The document discusses anaesthetic considerations for patients with chronic obstructive pulmonary disease (COPD). It defines COPD and its subtypes chronic bronchitis and emphysema. It describes taking a thorough history including dyspnea, cough, smoking history and current medications. The physical exam focuses on signs of respiratory distress and lung examination. Key investigations include spirometry, chest X-ray and blood gases which may show respiratory acidosis or chronic respiratory failure. Preoperative planning considers optimizing the patient's pulmonary status and intraoperative management focuses on lung-protective ventilation.

1. Anaesthetic considerations in
Patients with COPD.
Moderator – Dr Apurv Agarwal Sir ( Professor)
Presenter- Dr Sanika Shukla (JR2)

2. Contents
• Definition of COPD?
• Chronic Bronchitis V/S Emphysema
• Blue bloaters V/s pink puffers
• Etiopathogenesis of COPD
• History taking in a patient with COPD
• Grading of Dyspnea
• History of Smoking
• History of concurrent Medications
• Examination of a patient with COPD
• Investigation of a patient with COPD
• Spirometry
• Anaesthetic considerations
• Preoperative Anaesthetic
considerations
• Intraoperative Anaesthetic
considerations
• Ventilatory settings in COPD
• Perioperative Fluid Management
• Perioperative Bronchospasm
• Postoperative Considerations
• Regional Anaesthesia in COPD
• Acute Exacerbation of COPD

3. What is Chronic Obstructive Pulmonary
Disease?
• COPD a common preventable disease, is
characterised by persistent airflow
limitation that is usually progressive
and associated with an enhanced
chronic inflammatory response in the
airways and the lung to noxious particles
or gases.
• COPD includes
I. Chronic Bronchitis
II. Emphysema

4. CHRONIC BRONCHITIS
• Defined clinically as chronic
productive cough for 3 months
in each of 2 successive years in a
patient in whom other causes of
productive chronic cough have
excluded.
EMPHYSEMA
• Defined pathologically as the
presence of permanent
enlargement of the airspaces
distal to the terminal
bronchioles, by destruction of
their walls and without obvious
fibrosis.

5. Etiopathogensis of COPD
Tobacco smoke
Air pollution
Continued bronchial
irritation and inflammation
Breakdown of elastin in
connective tissue of
lungs
Chronic Bronchitis
Bronchial Oedema
Hyper-secretion of mucus
Chronic cough
Bronchospasm
Emphysema
Destruction of alveolar
septa
Airway Instabilty

6. Airway Obstruction
Air Trapping
Dyspnea
Frequent infections
Abnormal ventilation- perfusion ratio
Hypoxemia
Hypoventilation
Cor Pulmonale

7. Blue Bloaters
• Patients with chronic bronchitis present with productive cough on most
days in 3 consecutive months for at least 2 consecutive years.
• Recurrent exposure to irritants and air pullouts with pulmonary
infections (viral and bacterial ) are common and often associated with
bronchospasm.
• In patients with COPD, chronic Hypoxemia leads to pulmonary
vasoconstriction and eventually pulmonary hypertension and eventually
right ventricular failure, this combination of findings is often referred to as
‘blue bloaters’
• In the course of disease progression, patients gradually develop chronic
CO2 retention; the normal ventilation drive becomes less sensitive to
arterial CO2 tension and may be depressed by oxygen.

9. Pink puffers
• Disruption of the alveolar-capillary structure and loss
of the Alveolar structure leads to decreased
diffusion lung capacity, V/Q mismatch, impaired of
gas exchange.
• Also, normal parenchyma may become compressed
by the hyper inflated portions of the lung, resulting in
a further increase in the V/Q mismatch.
• Destruction of pulmonary capillaries in the alveolar
septa leads to mild to moderate pulmonary
hypertension. When dyspneic patients with
emphysema often purse their lips to delay the
closure of the small airways, which accounts for the
term “pink puffers” is often used

10. CHRONIC
BRONCHITIS
EMPHYSEMA
Age 40-45yrs 50-75yrs
Dyspnea Mild, late Severe, early
Cough Early,copious sputum Late, scanty
Infections Common Occasional
Cor Pulmonale Common Rare, terminal
Airway Resistance Increased Normal
Elastic Recoil Normal Decreased
CXR Prominent vessels, large
heart
Hyper inflated, tubular
heart
Apperance Blue bloaters Pink puffers

12. History Taking in a Patient in
COPD

13. History taking of a Patient of COPD
• The key indicators in the history of the patient are
Dysnpea that is Progressive ( worsens over time), characteristically
worsens with exercise, Persistent
Chronic cough
Chronic sputum production
History of exposure of risk factor- Tobacco Smoke/ Smoke from home
cooking and heating fuels / occupational dusts and chemical

