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WELCOME
COPD and Anaesthesia
Prepared by : Maj jayed
INTRODUCTION
 Common condition (mainly related to smoking &
Aging)
 Burden of the disease is increasing
 Will rank third by 2030 among worldwide
 Causes 100,000 deaths per year in US
 Pose a challenge to anaesthesiologist
 Intraoperative & postoperative pulmonary
complications are more common
 Can lead to icreased length of hospital stay &
SCOPE
 Copd and types
 Pathophysiology
 Treatment
 Anaesthetic consideration in copd patients
undergoing surgery
 Preoperative assessment
(examination/investigation)
 Preoperative preperation
 Planning of anaesthetic technique
 Prediction of post operative complication and
reduction strategies
 conclusion
COPD MORTALITY RATE
WORLDWIDE
Stomach Cancer
HIV
Suicide
6th
3rd
Source: Murray & Lopez. Lancet 1997
1990 2030
Ischaemic heart disease
Cerebrovascular disease
Lower resp infection
Diarrhoeal disease
Perinatal disorders
COPD
Tuberculosis
Measles
Road Traffic Accidents
Lung Cancer
PATHOPHYSIOLOGY,
DIAGNOSIS,
TREATMENT
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.
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 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)
 The presence of permanent enlargement of the
airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and
alveolar septa.
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
CHRONIC BRONCHITIS
EMPHYSEMA
RISK FACTORS
Host factors:
Genetic factors: Îą1 Antitrypsin Deficiency
Sex : Prevalence more in males
Age : Increases with
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
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 diame
•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 bronchio
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)
LUNG STRUCTURE AND FUNCTION
NORMAL LUNG
LUNG WITH COPD
PATHOGENESIS
Tobacco smoke & other
noxious gases
Inflammatory
response in
airways
Tissue Destruction
Impaired defense against tissue
destruction
Impaired repair mechanisms
Protease & Antiprotease
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 Vasoconstriction, Endothelial dysfunction
◦ Remodelling of arteries & capillary destruction
 Systemic effects
DIAGNOSIS
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
•Tachypnea
•Pursed lip breathing
•Adventitious
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
•<15 - 20%
Alpha-1 Antitrypsin levels
•Young COPD with Family History
GOLD CLASSIFICATION
Stage Characteristics
I: Mild FEV1/FVC < 70%
FEV1 > 80% predicted, with/without chronic
symptoms
II:
Moderate
FEV1/FVC < 70%
50% ≤ FEV1 < 80% predicted, with/without
chronic symptoms
III: Severe FEV1/FVC < 70%
30% ≤ FEV1 < 50% predicted, with/without
chronic symptoms
IV: Very
severe
FEV1/FVC < 70%
FEV1 < 30% predicted or < 50% predicted
plus chronic respiratory failure (PaO2 <
60mm Hg &/or PaCO2 > 50mm Hg)
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, Counsellin
& behavioural suppor
 Nicotine replacement
◦ Patches
◦ chewing gum
◦ Inhaler
◦ nasal spray
◦ lozenges
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 Respi
Care Med 2002; 166: 675–679.
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 INDICATION FOR LONGTERM
OXYGEN THERAPY(LTOT)
PaO2 mmHg SaO2 % LTOT indication Qualifying
condition
≤55 ≤88 Absolute None
55–59 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
Relief of arterial hypoxemia with
supplemental oxygen
administration is more effective
than any known drug therapy in
decreasing pulmonary vascular
resistance and pulmonary
hypertension
TREATMENT:SYMPTOMATIC MEASURES
 Bronchodilators:
◦ Anticholinergics
◦ Beta Agonists
◦ Methylxanthines
 Corticosteroids
 N-Acetyl Cysteine
 α1 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: EXECERBATIONS
Definition:
 An exacerbation of COPD is an event in the
natural course of the disease characterised
by a change in the patient’s baseline
dyspnoea, cough and/or sputum beyond
day-to-day variability sufficient to warrant a
change in management.
