Respiratory disease and anesthesia

RESPIRATORY DISEASES AND
ANESTHESIOLOGY
PG RESIDENT
Department of Anaesthesiology,SRG
Jhalawar

CONTENTS
Introduction
Pulmonary risk factors
Types of diseases
Obstructive
ASTHMA
C.O.P.D.
Chronic
Bronchitis
Emphysema
Restrictive
Intrinsic
Acute
Chronic
Extinsic
Pulmonary
embolism

Effect of pre-existing condition of
anesthesia is predictable.

Pulmonary risk factors
In the general surgery population, the incidence
of postoperative pulmonary complications
ranges from 2.0% to 5.6%
Two strongest predictors -operative site
-history of dyspnea

SMOKING
Smoking causes respiratory disease is well
known
Smoker ----------pulmonary compromise(
detcted by PFT )

ADVANCING AGE
• prevalence of pulmonary disease increase in closing
capacity.
(Closing capacity refers to the volume of gas present in the
lung at which small conducting airways begin to collapse) i.e.
The small airways begin to collapse at a higher volume/before
expiration is complete.
This also occurs with certain disease processes, such as
asthma, chronic obstructive pulmonary disease, and
pulmonary edema.
Any process that increases the Closing Capacity by increasing
the closing volume (CV) can increase an individual's risk of
hypoxemia, as the small airways may collapse during
exhalation, leading to air trapping and atelectasis.

OBESITY per se is not considered to increase the
incidence of postoperative pulmonary complications.
However, OBSTRUCTIVE SLEEP APNEA does
contribute to adverse perioperative outcomes.

SITE OF SURGERY
Near the diaphragm-------diaphragmatic dysfunction and a restrictive
ventilatory defect
Upper abdominal ------- significantly (>30%) decrease functional residual
capacity (FRC). This effect is maximal on the first postoperative day and
lasts up to 10 days.
Because
• Pain--------------------------------------
• Opioids
• Recumbent position
• Residual anesthetic effects
• Abdominal distention, and
• Restrictive dressings
PAIN causes rapid shallow breathing with an
ineffective cough
IMPAIRED MUCOCILIARY CLEARANCE leads to
micro-atelectasis and loss of lung volume.
Subsequent development of VENTILATION/
PERFUSION MISMATCH (shunt) produces
hypoxemia.

Hence even if you completely relieve the pain with
regional anesthesia , that will not completely
reverse, these abnormalities.
*Persistent microatelectasis and retention of
secretions favor the development of
postoperative pneumonia.

If patient has history of dysnea and no previous workup is available,
how to assess?

Pumonary
Disaeas
Restrictive
Interstitial Diseases
Idiopathic Pulmonary
Fibrosis
Sarcoidosis
Scoliosis
Obstructive
Asthma
COPD
Bronchiectasis

Obstructive Pulmonary Diseases
• Characteristic-resistance to airflow.
• More common than restrictive
• Obstructive diseases include -asthma
-emphysema
-chronic bronchitis
-cystic fibrosis
-bronchiectasis
-bronchiolitis
*An MMEF (Maximal Mid Expiratory Flow)of less than 70%
(forced expiratory flow [FEF25–75%]) is often the only
abnormality early in the course of these disorders.
(normal FEF25–75% -greater than 2.0 L/s)

• As the disease progresses, both forced expiratory volume
in the first second of exhalation (FEV1) and the FEV1/FVC
(forced vital capacity) ratio are less than 70% of the
predicted values.
• Elevated airway resistance and air trapping leads to
increase in residual volume and total lung capacity (TLC).
• Ascultatory feature-
mild obstruction = initially only by prolonged exhalation
Progressive obstruction =turbulent airflow=Wheezing.
expiratory
wheezing only
both inspiratory
and expiratory
wheezing
marked obstruction,
wheezing may be
absent when airflow
has nearly ceased

Preoperative Considerations
A.Pathophysiology
B. Treatment
Anesthetic Considerations
A.Preoperative Management
B. Intraoperative Management

A.Pathophysiology
• 5% to 7% affected.
• Characteristic - bronchiolar inflammation and hyperreactivity
• Clinically features-episodic attacks of dyspnea, cough, and wheezing.
• Reversible-YES
• What happens?-bronchial muscle constriction, edema and secretions.
• precipitated by -pollens, animal dander, dusts, pollutants, and various
chemicals like aspirin, Exercise, cold air, emotional excitement, and
viral infections.
• classification-
asthma
chronic
Intermittent(mild)
moderate
sever
acute

A. Pathophysiology
Involves -release of various chemical mediators and overactivity of the
parasympathetic nervous system.
Inhaled substances can initiate bronchospasm through both specific and
nonspecific immune mechanisms by degranulating bronchial mast cells
due to antigen binding to immunoglobulin E (IgE) on the surface of mast
cells causes degranulation.
Bronchoconstriction is the result of the subsequent release of histamine
bradykinin; leukotrienes C, D, and E; prostaglandins and chemotactic
factors.

