Veterinary Technician's Manual for Small Animal Emergency and Critical Care

Veterinary Technician’s Manual for

Small Animal Emergency and Critical Care

Companion website This book is accompanied by a companion website: www.wiley.com/go/norkus The website includes: •  Multiple-Choice Review Questions for each chapter •  Case Studies •  Powerpoints of all figures from the book for downloading

Veterinary Technician’s Manual for

Small Animal Emergency and Critical Care

Edited by Christopher L. Norkus, BS, CVT, VTS (ECC), VTS (Anesthesia)

Ross University School of Veterinary Medicine Basseterre, Saint Kitts, West Indies Cummings School of Veterinary Medicine at Tufts University North Grafton, Massachusetts

A John Wiley & Sons, Inc., Publication

This edition first published 2012 © 2012 by John Wiley & Sons, Ltd. Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical and Medical business with Blackwell Publishing. Registered office: John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial offices: 2121 State Avenue, Ames, Iowa 50014-8300, USA The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 9600 Garsington Road, Oxford, OX4 2DQ, UK For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/ wiley-blackwell. Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by Blackwell Publishing, provided that the base fee is paid directly to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payments has been arranged. The fee codes for users of the Transactional Reporting Service are ISBN-13: 978-0-8138-1057-7/2012. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Library of Congress Cataloging-in-Publication Data Veterinary technician’s manual for small animal emergency and critical care / edited by Christopher L. Norkus.     p. ; cm.   Includes bibliographical references and index.   ISBN-13: 978-0-8138-1057-7 (pbk. : alk. paper)   ISBN-10: 0-8138-1057-4 (pbk. : alk. paper)  1.  Veterinary emergencies.  I.  Norkus, Christopher L.   [DNLM: 1.  Emergency Treatment–veterinary.  2.  Pets.  SF 778]   SF778.V585 2011   636.089'6025--dc23 2011021941 A catalogue record for this book is available from the British Library. Set in 10/12 pt Sabon by Toppan Best-set Premedia Limited

Disclaimer The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation warranties of fitness for a particular purpose. No warranty may be created or extended by sales or promotional materials. The advice and strategies contained herein may not be suitable for every situation. This work is sold with the understanding that the publisher is not engaged in rendering legal, accounting, or other professional services. If professional assistance is required, the services of a competent professional person should be sought. Neither the publisher nor the author shall be liable for damages arising herefrom. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read.

1  2012

This book is dedicated to Charles P. Gandal, DVM I “kept the faith” after all these years. and The Ross University School of Veterinary Medicine Class of May 2011, “Pink for life.”

Contents

Contributors Preface Acknowledgment

ix xi xiii

Section 1: Initial Patient Management 1: Triage and Initial Assessment of the Emergency Patient Amy N. Breton

5

2: Shock and Initial Stabilization Jennifer Keefe

25

3: Venous Access Kara B. Trent

45

4: Monitoring the Critical Patient Trish Farry

63

5: Cardiopulmonary Cerebral Resuscitation Christopher L. Norkus

83

Section 2: Specific Organ System Disorders 6: Cardiovascular Emergencies Christopher L. Norkus

101

7: Respiratory Emergencies Dana Heath and Lori Baden Atkins

127

8: Gastrointestinal Emergencies Amy Campbell

151

9: Urogenital Emergencies Andrea M. Steele

177 vii

viii  Contents

10: Endocrine and Metabolic Emergencies Angela Randels

197

11: Hemolymphatic, Immunologic, and Oncology Emergencies Mary Tefend Campbell

221

12: Neurological Emergencies Sally R. Powell

263

13: Musculoskeletal, Integumentary, and Environmental Emergencies David Liss

283

14: Toxicological Emergencies Christopher L. Norkus

313

15: Reproductive Emergencies Jaime Maher

337

16: Ocular Emergencies Jonathan A. Esmond

355

17: Special Species and Avian Emergencies Kimm Wuestenberg

369

Section 3: Select Emergency/Critical Care Topics and Therapies 18: Critical Care Pharmacology David Liss

389

19: Fluid Therapy, Electrolyte, and Acid–Base Disorders David Liss

433

20: Anesthesia and Analgesia Jennifer K. Sager

465

21: Transfusion Medicine Lindan Spromberg

495

22: Nutrition for the Critically Ill Ann Elise Wortinger

523

Appendices Glossary Index

543 553 559

Companion website This book is accompanied by a companion website: www.wiley.com/go/norkus

