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Fisiologia degli scambi
gassosi durante circolazione
extracorporea
2009, Milano
Luciano Gattinoni, MD, FRCP
Università di Milano
Fondazione IRCCS- “Ospedale Maggiore
Policlinico, Mangiagalli, Regina Elena”
Milan, Italy
Oxygenation assessment:
the basics
Oxygenation
• Tension
• Content
• Assessment
Oxygenation
• Tension
• Content
• Assessment
The basic Physiology
Partial pressure (Tension)
Activity of the unbounded O2 molecules
In arterial blood PaO2
In venous blood PvO2
In alveoli PAO2
PAO2 = FIO2 * 713 – PACO2/RQ
Oxygenation
• Tension
• Content
• Assessment
102
100
Oxygen Saturation (%)
98
96
94
92
54 pts
90
88
r2 = 0.8973
86
p < 0.0001
84
82
80
0
50
100
150
PaO2 (mmHg)
200
250
300
Maximal binding capacity of hemoglobin
1 mole Hb (64500 gr/M)
binds
4 moles of oxygen (4 x 22.414 L at 0°C and 760 mmHg)
Therefore
89656 mL/64500 gr = 1.39 mLO2/grHb
The basic Physiology
Content
total amount of bounded and unbounded O2
molecules
In arterial blood
CaO2 = PaO2 x 0.003 + 1.39 x Hb x SataO2
In venous blood
CvO2 = PvO2 x 0.003 + 1.39 x Hb x SatvO2
In lung capillaries (Hp Sat=100%)
CcO2 = PAO2 x 0.003 + 1.39 x Hb x 1
Oxygen Transport (DO2)
DO2 = CaO2 x Qt
normally
1000 mL/L = 200 mL/L x 5 L
VO2 ≈ 1/4 - 1/5 of DO2
Venous O2 saturation ≈ 0.75 = 1- VO2/DO2
Oxygenation
• Tension
• Content
• Assessment
– PaO2/FiO2
– Right to left shunt
– Oxygenation Index (OI)
Anatomical shunt compartment
Gasless tissue
Right to Left Shunt
CcO2
CvO2
VCO2
CaO2
CvO2
CaO2 x Qt = CcO2 x (Qt-Qs)+CvO2 x Qs
Shunt =
(CcO2 – CaO2)
(CcO2 – CvO2)
Oxygenation Index
Oxygenation Index = (FIO2 * Mean Airway Pressure) / PaO2
Oxygenation index and severity of lung dysfunction
2–7 Normal or mild pulmonary dysfunction
8–9 Moderate pulmonary dysfunction
≥ 10 Severe pulmonary dysfunction
≥ 30 Need for ECMO
Fiser et al. J Heart Lung Transplant 2001;20:631–636.
As an example…
55
PaO2 60 mmHg
PaO2 50 mmHg
MAP 25 cmH2O
Oxygenation Index
50
45
50
56
63
40
71
67
35
83
60
P/F ratio
75
30
86
25
100
20
50
60
70
80
90
Oxygen fraction (%)
100
110
Carbon dioxide assessment:
the basics
Carbon dioxide
• Tension
• Content
• Assessment
Carbon dioxide
• Tension
• Content
• Assessment
The basic Physiology
Partial pressure (tension)
Activity of the unbounded CO2
molecules
In arterial blood PaCO2
In venous blood PvCO2
In alveoli PACO2
ETCO2
Carbon dioxide
• Tension
• Content
• Assessment
Contents
Total CO2 = sCO2 + HCO3- + CO3= + PrNHCOO- + NaCO3-
Simplifying
Total CO2 = 0.03 x PaCO2 + HCO3i.e.
Total CO2 = 0.03 x PaCO2 x (1 + 10pH-pK)
Remember
1 mMol/L = 2.24 mL%
CO2 content (mL%)
80
BE 0
BE -5
BE -10
BE -15
60
BE -20
40
20
20
40
60
80
PCO2 (mmHg)
100
120
Carbon dioxide
• Tension
• Content
• Assessment
Dead Space derivation
VA*PACO2 = VCO2
(VA+VDalv)*PETCO2 = VCO2
(VA+VDalv+VDanat)*PECO2 = VCO2
It is assumed that:
Alveolar PCO2 = Arterial PCO2
Physiological Dead
Space
(PaCO2 – PECO2)
PaCO2
Alveolar Dead Space
(PaCO2 – PETCO2)
PaCO2
Shunt effect
PcCO2=PACO2
PcCO2
PvCO2
VCO2
PaCO2
PvCO2
Greater the shunt, greater the difference between
alveolar and arterial CO2
PECO2
PCO2
cascade
PETCO2
PACO2
Ventilated/
perfused lung
PcCO2
PvCO2
Alveolar
VD/VT
Anatomic
VD/VT
VCO2
PaCO2
PvCO2
Artificial Lung
• Determinants of oxygenation
• Determinants of Decarboxylation
• The performance of the membrane
lung
Artificial Lung
• Determinants of oxygenation
• Determinants of Decarboxylation
• The performance of the membrane
lung
The oxygen charged by the
artificial lung depends,
for a given input saturation,
on the blood flow in the
device
Performance
Oxygenator
Input:
37°C
Hb 15 gr/dL
Sat IN 70%
Bovine blood
Remember that:
The output blood is fully oxygenated,
even at low extracorporeal gas flow
Oxygen transfer is greater with lower
input saturation
Oxygen transfer increases linearly with
extracorporeal blood flow
Artificial Lung
• Determinants of oxygenation
• Determinants of Decarboxylation
• The performance of the membrane
lung
In the venous blood the CO2
content is ≈ 45-50 mL%.
