This document discusses chronic obstructive pulmonary disease (COPD) and considerations for anesthesia. It defines COPD and describes related conditions like chronic bronchitis and emphysema. It covers risk factors, pathogenesis, pathophysiology including airway obstruction, hyperinflation, and gas exchange impairment. Clinical features, investigations, disease classification, and treatment approaches including smoking cessation and bronchodilators are summarized. Key points for anesthetists regarding airway challenges, ventilation/perfusion abnormalities, and development of auto-PEEP are highlighted.

1. COPD AND ANAESTHESTIC
CONSIDERATIONS
BY- DR NANDINI DESHPANDE
GUIDE- DR ASHISH PAREEK
SPECIAL CO- GUIDE- DR M.L.GUPTA
[PULMONOLOGIST]

2. CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
 Definition: Disease state characterized by airflow
limitation that is not fully reversible The airflow limitation is
usually progressive and is associated with an abnormal
inflammatory response of the lungs to noxious particles or
gases, primarily caused by cigarette smoking.
 According to GOLD [Global Initiative for chronic obstructive
disease],Chronic Obstructive Pulmonary Disease (COPD) is a
common, preventable and treatable disease that is characterized
by persistent respiratory symptoms and airflow limitation that is
due to airway and/or alveolar abnormalities usually caused by
significant exposure to noxious particles or gases.

3. CHRONIC
BRONCHITIS
EMPHYSEMA
PERIPHERAL AIRWAY
DISEASE
ASTHMA
BRONCHIECTASIS
PULMONARY
FIBROSIS
CYSTIC FIBROSIS

4.  Chronic Bronchitis: (Clinical Definition)
Chronic productive cough for 3 months in each of 2
successive years in a patient in whom other causes
of productive chronic cough have been excluded.
 Emphysema: (Pathological Definition)
The presence of permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and
without obvious fibrosis

5. COMPARATIVE FEATURES OF COPD
FEATURE CHRONIC BRONCHITIS EMPHYSEMA
Mechanism of airway
obstruction
Decreased Lumen d/t
mucus & inflammation
Loss of elastic recoil
Dyspnoea Moderate Severe
FEV1 Decreased Decreased
PaO2 Marked Decrease (Blue
Bloater)
Modest Decrease (Pink
Puffer)
PaCO2 Increased Normal or Decreased
Diffusing capacity Normal Decreased
Haematocrit Increased Normal
Cor pulmonale Marked Mild
Prognosis Poor Good

6. RISK FACTORS:
 Host factors:
•Genetic factors: Eg α1
Antitrypsin Deficiency
•Gender : Prevalence more
in males. ?Females
more susceptible
•Airway
Hyperresponsiveness
 Exposures:
•Smoking: Most Important
Risk Factor
•Passive/second hand
,smoking exposure
•Occupation
•Environmental pollution
•Recurrent
bronchopulmonary
infections

7. PATHOGENESIS:

8. PATHOPHYSIOLOGY AND IMPORTANT
CONSIDERATIONS TO THE ANAESTHETIST
 Airway obstruction :
 The major site of obstruction is found in the smaller conducting
airway (<2mm in diameter).
 Processes contributing to obstruction in the small conducting airway include
disruption of the epithelial barrier, interference with mucociliary clearance
apparatus that results in accumulation of inflammatory mucous exudates in
the small airway lumen, infiltration of the airway walls by inflammatory cells
and deposition of connective tissue in the airway wall.
 Fibrosis surrounding the small airway appears to be a significant contributor.
This remodeling and repair thickens the airway walls, reduces lumen caliber
and restricts the normal increase in calibre produced by lung inflation

9.  Increased resistance of the small conducting airway and increased
compliance of the lung as a result of emphysematous destruction, causes
the prolonged time constant.
 This constant is reflected in measurements of the FEV1 and its ratio to
forced vital capacity(FEV1/FVC),which are reliable screening tools
because they are affected by both airway obstruction and emphysema.
 Hyperinflation:
 In COPD there is often “air trapping” (increased residual volume and
increased ratio of residual volume to total lung capacity) and progressive
hyperinflation (increased total lung capacity) late in the disease.
Hyperinflation of the thorax during tidal breathing preserves maximum
expiratory airflow, because as lung volume increases, elastic recoil
pressure increases, and airways enlarge so that airway resistance
decreases.

