3. INTRODUCTION
ď Common condition (mainly related to smoking &
Aging)
ď Burden of the disease is increasing
ď Will rank third by 2030 among worldwide
ď Causes 100,000 deaths per year in US
ď Pose a challenge to anaesthesiologist
ď Intraoperative & postoperative pulmonary
complications are more common
ď Can lead to icreased length of hospital stay &
4. SCOPE
ď Copd and types
ď Pathophysiology
ď Treatment
ď Anaesthetic consideration in copd patients
undergoing surgery
ď Preoperative assessment
(examination/investigation)
ď Preoperative preperation
ď Planning of anaesthetic technique
ď Prediction of post operative complication and
reduction strategies
ď conclusion
7. DEFINITION
ď Disease state characterised by airflow
limitation that is not fully reversible
ď 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.
8. DEFINITION
ď Disease state characterised by airflow
limitation that is not fully reversible
ď 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.
10. COPD
Chronic Bronchitis: (Clinical Definition)
ď Chronic productive cough for 3 consecutive
months in each of 2 successive years in a patient
in whom other causes of productive chronic cough
have been excluded.
Emphysema: (Pathological Definition)
ď The presence of permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and
alveolar septa.
11. COMPARATIVE FEATURES OF COPD
Feature Chronic
Bronchitis
Emphysema
Mech of Airway
Obstruction
Decreased Lumen
d/t mucus &
inflammation
Loss of elastic recoil
Dyspnoea 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
14. RISK FACTORS
Host factors:
Genetic factors: Îą1 Antitrypsin Deficiency
Sex : Prevalence more in males
Age : Increases with
Airway hyperactivity,
Immunoglobulin E and asthma
15. Exposures:
â˘Smoking: Most Important Risk Factor
â˘Socioeconomic status
â˘Occupation
â˘Environmental pollution
â˘Perinatal events and childhood illness
â˘Recurrent bronchopulmonary infections
â˘Diet
16. PATHOPHYSIOLOGY
Pathological changes are seen in 4
major compartments of lungs:
ď central airways
ď Peripheral airways
ď lung parenchyma
ď pulmonary vasculature.
17. PATHOPHYSIOLOGY
Central Airways: (cartilaginous airways >2mm of internal
diameter)
â˘Bronchial glands hypertrophy
â˘Goblet cell metaplasia
â˘Airway Wall Changes:
â˘Inflammatory Cells
Squamous metaplasia of the airway epithelium
Increased smooth muscle and connective tissue
Peripheral airways (noncartilaginous airways<2mm internal diame
â˘Bronchiolitis
â˘Pathological extension of goblet cells and squamous metaplasia
â˘Inflammatory cells
â˘Fibrosis and increased deposition of collagen in the airway walls
Excessive
Mucus
production Loss of cilia and
ciliary
dysfunction
Airflow
limitation and
hyperinflation
18. PATHOPHYSIOLOGY
Lung parenchyma (respiratory bronchioles, alveoli and capillaries)
â˘Emphysema (abnormal englagement of air spaces distal to terminal bronchio
occurs in the parenchyma:
2 Types: Centrilobular and Panlobular
â˘Early microscopic lesion progress to Bullae over time.
â˘Results in significant loss of alveolar attachments, which contributes
to peripheral airway collapse
â˘Inflammatory cells
Pulmonary Vasculature:
â˘Thickening of the vessel wall and endothelial dysfunction
â˘Increased vascular smooth muscle & inflammatory infiltration of the vessel
wall
â˘Collagen deposition and emphysematous destruction of the capillary bed
Airflow
limitation and
hyperinflation
â˘Pulmonary
HTN
â˘RV dysfunction
(cor Pulmonale)
28. TREATMENT
ď Modifying natural history of Disease:
⌠Smoking cessation
⌠Long term oxygen therapy
ď Symptomatic:
⌠Bronchodilators
⌠Antibiotics
⌠Others
ď Pulmonary Rehabilitation
ď Nutrition
29. TREATMENT:SMOKING CESSATION
ď 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
ď Motivation, Counsellin
& behavioural suppor
ď Nicotine replacement
⌠Patches
⌠chewing gum
⌠Inhaler
⌠nasal spray
⌠lozenges
30. Effect of smoking and smoking
cessation on Lung Function:
Loss of lung function over 11 yrs in the Lung Health Study for continuous smokers
(âââ), intermittent quitters (âââ) and sustained quitters (âââ). 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 Respi
Care Med 2002; 166: 675â679.
