CHƯƠNG TRÌNH TỐI ƯU HÓA SINH LÍ SỬ DỤNG SVV & SI

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PHYSIOLOGIC OPTIMIZATION

PROGRAM USING SVV & SI

Yes No

Fluid Infusion

1 liter NS SI >Normal SI Low SI High
Pressor Inotrope/

Vasodilator Diuretic

Volume Responsive: SVV>13%

1 2 3

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Fluid therapy!!

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The Volume prescription Rx for the

Critically Ill and Injured

William T. McGee, M.D., M.H.A. 
FCCM, FCCP

Intensivist

Baystate Medical Center, Springfield, MA
Associate Professor of Medicine and Surgery

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Relevant Disclosures

Edwards Lifesciences

FloTrac/Vigileo/EV1000/ Clear
Sight

My cases; POPtm (free)
PICCO

LIDCO
Echo

Esophageal Doppler

Respirophasic change in SV
(SVV)

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What I won’t be able to do in

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Hospital mortality according to whether or not 
patients achieved AIFR, CLFM, both, or neither.

Murphy C V et al. Chest 2009;136:102-109

intensivist

surgeon

cardiologist

Fool guessing!

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Goals:

1. Volume management is the most

important part of care of the critically ill
(volume management is important )

2. POP provides a simple physiology based
way to accomplish it

3. Physiology based care is important in the
ICU

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A critique of fluid bolus

resuscitation in

severe sepsis

Andrew K. Hilton & Rinaldo Bellomo

Critical Care 2012, 16:302

BAD Fluids!

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•The Question we ask on rounds every
day….

•Do we want to give more IVF?!?!?!?!?
•Is the patient fluid responsive?!?!?!?!?

Fundamentally, will fluid increase the
patient’s stroke volume and therefore
increase oxygen delivery?

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Fluid ?

Pressor ?
Diuretic ?

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DO

2

= CO (CaO

2

)

CaO

2

= Hb (1.36 ccO

2

/gm)

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What percentage of ICU

patients are volume depleted

after 24hours?

1. Almost 0%
2. 25%

3. 50%
4. 75%

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Volume therapy critical care

perspective: 1 question

What is the impact on cardiac performance?
Requires a cardiac performance measure!

Ultimately

DO

2 is what we can control

regarding Organ perfusion and function.

Answer: Physiologic Optimization Program

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Is Volume Management

Important?

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Volume Status

Morbidity

/Mort

alit

y

Under Perfect Over

Relationship of Morbidity/Mortality 
to Volume Status

for High-Risk Patients

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Relationship of Morbidity/Mortality to
Volume Status for High-Risk Patients

30%
0%
Fluid Loading
B
Hypovolemia
Euvolemia
A C
Hypervolemia
D
SV
EDV
A
B
C
Per
io
p
er
ati
v
e 
M
o
rb
id
it
y

R
isk
50%
10%
A C
B
Hypovolemia
Euvolemia
Hypervolemia
Fluid Loading
IC
U
 M
o
rtal
it
y
 R
isk

D

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Functional Hemodynamics

The Study and use of the cardiopulmonary

interaction to assess physiology  Dynamic

measures of volume responsiveness Stroke
Volume Variation SVV and Pulse Pressure

Variation PPV

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Physiologic Basis of

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Ancient Chinese physicians
would assess a patient's pulse
for hours at a time to establish a
diagnosis. (Pulsologists) 2500 
BC

Muo Ching

Described, differentiated and
diagnosed pulses in 10

volumes of books.

They could recognize more
than 200 different variations of
pulse based on volume,

strength, and regularity.

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Definitions

SV/SI Stroke Volume/Stroke

Index: cardiac performance

measure

SVV Stroke Volume Variation:

volume responsiveness

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Mechanism of SVV

Time
Airw
ay
Pres
s
ure
Ar
ter
ial
Pr
es
s
ur
e

Positive Pressure Breath

↑ Intrathoracic pressure

↑ RV afterload

↓ RV Preload

Empty Pulmonary System

Delayed ↓↓ SV

Acute ↑ SV

↑ LV Preload

McGee, WT;J Int. Care Med 2009; 24(6) p352

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The increase of preload volume is equal: ∆ EDV1 = ∆ EDV2

starting point is not ∆ SV1 >> ∆ SV2

∆ SV (SVV) Starling Relationship:

Respiratory Variation in SV at Different 
Preloads

EDV
SV

small variation

large variation

∆ EDV1 ∆ EDV2

∆ SV1
∆ SV2

∆ EDV (preload) caused by mechanical ventilation

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SV – SVV Mirrors Frank-Starling EDV – SV Relationship
Preload Increases from A to B

60
65
70
75
80
85
90
95
100
105

140 160 180 200 220 240 260

EDV, (ml)
S
V
, 
(m
l)
60
65
70
75
80
85
90

95
100
105

0 5 10 15 20 25 30 35 40 45

SVV, (%)
S
V
, 
(m
l)

F-S relationship requires development; SV- SVV allows

prediction about preload dependent cardiac performance

A A

B B

McGee,Hatib CCM 2007;34

SVV high

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More variability
SVV high

Preload
Sweet spot Goal

Less variability
SVV low

SV/SVV pairs determine an individual’s position on
their Starling Curve

Sweet spot: max benefit from preload s volume
overload!

Provides a Goal for volume therapy.

