Review
Cardiopulmonary resuscitation: the science
University of Washington,
Division of Cardiology, Seattle,
Washington, USA
Correspondence to
Dr Peter J Kudenchuk, University
of Washington, Division of
Cardiology, Box 346422, 1959
NE Pacific Street, Seattle, WA
USA; p​ kudenchuk@​cardiology.​
washington.​edu
AWH and PJK contributed
equally.
Received 8 November 2017
Revised 9 December 2017
Accepted 15 December 2017
Published Online First
20 January 2018
To cite: Harris AW,
Kudenchuk PJ. Heart
2018;104:1056–1061.
1056   Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696
behind the hands
Andrew W Harris, Peter J Kudenchuk
ABSTRACT
Sudden cardiac arrest is a leading cause of death
worldwide. Despite significant advances in resuscitation
science since the initial use of external chest
compressions in humans nearly 60 years ago, there
continues to be wide variability in rates of successful
resuscitation across communities. The American Heart
Association (AHA) and European Resuscitation Council
emphasise the importance of high-quality chest
compressions as the foundation of resuscitation care.
We review the physiological basis for the association
between chest compression quality and clinical outcomes
and the scientific basis for the AHA’s key metrics for
high-quality cardiopulmonary resuscitation. Finally, we
highlight that implementation of strategies that promote
effective chest compressions can improve outcomes in all
patients with cardiac arrest.
Introduction
Sudden cardiac arrest is a leading cause of death
worldwide.1 2 Significant scientific advances have
transformed the care of the cardiac arrest victim in
the 57 years since Kouwenhoven and colleagues3
first reported the successful clinical use of closed-
chest compressions. The American Heart Associ-
ation (AHA) and European Resuscitation Council
each published guidelines in 2015 that reflect the
current state of the science of resuscitation. These
guidelines highlight the importance of high-quality
cardiopulmonary resuscitation (CPR) and empha-
sise the importance of effective chest compressions
as the foundation of resuscitation care.1 2 This
article will summarise the evidence supporting these
recommendations and the improved outcomes
achievable with high-quality CPR.
Importance of chest compressions
Defibrillation is regarded as the definitive inter-
vention for cardiac arrest due to ventricular fibril-
lation (VF) or pulseless ventricular tachycardia
(VT). Although success is high during the initial few
minutes after collapse, survival from witnessed VF/
VT cardiac arrest declines by approximately 10%
per minute that defibrillation is delayed. In such
circumstances, chest compressions are essential for
generating blood flow to the myocardium, brain
and other vital organs. Initial canine experiments of
external defibrillation in 1943 showed that applying
an electrical defibrillatory shock within 1–1.5 min
of onset of VF was highly successful in restoring
normal sinus rhythm, but less so after longer dura-
tions of the arrhythmia. Conversely, when cardiac
massage was administered prior to defibrillation,
the duration of VF preceding a successful shock
could be extended.4 There is an apparent synergistic
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
relationship between CPR and defibrillation clini-
cally, in that the rate of decline in survival with each
passing minute from collapse to defibrillation is cut
in half when CPR is performed.
A possible explanation for this phenomenon
arises from experimental animal work that seri-
ally assayed myocardial concentrations of ATP—a
high energy compound that drives cellular metab-
olism—during protracted periods of VF in the
absence of CPR. In this model, ATP concentra-
tions declined significantly over time, reaching
concentrations that were less than half of normal
after only 5 min of unsupported VF (figure 1).5
A corresponding time-dependent diminution in
the amplitude and apparent coarseness of the
VF waveform has also been observed in clinical
VF, such that in its late stages the arrhythmia is
often indistinguishable from asystole (figure 2).