Theoretically from 0.5 L of
blood it is possible to clear the
metabolic CO2 production
Carbon dioxide transfer as a function of blood input pCO2, at
different blood flow rates
Kolobow et al Trans. Am. Soc. Artif. Intern. Organs. 1977. 23: 17-21
Kolobow et al Trans. Am. Soc. Artif. Intern. Organs. 1977. 23: 17-21
Performance
Oxygenator
Input:
37°C
Bovine blood
PCO2 45 mmHg
Artificial Lung Performances
(11 pts)
Day 1
Day 10
1L
2L
Gas Flow
1.5 L
2.5 L
Input PO2
47 ± 12 mmHg
31 ± 10 mmHg
Input SatO2
76 ± 8
57 ± 7
Output PO2
530 ± 80 mmHg
479 ± 80 mmHg
Input PCO2
52.8 ± 8 mmHg
47.7 ± 8 mmHg
Output PCO2
35.4 ± 7 mmHg
29.0 ± 7 mmHg
17.4 mmHg
18.7 mmHg
Blood Flow
∆PCO2
CO2 clearance increases with:
Gas flow (primarily)
The logarithm of Blood Flow
Input PCO2
While in natural lung…
Content/Tension relationship
( mL/100mL whole blood)
20
100
54
∆C5
80
∆C5
15
49
%
∆P5
DP40
60
10
44
5
39
0
100 120 140
34
40
20
0
0
20
40
60 80
80
PO2
30
(mmHg)
35
40
PCO2
45
45
50
OXYGENATION
FiO2 =1.0 250 mL min-1
7000 mL min-1
PBF
Hb 15 g
Satv 82%
PvO2 47 mmHg
CO2 cont 52 mL
PvCO2 43 mmHg
Sata 98%
PaO2 110 mmHg
VO2
250
mL min-1
CO2 REMOVAL
VA 9500 mL min-1
1100 mL min-1
PBF
CO2 cont 34 mL
PaCO2 15 mmHg
VCO2
200
mL min-1
Gattinoni et al., European Advances in Intensive Care, 1983; 21: 97-117
gas flow 10 l/min
1 10
EC onset
4
120
9000
100
8000
VE
90
7000
-1
80
70
5000
60
4000
50
2
6000
PaCO (mmHg)
VE (mL*min )
110
PaCO2
40
3000
30
2000
20
1000
10
0
0
0
6
12
18
24
30
36
42
Time (h)
48
54
60
66
72
Oxygen transfer in artificial and natural lung:
Interaction
The model
Limits of oxygenation in V-V bypass
Consequences of loss of hypoxic
vasoconstriction
Oxygen transfer in artificial and natural lung:
Interaction
The model
Limits of oxygenation in V-V bypass
Consequences of loss of hypoxic
vasoconstriction
O2 natural lung
End-capillary blood
Intrapulmonary
shunt
Mixed-venous
Natural Lung
Arterial blood
Post
lung
Artificial Lung
O2 ECMO
Pre
lung
Body Tissues
VO2
Time course to
equilibrium
Arterial Oxygen Saturation (%)
98
Arterial Oxygen Saturation (%)
100
QECMO/Qtot 70%
Shunt 40%
96
94
92
90
88
QECMO/Qtot 10%
86
84
82
Mixed Venous Oxygen Saturation (%)
100
Mixed Venous Oxygen Saturation (%)
QECMO/Qtot 70%
95
90
85
80
75
QECMO/Qtot 10%
70
65
60
80
1
2
3
4
STEP
Shunt 40%
5
6
7
1
2
3
4
STEP
5
6
7
Time course to
equilibrium
Arterial Oxygen Saturation (%)
98
Mixed Venous Oxygen Saturation (%)
QECMO/Qtot 70%
Shunt 60%
Mixed Venous Oxygen Saturation (%)
Arterial Oxygen Saturation (%)
96
94
92
90
88
86
84
82
80
78
QECMO/Qtot 70%
95
90
85
80
75
70
65
QECMO/Qtot 10%
76
QECMO/Qtot 10%
60
1
2
3
4
STEP
Shunt 60%
5
6
7
1
2
3
4
STEP
5
6
7
The equilibrium is reached when O2
from artificial lung plus O2 from
natural lung equals O2 consumed by
tissues
VO2 = O2ECMO + O2NATURAL LUNG
96
420
94
400
92
380
90
360
88
340
86
Shunt 50%
ECMO blood flow 50%
CO 9 L/min
Hb 11 gr/dL
VO2 250 mL/min
84
82
320
300
280
80
260
78
240
1
2
3
4
STEP
5
6
7
VO2 (mL/min)
O2 transfer
Arterial Oxygen Saturation (%)
ECMO
mathematical model
Oxygen transfer in artificial and natural lung:
Interaction
The model
