UWORLD Cardio Pharm 3/14a Flashcards
Dobutamine receptor effect
- B1 agonist
- weak B2, a1 agonist
Dobutamine MoA
- Gs –> activate adenylyl cyclase –> + cAMP
- increase Na & Ca channel activation in nodes
Dobutamine effects
- increase contractility
- increase HR
- increase CO
- B2 > a1 = mild vasodilation –> decrease SVR
Dobutamine indications
- LV systolic dysfunction
- cardiogenic shock
Digoxin MoA
- inhibit Na/K ATPase
- decrease Na efflux
- decrease activity of Na/Ca exchanger
- decrease Ca efflux
- increased intracellular Ca
- activate vagus nerve
- increase parasympa tone
Digoxin effects
- positive inotropy
- slow conduction thru AV node
Digoxin toxicity
- nonspecific = nausea, ab pain, fatigue, dizziness, confusion, blurred vision, abnormal color perception
- cardiac arrhythmias = bradycardia, junctional escape beats (AV node block)
- hyperkalemia
chlorthalidone?
thiazide
thiazide MoA
- inhibit Na/Cl cotransporters in distal convoluted tubule
- decrease reabsorption of Na & Cl
Thiazide effects
- decrease intravascular volume
- reduce CO
- lower SVR
- lower BP
thiazides - raise? lower?
raise
- calcium
- uric acid
- glucose
- LDL
- TGs
lower
- sodium
- potassium
- magnesium
arteriolar vasodilators
hydralazine
minoxidil
arteriolar vasodilator effects
- reduce SVR
- lower BP
arteriolar vasodilator ADR
- stimulate baroreceptors = reflex sympa tone
- increased HR, contractility, CO
- stimulate RAAS = Na/fluid retention & peripheral edema
arteriolar vasodilator indications
- acute severely elevated BP
- combo with sympatholytics & diuretics for resistant HTN
digoxin indications
AF & flutter with RVR
sx of chronic systolic heart failure (pos inotropy)
Milrinone
selective PDE3 enzyme inihibitor
inotropic agent
Milrinone MoA
- inhibit PDE-3 in heart and vascular smooth muscle
- decrease rate of cAMP degradation –> + cAMP
- increased intracellular Ca in heart
Milrinone effects
- positive inotropy
- systemic arterial and venous dilation
- decrease BP
nitrates MoA
- converted to NO by vascular smooth muscle
- increase intracellular cGMP
- vascular smooth muscle relaxation
nitrates DDI
phosphodiesterase inhibitors
both cause increased cGMP –> extreme vasodilation
nitrates = increased cGMP PDEi = decreased degradation of cGMP
First dose hypotension
- ACEi ADR
- in pts with high plasma renin (vol depletion from diuretics, or heart failure)
- abrupt removal of ATII vasoconstriction –> decreased SVR –> drop in BP
avoid by starting at low dose and slowly titrating up