It is likely that the declining vigour of the VF
waveform is a result of consumption of high-en-
ergy phosphate molecules resulting in a progres-
sively energy-depleted myocardium. Another
possible expression of this energy-depleted state
is the heart’s poor contractile function after a
protracted period of VF has been terminated by
shock. This often results in asystole or pulse-
less electrical activity, and in fact serves as the
basis for creating such rhythms in experimental
models.6 7 By providing blood flow to the heart
during cardiac arrest, might CPR mitigate or even
reverse the loss of myocardial energetics associ-
ated with these changes in the VF waveform, poor
contractile function after shock, and ultimately
death? There is evidence to suggest this might be
the case.
In one such study, animals were subjected to
10 min of VF without CPR, then randomised to
either immediate defibrillation or to receive 3 min
of CPR before shock. VF amplitude and frequency
characteristics were sampled in all animals after
1 min of VF (without CPR), at 10 min (without
CPR) and again at 13 min (after a 3 min period of
CPR) in the group of animals that were randomised
to receive preshock CPR. These characteristics of
VF expectedly deteriorated during the untreated
period of VF, with the waveform becoming visu-
ally (and numerically) less coarse at 10 min than
at 1 min into the VF episode. Notably, these char-
acteristics improved significantly following 3 min
of chest compressions, which virtually brought
these parameters and the visual appearance of VF
back to its characteristics measured after 1 min
of VF (figure 2). Furthermore, after up to three
shocks, none of the animals in the group not
receiving CPR were resuscitated, compared with
50% of those receiving chest compressions prior

Figure 1 Bar graphs of myocardial adenine nucleotide concentrations
during normal sinus rhythm (NSR) and at various durations of untreated
ventricular fibrillation (VF). All tissue concentrations expressed in nmol/
mg protein (from Neumar et al5). Reproduced with permission from
Elsevier.
to defibrillation.8 Similar findings have emerged from clinical
studies that showed improved survival to hospital discharge
when CPR was provided for a prescribed time period before
defibrillation rather than an immediate shock approach in
patients with out-of-hospital cardiac arrest (OHCA) due to
VF.9
CPR mechanisms
Conventional CPR occurs in two phases, compression and
decompression (figure 3). External chest compression results
in arterial blood flow due to phasic changes in intrathoracic
pressure produced by the force generated by the hands. Impor-
tantly, in closed-chest CPR, the increased intrathoracic pressure
and reduced thoracic volume created by chest compressions
squeeze the heart itself and all blood-containing structures in
the chest, including the lungs and great vessels. Thus, conven-
tional CPR takes advantage of the entire chest, not just the
heart, as its ‘pump’. Chest compression leads to a relatively
uniform rise in the pressure of all intrathoracic vascular struc-
tures, and it is this pressure that ejects blood from the thorax
during this phase of CPR. Thoracic pressure is transmitted to
the body via the great arteries, but fortunately not via the great
veins where this is prevented by the closure of venous valves at
Figure 2 Typical changes in ventricular fibrillation (VF) waveform in
untreated VF (after 1 and 10 min) and after 3 min of cardiopulmonary
resuscitation-first (13 min) in swine. AMP, amplitude (in mV); MF,
VF median frequency (in Hz) (from Berg et al8). Reproduced with
permission from Elsevier.
Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696
Review
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
Figure 3 Haemodynamic effects of compression and decompression
phases of cardiopulmonary resuscitation. Compression phase creates
organ perfusion pressure (difference between aortic and extrathoracic
vein pressure). Decompression phase creates myocardial perfusion
pressure (difference between aortic and right atrial pressure). Data
adapted from Criley et al. Circulation. 1986; 74 (Suppl IV): 42-50.
the thoracic outlet. Were this not the case, high venous pres-
sures could neutralise the necessary gradient between arterial
and venous beds that is critical to organ perfusion.10 All told,
the greater the vigour of these chest compressions, the greater
the resulting cardiac (actually thoracic) output and magnitude
of cerebral blood flow.11
‘Diastole’ occurs during the decompression phase of the CPR
cycle—when the thorax is permitted to rebound to its normal
fully expanded configuration. While seemingly passive and unim-
portant, CPR decompression may be even more important than
its compression phase. During this phase, closure of the aortic
valve maintains an aortic pressure that is higher than intracar-
diac pressures, which fall precipitously beneath the closed valve,
driven by the ‘vacuum’ effect created by the recoiling thoracic
cage. This intrathoracic vacuum is what draws blood to return
back into the chest from the periphery, filling the heart, lungs
and great vessels in preparation for the next chest compression.