Limits of oxygenation in V-V bypass
Consequences of loss of hypoxic
vasoconstriction
ECMO
mathematical model
Arterial Oxygen Saturation (%)
100
Steady state
95
90
Shunt 40%
85
Shunt 50%
80
Shunt 60%
75
10
20
30
40
50
ECMO Blood Flow (%CO)
60
70
Oxygen transfer in artificial and natural lung:
Interaction
The model
Limits of oxygenation in V-V bypass
Consequences of loss of hypoxic
vasoconstriction
Anatomical shunt compartment
Gasless tissue
1.0
0.8
0.8
Functional shunt
Functional shunt
1.0
0.6
0.4
0.6
0.4
0.2
0.2
0.0
0.0
0.0
0.2
0.4
0.6
0.8
1.0
0.0
0.2
0.4
0.6
0.8
Anatomical shunt compartment
Anatomical shunt compartment
A
B
1.0
Cressoni M. et al. Crit Care Med. 2008 Mar;36(3):669-75.
400
PaO2/FIO2 (mmHg)
PaO2/FIO2 (mmHg)
400
300
200
100
300
200
100
0
0
0.0
0.2
0.4
0.6
0.8
1.0
0.0
0.2
0.4
0.6
0.8
Anatomical shunt compartment
Anatomical shunt compartment
A
B
1.0
Cressoni M. et al. Crit Care Med. 2008 Mar;36(3):669-75.
Hypoxic vasoconstriction
maintains oxygenation at
different degrees of
anatomical shunt
Perfusion Ratio
QS
QT
K
= Kx
=
Gr. non aerated tissue
Lung Total Weight (gr.)
Perfusion/ gr. non aerated tissue
Perfusion/ gr. Tot.
Assumptions: 1) Edema near homogeneously distributed
2) Qs perfuses only the non aerated tissue
HU > -100
HU > -300
Cressoni M. et al. Crit Care Med. 2008 Mar;36(3):669-75.
Perfusion Ratio
1) Size of the “bad” lung
Perfusion ratio
and its change
depend on
(R2 0.83)
2) Global perfusion
3) Hypoxic stimulus
(PsO2 = PvO20.38 x PAO20.42)
Decreasing the size
(recruitment)
Perfusion ratio ↑
Decreasing the CO
Perfusion ratio ↓
AS AVERAGE – It does not change
Hypoxic vasoconstriction
Theoretical model
100
PsO2 = PvO20.38 x PAO20.42
PVR max (%) = 100 x (PsO2-2.616)/(6.683 x 10-5 + PsO2-2.61)
PVR MAX (%)
80
60
40
FiO2 40%
FiO2 60%
FiO2 80%
FiO2 100%
20
0
0
20
40
PvO2
60
80
100
Therefore don’t be surprised
if providing 3-4 L ECMO
fully oxygenated blood flow,
arterial PaO2 and saturation
change minimally, since
functional shunt tends to
increase
Decarboxylation: interaction with
spontaneous and mechanical breathing
The lung rest concept
Control of breathing using an
extracorporeal membrane lung
Kolobow T, Gattinoni et al., Anesthesiology, 1977; 46: 138-141
Kolobow et al Trans. Am. Soc. Artif. Intern. Organs. 1977. 23: 17-21
This happens also in
spontaneously breathing men
during CO2 removal
Alveolar ventilation as a function of CO2 elimination
Gattinoni et al Anest. e Rianim. 1977. 18(4): 396-406
Gattinoni et al Anest. e Rianim. 1977. 18(4): 396-406
Control of intermittent positive pressure breathing
(IPPB) by extracorporeal removal of carbon dioxide
Gattinoni et al., Br. J. Anesth., 1978; 50: 753
Corso Teorico-Pratico
Trattamento
dell’Insufficienza Respiratoria Acuta
mediante Supporto Extracorporeo
Centro di Simulazione
Fondazione IRCCS Policlinico, Mangiagalli e Regina Elena
Milano
2009
Il circuito extracorporeo:
Tipologie possibili
Giorgio Iotti
Anestesia e Rianimazione 2
Pavia
Sistema Respiratorio
Lung Failure
Pump Failure
Insp
Esp
Scambiatore di Gas
Pompa
Inquadramento Diagnostico
Fisiopatologico
INSUFFICIENZA RESPIRATORIA
