Glottal patency during experimental cortical seizures in piglets

Systemically-induced seizures produce glottal airflow obstruction in anesthetized pigs, resulting in hypercapnia and respiratory acidosis. Cortically-induced seizures may be more representative of human seizure disorders. The purpose of this study was to describe glottal area patency (GAP) in piglets during cortically-induced seizures.

Nineteen spontaneously breathing, lightly anesthetized (alphaxalone-alphadolone IV) piglets (aged 10 +/- 2 days) were instrumented for recording nasal airflow, subglottic pressure, and electrocorticogram. Glottal visualization was achieved supraglottically using a 1.2-mm fiberoptic scope inserted through the thyrohyoid membrane. Following baseline-control, hypoxic-rebreathing, and new baseline recordings, seizures were induced using subcortical injections of crystalline penicillin G (100,000 units/ injection). Five consecutive-breath representative epochs were digitized from baseline-control, hypoxic-rebreathing, and seizure conditions. For each breath, GAP was measured at the onset of inspiratory pressure, peak of inspiratory effort (Ip), and onset of expiration.

The piglets were physiologic at baseline-control and new baseline conditions, and showed expected increases in ventilation and GAP during rebreathing experiments. GAP was maximum at Ip under baseline and rebreathing conditions, but was significantly decreased and airway resistances were increased during seizure conditions (p < 0.05, ANOVA).

Generalized seizure activity results in reduced GAP at the peak of inspiratory effort. Increased work of breathing during seizures is created by direct mechanical obstruction at the level of the larynx.