NEW CRITERIA OF GOLD ALONG WITH ANESTHETIC CONSIDERATION AND TECHNIQUE

1. COPD:-
brief clinical review and anesthetic
consideration
Presenter-Pawan Kumar Ray
Moderator-Dr. Virendra Kumar

2. FLOW OF CONTENT
 COPD- Definition,
Risk factors
Pathophysiology.
Diagnosis and assessment-
Old GOLD criteria
New GOLD criteria.
Management
 Acute exacerbation of COPD.
 Anesthetic consideration.

3. Chronic Obstructive Pulmonary Disease
Definition:
Disease state characterised 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.

4. COPD:Includes:
•Chronic Bronchitis
•Emphysema
•Peripheral Airways
disease
Doesn’t include
•Asthma, Asthmatic Bronchitis
•Cystic Fibrosis
•Bronchiactesis
•Pulmonary fibrosis due to other
causes

5. COPD
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.

6. Comparative features of COPD
 Feature Chronic Bronchitis Emphysema
 Cough Frequent With exertion
 Sputum Copious Scant
 Hematocrit Elevated Normal
 PaCO2 Often elevated(>40) Usually normal(<40)
 CXR Increased lung markings Hyperinflation
 Elastic recoil Normal Decreased
 Airway resistance Increased Normal to slightly increased
 Cor pulmonale Early Late

7.  Feature Chronic bronchitis emphysema
 Mech. of airway obstr. Decreased airway Loss of elastic recoil
 lumen due to mucus
 and inflammation
 Dyspnea Moderate Severe
 FEV₁ Decreased Decreased
 PaO₂ Marked decreased Modest decrease
 ‘blue bloater’ ‘pink puffer’
 Diffusing capacity Normal Decreased
 Prognosis Poor Good

8. Risk factors-
Host factos:
•Genetic factors: E.g. α1 Antitrypsin Deficiency
•Sex : Prevalence more in males.
?Females more susceptible
•Airway hyperactivity,
Immunoglobulin E and asthma
Exposures:
•Smoking: Most Important Risk Factor
•Socioeconomic status
•Occupation
•Environmental pollution
•Perinatal events and childhood illness
•Recurrent bronchopulmonary infections
•Diet

11. Pathophysiology:
Pathological changes are seen in 4 major
compartments of lungs:
central airways
Peripheral airways
lung parenchyma
 pulmonary vasculature.

12. Pathophysiology.
Central Airways: (cartilaginous airways >2mm of internal diameter)
•Bronchial glands hypertrophy
•Goblet cell metaplasia
•Airway Wall Changes:
•Inflammatory Cells
Squamous metaplasia of the airway epithelium
Increased smooth muscle and connective tissue
Peripheral airways (non cartilaginous airways <2mm internal diameter)
•Bronchiolitis
•Pathological extension of goblet cells and squamous metaplasia
•Inflammatory cells
•Fibrosis and increased deposition of collagen in the airway walls
Excessive
Mucus
production
Loss of cilia and
ciliary
dysfunction
Airflow
limitation and
hyperinflation

13. Lung parenchyma (respiratory bronchioles, alveoli and capillaries)
•Emphysema change occurs in the parenchyma:
Early microscopic lesion progress to Bullae over time.
•significant loss of alveolar attachments, which contributes
to peripheral airway collapse
•Inflammatory cells
Pulmonary Vasculature:
•Thickening of the vessel wall and endothelial dysfunction
•Increased vascular smooth muscle & inflammatory infiltration of the vessel wall
•Collagen deposition and emphysematous destruction of the capillary bed
Airflow limitation
and
hyperinflation
•Pulmonary HTN
•RV dysfunction
(cor Pulmonale)

14. Pathogenesis:
Tobacco smoke & other
noxious gases
Inflammatory
response in airways
Proteinase & Antiproteinase
imbalance
Oxidative
Stress
Alpha 1
antitrypsin
def.

16. Inflammatory cascade in COPD and asthma

18. Physiological Effects:
Mucous hypersecretion and cilliary dysfunction
 Goblet cell hyperplasia & squamous metaplasia
Airflow limitation and hyperinflation
 Airway remodelling
 Loss of elastic recoil
 Destruction of alveolar supports
 Accumulation of mucus, inflammatory cells & exudate
Gas exchange abnormalities: (Hypoxemia +/- Hypercapnia)
 Abnormal V/Q ratios
 Abnormal DLCO
Pulmonary hypertension
 Hypoxic Vasoconstriction, Endothelial dysfunction
 Remodelling of arteries & capillary destruction
 Systemic effects-Cor pulmonale, resp. and skeletal muscle wasting and
weight loss

