EMERGENCY PRESENTATIONS

Cardiorespiratory arrest What’s new?

Clive Weston
C New guidelines for the management of cardiorespiratory arrest
Omar Aldalati were published in 2010
C The importance of predicting and preventing cardiopulmonary
arrest within hospital has led to the development of critical care
outreach teams in many hospitals
Abstract
C Drugs play a limited role in advanced life support
Management of cardiorespiratory arrest is an essential skill to be acquired
C Devices that augment cardiopulmonary resuscitation are the
during core medical training. The requisite knowledge, skills, attitudes and
subject of randomized trials
behaviours to allow competent and appropriate performance of cardiopul-
C Post-resuscitation care pathways are being developed
monary resuscitation are outlined in recently updated national guidelines.
Successful resuscitation outcomes remain poor, but attention to detail is
important to provide optimal recovery. Current guidelines emphasize the These disappointing figures emphasize the importance of
importance of minimizing interruption of chest compressions and prompt prevention wherever possible.
delivery of shock when the rhythm is shockable. ‘Pure’ respiratory arrest e cessation of breathing with per-
sisting effective cardiac activity e may complicate respiratory
Keywords advanced life support; basic life support; cardiac arrest; diseases such as asthma, exacerbations of chronic pulmonary
cardiopulmonary resuscitation; defibrillation disease, airways obstruction, neuromuscular diseases and use of
respiratory suppressant drugs such as morphine and tramadol.
Techniques for CPR are also useful in the management of
arrest due to asphyxia, for example drowning.
Cardiorespiratory arrest is rapidly fatal without resuscitation.
Outside hospital, the underlying cause is often transient cardiac Principles of treatment
ischaemia resulting in ventricular fibrillation (VF) in a heart that,
while scarred or hypertrophied, is deemed ‘too good to die’. The principles of resuscitation comprise:
Untreated VF degenerates to asystole but can be successfully
appropriate use of ‘do not resuscitate’ orders
reversed with prompt life-supportive manoeuvres involving chest
rapid recognition that cardiorespiratory arrest has occurred
compressions, rescue breathing and defibrillation. ‘Non-shock-
a call to suitably trained personnel for help
able rhythms (asystole and pulseless electrical activity (PEA)) are
avoidance of danger to rescuers and victim
more common and more resistant to treatment, and recovery is
assessment of the circumstances of the collapse
unlikely unless an underlying cause can be recognized and
maintenance of sufficient coronary perfusion (during the
reversed. Long-term survival following pre-hospital cardio- relaxation phase of chest compressions) to allow subse-
respiratory arrest is unusual (<10% of cases), although this rises quent reversal of non-perfusing cardiac rhythms
to 30e40% in the subgroup whose arrests are witnessed, who
maintenance of cerebral perfusion (during the compres-
then receive bystander cardiopulmonary resuscitation (CPR) and sion phase of chest compressions) to avoid permanent
are in VF when a defibrillator is available at the scene. neurological damage following restoration of spontaneous
In hospital, sudden collapse is neither entirely unpredictable circulation (ROSC)
nor unpreventable. Although the patient has the advantage of
maintenance of oxygenation through continuous positive
rapid response from a ‘cardiac arrest team’, the outcome is poor; airways pressure (CPAP) or positive-pressure ventilation
the arrest is frequently a terminal event because of severe co-
correction of the underlying problem using cardiac moni-
morbidities and evidence of clinical decline over several hours. toring, defibrillation and drugs
Except when arrest occurs soon after hospitalization, the hospital
consideration of early coronary angiography and mild
cardiac arrest team is usually confronted with a non-shockable therapeutic hypothermia in those surviving out-of-hospital
rhythm. For cardiac arrests occurring in hospital only 17% cardiac arrest
patients survive to discharge (three-quarters with good neuro-
timely cessation of resuscitative attempts.
logical function) e the equivalent figure for those found in VF is The response to cardiorespiratory arrest is characterized by the
37%, but only 11% for those found in non-shockable rhythm.1 ‘chain of survival’ e early recognition and rapid delivery of basic
life support (BLS), defibrillation and advanced management. All
clinicians should possess BLS skills and, in the UK, all those
Clive Weston MA MB is Reader in Clinical Medicine at the College of completing specialist training must have an advanced life
Medicine, Swansea University, Wales, UK, where he has responsibilities support (ALS) certificate, with re-certification every 3 years.
for the education of undergraduate medical students. His research
interests include the early management of myocardial infarction.
Guidelines for CPR
Competing interests: none declared.
The International Liaison Committee on Resuscitation commis-
Omar Aldalati MD MRCP is Registrar in Cardiology with the Wales sioned an evaluation of the evidence underpinning the manage-
Deanery, UK. Competing interests: none declared. ment of cardiorespiratory arrest.2

MEDICINE 41:2 59 Ó 2013 Elsevier Ltd. All rights reserved.

