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Physiology of Assisted Ventilation
www.walidhabre.org
Walid Habre, MD, PhD Anesthesiological Investigations Unit
& Pediatric Anesthesia Unit Geneva University Hospitals and University of Geneva
I have no COI to disclose
How to address the challenges in anesthesia
General anesthesia promotes « Lung heterogeneity » Positive pressure ventilation has a cost
on various physiological variables
Soni N. Br J Anaesth. 2008;101:446-57
Pulmonary system
Cardiovascular system
Variable compliance- dependent ventilation
Compresses capillaries alter perfusion
Effect on surfactant Alter compliance
îVenous return
îLymphatic flow
îCardiac output îVentilation/Perfusion
ì Central Venous Pressure
Lymphatics
Outline
• Physiological characteristics • Physiological effects on the lung
• Cardio-respiratory interaction • Physiology effects and monitoring
Passive system (exchanger) - Airways:
* RESISTANCE : flow R = ΔP (P2-P1) Flow - Lungs - Alveoli:
* COMPLIANCE : Volume C = Volume ΔP’ (P2’-P1’)
Active system (pump) - Respiratory muscles
(diaphragm, accessory muscles…)
Respiratory system
2
Impedance of the respiratory system
Elastic forces
Necessary for the distension of an elastic structure
Elastance
Compliance
(1 / Elastance)
Resistive forces
Resistance to air flow
Inertance
Resistance resulting from tissue distorsion
MOLECULAR Surfactant
FONCTIONAL
Viscoelastic
properties
HAEMODYNAMIC
Capillaries
MORPHOLOGY Extracellular
Matrix
Molecular Lamellar bodies containing surfactant Alveolar lining fluid
SURFACTANT
Pneumocytes II
Pneumocytes I
ALVEOLI
Water molecules
High surface tension
Strong attractive forces
Alveolar Collapse
Reduces surface tension
Surfactant interperses the water molecules
Lung stability
Morphology
Suki B et al. Compr Physiol 2011; 1:1317-1351
Extracellular matrix
Elastin
Collagen
Fibroblast cells
Proteoglycans
Basement membrane
Function
Suki B et al. Compr Physiol 2011; 1:1317-1351
Viscoelasticity
of the lung
Collagen Elastin Coupling of the elastic and dissipative properties
Low strain Increase strain
INDIRECT EFFET Regulatoiry mechanism
(mediators, neuronal control)
Abrupt change in lung haemodynamics
Change in the mechanical properties of the lung
Haemodynamic
DIRECT EFFECT Mecanical interdependence
3
Outline
• Physiological characteristics • Physiological effects on the lung
• Cardio-respiratory interaction • Physiology effects and monitoring Pavone L et al. Critical Care 2007, 11:R104
Restrictive profile ê Fuctional residual capacity
Airway Closure Lung Collapse
Atelectasis
Postoperative respiratory complications
Anaesthesia
Surgery
Patients
Tusman G et al. Curr Opin Anaesthesiol 2012; 25:1-10
Postoperative respiratory complications
Decrease DO2
Ischemia-reperfusion lesions
Delirium
Wound infection
Arrhythmias/myocardial ischemia
Hypoxaemia Pneumonia
Macrophages dysfunction
Surfactant depletion
Bacterial development
Bacterial Translocation
Local inflammatory response/*VILI Local Hypoxia/hyperoxia
Local mechanical parenchymal stress/shear stress
Biotrauma
Cyclic recruitment
Alveolar distension
(*VILI: « ventilator induced lung injury »)
Grosse-Sundrup M et al. BMJ 2012;345:bmj.e6329
Hypoxemia : major cause of morbidity and mortality in the perioperative setting
Respiratory • Upper airway obstruction • Pneumothorax/hemothorax
Postoperative Reintubation
0
10
20
30
40
50
60
70
80
Pulmon
ary
Respir
atory
Céereb
ral
Haemod
ynam
ic
Pulmonary oedema
Pneumonia
Atelectasis
Inhalation
Factors contributing to lung injury
u Positive pressure effects on intrathoracic pressures
u Pressure and distribution of airflow into the alveoli
u Pressure, stretch, and the lung
u Surfactant functions
4
100% FiO2
ì Pressure gradient Intraalveolar-capillaries
Rapid diffusion of O2 across alveolar-capillary barrier
Loss in alveolar distending pressure
Elevated FiO2 at induction leads to rapid alveolar collapse independant of the carrier gas
Joyce CJ et al. J Appl Physiol 1999; 86: 1116-1125
Atelectasis by O2-absorption
Edmark L et al. Anesthesiology 2003; 98: 28-33
The kinetic of O2-absorption atelectasis is determined by the alveolar concentration
Rothen H. et al. Anesthesiology 1995; 82(4):832-842
After RM, 40% FiO2 : v delays significantly the recurrence of atelectasis (at least 40’) v î V/Q v ì relative perfusion to poorly ventilated lung units
The effect of gas composition on the recurrence of atelectasis after re-expansion
100% O2
Consequences of low FRC
Increased airway resistance Airway closure
Impaired gas exchange
Increased work of breathing 2
Chu, E et al. Crit Care Med 2004; 32:168-174.
