The Veterinary Nurse's Practical Guide to Small Animal Anaesthesia (VetBooks.ir) PDF

The Veterinary Nurse’s Practical Guide to Small Animal Anaesthesia ­ he Veterinary Nurse’s Practical Guide T to Small Animal Anaesthesia Edited by Niamh Clancy, Dip AVN (SA) DipHE CVN DipVN PGCert VetEd FHEA RVN Teaching Fellow, School of Veterinary Nursing, Royal Veterinary College, UK Deput...

The Veterinary Nurse’s Practical Guide to Small Animal Anaesthesia ­ he Veterinary Nurse’s Practical Guide T to Small Animal Anaesthesia Edited by Niamh Clancy, Dip AVN (SA) DipHE CVN DipVN PGCert VetEd FHEA RVN Teaching Fellow, School of Veterinary Nursing, Royal Veterinary College, UK Deputy Co-course director, Certificates in Advanced Veterinary Nursing, Royal Veterinary College, UK Anaesthesia Nurse, Queen Mother Hospital for Animals, Royal Veterinary College, UK This edition first published 2023 © 2023 John Wiley & Sons Ltd All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions. 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Identifiers: LCCN 2022049641 (print) | LCCN 2022049642 (ebook) | ISBN 9781119716921 (paperback) | ISBN 9781119716969 (adobe pdf) | ISBN 9781119717034 (epub) Subjects: MESH: Anesthesia—veterinary | Anesthesia—nursing | Analgesics—standards | Dog Diseases—nursing | Cat Diseases—nursing | Animal Technicians—standards Classification: LCC SF914 (print) | LCC SF914 (ebook) | NLM SF 914 | DDC 636.089/796 —dc23/eng/20221230 LC record available at https://lccn.loc.gov/2022049641 LC ebook record available at https://lccn.loc.gov/2022049642 Cover Images: © Ana Carina Costa, Carolina Palacios Jimenez, Niamh Clancy, Ioan Holban Cover design by Wiley Set in 9.5/12.5pt STIXTwoText by Straive, Chennai, India  v Contents List of Contributors xv Preface xvii 1 Pre-Anaesthetic Assessment and Premedication 1 Niamh Clancy ­Patient Assessment 3 History 3 Physical Examination 4 Cardiac and Thoracic Auscultation 4 Body Condition Scoring (BCS) 6 Hydration 7 Patient Temperament 7 Other Considerations 7 ­Premedication 9 Administration of Premedication 15 Acknowledgements 17 References 17 2 Interpreting Blood Results 19 Joanna Williams ­Haematology 19 Red Blood Cell Count and Packed Cell Volume (RBC and PCV) 19 High PCV 19 Low PCV 20 White Blood Cell (WBC) and Neutrophil Count 20 High Count 20 Low Count 20 Lymphocytes and Monocytes 21 Eosinophils and Basophils 21 Platelets 21 High Count 21 Low Count 21 ­Biochemistry 23 Proteins (TP, ALB, GLOB) 24 vi Contents High Levels (Hyperproteinaemia) 24 Low Levels (Hypoproteinaemia) 24 Hepatic Parameters (ALKP, ALT, BIL) 25 High Levels 25 Renal Parameters (CREA, BUN, InPHOS) 25 High Levels 25 Low Levels 26 Glucose (GLU) 26 High Levels (Hyperglycaemia) 26 Low Levels (Hypoglycaemia) 26 ­Electrolytes 26 Sodium (Na+) 26 High Levels 26 Low Levels 27 Potassium (K+) 27 High Levels 27 Low Levels 27 Calcium (Ca2+) 28 High Levels 28 Low Levels 28 ­Conclusion 29 References 29 3 Cardiovascular Physiology 31 Joanna Williams ­Blood Flow Through the Heart 32 ­Conduction Through the Heart 33 ­Vascular System 34 Pulmonic Circulation 34 Systemic Circulation 35 ­Cardiac Output 36 Stroke Volume 36 Heart Rate 38 ­Anaesthetic Considerations for Patients with Cardiovascular Disease 39 References 41 4 Respiratory Physiology and Ventilation 42 Ioan Holbon ­Respiratory Anatomy 42 Pulmonary Ventilation 43 Central Regulation of Respiration 44 Chemical Regulation of Respiration 44 ­Mechanics of Breathing 44 Inspiration 45 Expiration 45  Contents vii ­ he Effects of Anaesthesia on Normal Respiratory Physiology 45 T ­Indications for Ventilation 46 ­Initiation of Ventilation 48 ­Manual Ventilation 49 ­Mechanical Ventilation 50 ­Volume Cycling Versus Pressure Cycling Ventilation 51 ­Positive End-­expiratory Pressure (PEEP) and Alveolar Recruitment Manoeuvres (ARM) 53 4.1 ­Possible Harmful Effects of Artificial Ventilation 54 ­Ventilation Strategies to Prevent Some of the Possible Negative Effects of IPPV 57 On the Lungs 57 On the Cardiovascular System 57 On the Intracranial Pressure 57 On Blood Gas and Acid–Base Disturbances 57 ­Troubleshooting During Mechanical Ventilation 58 Anaesthetic Machine and Breathing System 58 Ventilators 58 Patient 58 ­Weaning the Patient Off the Ventilator 58 References 60 5 Blood Pressure Regulation and Monitoring 63 Leanne Smith ­What Factors Contribute to Blood Pressure 63 ­The Importance of Blood Pressure Regulation During Anaesthesia 64 ­How Do We Measure Blood Pressure? 66 Non-invasive/Indirect Blood Pressure Monitoring 66 Doppler 68 Oscillometric 69 High Definition Oscillometric (HDO) Devices 69 Invasive Blood Pressure Monitoring 70 ­Treatment of Hypotension Under General Anaesthesia 70 ­Drugs to Treat Hypotension 71 Positive Inotropes 73 Adrenaline/Epinephrine, Ephedrine, Dobutamine, Dopamine, Noradrenaline/ Norepinephrine 73 Vasopressors 73 Adrenaline/Epinephrine, Dopamine, Ephedrine, Noradrenaline/Norepinephrine, Phenylephrine, Vasopressin 73 Anticholinergics 74 Glycopyrolate, Atropine 74 ­Treatment of Hypertension Under General Anaesthesia 74 ­Summary 75 Quick Reference Terminology and Definitions 75 References 76 viii Contents 6 Capnography and Spirometry 78 Lisa Angell ­Capnography/Capnometry 78 ­Capnograph Device Options 79 ­Information Provided from a Capnograph 81 Carbon Dioxide 81 Interpretation of Carbon Dioxide Values 82 The Normal Capnogram 87 ­Analysis of the Capnogram 88 ­Common Abnormal Capnography Waveforms and Their Interpretation 89 ­Spirometry 95 Acknowledgements 95 References 96 7 Pulse Oximetry 97 Ana Carina Costa ­Introduction 97 ­How Does the Pulse Oximeter Work? 97 ­Data Interpretation 100 ­SpO2 and PaO2 100 ­Hypoxaemia 102 ­Plethysmograph 104 ­Anaemia and Abnormal Haemoglobin Forms 107 Anaemia 107 Methaemoglobin 108 Carboxyhaemoglobin 108 ­Tips and Tricks 108 ­Advanced Technology – Masimo Pulse Co-­Oximetry 111 References 111 8 Practical ECGs 113 Courtney Scales ­ECG Fundamentals 114 Normal Conduction 114 The ECG Machine 115 The ECG Cables 117 The ECG Complex 119 ­Common ECG Complexes and Rhythms 121 Sinus Rhythms 121 Normal Sinus Rhythm 122 Sinus Arrhythmia 122 Sinus Tachycardia 123 Sinus Bradycardia 124  Contents ix Supraventricular Arrhythmias 124 Atrial Fibrillation 125 Second Degree Atrioventricular Block 125 Third Degree Atrioventricular Block 127 Sick Sinus Syndrome 128 Ectopic Ventricular Complexes 128 Ventricular Premature Complex 129 Ventricular Escape Complex 131 Ventricular Arrhythmias 131 Ventricular Tachycardia 132 Accelerated Idiopathic Ventricular Rhythm 132 Ventricular Fibrillation 133 References 138 9 Fluid Therapy 139 Niamh Clancy ­Fluid Distribution and Composition 139 ­Movement of Fluid in the Body 141 ­Fluid Disturbances 142 Dehydration vs. Hypovolemia 143 ­Intravenous Fluid Therapy During the Peri-­Anaesthetic Period 145 ­Fluid Selection 146 Crystalloids 146 Hartmann’s Solution/Compound Sodium Lactate 146 Lactated Ringer’s Solution 148 Normal Saline 148 5% Dextrose Solution 148 Hypertonic Saline 148 Colloids 149 Gelatines 149 Dextrans 150 Hydroxyethylstarches (HES) 150 Albumin 150 Whole Blood 150 Plasma (Fresh/Fresh Frozen/Stored) 151 ­Fluid Supplementation 151 Potassium 151 Sodium Bicarbonate 152 Calcium 152 Glucose 152 ­Fluid Delivery Systems 153 Giving Sets 153 Fluid Pumps and Syringe Drivers 155 References 157 x Contents 10 Induction Agents 159 Ana Carina Costa ­Stages of General Anaesthesia 159 ­Injectable Anaesthetics 160 Propofol 160 Pharmacokinetic Properties 160 Pharmacodynamic Properties 161 Tips and Tricks 161 Special Considerations 162 Alfaxalone 162 Pharmacokinetic Properties 163 Pharmacodynamic Properties 163 Tips and Tricks 163 Special Considerations 163 Propofol and Alfaxalone Total Intravenous Anaesthesia – TIVA 164 Special Considerations 164 Ketamine 166 Pharmacokinetic Properties 167 Pharmacodynamic Properties 167 Tips and Tricks 168 Special Considerations 168 Co-­Induction 168 Special Considerations 169 Etomidate 170 Pharmacokinetic and Pharmacodynamic Properties 170 Special Considerations 171 Thiopental 171 ­Inhalational Anaesthesia Induction 171 Acknowledgements 172 References 173 11 Inhalant Anaesthetic Agents 175 Niamh Clancy ­Pharmacokinetics of Inhalant Agents 175 Distribution 175 The Inspired Concentration of Inhalants 176 Blood: Gas Solubility 176 Ventilation 177 Elimination 177 ­Minimal Alveolar Concentration (MAC) 177 ­The Ideal Inhalant Agent 179 ­Physiological Effects of Inhalant Agents 180 ­Isoflurane 182 ­Sevoflurane 182 ­Desflurane 183 ­Vaporisers 183 Saturated Vapour Pressure 183  Contents xi ­Desflurane 186 ­Position on the Back Bar 187 ­Key Fill Systems 187 ­Nitrous Oxide 190 Advantages and Clinical Uses 191 Disadvantages 191 ­Personal Safety 191 Monitoring of Exposure 192 Limiting of Exposure 192 References 192 12 Intubation 194 Carol Hoy ­Placement of an ETT 195 ­Equipment 196 ETT or Similar Device 196 Laryngeal Masks 197 Armoured ETT 198 Securing the ETT 199 Laryngoscope 199 A Stylet 199 Lidocaine 200 ­Technique 202 Confirming Placement 204 Inflating the Cuff 205 Cleaning ETT 206 ­Alternative Intubation Techniques 206 Nasotracheal Intubation 206 Intubation Using a Pharyngotomy 207 Retrograde Intubation 207 One Lung Intubation 207 Tracheostomy 208 ­Troubleshooting 208 Brachycephalic Patients 209 Equipment for Difficult Intubation 209 How to Deal with an ETT that Is Difficult to Remove 