31. TREATMENT:OXYGEN THERAPY
Long Term Oxygen Therapy(LTOT):
ď Improves survival, exercise, sleep and
cognitive performance.
ď Oxygen delivery methods include nasal
continuous flow, reservoir cannulas and
transtracheal catheter.
ď 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.
32. PHYSIOLOGICAL INDICATION FOR LONGTERM
OXYGEN THERAPY(LTOT)
PaO2 mmHg SaO2 % LTOT indication Qualifying
condition
â¤55 â¤88 Absolute None
55â59 89 Relative with qualifier âPâ Pulmonale,
polycythemia >55%
History of edema
âĽ60 âĽ90 None except with qualifier Exercise
desaturation
Sleep desaturation
not corrected by CPAP
Lung disease with
severe dyspnea
responding to O2
33. Relief of arterial hypoxemia with
supplemental oxygen
administration is more effective
than any known drug therapy in
decreasing pulmonary vascular
resistance and pulmonary
hypertension
35. SURGICAL TREATMENT
Bullectomy
⌠short-term improvements in
ď airflow obstruction
ď lung volumes
ď hypoxaemia and hypercapnia
ď exercise capacity
ď dyspnoea
Lung Volume Reduction Surgery
⌠potentially long-term improvement in survival
⌠short-term improvements in
ď Spirometry
ď lung volumes
ď exercise tolerance
ď dyspnoea
Lung Transplantation
36. COPD: EXECERBATIONS
Definition:
ď An exacerbation of COPD is an event in the
natural course of the disease characterised
by a change in the patientâs baseline
dyspnoea, cough and/or sputum beyond
day-to-day variability sufficient to warrant a
change in management.
Precipitating Causes:
ď Infections: Bacterial, Viral
ď Air pollution exposure
ď Non compliance with LTOT
37. COPD:EXECERBATIONS
Indication for Hospitalisation:
ď The presence of high-risk comorbid
conditions
⌠pneumonia,
⌠cardiac arrhythmia,
⌠congestive heart failure,
⌠diabetes mellitus,
⌠renal or liver failure
ď Inadequate response to outpatient
management
ď Marked increase in dyspnoea, orthopnoea
ď Worsening hypoxaemia & hypercapnia
ď Changes in mental status
ď Uncertain diagnosis.
38. COPD: EXECERBATIONS
Indication for ICU admission:
ď Impending or actual respiratory failure
ď Presence of other end-organ dysfunction
⌠shock
⌠renal failure
⌠liver failure
⌠neurological disturbance
ď Haemodynamic instability
39. TREATMENT
ď Supplemental Oxygen (if SPO2 < 90%)
ď Bronchodilators:
⌠Nebulised Beta Agonists,
⌠Ipratropium with spacer/MDI
ď Corticosteroids
⌠Inhaled, Oral
ď Antibiotics:
⌠If change in sputum characteristics
⌠Based on local antibiotic resistance
⌠Amoxycillin/Clavulamate, Respiratory Flouroquinolones
ď Ventillatory support: NIV, Invasive ventillation
41. ANAESTHETIC CONSIDERATION IN
COPD PTS UNDERGOING SUGERY
Patient Factors:
ď Advanced age
ď Poor general condition, nutritional status
ď Co morbid conditions
⌠HTN
⌠Diabetes
⌠Heart Disease
⌠Obesity
⌠Sleep Apnoea
ď Weak HPV, blunted Ventilatory
responses to hypoxia and CO2 retention
42. 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
response to hypoxia,
Increased Aspiration
Increased resp. failure
43. ANAESTHETIC CONSIDERATION IN
COPD PTS UNDERGOING SURGERY
