Heart failure, advanced/decompensated

Factors that may decrease theophylline clearance and lead to reduced dosage requirements include advanced age, bacterial or viral pneumonia, heart failure, liver dysfunction, hypoxemia from acute decompensation, and use of drugs such as cimetidine, macrolides, and fluoroquinolone antibiotics. 

Yamani MH, Haji SA, Starling RC, et al. Comparison of dobutamine-based and milrinone-based therapy for advanced decompensated congestive heart failure Hemodynamic efficacy, clinical outcome, and economic impact. Am Heart J. 2001 142 998-1002. 

In a randomized, open, parallel-group study of the hemodynamic effects of milrinone and glyceryl trinitrate in 119 patients with advanced decompensated heart failure, milrinone was significantly more effective than glyceryl trinitrate (7). Adverse effects caused the withdrawal of milrinone in three of the 58 patients who took it one had ventricular extra beats, one had renal insufficiency, and one had hypokalemia. Headache was the most common adverse effect in both groups, but was less common in those who took milrinone (12 versus 29%). 

Stage D heart failure includes patients with symptoms at rest that are refractory despite maximal medical therapy. This includes patients who undergo recurrent hospitalizations or cannot be discharged from the hospital without special interventions. These individuals have the most advanced form of heart failure and should be considered for specialized therapies, including mechanical circulatory support, continuous positive inotropic therapy, cardiac transplantation, or hospice care. The approach to treatment of patients with stage D heart failure is discussed in more detail in the section Treatment Advanced/ Decompensated Heart Failure. ... 

I Thiazide Diuretics. Thiazide diuretics such as hydrochlorothiazide block sodium and chloride reabsorption in the distal convoluted tubule (approximately 5% to 8% of filtered sodium). The thiazides therefore are relatively weak diuretics and infrequently are used alone in heart failure. However, as is reviewed in detail in the section Treatment Advanced/Decompensated Heart Failure under Diuretic Resistance, thiazides or the thiazide-like diuretic metolazone can be used in combination with loop diuretics to promote a very effective diuresis. 

D in the ACC/AHA classification scheme)."" " The terms decompensated heart failure and exacerbation of heart failure refer to patients with acute worsening of their baseline symptoms that is usually caused by volume overload and/or hypoperfusion. Irrespective of the term used, these forms of severe heart failure may be caused by progression of the underlying disorder or by other intercurrent events that result in worsening of the patient s symptoms. Early identification and aggressive management of patients with advanced heart failure hopefully will reduce morbidity, mortality, and cost of care. 

FIGURE 14-8. General treatment algorithm for advanced/decompensated heart failure based on clinical presentation. Intravenous vasodilators that may be used include nitroglycerin, nesiritide, and nitroprusside. (Adapted with permission from Am Heart J 1998 135 5293-309.)... 

PHARMACOLOGIC THERAPY OF ADVANCED OR DECOMPENSATED HEART FAILURE... 

Zineh I, Schofield RS, Johnson JA. The evolving role of nesiritide in advanced or decompensated heart failure. Pharmacotherapy 2003 23 1266-1280. 

Persons at greatest risk for NSAID hemodynamic nephropathy generally have pre-existing renal insufficiency, medical problems associated with high plasma renin activity (hepatic disease with ascites, decompensated congestive heart failure, or intravascular volume depletion), or systemic lupus erythematosus. Additional risk factors include atherosclerotic cardiovascular disease and diuretic therapy. The elderly are also at higher risk due to interaction of prevalent medical problems, multiple drug therapies, and reduced renal hemodynamics. Advanced age, however, has not been shown to be an independent risk factor for toxicity in limited trials in otherwise healthy elderly subjects. Combined NSAID and ACEl or ARB therapy is also a concern and should be avoided. 

STEMI (17). This landmark trial revealed that the use of early beta-blocker therapy in STEMI reduces the risks of reinfarction and ventricular fibrillation. However, there was a small increase in frequency of cardiogenic shock in patients randomized to the beta-blocker group. Therefore, beta-blockers should be contraindicated in patients presenting with a cardiogenic shock or decompensated congestive heart failure (CHF). Other relative contraindications to beta-blockers include advanced heart block, bradyarrythmias, and active asthma. Unless these contraindications are present, the (ACC/AHA) guidelines list oral beta-blocker therapy within 24 hours as a class I indication in patients with ACS (18). In patients presenting with left ventricular dysfunction after MI as defined by an ejection fraction <40%, carvedilol has been shown to reduce reinfarction rate and mortality in the Carvedilol Post Infarction Survival Control in Left Ventricular Dysfunction (CAPRICORN) trial when compared with placebo (19). 

Treatment strategies for progressive pulmonary venous hypertension should focus on treatment of the underlying disease. For patients with advanced decompensated systolic heart failure and secondary pulmonary hypertension, it is essential to reduce the pulmonary vascular resistance prior to heart transplantation to prevent acute RV failure of the donor heart. The use of continuous milrinone, occasionally nesirit-ide, and earlier intervention with mechanical circulatory device support (19) as a bridge to cardiac transplantation is considered a standard approach for this group of patients. Earlier intervention with valve repair or replacement for patients with mitral valve disease and aortic valve disease with associated pulmonary hypertension is recommended. 

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