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11 Cards in this Set

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  • Back
(C)ardene - Nicardipine

-medication blocks the movement of calcium into the smooth muscle cells surrounding the arteries of the body and the heart
-Since calcium promotes contraction of muscle, blocking calcium entry into the muscle cells relaxes the arterial muscles and causes the arteries to become larger.
-This lowers blood pressure, which reduces the work that the heart must do to pump blood to the body. Reducing the work of the heart
-also it leads to decreased myocardial contractility and decreased myocardial oxygen demand

-mix 25mg/250ml D5W
-initiate 5mg/hr
-titrate q 10min
-increments of 2.5mg/hr to desired MAP
-max dose 15mg/hr
-Dobutamine is predominantly a β1-adrenergic agonist
-Dobutamine also has mild β2 agonist activity, which makes it useful as a vasodilator.
-βeta agonist- inc cardiac output, by raising heart rate (positive chronotropic effect) and increasing impulse conduction and increasing contraction thus increasing the volume expelled with each beat (increased ejection fraction).
-while Alpha 1 receptors mediate vasoconstriction, Beta 2 receptors induce vasodilation in vascular smooth muscle
-Inodilator, used to stimulate beta receptors located in the blood vessels to cause vasodilation
-Systemic vascular resistance is usually decreased with administration of dobutamine.
-SBP 70-100mmHg with s/s of HF and pulmonary edema
-mix 250mg in 250ml D5W (1000mcg/ml)
-2-20mcg/kg/min, increase in 5-10mcg, up to 40mcg/kg/min
-a beta1-selective (cardioselective) adrenergic receptor blocking agent (beta blocker)
-activation of beta1 receptors in the SA node by norepi results in depolarization of the SA node and inc HR and contraction
-esmolol slows down HR and dec contraction
-has a very short duration of action

-mix 2.5g in 250ml D5W, initiate at 50mcg/kg/min q 5min
-increase at: 50, 100, 200, 300mcg/kg/min
-end point is max dose 300mcg/kg/min, HR<60 or MAP <80

(E - 3)00, 200, 100, 50mcg/kg/min
Es = 2 letters
molol = 5 letters
2.5g in 250ml
Sodium Nitroprusside
-Nitroprusside acts on vascular smooth muscle to reduce afterload
-Sodium nitroprusside (SNP) has potent vasodilating effects in arterioles and venules (arterioles more than venules).
-Mix 50mg in 250ml D5W
-Initiate at 0.2mcg/kg/min, titrate 0.1mcg/kg/min
-Titrate at 1mcg/kg/min once 1mcg is reached
-Max dose is 10mcg/kg/min
-Nitrates are venodilators, and primary effect is to dec preload
-Nitrates decrease the preload and mediate the volume of blood presented to the left ventricle
-direct smooth muscle relaxation of the coronary arteries, improves coronary blood flow and increasing myocardial oxygen supply
-dec myocardial oxygen demand by reducing preload

-Nitro gtt 50mg/250ml D5W
-Infuse 10mcg/min inc q 5min by 10mcg/min
-Dopamine is also an excellent inotrope, it is also a vasoconstrictor, it increases afterload in pt with HF and will decrease stroke volume
-doses of 5-10mcg/kg/min dopamine inc inotropy with significant chronotropy
-at high doses > 10mcg/kg/min alpha effects cause peripheral vasoconstriction
-smooth muscles of the arteries and veins have mostly alpha1 and alpha2 receptors (A for Arteries & A for Alpha)
-activation of alpha1 and alpha2 receptors in the arteries results in inc contraction by arteriolar smooth muscle and an inc BP
-dopamine inc inotropy with significant chronotropy

-at high doses > 10mcg/kg/min alpha effects cause peripheral vasoconstriction
-400mg/250ml D5W, begin 5mcg/kg/min
-Mannitol is an osmotic diuretic, it elevates blood plasma osmolality, and results in enhanced flow of water from tissues to plasma, as a result of osmosis (water flow from high to low concentration)
-contraindicated in renal failure, pulmonary edema, CHF, shock
-Plasma osmolality- a measure of the concentration of substances, Na, Cl, K, urea, glucose in the blood
-Osmolality of blood inc with dehydration
-Osmolality of blood dec with overhydration

-1gm/kg over 5-10min
-Calcium Channel Blocker
-These drugs exert a strong negative inotropic effect without the long term benefits of beta blockers decrease myocardial oxygen demand by decreasing afterload, contractility, and HR
-Calcium ions regulate contraction in smooth and cardiac muscle
-CCB inhibit the movement of Ca ions across myocardial and vascular smooth muscle
-this leads to decreased myocardial contractility and decreased myocardial oxygen demand
-CCB also improve coronary blood flow via direct smooth muscle relaxation
-they also cause peripheral vasodilation from direct smooth muscle relaxation

-initial bolus of 0.25mg/kg IV over 2min
-followed by infusion of 10mg/hr
150mg IV over 10 min for Atrial dysrhythmias
300mg IV ACLS, repeat 150mg IV x1, infusion 1mg/min
Mix 450mg/250ml D5W
-Contra: cardiogenic shock, bradycardia, 2nd and 3rd degree blocks, dont use with meds that prolong the QT interval
-SE: vasodilation, dec BP, dec HR, AV blocks, inc QT interval, VF and VT
-pedi, 5mg/kg
Ca Chloride
-Reverse the membrane potential effects of the elevated ECF K by administering calcium, which can immediately reverse the membrane excitability

-Calcium chloride – 10mg/kg, administer slowly at less than 100mg/min, it has triple the free Ca available than what Ca gluconate provides, do not administer in same line as NaHC03

-Calcium gluconate – 10mg/kg, administer slowly at less than 100mg/min

Magnesium sulfate
Preterm labor
-initial dose: 4gm in 100ml LR or NS over 15-30min
-infusion: 2gm/hr
-1-2gm over 2min
-infusion 1gm/hr