Ok, in part 1 I explained the many causes of rapid breathing, and in part 2 we went over one of them, hyperventilation syndrome. In part 3 I am going to briefly go over some other causes of rapid breathing.
I plan on using quite a few images and videos in my blog to assist the visual learner. I hope this helps.
Most COPD patients have chronic bronchitis so lets start by explaining chronic bronchitis. As Dr. Fink stated, this condition occurs when the bronchial tubes become inflamed, hints the term bronchitis. This is different from the common respiratory infection, also termed bronchitis, that may accompany cold symptoms. This condition is more associated with smokers. Check out this video for a pretty cool look at the effect of smoking on the alveoli.
Chronic bronchitis is defined clinically as a persistent cough that produces sputum(phlegm) and mucus, for at least three months in two consecutive years.- Wikipedia
- Emphysema leads to weight loss, Chronic bronchitis leads to weight gain
- Edema is usually absent with emphysema and present with chronic bronchitis
- Central cyanosis is particular to advanced chronic bronchitis
- Emphysema patients are usually thin waisted.
- Hyperresonance is more commonly percussed on emphysema patients
- JVD may be more present in chronic bronchitis patients(sign of pulmonary HTN)
- Right axis deviation, RVH, and atrial arrhythmias are more associated with chronic bronchitis.
Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. firstname.lastname@example.org
The treatment of acute asthma exacerbation consumes a significant portion of emergency medical services (EMS) system resources. Because few studies have addressed EMS treatment of asthma, most EMS providers model their approach to treatment on strategies thought to be effective in the emergency department. During the treatment of asthma, a patient’s history and current airway and respiratory status are important components of the initial assessment. Although the general evaluation may address a patient’s appearance, vital signs, mental status, level of fatigue, and ability to speak normally, the initial assessment of an asthmatic patient must focus specifically on his or her respiratory effort and quality and on objective measurement of the patient’s blood oxygenation. Inhaled beta-agonist therapy is the widely recommended first choice of treatment, but anticholinergic agents and steroids may also have roles. Although not routine treatments, parenteral magnesium and epinephrine may also be beneficial for certain patients. Endotracheal intubation is a procedure of last resort and should be reserved for patients at immediate risk of respiratory arrest. Finally, EMS providers must be alert to the danger of using a “treat and release” approach, as recommended by some protocols, in the treatment of acute asthma. The quick results and benefit that short-acting treatments provide can easily and erroneously lead a provider to believe that an attack has been adequately controlled when, in fact, a more serious exacerbation may be imminent. Treatment protocols, therefore, should discourage EMS personnel from this practice and advise them to always transport asthmatic patients they have treated to the hospital to undergo more extended care and monitoring.
When used correctly, CPAP has been shown to alleviate symptoms and decrease the need for intubation for patients with CHF, COPD and asthma. It is safe, portable and easy to apply. CPAP does not replace intubation, but rather is a less-invasive means of providing respiratory support while medications work to correct the underlying cause of distress.
BACKGROUND AND OBJECTIVE: Hyperinflation with a decrease in inspiratory capacity (IC) is a common presentation for both unstable and stable COPD patients. As CPAP can reduce inspiratory load, possibly secondary to a reduction in hyperinflation, this study examined whether CPAP would increase IC in stable COPD patients. METHODS: Twenty-one stable COPD patients (nine emphysema, 12 chronic bronchitis) received a trial of CPAP for 5 min at 4, 7 and 11 cmH(2)O. Fast and slow VC (SVC) were measured before and after each CPAP trial. In patients in whom all three CPAP levels resulted in a decreased IC, an additional trial of CPAP at 2 cmH(2)O was conducted. For each patient, a ‘best CPAP’ level was defined as the one associated with the greatest IC. This pressure was then applied for an additional 10 min followed by spirometry. RESULTS: Following application of the ‘best CPAP’, the IC and SVC increased in 15 patients (nine emphysema, six chronic bronchitis). The mean change in IC was 159 mL (95% CI: 80-237 mL) and the mean change in SVC was 240 mL (95% CI: 97-386 mL). Among these patients, those with emphysema demonstrated a mean increase in IC of 216 mL (95% CI: 94-337 mL). Six patients (all with chronic bronchitis) did not demonstrate any improvement in IC. CONCLUSIONS: The best individualized CPAP can increase inspiratory capacity in patients with stable COPD, especially in those with emphysema.