The parasympathetic nervous system plays a major role in maintaining
normal bronchial tone.
Vagal afferents in the bronchi are sensitive to histamine and multiple
noxious stimuli, including cold air, inhaled irritants, and instrumentation
(eg, tracheal intubation).
Reflex vagal activation results in bronchoconstriction
During an asthma attack, bronchoconstriction, mucosal edema, and
secretions increase resistance to gas flow at all levels of the lower
airways.

Prolonged or severe attacks –
• increase the work of breathing and can fatigue respiratory muscles.
• The number of alveolar units with low (V/Q) ratios increases, resulting
in hypoxemia.
• Tachypnea is likely and typically produces hypocapnia.
• high Paco2 indicates that the patient can no longer maintain the work
of breathing sign of impending respiratory failure
*A pulsus paradoxus and electrocardiographic signs of right ventricular
strain (ST-segment changes, right axis deviation, and right bundle-
branch block) are also indicative of severe airway obstruction.

Treatment
Drugs -β-adrenergic agonists
methylxanthines
glucocorticoids
anticholinergics
leukotriene modifiers,
mast- cell–stabilizing agents.
cromolyn sodium and nedocromil -preventing bronchospasm by
blocking the degranulation of mast cells.

Sympathomimetic (eg, albuterol)
• most commonly used for acute exacerbations. They β2-
agonist activity.
Methylxanthine
• theophylline has a narrow therapeutic range; therapeutic
blood levels are considered to be 10 to 20 mcg/mL. Lower
levels, however, may be effective. Aminophylline is the only
available intravenous theophylline preparation.
Anticholinergic agents produce bronchodilation through their
antimuscarinic action and may block reflex
bronchoconstriction.

Glucocorticoids
• for both acute treatment and maintenance therapy
• Have antiinflammatory and membrane-stabilizing effects.
• used in metered-dose inhalers for maintaince –
a. Beclomethasone
b. Triamcinolone
c. Fluticasone
d. Budesonide
Although they are associated with a low incidence of
undesirable systemic effects, inhaled administration does not
necessarily prevent adrenal suppression.
For acute sever attack- Intravenous hydrocortisone or
methylprednisolone followed by tapering doses of oral
prednisone.

Preoperative Management
1. evaluating patients of asthma- severity and recent course
of the disease, drugs he is taking
2. Find out if the patient is in optimum condition. Because
patients with poorly controlled asthma or wheezing are at
risk complications.
Conversely, well controlled asthma has not been shown to be
a risk factor for intraoperative or postoperative complications.
Complete resolution of recent exacerbations should be
confirmed by chest auscultation only then go ahead.
Patients with frequent or chronic bronchospasm should be
placed on an optimal bronchodilating regimen.

3. Look for chest radiograph features-
air trapping so hyperinflation -flattened diaphragm ,
• a small-appearing heart
• hyperlucent lung fields.
• bronchial wall thickening: peribronchial cuffing (non-
specific finding but may be present in ~48% of cases with
asthma 1)
4. Pulmonary Function Test— particularly expiratory airflow
measurements such as FEV1, FEV1/FVC, FEF25-75%, and peak
expiratory flow rate help in assessing the severity of airway
obstruction and reversibility after bronchodilator treatment.

IN CASE OF
EMERGENCY
SURGERY IN AN
ASTHMATIC
PATIENT

treated aggressively
1. oxygen,
2. aerosol of β2-agonists
3. intravenous glucocorticoids ----- improve function in few hours
Use Arterial blood gases for evaluating severity and adequacy of
treatment. Hypoxemia and hypercapnia are typical of moderate or
severe disease; even slight hypercapnia is indicative of severe air
trapping and may be a sign of impending respiratory failure.
Bronchodilators should be continued up to the time of surgery; these
include β-agonists, inhaled glucocorticoids, leukotriene modifiers, mast-
cell stabilizers, theophyllines, and anticholinergics.
Patients who receive chronic glucocorticoid therapy with more than 5
mg/d of prednisone should receive a graduated supplementation
schedule based on the severity of the illness and complexity of the
surgical procedure. Supplemental doses should be tapered to baseline
within 1 to 2 days.

