KATE CURTISCLAIR RAMSDEN

RAMON Z. SHABANMARGARET FRY

JULIE CONSIDINE

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KKAATTEE CCUURRTTIISS

FOR NURSES AND PARAMEDICS

EMERGENCY AND TRAUMA CARE

THIRD EDITION

EMERGENCY AND TRAUMA CARE 3e

FOR NURSES AND PARAMEDICS

Kate Curtis RN, GradDipCritCare, MNurs(Hons), PhD, FCENA

Professor Emergency and Trauma Care, University of Sydney, NSW, Australia

Clinical Nurse Consultant Emergency, Illawarra Shoalhaven Local Health District, Illawarra Health and Medical Research Institute, NSW, Australia

Honorary Professor, Faculty of Science, Medicine and Health, University of Wollongong, NSW, Australia

Honorary Professorial Fellow, The George Institute for Global Health, Sydney, NSW, Australia

Clair Ramsden RN, GradCertCardiol, MHealthcareEthics, MHlthServMgt

Associate Professor, University of Technology Sydney, NSW, Australia

Executive Director Operations, Nepean Blue Mountains Local Health District, NSW, Australia

Ramon Z. Shaban RN, CICP-E, BSc(Med), BN, GradCertInfCon, PGDipPH&TM, MEd,

MCommHealthPrac(Hons), PhD, FCENA, FACN

Professor and Clinical Chair of Infection Prevention and Disease Control, Susan Wakil School of Nursing and Midwifery and Marie Bashir Institute for Infectious Diseases

and Biosecurity, University of Sydney, NSW, Australia

Department of Infectious Diseases and Infection Control & Nursing, Midwifery and Clinical Governance Directorate, Western Sydney Local Health District, NSW, Australia

Editor-in-Chief, Australasian Emergency Care, College of Emergency Nursing Australia, NSW, Australia

Margaret Fry RN, NP, BSc(Nurs), MEd, PhD, FCENA

Professor of Nursing, University of Technology Sydney, Sydney, NSW, Australia

Director Research and Practice Development

Northern Sydney Local Health District Nursing and Midwifery Directorate, Sydney NSW, Australia

Adjunct Professor, University of Sydney, Sydney, NSW, Australia

Julie Considine RN, RM, GDipNurs(AcuteCare), GradCertHEd, MNurs, PhD, FACN, FCENA

Professor of Nursing, Deakin University – Eastern Health, Burwood, Victoria, Australia

Senior Editor, Australasian Emergency Care, College of Emergency Nursing Australasia, NSW, Australia

Director, Centre for Quality and Patient Safety Research – Eastern Health Partnership, Box Hill, Victoria, Australia

CONTENTSForeword xiPreface xiiAcknowledgments xiiiContributors xivReviewers xviii

SECTION 1

FOUNDATIONS OF EMERGENCY CARE

1 Emergency nursing in Australia and New Zealand 3Margaret Fry, Ramon Z. Shaban and Julie Considine

Introduction 3Emergency nursing 4Emergency departments 4Emergency service (re-)design of models of care 7Australasian nurse competency standards 8Development of emergency nursing professional bodies 8Emergency nurse specialisation 9Clinical roles 9Leadership and management 10Professional development 10

2 Paramedicine in Australia and New Zealand 17Paul Jennings

Introduction 17History of paramedicine 17Historical overview of paramedicine by jurisdiction 18Evolutions in pre-hospital care 20Air ambulance services 22Role of volunteers in pre-hospital care 22Current status of paramedicine 23Regulation of paramedicine 25The future of paramedicine 25

3 Clinical ethics for emergency healthcare 29Eleanor Milligan, Sarah Winch and David Hunter

Introduction 29Ethics: an ancient and evolving fi eld 30The ethical framework of emergency healthcare:

our moral commitments and obligations 31Ethical decision-making 32Sequelae—Another key value: taking care of yourself 36

4 Emergency care and the law 39Ruth Townsend

Introduction 39What is the law? 40Different types of laws 40Professional competency and patient safety 40The Coroner’s Court 41

Investigations and court 42Child Protection Act and mandatory reporting 44Documentation 45Confi dentiality 46Privacy 46Assault and consent 47Who may give consent when the patient can not 48Advance care directive 50Palliative care 50Medicines 50Mental health and involuntary detention 51Restraint 52Negligence 53Nurse practitioner responsibilities 54

5 Cultural considerations in emergency care 59Fiona Orr

Introduction 59Culture and what it means for healthcare workers 60What does the word ‘culture’ describe? 60Understanding the health–illness experience from the

patient’s perspective 61Matters specifi c to Australia 62Matters specifi c to New Zealand–Aotearoa 64

6 Patient safety and quality in emergency care 71Julie Considine, Ramon Z. Shaban, Margaret Fry, Kate Curtis, Clair Ramsden and Paul Jennings

Introduction 71Safety and quality frameworks 72Outcomes 72Structure of the ED 75Emergency care processes 78

7 Research for emergency care 87Julie Considine, Ramon Z. Shaban, Margaret Fry and Kate Curtis

Introduction 87Evidence-based practice 88Research and the process 88Method 92Data analysis 96Ethical considerations in research 97Results, conclusions and recommendations 97Dissemination and translation of research fi ndings 98Research priorities for emergency care 101

8 Patient and carer engagement and communication 107Judy Mullan and Pippa Burns

Introduction 107Health literacy 108

vi CONTENTS

Effective patient communication 108Targeting patient education about medication adherence 110Health promotion activities and disease prevention

strategies 110Verbal patient education and communication 110Written patient information 112Developing written patient information 113

SECTION 2

CLINICAL CONCEPTS AND SYSTEMS

9 Scene assessment, management and rescue 125Karel Habig

Introduction 125Safety fi rst—keeping you and the patient safe 126Scene management priorities—why an organised

scene is priceless 129Scene assessment 131Scene access 134Patient extrication 135Scene egress 137Management of specifi c hazards 137

10 Physiology and pathophysiology for emergency care 149Peter Moules

Introduction 149Homeostasis 150Oxygen transport 150Carbon dioxide transport 154Oxygen therapy 156Homeostatic temperature control 156Fluid and electrolyte balance in homeostasis 156Nervous system functions—Fright, fi ght and fl ight,

or Rest and digest 159Capillaries and nutritive blood fl ow 160Cellular metabolism 161Cell protection: the blood–brain barrier 162Shock 163Unique population groups 170

11 Clinical reasoning, problem-solving and triage 175Margaret Fry, Ramon Z. Shaban and Julie Considine

Introduction 175Clinical reasoning for quality emergency care 176Theoretical considerations 176Triage 180Triage decision making tools 181Triage nurse decision-making 182Triage nurse education 184Triage documentation and legal aspects 185Paramedic applications: patterns and protocols and

triage for problem-solving 186Special conditions 186Communicating for patient safety 188

12 Major incident preparedness and management 201Lisa Conlon, Alana Clements and Sam Willis

Introduction 202What is a mass-casualty incident? 202

Government planning for mass-casualty incidents 204The challenge for paramedics and other healthcare

providers 207Risk analysis in planning by hospitals 207The pre-hospital phase 208Hospital phase 215Debriefi ng 227Chemical–biological–radiological MCIs 227Likelihood of a CBR attack 227CBR agents and their effects 227Pre-hospital management of a CBR MCI 234Personal protective equipment 236Bioethical implications in triage 237Awareness training and education 237

13 Patient assessment and essentials of care 243Belinda Munroe and Claire Hutchinson

Introduction 243The assessment process 244The primary survey 244Assessment (clinical examination) 247Head-to-toe assessment 252Special considerations 259Communication 261Essentials of care 266Caring 266Personal hygiene and preventing complications 267Prevention of deconditioning 268Nutrition 269Elimination 269

14 Resuscitation 281Julie Considine and Ramon Z. Shaban

Introduction 281Identifi cation of and response to the deteriorating

patient 282Basic life support 285Advanced life support 289Care of families and family presence during

resuscitation 299

15 Stabilisation and transfer 307Daniel Martin

Introduction 307Intra- and inter-facility patient transport 308Types of transport 310Clinical coordination and communication 312Team preparation 313Principles of transport 314Monitoring and equipment 317Stressors of transport 322Debrief and post-mission review 324Psychological considerations 325

16 Clinical skills 329James Brinton, Wendy Fenton and Ben Meadley

Introduction 329Airway management 330Capnography/end-tidal carbon dioxide monitoring 338Cervical spine immobilisation 340Suctioning techniques 346

viiCONTENTS

Arterial blood gases 348Blood glucose level sampling 350Underwater-seal drains 351Respiratory function testing 353Cardiac monitoring 354Temporary cardiac pacing 356Vascular access 358Haemodynamic monitoring 363Central venous catheters 365Soft tissue injuries 367Casts 371Splinting 371Crutches and walking sticks 375Regional anaesthesia and nerve blocks 378Removal of objects 388Wound closure 393Eye emergencies 397

17 Minor injury and management 407Keryn Jones and Erica Rootham

Introduction 407Pre-hospital care 408Initial assessment 408Practical care 408Hospital/health facility care 408A systematic approach to injury assessment 409Injuries around the shoulder 409Injuries to the elbow, forearm and wrist 410Injuries of the hand and digits 413Injuries around the knee 416The lower leg, ankle and foot 418Injuries of the skin: wounds 422

18 Pain management 447Bill Lord and Wayne F. Varndell

Introduction 447Defi nition of pain 449Anatomy and physiology of pain 449Pathophysiology 451Patient assessment 452Management 455Anaesthesia 462

19 Organ and tissue donation 471Myra Sgorbini, Leigh McKay, Jane Treloggen and Carrie Alvaro

Introduction 471Donation and transplantation in Australia and

New Zealand 472Pathways of donation 473The procurement process 483Donor family care 484

20 End of life 489Linda Ora, Dwight A. Robinson and James V.R. Marshall

Introduction 489Cultural considerations 490Palliative care 490Advance care planning 491Sudden and unexpected death 492Sudden death of a child 492

Family presence during resuscitation 493Care of a deceased patient 493Post-mortem examination 494Mass casualty incidents 496Staff support 496

SECTION 3

EMERGENCIES

21 Respiratory emergencies 503Jeff Kenneally and Tracy Flenady

Introduction 503Respiratory failure 504Respiratory assessment 505Emergency care considerations for respiratory issues 510Support of respiratory function 514Non-invasive ventilation 516Invasive mechanical ventilation 519Acute pulmonary oedema 526Asthma 527Chronic obstructive pulmonary disease 529Pneumonia 532Pulmonary emboli 533Respiratory outpatient care programs 534Inhalation injuries 534Acknowledgement 538

22 Cardiovascular emergencies 545Marc Aquilina, Lesley Fitzpatrick and Margaret Fry

Introduction 545Anatomy and physiology 546Electrocardiogram interpretation 550Cardiac assessment 553Acute chest pain 554Acute coronary syndromes 560Cardiogenic shock 566Percutaneous coronary intervention 568Pharmacological management 569Cardiac dysrhythmias 572Cardiac pacing 584Chronic heart failure 585Acute pericarditis 587Aortic aneurysm 587Aortic dissection 589Hypertensive emergencies 589

23 Neurological emergencies 595Julie Considine

Introduction 595Anatomy and physiology of the nervous system 596Divisions of the nervous system 600Assessment of the patient with altered consciousness 602Investigations 605Delirium 608Transient ischaemic attacks 608Vertebrobasilar attacks 609Stroke 610Seizures 614Headache 616Infl ammatory brain conditions 619

viii CONTENTS

24 Gastrointestinal emergencies 625Wayne F. Varndell and Lesley Fitzpatrick

Introduction 625Anatomy and physiology 626General assessment 630Upper gastrointestinal emergencies 639Lower gastrointestinal emergencies 646

25 Renal and genitourinary emergencies 669Ann Bonner

Introduction 669Anatomy and physiology 670Patient assessment 673Physical assessment 674Specifi c conditions 678

26 Endocrine emergencies 695Thomas Buckley and Margaret Murphy

Introduction 695Anatomy and physiology 696Diabetes 701Hyperglycaemic, hyperosmolar syndrome 705Adrenal insuffi ciency 708Acute pituitary apoplexy 708Thyroid storm 709Myxoedema coma 710Cushing’s syndrome 711

27 Healthcare-associated infections and infectious diseases 717Ramon Z. Shaban, Deborough Macbeth, Phillip L. Russo, Brett G. Mitchell and Julie E. Potter

Healthcare-associated infection and infectious disease in emergency care 718

Overview of infection and infectious disease 719Breaking the chain—preventing infection 723Specifi c challenges for infection prevention in

emergency care 727

28 Environmental emergencies 739Ioana Vlad and Helena Halton

Introduction 740Temperature-related emergencies 740Heat-related emergencies 740Cold-related emergencies 744Drowning 749Atmospheric-pressure-related emergencies 750Diving emergencies 753Envenomations 755Antivenom 756Snakebite 756Snakes 759Spiders 762Other terrestrial envenomations 764Marine envenomations 764

29 Oncological and haematological emergencies 771Meredith Oatley and Ruth Dunleavey

Introduction 771Cancer incidence in Australia and New Zealand 771

Cancer pathophysiology 772Cancer and the immune system 773Cancer diagnosis and treatment 774Oncological emergencies 779Haematological emergencies 779Thrombocytopenia emergencies 789The patient who is bleeding 790Metabolic emergencies 794Non-metabolic oncological emergencies 795Venous access 799

30 Toxicological emergencies 807Ioana Vlad and Helena Halton

Introduction 807Demographics and common presentations 807Resuscitation 808Risk assessment 809Supportive care 810Investigations 812Gastrointestinal decontamination 812Enhanced elimination 814Antidotes 814Disposition 815Commonly ingested agents 815

