Mechanics and physiology of lung isolation/ one-lung ventilaion, Anaesthetic implications of one-lung ventilation and management strategies West zones of the lung Ventilation-perfusion mismatch, V-Q Hypoxic pulmonary vasoconstriction

1. DR. ARATI MOHAN BADGANDI
PROBLEMS OF OPEN
CHEST AND
PATHOPHYSIOLOGY OF
ONE-LUNG VENTILATION

2. INTRODUCTION
Principle of one lung ventilation is one lung for the surgeon
and one for the anesthetist.
The collapsed lung gives good access to surgeon and the
uncollapsed lung is used by the anesthetist to oxygenate.
Originally One Lung Ventilation was carried out to prevent
spillage of infected materials, mucous, tumour materials from
diseased Lung to normal Lung during Lung Surgeries.
GALES and waters first reported the use of selective Lung
Ventilation during thoracic surgeries in 1931.
1949 Carlens originated P.V.C disposable DLT.
Rowbatham introduced a DLT in 1962.

3. ADVANTAGES OF OLV
Independent channel for ventilation and suctioning.
Isolation of normal lung from diseased, thereby preventing
contamination by infected secretion, mucous, tumour
materials.
Independent collapse of lung to be operated and reexpansion
when needed.
Provides optional operating condition facilitating easy
approach; retraction of affected area with minimal stretching
and trauma to tissues.
Provides blood less field and shortens the duration of surgery.
Complete collapse of lung facilitates other surgeries - spinal,
laproscopic assisted vagotomy, oesophageal.
Avoids complication of prone position.

4. INDICATIONS OF OLV

6. TECHNIQUES OF PROVIDING OLV
In general three techniques are used-
1. DLT.(DOUBLE LUMEN TUBE).
2. Bronchial Blockers(univent tubes)
3. Single Luman Endobronchial tubes.
Arterial hypoxemia is the main pathophysiological change
during OLV.

7. Pathophysiology in awake patient
with closed chest in lateral
decubitus
During spontaneous ventilation the dependent lung is better
ventilated than the non-dependent one.
On induction of GA with NM paralysis both lungs move down
on the pressure volume curve.
Perfusion:
Dependent lung better perfused.
Blood flow to non dependent lung is decreased by 10%
Rt lung Bf :45% (55%)
Lt lung Bf :35% (45%)

12. PATHOPHYSIOLOGY IN Anesthetised
PATIENT WITH closed chest IN LDP
Perfusion : induction of anesthesia does not cause any change
in perfusion .
Ventilation : GA decreases FRC hence compliance
Mediastinum rests on dependent lung thus impeding
expansion.
Weight of abdominal contents pushing the diaphragm impedes
lower lung expansion.V/Q MISMATCH

13. Compression (with loss of FRC) of the dependent lung and
restriction of its excursion (decrease in compliance) by the
mediastinum.
Cephalad movement of the abdominal organs against the
flaccid diaphragm, and exaggerated flexed position with chest
rolls to free the axillary contents occurs in LDP.
The net result is that the non-dependent lung is better
ventilated - FRC 1.5 times that of the dependent lung.
This leads to (V/Q) mismatching, as the dependent lung is
better perfused and under ventilated and the non-dependent
lung is under perfused and better ventilated.
Gravity has no significant effect on distribution of ventilation
during IPPV in the lat. decubitus position.

14. PATHOPHYSIOLOGY OF ANAESTHETISED
PATIENT WITH OPEN CHEST IN LDP
Perfusion : not altered (dependent> nondependent).
Ventilation: upper lung is better ventilated as it is no longer
restricted by chest wall.
When the non-dependent hemithorax is opened, there is
further increase in FRC and compliance of the non-dependent
lung and a decrease of these parameters of the dependent lung
with two-lung ventilation.
This causes further deterioration of ventilation perfusion
mismatch.
When the non-dependent lung is collapsed, the blood flow to
that lung is not oxygenated leading to increased P (A-a) O2
gradient and impaired oxygenation.

