Pulmonary Atelectasis

Presented by Kang, ting-jui

 Introduction
General anesthesia is associated with impaired
oxygenation  pulmonary atelectasis was
suspected as the major cause
Decrease in lung compliance and the partial
pressure of arterial oxygen (PaO2)
Atelectasis occurs in the most dependent parts of
the lung of 90% of patients who are anesthetized
 gas exchange abnormalities and reduced static
compliance associated with acute lung injury 
perioperative morbidity
 Physiologic causes of atelectasis

Mechanisms:
Compression of lung tissue
Absorption of alveolar air
Impairment of surfactant function
 Compression atelectasis
Overall cephalad diaphragm displacement 
after anesthesia, the diaphragm is relaxed
Differential regional diaphragmatic changes
In an anesthetized patient breathing
spontaneously  the diaphragm moves the
most in the lower, dependent portion
During paralysis and positive-pressure
ventilation  the passive diaphragm is
displaced by the positive pressure preferentially
in the upper, nondependent portion
 Compression atelectasis
Shift of thoracic central vascular blood
into the abdomen  additional
dependent pressure arising from the
abdomen
Altered diaphragmatic dynamics 
phrenic nerve stimulation versus
isovolumic conditions in anesthetized
patients
 Gas resorption
Resorption atelectasis occur by two mechanisms
After complete airway occlusion  gas trapped
 gas uptake by the blood continues and gas
inflow is prevented  gas pocket collapses;
increases with elevation of FI02
Low ventilation relative to perfusion (low
[VA/Q] ratio) have a low partial pressure of
alveolar oxygen (PAO2)  when FIO2 increased,
PAO2 increases  oxygen moves from alveolar
to blood greatly  lung unit progressively
smaller
 Surfactant impairment
Stabilizing function of surfactant may be
depressed by anesthesia
Reduction in percent maximum lung volume
was proportional to the concentration of both
chloroform and halothane
Halothane anesthesia combination with high
oxygen concentration, caused increased
permeability of the alveolar– capillary barrier in
rabbit lungs
Increased tidal volume  cause release of
surfactant
Pathogenic mechanisms to
development atelectasis
Factors modulating the
formation of atelectasis
 Type of anesthesia
Atelectasis develops with both intravenous and
inhalational anesthesia, whether the patient is
breathing spontaneously or is paralyzed and
mechanically ventilated
Ketamine: not produce atelectasis when used
alone
Regional anesthesia: depend on the type and
extension of motor blockade
Reduces inspiratory capacity by up to 20%, and
expiratory reserve volume approaches zero
Less extensive blockade  closing capacity and
FRC remain unchanged
 Impact of time
The maximum decrease in FRC seems to occur
within the first few minutes of general anesthesia
During anesthesia for surgical operations on the
limb  FRC is not influenced further by depth or
duration of anesthesia
During abdominal or thoracic surgery,
pulmonary gas exchange deteriorates
progressively during the course of the operation
unable to determine the independent impact of
time on atelectasis as opposed to surgical
manipulation
 Effects of position
Changing from the upright to the supine
position results in a decrease of 0.5L in FRC
to 1.0L, even in the awake state
After anesthesia, FRC is reduced by a further
0.5L to 0.7L
Trendelenburg position resulting in further
decrease in FRC
Lateral decubitus position usually slight
increase in total lung FRC
Prone position may increase FRC slightly,
although this may not decrease atelectasis
 Effects of position
Distribution of ventilation is more uniform in
anesthetized patients in the prone position;
improves oxygenation in patients with ARDS
Atelectasis is more prominent after cardiac
surgery with cardiopulmonary bypass; not
related to increasing in pulmonary endothelial
permeability
Lung recruitment strategy and PEEP improves
oxygenation in patients after CPB
Intentionally inflate the patient’s lungs before
coming off CPB and directly visualize equal
expansion of the lungs
 Inspired oxygen
High oxygen concentration has been associated
with atelectasis formation
Increasing FIO2 at the end of surgery to 1.0
before extubation also causes additional
atelectasis
During routine induction of general anesthesia,
80% oxygen caused minimal atelectasis, but the
time margin before desaturation occurred was
significantly shortened compared with that of
100% oxygen
 Inspired oxygen
No difference in the incidence of postoperative
atelectasis if nitrous oxide in oxygen was used or
if air in oxygen was used
The very rare possibility of acute hypoxemia in
the event of difficulty with airway management
versus the common and predictable — but
generally mild—impact of hyperoxia-induced
atelectasis on later intraoperative gas exchange
A lower FIO2 to replace preoxygenation has not
been recommended
 Effects of age
Progressive age is not associated with increased
propensity for development of atelectasis
Young children (aged 1–3 yr) develop atelectasis
more readily greater thoracic wall compliance,
less outwardly directed lung distension forces
Children younger than 2yr prone to respiratory
failure and fatigue: type I and II muscle fibers are
not fully developed
Infant at greater risk for atelectasis because the
elastic supporting structure of the lung is
incompletely developed
 Body habitus
Obesity markedly reduced FRC and lung
compliance development of atelectasis 
worsens arterial oxygenation
The weight of the torso and abdomen make
diaphragmatic excursions more difficult—
especially when recumbent or supine—the
FRC decreases, intensified in paralysis with
neuromuscular blockade
Pregnancy also potentiates atelectasis
 Tidal volume
The use of low tidal volume in patients with
ARDS reduces stretch-induced lung injury in
patients with ARDS, improved patient survival
Low tidal volume increases atelectasis in the
absence of lung injury
The specific ―low-tidal-volume‖ approach was
actually associated with the development of
intrinsic PEEP
Pressure-controlled ventilation results in smaller
delivered tidal volumes when respiratory system
compliance is decreased may lead to atelectasis
and may go undiagnosed
 Preexisting lung disease
Smokers and patients with lung disease show
more pronounced gas exchange impairment
than healthy subjects
Only a small shunt and almost no atelectasis
develops in these patients, but they may have
severe VA/Q mismatch
COPD may make them resist collapse
Large regions with low VA/Q ratios that can
result, over time, in resorption atelectasis
 Effects of atelectasis