Precipitating Causes:
 Infections: Bacterial, Viral
 Air pollution exposure
 Non compliance with LTOT
COPD:EXECERBATIONS
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: EXECERBATIONS
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 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 CONSIDERATION IN
COPD PTS UNDERGOING SUGERY
Patient Factors:
 Advanced age
 Poor general condition, nutritional status
 Co morbid conditions
◦ HTN
◦ Diabetes
◦ Heart Disease
◦ Obesity
◦ Sleep Apnoea
 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
response to hypoxia,
Increased Aspiration
Increased resp. failure
ANAESTHETIC CONSIDERATION IN
COPD PTS 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
 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
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
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
↑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 P2
Right Parasternal heave
Tricuspid regurgitation
PREOPARETIVE
ASSESSMENT:INVESTIGATION
 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 XRAY
 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
PULMONARY FUNCTION TESTS:
Measureme
nt
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 
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
Litres
5
COPD
NORMAL
60%
3900
2350
COPD
80%
5200
4150
Normal
FEV1/FVC
FVC
FEV1
FVC
SPIROMETRIC TRACING OF
COPD PATIENTS
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
PREOPERATIVE PREPERATION
 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 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
DILATATION OF AIRWAYS:
 Bronchodilators:
 Only small increase in FEV1
 Alleviate symptoms by decreasing
hyperinflation & dyspnoea
 Improve exercise tolerance
Anticholinergics
Beta Agonists
Methylxanthines
ANTICHOLENERGICS:
 Block muscarinic receptors
 Onset of action within 30 Min
 Ipratropium –
◦ 40-80 μg by inhalation
◦ 20 μg/ puff – 2 puffs X 3-4 times
◦ 250 μg / ml respirator soln. 0.4- 2 ml X 4
times daily
 Tiotropium - long lasting
 Side Effects:
◦ Dry Mouth, metallic taste
◦ Caution in Prostatism & Glaucoma
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
 Formeterol, Bambuterol
METHYLXANTHINES
 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 COTICOSTEROIDS:
 Anti-inflammatory
 Restore responsiveness to β2 agonist
 Reduce severity and frequency of
exacerbations
 Do not alter rate of decline of FEV1
 Beclomethasone, Budesonide, Fluticasone
 Dose: 200 μg BD ↑ upto 400 μg QID
 > 1600 μg / day- suppression of HPA axis
PLANNING: ANAESTHETIC
TECHNIQUE
 COPD is not a limitation on the choice of
anaesthesia.
 Type of Anaesthesia doesn’t 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 N2O
•Sedation reqd. May compromise expiratory fn.
CONCERNS IN RA
Peripheral Nerve Blocks:
•Suitable for peripheral limb
surgeries
•Minimal respiratory effects
•Intersclanie 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.
•Technique of choice in perineal, pelvic
extraperitoneal
& lower extremities
•No benefit over GA in Intraperitoneal surgery,
CONCERNS IN GA
•Airway instrumentation & bronchospasm
•Residual NMB
•Nitrous Oxide
•Attenuation of HPV
•Respiratory depression with opioids, BZDs
•Airway humidification
PREDICTION OF
POSTOPERATIVE 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
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
CHOICE OF ANESTHESIA
Regional anaesthesia General
anesthesia
Spontaneous
ventilation
Spinal/Epidural anaesthesia Endotrachea
l intubation
with
controlled
ventilation
Sedation LMA
High Low  does not stimulate
the larynx, but does
offer some protection
for the trachea
 used for minor
surgery of the limbs
or body surface of
short duration (< 2
hrs)
When 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
General + Regional
 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.
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.
Monitoring
 Pulse oximetry
 Electrocardiogram
 Non-invasive blood pressure recordings
 if available, end-tidal carbon dioxide
measurement
 indwelling arterial catheter - for regular
ABGs in those patients at greatest risk
of periop pulmonary cx
Perioperative steroid
supplementation
 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.