14. Dyspnea Indicative of
COPD
Dyspnea indicative of
heart Failure
Wheezes and Ronchi Peripheral edema
Hyper-resonance to percussion Ascites and Raised JVP
Inadequate chest Excursion Orthopnea and PND
Barrel Chest, Cough with or
without expectoration
Elevated Troponin, creatinine
kinase.
Absence of Orthopnea Air hunger and feeling of
suffocation
Statements such as “Cannot take
a deep enough breath, it takes
more effort to breath
Radiograph shows increased
pulmonary vasculature and
interstial infiltrates
Radiography shows
hyperinflation, decreased
pulmonary vasculature, thickened
bronchial markings.

15. Grading of Dyspnea
( NYHA GRADING)

16. Roizen’s Criteria

17. METS SCORE
MET is defined as the amount of consumed oxygen at rest by a person,
which is approximately 3.5 ml O2/kg/min [5, 6]. This can then be used to
assess and quantify the functional capacity of an individual planned for
major non-cardiac surgery

18. Hirshmann classification of Respiratory disease
patients with hyper reactive airways

19. History of Smoking
• Duration and number of cigarettes smoked
per day are of importance and is expressed as
pack years.
• One pack = 20 cigarettes
• >40 pack years is high risk for post operative
pulmonary complications
• SMOKING INDEX- number of cigarettes/day x
total duration in years
• SI < 100 mild smoker
• SI 100-300 moderate smoker
• SI > 300 heavy smoker

20. Effects of General Anaesthesia on Smokers
• Central respiratory depression
• Reduced compliance
• Cranial shift of diaphragm
• Atelectasis
• Decreased FRC
• Impaired oxygen exchange
• Increased V/Q mismatch

21. Effect of smoking on different systems
• CVS
 Nicotine stimulates the adrenal medulla to secrete adrenaline.
Resets the aortic and carotid body receptors to maintain a higher
blood pressure.
 Stimulates the sympathetic system which results in an increase in
heart rate, blood pressure and peripheral vascular resistance.
Myocardial conntractility increased, increased oxygen demand

22. Effects on Respiratory System
• Irritants in smoke increase the mucus secretion . The mucus becomes
hyper viscous with altered elasticity.
• Cilia become inactive and are destroyed by ciliotoxins resulting into
impaired tracheobronchial clearance.
• Smoking leads to narrowing of small airways, causing an increase in
closing volume.
• Increase the proteolytic and elastolytic enzymes leading to loss of
elasticity and emphysema.

23. Other systems
• Tobacco smoke is also known to induce enzymes like cytochrome
P450 and this partially explains the PONV protecting effect of
smoking.
• Chronic exposure to nicotine leads to desensitisation of central
nicotine receptors which increases the tolerance to emetogenic
effects of surgery and anaesthesia.

24. Effects of smoking cessation
Time Durations Effects
12-24 hrs Decreases CO & Nicotine
levels
48-72 hrs COHb level normalised, ciliary
function improves
1-2 wks Decreased sputum production
4-6 wks PFTs improve
6-8 wks Immune function normalize
Decreases post op morbidity/

25. History of concurrent medications
• Patient can be on Bronchodilators, steroids, mycolytics agents.
BRONCHODILATORS
Classified as beta 2 agonists, xanthine derivatives, atropine derivatives,
mast cells inhibitors (used for prevention of an attack of bronchospasm )
and steroids.
ANAESTHETIC IMPORTANCE
1. Beta 2 agonist eg Salbutamol, terbutaline
oChronic use can produce hypokalemia there by prolonging the duration
of non depolarising and induce tachycardia and dysthymia.
oXanthines – can interact with halothane can produce dysthymia.
oSTEROIDS- There can be suppression of adrenal- cortical axis if the
patient is on prednisolone of >10 mg taken more than 10 days within 10
wks. These patients need supplemental doses of steroid before induction.
oChronic use can also produce Cushings Syndrome.

26. Examination of patient with
COPD

27.  BODY MASS INDEX ( BMI) – obesity (BMI
>30 kg/m2) decreases FRC with relative
increase in Closing Capacity producing
increase in intra pulmonary shunts and
decrease the pulmonary reserves.
• Patients with obesity are vulnerable during
the post operative period, particularly
when sedatives or opioids have been given.
Patients positioned supine are usually
susceptible to upper airway obstruction
• Postoperative continuous positive airway
pressure should be considered until the
patient can protect the airway and maintain
spontaneous ventilation without
obstruction.