The result is that the better the decompression, the stronger the
vacuum, the better the refilling, and ultimately the more thoracic
blood available for subsequent compression.
CPR diastole serves a second useful purpose that is often
unappreciated. All organs of the body are perfused during the
compression phase of CPR except, ironically, the heart itself,
which is not perfused by blood within its chambers, but rather by
the coronary arteries. Coronary blood flow is estimated by coro-
nary perfusion pressure (CPP), defined as the difference between
pressure in the aorta (where the coronary arteries originate) and
in the right atrium (where coronary venous blood ultimately
returns).12 During the compression phase of CPR, all intratho-
racic pressures including the aorta and all chambers of the heart
equalise with the compressive force of the hands, resulting in
no coronary blood flow between the aorta and right atrium.
Conversely, in CPR diastole, the higher aortic pressure above
its closed valve compared with the falling intrathoracic pressure
results in a positive CPP. It is this combination of compressive
force producing higher aortic pressures both in systole and in
diastole, along with its release causing a fall in intrathoracic
1057
 Review
Figure 4 Adjusted cubic spline of the relationship between chest
compression rates and the probability of survival to hospital discharge.
The adjusted model includes sex, age, bystander witnessed arrest,
Emergency Medical Services (EMS) witnessed arrest, first known
EMS rhythm, attempted bystander cardiopulmonary resuscitation,
public location and site location (y-axis). Probability of survival versus
average chest compression rate when other covariates are equal to the
population average. A histogram of the compression rates and number
of patients is included. Dashed lines show 95% CIs (from Idris et
al16). Reproduced with permission from Wolters Kluwer Health.
pressure, that results in optimal organ perfusion, including the
heart itself.
Saving the heart is an essential first step in resuscitation,
without which there can be no return of spontaneous circula-
tion (ROSC). Animal studies have shown that there is excellent
correlation between CPP and myocardial blood flow during
CPR.13 Furthermore, it has been noted that CPP during CPR
has significant prognostic implications on outcomes after
resuscitation. Among 100 patients in whom invasive aortic and
right atrial pressure measurements were obtained during CPR,
CPP was directly associated with the likelihood of achieving
ROSC. The 24 patients who achieved ROSC had a maximal
CPP of 25.6 mm Hg vs 8.4 mm Hg (P<0.0001); among those
not achieving a CPP of at least 15 mm Hg, none survived.14
These findings provide the physiological rationale for opti-
mising haemodynamics during CPR, in which the goal is to
improve cerebral and myocardial blood flow, achieve ROSC,
and ultimately increase survival with good neurological
outcome.
Acute coronary occlusion and/or severe coronary stenoses
are commonly found in patients with cardiac arrest. These
add to the challenge of achieving adequate coronary perfusion
during CPR and further underscore the importance of efforts
to optimise CPP. In some cases, emergent coronary revascu-
larisation and/or extracorporeal CPR may be required for
successful resuscitation, a discussion of which is beyond the
scope of this article.
