PHYSIOLOGY OF ONE

LUNG VENTILATION

MODERATOR- DR. NATARAJ

GUIDE- DR. NAGARAJ
SPEAKER- DR. ROHIT
ONE LUNG VENTILATION [OLV]
 OLV is a technique that allows mechanical isolation of
individual lung thereby independent functioning of
that lung.
 It improves surgical exposure during pulmonary and
extra pulmonary intra-thoracic procedures.
 If only dependant well perfused lung is ventilated ,
surgical access to Non Dependant Lung [NDL]
improves.
 However NDL is still perfused and Dependant Lung
[DL] is over perfused than ventilation leading to
venous admixture resulting in hypoxemia.
HISTORY
 OLV/Singlelung ventilation also called selective
intubation was first described in 1931 by Gale
and Waters using prototype double lumen
tube(DLT).
PHYSIOLOGICAL CONCERNS DURING ONE
LUNG VENTILATION
1. Pulmonary Circulation and Shunt
2. Ventilation and Dead Space
3. V/Q Mismatch
4. Lateral Decubitus Position [LDP]
5. Hypoxic Pulmonary Vasoconstriction [HPV]
6. Hypoxemia During OLV
7. Pulmonary Vascular Resistance and Right Ventricle
function
8. Peak Airway Pressure
9. Fluid Management
10. Effect of Anaesthetic Agents
WEST ZONES OF LUNG IN UPRIGHT
POSITION
THESE ZONES ARE NOT ABSOLUTE AND ARE
INTERCHANGEABLE BASED ON

 PERFUSION/ VOLUME STATUS

 CARDIAC CYCLE(SYSTOLE/DIASTOLE)

 DECUBITUS

 PRESSURE USED DURING VENTILATION

 PULMONARY VASCULAR RESISTANCE

 HETEROGENOUS HPV
BLOOD FLOW -LDP, AWAKE, CLOSED
CHEST, SPONTANEOUS BREATHING
RIGHT LUNG LEFT LUNG

 When the right lung  When the left lung is

is nondependent, it nondependent, it
should receive should receive
approximately 45 % approximately 35 %
of total blood flow as of total blood flow as
opposed to the 55 % opposed to the 45 %
of the total blood of the total blood
flow that it receives in flow that it receives in
the upright and the upright and
supine positions supine position.
VENTILATION-LDP,AWAKE, CLOSED CHEST,
SPONTANEOUSLY BREATHING
 Gravity also causes a vertical gradient in the pleural
pressure, ventilation is relatively increased in the
dependent compared with the non dependent lung.

 The dome of the lower diaphragm is pushed higher

into the chest thus contract more efficiently than the
dome of the upper diaphragm.
V/QMATCHING LDP,AWAKE,CLOSED
CHEST,SPONTANEOUSLY BREATHING

 Blood flow and ventilation are significantly greater in

the dependent lung than the non-dependent lung.

 As most of the perfusion is to the dependent lung,

the V/Q matching is maintained in the lateral position
similar to that of upright position.
LDP, ANAESTHETIZED, SPONTANEOUS
VENTILATION , CLOSED CHEST
 The induction of general anaesthesia does not cause
significant change in the distribution of blood low.

 Induction of general anaesthesia causes a reduction

in the volumes of both lungs secondary to a reduction
in FRC.

 Thereduction in volume in the dependent lung is

greater than that in the non-dependent lung because,
1. The cephalad displacement of the dependent
diaphragm by the abdominal contents is more
pronounced.

2. The mediastinal structures pressing on the

dependent lung or

3. poor positioning of the dependent side on the

operating table prevents the proper expansion of the
lung.
 These factors will move lungs to a lower volume on
the S-shaped volume–pressure curve .

 The nondependent lung moves to a steeper position

on the compliance curve and receives most of the
ventilation, whereas the dependent lung is on the flat
(noncompliant) part of the curve. This results in a
significant V/Q mismatch
ARTIFICIAL VENTILATION,CLOSED
CHEST
 Here, the highly curved diaphragm of the lower lung
is no longer actively contracting.
 Mediastinum rests on the lower lung and physically
impedes lower lung expansion.
 The weight of the abdominal contents pushing
cephalad, against the diaphragm is greatest in the
dependent lung.
 Suboptimal Patient positioning

All these lower lung expansion and

disproportionately decreases FRC.
LDP, AWAKE, BREATHING
SPONTANEOUSLY, OPEN CHEST
 Withthe non-dependent hemithorax open,
atmospheric pressure in that cavity exceeds the
negative pleural pressure in the dependent
hemithorax.

 Thisimbalance of pressure on the two sides of the

mediastinum causes a further downward
displacement of the mediastinum into the dependent
thorax.
Two complications can arise from the patient
breathing spontaneously with an open chest
1. MEDIASTINAL SHIFT
2. PARADOXICAL RESPIRATION

MEDIASTINAL SHIFT- More during inspiration

There is negative pressure in the intact
hemithorax, compared with the less negative
pressure of the open hemithorax, can cause the
mediastinum to move vertically downward and
push into the dependent hemithorax
 Thetidal volume in the dependent lung is decreased
by an amount equal to the inspiratory displacement
caused by mediastinal movement.

