Anesthesia in Obstructive pulmonary disease.

1. Anesthesia in Restrictive
Pulmonary disease
Dr. Tenzin Yoezer
KGUMSB

2. Introduction
• Characterized by decreased lung compliance
• Reduced lung volumes, esp TLC
• But has preserved expiratory flow rates
• Affects both lung expansion and compliance( i.e inability to
increase lung volume in proportion to an increase in pressure in
the alveoli)
• FEV1 and FVC are reduced – thus FEV1/FVC is normal
• Reduced lung compliance – increase work of breathing – rapid and
shallow breathing pattern
• Respiratory gas exchanged is maintained until disease is advanced

5. Introduction
• As disease advanced – reduced surface area for gas diffusion –
ventilation/perfusion mismatch and hypoxia
• TLC classify severity of the disease:
• Mild – TLC 65-85%
• Moderate – TLC 50- 65%
• Severe – TLC < 50%
• Other classification is by its causes

7. Restrictive lung disease
• Includes:
• Acute intrinsic pulmonary disorders
• ARDS, pneumonia, pneumonitis
• Chronic intrinsic pulmonary disease
• Interstitial lung disease
• Extra-pulmonary disorders
• Pleura, chest wall, diaphragm, neuromuscular dysfunction

8. Pulmonary edema
• Due to leakage of intravascular fluid into the interstitium of the lungs
and eventually into the alveoli
• Acute PE is due to:
1. increased capillary pressure(hydrostatic or cardiogenic)
2. increased capillary permeability

9. Pulmonary oedema
• Increased capillary permeability:
• Air-bronchogram
• High conc of protein and secretory products
• Associated with ARDS
• Increased capillary pressure :
• Bilateral symmetrical perihilar opacities(butterfly pattern) on CXR
• Cardiogenic PE – marked dyspnea, tachypnea, signs of SNS(HTN, tachycardia,
diaphoresis)

10. Neurogenic PE
• Seen in brain injury(after mins to hrs)- thus ay present perioperatively
• Mechanism:
• Brain injury – massive outpouring of sympathetic impulses
• Generalized vasoconstriction
• Shift of blood volume into pulmonary circulation
• Increased pulmonary capillary pressure
• Transduction of fluid into interstitium and alveoli
• Pulmonary HTN and hypervolemia also damages vessels
• DD- chemical pneumonitis

11. Drug-induced PE
• Especially with opioids(heroin) & Cocaine
• High permeability of capillary – high protein conc in the fluid
• Rx - supportive

12. High-altitude PE
• Occurs height ranging from 2500-5000 m
• Influenced by rate of ascent to that altitude
• Symptoms:
• gradual onset
• Typically within 48-72 h
• Fulminant PE may be preceded by less severe symptoms of acute mountain sickness
• Mechanism:
• Hypoxic pulmonary vasoconstriction - increases pulmonary vascular pressure – PE
• Rx :
• prompt descend
• Administration of oxygen
• Inhalation of nitric oxide

13. Re-expansion PE
• rRe-expansion of collapse lung following pneumothorax or pleural
effusion may lead to PE
• Factors that influence:
• Amount of air/fluid in pleural space - >1L increases risk
• Duration of collapse - >24 h increases risk
• Rapidity of re-expansion
• Content – high protein
• Rx - supportive

14. Negative pressure PE
• Develops following relief of acute upper airway obstruction-
laryngospasm, epiglottitis, tumor, obesity hiccups or OSA in
spontaneously breathing pt
• Also known as post-obstructive PE
• Spontaneous ventilation is necessary to create the marked negative
pressure
• Onset – few minutes to 2-3 h
• Presentation – tachypnea, cough, failure to maintain SpO2 > 95%
• DD – pulmonary aspiration, PE

