scholarly journals Ketamine Activates Breathing and Abolishes the Coupling between Loss of Consciousness and Upper Airway Dilator Muscle Dysfunction

2012 ◽  
Vol 116 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Matthias Eikermann ◽  
Martina Grosse-Sundrup ◽  
Sebastian Zaremba ◽  
Mark E. Henry ◽  
Edward A. Bittner ◽  
...  
Keyword(s):  
Power Spectrum ◽  
Eye Movement ◽  
Upper Airway ◽  
Muscle Dysfunction ◽  
High Dose ◽  
Loss Of Consciousness ◽  
Respiratory Drive ◽  
Airway Patency ◽  
Dilator Muscle ◽  
Ketamine Anesthesia

Background Procedural sedation is frequently performed in spontaneously breathing patients, but hypnotics and opioids decrease respiratory drive and place the upper airway at risk for collapse. Methods In a randomized, controlled, cross-over, pharmaco-physiologic study in 12 rats, we conducted acute experiments to compare breathing and genioglossus electromyogram activity at equianesthetic concentrations of ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist that combines potent analgesic with hypnotic action effects, versus propofol. In 10 chronically instrumented rats resting in a plethysmograph, we measured these variables as well as electroencephalography during five conditions: quiet wakefulness, nonrapid-eye-movement sleep, rapid eye movement sleep, and low-dose (60 mg/kg intraperitoneally) and high-dose ketamine anesthesia (125 mg/kg intraperitoneally). Results Ketamine anesthesia was associated with markedly increased genioglossus activity (1.5 to fivefold higher values of genioglossus electromyogram) compared with sleep- and propofol-induced unconsciousness. Plethysmography revealed a respiratory stimulating effect: higher values of flow rate, respiratory rate, and duty-cycle (effective inspiratory time, 1.5-to-2-fold higher values). During wakefulness and normal sleep, the δ (f = 6.51, P = 0.04) electroencephalogram power spectrum was an independent predictor of genioglossus activity, indicating an association between electroencephalographic determinants of consciousness and genioglossus activity. Following ketamine administration, electroencephalogram power spectrum and genioglossus electroencephalogram was dissociated (P = 0.9 for the relationship between δ/θ power spectrum and genioglossus electromyogram). Conclusions Ketamine is a respiratory stimulant that abolishes the coupling between loss-of-consciousness and upper airway dilator muscle dysfunction in a wide dose-range. Ketamine compared with propofol might help stabilize airway patency during sedation and anesthesia.

scholarly journals Effect of inhaled carbon dioxide on laryngeal abduction

2015 ◽  
Vol 118 (4) ◽  
pp. 489-494 ◽  
Author(s):  
Jonathan Cheetham ◽  
Amanda Jones ◽  
Manuel Martin-Flores
Keyword(s):  
Laryngeal Mask Airway ◽  
High Speed ◽  
Upper Airway ◽  
Laryngeal Mask ◽  
Maximal Response ◽  
High Temporal Resolution ◽  
Respiratory Drive ◽  
Laryngeal Function ◽  
Airway Patency ◽  
End Tidal

Hypercapnia produces a profound effect on respiratory drive and upper airway function to maintain airway patency. Previous work has evaluated the effects of hypercapnia on the sole arytenoid abductor, the posterior cricoarytenoid (PCA), using indirect measures of function, such as electromyography and direct nerve recording. Here we describe a novel method to evaluate PCA function in anesthetized animals and use this method to determine the effects of hypercapnia on PCA function. Eight dogs were anesthetized, and a laryngeal mask airway was used, in combination with high-speed videoendoscopy, to evaluate laryngeal function. A stepwise increase in inspired partial pressure of CO2 produced marked arytenoid abduction above 70-mmHg end-tidal CO2 (ETCO2) ( P < 0.001). Glottic length increased above 80-mmHg ETCO2 ( P < 0.02), and this lead to underrepresentation of changes in glottic area, if standard measures of glottic area (normalized glottic gap area) were used. Use of a known scale to determine absolute glottic area demonstrated no plateau with increasing ETCO2 up to 120 mmHg. Ventilatory parameters also continued to increase with no evidence of a maximal response. In a second anesthetic episode, repeated bursts of transient hypercapnia for 60 s with an ETCO2 of 90 mmHg produced a 43–55% increase in glottic area ( P < 0.001) at or shortly after the end of the hypercapnic burst. A laryngeal mask airway can be used in combination with videoendoscopy to precisely determine changes in laryngeal dimensions with high temporal resolution. Absolute glottic area more precisely represents PCA function than normalized glottic gap area at moderate levels of hypercapnia.

