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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
A state-of-the-art reference for all aspects of thoracic surgery in dogs and cats Written by two of the foremost experts in this area of surgery, Small Animal Thoracic Surgery encompasses both basic and advanced thoracic surgery for dogs and cats. It provides a host of well-illustrated techniques for thoracic surgery, including classic open surgery, minimally invasive surgery, thoracoscopy, and image-guided hybrid surgery. This comprehensive and detailed book will help improve outcomes of thoracic cavity operations in small animal patients. Small Animal Thoracic Surgery provides the most current and complete information available on this challenging area of surgery. The book offers guidance for treating the many disorders that can affect the canine and feline thoracic cavity, including pleural effusions, pneumothorax, hernias, heart disease, and more. Small Animal Thoracic Surgery: * Presents step-by-step descriptions of thoracic surgeries ranging from basic to advanced * Features high-quality illustrations that depict key steps for each procedure * Covers emerging minimally-invasive procedures, including thoracoscopy * Offers up-to-date information for surgical treatment of ailments of the heart and lungs * Provides video clips of procedures on a companion website An invaluable reference for veterinary surgeons, Small Animal Thoracic Surgery is also an ideal aid for general practitioners who perform some of the basic procedures in their clinics.
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Veröffentlichungsjahr: 2017
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Small Animal Thoracic Surgery
E. Christopher Orton, DVM, PhD
Diplomate, American College of Veterinary SurgeonsProfessorColorado State UniversityFort Collins, Colorado, U.S.A.
Eric Monnet, DVM, PhD
Diplomate, American College of Veterinary SurgeonsDiplomate, European College of Veterinary SurgeonsProfessorColorado State UniversityFort Collins, Colorado, U.S.A.
Illustrated by:
Molly Borman, MSwww.mborman.com
Thomas O. McCracken, MS
This edition first published 2018© 2018 John Wiley & Sons, Inc.
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The right of E. Christopher Orton and Eric Monnet to be identified as the authors of this work has been asserted in accordance with law.
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Library of Congress Cataloging-in-Publication Data
Names: Orton, E. Christopher, author. | Monnet, Eric, author. Title: Small animal thoracic surgery / by E. Christopher Orton, Eric Monnet ; illustrated by Molly Borman, Thomas O. McCracken. Description: Hoboken, NJ : Wiley, 2017. | Revised and updated version of: Small animal thoracic surgery / E. Christopher Orton ; illustrated by Thomas O. McCracken ; contributing author, James S. Gaynor. 1995. | Includes bibliographical references and index. | Identifiers: LCCN 2017030438 (print) | LCCN 2017031919 (ebook) | ISBN 9781118943434 (pdf) | ISBN 9781118943441 (epub) | ISBN 9781118943410 (cloth) Subjects: | MESH: Dog Diseases--surgery | Cat Diseases--surgery | Thoracic Surgical Procedures--veterinary | Thoracic Diseases--veterinary Classification: LCC SF991 (ebook) | LCC SF991 (print) | NLM SF 992.R47 | DDC 636.089/754--dc23 LC record available at https://lccn.loc.gov/2017030438
Cover Design: Wiley Cover Images: Illustrations by Molly Borman
This book is dedicated to our patients, who have been our greatest teachers, and their families,who have shown us the depth of the bond between species.
Christopher OrtonEric Monnet
CONTENTS
Cover Page
Title Page
Copyright Page
Preface
About the Companion Website
Section I General Principles
1 Cardiopulmonary Function
The Oxygen Pathway
Ventilation
Pulmonary Gas Exchange
Oxygen Saturation and Oxygen Content
Oxygen Delivery, Oxygen Consumption, and Oxygen Extraction
Cardiac Output
Heart Failure
Summary
References
2 Cardiopulmonary Monitoring and Supportive Care
Ventilation
Gas Exchange
Blood Pressure
Cardiac Output
Heart Rate and Rhythm
3 Instrumentation
Section II Thoracic Approaches
4 Thoracotomy
Intercostal Thoracotomy
Postoperative Management
References
5 Sternotomy
Postoperative Care
Reference
6 Minimally Invasive Thoracic Surgery
Minimal-Incision Thoracotomy
Video-Assisted Thoracoscopic Surgery (VATS)
Image-Guided Interventions
References
Section III Thoracic Wall and Pleural Space
7 Thoracostomy and Pleural Drainage
Thoracocentesis
Thoracostomy Tubes
Long-Term Pleural Drainage
References
8 Thoracic Wall
Structure and Function
Trauma
Thoracic Wall Neoplasia
Pectus Excavatum
References
9 Pleural Effusions
Structure and Function
Diagnosis
Pyothorax
Chylothorax
Neoplastic Pleural Effusion
References
10 Pneumothorax
Diagnosis
Treatment
References
Section IV General Thoracic Surgery
11 Thymoma and Mediastinal Masses
Diagnosis
Surgery for Cranial Mediastinal Masses
References
12 Esophagus
Structure and Function
Surgical Conditions of the Esophagus
Surgery of the Esophagus
References
13 Vascular Ring Anomalies
Types of Vascular Ring Anomaly
Diagnosis
Surgery
References
14 Trachea
Structure and Function
Temporary Tracheostomy
Permanent Tracheostomy
Traumatic Tracheal Injury
Tracheal Resection and Anastomosis
Tracheal Rupture
Tracheal Collapse
References
15 Lung
Structure and Function
Surgical Conditions of the Lung
Diagnosis
Surgery
References
16 Diaphragm
Structure and Function
Surgical Conditions of the Diaphragm
Surgery of the Diaphragm
Care after Surgery
References
Section V Cardiac Surgery
17 Pericardium
Structure and Function
Pathophysiology
Pericardial Effusion
Constrictive Pericarditis
References
18 Strategies for Cardiac Surgery
Beating Heart Surgery
Venous Inflow Occlusion
Cardiopulmonary Bypass
