Anesthesia in. Obstructive pulmonary disease.

1. ANESTHESIA IN
OBSTRUCTIVE
PULMONARY DISEASE
Dr. Tenzin Yoezer
KGUMSB

2. Characteristic of OAD
• Pry characteristics of these disorders is resistance to
airflow
• Decrease FEV1
• FEV1/FVC < 70% of predicted values
• Air-trapping and elevated airway resistance
• Thus, Increase RV and TLC
• Wheezing
• Turbulent airflow

3. Obstructive pulmonary diseases
• Obstructive pulmonary/respiratory disease is divided into
following for discussion of their influence on anesthetic
management:
• Acute upper respiratory infection(URI)
• Asthma
• Chronic bronchitis
• Cystic fibrosis
• Bronchiectasis
• Bronchiolitis

4. UPPER RESPIRATORY
INFECTION

5. Upper respiratory infection
• Every year 25 millions visit hospital because of URI
• 20 million days are absence from work
• 25 million days absence from school
• Thus it is likely there will be pt schedule for surgery
• Infections account for 95%
• Common pathogens – rhinovirus, coronavirus, influenza
virus, parainfluenza virus, RSV
• Non-infectious – allergic or vasomotor

6. URI
• Signs and symptoms
• Nonproductive cough
• Sneezing
• Rhinorrhea
• Bacterial infection:
• Fever
• Purulent nasal discharge
• Productive cough
• Malaise
• Tachypneic
• wheezing
• Toxic appearance

7. Management of anesthesia
• Most postop pulmonary complication occurs in pediatric
population with history of :
• Copious secretion
• Prematurity
• Parental smoking
• Nasal congestion
• Reactive airway disease
• ET intubation
• Airway surgery
• Limited data about adult population

8. Management of anesthesia
• Consultation with surgery for urgency of surgery is
necessary
• Stable pt or recovering – may manage safely
• Decision to make before cancelling – economic and
practical aspect
• If postponed – have to postpone for 6 weeks
• It takes 6 weeks to resolve airway reactivity

9. Anesthetic consideration
• Viral infections(during infectious period)
• Morphologic and functional changes in epithelium
• Tracheal mucociliary flow and pulmonary bactericidal
activity is decreased by GA
• Positive pressure ventilation – spread infection from upper
to lower respiratory infection
• Immune response of the body is altered by surgery and
anesthesia
• Reduction in B-lymphocyte numbers, T-lymphocyte responsiveness
and antibody production

10. Management
• Adequate hydration
• Reducing secretion
• Limiting manipulation of potentially sensitive airway
• Nebulize or topical local anesthetic application to vocal
cord
• LMA than ET tube

11. Adverse events:
• Transient hypoxia
• Laryngospasm
• Bronchospasm
• Airway obstruction
• Post-intubation croup
• Atelectasis
• Long-term complications have not been demonstrated

12. ASTHMA

13. Asthma
• Common disorder – 5- 7%
• Globally affects ~ 300 million
• Prevalence is increasing in developing countries –
urbanization and atmospheric pollution
• Pry characteristics – bronchiolar inflammation and hyper-
reactivity in response to various stimuli
• Airway obstruction is generally reversible
• Airway obstruction is due to bronchial smooth muscle
constriction, edema and increase secretion

14. Stimuli:
• Multi-factors : genetic and environmental causes
• Family history
• Maternal smoking
• Airborne substances - Pollen, animal dander, dust,
pollutants
• Drugs – NSAIDs, aspirin, sulfite, beta-antagonist
• Miscellaneous – emotion excitement(endorphins & vagal),
exercise, cold air, viral infection(rhinovirus and infantile
RSV)

15. Asthma classification
• Acute
• Chronic
• Intermittent(mild)
• Moderate
• Severe persistent

16. Pathophysiology
• Release of various chemical mediators and over-activity
of parasympathetic activity
• Antigen bind to IgE of mast cells – degranulation- release
of histamine, bradykinin, leukotrines C, D, and E, platelet
activating factors, PGE2, PGF2â, and PGD2, neutrophil
and eosonophil
• Causes bronchospasm
• Vagus afferent are sensitive to histamine and multiple
noxious stimuli.
• Reflex vagal activation results in bronchoconstriction
• Parasympathetic has diurnal variation, with peak airway
resistance occurring early in the morning (usually around
6 am)

17. Pathophysiology
• During attack, bronchoconstriction, mucosal edema and
secretion increase airway resistance to gas flow at all
levels of the lower airway
• As attack resolves, airway resistances first normalize in
large airways(mainstream, lobar, segmental and
subsegmental bronchi), and then in more peripheral
airways
• Therefore, during attack resolution expiratory flow rate is
reduced only at low lung volumes

