e200 - Correspondence
Declarations of interest
The authors declare that they have no conflicts of interest.
References
1. Harper NJN, Nolan JP, Soar J, Cook TM. Why chest com-
pressions should start when systolic arterial blood pres-
sure is below 50 mm Hg in the anaesthetised patient. Br J
Anaesth 2020; 124: 234e8
2. Garvey LH, Dewachter P, Hepner DL, et al. Management of
suspected immediate perioperative allergic reactions: an
international overview and consensus recommendations.
Br J Anaesth 2019; 123: e50e64
3. Harper NJN, Cook TM, Garcez T, et al. Anaesthesia, sur-
gery, and life-threatening allergic reactions: management
and outcomes in the 6th National Audit Project (NAP6). Br J
Anaesth 2018; 121: 172e88
4. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-
chest cardiac massage. JAMA 1960; 173: 1064e7
5. Lurie KG, Nemergut EC, Yannopoulos D, Sweeney M. The
physiology of cardiopulmonary resuscitation. Anesth
Analg 2016; 122: 767e83
6. Aagaard R, Granfeldt A, Botker MT, Mygind-Klausen T,
Kirkegaard H, Lofgren B. The right ventricle is dilated
during resuscitation from cardiac arrest caused by hypo-
volaemia: a porcine ultrasound study. Crit Care Med 2017;
45: e963e70
7. Jeffcoach DR, Gallegos JJ, Jesty SA, et al. Use of CPR in
hemorrhagic shock, a dog model. J Trauma Acute Care Surg
2016; 81: 27e33
© 2020 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
Why chest compressions should start when systolic blood pressure
is below 50 mmHg in the anaesthetised patient. Reply to Br J
Anaesth 2020; 124: e199e200
Jerry P. Nolan1, Jasmeet Soar2, Nigel J. N. Harper3 and Tim M. Cook1,*
1
Bath, UK, 2Bristol, UK and 3Manchester, UK
*Corresponding author. E-mail: timcook007@gmail.com
Keywords: anaesthesia; cardiopulmonary resuscitation; chest compressions; hypotension; pulseless electrical activity
EditordWe thank Granfeldt and Andersen1 for their interest in
our editorial. We agree that it is important to clarify that our
comments were specific to patients with cardiac electrical
activity compatible with perfusion. We implied this in our
DOI of original article: 10.1016/j.bja.2020.01.006.
8. Watts S, Smith JE, Gwyther R, Kirkman E. Closed chest
compressions reduce survival in an animal model of
haemorrhage-induced traumatic cardiac arrest. Resusci-
tation 2019; 140: 37e42
9. Paradis NA, Halperin HR, Zviman M, Barash D, Quan W,
Freeman G. Coronary perfusion pressure during external
chest compression in pseudo-EMD, comparison of systolic
versus diastolic synchronization. Resuscitation 2012; 83:
1287e91
10. Marill KA, Menegazzi JJ, Koller AC, Sundermann ML,
Salcido DD. Synchronized chest compressions for pseudo-
PEA: proof of concept and a synching algorithm. Prehosp
Emerg Care 2019: 1e9. https://doi.org/10.1080/
10903127.2019.1690605
11. White L, Rogers J, Bloomingdale M, et al. Dispatcher-
assisted cardiopulmonary resuscitation: risks for patients
not in cardiac arrest. Circulation 2010; 121: 91e7
12. Koster RW, Beenen LF, van der Boom EB, et al. Safety of
mechanical chest compression devices AutoPulse and
LUCAS in cardiac arrest: a randomized clinical trial for
non-inferiority. Eur Heart J 2017; 38: 3006e13
13. Beom JH, You JS, Kim MJ, et al. Investigation of compli-
cations secondary to chest compressions before and
after the 2010 cardiopulmonary resuscitation guideline
changes by using multi-detector computed tomography: a
retrospective study. Scand J Trauma Resusc Emerg Med 2017;
25: 8
14. Seung MK, You JS, Lee HS, Park YS, Chung SP, Park I.
Comparison of complications secondary to cardiopulmo-
nary resuscitation between out-of-hospital cardiac arrest
and in-hospital cardiac arrest. Resuscitation 2016; 98: 64e72
doi: 10.1016/j.bja.2020.01.008
Advance Access Publication Date: 1 February 2020
statement: ‘In ventricular fibrillation there is a clear need for
immediate defibrillation and chest compressions and during
asystole there is a clear need for chest compressions. What is less
clear is the clinical criteria, particularly during isolated severe
hypotension, which should prompt chest compressions in other
situations?’ However, we agree that this could have been
made clearer.