10.  Despite compensating for airway obstruction, hyperinflation can push the
diaphragm into a flattened position with a number of adverse effects.
 First, by decreasing the zone of apposition between the diaphragm and
the abdominal wall, positive abdominal pressure during inspiration is not
applied as effectively to the chest wall, hindering rib cage movement and
impairing inspiration.
 Second, because the muscle fibers of the flattened diaphragm are
shorter than those of a more normally curved diaphragm, they are less
capable of generating inspiratory pressures than normal.
 Third, the flattened diaphragm (with increased radius of curvature)
must generate greater tension to develop the transpulmonary pressure
required to produce tidal breathing.

11.  Gas exchange:
 Non‐uniform ventilation and ventilation‐perfusion mismatch are
characteristics of COPD, due to the heterogenous nature of the disease
process within airway and lung parenchyma.
 Ventilation/ perfusion (V/Q) mismatching causes reduction in PaO2 but
shunting is minimal.
 This finding explains the effectiveness of modest elevation of inspired
oxygen in treating hypoxemia due to COPD. Pao2 usually remains near
normal until FEV1 is decreased to 50% of predicted and elevation of
PaCO2 is not seen until FEV1 is <25%.
 Hypercapnia, if present, reflects both V/Q mismatching and alveolar
hypoventilation, the later resulting from both respiratory muscle
dysfunction and increased ventilatory requirements.
 Pulmonary hypertension severe enough to cause cor-pulmonale and right
heart failure is seen when there is marked decrease in FEV1<25% along
with chronic hypoxemia PaO2 <55 mmHg.

12. CONCEPT OF AUTO-PEEP
 Patients with severe COPD often breathe in a pattern that interrupts
expiration before the alveolar pressure has decreased to atmospheric
pressure.
 This incomplete expiration is due to a combination of factors which
include flow limitation, increased work of respiration and increased
airway resistance
 This interruption leads to an increase of the end‐expiratory lung volume
above the FRC. This PEEP in the alveoli at rest has been termed
auto‐PEEP or PEEP i.
 All these changes can cause difficulty in positive
pressure ventilation , increase in peak pressures,
development of auto –PEEP and impaired ventilation
and perfusion during anaesthesia.

13. CLINICAL FEATURES:
 Symptoms: Cough: Initially intermittent Present throughout the day
Sputum: Tenacious & mucoid Purulent Infection Dyspnea: Progressively
worsens, Persistent.
 Physical Examination:
 Respiratory Signs •Barrel Chest •Pursed lip breathing •Adventitious
Ronchi/Wheeze
 Systemic Signs •Cyanosis •Neck vein enlargement •Peripheral oedema
•Liver enlargement •Loss of muscle mass
 Exposure: Smoking, in pack years

15. INVESTIGATIONS:
 PULMONARY FUNCTION TESTS:
Diagnosis
Assessment of severity
Following progress Decreased
FEV1/FVC
Decreased FEF
(25-75%)
Increased RV

18.  ARTERIAL BLOOD GASES:
Arterial blood gases and oximetry may demonstrate resting or
exertional hypoxemia
Arterial blood gases provide additional information about alveolar
ventilation and acid-base status by measuring arterial Pco2 and pH .
The change in pH with Pco2 is 0.08 units/10 mmHg acutely and 0.03
units/10 mmHg in the chronic state .
The arterial blood gas is an important component of the evaluation
of patients presenting with symptoms of an exacerbation.

19.  CHEST RADIOGRAPH:

20.  CT SCAN:
Computed tomography (CT) scan is the current definitive
test for establishing the presence or absence of
emphysema.
 ECG:
Signs of RVH: RAD , p Pulmonale in Lead II ,Predominant
R wave in V1-3 , RS pattern in precordial leads

21. Bronchodilator Reversibility Testing
 Provides the best achievable FEV1 (and FVC) .
 Can be done on first visit if no diagnosis has been
made .
 Best done as a planned procedure: pre- and
postbronchodilator tests require a minimum of 15
minutes

22. Alpha-1 antitrypsin deficiency (AATD)
 The World Health Organization recommends that all patients with
a diagnosis of COPD should be screened once especially in areas
with high AATD prevalence.
 AATD patients are typically < 45 years with pan lobular basal
emphysema.
 Delay in diagnosis in older AATD patients presents as more
typical distribution of emphysema (centrilobular apical).
 A low concentration (< 20% normal) is highly suggestive of
homozygous deficiency.