210 ­Summary 210 References 210 13 The Anaesthetic Machine and Breathing Systems 212 Courtney Scales ­Introduction 212 ­Gas Supply 212 Oxygen Cylinders 214 Nitrous Oxide Cylinders 214 Oxygen Concentrators 215 Cylinder Manifold 216 xii Contents Liquid Oxygen 218 Pressure Gauges and Regulators 219 Alarms 220 Safety Features 220 ­The Anaesthetic Machine 225 Flowmeters 225 Back Bar 228 Common Gas Outlet 228 Oxygen Flush 229 ­Anaesthetic Machine Leak Test 229 ­Scavenging System 230 Active Scavenging System 231 Passive Scavenging System 232 ­Breathing Systems 234 ­Non-Rebreathing Systems 236 Fresh Gas Flow 237 Paediatric T-Piece 238 Bain 239 Lack 241 ­Rebreathing Systems 242 Circle Fresh Gas Flow Rates 244 Carbon Dioxide Absorbing 245 ­Hybrid System 247 Fresh Gas Flow 248 ­Breathing System Selection 248 ­Storage and Repeated Use of Breathing Systems 249 References 250 14 Anaesthesia Recovery 251 Courtney Scales ­Introduction 251 ­Preparing to Recover 251 ­Handover to the Recovery Team 253 ­Monitoring in the Recovery Period 254 ­Delayed Recovery 254 ­Sedation in the Recovery Period 255 ­Pain Management 257 ­Airway Management and Hypoxaemia 257 Airway Obstruction 257 Hypoxaemia 260 ­Temperature Management 261 Hypothermia 262 Hyperthermia 263 ­Haemodynamic Instability 264 ­Coexisting Disease Considerations 265 ­Conclusion 267 References 268  Contents xiii 15 Pain 269 Niamh Clancy and Claire Sneddon ­The Pain Pathway 271 Transduction 271 Transmission 272 Modulation 272 Projection 273 Perception 273 ­Pain Management 273 Opioids 274 Ketamine 275 Lidocaine 275 Alpha-­2-­Adrenergic Agonists 275 Non-­Steroidal Anti-­Inflammatory Drugs (NSAIDs) 276 Other Analgesics 276 Nursing Care for the Painful Patient 277 ­Pain Assessment 279 Pain Scoring Systems 282 Validation 283 Application of Pain Scales 284 Pitfalls of Pain Scoring Systems 287 Acknowledgements 294 References 294 16 Local Anaesthetic Techniques 296 Lisa Angell ­The Nervous System 296 ­Mechanism of Action 297 ­Performing Local Anaesthetic Techniques 299 ­Techniques for the Head 301 Techniques for the Upper Jaw and Nose 302 Maxillary Nerve Block 302 Infraorbital Nerve Block 303 Palatine Nerve Block 303 The Lower Jaw 303 The Mandibular Nerve Block 303 The Mental Nerve Block 303 ­Ocular Nerve Blocks 304 The Retrobulbar Block 304 ­Auricular Nerve Blocks 305 ­Techniques for the Forelimbs 306 Brachial Plexus Nerve Block 306 RUMM Block 307 ­Techniques for the Hindlimbs 308 The Epidural 308 Femoral, Sciatic, and Psoas Nerve Block 310 xiv Contents Bier’s Nerve Block 311 Digital Nerve Block 312 ­Thoracic Nerve Block 312 Intercostal Nerve Block 312 ­Techniques for Neutering 313 Testicular Block 313 Ovarian Pedicle 313 ­Other Techniques 314 The Erector Spinae Plane Nerve Block 314 Quadratus Lumborum Nerve Block 315 ­Local Anaesthesia for Post-­Operative or Chronic Pain Conditions 315 Wound Soaker Catheters 315 Intrapleural Analgesia 316 Epidural Catheters 316 ­Nursing Care for Patients Following Local Anaesthetic Techniques 316 Acknowledgements 317 References 317 17 Constant Rate Infusions and Calculations 319 Niamh Clancy ­What Are CRIs 319 ­Advantages of CRIs 320 ­Analgesia 321 ­Blood Pressure Regulation 322 ­Hypnosis 324 ­Administration 325 ­Calculations 327 Acknowledgements 331 References 331 18 Case Studies 333 Niamh Clancy ­Brachycephalic Patients 333 ­Renal Disease 336 ­Hyperthyroidism 339 ­Diabetes Mellitus 341 ­Hepatic Disease 343 ­The Aggressive Patient 345 ­Paediatric Patient 347 ­Geriatric 350 ­Respiratory Patient 352 ­Caesarean Section 355 ­Gastric Dilation-­Volvulus 357 ­Urethral Obstruction 359 ­Cardiac Disease 361 Acknowledgements 364 Index 365  xv List of Contributors Ana Costa, PG Cert AVN, NCert Anaesth, Ioan Holban, BSc (Hons) RVN NCert Physio, RVN Anaesthesia Department Queen Mother Anaesthesia Department Queen Mother Hospital for Animals Hospital for Animals Royal Veterinary College Royal Veterinary College Hawkshead Lane Hawkshead Lane AL9 7TA AL9 7TA UK UK Carol Hoy, VTS (Anaesthesia & Analgesia) Joanna Williams, BSc RVN PgCert (VetEd) Eye Veterinary Clinic Senior Nurse Marlbrook Anaesthesia Department Queen Mother Leominster Hospital for Animals HR6 0PH Royal Veterinary College USA Hawkshead Lane AL9 7TA Leanne Smith, BSc (Hons) UK PgCert (Veterinary Anaesthesia & Analgesia) RVN Claire Sneddon, RVN Royal Veterinary College Senior Nurse Hawkshead Lane Anaesthesia Department Queen Mother AL9 7TA Hospital for Animals UK Royal Veterinary College Hawkshead Lane Lisa Angell, VTS (Anaesthesia/Analgesia) AL9 7TA PgCert (VetEd) RVN UK Head Nurse Anaesthesia Department Queen Mother Courtney Scales, NCert Anaesth RVN Hospital for Animals Clinical Educator Royal Veterinary College Burtons Medical Equipment Ltd. Hawkshead Lane Pattenden Lane AL9 7TA Marden UK TN12 9QD UK xvi List of Contributors Niamh Clancy, Dip AVN (SA) HE Dip CVN Mother Hospital for Animals PgCert (VetEd) RVN Royal Veterinary College Teaching Fellow Centre for Hawkshead Lane Veterinary Nursing AL9 7TA RVN Anaesthesia Department Queen UK  xvii Preface The role of the veterinary nurse within the veterinary team has changed drastically since the infancy of the profession many years ago. With professional recognition in the United Kingdom (UK) came accountability for their conduct and the requirement to undertake continuing professional development. Every registered veterinary nurse (RVN) in the UK makes a declaration to ensure the health and welfare of animals committed to their care. As veterinary nursing has developed over the years, so too has the discipline of veterinary anaesthesia. The use of safer anaesthetic protocols, availability of monitoring equipment and the changes in the education of veterinary nurses, have all contributed to a reduction in mortality and morbidity of patients. Anaesthesia has become a large portion of the vet- erinary nurse’s role in the veterinary practice. While some revel in undertaking the task, it can be daunting to many. The RVN’s role in anaesthesia, under the veterinary surgeon’s direction, is to act as the eyes and ears of the veterinary surgeon, reporting any changes that may occur and reacting appropriately. RVNs also play a pivotal role in the recovery stages of the peri-­anaesthetic period and the pain assessment of patients under their care. Despite the RVN’s role in veterinary anaesthesia, currently, there is no practical guide to anaesthesia directed solely at the veterinary nurse. Although veterinary anaesthesia text- books do exist, they tend to focus strongly on pharmacology and are text-­heavy which may be better suited to the veterinary student studying for exams. While there are veterinary anaesthesia textbooks directed at the RVN, these are currently dated. The goal of the veteri- nary nurse’s practical guide to small animal anaesthesia is to provide the RVN in practice with a quick reference book that can be utilised in an emergency, while also being in-­depth enough that it can be used to research a topic. It is intended for both the experienced RVN, and those just starting their journey. All involved in the production of this textbook are RVNs who share a passion for anaes- thesia while having worked as specialist anaesthesia nurses at times during their careers. Many of the chapters provided have also been peer-­reviewed by European and American board specialists in anaesthesia and analgesia. We hope that this guide will become a useful tool for the RVN in practice and that it will help with the provision of anaesthesia that is safe and reduces mortality and morbidity.  1 1 Pre-Anaesthetic Assessment and Premedication Niamh Clancy The benefits of good history taking and a thorough clinical examination prior to general anaesthesia cannot be disputed and are vital to the delivery of a safe anaesthetic. Issues found during the pre‐anaesthetic assessment may cause the Veterinary Surgeon (VS) in charge of the case to change their anaesthetic plan and allow the Registered Veterinary Nurse (RVN) to prepare for any eventuality. This chapter will outline how the RVN can perform a thorough clinical examination, assign American Society of Anesthesiologists (ASA) status to a patient and how some concurrent health issues and medications may affect the choice of anaesthetic medications used. This chapter also sets to outline the aims of premedication and the advantages and disadvantages of many commonly used agents. Although the risk of mortality in veterinary anaesthesia has decreased in recent years, it is still substantial with Brodbelt et al. (2008) stating that 1 in 2000 dogs and 1 in 850 cats will face mortality. Being aware of a patient’s co‐morbidities before administration of any medications could potentially reduce these numbers greatly. Table 1.1 American Society of Anesthesiologists (ASA) scale for general anaesthesia. ASA scale Physical description Patient example 1 Healthy – no disease present Healthy patient for castration 2 Slight to mild systemic disease which Patient with stable diabetes mellitus for cataract is not limiting surgery 3 Moderate to severe systemic disease Uncontrolled diabetic patient or patient which limits normal function presenting with symptomatic heart disease 4 Very severe systemic disease that is a Patient with septic peritonitis for exploratory constant threat to life laparotomy 5 Moribund and not expected to live over Patient for gastric dilation and volvulus 24 hours without surgery correction surgery E Emergency Depicts surgery is emergency The Veterinary Nurse’s Practical Guide to Small Animal Anaesthesia, First Edition. Edited by Niamh Clancy. