The document outlines the definition, causes, symptoms, and management of asthma, including specific preoperative, intraoperative, and postoperative considerations. It details pulmonary function tests, treatment protocols for acute asthma attacks, and best practices for anesthesia management in asthmatic patients. The material emphasizes the importance of patient evaluation and individualized treatment plans to optimize respiratory function during surgical procedures.

1. Asthma and COPD
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2. Objectives
 Define asthma and Explain the cause of asthma
 List symptoms and signs of asthma
 Describe the general considerations for pt with asthma
 Explain the preoperative evaluation and preparation
 Describe the perioperative medications used to treat asthma
 List drugs safe for asthmatics
 Describe anaesthesia management of asthmatic patients
 Describe management of severe bronchospasm outside OR
 Describe management of severe bronchospasm during anaesthesia
 Manage asthmatic patients during the perioperative period
 Describe the postoperative care of asthmatic patients
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3. Introduction
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4. Normal values
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5.  Functional resdual capacity (FRC)
◦ 40% of TLV
◦ Pulmonary variables are optimized at FRC because of
better
 Work of breathing
 Vascular resistance
 Ventilation perfusion ratio
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6. Factors affecting lung volumes &
capacitis
 FRC increase is caused by hyperinflation,
emphysema, asthma
  TLC is caused by restrictive pulmonary
disease, interstitial fibrosis
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7. Dray spirometer (vitalography)
Used to record the forced expiratory spirogram which
includes
FVC = Forced vital capacity
Total volume expired under maximal effort
FEV1= Forced expiratory volume during one sec
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8. ◦ Vital capacity: Influenced by
 Strength of muscle
 Range of diaphragm motility
 Posture
 Compromising abdominal volume
 Chest deformity
 Pain
 Increased residual volume
 Bronchial asthma, emphysema)
 Reduction of total lung capacity
 Pneumothorax
 Pulmonary congestion
 Lung compliance
 Lung fibrosis
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9. Pulmonary function test (PFT)
1. Forced expiratory volume-1 (FEV1)
 Volume of air expired by the end of one second
 Fraction of vital capacity expelled in the first one second using
maximal expiratory effort
 Represents forced expiration
 It is effort dependent
 Normal value is 80% of FVC
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10. FEV1/FVC
◦ FEV1 Percent or (FEV1%)
◦ This number is the ratio of FEV1 to FVC
◦ It indicates what percentage of the total FVC was expelled
from the lungs during the first second of forced exhalation
◦ This number is called FEV1%, %FEV1 or FEV1/FVC
ratio.
◦ This PFT value is critically important in the diagnosis of
obstructive and restrictive diseases.
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11. Obstructive Pulmonary Disease
 Obstructive and restrictive diseases are the two
most common abnormal patterns as determined by
PFTs.
 Obstructive diseases include asthma, emphysema,
chronic bronchitis, cystic fibrosis, bronchiectasis,
and bronchiolitis.
 The primary characteristic of these disorders is
resistance to airflow.
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12.  Restrictive pulmonary diseases are characterized by
decreased lung compliance.
 Lung volumes are typically reduced, with
preservation of normal expiratory flow rates.
 Both FEV1 and FVC are reduced, but the
FEV1/FVC ratio is normal.
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13.  Restrictive pulmonary diseases include many acute
and chronic intrinsic pulmonary disorders, as well as
extrinsic (extrapulmonary) disorders involving the
pleura, chest wall, diaphragm, or neuromuscular
function.
 Reduced lung compliance increases the work of
breathing, resulting in a characteristic rapid but
shallow, breathing pattern
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14.  Elevated airway resistance and air trapping increase
the work of breathing.
 Respiratory gas exchange is impaired because of
ventilation/perfusion ( V/Q)imbalance.
 The predominance of expiratory airflow resistance
results in air trapping; residual volume and total lung
capacity (TLC) increase.
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15.  Wheezing is a common finding and represents
turbulent airflow.
 It is often absent with mild obstruction that may be
manifested initially only by prolonged exhalation.
 Progressive obstruction typically results first in
expiratory wheezing only, and then in both
inspiratory and expiratory wheezing.
 With marked obstruction,wheezing may be absent
when airflow has nearly ceased.
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16.  Obstructive lung diseases
◦ Difficulty in moving gas out of the lun
◦ There is high airway resistance
◦ Reduced FEV
◦ Reduced FEV/FVC ratio
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17. PFTS-OBSTRUCTIVE
PARAMETER Asthma Bronchitis Emphysem
 FVC dec dec dec
 FEV1 dec dec dec
 FEV1/FVC dec dec dec
 RV/TLC inc inc inc
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18. PFTS - RESTRICTIVE
PARAMETER INTRINSIC EXTRINSIC
 FVC dec dec
 FEV1 normal normal
 FEV1/FVC normal normal
 RV/TLC normal increased
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19. Maximal expiratory flow (MEF)
◦ Peak expiratory flow (PEF)
◦ The maximal flow rate of air during FEV1
◦ Normal value is 8 L/s
◦ It is reduced in bronchial asthma .
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20. Forced expiratory flow (FEF)
 The FVC expiratory curve is divided into quartiles:
therefore there is a FEF that exists for each quartile.
 The quartiles are expressed as FEF25%, FEF50%,
and FEF75% of FVC.
◦ FEF25% - Describes the volume of air (L/s) that was
forcibly expelled in the first 25% of the total FVC test.
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21. Maximal Voluntary Ventilation (MVV) –
 This value is determined by breathing in and out as
rapidly and fully as possible for 12 -15 seconds
 The total volume of air moved during the test can be
expressed as L/sec or L/min (150 l/min)
 Reflects the status of the respiratory muscles, compliance
of the thorax-lung complex, and airway resistance.
 Ventilation reserve index = (MVV-MV) x100
MVV
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22.  Breathing Frequency: Measured by
Observing chest movement
Stetography
Breathing frequency (f) =
=12 breaths /min in adults
 Minute ventilation (MV)
MV =Tv x f
 Alveolar Ventilation = (Tv-VD) x f
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23. Dead space volume (VD)
Anatomic VD: Approximated in two ways:
VD = VT ( PACO2-PECO2)
PaCO2
In health
 Anatomic DV =Physiologic DV
In diseases,
Physiologic VD= Anatomic VD+ volume of
nonfunctional alveoli.
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24. Asthma
Definition: Asthma is a reversible airflow obstruction due to
constriction of smooth muscles in the airway
Bronchial wall inflammation
- Mucus hyper secretion,
- Epithelial damage
- Airways constriction
Triggering factors:
-Exercise, cold air, viral infections, occupational exposure and
emotional stress) 6/22/2024 24

