Best of heart failure

6 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 ARBs are not as effective ACE inhibitors in the HF population and should be used when intolerance to ACE inhibitors is present. The V2 receptor antagonist, tolvaptan, can be considered in the setting of hyponatremia in HF exacerbation to improve sodium levels, decrease edema, and promote weight reduction in the short-term. Long term benefits have not been seen with V2 antagonists as per the EVEREST trial [43]. Nesiritide, a recombinant BNP with vasodilatory properties, gained popularity in the early 2000s when it showed improvement indyspnea and lowering of PCWP in theHFpopulation. ASCEND- HF trial in 2011 concluded nesiritide had a small, nonsignificant effect on dyspnea when used in combination with other medical therapies and that it was also associated with hypotension, limiting its use. This led to a decrease in popularity [44]. In HF patients with either ischemic or nonischemic cardiomyopathy with NYHA III–IV symptoms who are on optimal medical therapy, have poor LV function with EF <35%, QRS duration >120 ms, and are in sinus rhythm, cardiac resynchronization therapy has shown to be beneficial in decreasing mortality and hospitalizations [45]. Inotropes In patients with refractory HF who are not candidates for LVAD or transplantation, the continuous infusion of inotropes may be considered. The two commonly used inotropes used in the US include milrinone and dobutamine. It is important to note, however, that the mortality rate for patients who receive inotropes is more than 50% at 6 months [46]. The main two ways inotropes are used are either as palliative therapy in patients without another advanced HF option or as bridge to advanced therapies. Milrinone increases cyclic adenosine monophosphate within the cell, resulting in increased calcium levels and increased contractility. Milrinone also has the advantage of reducing afterload by causing peripheral vasodilation. However, vasodilation could be a problem if the patient is borderline hypotensive and potentially limit its use. However, symptomatic relief and improvement in dyspnea comes at a price. For example, The PROMISE trial, which randomized advanced HF patients to oral milrinone therapy vs. placebo, was stopped early due to a 28% increase in all-cause mortality and 34% increase in cardiovascular mortality in the oral milrinone group. Similarly, in the OPTIME-CHF trial, advanced HF patients were randomized to either IV milrinone or placebo. The milrinone group had a higher incidence of atrial arrhythmias and hypotension [47]. Dobutamine is a B1 and B2-adrenergic receptor agonist and helps improve myocardial contractility. Due to its B2 properties, it can induce hypotension by peripheral vasodilation. It has a relatively short half-life of 3 min. Due to an increase in mortality associated with dobutamine, it is only used for acute decompensated systolic failure and for improvement in symptoms. It is also used for palliative purposes. Like milrinone, dobutamine is pro-arrhythmic [47] (Table 4). Digoxin inhibits the Na-K ATPase pump which prevents the efflux of calcium out of the cell, causing an inotropic effect. Digoxin has been used widely for symptomatic relief and to decrease the frequency of HF admissions. Use of digoxin is a Class IIa indication in HF with reduced EF patients who are symptomatic despite optimal medical therapy. Digoxin does not cause hypotension and is commonly used in chronic HF patients who have underlying atrial fibrillation for rate control. However, despite its widespread use, digoxin has no survival benefit [47]. As prognosis for patients, going home on inotropes is very poor and they are not candidates for advanced therapies including transplantation or ventricular assist devices, thorough evaluation should be made taking into account patient preferences and whether they prefer hospice care, palliative support. It is also not unreasonable to have discussion about resuscitation [48]. Table 4. Parenteral drugs used for HFREF. Drug Initial dose(s) Maximum dose(s) Side effects Loop diuretics Furosemide 20–40 mg 160 mg 3–4×/day 40 mg/h Hypovolemia, hypokalemia, hypersensitivity, ototoxicity, contraction alkalosis Torsemide 10–20 mg 200 mg BID 20 mg/h Bumetanide 0.5–1 mg 4–8 mg 3–4×/day, 1–2 mg/h Thiazide diuretics Chlorothiazide 250 mg QD 250–500 mg 3–4×/day Hypotension, hypokalemia Inotropes Milrinone 0.125–0.75 mcg/kg/min 0.75/mcg/kg/min Arrhythmias, hypotension Dobutamine 0.5–20 μg/kg/min Typically 2.5–5 μg/kg/min 40 mcg/kg/min