RESPIRATORY CHANGES DURING
ANESTHESIA AND POSITIVE
DR DANISH OMAIR
MODERATOR- DR FERHAN
• The lung is regularly affected by anesthesia and mechanical
• This occurs even in healthy volunteers or patients with no
cardiopulmonary disease, and sometimes the dysfunction
can be severe enough to cause life-threatening hypoxemia.
• In patients with preexisting lung disease, gas exchange will
be further compromised in comparison to the awake state.
• Knowledge of the functional impairment that will ensue
during anesthesia and mechanical ventilation will make
possible ventilatory support that should, in the large
majority of patients, prevent any disastrous impairment in
RESPIRATORY FUNCTION DURING
• Anesthesia causes an impairment in pulmonary
function, whether the patient is breathing
spontaneously or is ventilated mechanically
after muscle paralysis.
• Impaired oxygenation of blood occurs in most
subjects who are anesthetized.
• It has therefore become routine to add oxygen
to the inspired gas so that the inspired oxygen
fraction (FIO2) is maintained at around 0.3 to 0.4.
• Despite these measures, mild to moderate
hypoxemia, defined as an arterial oxygen
saturation of between 85% and 90%, may occur
in approximately half of all patients undergoing
elective surgery, and the hypoxemia can last
from a few seconds to up to 30 minutes.
• About 20% of patients may suffer from severe
hypoxemia, or oxygen saturation below 81% for
up to 5 minutes.
• Lung function remains impaired postoperatively,
and clinically significant pulmonary
complications can be seen in 1% to 2% after
minor surgery in up to 20% after upper
abdominal and thoracic surgery.
• The first phenomenon that might be seen
with anesthesia is loss of muscle tone with a
subsequent change in the balance between
outward forces (i.e., respiratory muscles) and
inward forces (i.e., elastic tissue in the lung)
leading to a fall in FRC.
• This is paralleled by an increase in the elastic
behavior of the lung (reduced compliance)
and an increase in respiratory resistance.
• The decrease in FRC affects the patency of
lung tissue with the formation of atelectasis
(made worse with the use of high
concentrations of inspired oxygen) and
• This alters the distribution of ventilation and
matching of ventilation and blood flow and
impedes oxygenation of blood and removal
of carbon dioxide.
LUNG VOLUME AND RESPIRATORY
MECHANICS DURING ANESTHESIA
• LUNG VOLUME:
• FRC is reduced by 0.8 to 1.0 L by changing
body position from upright to supine, and
there is another 0.4- to 0.5-L decrease when
anesthesia has been induced.
• End-expiratory lung volume is thus reduced
from approximately 3.5 to 2 L, the latter
being close or equal to RV.
• The anesthesia per se causes a fall in FRC
despite maintenance of spontaneous breathing
and the decrease in FRC occurs regardless of
whether the anesthetic is inhaled or given
• Muscle paralysis and mechanical ventilation
cause no further decrease in FRC.
• The average reduction corresponds to around
20% of awake FRC and may contribute to an
altered distribution of ventilation and impaired
oxygenation of blood.
• The decrease in FRC seems to be related to
loss of respiratory muscle tone, which shifts
the balance between the elastic recoil force
of the lung and the outward force of the
chest wall to a lower chest and lung volume.
• Maintenance of muscle tone, as during
ketamine anesthesia, does not reduce FRC.
• FRC increases with age if weight and height
remain unaltered over the years
COMPLIANCE AND RESISTANCE OF
• Static compliance of the total respiratory system
(lungs and chest wall) is reduced on average from
95 to 60 mL/cm H2O during anesthesia.
• There is a decrease in compliance during
anesthesia when compared to awake states.
• There are also studies on resistance of the total
respiratory system and the lungs during
anesthesia, most of them showing a considerable
increase during both spontaneous breathing and
• This figure shows the cranial shift of diaphragm
and a decrease in transverse diameter of thorax
contribute to lowered FRC during anesthesia.
• Decreased ventilated volume (atelectasis and
airway closure) is a possible cause of reduced
• Decreased airway dimensions by lowered FRC
should contribute to increase airway resisitance.