You should know that-
• Anticholinergic agents are not customarily given unless very copious
secretions are present or if ketamine is to be used for induction of
anesthesia.In typical intramuscular doses, anticholinergics are not
effective in preventing reflex bronchospasm following intubation.
• The use of an H2-blocking agent (such as cimetidine, ranitidine, or
famotidine) is theoretically detrimental, since H2-receptor activation
normally produces bronchodilation; in the event of histamine release,
unopposed H1 activation with H2 blockade may accentuate
bronchoconstriction.
Stimulatators of bronchospasm: These include obstruction of the
tracheal tube from kinking, secretions, or an overinflated balloon;
bronchial intubation; active expiratory efforts (straining); pulmonary
edema or embolism; and pneumothorax.

Intraoperative Management
critical time -instrumentation of airway.
GA -noninvasive ventilation or regional anesthesia avoids this problem
but neither eliminates the possibility of bronchospasm The most critical
time for asthmatic patients under- going anesthesia is during
instrumentation of the airway.
• some clinicians believe that high spinal or epidural anesthesia may
aggravate bronchoconstriction by blocking sympathetic tone to the
lower airways (T1–T4) and allowing unopposed parasympathetic
activity.
• Pain, emotional stress, or stimulation during light general anesthesia
can precipitate bronchospasm
• Drugs often associated with histamine release (eg, atracurium,
morphine) should be avoided or given very slowly when used.
any induction agent can be used provided depth of anesthesia is
achieved before intubation.

Induction agents selection
• Sevoflurane usually provides the smoothest inhalation induction with
bronchodilation in asthmatics. Isoflurane and desflurane are more
pungent and may result in cough, laryngospasm, and bronchospasm
during inhalation induction.
• Thiopental may occasionally induce bronchospasm as a result of
exaggerated histamine release. Propofol and etomidate -suitable
induction agents
• Propofol –can cause bronchodilation.
• Ketamine - bronchodilating properties and is a good choice for
patients with asthma who are also hemodynamically unstable.
Ketamine should probably not be used in patients with high
theophylline levels, as the combined actions of the two drugs might
precipitate seizure activity.

How to blunt reflex bronchospasm?
Reflex bronchospasm can be blunted before intubation by an additional
dose of the induction agent, ventilating the patient with a 2 to 3 mini-
mum alveolar concentration (MAC) of a volatile agent for 5 min, or
administering intravenous or intratracheal lidocaine (1–2 mg/kg).
Note* - intratracheal lidocaine itself can initiate bronchospasm if an
inadequate dose of induction agent has been used.
-anticholinergic agent may block reflex bronchospasm, but causes
excessive tachycardia.
What about succinylcholine???
Although succinylcholine may on occasion induce marked histamine
release, it can generally be safely used in asthmatic patients.

Features of bronchospasm Intra operative
• Wheezing
• Capnography -delayed rise of the end-tidal CO2 value ( obstruction in
expiration)
(Do keep in mind…
In the absence of capnography, confirmation of correct tracheal
placement by chest auscultation can be difficult in the presence of
marked bronchospasm. )
• decreasing exhaled tidal volumes
• Severe bronchospasm -rising peak inspiratory pressures and
incomplete exhalation.
• plateau pressure may remain unchanged.

What to do?
• Set the Tidal volumes - 6 mL/kg
• Prolong the expiratory time TO AVOID AIR TRAPPING.
• Increasing the concentration of the volatile agent
• Aerosolized bronchodilator.
• Hydrocortisone
*Infusion of low-dose epinephrine may be needed if bronchospasm is
refractory to other interventions
*Deep extubation (before the return of airway reflexes) reduces the risk
of bronchospasm on emergence. Lidocaine as a bolus (1.5–2 mg/kg)
may help to obtund airway reflexes upon emergence.
.

(2)
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
airflow limitation that is not fully reversible

• COPD is the most common pulmonary disorder encountered in
anesthetic practice.
• prevalence -increases with age.
• Strong association- cigarette smoking
• *MMEF- Maximal Mid Expiratory Flow rate become abnormal before
symptoms of COPD appear.
• Predominance- male
• mixture of small and large airway disease (chronic bronchitis/
bronchiolitis) and parenchymal destruction (emphysema)
*Most patients with COPD are asymptomatic but show expiratory air-
flow obstruction upon PFTs.
In many patients, the obstruction has an element of reversibility, With
advancing disease, maldistribution of both ventilation and pulmonary
blood flow results in areas of low ( 􏰀 􏰀V/Q ) ratios (intrapulmonary
shunt), as well as areas of high ( 􏰀V/Q 􏰀 ) ratios (dead space).

