respiratory diseases , anaesthetic management

1. ANESTHESIA IN PATIENT
WITH RESPIRATORY
DISEASES
Dr. Radhwan H. AL-Khashab
Consultant anaesthesia & ICU
Assist. Prof.
2023
https://www.mosulitu.ahlamontada.net

2. Lecture outlines
1) Aims of preoperative praparation.
2) Anaesthetic consideration of obstructive & restrictive
lung problems.
3) Postoperative management.

3. Introduction
 Respiratory complications are common,
representing 10% of all post-operative
complications, accounting for significant morbidity,
mortality and financial cost.
 Preoperative pulmonary impairment are associated
with more marked intraoperative alterations in
respiratory function and higher rates of
postoperative pulmonary complications.
 COPD is currently the 4th leading cause of death in
the world

4. Preoperative risk factors
Patients related: Procedures related:
1. Age > 60 years.
2. ASA > II.
3. Congestive Heart Failure.
4. Preexisting pulmonary dis.(e.g.
PHT).
5. Cigarette smoking.
6. Alcohol use.
7. OSA.
8. Preoperative sepsis.
9. Hypoalbuminemia <3.5mg/dl.
10. Elevated renal function.
1) Emergency surgery.
2) Abdominal or thoracic surgery.
3) Prolonged duration of
anaesthesia > 2.5 hr.
4) Use of general anesthesia.
5) Laprascopic vs open surgery.
6) Residual muscle relaxant after
operation.

5. Other risk factors that include:
 Chronic kidney disease.
 Diabetes mellitus.
 Preoperative anemia (hemoglobin 10 g/dL) .
Advanced age is accompanied by:
1. Decreased elastic recoil of lung parenchyma.
2. Decreased chest wall compliance.
3. Decreased alveolar surface area.
4. Decreased respiratory muscle strength

6. Effct of anesthesia
 Instrumentation alters mucociliary function, promoting
retention of secretions.
 Administered drugs release circulating mediators causing
bronchoconstriction.
 There is decreased surfactant production.
 There is inhibition of alveolar macrophage activity.
 NMBA:Their use increases the risk for postoperative
desaturation and postoperative residual curarization
(PORC). Long-acting blockade agents can have residual
effects up to 7 days postoperatively, so better to use
medium acting muscle relaxant.

7.  Anaesthesia causes a respiratory impairment, whether the
patient is breathing spontaneously or is ventilated
mechanically.This impairment impedes the matching of
alveolar ventilation and perfusion .
 A triggering factor is loss of muscle tone that causes a fall in
the resting lung volume, functional residual capacity.This
fall promotes airway closure and gas adsorption, leading
eventually to alveolar collapse, & atelectasis.

8. Atelactasis during GA
 In most patients the atelectasis may not appear
severe.Thus in the average patient the atelectasis may
contain 15–20% of the lung tissue close to the diaphragm
and about 10% of the total lung tissue. In extreme cases
almost half the lung can be collapsed during anaesthesia.
 Atelectasis can persist for two days after major surgery but
disappears within 24 h after laparoscopy in non‐obese
subjects.

9. Types of atelectasis
1. Compression atelectasis occurs when the transmural
pressure distending the alveolus is reduced.
2. Absorption atelectasis occurs when less gas enters the
alveolus than is removed by uptake by the blood.
3. Loss‐of‐surfactant atelectasis occurs when the surface
tension of an alveolus increases because of reduced
surfactant action.

10. Gas exchange during GA
To ensure the maintenance of a normal arterial PO2, the
alveolar PO2 had to be as high as 200 mm Hg and this required
an inspired oxygen concentration (FIO2) of 35%. Since then it
has been commonly accepted that all general anaesthesia
should use at least 30–35% oxygen.

11. Ventilator Strategies
 There is strong evidence for the beneficial use of
lower tidal volumes have lower levels of circulating
inflammatory cytokines postoperatively , and may
have a lower instance of pneumonia.
 The use of positive end-expiratory pressure
(PEEP) is generally a safe strategy that reduces
the incidence and severity of atelectasis.