Contributors

Lori Baden Atkins, LVT, VTS (Emergency & Critical Care) Veterinary Medical Teaching Hospital Texas A&M University College Station, TX Amy N. Breton, CVT, VTS (Emergency & Critical Care) Veterinary Emergency & Specialty Center of New England Waltham, MA Amy Campbell, CVT, VTS (Emergency & Critical Care) Tufts Veterinary Emergency Treatment & Specialties Walpole, MA Mary Tefend Campbell, CVT, VTS (Emergency & Critical Care) Carriage Hills Animal Hospital and Referral Center Montgomery, AL Jonathan A. Esmond, RVT, VTS (Emergency & Critical Care) Advanced Critical Care & Internal Medicine Tustin, CA; Animal Emergency Clinic of the High Desert Victorville, CA

Trish Farry, CVN, VTS (Emergency & Critical Care), VTS (Anesthesia), Cert IV (TAA) School of Veterinary Science The University of Queensland Australia Dana Heath, RVT, VTS (Emergency & Critical Care), VTS (Anesthesia) Veterinary Medical Teaching Hospital Texas A&M University College Station, TX Jennifer Keefe, CVT, VTS (Emergency & Critical Care), VTS (Anesthesia) Angell Animal Medical Center Boston, MA David Liss, BA, RVT, VTS (Emergency & Critical Care) Veterinary Specialists of the Valley Woodland Hills, CA Jaime Maher, CVT, VTS (Emergency & Critical Care) Cummings School of Veterinary Medicine at Tufts University North Grafton, MA

ix

x  Contributors

Christopher L. Norkus, BS, CVT, VTS (Emergency & Critical Care), VTS (Anesthesia) Ross University School of Veterinary Medicine Basseterre, Saint Kitts, West Indies Cummings School of Veterinary Medicine at Tufts University North Grafton, MA Sally R. Powell, CVT, VTS (Emergency & Critical Care) MJR Veterinary Hospital at the University of Pennsylvania Philadelphia, PA Angela Randels, CVT, VTS (Emergency & Critical Care) VTS (Small Animal Internal Medicine) FIRST Regional Animal Hospital Chandler, AZ Jennifer K. Sager, BS, CVT, VTS (Anesthesia), VTS (Emergency & Critical Care) University of Florida College of Veterinary Medicine Gainesville, FL

Lindan Spromberg, BS, LVT, VTS (Emergency & Critical Care) PIMA Medical Institute Seattle WA Andrea M. Steele, BSc, RVT, VTS (Emergency & Critical Care) Ontario Veterinary College Health Sciences Centre Guelph, Ontario, Canada Kara B. Trent, CVT, VTS (Emergency & Critical Care), VTS (Anesthesia) VCA Veterinary Specialists of Northern Colorado Loveland, CO Ann Elise Wortinger, BIS, LVT, VTS (Emergency & Critical Care), VTS (Small Animal Internal Medicine) Sanford Brown College Dearborn, MI. Kimm Wuestenberg, CVT, VTS (Emergency & Critical Care), VTS (Small Animal Internal Medicine) Phoenix, AZ

Preface

Let’s face it. Our beloved household pets manage to get themselves into lots of trouble.

Essentially, our job in veterinary emergency and critical care medicine is to help get our animal friends out of harms’ ways 24 hours a day, 7 days a week, and 365 days a year. Veterinary Technician’s Manual for Small Animal Emergency and Critical Care serves to provide veterinary paraprofessionals with a cutting edge reference as to the pathophysiology, epidemiology, signs, diagnosis, treatment, and general nursing techniques of the most common veterinary emergencies. The book has been organized into sections following that of the qualifying exam for the Academy of Veterinary Emergency & Critical Care Technicians (AVECCT) and may be a helpful aid for those preparing to write the exam. The end goal of this work, however, is to become a critical and respected resource which expands the knowledge base of veterinary paraprofessionals and, ultimately, results in better patient care and increased know-how when seconds count to save lives. Christopher L. Norkus xi

Acknowledgment

A special thank you is necessary to my best friend Mark Holloway for his superior IT support in rescuing a majority of this book off of my dead laptop after I clumsily spilled soda on it. C.L.N.

xiii

Veterinary Technician’s Manual for

Small Animal Emergency and Critical Care

Section 1 Initial Patient Management

Amy N. Breton

Introduction One of the most important skills as a veterinary technician is the ability to be able to triage quickly and appropriately. Failure to triage appropriately may mean life or death for the patient.