ď Problems due to Disease
⌠Exacerbation of Bronchial inflammation
ď d/t Airway instrumentation
⌠preoperative airway infection
⌠surgery induced immunosuppression
⌠increased WOB
⌠Increased post operative pulmonary
complications
44. ď 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
ď Problems due to Surgery:
⌠Site : most important predictor of Post op
complications
⌠Duration: > 3 hours
⌠Position
45. PREOPERATIVE ASSESMENT
History:
⌠Smoking
⌠Cough: Type, Progression, Recent RTI
⌠Sputum: Quantity, color, blood
⌠Dyspnea
⌠Exercise intolerance
⌠Occupation, Allergies
⌠Symptoms of cardiac or respiratory failure
⌠Current Medication
⌠Frequency of exacerbation
⌠Hospitalization
⌠Concomitant disease
46. PREOPERATIVE
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
âWOB
⌠â RR, âHR
⌠Accessory muscles used
⌠Tracheal tug
⌠Intercostal indrawing
⌠Tripod sitting posture
47. ď Body Habitus
Obesity/ Malnourished
ď Active infection
⌠Sputum- change in quantity,
nature
⌠Fever
⌠Crepitations
â˘Respiratory failure
Hypercapnia
Hypoxia
Cyanosis
â˘Cor Pulmonale and
Right heart failure
Dependant edema
tender enlarged liver
â˘Pulmonary
hypertension
Loud P2
Right Parasternal heave
Tricuspid regurgitation
48. PREOPARETIVE
ASSESSMENT:INVESTIGATION
ď Complete Blood count
ď Serum Electrolytes
ď Blood Sugar
ď Urinalysis
ď ECG
ď Arterial Blood Gases
ď Diagnostic Radiology
⌠Chest X Ray
⌠Spiral CT
ď Preoperative Pulmonary Function Tests
⌠Tool for optimisation of pre-op lung function
⌠Not to assess risk of post op pulmonary complications
49. INVESTIGATIONS:CHEST XRAY
ď Overinflation
ď Depression or flattening of
diaphragm
ď Increase in length of lung
ď â size of retrosternal
airspace
ď â lung markings- dirty lung
ď Bullae +/-
ď Vertical Cardiac silhouette
ď â transverse diameter of
chest, ribs horizontal,
square chest
ď Enlarged pulmonary artery
50. PULMONARY FUNCTION TESTS:
Measureme
nt
Normal Obstructive Restrictive
FVC (L) 80% of TLC
(4800)
ďŻ ďŻ ďŻ
FEV1 (L) 80% of FVC ďŻ ďŻ
FEV1/FVC(%) 75- 85% N to ďŻ N to ď
FEV25%-
75%(L/sec)
4-5 L/ sec ďŻ N to ďŻ
PEF(L/sec) 450- 700 L/min ďŻ N to ďŻ
Slope of FV
curve
ďŻ ď
MVV(L/min) 160-180 L/min ďŻ N to ďŻ
TLC 6000 ml N to ď ďŻ
RV 1500 mL ď ďŻ
RV/TLC(%) 0.25 ď N
52. PREOPERATIVE ASSESSMENT:
INVESTIGATIONS
ECG
ď Signs of RVH:
⌠RAD
⌠p Pulmonale in Lead II
⌠Predominant R wave in V1-3
⌠RS pattern in precordial leads
Arterial Blood Gases:
ď In moderate-severe disease
ď 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
53. PREOPERATIVE PREPERATION
ď Cessation of smoking
ď Dilation of airways
ď Loosening & Removal of secretions
ď Eradication of infection
ď Recognition of Cor Pulmonale and treatment
ď Improve strength of skeletal muscles â
nutrition, exercise
ď Correct electrolyte imbalance
ď Familiarization with respiratory therapy,
education, motivation & facilitation of patient
care
54. EFFECTS OF SMOKING:
ď Cardiac Effects:
⌠Risk factor for development of cardiovascular disease
⌠CO decreases Oxygen delivery & increases myocardial
work
