Download Venous Return - Erasmus Critical Care

Venous Return
Jan Bakker
[email protected]
Erasmus MC University
Medical Center Rotterdam
• 45+ ICU beds in a 1300 bed hospital
• Trauma center, Only center allowed to do all transplantations in adults
and children
• ECMO center (last 5 mo: 20 patients)
• Admitting 2500 patients in ICU and 1000 in PACU
• 70% Mechanical Ventilation
• APACHE II: 20±9
Research
• Circulation: 10 PhD students
• Ventilation: 4 PhD students
• Ethics/EOL: 2 PhD students
Venous Retrun
‣Do you measure venous return in your
patients?
Cardiac Output
‣ Is not a physiological variable
‣ Product of Stroke Volume and Heart Rate
‣ When cardiac function is normal this is a
passive variable
‣ Major determinant is the return of blood to the
heart (venous return)
‣ Acute decreases are not well tolerated as
compensation mechanisms are limited
Main functions of the heart
‣
‣
Keep the right atrial pressure low
- facilitate venous return
Equal RV-output to LV-output
- Frank-Starling mechanism
Starling’ Law
The Starling mechanism provides the “fine tuning” to
match in-flow to out-flow
Consider a situation where the SV of the RV is 101 ml
and that of the LV is 100 ml (1% difference). Heart rate is
70 /min
In 1.5 hour the total blood volume would be in
the lungs!
S. Magder
Regulation of CO
‣ A healthy 25 year old donates one kidney to his sister
‣ In stable conditions CO is measured before donation
‣ Following complete recovery CO is measured again under stable
conditions
‣ Is the CO following the removal of one kidney
higher - similar - lower than before the
donation?
PS! Don’t consider the compensation mechanisms in the remaining kidney
heart rate? This is not easy to comprehend if one
nks in a ’cardiocentric’ manner and focuses on the
l-known formula learned by all physiologists: carc output ! stroke volume " heart rate.
effectively accommodate changes in venous return.
This conceptual framework is very helpful in explaining changes in cardiac output that occur during
exercise (when metabolic activity and blood flow to
skeletal muscles are increased), after eating a large
meal (which increases metabolic activity and blood
flow in the gastrointestinal system), and in many other
physiological conditions. In each of these circumstances, cardiac pumping ability plays a relatively
Distribution of cardiac
output
diac Output is th e Sum of Tissue an d Or gan
od Flow s
had shown Fig. 1 before asking this question, I
bt that anyone would have had difficulty answer-
FIG. 1 .
Relation sh ip betw een car diac output an d per iph er al blood flow r egula-
Microcirculation
Pulmonary circulation
CO2
CO2 production
CO2 flow
Expiration
Organ
O2 consumption
Circulation
O2 flow
Lungs
Inspiration
QCO2
VO2
Dilate
SV
HR
Recruit
Vt
F
O2
Starling’s Law
CVP
Output
Output
Starling J. Physiol 1914
CVP
RAP vs CO in exercise
RAP vs CO in exercise
1
Stressed volume
stressed
volume
unstressed
volume
stressed
volume
unstressed
volume
stressed
volume
unstressed
volume
Determinants of venous return
➢ RAP
➢ Vascular compliance
➢ Stressed volume
➢ Resistance to venous return
➢ Distribution of blood flow
Stressed volume
5 anesthetized, hypothermic (19oC) patients
3p Thoracic arch
2p Vena caval resections
Passive drainage of the RA-catheter after cardiac arrest
Stressed volume
1290±296 ml
20.2±1.0 ml/kg
Stressed volume is 30±17% of the total blood volume
Crit Care Med 1998;26(6):1061-1064
Mean Circulatory Filling
Pressure
The gradient for venous return is normally very small.
In this case it is only 4 mm Hg
Jean-François Georger
Olfa Hamzaoui
Anis Chaari
Julien Maizel
Christian Richard
Jean-Louis Teboul
Restoring arterial pressure
with norepinephrine improves muscle tissue
oxygenation assessed by near-infrared
spectroscopy in severely hypotensive septic
patients
Intensive Care Med (2010) 36:1882–1889
DOI 10.1007/s00134-010-2013-3
ORIGINAL
188
• 28 patients with septic shock
• Fluid resuscitated
Abstract Purpose: To examine
Received: 18 January 2010
Norepinephrine
to
increase
MAP>65
mm Hg of administration of
•
the consequences
Accepted:
19 July 2010
measured and served as controls.
Results: In healthy volunteers, StO2
Table online:
2 Macrocirculatory
variables
(mean ±on
SD)
in septic
StO
Published
6 August 2010
norepinephrine
muscle
tissue shockranged between 75 and 90% and StO
2 2
!patients
Copyright jointly held by Springer and
slopes ranged between 1.5
oxygenation in severely hypotensive recovery 95
ESICM 2010
and 3.4%/s. Administration of norseptic shock patients. Meth90 which was associated
ods: This was
a prospective
Jean-Louis Teboul is a member
of the norepinephrine
Before
After
norepinephrine epinephrine,
medical advisory board of Pulsion.
with an increase in MAP from 54 ± 8
observational (introduction/increase)
study conducted in a
(introduction/increase)
medical intensive care unit of a uni- to 77 ± 985mmHg (p \ 0.05), also
p<0.05
Electronic supplementary material
induced increases in CI from
versity
hospital.