19. Diagnosis
Clinical Features:
Symptoms:
Cough: Initially intermittent
Present throughout the
day.
Sputum: Tenacious & mucoid
Purulent Infection
Dyspnoea: Progressively
worsens, Persistent
Exposure: Smoking, other pollutants.
Physical Examination:
Respiratory Signs
•Barrel Chest
•Pursed lip breathing
•Adventitious
Ronchi/Wheeze
Systemic Signs
•Cyanosis
•Neck vein enlargement
•Peripheral edema
•Liver enlargement
•Loss of muscle mass

20. Investigations:
Spirometry
Diagnosis
Assessment of severity
Following progress
Chest Radiograph: To exclude other diseases
Emphysematous changes
Bronchodilator Reversibility
Exclude Bronchial Asthma
Alpha-1 Antitrypsin levels

21. Alpha-1 antitrypsin deficiency (AATD)
AATD screening
► 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 panlobular 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.

22. Diagnosis and Initial Assessment

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24. Assessment of airflow limitation
Spirometry is required to make the diagnosis; the presence of a
post-bronchodilator FEV1/FVC < 0.70 confirms the presence of
persistent airflow limitation.

27. GOLD Classification
Stage Characteristics
I: Mild FEV1/FVC < 70%
FEV1 ≤ 80% predicted, with/without chronic symptoms
II: Moderate FEV1/FVC < 70%
50% ≤ FEV1 ≤ 80% predicted, with/without chronic
symptoms
III: Severe FEV1/FVC < 70%
30% ≤ FEV1 ≤ 50% predicted, with/without chronic
symptoms
IV: Very
severe
FEV1/FVC < 70%
FEV1 < 30% predicted or < 50% predicted plus chronic
respiratory failure (PaO2 < 60mm Hg &/or PaCO2 > 50mm
Hg)

28. Assessmnet of copd
 Symptoms
 Degree of airway limitation using spirometry
 Risk of exacerbations
 Comorbidities.
Goals –
to determine the level of airflow limitation, the impact of
disease on the patient’s health status, and the risk of future events
(such as exacerbations, hospital admissions, or death), in order to
guide therapy.

29. Assessment of symptoms
 COPD assessment test (CAT)-an 8 item measure of health
impairment in COPD.
 Chronic Respiratory Questionnaire (CRQ)-self administered
questionnaire develop to measure clinical control in pt with
COPD.
 Modified Medical Research Council (m MRC)-breathlessness
measurement relates well to other measures of health status and
predict future mortality risk.

30. COPD assessment test (CAT)

32.  Previous versions of the GOLD guidelines classified patients by
FEV1 only.
 The new GOLD guidelines now grade patients (A-D)- based on
symptoms, airflow obstruction, and exacerbation history as follows:
 Symptom burden is measured by your choice of the modified
Medical Research Council questionnaire (mMRC) or the COPD
assessment test (CAT).

33. A = Low risk, low symptom burden
Low symptom burden (mMRC of 0-1 OR CAT score < 10)
&
FEV1 of 50% or greater (old GOLD 1-2) AND low
exacerbation rate (0-1/year).
B = Low risk, higher symptom burden
Higher symptom burden (mMRC of 2 or more OR CAT of 10
or more)
&
FEV1 of 50% or greater (old GOLD 1-2) AND low
exacerbation rate (0-1/year

34. C = High risk, low symptom burden
Low symptom burden (m MRC of 0-1 OR CAT score < 10)
&
FEV1 < 50% (old GOLD 3-4) AND/OR high exacerbation
rate (2 or more/year).
D = High risk, higher symptom burden
Higher symptom burden (mMRC of 2 or more OR CAT of 10
or more)
&
FEV1 < 50% (old GOLD 3-4) AND/OR high exacerbation
rate (2 or more/year)

35. Note that the assessment starts with categorization by symptom
burden, and then is refined by “risk” evaluation using FEV1
and/or exacerbation history.
Functionally, this means that patients can be categorized into
the higher risk groups (C and D) by either low FEV1 or
frequent exacerbations, or both

36. ABCD assessment tool

37. Once COPD has been diagnosed, effective management should be based on
an individualized assessment to reduce both current symptoms and future
risks of exacerbations

38. Identify And Reduce Exposure To Known Risk
Factors
► Cigarette smoking is the most commonly encountered and
easily identifiable risk factor for COPD, and smoking
cessation should be continually encouraged for all
individuals who smoke.
► Reduction of total personal exposure to occupational dusts,
fumes, and gases, and to indoor and outdoor air pollutants,
should also be addressed.

39. Pharmacologic treatment-
Pharmacologic therapies can reduce symptoms, and the risk and
severity of exacerbations, as well as improve health status and exercise
tolerance.
► Most of the drugs are inhaled so proper inhaler technique is of high
relevance.