⌠Catecholamine release, coronary vasoconstriction
⌠Decreased exercise capacity
ď Respiratory Effects:
⌠Major risk factor for COPD
⌠Decreased Mucociliary activity
⌠Hyperreactive airways
⌠Decreased Pulmonary immune function
ď Other Systems
⌠Impairs wound healing
55. 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
56. DILATATION OF AIRWAYS:
ď Bronchodilators:
ď Only small increase in FEV1
ď Alleviate symptoms by decreasing
hyperinflation & dyspnoea
ď Improve exercise tolerance
ďAnticholinergics
ďBeta Agonists
ďMethylxanthines
57. ANTICHOLENERGICS:
ď Block muscarinic receptors
ď Onset of action within 30 Min
ď Ipratropium â
⌠40-80 Οg by inhalation
⌠20 Îźg/ puff â 2 puffs X 3-4 times
⌠250 Οg / ml respirator soln. 0.4- 2 ml X 4
times daily
ď Tiotropium - long lasting
ď Side Effects:
⌠Dry Mouth, metallic taste
⌠Caution in Prostatism & Glaucoma
59. METHYLXANTHINES
ď Mode of Action
â inhibition of phospodiesterase,â cAMP, cGMP â
Bronchodilatation
⌠Adenosine receptor antagonism
⌠â Ca release from SR
ď Oral(Theophyllin) & Intravenous
(Aminophylline, Theophyllin)
⌠loading â 5-6 mg/kg
⌠Previous use â 3 mg/kg
⌠Maintenace â
ď 1.0mg/kg h for smokers
ď 0.5mg/kg/h for nonsmokers
ď 0.3 mg/kg/h for severely ill patients.
60. INHALED COTICOSTEROIDS:
ď Anti-inflammatory
ď Restore responsiveness to β2 agonist
ď Reduce severity and frequency of
exacerbations
ď Do not alter rate of decline of FEV1
ď Beclomethasone, Budesonide, Fluticasone
ď Dose: 200 Îźg BD â upto 400 Îźg QID
ď > 1600 Îźg / day- suppression of HPA axis
61. PLANNING: ANAESTHETIC
TECHNIQUE
ď COPD is not a limitation on the choice of
anaesthesia.
ď Type of Anaesthesia doesnât predictably
influence Post op pulmonary complications.
62. CONCERNS IN RA
Neuraxial Techniques:
â˘No significant effect on Resp function: Level
above T6 not recommended
â˘No interference with airway ď Avoids
bronchospasm
â˘No swings in intrathoracic pressure
â˘No danger of pneumothorax from N2O
â˘Sedation reqd. May compromise expiratory fn.
63. CONCERNS IN RA
Peripheral Nerve Blocks:
â˘Suitable for peripheral limb
surgeries
â˘Minimal respiratory effects
â˘Intersclanie techniques
contraindicated in severe
Pulmonary disease
64. CONCERNS IN RA
â˘Improved Surgical outcome:
ďBetter pain control
ďAttenuation of neuroedocrine respones to
surgery
ďImprovement of tissue oxygenation
ďMaintenance of immune function
ďFewer episodes of DVT, PE, stroke.
â˘Technique of choice in perineal, pelvic
extraperitoneal
& lower extremities
â˘No benefit over GA in Intraperitoneal surgery,
65. CONCERNS IN GA
â˘Airway instrumentation & bronchospasm
â˘Residual NMB
â˘Nitrous Oxide
â˘Attenuation of HPV
â˘Respiratory depression with opioids, BZDs
â˘Airway humidification
67. Patient Related:
â˘Age > 70 yrs
â˘ASA Class II or above
â˘CHF
â˘Pre-existing Pulmonary Disease
â˘Functionally Dependent
â˘Cigarette smoking
â˘Hypoalbuimnemia , 3.5g/dL
Procedure Related:
â˘Emergency Surgery
â˘Duration > 3 Hrs
â˘GA
â˘Abd, Thoracic, Head & Neck,
Nuero, Vascular Surgery
68.
