PMT, Kruse - Drugs for Heart Failure Flashcards
What type of agent is best used in systolic failure? wHy?
Inotropic agents (digoxin) directly treat myocardial dysfunction by increasing cardiac contractility.
What agents DO NOT improve survival?
Diuretics (except aldosterone does) and inotropic agents.
What are the three types of inotropic agents?
1) Cardiac glycosides - digoxin
2) Bipyridines - inamrinon and milrinone
3) B-agonists - dobutamine and dopamine
Digoxin:
- Agent and class
- Used for
- Pharmacokinetics
- Agent and class - Inotropic, cardiac glycoside
- Used for HF and afib
- Pharmacokinetics - oral and 1/day dose
Digoxin:
- MOA
- Desired physiological effects
- MOA - Inhibits membrane bound Na/K ATPase = increases Ca in SR
- Desired physiological effects: 1) increase contractility; 2) prolong AVN refractory period in supraventricular arrhythmias
Digoxin:
- Cardiac toxicity
- Other toxicity
- Cardiac - Arrhythmias and Tachycardia deteriorating into fibrillation is fatal.
- GI - anorexia/N/V/D
- CNS - hallucination, vision
Does SNS or PSN-mimetic effects dominate cardiac tissue at therapeutic levels of digoxin? What drug inhibits theses effects?
Parasympathomimetic effects.
Atropine inhibits
What electrolyte binds to the same sites as digoxin on Na/K ATPase? So, can use this electrolyte to do what?
Potassium. Use K to reduce digoxin toxic effects.
What increases risk of digoxin induced arrhythmias?
What do you give for a digoxin induced arrhythmia?
HyperCa and HypoMg
Mg
Inamrinone and milrinone
- Agent and class
- Used for
- Pharmacokinetics
- Agent and class - Cardiac glycoside, bipyridine
- Used for SHORT TERM support of circulation in SEVERE HF
- Pharmacokinetics - parenteral.
Inamrinone and milrinone
- MOA
- Desired physiological effects
- MOA - inhibition of PDE3, which increases cAMP
- Desired physiological effects - stimulate myocardial contractility and decrease LV afterload, which INCREASES CO
What two things have the same MOA as bipyridines?
Caffeine and theophylline (asthma meds, bronchodilator).
Inamrinone and milrinone toxicity, respectively.
Inamrinone - N/V/D, thrombocytopenia, liver enzyme changes.
Milrinone - arrhythmias
Dobutamine
- Agent and class
- Used for
- Pharmacokinetics
- MOA
- Desired physiological affects
- Toxicity
- Cardiac glycosides, B1-receptor AGONIST
- Used for systolic dysfunction and HF
- Pharmacokinetics - parenteral
- MOA - B1 receptor selective stimulator
- Desired physiological affects are increased SV and CO
- Toxicity - tachycardia and arrhythmia
Dopamine
- Agent and class
- Used for
- Pharmacokinetics
- MOA
- Desired physiological affects
- Toxicity
- Agent and class - cardiac glycoside, D1-receptor agonist
- Used for raising BP (limited use in HF patients)»_space; sepsis or anaphylaxis - in which circ failure dt vasodilation)
- Pharmacokinetics - parenteral
- MOA - D1 receptor selective stimulator
- Desired physiological affects - 1) low doses vasodilate, 2) Intermediate doses stimulate B-receptors on heart 3) high doses cause peripheral vasoconstriction (stims alpha)
- Toxicity - tachycardia, ischemia in CAD