18. Pathophysiology
• TLC, RV and FRC increases
• The number of alveolar with V/Q ratio increases
• Tachypnea – hypocapnia
• Normal or high PaCO2 indicates sign of impending
respiratory failure
• Pulsus paradoxus
• Right ventricular strain on ECG(ST changes, right axis
deviation, RBBB) – sign of severe airway obstruction

19. Treatment
• Beta-adrenergic agonist/ sympathomimetics agent
• Methylxanthines
• Glucocorticoids
• Anticholinergics
• Leukotriene modifiers
• Mast cell stabilizing agents
• Cromolyn sodium
• nedocromil

20. Anesthetic considerations
• Preop management
• Age at onset
• Severity of disease
• Recent course of the disease
• Disease optimization
• Triggering events
• Hospitalization for asthma
• Frequency of emergency department visits
• Need for intubation and mechanical ventilation
• Allergies
• Cough
• Sputum characteristics
• Current medication and its response
• Anesthetic responsive

22. Examination and investigations
General appearance
Use of respiratory and accessory muscles
Auscultation- wheezing or crepitation
CBC – eosinophil counts( often parallel with degree of airway
inflammation)
CXR – air-trapping, hyperinflation, flattened diaphragm, small appearing
heart, hyperlucent lung field
ECG: right ventricular strain or ventricular irritably
PFT – FEV1, FEV1/FVC, FEF25-75%, peak expiratory flow rate
Helps in assessing severity of the disease
Reversibility after the bronchodilator treatment.
Comparison with previous measurement are invaluable

25. Active asthma in emergency surgery
• Should be treated aggressive
• Oxygen
• Nebulization with beta2 agonist
• IV glucocorticosteroid
• ABG
• Hypoxia and hypercapnia – indication of moderate to
severe disease
• Even slight hypercapnia is indication for air trapping
and may be sign of impeding respiratory failure

26. Premedication
• Anticholinergic – not given usually
• H2 blocking – theoretically detrimental, though H2 receptor activation
causes bronchodilation but in the event of histamine release,
unopposed H1 receptor activation with H2 receptor blockade cause
bronchoconstriction
• Bronchodilators –continued up-to time of surgery
• (includes beta agonist, glucocorticoid steroids, leukotriene modifiers,
mast cell stabilizers, theophylines, anticholinergics)
• Pts with chronic glucocorticoid steroid > 5mg/d of prednisolones or its
equivalent or have been on high systemic dose within past 6 months -
should receive supplementation steroid based on severity of illness
and complexity of surgical procedure
• **HPA-adrenal suppression is unlikely if only inhaled corticoid is used
• Supplementation dose should tapered to baseline within 1-2 days

27. Ideal patient before surgery
• Free of wheezing
• PEFR > 80% predicted or pts personal best value

28. Intraop Mx
• Concerns :
• Airway stimulation during stimulation
• Pain
• Stress
• Light anesthesia
• Histamine releasing drugs(morphine, atracurium,
meperidine)
• All these causes bronchoconstriction
• Noninvasive ventilation and RA avoids airway stimulation
but doesn't’t eliminate risk of bronchospasm

29. Intraop mx
• Choice of anesthesia is less important if adequate depth is
achieved before intubation or surgical intubation
• High spinal or epidural anesthesia may aggravate
bronchoconstriction by blocking sympathetic tone of T1-T4 and
allowing unopposed parasympathetic activity
• Choice of induction agents:
• Propofol and etomidate – hemodynamically stable
• Propofol produces bronchodilation and smooth muscle
relaxation
• ** Thiopental causes bronchospasm as it releases histamine
• Ketamine is good choice in unstable patient(has
bronchodilatory effect)
• Caution: avoid ketamine in high theophyline levels – combined
effect increases seizure activity

30. Measures to prevent reflex bronchospasm
• Ventilating patient with 2-3 MAC Sevo for 5 mins
• ( Iso and Des are pungent and causes cough,
laryngospasm, bronchospasm)
• Lidocaine 1-2 mg/kg IV or intratracheal
• (if adeqaute dose for intratracheal is not given, it will
cause bronchospasm)
• Non-histamine releasing opioids – remifentanil, fentanyl
• *** opioid induced muscle rigidity – reduced lung
compliance and impair ventilation
• LMA than ET