12. Preoperative investigations
Routine preoperative laboratory testing may help identify patients at
increased risk.
Other than routine one we may do :
 Pulmonary function test (PFT) , A forced expiratory volume at one
second (FEV1) less than 60% of predicted has been identified as a
risk factor for postoperative complications.
 Blood gases analysis.
 Chest radiographs .
 Preoperative protein depletion is associated with altered pulmonary
dynamics and respiratory muscle function, which leads to a higher
rate of pneumonia , Patients with low serum albumin levels (less
than 30 g/L) have significantly increased rates of reintubation,
pneumonia, and failure to wean from mechanical ventilation

13. How we can reduce perioperative
respiratory complications?
Smoking cessation
Cigarette smoke can acutely reduce airway cilliary function
and increase carbon monoxide levels.
* It may take weeks to months to find an objective
improvement in respiratory function after smoking cessation.
* The best evidence would suggest that at least two months
is required before smoking abstinence reduces the risk of
pulmonary complications .

14. Anesthetic technique :
Significant reduction in mortality in those patients who
received neuraxial blockade or neuraxial blockade combined
with general anesthesia versus those who received general
anesthesia alone.
Pain control
Pulmonary compromise is most severe after upper abdominal
procedures. FEV-1 decreased by 60% compared to
preoperative levels. Pain can also influence respiratory
mechanics resulting in rapid, shallow breathing increasing the
work of breathing. Patients may also experience postoperative
diaphragm dysfunction.

15. Postoperative management:
This includes incentive spirometry, assisted cough,
percussion and vibration, deep suctioning and
ambulation.

16. Definition of COPD
 Chronic obstructive pulmonary disease (COPD) is a
spectrum of diseases that includes emphysema, chronic
bronchitis, and asthmatic bronchitis. It is characterized by
progressive increased resistance to breathing. Airflow
limitation may be caused by loss of elastic recoil or
obstruction of small or large (or both) conducting airways.
 The increased resistance may have some degree of
reversibility. Cardinal symptoms are cough, dyspnea, and
wheezing

17. Note
COPD patients desaturate more frequently and severely
than normal patients during sleep.This is due to the
rapid/shallow breathing pattern that occurs in all patients
during rapid-eye movement (REM) sleep. In COPD patients
breathing air, this is causes a significant increase in the
respiratory dead space/tidal volume (VD/VT) ratio and a fall
in alveolar oxygen tension (PAo2) and Pao2

18. Concurrent Problems That Should Be Treated
before Anesthesia in COPD Patients

19. Asthma
Chronic inflammation of the airways, associated with airway
hyperresponsiveness, which leads to
1. Recurring episodes of wheezing,
2. Coughing,
3. Breathlessness,
4. Chest tightness
5. Reversible airflow obstruction within the lung

20. The pathophysiology of asthma
Involves the local release of various chemical mediators in the
airway and, possibly, over activity of the parasympathetic
nervous system.
Bronchoconstriction is the result of the subsequent release of
histamine; bradykinin; leukotrienes ; platelet-activating factor;
prostaglandins (PG) PGE2, PGF2, and PGD2; and neutrophil and
eosinophil chemotactic factors.

21. Classification of asthma

22. 1.History of illness, drugs, frequency of attacks.
2.Preoperative examination is the forced expiratory time
(FET), which is assessed by auscultation during
expiration. FET values greater than 6 seconds correlate
with abnormal FEV1/FVC ratios.
3.Patients should be advised to cease smoking at least 8
weeks before surgery, and certain patients may benefit
from a brief course of corticosteroids.
4.Measurement of arterial blood gases is indicated if
there is any question about the adequacy of ventilation or
oxygenation.
Anesthetic Preoperative Management

23. Bronchodilators should be continued up to the time of
surgery. inhaled glucocorticoids, leukotriene blockers,
mast-cell stabilizers, theophyllines, and anticholinergics.
In general, benzodiazepines are the most satisfactory
agents for premedication. Anticholinergic agents are not
customarily given unless very copious secretions are
present or if ketamine is to be used for induction of
anesthesia.
Preoperative drug management

24. Intra operative Management
Anesthetic
A goal of induction and maintenance of anesthesia is to
suppress airway reflexes to avoid bronchoconstriction in
response to mechanical stimulation of the airways.
a. Regional Anesthesia. The use of regional anesthesia
when the operative site is suitable for this may avoid
instrumentation of the airway and tracheal intubation.
b. General Anesthesia. Induction of anesthesia with
propofol is preferable to induction with thiopental, which
is associated with a higher incidence of wheezing.
Ketamine may produce smooth muscle relaxation and
contribute to decreased airway resistance.