There are two main forms of COPD:
Chronic bronchitis-which involves a long-term cough with
mucus.
Emphysema,-which involves damage to the lungs over time.

Chronic Bronchitis
defined - presence of a productive cough on most days of 3 consecutive
months for at least 2 consecutive years.
Factors
• cigarette smoking
• exposure to air pollutants,
• occupational exposure to dusts,
• recurrent pulmonary infections,
• familial factors
Secretions from hypertrophied bronchial mucous glands and mucosal
edema from inflammation of the airways produce airflow obstruction.
Recurrent pulmonary infections (viral and bacterial) are common and
often associated with bronchospasm.
Intrapulmonary shunting and hypoxemia
Features
RV is increased, but TLC is often normal.

chronic hypoxemia leads to
1) Erythrocytosis,
2) pulmonary hypertension
3) Right ventricular failure (cor pulmonale)
“blue bloater” syndrome,
but less than 5% of patients with COPD fit this description
*In the course of disease progression, patients gradually develop
chronic CO2 retention; the normal ventilatory drive becomes less
sensitive to arterial CO2 tension and may be depressed by oxygen
administration .

Emphysema
irreversible enlargement of the airways distal to terminal bronchioles
and destruction of alveolar septa
diagnosis-CT of the chest.
*Mild changes with age
*if early - homozygous deficiency of α1-antitrypsin

Emphysema associated with smoking -due to a relative imbalance
between protease and antiprotease activities.
Types of emphysema
1. Centrilobular
2. Panlobular form.
CENTRILOBULAR - dilation or destruction of the respiratory bronchioles,
Assosication -tobacco smoking,
Predominant site - upper lobe
PANLOBULAR –dilation of the entire acinus,
Association- α1-antitrypsin deficiency
Predominantly - lower lobe distribution.

Loss of the elastic recoil
premature collapse
during exhalation
expiratory flow limitation
with air trapping
hyperinflation
What happens in Emphysema?
Destruction of
alveolar structure
decreased diffusion
lung capacity
(V/Q) mismatch
impairment of gas
exchange
normal
parenchyma
compressed by the
hyperinflated
further increase in
the (V/Q) mismatch

Patients characteristically have increases in RV, FRC, TLC, and the
RV/TLC ratio.
CO2 has higher diffusibility 􏰀􏰀 so,
elimination of CO2 is well preserved in early
stages
Chronic CO2 retention occurs slowly
results in a compensated respiratory acidosis
Arterial oxygen tension is usually normal or slightly
reduced
**Acute CO2 retention is a sign of impending respiratory
failure.

One more thing happens,
Destruction of pulmonary capillaries in the alveolar septa leads to the
development of mild to moderate PULMONARY HYPERTENSION.
Why are emphysema patienst some times called “pink puffers”?
When dyspneic, patients with emphysema often purse their lips to
delay closure of the small airways.

Treatment for COPD
• primarily supportive.
• Stop smoking to reduce decline of lung function.
• Do spirometry -assess the severity of airflow reduction
- check response to bronchodialator
• If responsive to bronchodialators,
A. when FEV1 is greater than 80% of predicted-use short-acting
bronchodilators
B. When FEV1 and symptoms worsen-use longer-acting
bronchodilators and inhaled corticosteroids
• Inhaled β2-adrenergic agonists, glucocorticoids, and ipratropium are
also used.

• If HYPOXEMIA –oxygen
• If CHRONIC HYPOXEMIA (Pao2 <55 mm Hg) and pulmonary
hypertension - low-flow oxygen therapy (1–2 L/min)
CO2 retention may be exacerbated in patients with reduced hypoxic
ventilatory drive.
Consequently, oxygen therapy is targeted to a hemoglobin oxygen
saturation of 90%.
• PULMONARY REHABILITATION may improve the functional status of
the patient by improving physical symptoms and exercise capacity.