PUMP FAILURE - IPERCAPNICA
Inquadramento Diagnostico
Fisiopatologico
INSUFFICIENZA RESPIRATORIA
PUMP FAILURE - IPERCAPNICA
LUNG FAILURE - IPOSSIEMICA
• The syndrome did not respond to usual
and ordinary methods of respiratory
therapy
• The syndrome did not respond to usual
and ordinary methods of respiratory
therapy
• Positive end-expiratory pressure (PEEP)
was most helpful in combating atelectasys
and hypoxemia
CPT
Volumi
Polmonari
Vtidal
FRC
Start
Plim
Pressioni
Alveolari
Ptidal
EEP
CPT
Volumi
Polmonari
Vtidal
FRC
Start
Plim
Pressioni
Alveolari
Ptidal
EEP
CPT
Volumi
Polmonari
Vtidal
FRC
Start
Plim
Pressioni
Alveolari
Ptidal
EEP
↓ Vt
CPT
Volumi
Polmonari
Vtidal
FRC
Start
Plim
Pressioni
Alveolari
Ptidal
EEP
↓ Vt
↑ Freq.
INSUFFICIENZA RESPIRATORIA
PUMP FAILURE - IPERCAPNICA
•
•
•
•
•
•
•
LUNG FAILURE - IPOSSIEMICA
Ossigeno
Ventilazione protettiva
↓ spazio morto
Pronazione
Manovre di reclutamento
iNO
Attività resp. spontanea
UTILIZZO OTTIMALE / MASSIMALE
DELL’ORGANO MALATO
Il gioco qualche volta non funziona…
• Anche con tutti i trucchi, le acrobazie e
le precauzioni che abbiamo imparato,
talvolta la sola POMPA ARTIFICIALE
non basta:
– Severa IPERCAPNIA
– Pericolosa IPOSSIEMIA
INSUFFICIENZA RESPIRATORIA
PUMP FAILURE - IPERCAPNICA
•
•
•
•
•
•
•
LUNG FAILURE - IPOSSIEMICA
Ossigeno
Ventilazione protettiva
↓ spazio morto
Pronazione
Manovre di reclutamento
iNO
Attività resp. spontanea
UTILIZZO OTTIMALE / MASSIMALE
DELL’ORGANO MALATO
SOSTITUZIONE con
ORGANO ARTIFICIALE
INSUFFICIENZA RESPIRATORIA
PUMP FAILURE - IPERCAPNICA
LUNG FAILURE - IPOSSIEMICA
Supporto Respiratorio Extracorporeo
• Prelevo del sangue
• Lo tratto con uno scambiatore di gas
Extra Corporeo a Membrana
Rimozione di CO2 (CO2R)
ECCO2R
+ Ossigenazione (O)
ECMO
• Reinfondo il sangue trattato
va ECMO
Rimozione di CO2
Ossigenazione
Assist. Cardiaca
JAMA 1979; 242:2193-6
Extracorporeal membrane oxygenation in severe acute respiratory
failure. A randomized prospective study.
Zapol WM, Snider MT, Hill JD, Fallat RJ, Bartlett RH, Edmunds LH,
Morris AH, Peirce EC 2nd, Thomas AN, Proctor HJ, Drinker PA, Pratt
PC, Bagniewski A, Miller RG Jr.
Nine medical centers collaborated in a prospective randomized study to
evaluate prolonged extracorporeal membrane oxygenation (ECMO) as a
therapy for severe acute respiratory failure (ARF). Ninety adult patients were
selected by common criteria of arterial hypoxemia and treated with either
conventional mechanical ventilation (48 patients) or mechanical ventilation
supplemented with partial venoarterial bypass (42 patients). Four patients in
each group survived. The majority of patients suffered acute bacterial or viral
pneumonia (57%). All nine patients with pulmonary embolism and six
patients with posttraumatic acute respiratory failure died. The majority of
patients died of progressive reduction of transpulmonary gas exchange and
decreased compliance due to diffuse pulmonary inflammation, necrosis, and
fibrosis. We conclude that ECMO can support respiratory gas exchange but
did not increase the probability of long-term survival in patients with severe
ARF.
