Kembara Xtra - Medicine - Acute Decompensated Heart Failure
Introduction The term "acute decompensated heart failure" (ADHF) refers to a diverse range of similar diseases that include new-onset or recurrent deterioration of cardiac pump performance. ADHF may be brought on by issues with the heart valves, pericardium, myocardium, or endocardium. This causes pulmonary congestion with elevated left atrial pressure, excessive fluid accumulation, and a decrease in cardiac output, which in turn causes a wide range of secondary symptoms. A new diagnosis of ADHF may occur or an existing case of chronic heart failure (HF) may get worse. This illness has been referred to by a number of names, including acute HF, acute HF syndrome, and acute decompensation of chronic HF. Prevention Incidence HF is the medical illness for which Medicare spends the most on diagnosis and treatment. Over 1 million hospital admissions each year in the United States are due to HF, which is the most prevalent reason for admission and readmission for patients over 65. About 50% of those with HF pass away within 5 years of their diagnosis. 90% of HF patients pass away within 10 years. A 37% death rate in the older population within a year has been reported in more recent research. Pathophysiology and Etiology Systolic and/or diastolic cardiac dysfunction are two possible pathophysiologic disorders that result in the clinical symptoms of HF. See "Chronic Heart Failure." Diastolic dysfunction is a compliance anomaly, while systolic dysfunction is an inotropic abnormality. – Recently, the words "HF with reduced," "HF with midrange," "HF with preserved," and "HF with improved LVEF" have been adopted, accordingly. Three clinical profiles of ADHF patients have also been recently described by American HF guidelines, which consider the patient's clinical symptoms, hemodynamics, and systemic perfusion: Patients with volume overload are typically caused by an acute hypertensive crisis and are characterized by pulmonary and/or systemic congestion. In patients with decreased cardiac output, shock, hypotension, and/or renal hypoperfusion may be present. Patients who exhibit shock and volume overload symptoms ● ADHF may be brought on by the following circumstances: - Myocardial disease: An acute trigger such as coronary artery disease (CAD), MI, toxic damage, immune-mediated and inflammatory damage, infiltrative illnesses, metabolic disturbances, or genetic abnormalities that causes a worsening of preexisting chronic HF. - Abnormal loading situations include high blood pressure, structural flaws in the valves and myocardium, pericardial and endomyocardial diseases, high output states, and volume overload. - Tachyarrhythmias, high-grade heart blocks, bradyarrhythmias, atrial fibrillation The most common reason for death in ADHF is dysrhythmia, which is followed by pump failure. The majority of patients take more than five drugs and have more than five comorbid conditions, including CAD, chronic renal disease, and diabetes. DIAGNOSIS without a gold-standard diagnostic test, necessitates a complex clinical approach: No one physical examination (PE), ECG, radiographic, or history finding can exclude HF. HISTORY The majority of patients had histories of HF, MI, uncontrolled HTN, and the other risk factors listed above. Only orthopnea and dyspnea upon exertion have excellent sensitivity but suffer from low specificity. With a positive likelihood ratio (LR) ranging from 1.6 to 13.0, S3 has the highest LR in relation to PE. No PE finding is more sensitive than 70%. Exam of the lungs reveals rales (crackles), occasionally wheezing, and Cheyne-Stokes respirations. Multiple Diagnoses pulmonary embolism, MI, tamponade, pneumothorax, acute respiratory distress syndrome, sepsis, chronic obstructive pulmonary disease (COPD), pneumonia, constrictive pericarditis, and high output states (anemia, hyperthyroidism) are all illnesses that should be ruled out before anything else. Laboratory Results Laboratory results are supplementary and aid in predicting the clinical course. First, check your blood pressure (BP) and other vital signs to rule out hemodynamic instability and cardiogenic shock symptoms. Next, have a look at your lab and imaging results. To assess for ACS, use cardiac troponins and the ECG. Be aware that most HF patients have increased troponins, frequently