A. Preoperative Management
1. Ask if –
recent changes in dyspnea, sputum, and wheezing.
2. Check FEV1-
Patients with an FEV1 less than 50% of predicted (1.2–1.5 L) usually
have dyspnea on exertion, whereas those with an FEV1 less than 25%
(<1 L in men) typically have dyspnea with minimal activity.
The latter finding, in patients with predominantly chronic bronchitis, is
also often associated with CO2 retention and pulmonary hypertension.
3. Do-
PFTs
chest radiographs(bullous changes ???)
arterial blood gas measurements,
cardiovascular evaluation(concomitant cardiac disease)

In contrast to asthma, only limited improvement in
respiratory function may be seen after a short period of
intensive preoperative preparation but you have to still do
them to reduce postoperative pulmonary complications
1. correcting hypoxemia
2. relieving bronchospasm
3. mobilizing and reducing secretions
4. treating infections
Patients at greatest risk of complications are those with
preoperative pulmonary function measurements less than
50% of predicted.

What about the Smokers??
Discuss the possibility that postoperative ventilation with both the
patient and the surgeon.
Smoking should be discontinued for at least 6 to 8 weeks before the
operation to decrease secretions and to reduce pulmonary
complications(increases mucus production and decreases clearance).
Both gaseous and particulate phases of cigarette smoke can deplete
glutathione and vitamin C and may promote oxidative injury to tissues.
24 h stop ( theoretically beneficial)-- effects on the oxygen-carrying
capacity of hemoglobin
acute inhalation of cigarette smoke releases carbon monoxide, which
increases carboxyhemoglobin levels, as well as nitric oxide, and nitrogen
dioxide, which can lead to formation of methemoglobin.

Long-acting bronchodilators and mucolytics should be
continued, including on the day of surgery.
COPD exacerbations should be treated aggressively.
Preoperative chest physiotherapy and lung expansion
interventions with incentive spirometry, deep breathing
exercises, cough, chest percussion, and postural drainage may
be beneficial in decreasing postoperative pulmonary
complications.

TYPE OF ANESTHEISA
• regional anesthesia is preferable to general anesthesia but high spinal
or epidural anesthesia can decrease lung volumes, restrict the use of
accessory respiratory muscles, and produce an ineffective cough,
leading to dyspnea and retention of secretions.
• Loss of proprioception from the chest and positions such as lithotomy
or lateral decubitus may accentuate dyspnea in awake patients.
• Concerns about hemidiaphragmatic paralysis may make interscalene
blocks a less attractive option in the lung disease patient.

VENTILATION
Preoxygenation prior to induction,prevents the rapid oxygen
desaturation often seen in these patients.
Unfortunately, bronchodilating anesthetics--- improves only
the reversible component of airflow obstruction; significant
expiratory obstruction may still present, even under deep
anesthesia.
Expiratory airflow limitation, especially under positive
pressure ventilation, may lead to air trapping, dynamic
hyperinflation, and elevated intrinsic positive end-expiratory
pressure (iPEEP).

Can lead to……
Dynamic hyperinflation may --volutrauma
--hemodynamic instability
-- hypercapnia
--acidosis.
How to mitigate this trapping of air ???
(1) allowing more time to exhale by decreasing both the
respiratory rate and inspiratory/ expiratory (I:E) ratio
(2) allowing permissive hypercapnia
(3) applying low levels of extrinsic PEEP
(4) aggressively treating bronchospasm.

Beware of inta-op hypotention!!!
Apart from the usual causes,PNEUMOTHORAX and RIGHT
HEART FAILURE due to hypercapnia and acidosis are to be
kept in mind.
PNEUMOTHORAX
A pneumothorax may manifest as hypoxemia, increased peak
airway pressures, decreasing TV, and abrupt cardiovascular
collapse unresponsive to fluid and vasopressor
administration.
***Nitrous oxide should be avoided in patients with bullae
and pulmonary hypertension.

About inhalational agents….
Inhibition of hypoxic pulmonary vasoconstriction by
inhalation anesthetics is usually not clinically apparent at
usual doses.
However, due to increased dead space, patients with severe
COPD have unpredictable uptake and distribution of
inhalational agents, and the end-tidal volatile anesthetic
concentration is inaccurate.

ARTERIAL CO2 ???
Although pulse oximetry accurately detects significant arterial
desaturation, direct measurement of arterial oxygen tensions
may be necessary to detect more subtle changes in
intrapulmonary shunting.
Moreover, arterial CO2 measurements can guide ventilation
because increased dead space widens the normal arterial-to-
end-tidal CO2 gradient.
Moderate hypercapnia with a Paco2 of up to 70 mm Hg may
be well tolerated in the short term, assuming a reasonable
cardiovascular reserve.
Be ready with the ionotrops for more compromised patients.