16. PATHOPHYSIOLOGY OF LDP & OLV-
V/Q MISMATCH
V/Q Mismatch is due to creation of an OBLIGATORY RT TO LT
TRANS PULMONARY SHUNT .
During 2 Lung Ventilation in LDP-60% of Cardiac Output (CO)
goes to dependent Lung and 40% to Non dependent Lung
Normal Venous admixture is 10% and is equally shared(5%+5%)
between two lungs.
So average percentage of CO participating in gaseous exchange
in Non-dependent-Lung is 35%; and in dependent Lung in 55%.
In OLV: the dependent lung ventilated with whole of tidal
volume and non-dependent lung in NOT Ventilated, but still
perfused.

17. The result is creation of an obligatory R-L TRANS
PULMONARY SHUNT through Non ventilated non dependent
lung that is 35% of CO-not oxygenated .
Un-inhibited H.P.V. reduce 50% of blood flow to the NON-
VENTILATED Lung - blood flow becomes 17.5% (35/2) and
shunt will be also 17.5% only.
If this is added to 5% of existing shunt the total shunt in NON-
VENTILATED Lung will be 22.5(17.5+5)%.
So altogether in OLV the shunt will be 27.5% (22.5+5) causing
impairement optimal PaO2.
Other factors like absorption atelectasis due to circum ferential
compression of dependent lung
Accumulation of secretion and fluid transudate (particularly in
prolonge surgery and anesthesia) in dependent lung low V/Q
and increase P(A-a) O2 gradient and impaired oxygenation.

19. Awake/closed chest Anesthetized

20. V-Q relationships in the anesthetized, open-chest and paralyzed patients in LDP

21. PHYSIOLOGY OF LDP & OLV-
V/Q MISMATCH
RECTIFIED BY:
Adequate ventilation to dependent lung- increase FIO2
Adjustment of I:E (1:2) ratio
RR to keep CO2 40mg Hg.(20% increase)
Limiting Inspiratory flow and Expiratory airway resistance
(unchanged Minute Ventilation)
Vigilent monitoring of peak inspiratory pressure. Sao2,PETCO2
if possible ABG.
Maintaining optimal CO
Suctioning of dependent lung as and when needed.
Avoiding Over enthusiastic Hyperventilation.

22. Hypoxemia in OLV
 FRC REDUCTION is another important cause of hypoxemia.
 Causes are-
1. In LDP-Shifting intra abdominal content, causes cephaled
shift of Diaphragm reducing FRC.
2. GA and the mechanical effects of ventilation.
3. Weight of sagging Mediastinum
4. Sub-optimal position of the patient with rolls and packs on
the operation table as shoulder support

23. Hypoxemia in OLV
CAN BE OPTIMISED BY:
Vigilent Monitoring of vital parameters
Optimal ventilatory settings of dependent lung so that-
inspiratory pressure not more than 30cm.
PEEP to the ventilated lung to recruit collapsed under
ventilated alevoli of dependent lung
will improve FRC/V/Q ratio and oxygenation

24. Hypoxemia in OLV
Application of CPAP to Non-Ventilated lung,
increases oxygenation by improving V/Q ratio and causing
vasoconstriction; then diversion of perfused blood to dependent
lung.
This can be possible only when there is no major leak of
bronchial tre as not helpful with broncho plural fistula and
massive pulmonary hemorrhage etc.,
Institution of both lung ventilation periodically in long surgical
procedure.
Maintaining optimal CO through out the procedure.

25. HYPOXIC PULMONARY VASOCONSTRICTION
 HPV is an auto regulatory mechanism that maintain Pao2 by
decreasing amount shunt flow through hypoxic non
ventilated lung.
 HPV primarily occurs in pulmonary arterioles of 200µm
diameter which are situated close to small bronchiole and
alveoli.
 Precise mechanism of HPV not known.
 Various theories have been put forth:
Direct action on pulmonary smooth muscle cells, sensed
by mitochondrial electron transport chain ,reactive oxygen
species(H2 O2superoxide ) acting as second messengers to
increase calcium content resulting in vasoconstriction.
Endothelial derived products potentiate (eg:leucotrines)
and attenuate (NO PGI2) HPV.

