CHF?

[Brandon O]

It's important to make the distinction between chronic conditions -- we're talking about CHF and COPD -- and acute exacerbations of these. The characteristic lung sounds of COPD are DIMINISHED breath sounds (perhaps some early inspiratory crackles). Wheezing is more of a sign of bronchoconstriction, which may be a component of COPD but isn't really the key factor (that's why albuterol etc can help these folks a little, but usually not a whole lot). Exacerbations of COPD, however, tend to have a largely reactive component, and they wheeze and respond to albuterol.

Symptomology in CHF is linked with volume status, but acute exacerbations aren't necessarily due to hypervolemia. For a given patient presentation of pulmonary edema, mo' volume may be associated with mo' problems (as Dr. Biggie put it), but isn't necessarily the main driving force, nor is reducing volume necessarily the first line treatment. You can be euvolemic or even hypovolemic but still be full of pulmonary edema due to increased vascular permeability or a highly adrenergic state. As mentioned, current thinking is mostly preload reduction, NIPPV, and go from there; starting with diuresis is working in the wrong timeline (missing the tree for the forest, as it were).

 

[Nova1300]

I'm gonna bet this lady with no history of liver disease, if she was truly jaundice, it was likely congestive hepatopathy from her heart failure. The rise in BP was more likely attributable to increased cardiac output after your application of a non-rebreather began better matching her myocardial oxygen demand, not the inhaled beta agonist.

If this patient had a history of COPD and is in respiratory failure, she should probably receive bronchodilators no matter what the underlying pathology. You are hypoxic, you need better gas exchange. Open the airways. Even if it's heart failure, what are you worried about? A little beta agonist making it to the failing heart?