Phenylephrine-induced hypertension acutely decreases genioglossus EMG activity in awake humans

1992 ◽  
Vol 72 (1) ◽  
pp. 110-115 ◽  
Author(s):  
E. Garpestad ◽  
R. C. Basner ◽  
J. Ringler ◽  
J. Lilly ◽  
R. Schwartzstein ◽  
...  

To investigate the relationship between systemic blood pressure (BP) and upper airway dilator muscle activity, we recorded genioglossus electromyograms (EMGgg) during pharmacologically induced acute increases in BP in five healthy humans (ages 27–40 yr). EMGgg was measured with perorally placed fine-wire electrodes; phasic EMGgg was expressed as percentage of baseline activity. Subjects were studied supine, awake, and breathing through a face mask with their mouths taped. End-tidal PCO2 was monitored with a mass spectrometer; minute ventilation was measured with a pneumotachograph. Digital BP was monitored continuously with the Penaz method (Finapres, Ohmeda). Mean arterial pressure (MAP) at baseline was 89 +/- 6 (SD) mmHg. Phenylephrine was infused until MAP reached 15–25 mmHg above baseline (107 +/- 7 mmHg). Recording was continued until MAP returned to baseline (90 +/- 7 mmHg). Elevated BP was associated with a significantly decreased phasic EMGgg (P less than 0.005). With return of MAP to baseline, phasic EMGgg returned toward normal (P less than 0.01). Minute ventilation and end-tidal PCO2 did not differ among conditions. Genioglossus activity appears to be influenced by acute changes in systemic BP. We speculate that BP elevations accompanying obstructive apneas during sleep may decrease upper airway tone and facilitate subsequent apneas.

2000 ◽  
Vol 89 (4) ◽  
pp. 1275-1282 ◽  
Author(s):  
Giora Pillar ◽  
Atul Malhotra ◽  
Robert B. Fogel ◽  
Josee Beauregard ◽  
David I. Slamowitz ◽  
...  

Although pharyngeal muscles respond robustly to increasing Pco 2 during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO2-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal Pco 2(Pet CO2 ) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO2(Pet CO2 = 6 Torr above the eupneic level) were also assessed during SWS ( n = 9) or stage 2 sleep ( n = 7). Pet CO2 increased spontaneously by 0.8 ± 0.1 Torr from stage 2 to SWS (from 43.3 ± 0.6 to 44.1 ± 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 ± 0.1 to 11.9 ± 0.3 l/min in stage 2 and 8.6 ± 0.4 to 12.7 ± 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of Pet CO2 (50.4 ± 1.6 Torr in stage 2, and 50.4 ± 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.


1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.


2006 ◽  
Vol 3 (3) ◽  
pp. 131-136 ◽  
Author(s):  
D.J. Marlin ◽  
V. Adams ◽  
A. Greenwood ◽  
E. Case ◽  
M. Roberts ◽  
...  

AbstractSeveral studies have shown that the placement of a face mask on a horse can have effects on ventilation, gas exchange and the cardiovascular system during exercise. The aim of the present study was to determine if airflow and ventilation measured with the same ultrasonic flowmeters were different during exercise between horses wearing half- (HM) and full-face (FM) masks. Five clinically healthy Thoroughbred horses with no history of respiratory disease were studied in an unbalanced crossover design. They were exercised on a treadmill at speeds between 1.7 and 11ms−1 on a 3° incline wearing both masks. The following variables were recorded: peak inspired (PIF) and peak expired flow rates (PEF), inspiratory tidal volume (VT), respiratory rate (fR ), inspiratory minute ventilation (VE), inspiratory time, (TI), expiratory time (TE ), total breath time (TT), end tidal oxygen (ETO2), end tidal carbon dioxide (ETCO2) and heart rate (HR). A mask by speed of exercise interaction term was not significant for any of the models. The PEF (mean difference 12.91s−1; lower and upper 95% CI 7.6 and 18.21s−1, respectively; P<0.0001) and ETO2 (mean difference 0.77%; lower and upper 95% CI 0.48 and 1.00%, respectively; P<0.0001) were significantly greater and ETCO2 was significantly lower (mean difference −1.3%; lower and upper 95% CI −2.0 and 0.7%, respectively; P<0.0001) with the FM compared with the HM. There was also a trend for inspired VE to be higher with the FM compared with the HM (mean difference 1021min−1; lower and upper 95% CI 26 and 1781 min−1, respectively; non-significant). We conclude that the HM may impair ventilation in the horse during exercise compared with the FM, despite the latter having a greater deadspace.