Influence of sleep on alae nasi EMG and nasal resistance in normal men

1993 ◽  
Vol 75 (2) ◽  
pp. 626-632 ◽  
Author(s):  
J. R. Wheatley ◽  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Sleep Onset ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Nasal Airway ◽  
Nasal Resistance ◽  
Rapid Eye Movement ◽  
Dilator Muscle ◽  
Stage 2 Sleep ◽  
Normal Men

The influence of sleep on the upper airway musculature varies considerably, with some muscles maintaining their activity at waking levels and others falling substantially. The influence of sleep on the alae nasi (AN), a dilator muscle of the nasal airway, has been minimally studied to date. Thus we determined the effect of non-rapid-eye-movement (NREM) sleep on the AN electromyogram and its relationship to nasal resistance (Rn) in nine normal supine males. Phasic inspiratory AN activity decreased from 20 +/- 6 arbitrary units during wakefulness to 5 +/- 1 arbitrary units (P < 0.001) at the onset of stage 2 NREM sleep and remained unchanged for two subsequent hours of NREM sleep. However, the Rn at the onset of NREM sleep remained similar to awake values (5.7 +/- 0.9 cmH2O.l-1 x s) and increased only after 1 h of NREM sleep (8.6 +/- 1.7 cmH2O.l-1 x s, P < 0.05), thus demonstrating little relationship to AN activity. We conclude that Rn increases slightly after 1 h of sleep, whereas AN activity decreases at stage 2 sleep onset. Thus AN activity has little influence on Rn during sleep.

Alae nasi electromyographic activity and timing in obstructive sleep apnea

1985 ◽  
Vol 58 (4) ◽  
pp. 1252-1256 ◽  
Author(s):  
P. M. Suratt ◽  
R. McTier ◽  
S. C. Wilhoit
Keyword(s):  
Eye Movement ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Esophageal Pressure ◽  
Emg Activity ◽  
Electromyographic Activity ◽  
Rapid Eye Movement ◽  
Rib Cage ◽  
Dilator Muscle ◽  
Obstructive Sleep

The alae nasi is an accessible dilator muscle of the upper airway located in the nose. We measured electromyograms (EMG) of the alae nasi to determine the relationship between their activity and timing to contraction of the rib cage muscles and diaphragm during obstructive apnea in nine patients. Alae nasi EMG were measured with surface electrodes and processed to obtain a moving time average. Contraction of the rib cage and diaphragm during apneas was detected with esophageal pressure. During non-rapid-eye-movement (NREM) sleep, there was a significant correlation in each patient between alae nasi EMG activity and the change in esophageal pressure. During rapid-eye-movement (REM) sleep, correlations were significantly lower than during NREM sleep. As the duration of each apnea increased, the activation of alae nasi EMG occurred progressively earlier than the change in esophageal pressure. We conclude that during obstructive apneas in NREM sleep, activity of the alae nasi increases when diaphragm and rib cage muscle force increases and the activation occurs earlier as each apneic episode progresses.

scholarly journals Pulmonary C-fiber activation attenuates respiratory-related tongue movements

2012 ◽  
Vol 113 (9) ◽  
pp. 1369-1376 ◽  
Author(s):  
Kun-Ze Lee ◽  
David D. Fuller ◽  
Ji-Chuu Hwang
Keyword(s):  
Upper Airway ◽  
Respiratory Drive ◽  
Adult Rats ◽  
Nerve Branch ◽  
Airway Patency ◽  
C Fibers ◽  
Tongue Muscles ◽  
C Fiber ◽  
Before And After ◽  
Tongue Movements