40. Bronchodilators in COPD
 Beta 2 Agonists
 Short Acting Beta 2 agonists (SABA)- Salbutamol,Terbutaline.
 Long Acitng Beta 2 agonists (LABA)-
Formoterol,Salmeterol,Indacaterol, Vilanterol
 Anticholinergics
 Short Acting Muscarinic Antagonist (SAMA)- Ipratropium
 ,Oxitropium
 Long Acting Muscarinic Antagonists (LAMA)- Tiotropium,
 Aclidinium, glycopyronnium,Umeclidinium)

41. © 2017 Global Initiative for Chronic Obstructive Lung Disease
Pharmacologic treatment algorithms

42. All Group A patients should be offered
bronchodilator treatment based on its
effect on breathlessness.
► This can be either a short- or a long-
acting bronchodilator.
► This should be continued if
symptomatic benefit is documented.
Group A

43. Initial -a long acting bronchodilator.
Long-acting inhaled bronchodilators are superior
to short-acting bronchodilators taken as needed
and are therefore recommended.
.
For patients with persistent breathlessness on
monotherapy the use of two bronchodilators is
recommended.
Group b

44. ► For patients with severe breathlessness
initial therapy with two bronchodilators may
be considered.
► If the addition of a second bronchodilator
does not improve symptoms, treatment
could be stepped down again to a single
bronchodilator.
► Group B patients are likely to have
comorbidities that may add to their
symptomatology and impact their
prognosis, and these possibilities should
be investigated.

45. Group C
► Initial therapy should consist of a single long acting
bronchodilator.
► LAMA is superior to the LABA regarding
exacerbation prevention, therefore to recommend
starting therapy with a LAMA in this group.
► Persistent exacerbations may benefit from adding a
second long acting bronchodilator (LABA/LAMA)
or using a combination of a long acting beta2-agonist
and an inhaled corticosteroid (LABA/ICS).
► As ICS increases the risk for developing pneumonia
in some patients, so primary choice is
LABA/LAMA.

46. Group D
Recommend starting therapy- LABA/LAMA combination
because:- LABA/LAMA combinations showed
superior results compared to the single substances.
If a single bronchodilator is chosen as initial treatment, a
LAMA is preferred for exacerbation prevention based
on comparison to LABAs.
A LABA/LAMA combination was superior to
LABA/ICS combination in preventing exacerbations and
other patient reported outcomes in Group D patients
Group D patients are at higher risk of developing
pneumonia when receiving treatment with ICS.

47. ► In some patients initial therapy with LABA/ICS may be the first choice.
► These patients may have a history and/or findings suggestive of asthma-COPD overlap.
► High blood eosinophil counts may also be considered as a parameter to support the use
of ICS,
► In patients who develop further exacerbations on LABA/LAMA therapysuggest two
alternative pathways:
Escalation to LABA/LAMA/ICS..
Switch to LABA/ICS.
 If LABA/ICS therapy does not positively impact exacerbations/symptoms, a
LAMA can be added.

48.  If patients treated with LABA/LAMA/ICS still have exacerbations the
following options may be considered:
► Add roflumilast in patients with an FEV1 < 50% predicted and chronic
bronchitis, particularly if they have experienced at least one
hospitalization for an exacerbation in the previous year.
► Add a macrolide. The best available evidence exists for the use of
azithromycin. Consideration to the development of resistant organisms
should be factored into decision making.

49. Oxygen Therapy
Long Term Oxygen Therapy(LTOT):
 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) <7.3 kPa (55 mmHg).
 The therapeutic goal is to maintain SpO2 >90% during rest,
sleep and exertion.

50. Physiological indications for long-term oxygen therapy
(LTOT)
PaO2 mmHg SaO2 % LTOT indication Qualifying
condition
≤55 ≤88 Absolute None
55–59 89 Relative with qualifier “P” Pulmonale,
polycythemia
History of edema
≥60 ≥90 None except with qualifier Exercise desaturation
Sleep desaturation not
corrected by CPAP
Lung disease with
severe dyspnea
responding to O2

52. Surgical Treatment
Bullectomy
 short-term improvements in
 airflow obstruction
 lung volumes
 hypoxaemia and hypercapnia
 exercise capacity
 dyspnoea
Lung Volume Reduction Surgery
 potentially long-term improvement in survival
 short-term improvements in
 Spirometry
 lung volumes
 exercise tolerance
 dyspnoea
Lung Transplantation

53. Non-Pharmacologic Treatment
► Education and self-management
Physical activity
Pulmonary rehabilitation programs
Exercise training
End of life and palliative care
Nutritional support
Vaccination-Vaccination against influenza (all COPD patients)
and pneumococcus (all COPD patients older than 65 or with
other cardiopulmonary disease)
Oxygen therapy