25. Clinical manifestations:
Wheezing
Shortness of breath
Cough and
Chest tightness
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26. Pathophysiology:
 The immunologic-inflammatory pathways involved in the
pathogenesis of asthma are complex and include lymphocytes,
immunoglobulin E, eosinophils, neutrophils, mast cells, leucotrienes,
and cytokines.
 These pathways are triggered and modified by extrinsic and
environmental factors such as allergens, respiratory infections,
smoke, and occupation-related exposure.
 Thus, asthma ultimately represents a dynamic interaction between
host and environmental factors
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27. Airway inflammation contributes to airway
hyperresponsiveness, airflow limitation, respiratory
symptoms, and disease chronicity.
In some patients, persistent changes in airway structure
occur, including sub-basement fibrosis, mucus hyper
secretion, injury to epithelial cells, smooth muscle
hypertrophy, and angiogenesis.
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28. Airway edema.
These include edema, inflammation, mucus hyper secretion and
the formation of mucus plugs, as well as structural changes
including hypertrophy and hyperplasia of the airway smooth
muscle.
These latter changes may not respond to usual treatment.
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29. Prevention of attacks
 Allergens that can be controlled by avoidance (e.g. animal
dander, dust, airborne moulds, and pollens) should be
eliminated.
 Nonspecific exacerbating factors (e.g. cigarette smoke,
odors, irritant fumes, and change in temperature,
atmospheric pressure, and humidity) should also be
investigated and avoided if possible.
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30. Treatments
 Drugs used to treat asthma include β-adrenergic
agonists, methylxanthines, glucocorticoids,
anticholinergics, leukotriene modifiers, and mast-
cell–stabilizing agents.
 Although devoid of any bronchodilating properties,
cromolyn sodium and nedocromil are effective in
preventing bronchospasm by blocking the
degranulation of mast cells.
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31. • Assessing the severity of the attack is paramount in
deciding management
◦ Bronchodilators should be used in orderly progression
◦ Decide when to start corticosteroids
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32. Cont.
 Treatment of the Acute Attack
 Mild acute attack: most can be managed as an outpatient
 Salbutamol aerosol (Ventolin®) two puffs every 20 minutes for
three doses is the 1st line of treatment.
 Adrenaline 1:1000 can be given in doses up to a maximum of
0.2 ml in children and 0.3ml in adults, repeated once or twice
in 20 to 30 min (if there is no hypertension or any other contra
indication). 6/22/2024 32

