The effect of diaphragm contraction on upper airway collapsibility

2013 ◽  
Vol 115 (3) ◽  
pp. 337-345 ◽  
Author(s):  
David R. Hillman ◽  
Jennifer H. Walsh ◽  
Kathleen J. Maddison ◽  
Peter R. Platt ◽  
Alan R. Schwartz ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Upper Airway ◽  
Dependent Manner ◽  
Phrenic Nerve Stimulation ◽  
Airway Patency ◽  
Airway Collapsibility ◽  
The Difference ◽  
Upper Airway Collapsibility

Increasing lung volume increases upper airway patency and decreases airway resistance and collapsibility. The role of diaphragm contraction in producing these changes remains unclear. This study was undertaken to determine the effect of selective diaphragm contraction, induced by phrenic nerve stimulation, on upper airway collapsibility and the extent to which any observed change was attributable to lung volume-related changes in pressure gradients or to diaphragm descent-related mediastinal traction. Continuous bilateral transcutaneous cervical phrenic nerve stimulation (30 Hz) was applied to nine supine, anesthetized human subjects during transient decreases in airway pressure to levels sufficient to produce flow limitation when unstimulated. Stimulation was applied at two intensities (low and high) and its effects on lung volume and airflow quantified relative to unstimulated conditions. Lung volume increased by 386 ± 269 ml (means ± SD) and 761 ± 556 ml during low and high stimulation, respectively ( P < 0.05 for the difference between these values), which was associated with peak inspiratory flow increases of 69 ± 57 and 137 ± 108 ml/s, respectively ( P < 0.05 for the difference). Stimulation-induced change in lung volume correlated with change in peak flow ( r = 0.65, P < 0.01). Diaphragm descent-related outward displacement of the abdominal wall produced no change in airflow unless accompanied by lung volume change. We conclude that phrenic nerve stimulation-induced diaphragm contraction increases lung volume and reduces airway collapsibility in a dose-dependent manner. The effect appears primarily mediated by changes in lung volume rather than mediastinal traction from diaphragm descent. The study provides a rationale for use of continuous phrenic stimulation to treat obstructive sleep apnea.

scholarly journals Effect of Head Elevation on Passive Upper Airway Collapsibility in Normal Subjects during Propofol Anesthesia

2011 ◽  
Vol 115 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Masato Kobayashi ◽  
Takao Ayuse ◽  
Yuko Hoshino ◽  
Shinji Kurata ◽  
Shunji Moromugi ◽  
...  
Keyword(s):  
Upper Airway ◽  
Normal Subjects ◽  
Target Concentration ◽  
Airway Patency ◽  
Head Elevation ◽  
Jaw Opening ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Head Flexion ◽  
Male Subjects

Background Head elevation can restore airway patency during anesthesia, although its effect may be offset by concomitant bite opening or accidental neck flexion. The aim of this study is to examine the effect of head elevation on the passive upper airway collapsibility during propofol anesthesia. Method Twenty male subjects were studied, randomized to one of two experimental groups: fixed-jaw or free-jaw. Propofol infusion was used for induction and to maintain blood at a constant target concentration between 1.5 and 2.0 μg/ml. Nasal mask pressure (PN) was intermittently reduced to evaluate the upper airway collapsibility (passive PCRIT) and upstream resistance (RUS) at each level of head elevation (0, 3, 6, and 9 cm). The authors measured the Frankfort plane (head flexion) and the mandible plane (jaw opening) angles at each level of head elevation. Analysis of variance was used to determine the effect of head elevation on PCRIT, head flexion, and jaw opening within each group. Results In both groups the Frankfort plane and mandible plane angles increased with head elevation (P &lt; 0.05), although the mandible plane angle was smaller in the free-jaw group (i.e., increased jaw opening). In the fixed-jaw group, head elevation decreased upper airway collapsibility (PCRIT ~ -7 cm H₂O at greater than 6 cm elevation) compared with the baseline position (PCRIT ~ -3 cm H₂O at 0 cm elevation; P &lt; 0.05). Conclusion : Elevating the head position by 6 cm while ensuring mouth closure (centric occlusion) produces substantial decreases in upper airway collapsibility and maintains upper airway patency during anesthesia.

