Cardiopulmonary monitoring at home: the CHIME monitor.

A new physiologic monitor for use in the home has been developed and used for the Collaborative Home Infant Monitor Evaluation (CHIME). This monitor measures infant breathing by respiratory inductance plethysmography and transthoracic impedance; infant electrocardiogram, heart rate and R-R interval; haemoglobin O2 saturation of arterial blood at the periphery and sleep position. Monitor signals from a representative sample of 24 subjects from the CHIME database were of sufficient quality to be clinically interpreted 91.7% of the time for the respiratory inductance plethysmograph, 100% for the ECG, 99.7% for the heart rate and 87% for the 16 subjects of the 24 who used the pulse oximeter. The monitor detected breaths with a sensitivity of 96% and a specificity of 65% compared to human scorers. It detected all clinically significant bradycardias but identified an additional 737 events where a human scorer did not detect bradycardia. The monitor was considered to be superior to conventional monitors and, therefore, suitable for the successful conduct of the CHIME study.

Cardiorespiratory events recorded on home monitors: Comparison of healthy infants with those at increased risk for SIDS.

CONTEXT: Home monitors designed to identify cardiorespiratory events are frequently used in infants at increased risk for sudden infant death syndrome (SIDS), but the efficacy of such devices for this use is unproven. OBJECTIVE: To test the hypothesis that preterm infants, siblings of infants who died of SIDS, and infants who have experienced an idiopathic, apparent life-threatening event have a greater risk of cardiorespiratory events than healthy term infants. DESIGN: Longitudinal cohort study conducted from May 1994 through February 1998. SETTING: Five metropolitan medical centers in the United States. PARTICIPANTS: A total of 1079 infants (classified as healthy term infants and 6 groups of those at risk for SIDS) who, during the first 6 months after birth, were observed with home cardiorespiratory monitors using respiratory inductance plethysmography to detect apnea and obstructed breathing. MAIN OUTCOME MEASURES: Occurrence of cardiorespiratory events that exceeded predefined conventional and extreme thresholds as recorded by the monitors. RESULTS: During 718 358 hours of home monitoring, 6993 events exceeding conventional alarm thresholds occurred in 445 infants (41%). Of these, 653 were extreme events in 116 infants (10%), and of those events with apnea, 70% included at least 3 obstructed breaths. The frequency of at least 1 extreme event was similar in term infants in all groups, but preterm infants were at increased risk of extreme events until 43 weeks' postconceptional age. CONCLUSIONS: In this study, conventional events are quite common, even in healthy term infants. Extreme events were common only in preterm infants, and their timing suggests that they are not likely to be immediate precursors to SIDS. The high frequency of obstructed breathing in study participants would likely preclude detection of many events by conventional techniques. These data should be important for designing future monitors and determining if an infant is likely to be at risk for a cardiorespiratory event.

Scanning electron microscopic changes in the morphology of rabbit pulmonary tissue biopsied following ischemia and reperfusion: a window of opportunity?

Reperfusion is known to cause tissue damage in ischemic pulmonary tissue. We investigated the time frame of this occurrence by examining electron microscopic changes in lung tissue. Isolated, perfused, and ventilated rabbit lungs (and heart) were placed en bloc in a 37 degrees C chamber and perfused through the pulmonary artery at 15 mm Hg pressure with oxygenated Krebs-Henseleit buffer, pH 7.4, 70 ml min(-1), for 20 min and the pulmonary pump and ventilator were stopped. The resultant ischemic state was maintained for 2 h, and reperfusion resumed with the same buffer. The lungs of four groups of rabbits (n = 5 per group) were each subjected to 30 min, 1, 2, and 4 h of reperfusion respectively. Upon completion, lungs were biopsied for scanning electron microscopy. Ischemic damage including the loss of lung architecture, and edema were seen. Reperfusion restored some of the tissue anatomy and the return to normalcy increased up to 1 h of reperfusion after which the damage increased with time. Results suggest that damage due to ischemia alone may be reversible. Initial recovery is due to the re-establishment of circulation. However, with time, the damage seen may be due to free radicals and with 4 h of reperfusion, cell death may have occurred.

