1 Respiratory Dzzd Anesth-1 (1)
Page 1: Introduction to Anesthesia in Respiratory Compromised Patients
Speaker: Dr. Brighton T. Dzikiti, PhD, MSC, BVSc
Focus: Anesthesiology in veterinary patients with respiratory compromise and pulmonary disease.
Page 2: Importance of Anesthesia in Respiratory Compromise
Highlights the significance of understanding respiratory issues in anesthesia practices.
Page 3: Respiratory Physiology
Complex Subject: Understanding respiratory physiology is vital for safe anesthetic practices.
Key Learning Outcomes:
Recognize life-threatening respiratory issues.
Treat appropriately based on knowledge.
Resource: Figures from "Respiratory Physiology" by West.
Page 4: Lecture Objectives
Learning Points:
Basic respiratory anatomy and physiology.
Causes of Hypoxemia: Understand five main causes of hypoxemia.
Interpret PaO2:FiO2 ratio and A-a gradient with normal values.
Understand Indications and physiologic effects of Intermittent Positive Pressure Ventilation (IPPV).
Describe anesthetic management for respiratory or pulmonary compromised patients.
Page 5: Anatomy of the Respiratory System
Airways:
Conducting Zone: Dead space, no gas exchange.
Respiratory Zone: Site of gas exchange characterized by a thin blood-gas barrier (less than 0.3um).
Pulmonary Circulation:
Low resistance; pulmonary artery (PA) pressure ~15 mmHg.
Page 6: Lung Volumes
Types of Lung Volumes:
Tidal Volume (TV): Volume of a normal breath.
Functional Residual Capacity (FRC): Remaining lung gas after normal expiration.
Vital Capacity: Maximum volume expelled after maximum inspiration.
Residual Volume: Remaining lung gas after maximal expiration.
Page 7: Diffusion and Fick’s Law
Diffusion Rate Factors:
Proportional to:
Tissue area.
Partial pressure difference.
Gas solubility in tissue.
Inversely Proportional to:
Tissue thickness.
Square root of molecular weight.
Page 8: Diffusion Rates of CO2 and O2
Key Fact: CO2 diffuses 20 TIMES faster than O2 due to higher solubility and similar molecular weight.
Page 9: Hypoxemia
Definition: PaO2 < 60 mmHg; correlates with SpO2 of approximately 90%.
Five Causes of Hypoxemia:
Hypoventilation.
Anatomic R to L shunt.
Low inspired O2 (FiO2).
Diffusion impairment.
Ventilation-perfusion (V/Q) mismatch.
Page 10: Hypoventilation
Definition: High PaCO2 (>45 mmHg).
Clinical Implications:
Causes hypoxemia with room air (FiO2 = 0.21).
May not cause hypoxemia if breathing 100% oxygen (FiO2 = 1.0).
Page 11: Anatomic R to L Shunt
Understanding Shunt:
Blood enters the arterial system without passing through ventilated lung areas.
Normal Shunt: Small amount (<5%).
Circulation Types:
Bronchial Arteries: Oxygenate lung.
Coronary Circulation: Supplies myocardium.
Page 12: Pathologic R to L Shunt
Conditions Leading to Shunt:
Reverse-flow patent ductus arteriosus.
Tetralogy of Fallot.
Pulmonary arteriovenous malformation.
Page 13: Low Inspired FiO2
Real-Life Examples:
Extreme Altitudes: Top of Everest.
Aviation Incidents: Aircraft decompression.
Anesthesia Note: Delivery of hypoxic gas mixture to anesthetic breathing systems.
Page 14: Diffusion Impairment
Characteristics:
Thickened blood-gas barrier; usually rare in veterinary species.
Associated Conditions:
Interstitial lung disease and pulmonary fibrosis.
Congestive heart failure leading to pulmonary edema.
Lifestyle factors like smoking.
Page 15: Ventilation-Perfusion Mismatch
V/Q Ratio:
V (Ventilation) vs. Q (Perfusion) should ideally be 0.8-1.
Decreased V or increased Q leads to severe V/Q mismatch, impacting gas exchange.
Page 16: V/Q Coefficient
Location Dependency:
Both perfusion and ventilation increase from top to bottom of the lung, with perfusion increasing more significantly.
V:Q ratio decreases from top to bottom.
Page 17: V/Q Relationships
Visualizing V/Q:
With no ventilation, blood perfusion is indicated, leading to normal V/Q ratios.
Page 18: Effects of V/Q Mismatching
Impact on Gas Levels:
V/Q mismatch affects both PaO2 and PaCO2.
Increased ventilation decreases PaCO2 but minimizes PaO2 improvements due to dissociation curves.
Page 19: Hypoxic Pulmonary Vasoconstriction (HPV)
Physiological Mechanism:
Regional alveolar hypoxia results in vasoconstriction of pulmonary arteries, redirecting blood flow to better-oxygenated areas.
Impact of Anesthetics:
Anesthetic drugs, especially inhalants, decrease this reflex, increasing V/Q mismatch and lowering PaO2:FiO2.
Page 20: Assessing Oxygenation
Assessment Importance:
Oxygenation can be abnormal even with normal PaO2 when breathing >21% oxygen.
Assessment Methods:
Alveolar-arterial O2 gradient and PaO2:FiO2 ratio.
Page 21: Alveolar Gas Equation
Equation:
PAO2 = FiO2 (PATM – PH20) – (PaCO2/R).
