QP, QS and other Cues Desiree Machado, - PowerPoint Presentation

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QP, QS and other Cues

Desiree Machado,

June 21

st

, 2018

Slide2

Disclosure

No COI

You will see a lot a good looking people!

No consents were obtained

Slide3

Objectives

Examine

physiological factors affecting balance of

circulations

2. Recognize specific scenarios and impact of an unbalanced

circulation

3.

Differentiate

 strategies tailored to individual anatomical 

characteristics

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And 4)

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Slide6

Something different

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Fetal circulation

But hey, this is a NICU talk…..

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Q=flow

Flow in fetal circulation:

Streaming, mixing and shunting

SV:

HLHS: RV suplies Transverse and descending aorta while ascending aorta is suplied retrograde fashion

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Physiological Factors Affecting QP:QS

Translate QP:QS to English, Portuguese…

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Translating QP:QS

CO: Preload, Intrinsic,

Afterload

CO= HR x SV….where SV=EDV-ESV

Flow= Ohm’s Law: Q=ΔP/RDriving Pressure Pulmonary Circulation: PAP (mean)-PWP

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Calculating PVR

PVR= (

Ppa

-PWP)/ CO (Wood units= dyn·s·cm−5)Factors:

1) Hagen-Poiseuille2) Muscle tone3) Elasticity4) Hormonal 5) Cellular (plat)

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Flow=CO

CO: Preload, Intrinsic,

Afterload

CO= HR x SV….where SV=EDV-ESV

Flow: Ohm’s Law: Q=ΔP/RDriving Pressure Systemic Circulation:

MAP-RAP (CVP)

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Calculating SVR

QP= (MAP-CVP)/ CO (

dyn·s·cm

−5)1)Hagen-Poiseuille 2) Muscle tone3) Elasticity

4)Hormonal 5)Cellular-receptors

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“An Oldie, but a Goodie”

Fick’s

Law: Diffusion of gas through a membrane

Fick’s Principle CO (7/9/1870)

:Blood flow to an organ can be calculated using a marker (oxygen) if you know:

Marker taken

up by the organ per unit

time

Marker in

arterial blood supplying the

organ (arterial O2)

Marker

in venous blood leaving the

organ (venous O2)

Adolf

Eugen

Fick

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Fick Equation:

Rate of indicator Out= Rate in + V

QC(out

)=

QC(in

) +V

Q= V/

C(out

-in)

If Oxygen:

Q= V

O

2

/

C

A

O

2

– C

V

O2Q= Oxygen consumption/AVDO2 difference

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Now to the “QP:QS”

Pulmonary blood flow:

QP= VO

2 C

AO2(PV sats) – C

V

O

2 (

Pulm

art

sats

)

Systemic blood flow

QS= VO

2

C

A

O

2(Aorta

sats

)

– CVO2 (RA sats)

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Simplifying..

QP=QS

VO2

= VO2 CAO

2

(PV

sats

)

– C

V

O

2

(

Pulm

artery

sats

)

C

AO2(Aorta sats) – CVO2 (RA sats)CAO2(Aorta sats) – CVO2 (RA sats) CAO2(PV sats)– CVO2 (Pulm artery sats) QP:QS= Aorta sats - RA sats

PV sats - Pulm art sats

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Simplified Fick

: SV case 1

Fick

:QP:QS= Ao sat- mixed venous sat

Pvenous sat- Parterial sat

HLHS: Ao sat= Part sat

Radial art

sats

: 80%

SvO2 (PICC IVC): 60%

Pulm

vein

Sats

(great lungs): 100%

PA

sats

: 80%

80%-60%

= 20/20= 1 (well balanced, QP:QS=1)

100%-80%

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Simplified Fick

: SV case 2

HLHS:

Ao sat= Part satRadial art

sats: 90%SvO2 (PICC IVC): 40%Pulm vein Sats (great lungs): 100%

PA

sats

: 90%

90%- 40%

= 50/10= 5 (QP:QS=5:1)

100%- 90%

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Now to the bedside

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Objectives

Examine

physiological factors affecting balance of

circulations

2. Recognize specific scenarios and impact of an unbalanced

circulation

3.

Differentiate

 strategies tailored to individual anatomical characteristics

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Management of Neonate SV

CAB …and QP:QS

NRP

ABCVascular access: Double Lumen UVC; UACPGE*

SV: What is the Problem? Decreased PBF?Excessive PBF and Poor perfusion?

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Decreased PBF

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SV with decreased PBF?

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Ductal

Patency

Good mixture

Optimize CaO2

Optimize CO (preload and contract)

Optimize PVR

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Now the Cues:

How to improve (temporize) PBF?

1)Optimize PVR (lung hygiene)

2)Improve DO2

3)Treat acidosis

4)Treat Hypoxia

(

caution…treat PV dessaturation)

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1) PVR

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2) DO2

DO2= CO

x

CaO2DO2= CO x [

Hb] (g/dL) x

1.34

(mlO

2

/g

Hb

)

x

O

2

FiO2

+ 0.0032

x

PaO2

(

torr

)Optimize VO2 (Decrease metabolic demand)-Prevent hyperthermia-Prevent aggitation (specially if high PVR)-Treat metabolic derangements

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Circulation, 1998

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3)Treat acidosis

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4)Treat Hypoxia*

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And if nothing else works….