31. Intraop Mx
• Use of NMD
• Though Sux releases histamine occasionally it is safe to use in asthma
• Use NDM with non-histamine releasing
• Theoretically, antagonism of NMB with anticholinesterase drugs could
precipitate bronchospasm due to stimulation of postganglionic cholinergic
receptors in airway muscles
• However it doesn’t occur due to simultaneous administration of anticholinergic
drugs
• Maintenance – volatile anesthetist due to its bronchodialating
properties
• Warm humidified gases are incorporated whenever possible – esp in
pt with exercise induced asthma
• Sufficient time must be provide for exhalation to prevent air-trapping
• Adequate hydration- airway secretion is less viscous

32. Intraop mx
• Extubation – deep extubation
• When it is contraindication for deep extubation:
• IV lidnocaine
• Inhaled bronchodilator

33. Intraop complication
• Bronchospasm
• Capnography –delayed/slow rise of ETCO2 waveform
• (severity of obstruction is inversely related to rate of rise
of ETCO2)
• Rising peak inspiratory pressure(PIP)
• Plateau pressure remain unchanged
• Incomplete exhalation
• Decreasing exhaled VT
• O/E - wheezing

34. • D/D of Bronchospasm(intraop wheezing &
bronchospasm)
• Mechanical obstruction of ET tube
• Tube kinking
• Secretions
• Overinflated balloon
• Bronchial intubation
• Inadequate depth of anesthesia
• Active expiratory efforts(straining)
• Decreased FRC
• Pulmonary edema
• Pulmonary aspiration
• Pulmonary embolism
• Pneumothorax
• Acute Asthmatic attack

35. Bronchospasm Mx
• Increase the conc of volatile agent/ propofol
• Administering short acting aerosolized bronchodilator via
ETT
• Suctioning secretion
• Infusion of low dose epinephrine & IV hydrocortisone in
refractory condition
• At the end of surgery patient should be free of wheezing
• Reversal agents doesn’t precipitate
• Sugamadex avoids issue of rising acetylcholine
• Deep extubation
• Lidocaine 1.5 – 2 mg/kg IV bolus before extubation

36. COPD

37. COPD
• Defined as a disease of progressive loss of alveolar tissue
characterized by airflow limitation that is not fully
reversible
• Mixture of small and large airway disease (chronic
bronchitis/bronchiolitis) and parenchymal
destruction(emphysema
• WHO predicts by 2030 COPD will be 3rd leading cause of
dead worldwide
• Prevalence increases with age
• Strongly associated with cigarette smoking
• Most are asymptomatic or mildly symptomatic
• In PFT shows expiratory airflow obstruction
• Advance disease – V/Q mismatched

38. Stimuli for COPD
• 1) Cigarette smoking
• 2) Occupation exposure to dust and chemical
• coal mining, gold mining, textile industry
• 3) Indoor and outdoor pollution
• 4) Recurrent childhood respiratory infection
• 5) Low birth-weight
• 6) Alpha 1 antitrypsin deficiency

39. COPD
• Pathological deterioration in elasticity or recoil within the
lung parenchyma
• Pathological changes that decrease the rigidity of the
bronchiolar wall – predispose them to collapse during
exhalation
• An increase in the gas flow velocity in narrowed bronchioli
– lowers the pressure inside the bronchioli – further favors
airway collapse
• Active bronchospasm and obstruction – increase
secretion
• Destruction of lung parenchyma– enlarges air sacs -
emphysema

40. Chronic bronchitis
• Defined as the presence of productive cough on most
days of 3 consecutive months for at least 2 consecutive
years.
• Risk factors: cigarette smoking, exposure to air pollutants,
occupational exposure to dusts, recurrent pulmonary
infections, and familial factors
• Secretion from hypertrophied bronchial mucous glands
and edema from inflammation of the airway produce
airflow obstruction.
• Recurrent viral and bacterial infection is common
• RV is increased
• TLC is normal
• Intrapulmonary shunt and hypoxia

41. • Chronic hypoxia leads to:
• Erythrocytosis
• Pulmonary HTN
• RVH
• Cor pulmonale
• Blue bloater syndrome
• Chronic CO2 retention

42. Emphysema
• Pathological disorder characterized by irreversible enlargement
of the airways distal to terminal bronchioles and destruction of
alveolar septa
• Diagnosis – CT chest
• Mild apical emphysematous – normal, clinically insignificant,
related to aging
• Significant emphysema – common, related to cigarette
smoking
• Young age – associated with homozygous deficiency of alpha 1
antitrypsin(protease inhibitor- prevents excessive activity of
proteolytic enzyme(elastase) in the lung)
• Enzyme is produced by neutrophil and macrophage in response to
infection and pollutants.
• Smoking causes imbalance between protease and
antiprotease activity