Hybrid Cardiac Surgery
References
19 Patent Ductus Arteriosus
Pathophysiology
Diagnosis
Indications for Surgery
PDA Ligation
Division of PDA
Expected Outcomes
References
20 Pulmonary and Aortic Valves
Pulmonary Stenosis and Pulmonary Outflow Obstructions
Subvalvular Aortic Stenosis
Aortic Insufficiency
References
21 Tricuspid and Mitral Valves
Congenital Tricuspid Valve Dysplasia
Mitral Regurgitation
References
22 Congenital Septal Defects
Ventricular Septal Defect
Atrial and Atrioventricular Septal Defect
Tetralogy of Fallot
References
23 Cor Triatriatum and Double-Chambered Right Ventricle
Cor Triatriatum
Double-Chambered Right Ventricle
References
24 Cardiac Neoplasia
Hemangiosarcoma
Intracavitary Cardiac Masses
Heart Base Tumors
References
25 Epicardial Pacemaker Implantation
Epicardial Pacing
Epicardial Pacemaker Implantation
Post-Operative Care
References
Index
WILEY END USER LICENSE AGREEMENT
List of Table
Chapter 9
Table 9.1
Chapter 21
Table 21.1
List of Illustrations
Chapter 1
Figure 1.1
Oxygen Pathway
Figure 1.2
Work of Breathing
Figure 1.3
Oxygen-Hemoglobin Saturation Curve
Figure 1.4
Cardiac Pressure-Volume Relationship
Figure 1.5
Cardiac Preload
Figure 1.6
Cardiac Afterload
Figure 1.7
Cardiac Contractility
Figure 1.8
Determinates of Cardiac Output
Figure 1.9
Heart Failure
Chapter 2
Figure 2.1
Pulse Oximetry and Capnography
Figure 2.2
Systemic Blood Pressure—Indirect Doppler
Figure 2.3
Systemic Blood Pressure—Direct Percutaneous
Figure 2.4
Systemic Blood Pressure—Direct Seldinger
Figure 2.5
Central Venous Pressure
Figure 2.6
Jugular Introducer Catheter
Figure 2.7
Swan-Ganz Pulmonary Catheter
Figure 2.8
Tachyarrhythmias
Chapter 3
Figure 3.1
Finochietto Retractors
Figure 3.2
Scalpel Handles and Blades
Figure 3.3
DeBakey Tissue Forceps
Figure 3.4
Scissors
Figure 3.5
Needle Holders
Figure 3.6
Angled Thoracic Forceps
Figure 3.7
Hand Retractors
Figure 3.8
Vascular Clamps
Figure 3.9
Tangential Vascular Clamps
Chapter 4
Figure 4.1
Intercostal Thoracotomy
Figure 4.2
Thoracotomy Retraction
Figure 4.3
Thoracotomy Closure
Chapter 5
Figure 5.1
Sternotomy
Figure 5.2
Extension of Sternotomy Approach
Figure 5.3
Closure of Sternotomy
Chapter 6
Figure 6.1
Minimal-Incision Thoracotomy
Figure 6.2
Endoscopes and Cable (© KARL STORZ GmbH & Co. KG)
Figure 6.3
Endoscopic Tower (© KARL STORZ GmbH & Co. KG)
Figure 6.4
0° and 30° Endoscopes
Figure 6.5
Thoracoscopic Ports
Figure 6.6
Instruments for Thoracoscopic Surgery
Figure 6.7
Articulating and Curved Endoscopic Stapling Devices
Figure 6.8
Thoracoscopic Approach—Intercostal
Figure 6.9
Thoracoscopic View—Subxyphoid Approach
Figure 6.10
Arndt Endobronchial Blocker with Adapter
Figure 6.11
Transapical Approach for Hybrid Cardiac Surgery
Figure 6.12
Transcatheter Mitral Valve Implantation
Chapter 7
Figure 7.1
Thoracocentesis
Figure 7.2
Thoracostomy Tube Placement
Figure 7.3
Finger-Cuff Suture
Figure 7.4
Small-Caliber Thoracostomy Tube with Guidewire
Figure 7.5
Bottle System for Continuous Drainage
Figure 7.6
Subcutaneous Pleural Drainage
Chapter 8
Figure 8.1
Basket-Weave Repair of Intercostal Laceration
Figure 8.2
External Splint for Flail Chest
Figure 8.3
Rib Fracture Repair
Figure 8.4
Thoracic Wall Resection
Figure 8.5
Latissimus Dorsi Rotation Flap
Figure 8.6
Mesh Reconstruction of Thoracic Wall
Figure 8.7
Plate Reconstruction of Thoracic Wall
Figure 8.8
Diaphragm Advancement for Thoracic Reconstruction
Chapter 9
Figure 9.1
Mediastinectomy
Figure 9.2
Caval-to-Atrial Conduit
Figure 9.3
Pulmonary Decortication
Figure 9.4
En bloc
Thoracic Duct Ligation
Chapter 10
Figure 10.1
Traumatic Pulmonary Bleb
Figure 10.2
Traumatic Pulmonary Hematoma
Figure 10.3
Emphysematous Bullae
Figure 10.4
Pulmonary Bleb
Chapter 11
Figure 11.1
Surgical Resection—Thymoma
Figure 11.2
Thoracoscopic Resection— Thymoma
Chapter 12
Figure 12.1
Esophagotomy
Figure 12.2
Transdiaphragmatic Gastrotomy
Figure 12.3
Esophageal Resection and Anastomosis
Figure 12.4
Esophageal In-Lay Patch from Diaphragm
Chapter 13
Figure 13.1
Types of Vascular Ring Anomaly
Figure 13.2
Endoscopic View of Persistent Right Aortic Arch
Figure 13.3
Surgery for Persistent Right Aortic Arch
Figure 13.4
Thoracoscopic Surgery for Vascular Ring Anomaly
Figure 13.5
Esophageal Resection for Vascular Ring Anomaly
Chapter 14
Figure 14.1
Tracheostomy Tubes
Figure 14.2
Tracheostoomy
Figure 14.3
Permenent Tracheostomy
Figure 14.4
Tracheal Resection and Anastamosis
Figure 14.5
Ring Tracheoplasty
Figure 14.6
Tracheal Stenting for Collapsing Trachea
Chapter 15
Figure 15.1
Canine Lung Lobes
Figure 15.2
Partial Lung Resection
Figure 15.3
Partial Lung Resection with Staples
Figure 15.4
Thoracoscopic Lung Biopsy—Loop Technique
Figure 15.5
Thoracoscopic Partial Lung Resection with Staples
Figure 15.6
Division of Pulmonary Ligament
Figure 15.7
Lung Lobectomy
Figure 15.8
Thoracoscopic Lung Lobectomy
Chapter 16
Figure 16.1
Diaphragmatic Hernia Repair
Figure 16.2
Transverse Abdominus Flap Repair of Diaphragm
Figure 16.3
Hiatal Hernia Repair
Chapter 17
Figure 17.1
Subtotal Pericardiectomy—Right Thoracotomy
Figure 17.2
Thoracoscopic Pericardial Window
Figure 17.3
Pericardial Window via Minimal-Incision Thoracotomy
Figure 17.4
Constrictive Pericarditis—Pericardiectomy and Epicardial Decortication
Chapter 18
Figure 18.1
Venous Inflow Occlusion
Figure 18.2
Heart-Lung Machine
Figure 18.3
Cardiopulmonary Bypass Circuit
Figure 18.4
Femoral Artery Cannulation
Figure 18.5
Aortic Cannulation
Figure 18.6
Bicaval Venous Cannulation
Figure 18.7
Right Atrial Cannulation—Right Thoracotomy
Figure 18.8
Right Atrial Cannulation—Left Thoracotomy
Figure 18.9
Cardioplegia Cannula and Aortic Crossclamp—Right Thoracotomy
Figure 18.10
Left Ventricular Vent—Right Thoracotomy
Figure 18.11
Hybrid Cardiac Approaches
Chapter 19
Figure 19.1
Patent Ductus Arteriosus Ligation.