We
included
28
The
online
version
of
this
article
SAP (mmHg)
86 ± 19
126 ± 18*
80 to 3.61 ± 1.28 L/min/
3.14 ± 1.03
(doi:10.1007/s00134-010-2013-3) contains septic shock patients that received
2
DAP
(mmHg)
38
±
7
52
±
8*
supplementary material, which is available early volume resuscitation. All were m (p \ 0.05), in StO2 from 75 ± 9
(mmHg)
54 ± 8 eligible for receiving
77 ±norepinephrine
9*
to MAP
authorized
users.
75 (p \ 0.05) and in StO2
to 78 ± 9%
introduction of
-1
Heart rate (min ) 98 ± 25 because of life-threatening
101 ± 28 hypoten- recovery slope from 1.0 ± 0.6 to
norepinephrine
70
Temperature (!C) 37.5 ± 1.4 sion and low diastolic
37.5 ± 1.3
1.5 ± 0.7%/s (p \ 0.05). Concluarterial
increase in the dose
2
CI (L/min/m )
3.1 ± 1.0 pressure. Muscle
3.6tissue
± 1.3*
oxygen satu- sions: Norepinephrine administraof norepinephrine
65at achieving a MAP higher
GEDVI (mL/m2)
687 ± 117 ration (StO2) and
730its±changes
156* during a tion aimed
than 65 mmHg in septic shock
EVLWI (mL/kg)
13 ± 9 vascular occlusion
13 test
± 7were mea60 life-threatening hypopatients with
SaO2 (%)
94 ± 5 sured at the level93of±the4 thenar
a near-infrared
spec- tension resulted in improvement of
PaO
± 73
115
± 63
J.-F.
Georger
! O. Hamzaoui !122
A. Chaari
! eminence using
2 (mmHg)
55
NIRS variables
measured at the level
troscopy
(NIRS)
device.
J. PaCO
Maizel ! C.
Richard
!
J.-L.
Teboul
(
)
after
)
before
40 ± 16
40 ± 15
2 (mmHg)
Transpulmonary thermodilution car- of the thenar eminence.
Service de réanimation médicale,
norepinephrine
norepinephrine
pH
7.34 ± 0.10diac index (CI)
7.33
± 0.10
Centre Hospitalo-Universitaire de Bicêtre,
and NIRS-derived
(introduction/increase)
ScvO2 Publique-Hôpitaux
(%)
± 9 variables were obtained
72 ± 7*before and Keywords Muscle (introduction/increase)
Assistance
de68
Paris,
tissue oxygen
EA 4046, Université Paris Sud,
saturation ! Norepinephrine !
after the mean arterial pressure
78,SAP
rue du
Général arterial
Leclerc, pressure, DAP diastolic arterial pressure, MAPSeptic
Fig.shock
1 Individual
values ! of the muscle tissue oxygen saturatio
systolic
! Microcirculation
(MAP) was increased by norepi94mean
270 Le arterial
Kremlin-Bicêtre,
France
(StO2) before
and during administration of norepinephrine in sept
pressure, CI cardiac
index,The
GEDVI
end-diaspectroscopy
nephrine.
baselineglobal
StO2 and
the Near-infrared
e-mail: [email protected]
stolic
volume index, EVLWI extravascular
lung water
index,variSaO2 patients. The eight patients who had already received norepinep
vascular occlusion
test-derived
Tel.:
?33-1-45213547
arterial
oxygen saturation, PaOables
pressure
of oxygen
of 17 healthy
volunteers
were in rine are represented by dotted lines. The grey cross-hatched zo
Fax:
?33-1-45213551
2 partial
Restoring arterial pressure
with norepinephrine improves m
oxygenation assessed by near-in
spectroscopy in severely hypote
patients
%
Jean-François Georger
Olfa Hamzaoui
Anis Chaari
Julien Maizel
Christian Richard
Jean-Louis Teboul
arterial blood, PaCO partial pressure of carbon dioxide in arterial represents the range of values of the StO measured in our group
Bakker et al. Ned Tijdschr Geneeskd 1996;140:2498-2502
Rare cause of shock
17 yr old, following liver transplantation
Admitted in other hospital with shock: hypovolemic?
Not responding to therapy
Massive amounts of vasopressors
Diagnosis: obstructive shock
due to compression of the
inferior vena cava
Rapid discontinuation of the
vasopressors
Uneventful recovery
Importance of venous
return
‣ Cardiac output is coupled to oxygen demand
‣ The primary mission of the heart is to facilitate venous return by
keeping RAP low to match LV-output to the demand for oxygen
delivery
‣ The determinant of venous return is the stressed volume
•
•
Increase in unstressed volume decreases CO
Increase in the resistance to venous return limit CO