Pressurizing the lungs during cardiopulmonaryresuscitation: a matter of life and breath
Every medical student learns during a first lumbar puncture that cerebrospinal fluid pressure falls with inspiration and rises with expiration.Fewer learn that these same respiratory oscillations in intrathoracicpressure also influence intracranial pressure (ICP), cerebral venousdrainage, and cerebral perfusion. More than a century ago, observations by Valsalva (1704),1 Quincke (1891),2 and Leonard Hill (1896)3established a physiological principle that remains highly relevanttoday: when intrathoracic pressure rises, venous return from thebrain may be impeded, ICP may increase, and cerebral perfusionpressure may fall.This principle has immediate implications during cardiopulmonaryresuscitation (CPR), when blood flow to the heart and brain isalready critically compromised. In this issue of Resuscitation,Segond et al. report that during conventional CPR continuous insufflation of oxygen (CIO) was associated with worse outcomes compared 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 inresuscitation science: how does each breath delivered during CPRaffect circulation?During cardiac arrest, even small pressure changes within thelungs can have large physiological consequences. Continuous positive intrathoracic pressure, whether generated by CIO or otherdevices, such as those producing positive end-expiratory pressure(PEEP), may impede systemic venous return, reduce cardiac fillingduring chest recoil, increase right-sided venous pressures, and promote cerebral venous congestion.4,5 The consequence may be a risein ICP and a reduction in coronary and cerebral perfusion at the verymoment these organs are most vulnerable to ischemia.The anatomical foundation for these interactio ns is well established.6 An extensive valveless paravertebral venous plexus formsa conduit betwee n the abdomen, thorax, spinal canal, and cranialvault.6 Pressure changes within the chest or abdomen can thereforebe transmitted rapidly to the intracranial compartment. During CPR,chest compressions, incomplete recoil, excessive positive-pressureventilation, abdominal pressure, or head-down positioning may allcontribute to elevated cerebral venous pressure and higherICP.4,6,7 Since cerebral perfusion pressure equals arterial pressureminus ICP, even modest increases in ICP may meaningfully reducebrain blood flow during low-flow states.Animal studies anticipated the clinical findings reported by Segondet al. Moore and colleagues, evaluating the Boussignac Cardiac ArrestDevice (B-card), demonstrated that CIO during CPR generated sustained positive intrathoracic pressure th roughout both compressionand decompression phases.8 This blunted the negative intrathoracicpressure normally created during recoil, impaired venous return,reduced cardiac refilling, and worsened cerebral hemodynamics. Thus,from a physiological perspective, worse clinical outcomes with CIOdescribed by Segond et al would not be unexpected.In many respects, continuous positive intrathoracic pressure generated by CIO is the physiological opposite of agonal respiration.Spontaneous gasping during cardiac arrest generates negativeintrathoracic pressure, enhancing venous return, lowering ICP,improving right-heart filling, and augmenting systemic and cerebralperfusion.4,9 Clinical and experimental observations have repeatedlyassociated gasping during cardiac arrest with improved survival andmarkedly better neurological outcomes.9 The inspiratory vacuumcreated by a gasp can be lifesaving. Continuou s positive pressurein the lungs may produce the reverse.The brain is especially susceptible to these effects. Enclosedwithin the rigid cranial vault, it tolerates ischemia poorly and has limited reserve for increases in pressure. Though not always appreciated, during CPR ICP rises sharply with each chest compressionand falls with each decompression.4,10 These pressure surges maybe exacerbated by excessive ventilation, incomplete chest recoil,or sustained positive intrathoracic pressure.4,10 In this setting eventransient high ICP levels may have dangerous physiological and clinical consequences.7Fortunately, the same physiology that explains harm also identifies opportunities for benefit. Several resuscitation strategies mayreduce ICP and improve cardio-cerebral perfusion: allowing full chestrecoil after each compression; avoiding excessive compression ratesand force; preventing hyperventilation and excessive tidal volumes;using active compression–decompression CPR; adding an impedance threshold device when appropriate; and, in selected settings,gradually elevating the head and thorax while maintaining forwardblood flow.4,10–15 Each strategy seeks to optimize pressure gradientsthat drive venous return and organ perfusion. When combined, theywork synergistically to reduce ICP, augment cerebral perfusion, andpreserve the brain.
