Bronchial asthma and COPD are chronic respiratory conditions characterized by airway inflammation and obstruction. Bronchial asthma involves reversible airflow limitation due to bronchospasm while COPD involves irreversible airflow limitation from lung damage. Key differences are that asthma typically presents earlier in life and has a family history, while COPD is mainly caused by smoking. Preoperative treatment aims to prevent bronchospasm during anesthesia and surgery by optimizing lung function and suppressing airway reflexes.

1. BRONCHIAL
ASTHMA/COPD/
ANAESTHETIC
IMPLICATIONS
Dr. Sanjeev Sharma
Dr. Richa Kumar

2. BRONCHIAL ASTHMA

3. ASTHMA
 Characterized by:
 1. chronic airway inflammation
 2. reversible expiratory airflow
obstruction
 3. bronchial hyperactivity
 Both large and small airway are
affected

4. EXTRINSIC ASTHMA INTRINSIC ASTHMA
Atopy- type 1 HS reaction adults
S. Ig E increased Local Ig E increased
Hereditary acquired
Family history present ----
Multisystem allergy ++
(rhinitis/eczema)
----
Asthma -mild Severe
onset : childhood Adult
SAMTER’S TRIAD: Intrinsic
asthma + nasal polyp +
aspirin sensitivity

5.  PATHOGENESIS:
1. Allergens- house dust mite Dermatophagoides pteronyssinus
2. Occupational exposure: Toulene isocyanate, fungal
amylase
3. Hygiene hypothesis: high socioeconomic status
4. Diet and disease: deficiency of antioxidants, anti-
inflammatory vitamin D, magnesium,Selenium, excess of omega6
FA
5. Drugs: aspirin, acetaminophen,(betablockers ppt.)
6. Infection: RSV , mycoplasma , chlamydia
7. Steroid effect: smoking causes decrease in steroids

6.  SIGNS AND SYMPTOMS:
 1.Episodic disease with acute exacerbations interspersed
with symptom free period
 Symptom : cough (m/c) followed by dyspnea  wheeze (
severe dyspnea), chest discomfort, air hunger
 Signs : Inspection: central mediastinum
Palpation: VF decreased (air retained)
Percussion: hyperresonanace
Auscultation: Rhonchi (I & E : biphasic)
HISTORY : previous intubation or admission in ICU , two or
more hospitalizations for asthma in past one year and
presence of coexisting diseases.

7.  INVESTIGATIONS:
1. CXR: m/c CXR is normal , hyperinflation
2. ECG: My show RVF during asthmatic attack
3. PFT: REVERSIBLE obstructive disease ( distinguishes it from COPD)
 increase in FEV1 by > 15 % from baseline after beta agonist inhaler
4. NO BREATH TEST : Normally: <25ppb ASTHMA >50ppb
5. ABG: type 1 respiratory failure > type 2 respiratory failure
Alveolar hypoxia
hyperventilatidecreasedPaCO2
(resp.alkalosis)
Ongoing fatigue hypoventilation increased PCo2
(resp. acidosis)

8.  SPIROMETERY: diag

9.  FEV1 and MMEF rate  direct measures of expiratory
airflow obstruction
Used to asses severity and to monitor the course of an
exacerbation of asthma
 Flow volume loops show characteristic downward scooping
of the expiratory limb of the loop.
 Severe asthmatic attack -FRC may increase substantially
-TLC usually remains within the
normal range
- Dco unchanged
 abnormalities in PFT may persist several days after an acute
attack of asthma despite absence of symptoms
 and also diagnosis can be suspected even when PFT is
normal as it is an episodic illness

10. SEVERI
TY
FEV1(%
PREDICTED
)
FEF (25%-
75%)
PaO2(mm
Hg)
PaCO2 (mm
Hg)
mild 65-80 60-75 >60 <40
moderat
e
50-64 45-89 >60 <45
marked 35-49 30-44 <60 >50
severe <35 <30 <60 >50

11.  ACUTE SEVERE BRONCHIAL ASTHMA:
 4 RESPIRATORY SIGNS 2 CARDIAC
SIGNS
RR> 24 / min HR> 120/min
Silent chest pulsus paradoxus
Presence of cyanosis
Unable to complete sentence

12.  TREATMENT:
 Main aim of treatment is preventing and controlling
bronchial inflammation rather than controlling or
preventing bronchospasm with BD therapy
 Table 9-4