The functional impact of pulmonary C-fiber activation on upper airway biomechanics has not been evaluated. Here, we tested the hypothesis that pulmonary C-fiber activation alters the respiratory-related control of tongue movements. The force produced by tongue movements was quantified in spontaneously breathing, anesthetized adult rats before and after stimulation of pulmonary C fibers via intrajugular delivery of capsaicin (0.625 and 1.25 μg/kg). Brief occlusion of the trachea was used to increase the respiratory drive to the tongue muscles, and hypoglossal (XII) nerve branches were selectively sectioned to denervate the protrusive and retrusive tongue musculature. Tracheal occlusion triggered inspiratory-related tongue retrusion in rats with XII nerves intact or following section of the medial XII nerve branch, which innervates the genioglossus muscle. Inspiratory-related tongue protrusion was only observed after section of the lateral XII branch, which innervates the primary tongue retrusor muscles. The tension produced by inspiratory-related tongue movement was significantly attenuated by capsaicin, but tongue movements remained retrusive, unless the medial XII branch was sectioned. Capsaicin also significantly delayed the onset of tongue movements such that tongue forces could not be detected until after onset of the inspiratory diaphragm activity. We conclude that altered neural drive to the tongue muscles following pulmonary C-fiber activation has a functionally significant effect on tongue movements. The diminished tongue force and delay in the onset of tongue movements following pulmonary C-fiber activation are potentially unfavorable for upper airway patency.

scholarly journals Differential Effects of Isoflurane and Propofol on Upper Airway Dilator Muscle Activity and Breathing

2008 ◽  
Vol 108 (5) ◽  
pp. 897-906 ◽  
Author(s):  
Matthias Eikermann ◽  
Atul Malhotra ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Flow Rate ◽  
Muscle Activity ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Apparent Paradox ◽  
Arterial Blood ◽  
Dilator Muscle ◽  
Spontaneously Breathing ◽  
Intact Rats

Background Anesthesia impairs upper airway integrity, but recent data suggest that low doses of some anesthetics increase upper airway dilator muscle activity, an apparent paradox. The authors sought to understand which anesthetics increase or decrease upper airway dilator muscle activity and to study the mechanisms mediating the effect. Methods The authors recorded genioglossus electromyogram, breathing, arterial blood pressure, and expiratory carbon dioxide in 58 spontaneously breathing rats at an estimated ED50 (median effective dose) of isoflurane or propofol. The authors further evaluated the dose-response relations of isoflurane under different study conditions: (1) normalization of mean arterial pressure, or end-expiratory carbon dioxide; (2) bilateral lesion of the Kölliker-Fuse nucleus; and (3) vagotomy. To evaluate whether the markedly lower inspiratory genioglossus activity during propofol could be recovered by increasing flow rate, a measure of respiratory drive, the authors performed an additional set of experiments during hypoxia or hypercapnia. Results In vagally intact rats, tonic and phasic genioglossus activity were markedly higher with isoflurane compared with propofol. Both anesthetics abolished the genioglossus negative pressure reflex. Inspiratory flow rate and anesthetic agent predicted independently phasic genioglossus activity. Isoflurane dose-dependently decreased tonic and increased phasic genioglossus activity, and increased flow rate, and its increasing effects were abolished after vagotomy. Impairment of phasic genioglossus activity during propofol anesthesia was reversed during evoked increase in respiratory drive. Conclusion Isoflurane compared with propofol anesthesia yields higher tonic and phasic genioglossus muscle activity. The level of respiratory depression rather than the level of effective anesthesia correlates closely with the airway dilator muscle function during anesthesia.

scholarly journals Upper Airway Dilator Muscle Weakness Following Intermittent and Sustained Hypoxia in the Rat: Effects of a Superoxide Scavenger