31 Dental, ear, nose and throat emergencies 831Tony Skapetis and Jacqueline Fong

Introduction 831Anatomy and physiology 832Patient assessment 834Dental emergencies 836Ear emergencies 844Nasal emergencies 848Throat emergencies 849Facial emergencies 851

32 Ocular emergencies and trauma 855Joanna McCulloch

Introduction 855Anatomy and physiology 856Patient assessment 862Ophthalmic examination 863Eye emergencies 866Trauma 872Chemical burns 879Glaucoma 881Central retinal artery occlusion 881Central (branch) retinal vein occlusion 882Ocular pharmacology 882

33 Gynaecological emergencies 887Diana Williamson

Introduction 887Anatomy and physiology 888Patient assessment 889Clinical presentations 891Ovarian emergencies 895Infections 896Sexually transmitted infections 897Common types of genital tumour 901

ixCONTENTS

Endometriosis 902Emergency contraception 902

34 Obstetric emergencies 907Nicole Watts and Allison Cummins

Introduction 907Obstetric emergencies 908Anatomy and physiology 908Recognition of the sick woman 910Maternal collapse 910Clinical presentations 913

35 Paediatric emergencies 933Dianne Crellin and Michelle McCarthy

Introduction 934Approach to paediatrics 934Assessment 941Triage 953Respiratory emergencies 954Cardiovascular emergencies 969Neurological emergencies 977Abdominal emergencies 980Rashes and soft-tissue infections 985Neonatal presentations 990Fever 991Trauma 993Pain management and procedural sedation 1002Health promotion 1007

36 Mental health emergencies 1031Nicholas Procter, Monika Ferguson, Graham Munro and Michael A. Roche

Introduction 1031Background 1032Prevalence of mental health admissions

in EDs 1033Supporting individuals in the out-of-hospital

environment 1033Pathways to the ED 1034Out-of-hospital assessment and management 1035ED triage assessment 1036After triage 1038Mental health conditions 1039Substance misuse and dual diagnosis 1044Suicide and self-harm 1045Other considerations when providing emergency

mental health care 1048Early intervention in aggression and mitigation

strategies to prevent unnecessary use of restraint and/or restrictive practices 1048

Cultural considerations when providing an emergency mental health response 1050

Collaboration and teamwork between mental health professionals 1051

37 People with disabilities 1059David Foley

Introduction 1059Defi nition of disability 1059Historical context 1060

Nature of problem in emergency care 1060National Disability Insurance Scheme and

New Zealand Disability Strategy 1060Broader implications 1060Aetiology and epidemiology of intellectual disability 1061Intellectual disability morbidity 1061Diagnostic overshadowing 1061Major emergency care issues for people with an ID 1064Assessment of the person with an ID 1065Particular clinical presentations 1073Communication with the person with an ID 1073

38 The older person 1081Glenn Arendts and Helen Rawson

Introduction 1081What is an older person? 1081Assessment of normal ageing 1082Conditions often seen in older people 1084Tips and tools: the geriatric assessment in the

emergency health setting 1086Discharge risk assessment 1088Futility criteria 1089Geriatric emergencies 1089The dying patient 1091Conclusion 1091

39 Violence, abuse and assault 1097Amber Preece, Russell Krieger and Sam Maalouf

Introduction 1098The child at risk 1098Intimate partner violence 1102Sexual assault 1105Elder abuse and neglect 1106

40 Alcohol, tobacco and other drug use 1113Michael A. Roche and Louise Keane

Introduction 1113Overview and background 1114Understanding ATOD problems 1115ATOD emergency assessment and screening 1117Engaging with the patient with an ATOD dependence 1118Major ATOD groups 1123Cannabis 1137Psychostimulants 1137Common psychostimulants 1138Some other drugs 1141

SECTION 4

MAJOR TRAUMA

41 Epidemiology of injury 1153Taneal Wiseman and Sarah Kourouche

Introduction 1153The burden of injury 1154History 1154Epidemiology of trauma in Australia and New Zealand 1155Trauma morbidity 1157Trauma determinants 1157Mechanisms of injury 1160

x CONTENTS

Effects of injury on society 1174Injury prevention 1175Tracking injury in Australia and New Zealand 1177Standardised clinical trauma management 1178Trauma specialist roles 1181

42 Major trauma initial assessment and management 1189Kellie Gumm

Introduction 1189Preparation 1190The trauma team 1192Initial resuscitation 1195Primary survey 1195Secondary survey 1216Tertiary survey 1216Ongoing nursing care in the ED 1218Criteria for early transfer 1220Family presence 1220Post-traumatic stress 1220

43 Traumatic brain injury 1227Joseph Sharpe and Travis Cole

Introduction 1227Epidemiology 1228Injury mechanism 1228Anatomy 1228Physiology 1228TBI classifi cations 1230Patient assessment and management 1235Mild traumatic brain injury 1243

44 Maxillofacial trauma 1251Robert J.W. Knight

Introduction 1251Anatomy and physiology 1252Injury mechanism 1256Patient assessment 1257Specifi c fracture management 1264

45 Thoracic and neck trauma 1275Elizabeth Walter and Benjamin Crook

Introduction 1275Anatomy and physiology 1276Patient assessment 1276Clinical interventions 1279Radiology 1280Fractures of the bony thorax 1282Pneumothoraces 1289Other thoracic injuries 1296Neck injuries 1305

46 Abdominal and genitourinary trauma 1315Kate King and Debra McDougall

Introduction 1315Epidemiology 1316Anatomy 1316Mechanism of injury 1318Initial assessment and management 1319

Investigations 1323Ongoing management 1326Management techniques 1326Specifi c organ injury 1328Genitourinary trauma 1333Genital injuries 1337Postoperative management 1340

47 Spinal trauma 1353Andrew N. Keygan

Introduction 1353Epidemiology 1354Anatomy and physiology 1354Mechanisms and associated injuries 1356Pre-hospital assessment and initial management 1358Spinal stabilisation 1360Ongoing patient assessment 1362Pharmacological management 1367Defi nitive care 1370Primary and secondary damage 1371Classifi cation of spinal cord injuries 1372Autonomic dysrefl exia/hyperrefl exia 1374The future 1375

48 Major orthopaedic and neurovascular trauma 1385Celine Hill, Belinda Atalla and Jessica Keady

Introduction 1385Anatomy and physiology 1386Patient assessment 1389Clinical interventions 1391Radiology 1391Pain management 1393Dislocations and subluxations 1393Traumatic amputations 1396Fractures 1398Mangled limbs 1409Pelvic fractures 1410Proximal femur and femoral neck fractures 1414Crush injury 1415Compartment syndrome 1418Fat embolism syndrome 1420Delayed complications 1421Infection prevention 1421Traction 1422Splints 1424Psychosocial aspects 1424

49 Burns trauma 1431Andrew J.A. Holland and Linda Quinn

Introduction 1431Epidemiology and aetiology of burns 1432Pathophysiology 1432Paramedic emergency and fi rst aid treatment 1434Burns shock and fl uid resuscitation 1436Inhalational injury 1438Burn wound assessment and management 1439Specifi c burn management 1441Burns in children 1443

Index 1449

Health and wellbeing are fundamental human rights. We all have the right to be healthy and to be well, regardless of our standing or station. Australia enjoys one of the most advanced and socially progressive healthcare systems in the world, and emergency and trauma care are fundamentally critical components of this system and, indeed, all healthcare systems globally. The same cannot be said, regrettably, for many other parts of the world where healthcare systems are underdeveloped, are chronically under-resourced and, in some cases, in contexts where human rights are disregarded, undervalued or absent.

Emergency clinicians play essential roles in complex and dynamic healthcare systems, and in doing so, they are presented with challenges that are peculiar to them and their specialty. They assess and initiate care for patients of all ages, with varying degrees of clinical urgency and severity, and where patients are typically undiagnosed and undifferentiated. They see and work with patients and their families at their most vulnerable, with an ever-increasing demand for healthcare that routinely outstrips supply and available resources.

Emergency and Trauma Care for Nurses and Paramedics 3e provides emergency clinicians with comprehensive, contemporary, practical and evidence-based information necessary to support the ever-increasing demands and needs of their professional practice.

Importantly, it serves as a guide for emergency clinicians to recognise the inherent value of each person, regardless of their background, where they live, what they look like, what they think, or what they may believe, as is said for all of their colleagues in the other health profes-sions. The delivery of modern healthcare, in particular emergency and trauma care, must be based on the fundamental human rights principles of dignity, equality and mutual respect across all cultures, religions and philosophies. The care that emergency clinicians provide must be such that patients and their families feel safe, believe they are treated fairly and appropriately, and that they have the ability to make genuine choices that affect the options and trajectory of their care.

It is my pleasure to congratulate the editors Kate Curtis, Clair Ramsden, Ramon Z. Shaban, Julie Considine and Margaret Fry and all contributing authors on this state-of-the-art text. Emergency and Trauma Care for Nurses and Paramedics 3e will be a valuable resource for everyone working in emergency care settings, irrespective of the setting, including emergency departments, other hospital-based environments and the pre-hospital setting.

I commend Emergency and Trauma Care for Nurses and Paramedics 3e to you as a leading resource to enable you to provide high-quality, safe, effective and timely emergency care to patients and their families for their human rights.

Professor Gillian Triggs Vice-Chancellor ’ s Fellow , University of Melbourne

Chair , Justice Connect

FOREWORD

Emergency and Trauma Care for Nurses and Paramedics 3e is a comprehensive, contemporary, practical and evidence-based resource for emergency and trauma nurses, paramedics and other healthcare workers, and students working in urban, rural and remote settings. It provides everyday clinicians with invaluable information relevant to their local practice environment that is informed by best-available global evidence. Our 85 contributing authors are recognised practitioners of standing in Australia or New Zealand and were chosen for their expertise to ensure relevant, practical information.

Emergency and Trauma Care for Nurses and Paramedics 3e is organised into four sections. Section 1 comprehensively documents the foundations and development of paramedic and emergency and trauma nursing practice, as well as the fundamentals of emergency care, including quality and safety, ethics, leadership and patient education. Section 2 addresses the clinical and health service system concepts of scene assessment, patient assessment, triage and the physiology of emergency care, and contains a chapter featuring essential clinical skills, which are cross-referenced throughout this edition. Section 3 then explores contemporary recognition and management of specifi c body system emergencies, including cardiovascular, respiratory, neurological and endocrine. Other areas of emergency are also covered in depth, including toxicology, envenomation and ocular and environmental emergencies, as well as end-of-life care. Emergency care for unique population groups, including the elderly, disabled, obstetric and paediatric patients, is also presented. Section 4 of the text provides a detailed review on major trauma assessment and management, examining trauma systems, trauma assessment and trauma to specifi c body regions.

Throughout the 49 chapters, cross references are made to other areas of the text that are of relevance. The 540 fi gures and 255 tables actively support the hands-on clinical approach of the text. Clinical assessment, physiology, decision-making and rationale for interventions of common and not-so-common emergency presentations are provided. Case studies are provided at the end of each chapter to enable consolidation of knowledge for practice.

Emergency and Trauma Care for Nurses and Paramedics 3e refl ects expert knowledge, published research and literature available at the time of production. It is important that readers continue to search for the most recent sources of appropriate information to guide their practice. To assist the reader in this, useful websites are also provided at the end of each chapter. Feedback from readers is welcome so as to facilitate the growth and development of the disciplines of emergency and trauma care and the professions who practise it.

We commend Emergency and Trauma Care for Nurses and Paramedics 3e to you in support of our shared efforts to provide high-quality, safe, effective and timely emergency care for patients and their families.

Kate Curtis Clair Ramsden

Ramon Z. Shaban Margaret Fry

Julie Considine July 2019

PREFACE

Marc Aquilina RN, GradDipNurs, GradCertCardiacNurs Cardiac Assessment Nurse Consultant , Illawarra Shoalhaven Local Health District , NSW , Australia

Glenn Arendts MBBS, MMed, PhD, FACEM Associate Professor , Emergency Medicine, School of Medicine, University of Western Australia , Perth , Western Australia , Australia

Ann Bonner RN, BAppSc(Nurs), MA, PhD Professor of Nursing , School of Nursing, Faculty of Health, Queensland University of Technology , Queensland , Australia Visiting Research Fellow , Kidney Health Service, Metro North Hospital and Health Service , Brisbane , Queensland , Australia

James Brinton RN, GradCertCritCare(Emergency) Clinical Nurse Consultant Surgery , Service Lead Emergency, Illawarra Shoalhaven Local Health District , Wollongong , NSW , Australia

Thomas Buckley RN, GradCertHPlo, CertICU, MNurs, PhD Associate Professor and Academic Leader Research Education , The University of Sydney Susan Wakil School of Nursing and Midwifery , Sydney , NSW , Australia

Pippa Burns BSc(Hons), MPH(Dist), GradCertManComm(Dist), PhD Lecturer , Research and Critical Analysis, School of Medicine, University of Wollongong , NSW , Australia

Alana Clements MNurs(EmergTrauma) Nurse Unit Manager A5 Surgical , Woollongong Hospital , NSW Health , Sydney , NSW , Australia

Travis Cole RN (Emerg), BSc(Nurs), GradCertEmerg, MNurs(AdvClPrac) Nurse Educator , The Townsville Hospital Emergency Department , Townsville , Queensland , Australia

Lisa Conlon RN, MNurs, PhD Director of Pre-registration Programs , The University of Sydney Susan Wakil School of Nursing and Midwifery , Sydney , NSW , Australia

Julie Considine RN, RM, GDipNurs(AcuteCare), GradCertHEd, MNurs, PhD, FACN, FCENA Professor of Nursing , Deakin University – Eastern Health , Burwood , Victoria , Australia Senior Editor , Australasian Emergency Care, College of Emergency Nursing Australasia , NSW , Australia Director , Centre for Quality and Patient Safety Research – Eastern Health Partnership , Box Hill , Victoria , Australia

