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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 DO2 CVP

CO SpO2 BP

Professor Brendan Smith.

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

Bathurst

NONE!!

www.learnhemodynamics.com

Why we need to

measure haemodynamics?

So we can use fluids,

HR SVR Hb

SV DO2 CVP

CO SpO2 BP

“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

Abnormal values in medicine are a sign of disease

Correcting the values is what we every day

We correct all sorts of abnormal values:-Blood pressure, glucose, urea levels, SpO2,

haemoglobin, electrolytes, temperature…

When the values return to normal we say “the patient is cured!”

Haemodynamics is just the same

Data Acquisition.

Haemodynamic data can be acquired in many ways

Trans-Thoracic Echocardiography Trans-Oesphageal Echocardiography

USCOM Doppler Examination Pulmonary Artery Catheter

PiCCO

?? Impedance/Conductance cardiography Etc…

Each has it’s own benefits and drawbacks, BUT…

However we obtain the raw data we still have a big problem… What all these figures mean?

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

Fluid? Vasopressor? Inotrope?

What you use when you don’t know what to use???

Terminology…

Fluid

Any liquid; crystalloid, colloid or blood product

Vasopressor (= α agonist)

Arterial vasoconstrictor e.g phenylephrine

Inotrope (= β1 agonist)

Mrs G.R – 36 years, 51 Kg. ?Acute Cholangitis.

BP on admission 72/34, HR 88 WCC 24.8, Temp 39.4

After 2L N/Saline BP 74/36, HR 86

What are you going to now?

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?

After litres of N/Saline:

BP 79/35 HR 89

SpO2 89% on 15L O2 Lactate 6.7

Now what?

Vasopressor? Inotrope? More Fluid? Call a doctor?!!

After 9L fluid;

(6L N/Saline, 3L Hartmann’s) BP 78/37, HR 94, Temp 39.1

Lactate 7.1

So what’s the problem?

“If giving one or two (or or 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”

“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

So what next?

www.learnhemodynamics.com

Fluid? Inotrope?

Vasopressor?

Cardiac Output Stroke Volume

Blood Pressure

Preload Inotropy Afterload

Hb SpO2

Oxygen Delivery – DO2

Heart Rate

SVR

www.learnhemodynamics.com

CO SVR

Vasopressors and DO2

BP = CO X SVR

CO

SVR

BP can only rise if inotropy is good and CO maintained

Otherwise CO & DO2 fall with vasoconstriction.

Pure vasopressors in shock

Three types of clinicians use them… - The ignorant

- The lazy

-The ignorant and lazy!!

(John Hinds 2016)

Inotropy.

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 –

1o Cardiac Conditions –

AMI, LVF, Cardiomyopathy

2o Myocardial Depression –

Septic shock, Pancreatitis, Pneumonia, DKA, Burns, Hypoxia, Crush Injury,

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

Evenomation,

Iatrogenic Antihypertensives, chemotherapy, electrolyte disorders, sedation, steroids,

anaesthetics…

Preload Inotropy Afterload

Why is inotropy so important? BP = SVR x HR x SV : SV x HR = CO

Fluid loading

Power of the heart

Blood Pressure

How we assess inotropy?

- We use surrogates of global cardiac function

- 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

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 we know we’ve reached them? If only we could measure inotropy!!

Preload Inotropy Afterload

Why is inotropy so important? BP = SVR x HR x SV : SV x HR = CO

Fluid loading

www.learnhemodynamics.com

Starling Curves and Inotropy Index (SMII)

+inotropy

Left ventricular end diastolic volume Stroke Volume Index 50 25 SV

SMII = 2.0

SMII = 1.8

SMII =1.4

SMII = 1.1

The echo showed a

hyperdynamic ventricle…

( = high Ejection Fraction)

High EF = good myocardial contractility

Actually, no it doesn’t!!

The echo also showed something else…

“Kissing Ventricle Sign”

ESV is determined by the balance of forces

between afterload and inotropy.

ESV is determined by the balance of forces

between afterload and inotropy.

Preload is not a significant factor in ESV.

SMII %Δ

www.learnhemodynamics.com

www.learnhemodynamics.com

But what’s normal?

Now we know what’s normal

we can start to treat the abnormal.

Because you don’t die with

Part

The Bathurst Universal

Haemodynamic Protocol

(BUSH)

So much for the theory –

what about the patient data?

