Copd and anaesthetic management

 INTRODUCTION
 DEFINATION
 RISK FACTORS
 PATHOGENESIS
 PATHOPHYSIOLOGY
 CLINICAL FEATURES
 INVESTIGATION
 TREATMENT
 EXACERBATIONS
 PREPRATION FOR ANAESTHESIA
 ANESTHETIC TECHNIQUE

 COPD is currently the fourth leading cause of death
in the world
 COPD is projected to be the 3rd leading cause of
death by 2020
 More than 3 million people died of COPD in 2012
accounting for 6% of all deaths globally.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE

 Prevalence of COPD higher in smokers and ex-smokers
compared to non-smokers
 Higher ≥ 40 year group compared to those < 40
 Higher in men than women.
 Globally, the COPD burden is projected to increase in
coming decades because of continued exposure to
COPD risk factors and aging of the population

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

Chronic Obstructive Pulmonary Disease (COPD) is a
common, preventable and treatable disease that is
characterized by persistent respiratory symptoms and
airflow limitation that is due to airway and/or alveolar
abnormalities usually caused by significant exposure to
noxious particles or gases
GOLD 2017 REPORT

COPD
Includes:-
I.CHRONIC BRONCHITIS
II.EMPHYSEMA
III.SMALLAIRWAY DISEASE

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
COPD

COPD: Risk factors
Host factors:
•Genetic factors: Eg. α1 Antitrypsin Deficiency
•Gender : Prevalence more in males.
?Females more susceptible
•Airway Hyperresponsiveness
Exposures:
•Smoking: Most Important Risk Factor
•Passive/second hand ,smoking exposure
•Occupation
•Environmental pollution
•Recurrent bronchopulmonary infections

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

PATHOLOGY
Pathological changes occur in 4 major areas of
lungs:-
Large airways
Small airways
Lung parenchyma
Pulmonary vasculature

Large 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
Small 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

Lung parenchyma (respiratory bronchioles, alveoli and capillaries)
•Emphysema (abnormal enlargement 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)

Copd and anaesthetic management

PATHOPHYSIOLOGY
I. Airway obstruction
 The major site of obstruction is found in the smaller
conducting airway (<2 mm in diameter).
 Processes contributing to obstruction in the small conducting
airway include disruption of the epithelial barrier, interference
with mucociliary clearance apparatus that results in
accumulation of inflammatory mucous exudates in the small
airway lumen, infiltration of the airway walls by inflammatory
cells and deposition of connective tissue in the airway wall.
 Fibrosis surrounding the small airway appears to be a
significant contributor. This remodelling and repair thickens
the airway walls, reduces lumen calibre and restricts the
normal increase in calibre produced by lung inflation.

 Increased resistance of the small conducting airway and
increased compliance of the lung as a result of
emphysematous destruction, causes the prolonged time
constant.
 This constant is reflected in measurements of the FEV1 and
its ratio to forced vital capacity(FEV1/FVC),which are
reliable screening tools because they are affected by both
airway obstruction and emphysema

 In COPD there is often “air trapping” (increased
residual volume and increased ratio of residual volume
to total lung capacity) and progressive hyperinflation
(increased total lung capacity) late in the disease.
 Hyperinflation of the thorax during tidal breathing
preserves maximum expiratory airflow, because as
lung volume increases, elastic recoil pressure
increases, and airways enlarge so that airway
resistance decreases.
Despite compensating for airway obstruction,
hyperinflation can push the diaphragm into a flattened
position with a number of adverse effects.
II. Hyperinflation

First, by decreasing the zone of apposition between the
diaphragm and the abdominal wall, positive abdominal
pressure during inspiration is not applied as effectively to
the chest wall, hindering rib cage movement and
impairing inspiration.
 Second, because the muscle fibers of the flattened
diaphragm are shorter than those of a more normally
curved diaphragm, they are less capable of generating
inspiratory pressures than normal.
 Third, the flattened diaphragm (with increased radius of
curvature) must generate greater tension to develop the
transpulmonary pressure required to produce tidal
breathing.

Auto positive end expiratory pressure [Intrinsic positive end
expiratory pressure (PEEPi)]
Patients with severe COPD often breathe in a pattern
that interrupts expiration before the alveolar pressure has
decreased to atmospheric pressure
 This incomplete expiration is due to a combination of
factors which include flow limitation, increased work of
respiration and increased airway resistance
 This interruption leads to an increase of the
end‐expiratory lung volume above the FRC. This PEEP
in the alveoli at rest has been termed auto‐PEEP or
PEEPi.