54. COPD and Comorbidities
► COPD often coexists with other diseases (comorbidities) that
may have a significant impact on disease course.
► In general, the presence of comorbidities should not alter COPD
treatment and comorbidities should be treated per usual
standards regardless of the presence of COPD.
► Lung cancer is frequently seen in patients with COPD and is a
main cause of death.
► Cardiovascular diseases are common and important
comorbidities in COPD

55.  Some common comorbidities occurring in patients with COPD with
stable disease include:
► Cardiovascular disease (CVD)
► Heart failure
► Ischaemic heart disease (IHD)
► Arrhythmias
► Peripheral vascular disease
► Hypertension
► Osteoporosis
► Anxiety and depression
► COPD and lung cancer
► Metabolic syndrome and diabetes
► Gastroesophageal reflux (GERD)
► Bronchiectasis
► Obstructive sleep apnea

56. Acute exacerbation of COPD
Definition:
 An exacerbation of COPD is an event in the natural course of the
disease characterised by a change in the patient’s baseline
dyspnoea, cough and/or sputum beyond day-to-day variability
sufficient to warrant a change in management
► They are classified as:
 Mild (treated with short acting bronchodilators only, SABDs)
 Moderate (treated with SABDs plus antibiotics and/or oral
corticosteroids) or
 Severe (patient requires hospitalization or visits the emergency room).
Severe exacerbations may also be associated with acute respiratory
failure.

57. Classification of hospitalized patients
No respiratory failure:
Respiratory rate: 20-30 breaths per minute; no use of accessory
respiratory muscles; no changes in mental status; hypoxemia
improved with supplemental oxygen given via Venturi mask 28-
35% inspired oxygen (FiO2); no increase in PaCO2.
 Acute respiratory failure — non-life-threatening: Respiratory
rate: > 30 breaths per minute; using accessory respiratory
muscles; no change in mental status; hypoxemia improved with
supplemental oxygen via Venturi mask 25-30% FiO2;
hypercarbia i.e., PaCO2 increased compared with baseline or
elevated 50-60 mmHg.

58.  Acute respiratory failure — life-threatening:
Respiratory rate: > 30 breaths per minute; using accessory
respiratory muscles; acute changes in mental status; hypoxemia
not improved with supplemental oxygen via Venturi mask or
requiring FiO2 > 40%; hypercarbia i.e., PaCO2 increased
compared with baseline or elevated > 60 mmHg or the presence
of acidosis (pH < 7.25).

59. Precipitating Causes:
.1) Infections:
Bacterial- Moraxella catarrhalis , Haemophilus influenza,
and Streptococcus pneumonia --most common organisms associated
with.
Other bacteria-e.g., Pseudomonas and Staphylococcus.
Viral- Rhinovirus and respiratory syncytial virus,influeza virus.
Atypical microorganisms such as Mycoplasma
pneumoniae and Chlamydia.
2)Air pollution exposure
3) Cardiac dysfunction mainly Acute left heart dysfunction
4)Non compliance with LTOT

60. THE WINNIPEG CRITERIA

61. management
• Oxygen thetapy
• Administer oxygen to raise the Pao2 above 60 mm Hg or the Sao2 above 90%.
• Use any of the following devices: standard dual prong nasal cannula, simple
facemask, Venturi mask, or nonrebreathing mask with reservoir and one-way
valve.
• Because oxygen administration may produce hypercapnia, arterial blood gases
and/or continuous EtCO2 and oxygen saturation monitoring.
• It may take 20 to 30 minutes from administration of supplemental
• oxygen for improvement to occur.
• If adequate oxygenation is not achieved or respiratory acidosis develops,
assisted ventilation may be required.

62. management
Bronchodilators-
short-acting β-agonists, and anticholinergic bronchodilators concept
that the smooth muscle reactivity, airway inflammation, and mucus
production characteristics of AECOPD.
Methylxanthines- such as theophylline (oral) and aminophylline
(parenteral), inhibit phosphodiesterases and enhance
 respiration in two ways: by improving the mechanics of breathing (at the
smooth muscle and diaphragm) and through an anti-inflammatory effect.
Anti-inflammatory (Corticosteroid) Therapy-
 use of a short course (5 to 7 days) of systemic steroids improves lung
function and hypoxemia and shortens recovery time in acute COPD
exacerbations
.

