Effect of mild hypercapnia on outcome and histological injury in a porcine post cardiac arrest model

Abstract

Aim of the study: To evaluate in an established porcine post cardiac arrest model the effect of a mild hypercapnic ventilatory strategy on outcome. Methods: The left anterior descending coronary artery was occluded in 14 pigs and ventricular fibrillation induced and left untreated for 12 min. Cardiopulmonary resuscitation was performed for 5 min prior to defibrillation. After resuscitation, pigs were assigned to either normocapnic (end-tidal carbon dioxide (EtCO 2) target: 35-40 mmHg) or hypercapnic ventilation (EtCO 2 45-50 mmHg). Hemodynamics was invasively measured and EtCO 2 was monitored with an infrared capnometer. Blood gas analysis, serum neuron-specific enolase (NSE) and high sensitive cardiac troponin T (hs-cTnT) were assessed. Survival and functional recovery were evaluated up to 96 h. Results: Twelve pigs were successfully resuscitated and eight survived up to 96 h, with animals in the hypercapnic group showing trend towards a longer survival. EtCO 2 and arterial partial pressure of CO 2 were higher in the hypercapnic group compared to the normocapnic one (p < 0.01), during the 4-hour intervention. Hypercapnia was associated with higher mean arterial pressure compared to normocapnia (p < 0.05). No significant differences were observed in hs-cTnT and in NSE between groups, although the values tended to be lower in the hypercapnic one. Neuronal degeneration was lesser in the frontal cortex of hypercapnic animals compared to the normocapnic ones (p < 0.05). Neurological recovery was equivalent in the two groups.

Mild hypercapnia improves brain tissue oxygen tension but not diffusion limitation in asphyxial cardiac arrest: an experimental study in pigs

“…In our study, there was a slightly increased MAP and ICP in mild hypercapnia group. The result of a higher MAP in the mild hypercapnic animals was consistent with previous studies [10,33]. However, there were studies suggesting no association between hypercapnia and MAP [13,34].…”

“…Previous studies showed asphyxial CA model causes more severe cerebral metabolism injuries and ischemic brain injury after asphyxial CA appears more severe and more widespread than VF model of the same duration [36,37]. Second, we defined mild hypercapnia as EtCO 2 between 45 and 50 mmHg based on previously published studies [10], which may be arbitrary, since the target EtCO 2 levels associated with potential benefit or harm are unknown. Third, we only assessed two different levels of EtCO 2 for a period of 12 h. Fourth, Pbto 2 is a focal measure, which could not represent the global monitor.…”

“…Recently, several studies have investigated the effect of mild hypercapnia on postcardiac arrest care; however, the results were not completely consistent [ 9 – 11 , 13 , 15 ]. The “Carbon Control after Cardiac Arrest (CCC) trial” found mild hypercapnia attenuated the release of NSE compared with normocapnia [ 11 ], whereas some experimental and randomized pilot trials did not observe the effect of mild hypercapnia on NSE or S100β [ 9 , 10 ]. Meanwhile, there was one consistent finding that mild hypercapnia increased regional cerebral tissue oxygen saturation (Scto 2 ) assessed by near-infrared spectroscopy (NIRS) [ 9 , 13 ].…”

“…A number of specific interventions have been demonstrated to improve outcomes of PCAS, of which the management of the partial pressure of arterial carbon dioxide (Paco 2 ) as a potential therapeutic target receives special attention [9][10][11]. Carbon dioxide is the major physiological regulator of cerebral blood flow (CBF), with higher Paco 2 causing increased brain perfusion [12].…”

“…Previous studies found mild hypercapnia increased cerebral oxygenation assessed by near infrared spectroscopy (NIRS) and attenuated the release of serum neuron specific enolase (NSE) [9,11,13]. However, the results were inconsistent and the potential mechanisms are unclear [10,14,15]. In addition, NIRS may not accurately reflect the cerebral oxygenation [16].…”