Treatment of Acute Decompensated Heart Failure PDF

Treatment of acute decompensated heart failure
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Author Wilson S Colucci, MD Section Editor Stephen S Gottlieb, MD James Hoekstra, MD Deputy Editor Susan B Yeon, MD, JD, FACC
Last literature review for version 16.1: January 31, 2008 | This topic last updated: January 31, 2008 INTRODUCTION Acute decompensated heart failure (HF) is a common and potentially fatal cause of acute respiratory distress. The clinical syndrome is characterized by the development of dyspnea associated with the rapid accumulation of fluid within the lung's interstitial and alveolar spaces, which is the result of acutely elevated cardiac filling pressures (cardiogenic pulmonary edema) [ 1] . Acute decompensated HF can also present as elevated left ventricular filling pressures and dypnea without pulmonary edema. Acute decompensated HF is most commonly due to left ventricular (LV) systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. However, a variety of conditions or events can cause cardiogenic pulmonary edema due to an elevated pulmonary capillary wedge pressure in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, particularly renovascular hypertension, and severe renal disease. Noncardiogenic pulmonary edema is a distinct clinical syndrome associated with diffuse filling of the alveolar spaces in the absence of elevated pulmonary capillary wedge pressure [ 1] . This disorder is discussed elsewhere [1] . (See "Noncardiogenic pulmonary edema"). General issues related to the management of acute decompensated heart failure will be reviewed here. The pathophysiology and evaluation of patients with acute decompensated HF and of the clinically stable patient with suspected heart failure (HF) is presented separately. ( See "Pathophysiology and evaluation of acute decompensated heart failure" and see "Clinical manifestations and evaluation of the patient with suspected heart failure"). GENERAL APPROACH The following recommendations are generally in agreement with those published in 2000 by the International Liaison Committee on Resuscitation (ILCOR) ( show algorithm 1) [2] . Similar recommendations for the management of pulmonary congestion in the setting of an acute myocardial infarction were published in 2004 by the American College of Cardiology and the American Heart Association (ACC/AHA) [3] . Acute versus chronic HF It is important to distinguish the management of acute decompensated HF from that of chronic HF. The treatment of chronic HF, particularly when due to systolic dysfunction, is built around therapies that have been shown to reduce long-term mortality (eg, ACE inhibitors and beta blockers). In contrast, the goals of the initial management of acute decompensated HF are hemodynamic stabilization, support of oxygenation and ventilation, and symptom relief [ 4] . Some of the cornerstones of chronic HF therapy should be avoided or used with caution in acute decompensated HF (eg, beta blockers), particularly during the period of initial stabilization. Later in the patient's course, such
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therapies may be initiated or reinstituted. Systolic versus diastolic dysfunction Among patients with chronic HF, long-term management strategies differ according to whether or not the patient has significant systolic dysfunction. ( See "Overview of the therapy of heart failure due to systolic dysfunction" and see "Treatment and prognosis of diastolic heart failure"). In the acute setting, however, some of the initial therapies are similar in systolic and diastolic HF, including the following: Supplemental oxygen and assisted ventilation, if necessary Diuresis Morphine sulfate in selected patients Vasodilator therapy in selected patients Some components of the initial treatment strategy are approached differently in patients with systolic versus diastolic HF. As an example, among patients with systolic dysfunction, some medications should be avoided or used with caution in the acute setting (eg, ACE inhibitors and beta blockers). In contrast, for patients with primarily diastolic dysfunction, treatment of hypertension and tachycardia are particularly important; as a result, ACE inhibitors and beta blockers may be useful. Inpatient monitoring Patients who are admitted to the hospital for the management of acute decompensated HF are at risk for hemodynamic instability and arrhythmias. Thus, close monitoring is necessary. Optimal standards are not defined and monitoring must be individualized, but should include the following: Regular assessment of heart rate, blood pressure and oxygen saturation. Telemetry is usually continued for at least 24 to 48 hours. This may be discontinued once the patients's hemodynamics, medication regimen, and electrolytes are stable. Monitoring volume status Effective fluid removal should be carefully monitored and clearly documented. Decompensated HF is associated with an exceptionally high rate of readmissions, which is due in part to inadequate fluid removal during the initial admission [ 5,6] . Fluid intake and output Determination of effective diuretic dosing should be confirmed by demonstration of a negative fluid balance. Daily weight Accurate intake and output assessments are often difficult to maintain. Daily assessment of patient weight may be the most effective method for documenting effective diuresis [7] . For accurate comparisons, daily measurements should use the same scale and should be performed at the same time each day, usually in the morning, prior to eating and after voiding. Swan-Ganz catheter A Swan-Ganz pulmonary artery catheter is not usually necessary for the evaluation or management of decompensated HF, but may be appropriate in selected cases. (See "Pathophysiology and evaluation of acute decompensated heart failure" section on Swan-Ganz catheter) Echocardiography Filling pressures may be estimated noninvasively by tissue doppler echocardiography. (See "Tissue Doppler echocardiography" section on Estimation of LV filling pressures). COMPONENTS OF THERAPY