Figure 19.2
Division of Patent Ductus Arteriosus.
Chapter 20
Figure 20.1
Transventricular Pulmonary Valvuloplasty
Figure 20.2
Pulmonary Patch-Graft
Figure 20.3
Pulmonary Valve Bypass
Figure 20.4
Transapical Aortic Valve Dilation
Figure 20.5
Aortic Valve Bypass
Figure 20.6
Heterotopic Aortic Valve Implantation
Chapter 21
Figure 21.1
Tricuspid Valve Replacement
Figure 21.2
Tricuspid Valve Repair
Figure 21.3
Mitral Valve Approaches
Figure 21.4
Mitral Valve Replacement
Figure 21.5
Mitral Ribbon Annuloplasty
Figure 21.6
Mitral Valve Repair—Artificial Chordae
Figure 21.7
Mitral Valve Repair—Edge-to-Edge
Chapter 22
Figure 22.1
Pulmonary Artery Banding
Figure 22.2
Ventricular Septal Defect Repair
Figure 22.3
Atrioventricular Septal Defect Repair
Figure 22.4
Modified Blalock-Taussig Shunt (Aorta to Pulmonary Artery)
Figure 22.5
Modified Blalock-Taussig Shunt (Subclavian Artery to Pulmonary Artery)
Figure 22.6
Tetralogy of Fallot Repair
Chapter 23
Figure 23.1
Cor Triatriatum Dexter Repair
Figure 23.2
Double-Chambered Right Ventricle Repair
Chapter 24
Figure 24.1
Right Auriculectomy
Figure 24.2
Intracavitary Cardiac Mass Removal
Chapter 25
Figure 25.1
Epicardial Electrode—Screw-In Type
Figure 25.2
Epicardial Electrode—Suture Type
Figure 25.3
Epicardial Pacemaker Implantation—Transdiaphragmatic
Figure 25.4
Bipolar Epicardial Pacemaker Implantation—Suture-Type Electrodes
Figure 25.5
Radiograph—Pacemaker Lead Detachment
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Preface
Thoracic surgery in small animals has grown in importance and prominence since the earlier publication of a book on the same subject. Several important advances in understanding of thoracic diseases and surgical technique have occurred, none more important than the development of minimally invasive techniques such as video-assisted thoracoscopic surgery.
In this first edition of a new and updated book on small animal thoracic surgery, emphasis has been placed on surgical technique, decision making, and perioperative care. We have endeavored to provide detailed descriptions of techniques that we have experience with and that have worked best in our hands. To this end, several new illustrations have been added to this new book, all beautifully drawn by Molly Borman. Her work blends seamlessly with the original illustrations by Thomas McCracken from the first book on the subject of small animal thoracic surgery. We are eternally grateful for the contributions of both of these talented individuals. Where alternate techniques and approaches exist, we have made every effort to reference the experience and techniques of others.
It is our hope that this textbook will prove useful to those seeking information from basic to advanced cardiothoracic surgery. As always, we welcome feedback from our colleagues who share our interest and passion for care of our small animal companions.
E. Christopher OrtonEric Monnet
About the Companion Website
This book is accompanied by a companion website:
www.wiley.com/go/orton/thoracic
The website includes:
• videos of the procedures described in the book.
Section IGeneral Principles
1Cardiopulmonary Function
E. Christopher Orton
A major function of the cardiopulmonary system is to deliver oxygen to tissues and eliminate carbon dioxide generated by tissue metabolism. To accomplish these functions, the respiratory and cardiovascular systems must act in close concert. Compromise of either system—or both systems—can adversely affect the outcome of animals undergoing thoracic surgery. The ability to quickly assess cardiopulmonary function and pinpoint the cause and severity of problems is firmly grounded in an understanding of cardiopulmonary physiology and pathophysiology. This ability is a core skill for those who undertake interventions in the thorax.
The Oxygen Pathway
The oxygen pathway is a clinically useful concept that provides a logical framework for evaluation and correction of disturbances in the cardiopulmonary system (Figure 1.1). It considers the transport of oxygen as a sequential, step-by-step process beginning with atmospheric oxygen and ending with oxygen delivery to tissues. Each step in the pathway is critically important and must be assessed independently to assure adequate overall cardiopulmonary function. The steps of the oxygen pathway can be viewed as a clinical checklist for monitoring cardiopulmonary function in animals before, during, and after thoracic surgery. Steps in the pathway include ventilation, pulmonary gas exchange, hemoglobin saturation, hemoglobin concentration, oxygen content, cardiac output, and oxygen delivery.
Figure 1.1 Oxygen Pathway
Ventilation
Ventilation is the mechanical process that causes air (a mixture of gases) to flow into and out of the lungs. Not all gas flow (L/min) into the respiratory system reaches areas of gas exchange; consequently, total ventilation or minute volume (VT) is divided between alveolar ventilation (VA), where gas exchange occurs, and dead space ventilation (VD).
