Learning objectives

After reading this article, you should be able to:

C recognize and treat cardiac arrest in adults according to current

national and international guidelines, understanding the

emphasis on good-quality chest compressions, minimizing

interruptions to chest compressions and good defibrillation

technique

C start post-resuscitation care after resuscitation from cardiac

arrest, including the use of therapeutic hypothermia

C understand the difficulties of prognostication in comatose

survivors of cardiac arrest.

INTENSIVE CARE

Cardiopulmonaryresuscitation andpost-resuscitation careKieron Rooney

Jasmeet Soar

AbstractSurvival following cardiac arrest depends on early recognition and treat-

ment. Current guidelines encourage good-quality chest compressions,

ventilation and defibrillation if appropriate. Interruptions to chest

compressions should be minimized. Successfully resuscitated patients

develop a ‘sepsis-like’ post-cardiac arrest syndrome. The intensive care

post-resuscitation ‘care bundle’ includes coronary reperfusion, control

of ventilation, circulatory support, glucose control, treatment of seizures

and therapeutic hypothermia. Prognostication in comatose survivors is

difficult. One-third of cardiac arrest survivors admitted to intensive care

are discharged home.

Keywords asystole; cardiac arrest; cardiopulmonary resuscitation; defi-

brillation; hypothermia; post-resuscitation care; pulseless electrical

activity; ventricular fibrillation

Introduction

Cardiac arrest survivors account for one in 17 intensive care unit

(ICU) admissions in the UK. This is a small proportion of the 50,000

cardiac arrests treated annually in the UK. Ventricular fibrillation

(VF) or pulseless ventricular tachycardia (VT) is the presenting

rhythmin mostout-of-hospital cardiacarrests. Early defibrillation is

the effective treatment for VF/VT and each minute of delay

decreases the chances of success by approximately 10%. Approxi-

mately 7e10% of out-of-hospital cardiac arrest victims survive to

hospital discharge. The incidence of in-hospital cardiac arrest is

about 1e4 per thousand admissions. In two-thirds of in-hospital

cardiac arrests, the first monitored rhythm is asystole or pulseless

electrical activity (PEA) and approximately 17% survive to hospital

discharge. One-third of cardiac arrests survivors admitted to ICU are

discharged from hospital. Overall, only 3% of all treated cardiac

arrests victims eventually return home.

The Chain of Survival

All four links in the Chain of Survival (Figure 1) must be strong

to improve survival from cardiac arrest.

Kieron Rooney MRCP FRCA is a specialist registrar in anaesthetics and

intensive care medicine at the Bristol School of Anaesthesia, UK.

Conflict of interest: none declared.

Jasmeet Soar FRCA is consultant in anaesthetics and intensive care

medicine at Southmead Hospital, North Bristol NHS Trust, UK. He is

chair of the Resuscitation Council UK. Conflicts of interest: none

declared.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 11:1 9

Early recognition and call for help

Out of the hospital, recognition of the importance of chest pain

and alerting the ambulance service can prevent cardiac arrest. In

the hospital, early identification of patients at risk of cardiac

arrest and alerting the resuscitation team or medical emergency

team (MET) may prevent cardiac arrest. Here, we cover the

issues following cardiac arrest.

Cardiopulmonary resuscitation

Diagnosis of cardiac arrest: gasping after a sudden cardiac

arrest (usually VF/VT) is common and can cause a delay in

starting CPR. In unconscious patients or during anaesthesia, the

exact moment when a PEA cardiac arrest occurs is often difficult

to recognize. Rescuers should look for signs of life, including

a pulse. If signs of life are absent or the rescuer is unsure, CPR

should be started. In anaesthetized or intensive care unit (ICU)

patients, the presence of monitoring will also help to make the

diagnosis but should not cause delays in starting CPR. Chest

compressions in a low cardiac output state are unlikely to be

harmful.

Chest compressions: chest compressions increase intra-thoracic

pressure and compress the heart directly to generate blood flow.