63.  oral or parenteral preparation.
 The effectiveness of ICS therapy depends heavily upon the patient's ability to
properly perform the aerosol delivery maneuvers, that may be difficult in the
dyspneic patient with an AECOPD episode
 Antibiotics
 the GOLD and American Thoracic Society COPD guidelines recommend
antibiotic use during these episodes .
 routine antibiotics shortened the severity and/or the duration of an AECOPD
episode.
 The choice of antibiotics depends on the likely organism.
 Treating an AECOPD episode early improves the speed of functional recovery.
 Ventilatory support: NIV, Invasive ventilation

64. Indications for Hospital Admission
 Marked increase in intensity of symptoms, such as sudden
development of resting dyspnea
 or inability to walk from room to room
 Failure of exacerbation to respond to initial medical management
 Significant comorbidities
 Newly occurring dysrhythmias, heart failure
 Frequent exacerbations and/or frequent relapse after ED
treatment
 Older age
 Insufficient home support

65. Indications for Intensive Care
Admission
 Severe dyspnea that responds inadequately to initial emergency
therapy
 Respiratory or ventilatory failure (current or impending) despite
supplemental oxygen and noninvasive positive-pressure
ventilation
 Decreasing level of consciousness or increasing confusion or
agitation
 Hemodynamic instability
 Presence of co morbidities leading to end-organ failure

66. Criteria for NIV Selection criteria –
 Acidosis (pH <7.36)/hypercapnia (Paco2 >50 mm Hg)/
 oxygenation deficit (Pao2 <60 mm Hg or Sao2 <90%)
 Severe dyspnea with clinical signs like respiratory muscle fatigue
 or increased work of breathing
 Exclusion criteria (any)
 Respiratory arrest
 Cardiovascular instability (hypotension, arrhythmias, myocardial infarction)
 Change in mental status; uncooperative patient
 High aspiration risk
 Viscous or copious secretions
 Recent facial or gastroesophageal surgery
 Craniofacial trauma
 Fixed nasopharyngeal abnormalities
 Burns

67. Indications for Intubation with Mechanical Ventilation
• Unable to tolerate noninvasive ventilation (NIV) or NIV failure
• Respiratory or cardiac arrest
• Respiratory failure
• Decreased consciousness or increased agitation
• Massive aspiration
• Persistent inability to remove respiratory secretions
• Hypotension
• Persistent hypoxemia despite optimal respiratory treatment
• Hemodynamic instability

70.  Anesthetic
considerations
in COPD.

71. ………. Preparation for
Anaesthesia

72. Anaesthetic Considerations -:
Patient Factors:-
 Advanced age
 Poor general condition
 Nutritional status
 Co-morbid conditions-
 HTN
 Diabetes
 Heart Disease
 Obesity
 Sleep Apnea
 Blunted Ventilatory responses to hypoxia and CO2 retention

73. Age Related Pulmonary Changes:
Pathological changes Effect Implications
Decreased efficiency of
lung parenchyma
Decreased VC
Increased RV
Respiratory Failure
Decreased Muscle strength Decreased Compliance,
FEV1
Poor cough
Infection
Alveolar septal destruction Decreased alveolar area Decreased gas exchange
Bronhchiolar damage Increased closing volume Air trapping
Decreased PaO2
Dilated upper airways Increased VD Decreased gas exchange
Decreased reactivity Decreased laryngeal
reflexes
Decreased vent response to
hypoxia, hypercarbia
Increased Aspiration
Increased resp. failure

74. 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

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

76. Pre-operative assessment:
History:-
 Smoking
 Cough: Type, Progression, Recent RTI
 Sputum: Quantity, color, blood
 Dyspnea
 Exercise intolerance
 Occupation
 Allergies
 Symptoms of cardiac or respiratory failure

77. Examination
Physical Examination: Better at assessing chance of post op
complications.
Airway obstruction
 hyperinflation of chest, Barrel chest
 Decreased breath sounds
 Expiratory ronchi
 Prolonged expiration: Watch & Stethoscope test, >4 sec
↑WOB
 ↑ RR, ↑HR
 Accessory muscles used
 Tracheal tug
 Intercostal indrawing
 Tripod sitting posture

78.  Body Habitus
-Malnourished
 Active infection
 Sputum- change in
quantity, nature
 Fever
 Crepitations
Respiratory failure
Hypercapnia
Hypoxia
Cyanosis
Cor Pulmonale and Right heart
failure
Dependant edema
tender enlarged liver
Pulmonary hypertension
Loud P2
Right Parasternal heave
Tricuspid regurgitation

79. Investigations-
 Complete Blood count
 Serum Electrolytes
 Blood Sugar
 Urinalysis
 ECG
 Arterial Blood Gases
 Diagnostic Radiology
 Chest X Ray
 Spiral CT
 Preoperative Pulmonary Function Tests
 Tool for optimisation of pre-op lung function
 Not to assess risk of post op pulmonary complications

80. Investigations: Chest X-Ray
 Overinflation
 Depression or flattening of
diaphragm
 Increase in length of lung
 ↑ lung markings- dirty lung
 Bullae +/-
 Vertical Cardiac silhouette
 ↑ transverse diameter of chest, ribs
horizontal, square chest
 Enlarged pulmonary artery with
rapid tapering

