Congestive Heart Failure PDF

Faculty of Pharmacy Department of Pharmacy Practice Course Name: Clinical Pharmacy and Pharmacotherapeutics II Code: PP905 Dr. Aliaa Osman PhD Holder of Clinical Pharmacy Head of Clinical Pharmacy Department, Ain Shams University Specialized Hospital Lecturer of Clinical Pharmacy Sinai Unive...

Faculty of Pharmacy Department of Pharmacy Practice Course Name: Clinical Pharmacy and Pharmacotherapeutics II Code: PP905 Dr. Aliaa Osman PhD Holder of Clinical Pharmacy Head of Clinical Pharmacy Department, Ain Shams University Specialized Hospital Lecturer of Clinical Pharmacy Sinai University  Clinical Pharmacy and Pharmacotherapeutics II II. Congestive Heart Failure Definition: Failure of the heart to maintain an adequate output (- - C.O) and congestion in the pulmonary and/or systemic circulation. Classes: Left-sided heart failure: cause pulmonary edema. Right-sided heart failure: cause systemic edema. Etiology: Hypertension Coronary artery disease Valvular heart Abnormal heart rhythms (arrhythmias) Overactive thyroid gland (hyperthyroidism) A severe decrease in red blood cells (anemia) Diseases that affect the heart muscle itself (cardiomyopathy) Diseases that cause cardiomyopathy include: Infection (viral, bacterial, AIDS, rheumatic fever, etc.) Toxins (alcohol, cocaine, radiation, chemotherapy, etc.) Nutritional deficiencies (thiamine deficiency causing beriberi) Connective tissue disorders (lupus, rheumatoid arthritis, etc.) Neuromuscular diseases (muscular dystrophy) Infiltrative (amyloidosis, sarcoidosis, cancer) Idiopathic (unknown) Familial Birth defects in the formation of the heart (congenital heart disease) Many other factors, called precipitating factors, include. Stopping prescribed medications Excessive intake of fluids or salt Uncontrolled hypertension Infection Heart attack Ischemia (lack of blood to heart muscle) Cardiac arrhythmia (abnormal heart rhythm) Anemia Pulmonary embolus (blood clot in lung) Hyperthyroidism (overactive thyroid) Hypoxia (low level of oxygen in blood usually due to lung disease) New heart valve malfunction Correction of congestive heart failure: The body compensates by maintaining the cardiac output. Sympathetic nerve stimulation Activation of renin-angiotensin-aldosterone system Activation of anti-diuretic hormone (ADH). Hypertrophy Symptoms of congestive heart failure:  Shortness of breath or difficulty breathing (dyspnea). ❑ Shortness of breath only with exertion (dyspnea on exertion) ❑ Shortness of breath while at rest ❑ Shortness of breath when lying down (orthopnea) ❑ Intermittent shortness of breath at night (paroxysmal nocturnal dyspnea) Edema Weight gain Fatigue Chest pain Acute pulmonary edema Diagnosis: Enlargement of the heart (cardiomegaly) A third heart sound (S3). Sound of fluid in the lungs during inspiration (Rales) Enlargement of the jugular vein in the neck (jugular venous distention). Enlargement of the liver (hepatomegaly). Edema. This is usually located in the legs, ankles, feet. The term "pitting edema" is often used because applying slight fingertip pressure produces a temporary pit which resolves quickly. Fast heart rate (tachycardia) Increased rate of breathing (tachypnea) High blood pressure (hypertension) Low blood pressure (hypotension). Cardiogenic shock. Fluid in the abdominal cavity (ascites) Fluid in the space between the lungs and the ribs (pleural effusion) Imaging: A chest X-ray (CXR) An electrocardiogram (EKG) An echocardiogram Treatment of the heart failure state: 1. Diet and rest  Na restriction  Absolute rest (disadvantages are thrombosis, pneumonia, psychosis, bed sores……) 2. Digitalis: ++ myocardial contractility without ++ in O2 consumption In cases refractory to diuretic and digitalis, add dilators. 