In part 1 I described the PH balance associated with the rapid breather. In part 2 we reviewed hyperventilation syndrome. In part 3 I gave a brief description of a chronic lunger, and how to treat them. In part 4 I am going to go over congestive heart failure(CHF). This happens to be one of my favorite topics.
Watch this video:
- Maybe the biggest clue would be a known history of CHF
- Peripheral edema would indicate right ventricular failure, which could indicate left ventricular failure.
- Crackles or rales both indicate pulmonary edema.
You may also suspect CHF based on patient’s medications, some medications a CHF patient might be on include:
- ACE Inhibitors (these are the drugs that end in “ril”, lisinopril, benazepril, ramipril…)
- Beta Blockers (these end in “lol”, labetalol, atenolol, carevedilol, metoprolol…)
- Diuretics (usually end in “ide” or “one”, furosemide, hydrochlorothiazide, metolazone…)
Don’t you hate it when the patient doesn’t know that they have CHF and are on all these meds? Here are some findings to help your differential diagnosis. If one of these is present, consider other cause.
- Hypotension (consider cardiogenic shock, or sepsis)
- Fever (consider pneumonia, or sepsis)
- Pleuritic chest pain (consider pulmonary embolism)
- Palpitations, irregular pulse (consider arrhythmia)
- For a complete differential diagnosis click here
One of the mistakes in the use of furosemide in acute pulmonary edema is the assumption that the patient is “fluid overloaded.” Studies have shown that many patients with pulmonary edema are actually euvolemic, or even hypovolemic, in the acute setting and that furosemide can cause rapid deleterious fluid shifts. Despite these facts, many medical providers continue to believe that patients with acute heart failure syndromes are volume overloaded, thus necessitating a diuretic.
Studies have also shown that when patients in heart failure are acutely given furosemide, preload and blood pressure are paradoxically increased in the initial 15–20 minutes. Conversely, in 1987, Hoffman demonstrated that the administration of furosemide alone, or in combination with morphine, added no benefit in the acute management of pulmonary edema and led to deleterious side effects, such as hypotension, and worsened clinical outcomes.
In addition to the established fact that some patients with pulmonary edema are not volume overloaded and that furosemide may cause worsening hemodynamics in the acute setting, evidence also suggests that we may be doing harm to patients because of incorrectly identifying pulmonary edema. Patients may have other medical conditions that can lead to acute shortness of breath, such as congestive heart failure (CHF), pneumonia, chronic bronchitis and emphysema. Many patients also have co-existing medical conditions.
In 2006, Jaronik et al studied the appropriateness of prehospital furosemide. They retrospectively identified all patients given this medication in the prehospital environment. The results were substantial. Of the 144 patients included in the study, 60 patients (42%) did not have any evidence of CHF during their hospital stay and 33 patients (23%) needed IV fluid administration from the dehydrating effects of furosemide.
That’s right, in case you haven’t heard, Lasix is not improving the outcome of your CHF, or presumed CHF, patients. In fact, Lasix is responsible for increased morbidity and mortality amongst these patients. That’s not all, here’s more from the same article.
[...]However, multiple studies demonstrate morphine’s potential dangers when used in patients with pulmonary edema. In 1987, Hoffman and Reynolds compared Lasix, nitroglycerin and morphine for the treatment of presumed pulmonary edema. Not only did this study demonstrate the potential for misdiagnosis of heart failure in the prehospital setting, as only 77% of patients received an emergency department (ED) or in-hospital diagnosis of CHF, it also demonstrated the potential for harm. They found adverse effects in the first hour of treatment only in patients who received morphine.Sacchetti et al also demonstrated a trend toward higher intubation rates and ICU admissions in patients receiving morphine.
In a recent study reported in the Emergency Medicine Journal in 2008, Peacock et al reviewed the ADHERE (Acute Decompensated Heart Failure National Registry) database in an attempt to compare the outcomes of patients who did and did not receive morphine during hospitalization for acute decompensated heart failure. This retrospective analysis demonstrated a higher rate of inotrope usage, longer hospitalization, higher need for mechanical ventilation, more ICU admissions and a greater mortality in the morphine group.
Although many studies evaluating morphine efficacy are often retrospective, the trend toward increased morbidity and mortality in patients receiving morphine for acute decompensated heart failure is fairly consistent. There’s no debate that the early aggressive treatment of patients presenting with acute decompensated heart failure can reduce morbidity and mortality; however, morphine does not appear to be the right medication.
Yep, Morphine seems to be a culprit too. Morphine and Lasix have remained in prehospital protocols based on theory. The research has shown that these theories were wrong. This is pretty hard for the old-timers to grasp, and the drugs are still being administered routinely. I predict they will fall in the way of stacked shocks, and MAST pants. The article also slams Lopressor, but I’ll save that for a different discussion. By the way, I have done the research on this, and these aren’t new statements, just finally being recognized.
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.
Bertini G et al. “Intravenous nitrates in the prehospital management of acute pulmonary edema.” Annals Of Emergency Medicine 30, no. 4 (October 1997)
STUDY OBJECTIVE: We sought to assess the effect of nitrates on prehospital mortality among patients with acute pulmonary edema (APE).[...] RESULTS: Overall prehospital mortality rate for APE in all patients was 7.8% (50 of of 640 patients). Mortality after 1984 was significantly lower than before (5.3% versus 13%, P < .01). Nitrates were effective in reducing mortality, even in hypotensive patients.[...]CONCLUSION: Our findings suggest that the use of intravenous nitrates improves short-term prognosis in APE.