vv ECMO
Rimozione di CO2
Ossigenazione
Kolobow T, Zapol W, Pierce J (1969) Trans Am Soc Artif Intern Organs 15:172-7
Anesth Analg 57: 470: 1978
av ECLA
(ILA Novalung)
Rimozione di CO2
A confronto
va ECMO
Rimozione di CO2
Ossigenazione
Assist. Cardiaca
vaECMO respiratoria: problemi
• Fortissima dipendenza dal supporto
extracorporeo
• Ridotta perfusione polmonare
• Scarsa ossigenazione del sangue in uscita
da VS (coronarie, tronchi sovraortici)
• Problemi di perfusione distale della zona
dipendente dall’arteria incannulata
• Embolizzazione sistemica
av ECLA
(ILA Novalung)
Rimozione di CO2
avECLA: vantaggi
• Bassa richiesta di tecnologia
– Semplicità
– Investimenti ridotti
– Facile trasportabilità
• Comunque necessari:
– Misuratore flusso extracorporea
– Flussimetro di precisione
– Hemochron (ACT)
avECLA: problemi
• Notevole aumento della richiesta di prestazione cardiaca
(shunt a-v)
• Dipendenza dalle condizioni emodinamiche del paziente
• Ridotta perfusione distale della zona dipendente
dall’arteria incannulata
• Dispersione di calore (scambiatore di calore assente)
• Facilità di passaggio di gas nella camera ematica
dell’ossigenatore (pressione transmembrana!!)
• Facilità di apposizioni trombotiche dell’ossigenatore
(flusso relativamente basso)
• Scarsa capacità di ossigenazione
avECLA: problemi
• Scarsa capacità di ossigenazione
• Se bisogna passare allo step successivo
(vvECMO), abbiamo fatto un grosso buco
in un’arteria!
vv ECMO
Rimozione di CO2
Ossigenazione
vvECMO: limiti
• Capacità di ossigenazione: non consente
un supporto totale
• Assistenza cardiaca: nessuna, se non
indiretta
Decapnizzatori
• vvECMO a bassissimo flusso
• Nessuna ossigenazione
• CO2 removal molto limitato
• Circuiteria da CRRT
– non eparinata
– Pompa sangue ?
– Concepita per uso discontinuo
– Cambi, tempo e impegno, costi
Conclusioni
• A voi le conclusioni sulla “ECMO
respiratoria” più appropriata oggi
La gestione del ventilatore ed
interazione con il bypass
Giuseppe Foti
Istituto Anestesia e Rianimazione
Università di Milano-Bicocca
dir. Prof. A. Pesenti
Ospedale S. Gerardo Monza
…….ma adesso che sono in bypass,
il ventilatore
serve ancora ?
VENTILAZIONE
OSSIGENAZIONE
Cosa succede alla partenza della
CEC
Rimozione > 70% VCO2
ATTENZIONE SHIFT pH e
PCO2 !!
• subito
– FR (sempre)
– TV (se necessario)
– I/E (attenzione)
• Guided by:
– EndTidalCO2
– EGA
• entro 10’
Se non serve più ventilare, perché
tengo il ventilatore ?
• Malgrado ECBF la PaO2 può essere
• ECBF/C.O.
• SvO2 Vasocostrizione ipossica
PO2 e PAP
PAP
SvO2
Flusso CEC
CEC SvO2
Se non serve più ventilare, perché
tengo il ventilatore ?
• Per Ossigenare
Come
• Tenendo aperto il polmone
Attenzione ai cambi bruschi di
Pmedia
FR = 30
FR = 15
Paw = [(30*1) + (15*1)] / 2 = 22.5
Paw = [(30*1) + (15*2)] / 3 = 20
30
30
1”
15
1”
1”
15
2”
Attenzione ai cambi bruschi di
Pmedia
• Evitare immediatamente la sovradistensione
• Ridurre Pplat < 30
• TV < 6 ml/Kg
NO GOOD
BETTER
Perché/Come contrastare i bruschi
cambi Pmedia ?
• Dereclutamento
(Plasmorrea/Capillary Leak)
• PEEP
• Evitando I/E
Strategie Ventilatorie in ECMO
(una guerra di religione)
Recruiter
Non Recruiter
High survival in adult patients with ARDS treated by
extracorporeal membrane oxygenation, minimal
sedation, and pressure supported ventilation
Linden V et al. ICM 2000; 26: 1630
17 patients
LIS 3.5
PaO2/FiO2 46 mmHg
Length of bypass 33-52 days
(conventional VV or VA 9/17)
PEEP 10 PSV 15
Survival Rate 76 %
lung rest settings were :
- peak inspiratory pressure 20–25,
- positive endexpiratory pressure 10–15,
- rate 10,
- FiO2 0・3.
Recruiter strategy
B.F.
PAW
Non Recruiter strategy
B.F.