At best, compressions achieve 25% of normal brain and

myocardium perfusion. The coronary perfusion pressure (CPP)

achieved during CPR correlates with restoration of spontaneous

circulation (ROSC). Each time chest compressions are stopped,

the CPP decreases rapidly. On resuming chest compressions, it

takes time to build up to the same CPP that existed just before

compressions were interrupted. The depth for chest compres-

sions in an adult is 4e5 cm and the rate is 100/min. The

compression to ventilation ratio is 30:2.

Advanced life support (ALS): the ALS algorithm gives a stan-

dardized approach to cardiac arrest treatment (Figure 2).

Airway and ventilation: tracheal intubation is the most reliable

airway during CPR when attempted by trained rescuers and

enables continuous chest compressions without pauses for

ventilations. The recommended ventilation rate is 10/min as

a higher rate decreases the CPP. Compared with bag-mask

ventilation, early ventilation with a supraglottic device reduces

� 2009 Elsevier Ltd. All rights reserved.

Figure 1

The advanced life support algorithm

Unresponsive?

Open airway

Look for signs of life

CPR 30:2

until defibrillator/monitor attached

Assess

rhythm

Call

resuscitation team

Non-shockable

(PEA/asystole)

Shockable

(VF/pulseless VT)

INTENSIVE CARE

the incidence of gastric distension and regurgitation. If a supra-

glottic airway (e.g. laryngeal mask airway, I-gel) has been

inserted, attempt continuous chest compressions without stop-

ping for ventilations. If excessive gas leakage results in inade-

quate ventilation of the patient’s lungs, interrupt chest

compressions to enable ventilation.

During CPR• Correct reversible

Defibrillation

Reproduced with permission from the Resuscitation Council UK

Immediately

resume

CPR 30:2

for 2 minutes

1 shock

150–360 J biphasic

or 360 J monophasic

Immediately

resume

CPR 30:2

for 2 minutes

causes*

• Check electrode

position and

contact

• Attempt/verify:

IV access and

Airway and oxygen

• Give uninterrupted

compressions

when airway

secure

• Give adrenaline

every 3–5 minutes

• Consider:

amiodarone,

atropine,

magnesium

*Reversible causesHypoxia

Hypovolaemia

Hypo/hyperkalaemia/metabolic

Hypothermia

Tension pneumothorax

Tamponade, cardiac

Toxins

Thrombosis (coronary or pulmonary)

Figure 2

Defibrillation creates a current across the myocardium and

depolarizes a critical mass of the cardiac muscle, simulta-

neously enabling the natural pacemaker tissue to resume

control. The pre-shock pause is the interval between stopping

chest compressions and delivering a shock. Every 5-s increase

in the pre-shock pause duration halves the chance of successful

defibrillation. To minimize the pre-shock pause self-adhesive

defibrillation pads should be applied whilst CPR is ongoing.

Before stopping chest compressions, the team should have

a clear plan of what to do if the rhythm is shockable. Identify

which team member will determine if the rhythm is shockable.

Identify who will charge the defibrillator if appropriate (issuing

the ‘stand clear’ order again whilst charging) and deliver the

shock. Identify which team member will resume chest

compressions immediately after the shock. Everyone should

‘stand clear’ on stopping chest compressions and ensure that

there is no oxygen flowing across the chest (leave tracheal

tubes or supraglottic devices attached to the breathing circuit

or bag device). All team members should wear gloves at all

times. If there are delays due to difficulties in rhythm analysis

or rescuers still in contact with the patient, chest compressions

should be resumed whilst another plan is made. The lengthy

pre-shock safety check (‘top, middle, bottom, self, oxygen

away’) is unnecessary and reduces the chance of successful

defibrillation.

Drugs: drug use during CPR is supported by very little evidence.