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.  ASA PHYSICAL STATUS CLASSIFICATION A guide for veterinary patients Health/Physical Status (not risk status) Definition Examples include but not limited to: Healthy (non-brachycephalic) patients with no underlying disease presenting for elective procedures such as neutering ASA Physical Status I* A normal healthy patient or simple fracture repair Anaemia - mild (PCV: 30-40% dogs, 25-30% cats) Epilepsy - controlled Brachycephalic considered healthy Gastrointestinal disease - mild/stable A patient with mild systemic disease Cardiac murmur - grade 1-2/6 - prior to full cardiac Geriatric patients considered otherwise healthy ASA Physical Status II* workup/with known cardiac disease (animal compensating well) Infection - mild/localised Dehydration - mild (4-6%) Obesity Endocrinopathy - stable Young (>12 weeks) patient considered otherwise healthy Anaemia - moderate (PCV: 20-30% dogs, 15-25% cats) Gastrointestinal disease - uncontrolled/unstable Brachycephalic with mild respiratory/gastrointestinal signs Hepatic disease - all but controlled/compensated Cardiac arrhythmia - all but controlled Infection - moderate/severe/systemic (e.g. pyometra) Cardiac disease - all but controlled/compensated A patient with severe systemic disease Pulmonary disease - all but controlled/compensated ASA Physical Status III* Cardiac murmur - grade 3/6 - prior to full cardiac (animal not compensating fully) workup/with known cardiac disease Pyrexia Dehydration - moderate (7-9%) Renal disease - all but controlled/compensated Endocrinopathy - uncontrolled/unstable Very young/Neonatal ( 45 mmHg), which hyperventilation should results in cerebral vasodilation be avoided in patients and increased cerebral blood with traumatic brain flow/volume, will further injury, as excessive increase ICP. vasoconstriction could lead to poor brain perfusion, which could pose a potential risk of further cerebral damage. Did You Know That A bloated stomach will impair ventilation and increase the likelihood of regurgitation (Clarke et al. 2014) and aspiration (Dugdale 2007a).  ­Ventilation Strategies to Prevent Some of the Possible Negative Effects of IPP 57 ­ entilation Strategies to Prevent Some of the Possible V Negative Effects of IPPV On the Lungs Use a ‘lung protective’ or ‘low stretch’ ventilation approach – that is the delivery of smaller tidal volumes, but at a more frequent respiratory rate to achieve adequate deliv- ery of minute ventilation. However, it is important to note that in the diseased lung the FRC is reduced, in addition, small tidal volumes will further affect the lung FRC and the likelihood of atelectasis formation (Dugdale 2007b). On the Cardiovascular System Minimising the magnitude and length of time there is positive pressure within the thorax, will result in less marked cardiovascular effects (Dugdale 2007a). This is to minimise mean intrapulmonary pressure and can be achieved by taking the following steps (Dugdale 2007b): Do not maintain positive pressure for longer than is necessary to deliver an adequate tidal volume. Aim for a relatively longer expiratory phase (an I : E ratio of 1 : 3). Minimise resistance to airflow, by using an appropriate length endotracheal tube for the patient being anaesthetised and avoid having too many angle connectors or sharp bends. Minimise the dead space in both the patient and the apparatus, as this reduces the vol- ume and pressure delivery requirements of the ventilator. Maintain an adequate plane of anaesthesia. An unnecessary deeper anaesthetic plane will significantly dampen the response of the baroreflex receptors, which would other- wise help with the cardiovascular system’s compensatory mechanisms (Dugdale 2007a). On the Intracranial Pressure In patients with suspected, or where there is clear evidence of raised ICP, controlled mild to moderate hyperventilation along with head elevation can offset the direct consequences of artificial ventilation on ICP, at least in the short term (Dugdale 2007a). Maintain EtCO2/PaCO2 towards the lower range of the normal limit at around 35 mmHg – this will result in reduced cerebral blood volume. Avoid excessive hyperventilation, excessive vasoconstriction can compromise cerebral oxygenation and may lead to further cerebral damage (Dugdale 2007b). On Blood Gas and Acid–Base Disturbances If respiratory acidosis or alkalosis is suspected based on capnometry readings or confirmed by blood gas analysis readjusting the ventilatory settings to either increase or decrease min- ute ventilation, will address alkalosis or acidosis. Aim to maintain normocapnia PaCO2 35–45 mmHg or EtCO2 in a similar range. 58 4 Respiratory Physiology and Ventilation When there is a suspicion of a large gradient/difference between PaCO2 and EtCO2, then running an arterial blood gas analysis to verify capnography readings is warranted (Dugdale 2007a). ­Troubleshooting During Mechanical Ventilation When troubleshooting issues with mechanical ventilation it can be broadly divided into the following categories: Anaesthetic Machine and Breathing System The machine and breathing system should be checked for leaks. Check that the anaesthesia machine is connected to an adequate source of O2 and has a vaporiser. Ventilators Ensure the ventilator is properly connected to either an electrical or pressurised gas source. Check all connections are free from leaks. Check that the ventilator settings are appropriate for the patient. Check for air leaks in the anaesthetic apparatus. Check that the O2 supply is connected. Patient Ensure that the air flows into both lungs during inspiration through auscultation and observation of the chest. Check there is no impairment to expiration such as sticky expiratory valves on a cir- cle system. Ensure depth of anaesthesia is appropriate as the patient will fight the ventilator if in a light plane of anaesthesia. If too light, further sedation can be administered. Check the patient’s perfusion – a decrease in blood flow to the lungs may cause V/Q mismatch which may lead to poor ventilation. ­Weaning the Patient Off the Ventilator The technique of weaning the patient off a ventilator can differ slightly depending on whether this is done at the end of the surgery and the patient is recovered or during the surgery/procedure.  ­Weaning the Patient Off the Ventilato 59 During the surgery: Decrease the depth of anaesthesia (only if safe to do so) to lighten the plane of the anaes- thetic -­this eventually will increase the likelihood of the patient’s responsiveness to the carbon dioxide chemoreceptors. Reduce the respiratory rate to allow the EtCO2/PaCO2 to increase; this eventually will stimulate spontaneous breathing. Switch off the ventilator when the patient is attempting to breathe spontaneously and con- tinue to assist ventilation manually until complete spontaneous ventilation recommences. At the end of surgery: Turn the volatile gas off (or stop total intravenous anaesthesia if this is the method of maintaining anaesthesia). Keep the same respiratory rate for a few minutes or just enough time to speed up the removal of inhalant anaesthetic from the patient. Reduce the respiratory rate to allow the EtCO2/PaCO2 to increase; ideally EtCO2 should be continuously monitored to prevent the development of excessive hypercapnia (EtCO2 > 60 mmHg), especially in neurological cases with increased ICP or any other conditions that would not tolerate hypercapnia (Hartsfield 2008). Switch off the ventilator when the patient is attempting to breathe spontaneously and continue to assist ventilation manually until complete spontaneous ventilation recom- mences and the patient can maintain normocapnia. Stimulate the patient such as turning/changing position. Excessive hypothermia may delay the weaning off procedure and could result in post anaesthetic respiratory depression. Therefore, in some extreme cases, it may be necessary that the patient is warmed up to a normal body temperature even before switching from control to spontaneous ventilation (Hartsfield 2008). Ventilation can seem like an overwhelming and daunting task, however, if the general principle of the mechanics of respiration are considered the VN can provide ventilation that is safe and effective. Table containing definitions of commonly used terms in respiratory physiology and ventilation. Definition Minute ventilation Total air that flows in and out of respiratory system in a minute. It can be calculated by multiplying the tidal volume by the respiration rate or number of breaths per minute. Tidal volume The volume of air that moves into and out of the lungs in one unforced breath. Alveolar ventilation The volume of fresh air that reaches the alveoli each minute. It is calculated by subtracting from the minute volume the air that does not reach the alveoli because of the anatomical dead space (the combined volume of the non-­exchanging airways). (Continued) 60 4 Respiratory Physiology and Ventilation (Continued) Definition Physiologic dead space Represents the sum of the alveolar dead space (non-­perfused