3.. Diuretics: Chlorothiazide or hydrochlorothiazide Frusemide and ethacrynic acid Spironolactone (remove potassium) 4. dilators: Nitrate Hydralazine Prazosin Captopril Na nitroprusside If no response, add. 5. Other inotropics: Dopamine & Dobutamine & Prenalterol Amrinone & Milrinone Aminophylline & Sulmazole I. Digitalis medications (digoxin, lanoxin) increase the force of contraction of the heart muscle and also control abnormal heart rhythms, especially atrial fibrillation and atrial flutter. Therefore, digitalis is most useful when someone with atrial fibrillation or atrial flutter has CHF. It improves heart function without increasing mortality. 1-unit Digitoxin = 0.1 mg 1-unit Digoxin = 0.25 mg 1-unit Digitoxin = 0.1 mg Preparation and dose 1. Loading dose: Initial digitalizing dose: full therapeutic dose = 12- 15 unit Rapid (24h): Moderate (3 days): 2 U X 3 times X 3 days Slow (7 days): 1 U X 3 times X 7 days Maintenance dose: dose needed to maintain the beneficial effects produced by initial digitalization (dose needed to replace the amount of digitalis metabolized or excreted every day)……………. ½- 2 U 2. Non loading dose: start with the maintenance dose …… in old and mild HF patients Action Contractility: ++ C.O. without increase O2. Strong short systole…….. Better emptying Long diastolic time ……… better filling Decrease stretch of cardiac muscle …………. More contraction Reduction of heart size Relief of venous congestion……. Decrease V.R. Rhythmicity: -- Chronotropic Small dose ……. inhibits S.A.N & delay AV conduction (By ++ vagal) Large dose ……inhibits S.A.N & delay AV conduction (By direct) Atropine can antagonize bradycardia in early digitalization as the vagal effect predominates, but after full digitalization atropine is without effect as the direct predominates. Automaticity: Toxic dose increases automaticity leading to V. Extrasystole V. Tachycardia V. Fibrillation ECG: 1. Long P-R …… slow conduction (AV conduction) 2. Short Q-T …… short duration of systole 3. Depress S-T 4. Flat (early toxicity) or inverted T wave 5. V. extrasystole or tachycardia Kidney: Diuretic only in CHF ++ C.O ……….. ++ R.B.F ……. ++ GFR ++ C.O ……….. ++ R.B.F …… decrease Renin ……. decrease angiotensin II ……….. decrease aldosterone. May compete with aldosterone. G.I.T: Nausea and vomiting ( local irritation & ++ C.T.Z) C.N.S: ++ vagal center, VMC, CTZ In toxic dose ……… hallucination, convulsion, visual disturbances Endocrine: Oestrogen like ……….. gynaecomastia Side effects: Early: Nausea, vomiting, and bradycardia < 60 b/min Late: 1. CVS: Bradycardia, heart block, increase automaticity in ventricle (extrasystole, V. tachycardia, V. fibrillation) 2. Extracardiac effects: 1. GIT: Nausea, vomiting 2. Eye: yellow green vision 3. Skin: Allergy 4. Gynecomastia: in male Treatment of digitalis arrythmias  Stop digitalis.  KCL  Heart block………….Atropine  V. Arrythmia with heart block……………diphenhydramine, propranolol, Lidocaine  Digitalis Abs (Digibind) The following increase digitalis toxicity Hypokalemia Hypomagnesemia Hypothyroidism Renal failure Hepatic failure Hypercalcemia Hyperacidosis Hyperthyroidism Old age Acute MI Contraindications: V. Tachycardia or extrasystole …………….. Fibrillation Partial H. block …………… complete H. block Renal diseases …………... (Digoxin) Hepatic disease ………….. (Digitoxin) II. Diuretics: This reduces the blood volume and the amount of blood that the heart has to pump, thereby reducing its workload. The goal is to maintain ideal weight by eliminating edema. III. Vasodilators IV. Other Inotropics 1. Amrinone and milrinone are phosphodiesterase inhibitors that increase the intracellular concentration of cAMP. This results in an increase of intracellular calcium and, therefore, cardiac contractility. 2. Beta-adrenergic agonists improve cardiac performance by causing positive inotropic effects and vasodilation. 3. Dopamine & Dobutamine are the most commonly used inotropic agent other than digitalis. Dobutamine leads to an increase in intracellular cyclic adenosine monophosphate (cAMP), which results in the activation of protein kinase. Slow calcium channels are one important site of phosphorylation by protein kinase. When phosphorylated, the entry of calcium ion into the myocardial cells increases, thus enhancing contraction. Thank You [email protected]