June 26, 2026
Pressurizing the lungs during cardiopulmonary
resuscitation: a matter of life and breath
Every medical student learns during a first lumbar puncture that cere
brospinal fluid pressure falls with inspiration and rises with expiration.
Fewer learn that these same respiratory oscillations in intrathoracic
pressure also influence intracranial pressure (ICP), cerebral venous
drainage, and cerebral perfusion. More than a century ago, observa
tions by Valsalva (1704),1 Quincke (1891),2 and Leonard Hill (1896)3
established a physiological principle that remains highly relevant
today: when intrathoracic pressure rises, venous return from the
brain may be impeded, ICP may increase, and cerebral perfusion
pressure may fall.
This principle has immediate implications during cardiopulmonary
resuscitation (CPR), when blood flow to the heart and brain is
already critically compromised. In this issue of Resuscitation,
Segond et al. report that during conventional CPR continuous insuf
flation of oxygen (CIO) was associated with worse outcomes com
pared with intermittent positive-pressure ventilation. Their findings,
that constant and continuous low-flow oxygen delivery is harmful,
renew attention to a central but often underappreciated question in
resuscitation science: how does each breath delivered during CPR
affect circulation?
During cardiac arrest, even small pressure changes within the
lungs can have large physiological consequences. Continuous posi
tive intrathoracic pressure, whether generated by CIO or other
devices, such as those producing positive end-expiratory pressure
(PEEP), may impede systemic venous return, reduce cardiac filling
during chest recoil, increase right-sided venous pressures, and pro
mote cerebral venous congestion.4,5 The consequence may be a rise
in ICP and a reduction in coronary and cerebral perfusion at the very
moment these organs are most vulnerable to ischemia.
The anatomical foundation for these interactio ns is well estab
lished.6 An extensive valveless paravertebral venous plexus forms
a conduit betwee n the abdomen, thorax, spinal canal, and cranial
vault.6 Pressure changes within the chest or abdomen can therefore
be transmitted rapidly to the intracranial compartment. During CPR,
chest compressions, incomplete recoil, excessive positive-pressure
ventilation, abdominal pressure, or head-down positioning may all
contribute to elevated cerebral venous pressure and higher
ICP.4,6,7 Since cerebral perfusion pressure equals arterial pressure
minus ICP, even modest increases in ICP may meaningfully reduce
brain blood flow during low-flow states.
Animal studies anticipated the clinical findings reported by Segond
et al. Moore and colleagues, evaluating the Boussignac Cardiac Arrest
Device (B-card), demonstrated that CIO during CPR generated sus
tained positive intrathoracic pressure th roughout both compression
and decompression phases.8 This blunted the negative intrathoracic
pressure normally created during recoil, impaired venous return,
reduced cardiac refilling, and worsened cerebral hemodynamics. Thus,
from a physiological perspective, worse clinical outcomes with CIO
described by Segond et al would not be unexpected.
In many respects, continuous positive intrathoracic pressure gen
erated by CIO is the physiological opposite of agonal respiration.
Spontaneous gasping during cardiac arrest generates negative
intrathoracic pressure, enhancing venous return, lowering ICP,
improving right-heart filling, and augmenting systemic and cerebral
perfusion.4,9 Clinical and experimental observations have repeatedly
associated gasping during cardiac arrest with improved survival and
markedly better neurological outcomes.9 The inspiratory vacuum
created by a gasp can be lifesaving. Continuou s positive pressure
in the lungs may produce the reverse.
The brain is especially susceptible to these effects. Enclosed
within the rigid cranial vault, it tolerates ischemia poorly and has lim
ited reserve for increases in pressure. Though not always appreci
ated, during CPR ICP rises sharply with each chest compression
and falls with each decompression.4,10 These pressure surges may
be exacerbated by excessive ventilation, incomplete chest recoil,
or sustained positive intrathoracic pressure.4,10 In this setting even
transient high ICP levels may have dangerous physiological and clin
ical consequences.7
Fortunately, the same physiology that explains harm also identi
fies opportunities for benefit. Several resuscitation strategies may
reduce ICP and improve cardio-cerebral perfusion: allowing full chest
recoil after each compression; avoiding excessive compression rates
and force; preventing hyperventilation and excessive tidal volumes;
using active compression–decompression CPR; adding an impe
dance threshold device when appropriate; and, in selected settings,
gradually elevating the head and thorax while maintaining forward
blood flow.4,10–15 Each strategy seeks to optimize pressure gradients
that drive venous return and organ perfusion. When combined, they
work synergistically to reduce ICP, augment cerebral perfusion, and
preserve the brain.
More than 25 years after early reports documented frequent and
harmful hyperventilation during CPR, ventilation remains one of the
least optimized components of resuscitation.10 We still lack practical
mechanical ventilatory systems specifically engineered for CPR that
supports ventilation and circulation, by providing controlled positive
pressure ventilation and generation of negative intrathoracic pres
sure during the chest recoil phase. That is one of several reasons
that automated mechanical ventilation devices are not recommended
in ILCOR and aligned American Heart Association guidelines.16 The
study by Segond et al. is therefore more than an observational
report. It is a reminder that during CPR, every breath changes
intrathoracic pressur e, every pressure change alters perfusion, and
those effects may influence whether a patient lives, dies, or survives
with an intact brain.
Declaration of competing interest
Keith Lurie MD is the co-inventor of multiple CPR devices including
devices for active compression decompression, inspiratory impe
dance during CPR, and patient positioning systems for head up
CPR. He is a founder and Chief Medical Officer of AdvancedCPR
Solutions, a company that makes resuscitation devices.
R E F ERENCES
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circulation. London: Churchill; 1896. - Lurie KG, Nemergut EC, Yannopoulos D, Sweeney M. The
physiology of cardiopulmonary resuscitation. Anesth Analg 2016;122
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during cardiopulmonary resuscitation using circulatory adjuncts is
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Keith G. Lurie*
Department of Emergency Medicine, University of Minnesota School
of Medicine, Minneapolis, MN, United States
Hennepin Healthcare Research Institute, Hennepin County Medical
Center, Minneapolis, MN, United States
AdvancedCPR Solutions, Edina, MN, United States
- Address: 701 Park Ave., Suite S3, Minneapolis, MN 55415-1623,
United States.
E-mail address: keithlurie@icloud.com,
Received 6 May 2026
Accepted 11 May 2026
https://doi.org/10.1016/j.resuscitation.2026.111134
© 2026 Elsevier B.V. All rights are reserved, including those for text
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