 Intravenous hydrocortisone 100mg 8
hourly is given starting with the
premedication.
 Over the next 5 days this is tapered to
their normal daily dose, where 100mg
intravenous hydrocortisone is equivalent to
25mg oral prednisolone.
Perioperative steroid supplementation
 Over the next 5 days this is tapered to
their normal daily dose, where 100mg
intravenous hydrocortisone is
equivalent to 25mg oral prednisolone.
 Intravenous steroids must replace oral
whilst these cannot be taken.
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
Drugs considered safe for airway hyperreactive
patients
Induction Propofol, etomidate, ketamine, midazolam
Opioids Pethidine,fentanyl, alfentanil
Muscle
relaxants
Vecuronium, suxamethonium, rocuronium
Volatile
agents
Halothane, isoflurane, enflurane, sevoflurane, nitrous oxide
Intubation
 Airway manipulation should be kept to
a minimum and take place only under
adequate anaesthesia.
 Endotracheal intubation using muscle
relaxants and controlled ventilation
Maintenance of anesthesia
 Avoid nitrous oxide if CXR showing –
cavity, emphysematous bulla
 In cases with severe airways
obstruction the ventilator rate may have
to be sufficiently low to allow the slow
expiration of asthma.
Recovery room
 The airway is vulnerable for up to 24
hours, and hypoventilation can occur for
up to 3 days.
 The airway is kept patent, and adequate
ventilation and oxygenation ensured
before discharge to the ward.
 All neuromuscular paralysis must be
reversed.
 If there are problems the patient will need
to go to the HDU or ICU.
 Otherwise, the patient is kept warm and
well hydrated, and maintain fluid balance
POSTOPERATIVE PULMONARY
COMPLICATIONS:
Risk Reduction Strategies:
Preoperative:
•Smoking cessation
•Bronchodilatation
•Control infections
•Patient Education
RISK REDUCTION STRATEGIES
Intraoperative:
•Minimally invasive surgery
•Regional Anaesthesia
•Duration < 3 Hrs
Post operative:
•Lung Volume Expansion Maneuvers
•Adequate Analgesia
POSTOPERATIVE PULMONARY
COMPLICATIONS:
Post Operative Analgesia:
 Opioids
 Paravertebral/Intercostal N Blocks
 Epidural Analgesia
◦ LA
◦ Opioids
 NSAIDS  Bronchospasm
POSTOPERATIVE PULMONARY
COMPLICATIONS:
Lung Expansion maneuvers:
 Incentive spirometry
 Deep breathing exercises
 Chest Physiotherapy & postural
drainage
 Intermittant Positive Pressure
Ventilation
 CPAP, BiPAP
 Early Ambulation
QUESTIONS?
CONCLUSION
 COPD is not a contraindication for any particular
anaesthsia technique if patients have been
appropriately stabilized.
 COPD patients are prone to develop
intraoperative and postoperative pulmonary
complications.
 Preoperative optimisation should include control
of infection, wheezing and prediction &
necessary measures for postoperative
Copd and anaesthesia

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Copd and anaesthesia

  • 3. INTRODUCTION  Common condition (mainly related to smoking & Aging)  Burden of the disease is increasing  Will rank third by 2030 among worldwide  Causes 100,000 deaths per year in US  Pose a challenge to anaesthesiologist  Intraoperative & postoperative pulmonary complications are more common  Can lead to icreased length of hospital stay &
  • 4. SCOPE  Copd and types  Pathophysiology  Treatment  Anaesthetic consideration in copd patients undergoing surgery  Preoperative assessment (examination/investigation)  Preoperative preperation  Planning of anaesthetic technique  Prediction of post operative complication and reduction strategies  conclusion
  • 5. COPD MORTALITY RATE WORLDWIDE Stomach Cancer HIV Suicide 6th 3rd Source: Murray & Lopez. Lancet 1997 1990 2030 Ischaemic heart disease Cerebrovascular disease Lower resp infection Diarrhoeal disease Perinatal disorders COPD Tuberculosis Measles Road Traffic Accidents Lung Cancer
  • 7. 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.
