Nitro, morphine and furosemide: they’ve been the Holy Trinity of emergent treatment of acute CHF since the 1960s, but does this cocktail actually work?
Recent advances in our understanding and treatment of acute congestive heart failure and acute pulmonary edema may spell the doom of prehospital administration of furosemide.
Congestive heart failure is one of the most prevalent forms of cardiac disease in the United States. Nearly 5 million Americans have the disease, and an additional 500,000 are diagnosed each year. It is the most common cause of hospitalizations in patients over age 65, and half of those diagnosed will be dead within five years. Each year 300,000 people die of the disease, and care for CHF patients represents 3–5% of the total U.S. healthcare budget.1 With the aging of the baby boomers and the resultant graying of America, those numbers will continue to rise.
Congestive heart failure (CHF) is a complex disease process, composed of four distinct clinical syndromes: acute pulmonary edema, hypertensive crisis, cardiogenic shock and chronic heart failure.
While all four will frequently be encountered by EMS providers, rarely will chronic heart failure require prehospital intervention, unless exacerbation of chronic CHF manifests itself as one of the other clinical syndromes.
For the purposes of this article, we will limit most of our discussion to the treatment of acute pulmonary edema.
Distilled to its essence, CHF is simply cardiac output insufficient to meet the demands of the body. It may manifest itself as right heart failure, in which a damaged right ventricle results in decreased blood flow to the lungs and backup of blood in the venous system, or it may manifest itself as left heart failure, resulting in impaired arterial blood flow and backup of blood in the pulmonary circulation. Mixed presentations are also common. It can develop over time as a chronic disease state or it may occur rapidly as a result of an acute disease process, such as severe sepsis or myocardial infarction.
Edema can result from one of two causes: increased capillary permeability or increased hydrostatic pressure. Edema resulting from increased capillary permeability, such as third-spacing from sepsis, is generally of a non-cardiogenic cause, and is beyond the scope of this article. Acute respiratory distress syndrome (ARDS) is an example. However, edema from increased hydrostatic pressure within the microvasculature usually results from a cardiogenic cause, e.g., CHF. If the increased pressure is in the venous system (right heart failure), plasma accumulates in the tissues, manifesting itself as peripheral edema and, if serious, in distended jugular veins and ascites. If the increased pressure is in the pulmonary vasculature, plasma accumulates in the extravascular pulmonary tissues, manifesting itself as pulmonary edema.
Whatever the cause, CHFers rarely call EMS because their feet are swollen. They call because they can’t breathe, which is why we have traditionally considered CHF a cardiac disease disguised as a respiratory condition. The bulk of prehospital treatment of CHF is aimed at treating the primary clinical manifestation of left heart failure: cardiogenic acute pulmonary edema (APE).
Acute Pulmonary Edema
The most common cause of cardiogenic APE is cardiac dysfunction—a dysrhythmia, valvular insufficiency or damage to the left ventricle, which may be chronic or acute. Chronic CHF is characterized by significant changes in the left ventricle’s structure, leading to problems with cardiac output and ejection fraction. These in turn cause a backup in the pulmonary circulation due to the left ventricle’s inability to pump blood forward, leading to an increase in hydrostatic pressure in the pulmonary circulation.1