69. CHOICE OF ANESTHESIA
Regional anaesthesia General
anesthesia
Spontaneous
ventilation
Spinal/Epidural anaesthesia Endotrachea
l intubation
with
controlled
ventilation
Sedation LMA
High Low ď does not stimulate
the larynx, but does
offer some protection
for the trachea
ď used for minor
surgery of the limbs
or body surface of
short duration (< 2
hrs)
ďWhen the patient
can breath
comfortably in the
supine position or on
their side
⢠Impair intercostal
muscle
function FRC &
risk of perioperative
basal atelectasis and
hypoxia.
indications -
below the
umbilicus and on
lower limbs
without
pulmonary
impairment
70. General + Regional
ď if general anaesthesia is required, the
addition of regional techniques can
reduce operative volatile anaesthetic
and post operative opioid
requirements and the likelihood of
respiratory complications.
71. Pre-medication
Antacids Antiemetic Analgesia Antisialogue Preoxygenatio
n
H2
antihistaminic
A/C to need COX
inhibitor
Anticholinergic
e.g.
glycopyrrolate
Humidified
oxygen
Use PPI Opiates
used with
caution
Epidural
analgesia
Nebulised with
salbutamol is
very important.
72. Monitoring
ď Pulse oximetry
ď Electrocardiogram
ď Non-invasive blood pressure recordings
ď if available, end-tidal carbon dioxide
measurement
ď indwelling arterial catheter - for regular
ABGs in those patients at greatest risk
of periop pulmonary cx
73. Perioperative steroid
supplementation
ď Patients who have received a course of
steroids in the 6 months before surgery, or
who are on maintenance therapy of
greater than 10mg of prednisolone a day,
are presumed to have adreno-cortical
suppression.
ď Intravenous hydrocortisone 100mg 8
hourly is given starting with the
premedication.
ď Over the next 5 days this is tapered to
their normal daily dose, where 100mg
intravenous hydrocortisone is equivalent to
25mg oral prednisolone.
74. Perioperative steroid supplementation
ď Over the next 5 days this is tapered to
their normal daily dose, where 100mg
intravenous hydrocortisone is
equivalent to 25mg oral prednisolone.
ď Intravenous steroids must replace oral
whilst these cannot be taken.
75. Inducing agents
Thiopentone
Propofol
Etomidate
Thiopentone Ketamine Volatile
anesthetics
BZDs &
Opioid
initial transient
apnoea
Thiopentone
increases
airway
reactivity
preserves
respiratory
drive
better at
maintaining
the airway
depress
respiratory
drive
decreasing
order :-
Enflurane>Des
flurane>Isoflur
ane>Sevoflura
ne>Halothane
depress
respiratory
drive and
response to
hypoxia and
hypercapnia
Morphine may
result in
histamine
release and
occasionally
bronchospasm
77. Intubation
ď Airway manipulation should be kept to
a minimum and take place only under
adequate anaesthesia.
ď Endotracheal intubation using muscle
relaxants and controlled ventilation
78. Maintenance of anesthesia
ď Avoid nitrous oxide if CXR showing â
cavity, emphysematous bulla
ď In cases with severe airways
obstruction the ventilator rate may have
to be sufficiently low to allow the slow
expiration of asthma.
79. Recovery room
ď The airway is vulnerable for up to 24
hours, and hypoventilation can occur for
up to 3 days.
ď The airway is kept patent, and adequate
ventilation and oxygenation ensured
before discharge to the ward.
ď All neuromuscular paralysis must be
reversed.
ď If there are problems the patient will need
to go to the HDU or ICU.
ď Otherwise, the patient is kept warm and
well hydrated, and maintain fluid balance
85. CONCLUSION
ď COPD is not a contraindication for any particular
anaesthsia technique if patients have been
appropriately stabilized.
ď COPD patients are prone to develop
intraoperative and postoperative pulmonary
complications.
ď Preoperative optimisation should include control
of infection, wheezing and prediction &
necessary measures for postoperative