Seri-IPo-HemoMonitoring-Izmir-'14 [Schreibgeschützt] · Comprehensive hemodynamic monitoring aids...
Transcript of Seri-IPo-HemoMonitoring-Izmir-'14 [Schreibgeschützt] · Comprehensive hemodynamic monitoring aids...
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Istvan Seri MD, PhD, HonDSidra Center of Excellence in NeonatologySidra Medical and Research Center
Weill-Cornell Medical College-Qatar, Doha, Qatar
Comprehensive Hemodynamic Monitoring in Neonates
IPOKRaTES Foundation – Clinical Course
Neonatal Hemodynamic Course - Singapore
Istvan Seri, MD, PhD, HonD has disclosed the following financial
relationships. Any real or apparent conflicts of interest related to the
content of this presentation have been resolved.
Affiliation / Financial Interest Organization
Educational Grant to support the
Neonatal Hemodynamics Club,
2013, 2014
Covidien Inc.; Mansfield, MA
Co-editorship of “Cardiology and
Neonatal Hemodynamics”; Book Royalty
Elsevier, Inc.; Philadelphia, PA
Disclosure Statement
Organ BF Distribution:
Vital OBF - O2 DeliveryNIRS – Cerebral rSO2
Doppler - US
BP = CO x SVR
Monitoring:
Blood pressure
measurements
Monitoring:
• Calculated (BP/CO);• Laser-Doppler;• Visible-light;
• NIRS
Monitoring:• Echocardiography;
• Impedance EC;• Pressure wave-form analysis;
• MRI
Systemic
Blood PressureDependent Variable
Systemic ResistanceIndependent variable
(Vasopressors, Lusitropes)
Systemic FlowIndependent variable
(Inotropes)
Organ BF Distribution:
Non-vital OBF - O2 Delivery
NIRS – Renal, intestinal, muscle rSO2
Doppler - US
O2 Delivery
O2 Demand
When blood flow regulation
exhausted:
1. ↑ Capillary recruitment (Visible light; Dark-field imaging)
2. ↑↑↑↑ O2 extraction (NIRS)
3. ↓↓↓↓ brain function (aEEG)
DEVELOPMENTAL HEMODYNAMICSBLOOD PRESSURE, BLOOD FLOW, BLOOD FLOW DISTRIBUTION, VASCULAR RESISTANCE
Soleymani et al, Expert Rev. Med. Devices 9, 501–511; 2012
↔
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1. Conventional assessment
a) Blood pressure, heart rate, O2 saturation
b) Indirect clinical & lab signs of CV function (Uv, CRT, ∆TC-P, BD, serum lactate)
2. Systemic and organ blood flow using
a) Echocardiography (LVO, RVO, SVC flow, PAP, EF, SF, MPI, VTI, PI, RI, etc)
b) Dilution techniques, direct & modified Fick methods, intra-arterial ultrasound probes, arterialpressure waveform analysis, electrical impedance cardiography, electrical cardiometry
c) NIRS, Laser Doppler, side-stream dark field imaging technology* (microvascular blood flow)
3. O2 delivery and consumption in tissues
a) Continuous wave differential or SR NIRS for CBF (∆CBV, absolute CBF, CFOE, TOI^)
b) SR NIRS for cerebral, renal intestinal and muscle oxygenation ([rSO2])
c) Visible light technology (buccal, other mucosal or skin blood flow)
4. Functional assessment (aEEG for brain activity)
5. MRI
6. Data collection requires use of real-time data acquisition systems
Assessment of cardiovascular function, organ perfusion, O2 delivery
and brain function in neonates at the bedside
Soleymani et al; Exp Rev Med Devices 2012; 9:501–511
Hypotheses:
1. Comprehensive hemodynamic monitoring aids in the
a. timely diagnosis
b. pathophysiology-targeted treatment of neonatal shock
2. Diagnosis and pathophysiology-targeted treatment of
neonatal shock especially in its early, compensated phase will
improve clinically relevant, short- and long-term outcomes
Comprehensive Hemodynamic Monitoring in Neonates
Comprehensive Hemodynamic Monitoring
Real-time, Comprehensive Monitoring and Data
Acquisition
1. In addition to conventional parameters (SpO2,HR, BP, RR,
