Chapt 25 - Pharm
Digoxin: dosage and admin / Oral Tablet / Adults / Pg 512
Digitalizing (Loading): RAPID: 0.75 - 1.25 mg (750 - 1250 mcg) divided into two or more doses, each adminstered at 6 to 8 hr intervals. SLOW: 0.125 - 0.5 mg (125 - 500 mcg) once daily for 7 days Maintenance: 0.125 - 0.5 mg (125 - 500 mcg) once daily
How should digoxin therapy be dosed? Pg 511
* DIGITILIZATION: is referring to the process of initiating a client on digoxing therapy. / digitalization is the saturation of body tissues with enough digoxing to improve the signs and symptoms fo heart failure or atrial fibrillation. * 2 METHODS OF DIGITALIZATION: rapid (fast) = requires hospt for the client slow (method) = ususally perscribed in an abulatory setting. * RAPID DIGITALIZATION (loading) : reserved for client who are in acute distress from heart failure. IF the client has not previously recvd any digoxin, IV digoxin is given in a divided dosease over a (24 HOUR PERIOD) * DIGOXIN MAY BE PERSCRIBED: 0.5 mg IV now and 0.25 mg IV every 6 hours for two doses (for a total of 1 mg), digoxin you want to give a loading dose of dig because pt is going to hospt w/ fast rate, you would give IV usually slow.
Digoxin Toxicity (Hyperkalemia) pg 514 Box 25-4
* Elevated potassium levels may also predispose to cardiac dysrhythmias n digoxin toxicity. Potential cause of hyperkalemia include renal insufficiency, increased dietary or IV potassium, ACE inhibitors, ARB's, Potassium sparing diuretics.
Digoxin Toxicity (Hypercalcemia) pg 514 Box 25-4
* Exccess calcium in teh presence of digoxin may cause SINUS BRADYCARDIA, AV conduction BLOCK, n ectopic dysrhythmia.
Digoxin Toxicity (Pathologic Conditions) pg 514 Box 25-4
* Kidney, liver, n severe heart disease are major factors in digoxin toxcity. Approx 80% of dig is excreted by the KIDNEYS.
Digoxin Toxicity (Potassium Loss) pg 514 Box 25-4
* Low potassium levels can increase digoxin cardiotoxicity. Becuz potassium inhibit the excitability of the heart, a depletion of body or myocardial potassium increased cardiac excitability. Low extracellular potassium is synergistic w/ digoxin n enhances ectopic pacemaker activity (dysrhythmias) * Reason for K+ Loss: - vomiting, diarrhea, or gastric suctioning - the use of various diuretics - poor dietary intake or severe dietary restrictions that decrease electrolyte intake can cause a loss of K+ - adrenal steroids cause K+ loss n Na+ retention. - surgical procedures associated w/ severe electrolyte disturbances. - the use of potassium free IV fluids can cause HYPOkalemia.
Digoxin Toxicity Pg. 513
* Obtaining an ECG is important to rule out dysrhytmias. * If dysrhytmias are noticed due to Digoxin, the toxicity can cause premature ventricular beats, paroxysmla atrial tachycardia w/ AV Block, progressing AV Blocks, n ventricular dysrhytmias suchas as ventricular tachycardia. * Other drugs can create digoxin toxicity, for example: loop diuretics and thiazide diuretics commonly result in HYPOKALEMIA / pt is already losing potassium with these meds, which puts them at risk for HYPOKALEMIA, then they take DIG and because of loop/thiazide make the pt prone to DIG Toxicity. (just be aware) * Look @ electrolyte assessment becuz alterations in calcium, magnesium, n particularly potassium can be life threatening to ventricular dysrhytmias in the pressce of elevated dig levels.
chronotropic
* action affect heart rate. * POSITIVE CHRONOTROPIC: effect is produced if the drug accelerate th eheart rate by increasing the rate of impluse formation in the SA Node. * NEGATIVE CHRONOTROPIC: drug has the opposite effect and slows the heart rate by decreasing impulse formation.
inotropic
* effect influence myocardial contractility. * POSITIVE INOTROPIC: effect strengthen or increase the force of myocardial contraction * NEGATIVE INOTROPIC: effect weaken or descrease the force of myocardial contraction.
