a physiological approach to one- lung ventilation … · a physiological approach to one-lung...
TRANSCRIPT
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A PHYSIOLOGICAL APPROACH TO ONE-LUNG VENTILATIONA. NEYRINCK, MD, PhDUniversity Hospitals Leuven
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OUTLINE
• physiology of lateral decubitus
• goals of one-lung ventilation
• lung collapse
• mechanisms and treatment of hypoxemia
• avoiding lung injury
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WELCOME TO…
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LATERAL DECUBITUS
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GOAL OF ONE-LUNG VENTILATION
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AVOID HYPOXEMIAAVOID LUNG
INJURYOPTIMIZE COLLAPSE
ONE-LUNG VENTILATION
PROTOCOLIZED APPROACH
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OPTIMIZING LUNG COLLAPSE
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OLV
LUNG ISOLATION LUNG SEPARATION
to avoid contamination withblood, pus, secretions, lavage
functional – to optimizesurgical exposure
DLT DLT
BBRIGHT LEFT
•lesion left main stem bronchus•(large thoracic aortic aneurysm)
•bilateral intervention•pneumectomy•sleeve lobectomy•lobectomy•lung transplantation(SLTX – SSLTX)
LEFT
•ETT – SLT in situ•unanticipated OLV required during procedure•(tracheal bronchus)•segmentecomy
•mediastinal surgery•esophagectomy•cardiac surgery•other non-pulmonary surgery requiring OLV
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DEVICE: DLT VERSUS BB
NarayanaswamyNarayanaswamyNarayanaswamyNarayanaswamy M et M et M et M et al.al.al.al. AnesthAnesthAnesthAnesth AnalgAnalgAnalgAnalg 2009;108:10972009;108:10972009;108:10972009;108:1097----1101110111011101
bronchial blocker: deflation of both lungs before inflation of BB
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GAS MIXTURE:DE-NITROGENATION
KoKoKoKo R et al. R et al. R et al. R et al. AnesthAnesthAnesthAnesth AnalgAnalgAnalgAnalg 2009 108: 10922009 108: 10922009 108: 10922009 108: 1092----6666
FiO2 = 0.4
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SUCTIONING
NarayanaswamyNarayanaswamyNarayanaswamyNarayanaswamy M et M et M et M et al.al.al.al. AnesthAnesthAnesthAnesth AnalgAnalgAnalgAnalg 2009;108:10972009;108:10972009;108:10972009;108:1097----1101110111011101
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AVOIDING HYPOXEMIA
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INCIDENCE
Author Year IncidenceTarhan et al. 1973 25%
Kerr et al. 1974 24%
Slinger et al. 1993 8%
Hurford et al. 1993 9%
Schwarzkopf et al. 2001 4%
Brodsky et al. 2003 1%
Ehrenfeld et al. 2008 10%
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SIGNIFICANCE: POCD
increased risk POCD when SctO2 < 65%
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PREDICTION OF HYPOXEMIA55 y.o. F, EmphysemaFEV1= 28%
60 y.o. M, Lung Ca.Non-smoker, FEV1= 98%
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PREDICTION OF HYPOXEMIA
• right versus left thoracotomy/scopy
• elastic recoil
o low FEV1: airtrapping
o prevention of atelectasis in dependent lung
o delayed collapse of non-dependent lung
o conflicting evidence
• preoperative PaO2
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PREDICTION OF HYPOXEMIA: DISTRIBUTION OF PERFUSION
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PREDICTION OF HYPOXEMIA: DISTRIBUTION OF PERFUSION
V/Q to the surgical side
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PREDICTION OF HYPOXEMIA: END-TIDAL CO2 DIFFERENCE
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MECHANISM OF HYPOXEMIA
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MECHANISM OF HYPOXEMIA
• right-to-left shunt
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DETERMINANTS OF HYPOXEMIA
• shunt equation
o Qs/Qt = (CcO2 – CaO2) / (CcO2 – CvO2)
o CaO2 = CcO2 – (CcO2 – CvO2) . (Qs/Qt)
• mixed venous oxygen content
o CvO2 = CaO2 – (VO2/Qt)
• CaO2 = CcO2 – (VO2/Qt) . (Qs/Qt)
(10(1 – Qs/Qt))
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DETERMINANTS OF HYPOXEMIA
• VO2 : oxygen consumption (mixed venous saturation)
• Qs/Qt: shunt fraction
• Qt: cardiac output
• CcO2: haemoglobin content – alveolar ventilation
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EFFECT OF SHUNT FRACTION AND APPROPRIATE MANAGEMENT
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SHUNT FRACTION
dependent lung
non-dependent lung
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CvO2
shunt fraction
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: HPV
• optimizes V/Q (reduction 40%)
• contraction smooth muscle
• PAO2 40-100 mmHg
• determinants: PAO2 and PvO2
• early response 15 min
• maximal response 4 h
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: HPV and ANESTHETIC TECHNIQUE
• Halothane/ Enflurane
• Isoflurane/ Desflurane/ Sevoflurane
• Total Intravenous Anesthesia (TIVA)
• Combined TEA plus General Anesthesia ?