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Supplemental oxygen and assisted ventilation Patients with acute decompensated HF should receive oxygen supplementation and, if necessary, assisted ventilation. We suggest considering initial therapies in the following order: Non-rebreather face mask delivering 100 percent oxygen. If respiratory distress and/or hypoxia persist, we suggest noninvasive positive pressure ventilation (NPPV) as the preferred initial modality of assisted ventilation as long as the patient does not have a contraindication (show table 1). This approach is supported by a meta-analysis of 15 clinical trials, which demonstrated both lower mortality and a reduced need for intubation with NPPV compared to conventional therapy [ 8] . Although the level of evidence is higher for continuous positive airway pressure (CPAP), there are no significant differences in clinical outcome between CPAP and noninvasive pressure support ventilation (NIPSV). (See "Noninvasive positive pressure ventilation in acute respiratory failure" , section on Cardiogenic pulmonary edema). Patients with respiratory failure who fail NPPV, do not tolerate or have contraindications to NPPV (show table 1) should be intubated for conventional mechanical ventilation. In such patients, positive end-expiratory pressure is often useful for improving oxygenation. ( See "Conventional mechanical ventilation" , and see "Positive end-expiratory pressure (PEEP)", section on Cardiac disease). Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 percent. Diuretics Patients with acute decompensated HF are usually volume overloaded. Even in the less common situation where cardiogenic pulmonary edema develops in a patient without significant volume overload (eg, with acute aortic or mitral valvular insufficiency), fluid removal with intravenous diuretics can relieve symptoms and improve oxygenation. (See "Use of diuretics in heart failure") Thus, patients with acute decompensated heart failure, regardless of the etiology, should be treated with intravenous diuretics as part of their initial therapy [ 7,9] . Rare exceptions include patients with severe hypotension or cardiogenic shock. In such cases, the underlying cause for hemodynamic instability should be sought and the patient may require mechanical ventilatory and hemodynamic support. ( See "Conventional mechanical ventilation" and see "Mechanical cardiac assistance" below). Most patients will also require additional diuresis through the course of their care, although volume status should be continually reassessed. Diuretic dosing Common initial intravenous doses of loop diuretics in patients with normal renal function include the following: Furosemide 40 mg intravenously Bumetanide 1 mg intravenously Torsemide 10 to 20 mg intravenously Diuretic dosing should be individualized. Patients who are treated with loop diuretics chronically are usually treated with a higher dose in the acute setting; diuresis may be achieved with an intravenous dose that is at least equivalent in milligrams to their maintenance dose (eg, 80 mg of intravenous furosemide for a patient who takes 80 mg orally daily). Peak diuresis typically occurs 30 minutes after administration. For patients who do not respond adequately to initial loop diuretic therapy, options include:
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Doubling the dose until a diuresis ensues or a maximum recommended dose is reached. ( See "Optimal dosage and side effects of loop diuretics" , section on Maximum effective dose). Addition of a thiazide diuretic to potentiate the effects of the loop diuretic. Chlorothiazide is the only thiazide in that can be given intravenously; however, its availability may be limited and a rapidly absorbed oral preparation, such as hydrochlorothiazide, is an alternative. (See "Treatment of refractory edema", section on Enhanced tubular sodium reabsorption). A continuous intravenous infusion of the loop diuretic. A Cochrane review of eight trials in 254 patients found that urine output was significantly greater with a continuous infusion, although the difference was modest (mean difference 271 mL per 24 hours) [10] . Less tinnitus and hearing loss occurred with continuous infusion. The review concluded that the available data were insufficient to confidently assess the relative merits of the two approaches. Hemodynamic effects By reducing intravascular volume, diuresis will eventually lower pulmonary capillary wedge pressures, and may reduce systemic pressures as well. However, furosemide and possibly other loop diuretics also have an initial morphine-like effect in acute pulmonary edema, causing venodilation that can decrease pulmonary congestion prior to the onset of diuresis [ 11] . This effect appears to be mediated by enhanced release of prostaglandins. (See "Use of diuretics in heart failure" Section on Morphine-like effect in acute pulmonary edema). Morphine sulfate Morphine sulfate may be administered intravenously at an initial dose of 2 to 4 mg over a three minute period and can be repeated if necessary at 5 to 15 minute intervals. Morphine reduces patient anxiety and decreases the work of breathing. These effects diminish central sympathetic outflow, leading to arteriolar and venous dilatation with a resultant fall in cardiac filling pressures [ 12,13] . It should be used with caution in patients with impending airway compromise. Vasodilator therapy Patients with acute cardiogenic pulmonary edema are often treated with vasodilators, usually nitrates, in an attempt to reduce preload and pulmonary capillary wedge pressure. Nitrates Nitrates are the most commonly used vasodilators. Options for nitrate therapy include: Transdermal nitroglycerin Topical nitroglycerin is often given as part of initial therapy. This preparation works within 30 minutes and has a peak effect at about two hours [ 14,15] . Intravenous