alveoli) and the conducting airway dead space (trachea, bronchi, bronchioles). Functional residual capacity The volume of air in the lungs between breaths when the lungs are at rest and no air is moving into or out of the lungs. I : E ratio Defined by the amount of time allocated for inspiration versus expiration. V/Q mismatch Refers to pulmonary parenchymal disease that leads to alveoli receiving decreased ventilation for the degree of perfusion (low V/Q) or no ventilation but ongoing perfusion (no V/Q or shunt). In small animal medicine, V/Q mismatch is associated with all forms of pulmonary parenchymal disease including pulmonary oedema, haemorrhage, and pneumonia. Alveolar surfactant A mixture of proteins and phospholipids into the thin fluid layer lining the inner surface of alveoli, and functions as a detergent by reducing the surface tension of the fluid layer, preventing alveolar collapse. Volutrauma Trauma caused by using higher than required volumes during artificial ventilation. Barotrauma Trauma caused by using higher than required pressures during artificial ventilation. Atelectasis Lung collapse. PaO2 Partial pressure of oxygen in arterial blood. PaCO2 Partial pressure of carbon dioxide arterial blood. SaO2 Saturation of haemoglobin with oxygen in arterial blood. SpO2 Saturation of haemoglobin with oxygen measured by a pulse oximeter. EtCO2 End-­tidal carbon dioxide. Hypoxia A PaO2 under 60 mmHg. Hypo/hyperventilate A decrease or increase in respiratory rate or volume. References Ambrosio, M.A., Carvalho-­Kamakura, T.P.A., Ida, K.K. et al. (2017). Ventilation distribution assessed with electrical impedance tomography and the influence of tidal volume, recruitment, and positive end-­expiratory pressure in isoflurane-­anesthetized dogs. Veterinary Anaesthesia and Analgesia 44 (2): 254–263.  References 61 Bumbacher, S., Schramel, J.P., and Mosing, M. (2017). Evaluation of three tidal volumes (10, 12 and 15 mL kg−1) in dogs for controlled mechanical ventilation assessed by volumetric capnography: a randomized clinical trial. Veterinary Anaesthesia and Analgesia 44 (4): 775–784. Clarke, K.W., Trim, C.M., and Hall, L.W. (2014). Anaesthesia of the dog: artificial ventilation. In: Veterinary Anaesthesia, 11e (ed. K.W. Clarke and C.M. Trim). London: Saunders Elsevier. De Monte, V., Grasso, S., De Marzo, C. et al. (2013). Effects of reduction of inspired oxygen fraction or application of positive end-­expiratory pressure after an alveolar recruitment maneuver on respiratory mechanics, gas exchange, and lung aeration in dogs during anesthesia and neuromuscular blockade. American Journal of Veterinary Research 74 (1): 25–33. Dugdale, A. (2007a). The ins and outs of ventilation 1. Basic Principles. In Practice 29 (4): 186–193. Dugdale, A. (2007b). The ins and outs of ventilation 1. Basic Principles. In Practice 29 (5): 272–282. Ewart, S.L. (2020). Overview of respiratory function: ventilation of the lungs. In: Cunningham’s Textbook of Veterinary Physiology, 6e (ed. B.G. Klein), 518–574. St. Louis, MO: Elsevier. Fantoni, D.T., Ida, K.K., Lopes, T.F.T. et al. (2016). A comparison of the cardiopulmonary effects of pressure controlled ventilation and volume controlled ventilation in healthy anesthetized dogs. Journal of Veterinary Emergency and Critical Care 26 (4): 524–530. Grubb, T. (2016). Respiratory compromise. In: BSVA Manual of Canine and Feline Anaesthesia and Analgesia, 3e (ed. T. Duke-­Novakovski, M. de Vries and C. Seymour), 314–328. Gloucester: BSAVA. Gwendolyn, L.C. (2008). Ventilation. In: Small Animal Anaesthesia and Analgesia (ed. L.C. Gwendolyn), 39–52. Oxford: Blackwell Publishing. Hammond, R. and Murison, P.J. (2016). Automatic ventilators. In: BSVA Manual of Canine and Feline Anaesthesia and Analgesia, 3e (ed. T. Duke-­Novakovski, M. de Vries and C. Seymour), 65–76. Gloucester: BSAVA. Hartsfield, S.M. (2008). Anaesthesia equipment. In: Small Animal Anaesthesia and Analgesia (ed. L.C. Gwendolyn), 3–23. Oxford: Blackwell Publishing. Lewis, R., Sherfield, C.A., Fellows, C.R. et al. (2017). The effect of experience, simulator-­ training and biometric feedback on manual ventilation technique. Veterinary Anaesthesia and Analgesia 44 (3): 567–576. https://doi.org/10.1016/j.vaa.2016.05.005. Marieb, E.N. and Hoehn, K.N. (2014). The respiratory system. In: Human Anatomy & Physiology, 9e, 865–905. London: Pearson. Mosing, M. (2016). General principles of perioperative care. In: BSVA Manual of Canine and Feline Anaesthesia and Analgesia, 3e (ed. T. Duke-­Novakovski, M. de Vries and C. Seymour), 13–23. Gloucester: BSAVA. Sjaastad, O.V., Hove, K., and Sand, O. (2003). Physiology of Domestic Animals, 1e, 89–427. Oslo: Scandinavian Veterinary Press. 62 4 Respiratory Physiology and Ventilation Further Reading Asorey, I., Pellegrini, L., Canfrán, S. et al. (2020). Factors affecting respiratory system compliance in anaesthetised mechanically ventilated healthy dogs: a retrospective study. Journal of Small Animal Practice 61 (10): 617–623. Borer-­Weir, K. (2014). An introduction to pharmacokinetics. In: Veterinary Anaesthesia, 11e (ed. K.W. Clarke, C.M. Trim and L.W. Hall), 65–79. London.: Saunders Elsevier. Bradbrook, C.A., Clark, L., Dugdale, A.H.A. et al. (2013). Measurement of respiratory system compliance and respiratory system resistance in healthy dogs undergoing general anaesthesia for elective orthopaedic procedures. Veterinary Anaesthesia and Analgesia 40 (4): 328–389. De Monte, V., Bufalari, A., Grasso, S. et al. (2018). Respiratory effects of low versus high tidal volume with or without positive end-­expiratory pressure in anesthetized dogs with healthy lungs. American Journal of Veterinary Research 79 (5): 496–504. De Wet, C. and Moss, J. (1998). Metabolic functions of the lung. Anesthesiology Clinics of North America 16 (1): 181–199. Fraser, M. (2003). Physiology relevant to anaesthesia. In: Anaesthesia for Veterinary Nurse (ed. E. Welsh), 15–33. Oxford: Blackwell Publishing. Hopper, K. and Powell, L.L. (2013). Basics of mechanical ventilation for dogs and cats. Veterinary Clinics of North America: Small Animal 43 (4): 955–969. Martin-­Flores, M., Cannarozzo, C.J., Tseng, C.T. et al. (2020). Postoperative oxygenation in healthy dogs following mechanical ventilation with fractions of inspired oxygen of 0.4 or >0.9. Veterinary Anaesthesia and Analgesia 47 (3): 295–300. McDonell, W. and Kerr, C.L. (2015). Physiology, pathophysiology, and anesthetic management of patients with respiratory disease. In: Veterinary Anaesthesia and Analgesia; The Fifth Edition of Lumb and Jones, 5e, pp. 513 (ed. K.A. Grimm, L.A. Lamont, W.J. Tranquilli, et al.). Oxford: Wiley Blackwell. Mosing, M., Staub, L., and Moens, Y. (2010). Comparison of two different methods for physiologic dead space measurements in ventilated dogs in a clinical setting. Veterinary Anaesthesia and Analgesia 37 (5): 393–400. Staffieri, F., Franchini, D., Carella, G.L. et al. (2007). Computed tomographic analysis of the effects of two inspired oxygen concentrations on pulmonary aeration in anaesthetised and mechanically ventilated dogs. American Journal of Veterinary Research 68 (9): 925–931.  63 5 Blood Pressure Regulation and Monitoring Leanne Smith It is important for veterinary nurses (VNs) to grasp how blood pressure is regulated and affected under general anaesthesia to enable us to understand, interpret, and report abnormalities accordingly. An underpinning knowledge of blood pressure physiology will enable us to consider how our patients’ regulatory mechanisms can be affected by anaesthetic drugs and will therefore empower us with the knowledge to work with veterinary surgeons to provide the safest possible anaesthetic protocols and monitoring. It is recommended that the reader understands common blood pressure terminology before reading this chapter, which is provided in the index. Reviewing the cardiovascular physiology in Chapter 3 of this book will also provide important background information. ­What Factors Contribute to Blood Pressure To visualise how blood pressure is regulated we should first picture the myocardium contracting. Cardiac muscle fibres shorten and the heart shrinks in size, creating a pressure elevation within the ventricles that pushes blood through a network of blood vessels (arteries, veins, and capillaries). The pressure exerted on the walls of blood vessels around the body is referred to as blood pressure. Blood pressure is therefore reliant on both the functionality of the heart, the circulatory blood volume, and the tension within the blood vessels themselves, as the wider these vessels are the less the pressure will be within them (Duke‐Novakovski and Carr 2015). Blood pressure can be calculated by multiplying cardiac output (CO) by systemic vascular resistance (SVR) and is therefore directly reliant on these two factors. Cardiac output is defined as the volume of blood pumped around the patient’s body per minute. Direct measurement of cardiac output is largely invasive and dangerous, requiring the placement of a Sanz‐Ganz catheter into the pulmonary artery which can cause occlusions, so it is often estimated by calculating a sum of heart rate (beats per minute) by stroke volume. Stroke volume can be defined as the volume of blood pumped from the left ventricle, per contraction. Stroke volume is affected