dromotropic
* effect refers to drugs that affect conduction velocity through specilized conducting tissues. * POSITIVE DROMOTROPIC: actions speeds conduction * NEGATIVE DROMOTROPIC: action delays conduction
How is digoxin used in the management of heart failure? pg 510
A heart in failure is no longer capable of supplying body tissue w/ adequate oxygen n nutrients or of removing metabolic waste products. Dig is used as a positive inotrope to increase myocardial contractility. The increased force of systolic contraction causes the ventriclees to empty more completely. When a slower heart rate is occuring caused by dig, this permits more complete filling in the ventricles and will result in the following: * Venous pressure falls, n the pulmonary n systemic congestion n their accompanying s/s are either diminished or eliminated. * Coronary circulation is enhanced, myocardial oxygen demandi s reduced, and the supply of oxygen n nutrients to the myocardium is improved. * Heart size is often decreased toward normal.
Common dose related adverse effects of DIGOXIN
ANOREXIA as well as nausea, bradycardia, visual disturbances mainifest by yellow vision, stomach pain, n dysrthymias. * Loss of appetite is ususally the 1st sign of toxicity; nausea, vomiting, n ab distress usually occur several days after teh anorexia.
Digoxin: dosage and admin / IV / Adults Pg 512
Digitalizing (Loading) 0.4 - 0.6 mg (400 - 600 mcg) initially, then 0.1 - 0.3 mg (100 - 300 mcg) q6-8h as needed. Maintenance: 0.125 - 0.5 mg (125 - 500 mcg) daily as a single dose or in divded doses daily
Digoxin: dosage and admin / Oral Capsule / Adults / pg 512
Digitalizing (Loading): RAPID: 0.4 - 0.6 (400-600 mcg), followed by 0.1 - 0.3 mg (100 - 300 mcg) q6-8hr as necessary SLOW: 0.05 - 0.35 mg (50 - 350 mcg) daily in two divided doses; repeat dose for 1-3 weeks to reach steady state serum levels Maintenance: 0.05 - 0.35 mg (50 - 350 mcg) PO once or twice daily, as necessary.
Digitalis is derived from the biennial flower
FOXGLOVE
digoxin (Lanoxin)
INDICATION: to treat heart failure n to slow ventricular rate in atrial fibrillation and atrial flutter. ADVERSE EFFECTS: heart block, bradycardia, ventricular fibrillation, n other cardiac dysrthymias, n serious electrolyte imbalances. SIDE EFFECTS: nausea, vomiting, diarrhea, dizziness, visual disturbances, rash, hallucinations, confusion, dizziness, n delirium.
Digibind (digoxin immune Fab) Pg 513
It is an ANTIDOTE for severe digoxing toxicity. * Digoxin immune fab binds and makes complex molecules with digoxin in the serum. These molecules are excreted by the kidneys. As more tissue digoxin is released into the serum to maintain equilibrium, it is bound and removed by this product, which rsults in lower levels ofdigoxin in serum and body tissues. * Adverse effects: close monitoring is necessary becuz the withdrawal of dig may result in decrease cardiac output, HF, n HYPOkalemia..
Digoxin posesses positive inotropic action, negative chronotopic action, and negative dromotropic action.
POSITIVE INOTROPIC ACTION: this is the main function of digoxin and it increases myocardial contractility. NEGATIVE CHRONOTROPIC AND NEGATIVE DROMOTROPIC ACTIONS: negative chronotropic- decreases heart rate, negative dromotropic- slow conduction velocity.
Box 25-3 (Determining Serum Digoxin Concentration)
The therapeutic serum digoxin concentration is dependent on indication. * For HF Management: the therapeutic range should be 0.8 to 2 ng/ml. * For dysrhythmias the therapeutic range should be 1.5 to 2.5 ng/ml. * Timing of Digoxin Levels: Digoxin levels should be obtained as trough levels (immediately before the next scheduled dose) * Remember digoxin serum levels are to be used just as a GUIDE, there has been cases where digoxin toxicity occurs with dosages less than 2 ng/ml
How is digoxin used in the management of atrial fibrillation? pg 511
therapeutic serum level should be b/w: 1.5 - 2.5 ng/ml. * dig is ideal for slowing ventricular rate because it increase the refractory period of the AV junction n slows conduction at this site, higher doses of dig are often required to achieve this effect, so with that said be sure to know that the therapetuic serum level should be 1.5 - 2.5 ng/ml.