Normal Values:
PAO2 ~100 mmHg breathing 21% O2, at sea level.
Page 22: Alveolar-Arterial O2 Gradient
Understanding Gradient:
Difference between PAO2 (calculated) and PaO2 (measured) should be less than 10-15 mmHg.
Values >15 indicate an oxygenation problem.
Page 23: PaO2 to FiO2 Ratio
Clinical Relevance:
A clinically useful measure of oxygenation ability, normal value ~500.
<500 indicates an oxygenation issue, commonly V/Q mismatch in anesthetized animals.
Page 24: Monitoring Oxygenation
Caution with SpO2 Readings:
SpO2 can read >90% until PaO2 drops below 60 mmHg.
Accurate assessment requires arterial blood gas analysis.
Page 25: Content of Oxygen in Blood
CaO2 Calculation:
CaO2 = (1.34 x [Hb] x SaO2) + (0.003 x PaO2).
Hemoglobin concentration primarily determines CaO2.
Page 26: Anemia and Hypoxemia
Clinical Insight:
Anemic patients might show normal PaO2 but can experience tissue hypoxia.
Increasing PaO2 is ineffective; must increase [Hb] instead.
Page 27: Factors Affecting Ventilation
Key Influences:
PaCO2, arterial pH, and PaO2 if <60 mmHg.
Other factors: pulmonary stretch receptors, body temperature, stress, anxiety, and pain.
Page 28: Control of Ventilation vs Anesthesia
Comparison: Examines differences in physiological controls versus anesthetic impacts.
Page 29: Drug Effects on Ventilation
Minimal Respiratory Depression:
Benzodiazepines, phenothiazines, α-2 agonists, opioids (varies by species).
Significant Depression:
Propofol, etomidate, alfaxalone, volatile anesthetics, and certain drug combinations.
Page 30: Controlled (Artificial) Ventilation
Intermittent Positive Pressure Ventilation (IPPV):
Can decrease PaCO2 and may improve PaO2 by resolving atelectasis, facilitating better V/Q matching.
PIP: Peak inspiratory pressure and PEEP: Positive end-expiratory pressure are crucial metrics.
Page 31: Options for Artificial Ventilation
Techniques Employed:
Manual IPPV, mechanical ventilators, Ambu bag usage during transport, and Demand Valve Devices for recovery.
Page 32: Disadvantages of IPPV
Physiological Impact:
Unlike natural inspiration relies on pressure gradients, IPPV can increase intrathoracic pressure, impeding venous return and blood pressure.
Page 33: Compounded Disadvantages of IPPV
Risks Involved:
Sees increased afterload, hypovolemic risks, pulmonary damage (including volutrauma and pneumothorax).
Page 34: Types of Respiratory Dysfunction
Classifications:
Airway obstruction (upper vs. lower), pneumonia/pulmonary edema, pleural effusion, pneumothorax, diaphragmatic hernia known collectively as extrapulmonary dysfunction.
Page 35: Anesthesia Considerations in Respiratory Diseases
Guidance:
Avoid elective anesthesia for animals with existing pulmonary disease.
Requires lung-protective ventilation strategies, especially during surgeries involving respiratory compromise.
Page 36: Approach to Dyspneic Animals
Sedation Recommendations:
Light sedation with butorphanol or benzodiazepines indicated to decrease anxiety and strain.
In cases of severe distress, consider induction and intubation, potential need for longer ventilation.
Page 37: Anesthesia in Dyspneic Patients
Emergency Management:
Immediate thoracocentesis for pleural effusion/pneumothorax.
IPPV may quickly counteract acute hypoxemia resulting from upper airway obstruction issues.
Page 38: Anesthetic Strategy for Compromised Patients
Management Techniques:
Pre-oxygenation, rapid sequence induction/intubation, and continuous monitoring of SpO2 during light-moderate sedation.
Use of arterial catheters for blood gas sampling, implementing lung-protective ventilation strategies.
Page 39: Special Considerations for Bulldogs
Brachycephalic Risks:
Conditions include long soft palate, stenotic trachea, everted laryngeal saccules affecting intubation.
Page 40: Anesthetic Management in Bulldogs
Protocols:
Monitor closely post-premedication, opt for small ET tubes, and conduct recovery in sternal position.
Prepare additional induction and intubation resources; delay extubation until alert.
Page 41: Managing Hypoxemia During Anesthesia
Actions for Improvement:
Clear any airway obstructions, proper positioning, and adjustments to PIP.
Consider bronchodilators if bronchoconstriction is suspected.
Page 42: Prevention of Re-expansion Pulmonary Edema
Protocol:
Maintain lower peak inspiratory pressures during IPPV to prevent complications.
Better to prevent than treat, especially with chronic conditions.
Page 43: Equine Colic and Hypoxemia
Challenges:
Severe V/Q mismatch in equine anesthetic scenarios, often due to physical constraints from abdomen pressure.
Page 44: Management of Hypoxemia in Equine Colic
Immediate Actions:
Prompt initiation of IPPV; careful balance between positive pressure and blood flow maintenance.
Page 45: Summary of Respiratory Anesthesia
Key Takeaways:
Pre-anesthetic stabilization, pre-oxygenation, rapid induction, continuous monitoring, and lung protective strategies are essential.
Page 46: Conclusion and Acknowledgments
Institution: Ross University School of Veterinary Medicine.
Expressing gratitude for attention and inquiries.