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Wet, Dry, or Even?
Some Ways of Looking at Volume Status without
a Pulmonary-Arterial Catheter
Anne K. Sutherland, MD
Critical Care Medicine
St. Barnabas Hospital
March 27, 2010
Pulmonary Arterial Catheter
PACs
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Pulmonary Artery Catheters are no longer
deemed to be an effective tool for monitoring
the volume status of the vast majority of
critically ill patients.
SUPPORT was an observational study of
critically ill patient by Conners et al that showed
PACs to be associated with increased mortality
and increased utilization of resources. (JAMA
1996)
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Harvey et al in the PAC-Man trial showed that
there was no difference in the mortality of
patients managed either with or without a PAC.
(Lancet, 2005)
FACTT
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The FACTT trial showed that PAC-guided therapy
did not improve survival or organ functions but was
associated with more complications than CVCguided therapy.
No difference in mortality between the liberal and
conservative fluid management
Conservative strategy improved lung function,
increased ventilator and ICU free-days
PAOP and CVP: No better than flip
of a coin
Osman et al CCM Jan 2007
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Retrospective study of all fluid challenges in 96
mechanically ventilated patients with severe sepsis
or septic shock between 2001 and 2004 who were
being monitored with a pulmonary arterial catheter.
Patients were given a volume challenge of 500 cc of
6% hydroxyethyl starch based on clinical signs of
hypoperfusion.
Patients were divided into groups of responders and
non responders based on whether or not the
cardiac index increased by 15%.
Results of Osman
Physical Exam
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Orthostatic hypotension – postural pulse increase of
>30 beats/min has a specificity for hypovolemia of
96% (McGee, JAMA, 1999)
Postural hypotension occurs in up to 10% of
normovolemic patients
Supine tacycardia is specific (96%), but insensitive
(~10%)
Supine hypotension is also specific and insensitive
(McGee, JAMA, 1999)
The problem: How do I decide if my
hypotensive septic patient needs
fluids, pressors, or an inotrope?
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Septic patients require volume
Giving pressors to an under-resuscitated patient
can cause tissue hypoxemia and ischemia
However, giving too much fluid may lead to
prolonged ventilatory support
Giving fluid is deleterious when the patient will
not respond to the fluids with an increase in
Cardiac output
The Perfect Volume Status Monitor
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Fast
Easy to learn
Validated in all critically ill patients. (medical,
surgical, trauma, neurosurgical on and off
positive pressure ventilaiton)
Available outside of the ICU, not require any
highly specialized equipment
Give an easy answer
Dynamic Methods to look at
Hemodynamics and Volume Status
in the MICU
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Take advantage of the Heart-Lung interactions
during positive pressure ventilation.
Arterial Line Monitoring with dynamic analysis
of the wave form and pulse pressure variability
Echocardiography to predict volume
responsiveness (not going to be covered in this 20
minute talk!)
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LV, IVC, SVC
Fluid Responsiveness
A patient who is fluid
responsive will have a
significant (>15%)
increase in CO in
response to a fluid
challenge.
This indicates that the
heart is on the steep
portion of the FrankStarling Curve
Volume Responsiveness in Critically
Ill patients
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Many of our critically ill, hypotensive patient are
on positive pressure ventilation
PPV causes changes in venous return, which is
accentuated in hypovolemic patients
It is possible to take advantage of the swings in
venous return in order to determine the fluid
responsiveness of hypotensive patients
2 major tools to look at this:
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Echo
Arterial Line – looking at changes in the pulse
contour, and in the pulse pressure
Positive Pressure and Venous
Return – Taking advantage of HeartLung Interactions
In a volume
resuscitated patient:
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Venous return does not
fall during inspiration on
PPV
Intrathoracic pressure is
positive
Intrabdominal pressure
also rises
Pressure gradient
between the abdomen
and thorax is maintained
Positive Pressure and Venous
Return – Taking Advantage of HeartLung Interactions
In volume depleted
patient on PPV:
Collapse of intra-abdominal
veins and SVC occurs as a
result of positive intrathoracic
pressure
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This results in a fall in
venous return RV stroke
volume, LV preload and
cardiac output
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Maximum SBP occurs during
inspiration in PPV
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Maximum RV pre-load occurs during expiration
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Additionally, there is an increased return of
blood from the lung to the LV during inspiration
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There is a lag secondary to pulmonary transit time,
which results in increased LV stroke volume during
inspiration
Pulmonary blood vessel compression
Decrease in left ventricular after-load
Interventricular effects:
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A decrease in RVSP in inspiration leads to increased LV
compliance which leads to an increase in LV pre-load
Min SBP occurs during expiration in
PPV
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Positive pressure during inspiration causes a
decrease in venous return, which results in
decreased right ventricular stroke volume
There is a lag of 2-3 heart beats secondary to
pulmonary transit time, which leads to the
decreased LV SV during expiration
Michard 2000 cont.
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The magnitude of
respiratory changes in
LV stroke volume and
pulse pressure should
be an indicator of
biventricular pre-load
dependence
40 septic, hypotensive
patients with a-lines
were studied on
positive pressure
ventilation
Michard, AJRCCM, 2000
Michard 2000 cont.
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The effects of volume
expansion upon CI as
measured with a PAC
was analyzed
Patients with a
baseline ΔPp >13%
were very likely to
respond to VE by
increasing CI by
>15% (ppv 94%)
Michard 2000 cont.