 EMERGENCY PRESENTATIONS

The resulting consensus document has been incorporated into tube. Ventilation should include an ‘inspiratory’ phase lasting
international guidelines.3 Whilst the basic principles governing 1 second with enough volume (often only 500e600 ml) to make
CPR remain constant, the revisions contain important practical the chest rise. There is no evidence that oxygen administration
changes based upon the following observations: through a non-secured airway is of benefit during basic life

early after onset of VF, chest compressions appear more support. Its use may lead to interruption in chest compressions,
important than ventilation and at present it is not recommended, except in cases of

the combination of inadequate or interrupted chest drowning. Excessive chest inflation increases intrathoracic
compressions with excessive ventilation reduces coronary pressure, decreases venous return, and reduces coronary and
and cerebral perfusion during CPR cerebral perfusion.

interruptions in chest compressions were frequent and At the 30:2 recommended ratio of compression and ventilation,
prolonged in previous guidelines; an extra 5-second delay 2 minutes of CPR will contain approximately five cycles. This rate
when performing a pre-shock safety check (‘stand clear!’) of compression requires substantial effort and, unless the rescuer
is associated with a halving in successful defibrillation is alone, someone else should take over compressions after

initial biphasic defibrillation terminates VF in approxi- 2 minutes or five cycles, if not before. Several mechanical devices
mately 90% of cases but, even when organized cardiac have been developed to augment, or replace, rescuer-delivered
rhythms ensue, immediate ROSC is rare. chest compressions (e.g. AutoPulse, LUCAS-CPR, impedance
threshold device ITD) and are undergoing trials. Such devices
Basic life support may be particularly useful during prolonged resuscitation
(e.g. cases of hypothermia or pulmonary embolism).
Recommended adult BLS is shown in Figure 1. Infrequent gasp-
ing ‘agonal’ breaths commonly occur early after cardiac arrest. If
in doubt, rescuers should act as if breathing is not normal and Advanced life support
start chest compressions. Health professionals often check for
The ALS algorithm is shown in Figure 2. CPR should continue as
a carotid pulse during the ‘breathing check’, but time should not
per BLS until the airway is secured, preferably by placement of
be wasted (no more than 10 seconds) and a pulse check should
an endotracheal tube. Thereafter, chest compressions (100e120/
coincide with assessing breathing. Two initial rescue breaths are
minute) should continue uninterrupted while ventilation
recommended only in obvious asphyxia, otherwise they delay
(10/minute) e with sufficient volume to observe the chest
the delivery of chest compressions and may deter bystander
rising e is commenced. Ventilations and compressions may then
resuscitation. Recent trials show no improvement in outcomes
be non-synchronized. Previously, in cases of prolonged arrest
when combined compressions and ventilation are compared with
a 2e3 minute period of BLS prior to defibrillation was felt to give
chest compressions alone.4 However ‘compression-only CPR’ is
a greater chance of ROSC. Randomized trials of this policy have
not recommended as standard treatment.
failed to show any benefit. So, while chest compressions and
The heel of the hand should be placed over the middle of
ventilation should continue until a defibrillator is available,
the lower half of the sternum. The preferred compression rate is
there should be no delay in delivering the first shock.
100e120/minute e faster rates are probably more effective
Without stopping compressions, adhesive defibrillator elec-
(though more tiring) e with compression depth 5e6 cm and
trodes should be placed; ‘right’ electrode to the right of the
release of all pressure between compressions. The ratio of
sternum just below the clavicle, ‘left’ electrode as far into the left
compressions to rescue breaths within one ‘cycle of CPR’ is 30:2
axilla as possible, not over breast tissue. It does not matter if the
unless the airway is secured with, for example, an endotracheal
electrodes are reversed. An analysis of cardiac rhythm should be
performed immediately and a single shock (150e200 J biphasic),
given if advised. Chest compressions are stopped only to assess
Adult basic life support cardiac rhythm (as ‘shockable’ or ‘non-shockable’). Compres-
Unresponsive? sions should be resumed while the defibrillator charges and
stopped just before the delivery of a shock. CPR should resume
Shout for help immediately after delivery of the shock, without a rhythm check,
and, unless signs of life become apparent, should continue for 2
Open airway
minutes before reassessment of cardiac rhythm. If organized
electrical activity appears, a check for a palpable pulse should
happen. Following 2 minutes of CPR, if a shockable rhythm
Not breathing normally?
persists, a second shock (150e360 J biphasic) should be deliv-
ered and CPR resumed. This ‘single-shock sequence’ significantly
Call 999
reduces time without chest compressions and is a major depar-
ture from previous guidelines. Only in the case of a witnessed
30 chest compressions
arrest in a monitored facility with immediate access to a defi-
brillator (e.g. a cardiac catheter laboratory or cardiac care unit)
2 rescue breaths; 30 compressions
should three rapid (‘stacked’) shocks without interposed cycles
Reproduced with the kind permission of the Resuscitation Council (UK). of CPR be given for persistent VF.
Neither vasopressors nor antiarrhythmics have proven long-
Figure 1 term benefit during resuscitation. A recent observational study