  • 8. 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.
  • 10. COPD Chronic Bronchitis: (Clinical Definition)  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)  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: •Smoking: Most Important Risk Factor •Socioeconomic status •Occupation •Environmental pollution •Perinatal events and childhood illness •Recurrent bronchopulmonary infections •Diet
  • 16. PATHOPHYSIOLOGY Pathological changes are seen in 4 major compartments of lungs:  central airways  Peripheral airways  lung parenchyma  pulmonary vasculature.
  • 17. 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 diame •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
  • 18. PATHOPHYSIOLOGY Lung parenchyma (respiratory bronchioles, alveoli and capillaries) •Emphysema (abnormal englagement of air spaces distal to terminal bronchio 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)
  • 19. LUNG STRUCTURE AND FUNCTION
  • 22. PATHOGENESIS Tobacco smoke & other noxious gases Inflammatory response in airways Tissue Destruction Impaired defense against tissue destruction Impaired repair mechanisms Protease & Antiprotease imbalance Oxidative Stress Alpha 1 antitrypsin def.
  • 23. 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 Vasoconstriction, Endothelial dysfunction ◦ Remodelling of arteries & capillary destruction  Systemic effects
  • 24. DIAGNOSIS Clinical Features: Symptoms: Cough: Initially intermittent Present throughout the day Sputum: Tenacious & mucoid Purulent Infection Dyspnoea: Progressively worsens Persistant Exposure: Smoking, in pack years
  • 25. PHYSICAL EXAMINATION Respiratory Signs •Barrel Chest •Tachypnea •Pursed lip breathing •Adventitious Systemic Signs •Cyanosis •Neck vein enlargement •Peripheral edema •Liver enlargement •Loss of muscle mass
  • 26. INVESTIGATIONS Spirometry •Diagnosis •Assessment of severity •Following progress Chest Radiograph: To exclude other diseases •Emphysematous changes Bronchodilator Reversibility •Exclude Bronchial Asthma •<15 - 20% Alpha-1 Antitrypsin levels •Young COPD with Family History
  • 27. GOLD CLASSIFICATION Stage Characteristics I: Mild FEV1/FVC < 70% FEV1 > 80% predicted, with/without chronic symptoms II: Moderate FEV1/FVC < 70% 50% ≤ FEV1 < 80% predicted, with/without chronic symptoms III: Severe FEV1/FVC < 70% 30% ≤ FEV1 < 50% predicted, with/without chronic symptoms IV: Very severe FEV1/FVC < 70% FEV1 < 30% predicted or < 50% predicted plus chronic respiratory failure (PaO2 < 60mm Hg &/or PaCO2 > 50mm Hg)
  • 28. TREATMENT  Modifying natural history of Disease: ◦ Smoking cessation ◦ Long term oxygen therapy  Symptomatic: ◦ Bronchodilators ◦ Antibiotics ◦ Others  Pulmonary Rehabilitation  Nutrition
  • 29. 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, Counsellin & behavioural suppor  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 (–––), 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 Respi Care Med 2002; 166: 675–679.
  • 31. 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.
  • 32. PHYSIOLOGICAL INDICATION FOR LONGTERM OXYGEN THERAPY(LTOT) PaO2 mmHg SaO2 % LTOT indication Qualifying condition ≤55 ≤88 Absolute None 55–59 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
  • 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
  • 34. TREATMENT:SYMPTOMATIC MEASURES  Bronchodilators: ◦ Anticholinergics ◦ Beta Agonists ◦ Methylxanthines  Corticosteroids  N-Acetyl Cysteine  Îą1 Antitrypsin augmentation  Vaccination  Others: No proven effect ◦ Leukotriene receptor antagonists/cromones ◦ Maintenance antibiotic therapy ◦ Immunoregulators ◦ Vasodilators: NO, CCB
  • 35. 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
  • 36. COPD: EXECERBATIONS Definition:  An exacerbation of COPD is an event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in management. Precipitating Causes:  Infections: Bacterial, Viral  Air pollution exposure  Non compliance with LTOT
  • 37. COPD:EXECERBATIONS 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.
