alexa Hemodynamic Response to Dynamic Changes in Upper Airway Impedance–A Volunteer Study
ISSN: 2155-6148

Journal of Anesthesia & Clinical Research
Open Access

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Hemodynamic Response to Dynamic Changes in Upper Airway Impedance–A Volunteer Study

Ottokar Stundner1,2, Thomas Danninger2, Isabelle Kao1, Peter Gerner2 and Stavros G Memtsoudis1*

1Department of Anesthesiology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York, USA

2Department of Anesthesiology, Perioperative Medicine and Intensive Care Medicine, Paracelsus Medical University, Austria

*Corresponding Author:
Stavros G. Memtsoudis, MD, PhD
Hospital for Special Surgery
Department of Anesthesiology
535 East 70th Street, New York, NY 10021, USA
Tel: (212) 606 1206
Fax: (212) 5174481
E-mail: [email protected]

Received date: April 05, 2013; Accepted date: March 27, 2013; Published date: May 29, 2013

Citation: Stundner O, Danninger T, Kao I, Gerner P, Memtsoudis SG (2013) Hemodynamic Response to Dynamic Changes in Upper Airway Impedance–A Volunteer Study. J Anesthe Clinic Res 4:317. doi: 10.4172/2155-6148.1000317

Copyright: © 2013 Stundner O, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Introduction: Intermittent airway obstruction may occurring both intubated and non-intubated critically ill patients due to endotracheal tube obstruction or kinking in the former and loss of oropharyngeal tone particularly during sedation in the latter patient group. Spontaneous breathing efforts against high airway resistance invoke shifts in intrathoracic pressure, which could potentially negatively affect cardiac performance. Previous studies utilized the Mueller Maneuver as a model for pathophysiologic changes during these episodes. However, this model only accounts for the state of maximum inspiration. To study progressive airway obstruction of various degrees, we devised an experimental setup allowing for a dynamic simulation and identification of associated short-term effects of breathing against discretely increasing airway resistance. Material and methods: 14 healthy volunteers (9 female, 5 male; mean age 27.8 ± 4.1 years, mean body mass index 26.1 ± 3.6 kg/m2) were asked to breathe through a set of endotracheal tubeswith decreasing internal diameter, while cardiovascular and hemodynamic parameters were recorded.StrokeVolume (SV) and Cardiac Index (CI) were recorded using thoracic bioreactance. Heart Rate (HR), non-invasive arterial blood pressure, oxygen saturation and spirometry parameters were also recorded. Results: Baseline SV, HR and CI averaged 99.8 ml, 69.5/min and 4.01 l/min/m2. During respiration through tubes with decreasing diameters, SV, HR and CI decreased significantly. At maximum airway resistance, SV, HR and CI averaged 90.7 ml, 65.0/min and 3.38 l/min/m2, representing mean percent changes from baseline of -9.1% (p=0.0041), -6.5% (p<0.0001) and -15.7% (p<0.0001). Strong inverse Pearson correlations were detectible between calculated additional airway resistance (Hagen-Poiseuille) and SV (R=-0.143, p=0.013), and CI (R=-0.147, p=0.011), respectively. Blood pressure, arterial oxygen saturation and spirometry parameters did not differ significantly. Conclusions: Increases in airway resistance were dynamically associated with significant hemodynamic deterioration. Ensuring the maintenance of airway patency is therefore an important factor to consider in hemodynamically unstable patients.

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