Explanation: The client comes to the emergency department with fatigue, shortness of breath, dry cough, and exertional dyspnea for 1 week; the client is homeless; medical history includes chronic heart failure, uncontrolled hypertension, coronary artery disease, and type 2 diabetes mellitus Vital signs: RR 22, SpOz 88% on room air; the client is dyspneic but can speak in full sentences; lung auscultation reveals decreased breath sounds at the lung bases and bilateral crackles; the client reports smoking 1 pack of cigarettes per day for 35 years; the client was hospitalized for pneumonia 6 months ago Vital signs: T 99 F (37.2 C), P 90, BP 170/100; continuous cardiac monitor shows sinus rhythm with occasional premature ventricular contractions; S1, S2, and S3 are heard on auscultation; bilateral lower extremity pitting edema is noted

Explanation: The findings all support the diagnosis of acute decompensated heart failure (ADHF): Crackles with auscultation: Indicative of pulmonary congestion due to fluid overload. Decreased capillary oxygen saturation: Reflects impaired gas exchange from fluid in the lungs. Elevated B-type natriuretic peptide (BNP): A level of 640 pg/mL is significantly elevated; BNP is released when the ventricles are stretched due to increased fluid volume. Left ventricular ejection fraction of 30%: Normal is 55 - 70%. This reduced EF confirms systolic dysfunction, common in ADHF. Lower extremity pitting edema: A classic sign of volume overload in right-sided or total heart failure.

Explanation: Dyshythmias due to structural changes (eg, cardiomegaly, ventricular hypertrophy) that alter electrical activity of the heart. Common dysrhythmias associated with HF include atrial fibrillation, life-threatening ventricular tachycardia, and ventricular fibrillation. • Acute kidney injury (AKI) due to hypoperfusion of vital organs (ie, decreased renal perfusion) secondary to decreased cardiac output. Decreased glomerular filtration can cause electrolyte imbalances (eg, hyperkalemia) related to AKI that can also be a precipitating factor for dyshythmias. • Pleural effusions can develop when fluid moves from capillaries to free spaces in the thoracic cavity as hydrostatic pressure in the pulmonary veins increases (back pressure).

Explanation: Expected interventions for acute decompensated heart failure (HF) focus on reducing cardiac workload and improving oxygenation. These include: • Daily weights should be performed to monitor fluid volume status and guide treatment. Ideally, daily weights should be performed at the same time of day, on the same scale, and with the client wearing the same amount of clothing. • Diuretics (eg, furosemide) prevent reabsorption of sodium and chloride in the kidneys, which increases fluid excretion in urine and decreases preload. Diuretics provide symptomatic relief by reducing pulmonary congestion and peripheral edema. These are the cornerstone of therapy and often a priority after oxygen therapy. • Fluid restriction is indicated to decrease circulating fluid volume and prevent excess strain on the heart. • Supplemental oxygen should be administered to improve oxygen delivery in clients with HF due to impaired gas exchange from pulmonary edema. • Antihypertensive medications reduce cardiac workload and improve contractility by lowering blood pressure (ie, afterload). Nebulized albuterol is a bronchodilator administered to improve oxygenation in clients with reactive airway disease (eg. asthma, chronic obstructive pulmonary disease). Bronchodilators will not improve oxygenation in clients with pulmonary edema and are not expected for treatment of HF.

Explanation: Pharmacologic management of heart failure (HF) focuses on reducing cardiac workload and improving cardiac output. • Beta-adrenergic antagonists ("beta blockers") (eg, carvedilol) reduce cardiac workload by inhibiting the action of catecholamines (eg, epinephrine, norepinephrine) on beta-adrenergic receptors in the heart. Beta blockers decrease myocardial oxygen demand by decreasing blood pressure and decreasing heart rate. • Angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril) alter the renin-angiotensin-aldosterone system by inhibiting conversion of angiotensin I to angiotensin II, thereby preventing the release of aldosterone. Aldosterone, an adrenal steroid hormone, retains sodium and water in addition to promoting vasoconstriction. By reducing circulating aldosterone, ACE inhibitors promote vasodilation and as a result decrease blood pressure. ACE inhibitors also decrease ventricular remodeling, an added benefit for clients with HF. • Loop diuretics (eg, furosemide) prevent reabsorption of sodium and chloride in the kidneys, which increases urine output and fluid excretion. Decreases in circulating fluid volume will decrease blood pressure and reduce pulmonary edema (ie, increase oxygen saturation), as well as decrease cardiac preload.