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

measures of volume responsiveness Stroke Volume Variation SVV and Pulse Pressure. Variation PPV[r]

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

Fluid therapy!!

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

Relevant Disclosures

Edwards Lifesciences

FloTrac/Vigileo/EV1000/ Clear Sight

My cases; POPtm (free) PICCO

LIDCO Echo

Esophageal Doppler

Respirophasic change in SV (SVV)

What I won’t be able to in

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

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

©2009 by American College of Chest Physicians

intensivist

surgeon

cardiologist

Fool guessing!

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

A critique of fluid bolus resuscitation in

severe sepsis

Andrew K Hilton & Rinaldo Bellomo

Critical Care 2012, 16:302

BAD Fluids!

•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?

Fluid ?

Pressor ? Diuretic ?

DO2 = CO (CaO2)

CaO2 = Hb (1.36 ccO2/gm)

What percentage of ICU

patients are volume depleted after 24hours?

1 Almost 0% 25%

3 50% 75%

Volume therapy critical care perspective: question

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

Ultimately DO2 is what we can control

regarding Organ perfusion and function

Answer: Physiologic Optimization Program

Is Volume Management Important?

Volume Status

Morbidity

/Mort

alit

y

Under Perfect Over

Relationship of Morbidity/Mortality to Volume Status

for High-Risk Patients

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

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

Physiologic Basis of

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

Definitions

SV/SI Stroke Volume/Stroke Index: cardiac performance

measure

SVV Stroke Volume Variation: volume responsiveness

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

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

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 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

SV

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

A

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)?

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%

POP: Goals vs.

No Goals (Chaos)

● Simulation/standardization

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

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%)

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%)

When SVV doesn’t help

● Irregular Rhythm

● Spontaneous Breathing

● Insufficient Pleural Pressure Change ● Tachycardia >135

When SVV is not useful

Cardiac performance SV/CO

∆ CO/SV

SVV provides additional information about volume

Give Fluids Assess Change in

CO/SV & DO2

May be problematic: Renal Failure

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

Assessing DO2 adequacy Clinical question?

O2 Extraction

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

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

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