless of Fi, (Other Patients ving cause for concern who do fot rieet above ciietia Abreviatons fit, faction of ried axyge GS 200 (1130) 3 234 2135 (2130) “A, aly and orentate, responds to voice or cnlused/agitcted,f response to pat U,unrespansive Abbreviations: BF blood presure: HR, Heart ce; BR, resprototy rte $p0;, peripheral oxygen slut: UC urine output hospital setting, The effectiveness of the MET con cept is significantly hampered by incomplete doc uumentation of patient observations. Gi importance of respiratory rate and urinary output, recording of these values is often poor. Education and redesigning traditional observation charts are often necessary to improve compliance. The relative success of chest reopening after car- diac arrest on the critical care unit cannot be repro- diced when chest reopening is undertaken on the ward. As the time out from surgery increases, the proportion of surgically remediable causes of car- diac arrest decreases exponentially. At this time, thromboembolic phenomena and cardiac failure are farmore common than bleeding or tamponade. Al patients reopened under such circumstances at the scene of arrest on Papworth wards in the past decade have died in hospital. Surgical reopening, trolleys have now been withdrawn from all ward areas and surgical reopening outside theatres and citical care units has been abandoned, ‘A minority of ward patients who arrest on the ‘wards may benefit from chest reopening. Scoop- ren the 2 ing these patients back to theatre has advantages for the patient, ward staff and arrest team. It also jves the surgeon the option af crashing back onto cre. Catheter laboratory arrests Invariably, VEIVP arrests in ae iatrogenic, amenable to very early defibrillation and associated with return of spontaneous circula: jon in more than 90% of cases, as well asa greater than 80% chance of survival to discharge. tn hos. pitals with a cardiac catheterization laboratory, the inclusion of catheter laboratory arrests in overall hospital statistics can significantly skew the overall hospital survival to discharge rate. In cases of coro. nary dissection or other surgically amenable con: ditions, early transfer to the operating theatre and emergency CPB should be considered. he catheter hboratory Postresuscitation care Hypothermia Mild hypothermia improves neurological outcome in comatose patients successfully resuscivated afterPEOSOIORY PRLOSOJOW —_QEOSE|OW TOO Prine: Ya To Caine (Meee Geography The geagraphical location and layout of cardiac surgical wards are both mpotant. Monitoring ECG monitoring s invaluable for detecting asystole and shackable mythms but less useul at detecting nonshockable rhythms causing PEA Prevention Nowheto the statement ‘Prevention is better than cure! mere true than inthe fied of esuscitetion. International studies have shown that many citicaly ill patients receive suboptimal care on the genesal wards. Many terminal ares's on general wards are preceded by unrecognized or inadequately treated deterioration in their vital signs. Consideration should be given to the preemptive transfer ol a deteriorating patient tothe citical care aiea The appropriate use of DNAR orders sianicantly reduces the incidence of unexpected cardiac anes. Early detection Outcomes ror witnessed arrests are beter than those where the inital arrest is undetected with erly detection, the propation af par VF/T anests higher and tne 0 delibilletion reduced. Fauipment £0 are now inreasnaly beng deployed in pblic ses. hey are now so prevlest tha 1S traning is being extended to include teaching on the use ofthese stiaightforwaid devices. There isa strong argument for putting semi-actomated éeibilato's on general medical and Suigcal wards. AED for n-hospital use should include an £C6 display and a manual overide facility for use by the cardia atest team, Accumulating evidence suggests thet biphasic detibillation waveforms may be superior to ‘manophasic wavelorms Training Resuscitation training should place greater emphasis on the identitcation af the atk patient and prevention of cardiac arests. Scenario-based trainng may be of value ‘Abbreviations: AID, automated extern defitilotar: BL, bast fe support: ONAR, do not attest resuscitation C6, lectocardogrop PE, pubelesselectical ct V,venticulrkbillaicn; WI, ventricular tochycaria, ‘out of hospital candiac arrest owing to VF. Mecha: nisms of action of therapeutichypothermia indude Key points reduced destructive enzyme actions, suppression of free radical actions and inhibition of release and uptake of excitatory transmiters. Cerebral metabolic rate decreases by approximately 7% for every 1°C reduction in temperature, ‘Therapeutichypothermiais, however, rarely used in the cardiac surgical critical care, mainly owing to concerns about arthythmias, hypotension, coag- ulopathy and infection. Interestingly, cardiac sur geons are increasingly using normothermic rather than hypothermic CPB for routine catdiac surgery. © The ALS algorithms require modification after catdiac surgery. © Consider the possibilty of undeslying VF in ‘systalic!atests and paced patients with apparent electromeckanical dissociation. © Look for epicardial pacing wires in bradycardic airests before giving atropine and epinephrine! © Resusctaton after caidlac surgery Is associated with better outcomes than resuscitation in ‘general hospitals 4BPROSKIOKY —PRESOFOW QCOsO,0v" 1.080 SECTION 1: Advis to critical ane FURTHER READING Buist MD, Moore GE, Bernard SA, et al. Eflects of a ‘medical emergency team on reduction of incidence of and mortality from unexpected cardiac ertests in hospital: preliminary study. BM) 2002:324:387-390, Goldhill DR, MeNarry AE, Mandersloot G, etal. A physiologically-based early warning score for aul patients: the association between score and outcome, Anaesthesia 2005;60: 547-553. “4 ‘The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia 1o improve the neurologic outcome after cardiac arrest.N Engl J Med 2002;346:549-556. Resuscitation Couneil Website. Available from: ‘worw resus org.uk Soar, Deakin CD, Nolan JP, et a. Furopean Resuscitation Council guidelines for resuscitation 2005, Section Cardiac arvest in special circumstances, Resuscitation 767 (Suppl. 1):S135-170.P2osojow — Qcosojow Tso Chapter 7 Transport of the cardiac critical care patient Introduction When critically il cardize patients are mowed, either Within the hospitalor between hospitals, the princi ples of safe transfer should be applied regardless of the distance travelled or the underlying diagnosis. eahigh level of expertise because further skilled help may not be readily available if problems occuren route. These transfers have significant associated risk and the tuansfer period has been shown (0 be one of the most hazardous phases in any episode of exit ical care. There must be a local strategy in place to ‘manage the process, so that safe and efficient coor: dination ean take place on a 24-hour basis Additional invasive monitoring and organ sup port before transfer may be required. Compactiech: nology to analyze blood gases and electrolytes dur ing uansfer is now readily available and should be used, especially during prolonged journeys. ‘Thrombolytic therapy, pacing and defibrillation have been shown to be both effective and safe dur- ing wansport. Bypass circuits and left ventricular assist devices Interhospital iransier in particular requi represent the custent extremes of car diac support during transfer, used only by selected specialist centres with fully trained medical, nursing and technical staffin attendance, In general, the aim of transfer is to upgrade the level of care or obiain appropriate specialist diag. nostic or treatment facilities, Transfer is associated with complications; even the physical movement fiom a bed 1 a suetcher or examination table may be hazanlous. Complications range in severity from minor t potentially life threatening and may be related to clinical, equipment or organizational problems. The