While extubation, make sure!
1. adequate pain control
2. Reversal optimum
3. absence of bronchospasm and secretions
4. absence of significant hypercapnia and acidosis
5. absence of respiratory depression due to residual
anesthetic agents.
***Patients with an FEV1 below 50% may require a period of
postoperative ventilation, particularly following upper
abdominal and thoracic operations.

• Characterized by -decreased lung compliance.
• Lung volumes - reduced, with preservation of normal
expiratory flow rates.
so
• FEV and FVC are reduced, but the FEV1/FVC ratio is
normal.
• Reduced lung compliance increases the work of breathing
so
• breathing becomes –rapid but shallow
* Respiratory gas exchange is usually maintained until the
disease process is advanced.

Restrictive lung
diseases
Acute intrinsic
pulmonary disorders
Chronic intrinsic
pulmonary disorders
Extrinsic restrictive
pulmonary disorders
• Pulmonary edema
(including ARDS)
• Infectious
pneumonia
• Aspiration
pneumonitis

PATHOPHYSIOLOGY of COPD
I. Airway obstruction –
The major site of obstruction is smaller conducting airway (<2
mm in diameter).
Processes causing obstruction 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 is 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)

COPD there is “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.
---------------------------------------------------------------------------------
--

ACUTE INTRINSIC PULMONARY DISORDERS
• Preoperative Considerations
• Anesthetic Considerations
B. B. Intraoperative Management

Acute intrinsic pulmonary disorders include
• Pulmonary edema (including ARDS)
• Infectious pneumonia
• Aspiration pneumonitis.

Preoperative Considerations for Acute intrinsic
pulmonary disorders
• Reduced lung compliance in these disorders is due to an
increase in extravascular lung water, from an increase in
either pulmonary capillary pressure or pulmonary capillary
permeability.
• Increased pressure occurs with left ventricular failure,
whereas fluid overload and increased permeability are
present with ARDS.
• Increases in permeability also occur following aspiration or
infectious pneumonitis.

Anesthetic Considerations for acute pulmonary disease
avoid elective surgery.
If emergency-- optimize oxygenation and ventilation.
1. Fluid overload –diuretics
2. Heart failure- treatment.
3. Large pleural effusions –drainage
massive abdominal distention -relieved by nasogastric suction
or drainage of ascites.
*Persistent hypoxemia may require mechanical ventilation.

• Increased inspired oxygen concentrations and PEEP may be required.
but
• decreased lung compliance results in high peak inspiratory pressures
during positive-pressure ventilation and increases the risk of
barotrauma and volutrauma.
so
• Tidal volumes ----reduced to 4 to 6 mL/kg, with a compensatory
increase in the ventilatory rate (14–18 breaths/min), even if the
result is an increase in end-tidal CO2.
• Airway pressure should generally not exceed 30 cm H2O.
Keep in mind….
Right ventricular function may be challenged due to to increases in
pulmonary vascular resistance secondary to permissive hypercapnia.

CHRONIC INTRINSIC PULMONARY DISORDERS
Also called interstitial lung diseases.
• Preoperative Considerations
• Anesthetic Considerations

characterized by –
1. an insidious onset
2. chronic inflammation of alveolar walls and perialveolar
tissue
3. progressive pulmonary fibrosis
Causes –
• hypersensitivity pneumonitis from occupational and
environmental pollutants,
• drug toxicity (bleomycin and nitrofurantoin)
• radiation pneumonitis,
• idiopathic pulmonary fibrosis
• sarcoidosis.
• Chronic pulmonary aspiration, oxygen toxicity, and severe
ARDS can also produce chronic fibrosis.

Patients typically present with dyspnea on exertion and
sometimes a nonproductive cough.
Symptoms of cor pulmonale are present only with advanced
disease.
Physical examination -reveal fine (dry) crackles over the lung
bases, and,
-in late stages, features of right
ventricular failure may be presesnt.
Chest Xray
ABG -mild hypoxemia with normocarbia.
PFTs -restrictive type and carbon monoxide diffusing
capacity is reduced.
ground-glass
Reticulo-
nodular
markings
honeycomb

Treatment
Stop disease process and stop exposure.
If the patient has chronic hypoxemia, oxygen therapy may be
started to prevent, or attenuate, right ventricular failure.