Anatomic dead space ventilation includes gas flow to anatomic areas not normally involved in gas exchange. Physiologic dead space includes anatomic dead space, as well as flow to alveoli that are ventilated but not receiving pulmonary blood flow. While anatomic dead space remains constant, physiologic dead space changes depending on the number of functioning alveoli. Furthermore, the ratio of VD to VA changes with the respiratory rate and tidal volume and cannot be easily determined clinically. For example, an animal that is panting increases VT and VD several-fold without necessarily changing VA. Thus, the adequacy of VA cannot be determined by just measuring VT.
Carbon Dioxide Tension
The primary drive for alveolar ventilation is arterial carbon dioxide tension (PaCO2). Under physiologic conditions, the central respiratory center drives VA to keep PaCO2 at about 40 mm Hg, regardless of the total amount of carbon dioxide produced (VCO2) based on the size, metabolism, and activity level of the patient. This relationship of PaCO2, VA, and VCO2 is described by Equation 1.2, where K is a conversion constant:
By definition, hypoventilation is present when VA fails to match VCO2, and as a result, PaCO2 increases (i.e., > 40 mm Hg for animals at sea level). Conversely, hyperventilation is present when VA exceeds what is necessary to eliminate VCO2 causing PaCO2 to decrease (i.e., < 40 mm Hg at sea level). Thus, in the clinical setting, adequacy of ventilation is determined by PaCO2 from a blood gas analysis. If PaCO2 is normal based on the regional normal value, then ventilation to the gas exchange regions of the lung is considered adequate. (Note: The regional normal value of PaCO2 is altitude dependent because animals that reside at higher altitudes increase relative VA to compensate for lower inspired oxygen tension.)
Alveolar Gas Equation
Because arterial oxygen tension (PaO2) cannot be higher than alveolar oxygen tension (PAO2), PAO2 is critically important to all subsequent steps in the oxygen pathway. PAO2 is not measured clinically, but can be estimated from the alveolar gas equation:
From above equation, it is apparent that PAO2 is a function of the inspired oxygen tension (PIO2), PaCO2 (and thereby VA), and the respiratory exchange ratio (R). The respiratory exchange ratio is the ratio of oxygen consumption (VO2) to VCO2. The respiratory exchange ratio can be determined by indirect calorimetry, but this is not routinely done in the clinical setting. In a study of dogs evaluated by indirect calorimetry, R was found to be 0.76 in postoperative or post-trauma dogs compared to an R of 0.84 in normal dogs [1]. For purposes of the above calculation, R is generally assumed to be 0.8. The PIO2 is determined by the fraction of inspired oxygen (FIO2, 0.21 in ambient air), barometric pressure (PB, 760 mm Hg at sea level), and the vapor pressure of water (PH2O, 47 mm Hg at 100% saturation and body temperature):
Thus, the PIO2 of room air at sea level is approximately 150 mm of Hg. From the above equation, it can be seen that either barometric pressure or FIO2 can alter PIO2, and, in turn, the PAO2. Substantial change in barometric pressure is most likely to result from residence at altitude, whereas FIO2 is altered clinically by administration of supplemental oxygen. Increasing FIO2 to 40% nearly doubles PIO2 and increases PAO2 without changing VA.
Alveolar ventilation is the other major determinant of PAO2. The alveolar gas equation predicts that an animal breathing room air at sea level with a PaCO2 of 40 mm Hg would have a PAO2 of approximately 100 mm Hg:
A rule of thumb, for every 1 mm Hg elevation in PaCO2, there will be approximately a 1.25 mm Hg decrease in PAO2 (and PaO2).
Hypoventilation
Adequate ventilation requires central respiratory centers, spinal pathways, peripheral respiratory nerves, primary respiratory muscles, pleural-pulmonary coupling, and pulmonary mechanics to be intact or normal. Hypoventilation occurs when any component of this pathway is disrupted or abnormal. Important causes of hypoventilation include depression or injury of the central respiratory center, injury or disease of the neuromuscular apparatus of ventilation, disruption of pleural-pulmonary coupling (e.g., pneumothorax), and/or abnormal pulmonary mechanics that increase the work of respiration to levels that cannot be sustained by the patient. The major determinants of respiratory work are airway resistance and lung compliance. Obstructive airway disorders or restrictive lung conditions, or both, increase respiratory work leading to hypoventilation when they are severe.
Breathing Patterns
Clinical assessment of ventilation should include observation of breathing. The first indication that a patient is hypoventilating may come from the simple observation that ventilatory excursions are poor. Information about abnormal pulmonary mechanics is gained from observation of the pattern of breathing. Animals adopt a respiratory rate and pattern that minimizes respiratory work. Normal breathing balances the major elastic force of lung compliance with the major viscous force of airway resistance. Elastic forces in the lung are minimized by a rapid and shallow breathing pattern, whereas resistance forces in the lung are minimized by a slow and deep breathing pattern (Figure 1.2). Thus, animals with restrictive lung diseases (e.g., pulmonary edema, interstitial pneumonia, pulmonary fibrosis, pleural effusion) will adopt a rapid and shallow breathing pattern, whereas animals with airway obstruction (e.g., laryngeal paralysis, bronchoconstriction) will tend to adopt a slow and deep pattern of breathing. Obstructive breathing patterns can be further assessed by observing of the phase of respiration that produces the most ventilatory effort. Upper airway obstruction causes an exaggerated effort during inspiration, whereas lower airway obstruction causes an exaggerated effort during expiration.
Figure 1.2 Work of Breathing
Tidal Volume and Minute Volume
Total ventilation can be measured directly with a respirometer attached to an endotracheal tube or tight-fitting mask. Tidal volume is the volume (mL) of gas expired during each breath and is normally at least 10 mL/kg of body weight. Minute volume (VT) is the total volume of gas expired each minute (L/min). If tidal volume or minute volume are low, there is a good possibility that ventilation is inadequate. However, because VT includes both VD and VA, measurement of a normal tidal volume or minute volume does not assure that VA is adequate.
