Flashcards for:
Drugs Used in Congestive Cardiac Failure

The sympathetic nervous system increases heart rate and contractility initially, and the Renin-Angiotensin-Aldosterone System (RAAS) is activated, causing vasoconstriction and fluid retention.

Digoxin toxicity can cause nausea, confusion, and arrhythmias. Treatment includes stopping the drug, correcting electrolyte imbalances, using antiarrhythmic drugs, Atropine for bradycardia, temporary pacing for heart blocks, and Digibind antibodies for severe cases.

Thiazides (mild diuretics), loop diuretics (strong diuretics like furosemide), and K+-sparing diuretics (e.g., spironolactone) are used to reduce blood volume and preload.

Digoxin increases intracellular calcium to improve contractility and is used in severe systolic dysfunction and CHF with atrial fibrillation. It requires careful monitoring for toxicity.

Phosphodiesterase inhibitors (e.g., Amrinone, Milrinone) are used short-term to increase cyclic AMP in severe heart failure. Long-term use is limited due to the risk of increased mortality.

The Frank-Starling Law states that the more the ventricle is filled with blood, the stronger it contracts within physiological limits. This leads to increased end-diastolic volume (EDV) and contractility.

A failing heart has decreased contractility, leading to reduced cardiac output (CO) despite higher end-diastolic volume (EDV).

ACE inhibitors and ARBs reduce preload by decreasing salt and water retention and reduce afterload by vasodilation. They also help manage RAAS to prevent pathological remodeling of the heart.

They are reserved for specific cases due to the risk of receptor downregulation when used long-term and are primarily used for acute phases of heart failure.

Diuretics and vasodilators like ACE inhibitors and angiotensin II receptor blockers (ARBs) are used to reduce preload.

LaPlace's Law states that the pressure generated by the heart is proportional to wall tension and inversely proportional to the radius of the ventricle. In a failing heart, an increased radius and stress reduce effective pressure generation.

The main goals are to reduce preload, reduce afterload, and improve contractility.

The typical stroke volume is 70 ml, and the end-diastolic volume (EDV) is around 140 ml in a healthy heart.

Initial management includes ACE inhibitors, ARBs, and diuretics to reduce preload and afterload, improve survival, and reverse pathological changes in the heart.

The heart is not pumping efficiently.