Sốc nhiễm khuẩn – Thời điểm sử dụng khoa học - Professor Brendan Smith

So we can use science to treat septic shock instead of dogma ... The scientific approach to septic shock…[r]

Septic Shock – Time to Use Science?

HR SVR Hb

SV DO2 CVP

CO SpO2 BP

Professor Brendan Smith

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

Vasopressors

And

Definition of shock:

“Any haemodynamic disturbance leading to inadequate perfusion and oxygenation

of the tissues.”

BP Low

Low SVR

High SVR

BP High

BP = CO x SVR

CO SVR

Vasopressors and DO

2

CO

SVR

BP can only rise if inotropy is good and CO is maintained

Otherwise

CO & DO

2

fall

with

vasoconstriction

.

The heart must have sufficient

inotropy

(contractility) to overcome

the increase in afterload produced

by vasoconstriction or

90%

of septic shock patients

have

depressed inotropy

.

Increasing SVR with vasopressors

reduces

SV, CO and DO

2

!!

We have been fooled by the

“

Blood Flow

depends on

Blood Pressure

”

Pure vasopressors in septic 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 presentations –

1

o

Cardiac Conditions

–

AMI, LVF, Cardiomyopathy

2

o

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…

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 totally unreliable indicators of cardiac function even in the hands of senior clinicians

How we titrate inotropes?

Noradrenaline -

↑

BP

but

↓

Flow

Dobutamine -

↓

BP

but

↑

Flow

Adrenaline -

↓

BP

and

↑

Flow

(Low dose)

Adrenaline -

↑

BP

and

↓

Flow

(High dose)

How can you titrate inotropes

Even more illogical…

How we juggle powerful inotropes

without measuring

inotropy!

Was it

low

before?

Is it

normal

now?

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!!

Total Inotropy = PE + KE

( = blood pressure + blood flow)

Inotropy = BPm x SV x 10-3 + x SV x 10-6 x ρ x Vm2

7.5 x FT 2 x FT

The Smith-Madigan Formula

The unit of inotropy is the Watt

British Journal of Anaesthesia – 2013

(doi: 10.1093 / bja / aet118)

U-S-C-O-M

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

SMII %Δ

SV

LVEDV

ΔSV

~75ml/m2l

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.

That’s the scientific way!

The

B

athurst

U

niversal

H

aemodynamic

P

rotocol

(BUSH)

The scientific approach to septic shock…

Measure the variable(s)

Compare to normal reference values Administer the treatment

Remeasure the variable(s)

Compare to normal reference values

When the value of the variable(s) is within normal limits, then we can say

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” – SSC Guidelines

We analysed for 8 possible outcomes which were not mutually exclusive:

Translator: You don’t need to translate all this,

but this is so you know what the abbreviations mean in the next few slides…

the variables we analysed for were:

Time taken to achieve haemodynamic stability – TTHS Morbidity (death)

Acute Heart Failure (AHF) Acute Renal Failure (ARF)

Acute Respiratory Failure (need for positive pressure ventilation – PPV) Time to completion of first round of antibiotics

Total fluid used in first 24 hours and first 48 hours Need to transfer patients to tertiary hospital (Sydney)

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

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…

Measure Haemodynamics ASAP

Especially Inotropy Index…

In patients with septic shock

CVP

measurement (and IVC imaging)

are

not reliable

measures of preload.

Saline

does not carry oxygen.

Vasopressors

do not increase

CO

and

DO

2

Inotropy

can be measured

easily.

If we use

science

, then treating septic

shock should be like clockwork

Logical, integrated and smooth.

HR SVR Hb

SV DO2 CVP

CO SpO2 BP

Thank you for listening.