Bạn không thể chết nếu các giá trị dưới đây bình thường - Professor Brendan Smith

The energy produced by cardiac contraction must be converted to either Potential Energy (PE) in the form of blood pressure or Kinetic. Energy (KE) in the form of blood flow[r]

You Don’t Die With Normal Numbers!

HR SVR Hb

SV DO 2 CVP

Professor Brendan Smith.

School of Biomedical Science, Charles Sturt University, Medical School of University of Notre Dame, Australia,

Bathurst, Australia.

Sydney

Conflict of Interest / Financial Considerations

Why do we need to measure haemodynamics?

So we can use fluids,

inotropes and vasopressors

in a logical way…

HR SVR Hb

SV DO 2 CVP

“If all the haemodynamic parameters are normal

then it is unlikely that you will die:

You die when these parameters are very abnormal”

Dr James Carmichael – Intensivist, 1981.

www.learnhemodynamics.com

Abnormal values in medicine are a sign of disease.

Correcting the values is what we do every day.

We correct all sorts of abnormal

values:-Blood pressure, glucose, urea levels, SpO2,

haemoglobin, electrolytes, temperature…

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When the values return to normal we say

“the patient is cured!”

Haemodynamics is just the same

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Data Acquisition.

Haemodynamic data can be acquired in many ways

Trans-Thoracic Echocardiography Trans-Oesphageal Echocardiography

USCOM Doppler Examination Pulmonary Artery Catheter

However we obtain the raw data

we still have a big problem…

What do all these figures mean?

How can we put it all together to help our patients?

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Fluid? Vasopressor? Inotrope?

What do you use when you don’t know

what to use???

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How would you treat this woman?

a) Give another 2L of N/Saline?

b) Use a vasopressor?

c) Use an inotrope?

d) Tell ED you’re busy on the ward round?

e) Hide until your shift ends?

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Maybe a bedside echo would help …

After 6 litres of N/Saline:

BP 79/35

HR 89SpO2 89% on 15L O2

“If giving one or two (or 3 or 4 or 5)

litres of normal saline didn’t result

in a sustained increase in BP or

oxygen delivery, why would the 7th

litre give you a different result?”

The “Fluid Non-responder”

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“Despite overwhelming data demonstrating the deleterious effects

of aggressive crystalloid-based resuscitation strategies, large-volume resuscitations continue to be the standard of care”

Bryan Cotton, Shock 2006; 26 (2): 115 - 121

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Cardiac Output Stroke Volume

BP can only rise if inotropy is good and CO maintained

Otherwise CO & DO 2 fall with vasoconstriction

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Pure vasopressors in shock

Three types of clinicians use them…

- The ignorant

- The lazy -The ignorant and lazy!!

(John Hinds 2016)

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Inotropy (myocardial contractility) as a

concept is well known to all clinicians but

not as a discrete quantity

Depressed inotropy is an important feature

of many ICU/ED presentations –

1 o Cardiac Conditions –

AMI, LVF, Cardiomyopathy

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2 o Myocardial Depression –

Septic shock, Pancreatitis, Pneumonia,

DKA, Burns, Hypoxia, Crush Injury,

Hypovolaemia, Anaemia, Thyroid Disorders, Hyperthermia, Hypothermia, Poisoning,

Preload Inotropy Afterload

Why is inotropy so important?

How do we assess inotropy?

- BP, HR, urine output, skin perfusion, capillary

refill, skin temperature, bowel sounds, Ejection

Fraction, sweating, … ??

- All of these are notoriously unreliable indicators

of cardiac function even in the hands of senior

clinicians.

www.learnhemodynamics.com

When should we use inotropes?

In >95% of cases this is done by

clinical judgment alone!

Which inotrope and how much?

What are our therapeutic targets?

How do we know we’ve reached them?

If only we could measure inotropy!!

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Measuring Inotropy.

Insert Vietnamese translation of

title here

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Preload Inotropy Afterload

Why is inotropy so important?

BP = SVR x HR x SV : SV x HR = CO

Fluid loading

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BP

Starling Curves and Inotropy Index (SMII)

The echo showed a

The echo also showed something else…

“Kissing Ventricle Sign”

Kissing Ventricles = Hypovolaemia.

Do you want to bet money on that?

ESV is determined by the balance of forces

between afterload and inotropy

Preload is not a significant factor in ESV.

ESV is determined by the balance of forces

between afterload and inotropy

Preload is not a significant factor in ESV.

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%Δ

SV

Fluid resuscitation depends on inotropy

Insert Vietnamese translation of title here

Insert Vietnamese translation here

Insert Vietnamese translation of title here

But what’s normal?

We have data from ~ 3,500 normal patients

from birth to 88 years.

Now we know what’s normal

we can start to treat the abnormal.

Because you don’t die with

normal numbers!

Part 2 Using the BUSH Protocol

The Bathurst Universal

Haemodynamic Protocol

(BUSH)

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So much for the theory –

what about the patient data?

