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Resuscitation

 

83 (2012) 925

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Resuscitation

j o

 

u

 

r n

 

a l

 

h o m

 

e p a g e

 

:

 

w w w . e l s e v i e r . c o m / l o c a t e / r e s u s c i t a t i o n

Editorial

CPR

 

cardiopulmonary

 

resuscitation

 

or

 

cerebral

 

perfusion

 

restoration

It

 

has

 

long

 

been

 

recognised

 

that

 

following

 

cardiac

 

arrest,

 

cere-

bral

 

oxygenation

 

falls

 

rapidly.

 

The

 

brain

 

is

 

a

 

metabolically

 

highly

active

 

organ

 

and

 

cell

 

death

 

begins

 

after

 

only

 

a

 

few

 

minutes

 

of

anoxia.

1

The

 

main

 

mode

 

of

 

death

 

following

 

resuscitation

 

from

 

car-

diac

 

arrest

 

remains

 

neurological

 

death.

2

Recent

 

guidelines

 

have

 

stressed

 

the

 

importance

 

of

 

continu-

ous

 

chest

 

compressions

 

in

 

order

 

to

 

maintain

 

coronary

 

perfusion

pressure.

3

This

 

has

 

led

 

towards

 

a

 

greater

 

emphasis

 

on

 

the

 

use

 

of

supraglottic

 

airway

 

devices

 

(SADs)

 

to

 

manage

 

the

 

airway

 

in

 

order

to

 

minimise

 

interruptions

 

in

 

chest

 

compressions.

A

 

paper

 

in

 

this

 

edition

 

of

 

resuscitation

 

shows

 

that

 

in

 

a

 

swine

model,

 

inflation

 

of

 

a

 

SAD

 

causes

 

impairment

 

in

 

carotid

 

artery

 

blood

flow.

4

This

 

has

 

been

 

shown

 

with

 

a

 

number

 

of

 

different

 

devices

 

all

 

of

which

 

have

 

inflatable

 

cuffs.

 

There

 

are

 

obvious

 

limitations

 

in

 

being

a

 

swine

 

model,

 

but

 

it

 

is

 

already

 

known

 

that

 

SADs

 

reduce

 

carotid

blood

 

flow

 

in

 

anaesthetised

 

humans

 

so

 

the

 

effects

 

are

 

probably

translatable.

5

In

 

addition

 

the

 

use

 

of

 

epinephrine

 

during

 

CPR

 

can

further

 

reduce

 

carotid

 

blood

 

flow.

6

This

 

leads

 

to

 

the

 

very

 

real

 

con-

cern

 

that

 

recent

 

changes

 

in

 

the

 

management

 

of

 

cardiac

 

arrest

 

will

lead

 

to

 

an

 

increased

 

number

 

of

 

survivors

 

but

 

those

 

survivors

 

will

be

 

in

 

a

 

poor

 

neurological

 

condition.

Should

 

the

 

management

 

of

 

cardiac

 

arrest

 

then

 

be

 

aimed

 

pri-

marily

 

at

 

minimising

 

neurological

 

damage

 

during

 

resuscitation?

Advances

 

such

 

as

 

extracorporeal

 

life

 

support

 

and

 

prehospital

 

cool-

ing

 

of

 

patients

 

would

 

suggest

 

that

 

this

 

may

 

be

 

the

 

direction

 

to

 

go.

The

 

concept

 

of

 

CPR

 

as

 

cerebral

 

perfusion

 

restoration

 

as

 

opposed

 

to

trying

 

to

 

maximise

 

coronary

 

perfusion.

So

 

the

 

pendulum

 

may

 

be

 

swinging

 

again

 

in

 

favour

 

of

 

brain

focussed

 

resuscitation

 

potentially

 

at

 

the

 

expense

 

of

 

coronary

 

perfu-

sion.

 

The

 

concept

 

of

 

focussing

 

resuscitation

 

on

 

the

 

brain

 

is

 

not

 

new,

we

 

have

 

attempted

 

abdominal

 

binding

 

and

 

leg

 

raises

 

to

 

improve

cerebral

 

blood

 

flow

 

for

 

over

 

twenty

 

years.