5

CHAPTER 1

1

Triage and Initial Assessment of the Emergency Patient

6  Chapter 1: Triage and Initial Assessment of the Emergency Patient

CHAPTER 1

Triage The term triage comes from the French word that means “to sort” and was first used in World War I to sort and classify wounded soldiers based on the severity of their wounds (Grossman 2003). Emergency departments started using organized triage systems in the 1960s when hospitals began to see more patients than they had available resources for (Grossman 2003).

Telephone Triage The initial triage may actually occur over the phone. Because the technicians cannot rely on their sense of touch, sight, and feel of the patient, technicians who are tasked to handle telephone calls should have strong clinical knowledge, excellent listening and communicating skills, and a sense of intuition (Grossman 2003). A telephone triage log of the calls should be kept. Because it is a legal document, the log should be stored for several years depending on the state laws. It is important to note that several court cases have occurred involving a pet owner and a veterinary clinic because of the advice that was given over the phone. Remember that the recommendations you offer to the client can have legal ramifications, and it is important that you document the conversation to protect both yourself and the clinic. Ideally, an organized system should be in place and all employees should follow the system (Grossman 2003). Each technician should ask the same initial questions of each

Box 1.1  Telephone Triage Questions • • • • •

Name, location, and telephone number of client Pet’s name, age, sex, breed, and weight Pertinent medical history Current medications Current complaint  How is your pet breathing?  What is the color of the gums?  What is the level of consciousness (LOC)?  Current rectal temperature? (if able)  Is the pet able to stand/walk? Other questions may include the following:

• • • • • • •

Is the pet eating? Is there vomiting, retching, or diarrhea? Is the abdomen distended or painful to the touch? Can the pet urinate? Are the urinations normal? Is there any bleeding? Where and how much? How much and when did the pet ingest the substance? How many and how long have the seizures been? Has there been any coughing?

CHAPTER 1

Initial Patient Management  7

Figure 1.1  Cases brought to the emergency room, such as this dog hit by a car, must be triaged and examined quickly to address immediate life threats.

client that calls in order to ensure that each call is handled in a thorough manner. After the initial information is gathered, the questions may vary depending on what the presenting complaint is. Each clinic may have a different policy on what advice can or cannot be given over the phone. No matter what the clinic’s policy is, all owners should be instructed to come in with their pet no matter how insignificant the problem may appear. Because of owner error in interpreting their pet’s condition, it is impossible to appropriately triage an animal over the phone. For example, owners frequently cannot tell if their pet is seizuring versus trembling out of fear. The safest suggestion is to always advise the owner to bring the pet into a veterinary hospital immediately. For legal purposes, it is important that the telephone triage log reflect this recommendation with each phone call. Any medical treatment suggested to clients over the phone must be documented in full in the telephone log. Once you have suggested to the clients that they bring in their pet for a medical treatment, you should provide the owners with information about how to safely transport their pet to the clinic (Davis 2008). This may include placing pressure on a bleeding wound, putting a quick bandage on a bleeding area, keeping the animal immobile, or instructing the owner how to make a muzzle at home to ensure he/she is kept safe. Telephone triage is also important because it allows the medical team to prepare for the arrival of the patient at the hospital and to organize resources (Davis 2008). Intravenous fluids, catheters, oxygen, and crash cart supplies can be readied prior to the patient’s arrival (Fig. 1.1).

Hospital Triage Every patient that enters into the emergency room should be triaged by a veterinary technician within a minute of its arrival. It is better to assume every patient is critical than to allow a critical animal to wait for a triage while it is declining in health. When triaging, it is important to be able to quickly assess each patient and to sort each into categories. All triage systems break down categories into either a three-, four-,

8  Chapter 1: Triage and Initial Assessment of the Emergency Patient

CHAPTER 1

Table 1.1  Triage level acuity systems

3 Levels

Wait/Reassessment Time

Condition Examples

Resuscitative Emergent Urgent

Immediately 10–45 minutes 30 minutes–2 hours

Cardiac arrest Fracture Abscess

4 Levels

Wait/Reassessment Time

Condition Examples

Resuscitative Emergent Urgent Nonurgent

Immediately 5–15 minutes 15–45 minutes 1–2 hours

Active seizures Serious laceration Eye injury Constipation

5 Levels

Wait/Reassessment Time

Condition Examples

Resuscitation Emergent Urgent Semi-urgent Routine

Immediately 5–15 minutes 15–45 minutes 1–2 hours 4 hours

Severe respiratory distress Urinary obstruction Vomiting/diarrhea (no blood) Minor laceration Suture removal