25. i. Intravenous or intratracheal injection of lidocaine (1 - 1.5
mg/kg), (1 - 3 minutes ) before tracheal intubation can
be helpful. Opioids may suppress the cough reflex and
deepen anesthesia. It may be preferable to use short
acting opioids that have limited risk of causing
postoperative respiratory depression, such as
remifentanil (continuous infusion of 0.05 to 0.1
mcg/kg/min).
ii. LMA insertion is less likely than endotracheal intubation to
result in bronchoconstriction.
iii. Drugs with limited ability to evoke the release of histamine
should be selected.
Although all opioids have some histamine-releasing
effects, fentanyl and analogous agents have been used
safely in asthma patients.

26. iv. Antagonism of neuromuscular blockade with
anticholinesterase drugs could precipitate bronchospasm
secondary to stimulation of postganglionic cholinergic
receptors in airway smooth muscle. Bronchospasm does can
be minimized by simultaneous administration of
anticholinergic drugs.

27. v. During mechanical ventilation in asthmatic patients, a slow
inspiratory flow rate provides optimal distribution of
ventilation relative to perfusion. Sufficient time for exhalation
is necessary to prevent air trapping. Humidification and
warming of inspired gases may be especially helpful.
vi. Maintenance of adequate hydration ensures less viscous
secretions in the airway.

28. vii. If possible, extubation should be performed while
anesthesia is still sufficient to suppress hyper reactive
airway reflexes. Suppressing airway reflexes and the risk of
bronchospasm by administration of intravenous lidocaine
or pretreatment with inhaled bronchodilators should be
considered.

29. Airflow obstruction during expiration is apparent
on capnography as a delayed rise of the end-
tidal CO2 value.

32. Differential diagnosis of
intraoperative bronchospasm & wheezing

33. Chronic Bronchitis
Presence of a productive cough on most days of 3 consecutive
months for at least 2 consecutive years.
Secretions from hypertrophied bronchial mucous glands and
mucosal edema from inflammation of the airways produce airflow
obstruction.
Intrapulmonary shunting is prominent, and hypoxemia is common.
In patients with COPD, chronic hypoxemia leads to erythrocytosis,
pulmonary hypertension, and eventually right ventricular failure (cor-
pulmonale); this combination of findings is often referred to as the
blue bloater syndrome.
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

34. Emphysema
Irreversible enlargement of the airways distal to terminal bronchioles
and destruction of alveolar septa.
Significant emphysema is nearly always related to cigarette smoking.
Less commonly, emphysema occurs at an early age and is associated
with a homozygous deficiency of alpha 1-antitrypsin.
Loss of the elastic recoil that normally supports small airways by radial
traction allows premature collapse during exhalation
Patients characteristically have increases in RV, FRC, TLC.

35. Large cystic areas, or bullae, develop in some patients.
Increased dead space is a prominent feature of emphysema.
Arterial oxygen tensions are usually normal or only slightly reduced;
CO2 tension is also typically normal.
When dyspneic, patients with emphysema often purse their lips to
delay closure of the small airways—which accounts for the term pink
puffers that is often used.

36. Treatment of COPD
Treatment for COPD is primarily supportive.
1.Cessation of smoking.
2.Inhaled B2-adrenergic agonists.
3.Glucocorticoids.
4.Ipratropium are very useful.
5.Oxygen therapy can dangerously elevate PaCO2 in
patients with CO2 retention; elevating PaO2 above 60 mm
Hg can precipitate respiratory failure.
6.When cor-pulmonale is present, diuretics are used to
control peripheral edema.

37. Anesthetic Preoperative
Management
Ask about recent changes in dyspnea, sputum, and
wheezing.
PFTs, chest radiographs, and arterial blood gas
measurements should be reviewed carefully.
preoperative interventions in patients with COPD aimed at
correcting hypoxemia, relieving bronchospasm, mobilizing
and reducing secretions, and treating infections may
decrease the incidence of postoperative pulmonary
complications.

38.  Smoking should be discontinued for at least 6–8
weeks before the operation to decrease secretions
and to reduce pulmonary complications.
 Preoperative chest physiotherapy (chest
percussion and postural drainage) and antibiotics for
patients with a change in sputum are beneficial in
reducing secretions.
 Bronchospasm should be treated with
bronchodilators.
 Patients with moderate to severe disease may benefit
from a perioperative course of glucocorticoids.