despite no evident myocardial ischemia. Liver function tests, electrolytes, TSH (new onset), glucose, and CBC. Transthoracic echocardiography is advised within 48 hours of the onset of hemodynamic instability in ADHF patients, and sooner if cardiac structure and function are unknown or may have changed since earlier tests. BNP and/or N-terminal fragment pro-BNP (NT-proBNP) measurements are advised for all patients with suspected ADHF and acute dyspnea when the etiology of the dyspnea is unknown but may be connected to ADHF. – BNP 100 effectively rules out HF with a sensitivity of 93.5% and a negative LR of 0.2. BNP >500 have an 89.8% specificity. BNP levels of 100 to 400 may signify HF or may be linked to many illnesses, including cardiac and noncardiac (such as pulmonary) problems. In the appropriate clinical situation, NT-proBNP readings >450 pg/mL for persons under 50, >900 pg/mL for people between 50 and 75, and >1,800 pg/mL for those over 75 are highly indicative of HF (sensitivity 90%, specificity 84%). Chest x-rays are used to examine the patient's lungs for congestion and to look for any cardiac or noncardiac disorders that could be the source of or contribute to their symptoms. Lung ultrasound (LUS) is becoming a useful method for the diagnosis of ADHF, with a positive LUS being defined as the presence of more than three B lines in each of the two bilateral lung zones, which has a specificity of 92.7% and an LR of 7.4. Other/Diagnostic Procedures When CAD is suspected, cardiac catheterization may be considered. In extreme situations of cardiogenic shock, pulmonary artery catheterization may be used to direct therapy. Interpretation of Tests HF's etiology affects cardiac pathophysiology. Management The purpose of treatment is to reduce symptoms, restrict cardiac and renal damage, restore oxygenation, enhance hemodynamics and organ perfusion, as well as discover the etiology or triggering causes. The 2017 ACC guidelines for the management of heart failure served as the basis for all of the suggestions below. prescription caution Numerous treatments have a negative effect on morbidity or death. In cases of fluid overload ADHF, diuretics are first given, and nitrates are then added as needed for early stabilization. After stabilizing the patient, it is important to identify precipitating causes and improve their chronic oral therapy while they are hospitalized. It is also important to identify patients who might benefit from revascularization. Finally, information must be given about dietary salt restriction, volume status self-assessment, and medications. In patients with impaired systolic function, the recommendation is to begin an ACE inhibitor, ARB, or ARNI once ADHF has stabilized. In some individuals, the use of a new drug called ivabradine has also been promoted, however there is no evidence that it lowers cardiovascular mortality. Avoid COX-2 inhibitors and NSAIDs. There are no prescribed class IA medications for ADHF. Initial Line In ADHF with systolic blood pressure (SBP) >90 mm Hg, consider vasodilators. If there are no contraindications, patients with hypertensive ADHF should get IV vasodilators as their first line of treatment to relieve congestion. It is ineffective to use in chronic HF. Vasodilators reduce systemic vascular resistance and ventricular filling pressure, which indirectly enhances heart function. - IV nitroglycerin (IV 10 to 20 g/min, rise to 200 g/min) may provide short-term benefits by reducing preload and afterload by widening peripheral capacitance and resistance arteries on vascular smooth muscle. - IV nitroprusside: Use caution while administering; start at 0.3 g/kg/min and work your way up to 5.0 g/kg/min. – IV ACE inhibitors have conflicting recommendations and ambiguous evidence. They are supposed to function by lessening both the preload and the afterload. All patients with ADHF and symptoms of fluid overload in hemodynamically stable individuals are advised to use IV loop diuretics (contraindicated if SBP 90 mm Hg, severe hyponatremia, or acidosis); if kidney disease is present, be wary of electrolyte abnormalities. Early in the course of ADHF, diuresis should be started; continuous infusion is no better than bolus; and high dose is not noticeably superior to low dose. - Furosemide (Lasix): Patients with new-onset ADHF should receive IV