Anaesthesia for Patients

with COPD
Teresa Gabriella Laurauli
Damar Nirwan Alby
Erika Agustina Kasdjono
COPD:
PATHOPHYSIOLOGY,
DIAGNOSIS, TREATMENT
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.
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.
COPD:
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
Comparative features of COPD
Feature Chronic Bronchitis Empysema
Mech of Airway
Obstruction
Decreased Lumen d/t
mucus &
inflammation
Loss of elastic recoil
Dysnoea Moderate Severe
FEV
1
Decreased Decreased
PaO
2
Marked Decrease
(Blue Bloater)
Modest Decrease
(Pink Puffer)
PaCO
2
Increased Normal or Decreased
Diffusing capacity Normal Decreased
Hematocrit Increased Normal
Cor Pulmonale Marked Mild
Prognosis Poor Good
COPD: Risk factors
Host factos:
Genetic factors: Eg. 1 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
Natural History:
Fig. 1. - The normal course of forced expiratory volume in one second (FEV1) over time ()
is compared with the result of impaired growth of lung function ( ) an accelerated decline
() and a shortened plateau phase (). All three abnormalities can be combined
(Kerstjens HAM, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age and
smoking status: facts, figures, and fallacies. Thorax 1997; 52: 820827.)
Pathophysiology:
Pathological changes are seen in 4
major compartments of lungs:

central airways
Peripheral airways
lung parenchyma
pulmonary vasculature.

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 (noncartilaginous 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
Pathophysiology:
Lung parenchyma (respiratory bronchioles, alveoli and capillaries)

Emphysema (abnormal englagement of air spaces distal to terminal bronchioles)
occurs in the parenchyma:
2 Types: Centrilobular and Panlobular
Early microscopic lesion progress to Bullae over time.
Results in 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)
Pathogenesis:
Tobacco smoke & other
noxious gases
Inflammatory
response in
airways
Tissue Destruction
Impaired defense against tissue
destruction
Impaired repair mechanisms
Proteinase & Antiproteinase
imbalance
Oxidative
Stress
Alpha 1
antitrypsin
def.
Physiological Effects:
Mucous hypersecretion and cilliary dysfunction
Goblet cell hyperplasia & squamous metaplasia
Airflow limitation and hyperinflation
Airway remodelling
Loss of eleastic 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 Vasoconstrictoin,Endothelial dysfunction
Remodelling of arteries & capillary destruction
Systemic effects
Diagnosi
s
Clinical Features:
Symptoms:
Cough: Initially intermittent
Present throughout the day
Sputum:
Tenacious & mucoid
Purulent Infection
Dyspnoea: Progressively worsens
Persistant
Exposure: Smoking, in pack years
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
Investigations:
Spirometry
Diagnosis
Assessment of severity
Following progress
Chest Radiograph: To exclude other
diseases
Emphysematous changes
Bronchodilator Reversibility
Exclude Bronchial Asthma
<20%
Alpha-1 Antitrypsin levels
Young COPD with Family History

Diagnosis

GOLD Classification
Stage Characteristics
I: Mild FEV
1
/FVC < 70%
FEV
1
80% predicted, with/without chronic symptoms
II: Moderate FEV
1
/FVC < 70%
50% FEV
1
80% predicted, with/without chronic
symptoms

III: Severe FEV
1
/FVC < 70%
30% FEV
1
50% predicted, with/without chronic
symptoms
IV: Very
severe
FEV
1
/FVC < 70%
FEV
1
< 30% predicted or < 50% predicted plus chronic
respiratory failure (PaO
2
< 60mm Hg &/or PaCO
2
>
50mm Hg)
Treatment
Modifying natural history of Disease:
Smoking cessation
Long term oxygen therapy
Symptomatic:
Bronchodilators
Antibiotics
Others
Pulmonary Rehabilitation
Nutrition
Treatment: Smoking Cessation
Need:
Most important cause
of COPD
Major risk factor for
atherosclerotic
vascular disease,
cancer, peptic ulcer
and osteoporosis.
Quitting smoking
slows progressive loss
of lung function &
reduces symptoms