Adapted from Grossman (2003), Quick Reference to Triage.

or five-tier system. While there is not a standard triaging system in veterinary medicine, most human medicine triage systems can be applied. In most human emergency departments in the United States, a triage acuity system is used to determine which patient can safely wait and which patient needs to be seen immediately (Hansen 2005). In 2001, the Emergency Nurses Association of the United States was surveyed to ask what type of triage acuity scale was used by each hospital (Hansen 2005). An overwhelming 69% of the emergency departments used a three-level scale (Hansen 2005). Only two years later, another study was conducted and found that only 47% of emergency departments were using a three-level triage system, while there was an increase to 20% for those that used four-level and 20% that used five-level systems (Hansen 2005; see Table 1.1). The general consensus is that there is a trend toward four- and five-tier systems in hospitals. No matter what system is used, one thing is certain: the system should be organized and everyone at the clinic should use it. In 1994, the animal trauma triage (ATT) scoring system was created (Table 1.2). The ATT scoring system is a way to classify and help predict the likelihood of a patient’s survival after a traumatic incident (Wingfield and Raffe 2002). The system classified six different categories (perfusion, cardiac, respiratory, eye/muscle integument, skeletal, and

Table 1.2  The animal trauma triage scoring system

Grade

Perfusion

Cardiac

Respiratory

Eye/Muscle Integument

Skeletal

Neurological

0

Mucous membrane (MM) pink/moist

HR:

Normal respiratory rate

Abrasions, lacerations: only partial thickness

Weight bearing on 3–4 limbs

Central: conscious and alert

Eyes: normal

No fractures or joint laxity

Mild increased respiratory rate and effort

Abrasions, lacerations: full thickness but no deep tissue involvement

Closed fracture

Mild increase upper airway sounds

Eye: corneal laceration/ ulcer

Temp: >100°F Pulses strong or bounding 1

MM pale pink or hyperemic Temp: >100°F Pulses fair

2

K9: 60–140 F: 120–200

Peripheral: normal

NSR

HR: K9:140–180 F: 200–260 NSR or Ventricular premature complexes PCs (160 bpm in large dogs, >180 bpm in small dogs, and >240 bpm in cats (Ettinger and Feldman 2005). Other proposed indications for drug treatment of ventricular excitability include when “R on T phenomena” is observed, when VPDs are highly polymorphic, or whenever CO appears compromised. Because ventricular flutter is a severe form of VT and rapidly deteriorates into ventricular fibrillation, it warrants immediate treatment. Although the causes and appearance of AIVR are the same as with VT, AIVR does not require treatment because the slower ventricular rate does not compromise ventricular filling time and therefore is generally well tolerated by the patient. Treatment for unstable VT and ventricular flutter are identical to that of VPDs. Lidocaine is often selected as an initial drug of choice in the dog, being initially administered at 2 mg/kg IV and repeated as necessary up to a total dose of 8 mg/kg. When the VT or ventricular flutter has converted to a more stable rhythm, a CRI of lidocaine at 40– 75 mcg/kg/min is selected (Rozanski and Rush 2007). If the lidocaine is initially ineffective, another drug should be selected. Because of concern of lidocaine toxicity in cats,

Specific Organ System Disorders  123

many either do not use lidocaine as their first choice of antiarrhythmic drug for VT and ventricular flutter in cats, often selecting propanolol instead, or just use lidocaine at a reduced dose. Patients who do not respond to drug therapy should also have their electrolyte levels checked with specific attention paid to potassium and magnesium. Deficiencies in these electrolytes may need to be corrected before drug therapy will be successful.

AV blocks AV blocks are disturbances of conduction between the atria and ventricle. Such conduction disturbances can be as simple as a delay or as profound as a complete stoppage. As a result, clinical signs can vary from nonexistent to potentially life-threatening. First degree AV block.  First degree AV block is a simple delay of conduction from the atria to the ventricles. Although conductance is slowed, each impulse does successfully cross to the AV node. A prolonged PR interval with a normal sinus appearing QRS complex is necessary for the diagnosis. There are no clinical manifestations of first degree AV block, and the arrhythmia requires no treatment. Second degree AV block.  Second degree AV block is the result of a complete but transient interruption of conductance from the atria to the ventricles. As a result, P waves are present for every QRS complex but a QRS complex does not exist for every P wave. Second degree AV block is further divided into two subclasses: Mobitz Type 1, which is characterized by a progressive lengthening of the PR interval which ultimately results in a P wave that occurs without a QRS complex (Fig. 6.18), and Mobitz Type 2, which demonstrates perfectly regular PR intervals for all QRS complexes, but one or more P wave lacks a corresponding QRS complex (Fig. 6.19). Depending on the ventricular rate and its impact on CO, clinical signs may be absent and require no treatment whatsoever or may produce exercise intolerance, lethargy, syncope, or hypoxic seizures (Stokes–Adams seizures) and require drug intervention.