1994 ◽  
Vol 77 (6) ◽  
pp. 2600-2605 ◽  
Author(s):  
T. Van der Touw ◽  
N. O'Neill ◽  
T. Amis ◽  
J. Wheatley ◽  
A. Brancatisano

We studied the effects of increasing respiratory drive on electromyographic (EMG) soft palate muscle (SPM) activity in nine anesthetized tracheostomy-breathing dogs during hypoxic hypercapnia (HH) with a 14% O2–8% CO2–78% N2 inspired gas mixture. Moving time average EMG activity was recorded from palatinus (PAL), levator veli palatini (LP), and tensor veli palatini (TP) muscles (with bipolar fine-wire electrodes) and diaphragm (DIA; with bipolar hook electrodes). During HH, peak inspiratory DIA activity increased from 18.8 +/- 1.3 to 30.1 +/- 2.0 arbitrary units and minute ventilation increased from 6.2 +/- 0.3 to 18.3 +/- 1.8 l/min (both P < 0.001). Phasic inspiratory, expiratory, and/or tonic EMG activity was present in each SPM during room air breathing (control) and increased during HH (P < 0.05), except for phasic inspiratory PAL and phasic expiratory TP activities. Peak inspiratory LP and TP activities increased during HH to 250 and 179% of control, respectively, and peak expiratory activity increased to 187, 235, and 181% of control in PAL, LP, and TP, respectively. These findings demonstrate respiratory-related regulation of SPM activity independent of local reflex control from the upper airway. However, the combined inspiratory and expiratory phasic recruitment of these muscles differs from the inspiratory recruitment of known upper airway dilator muscles.


1998 ◽  
Vol 84 (1) ◽  
pp. 3-12 ◽  
Author(s):  
S. Meza ◽  
E. Giannouli ◽  
M. Younes

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.


2005 ◽  
Vol 102 (1) ◽  
pp. 35-40 ◽  
Author(s):  
Mohamed Naguib ◽  
Abdulhamid H. Samarkandi ◽  
Khaled Abdullah ◽  
Waleed Riad ◽  
Saleh W. Alharby

Background The authors examined the notion that a reduction in succinylcholine dose from 1 mg/kg to approximately 0.6 mg/kg would allow a faster recovery of spontaneous ventilation and reduction in the incidence of hemoglobin desaturation during the period of apnea in simulated complete upper airway obstruction situations. Methods This prospective, randomized, double-blind study involved 60 patients. After preoxygenation to an end-tidal oxygen concentration &gt;90%, patients were anesthetized with 2 microg/kg fentanyl and 2 mg/kg propofol. After loss of consciousness, patients were randomly allocated to receive 0.56 or 1.0 mg/kg succinylcholine or saline (control group). Oxygen saturation was monitored continuously at the index finger. When the patient became apneic, the face mask was removed and the patient's airway was left unsupported. If the oxygen saturation decreased to 90%, the face mask was reapplied, and ventilation was assisted until the patient was awake. Time from injection of the study drug to the first visible spontaneous diaphragmatic movements was noted. Results Oxygen saturation decreased &lt;90% in 45%, 65%, and 85% of patients in the control, 0.56 mg/kg, and 1.0 mg/kg succinylcholine groups, respectively (P = 0.03). Corresponding times (mean +/- SD) to spontaneous of diaphragmatic movements were 2.7 +/- 1.2, 4.8 +/- 2.5, and 4.7 +/- 1.3 min, respectively. These times were longer (P &lt; 0.001) after either dose of succinylcholine compared with controls. Conclusions Reduction in succinylcholine dose from 1.0 mg/kg to 0.56 mg/kg decreased the incidence of hemoglobin saturation &lt;90% from 85% to 65% but did not shorten the time to spontaneous diaphragmatic movements. A significant fraction of patients would be at risk if there were failure to intubate and ventilate whether succinylcholine is administered or not and regardless of the dose of succinylcholine administered.


1992 ◽  
Vol 73 (2) ◽  
pp. 584-590 ◽  
Author(s):  
J. C. Leiter ◽  
S. L. Knuth ◽  
D. Bartlett

We investigated the quantitative relationships among pharyngeal resistance (Rph), genioglossal electromyographic (EMGge) activity, nasal resistance (Rna), and airflow in 11 normal men aged 19–50 while they were awake. We made measurements with subjects seated with the head erect, seated with the head flexed forward approximately 40 degrees, and supine. Each subject wore a face mask connected to a pneumotachograph to measure airflow. After topical anesthesia of the nose, two catheters for measuring nasal and pharyngeal airway pressures were passed through one nostril: the nasal pressure catheter was positioned at the nasal choanae, and the pharyngeal pressure catheter was positioned just above the epiglottis. We measured EMGge activity with an intraoral surface electrode. The subjects breathed exclusively through the nose while inhaling room air or rebreathing CO2. We measured Rph, Rna, airflow, and EMGge activity at approximately 90-ms intervals throughout each inspiration. Rph was invariant as head position was changed. At any given head position, EMGge activity rose as airflow increased, and Rph remained constant. In contrast, Rna increased as airflow increased. Because Rph was constant, EMGge activity was not correlated with Rph, but EMGge was positively correlated with Rna and airflow. On the basis of the stability of Rph in the face of marked changes in collapsing forces, we conclude that the dynamic interplay of posture, head and jaw position, and upper airway muscle activity quite effectively maintains pharyngeal patency, and interactions among these factors are subtle and complex.