39. Anesthetic Intra operative
Management
1. Pre-oxygenation prior to induction of general anesthesia
prevents the rapid oxygen desaturation often seen in these
patients.
2. The selection of anesthetic agents and general intraoperative
management are similar to those for asthmatic patients.
3. Ventilation should be controlled with small to moderate tidal
volumes and slow rates to avoid air trapping.
4. Humidified gases should be used if significant bronchospasm is
present and for long procedures (> 2 h).
5. Direct measurement of arterial oxygen tensions may be
necessary to detect more subtle changes in intrapulmonary
shunting.

40. Patients with pulmonary bullae are at high risk of developing
pneumothorax intraoperatively, particularly if ventilated with
positive pressure.
At the end of surgery, the timing of extubation should balance
the risk of bronchospasm with that of pulmonary insufficiency,
but evidence suggests that early extubation (in the operating
room) is beneficial.
Patients with an FEV1 below 50% are most likely to require a
period of postoperative ventilation, particularly following
upper abdominal and thoracic operations.

41. Intraoperative Complications That Occur with
Increased Frequency during Thoracotomy

42. Bronchiectasis.
A chronic suppurative disease of the airways, bronchiectasis
may cause expiratory airflow obstruction similar to that seen
with COPD.
1. Pathophysiology. Bacterial or mycobacterial infections are
presumed responsible for that illness.
2. Diagnosis. The history of a chronic cough productive of large
amounts of purulent sputum is highly suggestive of
bronchiectasis. Digital clubbing occurs in most patients with
significant bronchiectasis. Computed tomography (CT)
provides excellent images of bronchiectatic airways.

43. 3. Treatment. Bronchiectasis is treated with antibiotics
and postural drainage. Massive hemoptysis (>200 mL over
a 24-hour period) may require surgical resection of the
involved lung.
4. Management of Anesthesia.A double-lumen
endobronchial tube may be used to prevent spillage of
purulent sputum into normal areas of the lungs. Nasal
intubation should be avoided due to high rates of chronic
sinusitis.

44. Restrictive Pulmonary Disease
 Restrictive pulmonary diseases are characterized by decreased
lung compliance.
 Lung volumes are typically reduced, with preservation of normal
expiratory flow rates.
 Both FEV1 and FVC are reduced, but the FEV1/FVC ratio is high or
normal.
 Restrictive pulmonary diseases include many acute and chronic
illness involving the pleura, chest wall, diaphragm, or
neuromuscular function.
 Reduced lung compliance increases the work of breathing,
resulting in a characteristic rapid and shallow breathing pattern.

45. Acute Intrinsic Pulmonary
Disorders
 Acute intrinsic pulmonary disorders include pulmonary
edema (including the acute respiratory distress syndrome
[ARDS]), infectious pneumonia, and aspiration pneumonitis.
 Reduced lung compliance in these disorders is primarily due
to an increase in extravascular lung water, from either an
increase in pulmonary capillary pressure or an increase in
pulmonary capillary permeability
 Increased pressure occurs with left ventricular failure,
whereas fluid overload and increased permeability are
present with ARDS.

46. Anesthetic Preoperative
Management
In preparation for emergency procedures, oxygenation and
ventilation should be optimized preoperatively to the greatest
extent possible.
Fluid overload should be treated with diuretics; heart failure
may also require vasodilators and inotrops.
Persistent hypoxemia may require positive-pressure
ventilation and positive end-expiratory pressure (PEEP).

47. Anesthetic Intra operative
Management
High inspired oxygen concentrations and PEEP may be
required.
The decreased lung compliance results in high peak
inspiratory pressures during positive-pressure ventilation
and increases the risk of barotrauma and volumtrauma.
Tidal volumes for these patients should be reduced to 4–7
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.

48. Chronic Intrinsic Pulmonary
Disorders
Also often referred to as interstitial lung
diseases.Characterized by an insidious onset, chronic
inflammation of alveolar walls and progressive pulmonary
fibrosis.
Causes include : hypersensitivity pneumonitis from
occupational and environmental pollutants, drug toxicity
(bleomycin and nitrofurantoin), radiation pneumonitis,
idiopathic pulmonary fibrosis, autoimmune diseases, and
sarcoidosis.
Chronic pulmonary aspiration, oxygen toxicity, and severe
ARDS can also produce chronic fibrosis.

49. Patients typically present with dyspnea on exertion and
sometimes a nonproductive cough.
Symptoms of corpulmonale are present only with
advanced disease.
Physical examination may reveal fine (dry) crackles over
the lung bases and, in late stages, evidence of right
ventricular failure.
The chest radiograph show "ground-glass" appearance
and "honeycomb" appearance.
Arterial blood gases usually show mild hypoxemia with
normocarbia.
PFTs are typical of a restrictive ventilatory defect

50. Anesthetic Preoperative
Management
A history of dyspnea on exertion (or at rest) should be
evaluated further with PFTs and arterial blood gas analysis.
A vital capacity less than 15 mL/kg is indicative of severe
dysfunction.
A chest radiograph is helpful in assessing disease severity.