Key metrics for quality CPR
The AHA has identified five key metrics for high-quality CPR on
the basis of improved haemodynamics during CPR and improved
clinical outcomes: (1) chest compression rate, (2) chest compres-
sion depth, (3) chest compression fraction and minimising
pauses, (4) allowing full chest recoil, and 5) controlled ventila-
tion with avoidance of hyperventilation.1
1058
Chest compression rate (AHA recommendation: 100–120/min)
Early studies of chest compression rates in dogs showed higher
CPP, mean arterial pressure and improved rates of 24-hour
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
survival when randomised to receive chest compressions at a
rate of 120/min compared with 60/min.15 A recent study from
the Resuscitation Outcomes Consortium (ROC) corroborated
this association between chest compression rates with outcome
in 3098 patients with OHCA, among whom the probability of
survival to hospital discharge was highest at ~110–120 compres-
sions/min, with a notable decline in survival on each side of this
range (figure 4).16 The optimal compression rate represents a
balance that attempts to maximise key physiological parame-
ters during CPR. Because stroke volume is lower during CPR,
a higher compression rate is necessary to achieve a sufficient
cardiac output for organ perfusion. However, excessive chest
compression rates may also lead to reduced cardiac output in
shortening the diastolic time interval (‘CPR diastole’) required
for thoracic refilling and for myocardial perfusion. Furthermore,
an inverse association has been observed between chest compres-
sion rate and depth, especially at higher rates. In one study,
the mean chest compression depth deteriorated (<38 mm) in
more than 80% of patients when compression rates were >140/
min.16 Thus, maintaining rates within the recommended range
helps to optimise key physiological parameters and other
important CPR metrics.
Chest compression depth (AHA recommendation: 5–6 cm)
Like chest compression rate, compression depth is also associated
with clinical outcomes. In a large observational study of 9136
patients with OHCA from ROC, increasing chest compression
depth was associated with improved rates of ROSC and survival
to hospital discharge. The adjusted OR (95% CI) for survival
was 1.04 (1.00 to 1.08) per 5 mm increase in chest compres-
sion depth and 1.45 (1.20 to 1.76) for cases that were >38 mm
more than 60% of time, as compared with those outside this
range. There also appeared to be a plateau association between
compression depth and survival, with best outcomes seen at
depths between 40 and 54 mm (figure 5), and support current
guideline recommendations.17
Chest compression fraction and minimising pauses (AHA
recommendation: chest compression fraction ≥60%, minimise
pauses in chest compressions)
Interruptions in chest compressions have been shown to have
significant adverse effects on haemodynamics during resuscita-
tion. After pausing chest compressions, CPP quickly decreases
to zero and can take upwards of 15 or more compressions
to achieve the same magnitude to that present before the
pause.18 19 The duration of pauses in CPR can also influence
outcome. This was demonstrated in a large observational study
of 2006 patients with OHCA due to a shockable arrhythmia in
whom the adjusted odds of survival were 7% lower for every 5 s
increase in a preshock pause and 6% lower for every 5 s increase
in perishock (preshock and postshock) pause.20 Another study
found the durations of the longest perishock pause, longest
non-shock pause and longest pause for any reason were all asso-
ciated with decreased survival to hospital discharge, therefore
demonstrating that pauses at any point in resuscitation can be
detrimental (figure 6).21 Together, these studies indicate that
decreasing both the frequency and duration of interruptions in
CPR can improve outcomes.
Chest compression fraction represents the percentage of time
that chest compressions are performed in a pulseless patient
Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696

Figure 5 Covariate-adjusted survival to discharge by compression
depth, with 95% CIs. Red vertical dashed line represents highest
survival, and grey vertical dashed lines represent 15 mm interval with
highest survival (from Stiell et al17). Reproduced with permission from
Wolters Kluwer Health.
with cardiac arrest. Either frequent and/or longer pauses in chest
compressions manifest as a lower chest compression fraction. In
a prospective study of 506 patients with OHCA arrest due to a
shockable arrhythmia, a higher chest compression fraction prior
to the first defibrillation attempt was associated with improved
survival to hospital discharge. Patients with a chest compression
fraction of >60% had the highest survival, with an adjusted
OR for survival to hospital discharge of 1.11 (1.01 to 1.21) per
10% increase in chest compression fraction (figure 7).22 Chest
compression fraction is also a complex measure because of its
potential interaction with other CPR metrics such that its inter-
pretation in isolation from these other factors can prove to be
Figure 6 Survival to hospital discharge and duration of longest
overall pause in chest compressions (black), longest perishock pause
(grey) and longest non-shock pause (white). Numbers in bars represent
the number of patients. P<0.01 for each pause category (from Brouwer
et al21). Reproduced with permission from Wolters Kluwer Health.
Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696
Review
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
Figure 7 Smoothing spline representing the incremental probability of
survival corresponding to a linear increase in chest compression fraction
(CCF) (from Christenson et al22). Reproduced with permission from
Wolters Kluwer Health.
misleading. For example, a high or low chest compression frac-
tion does not necessarily trump the other qualities of CPR that
are essential to good outcome.23 This is why the AHA recom-
mends targeting a chest compression fraction of greater than
60% in the context of the totality of CPR metrics.24
Chest recoil (AHA recommendation: allow full chest recoil)
Permitting complete chest recoil during the decompression
phase of CPR is essential for refilling the chest and for adequate
myocardial perfusion. Incomplete chest recoil or leaving a
residual pressure on the chest (‘leaning’) results in an increase
in intrathoracic pressure when it needs to be at its minimum.
Among a group of animals that received standard chest compres-
sions with full chest recoil, followed by chest compressions
permitting only 75% of full chest recoil, CPP decreased by more
than a third during the period of incomplete chest recoil and
cerebral perfusion pressures by more than 50% (both P<0.05).25
Inattention to full recoil is an all too common problem during
resuscitation. The problem often arises as a result of fatigue,
whereby the chest compressor (who is usually leaning over the
patient while performing compressions) unintentionally uses the
patient’s chest as a resting table during the decompression phase
of CPR, rather than permit its full recoil. An observational study
of 108 adults with inhospital cardiac arrest at the University of
Pennsylvania used force-sensing devices during resuscitation to
detect 5 pounds of residual pressure (‘lean’) left on the chest
during the decompression phase of CPR. By this definition,
leaning was observed in 91% of the resuscitations, underscoring
its all-too-common occurrence.26
1059
 Review
Figure 8 Outcomes according to calendar year. Shown are the
frequency of return of spontaneous circulation (ROSC), survival to
hospital discharge and 1-year survival during each year during the
control and intervention periods, with 95% CIs. No temporal trends
were seen within each study period but rather improved outcomes
in the intervention period as compared with the control period (from
Kudenchuk et al28). Reproduced with permission from Wolters Kluwer
Health.
Controlled ventilation, avoiding hyperventilation (30:2 chest
compression:ventilation ratio prior to advanced airway; 10
breaths/min with advanced airway)
Prior to the placement of an advanced airway, the provision of
rescue breaths is associated with a trade-off between cardiac
output and blood oxygenation due to interruptions in chest
compressions.19 This is why interruptions for ventilation during
30:2 (30 chest compressions followed by 2 breaths) CPR need to
be brief—at most 2 s in duration. Care needs to be taken to avoid
hyperventilation particularly after placement of an advanced
airway, when the impression that patients in arrest need more
ventilation frequently results in hyperventilation, a potentially
lethal error.27 Each positive pressure breath, while providing
needed oxygen and clearance of carbon dioxide, also increases
intrathoracic pressure and compromises chest refilling. Excessive
ventilation can also alter pH balance, creating alkalosis and cere-
bral vasoconstriction. The impact these effects might have on
outcome was studied in an experimental model in which a group
of intubated animals undergoing CPR for VF were randomised
to a ventilation rate of 12 vs 30 breaths/min (supplemented with
carbon dioxide in a subgroup to maintain pH balance). Expect-
edly, the mean intrathoracic pressure was significantly lower
among the animals ventilated at a rate of 12 vs 30/min (7.1 vs
17.5 mm Hg, respectively; P<0.001). This higher intrathoracic
pressure resulted in an increase in right atrial diastolic pres-
sure and 28% decrease in CPP in the hyperventilated animals
(P<0.05). Notably, survival was significantly lower in the hyper-
ventilated animals (with or without receipt of supplemental
carbon dioxide).27 The AHA cautions that the lower cardiac
output during CPR requires less ventilation than normal—and
that 10 breaths per minute, each sufficient to make the chest
rise, are adequate. This approach offers the best balance between
meeting the patient’s ventilation needs without compromising
their haemodynamic demands.