23. GOLD CLASSIFICATION:
STAGE CHARACTERISTICS
Mild FEV1/FVC< 70%
FEV1< 80% predicted, with/without chronic
symptoms
Moderate FEV1/FVC< 70%
50%<FEV1< 80% predicted, with/without
chronic symptoms
Severe FEV1/FVC< 70%
30%<FEV1< 50% predicted, with/without
chronic symptoms
Very severe FEV1/FVC< 70%
FEV1< 30% predicted or <50% predicted plus
chronic respiratory failure (PaCO2<60 mmHg
or PaCO2>50 mmHg)

24. TREATMENT:
 Modifying natural history of Disease:
Smoking cessation
Long term oxygen therapy
 Symptomatic:
Bronchodilators
Antibiotics
 Pulmonary Rehabilitation
 Nutrition

25. SMOKING CESSATION:
 Time course Beneficial effects
 12-24 hours ↓ COHb levels and nicotine levels
 48-72 hours bronchociliary functions improve
 1-2 weeks sputum production
 4-6 weeks PFT improves
 6-8 weeks immune function and drug metabolism normalize
 8-12 weeks ↓overall perioperative morbidity

26. MANAGEMENT OF COPD STAGE I: MILD COPD
 Characteristics:
Treatment:
• FEV1 /FVC < 70%
• FEV1 > 80 %
predicted
• With or without
chronic
symptoms
Short-acting
bronchodilators
as needed

27. MANAGEMENT OF COPD STAGE II:
MODERATE COPD
 Characteristics:
Treatment:
• FEV1 /FVC < 70%
• 50% < FEV1<
80% predicted
• With or without
chronic
symptoms
• Short-acting
bronchodilators
as needed
• Regular
treatment with
one or more
long-acting
bronchodilators
• Rehabilitation

28. MANAGEMENT OF COPD STAGE III: SEVERE
COPD
 Characteristics:
Treatment:
• FEV1 /FVC < 70%
• 30% < FEV1<
50% predicted
• With or without
chronic
symptoms
• Short-acting bronchodilators
as needed
• Regular treatment with one
or more long-acting
bronchodilators
• Inhaled glucocorticosteroids
if repeated exacerbations
• Rehabilitation

29. MANAGEMENT OF COPD STAGE IV:
VERY SEVERE COPD
 Characteristics:
Treatment:
• FEV1 /FVC < 70%
• 30% < FEV1<
50% predicted
• Plus chronic
respiratory
failure
• Short-acting bronchodilators as
needed
• Regular treatment with one or
more long-acting bronchodilators
• Inhaled glucocorticosteroids if
repeated exacerbations
• Treat complications
• Rehabilitation
• Long-term oxygen therapy if
respiratory failure
• Consider surgical options

30. LONG TERM OXYGEN THERAPY:
 Improves survival, exercise, sleep and cognitive
performance.
 Oxygen delivery methods include nasal continuous
flow, reservoir cannulas and transtracheal catheter.
 Physiological indications for oxygen include an arterial
oxygen tension (PaO2 )<7.3kPa (55mmHg). The
therapeutic goal is to maintain spO2 >90% during rest,
sleep and exertion.

33. SURGICAL TREATMENT:
 Bullectomy -short-term improvements in
1. airflow obstruction
2. lung volumes
3. hypoxaemia and hypercapnia
4. exercise capacity
5. Dyspnoea
 Lung Volume Reduction Surgery -potentially long-term improvement in
1. survival
2. short-term improvements in Spirometry
3. lung volumes
4. exercise tolerance
5. dyspnoea
 Lung Transplantation

34. COPD : EXACERBATIONS:
 Definition: An exacerbation of COPD is an event in the
natural course of the disease characterized by a change in the
patient’s baseline dyspnea, cough and/or sputum beyond day-to-
day variability sufficient to warrant a change in management.
 Precipitating Causes:
 Infections: Bacterial, Viral
 Air pollution exposure
 Non compliance with LTOT

35. INDICATIONS FOR HOSPITALIZATION:
 The presence of high-risk comorbid conditions
1. Pneumonia
2. cardiac arrhythmia
3. congestive heart failure
4. diabetes mellitus
5. renal or liver failure
 Inadequate response to outpatient management
 Marked increase in dyspnoea, orthopnoea
 Worsening hypoxaemia & hypercapnia
 Changes in mental status
 Uncertain diagnosis.

