Anesthesia & Clinical Research
Open Access
ISSN: 2155-6148
ISSN: 2155-6148
Thomas Danninger, Stephen Haskins, Ottokar Stundner, Yan Ma, Jemiel Nejim, Sean Garvin and Stavros G Memtsoudis
Previous research suggests that increases in airway resistance are associated with a depression in a number of hemodynamic variables. In this study we evaluated the hypothesis that these changes may be in part associated and explainable with increases in pulmonary vascular pressures. We therefore examined the effect of increasing airway resistance on a number of cardiac parameters, and estimated pulmonary arterial pressures using transthoracic echocardiography (TTE) in spontaneously breathing healthy volunteers.
Methods: Subjects were connected to a bioreactance monitor capable of determining hemodynamic parameters including stroke volume (SV), and cardiac index (CI). Blood pressure (NIBP) was obtained non-invasively. Volunteers sequentially breathed for 2 minutes through endotracheal tubes (ETT) with decreasing internal diameters (ID) between 8.0 and 3.0 mm in order to simulate increasing airway resistance, while attached to spirometric equipment. A second measurement cycle was performed for validation. TTE was performed focusing on the estimation of pulmonary arterial pressures during the experiment. Statistical analyses were performed using the generalized estimating equations (GEE) method and Spearman correlation.
Results: All subjects were male, (mean age 29.8 years (SD 5.4), mean BMI 26.75 kg/m2 (SD 4.8)). Mean baseline SV and CI were 117.48 ml (SD 14.0) and 3.72 l/min/m2 (SD 0.7); both, SV and CI decreased significantly vs. baseline when breathing through ETT ID 3.0 (111.50 ml (SD 15.3), p=0.0016 and 3.51 l/min/m2 (SD 0.7), p=0.0007, respectively). For the same breathing cycles, no change in averaged systolic pulmonary arterial pressure (SPAP) was detected between baseline and ETT ID 3.0 (24.45 mm Hg (SD 5.1) vs. 24.87 mm Hg (SD 5.6), p=0.43).
Discussion: Although detecting hemodynamic alterations when simulating upper airway resistance in healthy volunteers, there was no significant change in systolic pulmonary arterial pressure (SPAP) seen. Further research is needed to investigate potential mechanisms associated to hemodynamic changes in response to increases in airway resistance.