nitroglycerin Patients who do not adequately respond to oxygen, loop diuretics, and morphine are typically treated with intravenous nitroglycerin (initial dose 5 g/min). Similar benefits have been described with high-dose intravenous isosorbide dinitrate, where available [16,17] . However, if hypotension occurs, the longer half-life of isosorbide dinitrate compared to intravenous nitroglycerin (four hours versus three to five minutes) is a major disadvantage. Intravenous nitroprusside The need for pronounced afterload reduction is an indication for nitroprusside (initial dose 0.25 to 0.5 g/kg per minute) as opposed to nitroglycerin [ 18] . Examples of such settings include hypertensive emergency, acute aortic regurgitation, acute mitral regurgitation, or acute ventricular septal defect. ( See "Drug treatment of hypertensive emergencies", section on Nitroprusside). The major limitation to the use of nitroprusside is its metabolism to cyanide. The accumulation of nitroprusside metabolites can lead to the development of cyanide, or rarely thiocyanate, toxicity which may be fatal. It also requires close and continuous blood pressure monitoring, and may cause reflex tachycardia. Thus, the use of nitroprusside is limited to selected patients, usually for durations of less than 24 to 48 hours. Nesiritide Although plasma brain natriuretic peptide (BNP) levels are increased in patients with HF,
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such patients typically are sodium avid and have increased systemic vascular resistance, primarily due to high levels of vasoconstrictors, such as angiotensin II and norepinephrine. Exogenous administration of recombinant human BNP (nesiritide) to patients with HF further increases plasma BNP concentrations and produces arterial and venous vasodilation. Initial clinical trials have demonstrated the efficacy of nesiritide in improving hemodynamic parameters and symptoms of heart failure. However, subsequent studies raised concerns about a potential adverse impact on mortality rate and a potential risk of worsening renal function. The possible role of nesiritide in the management of acute decompensated HF is presented separately. (See "Nesiritide in the treatment of acute decompensated heart failure"). ACE inhibitors and ARBs For patients with HF due to systolic dysfunction, ACE inhibitors and angiotensin receptor blockers (ARBs) are a mainstay of chronic therapy. ( See "Angiotensin II receptor blockers in heart failure due to systolic dysfunction: Therapeutic use" ). Among patients with acute decompensated HF, the role of angiotensin inhibition depends upon whether the patient is already receiving such therapy. Continued therapy For the majority of patients who have been treated with chronic ACE inhibitor or ARB therapy, maintenance oral therapy can be cautiously continued during an episode of decompensated HF. However, these medications should be decreased or discontinued in the following settings: Hypotension Acute renal failure Hyperkalemia With regard to hypotension, two additional points should be considered: Some patients with chronic HF and severe left ventricular systolic dysfunction tolerate relatively low blood pressures (eg, systolic blood pressure 90 to 100 mmHg). Such patients often tolerate chronic ACE inhibitor or ARB therapy and may tolerate these drugs in the acute setting as well. Patients with acute pulmonary edema may initially be hypertensive due to high catecholamine levels during the early period of distress. With initial therapy, blood pressure may fall rapidly and patients may become relatively hypotensive, particularly if they are aggressively diuresed. Thus, long-acting drugs, such as ACE inhibitors and ARBs, should be administered with caution the first few hours of hospitalization. Initiation of ACE inhibitors and ARBs There is little evidence regarding the safety and efficacy of initiating new ACE inhibitor or ARB therapy in the early phase of therapy of acute decompensated HF (ie, the first 12 to 24 hours) [4] . Major concerns with early therapy include: Patients with acute HF may develop hypotension and/or worsening renal function during initial therapy. Determining the pathogenesis of such complications becomes more difficult if an ACE inhibitor or ARB has also been given. The intravenous ACE inhibitor enalaprilat may have deleterious effects in patients with an acute myocardial infarction, especially when complicated by HF or aggressive diuresis [ 3,19] . Thus, intravenous enalaprilat should be avoided in patients with an acute infarction and probably in those
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with other causes of HF [3,4] . Early initiation of oral therapy is also not recommended, and should be avoided in patients at high risk for hypotension (eg, low baseline blood pressure or hyponatremia, which is a marker for increased activation of the renin-angiotensin system and therefore increased dependence upon angiotensin II for blood pressure maintenance). In addition, the aggressive diuretic therapy typically given for acute pulmonary edema may increase the sensitivity to ACE inhibition or angiotensin blockade. (See "Pathophysiology of heart failure: Neurohumoral adaptations" and see "Hyponatremia in heart failure"). Once the patient is stable, chronic oral therapy can be started. Beta blockers Beta blockers reduce mortality when used in the long-term management of such patients, but must be used extremely cautiously in patients with systolic dysfunction because of the potential to worsen acute HF due to systolic dysfunction. ( See "Use of beta blockers in heart failure due to systolic dysfunction"). Thus, in patients with systolic dysfunction and acute decompensated HF, we approach the use of beta blockers in the following manner: For patients on chronic beta blocker therapy, if the degree of decompensation is moderate-to-severe or if the patient is hypotensive, we withhold or decrease the dose of beta blocker during the early phase of treatment. In