Epi and Nitro for Respiratory Issues

[Aequitas]

Hello, this is my first post to this forum. I'm going through my 48 hr medic refresher, and it has brought to mind some questions.
Can anyone clarify why we use epi for asthma/COPD? While epi does dilate the bronchioles, it also indiscriminately constricts the vasculature and increases the HR. Conversely, nitro dilates the vasculature, making it easier for the lungs to remove fluid and put it in the vasculature. They have opposite physiological effects, but are both indicated in respiratory distress. Why not use albuterol in conjunction with nitro? Best of both worlds? Thanks!!!

 

[chaz90]

Epi is indicated in severe cases of respiratory distress secondary to asthma and COPD. It's used most often when more selective inhaled Beta agonists and anticholinergics aren't effective enough in resolving the issue. Nitroglycerin isn't indicated as pulmonary edema typically isn't a symptom of these bronchoreactive airway disorders. You may be thinking of CHF, where NTG and CPAP are considered the primary treatment modalities.

 

[Aequitas]

Thanks, that helps.

 

[Brandon O]

Come to think of it, that raises the question of why nitro isn't used for bronchospasm.

Is it ineffective at relaxing bronchial smooth muscle for some reason? (It's not like there aren't NO receptors there.) Or is there just too much of a hemodynamic effect to let you titrate it to the work of breathing in someone who's not also massively hypertensive?

 

[medicsb]

At lower doses, epinephrine can actually LOWER mean arterial pressure and systemic vascular resistance through its beta-2 effects on the peripheral arterioles. However, its beta-1 effects of increased inotropy and chronotropy are present, thus you don't actually see much of a change in systolic pressure, though diastolic can drop.

But, all that aside, epinephrine should only be used when respiratory distress is suspected to be due to bronchoconstriction. And it is of course recommended that it not be used in presence of known heart disease due to the effect on HR and inotropy, which could potentiate demand ischemia that could lead to infarction.

I imagine that NTG has some affect on airway smooth muscle (as it also does on GI smooth muscle - e.g. the esophagus), but I doubt it is of any clinical significance.