Dianne Crellin RN, NP, GradCertEmergNurs, GradDipAdvNurs(Paed), PhD Course Coordinator , Royal Children ’ s Hospital, Melbourne and The University of Melbourne , Parkville , Victoria , Australia

CONTRIBUTORS

Benjamin Crook RN(Emergency), BAppSc(Exercise&SportScience), MEd(Higher Ed) Academic , School of Nursing, Western Sydney University , NSW , Australia Clinical Nurse Educator , Emergency, Sutherland Hospital , NSW , Australia Academic , School of Nursing, Western Sydney University , NSW , Australia

Allison Cummins RM, GradCertMidwifery, MAEd, PhD Senior Lecturer in Midwifery , Faculty of Health, University of Technology Sydney , NSW , Australia

Kate Curtis RN, GradDipCritCare, MNurs(Hons), PhD, FCENA Professor Emergency and Trauma Care , University of Sydney , NSW , Australia Clinical Nurse Consultant Emergency , Illawarra Shoalhaven Local Health District, Illawarra Health and Medical Research Institute , NSW , Australia Honorary Professor , Faculty of Science, Medicine and Health, University of Wollongong , NSW , Australia Honorary Professorial Fellow , The George Institute for Global Health , Sydney , NSW , Australia

Ruth Dunleavey BSc(Hons)(Nurs) Clinical Research Nurse , Calvary Hospital , Kogarah , NSW , Australia

Wendy Fenton NP, MNurs Emergency Nurse Practitioner , Emergency Department, Wollongong Hospital , Wollongong , NSW , Australia

Monika Ferguson BPsych(Hons), GradCertSuicidePrevSt, PhD Lecturer in Mental Health , School of Nursing and Midwifery, University of South Australia , Adelaide , South Australia , Australia

Lesley Fitzpatrick RN, BSc(Nurs), MNurs Clinical Nurse Consultant , Emergency Department, Royal North Shore Hospital , St Leonards , NSW , Australia

Tracy Flenady RN, BNurs(Dist), PhD Academic Lecturer Researcher, 2nd year Co-ordinator (Bachelor of Nursing) , School of Nursing, Midwifery and Social Sciences, Higher Education Division, CQ University, North Rockhampton , Queensland , Australia

David Foley RN, BSc, MNurs, PhD Lecturer , Adelaide Nursing School, University of Adelaide , South Australia , Australia

Jacqueline Fong RN/NP, GradCertEd, MN(NP) Coordinator Master of Nursing (Nurse Practitioner) , The University of Sydney Susan Wakil School of Nursing and Midwifery , Camperdown , NSW , Australia

CONTRIBUTORS xv

Margaret Fry RN, BSc(Nursing), MEd(Adult), PhD Professor of Nursing , University of Technology Sydney, Northern Sydney Local Health District , Sydney , NSW , Australia

Kellie Gumm CNC, GradCert ITU, GradDipHlthProm, MEd, ACTN, TNCC Trauma Program Manager , The Royal Melbourne Hospital , Parkville , Victoria , Australia Senior EMST Coordinator , The Royal Australasian College of Surgeons , Melbourne , Victoria , Australia

Karel Habig BSc (Med), DipRTM, MBBS Prehospital and Retrieval Specialist and Lead Clinician , NSW Ambulance, Health Emergency and Aeromedical Services

Helena Halton RN, MNurs (Nurse Practitioner), GradCert(Emergency Nursing), GradDipNursPrac Nurse Practitioner/Coordinator of Masters of Nursing , Nurse Practitioner Course, School of Nursing and Midwifery, Edith Cowan University , Western Australia , Australia

Celine Hill RN, DipAppSci, GradCert Orthopaedics, MNurs(Trauma) Patient Safety Manager Shoalhaven Hospitals Group , Illawarra Shoalhaven Local Health District , Nowra , NSW , Australia

Andrew J A Holland BSc(Hons), GradCertEdStudies(Higher Ed), MBBS, PhD, FRCS(Eng), FRACS(Paed), FACS Professor of Paediatric Surgery , The University of Sydney School of Medicine, The Children ’ s Hospital at Westmead , NSW , Australia

David Hunter BA(Hons), MA, PhD Associate Professor of Medical Ethics , School of Medicine, Flinders University , Adelaide , South Australia , Australia

Claire Hutchinson RN, AdvDipHEdNurs, BSc(Hons)(Nurs), GradCertEmergency, MCN(Emergency) Clinical Nurse Consultant , Canterbury Emergency Department , Sydney , NSW , Australia

Paul Jennings BNurs, GradCertBiostats, GradDipHPE, MClinEpi, PhD Clinical Manager , Ambulance Victoria , Melbourne , Victoria , Australia

Keryn Jones BNurs, MEd Lecturer , Graduate Nursing Studies, University of Technology Sydney , NSW , Australia Emergency Nurse Practitioner , St George Hospital , Kogarah , NSW , Australia

Jessica Keady RN, BNurs, GradCertHlthMgt(Quality), MNurs(Acute Care) Nurse Manager , Patient Flow Unit, Western NSW Local Health District , NSW , Australia

Louise Keane RN, GradDipMentHlthNurs, CertDrugAlcoholAddiction Clinical Nurse Consultant , Drug and Alcohol Services, Drug and Alcohol Inpatient Unit, Royal North Shore Hospital , St Leonards , NSW , Australia

Jeff Kenneally ASM, BBus, CertMICA MICA Senior Team Manager Ambulance Victoria , Melbourne , Victoria , Australia Lecturer Paramedic Science , Victoria University , Melbourne , Victoria , Australia

Andrew Keygan RN, BNurs, MNurs(Emergency), MNursSc(Nurse Practitioner) Nurse Practitioner , Emergency Department, Tasmanian Health Service , Tasmania , Australia

Kate King RN, MNurs Clinical Nurse Consultant Trauma , John Hunter Hospital, New Lambton Heights , NSW , Australia Conjoint Lecturer , Faculty of Health, University of Newcastle , Newcastle , NSW , Australia

Robert J W Knight MBBCh, MRCS, MD, FRACS(Plast) Consultant Specialist Plastic , Reconstructive and Aesthetic Surgeon Consultant Specialist Craniomaxillofacial and Paediatric Plastic Surgeon Senior Clinical Lecturer , University of Wollongong , Sydney , NSW , Australia

Sarah Kourouche RN, MNurs Academic , The University of Sydney Susan Wakil School of Nursing and Midwifery , Sydney , NSW , Australia

Russell Krieger GradCertPubHlth, MBChB, FACEM Emergency Staff Specialist , Royal North Shore Hospital , St Leonards , NSW , Australia

Bill Lord BHlthSc(Pre-HospCare), MEd, PhD Associate Professor and Discipline Leader , Paramedicine, University of the Sunshine Coast, Sippy Downs , Queensland , Australia

Sam Maalouf BHlthSc(Paramedic) Qualifi ed Ambulance Paramedic , Ambulance Victoria , Melbourne , Victoria , Australia

Deborough Macbeth BNurs, MA(AppEthics), PhD Assistant Director of Nursing , Infection Control, Gold Coast Hospital and Health Service , Southport , Queensland , Australia

James Marshall DipAmbParamedStud, BA(Hons), MPH, MPA Paramedic Educator/Curriculum Development Program Offi cer , Ambulance Victoria , Melbourne , Victoria , Australia

Daniel Martin RN, BNurs(PracEmerg), GradCertEmerg, GradCertNursScRet, GradCertAeromedRet Nursing Director , MedSTAR Emergency Medical Retrieval, South Australia Ambulance Service Squadron Leader , Expeditionary Health Squadron, Royal Australian Air Force Associate Professor , College of Public Health, Medical and Veterinary Sciences, James Cook University , Queensland , Australia

Michelle McCarthy PGAcuteNursCare(Emerg), MNurs(NursePrac) Nurse Practitioner , Emergency Department, Royal Children ’ s Hospital , Parkville , Victoria , Australia

Joanna McCulloch RN, BA(Psych), BA(HlthSc), MNurs(NursePrac) Clinical Nurse Consultant Ophthalmology , Sydney Hospital and Sydney Eye Hospital , Sydney , NSW , Australia Adjunct Lecturer , School of Nursing, The University of Notre Dame , Sydney , NSW , Australia

Debra McDougall RN, GradCertEd, MNurs(AdvNursEd) Conjoint Lecturer Nursing , University of Newcastle , Newcastle , NSW , Australia

Leigh McKay RN, BAppSc(Nurs), GradCertCritCare, MPH Education Coordinator , NSW Organ and Tissue Donation Service , Sydney , NSW , Australia

CONTRIBUTORSxvi

Ben Meadley BAppSc(HumMove), DipParamedSci(PrehospCare), GradDipIntCareParamedic, GradDipEmergHlth(MICA), GradCertEmergHlth(Aeromed Retrieval) Lecturer in Paramedicine , Department of Community Emergency Health and Paramedic Practice, Monash University , Burwood , Victoria , Australia Intensive Care (MICA) Flight Paramedic , Ambulance Victoria , Victoria , Australia

Eleanor Milligan BA(Hons), BSc, GradDipEd, PhD, GAICD Professor Ethics and Professional Practice , School of Medicine, Griffi th University , Brisbane , Queensland , Australia

Brett Mitchell RN, BNurs, DipTropNurs, GradCertTeach, CertHlthMgt, MAdvPract, PhD Professor of Nursing , Avondale College of Higher Education , NSW , Australia Professor of Nursing , University of Newcastle , NSW , Australia

Belinda Mitchell (Atalla) RN, GradCertTrauma, GradCertOrthopaed, GradCertWoundCare Orthopaedic Clinical Nurse Consultant , Westmead Public Hospital , Westmead , NSW , Australia

Peter Moules RN, GradCertCritCare, GradCertHlthLeadMgt Clinical Nurse Specialist , Emergency, Wollongong Hospital, Wollongong , NSW , Australia Research Nurse , Susan Wakil School of Nursing and Midwifery, University of Sydney , NSW , Australia

Judy Mullan BPharm, BA, PhD, FSHPA Associate Professor, Director Centre for Health Research , Illawarra Shoalhaven Population (CHRISP) Deputy Director , Illawarra and Southern Practice Research Network, CHRISP, Australian Health Services Research Institute, University of Wollongong , NSW , Australia

Graham G. Munro RP, BHSc, GradCertEmergHlth, MHSM, PhD Senior Lecturer/National Course Coordinator Paramedicine , Australian Catholic University , North Sydney , NSW , Australia

Belinda Munroe RN(Emerg), MNurs(AdvPract), PhD Emergency Clinical Nurse Consultant , Illawarra Shoalhaven Local Health District , NSW , Australia Clinical Senior Lecturer , Sydney Nursing School, University of Sydney , NSW , Australia

Margaret Murphy RN, MH, MEd, GradDipCritCare, GradDipChangeMgt Clinical Nurse Consultant , Emergency Department, Westmead Hospital , Sydney , NSW , Australia

Meredith Oatley RN, GradCertCancerNurs, MNurs(NursePrac) Nurse Practitioner Medical Oncology , Northern Sydney Cancer Centre, Royal North Shore Hospital , St Leonards , NSW , Australia

Linda Ora RN, MPallC Clinical Nurse Consultant , Nepean Blue Mountains Local Health District , NSW , Australia

Fiona Orr RN, BHSc(Nurs), MLitt, PhD Director , International Activities, Faculty of Health, University of Technology Sydney , NSW , Australia

Julie Potter RN, ICUCert, MHSc(Ed), MN(Hons) Senior Research Offi cer , The University of Sydney Susan Wakil School of Nursing and Midwifery, Sydney and Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney Directorate of Nursing , Midwifery and Clinical Governance, Western Sydney Local Health District , NSW , Australia

Amber Preece BSW, MPS Senior Social Worker, Social Worker , Northern Sydney Local Health District , Sydney , NSW , Australia

Nicholas Procter RN, BA, GradDipAdultEd, MBA, PhD Professor and Chair : Mental Health Nursing , University of South Australia , Adelaide , South Australia , Australia

Linda Quinn RN, CertPaed, GradDipBurns Burns Advanced Nurse Consultant , Women ’ s and Children ’ s Hospital , Adelaide , South Australia , Australia

Clair Ramsden RN, GradCertCardiol, MHlthcareEthics, MHlthServMgt Associate Professor , University of Technology Sydney , NSW , Australia Executive Director Operations , Nepean Blue Mountains Local Health District , NSW , Australia

Helen Rawson RN, MSc, BSc(Hons), PhD Senior Research Fellow , Centre for Quality and Patient Safety Research – Monash Health Partnership, School of Nursing and Midwifery, Deakin University , Burwood , Victoria , Australia

Dwight Robinson RN, BNurs, GradCert(Emerg), MNurs(CritCareNurs) Manager , Emergency Management Unit, Liverpool Hospital , NSW , Australia Critical Care RN (ED & ICU) , Nepean Hospital, Nepean Blue Mountains Local Health District , NSW , Australia

Michael Roche RN, MHSc(Nurs), PhD Associate Professor in Health Services Management and Mental Health Nursing , Faculty of Health, University of Technology Sydney , NSW , Australia

Erica Rootham BNurs, GradCertEmergNurs, MNurs(NursePrac) Nurse Practitioner , Emergency Department, St George Hospital, Kogarah , Sydney , NSW , Australia

Philip L. Russo MClinEpid, PhD Director of Nursing Research , Cabrini Health , Melbourne , Victoria , Australia Associate Professor , School of Nursing and Midwifery, Faculty of Medicine and Health Sciences, Monash University , Melbourne , Victoria , Australia

Myra Sgorbini RN, GradCertICUNurs, GradCertHlthRes, MNurs(Hons) Clinical Nurse Consultant , Royal Prince Alfred Hospital , Sydney , NSW , Australia