33.  If the initial treatment fails, Aminophylline 250 mg IV
diluted in dextrose in water should be given slowly over
10-15 minutes, once.
 If the patient does not respond to one dose of
aminophylline IV, then the patient is declared to have
severe asthma, and should be admitted and managed
as in-patient.
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34. Cont.
 In patient management
 Patients who are diagnosed to have severe and life threatening
asthma need in patient management. Some may even need
admission to ICU.
 Signs of Severity of acute asthmatic attack
1) Tachycardia HR > 120/min , Tachypnea RR >30 min
2) Presence of pulsus paradoxus
3) Use of accessory muscles of respiration
4) Cyanosis

35. Cont.
6) Silent chest
7) Paradoxical movement of the chest and the abdomen
8) Presence of complications: Pneumothorax, atelectasis & etc.
9) Frequent interruption of speech to take a breath
10) Laboratory parameters
 PEFR < 50 % or FEV1 < 60 %
 PaO2 < 60mmof Hg or SaO2 < 90 %
 PaCO2 > 42 mmHg

36.  Specific drug Treatment
 Aminoplylline 1mg/kg/hr in a continuous IV infusion should be given.
 Corticosteroids should also be given IV e.g. Hydrocortisone 4mg/kg
IV every 4 hrs.
 When the patient improves the hydrocortisone be changed to
Prednisolone PO and the dosage should be tapered up on discharge.
 Patients who do not respond to aggressive drug therapy are
candidates for endotracheal intubation and Mechanical Ventilation for
which they should be admitted to an ICU.

37. Cont.
 Respiratory tract infections precipitating acute asthmatic
attack are predominantly viral; but if patients expectorate
yellowish, green or brown sputum, antibacterial therapy is
indicated. Ampicillin is the first line; alternatives are TTC,
erythromycin or cotrimoxazole.
 Chest x-ray is taken if there is suspicion of pneumonia or
complications.

38. Cont.
 Supportive Treatment
 O2 is always indicated for hospitalized patients.
 Fluid and electrolyte balance requires special attention because of
frequent occurrence of dehydration during acute asthmatic attack.
 However, over hydration may cause pulmonary edema and one
should be cautious in fluid administration.
 Anxiety is common in patients with severe acute asthmatic attack.
However this can be overcome when underlying hypoxia and feeling
of asphyxiation is treated.

39. Cont.
Maintenance Therapy (Chronic Treatment)
 Goal: to achieve a stable, asymptomatic state with
the best pulmonary function,using the list amount of
medication.
 Drug selection is based upon the severity of illness.

40. Preoperative assessment
History is elicited regarding :
– Frequency of attacks
– Time and duration of last attack
– Treatment that the patient is taking for asthma; steroids?
– Identification of precipitating factors e.g. weather, cold,
dust, medication etc.
– Exercise tolerance. Inability to climb at least two flights
of stairs indicates poor respiratory and/or cardiac
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41. Examinations
◦ Breathing rate and pattern
◦ Use of accessory muscles
◦ Fever may indicate active chest infection and a
prediction for bronchospasm intra- and
postoperatively
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42. Forced expiratory time
Simple screening test for prolonged exhalation is the forced
expiratory time (FET), which can be assessed by listening over
the trachea while the patient exhales forcibly and fully.
An FET > 6 s correlates with a substantially lowered FEV1/FVC
ratio and should initiate further investigation.
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43. Investigations
◦ Hgb, Full blood count
◦ Chest X-ray
◦ ECG, echocardiography (?)
◦ PFT: indicated in smokers, obese patients, patients
scheduled to undergo thoracic or upper abdominal
surgery, check improvement after bronchodilator
therapy
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44.  ABG: preserved for severely symptomatic patients
scheduled for pulmonary resection, to determine
possibility of respiratory failure and decide operability
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45. Patients with moderate or severe asthma can be provided
with a peak expiratory flow rate (PEFR) meter for home
assessment.
The normal range (200–600 litre per min)
Varies widely depending on age, gender, height, and
weight;
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46. The American Lung Association has suggested
 Green (80% of usual),
 Yellow (50–80% of usual), and
 Red zones (50% of usual) to alert patients about fluctuations
in their condition, and when to get medical attention.
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47. Preoperative optimization
Cessation of smoking should be enforced
Treatment with bronchodilators and inhaled steroids is
initiated based on the severity of asthma.
A chest consultation is obtained for advice regarding
optimization of therapy
Antibiotics and chest physiotherapy if infection is present
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48. Physical training with deep breathing exercises and
incentive spirometry prepares a patient for performing
respiratory maneuvers like deep breathing after surgery
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49. Goals of optimization
 Bronchospasm should be relieved
 No evidence of active chest infection
 It is prudent to postpone elective surgery for at least 4-6
weeks after respiratory infection in asthmatics as their
airways may remain hyper-reactive for this period
 Patient should be subjectively feeling comfortable
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50. 6/22/2024 50

