1. cause hypokalemia which increases the risk of digitalis arrhythmias; potassium supplements should be given prophylactically.
2. DRUG INTERACTION
2.1. Diuretics:
2.2. Verapamil, diltiazem, captopril, propafenone and amiodarone
2.3. increase plasma concentration of digoxin → plasma concentration of digoxin is doubled → toxicity can occur.
2.4. Adrenergic drugs:
2.4.1. can induce arrhythmias (both increase ectopic automaticity).
2.4.2. absorption is increased by atropinic drugs.
2.5. Propranolol, verapamil, diltiazem and disopyramide:
2.5.1. may additively depress A-V conduction and oppose positive inotropic action.
2.6. Digoxin
2.6.1. Q
2.7. Succinylcholine:
3. Cardiac Glycosides
3.1. This drug increase the contractality of the heart.
3.2. Mechanism of action
3.2.1. Inhibit Na + / K + ATPase enzyme
3.3. PHARMACOLOGICAL ACTIONS:
3.3.1. 1- Increase the force of myocardial contraction (+ve inotropic) leading to decrease in: heart size, venous pressure and edema 2- Slow heart rate ( -ve chronotropic ) by vagal stimulation
3.4. Therapeutic uses
3.4.1. - Congestive heart failure -Atrial arrhythmias: - Atrial flutter - Atrial fibrillation - Supraventricular tachycardia
3.5. Cardiac adverse effects
3.5.1. - digitalis-induced arrhythmias can cause any type of arrhythmia especially: - extrasystoles - coupled beats (Bigeminal rhythms ) - ventricular tachycardia or fibrillation - A.V.block, - cardiac arrest.
3.6. Calcium:
3.6.1. synergises with digitalis → precipitates toxicity.
3.7. Factors that increase digitalis toxicity: - Small Lean body mass - Renal diseases - Hypothyroidism - Hypokalemia - Hypomagnesemia - Hypercalemia
3.8. Extra cardiac adverse effects
3.8.1. -GIT : common ( the earliest signs of toxicity ): Anorexia,nausea, vomiting, diarrhea CNS: Headache, visual disturbances, drowsiness
4. First-line therapy -ACE inhibitors -Vasodilators -β blocker
5. 2 DISTINCT GOALS OF DRUG THERAPY
5.1. (a) Relief of congestive/low output symptoms: *ACE inhibitors *Vasodilators -nitrate,, nitroprusside,hydralazine *β blocker—Nebivolol, Carvedilol, Metoprolol, bisoprolol *Diuretics—Furosemide (Loop diuretic), thiazides * Positive Inotropic drugs—Digoxin, dobutamine
5.2. Second-line therapy -Diuretics -Positive Inotropic drugs
6. SEQUENCE-LINE OF THERAPY
7. can induce arrhythmias in digitalized patients.
8. (b) Arrest/reversal of disease progression and prolongation of survival: *ACE inhibitors, *β blockers *Aldosterone antagonist- Spironolactone, eplerenone
9. Heart Failure physiological abnormality is a cardiac output that is inadequate to meet the metabolic demands of the body, initially during exercise but, as the syndrome progresses, also at rest.
10. COMPENSATORY PHYSIOLOGYCAL
10.1. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of CHF and contribute to disease progression.
10.1.1. -Decrease contractility -Increase heart rate -Increase preload -Increase afterload -Increase workload of heart
11. MANAGEMENT
11.1. Acute decompensated heart failure
11.1.1. -In acute decompensated heart failure, the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs.
11.1.2. -This entails ensuring that airway, breathing, and circulation are adequate.
11.1.3. Positive inotropic drugs, very helpful in acute failure. Diastolic dysfunction does not usually respond optimally to positive inotropic drugs
11.2. Chronic management
11.2.1. -The goals of treatment for people with chronic heart failure are the prolongation of life, the prevention of acute decompensation and the reduction of symptoms, allowing for greater activity.
11.2.2. -Treatment strategies provide significant improvement in the relief of symptoms, exercise tolerance, and a decrease in the likelihood of hospitalization or death.
12. -Management of heart failure Treatment focuses on improving the symptoms and preventing the progression of the disease. -Treatments include lifestyle and pharmacological modalities.
13. Compensatory mechanisms: 1)Tachycardia and increased contractility through sympathetic nervous system activation. 2)The Frank-Starling mechanism, whereby increased preload increases stroke volume 3)Vasoconstriction (due to Activation of renin-angiotensin system) 4)Ventricular hypertrophy and remodeling.
14. INTRODUCTION
14.1. Due to Two types:
14.1.1. 2) Diastolic dysfunction - increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial disease, myocardial ischemia and MI, mitral or tricuspid valve stenosis and pericardial disease -results in ventricle does not fill adequately and decrease cardiac out put (Increased workload imposed on heart)
14.1.2. 1)Systolic dysfunction -reduction in muscle mass, dilated cardiomyopathies, and ventricular hypertrophy. -results in ventricle unable to pump blood effectively.