TCOM), continuous assessment of changes in systemic blood
flow (EV, US) and vital and non-vital organ blood flow
(NIRS, US) and peripheral perfusion (Laser Doppler) and
brain function (aEEG)
2. More data needed to establish
• Pathophysiologic and clinical relevance of neonatal shock
• Hemodynamic effectiveness of treatment
• Clinical relevance of hemodynamic effectiveness of treatment
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Sadaf Soleymani, MS
Hemodynamic Monitoring and Data Acquisition System
Patient Monitoring System #1
Computer
Data Acquisition System
Camera
Impedance Electrical Cardiometry
Modules for Modules for HR, BP, SPO2, RR, TCOM
Near Infrared Spectroscopy(NIRS)
Patient Monitoring System #2
(for additional channels)
aEEG
Laser Doppler (Peripheral BF)
0
100
200
300
400
500
600
700
800
900
LVO-ev LVO-echo
ᴏ
ᴏᴏ
Cardiac Output (m
L/m
in)
Continuous Non-Invasive Cardiac Output Measurements in
Neonates by Electrical Velocimetry (EV) - Comparison with
Echocardiography
EV’s Error percentage (EP) = 43.6%
ECHO’s precision = 30%
True precision of EV = 31.6%
115 paired measurements in 20 healthy term neonates on postnatal days #1 and 2
True PrecisionEV = √ [(EP)2 – (precisionecho)2]
Noori et al, Arch Dis Child Fetal-Neonatal Ed, 2012 Hot Topics, Washington, DC -
2013
ICON (Cardiac Output)
Continuous Web-Based Data Collection
Usual NICU Set-up
•EMR data charted hourly
•Data from Servers not getting to Viewer Workstations
•Data from additional devices not connected to monitors and do not reach collection workstations
Solution
•To record data continuously from patient monitosr and bedside equipment
•Continuous data recording can be accomplished in any number of beds
•Needs a DataBase
Execution
•Ensure system meets hospital standards
•Create a VM for DBase
•Viewer workstations with receiver software for HL7 data from Philips servers
•Bridges used for devices that are not connected to Philips server
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Philips MP70: Numeric: HR, BP, SPO2, TCOM, RRWaveform: ECG wave, BP wave
ICON: Cardiac Output (CO)
INVOS:Regional O2(rSO2)
Ventilators: (AVEA/ Servo-i)
CPC Virtual ServerCPC Virtual Server
CHLA NICCU Data Flow: Bernoulli System
Patient Monitor (MP70)Patient Monitor (MP70)
Bernoulli Multi Port BridgeBernoulli Multi Port Bridge
Bedside MonitorsBedside Monitors
Comprehensive Hemodynamic Monitoring
Examples
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Dopamine2 mcg/kg/min
0.9% SalineBolus (15 min)
Mechanisms of Action of Vasoactive Medications: VolumeEffect of saline bolus in a 1-day old 36-week’s gestation neonate
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Hemodynamic Parameters and Cerebral and Renal Regional
Tissue Oxygenation in a Very Preterm Infant during Postnatal Day
#1
Steady increase in CrSO2 despite no change or decreases in SPO2 (CO and pCO2 and continuously monitored)
(GA=26 weeks; BW=976 g) HR
SPaO2
RrSO2
CrSO2
MBP RR
Hemodynamic Effects of Positioning in Neonates
Neonates without congenital cardiac defects admitted to the NICU are eligible for enrollment.
Heart rate, stroke volume (SV) and cardiac output (CO) are monitored
continuously by electrical cardiometry (Aesculon, San Diego, CA).
Skin blood flow is continuously assessed on the forehead or foot using Laser Doppler technology (PeriFlux 5000, Ardmore, PA).
Statistical analysis: Wilcoxon matched-pairs signed-ranks test.
→ →
10min 10min 10min
Ma et al; AAP Meeting, Orlando, FL 2013
5010
015
020
0
beat
s/m
inut
e
Heart Rate
supine prone back to supine
p<0.01 p<0.01
.51
1.5
22.