51. Optimal anaesthetic technique
Pre-anaesthetic medication:
Morning dose of bronchodilators and inhaled steroids-
even in asymptomatic asthmatics decreases the incidence
of intra-operative bronchospasm
Benzodiazepines (diazepam 5-10 mg) are useful for
anxiolysis in patients unless they are overtly symptomatic
Adequate hydration is essential
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52. Anaesthesia Mx
 First case in the morning- to minimize fasting and
dehydration, and anxiety and bronchospasm
 Anaesthetic techniques with minimal airway manipulation-
spinal, epidural & nerve blocks are preferred over GA
GA:
Avoid- thiopentone, atracurium, d- tubocurarine,
mivacurium, morphine, desflurane and, if possible,
neostigmine
Preferred agents- ketamine, propofol, etomidate,
halothane, isoflurane and sevoflurane, fentanyl and
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53. If GA- intubation and instrumentation of the airway should
be avoided if possible
Intraop bronchospasm- increasing the inspired
concentration of inhaled anaesthetic, nebulized β2
sympathomimetics, intravenous steroids and ensuring
adequate depth of anesthesia.
Intravenous or subcutaneous bronchodilators may also be
administered (aminophylline 5-6 mg/kg or terbutaline 0.25
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54. The management of bronchospasm in step
wise approach
On suspecting bronchospasm
 Switch to 100% oxygen.
 Ventilate by hand
 Stop stimulation / surgery
 Consider allergy / anaphylaxis
 stop administration of suspected drugs / colloid /
blood products
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55. Immediate management; prevent hypoxia &
reverse bronchoconstriction
 Deepen anesthesia.
 If ventilation through ETT difficult/impossible, check
tube position and exclude blocked/misplaced tube.
 If necessary eliminate breathing circuit occlusion by
using self-inflating bag.
In non-intubated patients exclude laryngospasm and
consider aspiration.
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56. If the above supportive measures fail drug
therapy follows
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57. KEY FACTS: MANAGEMENT OF
INTRAOPERATIVE BRONCHOSPASM
 Deepen anesthesia with a volatile agent.
 Consider propofol, ketamine, and lidocaine to further
deepen anesthesia.
 Inhaled beta 2 agonists (many doses may be necessary for
adequate drug delivery)
 Avoid aminophylline.
 Parenteral corticosteroids to avoid recurrence
 Adjust ventilation to minimize barotrauma and gas
 trapping (limit peak pressure and prolong expiratory phase).
 Epinephrine may be necessary to provide adequate
stimulation of airway beta adrenoreceptors, especially if
anaphylaxis triggered bronchospasm.
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58. Extubation- after administration of intravenous lidocaine 1-1.5
mg/kg and inhaled bronchodilator
Adequate analgesia and oxygen supplementation in the post
anaesthesia care unit
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59. COPD
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60.  Define chronic obstructive pulmonary disease (COPD).
 Describe the cause of COPD
 Describe the pathophysiology of COPD
 List symptoms and signs of patient with COPD
 Describe preoperative assessment of patient with COPD
 Describe preoperative optimization of patient with COPD
 Describe the principle of perioperative anaesthesia
management
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61. COPD
COPD is a chronic progressive inflammatory condition
resulting in expiratory airflow limitation that is not fully
reversible.
The airway limitation (pulmonary component) is usually
progressive and associated with an abnormal inflammatory
response of the lung to noxious particles or gases and is not
fully reversible
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62.  Chronic obstructive pulmonary disease (COPD) affects
various structural and functional domains in the lungs.
 It also has significant extra-pulmonary effects, the so-
called systemic effects of COPD.
 Weight loss, nutritional abnormalities, and skeletal muscle
dysfunction are well-recognized systemic effects of
COPD.
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63. COPD is a disease of increasing public health importance around the
world. GOLD estimates suggest that COPD will rise from the sixth to
third most common cause of death world wide by 2020.
COPD includes:
(i) Emphysema a condition characterised by destruction and
enlargement of the lung alveoli;
(ii) chronic bronchitis a condition with chronic cough and phlegm; and
(iii) small airway disease in which small bronchioles are narrowed.
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64.  COPD is present only if chronic airflow obstruction occurs.
 Chronic bronchitis without chronic airflow obstruction is not
included with COPD
 Systemic inflammation in patients with COPD manifests
itself as enhanced activation of circulating inflammatory
cells and increased levels of pro-inflammatory cytokines and
acute-phase proteins, such as TNF-α and C-reactive protein
(CRP) 6/22/2024 64