Motivation,
Counselling &
behavioural
support
Nicotine
replacement
Patches
chewing gum
Inhaler
nasal spray
lozenges
Bupriopion
Effect of smoking and smoking
cessation on Lung Function:
Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers
(), intermittent quitters () and sustained quitters (). FEV1: forced expiratory
volume in one second
(Anthonisen NR et al,Lung Health Study Research Group.
Smoking and lung function of Lung Health Study participants after 11 years. Am J Respir Crit
Care Med 2002; 166: 675679.
Treatment: 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 (PaO
2
)
<7.3 kPa (55 mmHg). The therapeutic goal
is to maintain SpO2 >90% during rest,
sleep and exertion.
Physiological indications for long-term oxygen therapy
(LTOT)
PaO2 mmHg SaO2 % LTOT indication Qualifying
condition

55 88 Absolute None

5559 89 Relative with qualifier P Pulmonale,
polycythemia >55%
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
Treatment: Symptomatic Measures
Bronchodilators:
Anticholinergics
Beta Agonists
Methylxanthines

Corticosteroids
N-Acetyl Cysteine
1 Antitrypsin
augmentation
Vaccination
Others: No proven
effect
Leukotriene receptor
antagonists/cromones
Maintenance
antibiotic therapy
Immunoregulators
Vasodilators: NO,
CCB
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
COPD: Exacerbations
Definition:
An exacerbation of COPD is an event in the
natural course of the disease characterised
by a change in the patients baseline
dyspnoea, cough and/or sputum beyond
day-to-day variability sufficient to warrant a
change in management.
Precipitating Causes:
Infections: Bacterial, Viral
Air pollution exposure
Non compliance with LTOT
COPD: Exacerbations
Indication for Hospitalisation:
The presence of high-risk comorbid
conditions
pneumonia,
cardiac arrhythmia,
congestive heart failure,
diabetes mellitus,
renal or liver failure
Inadequate response to outpatient
management
Marked increase in dyspnoea, orthopnoea
Worsening hypoxaemia & hypercapnia
Changes in mental status
Uncertain diagnosis.
COPD: Exacerbations
Indication for ICU admission:
Impending or actual respiratory failure
Presence of other end-organ dysfunction
shock
renal failure
liver failure
neurological disturbance
Haemodynamic instability
Treatment
Supplemental Oxygen (if SPO
2
< 90%)

Bronchodilators:
Nebulised Beta Agonists,
Ipratropium with spacer/MDI

Corticosteroids
Inhaled, Oral

Antibiotics:
If change in sputum characteristics
Based on local antibiotic resistance
Amoxycillin/Clavulamate, Respiratory Flouroquinolones

Ventillatory support: NIV, Invasive ventillation



Optimal disease management entails redesigning standard medical care to integrate rehabilitative elements
into a system of patient self-management and regular exercise
In a nutshell
. PREPARATION
FOR ANAESTHESIA
Anaesthetic Considerations in patients
with COPD undergoing surgery:
Patient Factors:
Advanced age
Poor general condition, nutritional status
Co morbid conditions
HTN
Diabetes
Heart Disease
Obesity
Sleep Apnea
Weak HPV, blunted Ventilatory
responses to hypoxia and CO
2
retention
Age Related Pulmonary Changes:
Pathological
changes
Effect Implications
Decreased efficiency
of lung parenchyma
Decreased VC
Increased RV
Respiratory Failure
Decreased Muscle
strength
Decreased
Compliance, FEV
1

Poor cough
Infection
Alveolar septal
destruction

Decreased alveolar
area
Decreased gas
exchange
Brohchiolar damage Increased closing
volume
Air trapping
Decreased PaO
2

Dilated upper airways Increased V
D
Decreased gas
exchange

Decreased reactivity Decreased laryngeal
reflexes
Decreased vent
response to hypoxia,
hypercarbia
Increased Aspiration
Increased resp. failure
Anaesthetic Considerations in patients
with COPD undergoing surgery:
Problems due to Disease
Exacerbation of Bronchial inflammation
d/t Airway instrumentation
preoperative airway infection
surgery induced immunosuppression
increased WOB
Increased post operative pulmonary
complications
Anaesthetic Considerations in patients
with COPD undergoing surgery:
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 & CO
2

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


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
Pre-operative assessment: 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
Body Habitus
Obesity/ 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 P
2
Right Parasternal heave
Tricuspid regurgitation
Pre-operative assessment: Examination
Preoperative Assessment: 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
Investigations: Chest X-Ray
Overinflation
Depression or flattening of
diaphragm
Increase in length of lung
size of retrosternal airspace
lung markings- dirty lung
Bullae +/-
Vertical Cardiac silhouette
transverse diameter of chest,
ribs horizontal, square chest
Enlarged pulmonary artery with
rapid tapering in MZ
Pulmonary Function Tests:
Measureme
nt
Normal Obstructive Restrictive
FVC (L) 80% of TLC
(4800)