  • 38. COPD: EXECERBATIONS Indication for ICU admission:  Impending or actual respiratory failure  Presence of other end-organ dysfunction ◦ shock ◦ renal failure ◦ liver failure ◦ neurological disturbance  Haemodynamic instability
  • 39. 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
  • 41. ANAESTHETIC CONSIDERATION IN COPD PTS UNDERGOING SUGERY Patient Factors:  Advanced age  Poor general condition, nutritional status  Co morbid conditions ◦ HTN ◦ Diabetes ◦ Heart Disease ◦ Obesity ◦ Sleep Apnoea  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  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
  • 44.  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
  • 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 ↑WOB ◦ ↑ RR, ↑HR ◦ Accessory muscles used ◦ Tracheal tug ◦ Intercostal indrawing ◦ Tripod sitting posture
  • 47.  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
  • 48. PREOPARETIVE ASSESSMENT:INVESTIGATION  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
  • 49. INVESTIGATIONS:CHEST XRAY  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
  • 50. PULMONARY FUNCTION TESTS: Measureme nt 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  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
  • 51. FEV1 FEV1 FVC seconds 2 1 3 4 5 0 1 2 3 4 Litres 5 COPD NORMAL 60% 3900 2350 COPD 80% 5200 4150 Normal FEV1/FVC FVC FEV1 FVC SPIROMETRIC TRACING OF COPD PATIENTS
  • 52. 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
  • 53. PREOPERATIVE PREPERATION  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
  • 54. 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
  • 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:  Bronchodilators:  Only small increase in FEV1  Alleviate symptoms by decreasing hyperinflation & dyspnoea  Improve exercise tolerance Anticholinergics Beta Agonists Methylxanthines
  • 57. ANTICHOLENERGICS:  Block muscarinic receptors  Onset of action within 30 Min  Ipratropium – ◦ 40-80 Îźg by inhalation ◦ 20 Îźg/ puff – 2 puffs X 3-4 times ◦ 250 Îźg / ml respirator soln. 0.4- 2 ml X 4 times daily  Tiotropium - long lasting  Side Effects: ◦ Dry Mouth, metallic taste ◦ Caution in Prostatism & Glaucoma
  • 58. 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 Îźg inhalation  muscle tremors, palpitations, throat irritation  Terbutaline : ◦ oral 5 mg/ 0.25 mg s.c./ 250 Îźg inhalation  Salmeterol : ◦ Long acting (12 hrs) ◦ 50 Îźg BD- 200 Îźg BD  Formeterol, Bambuterol
  • 59. METHYLXANTHINES  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.
  • 60. INHALED COTICOSTEROIDS:  Anti-inflammatory  Restore responsiveness to β2 agonist  Reduce severity and frequency of exacerbations  Do not alter rate of decline of FEV1  Beclomethasone, Budesonide, Fluticasone  Dose: 200 Îźg BD ↑ upto 400 Îźg QID  > 1600 Îźg / day- suppression of HPA axis
  • 61. PLANNING: ANAESTHETIC TECHNIQUE  COPD is not a limitation on the choice of anaesthesia.  Type of Anaesthesia doesn’t predictably influence Post op pulmonary complications.
  • 62. 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 N2O •Sedation reqd. May compromise expiratory fn.