risk of a complication incicases with the extent of instrumentadion of the patient and the complexity of the machinery. It has been rec: ognized that the flequency of complications during transportis high and international effortshave been ‘made to improve the standards and organization of transport systems for the critically il, Current guidelines There are currently no specific guidelines relating to the transport of the critically il cardi patient, but general guidelines are valble, including from intensive care societies. Staff involved in the trans fer have a responsibility (0 ensure that they are adequately trained and experienced in the transfer procedure. Careful planning and detailed knowl edge of the equipment are vital to minimizing the tisk The transfer process Communication and control These are vital fist elements in the wansfer pro cess, The decision to move a critically ill patient must be made by» senior citi care doctow who can adequately assess the balance of isk wo benefit and plan the transfer. This may requite discussion with other tems inthe hospital, the receiving unit 45PEOSOIORY PLOSOJOW —_QEOSO|OW _TLOSO SECTION 1: Admission to critical care essential between named senior responsible m cal and nutsing personnel at both units. This can be a frustrating process, especially for smaller hospi: tals dealing with tertiary care centres. Ideally, there shoul be a dedicated telephone number that ean be used in the organization of the transfer Communication during transfer traditionally relies ely on the ambulance radio but in practice, phones are a particularly useful, quick and effective mode of communication and they should be carried by the transferring team. To avoid elec ‘tromagnetic interference, both phones and radios should beused at least 2 meters from all monitor ing and electrical clinical equipment. ‘Team members may have varying levels of expe rience and training in the transfer process and may benefitfrom a structured briefingbefore the transfer process starts, Initial assessment In general, critically ill patients tolerate transporta- tion poorly. Hypoxia and hypotension occur in at Teast 15% of transfers and may persist for sev- eral hours after artival atthe receiving hospital. In cases of inadequate resuscitation, equipment fail: ture, environmental delays or the transport vehicle being involved in an accident itself, uansportation can cause serious morbidity and mortality Thece is no risk model for predieting long-term ‘outcome in such patients. There have been attempts al risk scoring for these patients, but none have gained widespread acceptance. Fundamentally the mote deranged the physiology the higher the tsk. Preparation and packaging for transfer A checklist to avoid omissions is helpful and can be incorporated into the transfer documentation, Stabilization and meticulous preparation ate the keys to a successful transfer. All personnel should familiarize themselves with the patient, their previ ‘ous medical history and the current condition. The familiar concept of ‘optimization’ of perfusion and 45 ‘CHECKLIST Airway and NG tube Breathing and end-idal 0, Gredation an¢ invasive monitoring Disability cereal cllor and head injury cave Exposed, examined and equipment sorted out ané secute Family iniormed Fina considerations ‘Ask fornotes and x-ays? Bed confined? Continuity of care assured? ‘Diugs and spares? Documentation Everything secure? tissue oxygen delivery before any high-risk proce: dure should be applied o this group of patients Full clinical examination with special reference to on-going monitoring should be carried out. All possible sources of continuing blood loss and sep- is should have been located and controlled ifat all possible. Hypovolaemia is associated with greater risk of hypotension during moving: therefore, ade. quate filling and correction of intravascular volume should be ensured. If there is a risk that bleeding may continue despite best efforts or restart during transport, blood should be ordered and packaged for transport according to laboratory instructions, in general, if packed in an insulated box with ice it may be used for up to 4 hours. Neurological deficits should be noted both pre- and posttransport and any changes clearly doc- ied. Optimal respiratory function is funda mental. Ifspontaneous ventilation is compromised, intubation and mechanical ventilation must be ini- tiated before transport. Also, if the consciousness level is depressed or fluctuating or if the patient isPx osojovy QC OsojOW confused and agitated, cleave intubation should nf dhe sieway in tan. sit Facemask continuous positive airway press nnrely possible during transport, and patients who requive this for adequate oxygenation should « he electively intubated. Optini and adjusting inspired oxygen fraction should be performed before moving the patient, and blood pases checked, along with achest radiograph Adequate venous access must be in place. A uri nary catheter and nasogastiic tube should be con: be performed to prevent I ation of ventilation sidered, All ines and tubes must be securely fixed, with sutuies iFneces y- LCuansport by alr is cho: sen, chest drains need to be on a non-underwater drainage system and be easily accessible during transfer, This may be achieved by securely connect nga nasogastric drainage bagto thechest drain, and ensuring that this ic helaw the level of the hed at all times, If the chest drain is continuously bubbling because of an unresolved air leak, the underwater system should be retained and continuous suction during the transfer (at 5-7 kPa) prevents an enlarg. ing pneumothorax ‘The rewlts of recent investigations chest radiograph, other radiographs, haematol ‘ogy and biochemistry should be checked and car ried with the patient. All documentation, includ: ing referral letters, investigations, radiology reports, hard copies of radiographs and computed tomog: including phy scans, should be gathered and the receiving hospital recontacted before departure to confirm availability of the bed and give an estimated acrival time, This also allows an update of any changes in the patients’ condition, Monitoring ‘The standatd of monitoring should approach that expected within the hospital seting and minimum standards indude: + the continuous presence of appropriately rained stall + electrocardiograph (EC ORT OF THE CARDIAC CRITICAL CARE PATIENT + invasive blood pressure * arterial oxygen saturation; + end-tidal carbon dioxide in a ventilated patient and + teamperature, A disconnection alarm should be used whenever mechanical ventilators are used. Additionally, for cardiac patients there should be: + monlwr/defuillator plus paperjrecomder, + defibrillator pads: + quick4ook paddles or hands-free patches; and transcutaneous cardiac pacing facility Equipment Equipment must be suited to the environment namely, durable, lightweight and with sulficient battery life. monitored oxygensupply with asafery margin of at least 2 hours om the transfer time should be carried, Modern portable ventilators are sophisticated enough to allow relatively complex modes of ventilation, However, asurprisingamount of oxygen may be needed to drive theventilater, and this needs to be taken into account together with the inspiced oxy requitements forthe journey, There ate published nomograms that can assist with these calculations fraction when calculating the For longer transfers, a large margin of safety is required for unforeseen emergencies or delays en route, Portable monitors, with a single power source, combining oxygen saturation, EC invasive and noninvasive blood pressure are essen tial, A dedicated equipment bridge, containing ven- tilator, monitoring equipment and infusion devices and is becoming the method of choice for provid ing these requirements. This can be manufactured fairly simply locally, but must be robust enough © withstand the rigors of transport, compatible with stretchers and vehicle fittings and may nced formal clearance to be fitted in aircraft, There ate sophisticated commercial integrated equipment bridges available, but their complexity and incompatibility with most ambulances make a7PROSO}ONY ACOSO] THOS ‘oxygen requirement = 2 x transport time in minutes, (IV x flog + ventilator driving g3s) bxample. 