MANAGEMENT OF ACUTE HEART FAILURE PATIENTS PHASES OF CARE Phase I: Urgent/Emergent Care Phase II: Hospital Care Phase III: Predischarge Planning Phase IV: Postdischarge Management
PHASE IURGENT/EMERGENT CARE The initial goals in the management of a patient presenting with AHF are 1) to expeditiously establish the diagnosis 2) treat life-threatening abnormalities 3) Provide rapid symptom relief 4) Identify the cause and precipitating triggers for the episode. OXYGEN THERAPY In patients with severe hypoxemia (oxygen saturation [SaO2] <90%), oxygen
administration is recommended. Although oxygen saturation on presentation is inversely related to short-term mortality, inhaled oxygen (FiO2 0.4) may cause detrimental hemodynamic effects (such as hyperoxia-induced vasoconstriction) in patients with systolic dysfunction, so it is not routinely recommended for patients without hypoxemia. In patients with cardiogenic pulmonary edema, treatment with continuous positive airway pressure (CPAP) or noninvasive
intermittent positive-pressure ventilation (NIPPV) helps alleviate symptoms, optimizes physiologic variables, and reduces the need for invasive ventilation and mortality. CPAP typically is initiated with a positive endexpiratory pressure (PEEP) of 5 to 7.5 cm H2O, titrated to 10 cm H2O as needed for dyspnea relief and improvement in O2 saturation. Contraindications to the use of NIV include 1) Immediate need for endotracheal intubation (inability to protect the airway, life-threatening hypoxia) 2) lack of patient cooperation (altered sensorium, unconsciousness, anxiety, inability to tolerate mask).
Caution is indicated with use of these modalities in patients with-cardiogenic shock RV failure Severe obstructive airway disease. Potential side effects and complications include Anxiety Claustrophobia Dry mucous membranes Worsening RV failure Hypercapnea Pneumothorax Aspiration USE OF MORPHINE
Morphine may be useful in patients with severe anxiety or distress. It should be used cautiously or avoided, especially in the presence of hypotension, bradycardia, advanced atrioventricular block, or CO2 retention. Morphine use has been associated with increased likelihood of mechanical ventilation, requirement for intensive care unit (ICU) admission, prolonged hospital stay, and death in some retrospective analyses. LOOP DIURETICS
Intravenous loop diuretics are the most frequently administered pharmacologic agents for AHF more than 75% of patients in the emergency department receive intravenous diuretics Symptomatic patients with objective evidence of congestion consistent with pulmonary or systemic venous hypertension or edema should receive urgent diuretic therapy for rapid relief of dyspnea. VASODILATORS In the absence of hypotension, vasodilators
play an important role in the initial therapy of patients with pulmonary edema and poor oxygenation. A treatment strategy of early initiation of intravenous nitrate therapy in patients with severe cardiogenic pulmonary edema has been shown to reduce the need for mechanical ventilation and the frequency of myocardial infarction. INDICATIONS FOR HOSPITALIZATION Patients with evidence of severe decompensated heart failure including
hypotension, worsening renal function or altered mentation Dyspnea at rest associated with either tachypnea or, less commonly, significant hypoxemia (oxygen saturation <90%) Hemodynamically significant arrhythmia (most commonly atrial fibrillation either with rapid ventricular response or new onset) Acute coronary syndromes. Patients with worsened congestion, even in the absence of dyspnea and often reflected by significant weight gain (5 kg)
Other signs or symptoms of pulmonary or systemic congestion Newly diagnosed heart failure Complications of heart failure therapy (such as electrolyte disturbances, frequent implantable cardioverter-defibrillator [ICD] firings) Other associated comorbid conditions. Specific Clinical Presentations Atrial Fibrillation with Rapid Ventricular Response. Atrial fibrillation with rapid ventricular response is the most common tachyarrhythmia requiring treatment in patients with AHF. It may be difficult to determine with certainty whether the atrial fibrillation was a
trigger for AHF or whether progressive heart failure decompensation led to atrial fibrillation. Although the ventricular response frequently decreases in parallel with the relief of dyspnea, and consequent decreased sympathetic drive, additional therapy may be required. Immediate cardioversion generally is not indicated except in the unstable patient, as cardioversion while the patient remains significantly decompensated is associated with a high rate of recurrent atrial fibrillation.12 In patients with systolic dysfunction, intravenous digoxin (in the absence of an accessory pathway), cautious use of beta-blocker therapy, or amiodarone may be used. Diltiazem and other agents that suppress ventricular function should be avoided in patients with significant systolic dysfunction, but may be effective in patients with preserved function.
Right Ventricular Heart Failure The most common cause of RV heart failure in AHF is left-sided failure. Isolated RV heart failure is relatively rare and is generally due to acute RV infarction, acute pulmonary embolism, or severe pulmonary hypertension. Isolated RV heart failure caused by an acute RV infarction is best treated with early reperfusion, whereas hemodynamically significant pulmonary embolism may be treated with thrombolytics.
Hemodynamic stabilization by optimizing central venous pressures via carefully monitored fluid loading (target central venous pressure [CVP], approximately 10 to 12 mm Hg) and increasing RV systolic function with intravenous inotropic support under invasive hemodynamic guidance may also be necessary. Selective pulmonary artery vasodilation by inhaled (nitric oxide, prostacyclin analogues) or intravenous (prostacyclin analogues, sildenafil) agents may improve RV function through decreased afterload.