patients requiring inotropic support or those with severe volume overload, we withhold therapy. For patients who are not treated with beta blocker therapy chronically, we do not initiate a beta blocker in the early management of acute HF. However, the initiation of therapy prior to hospital discharge improves long-term beta blocker compliance without an increase in side effects or drug discontinuation. Prior to initiation of therapy, the patient should have no or minimal evidence of fluid retention and should not have required recent intravenous inotropic therapy. (See "Use of beta blockers in heart failure due to systolic dysfunction" , section on initiation of therapy). Inotropic agents Patients with systolic dysfunction who remain in pulmonary edema despite the above treatment, especially those with mild to moderate hypotension (systolic BP 80 to 100 mmHg), may benefit from intravenous (IV) inotropic support to improve cardiac performance and systemic perfusion. This is usually achieved by beta-agonist therapy ( dobutamine), a phosphodiesterase inhibitor (milrinone), or both [20,21] . These drugs can increase ventricular arrhythmias compared to the vasodilators [ 22] . (See "Inotropic agents in heart failure due to systolic dysfunction" and see "Use of vasopressors and inotropes"). The 2000 ILCOR guidelines on resuscitation and the 2004 ACC/AHA guidelines for the management of acute MI both suggested the selection of specific inotropes based upon the patients' blood pressure and whether or not there are signs and symptoms of shock (show algorithm 1) [2,3] . Inotropes that are commonly used in patients with HF include the following: Dobutamine Dobutamine acts primarily on beta-1 adrenergic receptors, with minimal effects on beta-2 and alpha-1 receptors. The hemodynamic effects of dobutamine include an increase in stroke volume, stroke work, and cardiac output, and modest decreases in systemic vascular resistance and pulmonary capillary wedge pressure [ 23,24] . Dobutamine is suggested in patients with hypotension who do not have clinical evidence of shock [ 2,3] . It should be started at 2.5 g/kg per min and, if tolerated, can be gradually increased to 15 g/kg per min. Dopamine The effects of dopamine are dose-dependent. At low doses of 1 to 3 g/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric
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artery beds. At 3 to 10 g/kg per min, dopamine also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate. Dopamine is suggested in patients with hypotension who also have clinical evidence of shock [2,3] . However, at medium-to-high doses, dopamine also stimulates alpha-adrenergic receptors, producing arterial and venous constriction which may further compromise systolic function and filling pressures. Therefore, dopamine should be reserved for hypotensive patients in whom an increase in arterial pressure is considered a priority. Milrinone Milrinone is a phosphodiesterase inhibitor that increases myocardial inotropy by inhibiting degradation of cyclic AMP. Other direct effects of milrinone include reducing systemic vascular resistance (via inhibition of peripheral phosphodiesterase) and improving left ventricular diastolic compliance [ 25,26] . All of these changes lead to an increase in cardiac index and decrease in left ventricular afterload and filling pressures. Patients should receive a loading dose of 50 g/kg over 10 minutes, followed by a maintenance dose of 0.375 to a maximum of 0.750 g/kg per min. Dose adjustment is required in the presence of renal insufficiency. ADDITIONAL CONSIDERATIONS In addition to the above treatments, several additional options and considerations may be relevant to selected patients. Arrhythmia management Both supraventricular and ventricular arrhythmias can occur in association with pulmonary edema. Atrial fibrillation Atrial fibrillation (AF) is a common arrhythmia, particularly in patients with underlying heart disease. Among patients with both HF and AF, there are several possible relationships: Acute HF can precipitate AF due to increases in left atrial pressure and wall stress. AF can cause acute HF, particularly if the ventricular response is rapid. ( See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm" ). AF may be chronic and not directly related to the acute HF decompensation. It is usually difficult to determine whether AF is the cause or result of acute HF. A reliable history of palpitations that clearly precede the decompensation suggests but does not prove that AF was the cause of the pulmonary edema. The treatment of AF depends upon whether or not it is associated with significant hemodynamic instability and whether or not it is believed to be the precipitant of HF decompensation. Rate control is often the preferred initial strategy for the following reasons: Because acute HF can precipitate AF, cardioversion prior to the resolution of acute HF will often be followed by early recurrence of AF. AF is often a chronic condition that is not contributing to the acute decompensation. However, if a rate control strategy is selected, the negative inotropic effects of beta blockers and nondihydropyridine calcium channel blockers can be problematic in patients with systolic dysfunction. For this reason, short-acting IV formulations of such drugs (eg, esmolol or diltiazem) are often used. In addition, digoxin is also potentially useful in this setting. In some patients with AF and acute HF, effective treatment of pulmonary edema results in slowing of the ventricular rate or spontaneous reversion of the arrhythmia. If AF persists, it is treated in the same