In the presence of hypovolaemia, it remains unclear
whether, in the beating heart, chest compressions will
improve cardiac output. We stated that in uncontrolled hae-
morrhage chest compressions could accelerate bleeding,
resulting in worse outcomes.2 Although chest compressions
are undoubtedly less effective in the presence of hypo-
volaemia, in the absence of uncontrolled bleeding they may
still increase perfusion in the presence of a beating heart and
very low BP. Granfeldt and Andersen1 cite a pig study in which
systolic synchronisation of chest compressions during
pseudo-pulseless electrical activity improved coronary perfu-
sion pressure.3 This was achieved in the controlled conditions
of an animal study and is unlikely to be achievable in clinical
practice. Whilst unsynchronised chest compressions may be
less effective, they may still improve coronary and cerebral
perfusion more than no chest compressions. Of interest, the
discussion of this paper includes the following statement,
which is supportive of the concepts we set out in our editorial:
‘When the P-EMD [pseudo-electromechanical dissociation]
pressures are very low, below 30 mmHg for instance, most forward
flow may be from CPR [cardiopulmonary resuscitation]. When the
intrinsic blood pressure is relatively higher, say above 50 mm Hg,
then the contribution from external chest compression might be
relatively small and the equation for perfusion similar to normal
hemodynamics.’ Whether, in the presence of hypovolaemia,
chest compressions are more effective after the onset of car-
diac standstill (which is associated with right ventricular
dilatation),4 as suggested by Granfeldt and Andersen,1 is un-
known to the best our knowledge.
We agree that it is important to consider carefully the po-
tential for harm caused by chest compressions. Granfeldt and
Andersen1 cite a study by Koster and colleagues5 as providing
more reliable evidence of the rate of injuries associated with
in-hospital cardiac arrest than the bystander study that we
cited.6 Serious or life-threatening damage was documented in
six (7.7%) of the 78 patients with in-hospital cardiac arrest in
the manual cardiopulmonary resuscitation (CPR) arm of that
study. Although serious resuscitation-related rib and sternum
damage was reported in 41% of patients in the manual CPR
arm of the study, it included both in- and out-of-hospital
cardiac arrests; the proportion of the injuries that occurred
after in-hospital cardiac arrest is not clear. We accept that this
study provides a more reliable indication of the injury rates
associated with in-hospital CPR; however, we doubt that it is
possible to extrapolate reliably from the relatively prolonged
episodes of in-hospital CPR to the relatively brief periods of
chest compressions that we would anticipate occurring in the
scenario we describe in our editorial.
© 2020 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
Correspondence - e201
We agree that the decision to start compressions is com-
plex. We highlighted in our editorial the primacy of other in-
terventions such as control of bleeding, infusion of intravenous
fluids, and administration of vasoactive drugs. When these
interventions are effective, there is no need for chest com-
pressions. While there is an argument for ‘individualised care’,
that does rather go against the whole approach to resuscitation
based on standardised practices and algorithms. However, it is
our view that a systolic BP of 50 mm Hg is a reasonable
threshold below which chest compressions should be
routinely started. Individualised care might involve the clini-
cian deciding to withhold chest compressions in exceptional
circumstances.
Declaration of interest
TC is a member of the associate editorial board of the British
Journal of Anaesthesia. The other authors have no conflicts to
declare.
References
1. Granfeldt A, Andersen LW. Starting chest compressions:
one pressure does not fit all. Br J Anaesth 2020; 124:
e199e200
2. Watts S, Smith JE, Gwyther R, Kirkman E. Closed chest
compressions reduce survival in an animal model of
haemorrhage-induced traumatic cardiac arrest. Resuscita-
tion 2019; 140: 37e42
3. Paradis NA, Halperin HR, Zviman M, Barash D, Quan W,
Freeman G. Coronary perfusion pressure during external
chest compression in pseudo-EMD, comparison of systolic
versus diastolic synchronization. Resuscitation 2012; 83:
1287e91
4. Aagaard R, Granfeldt A, Botker MT, Mygind-Klausen T,
Kirkegaard H, Lofgren B. The right ventricle is dilated dur-
ing resuscitation from cardiac arrest caused by hypo-
volemia: a porcine ultrasound study. Crit Care Med 2017; 45:
e963e70
5. Koster RW, Beenen LF, van der Boom EB, et al. Safety of
mechanical chest compression devices AutoPulse and
LUCAS in cardiac arrest: a randomized clinical trial for non-
inferiority. Eur Heart J 2017; 38: 3006e13
6. White L, Rogers J, Bloomingdale M, et al. Dispatcher-
assisted cardiopulmonary resuscitation: risks for patients
not in cardiac arrest. Circulation 2010; 121: 91e7
doi: 10.1016/j.bja.2020.01.008
Advance Access Publication Date: 18 February 2020