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For patients clinically diagnosed with

ARDS/ALI, what percentage have

hydrostatic; PCWP, pulmonary edema as

a contributing factor to their chest x-ray

picture and A-a gradient (oxygenation

defect)?

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Distribution of Pulmonary-Artery–Occlusion Pressure (Panel A) and Central 
Venous Pressure (Panel B) before Receipt of the First Protocol-Mandated

Instruction on Fluid Management.

The National Heart, Lung, and Blood Institute Acute Respiratory Distress 
Syndrome (ARDS) Clinical Trials Network. N Engl J Med 2006;354:2213-2224.

Many had hydrostatic pulmonary edema (30%)
Likely preventable; CI≥nl 97%

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POP: Goals vs.

No Goals (Chaos)

● Simulation/standardization

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PHYSIOLOGIC OPTIMIZATION

PROGRAM USING SVV & SV

Yes No

Fluid Infusion

1 liter NS SV Normal SV Low SV High

Pressor Inotrope/

Vasodilator Diuretic

Volume Responsive: SVV>10-15%

1 2 3

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Goals

Optimize perfusion and DO2
How:

1)Give volume until CO/SV

target/maximized (no increase)

2)Stop when SVV is low < 10-15% (13%)

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SI Normal: Pressor

Vasodilation, severe sepsis or septic shock

SI Low: Inotrope/Vasodilator

Low output state Echo?

SI High: Diuretic

Acute lung injury, ARDS, or previous massive
resuscitation (wet lungs)

The clinical impression of non-volume 
responsive patients along with the

stroke index directs therapy. 
1
2
3
P

A
T
H
W
A
Y
S

Non-volume responsive (SVV≤13%)

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When SVV doesn’t help

● Irregular Rhythm

● Spontaneous Breathing

● Insufficient Pleural Pressure Change
● Tachycardia >135

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When SVV is not useful

Cardiac performance SV/CO

∆ CO/SV

SVV provides additional

information about volume

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Give Fluids Assess Change in

CO/SV & DO

2

May be problematic:
Renal Failure

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Passive leg-raising test consists of measuring
the hemodynamic effects: ΔSV/CO of a leg

elevation up to 45o

45o

Semirecumbent position Passive leg raising

Responders get fluid

Non responders don’t! Improvement in SV requires 
other therapy

Teboul J-L and Monnet X. Prediction of volume responsiveness in critically ill patients
with spontaneous breathing activity. Curr Opin Crit Care. 2008:14(3);337

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Assessing DO2 adequacy

Clinical question?

O2 Extraction

No data exists that I am aware of that improving
DO2 is useful

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Goals

• SV cardiac performance measure: DO2

Individually assessed “adequate” baseline (OR)
or normal

• SVV volume responsiveness; α slope of F-S
Curve: if actively giving fluids goal

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CONCLUSION 2017 SVV/SV

Starling-ize our patients POP GDT

Optimization of volume therapy saves lives!
Manage volume therapy using physiology in

both directions

SV

More variability 
SVV is high

Less variability 
SVV is low

Preload

Sweet spot

GDT

No DO2 change

</div>

CHƯƠNG TRÌNH TỐI ƯU HÓA SINH LÍ SỬ DỤNG SVV & SI

PHYSIOLOGIC OPTIMIZATION

PROGRAM USING SVV & SI

<i><b>Fluid therapy!!</b></i>

<b>The Volume prescription Rx for the </b>

<b>Critically Ill and Injured</b>

<b>Relevant Disclosures</b>

What I won’t be able to do in

<b>Goals:</b>

A critique of fluid bolus

resuscitation in

severe sepsis

<b>DO</b>

<b>= CO (CaO</b>

<b>)</b>

<b>CaO</b>

<b>= Hb (1.36 ccO</b>

<b>/gm) </b>

<b>What percentage of ICU </b>

<b>patients are volume depleted </b>

<b>after 24hours?</b>

<b>Volume therapy critical care </b>

<b>perspective: 1 question</b>

<b>DO</b>

<b>Is Volume Management </b>

<b>Important?</b>

<b>Functional Hemodynamics</b>

<b>Physiologic Basis of </b>

<b>Definitions</b>

<b>SV/SI Stroke Volume/Stroke </b>

<b>Index: cardiac performance </b>

<b>measure</b>

<b>SVV Stroke Volume Variation: </b>

<b>volume responsiveness </b>

<b>Mechanism of SVV</b>

For patients clinically diagnosed with

ARDS/ALI, what percentage have

hydrostatic; PCWP, pulmonary edema as

a contributing factor to their chest x-ray

picture and A-a gradient (oxygenation

defect)?

<b>POP: Goals vs.</b>

<b>No Goals (Chaos)</b>

<b>PHYSIOLOGIC OPTIMIZATION </b>

<b>PROGRAM USING SVV & SV</b>

<b>Goals</b>

<b>1)Give volume until CO/SV </b>

<b>target/maximized (no increase)</b>

<b>2)Stop when SVV is low < 10-15% (13%)</b>

<b>Non-volume responsive (SVV≤13%)</b>

<b>When SVV doesn’t help</b>

When SVV is not useful

Cardiac performance SV/CO

<b>∆ CO/SV</b>

SVV provides additional

information about volume

<b>Give Fluids Assess Change in </b>

<b>CO/SV & DO</b>

Assessing DO2 adequacy

Clinical question?

O2 Extraction

Goals

CONCLUSION 2017 SVV/SV

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