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SHUNT: APPROACH TO NON-DEPENDENT LUNG
• insufflation
• CPAP
• IPAP (intermittent positive
airway pressure)
• modified CPAP
• HFJV
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: CPAP
Limited use during thoracoscopic procedures due to decreased visualisation
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: IPAP
• 6 aliquots of 70 ml
• 2lO2 – 2 sec – 8 sec
Russell Anaesth Intensive Care 2009
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: MODIFIED CPAP
Ku et al. JCVA 2009; 23: 850-852
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: HFJV• one-lung ventilation
o air-trappingo improved RV function
• as alternative for CPAPo optimal exposure
• to avoid one-lung ventilation (2-lung HFJV)o lower peak pressures
• Settings:o frequency +/- 180o pressure 1.8 – 2.2 baro higher PCO2 levels
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SHUNT: DEPENDENT LUNG
• HIGH TIDAL VOLUMES WITHOUT PEEP
• LOW TIDAL VOLUMES WITH PEEP
• RECRUITMENT BEFOR OLV
• PEEP• effect not predictable• evaluate oxygenation/compliance
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
PaO2mmHg
PEEP CPAPOLV PEEP+CPAP
Capan L, et al. Anesth Analg 59: 847, 1980, Lung Ca., FEV1= 70%Fugiwara M, et al. J Clin Anesth 13: 473: 2001, Esoph. Ca.
2LV
*
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
Auto-PEEP
Lower InflectionPoint
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
Auto-PEEP
Lower InflectionPoint
Total PEEP
• total PEEP increases less• dynamic hyperinflation
•shunt•hemodynamic collaps
•response not predictable
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
Auto-PEEP
Lower InflectionPoint
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
Auto-PEEP
Lower InflectionPoint
TotalPEEP
• total PEEP increases more• improved oxygenation
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
PEEP-responders (>20%) PEEP-NON-responders
not studied if PO2<60mmHgprediction not possibleno recruitment maneuvres
Hoftman et al. Ann Card Anaesth 2011; 14: 183-187
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
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SHUNT: APPROACH TO DEPENDENT LUNG: PEEP
• PEEP improves oxygenation
• mandatory when using lower volumes
• effect not predictable
o observe clinical effect on oxygenation
o observe improvement in compliance
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SHUNT: APPROACH TO NON-DEPENDENT LUNG: RECRUITMENT
RECRUITMENT
• 20 – 40 cmH2O• followed by PEEP• improves oxygenation• reduces inflammation• transient decrease in CO – significance?• repeated recruitment?
BEFORE OLV (2-LUNGS)
DEPENDENT LUNG (OLV)
NON-DEPENDENT LUNG (OLV
Unzueta et al BJA 2012Park et al EJA 2011; 28: 298-302
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TV 10 ml/kg
TV 5 ml/kg PEEP 5
TV 5 ml/kg PEEP 0
NO RECRUITMENT MANEUVERS!
Kim J Anesth 2012
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SHUNT: DEPENDENT LUNG –VASODILATORS (NO)
Wilson et al 1997
40 PPM no decrease in PVR no improvement oxygenation
Fradj et al 1999
20 PPM no decrease in PVR no improvement oxygenation
Rich et al 1994
20 PPM decrease in PVR when light PH (25-35 mmHg)
Moutafis et al 1997
20 PPM +Almitrine (16γ)
improved oxygenation
no effect on PAP and oxygenation in abscence of hypoxia or PHexcessive vasodilation by isoflurane or thoracic epidural?
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EFFECT OF CARDIAC OUTPUT AND APPROPRIATE MANAGEMENT
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CARDIAC OUTPUT
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CARDIAC OUTPUT
PaO2
Cardiac Output %
100
Qs/Qt
SvO2
100
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CARDIAC OUTPUT
• excessive increase in cardiac output
o �MvSO2 ��HPV
o �PAP ��perfusion of non-ventilated areas ��HPV
o inotropes ��HPV
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EFFECT OF OXYGEN CONSUMPTION AND APPROPRIATE MANAGEMENT
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OXYGEN CONSUMPTION
• lower oxygen consumption: higher MvSO2
• high dose anesthetics beneficial
o <>decrease in cardiac output
o high opiods – low anesthetic
• inotropes
o increase oxygen consumption
o <>effect on cardiac output more pronounced
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EFFECT OF CcO2 AND APPROPRIATE MANAGEMENT
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HEMOGLOBIN CONCENTRATION
• effect on CcO2
Hb 15
Hb 15
Hb 10Hb 10
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HEMOGLOBIN CONCENTRATION
• effect on CcO2
• hemodilution
o decreases PO2 in COPD patients
o effect on shunt - HPV?