Ramon Z. Shaban RN, CICP-E, BSc(Med), BN, GradCertInfCon, PGDipPH&TM, MEd, MCommHealthPrac(Hons), PhD, FCENA, FACN Professor and Clinical Chair of Infection Prevention and Disease Control , Susan Wakil School of Nursing and Midwifery and Marie Bashir Institute for Infectious Diseases and Biosecurity, University of Sydney , NSW , Australia Department of Infectious Diseases and Infection Control & Nursing, Midwifery and Clinical Governance Directorate, Western Sydney Local Health District , NSW , Australia Editor-in-Chief , Australasian Emergency Care, College of Emergency Nursing Australia , NSW , Australia

CONTRIBUTORS xvii

Joseph Sharpe RN(Trauma), BHlthSc, MNurs(Emerg) Clinical Nurse Consultant , The Townsville Hospital , Townsville , Queensland , Australia

Tony Skapetis BDS, MEd(Adult), PhD Clinical Director Education , Oral Health, Western Sydney Local Health District , NSW , Australia Clinical Associate Professor , Sydney School of Dentistry, Faculty of Medicine and Health, University of Sydney , NSW , Australia

Ruth Townsend BNurs, DipParaSc, GradCertVET, GradDipLegalPrac, LLM, PhD Senior Lecturer , Paramedic Law, Ethics, Professionalism and Research, School of Biomedical Sciences, Charles Sturt University , Bathurst , NSW , Australia

Jane Treloggen RN, DipMgt, BHSc(Nurs), ICUCert, MHSc(Nurs) Manager , NSW Tissue Banks, NSW Organ and Tissue Donation Service , Sydney , NSW , Australia

Wayne Varndell RN, MNurs(Res), BSc(Nurs), PGCE Clinical Nurse Consultant , Prince of Wales Hospital Emergency Department , Sydney , NSW , Australia Honorary Lecturer , Faculty of Health, University of Technology Sydney , NSW , Australia

Ioana Vlad MD, GradDipClinTox, DCH, VGDWH, FACEM Emergency Medicine Specialist , Clinical Toxicologist, Sir Charles Gairdner Hospital , Perth , Western Australia , Australia

Elizabeth Walter GradCertHlthLeadMgt, GradCertEmerg, Cert IV TAE, MNurs Clinical Nurse Coordinator , Emergency, The Sutherland Hospital , Caringbah , NSW , Australia

Nicole Watts RM, RN, MMid, GradDipMid Coordinator Bachelor of Midwifery , University of Technology Sydney , Sydney , NSW , Australia

Diana Williamson RN, DipHlthSc, GradCertEmerg, MCP(Emerg) Conjoint Lecturer University of Newcastle , Newcastle , NSW , Australia

Sam Willis BSc(Hons)ParamedicSc, MEd(Res), FHEA Senior Lecturer in Paramedicine , Charles Sturt University , Sydney , NSW , Australia

Sarah Winch RN, BA(Hons), PhD Associate Professor and Theme Lead , Medical Ethics, Law and Professionalism, Faculty of Medicine, The University of Queensland , Queensland , Australia

Taneal Wiseman RN, GradDipCritCareNurs, PhD Lecturer in Acute Care Nursing , The University of Sydney Susan Wakil School of Nursing and Midwifery , Sydney , NSW , Australia

Denise Blanchard RN, PhD

Associate Professor in Nursing , School of Nursing, Midwifery and Indigenous Health, Faculty of Science, Charles Sturt University , NSW , Australia

Pauline Calleja RN, GradCertHEd, BSc(Nurs), DipMgt, MAdvNursPrac, PhD, MACN, FCENA

Director of Post Graduate Nursing and Infection Prevention and Control programs, Senior Lecturer , School of Nursing and Midwifery, Griffi th University , Queensland , Australia

Karen Hammad RN, BN(Hons), GradDipEmergNurs, PhD

Consultant , World Health Organization

Senior Lecturer , Flinders University , Adelaide , South Australia , Australia

Martin Hopkins BA(Hons), PGCHE, MSc, RNursDip(Adult), PhD

Senior Lecturer , Murdoch University , Perth , Western Australia , Australia

Alex (Sandy) MacQuarrie RP, BSc, MBA

Senior Lecturer in Paramedicine , School of Medicine, Griffi th University, Gold Coast , Queensland , Australia

Robin Pap NDipEMC, BTechEMC, HDipHET, MScMed(EM)

Lecturer in Paramedicine , Western Sydney University , NSW , Australia

Minakshi Pearce RN, MIPH

Lecturer , Australasian College of Nursing and Midwifery, Charles Darwin University , Sydney , NSW , Australia

REVIEWERS Virginia Plummer RN, RM, CritCareCert, GradCertHlthProfEd, GradCertEmergHlth, MSc, PhD

Associate Professor Nursing and Midwifery , Monash University and Peninsula Health , Victoria , Australia

Joanne Porter GradDipCC, GradDipHSM, GradCertEd, MNurs, PhD, RN

Associate Professor , School of Nursing and Healthcare Professions, Federation University , Ballarat , Victoria , Australia

Julija Sipavicius BSN, MNurs(Lead), MNurs(NursePract)

Nurse Practitioner , Bone Marrow Transplantation, Department of Haematology, Royal North Shore Hospital , St Leonards , NSW , Australia

Penelope Sweeting RN, MN

Lecturer , College of Nursing and Midwifery, Charles Darwin University , Sydney , NSW , Australia

Karen Theobald RN, GradCert(Higher Ed), MHSc(Nurs), PhD

Associate Professor, Director of Academic Programs , Emergency Nursing Study Area and Coordinator, School of Nursing, Queensland University of Technology , Queensland , Australia

149

E s s e n t i a l s ● Physiological responses form the basis for signs and symptoms observed in emergency

patients. ● The sympathetic nervous system is activated and the parasympathetic nervous system

is slowed in most stressful situations. ● Shock is the process resulting from inadequate cellular perfusion. ● The ‘triad of death’ (acidosis, hypothermia and coagulopathy) is linked to death following

blood loss. ● The early assessment and identifi cation of abnormal physiology and shock are central

to the work of emergency clinicians. Early sets of vital signs can provide an indication of the existence of shock and provide clinical cues that guide interventions.

INTRODUCTION

Physiology in emergency care forms the basis of the many signs and symptoms displayed in patients who use emergency health services. Many research articles and textbooks have been published on the physiological phenomena of the stress response, or ‘general adaptation syndrome’ (GAS), fi rst introduced and popularised by Hans Selye. 1,2 Selye ’ s research identifi ed three very distinct phases within the GAS: alarm , resistance and exhaustion phases, triggered after the body ’ s exposure to injury or illness, resulting in the disruption of homeostasis. This chapter examines the physiological principles that apply to patients seen in the pre-hospital and hospital emergency department (ED) setting and forms the basis for all applicable chapters within this textbook.

CHAPTER 10

PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE PETER MOULES

150 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

Homeostasis Homeostasis may be defi ned as the body ’ s maintenance of a relatively constant internal environment in the face of an ever-changing external environment. Th e factors that are being kept relatively constant are called regulated variables . Examples include the concentration of virtually all blood chemicals, core tem-perature, partial pressure of carbon dioxide, vertical posture, withdrawal refl exes, blood pressure, blood glucose, energy usage, metabolic rate—even weight.

In general, these variables are regulated by negative feedback loops ( Fig. 10.1 ). In order for any variable to be kept relatively constant there has to be a feedback loop which corrects (or negates) any deviation of that variable from the set point. Th is is the healthy range for every variable.

In principle, every feedback loop must contain the following elements: ● set point—the level at which the regulated variable should

be maintained, as determined by a process that is connected to the control centre, i.e. the control centre has to have some knowledge of what the set point should be

● receptors—sensitive cells or tissues that measure or monitor the regulated variable; this together with the neural or hormonal signalling mechanism is the aff erent component

● control centre—compares the regulated variable with the set point and initiates the ‘error signal’

● error signal—a signal (electrical or chemical) initiated by the control centre in proportion to the diff erence between the regulated variable and the set point. Th e error signal brings about a response from the eff ector organ(s). Th is is the eff erent component

● eff ector organ(s)—the organ(s) that respond to the error signal and shift the regulated variable up or down towards the set point.

Effector organ(s)brings the regulatedvariable back to theset point

Start here.Follow the arrows in aclockwise direction

Monitored bydetectors(receptors)

Control centrecompares theactual value withthe set point

Set point

Regulatedvariable

Negativefeedback

Error signal

FIGURE 10.1 A negative feedback loop.

set point

regulated variable

FIGURE 10.2 A regulated variable oscillating around its set point.

As a consequence, regulated variables are always oscillating around a set point, as shown in Figure 10.2 .

If the regulated variable rises above the set point, this is monitored by receptors and the control centre compares this high value with the set point. Th e control centre sends an error signal to the eff ector organs to bring the regulated variable back towards the set point. Th e regulated variable then, generally, overshoots the set point; the lower value is detected by receptors and the control centre sends an error signal that causes the regulated variable to trend upwards, back to and over the set point, and so on.

A simple example is the control of core temperature when moving from a cool temperature to a slightly warmer one. Th e thermoreceptors in the hypothalamus constantly monitor the temperature of the blood. As it starts to warm, the control centre senses the diff erence between the temperature of the blood and the set point, and generates an error signal through the vascular portion of the sympathetic nervous system that controls the dilation and constriction of the small arterioles in the skin vascular beds. Dilation of these vessels allows the blood ’ s heat to radiate into the environment. If too much heat is lost, constriction of the same vessels helps conserve heat. At more extreme changes of temperature, other mechanisms such as sweating and shivering are recruited to assist cooling and warming.

If any part of a feedback loop is damaged or missing, a loss of homeostasis may result. Feedback loops can become pathologi-cal when, rather than taking the regulated variable back to the set point, it moves it further from the set point. Instead of negating the diff erence between the regulated variable and the set point, a pathological feedback loop will increase and amplify the diff erence. Th is is called positive feedback and is a central principle in the pathophysiology of emergency care.

An example will help to make the point. Consider a panic attack. A patient becomes aware of their own heart beating (normally this cannot be felt). Th e anxiety caused by these palpitations increases the release of adrenaline, which causes the heart to beat faster and with increased force, which causes more anxiety, more adrenaline release and yet more rapid and forceful palpitations: even though the patient is not in danger, the ‘fi ght or fl ight’ feedback mechanism has entered a vicious cycle.

Examples of some relevant regulated variables, receptors, control centres, error signals, eff ector organs and outcomes are shown in Table 10.1 .

Oxygen transport Th e atmosphere at sea level has a pressure of 760 mmHg. Twenty-one per cent of this is oxygen, which has a proportionate,

151CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

TAB

LE 1

0.1

Rec

epto

r pa

thw

ays

for

hom

eost

asis

REG

ULA

TED

VA

RIA

BLE

REC

EPTO

R

CO

NT

ROL

CEN

TR

E SE

T P

OIN

T

ERRO

R S

IGN

AL

EFFE

CTO

R

OR

GA

N(S

) R

ESU

LT

Art

eria

l par

tial

pres

sure

of

carb

on d

ioxi

de,

PaC

O 2

Cen

tral

ch

emor

ecep

tors

—ne

uron

s in

the

med

ulla

th

at a

re s

ensi

tive

to

CO

2 an

d hy

drog

en io

ns

Res

pira

tory

ne

uron

s in

the

po

ns a

nd m

edul

la

40 m

mH

g, de

term

ined

by

auto

mat

ic n

euro

ns

asso

ciat

ed w

ith t

he

resp

irat

ory

cent

res

Mod

ulat

ion

of

the

med

ulla

ry

resp

irat

ory

neur

ons

that

pr

ojec

t do

wn

the

spin

e

Inte

rcos

tal a

nd

diap

hrag

m m

uscl

esM

odul

atio

n of

the

rat

e an

d de

pth

of

resp

irat

ion

and

mai

nten

ance

of

PaC

O 2

at

the

set

poin

t

Plas

ma

osm

olar

ityH

ypot

hala

mic

os

mor

ecep

tors

—ne

uron

s th

at s

hrin

k or

sw

ell d

epen

ding

on

the

part

icle

con

tent

of

the

hypo

thal

amic

inte

rstit

ial

fl uid

. Thi

s ch

ange

s th

eir

fi rin

g pa

tter

ns

depe

ndin

g on

the

ir

degr

ee o

f hy

drat

ion

Para

vent

ricu

lar

hypo

thal

amic

ne

uron

s w

hose

ax

ons

proj

ect

to

the

post

erio

r pi

tuita

ry

App

rox.

300

Osm

.

Det

erm

ined

by

auto

mat

ic n

euro

ns

asso

ciat

ed w

ith t

he

hypo

thal

amic

co

ntro

l cen

tre

Mod

ulat

ion

of

the

secr

etio

n of

A

DH

Prim

arily

the

cel

ls

of t

he c

olle

ctin

g du

cts

in t

he k

idne

y

AD

H b

inds

to

V-2

rece

ptor

s in

the

ki

dney

col

lect

ing-

duct

cel

l mem

bran

es,

initi

atin

g an

intr

acel

lula

r se

cond

m

esse

nger

cA

MP

whi

ch p

rom

otes

the

m

anuf

actu

re a

nd in

stal

latio

n of

aq

uapo

rins

(w

ater

cha

nnel

s) in

the

api

cal

and

baso

late

ral c

ell m

embr

anes

. Thi

s in

crea

ses

thei

r pe

rmea

bilit

y to

wat

er

and,

pro

vidi

ng t

he k

idne

y m

edul

la is

of

a hi

gher

osm

olar

ity t

han

the

colle

ctin

g du

cts,

wat

er is

rea

bsor

bed

and

a m

ore

conc

entr

ated

uri

ne is

pro

duce

d.