1 hour transfer, minute volume 10 L/min Flo 0.6, ventilator diving gas 1 in, % Oxygen required = x 60% (10 0641) = Allowing for extra, this would requite 2 x sited cylinders or 1 x Fsied cylinder Oylinder capaciy 0,340 © 4601 LE 680 | F, 13601 Abbreviations: Fi, fraction of spied axygen MY, ‘minute volume them an impractical and expensive luxury. Alarms should be visible as well as audible. Suction and defibrillation should be immediately available. A. ‘warming blanket is also a consideration in cold cli. mates. A reasonable range and supply of medica tions should be carried with pumps o administer them, ensuring that all such devices have charged and spare batteries, (Some syringe drivers will run olf standard AA battery power) Interhospital management The safety of all those involved in the transfer is of paramount importance, Travelling in vehicles at high speed is hazardous; therefore, the crew's instructions must be followed. The team should censure that all equipment is adequately secured or stowed before setting off. Before vehicle departure, attendants should ensue thet the patient, the ven- tilator and monitoring and infusion devices are in view and accessible. They should secure themselves, using the seatbelts provided and should remain seated during the transfer if tall possible 48 Figure 7.1. Stretcher in an ambulance. The accompanying equipment snot secured and ais risk for both patient ané escorting stat When staff may be required to move outside the whicle onto the public highway, high visibility dothing must be worn, This should include a long- sleeved jacket with bands of retro reflective material surrounding the circumference Despite meticulous preparation, unexpected clin ical events may happen en route. Access for clinical intervention is not easy in a patient who is secured on a transfer stretcher, in a confined space, with monitoring atached and on the move. Stopping the vehide should always be considered if transport is by road. IFan attendant must perform a task while the vehicle is in motion, the ambulance crew must be informed. The attendant then adopts a kneelingPROSO}ONY ACOSO] THOS shooting during tiansler Common physiological changes Hypoxia, ardiac dysthythmia Hypotension Decrease in Glasgow Coma Scale Hypothermia Hypoglycemia Common equipment problems Exhaustion of oxygen supply Ventilator malfunction Loss of monitoring Loss of intvavencus access ‘Accidental extubation or tracheal tube blockage position within the ambulance, using one arm to hold on for stability, Ater the task has been com: pleted, the attendant should return toa secure seat In the past 15 years, technological support on ambulances has improved tremendously. Mostertt «al cre facilites can now be packaged into thecon- fines of an ambulance or small aircraft. It should be noted, however, that notall ambulance services possess equipment of the same sophistication Air ambulances and helicopters can sometimes appear to be an attractive alternative, However, the lack of familiarity with the environment and the high cost make the use of ai transport impractical in many countries. Some regions have integrated Jand and air ambulance services (Fixed-wing and helicopter) fora scattered population. The specifics ofairtransportare heyond the scape ofthis chapter refer to the further reading list for suggestions Receiving hospital and hand over Courtesy isessential when handing over. The patient the teaponsibilty-of the transfering per sonnel until safely delivered to a bed in the receiv ing hospital bed, with all monitoring in place and a completed hand over. The name and signature of the receiving doctor com ns the continuity of eare Table 7.4 Handover checklist HANDOVER ‘Acute problem ‘Belore admission to intensive care ‘curient clinical condition ‘Drugs/inlusions and documentation xaminaiion and any problems during tansport Fonily and provides a point of contact for future queries All documentation should be completed, including any undocumented transfer events. Post-transfer analysis On return to base, all equipment should be accounted for, electrical equipment back on charge and all documentation, including incident and audit forms, completed. Any debriefing required (for training purposes or i there have been prob lems with the transfer) should take placeas soon as practicable, Power supply AC power for monitoring can usually be sup plied from the vehicle inverter, if fited. If this power source is interrupted, the internal battery normally takes over. Clealy, the power require ments of all equipment intended for tensport use should be checked before the intended tanste and matched with the available power fac the availble ambulance or aircraft, Some ambu- ities on lance services have dedicated transfer vehicles with a 240v AC supply delivered through standard plug sockets, Transport of patients on an intra-aortic balloon pump Safe air transport of intra-aortic balloon pump IABP) has been validated mostly in the transfer of patients ftom peripheral hospitals © tertiary care 49Px osojovy QC OsojOW SECTION 1: Advis to critical ane centres. The most frequent problems encountered are uncoupling of tubing oF electronic connections and difficulties with helium cylinders, Experience with such transfers is limited to small numbers of patients, but studies report acceplable transfer out comes with few adverse incidents. INTRA-AORTIC BALLOON PUMP EQUIPMENT = Inua-aorth balloon pump with wansport support module. + Lead cable. Skin ECG © Transducer electrodes, © Invasive arterial presaure monitoring (there should be a dedicated separate arterial line in addition to that on the IABP), ‘= Balloon catheters (8 Fr gauge, 9.5 Fr gauge, with insertion kets). © Extension tubing + Adaptors to enable the connection of various brands of ballooa catheters to local equipment. = Spare helium cylinder * Operation manual + Stopcocks. * A GO-cesyring PRETRANSFER CHECKS Prepare the balloon pump for transport and con firm that the ECG lead cable and transducer are directly connected to the pump and in working ‘order. Check that there is enough battery time avail able with the IABP for the journey to the receiving, hospital or an external power source is available Acrange intravenous lines, drips, invasive lines and assist im the transfer of the patient from the bed to the suetcher. The transport wam should be skilled and experienced in the set-up, operation and (fou: bleshooting of the IABP. Transport of patients with pacing Temporary pacemakers (external and/or transve- nous) maybe in use External pacing pads should be 50 carried in caseof pacemaker failure and the transfer team should be familiar with the pacing function of the defibrillator Extracorporeal membrane oxygenation and transfer of extreme high-risk patients ‘The use of extracorporeal membrane oxygenation (ECMO) during transfer is reasonably well estab: lished in ceria spedalisi ceglonal services. for both adults and children. Transferring patients on ECMO is clearly complicated and resource dependent. Both venous-anterial and venovenous bypass have been used success(ully. Intethospital FCMO has also been reported for patients with cardiogenic shock unresponsive to conventional treatment. Some ECMO centres have their ewn dedicated sport team and have transferred patients «afely over long distances, despite significant respira tory and cardiovascular compromise, There is no demonstrated excess mortality in this group com pared to patients who are not moved Recently, pumpless extracorporeal lung assist has been used during transport of high-risk patients with severe adult respiratory distress system to specialist cenues, This is an ultracompact extra