Cardiac Arrest Management - PowerPoint Presentation

Slide1

Cardiac Arrest Management

Slide2

Last Time

Vasopressors

Inotropes

Slide3

Today

Post cardiac arrest management

Targeted Temperature Management (TTM)

Slide4

Case

54yr old tax lawyer

Collapses on Liverpool St Station

Anaethetist

on scene who finds AED

ROSC

afer

15min but patient remains unconscious

Brought to ED

Slide5

Priorities

Prevent further cardiac arrest

Define the underlying pathology

Limit organ damage

Predict non-survivors

Slide6

Ideally patients should be taken to a cardiac intervention

centre

with 24/7 capabilities

Slide7

Prevent Further Cardiac Arrest

Optimise

FiO

2

Target

sats

94-98% to avoid

hyperoxia

Decrease FiO

2

as soon as possible

Protective lung ventilation via ETT

Commence sedation

Ventilate to

normocapnia

Correct electrolyte abnormalities

Control glucose (

e.g

<10mmol/L)

Appropriate anti-

arrythmic

(

e.g

amiodarone

)

Slide8

Case Continued

The patient has been up on ICU for one hour

His wife has arrived and would like to know what’s going to happen next?

Slide9

Slide10

Define Underlying Pathology

Diagnose and treat underlying cause (PCI/thrombolysis)

Treat complications (

e.g

heart failure, hypotension, rib fractures, pneumothorax)

Cath

lab on ECMO or LUCAS if refractory arrest

Assess neurology

Slide11

Case Continued

Patient has come back to the unit following PCI

3 stents to a heavily narrowed LAD

Slide12

Cooling

Seems to get everyone hot under the collar

Although there are risks, they are largely theoretical

Instead, concerns about spending on infrastructure

Slide13

Theory behind cooling

Global ischaemia-reperfusion injury

Aim is to reduce:

Cerebral metabolism and oxygen demand

Apoptosis

Release of excitatory neurotransmitters

Cellular influx of Ca

2+

Inflammation

Free radical species

Intra and extra-cellular acidosis

Disruption of the blood-brain barrier

etc.

Slide14

Adverse effects of cooling

Bradycardia and arrhythmias

Electrolyte abnormalities

Impaired platelet function and coagulopathy

Depressed immune function

Reduced insulin sensitivity

Prolonged drug effects from decreased clearance

Slide15

Prior to 2013, the term “therapeutic hypothermia” was used

This was replaced with Targeted Temperature Management (TTM) after concerns that hypothermia wasn’t a necessary component

Slide16

Experimental animal data strongly supported cooling immediately after and perhaps before

intervention

NICE recommends cooling “as soon as possible after cardiac arrest”

1359 survivors of OHCA randomised to pre-hospital cooling or standard care (which included cooling in most)

Not associated with improved survival or neurological outcome.

Any cooling should take place once in hospital

Slide17

Cooling –

nothing new

1940’s

Knowledge of the deleterious effects of cerebral anoxia on brain volume noted

1950’s

Benefits of cooling on brain blood flow and volume noted

1950’s

Suggestion that cooling may be of benefit to the brain post cardiac arrest first investigated

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1959

27 patients with cardiac arrest

Excluded 8 as immediately perfectly healthy post-resus (did they really arrest?)

7

– no cooling

12 – cooled within 6 hrs of ROSC to 31-32 deg C

No cooling 1/7 survived (14%)

Cooling 6/12 survived (50%)

Survivors had no neurological deficit

Slide20

“Modern” Trials

We had to wait until the late 1990’s for further trails to be conducted – most published between 2000-2005

2 from the NEJM…

Bernard et al 2002

HACA Study Group 2002

Slide21

Bernard et al

4 hospital Australian randomised trial (Melbourne)

Included men >18 yrs and women >50 yrs (to minimise risk of cooling pregnant women)

Cardiac arrest initial rhythm VF

ROSC

Persistent coma

Excluded those with cardiogenic shock or other likely cause of coma (drugs, trauma, etc.)