 This phenomenon is called Mediastinal shift.

 Themediastinal shift can create circulatory and reflex

changes that may result in a clinical picture similar to
that of shock and tension pneumothorax.
PARADOXICAL RESPIRATION-

• During inspiration, the relatively negative

pressure in the intact hemi-thorax compared
with atmospheric pressure in the open hemi-
thorax can cause movement of air from the
nondependent lung into the dependent lung.
The opposite occurs during expiration.

• This reversal of lung movement with an open

chest during respiration has been termed
Paradoxical respiration.
• This gas movement reversal from one lung to
the other represents wasted ventilation and can
compromise the adequacy of gas exchange.

• Paradoxical breathing is increased by a large

thoracotomy or by an increase in airway
resistance in the dependent lung.

• PREVENTION- controlled positive pressure

ventilation OR adequate sealing
LDP, ANAESTHETIZED, SPONTANEOUSLY BREATHING,
OPEN CHEST
 Opening the chest has little impact on the distribution
of perfusion.

 However, the upper lung is now no longer restricted

by the chest wall and is free to expand.

 Thisresults in a further increase in V/Q mismatch as

the nondependent lung is preferentially ventilated,
owing to a now increased compliance.
LDP, ANAESTHETIZED, MUSCLE PARALYSIS,
CHEST OPEN
 Duringparalysis and positive-pressure ventilation,
diaphragmatic displacement is maximal over the
nondependent lung.

 Here,
there is the least amount of resistance to
diaphragmatic movement caused by the abdominal
contents.

 This
further compromises the ventilation to the
dependent lung and increases the V /Q mismatch.
OLV, ANAESTHETIZED, PARALYSED,
CHEST OPEN
 Theessential difference between two lung and one
lung ventilation is that during one lung ventilation the
non-ventilated lung has some blood flow.

 Therefore,
an obligatory shunt which is not present
during two lung ventilation is created .
BLOOD FLOW IN TLV VS OLV
 During two-lung ventilation [TLV] in the lateral
position, the mean blood flow to the nondependent
lung is assumed to be 40% of cardiac output, whereas
60% of cardiac output goes to the dependent lung.

 Normally, venous admixture (shunt) in the lateral

position is 10% of cardiac output and is equally
divided as 5% in each lung.

 Therefore, the average percentage of cardiac output

participating in gas exchange is 35% in the
nondependent lung and 55% in the dependent lung.
 OLV creates an obligatory right-to-left
transpulmonary obsolute shunt through the
nonventilated, nondependent lung because the V/Q
ratio of that lung is zero.

 In
theory, an additional 35% should be added to the
total shunt during OLV.

 However,assuming active HPV, blood flow to the

nondependent hypoxic lung will be decreased by 50%
and therefore it is (35/2) = 17.5%.
 Tothis, 5% must be added, which is the obligatory
shunt through the nondependent lung. Therefore the
total shunt in NDL is 22.5%

 Togetherwith the 5% shunt in the dependent lung,

total shunt during OLV is 22.5% in NDL + 5% in DL =
27.5%. This results in a Acceptable PaO2 of
approximately 150 mm Hg (FiO2 = 1).

 Because 72.5% of the perfusion is directed to the

dependent lung during OLV, the matching of
ventilation in this lung is important for adequate gas
exchange.
VENTILATION IN OLV
 The dependent lung is no longer on the steep
(compliant) portion of the volume–pressure curve
because of reduced lung volume and FRC.
 The causes for this reduction in FRC are:

1. General anaesthesia

2. Paralysis

3. pressure from abdominal contents

4. compression by the weight of mediastinal
structures
5. suboptimal positioning on the operating table.
 Other considerations that impair optimal ventilation
to the dependent lung include
1. absorption atelectasis,
2. accumulation of secretions, and

3. the formation of a transudate in the dependent

lung.

 Allthese create a low V/Q ratio and a large P(A–a)O2

gradient.
PREDICTORS OF IOH DURING OLV-INCIDENCE 4 -10%

•FUNCTIONAL STATUS(dyspnea, ASA score)

•PFT(FEV1),DLCO ,V/Q SCAN

•RT VS LT LUNG RESECTION(RT >LT)

• DISEASE AND EXTENT OF RESECTION

•TUMOUR CENTRAL(COMPRESSION ON SAME

SIDE(NDL) -LESS SHUNT VS PERIPHERAL TUMOUR

•USE OF CAPNOTHORAX IN VATS

•FACTORS AFFECTING HPV
ROLE OF HPV IN OLV
 HPV is a reflex contraction of vascular smooth muscle
in pulmonary circulation in response to low regional
partial pressure of oxygen(PAo2>>.mixed venous
Po2).