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fashion as AF in other situations. ( See "Overview of the presentation and management of atrial fibrillation"). Restoration of sinus rhythm should be considered in the following settings. ( See "Restoration of sinus rhythm in atrial fibrillation: Recommendations" , section on AF and unstable hemodynamics): If AF is associated with hypotension or evidence of cardiogenic shock. If AF is clearly the cause for pulmonary edema. If the response to effective therapy of pulmonary edema is slow or suboptimal. Patients should be begun on heparin prior to cardioversion, if possible. (See "Anticoagulation prior to and after restoration of sinus rhythm in atrial fibrillation" ). Ventricular arrhythmia Ventricular tachycardia during pulmonary edema is usually life-threatening. As a result, prompt electrical cardioversion or defibrillation is required. If the arrhythmia recurs after reversion, antiarrhythmic therapy with amiodarone or lidocaine may be effective. (See "Clinical features and treatment of ventricular arrhythmias during acute myocardial infarction" and see "Overview of the acute management of tachyarrhythmias", section on Monomorphic ventricular tachycardia). The development of ventricular fibrillation mandates prompt resuscitation. Mechanical cardiac assistance Patients with cardiogenic pulmonary edema who are also in cardiogenic shock should be considered candidates for mechanical circulatory support. These patients usually have a cardiac index less than 2.0 L/min per m2, a systolic arterial pressure below 90 mmHg, and a pulmonary capillary wedge pressure above 18 mmHg, despite adequate pharmacologic therapy. The two major mechanical modalities used in this setting are intraaortic balloon counterpulsation and an internally implanted left ventricular assist device. ( See "Intraaortic balloon pump counterpulsation" and see "Circulatory assist devices: Cardiopulmonary assist device and short-term left ventricular assist devices"). A novel form of mechanical assistance involves continuous aortic flow augmentation (CAFA) [ 27] . This system does not increase cardiac output directly, but may stimulate favorable hemodynamic changes (primarily through cardiac unloading). Details of this investigational approach are discussed separately. (See "Possibly effective emerging therapies for heart failure", section on Continuous aortic flow augmentation). Ultrafiltration Ultrafiltration is an effective method of fluid removal with advantages that include adjustable fluid removal volumes and rates, no effect on serum electrolytes, and decreased neurohormonal activity. (See "Continuous renal replacement therapies: Overview"). Patients with acute decompensated HF accompanied by renal insufficiency or diuretic resistance may benefit from ultrafiltration. Most studies have used a peripherally inserted ultrafiltration device that does not require central access, specialized nursing, or ICU admission [ 28-30] . In the RAPID-CHF trial, 40 patients with acute decompensated HF and renal insufficiency (serum creatinine 1.5 mg/dL [133 mol/L]) and/or anticipated diuretic resistance (high daily oral diuretic doses) were randomly assigned to receive usual care with or without ultrafiltration [ 28] . Ultrafiltration was associated with significant increases in fluid removal after 24 hours (4650 versus 2838 mL without ultrafiltration) and weight loss (2.5 versus 1.9 kg). In the UNLOAD trial, 200 patients hospitalized for acute decompensated HF were randomly assigned to
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ultrafiltration or to standard care including intravenous diuretics during the admission [ 29] . Unlike earlier studies, renal dysfunction and/or anticipated diuretic resistance were not entry criteria. Thus, this study included a less selected group of HF patients. The following findings were noted: At 48 hours, patients assigned to ultrafiltration had a significantly greater fluid loss (4.6 versus 3.3 liters with standard care). This difference may in part reflect the relatively modest level of diuretic therapy used in the standard care arm. At 90 days, patients assigned to ultrafiltration had significantly fewer HF rehospitalizations than patients assigned to standard care (0.22 versus 0.46 admissions per patient) and fewer unscheduled clinic visits (21 versus 44 percent with standard care). The rates of adverse events were similar in the two groups, although there was a higher incidence of bleeding in the standard care arm. While these data suggest that ultrafiltration is an effective method for fluid volume removal, it is not clear whether it provides an advantage in patients who respond adequately to standard intravenous diuretics or those who require more aggressive diuresis. In addition, given the relatively small body of data, it is not possible to assess the safety of ultrafiltration. At present, we reserve ultrafiltration for patients who do not achieve an adequate response to an aggressive diuretic regimen SUMMARY AND RECOMMENDATIONS The following summary and recommendations apply to the management of patients with acute decompensated HF. They are generally in agreement with those published in 2000 by the International Liaison Committee on Resuscitation (ILCOR) ( show algorithm 1) [2] . In the acute setting, management of patients with both systolic or diastolic dysfunction is similar (See "Systolic versus diastolic dysfunction" above ). Initial therapy includes the following: Supplemental oxygen and assisted ventilation if necessary Diuresis, usually with an IV loop diuretic In addition, most patients should also receive: Morphine sulfate Vasodilator therapy (eg, topical nitroglycerin in patients with mild or moderate symptoms) In selected patients with severe or refractory symptoms, the following additional therapies can be used: Intravenous vasodilators (eg, IV nitroglycerine or nesiritide). Intravenous positive inotropic agents Mechanical cardiac assistance Ultrafiltration Oxygen and ventilatory support Patients with acute decompensated HF and a decreased oxygen saturation should be treated with supplemental oxygen. For patients with significant hypoxia or respiratory distress, therapy is usually initiated with 100 percent oxygen via a nonrebreather facemask, and later titrated to patient comfort and an oxygen saturation of at least 90 percent.
