Laryngeal paralysis on receptor and reflex responses to negative pressure in the upper airway

1988 ◽  
Vol 74 (1) ◽  
pp. 25-34 ◽  
Author(s):  
O.P. Mathew ◽  
F.B. Sant'Ambrogio ◽  
G. Sant'Ambrogio
2010 ◽  
Vol 108 (6) ◽  
pp. 1619-1624 ◽  
Author(s):  
Danny J. Eckert ◽  
Julian P. Saboisky ◽  
Amy S. Jordan ◽  
David P. White ◽  
Atul Malhotra

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately −16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31 ± 4 vs. 31 ± 6 ms and peak amplitude 318 ± 55 vs. 314 ± 26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54 ± 7 ms, nadir amplitude 64 ± 6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.


2008 ◽  
Vol 104 (5) ◽  
pp. 1426-1435 ◽  
Author(s):  
Danny J. Eckert ◽  
R. Doug McEvoy ◽  
Kate E. George ◽  
Kieron J. Thomson ◽  
Peter G. Catcheside

Hypoxia can depress ventilation, respiratory load sensation, and the cough reflex, and potentially other protective respiratory reflexes such as respiratory muscle responses to increased respiratory load. In sleep-disordered breathing, increased respiratory load and hypoxia frequently coexist. This study aimed to examine the effects of hypoxia on the reflex responses of 1) the genioglossus (the largest upper airway dilator muscle) and 2) the scalene muscle (an obligatory inspiratory muscle) to negative-pressure pulse stimuli during wakefulness and sleep. We hypothesized that hypoxia would impair these reflex responses. Fourteen healthy men, 19–42 yr old, were studied on two separate occasions, ∼1 wk apart. Bipolar fine-wire electrodes were inserted orally into the genioglossus muscle, and surface electrodes were placed overlying the left scalene muscle to record EMG activity. In random order, participants were exposed to mild overnight hypoxia (arterial oxygen saturation ∼85%) or medical air. Respiratory muscle reflex responses were elicited via negative-pressure pulse stimuli (approximately −10 cmH2O at the mask, 250-ms duration) delivered in early inspiration during wakefulness and sleep. Negative-pressure pulse stimuli resulted in a short-latency activation followed by a suppression of the genioglossus EMG that did not alter with hypoxia. Conversely, the predominant response of the scalene EMG to negative-pressure pulse stimuli was suppression followed by activation with more pronounced suppression during hypoxia compared with normoxia (mean ± SE suppression duration 64 ± 6 vs. 38 ± 6 ms, P = 0.006). These results indicate differential sensitivity to the depressive effects of hypoxia in the reflex responsiveness to sudden respiratory loads to breathing between these two respiratory muscles.


2015 ◽  
Vol 118 (10) ◽  
pp. 1221-1228 ◽  
Author(s):  
Jayne C. Carberry ◽  
Hanna Hensen ◽  
Lauren P. Fisher ◽  
Julian P. Saboisky ◽  
Jane E. Butler ◽  
...  

This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine ( r2 = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.


2002 ◽  
Vol 30 (6) ◽  
pp. 804-806 ◽  
Author(s):  
H. Butterell ◽  
R. H. Riley

We present a case of negative pressure pulmonary oedema due to an overlooked cause. A 45-year-old female patient presented to the emergency department unconscious with severe pulmonary oedema. Subsequent investigations revealed a thyroid goitre causing significant tracheal compression. This case report highlights an extremely rare but potentially dangerous sequela of upper airway obstruction.


PEDIATRICS ◽  
1988 ◽  
Vol 82 (3) ◽  
pp. 520-521
Author(s):  
PAUL M. KEMPEN

To the Editor.— The current recommended therapy for patients with meconium aspiration consists of extensive suctioning of the oropharynx and nasopharynx after delivery of the head, with subsequent endotracheal intubation and deep suction with the endotracheal tube as the suction catheter. The upper airway is commonly cleared with a bulb syringe and/or a Delee suction device. With both the Delee and the currently recommended endotracheal suction methods, the physician's mouth is the source of negative pressure.


1990 ◽  
Vol 1 (2) ◽  
pp. 313-317
Author(s):  
Gloria Sonnesso

Negative pressure ventilation (NPV), a concept that was used in the 1940s through 1950s to support the victims of the polio epidemic, is regaining popularity. It is being used increasingly to intermittently support respiratory function in patients suffering from a variety of diseases. The use of NPV obviates the need for a surgically placed airway (if the patients’ upper airway is intact) and allows the patient to resume many of his or her normal activities. Several types of NPV are available for use and experimentation, and it is strongly recommended that the appropriate type for each patient be chosen. Nursing care of the patient on NPV is essentially the same as that of any chronically ventilator-dependent patient. Issues unique to the patient supported on NPV include: increased potential for aspiration, skin breakdown around the NPV site, and “tank shock.” Nursing plays an important role in identifying patients who may be candidates for NPV. Negative pressure ventilation may allow a formally hospital-bound patient the opportunity to be home with family and friends


2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Evan Harmon ◽  
Sebastian Estrada ◽  
Ryan J. Koene ◽  
Sula Mazimba ◽  
Younghoon Kwon

Upper airway obstruction is a potentially life-threatening emergency often encountered in the acute care, perioperative, and critical care settings. One important complication of acute obstruction is negative-pressure pulmonary edema (NPPE). We describe two cases of acute upper airway obstruction, both of which resulted in flash pulmonary edema complicated by acute hypoxic respiratory failure. Though NPPE was suspected, these patients were also found to have Takotsubo syndrome (TTS). Neither patient had prior cardiac disease, and both subsequently had a negative ischemic workup. Because TTS is a condition triggered by hyperadrenergic states, the acute airway obstruction alone or in combination with NPPE was the likely explanation for TTS in each case. These cases highlight the importance of also considering cardiogenic causes of pulmonary edema in the setting of upper airway obstruction, which we suspect generates a profound catecholamine surge and places patients at increased risk of TTS development.


1996 ◽  
Vol 80 (5) ◽  
pp. 1528-1539 ◽  
Author(s):  
C. A. Harms ◽  
Y. J. Zeng ◽  
C. A. Smith ◽  
E. H. Vidruk ◽  
J. A. Dempsey

We investigated the effects of negative pressure (NP) in the isolated upper airway (UA) in three unanesthetized dogs. The UA was isolated, and the dogs breathed through an endotracheal tube while wearing a fitted fiberglass snout mask. NP (-2 to -32 cmH2O) was applied in a square wave below the larynx or at the snout at end expiration and was held until inspiratory effort during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep. During all states of consciousness, NP applied to the UA prolonged expiratory time (TE) 1) below a threshold of -8 to -10 cmH2O, which coincided with closure of the oro- and/or velopharynx; and 2) in a progressive fashion at more negative pressures than threshold, up to a mean apneic length of 324% of the control value (or 13.9 s) at -30 cmH2O. TE prolongation was less during REM sleep at a given NP (P < 0.05). Augmented tonic genioglossal electromyographic activity also occurred with the applied NP during wakefulness and NREM sleep but not with REM sleep. NP (-20 to -32 cmH2O) applied as a brief pulse (300-500 ms) during NREM sleep caused transient airway occlusion, terminated the breath during inspiration, and prolonged TE when applied at end expiration. Central apneas always persisted beyond the termination of the UA closure. TE prolongation in response to NP persisted in the presence of a topical anesthetic nebulized through the UA sufficient to abolish the laryngeal gag reflexes. We conclude that UA closure and deformation will cause significant TE prolongation during all states of consciousness and activation of the genioglossus muscle during wakefulness and NREM sleep but not during REM sleep.


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