Effect of Blood Pressure Changes on Air Flow Dynamics in the Upper Airway of the Decerebrate Cat

1996 ◽  
Vol 84 (1) ◽  
pp. 128-134 ◽  
Author(s):  
Alexander H. Mayor ◽  
Alan R. Schwartz ◽  
James A. Rowley ◽  
Shannon J. Willey ◽  
Boyd M. Gillespie ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Airway Obstruction ◽  
Critical Pressure ◽  
Air Flow ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Nasal Resistance ◽  
Flow Limitation ◽  
Decerebrate Cat ◽  
Arterial Blood

Background Previous studies suggest that upper airway neuromuscular activity can be affected by changes in blood pressure via a baroreceptor-mediated mechanism. It was hypothesized that increases in blood pressure would increase upper airway collapsibility predisposing to airway obstruction at a flow-limiting site in the hypopharynx. Methods To examine the effect of blood pressure on upper airway function, maximal inspiratory air flow was determined through the isolated feline upper airway before, during, and after intravenous infusion of phenylephrine (10-20 micrograms.kg-1.min) in six decerebrate, tracheotomized cats. Inspiratory flow, hypopharyngeal pressure, and pressure at the site of pharyngeal collapse were recorded as hypopharyngeal pressure was rapidly decreased to achieve inspiratory flow limitation in the isolated upper airway. Pressure-flow relationships were used to determine maximal inspiratory air flow and its mechanical determinants, the upper airway critical pressure (a measure of pharyngeal collapsibility), and the nasal resistance upstream to the site of flow limitation. Results An increased mean arterial blood pressure of 71 +/- 16 mmHg (mean +/- SD) was associated with significant decrease in maximal inspiratory air flow from 147 +/- 38 ml/s to 115 +/- 27 ml.sec-1 (P < 0.01). The decrease in maximal inspiratory air flow was associated with an increase in upper airway critical pressure from -8.1 +/- 3.8 to -5.7 +/- 3.7 cm H2O (p < 0.02), with no significant change in nasal resistance. When blood pressure was decreased to baseline by discontinuing the phenylephrine infusion, maximal inspiratory air flow and upper airway critical pressure returned to their baseline values. Conclusions Increased blood pressure increased the severity of upper airway air flow obstruction by increasing pharyngeal collapsibility. Previous studies relating baroreceptor activity to neuromuscular regulation of upper airway tone, are consistent with this effect being mediated by afferent activity from baroreceptors. These findings warrant further study because they suggest the possibility that upper airway obstruction in postoperative patients could either be caused or exacerbated by an increase in blood pressure.

Collapsibility of the Upper Airway during Anesthesia with Isoflurane

2002 ◽  
Vol 97 (4) ◽  
pp. 786-793 ◽  
Author(s):  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
David R. Hillman
Keyword(s):  
Lung Volume ◽  
Critical Pressure ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Flow Limitation ◽  
Anesthetic Depth ◽  
Volume Collapse ◽  
End Tidal ◽  
Spontaneously Breathing

Background The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. Methods To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. Results The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. Conclusions Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

Assessment of Changes in Upper Airway Obstruction by Automatic Identification of Inspiratory Flow Limitation During Sleep

2009 ◽  
Vol 56 (8) ◽  
pp. 2006-2015 ◽  
Author(s):  
Christian Morgenstern ◽  
Matthias Schwaibold ◽  
Winfried J. Randerath ◽  
Armin Bolz ◽  
Raimon Jane
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Upper Airway Obstruction ◽  
Automatic Identification ◽  
Flow Limitation

Tracheal and neck position influence upper airway airflow dynamics by altering airway length

1993 ◽  
Vol 75 (5) ◽  
pp. 2084-2090 ◽  
Author(s):  
D. C. Thut ◽  
A. R. Schwartz ◽  
D. Roach ◽  
R. A. Wise ◽  
S. Permutt ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Critical Pressure ◽  
Upper Airway ◽  
Airflow Limitation ◽  
Nasal Resistance ◽  
Neck Flexion ◽  
Neck Extension ◽  
Neck Position ◽  
Mechanical Factors ◽  
Inspiratory Airflow Limitation