28. Signs of respiratory distress-
Tachypnea, use of accessory
muscles of respiration and
cyanosis
Pallor- anemia can exacerbate
the respiratory problems by
increasing the work of
breathing due to anemic
hypoxia

29. Respiratory System Examination in
COPD
Inspection
• Barrel shaped chest
• Horizontal Ribs
• Widened intercostal Spaces
• Abdominal Respiration
• Accessory muscles of respiration-
prominent and hypertrophied.
• Respiratory rate and pattern
• Measurement of chest- reduced
chest expansion <2cm in COPD
patients.
Palpation
• Tactile vocal fremitus decreased
PERCUSSION
• Hyperresonant, tympanic note
• Cardiac and hepatic dullness lost

30. AUSCULTATION
• Bronchial breath sounds may indicate
pneumonic consolidations or cavity.
• Decreased breath sounds heard over fibrosis,
collapse, pleural effusion and pneumothorax.
Added Sounds
• Crackles/ course crepts
• Ronchi

34. Investigations in COPD

35. Investigative findings in a patient with COPD
ECG – signs of RVH can be seen
oRAD ( Right axis deviation)
oP Pulmonale in lead 2
o Predominant R wave in V1-3
oRSR pattern in precordial leads

36. ABG
In moderate to severe disease increased PaCO2
level is a bad prognostic marker.
• Acute type 2 Respiratory Failure- Type 2 Acute Respiratory Failure
with low pH, high PaCO2 and normal bicarbonate levels
• Acute on Chronic type 2 Respiratory Failure – low pH, high PaCO2
and High bicarbonate levels
• Chronic Respiratory Failure- normal pH, raised PaCO2 and HCO3-

37. CHEST X ray

I. Depression or flattening of diaphragm
II. Increase in length of lung
III. Increase size of retrosternal airspace
IV. Increase lung marking- dirty lung
V. Vertical Cardiac silhouette
VI. Increased transverse diameter of the
chest, ribs horizontal
VII. Enlarged pulmonary artery with rapid
tapering in middle zone

38. Spirometry
• Spirometry is a method of assessing lung function by measuring the
volume of air that a patient can expel from the lungs after a
maximal expiration.
• FEV1. – volume of air expired in the first second
• FVC – total volume of air that can be forcibly exhaled in one breath
• VC – A volume of a full breath exhaled in the patients own time and
not forced. Often slightly greater than the FVC particularly in COPD.

39. Measure Normal Obstructive Restrictive
FVC(L) 80% of
TLC(4800)
Decreased Sev.
Decreased
FEV1(L) 80% of FVC Decreased Decreased
FEV1/FVC(
%)
75-80% Decreased Normal to
decrease
TLC 6000ml Normal to
increased
Decreased
RV 1500ml Increased Decreased

41. Anaesthetic Considerations in
COPD

42. Preoperative Anaesthetic Consideration
• Cessation of smoking
• Dilation of airways- use of inhaled steroids+ salbutamol 3 days pre-op
reduced the incidence of post- op bronchospasm
• Hydration and loosening of secretions
• Eradication of infection- treat infection with appropriate antibiotics-
In case of URTI ideally wait for 2-3 wks.
• Recognition of cor Pulmonale and its treatment.
• Incentive spirometery
• Familiarisation with respiratory therapy, education motivation and
facilitation of patient care.

43. Intraoperative concerns in GA
• Airway instrumentation and bronchospasm
• Residual NMB
• Respiratory depression with opioids, benzodiazepines
•
• Airway humidification.

44. 1) Preoxygenation prior to induction of general anaesthesia prevents
the rapid oxygen desaturation often seen in these patients.
2) Expiratory airflow limitation, especially under positive pressure
ventilation, May lead to air trapping, dynamic hyperinflation and
elevated intrinsic positive pressure end- expiratory pressure ( iPEEP)
3) Dynamic hyperinflation may result in lung injury, hemodynamic
instability, hypercapnia and acidosis.
• Allowing more time to exhale by decreasing both the respiratory rate
and inspiratory/ expiratory ( I:E) ratio.
• Treating Broncospasm.

45. Induction of anaesthesia

46. Maintenance of Anaesthesia
Muscle relaxant
 Prefer vecuronium , rocuronium
 Avoid atracurium, mivacurium , doxacurium ( histamine release)
 Volatile anaesthetic
 NO- caution in pulmonary Bullae , dilution of delivered O2
Inhalational agent- attenuate HPV
 Volatile anaesthetics produce Bronchodilation.( Halothane>
Enflurane>isoflurane> sevoflurane)

47. Ventilatory settings in COPD
• Aim is to maximise alveolar gas emptying
• Minimise DYNAMIC hyperinflation, iPEEP
• SETTINGS
Decrease minute ventilation- low frequency
Adequate expiration time
Reduce expiration flow resistance
• Humidification of gases
• Pressure controlled mode with decelerating flow

49. Use of N2O in the Perioperative period
• N2O is contraindicated in patients with pulmonary bullae
• Nitrous oxide is usually avoided during thoracic anaesthesia.