Arterial Carbon Dioxide Tension
Ultimately, clinical assessment of alveolar ventilation is based on the PaCO2. By definition, a patient is hypoventilating when hypercapnia (increased PaCO2) present. The most direct method of assessing PaCO2 is by arterial blood gas analysis. Alveolar ventilation should be considered inadequate when the PaCO2 is > 45 mm Hg for patients at or near sea level. Hypoventilation causes both hypoxemia and respiratory acidosis. Administration of supplemental oxygen (i.e., increasing the FIO2) corrects hypoxemia caused by hypoventilation by increasing the PIO2 and PAO2 (see the alveolar gas equation). Of course, administration of supplement oxygen does not correct the respiratory acidosis associated with elevated PaCO2, so it is important to correct the underlying cause(s) of hypoventilation even when animals are receiving supplemental oxygen.
End-Tidal Carbon Dioxide Tension
Because diffusion of carbon dioxide in the lung is highly efficient, PaCO2 and alveolar carbon dioxide tension (PACO2) are close to equal. The carbon dioxide tension of expired gas at the end of expiration closely approximates PACO2 and is termed end tidal carbon dioxide tension (PETCO2). The PETCO2 is measured clinically with a capnograph that samples expired gas continuously and reports the peak carbon dioxide tension at the end of expiration. Measurement of PETCO2 provides a clinical estimate of PaCO2, and therefore VA.
Pulmonary Gas Exchange
Pulmonary gas exchange is the collective process by which oxygen and carbon dioxide are exchanged between the alveolus and blood. Exchange of oxygen is complex and dependent on diffusion across the alveolar-capillary membrane, matching of alveolar ventilation and perfusion, and the amount of venous admixture to arterial blood. Ideally, PaO2 should be nearly equal to PAO2 predicted by the alveolar gas equation (i.e., 100 mm of Hg under physiologic conditions at sea level). Impaired pulmonary gas exchange is present when PaO2 becomes substantially less than the predicted PAO2. Because PaO2 can be measured directly and PAO2 can be calculated from measurable values, the degree of gas exchange impairment can be quantified by the alveolar-arterial oxygen difference (A-a PO2):
The A-a PO2 should be < 10 mm Hg for animals breathing room air. The normal A-a PO2 gradient increases 5 to 7 mm Hg for every 10% increase in FIO2. There are three basic mechanisms of gas exchange impairment: diffusion impairment, shunt, and ventilation-perfusion (VA/Q) mismatch.
Diffusion Impairment
Diffusion of oxygen across the alveolar-capillary membrane is directly proportional to the concentration gradient of oxygen across the membrane and the total membrane area; and inversely proportional to the membrane thickness. Adequate diffusion of oxygen is also a function of the time available to accomplish complete equilibration between the alveoli and blood. Under normal conditions, diffusion of oxygen in the lung is highly efficient and generally is complete by the time blood has traversed about one-fourth of the alveolar capillary bed. Thus, pulmonary disease must be severe before diffusion limits gas exchange. Diffusion impairment can result from diseases that affect the alveolar-capillary membrane such as pulmonary edema, interstitial pneumonia, or pulmonary fibrosis. However, because of the efficiency of gas diffusion, these conditions rarely cause hypoxemia by diffusion impairment in animals at rest.
The most important clinical cause of severe diffusion impairment is pulmonary thromboembolism (PTE), which impairs diffusion by decreasing the total membrane area available for oxygen diffusion. Because the cardiac output must be redirected to unobstructed pulmonary capillaries, the transit time available for diffusion is decreased, and this further contributes to diffusion impairment. A reciprocal consequence of pulmonary thromboembolism is an increase in dead space ventilation (VD/VT) resulting from the ventilation of unperfused alveoli. Dead space ventilation can be quantified by measuring the PaCO2 and mixed exhaled carbon dioxide tension (PECO2):
Determination of PECO2 requires collection of expired gases into a collection bag and analysis of carbon dioxide tension with an infrared analyzer. This determination is rarely performed in clinical patients. In theory, the increase in dead space ventilation could lead to an increase in PaCO2. However, carbon dioxide diffuses across the alveolar-arterial membrane about 20 times more rapidly than oxygen and is rarely if ever limited by diffusion.
Administration of supplemental oxygen can be expected to correct hypoxemia caused by diffusion impairment. It does so by increasing PAO2, and therefore the concentration gradient of oxygen across the alveolar-capillary membrane that drives diffusion. This explains why hypoxemia due to diffusion impairment, including pulmonary thromboembolism, is so responsive to administration of supplemental oxygen. This response to supplemental oxygen serves as a useful clinical observation that supports an assessment that hypoxemia is the result of this mechanism (e.g., PTE).
Shunt
Shunt occurs when unoxygenated venous blood bypasses viable gas exchange areas of the lung and mixes with oxygenated arterial blood. The resultant venous admixture produces hypoxemia. Shunt results from either a right-to-left cardiac shunt or pulmonary shunt. Examples of right-to-left cardiac shunt include ventricular septal defect with suprasystemic pulmonary hypertension and Tetralogy of Fallot. Pulmonary shunt results from perfusion of completely collapsed or fluid-filled alveoli. Shunt is an important cause of clinically significant hypoxemia. The magnitude of hypoxemia caused by shunt is a function of the ratio of shunt flow to total cardiac output, termed the shunt fraction (Qs/Q). Because venous admixture has no opportunity for gas exchange, hypoxemia arising purely from shunt is unresponsive to administration of supplemental oxygen. This physiologic reality distinguishes shunt from other causes of hypoxemia and serves as a useful clinical finding for diagnosing shunt as a contributing or sole mechanism of hypoxemia.
Shunt does not affect the PaCO2 until it becomes very severe. Thus, shunt usually does not result in hypercapnia. In fact, animals with shunt often have a low PaCO2 as a result of hypoxia-driven hyperventi- lation.
Ventilation-Perfusion Mismatch
Ventilation-perfusion (VA/Q) mismatch occurs when ventilation and blood flow are not closely matched in gas exchange units. The result is inefficient gas exchange and hypoxemia. If regions of the lung are ventilated but poorly perfused (i.e., high VA/Q), the functional result is wasted ventilatory effort that does not benefit gas exchange. Because regions of high VA/Q are associated with complete gas exchange, regions of high VA/Q do not directly contribute to impaired pulmonary gas exchange and hypoxemia. It does make gas exchange inefficient. In regions of the lung that are perfused but poorly ventilated (i.e., low VA/Q), the functional result is inadequate bulk flow of oxygen to alveoli to fully oxygenate blood as it flows through these regions. This results in admixture of poorly oxygenated blood from these exchange areas with blood that is more fully oxygenated from normal regions. The net result is overall hypoxemia. Low VA/Q mismatch is an important cause of hypoxemia in animals with pulmonary disease. Any pulmonary condition that disrupts ventilation but maintains blood flow to alveoli will result in low VA/Q mismatch and global arterial hypoxemia. Because alveoli are still at least partially ventilated in the setting of low VA/Q mismatch, the resultant hypoxemia is responsive to the administration of supplemental oxygen, depending on the magnitude of low VA/Q. In reality, pulmonary diseases that cause low VA/Q mismatch are usually accompanied by an increase in pulmonary shunt, explaining why many pulmonary conditions are only partially or poorly responsive to supplemental oxygen.