2013 ◽  
pp. 187-196 ◽  
Author(s):  
J. R. SKELLY ◽  
S. C. ROWAN ◽  
J. F. X. JONES ◽  
K. D. O’HALLORAN
Keyword(s):  
Muscle Fatigue ◽  
Respiratory Muscle ◽  
Upper Airway ◽  
Muscle Performance ◽  
Muscle Dysfunction ◽  
Dilator Muscle ◽  
Frequency Relationship ◽  
Superoxide Scavenger ◽  
Sustained Hypoxia

Obstructive sleep apnoea syndrome (OSAS) is a common disorder associated with upper airway muscle dysfunction. Agents that improve respiratory muscle performance may have considerable therapeutic value. We examined the effects of acute exposure to sustained and intermittent hypoxia on rat pharyngeal dilator muscle function. Additionally, we sought to test the efficacy of antioxidant treatment in ameliorating or preventing hypoxia-related muscle dysfunction. Isometric contractile and endurance properties of isolated rat sternohyoid muscle bundles were examined at 35 °C in vitro. Muscle bundles were exposed to one of four gas treatments: hyperoxia (control), sustained hypoxia (SH), intermittent hypoxia (IH) or hypoxia/re-oxygenation (HR), in the absence or presence of the superoxide scavenger – Tempol (10 mM). Stress-frequency relationship was determined in response to electrical stimulation (10-100 Hz in increments of 10-20 Hz, train duration: 300 ms). Muscle performance was also assessed during repetitive muscle stimulation (40 Hz, 300 ms every 2 s for 2.5 min). Compared to control, IH and HR treatments significantly decreased sternohyoid muscle force. The negative inotropic effect of the two gas protocols was similar, but both were of lesser magnitude than the effects of SH. SH, but not IH and HR, increased muscle fatigue. Tempol significantly increased sensitivity to stimulation in all muscle preparations and caused a leftward shift in the stress-frequency relationship of IH and SH treated muscles. Tempol did not ameliorate sternohyoid muscle fatigue during SH. We conclude that Tempol increases upper airway muscle sensitivity to stimulation but only modestly ameliorates respiratory muscle weakness during intermittent and sustained hypoxic conditions in vitro. Respiratory muscle fatigue during sustained hypoxia appears unrelated to oxidative stress.

Upper airway and respiratory muscle responses to continuous negative airway pressure

1989 ◽  
Vol 66 (3) ◽  
pp. 1373-1382 ◽  
Author(s):  
R. M. Aronson ◽  
E. Onal ◽  
D. W. Carley ◽  
M. Lopata
Keyword(s):  
Eye Movement ◽  
Airway Pressure ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Patency ◽  
Negative Airway Pressure ◽  
Muscle Responses

To determine upper airway and respiratory muscle responses to nasal continuous negative airway pressure (CNAP), we quantitated the changes in diaphragmatic and genioglossal electromyographic activity, inspiratory duration, tidal volume, minute ventilation, and end-expiratory lung volume (EEL) during CNAP in six normal subjects during wakefulness and five during sleep. During wakefulness, CNAP resulted in immediate increases in electromyographic diaphragmatic and genioglossal muscle activity, and inspiratory duration, preserved or increased tidal volume and minute ventilation, and decreased EEL. During non-rapid-eye-movement and rapid-eye-movement sleep, CNAP was associated with no immediate muscle or timing responses, incomplete or complete upper airway occlusion, and decreased EEL. Progressive diaphragmatic and genioglossal responses were observed during non-rapid-eye-movement sleep in association with arterial O2 desaturation, but airway patency was not reestablished until further increases occurred with arousal. These results indicate that normal subjects, while awake, can fully compensate for CNAP by increasing respiratory and upper airway muscle activities but are unable to do so during sleep in the absence of arousal. This sleep-induced failure of load compensation predisposes the airways to collapse under conditions which threaten airway patency during sleep. The abrupt electromyogram responses seen during wakefulness and arousal are indicative of the importance of state effects, whereas the gradual increases seen during sleep probably reflect responses to changing blood gas composition.