pulmonary gas exchange system that is perfused by the cardiac ouiput of the patient. It does not need extended technical support and, compared with ECMO, may be ea nel and vehicle requirements. Further evaluation is required jer in terms of person. Retrieval models Centalization of specialist services has led to the development of children’ retrieval services in major centres, Unfortunately, the same is not true for adult services despite some evidence that dedicated retrieval teams have reduced morbidity and early mortality, Further prospective investigations may prove the medical efficiency and cost effectiveness of such asystem,PEOSOIORY PLOSOJOW —_QEOSO|OW _TLOSO mnie 1. Identity regional hospitals, ‘Local ist with telephone numbers ‘Specialist Ist with telephone numbers 3. Wentiy kit trtrahospital ‘*Ventiator and powe' lead ‘Portable moniter and power lead ‘= 5yinge dives and power leas ‘= Spave batteries and extension lead ‘Transler bag + rugs bog ‘Oxygen and sel-inflating bag ‘#Persannel and porteng ‘Notes and radagraps 4. Identity personnel ‘Core specialty experience ‘*Aieway management ‘lonotopes ‘*Headinjures and trauma =Paedaties 6. Identify Training ‘Safely training ‘Everything not included in envronment specie training Team training ‘Incorporating semulated use of kit; safety dills and simulated emergencies. shoul include medical, nusing, paremedical and eviation personnel wheie appropriate Vehicle-specitic training ‘To include escape procedure; use offre extinguishers, engine cut-off and radio, 2, Ndentity key statt * Consultant authos7ing transler # Consultant authorizing reception Internospital ‘Ventiaior ard power lead + artable monitor and power lead *# Sjinge divers + Power inverter /adapter and spate bateries ‘Transfer bag + D1ug3 bog + Oxygen and selt-nflating bag ‘Personnel and portering + Notes and rdiogiaphs ‘ Documentation audit ‘orm 5, Familiarity with kit ‘Ventilator = Dugs = Syringe drivers © Monitor ‘Transducers ‘ Defirilator/extemnal pacer ‘ Specialst equipment (ECMO, ABP) 7. Quality contiot * Kit ched and e-spply «bug expiry dates + Staff cutendes and competencies Regular audit and feedback + Sypetvsion of utior sat 1.9 book review + Citica incident reporting system ‘0n-going equipment improvement and update ‘Abbrevitlans: EMO, extracorporeal memtvane oxygenation; ABP, traeatcballosn pump,PLOSOIOW’ PROSOFEVY _QEESE|OW Toso SECTION 1: Advis to critical ane Key points © Planning, traning and detailed knowledge of the equipment are vital to minimize the rks of transfer Early communication with the receiving unt is essential. ‘© tically il patients may tolerate transportation poetly and the team shouldbe prepared to intervene en route. ‘© stabilization and meticulous preparation are the keys to a successful transfer, FURTHER READING Advanced Life Support Group, Safe nansfer and serievat The practical approach, London: BM) Books; 2002 Intensive Care Society Standards, 2002 guidelines forthe transport of the critically ill adult. Available at: www icsac.uk/icmproffdawnloads) icstransport2002mem_pdf. Lutman D, Pewos AJ. How many oxygen cylinders doyou need to take on transport? A nomogram. for cylinder size and duration, Emerg Med J 2006;23:703-704, Markaki , Dalezios M, Chatzicostas G, ral Evaluation of a tisk score far interhospital transport of critically ill patients. Emerg Med 1 2006;23:313-317, Martin T. Handbook of patient transportation. London: Greenwich Medical Media: 2001Qe-0s0,0 SECTION 2 10 "1 12 13 14 15 16 W7 18 General considerations in laecemat lee Re Managing the airway AA, PEARCE AND 5, Mc{CORCELL Tracheostomy |. VARLEY AND fF. FALTER Venous access J-E. ARROWSMITH Invasive haemodynamic monitoring PA, WHITE AND A, KUEIN Pulmonary artery catheter 5. REX AND WF. SUHRE Minimally invasive methods of cardiac output and haemodynamic monitoring mM, THAYASOTHY Echocardiography and ultrasound 5.1, RUNNELS, K. VALCHANOY AND R. HALL Central nervous system monitoring 1M LEEMANS AND C.R. BAILEY Point of care analysis CC. WILLMOTT AND J.€, ARROWSINTH Importance of pharmacokinetics fA AND IA, FURLANUT Radiology N. SCREATON AND €. SATPLOSOIONY PROSOFEWY _QEESE|OW Toso Prine: ve To Come em autorskim Material chroniory prPROsojOvY —_QEOSO|OW 1.050, Managing the airway Introduction The provision of a patent airway from the exter: ral stmosph tothe lower trachea is commonly requited 1 facilitate mechanical ventilation in the critically il, A cuffed tracheal tube provides the highest degree of airway maintenance and protec: tion anal this is the most frequently wed device Core competencies for airway management inca diothoracie eiical careinclude relevant physiology and pharmacology, care of the intubated patient. strategies for intubation and extubation, intubation of a patient at risk of aspiration. the management of failed intubation and filed ventilation and spe- dialized techniques for lungisolstion. Physiology In normaladuts breathing ait, alveolar minuteven tation is approximately 3.5 L/min, The Pao For given inspired type conoentraion tan be alar Inted from the alveolar gas equation, A decrease in alveolar minuie ventilation will Hypexaemia secondary only 0 a reduction in minute ventilation can be treated easly by inceas ing the inspired oxygen. ‘Therelationship beoween Pao and Paco; Is more complex and isinfluenced by venous admixture and cardiac output, With a venous admixture or shunt fraction greater than 20% to 25%, it may prove Cchapter8 impossible to raise the Pao; to normal, even with 100% Inspired oxygen, The procedure of tracheal intubation is often undertaken to permit positive pressure ventilation when spontaneous respiration fails to. maintain gaseous homeostasis, Short periods of hypeventi: lation are inevitable during intubation and major airway interventions in critical care should always be preceded by a period of precxygenation. Preoxygenation Preaxygenation isthe term used for the procedure of breathing (or ventilation with) 100% oxygen to replace the nitrogen in the functional residual capacity with oxygen. This exygen store in the lungs ermitsalonger time for maior aeway interventions before the onset of hypoxaemia, and can be life sav ing, Breathing 100% inspired oxygen for 2 to 3 min. utes (3-5 time constants) is sufficient to raise the alveolar (or end-idal) oxygen to 90% 10 919% in normal patients During preoxygenation, the mask should fit tightly om the face the circuit should be high rebreathing of expired gas. The reservoir bag in the circuit should be distended and move with respiration. If the patient is already on contin uuous positive airway pressure. this should be left in situ and the inspired exygen increased 1 100%. the flow of oxygen into 10 Lmin) to avoidPROsojOvY —_QEOSO|OW 1.050, SECTION 2: Genera considerations in cardiothoracic ential care PAO: ~ F102 Py-Pyg0)- PACOVR. Figure &.1 Alveolar gas equation. Abbreviations: PB, barometric pressure (100 kPa at sea level; PH20, saturated ‘vapor pressure of water at 37°C (6.3 kPa); R,resratory quotient (0.8 on mixed diet), Preoxygenation provides a degree of safety dur ing intubation (and extubation). In critical care patients, oxygen consumption may behigh and the functional residual capacity volume small, result ing in much more rapid development of life: threatening hypoxaemia, Anaesthetic ogents Anaesthetic agents produce unconsciousness. Clin ically useful drugs are gien intravenously asa bolus cover 20 t030 seconds, act within one arm-brain cir cation time and have a dose-dependent ffect on length of unconsciousness. The main side effect are hypotension dueto eduction in peripheral vascular resistance and myocardial depression, peoPoFOL Propofol is the most commonly used induction agent and is also suitable for long-term sedation. (0, concentration in'apined ges 2 4 68 10 ‘Alveolar ventiation (min) (BTPS) Figure 8.2 Relaionship between alveolar minute Ventilation and Pc; fo: various inspired oxygen 56 4000 =r 3000 = Tomar 2000 \-=- Blood) = FRC 1000 + + 0 30 