ABSTRACT
BACKGROUND: Real-time detection and classification of apneic episodes remain significant challenges. This study explores the applicability of a novel method of monitoring the respiratory effort and dynamics for rapid detection and classification of apneic episodes. METHODS: Obstructive apnea (OA) and hypopnea/central apnea (CA) were induced in nine tracheostomized rats, by short-lived airway obstruction and administration of succinylcholine, respectively. Esophageal pressure (EP), EtCO2, arterial O2 saturation (SpO2), heart rate, and blood pressure were monitored. Respiratory dynamics were monitored utilizing three miniature motion sensors placed on the chest and epigastrium. Three indices were derived from these sensors: amplitude of the tidal chest wall displacement (TDi), breath time length (BTL), that included inspiration and rapid expiration phases, and amplitude time integral (ATI), the integral of breath amplitude over time. RESULTS: OA induced a progressive 6.42 ± 3.48-fold increase in EP from baseline, which paralleled a 3.04 ± 1.19-fold increase in TDi (P < 0.0012), a 1.39 ± 0.22-fold increase in BTL (P < 0.0002), and a 3.32 ± 1.40-fold rise in the ATI (P < 0.024). During central hypopneic/apneic episodes, each sensor revealed a gradual decrease in TDi, which culminated in absence of breathing attempts. CONCLUSION: Noninvasive monitoring of chest wall dynamics enables detection and classification of central and obstructive apneic episodes, which tightly correlates with the EP.
Subject(s)
Monitoring, Physiologic/instrumentation , Motion , Sleep Apnea, Obstructive/diagnosis , Animals , Blood Pressure , Disease Models, Animal , Heart Rate , Male , Monitoring, Physiologic/methods , Oximetry , Oxygen/chemistry , Pressure , Rats , Rats, Sprague-Dawley , Respiration , Sleep Apnea, Central/diagnosis , Succinylcholine/chemistry , Tidal Volume , Time Factors , TracheostomyABSTRACT
PURPOSE: Diagnosis of pneumothorax (PTX) in newborn infants has been reported as late. To explore diagnostic indices for early detection of progressing PTX, and offer explanations for delayed diagnoses. METHODS: Progressing PTX was created in rabbits (2.3 ± 0.5 kg, n = 7) by injecting 1 ml/min of air into the pleural space. Hemodynamic parameters, tidal volume, EtCO(2), SpO(2), blood gas analyses and chest wall tidal displacements (TDi) on both sides of the chest were recorded. RESULTS: (Mean ± SD): A decrease in SpO(2) below 90 % was detected only after 46.6 ± 11.3 min in six experiments. In contrary to the expected gradual increase of CO(2), there was a prolonged transient decrease of 14.2 ± 4.5 % in EtCO(2) (p < 0.01), and a similar decrease in PaCO(2) (p < 0.025). EtCO(2) returned back to baseline only after 55.2 ± 24.7 min, and continued to rise thereafter. The decrease in CO(2) was a mirror image of the 14.6 ± 5.3 % increase in tidal volume. The analysis of endotracheal flow and pressure dynamics revealed a paradoxical transient increase in the apparent compliance. Significant decrease in mean arterial blood pressure was observed after 46.2 ± 40.1 min. TDi provided the most sensitive and earliest sign of PTX, decreasing on the PTX side after 16.1 ± 7.2 min. The TDi progressively decreased faster and lower on the PTX side, thus enabling detection of asymmetric ventilation. CONCLUSIONS: The counterintuitive transient prolonged decrease in CO(2) without changes in SpO(2) may explain the delay in diagnosis of PTX encountered in the clinical environment. An earlier indication of asymmetrically decreased ventilation on the affected side was achieved by monitoring the TDi.