FEV
1
(L) 80% of FVC
FEV
1
/FVC(%) 75- 85% N to N to
FEV
25%-
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
FEV1
FEV1
FVC
seconds
2 1 3 4 5
0
1
2
3
4
L
i
t
r
e
s

5
COPD
NORMAL
60% 3900 2350 COPD
80% 5200 4150 Normal
FEV1/FVC FVC FEV1
FVC
Spirometric tracing in COPD patients
Maximum inspiratory and expiratory flow-volume
curves (i.e., flow-volume loops) in four types of airway
obstruction.
Preoperative Assessment: Investigations
ECG
Signs of RVH:
RAD
p Pulmonale in Lead II
Predominant R wave in V
1-3

RS pattern in precordial leads

Arterial Blood Gases:
In moderate-severe disease
Nocturnal sample in cor Pulmonale
Increased PaCO
2
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
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
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
Dilatation of Airways:
Bronchodilators:
Only small increase in FEV
1

Alleviate symptoms by decreasing
hyperinflation & dyspnoea
Improve exercise tolerance
Anticholinergics
Beta Agonists
Methylxanthines
Anticholinergics:
Block muscarinic receptors
Onset of action within 30 Min
Ipratropium
40-80 g by inhalation
20 g/ puff 2 puffs X 3-4 times
250 g / ml respirator soln. 0.4- 2 ml X 4
times daily
Tiotropium - long lasting
Side Effects:
Dry Mouth, metallic taste
Caution in Prostatism & Glaucoma

Beta Blockers:
Act by increasing cAMP
Specific
2
agonist
Salbutamol :
oral 2-4 mg/ 0.25 0.5 mg i.m /s.c 100-200 g
inhalation
muscle tremors, palpitations, throat irritation
Terbutaline :
oral 5 mg/ 0.25 mg s.c./ 250 g inhalation
Salmeterol :
Long acting (12 hrs)
50 g BD- 200 g BD
Formeterol, Bambuterol
Bronchodilators: methylxathines
Mode of Action
inhibition of phospodiesterase, cAMP, cGMP
Bronchodilatation
Adenosine receptor antagonism
Ca release from SR

Oral(Theophyllin) & Intravenous
(Aminophylline, Theophyllin)
loading 5-6 mg/kg
Previous use 3 mg/kg
Maintenace
1.0mg/kg h for smokers
0.5mg/kg/h for nonsmokers
0.3 mg/kg/h for severely ill patients.


Inhaled Corticosteroids:
Anti-inflammatory
Restore responsiveness to
2
agonist
Reduce severity and frequency of
exacerbations
Do not alter rate of decline of FEV
1
Beclomethasone, Budesonide, Fluticasone
Dose: 200 g BD upto 400 g QID
> 1600 g / day- suppression of HPA axis
. ANAESTHETIC
TECHNIQUE
Anaesthetic Technique
COPD is not a limitation on the choice
of anaesthesia.
Type of Anaesthesia doesnt predictably
influence Post op pulmonary
complications.
Concerns in RA
Neuraxial Techniques:
No significant effect on Resp function: Level above T6 not
recommended
No interference with airway Avoids bronchospasm
No swings in intrathoracic pressure
No danger of pneumothorax from N
2
O
Sedation reqd. May compromise expiratory fn.

Peripheral Nerve Blocks:
Suitable for peripheral limb surgeries
Minimal respiratory effects
Supraclavicular techniques contraindicated in severe
Pulmonary disease
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, blood Tx

Technique of choice in perineal, pelvic
extraperitoneal
& lower extremities
No benefit over GA in Intraperitoneal surgery,
or when high levels are needed
Concerns in GA
Airway instrumentation & bronchospasm
Residual NMB
Nitrous Oxide
Attenuation of HPV
Respiratory depression with opioids, BZDs
Airway humidification
Premedication
Sensitivity to the effect of respiratory
depressants
Opioids & Benzodiazepines - response to
hypoxia, hypercarbia
Bronchodilator puff / nebulisation, inhaled
steroids
Atropine ?: Should be individualised
Decreases airway resistance
Decreases secretion-induced airway reactivity
Decreases bronchospasm from reflex vagal
stimulation
Cause drying of secretions, mucus plugging
General Anaesthesia:
Induction
Opioids:
Fentanyl(DoC)
Morphine ,Pethidine
Respiratory Depression, Histamine release, Chest
tightness