60 90 129 180 Figure 8.3 Increase in oxygen stores with duration of reoxygenation, Time 0 = ait, It is an isopropylphenol formulated in soybean emubion; the solution is isotonic with a neuteal pH and supports bacterial growth so unused drag should be discarded after 6 hours. The bolus dose for induction is 1 19 2 mg/kg. HroMIDATE Promoted as the induction agent with the least cardiovascular depression, this imidazole deriva: ive is prepared in propylene glycol. The standard induction dose is 0.15 10 0.30 mg/kg. Unfortu nately, the drug is a powerful inhibitor of 11-8 and 17-a hydroxylation and interferes with synthe- sis of mineralo- and glucacorticoids, Deaths due to hypoadrenalism have been associated with infu: sions of the drug, and even single doses have a noticeable biochemical action. Some critical care uunitsdo not use the drug at all; some provide steroid coverifitisused, and othersallow only. asingledose. OTHER SEDATIVES Benzodiazepines may be used in the place of anaesthetic agents, particularly when the patient is already hypotensive or is already: vasodilated Agents such asmidazolam can be expected to reduce the blood pressure less than propofol or thiopen tone, but inadequate anaesthesia isa risk, and increased doses of opivids should be employed.PROsojOvY —_QEOSO|OW 1.050, opioids Opioids reduce the cardiovascular response tointe tation and prolong the duration of unconscious ness from the induction agent, bu and tend w exacerbate hypotension, Clinically use cause apnoea il, fal drags are fentanyl, 1104 gikg, and alfen 10 10 20 pike. Musde relaxants Tracheal intubation is usually possible only if the slottic closure reflex is obtunded. Muscle relaxants are commonly used for this purpose. The drugs are given after the induction agent and appropriate sedation must be continued to avoid the situation of a paralyzed patient who is aware but unable to move SUXAMETHONIUM, A rapidly acting depolarizing muscle relaxant, sux: amethonium has a duration of action of 310 6 min: ues, must be stored in the refiigerator and given in a dose of 10 to 1.5 mgikg. Its onset of action, econds, is accompanied by visible mus: de fasciculation. There are numerous side effects, such as transient hyper within 45 alaemia, particularly severe after major burns or spi cardia, Some physicians believe that the risks out weigh any benefits in the critical care setting al cord injury, and brady. ATRACURIUM AND CISATRACURIUM Auracurium and its monoisomeric form cisatra curium used non: depo for intubation and when muscle relaxation must be maintained. Atracurium, a benzylisoquinolinium compound, is not eliminated by renal or hepatic processes, butis broken down in the body by Hof- ‘mann degradation, which means tha the molecule falls apart under the influence of pH and tempera: ture, There is also nonspecific esterase metabolism, A long shelf lie for the drug is produced by ing it in the refrigerator with am aciel pH in the are the most commonly izing muscle relaxants in critical care both CHAPTER 8 MANAGING THE AIRWAY ampoule tn clinical use, itis administered in a bolus dose of 0.5 mg/kx and produces adequate muscle relaxation for intubation in 2 to 3 minutes Larger bolus doses (up to 1 mg/kg) can be used to speed up onset, but these larger doses produce ele- vated plasma histamine levels, which may produce adverse effecs, particularly hypotension, flushing and bronchospasm. Gisatracurium isan isomer that is three times more potent and does not cause his: VECURONIUM AND ROCURONIUM Both vecuronium and rocuronium are steroidal, pondepolarizing relaxants. Roaironium. in 3 dose 0f0.6 to 1.0 mg/kg, isgenerally acknowledgedas the drug with the fastest onset: it produces good con ditions for intubation in 60 seconds, Vecuronium does not release histami 1c, even in high doses of 0.2 mg/kg, Both drugs are mostly metabolized in the liver Airway management equipment Safe management requires immediately available equipment, aknovledgeable/sklledassistantanda back-up plan{protoco! for failed intubation. A di ficul airway tolley should also be available ‘The laryngeal mask may be more reliable as a means of veniilaion than the facemask and should always be considered in an unconscious oF para Iyzed patient in whom facemask ventilation is dif cult. Itdoes not protectthe airway againstaspitation of gstricconcents Management of the intubated patient After cardiac surgery, patients often artive in the critical care unit already intubated and ventilated icianat hand over should acquaint themselves with the following points + adequate fixation of the tube: + size of tracheal tube: + tbe inserted to correct depth; Thereceivingli + any difficulties with intubation,PROSO}ONY ACOSO] THOS Printer Ye To Come! SECTION 2: General considerations in cardiothoracic crvical care esr no te Facemask apnanraphy or oesophageal cetector device Oral end nasal airways Laryngeal mask Emergency crcothyrotomy kit Spare laryngoscope batteries / bulbs Magi forceps Suction catheters Catheter mount Tape erties for securing tube we working Syringe for inflating calf laryngoscones Introéucer (gum elasti: bougle) Tracheal tubes, ses 0-90 mm adequate initial settings for mechanical ventilation) ‘back-up ventilation bag with 100% oxygen immediately available; + equipment required for reintubation; and + appropriate pharmacological sedation, ‘The tube should be adequately fixed, usually by a tape encircling the head and tied to the tube, to avoid inadvertent removal or further insertion of the tube, The anaesthetist should specifically handover any difficulty during intubation, which should trigger special arrangements (staff or equip- ment) for extubation or reintubation. ‘Thecorreet depthofinsertion of a tracheal tube is ‘when the tip is approximately 2 cm above the carina. Insertion deeper than this risks endobronchial intu bation, either continuously or with movements of the head/neck. Clinical examination ought to show symmetrical bilateral chest expansion during inspiration, with equality of breath sounds over all regions of both lungs. Ifthere is any doubt, a chest radiograph should be performed, 58 Intubated ventilated patients are usually trans- ferred on 100% oxygen with manual ventilation by simple Waters or Mapleson C circuit The period of transfer onto mechanical ventilationis a time when critical incidents can occus. The mechanical venti latorshould be set according to the protocol of the individual unit and typical settings are as follows. + Tidal volume of 8 to 10 ml/kg + Rate of 10 10 12 breaths/min, + Inspiratoryexpiratory ratio of 1:2 +6096 inspired oxygen. + Positive end-expiratory pressure of 3 10 5 canl0, ‘+ Maximum peak inspiratory pressure of 30 cmH,0. ‘+ Minimum minute volume of 3 L/min, ‘Another means of ventilation should always be direcily available (stich as the circuit used for trans. fer) if there are problems with mechanical ventila- tion or desaturation, Thoracic patients are not commonly ventilated clectively after surgery and indeed it may be rela tively contraindicated, The bronchial stump suture or stapling line would be subjected to positive pres- sure, the risk of Infection is incteased and ait-leak from cut pulmonary surfaces will be more of a problem, intubation ‘The need to intubate a patient in the cardiothoracic critical care unit commonly indicates deterioration in cardiorespiratory function. Itis often a planned intervention, but may be necessary in a crisis situ- ation. Before attempting intubation, an adequately competent clinician should be found (usually an anaesthetist), and equipment, drugs, assistance and suction should be prepared, along with the mechan- ical ventilator itself Indications ‘The indications forintubation are failure of gaseous homeostasis with spontaneous respiration (pH.PROSO}ONY ACOSO] THOS eres Limited mouth opening (<3 cm) Limited alanto-occpital extension Large tongue ‘wollen floor of the mouth or neck Previous head neck surgery ‘ropharyngeal or lyngeal oedema/masses