III. GAS EXCHANGE
 Non‐uniform ventilation and ventilation‐perfusion mismatch are
characteristics of COPD, due to the heterogenous nature of the
disease process within airway and lung parenchyma.
 Ventilation/ perfusion (V/Q) mismatching causes reduction in
PaO2 but shunting is minimal.
 This finding explains the effectiveness of modest elevation of
inspired oxygen in treating hypoxaemia due to COPD. Pao2
usually remains near normal until FEV1 is decreased to 50% of
predicted and elevation of PaCO2 is not seen until FEV1 is <25%.

 Hypercapnia, if present, reflects both V/Q mismatching
and alveolar hypoventilation, the later resulting from
both respiratory muscle dysfunction and increased
ventilatory requirements.
 Pulmonary hypertension severe enough to cause
corpulmonale and right heart failure is seen when there
is marked decrease in FEV1 <25% along with chronic
hypoxaemia PaO2 <55 mm Hg.

CLINICAL FEATURES
Symptoms:
Cough: Initially intermittent
Present throughout the day
Sputum:
Tenacious & mucoid
Purulent Infection
Dyspnoea: Progressively worsens
Persistant
Physical Examination:
Respiratory Signs
•Barrel Chest
•Pursed lip breathing
•Adventitious
Rhonchi/Wheeze
Systemic Signs
•Cyanosis
•Neck vein enlargement
•Peripheral edema
•Liver enlargement
•Loss of muscle mass

 A "pink puffer" is a person where emphysema is the
primary underlying pathology.
 Emphysema results from destruction of the airways
distal to the terminal bronchiole which also includes the
gradual destruction of the pulmonary capillary bed and
thus decreased inability to oxygenate the blood.
 So, not only is there less surface area for gas exchange,
there is also less vascular bed for gas exchange but less
ventilation-perfusion mismatch than blue bloaters.
PINK PUFFER

 The body then has to compensate by
hyperventilation (the "puffer" part). Their arterial
blood gases (ABGs) actually are relatively normal
because of this compensatory hyperventilation.
 Eventually, because of the low cardiac output,
people afflicted with this disease develop muscle
wasting and weight loss.
 They actually have less hypoxemia (compared to
blue bloaters) and appear to have a "pink"
complexion and hence "pink puffer"

 A "blue bloater" is a person where the primary
underlying lung pathology is chronic bronchitis.
 Chronic bronchitis is caused by excessive mucus
production with airway obstruction resulting from
hyperplasia of mucus-producing glands, goblet cell
metaplasia, and chronic inflammation around bronchi.
BLUE BLOATER

 Unlike emphysema, the pulmonary capillary bed is
undamaged. Instead, the body responds to the increased
obstruction by decreasing ventilation and increasing cardiac
output. There is a dreadful ventilation to perfusion mismatch
leading to hypoxemia and polycythemia.
 In addition, they also have increased carbon dioxide
retention (hypercapnia). Because of increasing obstruction,
their residual lung volume gradually increases (the
"bloating" part).
 They are hypoxemic/cyanotic because they actually have
worse hypoxemia than pink puffers and this manifests as
bluish lips and faces-the "blue" part.

INVESTIGATIONS:-
1.PULMONARY FUNCTION TEST:
Diagnosis
Assessment of severity
Following progress
Decreased FEV1/FVC
Decreased FEF(25-75%)
Increased RV

Normal Trace Showing FEV1 and FVC
1 2 3 4 5 6
1
2
3
4
Volume,liters
Time, sec
FVC5
1
FEV1 = 4L
FVC = 5L
FEV1/FVC = 0.8

Spirometry: Obstructive Disease
Volume,liters
Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV1 = 1.8L
FVC = 3.2L
FEV1/FVC = 0.56
Normal
Obstructive

Time, seconds
FEV1 = 1.9L
FVC = 2.0L
FEV1/FVC = 0.95
1 2 3 4 5 6
5
4
3
2
1
Spirometry: Restrictive Disease
Normal
Restrictive
Volume,liters

Measurement Normal Obstructive Restrictive
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 
Slope of FV
curve
 
