Best of heart failure

5 is that ischemia accounts for more than 50% of cases [ 8 ]. In s HF cases had antecedent hypertension. An increased ratio of HDL cholesterol is associated with increased risk of develo study, 49%of the subjects who had underlying sleep apnea hadH noncompliance with HF medications, poor diet including high and fatty foods, can contribute to worsening of HF. Assessment of the Heart Failure Patient A number of criteria should be taken into consideration when with advanced HF including the number of previous admission tension, intolerance to angiotensin converting enzyme (ACE)/ blockers (ARB), and beta blockers, widening of the QRS co ness to biventricular pacing, worsening exertional tolerance, w tion, elevated HF biomarkers, and psychosocial factors. Common symptoms in HF patients include fatigue and d Dyspnea can range from shortness of breath with mild exerti paroxysmal nocturnal dyspnea. As such, patients report im ening in dyspnea marked by inability to walk a few block stairs as they move through the different classes of NY symptoms include lower extremity swelling, abdominal appetite, early satiety, drowsiness, and overall lack of energ ing and peripheral edema are common manifestations of flu more prevalent in the advanced HF population. Some o advanced HF include the following: need for inotropic sup medications, persistent hyponatremia, NYHA III–IV symp hospitalizations, and worsening renal function [ 6 , 11 ]. Sin disease, many patients adapt to their symptoms by decreasin duration of their activities of daily living. Because this occur of time, it is possible for HF patients to have advanced H significant symptoms or signs of HF. Physical exam findings associated with advanced HF inclu ular venous distention, rales on auscultation, hypotension, a The presence of jugular venous pressure (JVP) in HF patients ing. Data suggest that JVP is a reasonably good assessment o pressures in chronic HF patients. Sensitivity and specificity fo predict a pulmonary capillary wedge pressure >18 approac 80%, respectively [ 12 ]. JVP is a good prognostic marker as w analysis, elevated JVP was associated with an increased risk fo HF and increased risk of overall mortality. Presence of an S3 associated with worse outcomes [ 13 ]. Although the presence of is suggestive of severe HF and volume overload, the absence o 1 Management of Advanced Heart Failure: An Overview greatest bioavailability, more predictable diuretic response, and the longest half-life [38]. Thiazide diuretics may potentiate the effects of loop diuretics and so are sometimes used in combination to augment diuresis. IV chlorothiazide and oral metolazone are the thiazides often used in combination with loop diuretics. Metolazone has an added effect of acting on the proximal tubule which adds to its efficacy in advanced renal failure [39]. Combination therapy, however, should be used with caution and frequent monitoring as electrolyte abnormalities are common. When HF becomes refractory to loop diuretics, it is necessary to look for potential factors including medications which could be limiting their effect on the renal tubules. Uptitration of loop diuretics should then be pursued and switching from IV to a continuous infusion may be considered. Although the DOSE trial in 2011 showed that intermittent infusion of diuretics was not superior to continuous infusion, some clinicians prefer continuous infusion of loop diuretics as this may allow for more effective titration [40]. When ADHF patients are refractory to diuretics, ultrafiltration may be considered. This modality results in greater fluid removal and weight loss. The UNLOAD trial in 2007, which randomized hospitalized HF patients to IV diuretics or ultrafiltration, showed that ultrafiltration produced greater fluid removal, weight loss and reduced 90-day readmissions for HF [41]. However, in the setting of CRS and acute decompensated HF, the CARRESS-HF trial showed that ultrafiltration compared to medical therapy was associated with more adverse events and worsening of renal function. Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy [42]. Once optimal volume status is achieved and patients are optimized on ACE inhibitors and beta-blockers, vasodilators such as the combination of hydralazine and nitrates may be beneficial in reducing afterload. While vasodilators provide symptomatic relief and reduce filling pressures, the two drugs that may slow or reverse cardiac remodeling and disease progression are beta blockers and ACE inhibitors. ACE inhibitors are recommended for all stages of HF while beta blockers should be attempted. Table 3. Medications used for HFrEF. Drug Initial dose(s) Maximum dose(s) Side effects ACE inhibitors Captopril 6.25 mg TID 50 mg TID Cough, hyperkalemia, angioedema, impaired renal function Enalapril 2.5 mg BID 10–20 mg BID Lisinopril 2.5–5 mg QD 20–40 mg QD Beta blockers Bisoprolol 1.25 mg QD 10 mg QD Bradycardia, hypotension Carvedilol 3.125 mg BID 50 mg QD Carvedilol CR 10 mg QD 80 mg QD Metoprolol succinate extended release (metoprolol CR/XL) 12.5–25 mg QD 200 mg QD Angiotensin Receptor Blockers (ARBs) Candesartan 4–8 mg QD 32 mg QD Hyperkalemia, angioedema, impaired renal Losartan 25–50 mg QD 50–150 mg QD Valsartan 20–40 mg BID 160 mg BID ARNI Sacubitril/valsartan 49/51 mg BID (sacubitril/ valsartan) (may consider 24/26 mg BID as initial dose) 97/103 mg BID (sacubitril/ valsartan) Angioedema, hypotension, impaired renal function, hyperkalemia Aldosterone antagonists Spironolactone 12.5–25 mg QD 25 mg QD or BID Hyperkalemia, gynecomastia (spironolactone) Eplerenone 25 mg QD 50 mg QD I channel inhibitor Ivabradine 5 mg BID 7.5 mg BID Bradycardia, vision changes Isosorbide dinitrate and hydralazine Fixed-dose 20 mg isosorbide dinitrate/37.5 mg hydralazine TID 40 mg isosorbide dinitrate/ 75 mg hydralazine TID Headache, hypotension Isosorbide dinitrate and hydralazine separately 20–30 mg isosorbide dinitrate/25–50 mg hydralazine TID or QD 40 mg isosorbide dinitrate TID with 100 mg hydralazine TID