81. Indications for PFT
(American College of Physicians consensus statement)
 Cardiac, thoracic or upper abdominal surgery with a history
of dyspnea, smoking.
 Lower abdominal surgery with a history of
dyspnea, smoking and anticipated prolonged surgery.
 All patients undergoing lung resection
 Morbid obesity
 Any pulmonary disease
 Age > 70 years

82. Bedside PFTs-
 The cough test:- s/o underlying bronchitis.
The wheeze test:
Asked to take five deep inspirations/expirations,then auscultated between the
shoulder blades posteriorly to determine the presence or absence of wheezing.
 Maximum laryngeal height:-
 distance between the top of the thyroid cartilage and the suprasternal notch at the
end of expiration.
 < 4 cm--abnormal.
 accurate sign of obstructive airways disease compared to pulmonary function
tests.

83. Forced expiratory time (FET):.
> 6 seconds indicates severe expiratory airflow obstruction with %FEV1 < 50%.
correlates well with the forced expiratory time measured by spirometry.
 Sabrasez breath-holding time (BHT)-
 >40 seconds- normal
 20 to 30 seconds-compromised cardiopulmonary reserve.
 <20 seconds -very poor cardiopulmonary reserve.
 Single breath count test:
 asked to count out loud numbers from 1 onwards after a maximal
inspiration.
 normal -50 or more.
 <15 -severe impairment of vital capacity (VC).

84. Snider’s match test:
 Used to measure the patient’s maximum breathing capacity
(MBC). Place a lighted match stick at varying distances from the
patient’s mouth.
 Instruct the patient to sit, keep his mouth open and blow
(without pursing the lips) the candle off.
 22 cm  MBC >150 L/min
 15 cm MBC < 100 L/min
 7.5cm MBC < 50 L/min.

85. Investigations contd.
ECG
 Signs of RVH:
 RAD
 p Pulmonale in Lead II
 Predominant R wave in V1-3
 RSR1 pattern in precordial leads
Arterial Blood Gases:
 In moderate-severe disease
 Nocturnal sample in Cor Pulmonale-
 Increased PaCO2 is prognostic marker
 Strong predictor of potential intra-op respiratory failure & post op
Ventilatory failure
 Also, increased d/t post op pain, shivering, fever, respiratory depressants.

86. Exercise testing:
-expensive, cumbersome
-Not validated in nonthoracic surgery
-Parameter with greatest utility is decreased maximum
O2 consumption
α1 Antitrypsin levels:
-Non smokers
-Premature or basilar emphysema
-COPD with bronchiectasis
-family history of α1AT deficiency

87. Pre-operative preparation
 Cessation of smoking
 Dilation 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

88. Effects of smoking:
 Cardiac Effects:
 Risk factor for development of cardiovascular disease
 CO decreases Oxygen delivery & increases myocardial work
 Catecholamine release, coronary vasoconstriction
 Decreased exercise capacity
 Respiratory Effects:
 Major risk factor for COPD
 Decreased Mucociliary activity
 Hyperreactive airways
 Decreased Pulmonary immune function
 Other Systems
 Impairs wound healing.
 Chance of gastric aspiration.

89. Smoking cessation and time course of beneficial Effects
Time after smoking Physiological Effects
12-24 Hrs Fall in CO & Nicotine levels
48-72 Hrs COHb levels normalise
Airway function improves
1-2 Weeks Decreased sputum production
4-6 Weeks PFTs improve
6-8 Weeks Normalization of Immune function
8-12 Weeks Decreased overall post operative morbidity

90. Treatment: Smoking Cessation
 Motivation, Counseling & behavioral support
 Nicotine replacement
 Patches
 chewing gum
 Inhaler
 nasal spray
 lozenges
 Bupriopion

91. Dilatation of Airways:
 Bronchodilators:
 Only small increase in FEV1
 Alleviate symptoms by decreasing hyperinflation & dyspnoea
 Improve exercise tolerance
 Anticholinergics
 Beta Agonists
 Methylxanthines

92. Anticholinergics:
 Block muscarinic receptors
 Onset of action within 30 Min
 Ipratropium –
 40-80 μg by inhalation
 20 μg/ puff – 2 puffs X 3-4 times
 250 μg / ml respirator soln. 0.4- 2 ml X 4 times daily
 Tiotropium - long lasting
 Side Effects:
 Dry Mouth, metallic taste
 Caution in Prostatism & Glaucoma

93. Beta Blockers:
 Act by increasing cAMP
 Specific β2 agonist –
 Salbutamol :
 oral 2-4 mg/ 0.25 – 0.5 mg i.m /s.c ,100-200 μg inhalation
 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
 Formeterol, Bambuterol

94. Methylxathines:
 Mode of Action-
– inhibition of phospodiesterase,↑ cAMP, cGMP –
Bronchodilatation
 Oral(Theophyllin) & Intravenous (Aminophylline,
Theophyllin)
 loading – 5-6 mg/kg
 Maintenace –
 1.0mg/kg /h for smokers
 0.5mg/kg/h for nonsmokers
 0.3 mg/kg/h for severely ill patients.