51. Anesthetic Intra operative
Management
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, the inspired fractional concentration of oxygen
should be kept to the minimum concentration compatible with
acceptable oxygenation (SpO2 of > 88–92%).
High peak inspiratory pressures during mechanical ventilation
increase the risk of pneumothorax and should prompt smaller
than normal tidal volumes with a faster rate.

52. Extrinsic Restrictive Pulmonary Disorders
 Extrinsic restrictive pulmonary disorders alter gas
exchange by interfering with normal lung expansion.
 They include pleural effusions, pneumothorax, mediastinal
masses, kyphoscoliosis, pectus excavatum, neuromuscular
disorders, and increased intraabdominal pressure from
ascites, pregnancy, or bleeding.
 Marked obesity also produces a restrictive ventilatory
defect .
 Anesthetic considerations are similar to those discussed
for intrinsic restrictive disorders.

53. Pulmonary Embolism
 Pulmonary embolism results from the entry of blood
clots, fat, tumor cells, air, amniotic fluid, or foreign
material into the venous system. Venous stasis or
hypercoagulability is often contributory in such cases.
 Pulmonary embolism can also occur intraoperatively in
normal individuals undergoing certain procedures.

54. Anesthetic Preoperative
Management
 Patients with acute pulmonary embolism may present in the
operating room for placement of a caval filter or, rarely, for
pulmonary embolectomy.
 If the acute episode is more than 1 year old, the risk of
temporarily stopping anticoagulant therapy is probably small.

55. Anesthetic Intra operative
Management
 Vena cava filters are usually placed percutaneously under local
anesthesia with sedation.
 Decreased venous return during placement of the device can
precipitate hypotension.
 Patients presenting for pulmonary embolectomy are critically ill.
They are usually already intubated but tolerate positive-pressure
ventilation poorly. Inotropic support is necessary until the clot is
removed.
 They also tolerate all anesthetic agents very poorly. Small doses of
an opioid, etomidate, or ketamine may be used, but the latter can
theoretically increase pulmonary artery pressures.
Cardiopulmonary bypass is required.

56. Intra operative Pulmonary
Embolism
 Significant pulmonary embolism is a rare occurrence during
anesthesia.
 Air emboli are common.
 Fat embolism can occur during orthopedic procedures.
 Amniotic fluid embolism is a rare, unpredictable, and often fatal,
complication of obstetrical delivery .
 Thromboembolism may occur intraoperatively during prolonged
procedures.
 The clot may have been present prior to surgery or may form
intraoperatively; surgical manipulations or a change in the patient's
position may then dislodge the venous thrombus. Manipulation of
tumors with intravascular extension can similarly produce pulmonary
embolism.

57. Intra operative management of
PE
Intraoperative pulmonary embolism usually presents as:
1.unexplained sudden hypotension, hypoxemia, or bronchospasm.
2.A decrease in end-tidal CO2 concentration.
3.Elevated central venous and pulmonary arterial pressures.
4. Transesophageal echocardiogram may be helpful.
Management:
If air is identified in the right atrium, or if it is suspected, emergent
central vein cannulation and aspiration of the air may be life saving.
For all other emboli, treatment is supportive, with intravenous fluids
and inotropes.
Placement of a vena cava filter should be considered postoperatively.

58. Postoperative complications
1. Atelectasis.
2. Respiratory failure .
3. Pneumonia are the most common complications may
happen due to many factors :
 Postoperative pain
 Decreases sputum clearance.
 Bed rest.
 Poor chest physiotherapy (pre. & postoperative).

59. Postoperative lung expansion
A variety of techniques are available for postoperative lung expansion. This
includes
1. Postoperative pain control.
2. Incentive spirometry.
3. Assisted cough.
4. Percussion and vibration.
5. Deep suctioning.
6. Early Ambulation.
7. Fiberoptic bronchoscopy should be performed to remove the mucous
plugging.
8. Continuous positive airway pressure (CPAP) delivered via nasal cannula
or facemask and non-invasive ventilation (NIV) via facemask or helmet
improve oxygenation and help in re-expanding the collapsed lung.

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