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6h old, term, 2.7Kg, PA/VSD, prenatal diagnosis,

Apgar

3/5/5,

Sat 30-40%Intubated, 100% FiO2

iNO 20ppmHypotensive,

Metab

acidosis,

Lact

10,

Htc45

Epi

0.1mcg/kg/min

Echo:

closing DA (PGE 0.1)

Central ECMO, Flow 160ml/kg/min

OR

dol

4- 3mm Central

S

hunt

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SV with increased PBF and poor perfusion?

Ductal

Patency

Good mixture

Optimal CO

Optimal Coronary Perfusion Pressure

Increase PVR to favor SVR

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Now the Cues:

How to improve Systemic

B

lood Flow (QS)?

1)Optimize PVR (to the other side)

2)Improve DO2 and prevent

Hyperoxia

3)Relative Acidosis and

Hypercarbia

are your friends!

4) Decrease SVR

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1)Optimize PVR:

Your target is different now!

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2)Improve DO2 and prevent

Hyperoxia

DO2= CO

x CaO2DO2= CO x

[Hb] (g/dL)

x

1.34

(mlO

2

/g

Hb

)

x

O

2

FiO2

+ 0.0032

x

PaO2

(

torr)

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3) Relative acidosis is

your friend….

Resp

Acidosis

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Circ 2001

10 HLHS- Sedated and

paralysed

10min FiO2 17% followed by 10 min FiCO2 2.7%

QP:QS falls in both conditions

BUT DO2 in increased during

Hypercarbia

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4) Decrease SVR

49 SV

Preop

milrinone 1 (0.1-1.25) and FiO2 17% (14-20%)

Improved clinical status from day 0 to 4 (pH, lactate, Bicarb, PaO2)

Cong Heart

Dis

2011

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And if nothing else works….

Dr Fudge

Dr

Vyas

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2mo

, prenatal

dx

HLHS (MS/AS), coronary sinusoids-listed for Tx Worsening function and hypertension on PGE

Started milrinone (0.25)2 weeks: Sats

65%- low CO –

epi

0.02-5

CPAP -> BIPAP

2weeks:

Dessaturaions

50%- increased FiO2 requirements ->ECHO

Cath

- lab: ASD gradient25, LAP 34 ->

baloon

sept

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Honestly, this is very simplistic approach!

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Objectives:

Examine physiological factors affecting balance of circulations

2. Recognize specific scenarios and impact of an unbalanced circulation

3. Differentiate strategies tailored to individual anatomical characteristics

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Scenario 1

2dol @

adm

, 39+1w, Apgar 8/9, prenatal

dx HLHS (MA/AA), BW3.2Kg, -ve

serologies

, O-/O-, H-MRI N. Norwood-Sano

yesterday

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Scenario 2

1

dol @

adm, 38+2

w, Apgar 9/9, prenatal dx HLHS (MS/AA), BW3.05Kg, -ve

serol

, A+/O+

H-MRI: dol

2:

Focal acute

infarct

R PWM

Repeat MRI

dol

8: new

abnormal area in the high convexity right frontal corona

radiata

.

Clot LHV-IVC: UVC removed,

enoxap

startedRepeat MRI dol 14: new foci of restricted diffusion in the high right frontal region Repeat MRI dol 19: evolving, no hemorrhageOR TODAY (dol 21)!

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Management

Dol3-4: pulmonary

overcirculation

: CPAP, diuretics, hypotx- Ca drip

Dol5-15: off Ca, HFNC, diuretics, trophic feeds- ?Pneumatosis AXR -

resol

x24h. Grad ASD



15

Dol

16-20: worsening

overcirculation

- NPO,



diuretics

, HFNC



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Scenario 3

2dol @

adm

, 37+1w, Apgar 8/9, prenatal dx HLHS (MS/AA/coronary fistula), BW2.7Kg, -

ve serologies, H-MRI N. Cath dol2: significant coronary sinusoids

Listed for

HTx

(

ABOi

)

Dol3-20: significant

overcirculation

: CPAP->

BIPAP, diuretics

Dol

21: Hybrid-VAD @ 2.4Kg

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Current state

W: 3.5Kg

Po+NG

CMPAWaiting Tx

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1dol, 39+2w,

Apgar

8/9, prenatally diagnosed

ToF, BW2.8Kg, -ve serologies, PGE 0.05 at birth

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Clinical course

TET repair: VSD closure, RV-PA conduit (

dol

8)Failed to wean from CPB -> open chest and central ECMO cannulationECMO: 8 days -> Restrictive physiology

OR: 3.5mm Goretex Central Shunt Delayed chest closure: 8 days open chestExtubated

4 days later (total 20 days)

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The impact of

MultiD

care

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NPC-QIC

The impact of

MultiD

care

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Prolacta

Meet the Team

The impact of

MultiD care

No pictures: Dieticians Kelly and Katherine

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The impact of MultiD

care

Neuro

consortium

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THE REAL WORKFORCE

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Thank You!!

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