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For patients with acute decompensated HF and respiratory failure, we recommend a trial of noninvasive positive pressure ventilation (NPPV) if emergent intubation is not indicated, no contraindications to NPPV exist (show table 1), and personnel with experience in NPPV are available ( Grade 1A). (See "Supplemental oxygen and assisted ventilation" above , and see "Noninvasive positive pressure ventilation in acute respiratory failure" , section on cardiogenic pulmonary edema). Patients with respiratory failure due to acute decompensated HF who fail NPPV, do not tolerate NPPV, or have contraindications to NPPV (show table 1), require endotracheal intubation for conventional mechanical ventilation. ( See "Conventional mechanical ventilation" ). Fluid removal Patients with acute decompensated HF and pulmonary edema have symptomatic relief and improved oxygenation with fluid removal. In patients with acute decompensated HF and fluid overload, we recommend that initial therapy include an intravenous loop diuretic ( Grade 1B). (See "Diuretics" above). Dosing is individualized, determined largely by the patient's renal function and prior diuretic exposure. (See "Diuretic dosing" above). Bolus dosing with intravenous loop diuretics achieves adequate diuresis in most patients. For patients who do not have adequate fluid removal with this approach, options include: Continuous infusion of loop diuretic. Addition of a thiazide diuretic (preferably intravenous chlorothiazide if available) In addition, many HF patients are treated with a thiazide diuretic and/or an aldosterone antagonist as part of their chronic medical regimen. In most patients, these medications can be continued during an episode of acute decompensation, with appropriate monitoring of blood pressure, renal function, and electrolytes. Ultrafiltration is an option for patients refractory to diuretic therapy. ( See "Ultrafiltration" above). Morphine Although there is no evidence that morphine sulfate affects outcomes in patients with decompensated HF, morphine reduces patient anxiety and decreases the work of breathing. In patients with acute decompensated HF, we suggest morphine sulfate be administered intravenously at an initial dose of 2 to 4 mg over a three minute period and can be repeated if necessary at 5 to 15 minute intervals ( Grade 2C). (See "Morphine sulfate" above). Vasodilators Vasodilators, including nesiritide, nitroglycerin, and nitroprusside, can reduce filling pressures, improve symptoms, and facilitate diuresis. ( See "Vasodilator therapy" above). In patients with acute decompensated HF who are not hypotensive, we suggest the use of a vasodilator ( Grade 2C). (See "Vasodilator therapy" above). When using vasodilators in patients with acute decompensated HF, we favor the following approach: - Patients who are not in respiratory distress can usually be treated with topical nitroglycerin. - Patients with more severe HF, particularly if more precise dosing titration is desired should be treated with intravenous nitroglycerin. - In selected cases when there is a need for significant afterload reduction (eg, hypertensive emergency, acute aortic or mitral regurgitation), we use nitroprusside, although the risk of cyanide or thiocyanate toxicity limit its use. ( See "Drug treatment of hypertensive emergencies", section on
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Nitroprusside). Inotropes Patients with acute decompensated HF and systolic dysfunction who are hypotensive or who remain in pulmonary edema despite oxygen, diuresis, and, if tolerated, vasodilators, may benefit from intravenous inotropic support. (See "Inotropic agents" above, and see "Inotropic agents in heart failure due to systolic dysfunction"). ACE inhibitors/ARBs and beta blockers ACE inhibitors, ARBs, and beta blockers require special consideration in patients with decompensated heart failure. The approach to their use depends upon whether the patient has primarily systolic or diastolic dysfunction. ( See "Systolic versus diastolic dysfunction" above). Systolic dysfunction In patients with chronic HF due to systolic dysfunction the long-term use ACE inhibitors/ARBs and beta blockers reduces mortality, but there are short-term risks to the use of these medications in the setting of acute HF. ( See "ACE inhibitors and ARBs" above, and see "Beta blockers" above). We approach the use of these medications in this setting in the following manner: For patients who are not already taking an ACE inhibitor or ARB, we suggest that they not be initiated at the time of presentation with an episode of acute decompensated HF ( Grade 2C). An ACE inhibitor or ARB can usually be started within 24 to 48 hours, once the patient is hemodynamically stable. For patients who are not already taking a beta blocker, we suggest that they not be initiated at the time of presentation with an episode of acute decompensated HF ( Grade 2B). Beta blockers are generally started later than ACE inhibitors or ARBs, when the patient is euvolemic, usually shortly before discharge. A detailed discussion of the initiation of these medications, including dosing and sequence of initiation, is presented separately. (See "Overview of the therapy of heart failure due to systolic dysfunction", section on Pharmacologic therapy). For patients who are already taking an ACE inhibitor or ARB, we suggest that maintenance oral therapy be cautiously continued ( Grade 2C). However, the dose should be decreased or the drug discontinued if hypotension, acute renal failure, or hyperkalemia is present. ( See "Continued therapy" above). For patients who are already taking a beta blocker, management depends upon the clinical situation. Treatment may be maintained on the outpatient regimen, or the dose may be reduced or withheld. This decision is based upon the severity of the HF decompensation and the presence and degree of hypotension. (See "Beta blockers" above). Diastolic dysfunction As noted above, in the acute setting, patients with decompensated HF are treated similarly whether they have primarily systolic or diastolic dysfunction. In the chronic management of HF, however, patients with primarily diastolic dysfunction, are approached differently. In such patients, the long-term use of ACE inhibitors/ARBs and beta blockers does not have the same benefit as in patients with HF due to systolic dysfunction. However, the short term risks of beta blockers are also less concerning. In patients with diastolic dysfunction treatment of hypertension and tachycardia are particularly important, and the early use of beta blockers may be useful. ( See "Treatment and prognosis of diastolic heart failure").
