A common clinical syndrome characterized by sudden onset of dyspnea due to accumulation of fluid within the pulmonary interstitium and alveolar spaces, ref2242ed to as cardiogenic pulmonary edema.
Acute heart failure results from a rapid increase in cardiac filling pressures due to fluid overload in conjunction with left ventricle of dysfunction.
It may sometimes be caused by elevated left ventricular after load due to hypertension in the absence of frank fluid volume overload.
Hospitalization for acute heart failure manifests with high rates of re-hospitalization and mortality.
Acute heart failure is the most common diagnosis in the ED leading to hospitalization.
Acute decompensated heart failure
Refers to a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing, lower extremity swelling, and fatigue.
It is a common and potentially serious cause of acute respiratory distress.
It is caused by severe congestion of multiple organs by fluid that is accumulated due to the failing heart.
Acute decompensation can be caused by underlying medical illness: such as myocardial infarction, an abnormal heart rhythm, infection, or thyroid disease.
Treatment of ADHF consists of reducing the fluid level with diuretics and improving heart function with nitrates, or other treatments such as ultra-filtration may also be required.
Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity:
Exertional dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Acute pulmonary edema
Other symptoms of heart failure include chest pain/pressure and palpitations.
Patients with ADHF frequently have loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, nocturnal, and cerebral symptoms ranging from anxiety to memory impairment and confusion.
Chronic stable heart failure may decompensate: intercurrent illness, myocardial infarction, abnormal heart rhythms, uncontrolled hypertension, failure to maintain a fluid restriction, diet, or medication, anemia and hyperthyroidism, excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones.
Jugular venous distension is the most sensitive clinical sign for acute cardiac decompensation.
In acute decompensated heart failure, goals of treatment: re-establishimg adequate perfusion and oxygen delivery to end organs: propping up the head of the patient, giving oxygen to correct hypoxemia, administering morphine, diuretics, addition of an ACE inhibitor, use of nitrates and use of digoxin if indicated for the heart failure and if arrhythmic.
Supplemental oxygen may be administered if blood levels of oxygen are low.
Heart Failure Society of America, recommends that oxygen not be used routinely.
Initial management of acute decompensated heart failure usually includes some combination of a vasodilator such as nitroglycerin, a loop diuretic such as furosemide, and non-invasive positive pressure ventilation.
Common types of medications that are prescribed for heart failure patients include ACE inhibitors, vasodilators, beta blockers, aspirin, calcium channel blockers, and cholesterol lowering medications.
Nitrates such as nitroglycerin are often used as part of the initial therapy for ADHF.
Heart failure is usually associated with a volume overloaded state, and should be treated initially with intravenous loop diuretics.
Intravenous nitroglycerin is often used in addition to diuretic therapy to improve congestive symptoms, but volume status should still be adequately evaluated.
With diastolic dysfunction without systolic dysfunction, fluid resuscitation may improve circulation by decreasing heart rate, which will allow the ventricles more time to fill.
ADHF with severe pulmonary congestion and normal blood pressure requires urgent treatment, which should be initiated with intravenous loop diuretics.
In treating pulmonary edema to improve oxygenation, intravenous furosemide is generally the first line approach.
Loop diuretics may be combined with thiazide diuretics for a synergistic effect.
Diuretic therapy should be continued even in the face of worsening renal function.
Intravenous preparations are physiologically pref2242ed because of more predictable absorption due to intestinal edema.
Acute heart failure due to hypertension results from fluid redistribution as a consequence of basal constriction, increased cardiac work, and left ventricular dysfunction: vasodilator therapy is the treatment of choice to rapidly reduce ventricular afterload.
ACE inhibitors and angiotensin receptor blockers used acutely in ADHF are potentially harmful, as individuals with poor kidney perfusion are especially at risk for kidney impairment inherent with these medications.
Beta-blockers are discontinued or decreased with acutely decompensated heart failure and a low blood pressure, but are continued of beta-blockers if the blood pressure is adequate.
Inotropes are indicated if low blood pressure ( SBP < 90 mmHg ) is present.
Opioids have traditionally been used in the treatment of the acute pulmonary edema that results from acute decompensated heart failure, but little evidence to support this exists.
Continuous positive airway pressure using a face mask improves symptoms more quickly than oxygen therapy alone, and reduces the risk of death.
Severe respiratory failure may require endotracheal intubation and mechanical ventilation.
Ultrafiltration can be used to remove fluids with ADHF associated with kidney failure.
Heart failure due to acute aortic regurgitation is a surgical emergency associated with high mortality.
Heart failure may be caused by rupture of a ventricular aneurysm.
Procedures used to treat heart failure include: CABG, heart valve surgery, angioplasty, pacemaker, and heart transplant.
Mortality is unacceptably high in patients with acute heart failure, and much higher in patients with chronic heart failure with reduced left ventricular ejection fraction.
Among patients with acute heart failure, early intense and sustained vasodilatation therapy , compared with usual care, does not significantly improve outcome of all-cause mortality and acute heart failure rehospitalization at 180 days (GALACTIC trial).
Early initiation of high-dose intravenous nitrates targeted to arterial blood pressure versus high dose furosemide and noninvasive positive pressure ventilation improved outcomes in severe pulmonary edema, an acute heart failure phenotype that represents about 5% of all acute heart failure cases.
Approximately 20-30% of patients admitted for ADHF will experience a decline in kidney function during the hospitalization.