MEDICINE 41:2 60 Ó 2013 Elsevier Ltd. All rights reserved.

 EMERGENCY PRESENTATIONS

Adult advanced life support

Unresponsive?
Not breathing or only occasional gasps

Call resuscitation team

CPR 30:2
Attach defibrillator/monitor
Minimise interruptions

Assess rhythm

Shockable Return of spontaneous Non-shockable(pulseless

(VF/pulseless VT) circulation electrical activity/asystole)

Immediate post-cardiac arrest

1 shock treatment
• Use ABCDE approach
• Controlled oxygenation and
ventilation
• 12-lead ECG
Immediately resume • Treat precipitating cause Immediately resume
CPR for 2 minutes • Temperature control/ CPR for 2 minutes
Minimise interruptions therapeutic hypothermia Minimise interruptions

During CPR: Reversible causes:

• Ensure high-quality CPR: rate, depth, recoil • Hypoxia
• Plan actions before interrupting CPR • Hypovolaemia
• Give oxygen • Hypo-/hyperkalaemia/metabolic
• Consider advanced airway and • Hypothermia
capnography
• Continuous chest compressions when • Thrombosis – coronary or pulmonary
advanced airway in place • Tamponade – cardiac
• Vascular access (intravenous, • Toxins
intraosseous) • Tension pneumothorax
• Give adrenaline every 3–5 minutes
• Correct reversible causes

Reproduced with the kind permission of the Resuscitation Council (UK).

Figure 2

showed that pre-hospital administration of adrenaline arrest should be considered. These include hypoxia, hypo-
(epinephrine) was associated with an increased rate of ROSC, but volaemia, hyperkalaemia and other metabolic disturbances,
a reduced rate of survival and less chance of good functional hypothermia, tension pneumothorax, cardiac tamponade, toxic
outcome 1 month after the event.5 At present, pending results substances and thromboembolism. The routine use of sodium
from further studies, intravenous adrenaline (1 mg) and amio- bicarbonate is not recommended. It may have a role in cardiac
darone (300 mg) should be given upon recommencing arrest associated with hyperkalaemia or an overdose of tricyclic
compressions following the third shock in cases of resistant VF, antidepressants. Intravenous magnesium sulphate (1e2 g in
further doses of adrenaline being every 3e5 minutes thereafter 10 ml of glucose 5% over 5 minutes) may be of value, particu-
(i.e. after alternate shocks). larly in cases of polymorphic VT e ‘torsade de pointes’.
In cases of asystole or PEA, IV adrenaline should be given Palpation for arterial pulses and estimation of blood gases are
immediately and every 3e5 minutes thereafter (i.e. after every unreliable indicators of the efficacy of CPR. End-tidal carbon
2-minute cycle of CPR); atropine is no longer recommended. dioxide monitoring is a more effective non-invasive indicator of
During ALS, potentially reversible causes of cardiopulmonary ‘cardiac output’ generated during CPR, but is not widely performed.

MEDICINE 41:2 61 Ó 2013 Elsevier Ltd. All rights reserved.

