Hyperventilation-Induced Hypotension During Cardiopulmonary Resuscitation

Aufderheide, Tom P.; Sigurðsson, Garðar; Pirrallo, Ronald G.; Yannopoulos, Demetris; McKnite, Scott; Briesen, Chris von; Sparks, Christopher W.; Conrad, Craig J.; Provo, Terry A.; Lurie, Keith G.

doi:10.1161/01.cir.0000126594.79136.61

Cited by 725 publications

(448 citation statements)

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“…Estudos recentes demonstram que mesmo profissionais especializados falham na aplicação da técnica ideal 10 . Comumente observa-se ventilação excessiva, interrupção freqüente ou baixa freqüência das compressões torácicas, resultando em diminuição do débito cardíaco e da pressão de perfusão coronária 11,12 . Além disso, sua difusão em escala cada vez maior trás como conseqüência o aumento na prevalência de complicações relacionadas à manobra, com nítida predominância de traumas toráci-cos, dentre os quais destacam-se fraturas de costelas e esterno, pneumomediastino e pneumotórax 3,4,6,7 .…”

Section: Discussionunclassified

“…Essa alteração visa dar maior ênfase à manutenção da circulação, ao mesmo tempo em que poderá proporcionar menor risco de complicações relacionadas à ventilação artificial, seja devido à má técnica ou pelo potencial efeito maléfico de ventilação excessiva freqüentemente oferecida nesses casos ocasionando aumento da pressão intratorácica e intra-abdominal 6, 14,15,19 . No primeiro caso a conseqüência é a diminuição do retorno venoso às câmaras cardíacas reduzindo assim perfusão encefá-lica e coronariana 11,12,19 . No segundo a ventilação mecâ-nica é dificultada, podendo levar a hipoxemia, também contribuindo para uma diminuição do retorno venoso e do débito cardíaco, aumentando a lesão neurológica já existente e possibilitando a ocorrência de isquemia de ór-gãos intra-abdominais com risco de acidose metabólica e translocação bacteriana 19 .…”

Section: Discussionunclassified

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Ruptura gástrica por reanimação cardiopulmonar: relato de caso

Dias¹,

Mendes²,

Mello³

et al. 2006

Rev. bras. ter. intensiva

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Section: Discussionunclassified

Ruptura gástrica por reanimação cardiopulmonar: relato de caso

Dias¹,

Mendes²,

Mello³

et al. 2006

Rev. bras. ter. intensiva

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“…Ewy et al [162] demonstrated 50% ROSC and survival with CPR during a duration of VF up to 12 min before defibrillation using epinephrine. Aufderheide et al [163] demonstrated 86% survival in a porcine model after 6 min of VF and follow-up CPR. Hayes et al [164] evaluated ventilation scenarios in a swine model and reported 25-41% ROSC and survival after 8 min of uninterrupted VF followed by 3 cycles of 2 min of continuous chest compressions prior to defibrillation.…”

Section: The Experimental Model Of Cprmentioning

confidence: 98%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

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“…Dr. Thomas Aufderheide and associates made major contributions to CPR research, including their finding that hyperventilation during resuscitation efforts by EMS were common. They reported that the excessive frequency of positive pressure ventilations were harmful during resuscitation efforts, as they caused excessive increases in intrathoracic pressures, thereby decreasing venous return to the thorax and thus subsequent cardiac output 45, 46, 47…”

Section: Positive Pressure Ventilation Can Be Harmful During Resuscitmentioning

confidence: 99%

Cardiocerebral and cardiopulmonary resuscitation – 2017 update

Ewy

2017

Acute Medicine & Surgery

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Sudden cardiac arrest is a major public health problem in the industrialized nations of the world. Yet, in spite of recurrent updates of the guidelines for cardiopulmonary resuscitation and emergency cardiac care, many areas have suboptimal survival rates. Cardiocerebral resuscitation, a non‐guidelines approach to therapy of primary cardiac arrest based on our animal research, was instituted in Tucson (AZ, USA) in 2002 and subsequently adopted in other areas of the USA. Survival rates of patients with primary cardiac arrest and a shockable rhythm significantly improved wherever it was adopted. Cardiocerebral resuscitation has three components: the community, the pre‐hospital, and the hospital. The community component emphasizes bystander recognition and chest compression only resuscitation. Its pre‐hospital or emergency medical services component emphasizes: (i) urgent initiation of 200 uninterrupted chest compressions before and after each indicated single defibrillation shock, (ii) delayed endotracheal intubation in favor of passive delivery of oxygen by a non‐rebreather mask, (iii) early adrenaline administration. The hospital component was added later. The national and international guidelines for cardiopulmonary resuscitation and emergency medical services are still not optimal, for several reasons, including the fact that they continue to recommend the same approach for two entirely different etiologies of cardiac arrest: primary cardiac arrest, often caused by ventricular fibrillation, where the arterial blood oxygenation is little changed at the time of the arrest, and secondary cardiac arrest from severe respiratory insufficiency, where the arterial blood is severely desaturated at the time of cardiac arrest. These different etiologies need different approaches to therapy.

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Hyperventilation-Induced Hypotension During Cardiopulmonary Resuscitation

Abstract: Background-A clinical observational study revealed that rescuers consistently hyperventilated patients during out-ofhospital cardiopulmonary resuscitation (CPR).

Cited by 725 publications

References 14 publications

Ruptura gástrica por reanimação cardiopulmonar: relato de caso

Ruptura gástrica por reanimação cardiopulmonar: relato de caso

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Cardiocerebral and cardiopulmonary resuscitation – 2017 update

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