Adrenaline increases the CPP during CPR. Amiodarone given to

patients inVFrefractory to defibrillationattempts in thepre-hospital

setting improves survival to hospital admission. Drug administra-

tion and attempts at intravenous access should not cause delays in

defibrillation or excessive interruptions in chest compressions.

Reversible causes: identify and treat reversible causes during

CPR. These are divided into two groups of four based upon their

initial letterdeither H or T (Figure 2). Ultrasonography by

trained rescuers during CPR can help identify reversible causes

(e.g. cardiac tamponade).

ANAESTHESIA AND INTENSIVE CARE MEDICINE 11:1 10

Post-resuscitation care

Resuscitation from cardiac arrest triggers a systemic inflamma-

tory response syndrome (SIRS). The key components of this post-

cardiac arrest syndrome are as follows: 1) brain injury, 2)

myocardial dysfunction, 3) systemic ischaemia/reperfusion

response, and 4) the unresolved disease that caused the cardiac

arrest. A ‘bundle’ of early post-resuscitation care using the

ABCDE (Airway, Breathing, Circulation, Disability, Exposure)

approach improves survival. Prognosis cannot be based on the

circumstances surrounding cardiac arrest and cardiopulmonary

resuscitation. The decision to admit a comatose post-cardiac

arrest patient to ICU should be based predominantly on the

patient’s status before the cardiac arrest. Patients resuscitated

� 2009 Elsevier Ltd. All rights reserved.

INTENSIVE CARE

from cardiac arrest might benefit from admission to specific

cardiac arrest centres to optimize their chances of survival.

Airway and breathing: consider tracheal intubation, sedation

and controlled ventilation in patients with obtunded cerebral

function after ROSC. Hypocapnia, hypoxia and hyperoxia are

potentially harmful to the reperfused brain. Adjust oxygenation

and ventilation to achieve normal arterial oxygen saturation

(94e98%) and normocapnia.

Circulation: acute ST segment elevation or new left bundle

branch block and a typical history of acute myocardial infarction

are indications for reperfusion therapy. Percutaneous coronary

intervention (PCI) is the preferred technique for reperfusion. CPR

is not a contraindication to thrombolytic therapy if PCI is not

available. Haemodynamic instability is common after cardiac

arrest and often reverses within 48 h. Patients often require

fluids, inotropes and vasopressors to achieve haemodynamic

stability. An intra-aortic balloon pump (IABP) can also provide

mechanical assistance. Consider an infusion of an anti-

arrhythmic that restored a stable rhythm (e.g. amiodarone). Aim

to maintain serum potassium at 4.0e4.5 mmol/l and correct any

magnesium abnormalities.

Patients resuscitated from VF cardiac arrest outside the

context of proven acute ST segment elevation myocardial

infarction should be considered for an implantable cardioverter

defibrillator (ICD) before hospital discharge.

Disability and exposure: cerebral hyperaemia immediately

follows ROSC. This is followed 15e30 min later by global cere-

bral hypoperfusion. Normal cerebral autoregulation is lost,

leaving cerebral perfusion dependent on mean arterial pressure

(MAP). Hypotension can worsen any neurological injury. After

ROSC, attempt to maintain the MAP at the patient’s usual level.

Mild hypothermia suppresses many of the chemical reactions

associated with reperfusion injury. Unconscious adult patients

with spontaneous circulation after out-of-hospital VF cardiac

arrest should be cooled to 32e34 �C. Cooling should be started as

soon as possible and continued for at least 12e24 h. Cooling can

be initiated by rapidly infusing 30 ml/kg of cold (4 �C) crystal-

loid. There are many techniques to maintain hypothermia (e.g.

surface cooling and intravascular cooling devices). Induced

hypothermia can also be beneficial for other rhythms or in-

hospital cardiac arrest. Re-warm the patient slowly (0.25 �C/h)

and avoid hyperthermia. The risk of a poor neurological outcome

increases for each degree of body temperature over 37 �C.