36. INDICATION FOR ICU ADMISSION:
 Impending or actual respiratory failure
 Presence of other end-organ dysfunction
1. shock
2. renal failure
3. liver failure
4. neurological disturbance
 Haemodynamic instability

37. TREATMENT FOR COPD EXACERBATION:
 Supplemental Oxygen (if SPO2 < 90%)
 Bronchodilators:
1. Nebulised Beta Agonists,
2. Ipratropium with spacer/MDI
 Corticosteroids -Inhaled, Oral
 Antibiotics:
1. If change in sputum characteristics
2. Based on local antibiotic resistance
3. Amoxycillin/Clavulanate, Respiratory
Fluoroquinolones
 Ventilatory support: NIV, Invasive ventilation

38. PREPARATION FOR ANAESTHESIA:

39. Anaesthetic Considerations in patients
with COPD undergoing surgery:
Patient Factors:
 Advanced age
 Poor general condition, nutritional status
 Co morbid conditions :
1. HTN
2. Diabetes
3. Heart Disease
4. Obesity
5. Sleep Apnea

40. Problems due to Disease
 Exacerbation of Bronchial inflammation
 d/t Airway instrumentation
 preoperative airway infection
 surgery induced immunosuppression
 increased work of breathing
 Increased post operative pulmonary
complications

41.  Problems due to Anaesthesia:
1. GA decreases lung volumes, promotes V/Q mismatch
2. FRC reduced during anaesthesia
3. Anaesthetic drugs blunt Ventilatory responses to
hypoxia & CO2
4. Postoperative Atelectasis & hypoxemia
5. Postoperative pain limits coughing & lung expansion
 Problems due to Surgery:
1. Site : most important predictor of Post op
complications
2. Duration: > 3 hours
3. Position

42. PRE-OPERATIVE ASSESMENT:
 History:
1. Smoking
2. Cough: Type, Progression, Recent RTI
3. Sputum: Quantity, colour, blood
4. Dyspnoea
5. Exercise intolerance
6. Occupation, Allergies
7. Symptoms of cardiac or respiratory failure

43.  Examination:
1. Body Habitus:- Obesity/ Malnourished
2. Active infection
3. Sputum- change in quantity, nature
4. Fever
5. Crepitations
 Respiratory failure
1. Hypercapnia
2. Hypoxia
3. Cyanosis

44.  Cor Pulmonale and Right heart failure
1. Dependent oedema
2. tender enlarged liver
 Pulmonary hypertension
1. Loud P2
2. Right Parasternal heave
3. Tricuspid regurgitation

45. INVESTIGATIONS:
 Complete Blood count
 Serum Electrolytes
 Blood Sugar
 ECG
 Arterial Blood Gases
 Chest X Ray
 Spiral CT
 Preoperative Pulmonary Function Tests-specific and
nonspecific tests

46. INDICATIONS FOR PFT ‘S:
(AMERICAN COLLEGE OF PHYSICIANS CONSENSUS
STATEMENT)
 Cardiac, thoracic or upper abdominal surgery with a
history of dyspnoea, smoking
 Lower abdominal surgery with a history of dyspnoea,
smoking and anticipated prolonged surgery
 All patients undergoing lung resection
 Morbid obesity
 Any pulmonary disease
 Age > 70 years

47. PRE-OPERATIVE PREPARATION:
 Cessation of smoking
 Dilatation of airways
 Loosening & Removal of secretions
 Eradication of infection
 Recognition of Cor Pulmonale and treatment
 Improve strength of skeletal muscles – nutrition, exercise
 Correct electrolyte imbalance
 Familiarization with respiratory therapy, education, motivation
& facilitation of patient care