Direct

ECG

Lead II

Filter

20 mm/mv

Figure 6.18  An ECG tracing showing a Mobitz Type 1 second degree AV block. (Courtesy of Kristen Cooley, BA, CVT, VTS [Anesthesia].)

CHAPTER 6

Torsades de Pointes.  Torsades de Pointes is an uncommon form of VT that arises from a prolongation of the QT interval (Ettinger and Feldman 2005). The appearance of Torsades de Pointes on the ECG is that of a ribbon. Causes of the disturbance include hypokalemia, hypocalcemia, and antiarrhythmia drug toxicity (Ettinger and Feldman 2005). Treatment for the rhythm is highly specific and includes discontinuation of all antiarrhythmic drugs and administration of intravenous magnesium sulfate at 20–30 mg/kg IV slowly (Ettinger and Feldman 2005).

124  Chapter 6: Cardiovascular Emergencies T1 = – –T2 = 70.3F 05/18/2010 10:42:03 25mm/sec delay = 6 (0X) HR = – – SPO2 = – – 1) ECG 10mm/mv Lead II 2) AR1 –10–20mmHg ∗UNPLUGGED

Figure 6.19  An ECG tracing showing a Mobitz Type 2 second degree AV block. (Courtesy of Kristen Cooley, BA, CVT, VTS [Anesthesia].) 7:11:44 AM

CHAPTER 6

MEDTRONIC PHYSIO-CONTROL

P/N 804700

Figure 6.20  An ECG tracing showing a complete third degree AV block.

The common causes of second degree AV block may include high resting vagal tone, antiarrhythmic agents, opioids, alpha-2 adrenergic agonists, cardiac disease with atrial dilation, and AV nodal lesions (Ettinger and Feldman 2005). Treatment, if necessitated by diminished CO or clinical signs, is first directed at the underlying cause whenever possible. Acute drug therapy includes parasympatholytic agents (e.g., atropine, glycopyrrolate) and sympathomimetic agents (e.g., dopamine, dobutamine, isoproterenol, epinephrine). Cases that do not respond to drug therapy require pacemaker implantation. Third degree AV block.  Third degree AV block is a complete failure of conductance and total dissociation of the atria and the ventricles (Fig. 6.20). On ECG, there is no consistent PR interval. P waves occur variably with or without QRS complexes. In some cases, P waves may even occur during a QRS complex. The ventricular rate during third degree AV block is generally slow. As a result, marked lethargy, exercise intolerance, weakness, and syncope may result. Some patients may not always exhibit clinical signs (e.g., cats) and may not require treatment. The causes of third degree AV block include alpha-2 agonist administration, hyperkalemia, cardiac glycoside toxicity, Lyme disease, endocarditis, traumatic myocarditis, cardiomyopathies, endocardiosis, or myocardial fibrosis (Ettinger and Feldman 2005). Treatment for third degree AV block is aimed at the underlying cause. Drug therapy includes parasympatholytic agents (e.g., atropine, glycopyrrolate) and sympathomimetic agents (e.g., dopamine, dobutamine, isoproterenol, epinephrine) but is generally unrewarding. Symptomatic cases that fail to respond to drug therapy require pacemaker implantation.

References Ettinger, SJ, Feldman, EC. 2005. Textbook of Veterinary Internal Medicine, 6th ed. St. Louis, MO: Elsevier Saunders. Evans, H. 1993. Miller’s Anatomy of the Dog, 3rd ed. Philadelphia: Saunders.

Specific Organ System Disorders  125

CHAPTER 6

Goutal, C, Keri, I, Kenney, S. 2010. Evaluation of acute congestive heart failure in dogs and cats: 145 cases (2007–2008). J Vet Emerg Crit Care 20(3):330–337. Humm, K, Keenaghan-Clarke, E, Boag, A. 2009. Adverse events associated with pericardiocentesis in dogs: 85 cases (1999–2006). J Vet Emerg Crit Care 19(4):352–356. Moore, K, Morris, N, Dhupa, N, et al. 2007. Retrospective study of streptokinase administration in 46 cats with arterial thromboembolism. J Vet Emerg Crit Care 10(2):103–106. Oyama, MA, Rush, JE, Rozanksi, EA, et al. 2009. Assessment of serum N-terminal proB-type natriuretic peptide concentration for differentiation of congestive heart failure from primary respiratory tract disease as the cause of respiratory signs in dogs. J Am Vet Med Assoc 235:1319–1325. Plunkett, SJ. 2001. Emergency Procedure for the Small Animal Veterinarian, 2nd ed. Philadelphia: W.B. Saunders. Rozanski, EA, Rush, JE. 2007. Small Animal Emergency and Critical Care Medicine, 1st ed. London: Manson.