by various factors, including myocardial contractility The Veterinary Nurse’s Practical Guide to Small Animal Anaesthesia, First Edition. Edited by Niamh Clancy. © 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd. 64 5 Blood Pressure Regulation and Monitoring Blood pressure = cardiac output x systemic vascular resistance Heart rate X Stroke volume Vasomotor tone Contractility Venous return Preload Circulating blood volume Figure 5.1 A flow chart demonstrating the factors contributing to each part of the blood pressure calculation. and the amount of blood that enters the ventricle to be ejected (known as the preload). Many of the factors contributing to blood pressure also have related effects on each other; for example, vasomotor tone (therefore, SVR) can also influence the pre‐load, as smaller vessel diameters push more blood into the heart. A flow chart providing a summary of the components of blood pressure regulation and their relationships can be found in Figure 5.1 below and is discussed in more detail in Chapter 3 of this book. ­ he Importance of Blood Pressure Regulation T During Anaesthesia Healthy, conscious animals can auto‐regulate their blood pressure, meaning they are able to keep it within safe homeostatic ranges by autonomically altering the various contribut- ing factors accordingly (Schauvliege 2016). For example, if cardiac output drops slightly due to a reduction in pre‐load due to dehydration, the animal’s heart rate may elevate slightly to preserve blood pressure. Pre‐existing disease processes can affect a patient’s abil- ities to regulate their blood pressure. Therefore, identifying potential risk factors for blood pressure dysregulation (and stabilising where necessary) should be a consideration during the pre‐anaesthetic assessment. A patient with renal disease, for example, could have decreased renal autoregulation (Welsh 2009). Renal autoregulation can be defined as the physiological mechanism by which the body maintains a normal glomerular filtration rate and renal blood flow over a wide range of blood pressures. A decrease in renal autoregula- tion leads to an inability to maintain kidney perfusion and function during times of altered blood pressure, which can cause additional subsequent renal damage. Animals with car- diac disease may not have enough cardiovascular reserve to cope with the changes in hemodynamic stability during anaesthesia, and therefore recognition and stabilisation of such conditions is also pivotal prior to general anaesthesia (Schauvliege 2016). Refer to the case study section of this textbook for more information on anaesthesia for animals with specific conditions. Surgical interventions and anaesthetic drugs can also interfere with blood pressure regulation. A summary of the expected effects of commonly used anaesthetic  ­The Importance of Blood Pressure Regulation During Anaesthesi 65 agents on a patient’s blood pressure is provided in Table 5.1, and the reference ranges for normotension in cats and dogs are available in Table 5.2. Hypotension is a common anaesthetic concern, as most anaesthetic drugs will cause dose‐dependent cardiopulmonary depression by affecting vasomotor tone and/or cardiac output (Schauvliege 2016). Our patients are also often exposed to a risk of surgical haemorrhage, which will decrease the patient’s circulatory volume and therefore reduce Table 5.1 Some commonly used drugs in veterinary anaesthesia, and their potential effects on patients’ blood pressure. Drug name Effect on blood pressure Acepromazine Dose dependent vasodilation can reduce systemic vascular resistance, which can potentially cause a mild reduction in blood pressure. Dexmedetomidine/ Biphasic response: initial peripheral vasoconstriction elevates systemic Medetomidine vascular resistance, which can cause transient hypertension. A return to normotension or slightly reduced baseline readings may follow, as the centrally mediated effects can outlive the peripherally mediated effects. Volatile anaesthetic Reduces blood pressure due to dose dependent vasodilation, and a agents (i.e. isoflurane/ reduction in contractility. A common contributor to peri‐anaesthetic sevoflurane) hypotension. Propofol Reduces cardiac output and systemic vascular resistance. Patient does not maintain baro‐receptor response and therefore heart rate does not increase in response to hypotension. Alfaxalone Reduces cardiac output and systemic vascular resistance. Heart rate can reportedly increase in response to hypotension as the patient maintains a baroreceptor response. Therefore, may be preferred to propofol in animals with a low cardiac reserve. Ketamine As a solo injectable agent, central stimulation of the sympathetic nervous system can increase heart rate, cardiac output and therefore blood pressure. When given concurrently with other sedatives (e.g. Alpha‐2 adrenoceptor agonists), in severely compromised animals or at high intravenous doses ketamine may induce myocardial depression and therefore transient hypotension. Opioids Most opioids have little direct negative effect on cardiac contractility. However, when administered alongside other drugs can be associated with decreased cardiac function, including bradycardia and vasodilation at analgesic doses. Source: Chen and Ashburn (2015) and Schauvliege (2016). Table 5.2 Normal blood pressure ranges in dogs and cats. Reference ranges: blood pressure values Dogs Cats Systolic arterial pressure 90–140 mmHg 80–140 mmHg Diastolic arterial pressure 50–80 mmHg 55–75 mmHg Mean arterial pressure 60–100 mmHg 60–100 mmHg Source: Williamson and Leone (2012), pp. 134. 66 5 Blood Pressure Regulation and Monitoring pre‐load. Blood pressure is the essential driving force of organ perfusion, so when it drops below acceptable levels it can result in hypoperfusion (Schauvliege 2016). Hypoperfusion means that there is an inadequate delivery of oxygen and removal of waste products from tissues within the patient’s body. If unrecognised or untreated, hypoperfusion can lead to irreversible organ damage. In dogs and cats, a mean arterial blood pressure below 60 mmHg is defined as the renal threshold, and when pressures drop below this point, we risk imposing kidney damage to our patients due to hypoperfusion. Severe hypotension can also cause arrhythmias and cardiac arrest due to a reduced oxygen supply to the myocardium itself (Sierra and Savino 2015). A diastolic blood pressure below 40 mmHg has been noted to result in inadequate perfusion to the myocardium. We may also encounter hypertension in some anaesthetised patients due to underlying disease processes, pharmacological influences or from surgical nociception causing sympathetic nervous system (SNS) stimulation. SNS stimulation can greatly affect cardiovascular function by the release of neurotransmitters involved in the fight or flight response. If untreated, hypertension also greatly increases myocardial workload and therefore causes an elevated oxygen demand, which can cause ischaemia and subsequent arrhythmias or even potentially cardiac arrest (Schauvliege 2016). With prolonged exposure to hypertension, the force and friction can damage the delicate endothelium tissues lining the blood vessel walls. Additional consequences of sustained hypertension can include retinopathy, brain, and kidney damage‐ due to damage to the extremely delicate blood vessels and elevated workload (Schauvliege 2016). By noticing and addressing blood pressure fluctuations quickly, we can treat accordingly and reduce the likelihood of long‐ term organ damage being sustained. ­How Do We Measure Blood Pressure? It is important that blood pressure monitoring in the perioperative period is done as consistently and reliably as possible. Generally, either direct/invasive or indirect/non‐ invasive methods are used. Given the variability of the numbers generated by the various monitoring methodologies, it is advisable to use the same method in each patient to be able to identify trends successfully. The trend of the blood pressure recordings is often the predominant thing being monitored, as absolute numbers often are elusive (Williamson and Leone 2012). A summary of the advantages and disadvantages of the different blood pressure monitoring modalities is provided in Table 5.3. Non-invasive/Indirect Blood Pressure Monitoring Non‐invasive blood pressure (NIBP) monitoring is often quicker and easier to use than invasive methods and is more widely available in most practices. NIBP monitors use an occlusive pneumatic cuff, placed directly over a peripheral artery, and include oscillometric and Doppler techniques described below. It is of the utmost importance to ensure that the cuff size is correct for each patient, to minimise the risk of erroneous readings. The correct cuff size is usually defined as having a width of around 40% of the circumference of the patient’s limb in which is it being used (Welsh 2009). This is illustrated Figure 5.2. A cuff that is too narrow will cause an over‐estimation of blood pressure, and a cuff that is too  How Do We Measure Blood Pressure? 