13.  TREATMENT OF ACUTE EXACCERBATION:
 Oxygen inhalaltion upto 6 litres/min + short acting BD
 short acting Beta agonist
(Salbutamol)
 Short acting anticholinergic (Ipratropium)
 IV aminophylline bolus (6mg/kg) f/b infusion1mg/kg/hr)
 Muscle relaxant MgSO4 1-2 gm over 20 mins.
 Mechanical ventilation
 GA (halothane)

14. MANAGEMENT OF ANAESTHESIA
 Bronchospasm 0.2 % - 4.2% of all procedures involving G.A.
performed in asthmatic patients
 FACTORS predicting it: 1. type of surgery (Upper abdomen &
onco.)
 2. proximity of most recent asthmatic
attack
 PATHOLOGICAL MECHANISMS Involved: may be by G.A. or
direct mechanisms
1. 1. depression of cough reflex
2. 2. impairment of mucociliary clearance
3. 3. Reduction of palatopharyngeal muscle tone
4. 4. depression of diaphragmatic function
5. Increase in amount of fluid in airway wall
Increase airway
resistance by G.A

15.  Direct airway stimulation by:
1. Endotracheal intubation
2. Parasympathetic system activation
3. Release of neurotransmitters of pain ( substance P &
neurokinins)

16.  PREOPERATIVE ASSESSMEMT:
1. Disease severity
2. Effectiveness of current medications
3. Potential need for additional therapy before surgery
 THE GOAL is to formulate plan to prevent or blunt expiratory
flow obstruction.
 Clinical history: elicit the severity and characteristics of
asthma.1. Age of onset
2. Triggering events
3. Hospitalization for asthma (frequency of emergency visits & need for
intubation and mechanical ventilation)
4. Allergies
5. Cough
6. Sputum characteristics
7. Current medicarions
8. Anesthetic history

17.  Physical Exam.: General appearance: use of accessory ms.
Of resp.
Auscultation: wheezing/ crepitations
 Blood eosinophil counts often parallel with degree of airway
inflammation
 Airway hyperactivity provides an indirect assessment of
current status of disease
 PFT: FEV1 (before and after BD therapy)
 Risk factor for perioperative complications
1) FEV1 <70%
2) FEV1/ FVC <65% of predicted value

18. PREOPERATIVE THERAPY:
 Chest physiotherapy
 Antibiotic therapy
 Bronchodilator therapy
 These can improve reversible components of asthma
 Anticholinergics are individualized as they can increase viscosity of
secretions
 In selected patients preoperative course of oral corticosteroids may
be useful
 ABG: indicated if there is inadequacy of oxygenation or ventilation.
 Patients should be free of wheezing and should have PEFR >80%
or patients personal best value before surgery

19.  INTRAOPERATIVELY:
 During induction and maintainance of anaesthesia : airway
reflexes must be suppressed to avoid bronchoconstriction in
response to mechanical ventilation of hyperactive airways.
 Stimuli which do not evoke response can provoke
lifethreatenening bronchoconstriction in patients with asthma
GENERAL ANESTHESIA:
 INDUCTION:
1. Most often accomplished with IV induction agent
2. PROPOFOL > thiopentone ( thiopentone itself doesn’t cause
bronchospasm but inadequately suppresses airway reflexes so
ET intubation can cause bronchospasm)
3. KETAMINE produces bronchial smooth ms. Relaxation &
decreases airway resistance esp. in actively wheezing patients
BUT can increase airway secretions, can cause tachycardia,HTN
and increase pulmonary vascular resistance

20. MAINTENANCE:
 GOAL is to establish depth of anesthesia sufficient to
decrease airway reflexes so that nronchospasm is not ppt.
 Sevoflurane /halothane less pungent  less coughning
less
bronchospasm
 An alternative to decrease airway reflexes is IV or
intratracheal injection of LIDOCAINE (1-1.5mg/kg) 1-3
minutes before ET intubation
 OPIOIDS decrease airway reflexes and help to achieve deep
anesthesia
 REMIFENTANYL –ultrashort acting and does not accumulate
 Continuous infusion 0.05- 1 mg/kg

21.  Insertion of LMA is less likely to cause BC than insertion of
ETT
 LMA is better if patient is not at risk of aspiration
 Intraoperatively desirable level of arterial oxygenation and
CO2 removal is provided by mechanical ventilation
 Slow inspiratory flow rates
a) optimal distribution of ventilation relative to perfusion
b) sufficient time of exhalation  prevents air
trapping
 Humidification and warming of inspired gases may be
especially useful in patients with exercise induced asthma
 Liberal administration of fluid adequate hydration- less
viscous airway secretions removed easily