Alveolar-Arterial PO2 Gradient
The A-a PO2 can be calculated by measuring PaO2 and PaCO2 by blood gas analysis and inserting these values into Equation 1.6. The calculated A-a PO2 for animals breathing room air is normally < 10 mm of Hg. A calculated A-a PO2 of 30 mm of Hg or greater in animals breathing room air suggests significant impairment of gas exchange. Because the normal valve of A-a PO2 is affected by FIO2, the above normal valves do not apply to animals breathing supplemental oxygen. While normal values of A-a PO2 are reported for various levels of FIO2, it is often difficult to determine an accurate FIO2 in the clinical setting. Thus, blood gas analysis and calculation of A-a PO2 is most revealing when performed in animals breathing room air. The A-a PO2 has been shown to be an important predictor of survival in critically ill dogs [2].
Shunt Fraction (Qs/Q)
The magnitude of shunt can be determined by calculation of the shunt fraction from the oxygen saturation of arterial blood (SaO2), mixed venous blood (SvO2), and pulmonary capillary blood (ScO2) during breathing of pure oxygen:
The ScO2 is not measured directly, but is assumed to be 100% during breathing of pure oxygen. Ideally, the SvO2 sample should be obtained from a catheter in the pulmonary artery. Alternatively, the SvO2 can be approximated from a sample obtained from a central venous catheter. Shunt is the only mechanism of impaired gas exchange that persists during administration of 100% supplemental oxygen. A calculated Qs/Q > 10% is abnormal and indicates clinically important gas exchange impairment in animals breathing supplemental oxygen.
Oxygen Saturation and Oxygen Content
The PaO2 reflects the amount of oxygen dissolved in plasma. Dissolved oxygen is of course insufficient to meet metabolic demand for oxygen. Hemoglobin greatly increases the oxygen carrying capacity of blood. Arterial oxygen saturation (SaO2) is defined as the fraction or percent of total hemoglobin binding sites that are bond to oxygen in the arterial blood. The PaO2 is the principal determinant of SaO2.
The relationship between PaO2 and SaO2 is described by the oxygen-hemoglobin saturation curve(Figure 1.3). The affinity of hemoglobin for oxygen increases as more oxygen binds to it which gives the oxygen-hemoglobin curve its sigmoid shape. The shape of the oxygen-hemoglobin curve has important physiologic and pathophysiologic implications. The plateau phase of the curve causes hemoglobin to remain saturated over a wide of range oxygen tensions. The SaO2 is approximately 97% when the PaO2 is 97 mm of Hg. The SaO2 cannot be increased substantially by higher than normal PaO2 values. The steep phase of the oxygen-hemoglobin curve allows for efficient oxygen release in the peripheral tissues where oxygen tension normally decreases. A pathophysiologic implication of the steep phase of the curve is that small changes in PaO2 can have profound changes on SaO2 when arterial hypoxemia is present.
Figure 1.3 Oxygen-Hemoglobin Saturation Curve
The oxygen-hemoglobin curve can “shift” to the right or left reflecting changes in the overall affinity of hemoglobin for oxygen. A shift of the curve to the right decreases overall oxygen affinity of hemoglobin, whereas a shift to the left increases hemoglobin oxygen affinity. Conditions that shift the curve to the right include increased CO2 (Haldane effect), increased hydrogen ion concentration (Bohr effect), increased temperature, and increased 2,3-diphosphoglyerate. Interestingly, conditions that decrease hemoglobin affinity prevail in the peripheral tissues where unloading of oxygen is desirable. Because shifted curves converge in the plateau phase, a shift in the oxygen-hemoglobin curve has a more profound effect on the steep phase than on the plateau phase of the curve. For this reason, shifts in the curve have a greater physiologic effect on unloading of oxygen in the peripheral tissues than on loading of oxygen in the lung. Shifts in the oxygen-hemoglobin curve are quantified by measurement of the oxygen tension at which hemoglobin is 50% saturated (P50). Even though shifts in the oxygen-hemoglobin curve can have an important effect on pulmonary function, they are generally not assessed clinically. Nevertheless, it is useful for clinicians to be mindful of the possibility for such effects in their patients.
Arterial oxygen content (CaO2) is the total oxygen present in arterial blood measured in units of mL O2/100 mL (dL). Each gram of hemoglobin (Hgb) is capable of carrying 1.34 mL of molecular oxygen when fully saturated. Thus, the amount of oxygen bound to hemoglobin can be calculated by multiplying 1.34 (mL O2/gm), the hemoglobin concentration of blood (gm/dL), and SaO2 (%). Dissolved oxygen can be calculated from the PaO2. At sea level, dissolved oxygen is equal to 0.003 mL O2/dL blood/mm Hg PaO2. Thus, CaO2 is calculated as shown in Equation 1.9:
For an animal at sea level with a PaO2 of 97 mm of Hg, a SaO2 of 97%, and a hemoglobin concentration of 15 gm/dL, the CaO2 would be:
From this calculation, it is apparent that the contribution of dissolved oxygen to overall CaO2 is negligible and for clinical purposes can largely be ignored. Thus, the principal clinical determinants of CaO2 are SaO2 and hemoglobin concentration. Polycythemia and anemia can have an important impact on CaO2. Within limits, polycythemia is an important adaptive mechanism for physiologic (e.g., altitude) or pathophysiologic causes of chronic hypoxemia. Conversely, anemia substantially decreases CaO2. The effect that anemia has on CaO2 is sometimes under appreciated. In animals with a relatively normal cardiovascular system, deficits in CaO2 caused by anemia can be compensated for by an increase in cardiac output. However, if the cardiovascular system is compromised, as is often the case in critical patients, anemia can have an important adverse effect on O2 delivery. Thus, as a general rule, it is important to keep the hematocrit ≥ 30% in patients undergoing thoracic interventions.
