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Laboratory Assessment

Serum Electrolytes levels, which may be abnormal owing to causes such as fluid retention or renal dysfunction. Complete Blood Count which may indicate anemia or infection as potential causes of heart failure. Urinalysis which may reveal proteinuria, which is associated with cardiovascular disease. Blood Urea Nitrogen and Creatinine levels which may indicate decreased renal blood flow. Liver Function Tests which may show elevated liver enzyme levels and indicate liver dysfunction due to heart failure. Arterial Blood Gas values often reveal hypoxia (low oxygen level) because oxygen does not diffuse easy through fluid-filled alveoli. Respiratory alkalosis- may occur because of hyperventilation Respiratory acidosis- may occur because of carbon dioxide retention Metabolic acidosis may indicate an accumulation of lactic acid b-Type Natriuretic Peptide Levels BNP 100-500 pg/ml BNP >500 pg/ml HF probable HF very probable

BNP <100 pg/ml HF very improbable

Surgical Management Heart Transplantation is still the ultimate choice for heart failure Other surgical Therapies The most common ventricular reconstructive procedures include: Partial left ventriculectomy also known as heart reduction surgery-involves removing a triangle-shaped section of the weakened heart in the left lateral ventricle to reduce the ventricles diameter and decrease wall tension.

Endoventricular circular patch cardioplasty- the surgeon removes portions of the cardiac septum and left ventricular wall and grafts a circular patch (synthetic or autologous) into the opening. Acorn cardiac support device- is a polyester mesh jacket that is placed over the ventricles to provide support and to avoid overstretching the myocardial muscle. The material for the jacket has been used for other procedures, such as vascular grafts. The jacket appears to reduce hypertrophy of the heart muscle and assists with improvement of the ejection fraction. Myosplint- electrical stimulation of several tension pads (splints) on the outside of the ventricle changes it to a more normal shape to improve function.

Nonsurgical Management Gene Therapy- may be indicated for patients in end-stage heart failure who are not candidates for heart transplantation. This therapy replaces damaged genes with normal or modified genes by a series of injections of growth factor into the left ventricle. Cardiac resynchronization therapy- also called biventricular pacing, uses a permanent pacemaker alone or is combined with an implantable cardioverter/ defribillator. Electrical stimulation causes more synchronous ventricular contractions to improve ejection fraction, cardiac output and mean arterial pressure.

Pharmacological Management Angiotensin-converting enzyme and Angiotensin receptor blockers- patients with even mild heart failure resulting from left ventricular dysfunction should be given a trial of ACE inhibitors or ARBs Both ACE and ARBs improve function and quality of life for patients with heart failure. ACE inhibitors are the first-line drug of choice. Beta-adrenergic blockers- improve the condition of some patients in heart failure. It appears that prolonged exposure to increased levels of sympathetic stimulation and catecholamines worsens cardiac function. Beta-adrenergic blockade reverses this effect, improving morbidity, mortality, and quality of life for patients in heart failure.

Inotropic drugs- patients experiencing heart failure are candidates for IV drugs that increase contractility of the heart. Digoxin (Cardiac Glycoside)- provides symptomatic benefits for patients in chronic heart failure with sinus rhythm and atrial fibrillation. Dobutamine (Beta-adrenergic Agonists)- improves cardiac contractility and thus cardiac output and myocardial-systemic perfusion. Milrinone (Phosphodiesterase inhibitor)- this drug increases cyclic adenosine monophosphate, which enhances the entry of calcium into myocardial cells to increase contractile function. Levosimendan (Calcium-sensitizer)- it binds to troponin C in the heart muscle and therefore increases the contraction of the heart. Nitrates it causes primarily venous vasodilation but also a significant amount of arteriolar vasodilation. It also decreases the volume of blood returning to the heart and improves left ventricular function. Human B-type natriuretic peptide lowers pulmonary capillary wedge pressure and improves renal glomerular filtration.