Excitation of dorsal and ventral respiratory group neurons by phrenic nerve afferents

1987 ◽  
Vol 62 (3) ◽  
pp. 946-951 ◽  
Author(s):  
D. F. Speck ◽  
W. R. Revelette
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Afferent Input ◽  
Neuronal Responses ◽  
Onset Latency ◽  
Phrenic Nerve Stimulation ◽  
Group Iii ◽  
Neuronal Excitation ◽  
Dorsal Columns ◽  
The Difference

The projections of phrenic nerve afferents to neurons in the dorsal (DRG) and ventral (VRG) respiratory group were studied in anesthetized, paralyzed, and vagotomized cats. Extracellular recordings of neuronal responses to vagal nerve and cervical phrenic nerve stimulation (CPNS) indicated that about one-fourth of the DRG respiratory-modulated neurons were excited by phrenic nerve afferents with an onset latency of approximately 20 ms. In addition, non-respiratory-modulated neurons within the DRG were recruited by CPNS. Although some convergence of vagal and phrenic afferent input was observed, most neurons were affected by only one type of afferent. In contrast to the DRG, only 3 out of 28 VRG respiratory-modulated neurons responded to CPNS. A second study determined that most of these neuronal responses were due to activation of diaphragmatic afferents since 90% of the DRG units activated by CPNS were also excited at a longer latency by thoracic phrenic nerve stimulation. The difference in onset latency of neuronal excitation indicates an afferent peripheral conduction velocity of about 10 m/s, which suggests that they are predominately small myelinated fibers (group III) making paucisynaptic connections with DRG neurons. Decerebration, decerebellation, and bilateral transection of the dorsal columns at C2 do not abolish the neuronal responses to cervical PNS.

Effect of digitalis on the diaphragm in anesthetized dogs

1987 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
T. Chonan ◽  
H. Miki ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Stimulus Frequency ◽  
Dependent Manner ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Residual Capacity ◽  
Anesthetized Dogs

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Neostigmine/Glycopyrrolate Administered after Recovery from Neuromuscular Block Increases Upper Airway Collapsibility by Decreasing Genioglossus Muscle Activity in Response to Negative Pharyngeal Pressure

2010 ◽  
Vol 113 (6) ◽  
pp. 1280-1288 ◽  
Author(s):  
Frank Herbstreit ◽  
Daniela Zigrahn ◽  
Christof Ochterbeck ◽  
Jürgen Peters ◽  
Matthias Eikermann
Keyword(s):  
Neuromuscular Blockade ◽  
Lung Volume ◽  
Muscle Activation ◽  
Neuromuscular Block ◽  
Upper Airway ◽  
Acetylcholinesterase Inhibitors ◽  
Genioglossus Muscle ◽  
Pharyngeal Pressure ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Background Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function. Methods We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges. Results Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection. Conclusion Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.

Negative intrathoracic pressure decreases independently left ventricular filling and emptying

1989 ◽  
Vol 257 (1) ◽  
pp. H120-H131 ◽  
Author(s):  
J. Peters ◽  
C. Fraser ◽  
R. S. Stuart ◽  
W. Baumgartner ◽  
J. L. Robotham
Keyword(s):  
Stroke Volume ◽  
Nerve Stimulation ◽  
Lung Volume ◽  
Phrenic Nerve ◽  
Intrathoracic Pressure ◽  
Esophageal Pressure ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Phrenic Nerve Stimulation