43. Emphysema
• Types – centrilobular or panlobular
• Centrilobular(centriacinar):
• results from dilatation or destruction of respiratory bronchioles
• Associated with tobacco smoking
• Has predominates to upper lobe distribution
• Panlobular(Panacinar):
• even dilation and destruction of the entire acinus
• Associated with alpha 1 antitrypsin deficiency
• Has predominance to lower lobe distribution

44. Emphysema
• Loss of elastic recoil – premature collapse during exhalation –
airflow limitation – airway trapping and hyperinflation
• Increase RV, FRC, TLC, RV/TLC
• V/Q mismatch
• CO2 elimination is impaired only in severe V/Q mismatch since
CO2 is highly diffusible
• Chronic CO2 retention occurs slowly and compensatory
respiratory acidosis
• Therefore acute CO2 is sign of impending respiratory failure
• Arterial oxygen tension is normal or slightly reduced
• Pulmonary HTN develops due destruction of pulmonary
capillaries

45. Treatment of COPD
• Primarily supportive
• Cessation of smoking – lowers mortality by 18%,
eliminates or disappears symptoms of bronchitis
• Annual vaccination against influenza, pneumococcus
• Spirometry to assess severity of the disease and
response to bronchodilator
• Bronchodilator responsive pts –short acting
bronchodilator(when FEV1> 80% predicted), longer acting
and corticosteroid in severe

46. Treatment
• Oxygen therapy if PaO2 < 55 mm Hg, Hct > 55% or
evidence of cor pulmonale
• Goal – PaO2 > 60 mm Hg ( rate adjusted according to ABG or
pulse oximetry)
• Relief of arterial hypoxia with supplementation O2 therapy is more
effective than known drug therapy in decreasing pulmonary
vascular resistance and PHTN and preventing erythrocytosis
• Diuretics – if evidence of Right HF with Pleural edema
• Lung volume reduction
• Pulmonary rehabilitation
• Lung transplant

47. Anesthetic consideration in COPD
• Causes, course and severity of COPD
• Recent changes in dyspnea, sputum, wheezing
• Smoking hx
• Current medication
• Exercise tolerance
• FEV1 < 50% of predicted(1.2-1.5L) usually have dyspnea on exertion
• FEV1< 25%(<1L) have dyspnea with minimal activity
• Frequency of exacerbation
• Need for hospital admission
• Requirement for NIPPV or mechanical ventilation
• Associated disease due to smoking and COPD
• Diabetes, HTN, PVD, IHD,HF, Cardiac dysrhythmia, lung cancer,
Pulmonary hypertension

49. Preop investigation
• Value of routine PFT – controversial
• ABG & PFT – helps in predicting pulmonary function after lung
resection
• (but doesn’t help to predict likelihood of postop pulmonary
complication after non-thoracic sx)
• If periphery sx – no PFT needed
• Even if it is defined as high risk(FEV1 <70% predicted,
FEV1/FVC:< 60%, PaCO2 > 45) – can undergo lung resection
resection with acceptable risk
• Thus, PFT should be viewed as management tool to
optimize preoperative pulmonary function but not as a
means to predict risk

50. Other investigation
• ABG – Pco2 value
• Flow-volume loop
• CXR – to rule out other causes and to see complication
• ECG – Right ventricular strain
• Cardiac echo – in advanced disease to see RV function

52. Indication for PFT
1. Hypoxemia on room air or need for home oxygenation
therapy without known cause
2. Bicarbonate conc > 33 mEq/L or Pco2 > 50 mm Hg in pt
whose pulmonary disease has not been evaluated previously
3. Hx of respiratory failure resulting from problem that still exist
4. Severe shortness of breath attributed to respiratory disease
5. Planned pneumonectomy
6. Difficulty in assessing pulmonary function by clinical signs
7. The need to distinguish among potential causes of significant
respiratory compromise
8. The need to determine response to bronchodilator
9. Suspected pulmonary HTN

54. Preop optimization
• Correcting Hypoxia
• Relieving bronchospasm
• Mobilizing and reducing secretions
• Treating infection
• Patients with < 50% predicted PFT have high risk of
pulmonary complication
• Possibility of need of post op ventilator support should be
discuss with surgeon and patient

56. Cigarette smoking cessation
• Smoking cessation for at least 6-8 weeks before the
surgery- decreases secretion and reduces pulmonary
complications
• Smoking depletes glutathione and vitamin C – promote
oxidative injury
• Acute inhalation- release CO – increases carboxyHb level
, nitric oxide and N2 – formation of methHb

57. Cigarette smoking cessation
• Cessation for 12 h- benefits on oxygen carrying capacity
of Hb( P50 incrases from 22.9 to 26.4 mm Hg)
• Plasma level of carboxyHb decreases from 6.5% to ~ 1%(t1/2 of
CO is ~ 4-6 h)
• 6 weeks abstinence – return of normal immune function,
return of normal hepatic enzyme function
• Therefore optimum period of smoking cessation – 6-8
weeks
• Sx scheduled < 4 weeks – encourage to quit smoking,
offer behavioral support and pharmacotherapy(nicotine)
• However, there is risk of increase sputum production,
nicotine withdrawal, fear of handling stress, irritability,
sleep disturbances & depression.