• higher hematocrit (45%)
o predicts low PO2
o polycytemia due to higher shunt?
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ALVEOLAR VENTILATION AND FiO2
• effect on CcO2
• PAO2 = PiO2 – (PaCO2/RQ)
(increasing alveolar ventilation)
<> lower cardiac output<>increased shunting<>protective ventilation
increasing FiO2
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EFFECT OF TEA
• decrease in CO (sympathicolysis)
• decrease in HPV
• effect still unknown
• less influence when low dose LA and maintenance of CO
• ropivacaine 0.75%: �PO2
• dexmedethomidine: �PO2
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AVOIDING LUNG INJURY
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EVIDENCE OF LUNG INJURY
• epithelial lining fluid /broncho-alveolar lavage/systemic
Komatsu inflammation 2012
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EVIDENCE OF LUNG INJURY
• one-lung ventilation induces
o systemic inflammation
o pulmonary inflammation dependent lung
o pulmonary inflammation non-dependent lung
o indication for neutrophilic injury
o duration of one-lung ventilation• 100 – 300 min.
o Peak AwP > 35 CmH2O
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MECHANISM OF LUNG INJURY
Atelectrauma (open lung concept)•Repetitive opening and closure of atelectatic zones•recruitment and PEEP
Overdistention (baby lung)•volutrauma in functional reduced lung volume•reduction in tidal volume
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LUNG INJURY IS MULTIFACTORIAL
VENTILATION
EXCESS FLUIDADMINISTRATION
INFLAMMATION
CAPILLARY LEAKINTERSTITIAL FLUID
RIGHT HEART FAILURE
REDUCED LYMPH FLOW
ANATOMICAL RESECTION
REDUCED PULMONARY
VASCULAR BED
ALI/ARDS NODAL DISECCTION
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MECHANISM OF LUNG INJURY OLV
VENTILATED LUNG COLLAPSED LUNG SYSTEMIC
• hyperoxia•reactive oxygen species•oxygen toxicity
•hyperperfusion•endothelial damage•vasculare pressure
•ventilatory stress•volutrauma•atelectrauma•barotrauma
• OLV•ischemia/reperfusion•reexpansion•cytokine release•altered redox state
•Surgery•manipulation trauma•lymphatic disruption
• cytokine release•reactive oxygen species•overhydration•chemotherapy/radiation
ARDS/ALI
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MECHANISM OF LUNG INJURY OLV: RISK FACTORS• PATIENT
o poor postoperative predicted lung functiono preexisting lung injury
• trauma• infection• chemotherapy
o ethanol abuseo female gender
• PROCEDUREo lung transplantationo major resection (pneumonectomy > lobectomy)o esophagectomy – fluid administrationo transfusiono prolonged OLV (>100 min) Peak pressure > 35-40 cmH2Oo plateau pressure > 25 cmH2O
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MECHANISM LUNG RE-EXPANSION
• !low FiO2!
• !gradual opening!
non-dependent dependent
Leite JCTVA 2012
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MECHANISM OF LUNG INJURY: HISTORICAL FACTS AND PITFALLS• high tidal volumes 10 – 15 ml/kg
o oxygenationo “end-inspiratory alveolar recruitment”
• PPE (postpneumonectomy pulmonary edema)
• low tidal volume in ARDS is beneficial
• outcome? surrogate markers
• effect of protective lung ventilation on healthy lungs
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protective OLV
conventional OLV
OUTCOME
TV (ml/kg) – FiO2 –PEEP (cmH2O)
TV (ml/kg) –FiO2 – PEEP (cmH2O)
Ahn et al. Anaesth Intensive Care 2012
6 – 0.5 - 5 10 – 1 - 0 VATS –preoperative nl lung function
no difference inflammation-oxygenation-outcome
Yang Chest 2011
6 – 0.5 – 5VCV
10 – 1 – 0PCV
decreased infiltration-atelectasis. lower PO2 perop
Licker Crit Care 2009
5 – 0.6 - 6 7 – 0.6 - 3 retrospectiven = 500/group
decreased atelectasis – hospital stay – ICU admission
SchillingA&A 2005
5 - 0.8 - 0 10 – 0.8 - 0 reduced inflammation
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CONFLICT BETWEEN OXYGENATION AND PROTECTIVE VENTILATION?