95. 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
 Dose: 200 μg BD ↑ upto 400 μg QID
 > 1600 μg / day- suppression of HPA axis

96. Recommendations for steroids in perioperative patient
 Dose Surgery Recommended dose
 < 10 mg/day Minor/ Additional steroid cover not
 Moderate/Major required
 > 10 mg/day Minor surgery 25 mg of hydrocortisone at
 induction and normal
 medications postoperative
 > 10 mg/day Moderate surgery Usual dose preoperative and
 25 mg hydrocortisone IV at
 induction then 25 mg IV TDS for
 1 day then recommend
 preoperative dosage
 > 10 mg/day Major surgery Usual dose preoperative and 100
 mg hydrocortisone at induction then
 100 mg IV TDS for 2–3 days.

97. ………. AnaestheTIC Technique

98. Anaesthetic Technique
COPD is not a limitation on the choice of anaesthesia.
Type of Anaesthesia doesn’t predictably influence Post op
pulmonary complications.

99. Concerns in RA
 Neuraxial Techniques:
• No significant effect on Resp. function
• No interference with airway  Avoids bronchospasm
• No swings in intrathoracic pressure
• No danger of pneumothorax from N2O
• Sedation required. May compromise expiratory function.
 Peripheral Nerve Blocks:
• Suitable for peripheral limb surgeries
• Minimal respiratory effects
• Supraclavicular techniques contraindicated in severe pulmonary disease

100. Concerns in RA-
• Improved Surgical outcome:
Better pain control
Attenuation of neuroedocrine respones to surgery
Improvement of tissue oxygenation
Maintenance of immune function
Fewer episodes of DVT, PE, stroke
• Technique of choice in perineal, pelvic extra peritoneal
& lower extremities
• No benefit over GA in Intraperitoneal surgery,
or when high levels are needed.

101. Concerns in GA
• Airway instrumentation & bronchospasm
• Residual NMB
• Nitrous Oxide
• Attenuation of HPV
• Respiratory depression with opioids, BZDs
• Airway humidification

102. Premedication
 ↑ Sensitivity to the effect of respiratory depressants.
 Opioids & Benzodiazepines - ↓ response to hypoxia,
hypercarbia.
 Bronchodilator puff / nebulisation, inhaled steroids
 Atropine ?: Should be individualized
 Decreases airway resistance
 Decreases secretion-induced airway reactivity
 Decreases bronchospasm from reflex vagal stimulation
 Cause drying of secretions, mucus plugging

103. General Anaesthesia: Induction
 Thiopentone:
 Best to avoid
 Histamine release
 If barbiturates have to be usedoxybarbiturates(methohexitone).
 Propofol (DoC)
 Better suppression of laryngeal reflexes
 Hemodynamic compromise
 Agent of choice in stable patient
 Ketamine
 Bronchodilator
 Tachycardia and HT, may increase PVR
 Increased airway secretions

104. Intubation
 NMB :
 Succinyl Choline (1-2mg/kg)
 Vecuronium(0.08-0.10 mg/kg)
 Rocuronium (0.6-1.2 mg/kg )
 Attenuation of Intubation Response:
 IV lignocaine (1- 1.5 mg/kg) 90s prior to laryngoscopy
 Fentanyl 1-5 microgram/Kg
 Esmolol 100-150mg bolus
 Adequate plane of anaesthesia prior to intubation
 LMA Vs Endotracheal Tube
 Avoids tracheal stimulation
 P-LMA also allows for suctioning

105. Maintenance
 Muscle relaxant
 Prefer Vecuronium, Rocuronium, Cisatracurium
 Avoid Atracurium, Mivacurium, Doxacurium ( histamine
release)
 Volatile anaesthetic
 N2O  Caution in pulmonary bullae, dilution of
delivered O2
 Inhalational agents attenuate HPV
 Sevoflurane: non pungent, bronchodilator
 Halothane: Non pungent, bronchodilator.
Slower onset & elimination, Sensitises to
catecholamines

106. Maintenance
Ventialatory Strategy:
 Aim:
 Maximise alveolar gas emptying
Minimize dynamic hyperinflation, iPEEP
 Settings:-
 Decrease minute vent. Low frequency
 Adequate Exp time, Low I:E ratio, minimal exp.pause.
 Reduce exp.flow resistance
 Recruitment maneuvers
 Acceptance of mild hypercapnia & acidemia
 Humidification of gases
 Pressure Cycled mode with decelerating flow.