Oxygen Delivery, Oxygen Consumption, and Oxygen Extraction
Oxygen delivery (DO2) is the mL O2 delivered to the peripheral tissues each minute and is the product of CaO2 and cardiac output (Q):
Thus, maintenance of adequate DO2 requires adequate pulmonary function (PaO2), hemoglobin concentration, and cardiovascular function (Q). When hypoxemia (low PaO2) or low hemoglobin concentration cause low CaO2, oxygen delivery can be maintained by increasing cardiac output assuming that the cardiovascular system is capable. When DO2 is limited by low cardiac output, compensation is more difficult. Within limits, DO2 can be increased by increasing the hemoglobin concentration (e.g., polycythemia) or by increasing oxygen extraction.
Oxygen consumption (VO2) is the mL O2 consumed by tissues each minute and can be calculated by multiplying the difference between CaO2 and mixed venous oxygen content (CvO2) with cardiac output:
From the relationship in Equation 1.12, it can be seen that, in the setting of a low cardiac output, VO2 can be maintained by increasing the CaO2 – CvO2 difference (i.e., increasing oxygen extraction).
The oxygen extraction ratio is the proportion of oxygen consumed (VO2) to oxygen delivered (DO2):
Because cardiac output is in both the numerator and denominator, it cancels out. Thus, determination of O2 extraction ratio does not require actual measurement of cardiac output. Also, hemoglobin concentration can be assumed to be the same in arterial and mixed venous blood. As a result, calculation of O2 extraction can be simplified to:
Because the O2 extraction accounts for any deficits in SaO2 in the delivery of O2 to tissues, it becomes primarily an index of the adequacy of cardiac output. The utility of the O2 extraction is that it is independent of the patient size and does not require actual measurement of cardiac output. As such, the oxygen extraction ratio is a clinically useful method of assessing the adequacy of cardiac output. Under physiologic conditions at rest, oxygen extraction is about 0.25. When cardiac output becomes inadequate to meet the demands of the patient, O2 extraction increases. An O2 extraction ratio of > 0.4 suggests that cardiac output is inadequate.
Cardiac Output
The principal function of the cardiovascular system is the delivery of blood to the pulmonary and systemic circulations. This function is accomplished by pumping an adequate volume of blood to the pulmonary and systemic circulations (i.e., pulmonary and systemic cardiac output) and maintaining adequate pulmonary and systemic perfusion pressures.
Cardiac Output, Blood Pressure, and Vascular Resistance
The relationship of cardiac output (Q), mean arterial pressure (MAP), atrial pressure (AP), and vascular resistance (R) are described by:
This relationship shows that cardiac output is a direct function of the pressure difference that drives flow. In the pulmonary circulation this is the difference between mean pulmonary arterial pressure and left atrial pressure. In the systemic circulation this is the difference between mean systemic pressure and right atrial pressure. Cardiac output is inhibited by pulmonary and systemic vascular resistances in the pulmonary and systemic circulations, respectively. Rearranging this relationship demonstrates the determinants of mean arterial pressures for the pulmonary and systemic circulations
Vascular resistances are not measured directly, but can be calculated from Q, MAP, and AP:
As predicted by the Law of Poiseuille, vascular resistance is determined by the collective total cross-sectional vascular radius of resistance arteries (i.e., degree of vasoconstriction and vasodilation) and the viscosity of blood (i.e., hematocrit). The pulse pressure (Pp) is the difference between the systolic and diastolic blood pressures around the mean arterial pressure. The Pp is the principle determinant of the “strength” of a patient's peripheral pulse on palpation. The Pp is a direct function of the SV and inverse function of the collective compliance of the large elastic arteries (CA):
The most common cause for a diminished Pp or a “weak” pulse is a poor SV. Poor compliance or “stiffening” of the elastic conducting arteries can have the effect of elevating the Pp. Conditions such as patent ductus arteriosus or aortic insufficiency that allow rapid diastolic “run off” of blood dramatically lower diastolic blood pressure and thereby elevate the Pp. Together, the mean arterial pressure and pulse pressure determine the systolic arterial pressure, which is the major determinant of cardiac afterload.
Pressure-Volume Relationship
The cardiac cycle encompasses the electrical, pressure, volume, flow, and valve motion events that occur during one complete cardiac systole and diastole. During each cardiac cycle, the heart accomplishes two fundamental kinds of external work. It generates pressure (i.e., potential energy) and it ejects volume (i.e., kinetic energy). The relationship of these two events is illustrated by plotting instantaneous ventricular pressure and volume against each other to generate a ventricular pressure-volume plot (Figure 1.4). Pressure-volume plots form the basis of current understanding of cardiac physiology. Each loop of a pressure-volume plot represents one complete cardiac cycle and consists of the rapid diastolic and atrial filling phases, isovolumetric contraction phase, ejection phase, and isovolumetric relaxation phase. The important pressure endpoints are ventricular end-diastolic pressure (EDP) and ventricular systolic pressure (Ps). The principal volume endpoints are end-diastolic volume (EDV) and end-systolic volume (ESV). The difference between EDV and ESV is the stroke volume (SV). The area inside in pressure-volume loop represents the external work done by the heart in one cardiac cycle. The ejection fraction is the SV divided by EDV.