Comparison of apnea identified by respiratory inductance plethysmography with that detected by end-tidal CO(2) or thermistor. The CHIME Study Group.

As part of the Collaborative Home Infant Monitoring Evaluation (CHIME) we compared apnea identified by a customized home monitor using respiratory inductance plethysmography (RIP) with simultaneously recorded polysomnography-acquired nasal end-tidal CO(2) (PET(CO(2))) and nasal/oral thermistor in 422 infants during overnight laboratory recordings to determine concordance between techniques, sources of disagreement, and capacity of RIP to detect obstructed breaths within an apnea. Among 233 episodes of apnea identified by at least one method as >/= 16 s, 120 were observed by the CHIME monitor, 219 by PET(CO(2)), and 163 by thermistor. The positive predictive value of the CHIME-identified apnea was 89.2% (95% CI 83, 95) and 73% (95% CI 65, 81) for PET(CO(2)) and thermistor, respectively. However, the sensitivity of the CHIME monitor in identifying events detected by the other methods was only approximately 50%. Among 87 apnea events identified by all three techniques, no two methods showed high agreement in measurement of apnea duration: RIP and PET(CO(2)) (ICC = 0.54), RIP and thermistor (ICC = 0.13), PET(CO(2)) and nasal thermistor (ICC = 0.41). Among the 179 breaths identified by RIP as obstructed, 79.9% were judged to be obstructed on the PET(CO(2)) and 80.4% were judged to be obstructed on the thermistor channel. Among 238 breaths identified on PET(CO(2)) as obstructed, 54.2% were determined to be obstructed by RIP. Among 204 breaths identified on thermistor as obstructed, 55. 4% were determined to be obstructed by RIP. Reasons for discrepancies in apnea detection among channels included body movement, partial airway obstruction, and obstructed breaths. Despite these limitations the CHIME monitor provides an opportunity to record physiological data previously unavailable in the home.

Measurement of oxygen free radicals in a rabbit shock lung model. Effect of superoxide dismutase and retinol.

OBJECTIVES: To develop an isolated rabbit lung model in which oxygen free radical activity could be measured and to examine the effects on the model of oxygen free radical scavengers. DESIGN: Prospective, randomized study. SETTING: A clinical and basic research facility attached to a teaching hospital. PARTICIPANTS: Twenty-five New Zealand white rabbits weighing 3.5 to 4.5 kg. INTERVENTIONS: The mechanism of lung injury by oleic acid or by phorbol myristate acetate (20 ng/mL) plus polymorphonuclear neutrophils (PMA-PMN) in an ex vivo rabbit shock lung model may be the production of oxygen free radicals. Using a standard heart-lung preparation from these rabbits, baseline mean pulmonary artery pressure was maintained at 15 mm Hg and the mean airway pressure at 10 mm Hg. Experimental perfusates were infused over 30 minutes, followed by Krebs-Henseleit solution, pH 7.4. Dimethyl pyrroline oxide trapped oxygen free radicals, levels of which were measured by electron paramagnetic resonance spectroscopy. Lung injury was assessed by light and scanning electron microscopy and by lung weight. RESULTS: A 5-fold increase in pulmonary artery pressure (P < .001) and a nearly 3-fold increase in mean airway pressure (P < .001) were observed in both the oleic acid and PMA-PMN models. Superoxide dismutase (20,000 U/kg), but not retinol palmitate (2000 U), prevented lung injury, the increases in pulmonary artery pressure and mean airway pressure, and the increase in oxygen free radicals in the PMA-PMN model. There were no increases in oxygen free radicals in the control, oleic acid, or PMA-PMN/superoxide dismutase groups (n = 5 in each group). Maximum mean +/- SD increases in oxygen free radicals were 112 +/- 22 nmol/L in the PMA-PMN group (P < .003, n = 5) and 108 +/- nmol/L in the PMA-PMN/retinol group (P < .003, n = 5). CONCLUSIONS: The mechanism of lung injury in the PMA-PMN model is an increase in oxygen free radicals, because superoxide dismutase prevents both the rise in oxygen free radicals and lung injury. Administration of retinol does not prevent lung injury. Oleic acid produces injury not by an increase in oxygen free radicals but rather by another, unknown mechanism.