Anaesthesia for

Patients with COPD

Dr Sajith Damodaran

University College of Medical Sciences & GTB

Hospital, Delhi

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.

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COPD
Chronic Bronchitis: (Clinical Defnition)
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 Defnition)
The presence of permanent enlargement
of the airspaces distal to the terminal
bronchioles, accompanied by destruction
of their walls and without obvious fbrosis

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

FEV1

Decreased

Decreased

PaO2

Marked Decrease
(Blue Bloater)

Modest Decrease
(Pink Puffer)

PaCO2

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:

1. - The normal course of forced expiratory volume in one second (FEV1) over tim
mpared with the result of impaired growth of lung function ( ) an accelerated
and a shortened plateau phase (). All three abnormalities can be combined
tjens HAM, Rijcken B, Schouten JP, Postma DS. Decline of FEV1 by age and
king status: facts, fgures, 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:
Excessive
Mucus
Central Airways: (cartilaginous
airways
>2mm
of
Loss
of
cilia
production
internal diameter)
and ciliary
Bronchial glands hypertrophy
dysfunction

Goblet cell metaplasia

Squamous metaplasia of the airway epithelium
Increased smooth muscle and connective tissue
Airway Wall Changes:

Inflammatory Cells
Peripheral airways (noncartilaginous airways<2mm
internal diam
Airflow
Bronchiolitis
limitation
and
Pathological extension of goblet cells and squamous
metaplasia
hyperinflatio
Inflammatory cells
n
Fibrosis and increased deposition of collagen in the airway walls

Pathophysiology:

ng parenchyma (respiratory bronchioles, alveoli and capillaries)

mphysema (abnormal englagement of air spaces distalAirflow

to terminal bronch
limitation
curs in the parenchyma:
and
2 Types: Centrilobular and Panlobular
hyperinflatio
Early microscopic lesion progress to Bullae over time. n
Results in signifcant loss of alveolar attachments, which contributes
to peripheral airway collapse
flammatory cells
Pulmonary
HTN

Pulmonary Vasculature:
RV
Thickening of the vessel wall and endothelial dysfunction
dysfunction
Increased vascular smooth muscle & inflammatory(cor
infltration of
the vessel wall
Pulmonale)
Collagen deposition and emphysematous destruction of the
capillary bed

Pathogenesis:
Alpha 1
antitrypsin
def.
Proteinase &
Antiproteinase
imbalance

Tobacco smoke &

other noxious gases
Inc
r
Neu eased
Lym troph
il
Ma phocy s,
cro
pha tes &
ges

Inflammatory
response in
airways

Oxidativ
e Stress

Tissue Destruction
Impaired defense against tissue
destruction
Impaired repair mechanisms

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

Diagnosis
Clinical Features:

Physical Examination:
Symptoms:
Respiratory Signs
Cough: Initially intermittent
Present throughout the day Barrel Chest
Pursed lip breathing
Sputum:
Adventitious Ronchi/Wheeze
Tenacious & mucoid
Systemic Signs
Purulent Infection
Cyanosis
Dyspnoea: Progressively worsens Neck vein enlargement
Peripheral edema
Persistant
Exposure: Smoking, in pack

Liver enlargement
years Loss of muscle mass

Diagnosis
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

GOLD Classifcation
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)

Treatment
Modifying

natural history of Disease:

Smoking cessation
Long term oxygen therapy
Symptomatic:

Bronchodilators
Antibiotics
Others
Pulmonary
Nutrition

Rehabilitation

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:

f lung function over 11 yrs in the Lung Health Study for continuous smokers
intermittent quitters () and sustained quitters (). FEV1: forced expiratory
e in one second
onisen NR et al,Lung Health Study Research Group.
ng and lung function of Lung Health Study participants after 11 years. Am J Resp
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 (PaO2)
<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
condition
55

88

SaO2 %

Absolute

LTOT indication Qualifying

None

5559 89 Relative with qualifer

polycythemia >55%

P Pulmonale,

History of edema
60

90

None except with qualifer

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
Defnition:
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

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

In a nutshell

Optimal disease management entails redesigning standard medical care to integrate rehabilitative el
into a system of patient self-management and regular exercise

. 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 CO2 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, FEV1

Poor cough
Infection

Alveolar septal
destruction

Decreased alveolar
area

Decreased gas
exchange

Brohchiolar damage Increased closing

volume

Air trapping
Decreased PaO2

Dilated upper
airways

Increased VD

Decreased gas
exchange

Decreased
reactivity

Decreased
laryngeal reflexes
Decreased vent

Increased
Aspiration
Increased resp.

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 & 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

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

Pre-operative assessment: Examination

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 P2
Right Parasternal
heave
Tricuspid regurgitation

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:

Measurem
ent

Normal

Obstructiv Restrictive
e

FVC (L)

80% of TLC
(4800)

FEV1 (L)

80% of FVC

FEV1/FVC(%)

75- 85%

N to

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

Spirometric tracing in COPD patients

Litres

FEV1

FVC

FEV1/FV
C

Normal

4150

5200

80%

COPD

2350

3900

60%

FEV1

COPD
FVC

FEV1
NORMAL

FVC

5
1

seconds

Maximum inspiratory and expiratory flowvolume 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 V1-3
RS 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

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

Smoking cessation and time course of beneficial Effe

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

Normalisation of Immune function

8-12 Weeks

Decreased overall post operative

morbidity

Dilatation of Airways:
Bronchodilators:
Only small increase in FEV1
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 FEV1
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 signifcant effect on Resp function: Level above T6 no
recommended
No interference with airway Avoids bronchospasm
No swings in intrathoracic pressure
No danger of pneumothorax from N2O
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 beneft 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 humidifcation

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 O2
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
Humidifcation

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

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

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

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
NO
Difficult airway
Difficult
intubation

Deep

YES
Good airway - accessible
Easy intubation
No Residual NMB

Residual NMB

Normothermic

Full stomach

Not at increased risk of

aspiration

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
FEV1/FVC<70%
Preop PaCO2 > 50mm Hg

FiO2 & Ventillator 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

Post Operative Pulmonary

Complications:
Incidence:

6.8% (Range 2-19%)

(Sementa et al, Annals of internal Medicine,

2006,144:58195)

Include:

Atelectasis
Bronchopneumonia
Hypoxemia
Respiratory Failure
Bronchopleural fstula
Pleural effusion

Post Operative Pulmonary

Complications:
Patient Related:

Predictors
of
PPCs:

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,

Post Operative Pulmonary

Complications:
Specifc 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
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