 EMERGENCY PRESENTATIONS

Post-resuscitation care Predicting survival

Resuscitation that simply prolongs the process of dying within Factors associated with favourable outcome include the primary
hospital is difficult to justify, so while ROSC is a necessary arrhythmia at onset of the arrest, the rhythm present when CPR
prerequisite, the primary purpose of resuscitation is complete starts, provision of prompt, high-quality BLS, and early defibril-
recovery of the patient and subsequent discharge. There is lation when appropriate. Patient co-morbidities are important in
increasing evidence that care given early after the immediate final outcomes. Even when adjusted for known outcome
resuscitation can optimize long-term survival with full neuro- predictors, cardiac arrests at night and weekends carry a poorer
logical recovery. Post-resuscitation care may necessitate transfer prognosis, usually reflecting longer delays to treatment.15,16 Once
of survivors to specialized centres and the development of circulation is restored, there is no specific neurological sign or
specific treatment guidelines that aim to: test that reliably predicts poor outcome within the first 24 hours,

maintain physiologically normal intravascular fluid though the use of somatosensory evoked potentials may allow
volume early reliable prognostication in the future. Absence at 24 hours

restore tissue oxygenation and maintain normal blood in the unsedated comatose patient of pupillary, corneal and
glucose and pH e correcting hypercarbia, hypoxaemia and withdrawal reflexes, and motor responses is ominous, and the
avoiding hyperoxaemia (aiming for oxygen saturation of absence of all these at 72 hours reliably diagnoses brain death.
94e98%)3,6

maximize cardiac function through pharmacological When to stop
augmentation of blood pressure and early coronary angi-
In the absence of a ‘do not attempt resuscitation (DNAR)’
ography, and intervention in the absence of an obvious
directive, the decision to start CPR is usually straightforward.
non-cardiac cause of arrest e even in those with impaired
Stopping resuscitation is more difficult. ‘Termination of resusci-
consciousness7
tation’ (TOR) outside hospital should be considered when there

treat infection
has been no ROSC prior to transport, no shock delivered, no

prevent further neurological damage through improving
cardiac function, treatment of seizures with anti-
convulsants, reversal of hyperpyrexia and, in comatose
survivors, elective mild therapeutic hypothermia (e.g. to The resuscitation predictor score (RPS)
32e34  C for 12e24 hours)8,9
Use this table 15 minutes into a resuscitation where the following
Leading the arrest team are known:
Effective CPR requires team-work. The leader of the team,
C primary arrhythmia
frequently the senior attending physician, has responsibility for
C patient’s age
directing resuscitation according to guidelines. Lack of adequate
C primary mode of arrest (respiratory or cardiac)a
leadership e a failure to stand back calmly and direct others, and Variable 24-h
a failure of information transfer and resolution of conflict e is survival
associated with poorer performance.10,11 The leader needs to
liaise with senior anaesthetic and nursing staff, and, having PEA or asystole þ 70 years or older þ primary cardiac 4%
consulted with others, has the responsibility to stop resuscitation PEA or asystole þ 69 years or less þ primary cardiac 6%
and ensure adequate documentation of the various interventions, PEA or asystole þ 70 years or older þ primary 10%
facilitating a ‘debriefing’ of the rescuers and the sensitive respiratory
‘breaking of bad news.’ to relatives of the deceased. The intro- PEA or asystole þ 69 years or less þ primary 17%
duction of formal structured training in resuscitation has had respiratory
a positive impact of clinical management and outcome of cardiac VT or VF þ 70 years or older þ primary cardiac 12%
arrest.12 VT or VF þ 69 years or less þ primary cardiac 28%
VT or VF þ 70 years or older þ primary respiratory 29%
VT or VF þ 69 years or less þ primary respiratory b
Predicting arrest
Many in-hospital cardiorespiratory arrests are predictable and Note: the RPS scale is based on the following premise:
the shorter the resuscitation the greater the chance of survival (P < 0.001)
potentially avoidable e through recognition and immediate primary arrhythmias of VT/VF have a significantly higher survival rate than
reversal of antecedents, such as hypotension, hypoxaemia, PEA/asystole (P < 0.001)
metabolic or electrolyte disturbance, or cardiac ischaemia, and patients of 69 years or less are significantly more likely to survive (P < 0.001)
careful monitoring of patients who sustain a ‘false’ cardiac arrest where the primary mode of arrest is respiratory (as opposed to cardiac) the
survival rate is significantly improved (P ¼ 0.001).
call.13,14 Early detection, using early warning scoring (EWS) a
Refers to the initial mode of arrest. Was it a primary respiratory arrest or
systems should activate local escalation policies to provide a primary cardiac arrest?
b
prompt treatment and correct aberrant physiology. The UK has Not defined in scoring system due to insufficient data in original cohort.
Reproduced with permission from the BMJ Publishing Group, Cooper S, Evans
recently introduced a National EWS. Correction of aberrant
C. Resuscitation predictor scoring scale for inhospital cardiac arrests. Emerg
physiology may prevent subsequent arrest, but recognition of the Med J 2003; 20: 6e9.
acutely ill patient must also include an assessment of whether
CPR is appropriate. Table 1

MEDICINE 41:2 62 Ó 2013 Elsevier Ltd. All rights reserved.

