The document provides a detailed overview of anesthesia management for patients with asthma and chronic obstructive pulmonary disease (COPD), including definitions, causes, pathophysiology, and preoperative assessment strategies. It emphasizes the importance of understanding the dynamic interactions between environmental factors and these respiratory conditions, and outlines the necessary preoperative optimization techniques like smoking cessation and the use of bronchodilators. Additionally, it discusses the anesthetic techniques and medications preferred for managing these patients, aiming to minimize complications while ensuring effective ventilation and oxygenation during surgery.

1. ANESTHESIA FOR ASTHMAAND
COPD
MSC, 2009
1

2. outline
Asthma & COPD:
Definition
Causes
Pathophysiology
Signs & symptoms
Preoperative assessment & preparation
Anesthesia Mx and postoperative
considerations
2

3. Asthma
Definition:
-Asthma is a reversible airflow obstruction due to constriction of
smooth muscles in the airways
-Bronchial wall inflammation =>
- Mucus hyper secretion,
- Epithelial damage a
- Airways constriction
Triggering factors:
-Exercise, cold air, viral infections, occupational exposure and
emotional stress)
3

4. Clinical manifestations:
Wheezing
Shortness of breath
Cough and
Chest tightness
4

5. Phathophysiology:
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
5

6. 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.
6

7. Aspirin and other non-steroidal anti-inflammatory
drugs can also cause acute airflow obstruction in
some patients.
7

8. 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.
8

9. 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 reserve.
9

10. Examinations:
 Breathing rate and pattern
 Use of accessory muscles
 Fever may indicate active chest infection and a
prediction for bronchospasm intra- and
postoperatively
10

11. 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.
11

12. 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
 ABG: preserved for severely symptomatic patients scheduled for
pulmonary resection, to determine possibility of respiratory failure
and decide operability
12

13. 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;
what is relevant is how the PEFR varies from the patient’s own
baseline.
13

14. 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.
14

15. 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
15

16. Physical training with deep breathing exercises and
incentive spirometry prepares a patient for performing
respiratory maneuvers like deep breathing after surgery
16

17. 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
17

18. 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
18

19. 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 pethidine,
succinylcholine and vecuronium
19

20. 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 mg)
20

21. 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
21

22. 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
22

23. 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.
23

24. 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.
COPD is present only if chronic airflow obstruction occurs. Chronic
bronchitis without chronic airflow obstruction is not included with
COPD
24

25. 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)
25

26. Muscle impairment in COPD comprises loss of muscle
strength and/or endurance associated with loss of muscle
quantity and quality, respectively.
A major cause of reduced muscle quantity is muscle fiber
atrophy, especially the fast-twitch type fibers are affected .
The loss of muscle quality is primarily reflected by loss of
oxidative phenotype: a slow-to-fast or I-to-II fiber-type shift is
a consistent finding in lower-limb muscles of patients with
COPD, in which fiber type transitions seem to play an
important role.
26

27. 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 1 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:
27

28. 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 (FAM13A),
associated with the development of COPD in the COPD
gene study.
28

29. 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.
29

30. 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.
30

31. 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.
31

32. 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).
During spontaneous breathing, the high expiratory airway resistance, combined
with expiratory flow limitation, low elastic recoil, high ventilatory demands and
short expiratory time due to the increased respiratory rate, may not permit the
respiratory system to reach the elastic equilibrium volume (i.e., passive
functional residual capacity [FRC]) at end-expiration.
This phenomenon is commonly referred to as dynamic hyperinflation.
Thus, an elastic threshold load (intrinsic positive end expiratory pressure
[PEEPi]) is imposed on the inspiratory muscles at the beginning of inspiration
and increases the amount of the inspiratory effort needed for gas flow
32

33. 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.
33

34. 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.
34

35. 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.
35

36. Approximately, 10–30% of patients with moderate to
severe COPD have elevated pulmonary pressures and
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.
36

37. Pre-Operative Evaluation and Optimization
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.
History of smoking and presence of wheeze,
prolonged expiration increases the risk of post-
operative pulmonary complications (PPCs).
37

38. Age over 60 years, spirometry changes (FEV1 <1
L), duration of anesthesia (>3 h), surgeries of
upper torso, and use of nasogastric tube pre-
operatively increase the incidence of respiratory
events.
Electrocardiogram helps to rule out ischemic heart
disease in these patients.
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.
38

39. 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.
39

40. 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 (CPET).
Poor nutritional status with a serum albumin level <3.5
g/dl is a strong predictor of PPCs.
40

41. 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.
41

42. 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.
42

43. 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.
43

44. 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.
44

45. 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.
45

46. A comprehensive program 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.
46

47. Intra operative 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 anesthesia depends on the patient factors
(clinical state) and surgical factors (type and duration of
procedure).
General anesthesia and endotracheal intubation is
associated with increased morbidity.
47

48. 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.
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 anesthesia can seriously hinder
ventilation when not assisted.
48

49. There is increased risk of bronchospasm,
laryngospasm, hypoxemia and barotrauma during
general anesthesia in these patients.
Regional anesthesia, 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 anesthesia a popular
choice where ever feasible in these patients.
Combined spinal epidural anesthesia has been
successfully used as a sole anesthetic technique in
major abdominal surgeries in patients with COPD.
49

50. In spite of conflicts in opinion with regards to benefits of
epidural analgesia in COPD patients, recent evidence favours
use of thoracic epidural anesthesia 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% reduction in pulmonary function.
50

51. Mgt of patients under general anesthesia
During management of patients under general anesthesia,
tracheal intubation should be avoided by using the
laryngeal mask airway or similar device where possible.
Propofol, ketamine, or volatile anesthetics are the induction
agents of choice; barbiturates may sometimes provoke
bronchospasm.
Adjuvants to increase the depth of anesthesia and blunt
airway reflexes before intubation such as lidocaine or
opioids may be useful.
However, laryngotracheal lidocaine may be less useful, as
it might transiently increase airway resistance.
51

52. Volatile anesthetics are useful for maintenance of anesthesia due to their
excellent bronchodilation 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 anesthesia
due to fall in pre-load which is secondary to increased intrathoracic
pressure.
52

53. 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
53

54. 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 anesthesia is
approximately 0.2%.
Bronchospasm during anesthesia usually manifests as
prolonged expiration.
54

55. 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.
55

56. Intraoperatively, bronchospasm occurs most
commonly during the induction and maintenance
stages of anesthesia 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.
56

57. During the maintenance stage of anesthesia,
bronchospasm may result from an anaphylactic or
serious allergic reaction.
Following endotracheal intubation, wheezing is more
likely to occur when barbiturates are used as
anesthetic induction agents, compared with propofol,
ketamine or volatile anesthetics.
57

58. Auto-PEEP has been found to develop in most
COPD patients during one-lung anesthesia.
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.
58

59. 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.
Rarely, to facilitate this, it is necessary to apply manual external
pressure to the chest.
59

60. Post-Operative Care:
Analgesia and physiotherapy
Postoperative monitoring
Oxygen therapy
Ventilatory support using NIV
60

61. THANKS!
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