59. Preop therapy to reduce postop
complication
• Continue long acting bronchodilator, mucolytics,
anticholinergics, inhaled corticosteroid till day of surgery
• Preop chest physiotherapy
• Lung expansion interventions with incentive spirometry
• Deep breathing exercise
• Cough
• Chest percussion
• Postural drainage

60. Intraop Mx
• Regional anethesia is preferred- decrease the risk of
laryngospasm, bronchospasm, barotrauma & hypoxia
associated with positive pressure ventilation and
intubation
• But high SA/EA reduces lung volume, restrict the use of
accessory muscles, produce ineffective cough
• Thus RA is avoided in sensory requirement >T6 level
• Lithotomy or lateral decubitus – may accentuate dyspnea
in awake pts
• Interscalene block – hemidiaphragm paralysis

61. GA in COPD
• Rapidly eliminated volatile anesthetics are preferred
• Volatile anesthetics has bronchodilatory effect
• Desflurane causes irritation of bronchi and increased airway
resistance
• Emergence from anesthesia with inhalation agents can be
prolonged significantly in pts with significant airway obstruction
because air-trapping also traps the inhalational agent as they
try to flood out the various body compartments into the lung
• In that case IV anesthesia with propofol is preferred
• Opioids are less useful than inhaled anesthetics for
maintenance of anesthesia – associated prolonged ventilatory
effect
• Similar is seen with thiopental and midazolam

62. Use of NO
• Use with caution
• Possibility of enlargement or rupture of bullae – tension
pneumothorax
• Thus , Avoid NO with bullae and pulmonary HTN
• Limits inspired oxygen concerntration
• Inhibition of hypoxic pulmonary vasoconstriction by
inhalation agent is usually not apparent at usual dose

63. Intraop Mx
• Preoxygenation – prevents rapid desaturation
• Slection of agents – tailored to pt and goal of optimization
• Anesthetic bronchodilatory effect is not useful
• Under positive ventilation may lead to air trapping,
dynamic hyperinflation, elevated intrinsic positive end
expiratory pressure(iPEEP).
• Dynamic hyperinflation may lead to volutrauma,
haemodynamic instability, hypercapnia, acidosis
• Intraop hypotension(increase intrathoracic pressure-
decrease venous return- increase pulmonary HTN, RV
strain)
• (**other causes: pneumothorax, bronchopleural fistula,
right heart failure)

64. Identification of air trapping
• Capnography shows CO2 doesn't’t plateau but still
upsloping at the time of next breath
• Expiratory flow has not reach zero(baseline) before
initiation of next breath in the graph
• Advanced ventilator can detect using expiratory hold

65. Intervention to mitigate air trapping
• VT – 6-8 mL/kg
• Peak airway pressure - <30 cm H2O
• FiO2 titrated to keep SpO2 > 90%
• If immediate Rx is required – disconnect the pt from
ventilator for complete exhalation
• Decreasing RR
• Allowing more time to exhale by decreasing both
respiratory rate and inspiratory/expiratory(I:E) ratio
• Allowing permissive hypercapnia
• Applying low levels of extrinsic PEEP
• Aggressively treating bronchospasm

66. • Due to increase dead space, pt wit severe COPD have
unpredictable uptake and distribution of inhalation agents,
therefore end-tidal volatile anesthestic conc is inaccurate
• May need direct measurement of arterial oxygen tension
to detect more subtle changes in intrapulmonary shunting
• Pt with FEV1 < 50% may require postop ventilation
particularly following upper abdominal and thoracic
surgery.

67. Postoperative
• Aim – to prevent pulmonary complication by increasing
FRC and facilitating an effective cough
• Lung expansion maneuvers
• Deep breathing exercise
• Incentive spirometry
• Chest physiotherapy
• Positive pressure breathing techniques
• Postop neuraxial analgesia with opioids- doesn't cause
muscle weakness
• Ambulation – increases FRC, improves oxygenation

68. References
• Morgan and Mikhals 6th edition
• Stoelting Anesthesia and co-existing

69. THANK YOU