Slide22

Bernard et al

Randomly assigned (odd days – cooled, even days not cooled) to standard management with or without cooling

Started by the paramedics

Cooling – cooling ice packs

Standard –

“Correction of CV instability”

I

nvasive ventilation

Midazolam & vecuronium

PaO2 100mmHg, PaCO2 40mmHg

MAP 90-100,

T

hrombolytics (if required) & heparin

Lidocaine & K+ (target >4)

I

nsulin (glucose <10)

A

spirin to all

Slide23

Bernard et al

Cooled to 33 degrees

Packs removed

Kept paralysed to prevent shivering and kept at 33 until 12 hrs post-arrival at hospital

Actively rewarmed from 18 hrs post-arrival

Withdrawal of care at 72 hrs if no neurological recovery

Good outcome – normal to moderate disability

Slide24

Bernard et al

43 cooled

15 normal/minimal disability

6 moderate disability

0 severely disabled but awake

0 severely disabled but unconscious

22 dead

48.8% good outcome

p=0.046

34 not cooled

7

normal/minimal disability

2 moderate disability

1

severely disabled but awake

1

severely disabled but unconscious

23 dead

26.5% good outcome

Slide25

Bernard et al

no record of baseline neurological status prior to the event

no record of GCS on arrival in ED

good outcome: home or rehab facility at discharge (rather than a structured assessment)

positive outcome of trial would have been lost if 1 patient in good outcome group had a bad outcome

Slide26

HACA

Hypothermia

After

Cardiac

Arrest study group

Included

18-75yrs

<15 mins until resus started

Witnessed arrest, pulseless VT or VF

<60 mins until ROSC

Excluded

<30 deg on admission, coma before arrest, MAP <60 post arrest for >30 mins, hypoxaemia >15 mins post-arrest, terminal illness, coagulopathy

Slide27

HACA

Randomised, blinded outcome, controlled

Standard or standard + cooling

Standard therapy involved sedation for 32 hrs (no comment on ACS treatment)

Cooling – 32-34 deg C for 24 hrs

Passive rewarming

Slide28

HACA

Primary outcome – favourable neuro outcome

Pittsburg cerebral-performance category 1 or 2

1 – good recovery

2 – moderate disability

3 – severe disability

4 – veg state

5 – death

Slide29

HACA

Secondary endpoints

6 month mortality

Complications within 7 days:

Bleeding of any

severity

P

neumonia

S

epsis

P

ancreatitis

Renal failure

P

ulmonary oedema

S

eizures

Arrhythmias

Pressure sores

Slide30

HACA

Standard (138 pts)

Favourable neuro outcome 54/137 (39%)

Death 76/138 (55%)

Cooled (137)

Favourable neuro outcome

75/136 (55%)

P=0.009

Death

56/137 (41%)

P=0.02

Slide31

HACA

Slide32

HACA

no active temperature control — usual care group were not actually

normothermic

, they tended to be

hyperthermic

trial stopped early

only 8% of screened ED patients were included

Slide33

Cochrane Review 2010

“Conventional

cooling methods to induce mild therapeutic hypothermia seem to improve survival and neurologic outcome after

cardiac arrest”

Based on 5 papers (including the 2 we’ve just looked at)

Slide34

Clinical Recommendations

Resuscitation Council, ILCOR, AHA Guidelines – post-arrest care

Cool

Comatose survivors

of out-of-hospital cardiac arrest caused by

VF

(and pulseless VT but this is not in the guidelines)

Consider induced hypothermia for non-shockable rhythms

Slide35

Practice

Rapid induction of hypothermia

Stable and controlled maintenance

Controlled re-warming

Slide36

Methods of Cooling

Ice-cold Crystalloid at 20-40ml/kg bolus

Intra-vascular cooling catheters

Extra-corporeal circuits

Cooling blankets/pads

Cooling Helmet

Cold Air Tent

Ice packs

Few studies comparing feasibility and efficacy

No recommendations for a specific method as no study has evaluated implications on survival benefit

Slide37

When to Cool?

Animal studies suggest cooling during CPR or immediately after ROSC is associated with better organ preservation

Trials are coming…

Till then, aim to initiate cooling as soon as possible

Slide38

How long to Cool?

Recent studies maintained hypothermia for 24hrs, however, 12 hour protocols have been used

More studies are needed

Slide39

Re-warming

Rate of re-warming has not been studied, however, traditional recommendations are 0.3-0.5

0

C per hour

Avoid rebound hyperthermia

Slide40

But…

TTM Trial

17

th

November 2013

NEJM

Targeted temperature management at 33°C versus 36°C after cardiac arrest

Nielsen et al

Slide41

TTM Trial

Background

We don’t know what the target temperature should be

The HACA study standard treatment arm – lots of pyrexia

Was the cooling the source of benefit or was it just the avoidance of pyrexia?

