Heart Failure Drugs Pharm lecture PPT PDF

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Heart Failure Drugs Lecture PPT Pharm 3/20/19  Definition: Heart failure (HF) is a pathologic state in which the heart is unable to pump blood in sufficient amounts to meet the body’s metabolic needs ( cardiac output)  Systolic  Diastolic Diagnostic studies:  Diagnostic studies  BNP  Echocardiography to determine ejection fraction (EF) Causes of Heart failure:  Major causes:  Chronic hypertension  Myocardial infarction  Other causes  Valve deficiency  Atrial fibrillation/flutter  Aging of the myocardium  Most common cause of left-sided heart failure is left ventricular hypertrophy due to hypertension (HTN) Symptoms:  As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues  Left-sided heart failure  Pulmonary edema  Coughing  Dyspnea  Right-sided heart failure  Jugular vein distention  Ascites  Pedal edema Pitting pedal edema Jugular vein distention Classification of heart severity

Hear failure treatment guidelines:  According to the American Heart Association and the American College of Cardiology (2005) treatment of chronic heart failure should be directed at reducing the effects of the:  Renin-angiotensin-aldosterone system (RAAS)  Sympathetic nervous system (SNS) Drug classes used to treat HF:  Diuretics  Agents that inhibit the RAAS  ACE inhibitors (ACEI)  Drugs that inhibit the SNS  Beta-blockers  Others  Cardiac glycosides  B-type natriuretic peptides Goal of Drug therapy  Improve symptoms  Slow deterioration in myocardial function  Reduce mortality Terms to know  Positive inotropic drugs  Increase the force of myocardial contraction  Positive chronotropic drugs  Increase heart rate  Positive dromotropic drugs  Accelerate cardiac conduction  Compensated versus decompensate HF  Heart failure (HF) versus congestive heart failure (CHF)  Cardiac remodeling  Preload  Afterload

Loop Diuretics:  Mechanism of action:  Decreases Na, Cl, and K reabsorption in thick ascending limb of the loop of Henle in the nephron which results in profound diuresis.  Drug effects:  Reduced blood volume decreases venous pressure (preload) and arterial pressure (afterload). Reduced pulmonary and peripheral edema.  Examples:  furosemide (Lasix)  Indications:  Acute and chronic congestive HF  Dosages and Routes:  Oral: 20-80 mg/daily or BID; max dose 600 mg/day  IV: 20-40 mg/dose IV x 1, may increase by 20mg q 2 hours.  Adverse effects:  Hypokalemia (↑ risk of digoxin toxicity)  Severe hypotension  Nursing implications:  Assess patient’s fluid volume status  Assess vital signs  Assess labs  Patient education:  Avoid taking late in the afternoon due to nocturia.  Eat foods rich in potassium (bananas, oranges, potatoes, tomatoes, meats, fish, wheat bread, legumes). K+ supplement may be necessary  Report signs of hypokalemia (e.g. lethargy, weakness, leg cramps) to provider immediately.

ACE Inhibitors  Mechanism of action:  Inhibits ACE which prevents the conversion of angiotensin I to angiotensin II (a powerful vasoconstrictor). Also reduces aldosterone secretion. Suppress degradation of kinins (vasodilator).  Drug effects:  Arteriolar and venous dilation results in reduced preload, afterload, ↓ pulmonary & pedal edema, and increased cardiac output. ↑ kinins reduces cardiac remodeling.  Examples:  lisinopril (Prinvil), captopril (Capoten), enalapril (Vasotec)  Indications:  Cornerstone of HF therapy  Adverse effects:  Hypotension (0.9-6.7%)  Cough (9%)

 Hyperkalemia  Angioedema

Beta Blockers  Mechanism of action:  Protect heart from excessive sympathetic stimulation  Drug effects:  Improve LV ejection fraction (1-3 months), slow the progression of HF, reduce need for hospitalization, and prolong survivial.  Examples:  Carvedilol (Coreg), bisoprolol, sustained-release metoprolol (Toprol XL)  Dosages and routes:  WARNING: “Start low and go slow” as excessive beta blockade can reduce ventricular contractility.  Contraindications:  Heart block  Adverse effects:  Fluid retention/ worsening HF  Bradycardia/ heart block  Hypotension

Cardiac Glycosides     

Oldest group of cardiac drugs Comes from the foxglove plant Digoxin (Lanoxin) is the only cardiac glycoside available in the U.S. No longer used as first-line treatment Mechanism of action:  Inhibits the sodium-potassium adenosine triphosphatase pump. This cause an accumulation of calcium within the cardiac myocytes. The calcium then augments contractile force by facilitating the interaction of myocardial actin and myosin.  Drug effects:  Positive inotropic effect increases the force of ventricular contraction which increases cardiac output. Increased CO, can reverse all the overt manifestations of HF.

 Indications:  Second-line heart failure; atrial fibrillation  Precautions:  Lasix (secondary to risk of hypokalemia)  Adverse effects:  Digoxin toxicity  Cardiac dysrhythmia Narrow therapeutic window  digoxin (Lanoxin)

 Very narrow therapeutic window. Drug levels must be monitored  0.5 to 0.8 ng/mL (old upper limit 2 ng/mL)  Low potassium levels increase its toxicity. Electrolyte (serum K+) levels must be monitored.  Normal range 3.5 – 5 mEq / L Symptoms of digoxin toxicity:  HR below 60 or new irregular rhythm  Anorexia, nausea, vomiting  Vision changes: Halos, yellow tinged vision  Confusion  Digoxin should be discontinued by MD only – takes about 1 week for drug to be eliminated from the body Digoxin Overdose:  digoxin immune Fab (Digibind)  Therapeutic classification: antidotes  Pharmacologic classification: antibody  Indications: serious life-threatening over dosage with digoxin.  Action: an antibody produced in sheep that binds to unbound digoxin in serum.  Therapeutic effect: binding and subsequent removal of digoxin, preventing toxic effects in overdose. A baby sheep Cardiac Glycosides:  digoxin immune Fab (Digibind)  Therapeutic classification: antidotes  Pharmacologic classification: antibody  Indications: serious life-threatening over dosage with digoxin.  Action: an antibody produced in sheep that binds to unbound digoxin in serum.  Therapeutic effect: binding and subsequent removal of digoxin, preventing toxic effects in overdose. 

B-type Natriuretic Peptide  Mechanism of action/ Drug effects:  A synthetic form of BNP produced by recombinant DNA technology. Causes suppression of RAAS, suppression of SNS, direct dilation of arterioles and veins (↓ preload and ↓ afterload).  Examples:  nesiritide (Natrecor)  Indication/ Route:  Acutely decompensated CHF via continuous intravenous infusion only. Nursing implications/patient education  Digoxin  Take apical pulse for one minute before giving medication

 Hold dose and notify physician if bradycardia (heart rate less than 60 bpm) or new arrhythmias occur.  Check potassium level prior to giving medication  Check kidney function to ensure patient can excrete excess digoxin and avoid build up in body  Educate patient to notify physician of signs/symptoms of toxicity  Instruct patient to immediately report weight gain of 2 or more pounds in 1 day or 5 or more pounds in 1 week Evaluation of effectiveness  Increased urinary output  Decreased fatigue, edema, shortness of breath, dyspnea, and crackles  Improved peripheral pulses, skin color and temperature  Serum digoxin levels 0.5 to 0.8 ng/mL Clinical reasoning:  A patient has been receiving digoxin therapy for 2 months. During today’s visit, he tells you that he has been seeing yellowish rings around lights and has had no appetite. His latest blood potassium level is 5.6 mEq/L. What is the concern with this patient, and what should be done?...