67 Table 5.3 The advantages and disadvantages of the different blood pressure monitoring modalities. Monitoring modality Advantages Disadvantages Invasive blood Best reliability, even in patients Often difficult and time‐consuming placing pressure analysis with hypotension, arrhythmias arterial catheter, especially in small/very and bradycardia. sick patients. Updates in real time, with every More expensive equipment required. heartbeat. Risks to the patient, including haematoma Gives mean, systolic and formation, air embolism, blood loss, diastolic readings. systemic infection, and damage to adjacent Arterial catheter can be used for structures. blood sampling. Oscillometric Gives mean, systolic and Generally unreliable in patients less than (NIBP) diastolic readings. 5 kg. Can generate automated May not provide readings in patients readings at timed intervals‐ less experiencing vasoconstriction hypotension, technical skill required and less hypertension, bradycardia or arrhythmias. time consuming. Less handling required on conscious patients. Doppler (NIBP) Can be used to provide an Often advised to identify trends, rather audible pulse reading, to give a than a definitive blood pressure reading. real time assessment of pulse Gives only one reading; more closely rate and quality. associated with a mean reading in cats, and Equipment relatively cheap. systolic reading in dogs. Often more successful at More technically demanding and time obtaining blood pressure consuming. readings in hypotensive, More patient restraint required on bradycardic or arrhythmic conscious patients. patients. Readings may be challenging where Commonly used in very small peripheral vasodilation is profound (e.g. patients (less than 5 kg) following alpha‐2 agonist administration or including exotics. during hypovolaemic shock). Source: Williamson and Leone (2012) and Waddell and Brown (2015). wide will often under‐estimate (Welsh 2009). Many cuffs also specify where they should be placed in relation to the patient’s artery, also shown in Figure 5.3. Cuffs should be applied firmly but not tightly, as this will occlude blood flow and cause an underestimation of blood pressure and should not be secured with tape as this will prevent effective cuff infla- tion (Williamson and Leone 2012). NIBP readings can be obtained at multiple sites includ- ing forelimbs, hindlimbs, and the tail. Readings can also be affected by gravity; it is believed that for every 10 cm the cuff is placed above the patient’s right atrium, the pressure will be underestimated by approximately 7.36 mmHg, and for every 10 cm below the right atrium the blood pressure will be overestimated by around 7.36 mmHg (Welsh 2009). We should therefore consider patient positioning during NIBP measurement as this can contribute to inaccurate readings. The cuff should ideally be positioned on the limb at the level of the right atrium (Williamson and Leone 2012). 68 5 Blood Pressure Regulation and Monitoring Figure 5.2 Showing a cuff measure 40% of the circumference of a limb. Figure 5.3 Showing artery line on a blood pressure cuff. TOP TIP! Use your stethoscope against the Doppler unit, to allow more clear auscultation of arterial pulsation return. Doppler To obtain a blood pressure reading using a Doppler probe, the occlusive cuff is placed prox- imally to the site that the Doppler probe will be placed above a peripheral artery. The probe must be placed against a hairless patch of skin, and ultrasound gel applied onto the probe or skin to improve the signal quality. This is illustrated in Figure 5.4. The Doppler probe uses a piezoelectric crystal and relies on detecting the Doppler shift, whereby the frequency of the sound reflected by the arterial blood moving through the peripheral artery is different to the sound transmitted from the crystal (Welsh 2009). The shift in frequency is converted into an audible signal, meaning the patients arterial pulsations can be heard as a ‘whoosh’ sound. Once the cuff and probe are in place and an arterial pulsation is located, the hand piece known as the sphygmomanometer is used to inflate the cuff until the audible pulsation disappears. The pressure on the gauge of the sphygmomanometer at which the pulse becomes audible again is taken as the blood pressure reading. We must be careful how we interpret Doppler blood pressure readings; recent evidence has indicated  How Do We Measure Blood Pressure? 69 Figure 5.4 Area clipped for Doppler placement. that in feline patients the Doppler technique quite often underestimates the systolic arterial pressure, and the reading is more closely associated with the mean arterial pressure (Waddell and Brown 2015). In a canine patient it is suggested that the Doppler reading is more closely associated with the systolic blood pressure (Waddell and Brown 2015). Oscillometric Oscillometric blood pressure monitoring determines blood pressure by measuring pressure oscillations in a cuff placed around an extremity. Oscillometric monitors can detect pres- sure oscillations at various points throughout the cardiac cycle and can therefore provide systolic, diastolic, and mean blood pressures. Some monitors also record heart rate. It should be noted that Oscillometric blood pressure monitoring may be less reliable where hypotension, bradycardia, peripheral vasoconstriction, or arrhythmias are present, and often fails entirely to gain reliable readings in patients less than 5 kg in body weight (Waddell and Brown 2015). High Definition Oscillometric (HDO) Devices In recent years high definition oscillometric (HDO) devices have been growing in popular- ity in veterinary practices. These devices use a higher bit processor that allow for linear deflation of cuffs used. This is thought to improve accuracy in smaller patients. A study by Rysnik et al. (2013), showed that HDOs had good accuracy when compared to direct arte- rial blood pressure but poor precision. 70 5 Blood Pressure Regulation and Monitoring Invasive Blood Pressure Monitoring Invasive blood pressure (IBP) monitoring is largely considered the ‘gold standard’ blood pressure monitoring modality, often perceived as being the most reliable and offering consistent readings. However, data has shown that even direct blood pressures measurements in peripheral arteries can be conflicting with more central arterial pressures in cats (Parker et al. 2012) and dogs (Monteiro et al. 2013), and should therefore be interpreted accordingly. To measure IBP, firstly sterile skin preparation is performed, and then an arterial catheter is placed within the arterial lumen. This catheter is attached to a specialised t‐connector (flushed through with sterile saline) which is then connected to a transducer line feeding into the monitor. The patient’s arterial contractions cause displacement of the fluid within the connector, and the force of this displacement at various parts of the cardiac cycle gives us the pressure readings. Therefore, IBP monitoring offers systolic, mean, and diastolic arte- rial pressure recordings, alongside constant heart rate updates and an arterial waveform. Having an invasive arterial catheter gives the advantage of a constant measurement of blood pressure and heart rate, enabling us to identify changes instantaneously. IBP is useful in patients where rapid changes in blood pressure are anticipated, such as patients where sig- nificant haemorrhage is a concern during surgery, or if the patient is of a higher anaesthetic mortality risk. Once the arterial catheter has been placed, arterial blood samples can also taken, which can be used to determine other important parameters such as blood gas analy- sis, acid base balance, electrolyte levels, blood glucose and lactate levels (Poli 2017). It is important to note however that arterial cannulation does carry some risks to the patient, including haematoma formation, air embolism, thrombosis/distal ischaemia, blood loss, accidental arterial drug administration, systemic infection, and damage to adjacent structures (Summerfield 2019). In smaller or more critical patients also, gaining arterial access can be largely difficult and time consuming. ­Treatment of Hypotension Under General Anaesthesia Before attempting to treat hypotension, we should confirm the reliability of our readings by checking cuff size or location and using another modality if available. The choice of treatment option should be guided by an attempted identification of its underlying cause. In order to do this, it is important to consider the patients other parameters, concurrent disease processes and surgical implications. We should consider the patient’s blood pressure reading as part of the bigger picture, and where appropriate always think critically about the reliability of readings (especially where there is cause for skepticism, such as a poorly fitted or positioned blood pressure cuff). Identifying the causation to target treatment of hypotension can be difficult but is paramount to restore normotension effectively and safely. There are three underlying causes of hypotension; decreased cardiac output (by a reduced heart rate or stroke volume), decreased SVR, or a combination of these (Welsh 2009). An ideal starting point for trouble shooting is to focus on each individual blood pressure regulatory component and how abnormalities with each one may present, and how we could treat them.  ­Drugs to Treat Hypotensio 71 When attempting to identify the cause of hypotension, we must remember the compen- satory mechanisms at play. In a conscious patient without cardiovascular compromise, the varying aspects of the cardiac output calculation will largely compensate for each other. For example, if a patient has a reduced stroke volume due to a fluid deficit, we may see an elevation in heart rate to keep the cardiac output at a homeostatic equilibrium; one increases to keep the calculation outcome consistent (CO = HR × SV). These compensatory mechanisms are often dampened by anaesthetic drugs, and therefore interventions are often required. A tachycardic and hypotensive patient may therefore benefit from receiving an intravenous fluid bolus, which would increase the stroke volume and mean that the heart rate could return to normal. It helps to revert to the blood pressure and cardiac output calculations and examine which area of the equation could be the problem. For example, cardiac output is made up of heart rate and stroke volume; if the heart rate is low and the animal is unable to compensate for this fully by altering stroke volume, hypotension may be treated appropriately by initially reducing volatile agent usage so the animal can better compensate with vascular diameter and contractility or by using fluids to increase stroke volume. If this is unsuccessful then treating the low heart rate using anticholinergics (such as glycopyrrolate or atropine) may be a very sensible suggestion. Whether the systolic or diastolic pressures are low can also provide additional informa- tion during the diagnostic process; systolic pressure is generated during myocardial contrac- tion, and diastolic pressures are generated during the rest interval between. This information may therefore suggest that systolic pressures are largely affected by contractility and stroke volume, and diastolic pressures largely dependent on vascular resistance and circula- tory volume. ­Drugs to Treat Hypotension There are various treatment options to restore normotension under general anaesthesia, and accurately identifying the causation will enable the correct drug selection. The blood pressure regulating drugs available are often grouped by their mechanism of action; positive inotropes, vasopressors, positive chronotropes, and anticholinergics, with some drugs eliciting more than once mechanism of action. The receptor occupancy, clinical indications and effects of these drugs are demonstrated below in Table 5.4, and the main groups are introduced briefly below. Patients should always be monitored closely (including blood pressure and ECG analysis) after receiving blood pressure regulating drugs, as changes in cardiovascular status can happen rapidly and drastically. We must be aware that administering drugs that increase the myocardial workload by increasing contractility and/ or heart rate, will also increase myocardial oxygen demand. In severe cases myocardial oxygen depletion can cause arrhythmias or even cardiac arrest. Patients with pre‐existing cardiac disease especially may find it difficult to maintain haemodynamic stability in the presence of an increased cardiac output, and therefore more specialist advice and stabilisation is recommended. Before administering blood pressure regulating drugs patient depth should always be assessed, and volatile anaesthetic reduced as appropriate to decrease vasodilation. The option to antagonise current medications or correct fluid deficits should also precede further pharmaceutical intervention. It is important to note that 72 5 Blood Pressure Regulation and Monitoring Table 5.4 Drug names/classifications, their clinical indications and effects, alongside which receptors they use. Drug name and Receptors and effects of classification Clinical indication administration Adrenaline/ Shock (cardiogenic, vasodilatory) α1: vasoconstriction, Epinephrine Cardiac arrest increase contractility Positive inotrope Bronchospasm/anaphylaxis α2: vasoconstriction Vasopressor Symptomatic bradycardia or heart block β1: increase contractility, unresponsive to atropine or pacing increase HR, increase conduction speed β2: systemic vasodilation, bronchodilation Dobutamine Low CO (decompensated HF, cardiogenic β1: increase contractility, Positive inotrope shock, septic‐induced myocardial increase HR increase dysfunction and hypertrophic conduction speed cardiomyopathy) β2: systemic vasodilation, bronchodilation Dopamine Shock (cardiogenic, vasodilatory) α1: vasoconstriction, Positive inotrope Heart failure increase contractility Vasopressor Symptomatic bradycardia unresponsive to β1: increase contractility, Positive chronotrope atropine or pacing increase HR, increase conduction speed β2: systemic vasodilation, bronchodilation DA1: systemic vasoconstriction DA2: systemic vasoconstriction Ephedrine Mild hypotension α1: vasoconstriction, Positive inotrope increase contractility Vasopressor β1: increase contractility, increase HR, increase conduction speed Noradrenaline/ Shock (vasodilatory, cardiogenic) α1: vasoconstriction, Norepinephrine increase contractility Positive inotrope α2: vasoconstriction Vasopressor β1: increase contractility, increase HR, increase conduction speed β2: systemic vasodilation, bronchodilation Phenylephrine Hypotension (vagally mediated, α1: vasoconstriction, Vasopressor medication‐induced) increase contractility Increase MAP with AS and hypotension Decrease LVOT gradient in HCM  ­Drugs to Treat Hypotensio 73 Table 5.4 (Continued) Drug name and Receptors and effects of classification Clinical indication administration Vasopressin Shock (cardiogenic, vasodilatory) V1R: systemic Vasopressor Cardiac arrest vasoconstriction V2R: urine concentration Atropine Hypotension with concurrent bradycardia M1,2,3: bronchodilation, Anticholinergic tachycardia, vasoconstriction. Glycopyrronium Hypotension with concurrent bradycardia M1,2,3: bronchodilation, Anticholinergic tachycardia, vasoconstriction. Source: Credit, Jo Williams RVN. following the administration of blood pressure regulating drugs, depth should be watched closely as alterations in metabolic rate can occur. Positive Inotropes Adrenaline/Epinephrine, Ephedrine, Dobutamine, Dopamine, Noradrenaline/ Norepinephrine Inotropic drugs can alter the contractility of cardiac muscle, which will subsequently influence how effectively the heart can pump. By increasing contractility and heart rate, we improve our patients’ cardiac output and therefore blood pressure. Positive inotropes work by stimulating receptors that are part of the sympathetic (‘fight or flight’) nervous system (Sheppard 2001). The main desired effect of administering positive inotropes (increased contractility and heart rate) happens following activation of the beta‐1 receptors. Different inotropic drugs however also have varying effects on the other receptors. For example, adrenaline achieves increased contractility via beta‐1 activation but can also stimulate alpha receptors, and therefore may additionally cause peripheral vasoconstriction (particularly at higher doses), thus acting as a positive inotrope and a vasopressor at once. Dobutamine increases contrac- tility via beta‐1 activation but can also stimulate beta‐2 receptors, which can cause vasodila- tion. It is of the utmost importance to be aware of the varying effects of different inotropes to enable us to make an informed choice of which inotropic agent is to be used in certain patients. Inotropes also have a short half‐life, and therefore their prolonged use can be given only as continuous rate infusion (CRI) and should be decreased gradually before stopping. Vasopressors Adrenaline/Epinephrine, Dopamine, Ephedrine, Noradrenaline/Norepinephrine, Phenylephrine, Vasopressin Vasopressor drugs will elevate blood pressure by increasing vascular tone, and therefore increasing SVR. Many vasopressors elicit their effects by stimulation of alpha‐1 receptors, 74 5 Blood Pressure Regulation and Monitoring thus also having a positive inotropic effect by increasing contractility alongside causing vasoconstriction. Few also exist that work on alpha‐2 and V1R receptors and mediate vaso- constriction only. Vasopressors are only considered as a viable treatment option when a patient is experiencing profound vasodilation (such as during sepsis) and only once reduc- tion of volatile anaesthesia and intravenous fluid therapy have been ineffective at correct- ing blood pressure. Anticholinergics Glycopyrolate, Atropine Anticholinergics blocks the action of a parasympathetic neurotransmitter called acetylcholine. Acetylcholine has a vital role in regulating heart rate and rhythm but too much parasympathetic tone can cause bradycardia and hypotension. Thus, using these drugs inhibits the parasympathetic (‘rest and digest’) division of the nervous system‐ having multiple systemic effects including increased heart rate, reduced salivation, and reduced airway secretions. Anticholinergics are commonly required in veterinary anaesthesia, especially in paediatric patients where blood pressure regulation is strongly correlated with heart rate due to their immature cardiovascular systems having a reduced ability to compensate with lower heart rates. Many breeds of dog are also pre‐disposed to having high vagal tone, which means an over activity of the 10th cranial nerve which transmits parasympathetic innervation. These breeds of dog include brachycephalic breeds and dachshunds. Atropine is more commonly used in emergency situations