PAW
Non Recruiter strategy
• Low PEEP (5-10)
• LPS
– PSV
• High Blood Flow
– II° drainage cannula
• NO PNX
• Pulmonary Hypertension
– V-A bypass?
B.F.
Reclutamento e PAP
PAP
PVC
RMs = 70 cmH2O
Non Recruiter strategy
In 33 patients (49%), a second
access
cannula was needed to augment
ECMO support.
Recruiter strategy
•
•
•
•
RMs
PEEP Titration
SIGH
PNX ?
Opening and closing pressures
Paw > 35
50
cmH2O
to fully recruit
%
40
Opening
pressure
30
Closing
pressure
20
10
0
0
5
10 15 20 25 30 35 40 45 50
Paw [cmH2O]
Crotti et al. Am J Respir Crit Care Med 2001
Modern PEEP Titration
12
10
10
7
15
Spo2 e RM’s
• Problema risolto !
Era un’atelettasia
• e poi Ripeto e PEEP
•±
Pressione Rm’s
oppure aspetto
Quante RM’s ?
•
•
•
•
Pochissime se uso SIGH
In Controllata e Assistita
Che pressione ? quella di reclutamento
A chi ?
A quelli che reclutano
Effects of periodic lung recruitment maneuvers on gas exchange and
respiratory mechanics in mechanically ventilated ARDS patients.
G. Foti, M.Cereda, M.E. Sparacino, L. De Marchi,F. Villa, A. Pesenti
Intensive Care Med (2000) 26: 501-507
Pressione di reclutamento
Sigh (1 ogni 3 min)
SIGH
↑Oxygenation
↓ Qva/Qt
Monitoraggio
reclutamento
• EGA
–
–
–
–
P/F
PaO2 al 100%
Shunt
Rapporto B.F./C.O.
• Meccanica respiratoria
– Cpl, FRC
• Imaging
– Rx
– TC
Monitoraggio reclutamento
durante V-A bypass
• Quale sangue proviene dai polmoni ?
• Incannula la radiale dx
– Se attività cardiaca
– Sangue proveniente dal polmone naturale
Oh..oh…c’è un PNX
• Presto mettiamo drenaggio toracico
• Aspettiamo e convertiamoci
Oh..oh…c’è un PNX
• Non mi convertirò mai!
– Dg percutaneo
– Guidato scopia
– Identificazione eco
• Bene, non sbolla più
• Tiriamolo via
• Non rimuovete le frecce
durante CEC (…augh
(…augh))
Identificazione Ecografica PNX
Sono passate ormai 2
settimane…dobbiamo fare la tracheo.
• Se proprio non se ne può fare a meno
• Percutanea meglio che chirurgica
• Fantoni meglio delle altre
– Attenzione al tracheoscopio rigido
– Tecnica con fibroscopia flessibile
– Mantenete Paw con il tubino
– Sospendere/ridurre eparina
When a ALI/ARDS pts. can be
weaned to PSV from CMV ?
PaO2 > 80
PEEP < 15
Success
Failure
78%
22%
PaO2/FiO2
218±68
181±67
n.s.
Cst,rs
42 ± 15
30 ±16
< .05
(ml/cmH2O)
Vd/Vt
Days from
Tube
p
0.52 ±0.10 0.70 ±0.09
< .05
9.2 ±13.5 20.2 ±19.2
< .05
Cereda M, Foti G. et al. Crit Care Med 2000 Vol.28 n° 5; 1269-1275
BENEFICI Respiro Spontaneo in ARDS
spontaneous breathing
controlled ventilation, NMBA
Set: BIPAP+PSV, Pmax = 35-40cmH2O
Ti = 3-5 s.
RRBIPAP = 0.5-1 b.p.m.
ECMO per favorire il passaggio
al respiro assistito
• Quando è terminata fase iperacuta
– No capillary leak
• Per favorire reclutamento alveolare
• Per accelerare il weaning
• Dottore..dottore..la frequenza respiratoria – Aumenta PSV..mmm..no anzi
– Sedalo un pochino…..mmm….,aspetta
– Aumenta gas flow !
E se facessimo a meno
del ventilatore ?
2/87 Survival
in Intubated
because of Pneumonia
Ventilazione Diversamente
Invasiva (DIV)
1 Week
CEC
P/F 64
PEEP 15
GB 280
Plt 19.000
Start
CEC
P/F 104
PEEP 10
GB 1050
Plt 33.000
Pediatric ECMO Management:
Pulmonary
• Optimal ventilator settings vary
• Limit peak pressures to 30 cm
H2O
•
•
•
•
•
Delivered tidal volumes 4-6 cc/kg
Rate 5-10 breaths/minute
PEEP 12-15 cm H2O
Inspiratory time longer
Goal FiO2 0.21
Federico Pappalardo, MD
Department of Cardiothoracic and Vascular Anesthesia and Intensive Care
Università Vita e Salute San Raffaele Hospital, Milano
Hemorrhagic complications 54% (37/68)
•
•
•
•
•
ECMO cannulation site 22%
GI bleeding
10%
Respiratory tract
10%
Intracranial hemorrhage 9%
Genital bleeding
9%
Median amount of blood administered per patient
NO thromboembolic complications ???
