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It is a medication used to manage and treat heart failure and certain arrhythmias, and abortion. It is in the cardiac glycoside class of drugs. This article outlines the indications, action, and contraindications for digoxin as a valuable agent in managing heart failure and certain arrhythmias. This activity will highlight the mechanism of action, toxicity profile, and other vital factors, e.g., dosing, pharmacodynamics, pharmacokinetics, and monitoring, pertinent for members of the healthcare team in the management of patients who have been prescribed digoxin.

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Streptokinase can be useful in the management and treatment of acute ST-segment myocardial infarction, deep vein thrombosis, pulmonary embolism, arterial thrombosis or embolism, and arteriovenous cannula occlusion. It is in the thrombolytic class of medications. This activity reviews the indications, action, and contraindications for streptokinase as a valuable agent in the treatment of thrombotic and embolic disorders. This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the interprofessional team healthcare team in the treatment of patients with thrombotic and embolic events and related conditions. It is no longer commercially available in the United States.

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Others: Digitek, Digox, Lanoxicaps, Cardoxin

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All of digoxin's actions are mediated through its effects on Na-K ATPase. This enzyme, the “sodium pump,” is responsible for maintaining the intracellular milieu throughout the body by moving sodium ions out of and potassium ions into cells. By inhibiting Na-K ATPase, digoxin.

It causes increased availability of intracellular calcium in the myocardium and conduction system, with consequent increased inotropy, increased automaticity, and reduced conduction velocity

It indirectly causes parasympathetic stimulation of the autonomic nervous system, with consequent effects on the sino-atrial (SA) and atrioventricular (AV) nodes

It reduces catecholamine reuptake at nerve terminals, rendering blood vessels more sensitive to endogenous or exogenous catecholamines

It increases baroreceptor sensitization, with consequent increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure

It increases (at higher concentrations) sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves

It allows (at higher concentrations) progressive efflux of intracellular potassium, with consequent increase in serum potassium levels.

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It acts with plasminogen to produce an "activator complex" that converts plasminogen to the proteolytic enzyme plasmin. The t Â½ of the activator complex is about 23 minutes; the complex is inactivated, in part, by antistreptococcal antibodies. The mechanism by which dissociated streptokinase is eliminated is clearance by sites in the liver; however, no metabolites of streptokinase have been identified. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. Plasmin is inactivated by circulating inhibitors, such as (alpha)-2-plasmin inhibitor or (alpha)-2-macroglobulin. These inhibitors are rapidly consumed at high doses of streptokinase.

Intravenous administration has been shown to reduce blood pressure and total peripheral resistance with a corresponding reduction in cardiac afterload.

Intravenous infusion of Streptokinase is followed by increased fibrinolytic activity, which decreases plasma fibrinogen levels for 24 to 36 hours. The decrease in plasma fibrinogen is associated with decreases in plasma and blood viscosity and red blood cell aggregation. The hyperfibrinolytic effect disappears within a few hours after discontinuation, but a prolonged thrombin time may persist for up to 24 hours due to the decrease in plasma levels of fibrinogen and an increase in the amount of circulating fibrin(ogen) degradation products (FDP). Depending upon the dosage and duration of infusion of Streptokinase, the thrombin time will decrease to less than two times the normal control value within 4 hours, and return to normal by 24 hours.

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Heart Failure in Adults

It is indicated for the treatment of mild to moderate heart failure in adults. Moreover, it increases left ventricular ejection fraction and improves heart failure symptoms as evidenced by improved exercise capacity and decreased heart failure-related hospitalizations and emergency care, while having no effect on mortality. Where possible, it should be used in combination with a diuretic and an angiotensin-converting enzyme (ACE) inhibitor.

Heart Failure in Pediatric Patients

It increases myocardial contractility in pediatric patients with heart failure.

Atrial Fibrillation in Adults

It is indicated for the control of ventricular response rate in adult patients with chronic atrial fibrillation.

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Patients with Myocardial Infarction

It is indicated for use in the management of acute myocardial infarction (AMI) in adults, for the lysis of intracoronary thrombi, the improvement of ventricular function, and the reduction of mortality associated with AMI, when administered by either the intravenous or the intracoronary route, as well as for the reduction of infarct size and congestive heart failure associated with AMI when administered by the intravenous route. Earlier administration of Streptokinase is correlated with greater clinical benefit.

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Its use requires caution in cases of:

Hypercalcemia/hypocalcemia

Renal impairment

Diseased SA node

Bradycardia

AV block

Restrictive cardiomyopathy

Constrictive pericarditis

Thyroid disease  (Hypothyroidism leads to delayed drug clearance, and hyperthyroidism does the opposite.)

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The thrombolytic nature of streptokinase makes it contraindicated in patients with active internal bleeding, as it can worsen bleeding in some patients. It is also contraindicated in patients with severe uncontrolled hypertension, intracranial neoplasms, surgery within two months, recent stroke, and intraspinal surgery.

Streptokinase administered with extreme caution to those who have experienced recent trauma, coagulopathies or hematologic diseases, gastrointestinal bleeding, infective endocarditis, obstetric deliveries, diabetic hemorrhagic retinopathy, organ biopsies, or previous puncture of a non-compressible vessel.

Streptokinase is a pregnancy Category C medication; the effects of streptokinase on a fetus are unknown, and pregnant patients should only receive streptokinase to prevent life-threatening injury

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Cardiac arrhythmias

It may be desirable to reduce the dose of or discontinue digoxin for 1 to 2 days prior to electrical cardioversion of atrial fibrillation to avoid the induction of ventricular arrhythmias, but physicians must consider the consequences of increasing the ventricular response if digoxin is decreased or withdrawn. If digitalis toxicity is suspected, elective cardioversion should be delayed. If it is not prudent to delay cardioversion, the lowest possible energy level should be selected to avoid provoking ventricular arrhythmias.