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Michard – they used PPV as calculated
themselves by looking at the wave form, with
their own analysis
In the 40 patients studied, 9 patients were
paralyzed, and 8 more had to be temporarily
paralyzed for the readings.
Pulse Pressure Relationship to
Stroke Volume
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The compliance of the aorta is not a linear
relationship between pressure and volume
The same PPV may theoretically result from
large swing in volume in a patient with
compliant arteries, or smaller swings in SV in
stiff arteries
Wave reflection – pulse pressure from an a-line
is the combination of the incident pressure
wave and reflected wave from the periphery
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Damping
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Aortic flow during systole – outflow tends to be
Devices to Automatically analyze
waveforms – for SVV and PPV
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PiCCO
LiDCO/Pulse Plus
Flotrac/Vigilo
PiCCO
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PiCCO is a device made by Phillips that
enables continuous hemodynamic monitoring
using a femoral or axillary thermodilution a-line
(proprietary) and a central venous line.
Looks at both static and dynamic parameters:
1. Fluid responsiveness: SVV and PPV
2. CO measurement - transpulmonary thermodilution
and pulse contour analysis
3. Extravascular Lung Water Index
4. Global End-diastolic volume index
5. Cardiac Index
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Requires calibration with a thermal bolus, and
thus needs a special femoral a-line to determine
CO using transpulmonary dilution
PiCCO
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PPV – Pulse Pressure Variability – the
difference between systolic and diastolic
pressure throughout the respiratory cycle has
been shown to be able to predict fluid
responsiveness
An index of 13% discriminates between fluid
resonders (an increase in CO of >15%) and
non-responders
PPV has been shown to predict fluid
responsiveness in CABG patients, patients with
septic shock and ALI
On a PiCCO Monitor
PiCCO
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SVV – determined by analysis of the
continuous arterial pulse contour – uses the
area under the systolic curve for beat-to-beat
determination of stroke volume and their
variation over the respiratory cycle – can also
use for determining volume responsiveness
> 10% is considered to be responsive
PiCCO
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Marx et al in 2004 – with 10 septic patients
used PiCCO's calculation of SVV to determine
whether or not to volume load a patient. (all
patients were in sinus rhythm)
PiCCO was just as good as PAC as determining
whether or not a patient would respond to a
fluid bolus
LiDCO
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Made by the LiDCO group in London
Measures Cardiac output using a small dose of
lithium injected in the periphery and then
generating a arterial lithium concentration-time
curve by withdrawing blood past a lithium
sensor attached to the patient's a-line
It then uses proprietary software to calculate
continuous beat-to-beat cardiac output, by
analysis of the arterial blood pressure tracing.
FloTrac/Vigileo
No calibration needed, derives
measurements based on compliance
and patient characteristics (gender, age,
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height and weight – derived from experimental
cadaver data)
Measures the pulsitility of the arterial
waveform by calculating the standard
deviation of the arterial pressure wave
over a 20s period – multiplied by the
compliance
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The initial software autocalibrated every
20 minutes, leading to bad ROC when
compared to PACs – however it now
autocalibrates every minute.
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FloTrac and Cardiac Output
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FloTrac has been proven to be an acceptable
way of monitoring CO in patients undergoing
CABG (de Waal, CCM, 2007)
SVV as measured by FloTrac has been shown
to be higher in patients who responded to fluid
loading: 18 vs 4 (p <0.001) (Cannesson, Eur J of
Anesth, 2007)
Using FLoTrac to Guide Goal Directed Therapy in
High-Risk Elective Surgical Patients
Mayer et al. Critical Care 2010
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Randomized, Single-Center Study of 60 patients
Intra-operative GDT using a protocol based on enhanced
hemodynamic variables derived by the Flo-Trac/Vigileo device
reduced the LOS in high-risk patients undergoing major abdominal
surgery compared with a standard management protocol.
Both groups received the same amount of fluids, but the intervention
group received more colloid.
The incidence of complications was reduced in the enhanced
monitoring group.
No difference between the standard and enhanced monitoring
protocol groups was found with regard to ICU stay.
PULSE Study Group
PAC/PiCCO Use and Likelihood of Success Evaluation
Uchino et al 2006
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Multi-center observational study of 331 patients
with either a PAC or PiCCO (192 PiCCO 150
PAC, 11 with both)
No difference in outcomes either way (although the
PiCCO patients tended to be in positive fluid balance, and to be
on the vent longer)
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Demonstrates the difficulty in studying the effect
of a tool on outcomes – how you get data is
important – but what you do with it actually
affects patient outcome.
Intermittent Contin. Addit'l
Invasive
CO
CO
Variables
PiCCO
Plus
Femoral
Transpulm.
Every
thermistor
thermodiluti
-tipped
3s
on
catheter
Limits
Severe
GEDV,
Vasc.
Disease,
EVLW,
SVV, PPV IABP,
arrythmias
PulseCO/ Regular a- Transpulm.
Beat to
SVV
thermodiluti
Beat
LiDCO line
on
SVV/PPV,
IABP,
arrythmias
FloTrac/
Vigelo
Spont.
Breathing,
IABP
arrythmias
Regular aNone
line
Every
20s
SVV
Problems with Dynamic
Measurements
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Mechanical problems with a-line (dampening,
air bubbles, etc)
Arrhythmias – variation no longer a reflection of
changes due to mechanical ventilation (esp.
with patients with a-fib or frequent PVCs)
Small pleural pressure changes – ie in patients
with low tidal volumes, spontaneously breathing
or open chests.
Just because the patient has increased SVV or
PVV does not mean that she needs volume
expansion.