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We treated 45 septic shock patients

according to the BUSH Protocol

and

64 septic shock patients treated with

“usual care” – the controls

We analysed for 6 possible outcomes

which were not mutually exclusive

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Acute Heart Failure (AHF – ACC criteria)

Acute Renal Failure (ARF – RIFLE/oliguria/anuria)RRT (Requirement for dialysis)

Respiratory Failure (Need for IPPV / NIV)

Tertiary Transfer

Outcomes

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Demographics of BUSH and Non-BUSH Groups

Parameter BUSH Non–BUSH Significance

-TTHS = Time to haemodynamic stabilisation

Parameter BUSH Control P = Odds

TTAB = Time to completion of 1 st round of antibiotics

Effects of Noradrenaline Use on Day One

Parameter NA used NA not used Significance Odds Ratio (95% CI)

Number of patients (%) 52 (47 · 7%) 57 (52 · 3%)

Mean APACHE IIIJ (sd) 70 · 85 (31 · 8) 54 · 4 (26 · 8) P=0 · 004 -

Mean ROD score (sd) 0 · 300(0 · 267) 0 · 175(0 · 157) P=0 · 003 -

Mortality n = (%) 7/52 (13 · 5%) 20/57 (35 · 1%) P<0 · 01 3 · 47 (1 · 32–9 · 09) TTHS–hours (sd) 4 · 67 (9 · 44) 19 · 14 (13 · 05) P<0 · 001 -

Acute Heart Failure 8/52 (15 · 4%) 25/57 (43 · 9%) P=0 · 001 4 · 29 (1 · 72–10 · 75) Acute Renal Failure 12/52 (23 · 1%) 39/57 (68 · 4%) P<0 · 001 7 · 25 (3 · 08–16 · 95) RRT 2/52 (3 · 8%) 4/57 (7 · 0%) P=0 · 460 -

PPV 15/52 (28 · 8%) 21/57 (36 · 8%) P=0 · 380 -

Tertiary Transfer 5/52 (9 · 6%) 13/57 (22 · 8%) P=0 · 065 -

Fluids Day 1–litres(sd) 4 · 96 (1 · 32) 7 · 20 (1 · 15) P<0 · 001 -

Fluids Day 2–litres(sd) 8 · 18 (1 · 90) 11 · 33 (1 · 59) P<0 · 001 -

Effects of Noradrenaline Use on Day One

Predictors of Outcome for All Patients

Significance of Variables P =

Death AHF ARF RRT PPV Transfer

APACHE IIIJ Score ns ns ns ns ns ns

ROD Score ns ns ns ns ns ↑0 · 031 Age ns ns ns ns ns ns

Sex ns ns ns ns ns ns

Time to Antibiotic ↑0 · 006 ↑0 · 001 ↑0 · 001 ↑0 · 001 ↑0 · 003 ns

TTHS ↑0 · 018 ↑0 · 001 ↑0 · 001 ns ns ns

Medical v Surgical ns ns ns ns ns ↑0 · 014 Use of Inotrope Day 1 ↓0 · 009 ↓0 · 001 ↓0 · 001 ns ns ns

Volume of Fluid Day 1 ↑0 · 014 ↑0 · 003 ↑0 · 001 ns ns ns

Use of Inotrope Day 2 ns ns ns ns ns ns

Volume of Fluid Day 2 ↑0 · 033 ns ns ns ns ns

BUSH Protocol ↓0 · 001 ↓0 · 001 ↓0 · 001 ↓0 · 033 ↓0 · 015 ↓0 · 004

Predictors of Outcome

Were we pleased with the outcome?

Mortality reduced to under 7%!!

The lowest mortality from septic shock

in the world!

Take Home Messages…

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Fluid Resuscitation…

If the first 20ml/kg doesn’t work,

(i.e produce a sustained increase in BP)

why waste time

giving further

fluid boluses?

Go to Plan B…

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You have to escalate your care…

Broad-spectrum antibiotics

Arterial access ASAP Central venous access ASAP ( but don’t delay giving inotropes ) Consider intraosseous line???

Don’t drown the patient!

Get help!

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Measure Haemodynamics ASAP

Especially Inotropy Index…

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Put the puzzle together…

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In resuscitation of patients with shock

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If all else fails, remember…

But it’s too

hard to

learn the

USCOM!

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Thank you!

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The following slides are all for answering potential questions They do not need to be translated unless you want to do that

or keep copies of these slides for your own use.

Several slides are duplicated – the second copy of the slide

is so that it can be translated in to Vietnamese if needed but keep the English copy of each slide as well so I can use them.

Measuring Inotropy.

Conservation of Energy

The energy produced by cardiac contraction must be converted to either Potential Energy (PE) in the form of blood pressure or Kinetic

Energy (KE) in the form of blood flow.

But can we measure PE & KE?

Is the measurement reliable?

How long does it take?

Can we monitor Rx with it?

Conservation of Energy

The energy produced by cardiac contraction must be converted to either Potential Energy (PE) in the form of blood pressure or Kinetic

Energy (KE) in the form of blood flow.

But can we measure PE & KE?

Is the measurement reliable?

How long does it take?

Can we monitor Rx with it?