1880 mL
Overall adult ECLS Survival
ELSO Registry (100 centers)
Respiratory
53%
Cardiac
32%
eCPR
37%
THROMBIN GENERATION/EFFECTS
* Tissue Factor
Contact
(XIIa)
BTG, PF4
(TF:VIIa)
ATIIIIX
* TFPI
ATIII
IXa
X
Platelets
FV, FVIII, FXI
ATIII
Xa
VIIIa, Ca++ , PL
activation/consumption
FXIa, FVa/FVIIIa
FVi,
FVIIIi
Protein C
Va, Ca++, PL
APC
THROMBIN
Prothrombin
* Thrombomodulin
XIII
FPA
bradykinin
PT fragment 1.2
EC
ATIII
* tPA
tPA:PAI1
Fibrinogen
TAT
* PAI1
FSP
Fibrin (M)
Fibrin (Ps)
XIIIa
Plasminogen
PLASMIN
-2-antiplasmin
D-dimer
PAP complexes Platelet GP1b
*
Fibrin (Pi)
1. Initiation phase
Injury of vessels wall
leads to contact
between blood and
subendothelial cells
Tissue factor (TF) is
exposed and binds to
FVIIa or FVII which
is subsequently
converted to FVIIa
The complex between
TF and FVIIa activates
FIX and FX
FXa binds to FVa on the
cell surface
2. Amplification phase
The FXa/FVa complex
converts small amounts
of prothrombin into
thrombin
The small amount of
thrombin generated
activates FVIII, FV, FXI
and platelets locally.
FXIa converts FIX
to FIXa
Activated platelets
bind FVa, FVIIIa
and FIXa
3. Propagation phase
The FVIIIa/FIXa complex
activates FX on the
surfaces of activated
platelets
FXa in association with
FVa converts large
amounts of prothrombin
into thrombin creating a
“thrombin burst”.
The “thrombin burst”
leads to the formation
of a stable fibrin clot.
ASA, Dipyridamol, Clopidogrel
Heparin
Coumadin
PAT
aPTT
INR
TEG
• Haemostasis starts with the interaction between TF
and FVIIa on the surface of subendothelial cells.
• The small amount of thrombin generated during the
amplification phase activates platelets locally on
whose surface the subsequent reactions take place.
• The resulting thrombin burst results in the
formation of a stable clot.
Activation Balance
Inappropriate
Site
Inappropriate
Amount
Inappropriate Control
Thrombosis
DVT/PTE
MI
Stroke
Bleeding
Transfusion
Contact activation : interface of blood with
nonendothelial surface
Pericardial activation : mediated by trasfusion of
pericardial blood
Mechanical consumption : shear forces imposed by
circuit’s component
Anticoagulation Management
Pulsatile, axial or centrifugal device
Cannulation (apical, atrial)
Coagulation disease (anti-phospholipid antibodies,..)
Heart disease (acute infarction, icmp, myocarditis,
dcmp)
Cardiac rhythm (fibrillation)
Age (children)
Anticoagulation Management
safe
Anticoagulation management
low costs
simple
Heparin
Heparin activates
platelets directly
-GP IIb/IIIa activated
-P-selectin expressed
Heparin can induce
an immune response
in the form of
HIT/HITTS and lead to
thrombocytopenia and
thrombosis
Activated
Platelet
Heparin
+
GP IIb/IIIa
Thrombin
Thrombin
Thrombin
Heparin inactivated by
Platelet Factor 4 (PF4)
Thrombin
Fibrin
Heparin
+
Platelet
Factor 4
Antibodies
Heparin exhibits
a nonlinear
dose-response.
2
Thrombin
Heparin
Heparin cannot
bind clot-bound
thrombin
P
1
2
P
Thrombin
P
Heparin binds to
plasma proteins and
cells
P-selectin
2
Thrombin
1
P
P
1
Fibrin
PP
ACT
Low concentrations of
heparin increase the
affinity of thrombin for
fibrin.