Improved CPR quality and outcomes
The AHA’s guidelines for CPR focus on optimising the key
performance metrics discussed above. Large, observational
studies have shown that the incorporation of these recommen-
dations can lead to improved outcomes for patients with cardiac
1060
arrest. In 2005, the AHA recommended several changes to resus-
citation protocols to increase the proportion of time devoted to
chest compressions. In advance of these changes, resuscitation
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
protocols for King County, Washington, were instituted that
closely corresponded with these new AHA guidelines. In two
subsequent observational studies from King County, significant
improvements in survival associated with this change in protocol
were seen among patients with cardiac arrest due to either
shockable or non-shockable rhythms. For example, among 509
patients with OHCA due to bystander-witnessed VF, significant
reductions in postshock pauses in CPR, along with an increase
in chest compression fraction, were observed between the time
periods before and after the change in CPR protocol, resulting
in significantly improved survival (adjusted OR (95% CI) 1.75
(1.14 to 2.69)).24 Similarly, among 3960 patients with OHCA
due to a non-shockable rhythm, survival to hospital discharge
increased from 4.6% to 6.8% (P=0.004) and 1-year survival
from 2.7% to 4.9% (P=0.001) (figure 8), in association with
similar improvements in ‘hands-on’ time during the intervention
period.28 Such findings indicate that ‘CPR works’ but that ‘better
CPR works even better’.
Implications on life-saving
Cardiac arrest remains a significant public health issue.
Multiple clinical trials of advanced interventions for cardiac
arrest have been attempted with variable success. It has become
clear that high-quality CPR with effective chest compressions
is the foundation of all successful resuscitation efforts. While
survival after cardiac arrest in many communities remains
poor, this problem is clearly remediable. Improvements in CPR
practice can lead to substantial improvement in outcome.24 28
By incorporating clinical guidelines into practice, thousands
of lives can be saved each year with little more than correctly
applying human hands.
Contributors The authors contributed equally to the writing of this manuscript.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the
article) 2018. All rights reserved. No commercial use is permitted unless otherwise
expressly granted.
References
1 Kleinman ME, Brennan EE, Goldberger ZD, et al. Part 5: Adult Basic Life Support and
Cardiopulmonary Resuscitation Quality. Circulation 2015;132:S414–35.
2 Perkins GD, Handley AJ, Koster RW, et al. European resuscitation council guidelines
for resuscitation 2015: section 2. Adult basic life support and automated external
defibrillation. Resuscitation 2015;95:81–99.
3 Kouwenhoven WB, Jude JR, Knickerbocker GG, et al. Closed-chest cardiac massage.
JAMA 1960;173:1064–7.
4 Gurvich NL, YUNIEV GS. Restoration of heart rhythm during fibrillation by a condenser
discharge. Am Rev Sov Med 1947;4:252–6.
5 Neumar RW, Brown CG, Van Ligten P, Baker P, et al. Estimation of myocardial ischemic
injury during ventricular fibrillation with total circulatory arrest using high-energy
phosphates and lactate as metabolic markers. Ann Emerg Med
1991;20:222–9.
6 Thijs LG, Vincent JL, Weil MH, et al. A closed-chest model for the study of
electromechanical dissociation of the heart in dogs. Resuscitation
1982;10:25–32.
7 Vincent JL, Thijs L, Weil MH, et al. Clinical and experimental studies on
electromechanical dissociation. Circulation 1981;64:18–27.
8 Berg RA, Hilwig RW, Kern KB, et al. Precountershock cardiopulmonary resuscitation
improves ventricular fibrillation median frequency and myocardial readiness for
successful defibrillation from prolonged ventricular fibrillation: a randomized,
controlled swine study. Ann Emerg Med 2002;40:563–71.