Sividor or high dysphagia Oropharyngeal bes < 7.2; Pao; < 7-8 kPa on 60% inspired oxygen), excessive work of breathing or tiredness, cardiovas cular instability with hypotension, decreased level ‘of consciousness or other causes of inability to pro: {ect of maintain the airway, Prediction of difficult direct laryngoscopy Oral intubation by direct laryngoscopy is easy in ‘most patients, but may be very sible on occasion. A brief airway evaluation should look for common predictors of difficulty and itis ‘wise then to enlist more senior hep. ficult or impos: Oral or nasal intubation? ral intubation is common, but nasotrachealtube may sometimes better tolerated by the patient and more stable in position. Disadvantages of nasotra- cheal intubation include nasal haemorrhage, the requirement fora smaller tube, the risk of atransient bacteraemia, the development of paranasal infec: tion and mucosal ulceration, Tracheal tubes ‘Tracheal tubes are made from polyvinyl chloride, sized by the internal diameter of the lumen in mib: limetersand designed for single use, When removed (CHAPTER & MANAGING THE AIRWAY from the packaging, the tubes are uncut and the length can be seen from the markings in centime- ters from the tip. Appropriate sizes for use in adult critical care are 8.0 mm for women and 9.0 mm for men. Along tube allows flexibility in depth ofinse tionand accommodates facial swelling (particulariy in burns or oedema associated with anaphylactoid- type reactions), but risks being inserted to0 far into the airway resulting in endobronchial intubation, For normal-sized adult patients, itis common for the tube to becut at 24 t0 26 cm expecting the depth Of insertion (measured in centimeters at the angle of the mouth) to be 20.0 23 em. The cuffof the tube is described as ‘high volume, low-pressure‘to indicate that the seal with the tra cheal wall is made by a large surface area of cuff but low intracuff pressure. A high cuff pressure leads to impaired tracheal mucesal blood flew and the cuff pressure should be only slightly more than that required to produce a seal atthe inflation pressures used during ventilation, The cuff does not prevent all fluid leaking past it particulary if there is cok superior to it umn of f Technique of direct laryngoscopy The mosi common technique of oral intubation is to use the curved Macintosh laryngoscope blade. The laryngoscope blade (usualy standard or long lengsh) is held in the left hand, inserted slightly the right side of the mouth to distract the tongue to the leftand slowlyadvanced inthe midline over the base of the tongue unl the epighots is visualized Therip ofthe blade is manceuvied into the valecula anda vector of forces applied to distactihe tongue from the line of sight. In most patients, correct laryngoscopy technique allows a clear view of the laryngeal inlet and the lubricated tracheal tube can be placed through the glottic aperture under direct vision. In 5% t 8% of the normal population, it is possible 10 see only the epiglottis and this makes insertion of the tracheal tube move difficult, The frst manoeuvie 59PROSO}ONY ACOSO] THOS SECTION 2: General considerations in cardiothoracic crvical care 8.4 Intubating Uma ‘used to improve the view is external laryngeal manipulation, The most successful single move: ment is pressure on the thyroid cartilage to move the larynx backwards, upwards and o the rightof the patient (BURP) If passage of the tubes stil difficult, ‘an introducer or gumelastic bougie should be tried. Use of the introducer (gum-elastic bougie) This may be used even If the cords are not well visualized, and the target is estimated using expe. rience and knowledge of anatomy. The introducer should be held at about 25 to 30 cm in the right, hhand with the tp angled anteriotl. The introducer should be advanced s0 as 10 slide the sp along the undersurface of the epiglottis in the midline and continuing to advance without undue force. Keeping the laryngoscope blade in situ, the tracheal tube is advanced over the introducer and if hold ‘up occurs the tube is withdrawn slightly, rotated 90 degrees anticlockwise and readvanced, The 1ota tion alters the orientation of the tip of the tube, ‘which otherwise commonly impacts on the sight vocal cord. Confirmation of tracheal versus ‘oesophageal intubation It is essential after intubation to confirm that the tube is within the trachea and not the oesophagus. Occasionally, itis obvious when applying positive pressure ventilation that the chest does not move 60 nd a gurglingsound is heard indicating the tube is placed oesophageally. Unfortunately. all the clinical signsof successful tracheal intubation ~ chest move. ment, breath sounds, correct ‘eel’ of the inflating bag, nisi may occur with oesophageal intubation. of the tube and normal compliance VISUAL CONFIRMATION The ube is seen on disect laryngoscopy passing between the vocal cords or at least superiorly to the interarytenoid groove, CAPNOGRAPHY ‘The best test of tracheal placement is the monitor ing of six successive, sustained respiratory carbon dioxide traces on the capnograph. Some carbon dioxide can be detected with oesophageal incuba: tion iffacemask venti sw hasinflated the stomach with exhaled gas or ifa carbonated drink has been recently ingested but the CO; is rapidly washed out by ventilation so the end-tidal value declines with cach breath, Errors with cspnography are always ‘fail-safe’ ~ the capnograph will not confirm tra cheal intubation when this is not present ~ but failure to attach the capnograph, a nonfunction: ing gystem or blocked sampling line means that successful tracheal intubation is not accompanied by detectable respiratory gis COs. During cardiac arrest, pulmonary blood flaw, and hence end-tidal CO,, are low. Rapid sequence induction A rapid sequence induction may be nesessary to minimizethe risk of aspiration of gastric contents at thetime of induction of anaesthesia and intubation Ie involves the rapid induction of anaesthesia and muscle relaxation, the application of crioid force afierloss of consciousness, intubation with acuffed tube and removal of cricoid force only after intuba- tion of the trachea has been verified, It should be considered forall patients in a critical care area who require imubation and may be a increased risk ofPROsojOvY —_QEOSO|OW 1.050, aspiration. This particularly applies if a full stom: ach is suspected, such as nasogastric feeding only recently discontinued or the presence of abdomi nal distentionjileus, CRICOID PRESSURE Cricoid pressu ‘on the cricoid cartilage and appiving force posteri crly to move the cricoid ring against the bodies of is performed by placing two fingers the cervical vertebrae. The force should be applied to the cricoid cartilage, the most inferior laryngeal structure, and not to the thyroid cartilage, which is the most prominent, Failed intubation Intubation by direct laryngoscopy will prove diffi cult in 296 to 5% of patients. f difficulty is encoun: tered, further attempts at ditect laryngoscopy may be attempted only after reoxygenation, However, repeated attempts may lead to airway oedema, and prolonged deoxygenation has deleteriouseffects on the patient. Therefore, after more than one failed attempt senior assistance should be urgently sum: moned. The immediate requirement is oxygenation and itis useful o place alaryngeal mask (ocreturn to the facemask) and ventilate with 100% oxygen. This is usually successful, but may fail in the presence of slottic oedema; in this instance, it iy necessary to proceed to the failed intubation and failed venti lation protocol, which obviously carties significant tisk, If ver ation by laryngeal mask (or facemask) is possible and oxygenation is satisfactory. intuba: tion istequired by another technique. There arefour common approaches Intubation through the laryngeal mask Intubation can be undertaken through the clas sic laryngeal mask.’The most successful techniques used are fiberoptic assisted o the employment