IV digitalis?

Besides knowing the effects and uses of the drug be aware of the odd things that it is likely to do because that is what instructors usually like to develop questions about. It it s drug that is derived from a plant called purple foxglove, or Digitalis purpurea. Digitalis is considered a poison. Overdose, or toxicity produces the following symptoms (you better know these): nausea, vomiting, anorexia, diarrhea, abdominal pain, wild hallucinations, delirium, and severe headache. Later symptoms include irregular and slow pulse, tremors, various cerebral disturbances, especially of a visual nature (unusual color visions with objects appearing yellowish to green, and blue halos around lights), convulsions, and deadly disturbances of the heart including heart block, bradycardia or tachycardia. The drug digoxin immune FAB (Digibind) is the antidote for digoxin toxicity or poisoning.

The cardiac glycosides increase the force of myocardial contractions, increase the effect of diuretics which eliminate excess sodium and water and also increase the effect of vasodilator drugs which indirectly increase the amount of blood pumped by the heart (cardiac output). They are used in treating atrial fibrillation and congestive heart failure. Digoxin is excreted more rapidly than digitoxin.

You will usually only see digitalis used in the form of digoxin or digitoxin. All forms of digitalis are cardiac glycosides. Digoxin (Lanoxin) is a digitalis preparation derived from the plant species Digitalis lanata. Digitoxin is derived from Digitalis purpurea. The difference between the two is in their rate of absorption and duration of action. They are slowly metabolized and excreted so serum drug levels are routinely done to monitor and measure the amount of this drug in patients so the dosage can be adjusted as necessary. Food delays the absorption of the digitalis from the GI track when it is taken orally but does not interfer with the extent of the amount of the drug that is eventually absorbed. Half-life of digoxin is 1.5 to 2 days; half-life of digitoxin is 5 to 7 days. Digoxin is excreted via the urinary tract; Digitoxin is lipid soluable and must be metabolized by the liver. Digitalis works by inhibiting sodium-potassium ATPase. This results in an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of sodium-calcium exchange. This increased intracellular calcium gives a positive inotropic effect. Obviously, if given IV, it will go into action slightly faster than given orally.

It interacts with glucosteriods causing potentiation of the action of the digitalis that leads to hypokalemia which can lead to possible digitalis toxicity. When it's administered with anitfungal or antiviral drugs and antineoplastics it induces potassium loss, hypokalemia, potentiates cardiac arrhythmias and digitalis toxicity.