Heart failure is a long, progressive disease with its ultimate fate being remodeling of the heart through hypertrophy and fibrosis of muscle tissue. The heart fails as a pump, leading to decreased cardiac output. Forward failure is a systolic dysfunction, inability to pump forward to maintain cardiac output (CO), decreased blood pressure (BP) is main consequence, BP = CO x peripheral resistance (PR). Basically, this involves the heart not pumping well against an increased afterload.
Backward failure is a diastolic dysfunction due to inadequate relaxation to permit filling, causes cardiac and pulmonary congestion with fluid accumulation. The ability to pump forward may increase when filling pressure is increased
For example, this occurs when there is cardiac congestion. CHF usually involves both aspects, plus ventricular hypertrophy and remodeling, involving an increase in connective tissue, which is not good for the heart.
1. Gastrointestinal irritation, nausea, vomiting, diarrhea, stimulates CTZ
2. Visual effects involves blurring and halo effect
3. Central nervous system (CNS) effects include confusion, hallucinations, and psychosis
4. Cardiac arrhythmic effects involve bradycardia, AV block, pre-ventricular contractions, ventricular tachycardia, and ventricular fibrillation
Electrolyte and drug interactions involve the following:
1. Hypokalemia is caused especially by potassium-losing diuretics, which increases digoxin toxicity
2. Hyperkalemia is caused especially by ACE inhibitors and potassium-sparing diuretics, which reduces digoxin toxicity
3. Hypercalcemia and increased intracellular calcium increases digoxin effects and toxicity
4. Hypermagnisum reduces digoxin toxicity
5. Quinidine increases digoxin toxicity
This list is important for the upcoming evaluation