Total Inotropy = PE + KE ( I = Eblood pressure + Eblood flow)

Inotropy = BPm x SV x 10 -3 + 1 x SV x 10 -6 x ρ x V 2

7.5 x FT 2 x FT

(The Smith-Madigan Formula)

The SI unit of inotropy is the Watt

Total Inotropy = PE + KE ( I = Eblood pressure + Eblood flow)

Inotropy = BPm x SV x 10 -3 + 1 x SV x 10 -6 x ρ x V 2

7.5 x FT 2 x FT

(The Smith-Madigan Formula)

The SI unit of inotropy is the Watt

Inotropy Index

But how do we judge inotropy in patients of varying size,

e.g large and small adults, children, infants?

By analogy to cardiac index which is –

Cardiac Index = Cardiac Output

Body Surface Area

Smith-Madigan Inotropy Index = Inotropy

BSA

The SI unit of SMII is therefore W/m 2

Inotropy Index

But how do we judge inotropy in patients of varying size,

e.g large and small adults, children, infants?

By analogy to cardiac index which is –

Cardiac Index = Cardiac Output

Body Surface Area

Smith-Madigan Inotropy Index = Inotropy

BSA

The SI unit of SMII is therefore W/m 2

Smith-Madigan Inotropy Index

Smith-Madigan Inotropy Index

Or you can just look at the echo….

Imaging the IVC?

Dilated IVC

Imaging the IVC?

Dilated IVC

IVC appearance and CVP…

CVP has no correlation with blood volume!

C V P

Deficit or Excess Blood Volume

CVP has no correlation with blood volume!

C V P

Deficit or Excess Blood Volume

Chest 2008; 134: 172-8

•… “a very poor relationship between

CVP and blood volume”…

•… “inability of the CVP/∆CVP to

predict haemodynamic response to a

fluid challenge”

Chest 2008; 134: 172-8

•… “a very poor relationship between

CVP and blood volume”…

•… “inability of the CVP/∆CVP to

predict haemodynamic response to a

fluid challenge”

Chest 2008; 134: 172-8

• CVP should NOT be used to make

clinical decisions regarding fluid

management…

• …CVP should NO longer be routinely

measured in the ICU, Operating Theatre

or Emergency Department…

Chest 2008; 134: 172-8

• CVP should NOT be used to make

clinical decisions regarding fluid

management…

• …CVP should NO longer be routinely

measured in the ICU, Operating Theatre

or Emergency Department…

JVP / CVP

- Only looking at the right side of the heart

- Tells us little about left heart preload

- Tricuspid valve integrity? Stenosis and

regurgitation both lead to errors

- Arrythmias lead to error

- Even right ventricular pressure tells us little about right ventricular volume

JVP / CVP

- Only looking at the right side of the heart

- Tells us little about left heart preload

- Tricuspid valve integrity? Stenosis and

regurgitation both lead to errors

- Arrythmias lead to error

- Even right ventricular pressure tells us little about right ventricular volume

Pulmonary artery catheter

What pressure should we use?

PA Diastolic Pressure (PADP)?

PA Wedge Pressure (PAWP)?

PA mean Pressure (PAPm)?

Is the catheter in the right place?

What about IPPV, PEEP, pulmonary vascular patency, vasoconstriction, shunts,

arrythmias, mitral valve problems….etc

Pulmonary artery catheter

What pressure should we use?

PA Diastolic Pressure (PADP)?

PA Wedge Pressure (PAWP)?

PA mean Pressure (PAPm)?

Is the catheter in the right place?

What about IPPV, PEEP, pulmonary vascular patency, vasoconstriction, shunts,

arrythmias, mitral valve problems….etc

Attempts to measure left ventricular end

diastolic pressure - LVEDP

Left ventricular preload is strictly the left

ventricular end diastolic volume – LVEDV

Ventricular end diastolic pressure only acts

as an acceptable surrogate if we know the ventricular compliance

Attempts to measure left ventricular end

diastolic pressure - LVEDP

Left ventricular preload is strictly the left

ventricular end diastolic volume – LVEDV

Ventricular end diastolic pressure only acts

as an acceptable surrogate if we know the ventricular compliance

Passive Leg Raising - ↑ SV

Stroke volume increases from

26ml to 35ml = 34%

Patient still on left side of Starling Curve.Patient will respond to volume loading.Passive Leg Raising test can be repeated

after fluid bolus

Stroke volume increases from

26ml to 35ml = 34%

Patient still on left side of Starling Curve.Patient will respond to volume loading.Passive Leg Raising test can be repeated

after fluid bolus

FTc = Preload

FTc is also affected by two other factors –

Inotropy - shortens FTc Afterload – prolongs FTc

Once you know inotropy and afterload then you have a great (and simple!)

measure of preload…

FTc is also affected by two other factors –

Inotropy - shortens FTc Afterload – prolongs FTc

Once you know inotropy and afterload then you have a great (and simple!)

measure of preload…

Can basic physiology help us?

Inotropy

Cardiac Output Stroke Volume

Cardiac Output Stroke Volume