107. Maintenance
 Monitoring-
 ECG, NIBP
 Pulse Oximetry
 Capnography
 Neuromuscular Monitoring
 Depth of Anaesthesia
 Intraoperative IV Fluids
 Excessive IV volume  Water accumulation & tissue edema 
Respiratory/heart failure
 Haemodynamic goal directed fluid loading
 Restrictive fluid administration

108. Intraoperative Increased PIP-
 Bronchospasm
 Light anaesthesia, coughing, bucking
 Obstruction in the circuit
 Blocked / kinked tube
 Endobronchial intubation
 Pneumothorax
 Pulmonary embolism
 Major Atelectasis
 Pulmonary edema
 Aspiration pneumonia
 Head down position, bowel packing

109. Management of intraoperative bronchospasm
 Increase FiO2
 Deepen anaesthesia
 Commonest cause is surgical stimulation under light anaesthesia
 Incremental dose of Ketamine or Propofol
 Relieve mechanical stimulation
 endotracheal suction
 Stop surgery
 β2 agonists – Nebulisation or MDI
 s/c Terbutaline, iv Adrenaline
 intravenous Aminophyline
 Intravenous corticosteroid indicated if severe bronchospasm
 IV MgSO4 can also be used.

110. Reversal/ Recovery:
 Neostigmine - may provoke bronchospasm
 Atropine 1.2-1.8mg or Glycopyrrolate 0.6mg before
Neostigmine
 Tracheal toileting
 Extubation : deep or awake?
 Deep extubation may reduce chance of bronchospasm
Deep
Difficult airway
Difficult
intubation
Residual NMB
Full stomach
Good airway - accessible
Easy intubation
No Residual NMB
Normothermic
Not at increased risk of
aspiration
NO YES

111. Post operative care-
 ↑ Risk of Post op pulmonary complications
 Postoperative analgesia –
• Parenteral NSAIDS
• Neuraxial drugs
• Nerve blocks
• PCA
 Post-operative respiratory therapy –
• Chest physiotherapy & postural drainage
• Voluntary Deep Breathing
• Incentive Spirometry

112. Post operative care
 Mechanical Ventilation:
 Indications:
 Severe COPD undergoing major surgery
 FEV1/FVC<70%
 Preop. 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 maneuvers

113. Post Operative Pulmonary Complications:
 Incidence: 6.8% (Range 2-19%)
 Include:
 Atelectasis
 Bronchopneumonia
 Hypoxemia
 Respiratory Failure
 Bronchopleural fistula
 Pleural effusion

114. Predictors-
Predictors of
PPCs:
Patient Related:
•Age > 70 yrs
•ASA Class II or above
•CHF
•Pre-existing Pulmonary Disease
•Functionally Dependent
•Cigarette smoking
•Hypoalbuminemia <3.5g/dL
Procedure Related:
•Emergency Surgery
•Duration > 3 Hrs
•GA
•Abd, Thoracic, Head &
Neck,Neuro, Vascular Surgery

115. Specific Risk Factors:
 COPD
 Bronchial Asthma
 GA
 OSA
 Advanced age
 Morbid Obesity(BMI > 40)
 Functional limitation
 Smoking > 20 Pack year
 Alcohol consumption (>60ml ethanol/day)

116. Risk Reduction Strategies:
Preoperative:
•Smoking cessation
•Bronchodilatation
•Control infections
•Patient Education
Intraoperative:
•Minimally invasive
surgery
•Regional Anaesthesia
•Duration < 3 Hrs
Post operative:
•Lung Volume Expansion Maneuvers
•Adequate Analgesia

117. Lung Expansion maneuvers:-
 Incentive spirometry
 Deep breathing exercises
 Chest Physiotherapy & postural drainage
 Intermittent Positive Pressure Ventilation
 CPAP, BiPAP
 Early Ambulation

118. take home message
 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 anaesthsia
technique if patients have been appropriately stabilised.
 COPD patients are prone to develop intraoperative and
postoperative pulmonary complications.
 Preoperative optimisation 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

119. Thank you

120. Pulmonary Function Tests:
Measure Normal Obstructive Restrictive
FVC (L) 80% of TLC
(4800)
  
FEV1 (L) 80% of FVC  
FEV1/FVC(%) 75- 85%  N to 
FEV25%-
75%(L/sec)
4-5 L/ sec  N to 
PEF(L/sec) 450- 700 L/min  N to 
Slope of FV
curve
 
MVV(L/min) 160-180 L/min  N to 
TLC 6000 ml N to  
RV 1500 mL  
RV/TLC(%) 0.25  N