Cor

e te

mpe

ratu

reH

ypot

hala

mic

te

mpe

ratu

re r

ecep

tors

w

hich

cha

nge

thei

r di

scha

rge

patt

erns

de

pend

ing

on t

he

tem

pera

ture

of

the

perf

usin

g bl

ood

Hyp

otha

lam

ic

neur

ons

who

se

axon

s co

nnec

t to

th

e va

scul

ar

com

pone

nt o

f th

e sy

mpa

thet

ic

nerv

ous

syst

em

37°C

, det

erm

ined

by

aut

omat

ic

neur

ons

asso

ciat

ed

with

the

hy

poth

alam

ic

cont

rol c

entr

e

Mod

ulat

ion

of

disc

harg

e do

wn

the

sym

path

etic

ne

rves

whi

ch

cont

rol fl

ow

in

the

cuta

neou

s ci

rcul

atio

n

The

art

erio

les

in

the

derm

is o

f th

e sk

in

An

incr

ease

in c

ore

tem

pera

ture

res

ults

in

cut

aneo

us v

asod

ilatio

n; a

dec

reas

e in

co

re t

empe

ratu

re r

esul

ts in

cut

aneo

us

vaso

cons

tric

tion

Sodi

um a

nd

pota

ssiu

m—

shor

t ro

ute

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pla

sma

sodi

um o

r hi

gh p

lasm

a po

tass

ium

st

imul

ate

the

glom

erul

osa

cells

of

the

adre

nal g

land

Glo

mer

ulos

a ce

lls

of t

he a

dren

al

glan

d

Na + a

ppro

x.

140

mm

ol/L

; K +

appr

ox 4

–5 m

mol

/L.

Det

erm

ined

by

the

glom

erul

osa

cells

of

the

adre

nal g

land

Ald

oste

rone

se

cret

ion

Tubu

lar

cells

of

the

dist

al c

onvo

lute

d tu

bule

of

the

kidn

ey

Ald

oste

rone

bin

ds t

o nu

clea

r re

cept

ors

and

stim

ulat

es t

he t

rans

crip

tion

of m

ore

Na + -K

+ -AT

Pase

pum

ps. T

hese

ret

riev

e m

ore

Na + f

rom

the

fi lt

rate

and

allo

w K

+ lo

ss

152 SECTION 2 CLINICAL CONCEPTS AND SYSTEMSTA

BLE

10.

1 R

ecep

tor

path

way

s fo

r ho

meo

stas

is—

cont

’d

REG

ULA

TED

VA

RIA

BLE

REC

EPTO

R

CO

NT

ROL

CEN

TR

E SE

T P

OIN

T

ERRO

R S

IGN

AL

EFFE

CTO

R

OR

GA

N(S

) R

ESU

LT

Sodi

um a

nd

pota

ssiu

m—

long

ro

ute

A d

rop

in b

lood

pr

essu

re o

r vo

lum

e or

a

low

erin

g of

pla

sma

sodi

um s

timul

ates

the

ce

lls o

f th

e JG

A in

the

ki

dney

Cel

ls o

f th

e JG

AN

a + app

rox.

14

0 m

mol

/L; K

+ ap

prox

. 4–5

mm

ol/L

.

Det

erm

ined

by

cells

of

the

JG

A

Ren

in s

ecre

tion

→ a

ngio

tens

in I

fo

rmat

ion

→

angi

oten

sin

II fo

rmat

ion

→

stim

ulat

es

aldo

ster

one

secr

etio

n fr

om

glom

erul

osa

cells

of

adr

enal

gla

nd

Tubu

lar

cells

of

the

dist

al c

onvo

lute

d tu

bule

of

the

kidn

ey

Ald

oste

rone

bin

ds t

o nu

clea

r re

cept

ors

and

stim

ulat

es t

he t

rans

crip

tion

of m

ore

Na + -K

+ -AT

Pase

pum

ps. T

hese

ret

riev

e m

ore

Na + f

rom

the

fi lt

rate

and

allo

w K

+ lo

ss

Cal

cium

(C

a 2 + )

Low

cal

cium

det

ecte

d by

cel

ls o

f th

e pa

rath

yroi

d gl

and

Cel

ls o

f th

e pa

rath

yroi

d gl

and

App

rox

5 m

Eq.

Det

erm

ined

by

cells

of

the

par

athy

roid

gl

and

Secr

etio

n of

pa

rath

yroi

d ho

rmon

e

(i) B

one,

rel

ease

s so

me

Ca 2 +

fro

m

bone

(ii)

Gut

, enh

ance

s C

a 2 + a

bsor

ptio

n fr

om t

he g

ut

(iii)

Kid

ney

tubu

le

cells

, enh

ance

Ca 2 +

re

abso

rptio

n fr

om

kidn

ey fi

ltra

te

Rai

ses

plas

ma

calc

ium

leve

ls

Hig

h pl

asm

a ca

lciu

m

stim

ulat

es in

ters

titia

l ce

lls in

the

thy

roid

gl

and

Inte

rstit

ial c

ells

of

the

thyr

oid

glan

dA

ppro

x. 5

mM

.

Det

erm

ined

by

inte

rstit

ial c

ells

of

the

thyr

oid

Secr

etio

n of

ca

lcito

nin

Opp

oses

re

abso

rptio

n of

C

a 2 + f

rom

bon

e

Low

ers

plas

ma

calc

ium

leve

ls

Hyd

roge

n io

ns

and

bica

rbon

ate

ions

The

res

pira

tory

sys

tem

co

ntro

ls h

ydro

gen

ions

an

d bi

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153CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

or partial pressure , of 0.21 × 760 = 160 mmHg. If this atmosphere is in contact with a body of fl uid, the partial pressure of that particular gas dissolved in the fl uid will equilibrate. Th e partial pressure can be thought of as the ‘driving force’ that causes the gas to dissolve in the fl uid. Th e amount of gas in the fl uid depends on other factors as well, in particular, the solubility.

Unlike carbon dioxide, oxygen is not very soluble in water or plasma. At 37°C, only 1.5% of the oxygen carried by 100 mL of blood is dissolved in plasma. Th e only reason that blood can carry a signifi cant amount of oxygen is the presence of approxi-mately 15 g of haemoglobin per 100 mL of blood. Th e hae-moglobin is contained in the red blood cells. Haemoglobin is a globular protein with four subunits, each of which has a central iron atom capable of binding reversibly with one oxygen molecule, with an S-shaped affi nity curve ( Fig. 10.3 ).

Under experimental conditions it is possible to vary the partial pressure of oxygen in blood, and measure the resulting amount of bound oxyhaemoglobin as a percentage of total haemoglobin. Th is is termed the oxygen saturation . A gradient exists between alveolar air, across the alveolar wall, into the blood. At sea level, breathing room air, the typical partial pressure of oxygen in the arterial blood (PaO 2 ) in a healthy person is about 100 mmHg ( Fig. 10.4 ).

Th e oxygen–haemoglobin dissociation curve turns out to be S-shaped rather than linear. Th e shape of this curve (with a fl at top) is primarily due to the fact that when all the haemoglobin

molecules are carrying four oxygen molecules, no more oxygen can be carried by blood, except if dissolved in the plasma. Th is dissolved amount is very small (0.3 mL O 2 /100 mL plasma at 100 mmHg PaO 2 ). Each gram of haemoglobin can combine with a maximum of about 1.34 mL of oxygen, so an individual with 15 g of haemoglobin per 100 mL of blood can carry about 20 mL of oxygen per 100 mL of blood. 3 It can be seen that

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20181614121086420

60 80Pressure of oxygen in blood (PaO2) (mmHg)

1204020 100 140

O2 bound with haemoglobin

FIGURE 10.3 Effect of PaO 2 on the quantity of oxygen bound with haemoglobin in each 100 mL of blood. 3

FIGURE 10.4 Exchange of gases at the alveolus and the body tissues with blood and transport of oxygen and carbon dioxide. 4

Deoxygenated veins,upper torso

Deoxygenated veins,lower torso Oxygenated arteries,

lower torso

Oxygenated arteries,upper torso

Capillaries

Venous blood Arterial blood

Ambient air

PCO2 46 mmHg

PO2 40 mmHg

PCO2 40 mmHg

PO2 100 mmHg

PCO2 0.2 mmHg

PO2 160 mmHg

154 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

Th e bicarbonate ions produced in this way diff use out of the red cells and are replaced by chloride ions. In lung capillaries, the opposite of this happens: bicarbonate ions are converted back into carbon dioxide and carbon dioxide fl ows down a concentration gradient out of the blood and into the alveoli of the lungs. As a result of this increased solubility and chemical buff ering capacity in plasma and red blood cells, the carriage of CO 2 is more or less linearly proportional to its partial pressure. In arterial blood, there is a partial pressure (PaCO 2 ) of about 40 mmHg (5.3 kPa), which represents around 400 mL of carbon dioxide per 100 mL of blood.

Capnography Arterial PaCO 2 can be estimated by infrared assay of end-expiratory air samples. Th is air, essentially alveolar air, in normal haemodynamic and pulmonary states has a PCO 2 approximately 1–5 mmHg (0.14–0.68 kPa) below that of arterial blood. End-expiratory, or end-tidal, CO 2 (EtCO 2 ) refl ects a combination of the arterial CO 2 level and the amount of pulmonary perfusion.

Capnography is the real-time graphical representation of sampled CO 2 in air inspired and expired by the patient. It has become a standard monitoring tool for intubated patients in the pre-hospital setting and ED for several reasons. First, the presence of expired CO 2 confi rmed by the monitor waveform ( Fig. 10.6 ) indicates that the endotracheal tube is in the trachea and not the oesophagus. 5 Second, in brain-injured patients, for example, controlling ventilation to maintain arterial PCO 2 in normal ranges has been associated with improved outcomes. Lastly, the level of expired CO 2 during steady ventilation is a refl ection of pulmonary perfusion and hence a useful indica-tor of cardiac output. 6 During cardiac arrest, for example, the EtCO 2 can refl ect the adequacy of CPR. (For more informa-tion regarding capnography and EtCO 2 monitoring, refer to Chapter 14 .)

Regions of the lung ventilated but not perfused are known as ‘dead space’, and this increases as a result of decreased pul-monary perfusion. Th ese areas do not contribute to gas exchange between the blood and the atmosphere and thus decrease the effi ciency of the lung as a functional unit. An increase in dead space results in an increased gradient between arterial CO 2 and end-expiratory CO 2 (increased PaCO 2 in relation to EtCO 2 ). As the gradient between EtCO 2 and PaCO 2 may be signifi cant in ill or injured patients, it is good practice to obtain a measure of arterial PCO 2 and correlate this with the EtCO 2 . Some examples of the clinical scenarios that aff ect PaCO 2 :EtCO 2 gradient include: decreased pulmonary blood fl ow (low cardiac output states); pulmonary embolism; cardiac arrest; PEEP; hypovolaemia; and lateral decubitus positioning. 6

the vast majority of oxygen carried by the blood is bound to haemoglobin, thus even if the oxygen saturation approaches 100% a reduction in haemoglobin will lead to a reduction in the amount of oxygen delivered to tissues.

Symptoms of cardiac ischaemia may result from severe anaemia. No amount of supplemental oxygen will compensate for the reduced oxygen carriage in such a patient. As foreshad-owed above, another trick that haemoglobin has up its molecular sleeve is that its affi nity for oxygen changes depending on the environment in which it is operating. Most of the time it fl ows from the lungs saturated with oxygen and is then pumped through working vascular beds, the tissue of which has relatively low metabolic rates. On average, each haemoglobin molecule delivers only one oxygen molecule to the tissue and goes back to the heart and lungs still three-quarters saturated.

But in hardworking tissue like exercising muscle, the tissue is hot and acidic. Th is environment twists the haemoglobin molecule a touch and reduces the affi nity between oxygen and haemoglobin so that more than one oxygen molecule is liberated from each haemoglobin molecule ( Fig. 10.5 ). In extremely hot acidic working muscle, all the oxygen is stripped off the hae-moglobin. In this way the oxygen supply to tissue can be increased four-fold without an increase in blood supply.

Carbon dioxide transport Carbon dioxide does not bind to haemoglobin at the same sites as oxygen. It is carried as carbamino (N–COO – ) compounds on all the blood protein molecules, including haemoglobin, but this only accounts for 18% of carbon dioxide carriage. Five per cent of carbon dioxide is carried dissolved in the plasma. Approximately 77% of carbon dioxide is carried as bicarbonate ions that result from the chemical reaction between carbon dioxide and water. Carbon dioxide easily diff uses into red cells and is hydrated by the enzyme carbonic anhydrase, producing carbonic acid which ionises into bicarbonate ions and hydrogen ions:

CO H O H CO HCO H2 2 2 3 3+ ↔ ↔ +− + (a)

PRACTICE TIP

Capnography is used in EDs in a variety of scenarios, including sedation monitoring (especially in procedural sedation), ventilation monitoring and endotracheal tube confi rmation, assessing adequacy of CPR, diagnosis through waveform interpretation (such as bronchospasm), and detection of respiratory dead space.

0

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Pressure of oxygen in blood (PaO2) (mmHg)

FIGURE 10.5 Shift of the oxyhaemoglobin dissociation curve to the right caused by an increase in hydrogen-ion

concentration (decrease in pH). 3

BPG: 2,3-bisphosphoglycerate.

155CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

sensitive to arterial PaCO 2 , [H + ] and also PaO 2 , but only if oxygen drops to dangerously low levels. Th is hypoxic sensitivity and the associated respiratory drive are, essentially, emergency devices. Hyperventilation (may be voluntary or caused by anxiety or fever) blows off carbon dioxide. PaCO 2 may by reduced to as low as 20 mmHg (2.6 kPa; normally 40 mmHg, 5.3 kPa), thus reducing the respiratory drive. Hyperventilation cannot, however, increase the amount of oxygen carried in arterial blood if all the haemoglobin is already fully saturated and has no further carrying capacity. Consider the eff ects of hyperventilation on the equation:

CO H O H CO HCO H2 2 2 3 3+ ↔ ↔ +− + (a)

As carbon dioxide is ‘blown off ’, the equation will be pulled from right to left reducing the concentration of HCO 3 – and H + (i.e. the pH will increase—respiratory alkalosis).

Consider the eff ects of breath-holding or hypoventilation on the same equation: carbon dioxide will accumulate and push the equation from left to right, thus increasing the concentration of HCO 3 – and H + (i.e. the pH will decrease—respiratory

Oxygen/carbon dioxide homeostasis Due to the crucial role of CO 2 in the maintenance of acid–base balance via carbonic anhydrase, the respiratory system controls PaCO 2 very tightly ( Fig. 10.7 and Table 10.1 ).

When the PaCO 2 gets above 40 mmHg (5.3 kPa), there is a refl ex increase in the rate and depth of respiration, so more carbon dioxide diff uses from the blood into the alveoli and is ‘blown off ’. When the PaCO 2 drops below 40 mmHg (5.3 kPa), there is a refl ex decrease in the rate and depth of respiration, so more carbon dioxide is retained. Th e respiratory muscles, the diaphragm and the intercostals, are the eff ector organs. Th ey are driven by motor neurons in the spinal cord, which are in turn driven by descending motor neurons that originate in the medulla oblongata. In the medulla and pons are respiratory centres; they consist of pacemaker cells which determine the rate of respiration, and amplifi er circuits which determine the depth of respiration. Th ese respiratory centres are infl uenced by central chemoreceptors that are sensitive to PaCO 2 and hydrogen–ion concentration ([H + ]), and by peripheral chemo-receptors situated in the aortic arch and carotid bodies that are

Set pointRegulated variable = plasma PaCO2 (partial pressure of carbon dioxide)

Error signal (motor neuron action). Potentials flow from the medulla to the respiratory muscles (effector organs) proportional to the difference between the actual blood CO2 and the set point

Increased rate and depth of respiration blows off more CO2 and the blood CO2 decreases towards the set point

Start here.Follow the arrows in a clockwise direction

Detected by CO2 receptors in the central chemoreceptors in medulla

Increasing amount of CO2 in the blood

Negative feedback

Respiratory centres in themedulla compare theelevated CO2 with the setpoint

FIGURE 10.7 The respiratory system ’ s homeostatic control of blood carbon dioxide.

FIGURE 10.6 Normal � ndings on a capnogram. 6

50

0A B

CD

E

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bon

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ide,

mm

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156 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

climates, the skin serves as an adjustable radiator for heat loss and heat retention and, depending on the requirement to either eliminate or retain heat, blood is redistributed either to or from the peripheral skin circulation. A change in temperature below the ‘set point’ of the body ’ s thermostat is detected by skin and hypothalamic receptors, and results in vasoconstriction of the skin arterioles, reducing the rate of heat loss. Conversely, if the body core starts to heat up vasodilation results, increasing skin blood fl ow and dissipating excess heat into the environment. In low-melanin persons this can be seen as a change in skin colour—pale in cold and pink in warm environments.

In response to more extreme changes in temperature, other mechanisms are used to warm or cool the body. As ambient temperature approaches body temperature, radiant heat loss becomes less eff ective and is augmented by sweating and evapora-tive cooling. Th e sweat glands are also under the control of the sympathetic nervous system. When water evaporates it has to draw heat from the skin to change it from a liquid to a gas. Th is can provide a cooling eff ect, even if the ambient temperature is above body temperature. However, the eff ectiveness is reduced in the presence of humid heat, and excessive sweating also reduces plasma volume, serum sodium and potassium and urinary output (see Chapter 28 on environmental emergencies). Individuals acclimatise to heat over several days to weeks, with an increase in sweat production and a reduction in sweat sodium losses.

When the body is exposed to extreme cold, the drop in core temperature detected in the hypothalamus results in shivering—involuntary contractions of skeletal muscles that produce some waste heat. At the same time the contraction of the arrector pili muscles at the base of each hair follicle (goose-bumps) is an ancient refl ex harking back to our evolutionary heritage when humans were a lot hairier. Th e generalised erection of body hair improves the skin ’ s insulating properties.

Fluid and electrolyte balance in homeostasis Th e amount of fl uid, water and the concentration of electrolytes are all under the control of homeostatic mechanisms. Ultimately

acidosis). Th erefore, in the ordinary daily moment-to-moment control of the blood gases oxygen and carbon dioxide, the regulated variable is, largely, carbon dioxide. If the arterial PaCO 2 is kept at around 40 mmHg (5.3 kPa) then the blood, ordinarily, will be close to fully saturated with oxygen. If the respiratory system is compromised, for example, by brain injury, and respira-tion is reduced, the brain becomes relatively insensitive to the rising carbon dioxide levels and at a certain point the peripheral chemoreceptors, which alone monitor oxygen content of arterial blood, kick in and provide a signifi cant drive to respiration. As noted above, this is an emergency mechanism that may lead to intermittent (Cheyne-Stokes) breathing patterns. Th e oxygen-sensitive peripheral chemoreceptors do not provide a signifi cant amount of drive to the respiratory centres until the arterial blood is approaching the PaO 2 of venous blood (PaO 2 40–50 mmHg, 5.3–6.6 kPa), by which time cyanosis may well be evident.

In chronic respiratory acidosis (lasting more than an hour or so), the kidney tubule cells progressively increase their expul-sion of hydrogen ions into the urine and retain bicarbonate ions in the plasma in an attempt to maintain normal pH levels in the blood. A more comprehensive discussion of the measure-ment of acid–base balance and interpretation of arterial and venous blood gases is provided in Chapter 16 Clinical skills and Chapter 21 Respiratory emergencies.

Oxygen therapy Th e provision of oxygen at a greater concentration than room air (i.e. above 21%) is a commonly performed procedure in emergency situations. Very high concentrations of oxygen are also toxic. Particularly in premature infants, breathing 100% oxygen can damage lung tissue due to the activity of oxygen-free radicals (atomic oxygen) that occur in the gas. Th e unpaired electrons of atomic oxygen damage structural and functional proteins in the lung. However, in the fi rst 24 hours it is important to titrate oxygen delivery according to oxygen saturation measure-ments, but oxygen should not be withheld for fear of toxicity in adults. 7

Th e most common delivery devices used in emergency environments are nasal cannulae, masks or masks with reservoir bags. Th e approximate percentage oxygen delivery for each device is presented in Table 10.2 . 7

Hospitals are also increasingly employing high-fl ow nasal prongs in the treatment of hypoxic respiratory conditions. Th ese devices provide warmth and humidifi cation to the fl ow supplied. Th ey can supply between 1 and 60 L of fl ow, with oxygen concentrations between 0.21 and 1. Th ese devices can provide PEEP of up to 7.4 cmH 2 O. 8

Homeostatic temperature control In normal health, core body temperature is a regulated vari-able. Th e normal body temperature (recorded via a tympanic thermometer) is in the range of 35.4–37.8°C, and has a slight diurnal variation. 9 Th e detectors and control centre are temperature-sensitive receptors in the skin, and specialised neurons in the hypothalamus. In other species, and in human infants, metabolically active ‘brown’ adipose tissue plays a role in temperature homeostasis. In adults, the principal eff ector organs are the blood vessels and sweat glands in the skin. In temperate

TABLE 10.2 O 2 delivery systems 7

APPARATUS OXYGEN FLOW (L/MIN)

OXYGEN CONCENTRATION (%)

Nasal catheters 1–4 24–40

Semi-rigid mask 6–15 35–60

Semi-rigid mask with double O 2 supply

15–30 Up to 80

Semi-rigid mask with reservoir bag

12–15 60–90

High-fl ow nasal catheter

1–70 21–100

157CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

as the term ‘natriuretic’ suggests (from the Latin word for sodium, ‘natrium’), also antagonises the eff ects of aldosterone and reduces renin production (see next section) and promotes the loss of sodium, and hence water, from the kidney by reducing reabsorp-tion in the distal convoluted tubule. Finally, it has vasodilatory properties and eff ects on fat metabolism.

In the face of congestive cardiac failure, the fi lling pressures of the heart increase abnormally, and myocardium can become hypertrophic in response. In addition to its benefi cial modulation of blood volume in this situation, ANP is thought to have a protective eff ect on cardiac muscle by directly limiting this ‘remodelling’.

Electrolytes Sodium and potassium Th e levels of sodium and potassium in the blood are ultimately controlled by action of the steroid hormone aldosterone, mainly on the distal convoluted tubules of the kidney. Essentially, aldosterone binds to nuclear receptors in the nuclei of tubular cells and promotes the transcription of genes for specifi c proteins that increase the number of sodium channels in the cell mem-branes and also increase the number of sodium-potassium-ATPase pumps in the basolateral membrane that pump sodium back in to the kidney capillaries and allow potassium to be lost in the urine. Th e relative abundance of aldosterone will determine how much sodium is being retained and potassium is lost, and vice versa.

Th ere are two feedback loops that control the secretion of aldosterone from the adrenal cortex. First, the cells of the adrenal cortex itself sense reductions in plasma sodium levels and secrete aldosterone as a response. Second, some sensitive tissue (the juxtaglomerular apparatus, JGA), lodged between the glomeruli and the distal convoluted tubules of the kidney, senses the loss of sodium and releases the enzyme renin as a result. Renin, when released into the plasma, converts angiotensinogen into angiotensin I; this is converted in turn by angiotensin-converting enzyme (ACE) into angiotensin II, which causes the release of aldosterone from the adrenal cortex. In addition, angiotensin II causes vasoconstriction of arterioles and venules ( Fig. 10.8 ).

the kidney is the main eff ector organ. Life processes depend on water and electrolytes being kept within strict limits.

Water An increase in osmotic pressure (i.e. particle concentration in the blood) is caused, for example, by a loss of water when sweating is detected by osmoreceptors in the hypothalamus. Essentially the osmoreceptors are neurons that swell or shrink depending on the solute concentration of the perfusing fl uid and change their electrical discharge rates as a result. Th e information is processed by the nearby control centre, also in the hypothalamus. Th e nerves that emerge from the control centre descend to the posterior pituitary and secrete the peptide antidiuretic hormone (ADH), also known as vasopressin. Th e ADH is secreted into the bloodstream and ultimately binds to V-2 receptors, mainly on the collecting ducts deep in the medulla of the kidney. Th e ADH-receptor complex initiates the manufacture of the second messenger cyclic adenosine monophosphate (cAMP) in the cytoplasm of cells, which in turn brings about the incorpora-tion of aquaporins—water pores—in the apical and basolateral membranes of the collecting duct tubules. Th is increases the permeability of the membranes, allowing water to be drawn back into the relatively hyperosmotic (dry) kidney medulla and subsequently back into systemic circulation. A concentrated urine is produced; it has up to four times the osmotic concentration of blood. Th e hypothalamus also governs the subjective feeling of thirst, leading to increased oral water intake.

Excess water has the opposite eff ect: in the presence of hypo-osmolar plasma ADH secretion is inhibited and excess water is allowed to pass through the collecting ducts producing a dilute urine (see Table 10.1 ).

Th e osmoreceptors in the hypothalamus are not the only receptors involved in the ADH refl ex. Baroreceptors in the aortic arch and at the bifurcation of the carotid arteries detect pressure. If the pressure is lowered due to blood loss or dehydra-tion, the reduced pressure also results in increased ADH release from the posterior pituitary and retention of water. Th is accounts for about 10–15% of the response.

Importantly, both ADH and the baroreceptor refl ex cause vasoconstriction of both the resistance vessels (arterioles) and the capacitance vessels (venules). Sensibly, when faced with loss of blood volume the vasculature contracts, both keeping the pressure up on the arterial side and reducing the capacitance on the venous side. Th is accommodates the reduced circulating volume and preserves venous return of blood to the heart.

As noted earlier, the constriction of the arterioles generally reduces the capillary blood hydrostatic pressure, and so tissue fl uid is drawn into the circulation in capillaries where the osmotic pressure of the blood exceeds the capillary hydrostatic pressure. Th is bolsters blood volume.

Th e antidiuretic eff ect of ADH and the baroreceptors is opposed to some extent by atrial natriuretic peptide (ANP). ANP is secreted by the atria of the heart in response to stretch, and therefore helps regulate intravascular volume. Th e secretion of ANP is inhibited when blood volumes are reduced and venous return to the heart reduced. When venous return increases, ANP secretion follows suit. ANP antagonises the eff ects of ADH by inhibiting its release, both from the posterior pituitary and at its site of action in the collecting duct of the kidney. ANP,

PRACTICE TIP

The Renin-Angiotensin-Aldosterone (RAA) system plays an important role in regulating blood volume and systemic vascular resistance, thus affecting cardiac output and arterial pressure.

In this way, the kidneys play a major primary role in maintaining homeostatic blood pressure.

Calcium Ninety-nine per cent of the body ’ s calcium is in the form of calcium phosphate in bone. Calcium in plasma exists in an ionised, or free, form and an electrically neutral form bound to albumin and other plasma proteins. Only the ionised form is biologically active, and is important for many cellular functions, including nerve transmission, blood coagulation and muscle contraction. A reduction in plasma albumin or acidosis tends to favour an

158 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

tubules of the kidney and the loops of Henle. Th ese tubes convey the glomerular fi ltrate through the kidney, and the cells of these tubes are sensitive to plasma and tubular levels of magnesium and reabsorb magnesium as required. Th is may vary from almost total reabsorption during time on a low-magnesium diet to low reabsorption on a high-magnesium diet.

