Best of heart failure

2 in particular, classifies patients into rogressive worsening of symptoms t daily activities, and multiple hospi- ptimal HF therapy. Recurrent hospi- uropean EPICAL registry of more d that patients were admitted to the spent nearly 28 days per year in the ms at rest despite being on medical venous (IV) inotropic therapy, ven- lantation. Similarly, New York Heart nto class I–IV based on the severity noted by marked limitation of phys- hysical activity without discomfort, all into NYHA Class III–IV catego- ms of HF, it is imperative to find the F is extensive, some of the common ons, thyroid dysfunction, ischemia, and hypertension. Of note, however, ailure but no structural disease or nt but patient is asymptomatic nt along with symptoms apy and requiring advanced interventions f daily living without experiencing any ctivities of daily living ity triggers symptoms of HF g fatigue, inability to ambulate G. Murtaza and W. G. Cotts manifestations of fluid overload and are more prevalent in the advanced HF population. Some of the indicators of advanced HF include the following: need for inotropic support, intolerance to medications, persistent hyponatremia, NYHA III–IV symptoms, multiple HF hospitalizations, and worsening renal function [6, 11]. Since HF is a chronic disease, many patients adapt to their symptoms by decreasing the frequency and duration of their activities of daily living. Because this occurs over a long period of time, it is possible for HF patients to have advanced HF in the absence of significant symptoms or signs of HF. Physical exam findings associated with advanced HF include an S3 gallop, jugular venous distention, rales on auscultation, hypotension, and cardiac cachexia. The presence of jugular venous pressure (JVP) in HF patients is an important finding. Data suggest that JVP is a reasonably good assessment of elevated left-sided pressures in chronic HF patients. Sensitivity and specificity for an elevated JVP to predict a pulmonary capillary wedge pressure >18 approaches nearly 81% and 80%, respectively [12]. JVP is a good prognostic marker as well. In a multivariate analysis, elevated JVP was associated with an increased risk for hospitalization for HF and increased risk of overall mortality. Presence of an S3 heart sound is also associated with worse outcomes [13]. Although the presence of rales in HF patients is suggestive of severe HF and volume overload, the absence of rales does not rule out significantly elevated pulmonary capillary wedge pressures (PCWP). In one study, pulmonary rales were auscultated in only 19% of patients and lower extremity edema was only presented in 23% of the patients with PCWP >22 mmHg [12]. As a result, a patient with advanced HF can present without any evidence of fluid overload on physical examination and yet still have an elevated pulmonary capillary wedge pressure and an elevated central venous pressure. Therefore, it is important to keep in mind the potential role for invasive assessment of hemodynamics in this population. Although there are limitations to the physical exam, it should not be abandoned in the patient with heart failure. As such, it is useful to classify patients into four quadrants of HF as proposed by Lynne Warner Stevenson to aid in the assessment of advanced HF patients (Fig. 1). This classification takes into account the presence or absence of elevated filling pressures and adequate or limited organ perfusion. Briefly, it is interpreted as follows: warm and dry, indicating adequate perfusion and volume status; warm and wet, indicating adequate perfusion but congestion; cold and dry, indicating inadequate perfusion and normal filling pressures; and, cold and wet, indicating both inadequate perfusion and congestion [14, 15]. For example, a warm and wet patient is unlikely to need any inotropes and may only require diuresis and subsequent escalation of medical therapy. The cold patient, however, may require inotropic support or mechanical support. Therapy can be tailored to each patient’s specific hemodynamic profile as well as comorbid conditions and on the severity of HF. Imaging, Laboratory Evaluation, and Invasive Hemodynamic Monitoring Some of the common baseline tests ordered to assess HF include blood urea nitrogen and creatinine to assess for renal function in the setting of HF. An electrolyte panel may reveal hyponatremia in the volume overloaded patient and may suggest acid–base disturbances such as an elevated carbon dioxide level due to diuresis. A complete blood count is routinely checked to assess for anemia which is not uncommon with chronic disease and can affect the oxygen carrying capacity of blood. In more critically-ill patients, a lactic acid level may aid in determining end-organ damage as the body switches to anaerobic metabolism in cardiogenic shock. Thyroid function testing is usually done to assess for hyper- or hypothyroid states that may cause or exacerbate HF. Iron studies can be checked if there is a suspicion for an iron overload state like hemochromatosis or to further assess an anemic state. A sleep study can be performed to assess for both central and obstructive sleep apneas. The presence of an infiltrative disease like sarcoidosis or amyloidosis can often be identified withmagnetic resonance imaging/ echocardiography or an endomyocardial biopsy. An echocardiogram can point towards an underlying infiltrative disease with the presence of increased ventricular wall thickness, diastolic dysfunction, and restrictive pathology. These echocardiographic findings along with a high clinical suspicion for an infiltrative process would warrant an MRI for further evaluation. Because coronary artery disease (CAD) is a common cause of HF, either noninvasive imaging or coronary angiography can be helpful to diagnose CAD. Elevation of cardiac troponins may correlate withmyocyte loss and deterioration of LV systolic function. Persistent elevation of troponins in this patient population likely is related to continuous ventricular remodeling Table 1. ACC/AHA classification of HF. AHA/ACC classification Stage A Patient at high risk for heart failure but no structural disease or symptoms present Stage B Structural heart disease present but patient is asymptomatic Stage C Structural heart disease present along with symptoms Stage D HF refractory to medical therapy and requiring advanced interventions Table 2. NYHA classification of HF. NYHA classification Symptoms Class 1 Able to perform usual activities of daily living without experiencing any symptoms of HF Class II Some limitations in performing activities of daily living Class III Comfortable at rest but any activity triggers symptoms of HF Class IV Symptoms of HF at rest including fatigue, inability to ambulate