22.  Skeletal muscle relaxants with NDMR
 Drugs with limited ability to release histamine should be
selected
 At the end of surgery removal of ETT while anesthesia is
still sufficient to suppress hyperactive airway reflexes is
preferred known as “ DEEP EXTUBATION”
 when above is not possible then intravenous lidocaine or
pretreatment with BD is considered

23.  INTRAOPERATIVE BRONCHOSPASM:
 Table 9-6

24.  Treatment with bronchodilator drugs should not be
started until cause of wheezing including
mechanical obstruction of breathing circuit , the
airway or ETT is considered
 BD beta 2 agonist corticosteroid
 In case of emergency surgery in asthmatic patients
regional anesthesia may be preferable .

25. COPD

26. COPD
 Mainly related to smoking
 Characterized by progressive development of airflow
limitations which is not fully reversible
 It causes following pathological changes:
1. Pathological deterioration in elasticity or RECOIL within lung parenchyma
2. Decrease rigidity of bronchial wall predisposing to collapse during exhalation
3. Increase gas velocity in narrowed bronchioli lowers pressure increase
collapse
4. Active bronchospasm & obstruction from increased pulmonary secretions
5. Destruction of lung parenchyma enlargement of air sacs development of

27. Feature Chronic Bronchitis Emphysema
Mechanism of
airway
obstruction
Decreased airway lumen
due to mucus and
inflammation
Loss of elastic recoil
Dyspnea moderate severe
FEV1 decreased decreased
PaO2 Marked decrease
“BLUE BLOATERS”
Modest decrease
“PINK PUFFERS”
PaCO2 increased Normal or decreased
Diffusing
capacity
normal decreased
Hematocrit increased normal
Cor-pulmonale MARKED mild
Prognosis POOR Good
CHRONIC BRONCHITIS is defined as
sputum production for 3 months or more
In each 2 successive years or more

28.  Risk factors for development of COPD:
1. Cigarette smoking
2. Pulmonary infections
3. Occupational exposure to dust (coal mining. Gold mining)
4. Genetic factors (alpha1 antitrypsin deficiency increase in
elastase activity)
Signs and symptoms:
 vary with severity of COPD
 C/F: normal findings > tachypnea, prolonged expiratory
phase,
decreased breath sounds and expiratory wheezing.
Chronic productive cough (bronchitis)
Progressive limitation of exercise
Dyspnea, (emphysema), orthopnea(D/D= CHF)
History of smoking for long time
expiratory flow rate obstruction

29.  PFT :
 Decrease in FEV1/FVC
 Much decrease in FEF 25%-75% (MMEF)
 Increased residual volume
 Normal to increased FRC and TLC increased work of
breathing
 Irreversible obstructive disease (increase in FEV1 by <12%
after beta agonist)
 CXR:
 May be normal
 Hyperlucency/ arterial vascular deficiency in lung periphery
and hyperinflation
 Loss of normal dome of diaphragm (flat diaphragm)
 Bullae ++  emphysema
 Bronchitis rarely diagnosed by CXR
 Tubular heart ( compression by hyperinflated airway)

30.  Table 9-8

31.  TREATMENT :
1. Cessation of smoking and oxygen supplementation
2. Drug therapy with bronchodilators, treatment of associated
infections, annual vaccination for influenza, /
pneumococcal ,diuretics in cor-pulmonale but chloride
depletion should be avoided
3. Lung volume reduction therapy- surgical removal of over
distended lung tissue.

32. MANAGEMENT OF ANESTHESIA
 PREOPERATIVE:
 History and physical examination provides more
accurate assessment for postoperative pulmonary
complications than PFT or ABG
 Predictors of increased risk of post operative
complications:
1. History of poor exercise tolerance ,
2. chronic cough ,
3. unexplained dyspnea combined with diminished
breath sounds,
4. wheezing and
5. prolonged expiratory phase

33.  PFT:
 Value of routine PFT is controversial
 May be useful for predicting lung function following lung
resection but not reliable for predicting postop pulmonary
complications after non-thoracic surgery
 If there is doubt then simple spirometry with measurement of
FEV1 is sufficient (FEV1 is Prognostic marker of COPD)
 FEV1/FVC is a sensitive marker of COPD
 In patients with COPD there is reduction in expiratory flow
rates at any given lung volume
 Residual volume is increased due to air trapping