Upper airway obstruction during sleep is characterized by inspiratory airflow limitation and reductions in maximal inspiratory airflow (VImax). To determine how mechanical factors modulate VImax, we analyzed pressure-flow relationships obtained in the isolated upper airway of paralyzed cats. VImax and its determinants, the pharyngeal critical pressure (Pcrit) and the nasal resistance (Rn) upstream to the flow-limiting site (FLS), were measured as caudal tracheal displacement, neck position, and airway length were systematically varied. As the proximal tracheal stump was displaced caudally, graded increases in VImax from 145.3 +/- 90.8 (SD) to 285.9 +/- 117.5 ml/s (P < 0.02) and decreases in Pcrit from -3.0 +/- 3.0 to -9.5 +/- 3.4 cmH2O (P < 0.002) were seen without any significant change in Rn. During neck flexion, significant decreases in VImax from 192.1 +/- 68.5 to 87.2 +/- 48.4 ml/s (P = 0.001), increases in Pcrit from -5.3 +/- 2.03 cmH2O to -1.6 +/- 1.4 cmH2O (P < 0.001), and decreases in Rn from 29.7 +/- 12.2 cmH2O.l-1.s to 16.2 +/- 8.9 cmH2O.l-1.s (P < 0.001) were noted compared with the neutral or extended neck position. Relative to the neutral airway length, upper airway length was found to decrease by 1.15 +/- 0.14 cm during neck flexion and to lengthen by 0.45 +/- 0.12 cm during neck extension. When tracheal displacement and neck position were altered, VImax and Rn correlated directly and Pcrit correlated inversely with airway length (P < 0.001). We conclude that alterations in airflow mechanics with caudal tracheal displacement and changes in neck positions are primarily due to alterations in airway length.

scholarly journals Leptin receptor expression in the dorsomedial hypothalamus stimulates breathing during NREM sleep in db/db mice

SLEEP ◽  
2021 ◽  
Author(s):  
Huy Pho ◽  
Slava Berger ◽  
Carla Freire ◽  
Lenise J Kim ◽  
Mi-Kyung Shin ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Leptin Receptor ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Upper Airway Obstruction ◽  
Co2 Production ◽  
Dorsomedial Hypothalamus ◽  
Leptin Signaling ◽  
Arterial Blood ◽  
Obesity Hypoventilation

Abstract Study Objectives Obesity leads to obstructive sleep apnea (OSA), which is recurrent upper airway obstruction during sleep, and obesity hypoventilation syndrome (OHS), hypoventilation during sleep resulting in daytime hypercapnia. Impaired leptin signaling in the brain was implicated in both conditions, but mechanisms are unknown. We have previously shown that leptin stimulates breathing and treats OSA and OHS in leptin- deficient ob/ob mice and leptin-resistant diet-induced obese mice and that leptin’s respiratory effects may occur in the dorsomedial hypothalamus (DMH). We hypothesized that leptin receptor LepR b–deficient db/db mice have obesity hypoventilation and that restoration of leptin signaling in the DMH will increase ventilation during sleep in these animals. Methods We measured arterial blood gas in unanesthetized awake db/db mice. We subsequently infected these animals with Ad-LepR  b or control Ad-mCherry virus into the DMH and measured ventilation during sleep as well as CO2 production after intracerebroventricular (ICV) infusions of phosphate-buffered saline or leptin. Results Awake db/db mice had elevated CO2 levels in the arterial blood. Ad-LepR  b infection resulted in LepR  b expression in the DMH neurons in a similar fashion to wildtype mice. In LepR  b-DMH db/db mice, ICV leptin shortened REM sleep and increased inspiratory flow, tidal volume and minute ventilation during NREM sleep without any effect on the quality of NREM sleep or CO2 production. Leptin had no effect on upper airway obstruction in these animals. Conclusion Leptin stimulates breathing and treats obesity hypoventilation acting on LepR b-positive neurons in the DMH.

Accelerometry of Adductor Pollicis Muscle Predicts Recovery of Respiratory Function from Meeting Abstracts

2003 ◽  
Vol 98 (6) ◽  
pp. 1333-1337 ◽  
Author(s):  
Matthias Eikermann ◽  
Harald Groeben ◽  
Johannes Hüsing ◽  
Jürgen Peters
Keyword(s):  
Airway Obstruction ◽  
Neuromuscular Blockade ◽  
Forced Vital Capacity ◽  
Respiratory Function ◽  
Vital Capacity ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Upper Airway Obstruction ◽  
Residual Paralysis ◽  
Adductor Pollicis Muscle