Figure 1.4 Cardiac Pressure-Volume Relationship
Stroke Volume (Preload, Afterload, Contractility)
Cardiac output is the product of stroke volume and heart rate. Stroke volume is critically important to the maintenance of adequate cardiac output. Stroke volume, in turn, is determined by three important independent variables: preload, afterload, and contractility. Preload encompasses the Frank-Starling principle of the heart. On a cellular basis, preload is determined by the amount of diastolic strain on each cardiomyocyte. Within limits, the greater the diastolic strain, the more forceful the cardiac contraction. On a whole heart basis, preload is reflected by the EDV and EDP (Figure 1.5). On a beat-to-beat basis, the greater the EDV and EDP, the greater the preload. Since ESV does not change with preload, the net result of an increase in preload is an increase in stroke volume, and vice versa. Factors that determine preload are the mean filling pressure of the circulation and the vascular resistance. The mean filling pressure of the circulation is the pressure in the cardiovascular system at zero flow and the theoretical pressure that drives flow of venous blood back to the heart. Mean filling pressure is largely determined by blood volume and venous vascular tone. The mean filling pressure has a direct relationship with preload. Vascular resistance has an inverse relationship with preload. Increases in vascular resistance decrease venous return to the heart and therefore decrease preload and stroke volume. Thus, the determinants of preload reside within the circulation, not in the heart. Afterload is the systolic stress that the ventricular wall must overcome before it can eject volume. The determinants of ventricular systolic wall stress, and therefore cardiac afterload, are predicted by the LaPlace relationship:
Figure 1.5 Cardiac Preload
On a beat-to-beat basis, afterload is a function of Ps. On a chronic basis, cardiac remodeling (e.g., ventricular dilation and/or wall thickening) also affects afterload. Thus, beat-to-beat afterload is determined by events outside of the heart (i.e., mean arterial pressure and pulse pressure). Afterload has an inverse relationship with stroke volume (Figure 1.6). As afterload increases, stroke volume deceases, and vice versa. In theory, changes in afterload have a minimal effect on external cardiac work (area within the pressure-volume loop). A way to think about afterload is that it reflects the distribution of external cardiac work between generation of pressure and ejection of volume. As the heart is required to generate a higher systolic pressure (i.e., higher afterload), less work is leftover for the ejection of stroke volume.
Figure 1.6 Cardiac Afterload
Contractility, also known as inotropic state, represents the intrinsic contractile state of the heart independent of preload and afterload. On a beat-to-beat basis, contractility is largely a function of the amount of sympathetic (β) influence on the heart. Contractility is also affected by the diseases of the myocardium, cardiac drugs, and cardiac mass. Changes in cardiac mass through cardiac hypertrophy have a direct effect on the global contractility of the heart. Contractility has a direct relationship with stroke volume (Figure 1.7). The greater the contractility or inotropic state, the greater the stroke volume. On a pressure-volume loop, contractility is reflected by changes in the slope of the end-systolic pressure-volume relationship (ESPVR). The net result is a change in the ESV for given loading conditions.
Figure 1.7 Cardiac Contractility
Through the effects of preload, afterload, and contractility, maintenance of cardiac output is a complex interaction of acute and chronic physiologic and pathophysiologic changes in the heart and circulation (Figure 1.8). Understanding these interactive relationships is important for troubleshooting and managing cardiovascular function in the clinical setting.
Figure 1.8 Determinates of Cardiac Output
Heart Failure
Heart failure is present when cardiac output is inadequate despite adequate ventricular end-diastolic pressures or when adequate cardiac output can only be maintained at the expense of elevated end-diastolic pressures. Heart failure results from the combined effects of acute or chronic cardiac insufficiency and compensatory neuroendocrine mechanisms. Heart failure manifests as either organ dysfunction secondary to low cardiac output (termed low output heart failure or forward heart failure) or congestion of organs behind the heart (termed congestive heart failure or backward heart failure), or both (Figure 1.9). Congestion is manifested behind the left heart by pulmonary edema or pleural effusion; or behind the right heart as ascites, peripheral edema, or pleural effusion.
Figure 1.9 Heart Failure
The stretch or load on myocardial fibers just prior to contraction profoundly influences the degree of myocardial fiber shortening. This load or stretch prior to contraction is the cellular basis of preload. End-diastolic pressure in the heart reflects the amount of stretch or preload on the ventricle prior to contraction and in turn are an important determinant of cardiac output. The Frank-Starling curve describes the direct relationship between cardiac output and end-diastolic pressures in the heart.
Cardiac output and ventricular end-diastolic pressure are not only functionally related, but are the physiologic parameters directly responsible for the two adverse manifestations of heart failure; namely, inadequate perfusion and congestion. Initially, impaired cardiac function narrows the cardiac reserve (i.e., the ability to increase cardiac output during activity or exercise). The clinical manifestation is exercise or activity intolerance. Eventually, cardiac output can become low enough that it fails to meet metabolic needs of organ systems and tissues even at rest. If this happens acutely, the patient may manifest low output heart failure. Organ and tissue dysfunction become apparent. The patient is “cold” rather than “warm.” While ventricular end-diastolic pressure exerts a positive influence on cardiac output, it also is the effective downstream pressure that resists venous return to the heart. Congestion occurs when end-diastolic pressure elevates capillary hydrostatic pressure to the point where a net efflux of water from capillaries to the interstitial space occurs. The result is edema of the organs and tissues behind the failing heart. The patient is “wet” rather than “dry.”
Cardiac insufficiency is caused by one or a combination of four basic mechanisms: primary myocardial failure, hemodynamic overload, diastolic dysfunction, or cardiac arrhythmias. Progression of heart disease can be arbitrarily divided into three phases. The first phase of heart disease occurs when an initiating cardiac injury or insufficiency is present. If the initiating cardiac insufficiency is acute and overwhelming, then low output heart failure may ensue. More often in animals the cardiac insufficiency is not initially overwhelming or lethal, but rather slowly progressive. In this case, the presence of heart disease may be signaled only by the presence of physical findings such as abnormal heart sounds or murmurs, and not be associated with overt symptoms of heart failure other than possible activity or exercise intolerance.
The second phase of heart disease is hallmarked by activation of the neuroendocrine response to cardiac insufficiency. This neuroendocrine response ensures that blood pressure and cardiac output are maintained principally through the retention of vascular blood volume and the constriction of arteries and veins. Cardiac hypertrophy generally begins during this phase, particularly when the initiating cardiac insufficiency results from hemodynamic overload. The type of cardiac hypertrophy depends on the nature of the cardiac insufficiency. During this phase, clinical evidence of cardiac insufficiency in the form of cardiomegaly occurs, although overt signs of heart failure still may not present. Symptoms would still be mostly associated with reduced activity or exercise capacity.
Although the neuroendocrine response is initially adaptive, ultimately this response becomes maladaptive. This is the third phase of heart failure. During this phase, the neuroendocrine response “overcompensates,” producing high end-diastolic pressures primarily through the retention of blood volume. The result is congestion in the form of tissue and organ edema. Inappropriate arterioconstriction is also present during this phase, contributing to poor tissue perfusion. This state is termed congestive heart failure. It is possible in advanced cases of cardiac insufficiency for both congestive heart failure and low output heart failure to be present.