ATELECTASIS AND AIRWAY CLOSURE
• ATELECTASIS: In their classic paper, Bendixen
and coworkers proposed “a concept of
atelectasis” as a cause of impaired oxygenation
• They had observed a successive decrease in
compliance of the respiratory system and a
similar successive decrease in arterial
oxygenation in both anesthetized humans and
• This was interpreted as formation of atelectasis.
• Atelectasis appears in approximately 90% of all
patients who are anesthetized.
• It is seen during spontaneous breathing and after
muscle paralysis and whether intravenous or
inhaled anesthetics are used.
• Thus, 15% to 20% of the lung is regularly collapsed
at the base of the lung during uneventful
anesthesia, before any surgery has even been done.
• Abdominal surgery does not add much to the
atelectasis, but it can remain for several days in the
• It is likely that it is a focus of infection and can
contribute to pulmonary complications.
• It may also be mentioned that after thoracic
surgery and cardiopulmonary bypass, more
than 50% of the lung can be collapsed even
several hours after surgery.
• The amount of atelectasis decreases toward
the apex, which is mostly spared (fully
• There is a weak correlation between the size of
the atelectasis and body weight or body mass
index (BMI), with obese patients showing larger
atelectatic areas than lean ones do.
• Although this was expected, it came as a surprise
that the atelectasis is independent of age, with
children and young people showing as much
atelectasis as elderly patients.
• Another unexpected observation was that
patients with COPD showed less or even no
atelectasis during the 45 minutes of anesthesia
that they were studied.
• The mechanism that prevents the lung from
collapse is not clear but may be airway closure
occurring before alveolar collapse takes place,
or it may be an altered balance between the
chest wall and the lung that counters a
decrease in lung dimensions
PREVENTION OF ATELECTASIS DURING
• Several interventions can help prevent atelectasis or
even reopen collapsed tissue, as discussed in the
• 1)PEEP: The application of 10–cm H2O PEEP has been
tested in several studies and will consistently reopen
collapsed lung tissue.
• This is more likely an effect of increased inspiratory
airway pressure than of PEEP per se.
• However, some atelectasis persists in most patients.
Whether a further increase in the PEEP will reopen this
tissue was not analyzed in these studies.
• PEEP, however, does not appear to be the ideal
• First, shunt is not reduced proportionately, and arterial
oxygenation may not improve significantly.
• The persistence of shunt may be explained by a
redistribution of blood flow toward more dependent
parts of the lungs when intrathoracic pressure is
increased by PEEP.
• Under such circumstances, any persisting atelectasis in
the bottom of the lung receives a larger share of the
pulmonary blood flow than without PEEP.
• Furthermore, increased intrathoracic pressure
will impede venous return and decrease cardiac
• This results in a lower venous oxygen tension for
a given oxygen uptake and reduces arterial
• Second, the lung recollapses rapidly after
discontinuation of PEEP.
• Within 1 minute after cessation of PEEP, the
collapse is as large as it was before the
application of PEEP.
• During mechanical ventilation with zero end-
expiratory pressure (ZEEP), perfusion goes mainly
to the lower lung, but there is still perfusion of
the upper lung, with the average distribution to
the upper lung being 33% to 40% of total lung
• With a general PEEP of 10 cm H2O, perfusion is
squeezed down to the lower lung, and there may
be almost no perfusion at all in the upper lung.
• This causes a dramatic dead space–like effect.
• If, on the other hand, PEEP is applied
selectively to the lower lung, in this example
10 cm H2O, perfusion might be redistributed
to the upper lung so that a more even
distribution between the two lungs can be
2)MAINTENANCE OF MUSCLE TONE
• Use of an anesthetic that allows maintenance of
respiratory muscle tone will prevent atelectasis
• Ketamine does not impair muscle tone and does
not cause atelectasis.
• This is the only anesthetic thus far tested that
does not cause collapse.
• However, if muscle relaxation is required,
atelectasis will appear as with other anesthetics.
• The use of a sigh maneuver, or a double VT, has
been advocated to reopen any collapsed lung
• However, the atelectasis is not decreased by a
double VT or by a sigh up to an airway pressure of
20 cm H2O.
• Not until an airway pressure of 30 cm H2O is
reached does the atelectasis decrease to
approximately half the initial size.
• For complete reopening of all collapsed lung
tissue, an inflation pressure of 40 cm H2O is
• Such a large inflation corresponds to a maximum
spontaneous inspiration, and it can thus be called
a VC maneuver.