48. DRUGS COMMONLY ENCOUNTERED:
 Anticholinergics:
 Block muscarinic receptors
 Onset of action within 30 Min
 Ipratropium – MDI:- 17 mcg/puff, 200 puffs/ canister -2-3 puffs every 6hours
 NEBULIZER:- 0.25mg/ml(0.025%)- 0.25mg every 6hours
 Ipratropium bromide is generally preferred to the short acting beta-2-agonists
as a first-line agent because of its longer duration of action and absence of
sympathomimetic side effects
 Tiotropium - long lasting
 Side Effects: Dry Mouth, metallic taste
 Caution in Prostatism & Glaucoma

49. Beta Agonists:
 Act by increasing cAMP
 Specific β2 agonist – Salbutamol : oral 2-4 mg,
0.25 – 0.5 mg i.m /s.c and 100-200 μg inhalation
 Side – effects: muscle tremors, palpitations, throat
irritation
 Terbutaline : oral 5 mg/ 0.25 mg s.c./ 250 μg
inhalation
 Salmeterol : Long acting (12 hrs) , 50 μg BD- 200 μg
BD

50.  Methylxanthines :
 Mode of Action – inhibition of phospodiesterase,↑ cAMP,
cGMP – Bronchodilatation
 Adenosine receptor antagonism
 ↑ Ca release from SR
 Intravenous (Aminophylline, Theophylline)
 loading – 5mg/kg
 Maintenance – 0.5mg/kg/h

51. Inhaled Corticosteroids:
 Anti-inflammatory
 Restore responsiveness to β2 agonist
 Reduce severity and frequency of
exacerbations
 Do not alter rate of decline of FEV1
 Beclomethasone, Budesonide, Fluticasone

52. ANAESTHETIC TECHNIQUE……..

53. Choice of anaesthesia
depends on the
1. Patient factors(clinical state)
2. Surgical factors(type and duration
of procedure)

54. CONCERNS IN REGIONAL ANAESTHESIA:
 NEURAXIAL TECHNIQUES:
• No significant effect on Respiratory
function
• Level above T6 not recommended
• No interference with airway
• Avoids bronchospasm
• No danger of pneumothorax from N2O

55.  PERIPHERAL NERVE BLOCKS:
• Suitable for peripheral limb surgeries
• Minimal respiratory effects
• Supraclavicular techniques are
contraindicated in severe pulmonary
disease
• Interscalene block remains a concern
due to ipsilateral phrenic nerve
paralysis and loss of sympathetic tone
due to stellate ganglion block resulting
in bronchospasm

56.  Thoracic epidural anesthesia using low
concentrations of local anaesthetic agents and low
doses of opiates suppresses both the afferent
nociceptive inputs and the efferent sympathetic output
thus preserving the respiratory muscular activity and
the HPV response. It also improve ventilatory
mechanics resulting in decreased airway resistance,
lower work of breathing and better preservation of
inspiratory and expiratory capacities allowing lung
recruitment maneuvers and voluntary drainage of
secretions

57. CONCERNS IN GENERAL ANAESTHESIA:
 General anesthetic agents, opiates, myorelaxants as well as
mechanical ventilation are known to interfere with the
respiratory system.
 The combined effects of the supine position, GA and
thoracic/abdominal incision produce an immediate decline in
lung volumes with atelectasis formation in the most
dependent parts of the lung .
 Pre-oxygenation should be used in any patient who is
hypoxic on air before induction. In patients with severe COPD
and hypoxia, CPAP during induction may be used to improve
the efficacy of pre-oxygenation and reduce the development
of atelectasis.

58.  Upper airway instrumentation( eg tracheal intubation) may
trigger vagally-mediated reflex bronchoconstriction thereby
promoting the expiratory collapse of the peripheral airways with
incomplete lung alveolar emptying
 To attenuate the Broncho constrictive reflex due to endotracheal
intubation or suctioning, prophylactic treatment with lidocaine(IV
or inhaled) and/or a beta2-adrenergic agonist are recommended
in COPD patients with bronchospastic response
 Volatile anaesthetics like halothane [best], sevoflurane are
useful for maintenance of anaesthesia due to their excellent
Broncho dilating properties with the possible exception of
desflurane and isoflurane. Both desflurane and isoflurane may
cause irritation of the bronchi because of their pungent odour
and increase the airway resistance so there may be an advantage
to choosing a less irritating agent such as sevoflurane for
induction and emergence in cases of severe airway reactivity.