34.  Even in patients with high risk of by Spirometry (FEV1 < 70%
of predicted , FEV1/FVC <65%) or ABG (PaCO2 > 45
mmHg) can undergo surgery including lung resection with
acceptable risk of post operative complications.
 PFT can be used to optimize preoperative pulmonary
function and not to predict postoperative risk of
complications.
 PFT indications:1. Hypoxemia on R.A. requiring oxygen without a known cause
2. Bicarbonate conc. > 33 meq/L or PaCO2 >50mmHg
3. History of respiratory failure resulting from problem that still exists
4. Severe SOB attributable to respiratory disease
5. Planned pneumonectomy
6. Difficulty in assessing pulmonary function by clinical signs
7. To distinguish among potential causes of respiratory compromise
8. To determine response to bronchodilator therapy
9. Suspected pulmonary HTN

35.  In patients with advanced pulmonary disease right
ventricular function must be assessed by clinical
examination and echocardiography.
 Bed side tests?????????????????????????

36.  EVALUATION OF RISK FACTORS FOR
POSTOPERATIVE PULMONARY
COMPLICATIONS:
 Table 9-9

37. ALGORITHM FOR DECREASING PULMONARY
COMPLICATIONS
 Figure 9-5 page 192

38.  9-10

39.  9-11
Increases BP ,HR, PVR
CO shifts O2-Hb to left
Increases production of Hb,
RBC,WBC, Platelets, fibrinogen
Increases hematocrit

40. ACUTE EFFECTS OF SMOKING
CESSATION
 The A/E of CO on O2 carrying capacity and nicotine on CVS
are short lived
 Elimination T1/2 of CO= 4-6 hours when breathing R.A
 Sympathomimetic effects of nicotine on heart lasts 20-30
mins.
 Within 12 hours of smoking cessation:
A. P50 ( PaO2 at which Hb is 50%) saturated is increased
from 22.9-26.4 mmHg
B. Plasma levels of carboxy Hb decreases from 6.5% to
approx. 1%
 CO may have negative inotropic effect
 Despite these favourable effects on carboxyHb, postop

41. INTERMEDIATE TERM EFFECTS
 Cigarette smoking causes:
 mucus hypersecretion
 Impairment of mucociliary transport
 Narrowing of small airways
 Interferes with normal immune mechanism
 Stimulate hepatic enzymes
 These effects take weeks to improve after smoking
cessation and improvement in these are related to
decrease in postoperative pulmonary complications
 Return of normal immune function and hepatic
enzymeactivity requires 6 weeks or longer

42.  Optimal timing for smoking cessation before surgery
is unclear
 It is suggested to be 4-8 weeks
 Despite clear long term advantages, there are
disadvantages to smoking cessation in immediate
postoperative period including:
1. Increase in sputum production
2. Fear of inability to handle stress
3. Nicotine withdrawal : irritability , restlessness, sleep
disturbances and depression

43.  Many methods aid in smoking cessation:
 Mostly involves counseling and pharmacotherapy
 Nicotine replacement therapy with various delivery
systems is available ( pathches,inhalers, nasal
sprays,lozenges and gum)
 Atypical antidepressant BUPROPION in a sustained
release formulation can be used.
 This is started 1-2 weeks before smoking is stopped.
 Earlier the intervention before surgery, more effective it
is in reducing post-operative complications and
maintaining abstinence

44.  INTRAOPERATIVE:
 The choice of anaesthetic technique or specific anesthetic
drugs does not seem to alter incidence of post operative
pulmonary complications
 Studies reflect complications in G.A > Regional but nature
and complexities of surgeries is not reflected
 It is suggested that post operative complications are
associated with surgeries lasting >3 hours

45. REGIONAL ANESTHESIA:
1. Suitable in operations that do not invade peritoneum
2. surgery of extremeties
3. Lower abdominal surgeries
 Via peripheral nerve blocks carries lower risk of pulmonary
complications than either spinal or GA
 Useful in COPD patients only if large doses of sedatives and
anxiolytics will not be required
 COPD patients are extremely sensitive to resp. depressant
effect of sedatives
 Above T6 is not recommended impair resp. efforts
requiring active exhalation clinically manifested as
inadequate cough

46.  GENERAL ANESTHESIA:
 Often accomplished with VOLATILE ANESTHETICS
 Useful as these are rapidly eliminated (desflurane and
sevoflurane)  residual resp. depression is diminished
 Also cause BD relieve bronchospasm
 Desflurane causes airway irritation
 Sevoflurane is preferred
 N2O can be used but has disadvantages:
 Expand pulmonary bullae  rupture pneumothorax
 Imposes limitation on inspired oxygen concentration
 May attenuate regional HPV more shunting t/t : increase
FIO2

