Ezra A. Amsterdam

Society of Chest Pain Centers recommendations for the evaluation and management of the observation stay acute heart failure patient-parts 1-6.

Making the definitive diagnosis of heart failure in the acute care setting can be difficult. In the emergency department this needs to be done rapidly, frequently, and accurately, without access to a patient’s health records and while simultaneously initiating the appropriate diagnostic and therapeutic interventions. This section reviews the diagnostic strategies available to the physician confronted with a patient in whom the differential diagnosis includes acute heart failure. (Crit Pathways in Cardiol 2008;7: 91–95) Making the Diagnosis of Heart Failure When Patients Present With Symptoms Possibly Related to Acute Heart Failure Making the definitive diagnosis of heart failure (HF) in the acute care setting can be difficult. In the emergency department (ED) this needs to be done rapidly, frequently without access to a patient’s health records while simultaneously initiating the appropriate diagnostic and therapeutic interventions. The physician must determine the etiology of symptoms in patients with suspected HF based on the initial history, physical examination, diagnostic studies (laboratory data, electrocardiogram, and radiography), as well as response to empiric therapy. PubMed was searched in a systematic manner using a combination of search terms relevant to each topic specific to early diagnosis available in the emergency department setting. References from articles and guidelines so identified were also evaluated for additional pertinent literature. The Initial History and Physical Examination The most common symptom of HF is dyspnea. However, dyspnea is also common in the general population. Even in well persons, a lack of physical fitness may result in exertional dyspnea. Multiple other medical conditions also produce dyspnea, including chronic obstructive pulmonary disease (COPD), asthma, pneumonia, and myocardial ischemia (Table 1). In several studies and registries of presumed HF, up to 40% of patients had a history of COPD. Therefore, in the acute care setting, a chief complaint of dyspnea is very nonspecific. Other components of a complete history include assessment of abdominal distention, paroxysmal nocturnal dyspnea, orthopnea, fatigue, weakness, nausea, and vomiting. The presence of paroxysmal nocturnal dyspnea, orthopnea, or dyspnea on exertion increases the likelihood of HF, whereas their absence decreases its likelihood. One of the more reliable indicators that dyspnea is due to an acute exacerbation of HF is a previous history of HF. However, approximately 20% of patients admitted with acute heart failure have a history of COPD. A history is most beneficial when combined with other information but by itself will make the accurate diagnosis of HF challenging. Auscultation for an S3 gallop, assessment for jugular venous distension (JVD), auscultation for pulmonary rales, and assessment for leg edema should be part of the initial evaluation of a patient with suspected HF, and the presence of these signs increases the likelihood of HF. The absence of rales, edema, or JVD lowers the probability of HF. An S3 is difficult to detect in the emergency department. Electronic identification of an S3 should improve detection and diagnosis of HF, although studies have yet to show an effect on patient outcome.

Pathophysiology and Definition of the Acute Coronary Syndromes

The acute coronary syndromes include ST elevation myocardial infarction, non-ST elevation myocardial infarction, and unstable angina. The latter two conditions are distinguished by evidence of myocardial infarction based on the elevation of cardiac injury markers. The underlying pathophysiology in the great majority of patients with ACS is atherothrombosis, which encompasses chronic coronary atherosclerotic disease and superimposed acute thrombotic occlusion. Rupture of a coronary atherosclerotic plaque initiates platelet activation and thrombotic coronary occlusion as well as a cascade of clotting mechanisms and inflammatory agents that contribute to myocardial ischemia and necrosis. Patients typically present with chest discomfort but a variety of ischemic equivalents may also predominate (dyspnea, lightheadedness, and cardiac failure). Typically, total coronary occlusion is associated with ST-segment elevation and elevation of injury markers of necrosis. With partial occlusion, there are usually ST and/or T wave abnormalities. All ACS patients are treated with intensive antithrombotic and anticoagulation therapy, as well management of associated problems such as ischemia heart failure and arrhythmias. Optimal treatment of ST elevation infarction is urgent coronary reperfusion, preferably by percutaneous coronary intervention (PCI). Non-ST elevation ACS patients receive comprehensive medical therapy and the majority undergo invasive evaluation within 48 hours of admission to determine their suitability for revascularization by PCI (˜90% of patients) or coronary bypass surgery (˜10% of patients). Of importance is the finding that, although mortality and morbidity of ST elevation infarction are higher than with non-ST elevation ACS during the acute phase, long-term prognosis is worse with non-ST elevation ACS. Therefore, intensive, acute, and long-term management of all patients with ACS is crucial and includes antithrombotic therapy, management of coronary risk factors, and treatment of associated cardiac conditions.