7

Respiratory Emergencies

CHAPTER 7

Dana Heath and Lori Baden Atkins

Introduction Respiratory disorders are common in small animals and account for a significant number of emergency visits and hospitalizations. Respiratory distress or dyspnea may be a direct result of toxin exposure, trauma, an acute exacerbation of chronic conditions, secondary to infectious processes, or fluid shifts. Patients in respiratory distress are often anxious and are easily stressed. Physical examination, diagnostics, and treatments may need to be staged and the patient allowed to rest in an oxygen-rich environment between procedures. Overzealous handling of respiratory distress patients, particularly felines, may significantly worsen dyspnea and can have fatal consequences.

127

128  Chapter 7: Respiratory Emergencies

CHAPTER 7

Anatomy of the Respiratory System The main function of the respiratory system is to provide the body with a continuous source of gas exchange between the inspirited air and the circulatory system. This gas exchange system includes supplying the body with oxygen during inspiration and removing carbon dioxide (CO2) during expiration. Room air at sea level contains 21% oxygen. Upon inspiration, oxygen enters the body through the nose or mouth, travels through the pharynx and on to the trachea. The trachea enters the chest thoracic cavity and then divides at the carina into two bronchi and enters the lungs. Each bronchi serves to provide oxygen to one lung; the left bronchi supporting the left lung and the right bronchi supporting the right lung. The left lung is made up of a cranial, middle, caudal, and accessory lung lobe. The left lung, however, is composed only of a cranial and caudal lobe, with the cranial lobe having a cranial and caudal portion. With each lung lobe, their respective bronchi then divide further into smaller bronchioles. Finally at the end of each smaller bronchiole are clusters of alveoli. It is here at the alveoli where gas exchange with the circulatory system occurs via the alveolar–capillary membrane. The pleura is a thin membrane that encases the lungs and covers the inner walls of the thoracic cavity. This membrane is covered with a thin film of serous fluid, which provides lubrication as the lungs expand and contract within the thoracic cavity. The area within the pleura is called the pleural cavity and is normally in a state of negative pressure. This negative pressure or vacuum causes the lungs to expand and contract in conjunction with the expansion and contraction of the thoracic cavity. Loss of the normal negative pressure within the thoracic cavity typically results in respiratory distress and may lead to collapse of one or more lung lobes.

Mechanics of Normal Respiration Normal respiration is dependent upon the contraction and relaxation of the diaphragm, the contraction and relaxation of the chest and abdominal muscles, and the negative pressure that exists within the pleural cavity. Inspiration occurs as contraction of the diaphragm, and forward, outward movement of the ribs and chest muscles enlarge the thoracic cavity. The abdominal muscles relax, allowing the abdominal organs to move caudally as the diaphragm contracts. The expansion of the thoracic cavity causes expansion of the lungs, and air is drawn in through the bronchial tree and into the alveoli. Following inspiration, the muscles of the abdomen contract and push the abdominal organs forward into the caudal aspect of the diaphragm. The diaphragm is pushed forward into the thoracic cavity as it returns to its normal, resting position. The muscles of the chest draw the ribs inward toward the chest. These actions decrease the size of the thoracic cavity and expel air out of the lungs in expiration.

Respiratory Physiology Delivery of Oxygen Adequate tissue oxygenation is governed by a combination of processes including external respiration, oxygen transport, and internal respiration. Any impairment of these processes

may lead to inadequate oxygenation of the tissues and subsequent cellular damage or death. External respiration involves the inhalation of oxygen into the lungs, diffusion of oxygen molecules onto the red blood cells, and exhalation of CO2. During normal respiration, air is drawn into the nasal passages where is it warmed and humidified as it passes over the nasal turbinates en route to the lungs. Once air reaches the alveoli, oxygen diffuses through the alveolar–capillary membrane, where it binds with the hemoglobin (Hb) in the red blood cells (RBCs) to form oxyhemoglobin (HbO2). Oxygen transport involves the ability to move oxygen from the alveoli to the tissues. Hb is the primary carrier of oxygen; each molecule has the capacity to carry four oxygen molecules. Under normal physiological conditions, it is assumed that Hb will bind oxygen to all four sites and will have an oxygen saturation (SaO2) of >97%. Once oxygen is bound by Hb, it is transported to the tissues as blood is circulated throughout the body by the cardiovascular system. At the cellular level, oxygen molecules disassociate from the Hb and diffuse into the cells. Approximately 80%–90% of the oxygen diffused into the cell is consumed by the mitochondria during production of adenosine triphosphate (ATP), which is then utilized by cell for energy.