Homeostatic acid–base regulation All biological enzyme systems are dependent on a very tight control of acid–base balance for optimal function. pH is a mathematical expression of the degree of acidosis or alkalosis in a solution:

pH H= − log [ ]10 (b)

Hence for each decrease in pH by 1, there is an increase in hydrogen ion concentration by a factor of 10. Th e physiological range of plasma pH is 7.35 to 7.45. Two interrelated systems, the respiratory system and the renal system, are responsible for maintaining this critical acid–base balance, by contributing hydrogen ions or bicarbonate ions to the various buff ers present in body fl uid. A buff er is a system of molecules that exists in equilibrium in a solution, and which, by gaining or losing a bicarbonate or a hydrogen ion in response to an alkali or acid load, tends to resist changes in pH. An important example was outlined above in the case of carbon dioxide and bicarbonate, catalysed by carbonic anhydrase. By increasing or decreasing ventilation, the respiratory system has the capacity to blow off or retain carbon dioxide and hence can control pH over a course of minutes to hours.

Th e kidney, by altering the acidity of urine, has an even more profound infl uence on body pH maintenance, albeit exerted over

increase in the ionised, active form. Conversely, alkalosis tends to decrease ionised calcium. A clinical example is respiratory alkalosis caused by hyperventilation. Th e profound reduction in ionised calcium causes paraesthesia and tetany of skeletal muscles, which is reversible once normal ventilation is restored.

Th e total concentration of calcium in plasma is controlled by two hormones—parathyroid hormone (PTH) and calcitonin—secreted, respectively, by the parathyroid gland and the interstitial cells of the thyroid gland. When plasma calcium starts to drop this is detected by the cells of the parathyroid gland and increased amounts of PTH are released. PTH has three actions: 1. It stimulates the synthesis of calcitriol, which increases the

number of calcium pumps in the gut epithelium, thereby increasing the absorption of calcium from the gut.

2. It binds to PTH receptors in the kidney tubules and via a second messenger increases the number of calcium pumps in the tubules, thereby increasing the reabsorption of calcium from the kidney tubules back into the blood.

3. It recruits calcium from bone by stimulating the recruitment of osteoclasts.

As the plasma calcium concentration rises, the release of PTH is progressively inhibited and the release of calcitonin is progres-sively stimulated.

Calcitonin opposes the eff ects of PTH. Th ere is some evidence that, paradoxically, pulsatile release of PTH and some PTH fragments have the eff ect of increasing calcium deposition in bone rather than decreasing it. 10 Magnesium Th e control of plasma magnesium concentration is primarily under the control of the tubular cells of the proximal convoluted

FIGURE 10.8 The Renin-Angiotensin-Aldosterone system

Decreased perfusion detected in the juxta-glomerular apparatus of the kidneys stimu-lates RENIN production and release

The lungs and kidneys respond to ANGIOTENSIN Iby releasing angiotensin converting enzyme (ACE), whichconverts ANGIOTENSIN I to ANGIOTENSIN II

ANGIOTENSIN II leads to a cascade ofeffects; reabsorption of sodium and chloride,excretion of potassium, and retention of wa-ter in the renal tubules: aldosterone secretionfrom the adrenal cortex further contributesto the retention of water: vasoconstriction ofthe arterioles leading to an increase in bloodpressure: and anti diuretic hormone (ADH)secretion from the pituitary gland, whichstimulates the renal collecting ducts to reab-sorb water

RENIN acts on the liver protein angiotensi-nogen, converting it to ANGIOTENSIN I

159CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

of the arterioles of non-essential vascular beds—as in the gut, skin, kidneys and liver—while beta-adrenergic receptors respond by relaxing muscle arterioles and increasing the heart rate and contractile force of myocardium. Th e background vascular tone of muscle arterioles is simultaneously reduced by centres in the medulla oblongata. Th e resultant eff ect is to raise blood pressure, increase cardiac output and divert blood away from the temporarily non-essential organs to skeletal muscle.

In the liver, muscle and adipose tissue, adrenergic recep-tor stimulation leads to an increase in available levels of glucose and free fatty acids, as an immediate source of energy. In the lungs, beta-2 receptors lead to dilation of bronchial smooth muscle.

In extreme situations, excess adrenaline and noradrenaline can cause evacuation of the contents of the upper and lower digestive tract while the activity of the rest of the intestines is dramatically slowed, as blood is diverted from non-essential vascular beds to working muscle. Th e circulating adrenaline and noradrenaline also bring about increased alertness, anxiety and, at high levels, cognitive impairment, and sometimes nausea associated with slowing gastric motility.

Sympathetic activation also increases the secretion of adrenocorticotrophic hormone (ACTH) from the anterior pituitary gland, which increases the secretion of steroids from the adrenal cortex. Th is has the eff ect of inhibiting infl ammation, retaining water and sodium and breaking down proteins and fats for their energy content.

Parasympathetic nervous system Th e sympathetic nervous system is countered by the aptly named parasympathetic nervous system. Nearly every organ system has a dual supply of sympathetic and parasympathetic nerves which have largely opposite eff ects on the organs in question. A major exception is the vast majority of blood vessels which have, primar-ily, only sympathetic innervation.

Th e outfl ow of parasympathetic nerves from the central nervous system is mainly contained in the cranial nerves which service the head and most of the thorax and abdomen (via the vagus nerve). Th ere is a small outfl ow in the sacral nerves at the base of the spine which service the bladder, genitals and the distal end of the digestive tract.

Th e sympathetic nerve endings generally secrete noradrenaline onto their target cells, while the parasympathetic nerve endings secrete acetylcholine.

Th e target organs have specifi c adrenergic and cholinergic receptors in their cell membranes to which the noradrenaline and acetylcholine specifi cally bind. Th is brings about changes in the target cells’ activity by activating ‘second messengers’ in the cells and/or by opening ion channels in the cell membranes. An example of this is the heart. It has both a sympathetic and a parasympathetic nerve supply. Both the sympathetic and the parasympathetic nerves are continuously secreting small amounts of noradrenaline and acetylcholine onto heart muscle. In cardiac pacemaker cells—for example, the sinoatrial node—an electrical potential diff erence is maintained across the cell membrane. Th is is due to the opposing eff ects of potassium and sodium ion concentrations in the intracellular compared with the extracellular fl uid. A membrane protein ‘pump’ maintains the potential diff erence, termed polarisation. Th e resting electrical

a longer time frame of hours to days. Th e renal tubule has several mechanisms to control H + excretion and HCO 3 – reabsorption, in response to pH, sodium and potassium concentration and hormonal infl uences. Essentially, carbon dioxide is distributed evenly through the kidney, but inside tubular cells the enzyme carbonic anhydrase catalyses a chemical reaction between carbon dioxide and water. Th is results in the production of bicarbonate ions and hydrogen ions (as in Equation a). Th e hydrogen ions are pumped by an ATP-powered proton pump into the tubular fl uid where they are mostly buff ered by phosphate and ammonium ions. Th e bicarbonate is retrieved into the peritubular capillar-ies and then into the systemic circulation. Th e buff ered and unbuff ered hydrogen ions are voided in the urine.

Nervous system functions—Fright, fi ght and fl ight, or Rest and digest Th e nervous system has structural and functional components. Structurally, the central nervous system (CNS) comprises the brain and spinal cord and the peripheral nervous system is comprised of aff erent (signalling towards the brain, or sensory) and eff erent (signalling from the brain, or motor) nerves. Th e 31 spinal nerves serve as both aff erent and eff erent pathways, or mixed nerves. Functionally the peripheral nervous system is comprised of the enteric, somatic and autonomic nervous systems. Th e enteric nervous system controls the gastrointestinal tract, independently, or in coordination with the autonomic nervous system (parasympathetic and sympathetic branches). Th e somatic nervous system is associated with skeletal muscle and movement. Th e autonomic nervous system is comprised of the sympathetic and parasympathetic nervous systems.

Sympathetic nervous system Physiologically, emergencies are generally accompanied by the activation of the sympathetic nervous system (SNS). Th e resulting secretions of noradrenaline from sympathetic nerve endings, adrenaline from the adrenal medulla and cortisol from the adrenal cortex have a profound eff ect on the functioning of all organ systems. In evolutionary terms, the sympathetic nervous system prepares the body for physical activity: to fi ght or to run.

Th e sympathetic nerves fl ow out of the spinal cord between the fi rst thoracic and second lumbar vertebrae, synapse in the paravertebral ganglia and extend postsynaptic fi bres back up to the head and down to the organs of the thorax and abdomen, the arms and the legs. Th e sympathetic nervous system is also directly wired to the adrenal medulla, which, when stimulated, secretes adrenaline and some noradrenaline directly into the bloodstream. Th ese bind to receptors on cell membranes in addition to the noradrenaline that is secreted by the sympathetic nervous system.

In most physiologically stressful situations, the sympathetic nervous system is activated and the parasympathetic nervous system slows. Th e majority of noradrenaline in a stress response is secreted from the sympathetic nerve endings. Th e adrenal medulla secretes adrenaline:noradrenaline in approximately 4 : 1 ratio. Th e noradrenaline and adrenaline then fl ood into the bloodstream to bind to any available receptors. Th e eff ect at a cellular level diff ers according to the subtype of adrenergic receptor activated by these hormones in various end organs. In the cardiovascular system, alpha-adrenergic receptors respond by causing a constriction

160 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

transmitters bind to very similar receptors on the gut cell membranes as on cardiac cells, they are linked to diff erent second messengers and ion channels, and consequently mediate diff erent cellular responses.

Th e sympathetic nerve terminals may also directly inhibit the output of parasympathetic nerve terminals, through pre-synaptic inhibition. Put simply, the parasympathetic nervous system plays the major role in our vegetative being—digesting food, for example, while the sympathetic nervous system mediates ‘fi ght or fl ight’.

For a summary of the anatomical structures, and function of the autonomic nervous system see Table 10.3 .

Capillaries and nutritive blood fl ow During activation of the sympathetic nervous system the blood fl ow to non-essential organs is dramatically reduced. Normally organs are adequately supplied with oxygen, glucose, amino acids and fats and produce by-products of cellular metabolism, such as carbon dioxide, lactate and other acids. Tissue perfusion through these capillary beds is tightly regulated at both a central and a local level. Th e sympathetic nervous system generally ensures an adequate fl ow of blood to organs by controlling the diameter of the feeding arterioles. In the perfused tissues, most of the time, the majority of the capillaries are actually closed off by pre-capillary sphincters, which only open when waste products accumulate in the surrounding tissue. Under increased demand, metabolic by-products accumulate, leading to dilation of these sphincters and hence increased local blood supply.

Oxygen, carbon dioxide, fats and urea are fat-soluble and can diff use easily through capillary endothelium down their respective concentration gradients. Water-soluble components have to be fi ltered through 4-nm clefts in the capillary wall. Th is allows the fl ow of water and small molecules (glucose, amino acids, ions, etc.), but not proteins, through the capillary walls. Th e

potential of the inside of the cell membrane compared to the outside is about –70 mV, comparable to other excitable cells. Highly regulated protein ‘channels’ allow specifi c ions to fl ow back down their concentration and/or electrical gradients leading to depolarisation. If a cell depolarises enough and reaches ‘threshold’, an ‘action potential’ is propagated by the pacemaker and conducting cells and that initiates contraction of the myocardium. Th e rate of discharge is aff ected by both the degree of baseline electrical polarisation across the cell membrane and the amount of channel leakage leading the cell to reach its threshold for action potential propagation. Th e sympathetic nerves thus increase the heart rate by speeding up the depolarisa-tion of the pacemaker cells slightly (a few extra sodium channels are opened) and the parasympathetic nerves slow it down by hyperpolarising the cells slightly (a few extra potassium channels are opened). Th e resulting heart rate is essentially a net result of opposing sympathetic and para-sympathetic activity.

PRACTICE TIP

ATROPINE is an anticholinergic (muscarinic acetylcholine receptor antagonist). Acetylcholine is the main parasympa-thetic neurotransmitter.

ATROPINE , therefore, blocks the cardiac actions of the parasympathetic nervous system in the short term, and thus leads to a rise in heart rate.

TABLE 10.3 The functions of the autonomic nervous system

ORIGIN OF EFFERENT PATHWAY PARASYMPATHETIC ORGAN SYMPATHETIC

ORIGIN OF EFFERENT PATHWAY

Cranial Constricts pupils Eyes Dilates pupils Thoracic

Cranial Stimulates salivation Salivary Glands Inhibits salivation Thoracic

Cranial Decreases heart rate Heart Increases heart rate Thoracic

Cranial Constricts bronchi Lungs Dilates bronchi Thoracic

Cranial Stimulates digestion Stomach Inhibits digestion Thoracic, Lumbar

Cranial Stimulates bile release Liver, Gall Bladder Stimulate glucose release Thoracic, Lumbar

Cranial Kidneys Stimulate adrenaline and noradrenaline release

Thoracic, Lumbar

Cranial, Sacral Stimulates peristalsis and secretion

Intestines Inhibit peristalsis and secretion

Thoracic, Lumbar

Sacral Contracts bladder Bladder Relax bladder Lumbar

Sacral Stimulates Sex organs Inhibits Lumbar

Th e gastrointestinal tract also has a dual innervation, but in this instance the parasympathetic nervous system increases peristaltic activity and other aspects of digestion in the gut from the stomach to the colon while noradrenaline secreted by the sympathetic nervous system slows it down. Although the

161CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

As we saw earlier, accumulation of CO 2 and various acids leads to relaxation of precapillary sphincters, allowing access to the perfusing blood. Flow is sluggish, but there is fl ow. Second, the acidic waste products cause haemoglobin to dissociate from most of the oxygen it is carrying, and consequently the perfusing blood can deliver up to four times as much oxygen to the tissue as it normally would. Similarly, hypoxic and acidic haemoglobin can take up and remove proportionately more carbon dioxide than in normal conditions. So even at a quarter of the normal fl ow, oxygen supply would remain adequate and carbon dioxide removal would keep pace. For details, see the previous sections on oxygen and carbon dioxide transport.