Background Residual paralysis increases the risk of pulmonary complications but is difficult to detect. To test the hypothesis that accelerometry predicts effects of residual paralysis on pulmonary and upper airway function, the authors related tests of pulmonary and pharyngeal function to accelerometry of adductor pollicis muscle in 12 partially paralyzed volunteers. Methods Rocuronium (0.01 mg/kg + 2-10 microg x kg-1 x min-1) was administered to maintain train-of-four (TOF) ratios (assessed every 15 s) of approximately 0.5 and 0.8 over a period of more than 5 min. The authors evaluated pharyngeal and facial muscle functions during steady state relaxation and performed spirometric measurements every 5 min until recovery. Upper airway obstruction was defined as a mean ratio of expiratory and inspiratory flow at 50% of vital capacity of greater than 1. The TOF ratio associated with "acceptable" pulmonary recovery (forced vital capacity and forced inspiratory volume in 1 s of &gt; or =90% of baseline) was calculated using a linear regression model. Results At peak blockade (TOF ratio 0.5 +/- 0.16), forced inspiratory flow was impaired (53 +/- 19%) to a greater degree than forced expiratory flow (75 +/- 20%) with a mean ratio of expiratory and inspiratory flow at 50% of vital capacity of 1.18 +/- 0.6. Upper airway obstruction, observed in 8 of 12 volunteers, paralleled an impaired ability to swallow reported by 10 of 12 volunteers. In contrast, all volunteers except one could sustain a head lift for more than 5 s. The authors calculated that a mean TOF ratio of 0.56 (95% confidence interval, 0.22-0.71) predicts "acceptable" recovery of forced vital capacity, whereas forced inspiratory volume in 1 s was impaired until a TOF ratio of 0.95 (0.82-1.18) was reached. A 100% recovery of TOF ratio predicts an acceptable recovery of forced vital capacity, forced inspiratory volume in 1 s, and mean ratio of expiratory and inspiratory flow at 50% of vital capacity in 93%, 73%, and 88% of measurements (calculated negative predictive values), respectively. Conclusion Impaired inspiratory flow and upper airway obstruction frequently occur during minimal neuromuscular blockade (TOF ratio 0.8), and extubation may put the patient at risk. Although a TOF ratio of unity predicts a high probability of adequate recovery from neuromuscular blockade, respiratory function can still be impaired.

Effect of tracheal and tongue displacement on upper airway airflow dynamics

1996 ◽  
Vol 80 (6) ◽  
pp. 2171-2178 ◽  
Author(s):  
J. A. Rowley ◽  
S. Permutt ◽  
S. Willey ◽  
P. L. Smith ◽  
A. R. Schwartz
Keyword(s):  
Mechanical Model ◽  
Critical Pressure ◽  
Interactive Effect ◽  
Upper Airway ◽  
Independent Effect ◽  
Nasal Resistance ◽  
Large Decrease ◽  
Pressure Flow ◽  
Tongue Displacement

We have previously shown that caudal tracheal displacement alters the airflow dynamics of the upper airway. In the present study, we specifically examined the effects of tongue and tracheal displacement on upper airway airflow dynamics. To determine how tongue and tracheal displacement modulate maximal inspiratory airflow (VImax), we analyzed the pressure-flow relationships obtained in the isolated upper airway of paralyzed cats. VImax and its determinants, the pharyngeal critical pressure (Pcrit) and the nasal resistance (Rn) upstream to the flow-limiting site, were measured as tongue displacement and tracheal displacement were systematically varied. Four results were obtained: 1) there was no independent effect of tongue displacement on VImax, Pcrit, or Rn; 2) there was an increase in VImax with 2 cm of tracheal displacement, which was associated with a decrease in Pcrit and an increase in Rn; 3) there was an interactive effect of tongue and tracheal displacement on VImax and Pcrit but not on Rn; and 4) there was a large increase in VImax with tongue displacement > 2.5 cm with the trachea nondisplaced, which was associated with a large decrease in Pcrit and a large increase in Rn. We conclude that tongue and tracheal displacement exert differing influences on airflow dynamics and present a mechanical model of the upper airway that explains these results.

Effect of upper airway obstruction on blood pressure variability after stroke

2004 ◽  
Vol 107 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Peter M. TURKINGTON ◽  
John BAMFORD ◽  
Peter WANKLYN ◽  
Mark W. ELLIOTT
Keyword(s):  
Blood Pressure ◽  
Airway Obstruction ◽  
Acute Stroke ◽  
Upper Airway ◽  
Upper Airway Obstruction ◽  
Stroke Patients ◽  
Sleep Study ◽  
Ischaemic Brain ◽  
Respiratory Disturbance ◽  
The Impact