Other side effects

nausea

vomiting

diarrhea

stomach pain

fast, slow or uneven heart rate

lightheadedness

bloody or black, tarry stools

confusion, weakness

hallucinations

unusual thoughts or behavior

breast swelling or tenderness

blurred vision

yellowed vision

Common side effects in children

stomach pain

weight loss

growth delay

behavioral changes

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Bleeding

The reported incidence of bleeding (major or minor) has varied widely depending on the indication, dose, route and duration of administration, and concomitant therapy.

Allergic Reactions

Mild or moderate allergic reactions may be managed with concomitant antihistamine and/or corticosteroid therapy. Severe allergic reactions require immediate discontinuation of Streptokinase, with adrenergic, antihistamine, and/or corticosteroid agents administered intravenously as required.

Respiratory System

There have been reports of respiratory depression in patients receiving Streptokinase. In some cases, it was not possible to determine whether the respiratory depression was associated with Streptokinase or was a symptom of the underlying process. If respiratory depression is associated with Streptokinase, the occurrence is believed to be rare.

Other side effects

nausea

headache

dizziness

low blood pressure

mild fever

rash

itching

flushing

muscle or bone pain

shivering

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Digoxin. (2021, July 18). NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK556025/

Side Effects of Lanoxin (Digoxin Tablets), Warnings, Uses. (2021, April 14). RxList. https://www.rxlist.com/lanoxin-tablets-side-effects-drug-center.htm#consumer

Wilson, B.A., Shannon, M.T., Shields, K.M., & Stang, C.L. (2007).  Prentice Hall Nurse's Drug Guide 2007 (pp. 513-516).  Upper Saddle River, NJ: Pearson Prentice Hall.

Lehne, R.A. (2010). Pharmacology for nursing care (7th ed., pp. 522-527, 548-549).  St. Louis: Saunders Elsevier.

Streptase (Streptokinase): Uses, Dosage, Side Effects, Interactions, Warning. (2021, March 23). RxList. https://www.rxlist.com/streptase-drug.htm#description

American Heart Association. (2006). Handbook of Emergency Cardiac Care (p. 36, 52). Salem, MA: AHA.

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Drug Interactions:  1) Thiazide diuretics and loop diuretics promote dig-induced dysrhythmias by depleting potassium; 2) With digoxin, beta blockers and calcium channel blockers decrease contractility and heart rate; 3) Sympathomimetics (beta-adrenergic agonists) enhance heart rate and contractility; 4) Serum digoxin levels from oral doses are decreased by cholestyramine, kaolin-pectin, Neomycin, or sulfasalazine; 5) Serum digoxin levels are increased by aminoglycosides, colestipol, azithromycin, clarithromycin, erythromycin, omeprazole, tetracycline, alprazolam, amiodarone, captopril, diltiazem, nifedipine, nitrendipine, propafenone, quinidine, verapamil.

Drug IV Incompatibilities:  dobutamine, doxapram, amiodarone

Monitor blood pressure and apical pulse prior to administration.

Cardiac monitor should be used on patients receiving digoxin, especially loading doses.

Monitor serum digoxin levels closely, especially if receiving antibiotic therapy.

Monitor serum electrolytes, especially potassium.

Check for toxicity if visual or GI disturbances occur.

If DIGOXIN TOXICITY occurs with DYSRHYTHMIAS

Discontinue any digitalis medications and any potassium depleting diuretics.

Check serum potassium level.

Phenytoin or lidocaine can be used as antidysrhythmic medications [Do Not Use Quinidine or Amiodarone.].   Atropine can be used for bradycardias or AV blocks.  Fab antibody agents  can be administered carefully intravenously.

Avoid electrical cardioversion if patient is receiving digoxin unless condition is life-threatening.  Then use lower doses (10-20 joules).

Emphasize to patient the importance of taking digoxin as prescribed at regular intervals and not missing doses.

Advise the patient not to breastfeed while taking Digoxin.

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Drug Interactions:  1) Anticoagulants like heparin or enoxaparin increase the risk of bleeding; 2) Aminocaproic acid reverses the action of streptokinase

Drug Incompatibilities:  Do not use infusion IV line for other medications or therapies.

Screen patient carefully for possible contraindications prior to fibrinolytic therapy.

Obtain baseline lab data for aPTT, PT, INR, Hct, Hgb, and platelets prior to beginning streptokinase therapy.

Avoid any invasive procedures on patient during therapy and for 2 hours following therapy.

Monitor the patient for signs of bleeding every 15 minutes during therapy and hourly for next 8 hours following therapy.

Notify physician STAT if signs of anaphylaxis or allergic reaction begin to occur.

Maintain continuous cardiac monitoring during therapy and at least for the next eight hours to watch for reperfusion dysrhythmias.

Reperfusion dysrhythmias rarely require treatment, but appropriate resuscitation medications and equipment should be at the bedside.

Note for evidences of reperfusion include 1) relief of chest pain, 2) reperfusion dysrhythmias, 3) return of ST segments to baseline in affected leads, and 4) peaking of serum CK-MB

Watch for neurological alterations (like change in mental status, level of consciousness, seizures, hemiparesis/hemiplegia, changes in pupils, etc.) which may indicate cerebral hemorrhage.

Do not administer any injections, draw blood specimens (especially not arterial), or perform any other form of venipuncture during fibrinolytic therapy.

Do not use noninvasive blood pressure monitoring on patient during fibrinolytic therapy.