Ionized hypocalcemia during prolonged cardiac arrest and closed-chest CPR in a canine model

Cairns, Charles B.; Niemann, James T.; Pelikán, P.; Sharma, Jay

doi:10.1016/s0196-0644(05)81466-0

Cited by 41 publications

(16 citation statements)

References 28 publications

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“…Ionized calcium also decreased significantly during the early postresuscitation period. Ionized hypocalcemia following cardiac arrest and prolonged resuscitation has previously been reported (23)(24)(25). In the present study, the observed decrease in ionized calcium, although statistically significant, did not appear to independently affect cardiac contractility.…”

Section: Discussionsupporting

confidence: 62%

Tumor necrosis factor-α is associated with early postresuscitation myocardial dysfunction

Niemann

Garner

Lewis

2004

Critical Care Medicine

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Section: Discussionsupporting

confidence: 62%

Tumor necrosis factor-α is associated with early postresuscitation myocardial dysfunction

Niemann

Garner

Lewis

2004

Critical Care Medicine

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“…The loss of blood flow caused by CA is widely acknowledged to cause a metabolic pathology, but we struggle to measure the effect of this pathology at the bedside. The cessation of blood flow during CA stops delivery of metabolic substrates and removal of metabolic waste products, rapidly causing a variety of metabolic disorders including loss of ATP, acidemia, hypercarbia, hyperlactemia, loss of the adenosine pool, loss of ion gradients, and loss of water control 5, 6, 7, 8, 9…”

Section: Introductionmentioning

confidence: 99%

Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post–Cardiac Arrest Rat: A Novel Metabolic Phenotype

Shinozaki

Becker

Saeki³

et al. 2018

JAHA

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BackgroundThe concept that resuscitation from cardiac arrest (CA) results in a metabolic injury is broadly accepted, yet patients never receive this diagnosis. We sought to find evidence of metabolic injuries after CA by measuring O2 consumption and CO2 production (VCO 2) in a rodent model. In addition, we tested the effect of inspired 100% O2 on the metabolism.Methods and ResultsRats were anesthetized and randomized into 3 groups: resuscitation from 10‐minute asphyxia with inhaled 100% O2 (CA–fraction of inspired O2 [FIO2] 1.0), with 30% O2 (CA‐FIO 2 0.3), and sham with 30% O2 (sham‐FIO 2 0.3). Animals were resuscitated with manual cardiopulmonary resuscitation. The volume of extracted O2 (VO 2) and VCO 2 were measured for a 2‐hour period after resuscitation. The respiratory quotient (RQ) was RQ=VCO 2/VO 2. VCO 2 was elevated in CA‐FIO 2 1.0 and CA‐FIO 2 0.3 when compared with sham‐FIO 2 0.3 in minutes 5 to 40 after resuscitation (CA‐FIO 2 1.0: 16.7±2.2, P<0.01; CA‐FIO 2 0.3: 17.4±1.4, P<0.01; versus sham‐FIO 2 0.3: 13.6±1.1 mL/kg per minute), and then returned to normal. VO 2 in CA‐FIO 2 1.0 and CA‐FIO 2 0.3 increased gradually and was significantly higher than sham‐FIO 2 0.3 2 hours after resuscitation (CA‐FIO 2 1.0: 28.7±6.7, P<0.01; CA‐FIO 2 0.3: 24.4±2.3, P<0.01; versus sham‐FIO 2 0.3: 15.8±2.4 mL/kg per minute). The RQ of CA animals persistently decreased (CA‐FIO 2 1.0: 0.54±0.12 versus CA‐FIO 2 0.3: 0.68±0.05 versus sham‐FIO 2 0.3: 0.93±0.11, P<0.01 overall).Conclusions CA altered cellular metabolism resulting in increased VO 2 with normal VCO 2. Normal VCO 2 suggests that the postresuscitation Krebs cycle is operating at a presumably healthy rate. Increased VO 2 in the face of normal VCO 2 suggests a significant alteration in O2 utilization in postresuscitation. Several RQ values fell well outside the normally cited range of 0.7 to 1.0. Higher FIO 2 may increase VO 2, leading to even lower RQ values.

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“…Rescue ventilation is not necessary during primary cardiac arrest and this can be argued based on two observations. First, victims of a cardiac arrest are not oxygen-depleted in contrast to patients with respiratory arrest 27 28 29 30. Second, the incidence of drowning is far less than the incidence of cardiac arrest as a cause of out-of-hospital death.…”

Section: Early Mouth-to-mouth Ventilation Is Not Necessary As the Artmentioning

confidence: 99%

“…The underlying problem during cardiac arrest is the lack of blood flow to the vital organs rather than low oxygen content in the blood. Blood that is not circulated owing to cardiac arrest will maintain adequate oxygenation 27 28 29 30. We are not saying that oxygen delivery is not important during cardiac arrest.…”

Section: Early Mouth-to-mouth Ventilation Is Not Necessary As the Artmentioning

confidence: 99%

Rationale for continuous chest compression cardiopulmonary resuscitation

Ramaraj

Ewy

2009

Heart

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Every year more than a million cardiac arrests are documented in the industrialised nations of the world, with the majority occurring in settings outside hospital. A major factor in survival after out-of-hospital cardiac arrest (OHCA) is early institution of bystander resuscitation efforts. Sadly, the majority of OHCAs do not receive bystander resuscitation for a variety of reasons. One of them is the requirement for mouth-to-mouth (MTM) ventilation. The 2008 American Heart Association recommendation for "hands only" or continuous chest compression cardiopulmonary resuscitation (CPR) for untrained lay people was a welcome change. However, evidence indicates that MTM and other forms of positive pressure ventilation should be eliminated for all bystanders responding to primary cardiac arrest (unexpected witnessed collapse in an unresponsive person). The requirement for MTM ventilation may well be indicated for patients with respiratory arrest but is detrimental during early resuscitation efforts by anyone providing CPR to patients with primary cardiac arrest. This article provides rationale for continuous chest compression CPR by all bystanders.

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Ionized hypocalcemia during prolonged cardiac arrest and closed-chest CPR in a canine model

Cited by 41 publications

References 28 publications

Tumor necrosis factor-α is associated with early postresuscitation myocardial dysfunction

Tumor necrosis factor-α is associated with early postresuscitation myocardial dysfunction

Dissociated Oxygen Consumption and Carbon Dioxide Production in the Post–Cardiac Arrest Rat: A Novel Metabolic Phenotype

Rationale for continuous chest compression cardiopulmonary resuscitation

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