due to its rapid onset of action, Glycopyrrolate, however, has a longer duration of action. It is important to note that when administering anticholinergics, it is common to see a brief initial worsening of bradycardia associated with atrio‐ventricular blockade as the heart rate is attempting to speed up. This will usually rectify itself but can be followed with a subsequent secondary dose of anticholinergic if the bradycardia is extreme or unchanging. Temporary tachycardia may follow the administration of anticholinergics, and therefore myocardial oxygen demand will be increased as previously discussed. ­Treatment of Hypertension Under General Anaesthesia Hypertension is uncommon in the adequately anaesthetised patient, largely because of the negative cardiovascular effects of inhalant anaesthetics (AAHA 2020). Blood pressure cuff size and position should be assessed. It could be suggested to double check blood pressure at a different location or using a different modality if erroneous readings are suspected. Upon confirming that the pressure reading is reliable, a light plane of anaesthesia should be ruled out. This can be done by checking the patient’s eye positioning, jaw tone and palpebral reflex. If a light plane of anaesthesia is expected, even though adequate volatile agent is being supplied, we should check for errors such as a leaking or misplaced endotracheal tube or system leak. If no errors are found, we could consider ventilating our patient to increase volatile agent uptake or supplementing sedative drugs following  Quick Reference Terminology and Definitions 75 veterinary direction. If depth of anaesthesia is adequate, we should consider nociception as a cause and discuss additional analgesia with the veterinary surgeon. Hypoxaemia and hypercarbia have also been described as a potential causation for hypertension and should be ruled out accordingly by capnography and pulse oximetry analysis (AAHA 2020). If reliable hypertension persists but the patient appears to be adequately anaesthetised and receiving appropriate analgesia, we should consider whether underlying disease processes may be present and perform investigations as required. Hypertension is common with many systemic disease processes, including endocrine disorders such as diabetes mellitus, hyperthyroidism and hyperadrenocorticism. ­Summary VNs should ensure that they monitor blood pressure reliably and consistently throughout the peri‐operative period. The VN must be confident in how to fit a blood pressure cuff appropriately, and whether we are using the appropriate modality for the size of patient we have, and the health status of the animal. They should also be confident that the blood pressure reading obtained is reliable before initiating further treatment. The patient’s blood pressure should be regulated within set limits as specified in Table 5.2, wherever possible as both hypotension and long‐term hypertension can lead to irreversible organ damage. The VN must remember that volatile anaesthetic agents influence blood pressure through vasodilation, and excessive depth should always be considered as a cause for hypotension. It is vital to target the treatment of blood pressure abnormalities according to the suspected cause. The VN should be aware of the different blood pressure regulating drugs available, and the physiological reactions to anticipate following administration. Quick Reference Terminology and Definitions Systolic blood pressure (SBP) is the pressure within vessels during heart contraction, where oxygen‐rich blood is being pumped into the blood vessels through the aorta. Diastolic blood pressure (DBP) is the pressure within vessels between contractions, when the myocardium is relaxed. Mean arterial pressure (MAP) is defined as the average pressure in a patient’s arteries during one cardiac cycle. MAP is calculated by the following equation: (2(DBP) + SBP)/3, to reflect the fact that the cardiac cycle spends more time in diastole than systole. Hypotension: A blood pressure lower than that required to maintain adequate organ perfusion. We classify hypotension as mild (MAP 45–60 mmHg) or severe (MAP 160 bpm in dogs and >220 bpm in cats (Robinson and Borgeat 2016). Under anaes- thesia, a patient that develops sinus tachycardia should prompt investigation. It is usually in response to sympathetic stimuli (pain), inadequate anaesthesia depth or hypovolemia and hypotension (bleeding). Particular drug administration may also cause sinus tachycar- dia e.g. ketamine or atropine. Tachycardia will reduce the time that the ventricles can fill, which will eventually decrease cardiac output. A fast heart rate requires an increase in myocardial oxygen consumption, but with poor perfusion from the poor ventricular filling time, it can put the heart at risk of life‐threatening arrhythmias if left untreated. Figure 8.9 Sinus tachycardia. Photo credit: Emilia Vukoja. 124 8 Practical ECGs Figure 8.10 Sinus Bradycardia with double-counting (in green) compared to the pulse rate from the pulse oximeter (yellow) – Note that the depolarisation throughout the myocardium is not slow, just its frequency. Sinus Bradycardia In sinus bradycardia, the P‐QRS‐T waves and complexes are normal, but they are conducted at a slower rate than what is expected for the patient breed, life‐stage, and athleticism. Sinus bradycardia is shown in Figure 8.10. It can be defined as a rate of 3 R‐R intervals are absent). Due to the delay in the firing of the SA node, the main pacemaker, pacemaker tissue within the ventricles depolarises independently due to its own lower intrinsic rate. A ventricular escape complex is often referred to as a rescue beat, otherwise, death would be imminent. If there is a series of escape complexes, then this is called an escape rhythm, usually at a rate of 30–40 bpm. As the escape complex is ventricular in origin, there will not be a P wave associated with it and no conduction through the AV node, therefore the complex will be wide and bizarre. A ventricular escape complex is shown in Figure 8.19. It can be seen in dogs that have a heart rate of 30–40 bpm or in cats that have a heart rate of 80–120 bpm (Robinson and Borgeat 2016). Treatment is aimed to correct the bradycardia. A ventricular escape complex should not be treated with lidocaine. A VPC and an escape complex have the same morphology, but it is the timing difference that defines if it is premature (VPC) or after a long pause. Figure 8.19 Ventricular escape complex. Ventricular Arrhythmias As mentioned previously, different parts of the conductive pathway have their own intrin- sic rates which can generate an impulse before the SA node (the pacemaker) discharges. If the ventricles depolarise without the impulse coming through the AV node, the QRS com- plex is wide and bizarre in its morphology. Changes in the patient’s autonomic tone or a systemic inflammatory response may be responsible for ventricular arrhythmias (including an isolated VPC, bigeminy or trigem- iny). This may be seen in a patient without cardiac disease that has undergone abdominal surgery such as patients that have had GDV surgery, or have splenic, gastrointestinal or hepatic disease (Robinson and Borgeat 2016). Three common ventricular arrhythmias that may be seen under anaesthesia are: Ventricular tachycardia Accelerated idiopathic ventricular rhythm (AIVR) Ventricular fibrillation 132 8 Practical ECGs Ventricular Tachycardia Ventricular tachycardia (VT) is when there are four or more VPCs in succession. It can be further classified as paroxysmal VT if there are only a short burst of VPCs, or as sustained or unsustained (e.g. lasting 30 seconds, respectively). The heart rate is usually over 180 bpm, but can often be between 200 and 300 bpm. This fast and uncoordinated rate does not allow the ventricles to fill with blood. This type of arrhythmia is often haemodynami- cally unstable, if not already pulseless. VT can be treated with a common 1b antiarrhythmic agent such as lidocaine (a 2 mg kg−1 slow IV bolus over 1–2 minutes). This aims to disrupt the sodium channels in the heart and slow down the rate of ventricular depolarisation. The bolus can be repeated after 10 min- utes to a maximum of 8 mg kg−1. A lidocaine CRI can also be administered at a rate of 25–100 mcg/kg/minute in dogs (Robinson and Borgeat 2016). Care should be taken when using lidocaine in cats as they are more at risk of toxicities from lidocaine. If the VT becomes polymorphic, i.e. ventricular complexes that have many different ampli- tudes and widths, this may put the patient at risk of VF and death (Robinson and Borgeat 2016). Ventricular tachycardia is shown in Figure 8.20. Figure 8.20 Ventricular tachycardia. Accelerated Idiopathic Ventricular Rhythm AIVR has previously been described as ‘slow VT’ as the ventricular morphology is s­ imilar. An AIVR is in between an escape rhythm and VT, often at a rate of 100–200 bpm. The QRS com- plexes are wide and bizarre, but as the heart rate is normal for that patient in comparison to a VT, there is adequate time for the ventricles to fill. AIVR is shown in Figure 8.21. Systemic causes for AIVR include anaemia and opioids that slow the SA discharge rate. AIVR is usually self‐limiting and haemodynamically stable, not requiring treatment. However, if the AIVR is affecting the blood