Acute Coronary Syndromes Acute coronary syndromes may be the underlying trigger in patients presenting with AHF, but the diagnosis is confounded by the high prevalence of elevated troponins associated with AHF itself. These patients may present with chest discomfort, electrocardiographic changes consistent with ischemia, and elevated serum troponin. Aggressive therapy for acute coronary syndrome (ACS) should be rapidly instituted . In the absence of Cardiogenic shock, inodilators should be avoided in patients with ACS and those with significant asymptomatic coronary disease, because experimental
data have shown that they can cause necrosis of ischemic and/or hibernating myocardium. Cardiogenic Shock Cardiogenic shock is characterized by marked hypotension (SBP <80 mm Hg) lasting more than 30 minutes, associated with severe reduction of cardiac index (usually <1.8 L/min/m2) in spite of adequate LV filling pressure (PCWP >18 mm Hg), resulting in organ hypoperfusion. Mechanical complications of acute myocardial infarction (AMI) such as mitral regurgitation, cardiac rupture with ventricular septal defect or tamponade, and isolated RV infarct also may be causes in this setting.
Intravenous inotropes or even vasoconstrictors may be required in these patients, with mechanical circulatory support, such as with an intra-aortic balloon pump (IABP) or LV assist device (LVAD), for critical refractory cases, as a bridge to heart transplantation or other mechanical intervention. Phase II: Hospital Care The goals in management of the patient with AHF during the hospitalization phase are 1) to complete the diagnostic and acute therapeutic processes that were initiated at the time of initial presentation 2) to optimize the patients
hemodynamic profile and volume status and control clinical symptoms 3) to initiate or optimize chronic HF therapy. Monitoring of daily weights, fluid intake and output, and vital signs, including orthostatic blood pressure, as well as a daily assessment of symptoms and signs, is crucial. Laboratory monitoring should include daily analysis of electrolytes and renal function. Diagnostic evaluations should include an echocardiogram and evaluation for myocardial ischemia, if clinically indicated.
Dietary sodium restriction (to 2 g daily) and fluid restriction (to 2 L daily) may be useful to help treat congestion. Venous thromboembolism prophylaxis is indicated in all patients unless a clear contraindication is recognized. Most outpatient medications should be continued during hospitalization. In patients with worsening renal function, ACE inhibitors, ARBs, ARNIs and mineralocorticoid receptor antagonists often are withheld. Patients admitted on beta blockers had a lower occurrence of ventricular arrhythmias, a shorter
length of stay, and reduced 6-month mortality compared with those not receiving it so patients should therefore continue beta blocker therapy during hospitalization for AHF, unless significant hypotension or cardiogenic shock is present. To provide education and behavioral therapies to patients. Comorbid conditions should be aggressively addressed because these often complicate heart failure management. The Cardiorenal Syndrome in Hospitalized Patients
Represents one of the clinical state in which the volume overload of heart failure is resistant or refractory to treatment because of progressive renal insufficiency. A commonly used practical definition is an increase in serum creatinine above 0.3 mg/dL (or 25% decreases in GFR) despite evidence of persistent clinical or hemodynamic congestion. By this definition, the cardiorenal syndrome occurs in approximately 25% to 35% of the patients admitted with AHF, associated with longer lengths of stay and higher postdischarge mortality rates. It emphasizes the importance of persistent congestion, because multiple studies have suggested that changes in renal function during successful decongestion therapy usually are
transient and may not be associated with adverse outcomes. Estimated GFR (eGFR) should be calculated in patients with AHF. Arterial underfilling resulting from overdiuresis or low cardiac output does not appear to be the most frequent primary cause of worsening renal function, although hypotension can be an important factor. Increasing doses of diuretics typically are required, although diuretic resistance may be profound. The degree of diuretic resistance , sometimes quantified as diuretic efficiency is known to be associated with increased LOS and adverse prognosis. Although ultrafiltration often is considered in this scenario,
clinical trial data have not supported the efficacy or safety of this approach. Overall, the appropriate management of patients with cardiorenal syndrome remains a major unmet clinical challenge in AHF. Phase III: Predischarge Planning The predischarge phase focuses on the goals of evaluating readiness for discharge, optimizing chronic oral therapy, minimizing the side effects of treatments, and ultimately preventing early readmission and improving symptoms and survival.
Persistent clinical congestion at discharge was associated with a high risk for rehospitalization. Elevations of discharge BNP level have been shown to be associated with risk for subsequent rehospitalization. Pharmacologic therapies known to improve longterm outcomes in chronic heart failure, such as use of beta blockers, ACE inhibitors, and mineralocorticoid receptor antagonists, should be initiated as soon as reasonable during the hospitalization and before discharge in hemodynamically stable, appropriate patients.
Phase IV: Postdischarge Management A series of studies also have investigated the benefits of postdischarge support, especially patient-centered discharge instructions, transition coaches, follow-up telephone calls, and early physician follow-up evaluation, although results of these studies have been mixed in terms of impact on outcomes. A follow-up appointment is optimally scheduled within approximately 7 to 10 days after discharge, but an earlier follow-up visit (in less than a week) should be considered for patients with high-risk
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