Oxygenation and Hemodynamics during Chest Compressions in a Lamb Model of Perinatal Asphyxia Induced Cardiac Arrest

Abstract

The current guidelines recommend the use of 100% O2 during resuscitation of a neonate requiring chest compressions (CC). Studies comparing 21% and 100% O2 during CC were conducted in postnatal models and have not shown a difference in incidence or timing of return of spontaneous circulation (ROSC). The objective of this study is to evaluate systemic oxygenation and oxygen delivery to the brain during CC in an ovine model of perinatal asphyxial arrest induced by umbilical cord occlusion. Pulseless cardiac arrest was induced by umbilical cord occlusion in 22 lambs. After 5 min of asystole, lambs were resuscitated with 21% O2 as per Neonatal Resuscitation Program (NRP) guidelines. At the onset of CC, inspired O2 was either increased to 100% O2 (n = 25) or continued at 21% (n = 9). Lambs were ventilated for 30 min post ROSC and FiO2 was gradually titrated to achieve preductal SpO2 of 85–95%. All lambs achieved ROSC. During CC, PaO2 was 21.6 ± 1.6 mm Hg with 21% and 23.9 ± 6.8 mm Hg with 100% O2 (p = 0.16). Carotid flow was significantly lower during CC (1.2 ± 1.6 mL/kg/min in 21% and 3.2 ± 3.4 mL/kg/min in 100% oxygen) compared to baseline fetal levels (27 ± 9 mL/kg/min). Oxygen delivery to the brain was 0.05 ± 0.06 mL/kg/min in the 21% group and 0.11 ± 0.09 mL/kg/min in the 100% group and was significantly lower than fetal levels (2.1 ± 0.3 mL/kg/min). Immediately after ROSC, lambs ventilated with 100% O2 had higher PaO2 and pulmonary flow. It was concluded that carotid blood flow, systemic PaO2, and oxygen delivery to the brain are very low during chest compressions for cardiac arrest irrespective of 21% or 100% inspired oxygen use during resuscitation.

Excess cerebral oxygen delivery follows return of spontaneous circulation in near-term asphyxiated lambs

“…Our findings of a rapid, transient increase in carotid artery flow and oxygen delivery following ROSC are consistent with previous lamb studies in the transitional period 14 – 17 . Studies in asphyxiated lambs and piglets receiving 100% FiO 2 found higher cerebral tissue levels of oxygen than those in lambs that received 21% FiO 2 14 , 32 .…”

“…While high levels of alveolar partial pressure of oxygen may be achieved during CPR in 100% FiO 2 , pulmonary flow is low despite chest compressions, so blood oxygen content is likely to be low 17 . Similarly, antegrade carotid flow is limited to the compression phase and oxygen delivery to the brain is likely to remain low until ROSC 17 . Maximising blood oxygen content during the low-output state that characterises the need for CPR may shorten the duration of severe cerebral hypoxia.…”

“…However, most full-term infants with perinatal asphyxia have compliant lungs at birth. It is likely that the necessary increase in pulmonary blood flow can be achieved while minimising supplemental oxygen use and risk of hyperoxic injury 17,55,56 . This should be the subject of further investigation in a transitional model of severe asphyxia like the one we report here.…”

“…In response to severe hypoxic-ischaemia, cardiac output is redistributed to prioritise oxygen delivery to the brain through dilation of the cerebral vasculature. Lamb experiments have previously shown a rapid increase in both cerebral blood flow and oxygen delivery following ROSC [14][15][16][17] . The adequacy of oxygen delivery however is related to oxygen consumption.…”

Relationship between Brain Injury and Clinical Biomarkers in Hypoxic-Ischemic Newborn Piglets

“…This transient recovery is followed by a secondary deterioration involving a failure of oxidative metabolism (secondary phase) [5][6][7], which is associated with excitotoxic edema, seizures, cerebral hyperperfusion, and ultimately, brain cell death [8]. The term HIE is preferred over perinatal asphyxia [9], and clinical markers, such as fetal heart rate variability [10], blood gases from umbilical cord or Apgar scores, among others, are required to determine the risk of developing brain injury [11]. These clinical markers are currently being used in the clinical setting with approximately 80% sensitivity and specificity [12].…”