Anesthetic considerations for Chronic Intrinsic Pulmonary
Disorders
Focus on
• disease process and
• the degree of pulmonary impairment
If history of dyspnea is present, do
PFTs and ABG analysis and chest Xray for severity
-----Normal vital capacity is >70 mL/kg
A vital capacity of less than 15 mL/kg is indicative of severe
dysfunction

complicated because
their predisposition to hypoxemia and
their need for controlled ventilation
The reduction in FRC (and oxygen stores) predisposes these patients to
rapid hypoxemia following induction of anesthesia.
Because these patients may be more susceptible to oxygen-induced
toxicity, particularly patients who have received bleomycin, the inspired
fractional concentration of oxygen should be kept to the minimum
concentration compatible with acceptable oxygenation (Spo2 of >90%).
Protective ventilation strategies employed in ventilated patients in the
intensive care unit should be continued through to the operating room.

Nitric oxide may be used to reduce pulmonary vascular
resistance and reduce the work of the right ventricle.
***Extracorporeal membrane oxygenation (ECMO) is
increasingly used in the management of acute respiratory
failure.
Following anticoagulation, blood is drained from venous
cannulae and delivered to a membrane oxygenator.
Oxygenated blood can then either be returned either to the
venous system, if cardiac function is preserved, or pumped
into the arterial circulation, bypassing the heart and lungs.
Consequently, ECMO can provide transient support for both
cardiac and pulmonary failure.

EXTRINSIC RESTRICTIVE PULMONARY
DISORDERS
interfering with lung expansion.
E.g-pleural effusions, pneumothorax, mediastinal masses,
kyphoscoliosis, pectus excavatum, neuromuscular disorders,
and increased intraabdominal pressure from ascites,
pregnancy, or bleeding.
Anesthetic considerations are similar to those discussed for
intrinsic restrictive disorders.

A. Pathophysiology
B. Diagnosis
C. Treatment and Prevention
C. C. Intraoperative Pulmonary Embolism

Can occur from –
• blood clots
• Fat
• tumor cells
• air
• amniotic fluid
• foreign material
Site of origin - lower extremities, pelvic veins, or, less
commonly, the right side of the heart

Factors associated with deep venous thrombosis and
pulmonary embolism.
• Prolonged bed rest
• Postpartum state
• Fracture of the lower extremities Surgery on the lower
extremities Carcinoma
• Heart failure
• Obesity
• Surgery lasting more than 30 min
• Hypercoagulability
• Antithrombin III deficiency Protein C deficiency Protein S
deficiency
• Factor V Leiden mutation

A. Pathophysiology
• Increase in dead space should theoretically increase
Paco2.
However,
in practice, hypoxemia is more often seen.
• Pulmonary emboli acutely increase pulmonary vascular
resistance by reducing the cross-sectional area of the
pulmonary vasculature, causing reflex and humoral
vasoconstriction.
• Localized or generalized reflex bronchoconstriction
further increases areas with low (V/Q) ratios.
• The net 􏰀􏰀effect is an increase in (V/Q) mismatch and
hypoxemia.

The affected area loses its surfactant within hours and may
become atelectatic within 24 to 48 h.
Pulmonary infarction occurs if the embolus involves a large
vessel and collateral blood flow from the bronchial circulation
is insufficient for that part of the lung (incidence <10%).
In previously healthy persons, occlusion of more than 50% of
the pulmonary circulation (massive pulmonary embolism) is
necessary before sustained pulmonary hypertension is seen.

Patients with preexisting cardiac or pulmonary disease can
develop acute pulmonary hypertension with occlusions of
lesser magnitude.
A sustained increase in right ventricular afterload can
precipitate acute right ventricular failure and hemodynamic
collapse.
If the patient survives acute pulmonary thromboembolism,
the thrombus usually begins to resolve within 1 to 2 weeks.

B. Diagnosis
Clinical manifestations
• sudden tachypnea and dyspnea
• chest pain
• hemoptysis (When lung infarction has occurred).
• auscultation –Wheezing
*Remember that symptoms can be nos-specific unless massive
embolism has occurred.
ABG- mild hypoxemia with respiratory alkalosis (the latter due to an
increase in ventilation).
Chest Xray –
• normal/ area of oligemia (radiolucency),
• a wedge-shaped density with an infarct,
• atelectasis with an elevated diaphragm,
• an asymmetrically enlarged proximal pulmonary artery with acute
pulmonary hypertension.