• Because a VC maneuver may result in adverse
cardiovascular events, the dynamics in resolving
atelectasis during such a procedure was analyzed.
• It was found that in adults with healthy lungs,
inflation of the lungs to +40 cm H2O maintained
for no more than 7 to 8 seconds may re-expand
all previously collapsed lung tissue.
4)MINIMIZING GAS RESORPTION
• Ventilation of the lungs with pure oxygen after a VC
maneuver that had reopened previously collapsed
lung tissue resulted in rapid reappearance of the
• If, on the other hand, 40% O2 in nitrogen is used for
ventilation of the lungs, atelectasis reappears
slowly, and 40 minutes after the VC maneuver only
20% of the initial atelectasis had reappeared.
• Thus, ventilation during anesthesia should be done
with a moderate fraction of inspired oxygen (e.g.,
FIO2 of 0.3 to 0.4) and should be increased only if
arterial oxygenation is compromised.
• The striking effects of oxygen during anesthesia
raised the question of whether “preoxygenation”
during induction of anesthesia has an effect on the
formation of atelectasis.
• Breathing of 100% O2, just for a few minutes before
and during commencement of anesthesia,
increases the safety margin in the event of difficult
intubation of the airway with prolonged apnea.
• However, there turned out to be a price for it.
• Avoidance of the preoxygenation procedure
(ventilation with 30% O2) eliminated atelectasis
formation during induction and subsequent
• Preoxygenation can also be provided without
producing atelectasis if undertaken with
continuously increased airway pressure, as with
continuous positive airway pressure (CPAP).
• By applying CPAP of 10 cm H2O, Rusca and
associates could induce anesthesia on 100% O2
without any substantial atelectasis formation.
• This technique might provide the greatest safety
without atelectasis formation but it requires a
tight system and might be complicated in clinical
• In addition to atelectasis, intermittent closure
of airways can be expected to reduce the
ventilation of dependent lung regions.
• Such lung regions may then become “ low
Va/Q ” units if perfusion is maintained or not
reduced to the same extent as ventilation.
• Airway closure increases with age, as does
perfusion to “low- Va/Q ” regions.
• Because anesthesia causes a reduction in FRC
of 0.4 to 0.5 L, it may be anticipated that
airway closure will become even more
prominent in an anesthetized subject.
DISTRIBUTION OF VENTILATION
• Redistribution of inspired gas away from dependent to
nondependent lung regions has been observed in
anesthetized supine humans by isotope techniques.
• With the use of a radiolabeled aerosol and SPECT,
ventilation was shown to be distributed mainly to the
upper lung regions, and there was a successive
decrease down the lower half of the lung.
• Moreover, there was no ventilation at all in the bottom
of the lung, a finding corresponding to the distribution
of atelectasis that was simultaneously observed by CT .
• PEEP increases dependent lung ventilation in
anesthetized subjects in the lateral position,
so the distribution of ventilation is more
similar to that in the awake state.
• Similar findings of more even distribution
between the upper and lower lung regions
have also been made in supine anesthetized
humans after previous inflation of the lungs,
similar to PEEP.
DISTRIBUTION OF LUNG BLOOD FLOW
• A successive increase in perfusion down the lung,
from the ventral to the dorsal aspect, was seen,
with some reduction in the lowermost region.
• PEEP will impede venous return to the right heart
and therefore reduce cardiac output.
• It may also affect pulmonary vascular resistance,
although this may have less of an effect on
• In addition, PEEP causes a redistribution of blood
flow toward dependent lung regions.
• By this means, upper lung regions may be
poorly perfused, thereby causing a dead
• Moreover, forcing blood volume downward to
the dorsal side of the lungs may increase
fractional blood flow through an atelectatic
• Several inhaled anesthetics have been found to inhibit
HPV in isolated lung preparations. However, no such
effect has been seen with intravenous anesthetics
• The HPV response may thus be obscured by
simultaneous changes in cardiac output, myocardial
contractility, vascular tone, blood volume distribution,
blood pH and CO2 tension, and lung mechanics.
• In studies with no gross changes in cardiac output,
isoflurane and halothane depress the HPV response by
50% at a MAC of 2 .