Decreased compliance
Impaired oxygenation
Pulmonary vascular resistance increase
Lung injury
 Postoperative period
Atelectasis can persist for 2 days after major
surgery
The lung dysfunction is often transient; may be
related to reduction in FRC
Postoperative mechanical respiratory abnormality
after abdominal or thoracic surgery is a restrictive
pattern with severely reduced inspiratory
capacity, vital capacity, and FRC pain control in
preventing postoperative atelectasis
Atelectasis and pneumonia are often considered
together because the changes associated with
atelectasis may predispose to pneumonia
 Detection of atelectasis
Conventional chest radiography
Computed tomography
Magnetic resonance imaging
Ultrasonography
Intravital microscopy
Cytokine profile
 Prevention / reversal of atelectasis
Healthy lungs
Reversible by passive hyperinflation (i.e., three
successive inflations: a pressure of 20cmH2O for
10s; then a pressure of 30cm H2O for 15s; and
third, a pressure of 40 cm H2O sustained for 15s)
High initial pressures are needed to overcome the
anesthesia-induced collapse and that PEEP of 5cm
H2O or more is required to prevent collapse
No evidence of barotrauma or pulmonary
complications occurred in the high initial airway
pressure
 Prevention / reversal of atelectasis
Injured lungs
Large tidal volumes, high peak airway pressures,
and end-expiratory alveolar collapse with cyclic
reopening have all been proposed as deleterious
Calculated the inflection point from a pressure–
volume curve, and PEEP was preset at 2cm H2O
above the inflection point
Recruiting maneuver: continuous positive airway
pressures of 35–40cm H2O for 40 s followed by a
return to previous PEEP levels
Optimum overall cardiopulmonary interaction
Only in patients with early ARDS
 Treating atelectasis in the
postoperative period
Encourage or force patients to inspire deeply
Method: intermittent positive-pressure
breathing, deep-breathing exercises, incentive
spirometry, and chest physiotherapy
A simple posture change from supine to seated
Thoracic or sternal traction, the use of
intravenous aminophylline as successful
treatments of atelectasis in a number of case
reports
 HAVE A
NICE DAY