Cyclic opening and closing from ZEEP: Greater increases BAL cytokines than atelectasis. High-volume ventilation, over time: Degree of overdistension is more associated with increases in BAL cytokines than cyclic opening and closing alone
Repetitive intermittent stretch or constant stretch
stimulates greater release of inflammatory mediators ?
5
Increased cytokine production Increase white cell sequestration
Cyclic opening & closing Stress and shear forces
Over-distension of alveoli
Notion of Energy load to the respiratory system and dynamic alveolar strain
Energy load to the respiratory system comprises: - A static component, due to PEEP and PEEP volume
(potential energy):
Static energy load = PEEP x PEEP volume/2
- A dynamic cyclic component, due to driving pressure and tidal volume above PEEP (kinetic energy):
Dynamic energy load = (PEEP + Peak pressure) x TV/2 (Peak pressure −PEEP) x TV/2 + (PEEP x TV)
Protti A et al. Int Care Med Exp 2015; 3:34
Protti A et al. Int Care Med Exp 2015; 3:34
Average inspiratory capacity: TLC-FRC
Lower limit of inspiratory capacity = threshold for VILI
The dynamic component impact VILI
Above inspiratory capacity stress è rupture may occur In healthy lungs, PEEP is protective only if
associated with a reduced tidal volume otherwise, it has no effect or is harmful
Innovative concept: Role of driving pressure
Odds of postoperative pulmonary complications according to response of driving pressure after increase of PEEP
Neto AS et al. The Lancet Resp Med 2016; 4: 272-280
Driving pressure = specific tidal volume
.
VT/Crs
‘Specific’ tidal volume Tidal volume standardized for the end-expiratory lung volume
EELV
VT/EELV
STRAIN
6
Optimal PEEP
ì PEEP
ì or ≈ Driving pressure
î Driving pressure Lung recruitment & ì aerated lung tissue
VT Constant
No lung recruitment Lung tissue overstretched
K-edge subtraction synchrotron imaging: allows assessment of STRAIN
Ek = 34.56 keV Inonization energy of Xenon
Substraction image
103
102
101
100
10-1
Xenon
Bone Tissue
20 40 60 80 Energy (keV)
Mass attenuation µ/ρ (cm2/g)
Marked absorption by Xenon
Negligeable Absorption by Xenon
Bayat S. et al, Phys Med Biol 2001;46:3287-99
• The color codes represent the specific ventilation
• The Coefficient of variation reflects spatial ventilation heterogeneity
• Time constant of alveolar units to fill and empty Xenon
Xe I
Porra et al. Am J Respir Crit Care Med 2012;185: A3679
Regional lung Ventilation and Blood Volume are heterogeneous in normal lung
(CV=SD/mean)
Demonstration of small length-scale heterogeneity of regional ventilation and perfusion Atomic force microscopic (AFM) images of three different rat surfactants deposited on mica
Mechanical ventilation with injurious conditions
Panda AK et al. Am J Respir Cell Mol Biol 2004; 30: 641-650
Alteration number and size of LC domain structures at the air–liquid interface
ATELECTASIS TRAPPING
PA
NA
HI
High sV Normal sV Low sV High sV Normal sV Low sV High sV Normal sV Low sV
1000 500 0 -500 -1000
15
10
5
0
Cat
egor
y
Den
sity
(H
U)
sV
(1/
min
)
1/min
HU
.
