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:

  1. Hypoventilation.

  2. Anatomic R to L shunt.

  3. Low inspired O2 (FiO2).

  4. Diffusion impairment.

  5. 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.