Slide42

Patients

>18 years old

GCS <8 on hospital admission after OOH cardiac arrest

Any presenting rhythm

Presumed cardiac cause of arrest

>20

mins

of spontaneous circulation after arrest

Excluded

>2

hrs

between ROSC and screening to include in trial

Unwitnessed arrest with asystole as presenting rhythm

Suspected or known CVA or IC bleed

<30°C

Slide43

Methods

Multicentre

Randomly assigned to 33 vs.

36°C

Treating clinicians were aware of trial arm

Investigators and those performing neurological testing and prognostication were

not

36hrs – cooled rapidly (various methods) to target temp for 24hrs

Gradual rewarming (<0.5°C/

hr

) to 37°C

Sedation off at 36hrs

Kept <37.5°C until 72hrs

Slide44

Prognostication and withdrawal

If still unconscious…

72hrs after the end of the intervention

Neurological examination and recommendation regarding continuing care made

Slide45

Outcome measures

Primary

All cause mortality until 180 days after enrolment

900 patients needed

Secondary

Poor neurological function

Mortality at 180 days

Adverse events

Slide46

Results

Mortality during trial period

33°C – 50%

36°C – 48% (p=0.51)

Neurological outcome

CPC

33°C – 54%

36°C – 52% (p=0.78)

Mod Rankin

33°C – 52%

36°C – 52% (p=0.87)

Dead at 180 days

33°C –

48%

36°C –

47% (p=0.92)

Slide47

Adverse events

More adverse events in the 33°C group (93% vs. 90% - p=0.09)

Hypokalaemia more likely in the

33°C group

(19%

vs.

13%

-

p=0.02)

Causes of death similar between the groups

Slide48

Conclusion

No benefit in cooling to 33°C over 36°C

Slide49

Issues with the trial

No comment on ACS treatments

This

trial also advocated active prevention of fever until 72hrs – not done

before

Slide50

My thoughts

Well designed, well conducted, adequately powered and well reported trial

Followed international recommendations for further research into this

subject

It doesn’t tell us where the real benefit from cooling comes from

Is it simply fever prevention?

Is it through sedation and giving the brain a break?

Is it just good quality ICU care?

Slide51

How Should This Change Practice?

There’s no role for TTM, you just need to avoid fever

If TTM does improve survival, then T36 is probably most appropriate

And you should use as sophisticated equipment as you have available

Slide52

NUH Post Cardiac Arrest Care

Standard ICU admission criteria have to be met – they must have the physiological reserve to survive and rehabilitate to an acceptable

QoL

(as far as we can ascertain)

All post-arrest patients

(In theory all should go through the cardiac cath lab)

Sedate for 24 hours with cooling to 35 degrees

Chosen because our own audit data shows this means real temperatures are around 1 degree higher than target

ACS treatment as indicated

Sedation off at 24 hours

Try to maintain normothermia for further 2 days

Slide53

Effects of Therapeutic Hypothermia

Bradycardia

Hypotension

Decreased cardiac output

AF common

Severe dysrhythmias more common below T30

Slide54

Effects of Therapeutic Hypothermia

K+ and Mg2+ will fall (treat)

Low WBC, high PT/APTT and LFTs (don’t treat)

Drug metabolism generally slowed

Rectal temperature lags behind true core temperature

Use nasopharyngeal or

oesophageal

temperature probe

Slide55

Limit Organ Damage –other measures

Control shivering

Invasive monitoring

Inotropes/vasopressors

Target MAP>70: some target MAP>80 to ensure adequate CPP, others (Bernard) advocate SBP>120mmHg

Slide56

Case Continued

96hrs post admission

Off all sedation and tube tolerant.

Spontaneously breathing

GCS E1VTM2

Slide57

Prognosticate at Day 5

Clinical examination including GCS, pupillary and corneal reflex

SSEP and EEG

Biomarkers for brain damage NOT useful

Slide58

Discontinue Active Care

Brain death

Severe myoclonus in the first 24hrs and absence of N2O-peak on SSEP

Motor score 1-2 and absence of N20 peak on SSEP

Motor score 1-2 with treatment refractory status

epilepticus

Motor score 1-2, re-examine daily and withdraw if doesn’t improve and metabolic/pharmacological problems ruled out

Slide59

Summary

Patients should be taken 24/7 to cardiac intervention

centre

Lower FiO

2

as soon as possible

Normal pCO

2

SBP to 120mmHg with

pressor

Sedate

Maintain

T35

Prognosticate D5

Cath

lab on LUCAS or ECMO if refractory arrest