5
ml/k
g
Stroke Volume
supine prone back to supineN = 30 N = 30
Outlier
Maximum (within 1.5x IQR)
Upper Quartile
Median
Lower Quartile
Minimum (within 1.5x IQR)
Outlier
Box and whisker plot
Neonatal Hemodynamic Monitoring:
Hemodynamic Effects of Positioning in Neonates
Ma et al; AAP Meeting, Orlando, FL 2013
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p<0.01 p<0.01
0.5
11.
5
perf
usio
n un
it
Skin Blood Flow Index
supine prone back to supine
p<0.01 p<0.05
.1.2
.3.4
.5m
mH
g / m
l / k
g
Calculated SVR Index
supine prone back to supine
N=21
N = 30 N = 21
p=0.09
p=0.08
2040
6080
100
mm
Hg
Blood Pressure
supine prone back to supineSBP DBP MBP
N=21
p<0.01 p<0.01
100
150
200
250
300
ml/k
g/m
in
Cardiac Output
supine prone back to supineN = 30 N = 21
Ma et al; AAP Meeting, Orlando, FL 2013
Hemodynamic Effects of Positioning in Neonates
Conclusion
Short term prone positioning is associated with significant
changes in cardiovascular function
1. Decreased stroke volume and cardiac output
2. Decreased skin blood flow
3. Increased calculated vascular resistance
4. However, it’s unclear why HR does not increase to compensate for
the decreased CO and BP (DBP) increases at the same time.
Neonatal Hemodynamic Monitoring:
Hemodynamic Effects of Positioning in Neonates
Ma et al; AAP Meeting, Orlando, FL 2013
Cerebral and renal regional O2 saturations during arterial desaturation
episodes in ≤3-day old ELBW infants (n=7)
Duration of Desaturations: 8±±±±3 minutes
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Renal and Cerebral rSO2 vs. SPO2 % Change
0,0
0,1
0,2
0,3
0,4
0,5
0,6
0,7
0,8
0,9
0 0,2 0,4 0,6 0,8
rSO
2Change
SPO2 change
Renal
Cerebral SPO2 = 20.5% ±13.6
CrSO2=24.2% ±15.8
RrSO2=41.0% ±19.8*
* = p<0.05
Soleymani et al. PAS, 2012
Gestational Age 25.9 ±1.7 weeks
Birth Weight 899 ±152 g
Duration of Desaturations 8 ±3 minutes
Results
While the decreases in SPO2 and CrSO2 were similar (20.5 vs. 24.2%), the decrease in RrSO2 was close to twice that of CrSO2 (41.0 vs. 24.2%)
Conclusion
In response to decreases in SPO2, blood flow decreases in the kidneys while cerebral blood flow is likely maintained
Cerebral and renal regional O2 saturation during arterial desaturation
episodes in ELBW neonates during the first postnatal days
Soleymani et al. PAS, 2012
MR-COMPATIBLE INCUBATOR, VENTILATOR AND
MONITORING SYSTEM
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Fore- and Hindbrain Blood Flow
Response to Changes in O2 or CO2
Delivery in Adults and Neonates
Simultaneous MRI - NIRS
• Perfusion and blood flow changes assessed by MRI using BOLD signal and phase contrast method, respectively.
• Changes in tissue perfusion assessed by NIRS
IPoKRATES -Rio 2013
Phases of Neonatal Shock
Compensated phase
Heart rate; Urine output; No change in blood pressure;
Blood flow distributed to vital organs (brain, heart, adrenal glands) at the
expense of non-vital organ perfusion
Uncompensated phase
Heart rate; Urine output; Blood pressure
Blood flow in all organs, tissue hypoperfusion and acidemia develop
Irreversible phase
Irreversible cellular damage
Phases of Neonatal Shock
Compensated phase
Heart rate; Urine output; No change in blood pressure;
Blood flow distributed to vital organs (brain, heart, adrenal glands) at the
expense of non-vital organ perfusion
Uncompensated phase
Heart rate; Urine output; Blood pressure
Blood flow in all organs, tissue hypoperfusion and acidemia develop
Irreversible phase
Irreversible cellular damage
During compensated phase of shock when BP is maintained in the
normal range, organ blood flow is determined by organ assignment:
1. Vessels in vital organs (brain, heart, adrenal glands) vasodilate when
perfusion pressure falls
2. Vessels in non-vital organs vasoconstrict when perfusion pressure falls
Thus, if patient is stressed but not hypotensive, cerebral blood flow
is maintained
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1. What is the explanation for the documented
decrease in CBF in normotensive very preterm
neonates during the first postnatal day?
