INTENSIVE CARE
Cardiopulmonary
resuscitation and
post-resuscitation care
Kieron Rooney
Jasmeet Soar
Abstract
Survival 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
rhythm in most out-of-hospital cardiac arrests. 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
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.
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
9 Ó 2009 Elsevier Ltd. All rights reserved.
 INTENSIVE CARE

The advanced life support algorithm

Unresponsive?

Open airway
Look for signs of life

Call
resuscitation team
Figure 1
CPR 30:2
until defibrillator/monitor attached
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- Assess
ping for ventilations. If excessive gas leakage results in inade- rhythm
quate ventilation of the patient’s lungs, interrupt chest
Shockable Non-shockable
compressions to enable ventilation. (VF/pulseless VT) (PEA/asystole)
During CPR
Defibrillation • Correct reversible
Defibrillation creates a current across the myocardium and causes*
depolarizes a critical mass of the cardiac muscle, simulta- 1 shock • Check electrode
150–360 J biphasic position and
neously enabling the natural pacemaker tissue to resume
or 360 J monophasic contact
control. The pre-shock pause is the interval between stopping
• Attempt/verify:
chest compressions and delivering a shock. Every 5-s increase IV access and
in the pre-shock pause duration halves the chance of successful Immediately Airway and oxygen Immediately
defibrillation. To minimize the pre-shock pause self-adhesive resume • Give uninterrupted resume
defibrillation pads should be applied whilst CPR is ongoing. CPR 30:2 compressions CPR 30:2
Before stopping chest compressions, the team should have for 2 minutes when airway for 2 minutes
a clear plan of what to do if the rhythm is shockable. Identify secure
• Give adrenaline
which team member will determine if the rhythm is shockable.
every 3–5 minutes
Identify who will charge the defibrillator if appropriate (issuing • Consider:
the ‘stand clear’ order again whilst charging) and deliver the amiodarone,
shock. Identify which team member will resume chest atropine,
compressions immediately after the shock. Everyone should magnesium
‘stand clear’ on stopping chest compressions and ensure that
there is no oxygen flowing across the chest (leave tracheal *Reversible causes
tubes or supraglottic devices attached to the breathing circuit Hypoxia Tension pneumothorax
or bag device). All team members should wear gloves at all Hypovolaemia Tamponade, cardiac
times. If there are delays due to difficulties in rhythm analysis Hypo/hyperkalaemia/metabolic Toxins
Hypothermia Thrombosis (coronary or pulmonary)
or rescuers still in contact with the patient, chest compressions
should be resumed whilst another plan is made. The lengthy Reproduced with permission from the Resuscitation Council UK
pre-shock safety check (‘top, middle, bottom, self, oxygen
away’) is unnecessary and reduces the chance of successful Figure 2
defibrillation.
Post-resuscitation care
Drugs: drug use during CPR is supported by very little evidence. Resuscitation from cardiac arrest triggers a systemic inflamma-
Adrenaline increases the CPP during CPR. Amiodarone given to tory response syndrome (SIRS). The key components of this post-
patients in VF refractory to defibrillation attempts in the pre-hospital cardiac arrest syndrome are as follows: 1) brain injury, 2)
setting improves survival to hospital admission. Drug administra- myocardial dysfunction, 3) systemic ischaemia/reperfusion
tion and attempts at intravenous access should not cause delays in response, and 4) the unresolved disease that caused the cardiac
defibrillation or excessive interruptions in chest compressions. arrest. A ‘bundle’ of early post-resuscitation care using the
ABCDE (Airway, Breathing, Circulation, Disability, Exposure)
Reversible causes: identify and treat reversible causes during approach improves survival. Prognosis cannot be based on the
CPR. These are divided into two groups of four based upon their circumstances surrounding cardiac arrest and cardiopulmonary
initial letterdeither H or T (Figure 2). Ultrasonography by resuscitation. The decision to admit a comatose post-cardiac
trained rescuers during CPR can help identify reversible causes arrest patient to ICU should be based predominantly on the
(e.g. cardiac tamponade). patient’s status before the cardiac arrest. Patients resuscitated

ANAESTHESIA AND INTENSIVE CARE MEDICINE 11:1 10 Ó 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
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, Eikeland H. The chain of survival. Resuscitation 2006; 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 on Resuscitation; 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).
11 Ó 2009 Elsevier Ltd. All rights reserved.