65. Risk factors
Cigarette smoking: Retrospective studies => 80% of COPD
have significant exposure to tobacco smoking
The decline in the volume of air exhaled in the forced
expiratory volume at one s (FEV1), in a dose response
relationship to the intensity of cigarette smoking.
Effects of passive smoking on COPD is unclear
Increased airway responsiveness to various exogenous
stimuli Respiratory, infections, Occupational exposures:
6/22/2024 65

66. Exposure to dust at work e.g. coal mining, gold mining and
cotton textile dust Ambient air pollution,
Genetic:
Severe anti-trypsin (α1 AT) deficiency is a proven genetic
risk factor for COPD.
A recent study has found a genetic variant associated with
the development of COPD in the COPD gene study.
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67. Pathophysiology
 COPD is a combination of inflammatory small airway
disease (obstructive bronchiolitis) and parenchymal
destruction (emphysema) and affects central and peripheral
airway, lung parenchyma and pulmonary vasculature.
 This leads to poorly reversible narrowing of the airway,
remodeling of airway smooth muscle, increased numbers of
goblet cells and mucus-secreting glands and pulmonary
vasculature changes resulting in pulmonary hypertension.
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68. Airway obstruction
The major site of obstruction is found in the smaller conducting airway (<2 mm
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.
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69. Fibrosis surrounding the small airway appears to be a significant
contributor.
This remodelling and repair thickens the airway walls, reduces lumen
calibre and restricts the normal increase in calibre produced by lung
inflation.
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70. Dynamic hyperinflation
In COPD there is 'air trapping' (increased residual volume
and increased ratio of residual volume to total lung
capacity) and progressive hyperinflation (increased total
lung capacity).
This phenomenon is commonly referred to as dynamic
hyperinflation
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70

71. Respiratory muscle dysfunction
Hyperinflation can push the diaphragm in to a flattened
position with a number of adverse effects:
In COPD dynamic hyperinflation, excessive resistive load
and high ventilatory demands are factors leading to
respiratory muscle dysfunction.
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72. Gas exchange impairment
PaO2 usually remains near normal until FEV1 is decreased to
50% of predicted and elevation of PaCO2 is not seen until FEV1
is <25%.
Pulmonary hypertension severe enough to cause corpulmonale
and right heart failure is seen when there is marked decrease in
FEV1 <25% along with chronic hypoxaemia PaO2 <55 mm Hg.
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73. Extra-pulmonary effects
It also has significant extra-pulmonary effects, the so-called systemic
effects of COPD.
Weight loss, nutritional abnormalities and skeletal muscle dysfunction are
well-recognised systemic effects of COPD.
Cardiovascular dysfunction is usually related to acute and chronic blood
gas derangement, dynamic hyperinflation and increased right ventricular
afterload.
Pulmonary hypertension is increasingly being recognised as a contributing
factor to the morbidity, and mortality associated with COPD.
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74.  Approximately, 10–30% of patients with moderate to
severe COPD have elevated pulmonary pressures
 severe acidosis occurs in <5% of patients.
 Left ventricular dysfunction is commonly associated as
these patients are frequently old and suffer from several
risk factors for coronary artery disease.
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75. Pre-Operative Evaluation
Pre-operative evaluation aims at finding out the degree of
impairment, identification of modifiable risk factors and their
optimization which can influence the perioperative outcome.
Upper respiratory infections should be ruled out and treated
as a cause of increased secretions and airway hyper-
reactivity.
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76. History of smoking and presence of wheeze, prolonged
expiration increases the risk of post-operative pulmonary
complications (PPCs).
Age over 60 years, spirometric changes (FEV1 <1 L), duration
of anaesthesia (>3 h), surgeries of upper torso, and use of
nasogastric tube pre-operatively increase the incidence of
respiratory events.
Electrocardiogram helps to rule out ischaemic heart disease in
these patients. 6/22/2024 76

