Respiratory Rate

Respiratory rate was increased in patients who presented to our hospital emergency department because of asthma. One hour after bronchodilator therapy had been initiated, the rate declined signifi­cantly, but still remained above that of nonasthmatic patients in the emergency room. When we provoked asthma in the laboratory, using methacholine inhala­tion or treadmill exercise, despite significant reduc­tions in FEVb respiratory rate in asthmatic subjects was no different from healthy control subjects who had also been subjected to methacholine inhalation and exercise.

Although hyperventilation is a well-recognized, characteristic feature of acute asthma, investigators have not always agreed whether such patients should achieve this increase by breathing rapidly, deeply or both. It has been argued by some that slow, deep respirations minimize the work of breathing and is the pattern most commonly observed clinically. By con­trast, Roussos and Macklem have claimed that an attack of asthma is accompanied by a pattern of rapid, shallow breathing, even in the presence of reduced dynamic compliance, a pattern that may be a result of enhanced vagal activity. Tobin et al noted that breath­ing frequency was normal in his group of symptomatic asthmatic patients. tadalis sx 20

Our study may offer an explanation for these apparently conflicting viewpoints: naturally occurring attacks of asthma are accompanied by increased respiratory rates but episodes of acute airways obstruction induced in the laboratory are not. What then accounts for the distinctively rapid respiratory rate of acute asthma seen in the emergency room? It might be argued by some that emotional or psychological stress accounts for the phenomenon. However, we noted no increase in respiratory rate among nonasthmatic emergency room patients exposed to a similarly stressful environment. One might also postulate that hypoxemia is responsible for the observed increase in respiratory rate. However, most of our asthmatic patients were given supplemental oxygen in the emergency room and it is unlikely that they were hypoxemic at the time of our assessments. Moreover, there is evidence that the mild hypoxemia of acute asthma has little effect on ventilation and no measurable effect on respiratory rate. Freedman studied a group of asth¬matics with a mean FEVt of 43 ±16 percent of predicted and a mean oxygen saturation of 89 ±5 percent. While supplemental oxygen increased mean oxygen saturation to 95 ±2 percent, respiratory rate remained unchanged (22 ± 1 and 21 ± 1 breaths/min, respectively).

Is respiratory rate simply an indicator of the severity of airflow obstruction? If this were so, the difference in respiratory rate between asthmatic patients seen in the emergency room and asthmatics studied in the laboratory would simply be a consequence of more severe airflow obstruction observed in the former setting. Although both emergency room and labora¬tory-studied asthmatic patients were symptomatic with wheezing and dyspnea, mean FEV1 was lower in the former (1.42 ± 0.50 L vs a mean postmethacholine FEV1 of 2.12 ± 0.53 L). This explanation is not entirely satisfactory for three reasons. First, Chadha et al have monitored respiratory rate with inductive plethysmography in a group of asthmatic subjects while they provoked more severe airways obstruction with methacholine than we did in the current study. Despite a mean FEV1, just 45 percent of predicted and comparable to that seen in our emergency room patients, they observed no increase in respiratory rate. Second, the inverse correlations we observed between pre- treatment respiratory rate and pretreatment airflow indices were little more than vague trends achieving statistical significance by virtue of the relatively large number of subjects involved. Following treatment, respiratory rate remained abnormally high as compared to control subjects, but any hint of correlation between respiratory rate and airflow measurements disappeared. Clearly, respiratory rate and measures of FEV1 or PEFR are not redundant 1:1 correlates. Finally, the two asthmatic patients in our study who showed the most marked response to inhaled methacholine had a decline in FEV! of 49 percent (similar to pretreatment values we saw in the emergency room) but no change in respiratory rate. levitra professional