EFFECTS OF ANESTHETICS ON
• Spontaneous ventilation is frequently reduced
• Thus, inhaled anesthetics, as well as barbiturates
for intravenous use, reduce sensitivity to CO2.
• The response is dose dependent and entails
decreasing ventilation with deepening
• Anesthesia also reduces the response to hypoxia.
• Attenuation of the hypoxic response may be
attributed to an effect on the carotid body
• The effect of an anesthetic on respiratory muscles
• Rib cage excursions diminish with deepening
• The normal ventilatory response to CO2 is
produced by the intercostal muscles, with no
clear increase in rib cage motion with CO2
rebreathing during halothane anesthesia.
• Thus, the reduced ventilatory response to CO2
during anesthesia is due to impeded function of
the intercostal muscles.
FACTORS THAT INFLUENCE
RESPIRATORY FUNCTION DURING
• FRC is reduced to the same extent during anesthesia,
regardless of whether a muscle relaxant is used, and
atelectasis occurs to almost the same extent in
anesthetized spontaneously breathing subjects as during
• Furthermore, the cranial shift of the diaphragm, as
reported by Froese and Bryan in their classic paper, was of
the same magnitude both during general anesthesia with
spontaneous breathing and with muscle paralysis, even
though a difference in movement of the diaphragm from
the resting position was noted.
• Thus, during spontaneous breathing, the
lower, dependent portion of the diaphragm
moved the most, whereas with muscle
paralysis, the upper, nondependent part
showed the largest displacement.
2)INCREASED OXYGEN FRACTION(FiO2)
• Anjou-Lindskog and associatesinduced
anesthesia on air (FIO2 of 0.21) in middle-aged to
elderly patients during intravenous anesthesia
before elective lung surgery and found only small
shunts of 1% to 2%.
• When FIO2 was increased to 0.5, an increase in
shunt of 3% to 4% was noticed.
• In another study on elderly patients during
halothane anesthesia , an increase in FIO2 from
0.53 to 0.85 caused an increase in shunt from 7%
to 10% of cardiac output.
• Supine : when conscious person changes
from erect to supine position, FRC decreases
by 0.5-1L, because abdominal viscera press
against the diaphragm and 4 cm cephaloid
shift of diaphragm occurs.
• During anesthesia, cephaloid shift of
diaphragm is due to muscle paralysis.
• During IPPV, gas moves along the line of least
resistance, to the less congested and more
compliant substernal units of the superior
lungs are inflated preferentially .
• Gravity increases perfusion of dependent i e
posterior lung segments.
• Spontaneous ventilation favors dependent
lung segments and controlled ventilation
favors independent i e anterior segments.
• Prone : compression of abdominal and thorax
decreases total lung compliance and increase
work of breathing.
• Mechanical ventilation in prone position
improves oxygenation in ALI/ARDS, as it re-
aerates the dorsal lung units.
• Lateral decubitus: there is decrease volume of
dependent lung but there is increase in perfusion.
Decrease ventilation to dependent lung in
• Tredlenberg: decrease in lung capacities due
to shift of abdominal viscera, increase V/Q
mismatch and atelectasis, decrease FRC and
• It is well known that arterial oxygenation is
further impeded with increasing age of the
• Shunt and formation of atelectasis does not
increase with age in adults.
• In contrast, there appears to be increasing V/Q
mismatch with age, with enhanced perfusion
of low VA/Q regions both in awake subjects and
when they are subsequently anesthetized.
• Thus, the major cause of impaired gas
exchange during anesthesia at ages younger
than 50 years is shunt, whereas at higher ages
• Obesity worsens the oxygenation of blood.
• A major explanation appears to be a markedly
reduced FRC, which promotes airway closure to a
greater extent than in a normal subject.
• The use of high inspired oxygen concentrations
will promote rapid atelectasis formation behind
• The shorter time until desaturation during
induction of anesthesia, as observed in morbidly
obese patients, may also be prevented by PEEP or
• This can be explained by the increase in lung
volume by PEEP or CPAP so that more oxygen is
available for diffusion into the capillary blood. 47
PRE-EXISTING LUNG DISEASE
• Smokers and patients with lung disease have
more severe impairment of gas exchange in the
awake state than healthy subjects do, and this
difference also persists during anesthesia.
