UPDATE ON
MINIMALLY INVASIVE
HEMODYNAMIC
MONITORIZATION
Gozde Demiralp, MD
Department of Anesthesiology
Division of Critical Care Medicine
University of Oklahoma, College of Medicine
Oklahoma City, Oklahoma
•  I have no affiliations to disclose.
•  There will be display of new technologies and monitors
during this presentation. All the opinions that will be
displayed here reflects scientific data that is supported by
literature.
Disclosure
Outline:
Optimization of Fluid Therapy in ICU & OR.
How to Assess Volume Responsiveness in 2014 ?
New vs. Old. (CVP, PAOP, PLR, PPV,SPV, SVV)
Minimally Invasive Cardiac Output Measurements
What is out and available?
Why Does Cardiac Output Matter ? :
Monitoring critically ill patients:
What are we really worried about?
“Tissue Hypoperfusion”
What do we really want to monitor?
“Adequate Oxygen Delivery”
Definition of Shock:
“Inadequate tissue perfusion
affecting multiple organ systems.”
Why does Cardiac Output Matter ?:
Oxygen Delivery (DaO2) = CaO2 x CO x 10
= 1000 ml/min
Arterial Oxygen Content (CaO2)
= (0.0138 x Hgb x SaO2) + (0.0031 x PaO2 )
= 20.1 ml/dl
Cardiac Output (CO)
= SV x HR
=4-8 L/min
Would “Standard” ASA
Monitors be Enough to ASSESS
•  Heart Rate (HR)
Cardiac Output and/or
•  Blood Pressure ( Noninvasive vs.
Invasive)
Volume Responsiveness? •  Central Venous
Pressure (CVP)
•  Pulmonary Artery Catheters
(PACs)
HOW TO ASSESS
Volume Responsiveness
IS PATIENT VOLUME RESPONSIVE?
•  Primary resuscitation question is whether the
patient will increase their cardiac output in
response to intravascular volume infusion or
not.
•  Would “Standard” ASA Monitors be Enough to
Assess VOLUME RESPONSIVENESS ?
How to Assess Volume Responsiveness?
Central Venous Pressure
(CVP):
Is it good for anything ?
24 Studies , 803 patients
Systematic Review of Medline, Embase, Cochrane Databases between
1966-2007.
“CVP is a measure of right atrial pressure alone;
and not a measure of blood volume or ventricular
preload.”
Conclusions:
•  This systematic review demonstrated a very poor relationship
between CVP and blood volume as well as the inability of
CVP/CVP to predict the hemodynamic response to a fluid
challenge.
•  CVP should not be used to make clinical decisions regarding
fluid management.
(CHEST 2008; 134:172–178)
Prospective, Non Randomized Non Blinded Interventional Study
Group 1 & 2 ( Invasive w PAC vs. Non Invasive w TTE) ( 12 vs. 32 subjects)
Comparison of pressure derived preload indexes and volumetric preload indexes on
healthy volunteered subjects.
Fluid Challenge: 3L Normal Saline Infusion in 3 hours.
Even in healthy subjects,
“Cardiac Compliance” is
highly variable .
There is no predictable
relationship between static
pressure based preload
indices and volumetric
preload indices.
Passive Leg Raising Test
PLR Test Predicts Preload Responsiveness
Pulse Pressure Variation
(PPV)
Systolic Pulse Variation
(SPV)
“Swing on the Arterial Line”
•  Systemic Review of Literature
•  Review of studies to evaluate how predictive PPV, SPV and
SVV are to detect volume responsiveness and to compare static
fluid status indices.
•  29 Studies = 685 patients
Limitations:
PPV/SPV/SVV still won’t
give any ideas about global
heart function !
Echocardiography to
evaluate overall cardiac
function is recommended.
Minimally Invasive
Measurement of
Cardiac Output
Thermo Dilution
(by itself or combination)
Dye/Indicator Dilution
(by itself or combination)
Arterial Pulse Pressure
Analysis**
Pulmonary Artery Catheters (PACs):
Studies overall the years had conflicting results w PACs.
•  Increased Mortality ?
•  Multiple RCTs were conducted.
•  Conclusion:
No difference in LOS in the ICU
No difference in Mortality
No benefit, no harm
•  “There is no guided therapy tailored towards PAC use.”
•  “PAC is a diagnostic tool,
not a therapeutic one.”
Newer Technologies:
Transpulmonary Thermodilution Methods:
•  PiCCO & PiCCO2
•  VolumeView
(Pulsion Medical Systems)
(Edwards Life Sciences)
Lithium Dilution Technique:
•  LiDCO /LiDCOplus/LiDCOrapid
(LiDCO limited)
Ultrasound Indicator Dilution
•  COstatus
(Transonic Systems, Inc.)