TLC 6000 ml N to  
RV 1500 mL  
RV/TLC(%) 0.25  N

GOLD Criteria for COPD Severity

 Arterial blood gases and oximetry may demonstrate
resting or exertional hypoxemia
 Arterial blood gases provide additional information
about alveolar ventilation and acid-base status by measuring
arterial Pco2 and pH. The change in pH with Pco2 is 0.08
units/10 mmHg acutely and 0.03 units/10 mmHg in the
chronic state
 The arterial blood gas is an important component of the
evaluation of patients presenting with symptoms of an
exacerbation.
2.ARTERIAL BLOOD GAS ANALYSIS

3. CHEST RADIOGRAPH:
 Obvious bullae, paucity of parenchymal markings, or
hyper- lucency suggests the presence of emphysema
 Increased lung volumes and flattening of the
diaphragm suggest hyperinflation but do not provide
information about chronicity of the changes

4. CT SCAN:-
 Computed tomography (CT) scan is the current
definitive test for establishing the presence or absence
of emphysema

5.ECG
Signs of RVH:
 RAD
 p Pulmonale in Lead II
 Predominant R wave in V1-3
 RS pattern in precordial leads

6.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.

7.Bronchodilator Reversibility Testing
Provides the best achievable FEV1 (and FVC)
Can be done on first visit if no diagnosis has been
made
Best done as a planned procedure: pre- and post-
bronchodilator tests require a minimum of 15
minutes

Preparation
 Tests should be performed when patients are clinically
stable and free from respiratory infection
 Patients should not have taken:
 inhaled short-acting bronchodilators in the previous
six hours
 long-acting bronchodilator in the previous 12 hours
 sustained-release theophylline in the previous 24
hours

Spirometry
 FEV1 should be measured (minimum twice, within 5%
or 150ml) before a bronchodilator is given
 The bronchodilator should be given by metered dose
inhaler through a spacer device or by nebulizer to be
certain it has been inhaled
 The bronchodilator dose should be selected to be high
on the dose/response curve

Spirometry (continued)
 Possible dosage protocols:
 400 µg β2-agonist, or
 80-160 µg anticholinergic, or
 the two combined
 FEV1 should be measured again:
 15 minutes after a short-acting bronchodilator
 45 minutes after the combination

Results
 An increase in FEV1 that is both greater
than 200 ml and 12% above the pre-
bronchodilator FEV1 (baseline value) is
considered significant

Flow Volume Curve
Expiratory
flow rate
L/sec
Volume (L)
FVC
Maximum
expiratory flow
(PEF)
Inspiratory
flow rate
L/sec
RVTLC

Flow Volume Curve Patterns
Obstructive and Restrictive
Obstructive Severe obstructive Restrictive
Volume (L)
Expiratoryflowrate
Expiratoryflowrate
Expiratoryflowrate
Volume (L) Volume (L)
Steeple pattern,
reduced peak
flow, rapid fall off
Normal shape,
normal peak flow,
reduced volume
Reduced peak
flow, scooped out
mid-curve

TLC
RV
Expiratory
flow rate
L/sec
Volume (L)
Inspiratory
flow rate
L/sec

Combined Assessment of COPD: provides a rubric for combining
these assessments to improve management of COPD.
• Symptoms:
Less Symptoms =(mMRC 0-1 or CAT < 10)=patient is (A) or (C)
More Symptoms=(mMRC ≥ 2 or CAT ≥ 10)=patient is (B) or (D)
• AirflowLimitation:
Low Risk =(GOLD 1 or 2)=patient is (A) or (B)
High Risk=(GOLD 3 or 4)=patient is (C) or (D)
• Exacerbations:
Low Risk: ≤ 1 per year and no hospitalization for exacerbation:
patient is (A) or (B)
High Risk: ≥ 2 per year or ≥ 1 with hospitalization: patient is (C) or
(D)
8. Combined Assessment of COPD:-

ABCD Assessment Tool
Example
 Consider two patients:
 Both patients with FEV1 < 30% of predicted
 Both with CAT scores of 18
 But, one with 0 exacerbations in the past year and the other
with 3 exacerbations in the past year.
 Both would have been labelled GOLD D in the prior classification
scheme.
 With the new proposed scheme, the subject with 3 exacerbations in
the past year would be labelled GOLD grade 4, group D.
 The other patient, who has had no exacerbations, would be
classified as GOLD grade 4, group B.