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REFERENCES
1. 2. Ware, LB, Matthay, MA. Clinical practice. Acute pulmonary edema. N Engl J Med 2005; 353:2788. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 7: Section 1: Era of reperfusion (Acute Myocardial Infarction). The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 102:I172. Antman, EM, Anbe, DT, Armstrong, PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Available at: www.acc.org/qualityandscience/ clinical/statements.htm (accessed August 24, 2006). Gheorghiade, M, Zannad, F, Sopko, G, et al. Acute heart failure syndromes: current state and framework for future research. Circulation 2005; 112:3958. Ashton, CM, Kuykendall, DH, Johnson, ML, et al. The association between the quality of inpatient care and early readmission. Ann Intern Med 1995; 122:415. Konstam, MA. Relating quality of care to clinical outcomes in heart failure: in search of the missing link. J Card Fail 2001; 7:299. Hunt, SA, Abraham, WT, Chin, MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation 2005; 112:e154. Masip, J, Roque, M, Sanchez, B, et al. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta-analysis. JAMA 2005; 294:3124. Stampfer, M, Epstein, SE, Beiser, GD, Braunwald, E. Hemodynamic effects of diuresis at rest and during intense upright exercise in patients with impairedcardiac function. Circulation 1968; 37:900. Salvador, D, Rey, N, Ramos, G, Punzalan, F. Continuous infusion versus bolus injection of loop diuretics in congestive heart failure. Cochrane Database Syst Rev 2004; 1:CD003178. Dikshit, K, Vyden, JK, Forrester, JS, et al. Renal and extrarenal hemodynamic effects of furosemide in congestive heart failure after acute myocardial infarction. N Engl J Med 1973; 288:1087. Hsu, HO, Hickey, RF, Forbes, AR, et al. Morphine decreases peripheral vascular resistance and increases capacitance in man. Anesthesiology 1979; 50:98. Pur-Shahriari, AA, Mills, RA, Hoppin, FG Jr, Dexter, L. Comparison of chronic and acute effects of morphine sulfate on cardiovascular function. Am J Cardiol 1967; 20:654. Melandri, G, Semprini, F, Branzi, A, Magnani, B. Comparative haemodynamic effects of transdermal vs intravenous nitroglycerin in acute myocardial infarction with elevated pulmonary artery wedge pressure. Eur Heart J 1990; 11:649. Bolognese, L, Sarasso, G, Rognoni, G, et al. Sustained beneficial hemodynamic effects of low transdermal nitroglycerin doses compared with placebo in patients with congestive heart failure. Clin Cardiol 1988; 11:79. Cotter, G, Metzkor, E, Faigenberg, Z, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998; 351:389. Sharon, A, Shpirer, I, Kaluski, E, et al. High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000; 36:832. Palmer, RF, Lasseter, KC. Drug therapy. Sodium nitroprusside. N Engl J Med 1975; 292:294. Sigurdsson, A, Swedberg, K. Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction. Eur Heart J 1994; 15 Suppl B:14.
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4. 5. 6. 7.
8. 9.
10. 11.
12. 13. 14.
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18. 19.
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20.
Gage, J, Rutman, H, Lucido, D, et al. Additive effects of dobutamine and amrinone on myocardial contractility and ventricular performance in patients with severe heart failure. Circulation 1986; 74:367. Mager, G, Klocke, RK, Kux, A, et al. Phosphodiesterase III inhibition or adrenoreceptor stimulation: Milrinone as an alternative to dobutamine in the treatment of severe heart failure. Am Heart J 1991; 121:1974. Burger, AJ, Elkayam, U, Neibaur, MT, et al. Comparison of the occurrence of ventricular arrhythmias in patients with acutely decompensated congestive heart failure receiving dobutamine versus nesiritide therapy. Am J Cardiol 2001; 88:35. Liang, CS, Sherman, LG, Doherty, JU, et al. Sustained improvement of cardiac function in patients with congestive heart failure after short-term infusion of dobutamine. Circulation 1984; 69:113. Unverferth, DV, Magorien, RD, Altschuld, R, et al. The hemodynamic and metabolic advantages gained by a three-day infusion of dobutamine in patients with congestive cardiomyopathy. Am Heart J 1980;100:622. Simonton, CA, Chatterjee, K, Cody, RJ, et al. Milrinone in congestive heart failure: Acute and chronic hemodynamics and clinical evaluation. J Am Coll Cardiol 1985; 6:453. Anderson, JL. Hemodynamic and clinical benefits with intravenous milrinone in severe chronic heart failure: Results of a multicenter study in the United States. Am Heart J 1991; 121:1956. Konstam, MA, Czerska, B, Bohm, M, et al. Continuous aortic flow augmentation: a pilot study of hemodynamic and renal responses to a novel percutaneous intervention in decompensated heart failure. Circulation 2005; 112:3107. Bart, BA, Boyle, A, Bank, AJ, et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: the Relief for Acutely Fluid-Overloaded Patients With Decompensated Congestive Heart Failure (RAPID-CHF) trial. J Am Coll Cardiol 2005; 46:2043. Costanzo, MR, Guglin, ME, Saltzberg, MT, et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol 2007; 49:675. Costanzo, MR, Saltzberg, M, O'Sullivan, J, Sobotka, P. Early ultrafiltration in patients with decompensated heart failure and diuretic resistance. J Am Coll Cardiol 2005; 46:2047.
