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Pharmacology [CVS] 12- Heart Failure Treatment [Part 2- Digoxin – Dobutamine – Dopamine – Milrinone]

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In the previous lecture we’ve discussed the first part in the treatment options of heart failure in this lecture we’ll talk about the second part which is the anatropic drugs we’ll go through three groups digitalis glycosides beta agonists and phosphate ester ace inhibitors we’ll talk about their mechanisms trade names and uses positive inotropic agents enhance

The force of contraction of the heart so they increase cardiac output although these drugs act by different mechanisms the inotropic action is the result of an increased cytoplasmic calcium concentration that enhances the contractility of cardiac muscle again when calcium concentration increase force of contraction increases and cardiac output increases which we

Need to manage heart failure the first group in this category is cardiac glycosides or also known as digitalis glycosides they are a group of chemically similar compounds that come from the digitalis plant or known as fox glove the most widely used agent is digoxin now let’s discuss the exact mechanism of this agent at a cellular level there is a membrane-bound

Catalytic enzyme called sodium potassium atpase enzyme this enzyme hydrolyze atp to produce energy and this energy is needed for sodium to get out of the cell in exchange with potassium digoxin inhibit this enzyme so intracellular sodium concentration will increase so what happens is that sodium has to go out so cardiac fibers possess another mechanism which is

Exchange the intracellular sodium for extracellular calcium so the cardiac fibers will extrude sodium in exchange with calcium without consuming energy leading to increased intracellular calcium and inhibition of extrusion of calcium outside the cells and also releasing calcium stored in the sarcoplasmic reticulum all this will increase the concentration of calcium

Intracellularly so myocardial contractility will increase increasing the cardiac output vagal tone is also enhanced so both heart rate and myocardial oxygen demand decrease digoxin slows conduction velocity through the av node making it useful for atrial fibrillation digoxin therapy is indicated in patients with severe heart failure with reduced ejection fraction

After initiation of ace inhibitor beta blocker and diuretic therapy digoxin is available in oil and injectable formulations it has a long half-life of 30 to 40 hours it is mainly eliminated intact by the kidney requiring dose adjustment in renal dysfunction very important to know that digoxin has a very narrow therapeutic index antioxidant toxicity is one of the

Most common adverse drug reactions leading to hospitalization anorexia nausea and vomiting may be initial indicators of toxicity patients may also experience blurred vision yellowish vision xanthopsia and various cardiac arrhythmias decreased levels of serum potassium known as hypoglymia predispose a patient to dejockson toxicity because digoxin normally competes

With potassium for the same binding site on the sodium potassium atpase pump so how toxicity can be managed toxicity can often be managed by discontinuing digoxin determining serum potassium levels and replenishing potassium if indicated severe toxicity resulting in ventricular tachycardia may require administration of antiarrhythmic drugs and the use of antibodies

To digoxin digoxin immune fab which bind and inactivate the drug digoxin should also be used with caution with other drugs that may cause hypokalemia such as thiazide or loop diuretics and with drugs that slow av conduction such as beta blockers brypamil and diltiaism the second group of the anatropic drugs is beta agonists such as dobutamine and dopamine improve

Cardiac performance by causing positive inotropic effects and vasidylation dobutamine is the most commonly used anatropic agent other than digoxin beta-adrenergic agonists lead to an increase in intracellular cyclic adenosine monophosphate or camp which results in the activation of protein kinase protein kinase then phosphorylates slow calcium channels thereby

Increasing entry of calcium ions into the myocardial cells and enhancing contraction both drugs must be given by intravenous infusion and are primarily used in the short-term treatment of acute heart failure in the hospital setting and the last group we’ll talk about today is phosphatiesterase inhibitors such as melanon like beta adrenergic agonists it increases

The intracellular concentration of camp this results in an increase of intracellular calcium and therefore cardiac contractility that’s all for now about heart failure we are waiting for your comments and opinions about this topic in the next lecture we’ll start talking about cardiac arrhythmias so subscribe and wait for the upcoming videos

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Pharmacology [CVS] 12- Heart Failure Treatment [Part 2- Digoxin – Dobutamine – Dopamine – Milrinone] By Medical Videos [ ANIMATED ]