Cardiac signs –
• tachycardia
• wide fixed splitting of the S2 heart sound
• Hypotension
• elevated central venous pressure (right ventricular failure)
ECG –tachycardia
may show signs of acute cor pulmonale,
[ new right axis deviation,
right bundle- branch block,
tall peaked T waves]
USG-deep venous thrombosis in lower limb.
INTRA OP- difficult to diagnosis

IF YOU suspect, order following
CT angiography
Echocardiography can assist in the diagnosis.
- Right ventricular overload can be seen.
Sometimes clot can be seen in the right heart and pulmonary
artery confirming the diagnosis.
At other times, only the signs of right ventricular overload are
seen (eg, tricuspid regurgitation, right ventricular dilation).
The left ventricle may be relatively under-loaded secondary
to the inadequate delivery of blood

C. Treatment and Prevention
best treatment for perioperative pulmonary embolism is prevention.
regimens for DVT prophylaxis are -heparin (unfractionated heparin
5000 U subcutaneously every 12 h begun preoperatively or immediately
postoperatively in high-risk patients),
enoxaparin,
fondaparinux, and,
early ambulation after surgery.
Patients at risk for thrombophilia are treated with warfarin.
Newer anticoagulants such as factor Xa inhibitors (eg, rivaroxaban,
apixaban) and the direct thrombin inhibitor dabigatran will likely assume
a greater role in DVT prophylaxis.
The use of intermittent pneumatic compression of the legs may
decrease the incidence of venous thrombosis in the legs, but not in the
pelvis or the heart.

After a pulmonary embolism,
parenteral anticoagulation therapy is given.
Low-molecular- weight heparin (LMWH) or fondaparinux
are now preferred over intravenous unfractionated heparin
for initial anticoagulation.
All patients should start warfarin also and the two should
overlap for a minimum of 5 days.
The international normalized ratio should also be within the
therapeutic range (>2.0) for at least 24 h before
discontinuation of parenteral DVT prophylaxis.
Warfarin should be continued for 3 to 12 months.

Thrombolytic therapy is indicated in patients with massive
pulmonary embolism and hypotension.
Recent surgery and active bleeding are contraindications to
anticoagulation and thrombolytic therapy.
In these cases, an inferior vena cava filter may be placed to
prevent recurrent pulmonary emboli.
Pulmonary embolectomy may be lifesaving for
hemodynamically unstable patients with massive embolism in
whom thrombolytic therapy is contraindicated or ineffective.

• Patients with acute pulmonary embolism come for
placement of an inferior vena cava filter, or for pulmonary
embolectomy. In most instances, the patient will have a
history of pulmonary embolism and presents for unrelated
surgery; in this group of patients, the risk of interrupting
anticoagulant therapy perioperatively is unknown.
• If the acute episode is more than 1 year old, the risk
associated with temporarily stopping anticoagulant
therapy is probably small.
• Moreover, except in the case of chronic recurrent
pulmonary emboli, pulmonary function has usually
returned to normal. Just prevent new episode.

• Vena cava filters are usually placed percutaneously under
local anesthesia with sedation.
• Patients presenting for emergency pulmonary
embolectomy are critically ill.
• They are usually already intubated, but tolerate positive-
pressure ventilation poorly.
• Inotropic support is usually necessary until they are placed
on cardiopulmonary bypass to facilitate clot removal.
• Inotropic support may be required to separate from
cardiopulmonary bypass.

Intraoperative Pulmonary Embolism
Significant is rare
Diagnosis requires a high index of suspicion.
Air emboli are common but are often overlooked unless large
amounts are entrained.
Fat embolism, microthrombi and bone debris-- orthopedic
procedures
amniotic fluid embolism – rare
-complication of late pregnancy and
delivery
- unpredictable
- and often fatal

Thromboembolism may occur intraoperatively during
prolonged procedures.
Presentation –
• sudden cardiovascular collapse
• hypoxemia, or bronchospasm.
• decrease in end-tidal CO2 concentration is suggestive of
pulmonary embolism but is not specific.
• Invasive monitoring may reveal ----elevated central venous
pressure.
• Depending on the type and location of an embolism, a
transesophageal echocardiogram can be done; this may not
reveal the embolus but will often demonstrate right heart
distention and dysfunction.

• If air is identified in the right atrium, or if it is suspected,
emergent central vein cannulation and aspiration of the air
may be lifesaving.
• For all other emboli, treatment is supportive, with
intravenous fluids and inotropes.
• Placement of a vena cava filter may be considered
postoperatively.

Respiratory disease and anesthesia

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Respiratory disease and anesthesia

Similar to Respiratory disease and anesthesia (20)

Recently uploaded

Recently uploaded (20)

Respiratory disease and anesthesia