Seizures and/or myoclonus occur in approximately 40% of

comatose patients with ROSC. Prolonged seizures cause cerebral

injury and should be controlled with benzodiazepines,

phenytoin, propofol, or a barbiturate. Clonazepam is the treat-

ment of choice for myoclonus. Seizures and myoclonus per se are

not related significantly to outcome, but status epilepticus and, in

particular, status myoclonus, are associated with a poor

outcome. Consider continuous EEG monitoring to detect seizures

in patients requiring neuromuscular blockade.

Both a high and a low blood glucose after ROSC is associated

with a worse outcome. Normoglycaemia aiming at a moderate

glucose target (less than 10 mmol/l) and avoiding hypoglycaemia

(less than 4 mmol/l) has recently been recommended.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 11:1 11

Prognostication: by three days after the onset of coma relating to

cardiac arrest, 50% of patients with no chance of ultimate

recovery have died. The absence of corneal or pupil light reflexes

and an absent or extensor motor response to pain on day three

are independently predictive of a poor outcome (death or vege-

tative state) with very high specificity.

Median nerve somatosensory evoked potentials in normo-

thermic patients, comatose for at least 72 h after cardiac arrest,

predict poor outcome with 100% specificity. Bilateral absence of

the N20 component of the evoked potentials in comatose patients

with coma of hypoxiceanoxic origin is uniformly fatal. The N20

component is a negative deflection with a latency of 20 ms seen

in the waveform recorded by a scalp electrode on the

contralateral cortex. A normal or grossly abnormal EEG predicts

outcome reliably, but an EEG between these extremes is unreli-

able for prediction of prognosis.

Prognosis

In the UK, approximately one-third of ICU admissions after

cardiac arrest survive to hospital discharge. Most (80%) return to

their normal residence. The quality of life for most adult survi-

vors of cardiac arrest is good. Even those with good apparent

survival are at risk of depression, memory impairment and post-

traumatic stress disorder. A

FURTHER READING

Nolan JP, Laver SR, Welch CA, Harrison DA, Gupta V, Rowan K. Outcome

following admission to UK intensive care units after cardiac arrest:

a secondary analysis of the ICNARC Case Mix Programme Database.

Anaesthesia 2007; 62: 1207e16.

Nolan J, Soar J, EikelandH. The chainof survival.Resuscitation2006;71:270e1.

Nolan JP, Deakin CD, Soar J, Bottiger BW, Smith G. European Resuscitation

Council guidelines for resuscitation 2005. Section 4. Adult advanced

life support. Resuscitation 2005; 67: S39e86.

Nolan JP, Soar J. Airway and ventilation techniques. Curr Opin Crit Care

2008; 14: 279e86.

Nolan JP, Soar J. Defibrillation in clinical practice. Curr Opin Crit Care 2009;

15: 209e15.

Nolan JP, Neumar RW, Adrie C, et al. Post-cardiac arrest syndrome: epidemi-

ology, pathophysiology, treatment, and prognostication. A Scientific

Statement from the International Liaison Committee onResuscitation; the

American Heart Association Emergency Cardiovascular Care Committee;

the Council on Cardiovascular Surgery and Anesthesia; the Council on

Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical

Cardiology; the Council on Stroke. Resuscitation 2008; 79: 350e79.

Sandroni C, Nolan J, Cavallaro F, Antonelli M. In-hospital cardiac arrest:

incidence, prognosis and possible measures to improve survival.

Intensive Care Med 2007; 33: 237e45.

Soar J, Nolan JP. Mild hypothermia for post cardiac arrest syndrome. BMJ

2007; 335: 459e60.

USEFUL WEBSITES

European Resuscitation Council, www.erc.edu (accessed 17 Aug 2009).

International Liaison, Committee on Resuscitation, www.americanheart.

org/ILCOR (accessed 17 Aug 2009).

Resuscitation Council UK, www.resus.org.uk (accessed 17 Aug 2009).

� 2009 Elsevier Ltd. All rights reserved.