Arterial Pressure Waveform
Analysis
Arterial Pressure Waveform-
Derived CO Measurements
Pulse Power Analysis
LiDCO Systems
Pulse Contour Analysis
PiCCO Systems
Pressure Recording Analytical
Method
(PRAM)
FloTrac Vigileo
Arterial Pressure Waveform
Analysis
Requires CVL and Standart
A-line
Pulse Power Analysis
(LiDCO)
Initial Calibration as well as
Periodic Calibration Needed.
Requires CVL and Femoral
A-line (Dicrotic Notch)
Pulse Contour Analysis
(PiCCO)
Initial Calibration as well as
Periodic Calibration Needed
Pressure Recording Analytical
Method
(PRAM = FLOTRAC)
Requires A-line
Auto Calibration
(Accuracy?)
Arterial Pressure Waveform
Analysis
Limitations of
arterial pressure
waveform analysis:
1.Intrathoracic Hemorrhage
2. Intra Cardiac Shunts
3. Lithium Salts
4. Muscle Relaxants
5. Low SVR States
6. Arrhythmias
7.Limitations of Heart Lung
Interaction
8. IABP
New Terminology with New Techniques:
New Players :
GEDV
ITBV
EVLW
ITTV: Intra Thoracic Thermal Volume
ITBV: Intra Thoracic Blood Volume
PTV: Pulmonary Blood Volume
GEDV: Global End Diastolic Volume
EVLW: Extra Vascular Lung Water
Global End
Diastolic
Volume
GEDV
Prospective Clinical study in Medical ICU
Total 36 Septic Shock Patients with CVL and Fem Aline
PiCCO Systems to assess CI and GEDV.
(Single Indicator-Cold Saline-Dilution = Transpulmonary Dilution)
Comparison of GEDV, CVP and CI after Volume Loading and Dobutamine
Results:
1.  GEDV = Four Chamber Blood Volume = Serves as an indicator of preload
on septic patients.
2.  Changes in GEDVI correlates well with both Stroke Volume Index (SVI) and
Cardiac Index (CI).
3.  Changes in CVP, however, did not correlate well with either SVI or CI. ( It
increased regardless without any end points)
4.  Preinfusion GEDVI was significantly lower in patients who had a “positive”
response compared to “negative” response volume overloading.
5.  GEDVI didn’t increase with Dobutamine infusion, whereas CI, SVI and HR
increased. ( CVP also remained unchanged)
Frank-Starling Mechanism:
Greater the Preload, Greater Increase in SV.
With this study:
Preinfusion GEDVI index significantly correlates
with percentage increase of SVI.
Intra Thoracic
Blood Volume
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2012 Crit Care Med
Prospective Randomized Clinical Trial
120 Patients ( Septic & Non septic)
To receive either PAC or Transpulmonary Dilution Technique
To compare two techniques via comparison of ventilator free
days and LOS in ICU among two groups.
End point of Resuscitation:
EVLW < 10 ml/kg
GEDV < 850 ml/m2
PAOP< 18-20 mmHg.
Results
No difference between two groups in regards to LOS in ICU or
Ventilator free days.
No difference in mortality or other organ dysfunctions among two
groups.
TPTD group ended up receiving more fluid and remained on ventilator
longer days in Non Septic Shock group – likely secondary to fluid overload
and/or cardiac comorbidity.
Extra Vascular
Lung Water
EVLW
Extravascular Lung Water
•  Abnormal accumulation of fluid in the extravascular
space of the lung =
•  “Pulmonary Edema Quantification”
•  Can be due to increased pulmonary hydrostatic pressures
vs. increased capillary permeability. ( ARDS, ALI vs.
Cardiogenic)
•  Why do we care about EVLW?
WHY DO WE CARE ABOUT EVLW?
EVLW
EVLW
•  EVLW Normally 3-7 ml/kg.
•  > 10ml/kg is considered abnormally high and associated
with poor outcomes.
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How to calculate EVLW ?
•  Double Indicator (Thermo- Dye) Thermo Dilution
Technique
•  Single Indicator (Thermo) Thermo Dilution Technique
(PulseCO Method)
•  Others ( Not available as bedside monitor):
Quantitative CT
Positron Emission Tomography Scan
Magnetic Resonance Imaging
Both Dual Indicator TD and Transpulmonary TD techniques
correlated well with gravimetric measurements of EVLW.
Both Available at Bedside.
Diagnostic Value:
Detection of Pulmonary Edema
Better Characterization of Patients with ARDS
Therapeutic Value:
Guiding Fluid Therapy
Limitations of Dilution
Methods During Assessment Of EVLW:
1.  Pulmonary Resection
2.  Pulmonary Flow Obstruction ( Macro/ Micro)
3.  Focal Lung Injury
EVLW
Other Hemodynamic Monitors for ICU2
Contact Info:
Gozde Demiralp, MD
[email protected]
Assistant Professor of Anesthesiology
Department of Anesthesiology
Division of Critical Care Medicine
University of Oklahoma, College of Medicine