Responses to negative pressure surrounding the neck in anesthetized animals

1990 ◽  
Vol 68 (1) ◽  
pp. 154-160 ◽  
Author(s):  
A. D. Wolin ◽  
K. P. Strohl ◽  
B. N. Acree ◽  
J. M. Fouke
Keyword(s):  
Negative Pressure ◽  
Airway Resistance ◽  
Upper Airway ◽  
Transmural Pressure ◽  
Positive Pressure ◽  
Respiratory Drive ◽  
Airway Wall ◽  
Airway Patency ◽  
Upper Airway Resistance ◽  
Continuous Positive Pressure

Continuous positive pressure applied at the nose has been shown to cause a decrease in upper airway resistance. The present study was designed to determine whether a similar positive transmural pressure gradient, generated by applying a negative pressure at the body surface around the neck, altered upper airway patency. Studies were performed in nine spontaneously breathing anesthetized supine dogs. Airflow was measured with a pneumotachograph mounted on an airtight muzzle placed over the nose and mouth of each animal. Upper airway pressure was measured as the differential pressure between the extrathoracic trachea and the inside of the muzzle. Upper airway resistance was monitored as an index of airway patency. Negative pressure (-2 to -20 cmH2O) was applied around the neck by using a cuirass extending from the jaw to the thorax. In each animal, increasingly negative pressures were transmitted to the airway wall in a progressive, although not linear, fashion. Decreasing the pressure produced a progressive fall in upper airway resistance, without causing a significant change in respiratory drive or respiratory timing. At -5 cmH2O pressure, there occurred a significant fall in upper airway resistance, comparable with the response of a single, intravenous injection of sodium cyanide (0.5-3.0 mg), a respiratory stimulant that produces substantial increases in respiratory drive. We conclude that upper airway resistance is influenced by the transmural pressure across the airway wall and that such a gradient can be accomplished by making the extraluminal pressure more negative.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Phasic respiratory modulation of pharyngeal collapsibility via neuromuscular mechanisms in rats

2012 ◽  
Vol 112 (5) ◽  
pp. 695-703 ◽  
Author(s):  
Ying Cao ◽  
Michelle McGuire ◽  
Chun Liu ◽  
Atul Malhotra ◽  
Liming Ling
Keyword(s):  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Sprague Dawley ◽  
Lung Inflation ◽  
Sprague Dawley Rats ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Before And After ◽  
Patients Experience

Obstructive sleep apnea patients experience recurrent upper airway (UA) collapse due to decreases in the UA dilator muscle activity during sleep. In contrast, activation of UA dilators reduces pharyngeal critical pressure (Pcrit, an index of pharyngeal collapsibility), suggesting an inverse relationship between pharyngeal collapsibility and dilator activity. Since most UA muscles display phasic respiratory activity, we hypothesized that pharyngeal collapsibility is modulated by respiratory drive via neuromuscular mechanisms. Adult male Sprague-Dawley rats were anesthetized, vagotomized, and ventilated (normocapnia). In one group, integrated genioglossal activity, Pcrit, and maximal airflow (Vmax) were measured at three expiration and five inspiration time points within the breathing cycle. Pcrit was closely and inversely related to phasic genioglossal activity, with the value measured at peak inspiration being the lowest. In other groups, the variables were measured during expiration and peak inspiration, before and after each of five manipulations. Pcrit was 26% more negative (−15.0 ± 1.0 cmH2O, −18.9 ± 1.2 cmH2O; n = 23), Vmax was 7% larger (31.0 ± 1.0 ml/s, 33.2 ± 1.1 ml/s), nasal resistance was 12% bigger [0.49 ± 0.05 cmH2O/(ml/s), 0.59 ± 0.05 cmH2O/(ml/s)], and latency to induced UA closure was 14% longer (55 ± 4 ms, 63 ± 5 ms) during peak inspiration vs. expiration (all P < 0.005). The expiration-inspiration difference in Pcrit was abolished with neuromuscular blockade, hypocapnic apnea, or death but was not reduced by the superior laryngeal nerve transection or altered by tracheal displacement. Collectively, these results suggest that pharyngeal collapsibility is moment-by-moment modulated by respiratory drive and this phasic modulation requires neuromuscular mechanisms, but not the UA negative pressure reflex or tracheal displacement by phasic lung inflation.

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.

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