To measure insensible fluid loss from silicone membrane oxygenators during extracorporeal membrane oxygenation (ECMO), an in vitro system was used. A standard neonatal ECMO circuit (Avecor) was connected to a noncompliant reservoir, which was then primed with normal saline. The experiment was conducted by using two silicone oxygenators (Avecor 0.4 and 0.8 m2), three gas flow rates (0.5, 1.0, and 2.0 L/min) (sweep), and two fluid flow rates (200 and 400 ml/min). Two methods were used to measure the water loss. One method was to replace the water to the noncompliant circuit by using a calibrated burette, and the other method was to collect condensed water after cooling the postmembrane sweep gas to 0 degrees C. The influence of the amount of sweep, fluid flow rate, size of membrane, and inlet and outlet sweep gas temperatures on measured water loss was statistically determined. The amount of water loss correlated with sweep (r2 = 0.81; p<0.00001) but was not related to the fluid flow rate, membrane size, or inlet and outlet sweep gas temperature. The average daily fluid loss measured with replacement and collection methods for each liter of sweep per minute were 72.0+/-12.6 and 62.3+/-10.0 ml, respectively. This information may be applied to clinical practice to accurately manage fluid balance in the sick neonate on ECMO.

No abstract

Pulmonary artery (PA) mixed venous saturation (SvO2) has become a crucial monitor in the adult intensive care unit, but is not used in neonates because of the difficulty in PA catheterization. We evaluated the possibility of utilizing the right atrial venous oxygen saturation (RAvO2), which is easily accessed in the neonate, as a monitor of the effects of mechanical ventilation and intravascular volume in an animal model selected to be the size of the human neonate. A continuous RAvO2 monitoring catheter was placed into the right atrium of 16 normal rabbits (2.2 to 4.1 kg). Oxygen delivery was manipulated by alterations in peak inspiratory pressure (PIP) (n = 6), positive end-expiratory pressure (PEEP) (n = 6), or by progressive hypovolemia (n = 4). RAvO2 decreased with onset of mechanical ventilation alone from 69% +/- 6% to 61% +/- 5% (P < .01). As the PIP was increased from 12 to 21 cm H2O, the RAvO2 progressively decreased from 59% +/- 4% to 49% +/- 6% (P < .05). As the PEEP was increased from 3 to 9 cm H2O, the RAvO2 progressively decreased from 64% +/- 5% to 33% +/- 16% (P < .01). RAvO2 approached baseline after return to continuous positive airway pressure (CPAP) of 3 cm H2O. Progressive phlebotomy to a total of 10 mL/kg resulted in a decrease in RAvO2 from 70% +/- 6% to 27% +/- 5% (P < .001). Volume resuscitation resulted in an increase in RAvO2 to near baseline. Peripheral arterial oxygen saturation remained at a constant 100% throughout each protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Healthy lambs are capable of maintaining effective cardiac output in the presence of moderate arteriovenous shunts (15%). AV-ECMO may provide efficient ventilatory support in the neonatal population with hypercapnia. The amount of oxygen delivery with AV-ECMO depends on arterial desaturation.

Aiming at a better understanding of the pathophysiologic basis of perinatal encephalopathy, we evaluated patterns of tissue oxygenation during hypoxia and hyperoxia. We utilized both laserspectroscopy and invasive tissue-Po2 microneed measurements synchronously in five newborn lambs (141-143 days of gestation). The model of artificial placentation provided defined changes of the blood gases, using a extracorporeal circuit with interposition of membrane lung. During hyperoxia, the Po2 at the blood outlet port of the lung was raised to > 300 mmHg for five minutes. During hypoxia, Po2 was diminished as oxygen at the gas phasis was replaced by nitrogen. After the induction of hyperoxia, a rise of tissue-Po2 was observed. The synchronously recorded data of the laserspectroscopy showed adequately rising HbO2 values in concordance (r = 0.97, p < 0.001). As a constant finding we did not observe Cyt-aa3 changes during induced hyperoxia with tissue-Po2 values of < 40 mmHg. Furthermore, no changes in blood volume occurred in this case. A different pattern of the laserspectroscopic parameters was found when the tissue-Po2 rose above a value of > 40 mmHg and Cyt-aa3 rose after a lag-time occurred. During induced hypoxia an immediate fall of tissue-Po2 corresponding with a fall of HbO2 in the spectroscopic tracing occurred (r = 0.87, p < 0.001). A fall of the Cyt-aa3 level was seen with a lag-time when the tissue-Po2 had reached values of below 10 mmHg. In addition, a rise of blood volume was recorded in all cases of induced hypoxia. In conclusion, the results indicated that cellular redoxe state remains stable over a large range of oxygen partial pressure changes.

Mild hypothermia in rats, induced by a sustained pentobarbital anesthesia, reduces ventilation without compromising arterial oxygenation or acid-base balance, as measured at body temperature. Theoretically, our observations in spontaneously breathing rats imply that a combination of mild hypothermia with anesthesia could be safely utilized to maintain adequate ventilation, using relatively low minute ventilation. We speculate that such a maneuver, if applied during mechanical ventilation, may prevent secondary pulmonary damage by allowing the use of lower ventilator volume-pressure settings.

No abstract

A relatively long-term exogenous hypercapnia can significantly increase oxygen-carrying capacity in normal ventilated dogs. Whether this effect can occur during permissive hypercapnia because of controlled ventilation in patients warrants investigation.