+
Platelet
Cell
PP
Cell
PP
Heparin dose
UFH continues to dominate ECMO anticoagulation:
• rapidly acting
• easily reversible
• inexpensive
• widely available
• well tollerated by pediatrics and adults
• needs cofactor AT, produce inhibition of factor Xa, thrombin and TF
• thrombin bound to clot or surface of the circuit is not inhibited by AT-UFH complex
Bound thrombin activate clotting and thrombin generation
GREATER UFH NEEDS
Increased Heparin to
Preserve Haemostasis
• High Heparin had
reduced:
– Prothrombin activation
β−Thromboglobulin
5000
D-Dimer ( ng / ml )
4000
3000
2000
Control
High Hep
Despotis et al Thromb Hemostasis 1996;76:902-8
The effectiveness of anticoagulation worsens with the duration of
ECMO (6 days freedom from thromboembolic events)
Management of ECMO anticoagulation partially derived from the
experiences of CPB
The popular range for the ACT with UFH during ECMO is 180 to
220 sec
aPTT is a valuable tool to assess anticoagulation in situation that do
not require high heparin dosing such as ECMO
In very ill patients requiring continuous infusion of UFH the ACT can
not delineate between low and moderate level of anticoagulation
compared with aPTT
Dosage of Acetylsalicylacide
Dosage of Acetylsalicylacide
Low dosage:
Thromboxane A2 (platelet)
-> reduction of aggregation
High dosage:
Prostacyclin (endothelium)
-> increasing aggregation
High dosage:
Prostaglandin (stomac)
-> increasing GI-bleeding
Platelets and shock
400
350
300
250
200
150
100
50
600
0
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
500
400
Grafic 1.: LVAD and RHF
300
200
600
100
500
0
1
2
3
4
5
400
Grafic 3.: TAH survival
300
200
100
0
1
2
3
4
5
6
Grafic 2.: LVAD survival
7
8
9
10
11
12
13
14
15
16
6
7
8
9
10
11
12
13
14
15
16
17
Platelets and shock
“Platelet transfusion represents a major part of
management of ECMO patients”
“Recurrent platelet dysfunction on ECMO”
“Frequent platelets transfusions even with
normal platelet count”
“The more critically ill the patient, the more likely
platelets have been given”
LABORATORY TESTING
• Antigen assays
- ELISA detects antibodies
reactive against the
PF4/Heparin complex
- High sensitivity (90-98%)
- High negative predictive
value
- Moderate positive predictive
value
- The magnitude of a positive
ELISA can be diagnostically
useful
•
-
Activation/Functional assays
SRA (Serotonin release assay)
Platelet aggregation assay
Detect the presence of
antibodies that activate platelets
in the presence of heparin
High sensitivity (>95%)
High negative predictive value
Moderate positive predictive
value
The magnitude of a positive
ELISA can be diagnostically
useful
The presence of HIT antibodies does not necessarily
predict the development of clinical HIT!!
LABORATORY TESTING
There is no single laboratory test that perfectly correlates
with a clinical diagnosis of HIT, because there is currently no
test with 100% sensitivity and specificity for the detection of
pathogenic HIT antibodies
Do
STOP heparin
Switch to alternate anticoagulant
Don’t Do
No warfarin (Vit K if warfarin given)
No prophylactic platelets
Dx
HIT antibodies
Ultrasound for lower-limb DVT
DTI
COO-
+H
BIVALENT DTI
3N
+H N
3
Lepirudin
Bivalirudin
Argatroban
RENAL
ENZIMATIC>RENAL
IRREVERSIBLE
REVERSIBLE
REVERSIBLE
+
++
++++
+++
+
-
Elimination
Binding
UNIVALENT DTI
Effect on INR
Immunogenicity
HEPATIC
Bivalirudin
Reversible binding to thrombin - BIVALENT DTI
Blocks activation by thrombin of fibrinogen, Fact. V,VIII,XIII
and platelets
Cleaved by circulating proteases
Half-life 25-30’
Proteolytic clevage by thrombin (80%)
Removal by haemofiltration
AVOID STASIS
Set up
Albumin in priming
Consider UF in presence of lung injury and/or capillary leak
syndrome
Heparin bolus 1000 UI after cannulation, then check for bleeding
If bleeding <50 cc/h start heparin infusion to a target
ACT 180-200, aPTT 60 sec
If bleeding on heparin > 50 ml/h stop
2 UI/mL of heparin in the priming
Weaning
ACT >200
ECMO circuit change
Plasma leak
Hemolysis likely if:
• Pressure > 300 mmHg on arterial cannula
• Negative pressure > 200 on the venous cannula
• LDH>1000 mg/dL and FHb >40 mg/dL in two samples within 24h
Thrombi
Check HIT
Thrombocytopenia
Sistematically every 8-10 days
Weaning
Always keep 0.5L flow (risk of thrombosis)
If flow is stopped for definitive evaluation
(30 min. observation)
give heparin 10000 UI before lines clamping
Recirculation
Figure 1.: RVAD Impeller after 33 days of support
Figure 2.: RVAD Impeller after 3 days of low flow support
Similar
European Respiratory Society Annual Congress 2012
European Respiratory Society Annual Congress 2012