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:

[e-mail]

(M.

Thomas)

8

May

2012

0300-9572/$

–

see

front

matter ©

2012 Elsevier Ireland Ltd. All rights reserved.

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