59.  Emergence from anesthesia with inhalational agents
can be prolonged significantly ,especially in patients
with significant airway obstruction, because air
trapping also traps inhalational agents as they flood
out of the body’s compartments into the lungs .
 Nitrous oxide can be administered in combination with
a volatile anesthetic. When nitrous oxide is used, there
is the potential for passage of this gas into pulmonary
bullae. is could lead to enlargement or even rupture of
the bullae, resulting in development of a
pneumothorax.
 Another potential disadvantage of nitrous oxide is the
limitation on the inspired oxygen concentration that it
imposes.

60.  Opioids may be less useful than inhaled anesthetics for maintenance
of anesthesia in patients with COPD because they can be associated
with prolonged ventilatory depression as a result of their slow rate
of metabolism or elimination.
 An endotracheal tube bypasses most of the natural airway
humidification system, so humidification of inspired gases and use of
low gas flows are needed to keep airway secretions moist.
 General anesthesia exceeding 2.5–4 hours has been identified as a
strong predictor of PPCs .Indeed, prolonged exposure to general
anesthetics alters the immune defenses and gas exchange capacity
mainly by depressing the alveolar macrophage function, interfering
with surfactant production, slowing of the muco-ciliary clearance and
increasing the permeability of the alveolar-capillary barrier.
 Management of ventilation during general anaesthesia should be
aimed at reducing the dynamic hyperinflation, PEEP i, and air
trapping. Harmful effects of air trapping include hypotension,
barotrauma and volume trauma to the lungs, hypercapnia, and
acidosis

61.  Measures to reduce air trapping include use of smaller
tidal volumes and lower respiratory rates, with more
time for expiration.
 Shortening the inspiratory time increases the peak
inspiratory flow thereby facilitating better ventilation
of all alveoli.
 Tidal volumes of 6 to 8 mL/kg combined with slow
inspiratory flow rates minimize the likelihood of
turbulent air flow and help maintain optimal
ventilation/perfusion matching .
 Slow respiratory rates (6 to 10 breaths per minute)
provide sufficient time for complete exhalation to
occur, which is particularly important if air trapping is
to be minimized. Slow rates also allow sufficient time
for venous return and are less likely to be associated
with undesirable degrees of hyperventilation .

62.  Application of external PEEP has been shown to decrease
the effort of triggering breaths in patients breathing
spontaneously on assisted modes of ventilation.
 Even during controlled ventilation, external PEEP that is
less than or equal to PEEP i, is not found to significantly
increase the alveolar pressure.
 Pressure controlled ventilation, by virtue of its
decelerating flow reduces peak inspiratory pressure and
allows for more uniform distribution of tidal volume and
improvement of static and dynamic compliance .
 Residual neuromuscular blockade persisting after
anesthesia emergence has been incriminated in deficient
coughing, depressed hypoxic ventilatory drive and “silent”
inhalation of gastric contents
 Restrictive fluid administration decreases risk of
pulmonary oedema, it has been accepted in thoracic surgery
and showed good outcomes after major abdominal
interventions.

63. INTRAOPERATIVE INCREASED PIP:
1. Bronchospasm
2. Light anaesthesia, coughing, bucking
3. Obstruction in the circuit
4. Blocked / kinked tube
5. Endobronchial intubation
6. Pneumothorax
7. Pulmonary embolism
8. Major Atelectasis
9. Pulmonary oedema
10. Aspiration pneumonia

64. INTRAOPERATIVE BRONCHOSPASM:
 Bronchospasm during anaesthesia usually manifests as prolonged
expiration .
 Expiratory wheeze may be auscultated in the chest or heard in the
breathing circuit due to movement of the gas through narrowed
airway .
 Breath sounds may be reduced or absent.
 With intermittent positive pressure ventilation, peak airway
pressures are increased, tidal volumes reduced, or both.
 In severe bronchospasm, wheeze may be quiet or absent due to
cessation of movement of air