CO2 CO2 is the major by-product of cellular oxygen metabolism. Although often thought of as a waste product, CO2 actually plays a significant role in maintaining acid–base balance. CO2 combines with water (H2O) to form carbonic acid, which quickly dissolves into hydrogen ions (H+) and bicarbonate ions (HCO3−). The pH is directly affected by the ratio of CO2 to HCO3−. The primary route for excretion of CO2 is through exhalation following transport to the alveoli. After conversion of CO2 into HCO3−, a chloride shift occurs as HCO3− are released into the plasma by the RBCs in exchange for chloride ions. Bicarbonate is transported to the alveoli in the plasma, where it combines with hydrogen ions to form carbonic acid, and is then separated into CO2 and water. The CO2 diffuses across the alveolar–capillary membrane and is exhaled as a waste gas. A small amount (∼20%) of CO2 binds to Hb as carbaminohemoglobin and is exchanged for oxygen at the alveoli without further chemical conversion.

Hypoxemia versus Hypoxia There are a number of terms used to describe oxygenation and ventilation; an understanding of these terms is essential. Oxygenation—Saturation with oxygen. Ventilation—The exchange of oxygen and CO2 through inhalation and exhalation. Hypoxemia—Deficiency of oxygen within the blood. Patients breathing room air at sea level are considered hypoxemic when the partial pressure of oxygen in arterial blood (PaO2) is less than 80 mmHg. Hypoxia—Decreased oxygenation of the tissues. Anemic hypoxia—Decreased oxygenation of the tissues secondary to decreased level of Hb. Anemic hypoxia may also be observed in conditions where the Hb

CHAPTER 7

Specific Organ System Disorders  129

130  Chapter 7: Respiratory Emergencies

is unable to bind and transport oxygen such as methemoglobinemia and carboxyhemoglobinemia. Ischemic hypoxia—Decreased oxygenation of the tissues secondary to decreased perfusion. Ischemic hypoxia may be global as demonstrated by hypovolemic or cardiogenic shock or local as demonstrated by thromboembolic disease.

CHAPTER 7

Causes of Hypoxemia Hypoxemia may be caused by any number of conditions that interfere with the body’s ability to access oxygen during respiration and transport the oxygen molecules to the RBCs. A decreased fractional inspired oxygen concentration (FiO2) may result in hypoxemia. A healthy patient breathing room air (FiO2 = 21%) is expected to have a PaO2 of 80–100 mmHg (PaO2 = 4−5 × FiO2). This is sometimes referred to as the 5 times inspired rule. When the concentration of inspired oxygen is decreased, the patient’s PaO2 should decrease in a corresponding manner. Increasing the percentage of inspired oxygen easily treats this form of hypoxemia. Hypoventilation may result in hypoxemia as CO2 replaces oxygen within the alveoli, with a subsequent decrease in the PaO2. Hypoventilation is manifested by an increase in the partial pressure of CO2 in arterial blood (PaCO2); patients with a PaCO2 > 40 mmHg are considered to be hypoventilating. Oxygen therapy may be temporarily beneficial in the hypoventilatory patient, but definitive treatment requires assisted or mechanical ventilation to allow the removal of CO2. The arterial CO2 concentration provides the primary impetus for alveolar ventilation. In the normal patient, ventilation increases as the PaCO2 rises and conversely decreases as the PaCO2 falls. This homeostatic mechanism may not be functional in certain conditions and disease states including depression of the respiratory center by certain drugs or anesthetics, diseases affecting the central nervous system (CNS), and diseases of the respiratory muscles or chest wall. Patients with these conditions are not able to compensate by increasing ventilation as the PaCO2 rises. Oxygen therapy, without assisted ventilation, should be used cautiously in these patients. In the presence of severe hypercapnia (PaCO2 > 80 mmHg), regulation of ventilatory drive in response to CO2 fails and hypoxia becomes the trigger for ventilation. Hypoxemia is often secondary to conditions that interfere with oxygen diffusion through the alveoli and into the capillaries. Diffusion is typically discussed as the relationship between alveolar ventilation (V) and pulmonary blood flow or perfusion (Q); inequality in this relationship denotes impaired diffusion and is termed V/Q mismatch. Pulmonary thromboembolism results in a very high V/Q mismatch as the lung is adequately oxygenated while perfusion is decreased. Asthma, pneumonia, pulmonary edema, and any other pulmonary disease that results in poor ventilation or partial alveolar collapse may result in a low V/Q mismatch due to decreased oxygen availability with adequate perfusion. Other causes of V/Q mismatch include pulmonary dead space and pulmonary shunting. Oxygen therapy may be efficacious for low V/Q mismatch but frequently needs to be augmented by positive end expiratory pressure (PEEP) in order to maximize the oxygen delivery to the alveoli.