 EMERGENCY PRESENTATIONS

bystander-initiated CPR, and when the arrest was unwitnessed. If 9 Hypothermia after Cardiac Arrest Study Group. Mild therapeutic
these patients are transported to hospital further resuscitative hypothermia to improve the neurologic outcome after cardiac arrest.
efforts are nearly always unsuccessful. Within hospital, there are N Engl J Med 2002; 346: 549e56.
no hard and fast rules for cessation. A survival prediction 10 Marsch SC, Muller C, Marquardt K, et al. Human factors affect the
nomogram (Table 1) based upon a resuscitation predictor scoring quality of cardiopulmonary resuscitation in simulated cardiac arrests.
(RPS) scale has been developed and it is acceptable to consider Resuscitation 2004; 60: 51e6.
stopping as early as 15 minutes after commencement in the 11 Cooper S, Wakelam A. Leadership of resuscitation teams: ‘lighthouse
absence of ROSC. Because of rare cases of ROSC after cessation of leadership’. Resuscitation 1999; 42: 27e45.
resuscitative efforts, it is advisable to monitor the patient 12 Mosley C, Dewhurst C, Molly S, Shaw BN. What is the impact of
passively for 10 minutes before confirming death.17 A structured resuscitation training on healthcare practitioners, their
clients and the wider service? A BEME systematic review: BEME Guide
No. 20. Med Teach 2012; 34: e349e85.
13 Kause J, Smith G, Prytherch D, et al. A comparison of antecedents to
REFERENCES cardiac arrests, deaths and emergency intensive care admissions in
1 Meaney PA, Nadkarni VM, Kern KB, et al. Rhythms and outcomes of Australia and New Zealand, and the United Kingdomethe ACADEMIA
adult in-hospital cardiac arrest. Crit Care Med 2010; 38: 101e8. study. Resuscitation 2004; 62: 275e82.
2 Hazinski MF, Nolan JP, Billi JE, et al. International Consensus on 14 Kenward G, Robinson A, Bradburn S, Steeds R. False cardiac
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care arrests: the right time to turn away? Postgrad Med J 2007; 83:
Science with Treatment Recommendations. Circulation 2010; 122: 344e7.
S250e75. 15 Peberdy MA, Ornato JP, Larkin GL, et al. Survival from in-hospital
3 Resuscitation Council UK. Resuscitation guidelines 2010. London: cardiac arrest during nights and weekends. J Am Med Assoc
Resuscitation Council UK, 2010. Bo € ttiger BW, Koster RW, Bossaert L.
2008; 299: 785e92.
Chest-compression-only versus standard CPR. Lancet 2011; 377: 716.
16 Chan PS, Krumholz HM, Nichol G, et al. Delayed time to defi-
4 Hallstrom A, Cobb L, Johnson E, Copass M. Cardiopulmonary resus- brillation after in-hospital cardiac arrest. N Engl J Med 2008; 358:
citation by chest compression alone or with mouth-to-mouth venti- 9e17.
lation. N Engl J Med 2000; 342: 1546e53. 17 Cooper S, Duncan F. Reliability testing and update of the Resus-
5 Hagihara A, Hasegawa M, Abe T, et al. Prehospital epinephrine use citation Predictor Scoring (RPS) Scale. Resuscitation 2007; 74:
and survival among patients with out-of-hospital cardiac arrest. J Am 253e8.
Med Assoc 2012; 307: 1161e8.
6 Kilgannon JH, Jones AE, Shapiro NI, et al. Association between FURTHER READING
arterial hyperoxia following resuscitation from cardiac arrest and in- 2010 International consensus on cardiopulmonary resuscitation and
hospital mortality. J Am Med Assoc 2010; 303: 2165e71. emergency cardiovascular care science with treatment recommenda-
7 Nolan JP, Lyon RM, Sasson C, et al. Advances in the hospital tions. Circulation 2010; 122(suppl 2).
management of patients following an out of hospital cardiac arrest. Resuscitation Council UK guidelines 2010. Available at: http://www.resus.
Heart 2012; 98: 1201e6. org.uk/pages/guide.htm (accessed August 2012).
8 Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survi- For information regarding the Resuscitation Council (UK) iPhone appli-
vors of out-of hospital cardiac arrest with induced hypothermia. cation (including customer reviews and free download) see: http://
N Engl J Med 2002; 346: 557e63. itunes.apple.com/gb/app/iresus/id335355440?mt¼8.

MEDICINE 41:2 63 Ó 2013 Elsevier Ltd. All rights reserved.