50. Perioperative fluid management
• Excessive IV volume can lead to water accumulation and tissue edema
resulting in respiratory/heart failure.
• Hemodynamic goal directed fluid loading
• Restrictive fluid administration in cor pulmonale
• Total positive fluid balance in the first 24hrs peri-op should not
exceed 20mg/kg
• Monitoring of urine output > 0.5 ml/kg/hr is necessary

51. Causes of Perioperative
Bronchospasm
• Light anaesthesia, coughing, bucking
• Obstruction in the circuit
• Blocked/kinked ET tube
• Aspiration Pneumonia
• Head down position, bowel packing.

52. Management of intra operative
bronchospasm
• Sudden increase in resistance to
ventilation or peak inspiratory
pressure on ventilator.
• Management- cut off N2O, give
100% O2, deepening of
Anaesthesia with volatile agents
and muscle relaxants
• If bronchospasm persists
institution of bronchodilator
therapy
 long acting beta 2 agonist
Corticosteroids
Xanthines
Inj Lignocaine
Inj Ketamine

53. Postoperative Anaesthetic
Consideration

54. Predictors of Post Operative Pulmonary
Complications
• Age of the patient more than 70yrs
• ASA class 2 and above
• CHF
• Pre-existing Pulmonary Disease
• Cigarette smoking
• Hypoalbuminemia( <3.5 g/dl)
 Procedure Related
• Emergency Surgery
• Duration >3 hrs
• GA
• Abdominal, Thoracic, Head & Neck, Neuro, Vascular Surgery

55. Post Operative Anaesthetic Complications
Pulmonary complications
• Atelectasis
• Bronchopneumonia
• Pneumothorax and tension pneumothorax
• Hypoxemia
• Post op respiratory failure
Cardiovascular complications
• right sided heart failure
• Dysthymia

56. Postoperative measures to minimise
pulmonary complications in at-risk
patients
• Early mobilisation
• Lung expansion manoeuvres- consider CPAP in high risk patients
• Adequate pain control- consider epidural analgesia in high risk
patients
• Selective use of nasogastric decompression and total parental
nutrition
• DVT Prophylaxis

57. Post operative
Analgesia
• Parental NSAIDS
• Neuraxial Drugs
• Nerve Blocks
Post operative respiratory
therapy and Lung Expansion
Maneurves
• Chest physiotherapy and
postural drainage.
• Intensive Spirometry
• Deep breathing exercises
• CPAP/ BiPAP
• Early Ambulation

58. Regional Anaesthesia in
COPD

59. Techniques of regional anaesthesia
• Spinal anaesthesia
• Epidural anaesthesia
• Peripheral nerve blocks

60. Advantages of regional anaesthesia
• Better pain control
• Accentuation of neuroendocrine responses to surgery
• Improvement of tissue oxygenation
• Maintenance of immune functions
• Fewer episodes of deep venous thrombosis, pulmonary embolism.

61. Limitations Regional Anaesthesia in COPD
• Although regional anaesthesia is often considered preferable to
general anaesthesia, high spinal or epidural anaesthesia can
decrease lung volumes, restrict the use of accessory respiratory
muscles and produce an effective cough, leading to dyspnea and
retention of secretions.
• Loss of proprioception from the chest and position such as Lithotomy
or lateral decubitus may accentuate Dyspnea in awake patients.
• Concerns about hemidiaphragmatic Paralysis may make inter-
scalene blocks a less attractive option in Lung patient patients.

62. Spinal and epidural anaesthesia
• No significant effect on respiratory function- level above T6 not
recommended
• No interference with the airway, therefore, it avoids bronchospasm
• No fluctuation in intrathoracic pressure
• No risk of pneumothorax from N20
• Avoid the use of sedation as it can compromise expiratory functions

63. Para vertebral block
• Effective modality to
provide pain relief
• Can be done by the
anaesthesiologist before
the start of surgery
• Offers several technical and
clinical advantages and is
indicated for anaesthesia
when the afferent pain
input is predominantly
unilateral from the chest or
the abdomen

64. Thank-you
References- Morgan and Mikhail Chinical
Anaesthesiology
Millers Anaesthesia
Washingtons manual of Critical care
Harrisions Princples of Internal Medicine