7

These

 

techniques

 

how-

ever

 

have

 

never

 

translated

 

into

 

an

 

improved

 

outcome

 

for

 

patients.

8

Then

 

if

 

we

 

were

 

to

 

utilise

 

only

 

level

 

one

 

evidence

 

in

 

cardiac

 

arrest

management

 

then

 

we

 

would

 

have

 

little

 

in

 

our

 

armoury.

What

 

is

 

concerning

 

considering

 

the

 

amount

 

of

 

healthcare

resource

 

that

 

is

 

used

 

in

 

the

 

management

 

of

 

cardiac

 

arrest,

 

is

 

how

little

 

is

 

known

 

regarding

 

the

 

incidence

 

of

 

carotid

 

disease

 

as

 

either

a

 

cause

 

or

 

an

 

incidental

 

finding

 

following

 

cardiac

 

arrest.

 

Carotid

disease

 

has

 

a

 

high

 

incidence

 

in

 

patients

 

with

 

coronary

 

artery

 

dis-

ease

 

reported

 

as

 

high

 

as

 

40%

 

and

 

in

 

these

 

patients

 

there

 

is

 

a

 

higher

incidence

 

of

 

myocardial

 

events

 

even

 

following

 

revascularisation.

9

It

 

is

 

highly

 

likely

 

therefore

 

that

 

patients

 

following

 

cardiac

 

arrest

are

 

at

 

high

 

risk

 

of

 

impaired

 

carotid

 

blood

 

flow

 

even

 

with

 

ade-

quate

 

cardiac

 

output.

 

Further

 

impairing

 

that

 

flow

 

with

 

SADs

 

and

epinephrine

 

could

 

have

 

serious

 

consequences.

 

The

 

reasons

 

for

 

the

large

 

variations

 

in

 

neurological

 

outcome

 

following

 

cardiac

 

arrest

remain

 

unclear,

 

and

 

it

 

is

 

entirely

 

plausible

 

that

 

altered

 

cerebral

blood

 

flow

 

is

 

a

 

factor

 

in

 

this.

Further

 

research

 

into

 

the

 

effects

 

of

 

SADs

 

on

 

carotid

 

blood

 

flow

is

 

required.

 

It

 

would

 

be

 

useful

 

to

 

know

 

if

 

devices

 

with

 

no

 

inflat-

able

 

cuffs

 

such

 

as

 

the

 

iGEL

 

(Intersurgical,

 

Wokingham,

 

UK)

 

have

 

the

same

 

potential

 

to

 

cause

 

alterations

 

in

 

blood

 

flow.

 

It

 

is

 

also

 

important

to

 

understand

 

if

 

the

 

reductions

 

in

 

carotid

 

blood

 

flow

 

are

 

associated

with

 

reduced

 

cerebral

 

blood

 

flow

 

or

 

if

 

there

 

is

 

compensation

 

via

the

 

vertebral

 

arteries.

One

 

of

 

the

 

most

 

important

 

issues

 

that

 

this

 

paper

 

points

 

to

 

is

 

the

ultimate

 

outcomes

 

we

 

are

 

aiming

 

for

 

in

 

the

 

management

 

of

 

cardiac

arrest.

 

Long

 

term

 

good

 

neurological

 

outcome

 

has

 

to

 

be

 

the

 

ultimate

focus

 

of

 

all

 

clinicians

 

involved

 

in

 

resuscitation,

 

and

 

it

 

is

 

reassuring

that

 

this

 

has

 

been

 

recognised

 

in

 

the

 

recommended

 

outcomes

 

of

resuscitation

 

trials.

10

1.

 

Conflict

 

of

 

interest

We

 

report

 

no

 

conflict

 

of

 

interest.

References

1.

 

Lipton

 

P.

 

Ischemic

 

cell

 

death

 

in

 

brain

 

neurons.

 

Physiol

 

Rev

 

1999;79:1431–568.

2.

 

Laver

 

S,

 

Farrow

 

C,

 

Turner

 

D,

 

Nolan

 

J.