65.  With capnography, narrowed
airway and prolonged
expiration result in a delayed
rise in end‐tidal carbon
dioxide, producing a
characteristic ‘shark fin’
appearance

66.  Intraoperatively, bronchospasm occurs most commonly during the
induction and maintenance stages of anaesthesia and is less often
encountered in the emergence and recovery stages .
 Bronchospasm during the induction stage is most commonly
caused by airway irritation, often related to intubation.
 During the maintenance stage of anaesthesia, bronchospasm may
result from an anaphylactic or serious allergic reaction. Following
endotracheal intubation, wheezing is more likely to occur when
barbiturates are used as anaesthetic induction agents, compared
with propofol, ketamine or volatile anaesthetics

67. Inhalational: isoflurane,
desflurane [ due to
pungent odour]
IV Induction drugs:
thiopentone, etomidate
Opioids: morphine,
pethidine
Muscle relaxants:
atracurium,
mivacurium[>histamine
release],
succinylcholine[<histamine
]
Anaesthetic
drugs
causing
bronchospas
m

68. Inhalational:
sevoflurane[sweet-
smelling],halothane [best
bronchodilator]
IV Induction drugs:
propofol[ haemodynamically
stable patients] , ketamine[
haemodynamically unstable
patients]
Opioids: fentanyl
Muscle relaxants:
cisatracurium ,
vecuronium , rocuronium
Anaesthetic
drugs
preferred in
COPD patients

69. MANAGEMENT OF INTRAOPERATIVE
BRONCHOSPASM:

71.  Increase FiO2 to 100%
 Deepen the plane of anaesthesia - Commonest cause is
surgical stimulation under light anaesthesia
 Relieve mechanical stimulation - endotracheal suction,
Stop surgery
 β2 agonists – Nebulisation or MDI
1. s/c Terbutaline, iv Adrenaline
 intravenous Aminophylline:-5mg/kg IV over 20min then
0.5mg/kg/h infusion
 Intravenous corticosteroid(hydrocortisone 200mg)
indicated if severe bronchospasm

72. POST-OPERATIVE PULMONARY
COMPLICATIONS:
1. Atelectasis
2. Aspiration pneumonitis
3. Ventilator associated pneumonia[VAP]
4. Deep vein thrombosis and pulmonary
embolism

74. POST-OPERATIVE CARE:
 Mechanical Ventilation:
Indications:
1. Severe COPD undergoing major surgery
2. FEV1 /FVC<70%
3. Pre-op PaCo2> 50mm Hg
FiO2 & Ventilator settings adjusted to maintain PaO2 60- 100
mm Hg & PaCO2 in range that maintains pH at7.35- 7.45
 Continue Bronchodilators
 Oxygen therapy
 Lung Expansion manoeuvres

75. RISK REDUCTION STRATEGIES:
PRE-OPERATIVE:
• Cessation of smoking for at least 6 weeks
• Treat evidence of expiratory airflow obstruction
• Treat respiratory infection with antibiotics
• Initiate patient education regarding lung expansion
maneuverers [incentive spirometry, chest
physiotherapy, deep breathing exercises, postural
drainage]

76. INTRAOPERATIVE:
• Minimally invasive
surgery
• Consider regional
anaesthesia
• Avoid surgical
procedures lasting
>3 hours
POST-OPERATIVE:
• Incentive
spirometry
• CPAP or NIV
ventilation
• Voluntary deep
breathing
• Analgesia
[neuraxial
opioids,
intercostal nerve
blocks, patient –
controlled
analgesia]
• Ambulation

77. SUMMARY:
 COPD is a progressive disease with increasing irreversible
airway obstruction.
 Cigarette smoking is the most important causative factor for
COPD.
 Smoking cessation & LTOT are the only measures capable of
altering the natural history of COPD.
 COPD is not a contraindication for any particular anaesthesia
technique if patients have been appropriately stabilized.
 COPD patients are prone to develop intraoperative and
postoperative pulmonary complications.
 Preoperative optimization should include control of infection
and wheezing.
 Postoperative lung expansion maneuvers and adequate post op
analgesia have been proven to decrease incidence of post op
complications.