Th e reduction in the supply of glucose and amino acids is countered by the eff ects of the stress hormone cortisol (from the adrenal cortex), which promotes the breakdown of cellular glycogen to glucose and also promotes the breakdown of some cellular protein to amino acids, both of which can be used to generate adenosine triphosphate (ATP) through glycolysis and through the Krebs cycle. Th is can supply some of the metabolic needs of cells in under-perfused tissues, but prolonged under-perfusion leads to cell starvation, cell death and ultimately multiple-organ failure.

Cellular metabolism Th e internal environment of cells is quite diff erent from the tissue fl uid that surrounds them. Forty per cent of the energy we extract from our diet is expended in maintaining the diff erence between the intracellular and extracellular environments.

Just about all cellular machinery use energy stored in the form of adenosine triphosphate (ATP). Th e whole process of carbohydrate metabolism is directed towards the extraction of energy from sugars and the manufacture of ATP, in which the extracted energy is temporarily stored, then used for virtually all cellular processes. Primary among these is the operation of the ion pumps that actively pump sodium ions out of cells and potassium ions into cells, both up a concentration gradient. Not only does this generate an ion imbalance across the cell membrane (low sodium inside, high sodium outside), but it also creates a negative electrical potential of nearly one-tenth of a volt between the inside and the outside of the cell. Th e rest of the energy is used in the manufacture of all the other molecular structures inside the cell. Many proteins are biological catalysts, or enzymes, which foster the conversion of ATP into adenosine diphosphate (ADP). Th e reconversion of ADP into ATP requires energy input. Th is is achieved by other enzymes that work in a series of steps to break down some form of metabolic fuel, such as simple carbohydrates (sugars), fatty acids, proteins or ketone bodies. Th us, ATP can be thought of as the ‘universal energy currency’ of the body.

Th ere are generally two processes inside cells which harvest the energy contained in the chemical bonds of sugars. Th e fi rst is the anaerobic process. Cells lacking mitochondria, or suffi cient oxygen for normal metabolic processes, use glycolysis . Th is involves a series of reactions to convert glucose to pyruvate, with a net gain of 2 ATP molecules for every glucose molecule. Without suffi cient oxygen pyruvate is converted to lactic acid. If left untethered (as in shock or cardiac arrest) lactic acid increases and is detectable in large quantities in the blood as lactate. If this process only occurs for a short period, as in strenuous

proteins and other large molecules remaining in plasma are an important determinant of fl uid equilibrium between the blood and extravascular tissue. By raising ‘oncotic pressure’ (a form of colloid osmotic pressure exerted by proteins, notably albumin, in the blood that pulls water into the circulatory system) they cause a tendency for fl uid to move across the capillary wall into the vascular space. Opposing this is the capillary hydrostatic pressure , equal to the diff erence between capillary blood pressure and tissue pressure. At the arterial end of the capillary beds the hydrostatic pressure is greater than the colloid osmotic pressure and there is net fl ow of water and solute into the extravascular tissue. At the venous end of the capillary beds the hydrostatic pressure has fallen beneath the colloid osmotic pressure, and now there is a net fl ow of water and its dissolved components back into the capillaries. Hundreds of litres of fl uid are shifted across capillary walls each day, but the process is usually fi nely balanced. A slight excess, roughly 500 mL per day, fl ows out into extravascular tissue and is collected and recirculated by the lymphatic system, ultimately draining via the cisterna chyli into the left supraclavicular vein.

If capillary hydrostatic pressure is elevated past a certain point, fl uid will fi lter out through the 4-nm clefts in the capillary walls, accumulate in the extravascular tissues and cause swelling. Th e disturbance in this balance of oncotic and hydrostatic pressures is known as oedema. Capillary venous pressure might be elevated, as in the case of congestive cardiac failure or venous obstruction from thrombosis. Alternatively, the capillary hydrostatic pressure can be lower than normal; for example, by hepatic failure, malnutrition, protein-losing renal diseases, or blockage, for example, by malignant infi ltration. Th en the protein in the blood can draw liquid out of the tissues and bolster blood volume. Th e section below on hypovolaemic shock is a case in point.

Another means of transporting blood molecules into the tissues is vesicular transport . Th is is used for transporting large molecules, especially proteins, out of capillaries and into the extracellular space. Proteins such as insulin, or any of the anterior pituitary hormones, are too large to get out of the 4-nm clefts in the capillary walls. Instead they bind to the surface of the endothelial cells lining the capillaries and are then surrounded by endothelial cell membrane, which forms a tiny vesicle around the protein. Th e vesicle then travels through the endothelial cell to the outer membrane and the contents are discharged into the tissue surrounding the capillary (the extravascular space). Th ese transport mechanisms are protein-specifi c and highly regulated.

Physiological responses to tissue hypoperfusion Tissue hypoperfusion may result from a systemic shock state, such as hypovolaemia, or may result from activation of the sympathetic nervous system in susceptible organs. Mecha-nisms exist to mitigate against this low fl ow state, with the dual problems of reduced oxygen and nutrient delivery, and reduced waste product removal. Commonly the blood fl ow is reduced to 25% of the normal blood fl ow, potentially reduc-ing the supply of vital nutrients and reducing the removal of toxic wastes. Th e supply of water, soluble nutrients and those requiring vesicular transport will be reduced in proportion to the reduction in blood fl ow. Th e fat-soluble components fare a little better.

162 SECTION 2 CLINICAL CONCEPTS AND SYSTEMS

(a low arterial blood pH in the presence of a low bicarbonate level) and hyperkalaemia.

In addition, some of the cellular contents may appear in the blood. Depending on the type of tissue involved, specifi c intracellular contents might have diagnostic utility. For example, pancreatic cells contain a variety of powerful digestive enzymes that can damage the protein and lipid components of surrounding tissue in an amplifying cascade of necrosis that characterises severe pancreatitis. One of these proteins is lipase, which when detectable in large quantities confi rms the diagnosis.

exercise, lactic acid is reconverted to pyruvate, and used by the liver to create glucose in gluconeogenesis .

Th e second process is aerobic. Aerobic metabolism occurs in the cells ’ mitochondria. Th is process converts glucose to ATP with the use of oxygen. Th e end result of this process is between 36 and 38 ATP molecules. Th e by-products of this are CO 2 and H 2 O, which are generally harmless and easily eliminated from the body. 11

Cell deterioration Under-perfused tissues are on the verge of oxygen starvation and frequently glycolysis alone cannot generate enough ATP to maintain cellular processes. Th is under-perfusion may result from a global abnormality, such as asphyxia or haemorrhagic shock, or from local disruption of blood supply, such as during a stroke or myocardial infarct. Th e fi rst thing that happens is that the energy-dependent sodium–potassium exchange pump slows. Th en the cell membranes start to lose their voltage and the membrane potential is gradually lost. Th is depolarisation can lead to catastrophic consequences for the cells in question and for the cells in the vicinity of the dying cells. A small number of dying cells can, literally, kill thousands of adjacent cells by inadvertently initiating a massive amplifi cation of the initial disturbance. Th is amplifi cation is called a ‘cascade’ eff ect. Th e important cascade eff ects on a cellular level may be electrical or chemical. Electrical and chemical cascades Electrical anomalies occur in excitable cells, such as nerve cells and cardiac muscle. As the sodium-potassium-ATPase pumps fail and the cell starts to depolarise, the cell may experience electrical ‘death shudders’ in the form of abnormally triggered action potentials that stimulate other cells in the vicinity to follow suit. If confi ned to a small area of myocardium, this abnormal pacemaker is termed an ectopic focus. Spread of the action potential through the heart ’ s conducting system and myocardium would give a mistimed but coordinated contraction called an ectopic beat. Under more critical conditions a greater amount of myocardial tissue may have a reduced threshold for action potential propagation. Abnormal electrical activity might spread in an uncoordinated fashion, causing sustained ventricular fi brillation rather than eff ective rhythmic contractions.

Pathological depolarisation may precipitate calcium entry into the cell by the uncontrolled opening of voltage-regulated calcium channels in the plasma membrane, the endoplasmic reticulum and the mitochondria. Th e infl ux of calcium has a deleterious cascade eff ect on a number of cellular functions. Th ese include maintaining the integrity of the mitochondrial membrane, cellular metabolism, neurotransmitter release in the nervous system and control of muscle cell contraction and relaxation.

Loss of cell contents Th e process of cellular death in an uncontrolled, widespread manner is termed necrosis. Th is is distinct from the orderly removal of individual senescent cells, termed apoptosis. One of the hallmarks of cellular necrosis is release of intracellular contents, such as potassium, intracellular enzymes and lactate. Clinically, the release of contents from a signifi cant mass of dying cells may be detected by the presence of metabolic acidosis

PRACTICE TIP

Pathology results that raise suspicion of cellular necrosis include: • hyperkalaemia • lactate • metabolic acidosis (low blood pH and bicarbonate) • creatine kinase (muscle cells, especially after crush injury) • troponin (cardiac muscle) • lipase (pancreatic cells)

Th e release of potassium from dying cells will also aff ect the electrical activity of neighbouring cells. Th is is because membrane potential is primarily due to the ratio of the intra-cellular and extracellular potassium concentrations. If cells lose potassium into the extracellular space, the remaining cells will have a reduced ratio of potassium inside and outside the cell membrane, and consequently will have a lower (less-negative) membrane potential. Th is may tip adjacent cells into cell death, causing the release of even more potassium and hence initiating a potassium cascade.

Nerve cells may become ischaemic during a stroke, or due to systemic hypoxia. Normal cellular function rapidly ceases. Within minutes, ongoing ischaemia causes the neurons to release excess glutamate (an excitatory amino acid neurotransmitter) as their electrical potential fails. Th is binds to and opens NMDA ( N -methyl- D -aspartate) receptor-mediated calcium-ion channels in neighbouring cells, initiating a calcium cascade (see above), which causes the release of even more glutamate. Th is release results in a synergistic calcium and glutamate cascade, which propagates through nervous tissue, damaging cells in addition to those areas deprived of oxygen during the initial insult.

Cell protection: the blood–brain barrier Specifi c tissues in the body depend on a tightly regulated environment to maintain optimal function. Th e most important example of this is the central nervous system (CNS), where we have seen that the orderly function of neurons is highly sensitive to changes in the extracellular milieu. Th e evolution of these intrinsically excitable cells was associated with the co-evolution of a protective barrier that tightly regulates the passage of molecules into the vicinity of the neurons.

Th e physical form of the blood–brain barrier comprises non-nerve cells (glial cells), called astrocytes , found throughout the nervous system. Th ese cells interpose themselves between the perfusing capillaries and the neurons by wrapping their cytoplasmic processes around both capillary and nerve cells

163CHAPTER 10 PHYSIOLOGY AND PATHOPHYSIOLOGY FOR EMERGENCY CARE

regions of the nervous system, allowing the cells of the hypo-thalamus to sample the vascular components of blood and respond to any homeostatic imbalances that might be occurring. See the sections below on the control of plasma electrolytes, water and acid–base balance.

Shock Shock refers to an insuffi cient circulatory state leading to inad-equately perfused body tissues. Th e lack of oxygen and nutrients and the non-removal of waste products impair normal metabolism. Th e cells cannot generate enough ATP for their metabolic require-ments and are consequently prone to cell death. When cells die, as outlined in the cell deterioration section earlier in the chapter, their membranes allow the cell contents to leak into the extracellular space and generate an even more toxic environment for the adjacent cells—resulting in even more cell death. Th is is yet another example of a positive (vicious-circle) feedback mechanism ( Fig. 10.9 ). A review of the normal functioning of the cardiovascular system will demonstrate the major reasons for inadequate perfusion. In order to function adequately, the cardiovascular system requires the following components: ● an adequate blood volume with suffi cient

oxygen-saturated haemoglobin that is circulating through the arteries, arterioles, capillaries, venules and veins

and acting as a cellular intermediary between the two. Th e CNS capillaries are relatively impermeable and have far fewer clefts between their endothelial cells than in other parts of the body. Most of the transport is by carrier-mediated facilitated diff usion through the endothelial cells themselves rather than through the clefts; thus, the barrier can be highly selective in terms of the number of carriers that are manufactured by the cells forming the blood–brain barrier.

Water-soluble nutrients (glucose, amino acids, etc.) have specifi c carriers to supply the brain cells. In addition, some substances surplus to requirement are actively pumped out of the brain back into the capillaries. Conversely, the blood–brain barrier presents little impediment to fat-soluble substances, so oxygen, carbon dioxide, urea, etc. will diff use in or out down their concentration gradients. Drugs that are highly lipid soluble are therefore more able to penetrate the blood–brain barrier and gain access to the CNS.

When damaged, the blood–brain barrier can lose its integrity, exposing the neurons to a less highly regulated extracellular environment. Normally excluded toxins may accumulate; in addition, lipid insoluble drugs may now have an eff ect on the CNS.

Th e blood–brain barrier is not uniform. Th e blood vessels in the hypothalamus are more permeable than most of the other

Decreased systemic blood flow

Increasedcapillary

permeability

Decreased nutrition of tissuesDecreased cardiac nutrition

Decreased nutrition of brain

Decreased venous return

Decreasedblood volume

Tissue ischaemia

Decreased cardiac output

Decreased arterial pressure

Decreased vasomotoractivity

Cardiac depression

Vascular dilation

Venous poolingof blood

Decreased nutritionof vascular system

Release oftoxins

Intravascular clotting

FIGURE 10.9 Different types of positive feedback that can lead to the progression of shock. 3