2. Why do very preterm neonates mostly
develop P/IVH during the second or third
postnatal day?
Questions
Pathophysiology of Brain Injury in Very Preterm
Neonates
1. Proposed mechanisms of brain injury during transition
a. Developmental regulation of vital organ assignment of
forebrain (answer to Question #1)
b. Hypoperfusion-reperfusion cycle (answer to Question #2)
2. Pathophysiology-targeted prevention and treatment
approaches
Hernandez MJ et al. CBF, effects of nerves and neurotransmitters. Heistad DD, Marcus ML (Ed). Elsevier; 1982; p. 359–66
Normoxia
Hypoxia
Changes in fore- and hindbrain vascular resistance in response
to hypoxia in beagle pups
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*
Postnatal Age (h)
Decreased CBF in ELBW neonates immediately after delivery
Cerebral tissue O2
saturation (CrSO2)-NIRS:
CrSO2 is directly related to CBF if SpO2 and metabolic rate are comparable and stable, respectively.
(Lemmers et al – shown with permission)
<28 weeks 28-29 weeks 30-31 weeks
CrS
O2(%
)
Cerebral Fractional O2 Extraction (CFOE) by
NIRS:
CFOE is inversely related to CBF as long as metabolic rate and SPsO2 are unchanged.
(Kissack et al. J Cereb B Flow Metab; 2005; 25:545)
CFOE
Postnatal days
↓↓↓↓ FiO2
NIRS
Simultaneous Use of MRI - NIRS
↓↓↓↓ FiO2
MRI
Hindbrain-NIRS
Functional
Activity
Functional
Activity
Borzage et al; Preliminary data, 2012
Neonate
Adult
↓↓↓↓FiO2
FiO2 = 0.12
HYPOXIC CHALLENGE IN ADULT AND NEONATAL FOREBRAIN
NIRS
Forebrain
Borzage et al; Preliminary data, 2012
Neonate
Adult
BOLD –MRI
Fore-an
d Hindbrain
↓↓↓↓FiO2
FiO2 = 0.12
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Blood Flow Changes in Adult Fore- and Hindbrain during CO2
Challenge by Phase Contrast MRI
-1
0
1
2
3
1 2 3 4 5 6 7 8
∆Flow [ml/s]
Forebrain Flow Hindbrain Flow
Carbon Dioxide
P<0.05 vs baseline
Time (minutes)= Carotid and basilar arteries
= Vertebral and basilar arteries Borzage et al; Preliminary data, 2013
INVESTIGATORS
CHLA-USC faculty International Collaborations
Philipe Friedlich, MD, MEpi, MBA Barna Vasarhelyi, PhD
Shahab Noori, MD Tivadar Tulassay, MD, DSciRowena Cayabyab, MD Lola Stavroudis, MDMac Ebrahimi, MD Anita Aperia, MDPierre Wong, MD Ann-Christine Eklof, PhDBijan Siassi, MD Alejandro Bertorello, MDRangasamy Ramanathan, MD Gianni Celsi, MD
Frank van BelPetra LemmersFlora Wong
CHLA-USC fellows/residents National Collaborations
Shazia Bohmbal, MD Michael Wider, PhD (Somanetics)Bonnie Tam, MD Sandra L Drake, PhD (Somanetics)Amin Addie, MD Erin A Booth, PhD (Somanetics)Karine Barzaghyen, MD Jackie Evans, MD
Soraya Abbasi, MD
CHLA-USC PhD students Jeffrey Gerdes, MDMatt Borzage Barbara Ballermann, MDSadaf Soliemani Steven R Gullans, PhD
Barry Brenner
International FellowsRaul Nachar, MD, Valerio Romano, MD
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COMPREHENSIVE HEMODYNAMIC MONITORING
QUESTIONS?