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

Death

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

Demographics of BUSH and Non-BUSH Groups

Parameter BUSH Non–BUSH Significance

Number of patients 45 64 –

Age – years (sd) 62·0 (17·1) 68·3 (14·7) P=0·542 (ns) Weight kg (sd) 83·2 (13·1) 81·8 (16·2) P=0·742 (ns)

Male n = 28/45 (62·2%) 31/64 (48·4%) P=0·176 (ns) Mean APACHE IIIJ (sd) 61·09 (26·9) 63·06 (32·7) P=0·740 (ns) Mean ROD (sd) 0·232 (0.23) 0·236 (0.22) P=0·922 (ns)

Origin (Ward/ED/OT) 11/32/2 14/50/0 P=0·477 (ns) Medical/Surgical (%) 35/45 (77·7%) 58/64 (90·6%) P=0·057 (ns) MAPinit - mmHg (sd) 56·3 (5·3) 57·2 (4·9) P=0·792 (ns) SpO2 init - % (sd) 88·6 (4·2) 87·7 (4·6) P=0·803 (ns)

Demographics

Outcomes…

Parameter BUSH Control P = Odds Ratio

n = 45 64 - -TTHS

(hours) 1.25 19.9 <0.001 -Mortality 3 (6.7%) 25 (39%) <0.001 13.7

AHF 2 (4.4%) 31 (48.4%) <0.001 20.0 ARF 4 (8.9%) 47 (73.4%) <0.001 28.6 PPV 9 (20%) 27 (42.1%) 0.017 2.92

Parameter BUSH Control P = Odds Ratio

n = 45 64 - -TTAB

(hours) 0.63 4.28 <0.001 -Total Fluid

24 hours 4.44 L 7.32 L <0.001 -Total Fluid

48 Hours 7.57 L 11.49 L <0.001 -Tertiary

Transfer 2 (4.4%) 16 (25%) <0.001 7.1 RRT 0 (0%) 6 (9.5%) 0.033

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 -

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 ↓0·009 ↓0·001 ↓0·001 ns ns ns

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

Use of Inotrope Day ns ns ns ns ns ns

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

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

Were we pleased with the outcome? Mortality reduced to under 7%!!

The lowest mortality from septic shock

Take Home Messages…

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…

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!

Measure Haemodynamics ASAP

Especially Inotropy Index…

Put the puzzle together…

In resuscitation of patients with shock

But it’s too hard to

learn the USCOM!

Thank you!

Questions?

The following slides are all for answering potential questions They not need to be translated unless you want to that or keep copies of these slides for your own use

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?

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?

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

Inotropy = BPm x SV x 10-3 + x SV x 10-6 x ρ x V2

7.5 x FT 2 x FT

(The Smith-Madigan Formula)

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

Inotropy = BPm x SV x 10-3 + x SV x 10-6 x ρ x V2

7.5 x FT 2 x FT

(The Smith-Madigan Formula)

Inotropy Index

But how 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

Inotropy Index

But how 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

Smith-Madigan Inotropy Index

Normal Controls

1.6 – 2.2 W/m2

Left Ventricular Failure

0.4 – 0.9 W/m2

Septic Shock

Smith-Madigan Inotropy Index

Normal Controls

1.6 – 2.2 W/m2

Left Ventricular Failure

0.4 – 0.9 W/m2

Septic Shock

Imaging the IVC?

Imaging the IVC?

CVP has no correlation with blood volume!

Fluid depleted Fluid overloaded

C V P

CVP has no correlation with blood volume!

Fluid depleted Fluid overloaded

C V P

Chest 2008; 134: 172-8

•… “a very poor relationship between CVP and blood volume”…

•… “inability of the CVP/∆CVP to

Chest 2008; 134: 172-8

•… “a very poor relationship between CVP and blood volume”…

•… “inability of the CVP/∆CVP to

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

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

Preload

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

Preload

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

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,

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,

PAC

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

PAC

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

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

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

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!)

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!)

Can basic physiology help us?

SV

LVEDV

ΔSV

~75ml/m2l

Cardiac Output Stroke Volume

Blood Pressure

Preload Inotropy Afterload

(Hb) SpO2

Oxygen Delivery – DO2

Heart Rate

Cardiac Output Stroke Volume

Blood Pressure

Preload Inotropy Afterload

(Hb) SpO2

Oxygen Delivery – DO2

Heart Rate