Causes of Hypoxia Hypoxia frequently develops following hypoxemia, unless effective intervention is employed. Anemia is a common initiator of hypoxia. Any functional decrease in the

number of RBCs or the Hb concentration of the RBCs results in a net decrease in the oxygen-carrying capacity of the blood. The normal Hb concentration for dogs and cats is ∼12–15 g Hb/dL. Additionally, any chemical change that impairs the Hb from binding with oxygen molecules may cause a significant decrease in the oxygen-carrying capacity of the blood. Patients exposed to carbon monoxide will form carboxyhemoglobin. Due to its high affinity for Hb (∼218× greater than oxygen), carbon monoxide will bind to the Hb molecules, rendering them nonfunctional in an oxygen-carrying capacity. Methemoglobinemia may be observed secondary to acetaminophen toxicity in cats and other toxins such as nitrites, phenol, sulfites, and naphthalene in both cats and dogs. Every 1.5 g/dL of methemoglobin is equivalent to a 5 g/dL decrease in functional Hb. Treatment of anemic hypoxia should involve replacement of functional RBCs or Hb through blood transfusion or Oxyglobin® (OPK Biotech LLC, Cambridge, MA) and concurrent oxygen supplementation. Treatment of the underlying cause of anemia is typically required to achieve a long-term positive outcome. Ischemic hypoxia results from inadequate perfusion, resulting in decreased tissue oxygenation. Conditions such as hypovolemic shock, circulatory failure, and severe hemorrhage classically result in decreased tissue perfusion throughout the body and a corresponding decrease in the delivery of oxygen to the tissues. Localized hypoxia may result from loss of perfusion to specific organs or regions as seen in thromboembolic disease. Treatment of ischemic hypoxia involves increasing perfusion. In addition to volume replacement, effective treatment of hypovolemic shock must also address the underlying cause. Bleeding due to laceration may be controlled by the use of a pressure bandage, while hemorrhage caused by hepatic or splenic rupture will typically require immediate surgical intervention. Treatment of circulatory failure must focus on improving cardiac output, thereby restoring tissue perfusion and oxygenation. Oxygen therapy should be instituted concurrently with restoration of perfusion.

Assessment of Oxygenation and Ventilation Observation of either increased or depressed respiratory effort is a common indicator of hypoventilation and possible hypoxemia. Conditions that lead to decreased lung compliance such as pneumonia, pleural effusion, and pulmonary edema are typified by a pattern of rapid, shallow breathing; obstructive conditions such as asthma and laryngeal paralysis are characterized by slow, deep breaths. Observations should be made regarding the phase of ventilation requiring increased effort: is the patient working harder during the inspiratory phase or the expiratory phase? Increased inspiratory effort is consistent with diseases of the upper airway such as laryngeal paralysis while increased expiratory effort is associated with obstructive conditions of the lower airway such as asthma. Observation of a significant abdominal effort with minimal thoracic excursions during ventilation may be indicative of hypoventilation. Dyspneic patients frequently modify their posture to reduce airway resistance; elevation of the head and extension of the neck straightens the trachea while abduction of the elbows minimizes compression of the chest wall. Physical evaluation of the clinically dyspneic patient must be approached with caution, especially in the cat. These patients are often very unstable; diagnostics and treatments are usually performed in stages to avoid further stress to the patient. Mucous membrane (MM) color and capillary refill time (CRT) may be easily assessed and may yield significant

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Specific Organ System Disorders  131

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information regarding the patient’s oxygenation and perfusion status. Cyanotic mucous membranes indicate severe hypoxemia; the SaO2 of arterial blood is typically