47.  OPIOIDS less useful than inhaled anesthetics for
maintenance of anesthesia in COPD pts prolonged
respiratory depression
 CONTROLLED MECHANICAL VENTILATION:
 TV- 6-8 ml/kg
 Slow inspiratory flow rate
 Slow rates also allows sufficient time for venous return
 Phenomenon of air trapping is enhanced when PPV applied
but insufficient time for complete exhalation is there
increased intrathoracic pressure  decrease VR
transmission of pressure to pulmonary artery RV
strainRV impinges on filling of LV
 Hyperventilation direct pressure on heart  limiting
diastole even if adequate preload is there
Less turbulent flow
Helps to maintain optimum V/Q

48.  AIR TRAPPING detected during MV intraoperatively by
following methods:
 Capnography
 Direct measurement of flow
 PEEP measurement
 The patient can be briefly disconnected from ventilator to
see whether BP increases when PEEP is eliminated
 The HAZARD OF BAROTRAUMA should be considered in
presence of bullae
 If spontaneous breathing is permitted  consider COPD
patients have greater resp. depression by volatile
anesthetics

49. POST-OPERATIVE MANAGEMENT:
 Prophylaxis against the development of post-
operative complications is based upon:
1. Maintaining adequate lung volumes, esp. FRC
2. Facilitating enough cough
3. Adequate Analgesia
4. Deep venous thrombosis prophylaxis- polycythemia,
intraop. Hypothermia, preop immobility makes
patients vulnerable to DVT and PE
5. Early mobilization and enteral feeding.
6. Severe COPD may require mechanical ventilation
7. Right ventricular dysfunction/ failure may be a
complication so should be watched for.

50.  LUNG EXPANSION MANEUVERS:
1. Deep breathing exercises
2. Incentive spirometery- simple and inexpensive / requires pt.
Cooperation/ before surgery> after
surgery
3. Chest physiotherapy
4. Positive pressure breathing techniques- reserve for patients who
cannot do deep breathing exercises &
incentive spirometery
 These techniques decrease risk of atelectasis by increasing lung
volume
 All maneuvers decrease post op pulm. Complications two folds as
compared to no therapy

51. POST OPERATIVE NEURAXIAL ANALGESIA
Large incision  decreases FRC & decreases sputum
clearance due to pain
 Post operative neuraxial analgesia with opioids may permit
early tracheal extubation
 Less complications
 Early ambulation is possible aids increase in FRC and improves
oxygenation (by improving V/Q ratio)
 Particularly useful after intrathoracic and intraabdominal surgeries
 Quality of analgesia superior to parenteral opioids (no
documentation on superiority in preventing post operative pulm.
Complications)
 Breakthrough pain can be managed by systemic opioids by bolus
or patient controlled analgesia

52. MECHANICAL VENTILATION
 Continued MV may be necessary in pt. with severe COPD who have
undergone major abdominal surgery or intrathoracic surgery.
 FEV1/FVC <0.5
 Or preoperative PaCO2 >50 mmHg
 Continuous PPV decreases work of breathing and air trapping
 If PaCO2 is increased for long period it is important NOT to correct
hypercarbia too quickly metabolic alkalosis cardiac dysarrythmias, CNS
irritability and even seizures
 When continued MV is necessary:
 PaO2 =60-100mg, arterial pH at 7.35-7.45
 Reduction of RR and I:E ratio allows more time for exhalation  reduces
likely hood of air trapping
 D/A: can also lower TV & minute ventilation  can exaccerbate
hypercapnia, hypoxemia & acidosis
Likely to need
Postoperative MV

53. CHEST PHYSIOTHERAPY:
 A combination of chest physiotherapy and deep breathing
exercises taught during preoperative period decreases post-
op complications
 Vibrations produced dislodgement of mucous plug from
peripheral airways
 Appropriate positioning facilitates elimination of loosened
mucus

54.  Patients with preoperative respiratory diseases are at
increased risk of perioperative respiratory complications.
 Postoperative complications contribute to morbidity,
mortality and increased hospital stay
 Pulmonary complications also play an important part in
determining long term mortality after surgery
 Modification of disease severity and optimization of patient
before surgery decrease the incidence of these
complications

55. THANKYOU!!