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18 Cards in this Set

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Digitalis: Digoxin
any of the steroid or steroid glycoside that exert positive inotropic and electrophysiologic effect on heart

Primary agent used clinically is called DIGOXIN
used to enhance CO during CHF but no effect on CO of normal pt.

used to trt supraventricular cardiac arrhythmias (tox may also cause arrhythmias)
Digoxin vs. digitoxin
Digitoxin does not have a 12' hydroxyl group that digoxin does.

Digitoxin has better oral bioavailability, slower onset of action, reach peak in 4-6 hrs (vs. digoxin in 1.5- 4 hrs). It's is highly protein bound (97% vs. 23% for digoxin) Better Therapeautic plasma conc. (14-26) then digoxin (.5-1.2) and toxic plasma conc also better, 34 vs >2.4 for digoxin.
Why is digoxin not so great in emergency?
Peak effect takes hours, upto 4 hours for digoxin or 6 hours for digitoxin (IV)
Digoxin elimination and renal status
T1/2 is 1.6 dz but depends on renal function, and clear slowly with age and renal dysfunction.

May clear faster in some where it is also metabolized by gut bacteria
Digoxin: Drug interractions
Most important ones are certain antiarrhythmia drugs: Quinidine, Verapamil, Amiodarone... these drugs cause [digoxin] to double.

So decrease digoxin dose by 50% and monitor serum levels as necessary.
Digoxin: Mechanism
normally Na-K ATPase maintains sodium gradient within the cell by removing Na from cell and bringing in K. The Low Na in the cell allows for Na-Ca exchange where Na flows into the cell and Ca is kicked out of the cell.

When Na-K ATPase is out of business by digoxin binding and inhibiting Na-K ATPase pump, the Na builds up in the cell and so intracellular Na gradient is high and extracellular Na doesn't go in, and can't kick out Ca, hence leading to ACCUMULATION OF CALCIUM

This causes increase in force and velocity of contraction.
Digoxin and hypokalemia
since digoxin binds the same site as K, in hypokalemia, digoxin can more readily bind and disable the Na, K ATPase and its action is enhanced.
Digoxin Effects: Pt with Heart Failure
positive inotropic action causes >> Increase CO > increase renal perfusion > enhanced sodium excretion and reduction in edema.

Enhanced CO > Increased EF > decrease cardiac filling pressure > reflex reduction in HR and peripheral resistance > Sx improvement

Decreased venous pressure and LV end diastolic vol allows distended heart to return to smaller, more normal size and relieve edema.
Digitalis and O2 consumption
while increase contractility cause more o2 consumption, this is offset by decrease in HR and Heart size.
Digitalis in normal pts
Digitalis posses DIRECT VASOCONTRICTOR action, which causes incrase peripheral resistance in normal pts, but increased inotropic state of the heart doesn't translate to increase CO because of increase Afterload.

In pts with CHF, their peripheral resistance is already high due to compensatory vasocontriction, so the inotropic effects are realized.
Digoxin and CHF
should be used in pts with LV systolic dysfunction (dilated cardiomyopathy) usually doe to ischemia or infarct, myocarditis, toxins, or chronic mechanical overload. Used to treat Type II, III and IV heart failure symptoms.

Digoxin as Anti-Arrhythmic drug
Mech: enhance vagal tone (increase baroreceptor sensititivy, increase heart sensitivity to Ach, slow AV nodal conduction)

used in ATRIAL fibrillation, atrial flutter, Paroxysmal supraventricular tachcarydia (PSVT).
Digitalis Toxicity
Predisposing factors: DECREASED plasma K (or Mg) and increased plasma Ca

Renal (digoxin) or hepatic (digitoxin) dysfunctin.


Drug Interractions: verapamil, diltiazem, beta blockers, Kaliuretic diuretics, sympathomimetics
Digitalis: manifestations of toxicity
Arrhythmias, anorexia, nausea (stim. of area postrema), visual changes such as distortion of color vision or appearance of Halos on dark, headache, fatique, depression, confusion.
Arrhthmias as Toxic effect of digitalis
toxic dose can cause most any type of arrhythmias or conduction block.

Mech: Neurally via activatin of both Symp and parasymp nerve to heart.

Directly, by overinhibition of too many Na, K ATPases, causing alt. in Ca, K and Na fluxes.

The neural and direct effect synergize resulting in AV dissociation and arrhythmias.
Therapy for Digoxin toxicity
STOP drug, ECG monitoring, correct electrolytes, Low K or Mg common, High K likely to be fatal, Use atropine (pacing contraindicated)

Give Fab "Digibind", MgSO4
Other inotropic agents
symp amines (dopamine, dobutamine), PDE3 inhibitor (3 is spec for heart, leads to elecated intracellular Ca).