TREATMENT
 Modifying natural history of Disease:
Smoking cessation
Long term oxygen therapy
 Symptomatic:
Bronchodilators
Antibiotics
Others
 Lung Volume Reduction surgery

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

Effects of smoking:
 Respiratory Effects:
 The irritant smoke decreases ciliary motility and increases sputum
production.
 Thus these patients have a high volume of sputum and decreased
ability to clear it effectively
 Exposure to smoke increases synthesis and release of elastolytic
enzymes from alveolar macrophages,causes damage to lung
parenchyma
 Further damage to the lung tissue is probably caused by reactive
metabolites of oxygen,such as hydroxyl radicles and hydrogen
peroxide,which are usually used by the macrophages to kill
microorganisms

 Early in the disease , mild V/Q mismatch,bronchitis and
airway hyperactivity are the primary problems. Later these
problems are accompained by the hallmarks of COPD:Gas
trapping, flattened diaphragmatic configuration(which
decreases the diaphragm’s efficiency), and barrel chest
deformity
Cardiac Effects:
Risk factor for development of cardiovascular disease
CO decreases Oxygen delivery & increases myocardial
work
Catecholamine release, coronary vasoconstriction
Decreased exercise capacity
Other Systems
Impairs wound healing

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 Normalisation of Immune function
8-12 Weeks Decreased overall post operative morbidity

 Smoking patients should be advised to smoking
2 months prior to elective operations to maximize the
effects of smoking cessation, or for at least 4 weeks to
benefit from improved mucociliary function and some
reduction in post pulmonary complications.
 If patient cannot stop smoking for 4 to 8 weeks
preoperatively, it is controversial whether they should
be advised to stop smoking 24 hours preoperatively. A
24 hour smoking absitnence would allow
carboxyhemoglobin levels to fall to normal but may
increase the risk of post pulmonary complications

LONG TERM OXYGEN THERAPY
 Long-term oxygen therapy(home oxygen therapy) is
recommended if the Pao2 <55 mmHg, the hematocrit >55% or
there is evidence of cor pulmonale
 The goal of supplemental oxygen administration is to achieve a
Pao2 between 60 and 80 mmHg. This goal can usually be
accomplished by delivering oxygen through a nasal cannula at
2L/min. The flow rate of oxygen is titrated as neeeded according
to arterial blood gas or pulse oximetry measurements
 Relief of arterial hypoxemia with supplemental oxygen
administration is more effective than any known drug therapy in
decreasing pulmonary vascular resistance and pulmonary
hypertension and in preventing erythrocytosis

Symptomatic Measures
 Bronchodilators:
 Beta Agonists
 Anticholinergics
 Bronchodilators are the
mainstay of drug therapy for
COPD. Bronchodilators
cause only a small increase
in FEV1 but may alleviate
symptoms by decreasing
hyperinflation and dyspnea.
COPD is more effectively
treated by anticholinergic
drugs than by beta2 agonists.
 Corticosteroids
 N-Acetyl Cysteine
 α1 Antitrypsin augmentation
 Others:Vaccination(influenza
vaccine,pneumococcal
vaccine)

COPD: Exacerbations
Definition:
Exacerbations are episodes of increased dyspnea and cough and
change in the amount and character of sputum. They may or
may not be accompanied by other signs of illness, including
fever, myalgias, and sore throat.
Precipitating Causes:
 Infections: Bacterial, Viral
 Air pollution exposure
 Non compliance with LTOT

►Classified as:
 Mild (treated with SABDs only)
 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.
Assessment of Exacerbation Risk

Treatment
Supplemental Oxygen (if SPO2 < 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

………. 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

 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

 Problems due to Anaesthesia:
 GA decreases lung volumes, promotes V/Q mismatch
 FRC reduced during anaesthesia
 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

 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
Pre-operative assessment: Examination

Preoperative Assessment: Investigations
 Complete Blood count
 Serum Electrolytes
 Blood Sugar
 ECG
 Arterial Blood Gases
 Diagnostic Radiology
 Chest X Ray
 Spiral CT
 Preoperative Pulmonary Function Tests-specific and
nonspecific tests

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

Anticholinergics:
 Block muscarinic receptors
 Onset of action within 30 Min
 Ipratropium –
 MDI:- 17 mcg/puff, 200 puffs/ canister -2-3 puffs every
6hours
 NEBULIZER:- 0.25mg/ml(0.025%)- 0.25mg every 6hours
 Ipratropium bromide is generally preferred to the short-
acting beta-2-agonists as a first-line agent because of its
longer duration of action and absence of sympathomimetic
side effects
 Tiotropium - long lasting
 Side Effects:
 Dry Mouth, metallic taste
 Caution in Prostatism & Glaucoma