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22.
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25. 26. 27.
28.
29. 30.
GRAPHICS
The acute pulmonary edema, hypotension, and shock algorithm
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Adapted from Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2000; 102:I-189.
Contraindications to NPPV
Cardiac or respiratory arrest Nonrespiratory organ failure
Severe encephalopathy (eg, GCS <10) Severe upper gastrointestinal bleeding Hemodynamic instability or unstable cardiac arrhythmia
Facial or neurological surgery, trauma, or deformity Upper airway obstruction Inability to cooperate/protect airway Inability to clear secretions High risk for aspiration
Reproduced with permission from International Concensus Conferences in Intensive Care Medicine:Noninvasive positive pressure ventilation in acute respiratory failure.Am J Respir Crit Care Med 2001; 163:288. Copyright 2001 American Thoracic Society.
Grade 1A recommendation
A Grade 1A recommendation is a strong recommendation, and applies to most patients in most circumstances without reservation. Clinicians should follow a strong recommendation unless a clear and compelling rationale for an alternative approach is present.
Explanation:
A Grade 1 recommendation is a strong recommendation. It means that we believe that if you follow the recommendation, you will be doing more good than harm for most, if not all of your patients. Grade A means that the best estimates of the critical benefits and risks come from consistent data from well-performed, randomized, controlled trials or overwhelming data of some other form (eg, well-executed observational studies with very large treatment effects). Further research is unlikely to have an impact on our confidence in the estimates of benefit and risk.
Recommendation grades 1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients 2. Weak recommendation: Benefits and risks closely balanced and/or uncertain Evidence grades A. High-quality evidence: Consistent evidence from randomized trials, or overwhelming evidence of some other form B. Moderate-quality evidence: Evidence from randomized trials with important limitations, or very strong evidence of some other form C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws For a complete description of our grading system, please see the UpToDate editorial policy that can be found by clicking on Help, and
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Grade 1B recommendation
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Explanation:
A Grade 1 recommendation is a strong recommendation. It means that we believe that if you follow the recommendation, you will be doing more good than harm for most, if not all of your patients. Grade B means that the best estimates of the critical benefits and risks come from randomized, controlled trials with important limitations (eg, inconsistent results, methodologic flaws, imprecise results, extrapolation from a different population or setting) or very strong evidence of some other form. Further research (if performed) is likely to have an impact on our confidence in the estimates of benefit and risk, and may change the estimates.
Recommendation grades 1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients 2. Weak recommendation: Benefits and risks closely balanced and/or uncertain Evidence grades A. High-quality evidence: Consistent evidence from randomized trials, or overwhelming evidence of some other form B. Moderate-quality evidence: Evidence from randomized trials with important limitations, or very strong evidence of some other form C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws For a complete description of our grading system, please see the UpToDate editorial policy that can be found by clicking on Help, and then About UpToDate
Grade 2C recommendation
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Recommendation grades 1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients 2. Weak recommendation: Benefits and risks closely balanced and/or uncertain Evidence grades A. High-quality evidence: Consistent evidence from randomized trials, or overwhelming evidence of some other form B. Moderate-quality evidence: Evidence from randomized trials with important limitations, or very strong evidence of some other form C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws For a complete description of our grading system, please see the UpToDate editorial policy that can be found by clicking on Help, and then About UpToDate.
Grade 2B recommendation
A Grade 2B recommendation is a weak recommendation; alternative approaches may be better for some patients under some circumstances.
Explanation:
A Grade 2 recommendation is a weak recommendation. It means "this is our suggestion, but you may want to think about it." It is unlikely that you should follow the suggested approach in all your patients, and you might reasonably choose an alternative approach. For Grade 2 recommendations, benefits and risks may be finely balanced, or the benefits and risks may be uncertain. In deciding whether to follow a Grade 2 recommendation in an individual patient, you may want to think about your patient's values and preferences or about your patient's risk aversion.
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Grade B means that the best estimates of the critical benefits and risks come from randomized, controlled trials with important limitations (eg, inconsistent results, methodologic flaws, imprecise results, extrapolation from a different population or setting) or very strong evidence of some other form. Further research (if performed) is likely to have an impact on our confidence in the estimates of benefit and risk, and may change the estimates.
Recommendation grades 1. Strong recommendation: Benefits clearly outweigh the risks and burdens (or vice versa) for most, if not all, patients 2. Weak recommendation: Benefits and risks closely balanced and/or uncertain Evidence grades A. High-quality evidence: Consistent evidence from randomized trials, or overwhelming evidence of some other form B. Moderate-quality evidence: Evidence from randomized trials with important limitations, or very strong evidence of some other form C. Low-quality evidence: Evidence from observational studies, unsystematic clinical observations, or from randomized trials with serious flaws For a complete description of our grading system, please see the UpToDate editorial policy that can be found by clicking on Help, and then About UpToDate.
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