  • 63. CONCERNS IN RA Peripheral Nerve Blocks: •Suitable for peripheral limb surgeries •Minimal respiratory effects •Intersclanie techniques contraindicated in severe Pulmonary disease
  • 64. CONCERNS IN RA •Improved Surgical outcome: Better pain control Attenuation of neuroedocrine respones to surgery Improvement of tissue oxygenation Maintenance of immune function Fewer episodes of DVT, PE, stroke. •Technique of choice in perineal, pelvic extraperitoneal & lower extremities •No benefit over GA in Intraperitoneal surgery,
  • 65. CONCERNS IN GA •Airway instrumentation & bronchospasm •Residual NMB •Nitrous Oxide •Attenuation of HPV •Respiratory depression with opioids, BZDs •Airway humidification
  • 66. PREDICTION OF POSTOPERATIVE 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
  • 67. 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
  • 68.
  • 69. CHOICE OF ANESTHESIA Regional anaesthesia General anesthesia Spontaneous ventilation Spinal/Epidural anaesthesia Endotrachea l intubation with controlled ventilation Sedation LMA High Low  does not stimulate the larynx, but does offer some protection for the trachea  used for minor surgery of the limbs or body surface of short duration (< 2 hrs) When 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  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  Pulse oximetry  Electrocardiogram  Non-invasive blood pressure recordings  if available, end-tidal carbon dioxide measurement  indwelling arterial catheter - for regular ABGs in those patients at greatest risk of periop pulmonary cx
  • 73. Perioperative steroid supplementation  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.  Intravenous hydrocortisone 100mg 8 hourly is given starting with the premedication.  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  Over the next 5 days this is tapered to their normal daily dose, where 100mg intravenous hydrocortisone is equivalent to 25mg oral prednisolone.  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
  • 76. Drugs considered safe for airway hyperreactive patients Induction Propofol, etomidate, ketamine, midazolam Opioids Pethidine,fentanyl, alfentanil Muscle relaxants Vecuronium, suxamethonium, rocuronium Volatile agents Halothane, isoflurane, enflurane, sevoflurane, nitrous oxide
  • 77. Intubation  Airway manipulation should be kept to a minimum and take place only under adequate anaesthesia.  Endotracheal intubation using muscle relaxants and controlled ventilation
  • 78. Maintenance of anesthesia  Avoid nitrous oxide if CXR showing – cavity, emphysematous bulla  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  The airway is vulnerable for up to 24 hours, and hypoventilation can occur for up to 3 days.  The airway is kept patent, and adequate ventilation and oxygenation ensured before discharge to the ward.  All neuromuscular paralysis must be reversed.  If there are problems the patient will need to go to the HDU or ICU.  Otherwise, the patient is kept warm and well hydrated, and maintain fluid balance
  • 80. POSTOPERATIVE PULMONARY COMPLICATIONS: Risk Reduction Strategies: Preoperative: •Smoking cessation •Bronchodilatation •Control infections •Patient Education
  • 81. RISK REDUCTION STRATEGIES Intraoperative: •Minimally invasive surgery •Regional Anaesthesia •Duration < 3 Hrs Post operative: •Lung Volume Expansion Maneuvers •Adequate Analgesia
  • 82. POSTOPERATIVE PULMONARY COMPLICATIONS: Post Operative Analgesia:  Opioids  Paravertebral/Intercostal N Blocks  Epidural Analgesia ◦ LA ◦ Opioids  NSAIDS  Bronchospasm
  • 83. POSTOPERATIVE PULMONARY COMPLICATIONS: Lung Expansion maneuvers:  Incentive spirometry  Deep breathing exercises  Chest Physiotherapy & postural drainage  Intermittant Positive Pressure Ventilation  CPAP, BiPAP  Early Ambulation
  • 85. CONCLUSION  COPD is not a contraindication for any particular anaesthsia technique if patients have been appropriately stabilized.  COPD patients are prone to develop intraoperative and postoperative pulmonary complications.  Preoperative optimisation should include control of infection, wheezing and prediction & necessary measures for postoperative