of the Ainuve catheter, A size 6.0 mm tube is suit able for asize3 laryngeal mask airway (LMA) anda 7.0 mam for size 4 LMA, Intubating laryngeal mask The intubating LMA (ILMA) cm curved metal stem with a handle a bow! with an epiglottic elevator bar, dedicated wire spiraled tubes with a novel bevel and a stabilizing rod. The IMA bation and can also be used with a fiberscope ts of a tightly ihe most successful blind method of Intu- Fiberoptic intubation The Mexible Aberscope my be used w inubate through the nose or mouth, butskllis required and there may notbe asuitablefiberscope inthe critical careunit. There atea numberof oal airways, suchas the Berman airway, which may make orl fiberop tic intubation easier, hut the sll requited may be particularly high in cttical care where blood and secretions degrade the viewand oedema distorts the anatomy. Percutaneous tracheostomy In a patient in whom intubation by a senior clin ician has failed in the critical care unit, there is @ good case forimmedia tracheostomy, maintaining the airway during the procedure by laryngeal mask crsation of a percutaneous Failed ventilation The process of tracheal intubation in critical care appears © be more hazardous than during elective anaesthesia, pious oropharyngeal secretions or blood in the oropharynx, airway oedema, poor or basic equipment, inadequate assistance, imperfect muscle relaxation, poor cardiorespiratory reserve and relatively inexperienced nenanaesthetists may be responsible. At least or e serious complication occurs in approximately 25% of patients! E it is not possible wo maintain oxygen saturations cd ventilation isthe clinical scenario in which above 90% with 100% oxygen (if the saturations 6PEOSOIORY PLOSOJOW —_QEOSE|OW _TLOSO Prine: Ya To Caine SECTION 2: General considerations in cardiothoracic crvical care ‘were above this value ally), oF reverse signs of inadequate ventilation, by use of the facemask or laryngeal mask. ‘The situation of ‘can’tventilate-can’tintubate’ is, managed by inuoduction of exygen directly into the er by emergency cricothyrotomy or tra- cheostomy, Cricothyrotomy is quickerandis under- taken through the cricothyroid membrane, which is superticial easily located, relatively avascular and inferior to the vocal cords. There are thiee types of ricothyrotomy: small needle, arge-bore cannula (+4 mm diameter) and surgical + Needles or cannulae are placed through the cricothyroid membrane and directed caudally into the trachea. Air should be aspirated freely through the inserted cannula to confirm location within the trachea, Ifa needle or small cannula is used the resistance 1 gas flow is high and high pressure oxygen (2-4 Bar, 200-400 kPa) is required to allow sufficient ventilation to, remove CO, Exhalation is through the upper airway, which must be mi trachea tained open. ‘= Large-bore cannulae with an internal diamecer greater than 4 mm allow adequate inspiration with a standard breathing system (and pressure- limiting valve shut) and exhalation can occur through the cannula, ‘© "The surgical approach is to make an incision, open the airway by means ofa hook on the cricoid cartilage and passa 5-to G-mm tube directly into the airway. Complications of emergency cricothyrotomy include failue of technique, barotrauma wi pneumothorax or pneumomediastinum, bleed or damage to the larynx or surrounding structures figure 8.6 Layge-bae ckothyotomy cannula with an internal diameter of less than 4 mm. Changing the tube ‘Tracheal tubes sometimes need changing, com: monly ifaleakdevelopsin the cuff. the saiest proce- dureistoassemblethe intubation ‘kiandcheck the Figute 85. ricthyotomy cannula with an internal new tube, preoxygenate for 3 minutes, suction the diameter of 2 mm. oropharynx, ensure abolition of the glotic closure 6PROsojOvY —_QEOSO|OW 1.050, ‘flex by additional muscle relaxation and under take direct laryngoscopy. A tube-exchange catheter is passed through the in situ (ube until its ip is near the carina and the defective tube remaved, The now tube is passed ‘over the inserted catheter or introducer. Placing an introducer or ube-exchange catheter through the initial tabe avoids the problem of taking the defec tive tube ou but being unable to inteoduce the new lung separation In anaesthetic practice during thoracic surgery; Its common to undertake differential lang ventilation, primarily to allow collapse of the lung for surgi: cal access in the appropriate hemithorax. Usually the specialized tubes or blockers are removed or replaced at the end of surgery. However, there are rare indications within the citcal care unit forinite atingor continuinglungseparation,eitherto protect 2 ‘good’ lung from a contralateral disease process or control ventilation to each lung individually. The {wo most common techniques for providing lung separation are double-lumen tubes and bronchial blockers double-lumen tubes ‘These tubes contain two separate limbs, one thai resides in the bronchus and the otherin the trachea. “The tubes are known as ither ‘eit’or ‘tight! to ind «ate the endobronehial component. The bronchial cuff of a right double-lumen tube must incorpo. rate a slit or orifice to allow ventilation the upper lobe and the positioning of a right double-lumen tube ig more difficult than for a lef. The dispos: able double-lumen tubes are sized in French gauge (extemal circumference in mm) with 35 or 37 Fr being suitable for women and 39 or 41 Fr for is 29 cm for the average man and 27 cm for a The depth ofinsertion, messured atthe weth CHAPTER 8 MANAGING THE AIRWAY Bronchial blocker A bronchial blockers long, narrow catheter witha distal cuf.Itis designed to be placed under fiberop- tic control through a single lumen tube into the bronchus, where inflation of the cuff occludes the bronchus Extubation Extubation is the process of removal of the tracheal tube, after which the patient maintains and pro- airway. Various preconditions exist before extubation can be considered tectsthi * Mechanical ventilation is no longer required, + Theres cardiorespicatory stability. + The patient is alert enough to maintain their airway + There is satisfactory spontaneous ventilation, + The inspired oxygen is 40% to 60% oF lower. + The work of breathing is satisfactory and can be maintained. The extubation strategy encompasses the plan for extubation and management for reintubation should extubation fail. Equipment for reimtubation should be assembled, the nasogastric tube present should be suctioned to reduce the likelihood of aspiration and the inspited oxygen incre 100% for at least 3 minutes, Wh tions are present, itis helpful to apply positive pres- sure and temporarily deflate the cuff to force secre- tions above the cuff into the oropharynx, where copious secre they can be suetioned, At the point of extubation, the fixation tape is untied or cut, positive pres sure (approximately 20-30cm HO) is applied, the ‘cuff rapidly deflated and the tube removed. A face ‘mask should be applied attached to the Waters cuit with 100% inspired oxygen and adequacy of spontaneous respiration confirmed before transfer- Fing the patient onto a medium oxygen concentta- tion facemask. [eis wise to keep nil orally for 110 2 houts so that full laryngeal competence can be regained cyPLOSOIONY PROSOFEWY _QEESE|OW Toso Printer: Vi To Come SECTION 2: Genera considerations in cardiothoracic ential care Key points # Induction of anaestesa ane newomuscutar blockade shouldbe used to faclitate tracheal intubation, except in the utmost emergency, such as cardiac arrest. 