77. Although not regularly recommended in stable COPD
patients, (NICE guidelines) chest X-ray is useful to rule
out lower respiratory infection and occult malignancy in
patients showing recent deterioration in symptoms.
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78. The presence of extensive bullous disease on a chest X-ray highlights
the risk of pneumothorax.
FEV1, FVC and the ratio of the two will help us differentiate between
obstructive and restrictive pathology.
In patients undergoing lung resection, a FEV1 below 60% has been
shown to carry a two to threefold increased risk for operative mortality
and major respiratory complications.
Presence of pulmonary hypertension worsens prognosis.
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79. Arterial blood gas measurement is useful in patients with marked
symptoms, PaCO2>45 mm Hg and PaO2 <60 mm Hg (on room air) are
both associated with a worse prognosis.
Clinical assessment of functional status with simple and safe tests such
as stair climbing and the 6 min walk test correlates well with more
formal exercise testing.
A more objective way of assessing functional ability of patient is
cardiopulmonary exercise testing.
6/22/2024 79

80. Pre-operative optimization
Pre-operative optimization of these patients include cessation of smoking,
improvement of pulmonary functions using bronchodilators and steroids,
pre-operative chest physiotherapy and training of patient with lung
expansion maneuvers.
Reversible components of COPD such as bronchospasm, infections, and
pulmonary edema should be actively looked for and treated aggressively.
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81. Cessation of smoking is an important measure to reduce
perioperative pulmonary complications in COPD patients.
Maximum benefit is obtained if smoking is stopped at least 8 weeks
before surgery.
with some studies showing increased risk with cessation <8 weeks
before surgery is associated with increased risk of post-operative
complications, whereas other study showed decreased incidence of
complications with >4 weeks of cessation.
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82. Anticholinergic bronchodilators such as ipratropium, block
vagus nerve-mediated bronchoconstriction, which is an
important component of bronchospasm in patients with
COPD, and hence are more useful in patients with COPD
If resistant to anticholinergics, add β2 adrenoreceptor
agonists such as salbutamol, terbutaline helps in reversing
bronchospasm 6/22/2024 82

83. Oral theophylline is occasionally used in the treatment of severe COPD or in those
unable to use inhaled therapy;
IV aminophylline is used during perioperative management of these patients.
Inhaled anaesthetics, particularly halothane, may sensitize the heart to the toxic
effects of theophylline.
Doxofylline, a next generation methylxanthine has shown similar or better efficacy
than theophylline in relieving spasm both in adult and paediatric age group with lesser
cardiovascular, nervous and gastrointestinal side effects due to its reduced affinity
towards adenosine A1 and A2 receptors.
6/22/2024 83

84. The role of oral or inhaled mucolytic therapy in COPD is controversial,
though the recent evidence favours its use in COPD.
It may be helpful, particularly in those with increased secretions with
minimal side effects and its continuation is found to reduce the incidence
post-operative complications in these patients.
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85. A comprehensive programme of pulmonary rehabilitation, featuring
physiotherapy, exercise, nutrition and education, can improve the
functional capacity of patients with severe COPD.
Prophylactic use of antibiotics without bacteriological confirmation of
infection is not recommended but every lung infection should be properly
treated before surgery.
Benzodiazepine pre-medication should be used cautiously, since it can
blunt response to hypoxia and hypercarbia in addition to reduction in
respiratory drive.
6/22/2024 85

86. Intraoperative Management
The primary goal of anesthesia in these patients is to maintain
oxygenation and ventilation and minimize airway manipulation to
prevent complications.
Type of anaesthesia:
Choice of anaesthesia depends on the patient factors (clinical state)
and surgical factors (type and duration of procedure).
General anaesthesia and endotracheal intubation is associated with
increased morbidity.
6/22/2024 86