15. Negative pressure PE
• Mechanism:
• Vigorous inspiratory effort against an obstructive airway obstruction
• Development of high negative intra-pleural pressure
• Decreases the interstitial hydrostatic pressure
• Increases venous return and left ventricular afterload
• Intense activation SNS - central displacement of blood
• This all increases trans-capillary pressure gradient – PE
• Rx – self limited
• Administration of oxygen
• Radiological changes resolves within 12-48 h

16. Anesthetic management
• Elective case should be delayed until cardiopulmoary disorders are
optimized
• Usually they are critically ill
• Need ICU ventilator for intraop mx
• Though there is define intra op ventilationmx, acute lung injury
protocol is followed as they is risk of developing barotrauma
• Low VT – 6 mL/kg
• RR – 14-18
• End-inspiratory pressure < 30 cmH2O

17. Acute intrinsic pulmonary disorders
• Preop considerations
• Reduced lung compliance is primarily due to increase in extravascular
lung water
• Increase pulmonary pressure/ increase capillary leakage

18. Acute intrinsic pulmonary disorders
• Preop Mx
• Should be elective case
• If emergency procedure – optimize ventilation and oxygenation
preoperatively
• Fluid overload – treat with diuretics
• Treat heart failure
• Large pleural effusion – drainage
• Massive abdominal distension – NG aspiration

19. Introp mx
• Selection of anesthetic agent depends to each pt
• Critically ill pts like ARDS, cardiogenic pulmonary oedema, pneumonia
need. Continuation of periop intensive care
• Need increase inspired oxygenation conc and PEEP
• Decrease lung compliance leads to high peak inspiratory pressure
during positive-pressure ventilation – increase risk of barotrauma and
volutrauma
• VT should be reduced to 4-6 mL/kg with compensatory increase in RR
• Airway pressure should be < 30 cm H20
• Risk of right ventricular failure due to increased pulmonary vascular
resistance secondary to permissive hypercapnia

20. Chronic intrinsic pulmonary disorders
• Chronic inflammatory
• Insidious onset
• Often referred as interstitial lung diseases
• Causes:
• Occupational environemental pollutants
• Drug toxicity(bleomycin and NFT)
• Radiation pneumonitis
• Idiopathic pulmonary fibrosis
• Autoimmune diseases
• Sarcoidosis
• Chronic pulmonary aspiration
• Oxygen toxicity
• Severe ARDS

21. Preop consideration
• Dyspnea on exertion
• Nonproductive cough
• Advanced disease – cor pulmonale
• Fine(dry) crackles over lung bases
• Late stage – Right ventricular failure
• CXR – ground glass appearance and honey comb appearance
• ABG – mild hypoxia with normocarbia
• PFT – restrictive type
• Carbon monoxide diffusing capacity is reduced

22. Anesthetic consideration
• Preop Mx
• Focus on underlying disease and its severity
• History of dyspnea on exertion is evaluated further with PFT and ABG
• Vital capacity < 15 mL/kg – indication of severe dysfunction
• (normal - > 70 mL/kg)
• CXR is helpful in assessing disease severity

23. Intraop Mx
• Their management is complicated by predisposition to hypoxemia
and need for controlled ventilation
• Reduce FRC
• Susceptible for oxygen toxicity
• cautious with pt who receive with Bleomycin
• FiO2 should be kept minimal compatible with acceptable oxygenation(SpO2 >
90%)
• Continue intensive protective lung care in the introp mx
• Nitric oxide may be used to reduce pulmonary vascular resistance and
reduce the work of right ventricle

24. Intraop Mx
• ECMO( extracorporeal membrane oxygenation) is increasingly used in
acute respiratory failure mx
• Following anticoagulation, blood is drained from venous and
delivered to membrane exchanger
• Oxygenated blood is return to venous system if cardiac function is
preserved, or pumped into arterial circulation bypassing the heart
and lung
• It transiently supports both cardiac and lung function

25. References
• Morgan 6th edition
• Stoelting anesthesia and co-existing diseases