 

Mode

 

of

 

death

 

after

 

admission

 

to

 

an

 

inten-

sive

 

care

 

unit

 

following

 

cardiac

 

arrest.

 

Intensive

 

Care

 

Med

 

2004;30:2126–8.

3. Lim

 

SH,

 

Shuster

 

M,

 

Deakin

 

CD,

 

et

 

al.

 

Part

 

7:

 

CPR

 

techniques

 

and

 

devices:

 

2010

International

 

Consensus

 

on

 

Cardiopulmonary

 

Resuscitation

 

and

 

Emergency

Cardiovascular

 

Care

 

Science

 

with

 

Treatment

 

Recommendations.

 

Resuscitation

2010;81(Suppl.

 

1),

 

e86–92.

4. Segal

 

N,

 

Yannopoulos

 

D,

 

Mahoney

 

BD,

 

et

 

al.

 

Impairment

 

of

 

carotid

 

artery

 

blood

flow

 

by

 

supraglottic

 

airway

 

use

 

in

 

a

 

swine

 

model

 

of

 

cardiac

 

arrest.

 

Resuscitation

2012;83:1025–30.

5.

 

Colbert

 

SA,

 

O’Hanlon

 

DM,

 

Flanagan

 

F,

 

Page

 

R,

 

Moriarty

 

DC.

 

The

 

laryngeal

 

mask

airway

 

reduces

 

blood

 

flow

 

in

 

the

 

common

 

carotid

 

artery

 

bulb.

 

Can

 

J

 

Anaesth

1998;45:23–7.

6.

 

Burnett

 

AM,

 

Segal

 

N,

 

Salzman

 

JG,

 

McKnite

 

MS,

 

Frascone

 

RJ.

 

Potential

 

nega-

tive

 

effects

 

of

 

epinephrine

 

on

 

carotid

 

blood

 

flow

 

and

 

ETCO(2)

 

during

 

active

compression-decompression

 

CPR

 

utilizing

 

an

 

impedance

 

threshold

 

device.

Resuscitation

 

2012;83:1021-4.

7.

 

Koehler

 

RC,

 

Chandra

 

N,

 

Guerci

 

AD,

 

et

 

al.

 

Augmentation

 

of

 

cerebral

 

perfusion

by

 

simultaneous

 

chest

 

compression

 

and

 

lung

 

inflation

 

with

 

abdominal

 

binding

after

 

cardiac

 

arrest

 

in

 

dogs.

 

Circulation

 

1983;67:266–75.

8.

 

Koster

 

RW,

 

Sayre

 

MR,

 

Botha

 

M,

 

et

 

al.

 

Part

 

5:

 

Adult

 

basic

 

life

 

support:

 

2010

International

 

consensus

 

on

 

cardiopulmonary

 

resuscitation

 

and

 

emergency

cardiovascular

 

care

 

science

 

with

 

treatment

 

recommendations.

 

Resuscitation

2010;81(Suppl.

 

1),

 

e48–70.

9.

 

Komorovsky

 

R,

 

Desideri

 

A.

 

Carotid

 

ultrasound

 

assessment

 

of

 

patients

 

with

 

coro-

nary

 

artery

 

disease:

 

a

 

useful

 

index

 

for

 

risk

 

stratification.

 

Vasc

 

Health

 

Risk

 

Manag

2005;1:131–6.

10.

 

Becker

 

LB,

 

Aufderheide

 

TP,

 

Geocadin

 

RG,

 

et

 

al.

 

Primary

 

outcomes

 

for

 

resuscita-

tion

 

science

 

studies.

 

Circulation

 

2011;124:2158–77.

Matt

 

Thomas

R.

 

Jonathan

 

Hadfield

Intensive

 

Care

 

Unit,

 

University

 

Hospitals

 

Bristol,UK

Corresponding

 

author.

E-mail

 

address:

Matthew.Thomas@UHBristol.nhs.uk

 

(M.

 

Thomas)

8

 

May

 

2012

0300-9572/$

 

 

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front

 

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 2012 Elsevier Ireland Ltd. All rights reserved.

http://dx.doi.org/10.1016/j.resuscitation.2012.05.002