Propofol (DoC)
Better suppression of laryngeal reflexes
Hemodynamic compromise
Agent of choice in stable patient

Ketamine
Bronchodilator Catecholamine release, neural
inhibition
Tachycardia and HT, may increase PVR
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
Maintenance

Muscle relaxant
Prefer Vecuronium, Rocuronium, Cisatracurium
Avoid Atracurium, Mivacurium, Doxacurium (
histamine release)

Volatile anaesthetic
NO Caution in pulmonary bullae, dilution of
delivered O
2

Inhalational agents attenuate HPV
Sevoflurane: non pungent, bronchodilator
Halothane: Non pungent, bronchodilator.
Slower onset & elimination, Sensitises to
catecholamines

Maintenance
Ventialatory Strategy:
Aim: Maximise alveolar gas emptying
Minismise 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.


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
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

2
agonists Nebulisation or MDI
s/c Terbutaline, iv Adrenaline
intravenous Aminophyline
Intravenous corticosteroid indicated if severe
bronchospasm
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 YE
S
Post operative care
Risk of Post op pulmonary complications

Postoperative analgesia
Parenteral NSAIDS
Neuraxial drugs
Nerve blocks
PCA

Postoperative respiratory therapy
Chest physiotherapy & postural drainage
Voluntary Deep Breathing
Incentive Spirometry
Post operative care
Mechanical Ventilation:
Indications:
Severe COPD undergoing major surgery
FEV
1
/FVC<70%
Preop PaCO
2
> 50mm Hg
FiO
2
& Ventillator settings adjusted to
maintain PaO
2
60-100 mm Hg & PaCO
2
in
range that maintains pH at7.35-7.45
Continue Bronchodilators
Oxygen therapy
Lung Expansion maneuvers


Post Operative Pulmonary
Complications:
Incidence: 6.8% (Range 2-19%)
(Sementa et al, Annals of internal Medicine, 2006,144:581
95)
Include:
Atelectasis
Bronchopneumonia
Hypoxemia
Respiratory Failure
Bronchopleural fistula
Pleural effusion


Post Operative Pulmonary
Complications:
Predictors of
PPCs:
Patient Related:
Age > 70 yrs
ASA Class II or above
CHF
Pre-existing Pulmonary Disease
Functionally Dependent
Cigarette smoking
Hypoalbuimnemia , 3.5g/dL
Procedure Related:
Emergency Surgery
Duration > 3 Hrs
GA
Abd, Thoracic, Head & Neck,
Nuero, Vascular
Surgery
Post Operative Pulmonary
Complications:
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)


Post Operative Pulmonary
Complications:
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
Post Operative Pulmonary
Complications:
Post Operative Analgesia:
Opioids
Paravertebral/Intercostal N Blocks
Epidural Analgesia
LA
Opioids
NSAIDS Bronchospasm
Post Operative Pulmonary
Complications:
Lung Expansion maneuvers:
Incentive spirometry
Deep breathing exercises
Chest Physiotherapy & postural
drainage
Intermittant Positive Pressure
Ventilation
CPAP, BiPAP
Early Ambulation
Summary:
COPD is a progressive disease with increasing
irreversible airway obstruction.
Cigarette smoking is the most important causative
factor for COPD
Smoking cessation & LTOT are the only measures
capable of altering the natural history of COPD.
COPD is not a contraindication for any particular
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 complications.
References:
Stoeltings Anaesthesia & Coexisting Disease, 5
th
Ed.
Standards for Diagnosis & Management of COPD Patients,
American Thoracic Society & European Respiratory Society
Global Initiative for COPD
Refresher course lectures, 57
th
National Conference of ISA
COPD: Perioperative management, M.E.J. Anesth 2008 19(6)
Post Operative Pulmonary Complications, IJA April 2006
Periop Management of patients with COPD: Review, IJ
COPD 2007:2(4) 493:515
Harrisons Principles of Medicine, 16
th
Ed
Principles of respiratory Care, Egans, 9
th
Ed
Millers Anaesthsia, 7
th
Ed
Irwin & Rippes Intensive care medicine, 6
th
Ed.
Clinical Application of Mechanical Ventilation, David W
Chang, 3
rd
Ed