Beta Agonists:
 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

Methylxathines
 Mode of Action
– inhibition of phospodiesterase,↑ cAMP, cGMP –
Bronchodilatation
 Adenosine receptor antagonism
 ↑ Ca release from SR
 Intravenous (Aminophylline, Theophyllin)
 loading – 5mg/kg
 Maintenace – 0.5mg/kg/h

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

………. Anaesthetic Technique

 Choice of anaesthesia depends on the
1. Patient factors(clinical state)
2. Surgical factors(type and duration of
procedure)

Concerns in Regional Anesthesia
Neuraxial Techniques:
•No significant effect on Respiratory function:
Level above T6 not recommended
•No interference with airway  Avoids bronchospasm
•No danger of pneumothorax from N2O
Peripheral Nerve Blocks:
•Suitable for peripheral limb surgeries
•Minimal respiratory effects
•Supraclavicular techniques contraindicated in severe pulmonary
disease
•Interscalene block remains a concern due to ipsilateral phrenic
nerve paralysis and loss of sympathetic tone due to stellate
ganglion block resulting in bronchospasm

Concerns in Regional Anesthesia
•Thoracic epidural anesthesia using low concentrations of
local anaesthetic agents and low doses of opiates
suppresses both the afferent nociceptive inputs and the
efferent sympathetic output thus preserving the respiratory
muscular activity and the HPV response. It also improve
ventilatory mechanics resulting in decreased airway
resistance, lower work of breathing and better preservation
of inspiratory and expiratory capacities allowing lung
recruitment manoeuvres and voluntary drainage of
secretions

Concerns in General Anesthesia
 General anesthetic agents, opiates, myorelaxants as well as
mechanical ventilation are known to interfere with the
respiratory system
 The combined effects of the supine position, GA and
thoracic/abdominal incision produce an immediate decline in
lung volumes with atelectasis formation in the most dependent
parts of the lung
 Pre-oxygenation should be used in any patient who is hypoxic
on air before induction. In patients with severe COPD and
hypoxia, CPAP during induction may be used to improve the
efficacy of pre-oxygenation and reduce the development of
atelectasis

 Upper airway instrumentation( e.g tracheal intubation) may
trigger vagally-mediated reflex bronchoconstriction thereby
promoting the expiratory collapse of the peripheral airways
with incomplete lung alveolar emptying
 To atteunate the bronchoconstrictive reflex due to endotracheal
intubation or suctioning, prophylactic treatment with
lidocaine(IV or inhaled) and/or a beta2-adrenergic agonist are
recommended in COPD patients with bronchospastic response
 Volatile anaesthetics are useful for maintenance of anaesthesia
due to their excellent bronchodilating properties with the
possible exception of desflurane. Desflurane may cause
irritation of the bronchi and increased airway resistance so there
may be an advantage to choosing a less irritating agent such as
sevoflurane for induction and emergence in cases of severe
airway reactivity

 Emergence from anesthesia with inhalational agents can be
prolonged significantly ,especially in patients with significant
airway obstruction, because air trapping also traps inhalational
agents as they flood out of the body’s compartments into the
lungs
 Nitrous oxide can be administered in combination with a
volatile anesthetic. When nitrous oxide is used, there is the
potential for passage of this gas into pulmonary bullae. is could
lead to enlargement or even rupture of the bullae, resulting in
development of a pneumothorax. Another potential
disadvantage of nitrous oxide is the limitation on the inspired
oxygen concentration that it imposes

 Opioids may be less useful than inhaled anesthetics for
maintenance of anesthesia in patients with COPD
because they can be associated with prolonged
ventilatory depression as a result of their slow rate of
metabolism or elimination
 An endotracheal tube bypasses most of the natural airway
humidification system, so humidification of inspired
gases and use of low gas flows are needed to keep airway
secretions moist

 General anesthesia exceeding 2.5–4 hours has been
identified as a strong predictor of PPCs .Indeed,
prolonged exposure to general anesthetics alters the
immune defenses and gas exchange capacity mainly by
depressing the alveolar macrophage function, interfering
with surfactant production, slowing of the muco-ciliary
clearance and increasing the permeability of the
alveolar-capillary barrier
 Management of ventilation during general anaesthesia
should be aimed at reducing the dynamic hyperinflation,
PEEPi, and air trapping. Harmful effects of air trapping
include hypotension, barotrauma and volume trauma to
the lungs, hypercapnia, and acidosis