Mapping of regional ventilation in the lung Baseline Surfactant depletion
Bayat S. & Habre W. et al. Anesthesiology 2013; 119:89-100
PEEP 3 PEEP 3 PEEP 3 PEEP 9 PEEP 9
Porra L & Habre W et al. Eur J Anaesth 2016; in Press
Assessing strain from regional ventilation during VCV and PRVC
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At low tidal volume: 7ml/kg & PEEP of 5 cmH2O
Similar regional strain between VC and PRVC
Porra L & Habre W et al. Eur J Anaesth 2016; in Press
Clinical implications
Keeping driving pressure ideally below 13 cmH2O
Titrate PEEP and VT
Optimize gas exchange
Paw (cmH20)
30
Sec.
20
0
10
Paw (cmH20)
Sec.
30
20
0
10
Limited and constant inspiratory pressure
High end-inspiratory airway pressure
Difficulties to obtain equilibrium between Paw and Palv
Plateau pressure reached quicker Allows enough time for equilibrium
Peak airway pressure is lower with a decelerating flow Outline
• Physiological characteristics • Physiological effects on the lung
• Cardio-respiratory interaction • Physiology effects and monitoring
2 Lansdorp B et al. Crit Care Med 2014; 42(9):1983-1990.
Mechanical Ven+la+on-‐Induced Intrathoracic Pressure Distribu+on and Heart-‐Lung Interac+ons
Cardiopulmonary interaction variability
Baseline volume status
Vasomotor tone
Cardiac pump function
8
Effect of positive pressure on venous return Venous return is proportional to the gradient pressure: Mean systemic pressure minus the right atrial pressure (Vs –PRA)
ì PIP
ì PRA
î ΔP
î Venous return
Fessler HE et al. 1992: 146: 4-10
PEEP alters venous return curve by increasing the upstream pressure
ZEEP
PEEP 10
RV Preload
Paw IVC flow
Murphy BA et al. Respir Care. 2005 Feb;50(2):262-74;
ì Pleural pressure
ì Transpulmonary pressure
î RV preload
î RV ejection î LV preload
î LV ejection
î LV afterload
ì RV afterload
ì LV preload ì LV ejection
Systolic pressure Pulse pressure
Aortic blood velocity minimum during expiratory period
Systolic pressure Pulse pressure
Aortic blood velocity minimum at the end of the inspiratory period
Michard F et al. Crit Care 2000; 4:282–289
Hemodynamic effects of mechanical insufflation
Lansdorp B et al. Crit Care Med 2014; 42(9):1983-1990
Pressure-Volume loops
Kasper Kyhl et al. Am J Physiol Heart Circ Physiol 2013;305:H1004-H1009
Effect of positive-pressure ventilation on cardiac chamber volumes
ì PPV
î cardiac volumes
9
Roberson RS Best Pract Res Clin Anaesth 2014; 28: 407-418
Respiratory variation and cardiopulmonary interactions Outline
• Physiological characteristics • Physiological effects on the lung
• Cardio-respiratory interaction • Physiology effects and monitoring
III II I 0 0
III
II I 0 0
ETCO2
The slope of phase III is closely related to the ventilation/perfusion ratio of the lungs
CO2 production Metabolic rate
Elimination (VA) Ventilation/Perfusion
Continuously rising CO2 rather than Plateau indicates a V/Q abnormality
αIII correlates with spirometric indices (FEV1) Clinical observations suggest that αIII reflect airway properties Raw (cmH2O.s/l)
0 10 20 30 40
Cap
nogr
am p
hase
III s
lope
(m
mH
g/s)
0
1
2
3
4
5
6
7
369
H<13 cmH2O/l (mean-SD)
H>42 cmH2O/l (mean+SD)
Relationship between airway resistance and capnograph phase III slope
Peták F et al. Eur Respir J 2010; 36s, 54: 944s.