87. The fall in FRC and atelectasis noted in normal patients
may also be seen in patients with chronic bronchitis.
However, in patients with emphysema, the PEEPi, loss of
elastic recoil, chest wall stiffness and relaxation of
abdominal muscles result in maintenance of alveolar
patency preventing atelectasis.
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88. Diaphragmatic position, presence of alveoli at the upper flat end of the
alveolar compliance curve, all increase the work of breathing and hence
depression of ventilation under anaesthesia can seriously hinder
ventilation when not assisted.
There is increased risk of bronchospasm, laryngospasm, hypoxemia
and barotrauma during general anaesthesia in these patients.
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89. Regional anaesthesia, including central neuraxial block eliminates
the need for airway manipulation and was associated with 50%
reduction in PPCs in a study.
These factors make regional anaesthesia a popular choice where
ever feasible in these patients.
Combined spinal epidural anaesthesia has been successfully used
as a sole anaesthetic technique in major abdominal surgeries in
patients with COPD.
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90. In spite of conflicts in opinion with regards to benefits of epidural
analgesia in COPD patients, recent evidence favours use of thoracic
epidural anaesthesia and analgesia in these patients to reduce post-
operative complications.
Use of interscalene block in patients with COPD remains a concern
due to ipsilateral phrenic nerve paralysis and loss of sympathetic tone
due to stellate ganglion block resulting in bronchospasm.
Hence it is contraindicated in patients who cannot tolerate 25%
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91. Management of patients under general
anesthesia
During management of patients under general anaesthesia, tracheal
intubation should be avoided by using the laryngeal mask airway or
similar device where possible.
Propofol, ketamine, or volatile anaesthetics are the induction agents
of choice; barbiturates may sometimes provoke bronchospasm.
Adjuvants to increase the depth of anaesthesia and blunt airway
reflexes before intubation such as lidocaine or opioids may be
useful.
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92. Volatile anaesthetics are useful for maintenance of anaesthesia due to
their excellent bronchodilating properties with the possible exception of
desflurane.
Pre-oxygenation should be used in any patient who is hypoxic on air
before induction.
In patients with severe COPD and hypoxia, continuous positive airway
pressure (CPAP) during induction may be used to improve the efficacy
of pre-oxygenation and reduce the development of atelectasis.
Haemodynamic compromise can occur following general anaesthesia
due to fall in pre-load which is secondary to increased intrathoracic
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93. Harmful effects of air trapping include hypotension,
barotrauma and volume trauma to the lungs, hypercapnia,
and acidosis.
Measures to reduce air trapping include use of smaller tidal
volumes and lower respiratory rates, with more time for
expiration.
Use of low tidal volumes during major abdominal surgeries
reduces the risk of post-operative complications
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94. Intra-operative problems
Bronchospasm: Perioperative bronchospasm in patients with reactive
airway disease is relatively uncommon.
In patients with well-controlled asthma and COPD the incidence is
approximately 2%. The overall incidence of bronchospasm during
general anaesthesia is approximately 0.2%.
Bronchospasm during anaesthesia usually manifests as prolonged
expiration.
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95. 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.
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96. 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.
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97. Following endotracheal intubation, wheezing is more
likely to occur when barbiturates are used as anaesthetic
induction agents, compared with propofol, ketamine or
volatile anaesthetics.
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98. Auto-PEEP has been found to develop in most COPD
patients during one-lung anaesthesia.
Paradoxically it has been found that small amount of
added PEEP (e.g., 5 cm H2O) can decrease PEEPi and
hyperinflation in many ventilated COPD patients.
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99. Ways of reducing intra-operative PEEPi and
haemodynamic instability:
Allowing more time for exhalation.
Reducing the respiratory rate or the I:E ratio (typically to 1:3–1:5),
with a long expiratory time to allow complete exhalation and reduce
'breath-stacking' and PEEPi.
If bronchospasm is severe, only 3–4 breaths/min may be possible
with full expiration-it is useful to either auscultate or listen at the end
of the disconnected endotracheal tube to confirm that expiration has
finished, before commencing the next breath.
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100. Post-Operative Care
 Analgesia and physiotherapy
Postoperative monitoring
Oxygen therapy
Ventilatory support using NIV
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101. Questions ???
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