26. Factors determining HPV are:
1. Distribution Hypoxia (in non ventilated lung) causing
vasoconstriction and directing CO to normoxic lung and
reducing shunt fraction.
2. Atelectasis of non ventilated lung-causing increased PVR and
vasoconstriction and direct blood flow to normoxic lung, then
decreasing shunt traction.
3. Vasodilator drugs directly inhibits HPV but indirectly by
decreasing CO and lower Pvo2 thereby producing potent
stimulation of HPV in normoxic lung and offset HPV in the
original hypoxia lung and results in no flood diversion from
more obviously Hypoxia Lung.

27. 4. Vasoconstrictors will preferentially constricts pulmonary
vessels perfusing both lung segments and may direct blood to
hypoxia lung due to vasoconstriction in normoxic lung vascular.
5. Selectively decreasing FiO2 in normoxic compartment (1 to .5 to
.3) causes on increase in vascular resistance there by decreasing
blood flow diversion from hypoxic lung to normoxic lung.

29. Diagram of the tracheo bronchial tree

30. DLTs,
bronchial blockers, or
 single-lumen endobronchial tubes (SLTs)
Lung-Isolation Techniques

31. Carlens, a left-sided + a carinal hook
a right-sided Carlens tube
Bryce-Smith, no hook but a slotted cuff/Rt
Robertshaw, most widely used
1. Type:
All have two lumina/cuffs, one terminating in the trachea and the
other in the mainstem bronchus
Right-sided or left-sided available
Available size: 26F, 28F, 32F ,35F, 37F, 39F, 41F.

32. Double lumen endotracheal
tubes
Selection of Double-Lumen Tube Size Based on Adult Patients’ Sex and Height
Sex
Height (cm) Size (Fr)
Female <160 (63 in.) * 35
Female >160 37
Male <170 (67 in.) † 39
Male >170 41

33. INDICATIONS FOR RT DLTs
*exophyptic tumour that compresses the entrance of lt
bronchus
*intraluminal tumour near entrance of lt bronchus
*lt-sided tracheo broncheal disruption
*descending thoracic aortic aneurysm compressing the main
stem bronchus.

35. Insert tip of tube through cords and immediately rotate 90 degrees in direction of
bronchus you are aiming to intubate.
2. Advance tube until comes to a halt. (No xs force needed).
3. Inflate tracheal cuff until air leak disappears & check both lungs ventilate (just as you
would a single lumen tube).
4. Clamp tracheal lumen & check that only opposite side of chest moves and has air
entry. Remember to open cap on clamped side so air can escape and lung collapse. You
should feel a ‘whoosh’ of air as lung collapses. Make sure your clamp is proximal to the
open cap or you will have trapped the air in the lung.
5. Inflate bronchial cuff until no leak is heard via tracheal lumen. Need about 2 mls air
6. Repeat 4. By clamping bronchial lumen instead of tracheal.
7. Switch on ventilator and collapse lung to be operated on. Check
you can achieve a reasonable tidal volume without excessive
pressure and that the capnograph trace has not changed compared
to 2-lung ventilation.
INSERTION TECHNIQUE

37. Bronchial blockers

38. These devices are either within a modified SLT as an enclosed bronchial
blocker (Torque Control Blocker Univent; Vitaid, Lewinston, NY) or are used
independently with a conventional SLT,
the Arndt wire-guided endobronchial blocker (Cook Critical Care, Bloomington, IN),
Cohen tip-deflecting endobronchial blocker (Cook Critical Care, Bloomington, IN),
and the Fuji Uniblocker (Vitaid, Lewinston, NY).
Bronchial blockers

39. Characteristics of the Cohen, Arndt, and Fuji Bronchial Blockers
Cohen
Blocker
Arndt Blocker
Fuji
Uniblocker
Size 9 Fr 5 Fr, 7 Fr, and 9 Fr 5 Fr, 9 Fr
Balloon shape Spherical Spherical or elliptical Spherical
Guidance
mechanism
Wheel
device to
deflect the
tip
Nylon wire loop that is
coupled with the
fiberoptic
bronchoscope
None,
preshaped tip
Smallest
recommended ETT
for coaxial use
9 Fr (8.0
ETT)
5 Fr (4.5 ETT), 7 Fr
(7.0 ETT), 9 Fr (8.0
ETT)
9 Fr (8.0
ETT)
Murphy eye Present Present in 9 Fr Not present
Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID

40. Arndt Endobronchial Blocker
set
Invented by Dr. Arndt, an anesthesiologist
Ideal for diff intubation,
pre-existing ETT and postop ventilation needed
Requires ETT > or = 8.0 mm
Similar problems as Univent
Inability to suction or ventilate the blocked lung

42. It is useful when it is not possible to place a DLT or in situations where the patient
has already been intubated with a single lumen tube.
It has the appearance of a hollow bougie with a cuff.
The blocker has a guidewire in its lumen, the end of which can be hooked over a
bronchoscope so the blocker can be inserted under direct vision into the
lung that is to be collapsed.
This guidewire needs to be removed before air can be withdrawn from the blocker
and hence collapse the lung.
A disadvantage is that once the guidewire on the device has been
withdrawn,
it cannot be reinserted so the blocker cannot be reused or repositioned in
the patient.
INSERTION TECHNIQUE

43. Univent Tube
Developed by Dr. Inoue
Movable blocker shaft in external lumen of a single-
lumen ET tube
Easier to insert and properly position than DLT (diff
airway, C-s injury, pedi or critical pts)
No need to change the tube for postop ventilation
Selective blockade of some lobes of the lung
Suction and delivery CPAP to the blocked lung

45. Bronchial blockers (BB)
Arndt
Cohen
Fuji
Size selection rarely an
issue
Easily added to regular
ETT
Allows ventilation during
placement
Easier placement in
patients with difficult
airways and in children
Postoperative two-lung
ventilation by
withdrawing blocker
Selective lobar lung
isolation possible
CPAP to isolated lung
possible
More time needed for
positioning
Repositioning needed more
often
Bronchoscope essential for
positioning
Non optimal right lung
isolation due to RUL anatomy
Bronchoscopy to isolated lung
impossible
Minimal suction to isolated
lung
Difficult to alternate OLV to
either lung
Advantages
Disadvantages

46. Univent tube Same as BBs
Less repositioning
compared with BBs
Same as for BBs
ETT portion has higher air flow
resistance than regular ETT
ETT portion has larger diameter
than regular ETT
Endobronchial
tube
Like regular ETTs,
easier placement
in patients with
difficult airways
Longer than
regular ETT
Short cuff
designed for lung
isolation
Bronchoscopy
necessary for placement
Does not allow for
bronchoscopy,
suctioning or CPAP to
isolated lung
Advantages disadvantages

47. Positioning
The majority of thoracic procedures are performed with the patient in
the lateral position, most often the lateral decubitus position, but,
depending on the surgical technique, a supine, semisupine, or semiprone
lateral position may be used .These lateral positions
have specific implications for the anesthesiologist.

48. Complications associated with
position
Dependent Arm (Compression Injuries)
 Arm directly under thorax
 Pressure on clavicle into retroclavicular space
 Cervical rib
 Caudal migration of thorax padding into the axilla *
Nondependent Arm (Stretch Injuries)
Lateral flexion of cervical spine
Excessive abduction of arm (>90%)
S emiprone or semisupine repositioning after arm fixed to
a support

49. Neurovascular Injuries Specific to the Lateral Position:
Dependent eye
Brachial plexus
Circulation
Dependent ear pinna
Cervical spine in line with thoracic spine
Dependent arm:
Nondependent arm * :
Dependent and nondependent suprascapular nerves
Nondependent leg: sciatic nerve
Dependent leg:
Peroneal nerve
Circulation

50. Predictive post-operative
respiratory asseament

51. lculated as
Preoperative FEV1 х(1-nosegmentsremoved/19)
A PPOfev1 < 1 lt= retention of sputum
 <800ml= contrindication( vent dependent)
<40%= perioperative complication.
ppoDLCO= PREOPERATIVE DLCOх( 1- no segments removed/19)

54. SUMMARY
On conclusion ventilation of One Lung with 100%O2, the
application of CPAP to Non ventilated lung and
intermittent positive pressure to dependent lung counter
act any drug mediated effects of HPV and maintain PaO2.
So maintaining uninhibited HPV is very important for
maintaining normal V/Q and Pao2.

55. THANK
YOU