The Raw - αIII relationship is influenced by the elastic recoil of the respiratory system
High sensitivity in case of small respiratory elastance Emptying of the alveoli is determined by the small
airway geometry: » at low lung volumes/pressures: sequential
» at high lung volumes/pressures: parallel
Low sensitivity in case of stiff respiratory tissues Lung emptying is parallel, determined by the high elastic
recoil independently of the small airway geometry
Components contributing to the impedance of the respiratory system
• Elastic forces: – Distension of an elastic structure
– Elastance (E) and Compliance (1/E):
Crs (ml/cmH2O) = Volume/Pplat-PEEP
• Resistive forces: – Resistance to airflow:
Rrs (cmH2O.L-1.s) = (PIP-Pplat)/Flow
• Inertive forces: – Pressure required to accelerate and decelerate
the intrapulmonary gas (Important at high frequencies)
10
Volume (ml)
Pressure (cmH2O)
Inspiration
Expiration
Crs: ΔV/ΔP
Low compliance
High compliance
Pression-Volume curve: Expresses the mechanical properties
Dynamic pressure-volume curve includes the resistive and convective acceleration components of the flow
Monitor the pressure
Volume controlled mode
Pressure controlled mode
Monitor the volume
ΔV
Vol
ume
(ml)
Pressure (cmH2O)
ΔP
Vol
ume
(ml)
Pressure (cmH2O)
ΔP
ΔV Beginning of dynamic inflation: Evidence on lung recruitment
from tidal volume independent of PEEP
End of dynamic inflation: Evidence on lung overdistension
Upper inflection point
PEEP
PIP (Pmax)
Pplat
resistance flow
compliance tidal volume
end-inspiratory alveolar pressure
Analysis of airway pressure wave during VCV Strictly in constant flow mode
Stress index
Grasso S et al. Crit Care Med 2004; 32: 1018-1027
SI < 1: Recruitment Lower part of the P/V curve
ΔP
ΔV
SI > 1: overdistension Upper part of the P/V curve
ΔP
ΔV
Estimate changes in Crs and Rrs from the pressure curve analysis
Pmax
Pplat P resistive
Pelastic Peep
Low compliance
Elevated Pplat
High resistances
ñRrs
Constant flow inflation
Use flow/time curves to set Ti and Te: reflects recruitment and total exhalation
Flow
Time
Back to 0
TI
TE
îDriving pressure
Large regional variation in both recruitment and over-inflation within
and between the lungs
11
Schiller, H et al. Crit Care med 2003; 31(4):1126-1133 DiRocco JD et al. Intensive Care Med. 2007 ;33(7):1204-11 Jeon K et al. J Korean Med Sci. 2007;22(3):476-83.
Alveolar recruitment and derecruitment take place at different pressures, and the use of deflation limbs of P-V curves has greater inference to alveolar derecruitment than inflation limbs.
Apply a « Lung Protective » strategy Target a tidal volume of 6-7 ml/kg based on ideal weight
Avoid increase driving pressure : VT/EELV Restore FRC and optimize PEEP by assessing driving pressure Allow permissive hypercapnia: 6 kPa
Adolescent of 162 cm, 132 kg Lung volume: 3245 ml
Adolescent of 161 cm, 47 kg Lung volume: 3364 ml
Courtesy from Jaber S.
Protection of the lung against the harmful effects of positive pressure ventilation could be more important than optimising gas exchange
The use of heart-lung interactions during mechanical ventilation to assess fluid responsiveness
derived from analysis of arterial waveform
Stroke volume variation (SVV)
derived from pulse contour analysis
Systolic pressure variation (SPV) Pulse pressure variation (PPV)
Predicting fluid responsiveness in children: is it realistic ?
• The Starling curve: does it exist in neonates? – YES ! But it is shifted to the left
• Are classical static variables reliable? – No ! Very poor predictors
• Dynamic variables derived form heart-lung interaction: are they good predictors? – Value of Aortic Peak Flow velocity
Comparison of the areas under the ROC curve for dynamic variables
Aortic Peak Flow Velocity
12
Monitoring oxygenation and Cardiac output Importance of assessing adequacy of tissue oxygenation
Soni N. Br J Anaesth. 2008;101:446-57
NIRS
SvO2
SpO2
Goal-Oriented approach
Blood Pressure
Cardiac output
Intravascular volume
ìoxygen delivery index optimize oxygen transport
Improve outcome in high risk patients
O2 Hb