• Interestingly, smokers with moderate airflow
limitation may have less shunt than lung-healthy
• Thus, in patients with mild to moderate
bronchitis who were to undergo lung surgery or
vascular reconstructive surgery in the leg, only a
small shunt was noticed.
• In patients with chronic bronchitis studied by MIGET
and CT, no or very limited atelectasis developed during
anesthesia and no or only minor shunt.
• However, a considerable Va/Q mismatch was seen
with a large perfusion fraction to low Va/Q regions.
• A possible reason for the absence of atelectasis and
shunt in these patients may be chronic hyperinflation,
which changes the mechanical behavior of the lungs
and their interaction with the chest wall such that the
tendency to collapse is reduced.
• The ventilatory effects of regional anesthesia depend
on the type and extension of motor blockade .
• With extensive blocks that include all of the thoracic
and lumbar segments, inspiratory capacity is reduced
by 20% and expiratory reserve volume approaches
• Diaphragmatic function, however, is often spared,
even in cases of inadvertent extension of subarachnoid
or epidural sensory block up to the cervical segments.
• Skillfully handled regional anesthesia affects
pulmonary gas exchange only minimally.
• Arterial oxygenation and carbon dioxide
elimination are well maintained during spinal
and epidural anesthesia.
• This is in line with the findings of an
unchanged relationship of CC and FRC and
unaltered distributions of ventilation-
perfusion ratios during epidural anesthesia.
LUNG FUNCTION AFTER CARDIAC
• Cardiac surgery produces the largest atelectasis in the
postoperative period .
• Cardiac surgery is generally undertaken with both lungs
collapsed and the patient connected to an extracorporeal
pump and oxygenator.
• If no precautions are taken in the immediate postoperative
period, the lung will recruit slowly, and more than half the
lung may be collapsed 1 to 2 days later with a shunt that is
around 20% to 30% of cardiac output.
• A recruitment maneuver consisting of inflating the lungs to
an airway pressure of 30 cm H2O for a 20-second period is
sufficient to reopen the collapsed lung.
• This lower airway pressure will do the same
job as 40 cm H2O in patients undergoing
abdominal surgery because the maneuver is
undertaken with an open chest before closure
and return to mechanical ventilation.
RESPIRATORY FUNCTION DURING ONE
• In lung surgery, oxygenation may be a challenge
even during anesthesia.
• One lung is non-ventilated but still perfused, and
in the postoperative period, restoration of lung
integrity and ventilation/perfusion matching may
take time .
• The technique of one-lung anesthesia and
ventilation means that only one lung is ventilated
and provides oxygenation of blood, as well as
elimination of carbon dioxide from the blood.
• Persisting perfusion through the nonventilated
lung causes a shunt and decreased PaO2 .
• However, the dependent, ventilated lung will
also contribute to the impeded oxygenation
by formation of atelectasis in the dependent
• There are reasons to also consider a
recruitment maneuver in one-lung ventilation
• The alveolar recruitment strategy(ARS) maneuver
was executed by increasing peak airway pressure
minute by minute from 25 to 30, 35, and finally
40 cm H2O and simultaneously increasing PEEP
from 5 to 10, 15, and finally 20 cm H2O.
• Airway pressure was then reduced to a peak of
25 and PEEP to 5 cm H2O.
• This resulted in an increase in PaO2 from 217 to
470 mm Hg after ARS.
• Shunt can be seen in lower lung during two-
lung ventilation, but both in lower lungs and
in all of upper lung during one- lung
• In one- lung ventilation, upper non ventilated
lung will act as a shunt region as well as lower
part of dependent lung.
RESPIRATORY EFFECTS OF IPPV WITH
ZEEP OR PEEP
• IPPV results in minor changes in the spatial
distribution of ventilation which is only
relevant in pts with ALI.
• PEEP increases lung volume, re expands
collapsed alveoli and therefore improves
ventilation in these areas.
• Both delivery of IPPV and PEEP results in
apparatus deadspace which may or may not
influence the overall deadspace.
• There is slight worsening of V/Q ratios with IPPV
but this is often not significant.
• PEEP increases FRC whilst IPPV with ZEEP does
• IPPV and PEEP do not change oxygenation in
healthy pts but may have significant benefits in
decreased pts, as it increases FRC above closing
capacity, reducing airway resistance and
improving recruitment and maintaining patency
in alveolar units.