Approx. 60% of acute stroke patients have periods of significant UAO (upper airway obstruction) and this is associated with a worse outcome. UAO is associated with repeated fluctuation in BP (blood pressure) and increased BP variability is also associated with a poor outcome in patients with acute stroke. UAO-induced changes in BP, at a time when regional cerebral perfusion is pressure-dependent in areas of critically ischaemic brain, could explain the detrimental effect of UAO on outcome in these patients. The aim of the present study was to examine the relationship between UAO and BP variability in patients with acute stroke. Twelve acute stroke patients and 12 age-, sex- and BMI (body mass index)-matched controls underwent a sleep study with non-invasive continuous monitoring of BP to assess the impact of UAO on BP control after stroke. Stroke patients had significantly more 15 mmHg dips in BP/h than the controls (51 compared with 6.7 respectively; P<0.004). Stroke patients also demonstrated significantly higher BP variability than the controls (26.8 compared with 14.4 mmHg; P<0.001). There were significantly more 15 mmHg dips in BP/h in stroke patients who had significant UAO than those who did not (85.7 compared with 29.5 respectively; P<0.032). Furthermore, stroke patients without UAO (RDI <10, where RDI is respiratory disturbance index) had significantly more 15 mmHg dips in BP/h than the controls (29.5 compared with 6.7 respectively; P<0.037). There was a positive correlation between the severity of UAO (RDI) and 15 mmHg dips in BP/h (r=0.574, P<0.005) in stroke patients. Our results suggest that UAO alone does not explain BP variation post-stroke, but it does play an important role, particularly in determining the severity of the BP fluctuation.

Analysis of Inspiratory Flow Shapes in Patients With Partial Upper-Airway Obstruction During Sleep

CHEST Journal ◽  
2001 ◽  
Vol 119 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Tero Aittokallio ◽  
Tarja Saaresranta ◽  
Päivi Polo-Kantola ◽  
Olli Nevalainen ◽  
Olli Polo
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Upper Airway Obstruction ◽  
Partial Upper Airway Obstruction

Tracheostomy and respiratory dead space in emphysema

1964 ◽  
Vol 19 (1) ◽  
pp. 92-96 ◽  
Author(s):  
Herman F. Froeb ◽  
Byong M. Kim
Keyword(s):  
Airway Obstruction ◽  
Dead Space ◽  
Arterial Oxygen Saturation ◽  
Upper Airway ◽  
Alveolar Ventilation ◽  
Upper Airway Obstruction ◽  
Arterial Oxygen ◽  
Lower Airway ◽  
Arterial Blood ◽  
Lower Airway Obstruction

Acute experimentation to judge the effects of reduction of dead space with tracheostomy breathing was performed on four subjects with lower airway obstruction (bronchitis and emphysema) and on two subjects with upper airway obstruction (carcinoma of the larynx and tracheal stenosis). With tracheostomy breathing, the reduction in dead space led to a decrease in minute ventilation except in the two patients with upper airway obstruction. Alveolar ventilation decreased except when alveolar hypoventilation was present to start with. There was no change or an increase in Pacoco2 and H+ in the subjects with lower airway obstruction and small increases in arterial oxygen saturation and Paoo2 occurred. A decrease in Pacoco2 and H+ occurred in one of two patients with upper airway obstruction. Reduction of dead space per se with tracheostomy breathing brings about small changes in alveolar ventilation and gas exchange in the lungs of patients with chronic bronchitis and emphysema. Note:(With the Technical Assistance of Roy Engstrom, Mabel Pearson, and Tom Purcell) physiological dead space and tracheostomy; arterial blood gases with tracheostomy breathing; tracheostomy versus mouth breathing; emphysema and tracheostomy breathing Submitted on February 11, 1963

Collapsibility of the Upper Airway at Different Concentrations of Propofol Anesthesia

2005 ◽  
Vol 103 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Peter R. Eastwood ◽  
Peter R. Platt ◽  
Kelly Shepherd ◽  
Kathy Maddison ◽  
David R. Hillman
Keyword(s):  
Upper Airway ◽  
Inspiratory Flow ◽  
Electromyographic Activity ◽  
Flow Limitation ◽  
Genioglossus Muscle ◽  
Airway Collapsibility ◽  
Effect Site Concentration ◽  
Intramuscular Electrodes ◽  
Upper Airway Collapsibility ◽  
Spontaneously Breathing

Background This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it. Methods Upper airway collapsibility was determined from pressure-flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 mug/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 +/- 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects. Results With increasing depth of anesthesia, (1) critical closing pressure progressively increased (-0.3 +/- 3.5, 0.5 +/- 3.7, and 1.4 +/- 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 microg/ml respectively; P &lt; 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 +/- 9.9% of maximum at 2.5 microg/ml to 0.8 +/- 0.5% of maximum at 6.0 microg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 microg/ml but not at propofol concentrations of 4.0 and 6.0 microg/ml, whereas phasic EMGgg was unchanged. Conclusions Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

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