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Changes in Physiological Variables During Slow‐ and Rapid‐Onset Airway Obstruction in Swine
Author(s) -
Blackburn Megan Bardgett,
Nawn Corinne
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.728.4
Subject(s) - medicine , airway obstruction , heart rate , blood pressure , cardiology , anesthesia , clamp , airway , mechanical engineering , clamping , engineering
Airway compromise is a significant cause of death in emergency and battlefield settings. While novel airway management devices are available, there is no reproducible animal model of airway obstruction for testing these new product solutions. The goals of this study were to develop a slow‐ and rapid‐onset model of airway obstruction and compare changes in blood gas and cardiovascular parameters. Female swine were anesthetized, intubated, and instrumented for blood sampling and arterial blood pressure and heart rate recordings. Pigs were allowed to breathe spontaneously and a hemostatic clamp on the endotracheal tube was either slowly ratcheted closed over 30 minutes (slow‐onset) or fully clamped immediately (rapid‐onset) until a real‐time pulse oximeter reading of 70% or below was attained. Maximal decreases in blood oxygen saturation (Slow: −66±10% vs Fast: −49±5%) and oxygen partial pressure (Slow: −70±14 mmHg vs Fast: −96±12 mmHg) did not differ (P>0.05) between slow and rapid‐onset obstructions. In contrast, the increase in CO 2 partial pressure was significantly greater during slow (23±1 mmHg) vs rapid (13±2 mmHg, P<0.001) obstruction. Surprisingly, mean arterial pressure did not change significantly from baseline during either slow‐(Baseline: 109±8 mmHg vs Obstruction: 112±12 mmHg) or fast‐onset (Baseline: 105±7 mmHg vs Obstruction: 104±8 mmHg) obstruction. Heart rate significantly increased during slow‐onset obstruction (Baseline: 70 ± 8 bpm vs Obstruction: 88±11 bpm, P<0.05) but was unchanged during fast‐onset obstruction (Baseline: 72±7 bpm vs Obstruction: 80±5 bpm). The changes in mean arterial pressure (Slow: 3±9 mmHg vs Fast: −1±5 mmHg) and heart rate (Slow: 19±5 vs Fast: 8±6 mmHg, p=0.09) were not significantly different between groups. In conclusion, our model of slow‐ and fast‐onset airway obstruction induced significant hypoxemia and hypercapnia similar to what is expected during airway compromise and shows promise for use in testing components of airway management devices. Further studies are needed to determine whether obstruction for longer time periods (to induce a greater reduction in real‐time pulse oximetry blood oxygen levels) will cause greater cardiovascular changes.