The Effect of Incremental Airway Resistance on Cardiac Performance and Pulmonary Pressure in Spontaneously Breathing Volunteers

Thomas Danninger Stephen Haskins

doi:10.4172/2155-6148.1000360

Abstract

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.

Highlights

Obstructive Sleep Apnea (OSA) has become a major problem throughout the United States, affecting approximately 1 in 4 men and 1 in 10 women [1]
While many clinicians have focused on hypoventilation and desaturation events, some researchers point to the potential association of airway obstruction and adverse hemodynamic consequences as a reason for complications
A nose clip was applied and subjects were asked to breathe through a mouthpiece which was attached to a device recording spirometry data and ent-tidal CO2 data (EtCO2; Datex Ohmeda, Madison, WI)

Summary

Introduction

Obstructive Sleep Apnea (OSA) has become a major problem throughout the United States, affecting approximately 1 in 4 men and 1 in 10 women [1]. While a number of studies describe and explain the long-term cardiovascular consequences especially on pulmonary arterial pressures associated with repeated airway obstruction [2,3], only limited data exist evaluating a direct, short-term relationship between increased airway resistance and changes in stroke volume (SV) and cardiac index (CI), respectively [4]. This is important as pre-existing pulmonary hypertension has been suggested to be a major risk factor for complications in the postoperative period, likely due to worsening of right heart strain [5]. Specific goals were (1) to examine the effect of increasing airway resistance on a number of cardiac parameters and (2) to determine if the detected hemodynamic alterations were associated with changes in estimated pulmonary arterial pressures obtained using transthoracic echocardiography (TTE)

Methods

Results

Conclusion