More than 25 years after early reports documented frequent andharmful hyperventilation during CPR, ventilation remains one of theleast optimized components of resuscitation.10 We still lack practicalmechanical ventilatory systems specifically engineered for CPR thatsupports ventilation and circulation, by providing controlled positivepressure ventilation and generation of negative intrathoracic pressure during the chest recoil phase. That is one of several reasonsthat automated mechanical ventilation devices are not recommendedin ILCOR and aligned American Heart Association guidelines.16 Thestudy by Segond et al. is therefore more than an observationalreport. It is a reminder that during CPR, every breath changesintrathoracic pressur e, every pressure change alters perfusion, andthose effects may influence whether a patient lives, dies, or surviveswith an intact brain.Declaration of competing interestKeith Lurie MD is the co-inventor of multiple CPR devices includingdevices for active compression decompression, inspiratory impedance during CPR, and patient positioning systems for head upCPR. He is a founder and Chief Medical Officer of AdvancedCPRSolutions, a company that makes resuscitation devices.R E F ERENCES
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Quincke H. Die Lumbalpunktion des hydrocephalus. Berl KlinWochenschr 1891;28:929–33.
Hill LE. Physiology and pathol ogy of the cerebralcirculation. London: Churchill; 1896.
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Guerci AD, Shi AY, Levin H, Tsitlik J, Weisfeldt ML, Chandra N.Transmission of intrathoracic pressure to the intracranial spaceduring cardiopulmonary resuscitation in dogs. Circ Res 1985;56(1):20–30.
Mokri B. The Monro–Kellie hypothesis: appli cations in CSF volumedepletion. Neurology 2001;56(12):1746–8.
Moore JC, Lamhaut L, Hutin A, et al. Evaluation of the Boussignaccardiac arrest device (B-card) during cardiopulmonary resuscitationin an animal model. Resuscitation 2017;119:81–8. https://doi.org/10.1016/j.resuscitation.2017.08.004. Epub 2017 Aug 9. PMID:28800887.
Debaty G, Labarere J, Frascone RJ, et al. Long-term prognosticvalue of gasping during out-of-hospital cardiac arrest. J Am CollCardiol 2017;70(12):1467–76. https://doi.org/10.1016/j.jacc.2017.07.782. PMID: 28911510.
Aufderheide TP, Lurie KG. Death by hyperventilation: a common andlife-threatening problem during cardiopulmonary resuscitation. CritCare Med 2004;32(9 Suppl):S345–51. https://doi.org/10.1097/01.ccm.0000134335.46859.09. PMID: 15508657.
Pirrallo RG, Aufderheide TP, Provo TA, Lurie KG. Effect of aninspiratory impedance threshold device on hemodynamics duringstandard cardiopulmonary resuscitation. Resuscitation 2005;66(1):13–20.
Aufderheide TP, Frascone RJ, Wayne MA, et al. Standardcardiopulmonary resuscitation versus active compressiondecompression cardiopulmonary resuscitation with augmentation ofnegative intrathoracic pressure for out-of-hospital cardiac arrest: arandomised trial. Lancet 2011;377(9762):301–11. https://doi.org/10.1016/S0140-6736(10)62103-4. PMID: 21251705; PMCID:PMC3057398.
Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects ofincomplete chest wall decompression during cardiopulmonaryresuscitation on coronary and cerebral perfusion pressures in aporcine model of cardiac arrest. Resuscitation 2005;64(3):363–72.https://doi.org/10.1016/j.resuscitation.2004.10.009. PMID:15733767.
Moore JC, Segal N, Lick MC, et al. Head and thorax elevation duringactive compression decompression cardio pulmonary resuscitationwith an impedance threshold device improves cerebral perfusion in aswine model of prolonged cardiac arrest. Resuscitation2017;121:195–200.
Moore JC, Pepe PE, Scheppke KA, et al. Head and thorax elevationduring cardiopulmonary resuscitation using circulatory adjuncts isassociated with improved survival. Resuscitation 2022;179:9–17.
Greif R, Bray JE, Dja¨rv, et al. 2024 international consensus oncardiopulmonary resuscitation and emergency cardiovascular carescience with treatment recommendations: summary from the BasicLife Support ; Advanced Life Support; Pediatric Life Support;Neonatal Life Support; Education, Implementation, and Teams; andFirst Aid Task Forces. Circulation 2024;150(24). https://doi.org/10.1161/cir.0000000000001288.Keith G. Lurie*Department of Emergency Medicine, University of Minnesota Schoolof Medicine, Minneapolis, MN, United StatesHennepin Healthcare Research Institute, Hennepin County MedicalCenter, Minneapolis, MN, United StatesAdvancedCPR 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 2026Accepted 11 May 2026https://doi.org/10.1016/j.resuscitation.2026.111134© 2026 Elsevier B.V. All rights are reserved, including those for textand data mining, AI training, and similar technologies
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