1983 ◽  
Vol 54 (6) ◽  
pp. 1590-1596 ◽  
Author(s):  
W. A. Carlo ◽  
R. J. Martin ◽  
E. F. Abboud ◽  
E. N. Bruce ◽  
K. P. Strohl

A coordinated activation of upper airway and chest wall muscles may be crucial in maintaining airway patency and ventilation. The alae nasi (AN) and diaphragm (DIA) electromyograms (EMG) were recorded with surface electrodes in 17 unsedated healthy preterm infants during both active (AS) and quiet sleep (QS). Airflow was measured via a nasal mask pneumotachograph and integrated to obtain tidal volume. Studies were performed during inhalation of room air and mixtures of 2 and 4% CO2 in air. In room air, phasic AN EMG accompanied 45 +/- 7% of breaths during AS compared with 14 +/- 5% of breaths during QS (P less than 0.001); however, with inhalation of 4% CO2 the incidence of AN EMG increased to comparable levels in both sleep states. During room air breathing onset of AN EMG preceded that of the DIA EMG and inspiratory airflow by 41 +/- 8 ms (P less than 0.01) and 114 +/- 29 ms (P less than 0.05), respectively. Peak AN activity preceded peak DIA activity by 191 +/- 36 ms (P less than 0.01). Alteration in sleep state or increasing chemical drive did not significantly alter these temporal relationships. Nevertheless, with each increase in end-tidal CO2, peak DIA EMG and tidal volume increased while peak AN EMG only showed a consistent increase during 4% CO2 inhalation. We conclude that although there exists a mechanism that temporally coordinates AN and DIA activation, the amount of AN EMG activity with each breath is not clearly correlated with DIA activation, which may contribute to the high incidence of respiratory dysrhythmias in preterm neonates.


1991 ◽  
Vol 71 (6) ◽  
pp. 2283-2291 ◽  
Author(s):  
J. R. Wheatley ◽  
T. C. Amis ◽  
L. A. Engel

The influence of nasal airflow, temperature, and pressure on upper airway muscle electromyogram (EMG) was studied during steady-state exercise in five normal subjects. Alae nasi (AN) and genioglossus EMG activity was recorded together with nasal and oral airflows and pressures measured simultaneously by use of a partitioned face mask. At constant ventilations between 30 and 50 l/min, peak inspiratory AN activity during nasal breathing (7.2 +/- 1.4 arbitrary units) was greater than that during oral breathing (1.0 +/- 0.3 arbitrary units; P less than 0.005). In addition, the onset of AN EMG activity preceded inspiratory flow by 0.38 +/- 0.03 s during nasal breathing but by only 0.17 +/- 0.04 s during oral breathing (P less than 0.04). When the subject changed from nasal to oral breathing, both these differences were apparent on the first breath. However, peak AN activity during nasal breathing was uninfluenced by inspiration of hot saturated air (greater than 40 degrees C), by external inspiratory nasal resistance, or by changes in the expiratory route. The genioglossus activity did not differ between nasal and oral breathing (n = 2). Our findings do not support reflex control of AN activity sensitive to nasal flow, temperature, or surface pressure. We propose a centrally controlled feedforward modulation of phasic inspiratory AN activity linked with the tonic drive to the muscles determining upper airway breathing route.


1988 ◽  
Vol 65 (6) ◽  
pp. 2434-2439 ◽  
Author(s):  
W. A. Carlo ◽  
R. J. Martin ◽  
J. M. Difiore

Because neonatal apnea is frequently associated with airway obstruction, we compared relative changes in activity between various upper airway muscles and the diaphragm during hypercapnic stimulation. The technique of hyperoxic CO2 rebreathing was employed in 17 healthy, sleeping preterm infants studied at a postnatal age of 32 +/- 12 days. Surface diaphragm (DIA) electromyograms (EMGs) were recorded in all infants, and noninvasive measurements of posterior cricoarytenoid (PCA), genioglossus (GG), and alae nasi (AN) EMGs were analyzed in 11, 9, and 8 infants, respectively. During the control period, consistent phasic EMGs were recorded from the DIA in all infants and from the PCA in 8 infants, but from the GG and AN each in only one infant. During CO2 rebreathing, minute ventilation and end-tidal CO2 increased linearly as CO2 rose from 31 +/- 5 to 51 +/- 5 Torr. DIA and PCA EMGs also had proportional and comparable increases throughout rebreathing. In contrast, both GG and AN responses differed from the DIA and PCA (P less than 0.001) and exhibited minimal or absent responses at low levels of hypercapnia. Consistent GG and AN EMGs appeared at comparable levels of end-tidal CO2 (47 +/- 5 and 45 +/- 5 Torr, respectively) and subsequently increased linearly in most infants. We conclude that during CO2 rebreathing the initially delayed and subsequently linear responses of the GG and AN EMGs indicate a high CO2 threshold for these muscles.


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