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16 Cards in this Set

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Cardiac Glycosides-mechanism of action
Inhibit Na/K ATPasa--increased Ca2+ in SR-increased Ca2+ release & binding to troponin-tropomyosin moves allowing actin/myosin interaction--increased contractile force & CO

Central Vagal stimulation via PANS--facilitation of muscarinic activity and sensitation to baroreceptors
Decreased sympathetic activity

High doses:
Sympatomimetic (Beta 1 like)+ chronotropy, dromotropy and inotropy
Do Cardiac Glycosides improve survival
No. (ACE/ARB's usually 1st choice to treat HF)
Drugs that can cause Drug Induced SLE

hydralazine,isoniazid, procainamide, penicillamine, phenytoin chlorpromazine, sulfasalazine, methyldopa, and quinidine
(usually after taking the drug at least ~3-6 months)

ANA antibody/ anti-histone antibody
it's not HIPPP to have lupus
Most widely used cardiac glycoside (digitalis drug)
Inhibits Na/K ATPase-Ca2+ increased-greater cardiac contractibility (+inotropy)
Vagal stimulation-decreased SA nodal rate
Sympatomimetic (Beta 1 like)+ chronotropy, dromotropy and inotropy
T1/2 20-40 h, renal cl, 25% protein bound, Vd 6 L/kg
like digoxin but longer T 1/2, hepatic cl, more protein bound
T 1/2 120-160 (vs. 20-40)
CL Hepatic (vs. renal)
Vd 0.6 L/kg (v.s 6)
Protein Binding 90% (vs. 25%)
Digitalis Toxicity
Narrow therapeutic window.
Hypokalemia enhances dig activity ("digitalis pump is inhibited by K+) and hyperkalemia decreases effects

Signs: Anorexia, nausea, EKG (decreased QT interval, T wave inversion, PVB's, bigeminy)
CNS-disorientation, visual "halos", hallusinations
EKG changes in Digitalis Toxicity
EKG (decreased QT interval, T wave inversion, PVB's, bigeminy)
Signs of severe Cardiac (Digitalis) Toxicity
SVT's, AV nodal tachycardia or AV block
VT or VF
Management of Digitalis Toxicity
Adjust electrolytes (made worse with low K+ and Mg and high Ca2+)
Use antiarrhytmics (lidocaine, phenytoin-class 1B)
digitalis Fab antibodies (Digibind)
Cardiovert only if VF
Drug interactions that may cause digitalis toxicity
low K+, Mg and high Ca2+ (diuretics), quinidine, amiodarone, verapamil, NSAIDs, symptamomimetics and some antibiotics (erythromycin)

* no dig for WPW pt's
Inamrinone (Amrinone)
The cyclic AMP–phosphodiesterase (PDE) inhibitors

Inhibit PDE--increased cAMP (via decreased degradation)-- positive inotropy and vasodilation

short term support of advanced cardiac failure
Amrinone causes thrombocytopenia (10%) and milrinone may decrease survival in heart failure
First choice treatment in heart failure
ACE inhibitors

low dose 2< micrograms/kg per minute

Intermediate 2-5

High 5-15
Endogenous Catecholamine

Low dose: vasodilation-via cAMP and D2 causing decreased NE and alpha adrenergic tone (D2 receptors prominent in renal & splancnic vascular beds. (increased GFR)

Also direct effects on renal tubular epithelial cells that promote diuresis

Intermediate: stimulates beta receptors on the heart and vascular sympathetic neurons (cardiac contractibility)

High: no good for CHF. Too much vasoconstriction--increased afterload
B agonist
Racemic mix. Both stimulate B1 & B2. - form also alpha 1

increase in stroke volume (positive inotrop)

No effect on D2--so no independent GFR increase (increase proportional to increase in CO)

SE: tachycardia and arrhythmias, tolerance
Vascular selective CCA
Non-selective beta blocker-decreased refractory pump failure & sudden death

(bisprolol-Beta 1 selective--also survival benefit) and spironolactone (diuretic)

Combine tx w/ ACEI