 Thus diverts blood area atelectatic/hypoxic alveoli

to better ventilated alveoli minizing shunt. Response
is greatest in distal pulmonary arteries.
BIPHASIC NATURE OF HPV

 Phase 1 begins within a few seconds and is complete at 15 min. With moderate hypoxia
(Po2 30 to50mmHg),sustained for more than 30 to 60 min, phase 2 of HPV begins- with
further increase in pulmonary vascular resistance(PVR) is seen,reachinfg peak at 2hrs.
 It can also be seen from figure that when normoxia returns after a sustained period of
hypoxia, PVR does not immediately return to baseline, indicating a mechanism that
takes hours to reverse.
 Greater hypoxemia when alternatively two lung are to be operated in same time.
The greatest impact of HPV is seen
when the percentage of lung that is
hypoxic is intermediate(between
30-70%)as seen in OLV
Hypoxemia during OLV.

An arterial oxygen saturation of less than 90% with

an Fio2 of 1.0 is commonly accepted as a level at which
some intervention by the attending anesthesiologist is
required.

 Currently Incidence 5% previously = 25% as several

advances have reduced the outcome

1.Use of FOB to position DLTs and BBs led to better

ventilation during OLV
2.better understanding physiology of OLV
3.improved anesthetic agents (halothane had high
incidence of of desaturation)
FACTORS AFFECTING HPV
Augmenting Inhibiting
 very high or very low pulmonary artery
 low Alveolar paO2 > mixed pressures
venous saturation  high or very low mixed venous PO2
 Atelectasis  HighC.O,Hypocapnia,Hypothermia
 at FRC- lowest PVR  vasodilators such as nitroglycerin,
 Low CO nitroprusside, PDI (milrinone , amrinone
 Anaemia AND sildenafil), β-adrenergic agonists,
CCB, Inhaled NO
 Almitrine
 Acetazolamide-PASMCs,
 Patients with prior respiratory
disease have greater HPV
 Steriods ,Endothelin antagonists –
Bosentan, sitaxsentan)
 AC enzyme inhibitors or AT II receptor
blockers
 activation of epidural
 inhalation anaesthetics(ether ?N2O
halothane).higher MAC (of other inhaled
anaesthetics)
Schematic relation between Pao2 and cardiac output
during one-lung ventilation (OLV). As cardiac output decreases
below baseline, arteriovenous shunt (Q˙ s/Q˙ t) decreases,
but the mixed venous oxygen saturation ( SvO2 ) also
decreases resulting in a net decrease in Pao2. Conversely,
raising cardiac output above baseline tends to increase not
only SvO2 but also Q˙ s/Q˙ t, and the net result again is a decrease in
Pao2. Pao2 = arterial oxygen tension
OTHER MODIFIERS OF HPV
 Surgical retraction can assist HPV by increasing PVR
in the operative lung,
 However, the release of vasoactive substances
secondary to the manipulation may conversely result in
an inhibition of HPV .
 Ligation of pulmonary vessels during lung resection
results in the permanent exclusion of vascular territory
and thereby a reduction in shunt flow .
 The side of surgery influences the extent of shunt flow,
as the larger right lung receives a 10% higher proportion
of CO than the left lung.
 Positioning is important as the lateral decubitus
position allows for a gravity induced reduction in
shunt flow to the nondependent lung.

 Procedures that call for supine positioning, on the

other hand, are hampered by higher shunt flow to
the nondependent lung and may have higher rates of
intraoperative desaturations.

 Similarly, addition of a head-down tilt to the left

lateral position has been shown to worsen
oxygenation during OLV, likely due to dependent lung
compression by abdominal contents.
MANAGEMENT OF ONE LUNG VENTILATION
 Thoroughly denitrogenate the operative lung before
collapse

 Continue TLV as long as possible

 Recruitmentmanoeuvre (holding the lung at peak

end expiratory pressure of 20cm H2O for 12 to 20
sec) immediately after the start of OLV to decrease
atelectasis

 Increase expiratory phase if auto peep is likely

 allowpermissive hypercapnia
 Avoid over-inflation

 Avoid ? N2O/higher MAC of volatile anaesthetics

 Peep for dependant lung and CPAP for NDL

 Crystalloids <3l in first 24hrs.blood loss replaced by

blood or colloids.Excessive crystalloids may
contribute to intrapulmonary shunting in DL
resulting in lower lung syndrome-gravity dependant
transdudation.
 Patients with obstructive pathology may develop
intrinsic PEEP.
 In these patients, the application of external PEEP
may lead to unpredictable levels of total PEEP.
 Although the management of one-lung ventilation
has long included the use of 100% oxygen, evidence
of oxygen toxicity has accumulated both
experimentally and clinically.
 some clinicians recommend titrating Fio2 to maintain
the oxygen saturation above 90%, especially in
patients who have undergone adjuvant therapy and
are at risk of developing ALI.
REFERENCES

 MILLERS ANAESTHESIA
 BARASCH CLINICAL ANAESTHESIA

 MORGAN AND MIKHIAL ANAESTHESIA

 BENUMOFF’S

 Hypoxic Pulmonary Vasoconstriction, Physiology and

Anesthetic Implications, by Andrew B. Lumb, and
Peter Slinger.
THANK
YOU