9 Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary resuscitation
prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA
1999;281:1182–8.
Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696

10 Fisher J, Vaghaiwalla F, Tsitlik J, et al. Determinants and clinical significance of jugular
venous valve competence. Circulation 1982;65:188–96.
11 Niemann JT. Differences in cerebral and myocardial perfusion during closed-chest
resuscitation. Ann Emerg Med 1984;13:849–53.
12 Idris AH, Becker LB, Ornato JP, et al. Utstein-style guidelines for uniform reporting of
laboratory cpr research. Circulation 1996;94:2324–36 http://​circ.​ahajournals.o​ rg/​
content/​94/​9/​2324.​abstract.
13 Halperin HR, Tsitlik JE, Guerci AD, et al. Determinants of blood flow to vital organs
during cardiopulmonary resuscitation in dogs. Circulation
1986;73:539–50.
14 Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the
return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA
1990;263:1106–13.
15 Feneley MP, Maier GW, Kern KB, et al. Influence of compression rate on initial success
of resuscitation and 24 hour survival after prolonged manual cardiopulmonary
resuscitation in dogs. Circulation 1988;77:240–50.
16 Idris AH, Guffey D, Aufderheide TP, et al. Relationship between chest compression
rates and outcomes from cardiac arrest. Circulation 2012;125:3004–12.
17 Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth
during out-of-hospital cardiac arrest resuscitation of adult patients? Circulation
2014;130:1962–70.
18 Steen S, Liao Q, Pierre L, et al. The critical importance of minimal delay between
chest compressions and subsequent defibrillation: a haemodynamic explanation.
Resuscitation 2003;58:249–58.
19 Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting
chest compressions for rescue breathing during cardiopulmonary resuscitation for
ventricular fibrillation cardiac arrest. Circulation 2001;104:2465–70.
Harris AW, Kudenchuk PJ. Heart 2018;104:1056–1061. doi:10.1136/heartjnl-2017-312696
Review
20 Cheskes S, Schmicker RH, Verbeek PR, et al. ThE impact of peri-shock pause on
survival from out-of-hospital shockable cardiac arrest during the resuscitation
outcomes consortium PRIMED trial. Resuscitation 2014;85:336–42.
Heart: first published as 10.1136/heartjnl-2017-312696 on 20 January 2018. Downloaded from http://heart.bmj.com/ on 4 July 2018 by guest. Protected by copyright.
21 Brouwer TF, Walker RG, Chapman FW, et al. Association between chest compression
interruptions and clinical outcomes of ventricular fibrillation out-of-hospital cardiac
arrest. Circulation 2015;132:1030–7.
22 Christenson J, Andrusiek D, Everson-Stewart S, et al. Chest compression fraction
determines survival in patients with out-of-hospital ventricular fibrillation. Circulation
2009;120:1241–7.
23 Cheskes S, Schmicker RH, Rea T, et al. Chest compression fraction: a time dependent
variable of survival in shockable out-of-hospital cardiac arrest. Resuscitation
2015;97:129–35.
24 Rea TD, Helbock M, Perry S, et al. Increasing use of cardiopulmonary resuscitation
during out-of-hospital ventricular fibrillation arrest: survival implications of guideline
changes. Circulation 2006;114:2760–5.
25 Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall
decompression during cardiopulmonary resuscitation on coronary and cerebral
perfusion pressures in a porcine model of cardiac arrest. Resuscitation
2005;64:363–72.
26 Fried DA, Leary M, Smith DA, et al. The prevalence of chest compression leaning
during in-hospital cardiopulmonary resuscitation. Resuscitation
2011;82:1019–24.
27 Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension
during cardiopulmonary resuscitation. Circulation 2004;109:1960–5.
28 Kudenchuk PJ, Redshaw JD, Stubbs BA, et al. Impact of changes in resuscitation
practice on survival and neurological outcome after out-of-hospital cardiac arrest
resulting from nonshockable arrhythmias. Circulation 2012;125:1787–94.
1061