The mechanism for the fall in left ventricular (LV) stroke volume with normal and obstructed inspiration is controversial with changes proposed in LV preload and afterload. During respiration extending over several cardiac cycles, changes in both LV filling and emptying could occur, rendering demonstration of any responsible mechanism difficult. To evaluate the independent effects of negative intrathoracic pressure (NITP) on LV filling and emptying, we have analyzed the effects of NITP confined to either diastole or systole using electrocardiogram (ECG)-triggered phrenic nerve stimulation in six anesthetized closed-chest dogs. Lung volume was either maintained by completely obstructing the airway or allowed to increase during NITP. With diastolic NITP and the airway obstructed during phrenic nerve stimulation, LV filling volume (integrated mitral flow) significantly decreased (-37 +/- 6.1% SE) associated with increases in LV and right atrial filling pressures at end diastole relative to both atmospheric and esophageal pressures. Right atrial pressure relative to either atmospheric or esophageal pressure increased significantly more than left atrial pressure. The ensuing LV stroke volume (integrated ascending aortic flow) decreased significantly (-30.8 +/- 5.9%). With NITP confined to systole and at constant LV preload, LV stroke volume also decreased (-12.9 +/- 2.5%) associated with an increase in LV systolic pressure relative to esophageal pressure. Similar significant changes were observed despite a smaller fall in esophageal pressure when lung volume was allowed to increase during either diastolic or systolic NITP. We conclude that 1) NITP confined to diastole decreases LV filling and the ensuing LV stroke volume, most likely by ventricular interdependence; 2) NITP confined to systole also decreases LV stroke volume, presumptively by imposing an increased afterload on the LV; 3) both diastolic and systolic mechanisms should contribute to a decreased LV stroke volume during normal and obstructed inspiration; and 4) if the effects of intrathoracic pressure changes were to extend over several cardiac cycles, mechanisms exist to account for either increases or decreases in LV volumes.

Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

2004 ◽  
Vol 83 (9) ◽  
pp. 718-722 ◽  
Author(s):  
T. Ayuse ◽  
T. Inazawa ◽  
S. Kurata ◽  
I. Okayasu ◽  
E. Sakamoto ◽  
...  
Keyword(s):  
Maxillofacial Surgery ◽  
Mouth Opening ◽  
Upper Airway ◽  
Airflow Limitation ◽  
Airway Patency ◽  
Anesthetic Agents ◽  
Airway Collapsibility ◽  
Maximal Mouth Opening ◽  
Inspiratory Airflow Limitation ◽  
Upper Airway Collapsibility

Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to −3.6 ± 2.9 cm H2O compared with −8.7 ± 2.8 (p = 0.002) for closed mouths and −7.2 ± 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 ± 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

Relative contribution of neurotransmission failure to diaphragm fatigue

1990 ◽  
Vol 68 (1) ◽  
pp. 174-180 ◽  
Author(s):  
J. H. Kuei ◽  
R. Shadmehr ◽  
G. C. Sieck
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Neural Stimulation ◽  
Muscle Stimulation ◽  
Phrenic Nerve Stimulation ◽  
Relative Contribution ◽  
The Difference ◽  
Second Procedure ◽  
Phrenic Stimulation ◽  
Diaphragm Fatigue

Two procedures were used to estimate the relative contribution of neurotransmission failure (NF) to fatigue of the rat diaphragm at different rates of phrenic nerve stimulation. In one, direct muscle stimulation was intermittently superimposed on neural stimulation of the diaphragm, and the relative contribution of NF was estimated by the difference in generated tension. In a second procedure, diaphragm fatigue was induced by using either direct muscle stimulation (with complete blockade of the neuromuscular junction by d-tubocurare) or phrenic nerve stimulation. The relative contribution of NF to diaphragm fatigue was then estimated by comparing the force loss during these two modes of stimulation. With both procedures, it was observed that 1) the relative contribution of NF to diaphragm fatigue was less than 45% at each frequency of phrenic nerve stimulation; 2) the relative contribution of NF to diaphragm fatigue increased at higher rates of phrenic stimulation, reaching a maximum at 75 pulses/s; and 3) the relative contribution of NF to diaphragm fatigue reached a plateau after 2 min of repetitive stimulation.

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