 Measures to reduce air trapping include use of smaller tidal
volumes and lower respiratory rates, with more time for expiration
 Shortening the inspiratory time increases the peak inspiratory flow
thereby facilitating better ventilation of all alveoli
 Tidal volumes of 6 to 8 mL/kg combined with slow inspiratory
flow rates minimize the likelihood of turbulent air flow and help
maintain optimal ventilation/perfusion matching
 Slow respiratory rates (6 to 10 breaths per minute) provide
sufficient time for complete exhalation to occur, which is
particularly important if air trapping is to be minimized. Slow
rates also allow sufficient time for venous return and are less
likely to be associated with undesirable degrees of
hyperventilation

 Application of external PEEP has been shown to decrease the
effort of triggering breaths in patients breathing spontaneously
on assisted modes of ventilation. Even during controlled
ventilation, external PEEP that is less than or equal to PEEPi,
is not found to significantly increase the alveolar pressure
 Pressure controlled ventilation, by virtue of its decelerating
flow reduces peak inspiratory pressure and allows for more
uniform distribution of tidal volume and improvement of static
and dynamic compliance

 Residual neuromuscular blockade persisting after
anesthesia emergence has been incriminated in deficient
coughing, depressed hypoxic ventilatory drive and
“silent” inhalation of gastric contents
 Restrictive fluid administration decreases risk of
pulmonary oedema, it has been accepted in thoracic
surgery and showed good outcomes after major
abdominal interventions

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

 Bronchospasm during anaesthesia usually manifests as prolonged
expiration
 Expiratory wheeze may be auscultated in the chest or heard in
the breathing circuit due to movement of the gas through
narrowed airway
 Breath sounds may be reduced or absent.
 With intermittent positive pressure ventilation, peak airway
pressures are increased, tidal volumes reduced, or both.
 In severe bronchospasm, wheeze may be quiet or absent due to
cessation of movement of air
Intraoperative bronchospasm

 With capnography, narrowed airway and prolonged expiration
result in a delayed rise in end‐tidal carbon dioxide, producing a
characteristic ‘shark fin’ appearance

 Intraoperatively, bronchospasm occurs most commonly during
the induction and maintenance stages of anaesthesia and is less
often encountered in the emergence and recovery stages
 Bronchospasm during the induction stage is most commonly
caused by airway irritation, often related to intubation.
 During the maintenance stage of anaesthesia, bronchospasm
may result from an anaphylactic or serious allergic reaction.
Following endotracheal intubation, wheezing is more likely to
occur when barbiturates are used as anaesthetic induction
agents, compared with propofol, ketamine or volatile
anaesthetics

Management of intraoperative bronchospa
 Increase FiO2
 Deepen anaesthesia
 Commonest cause is surgical stimulation under light anaesthesia
 Relieve mechanical stimulation
 endotracheal suction
 Stop surgery
 β2 agonists – Nebulisation or MDI
 s/c Terbutaline, iv Adrenaline
 intravenous Aminophyline:-5mg/kg IV over 20min then 0.5mg/kg/h
infusion
 Intravenous corticosteroid(hydrocortosone 200mg) indicated if severe
bronchospasm

Post Operative Pulmonary
Complications:
Include:
 Atelectasis
 Aspiration pneumonitis
 Ventilation associated pneumonia
 Deep vein thrombosis and pulmonary embolism

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

Complications:
Post Operative Analgesia:
 Opioids
 Paravertebral/Intercostal N Blocks
 Epidural Analgesia
 LA
 Opioids

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
1) Harrison’s principles of internal medicine-19th edition
2) Robbins Basic Pathology- 9th edition
3) Stoelting’s Anesthesia and coexisting diseases- 2nd south asia edition
4) Clinical anesthesia-Barash, 7th edition
5) COPD: Perioperative management, M.E.J. Anesth 2008
6) Post Operative Pulmonary Complications, IJA April 2006
7) Perioperative Management of patients with COPD: Review, IJ COPD
8) Anaesthesia for patient with chronic obstructive pulmonary disease.
Indian J Anaesth 2015
9) http://goldcopd.org

World COPD Day
November 16, 2016
http://goldcopd.org/world-copd-day/

Copd and anaesthetic management

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