4 When an intubated patent arrives in intensive are unit, adequate handover should include 24 hours) at 5% for first-time coronary artery bypass grafting and more than 109% for other cardiac surgery. If mechanical ventilation is still required after 10 {0 14 days, then a tracheostomy is con monly performed. Many clinicians would also con. sideritnecessary after two failed attempts attracheal extubation, Prolonged ventilation or failed extuba tion may be due to + excessive secretions, persistent chest infection; + reduced compliance, such as after acute lung injury + high onygen requirements; or + tracheostomy is also often performed in cases of obtunded neurological state (e.g, after stroke) orreduced airway protection re- flexes Chapter9 Contraindications There are no absolute contraindications to tra cheestomy. Relative contraindications include: + previous neck surgery or radiation, because distorted anatomy could lead (o damage of associated anatomical structures, including vascular injury, + impaired coagulation (should be corrected before procedure); + high oxygen requirements, high positive end-expiratory pressure (PEEP) or airway pressures (may be difficult to ventilate effectively during the procedure), Timing There is no consensus about the best timing for tracheostomy. The decision to proceed is based on Fiek-benefit analysis, but the main deteeminant is usually the number of days of mechanical venti lation and tracheal intubaion that is prediced 1 be required. The cutoff point may vary, but most commonly is 10 10 14 days, After this time, chronic inflammation and damage to the oropharynx and larynx from the endotracheal tube is likely to cause long-term sequelae. The advocates of early tracheostomy. (within 7 days) have shown that this reduces the duration of mechanical ventilation, and duration of stay in critical care, However, this has not been shown 1 improve survival or decrease chest infections.PROSO}ONY ACOSO] THOS SECTION 2: General considerations in cardiothoracic crvical care Pree Facilation of repeated suctioning of the tracheobronchial tee Emme Reduced dead space and airways resistance, Reduced complications related to translavyngeal intubation: laryngeal oedema, sinus, mucosal uiceration, vocal cord dysfunction, subgiotic stenosis and tracheomalacia Incteased patient comfort and better oral hygiene. May allow speech ard swallowing ten allows discontinuation of sedation and neurological assessment, Patients are rarely able to give informed consent fortracheostomy placement, but a8 a matter of cour tesy; relatives should be informed of the reasons for the procedure, and of the advantages and disad. vantages. In some countries, specific actions must be taken to comply with curtent law in relation to consent. Complications A tracheostomy is not a benign intervention and can ni paciens as, inching dest CeNph cations can be divided into immediate, early and late. Immediate complications + Hypoxaemia owing to aitway obstruction uring the procedure, loss of PEEP and reduced tidal volume. + Intraoperative bleeding from the thyroid gland and from vesselsin the operative field. + Pneumothorax or pneumomediastinum are the result of direct injury to the pleura or the lung apex, orcreation of a false lumen during insertion of the tracheostomy cannula. + Injury to surrounding structures, including recurrent laryngeal nerve, the great vessels and the oesophagus, 66 + ‘Tracheal tear, + Airembolism. This is critical in patients with, mechanical assist devices because the device «will fail to function, + Fire; use of diathermy in an oxygen-enriched environment when the trachea is open may lead to flash fire and airway damage. farly complications + Obstruction by mucus plug, blood clot or mucosal flap (rare), + Displacement, leading 0 loss ofthe airway. Immediate oral reinuubaion may be required if the stoma was performed fewer than 7 to 10 days eatier and cannot be recannulated. + Localized stomal infection (may be less common after percutaneous technique). Late complications + Tracheomalacia, + Tracheal stenosis + Tracheoesophageal fistula, ‘+ Granulation tissue (with airway obstru + Scarring. nn). Technique: percutaneous or surgical A tracheostomy can be created either surgically or using a percutaneous dilatational technique, and neither has so far proven superior to the other despite passionate arguments by their respective proponents Percutaneous dilatational technique is a quicker procedure, usually performed by the critical care team at the bedside; therefore, transfer to theatre is not required. It operative and early complications = certainly less bleedingis seen and lower infection rates havebeen reported. Torrential haemorthage during the proce- dure, although rare, may becatastrophic and neces- sitatestransferto theatre andinvolvementof the sur sical team, Cosmetic appearance may be better, bu studies assessing long-ierm complications such as tbe associated with less intraPROSO}ONY ACOSO] THOS ‘Abnormal or pootly palpable midline neck anatomy. Show neck, dificulty palpating cried catlage above the sternum, even wit the neck extended. Need for emergency procedure Coaculopathy or thrambocytopaenia Enlaiged hyo gland Obesity (ultrasound guidence to locate anatomical landmarks may be tsed) tracheal narrowing owing to overgranulation have been equivocal If a percutaneous dilatational technique is car sied out, proper training is essential. Use of fiberop: tic bronchoscopy to confirm optimal placement is mandatory, and anaesthesia and muscle paralysis are also required; an anaesthetist not undertaking the procedure should perfon Without consensus, local preference and resour cesoften determine practice in individual units, Car diothoracic surgeons may prefer open surgical tech. nique because of perceived lower infection rate of sternotomy wound, although this is not proven Choice of tube ‘A small tube increases air flow resistance, making ‘weaning ftom the ventilator more difficult. How: ever, the maximum diameters restricted by the size Of the trachea, As a rule the diameter of the tube should be approximately three fourths that of the trachea. The length of the tube is important: + t00 short tubes might abut the posterior tracheal wall, which may cause obstruction and ulceration; * too long tubes might erode the anterior tracheal wall by curving in a forward direction, which ‘can cause erosion and haemorrhage from the Innominaweartery. CHAPTER 9 TRACHEOSTOMY A variety of materials are used 10 make the tracheostomy cannula. Poivinyl chloride is ther- mosensitive and inexpensive, but may retain bac- teria, Silicone, although more expensive, is softer and less prone to tain bacteria and secretions. Sil ver tubes may occasionally be used. when the tra- cheostomy is requited for several months or if the patient isto be discharged home with itn sit “The tube inserted during the procedure is almost invariably cuted and consists of a single cannula Once thetracheosiomy trac hashealed (7-10 days), the first tube change can be performed. Ifthe tube diameter allows, the new tube should consist of an inner and outer cannula, ‘The inner tube can be cleaned or replaced as necessary, reducing the chance of occlusion with secretions. In the emer ‘gengy situation ofa blocked airway, the inner tube is easily removed patients are preferably discharged tothe ward with such atube. An innercannula, hov- ‘ever, decreases the inner diameter by up jo 1.5 mm, Increasing the resistance. [As the patient's recovery progresses, modifica tions may be made to the tracheostomy to enable phonation and swallowing Thecuffean be deflated, at fist temporarily. This allows airflow past the tra- cheostomy, reducing airway resistance, It may also facilitate swallowing; the inflated cuff can ‘anchor’ the larynx and occlude the oesophagus. A fenes- trated tube is often preferred after the first tube change. This allows greater airflow through the tra cheostomy and through the vocal cords, thusallow- ing the return of phonation. A speaking valve is a one-way valve that caps the tracheostomy tube externally. Tt allows inspiration through the tra cheostomy tube, but closes on expiration, thus directing airflow through the larynx. Postoperative care Security of the new tracheostomy is paramount. The original tube is left sutured in place for 5 10 7 days to allow the wact 10 form. There is com- monly a degree of racheitisafier he procedure, ant o7