Rozé BJA 2012
LOWER PO2
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PROTECTIVE LUNG STRATEGY• low tidal volume
o 4-6 ml/kg
• PEEPo 5-10 cmH2O
• PROTECTIVEo lower shunt fractiono improved oxygenationo less atelectasiso lower cytokine release
Yang et al Chest 2011; 139: 530-537Schilling et al A&A 2005; 101: 957-965
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lung recruitment maneuver before OLV andventilation with a VT of 5 ml/kg during OLV isassociated with a more homogeneous distributionof lung tissue in the dependent ventilated lung
Kozian et al. Anesth 2011; 114: 1025-1035
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MODE OF VENTILATION
• up to date no clear benefit for PCV or VCV
• more homogeneous distribution with PCV?
• historical impact of limited AwP
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MODE OF VENTILATION
Rozé H et al. Br. J. Anaesth. 2010;105:377-381
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MODE OF VENTILATION
Rozé H et al. Br. J. Anaesth. 2010;105:377-381
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HYPERCAPNIA?
• consequence of protective ventilation
• reduces inflammation
o subset analysis of ARDS Networko �alveolar-systemic cytokine release
o �neutrophil accumulation
o �radical injury
• improves tissue oxygenation
• improves SjO2 (50 mmHg)
• hypocapnia: induces acute parenchymal lung injury
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EFFECT OF ANESTHETICS ON INFLAMMATION
• VOLATILE ANESTHETICS REDUCE INFLAMMATION
o sevoflurane vs propofol• �plasma IL-6• Lee JCTVA 2012• �BAL IL-6 • Sugasawa J Anesth 2012• �BAL IL-6, TNF-a, IL-8• De Conno Anesthesiology 2009
o isoflurane vs propofol• �plasma and BAL IL-8 and TNF-a• Mahmoud Anesthesiol Res Pract 2011
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Schilling Anesthesiology 2011
EFFECT ON CLINICAL OUTCOME ?
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TAILORED -PROTOCOLIZED APPROACHONE SIZE DOES NOT FIT ALL
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parameter target remark
Fi02 0.9 - reduce to 0.5 if possible (after onset of HPV)
•adjust 5 min prior to OLV •less inflammation with lower FiO2•re-inflation of non-dependent lung with air + recruitment
Tidal Volume 4-6 ml/kg •reduce stretch
Respir Rate increase to maintain MV •cave: increased Vd: higher RR necessary to maintain Va•cave: airtrapping if inadequate E-time: decrease RR•obstructive: I:E = 1:3 / restrictive: I:E = 1:1
Pplat AwP limit to 25-30 cmH20 •allow hypercapnia if necessary•air leak with BB when higher than 25 cmH20
PEEP 5-10 cmH20 •titrate to oxygenation (LIP)•reduces atelectasis – shear-stress•consider auto-PEEP•consider recruitment
PCO2 40 – 60 mmHg •permissive hypercapnia is protective•permissive hypercapnia in case of airtrapping or high Pplat AwP
ventilatory mode PCV -VCV •until now, no evidence for beneficial effect of a specific mode. allow PpeakAwP to be higher during VCV•cave: pressure in circuit is higher than alveolar pressure.
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HYPOXIA
1. increase FiO2 to 1.02. check position DLT/BB3. optimize cardiac output
• preload: 250-500 CC colloids• contractility• arrhytmias
4. recruitment dependent lung• AwP 20-30 cmH20 during 30 sec• followed by PEEP• cave: reduction in C.I.
5. optimize PEEP dependent lung towards LIP (� or �)6. CPAP to non-dependent lung
• recruitment first• 5-10 cmH20• NOT during VATS (surgical exposure)
7. intermittent inflate non-dependent lung (communicate with surgeon)8. partial ventilation of non-ventilated lung
• lobar re-inflation• selective lobar collapse (BB)• oxygen insufflation (consider insufflation in surgical field, cave combustion)• (high frequency ventilation)
9. reduce blood flow to non-ventilated lung• clamping of pulmonary artery (cave increased afterload to right ventricle)• (inhaled NO) (lowering IV or inhalational anesthesia)
10. maintain oxygen carrying capacity11. (ECMO as rescue)
MILD/GRADUAL (90%) SEVERE (<85%)
1. resume 2-lung ventilation2. (communicate with surgeon)3. increase FiO2 to 1.04. check position DLT/BB
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THANK YOU