boluses of 20 to 40 mg. – If using furosemide (Lasix) on a long-term basis, the first IV dose should be greater than or equivalent to the long-term oral dose (1.0 to 2.5 times home dose). Keep an eye out for proper urine production. – Alternative loop diuretics include bumetanide and torsemide. – Consideration should be given to adding a second kind of diuretic, either orally (metolazone or spironolactone) or intravenously (chlorothiazide), if congestion does not improve with initial diuretic therapy. Thiazides combined with loop diuretics may be helpful if diuresis is ineffective. If there is an extreme volume overload, loop diuretics may be used with hydrochlorothiazide [HCTZ] (25 mg PO) and spironolactone or eplerenone (25 to 50 mg PO). When loop diuretics are ineffective, metolazone (Zaroxolyn): 2.5 to 20.0 mg/day PO can be given as a second, synergistic diuretic. It may also be more effective than other thiazides for patients with renal failure. Bilevel positive airway pressure (BIPAP)/NPPV: NPPV reduces early mortality, intubation rate, and symptom severity in ADHF. This is a level A recommendation with pulmonary edema clinical proof. Next Line Tolvaptan is being researched as a treatment for severe hypervolemic hyponatremia that is resistant to medical intervention and water restriction. Inotropes are only prescribed to individuals who have severe systolic dysfunction, which most frequently occurs in hypotensive ADHF. - Phosphodiesterase inhibitors (milrinone, enoximone) reduce pulmonary resistance; they can be taken by people on -blockers, but they may raise the medium-term death rate in those with coronary artery disease (CAD). Milrinone specifically has ionotropic and vasodilatory actions without stimulating the heart's adrenergic receptors. - Avoid dobutamine infusions of 2 to 20 g/kg/min in patients who are in cardiogenic shock or who have tachyarrhythmias. Consider low-dose dopamine infusion (3 to 5 g/kg/min). - When compared to a placebo, levosimendan (a calcium sensitizer) improves hemodynamic parameters but not survival. In individuals who have cardiogenic shock despite receiving treatment with another inotrope, consider vasopressors. Nesiritide, a BNP analog, is not advised due to greater rates of hypotension, no benefit on mortality, or higher rates of rehospitalization. Renal replacement therapy with ultrafiltration is not advised for everyday use. The sickest group of ADHF patients may benefit from venoarterial extracorporeal membrane oxygenation (ECMO). ECMO has served as a stopgap measure before transplantation or prolonged mechanical assistance. Furthermore Treated Oxygen: Start treatment as soon as possible, ideally titrating to an arterial oxygen saturation of >92% (90% if you have COPD). Transfusion is used to treat anemia; a conservative trigger Hgb level of 8 is preferred. According to a Cochrane review, one fatality can be prevented for every 14 ADHF patients who receive NPPV treatment and one for every nine ADHF patients who receive CPAP treatment. If at all possible, steer clear of mechanical ventilation for patients with right HF. ● For maintenance therapies, see "Heart Failure: Chronic". Surgical Techniques if valvular disease is the cause, heart valve replacement; if necessary, PCI/CABG for patients with CAD/MI. Admission Considerations for admission criteria include: - Evidence of severely decompensated HF, including: dyspnea at rest, worsening renal function, altered mental status, concurrent arrhythmia, and acute coronary syndrome – Consider an observation unit stay if the following criteria are met: SBP >120 mm Hg, RR 32 breaths/min, BUN 40 mg/dL, creatinine 3.0 mg/dL, no evidence of ischemia or elevated troponins, BNP 1,000, N-type pro-BNP 5,000, and the clinical impression that the patient could be discharged in the next 24 hours. Improved symptoms, SBP normalized at 100 to 120 mm Hg, excellent urine output, serum sodium >135 mEq/L, and HF outpatient education are required for discharge. Patient Follow-Up Monitoring Early follow-up and interdisciplinary treatment to lower death and hospitalization rates. Teach medicine, activity, daily weight (and how to modify a diuretic); monitoring and self-care. See "Chronic Heart Failure. Arrhythmia, pulmonary edema, hyponatremia, and mortality are complications.
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