Acute Decompensated CHF
Case: 62 year old female with history of hypertension called EMS for shortness of breath worsening over past 48 hours. Denies overt chest pain. Symptoms are worse with walking > 10 feet. She is compliant with medications.
The patient is found to be tachypneic, and hypertensive. One exam she has rales bilaterally at the bases. The paramedic starts an IV and obtains a 12-Lead ECG which is normal. The paramedic then states that the plan is to give sublingual nitroglycerin and IV furosemide while setting up the CPAP.
JFRD SOG 430.2203
Treatment algorithm for patients experiencing shortness of breath from suspected CHF includes the administration of:
- Sublingual nitroglycerin: 0.4 mg SL q 5 minutes
- Lasix 20-40 mg IV/IO
- Morphine 2-4 mg IV/IO
While acute pulmonary edema due to CHF does have a fairly classic presentation, uncovering the true etiology of symptoms in the field can be difficult. Other possible diagnoses (COPD, MI, PE, pneumonia, mitral valve prolapse) may also be present, and the lack of extensive resources in the field may place these patients at risk if the standard treatment results in decompensation.
Currently, the ACEP standard for the treatment of acute heart failure includes NIPPV, IV nitrates and furosemide. The inclusion of furosemide in the treatment algorithm is aimed at alleviating hypervolemia, which may be the cause of the patient’s symptoms. Unfortunately, many patients who initially present to the hospital with symptoms suggesting CHF may in fact be suffering from another disease process, possibly one which has caused them to become hypovolemic. In addition, even well controlled CHF patients, who are in fact euvolemic or slightly hypovolemic, can experience acute pulmonary edema. For these reasons, giving furosemide without further evaluation to determine the patient’s volume status should be done with caution. Given the effectiveness of NIPPV and nitrates, these should be utilized up front to stabilize the patient until the true nature of illness is better understood.
In addition, the administration of morphine for the treatment of acutely decompensated heart failure has come into question. The initial addition of morphine in the treatment algorithm was in response to animal models which showed is vasodilatory effects. Subsequent studies have not only found this effect to be minimal, transient, and primarily due to a histamine response, but have also associated morphine’s use with increased intubation rates, ICU stay, and mortality.
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