What is the toxicity of digoxin?
Can it really bring the heartbeat to a dead stop? Is this true, literally? Is it just one extra dose or is it like a dozen or more overdoses which can do this? How narrow is the margin?
Asked by Ken Emenaha 1 month ago.
Digoxin's narrow therapeutic range (0.8 to 2 ng/ml) makes toxicity quite common: It's estimated to be present in 5% to 20% of all hospitalized patients on digoxin. Testing serum drug levels about 8 hours after each drug administration helps detect toxicity. Log and report digoxin levels greater than 2 ng/ml and a heart rate below 60 bpm; these are key indicators of digoxin toxicity, though many patients who are on digoxin routinely have heart rates below 60 bpm. Renal insufficiency, drug interaction, hypercalcemia, hypokalemia, hypomagnesemia, hypothyroidism, and advanced age all increase the risk of digoxin toxicity. (See Raising the Risks for common drugs that can cause problems.) Gastrointestinal symptoms of toxicity include anorexia, nausea, and vomiting. Neurologic symptoms include headaches, malaise, fatigue, neuralgic pain, dementia, seeing yellow or green halos around objects, and seizures. Cardiac signs include functional rhythms, heart blocks, ventricular rhythms, acute tachycardia, and bradycardia. Answered by Truman Nagelkirk 1 month ago.
Please see the web pages for more details on Digoxin. Answered by Lashawn Ryckman 1 month ago.
How does digoxin toxicity cause both hyper and hypokalemia?
Followup: Why do patients who are on chronic digoxin therapy present with hypokalemia when they have digoxin toxicity?
Asked by Noble Williamis 1 month ago.
Digoxin is a medication utilized for the A.) treatment of supraventricular tachycardia specifically Atrial Fibrillation, and more controversially, B.) for the treatment of left ventricular insufficiency. It is a cardiac glycoside manufactured and derived from the Foxglove plant. It inhibits the Sodium-Potassium ATPase, similarly known as the Sodium-Potassium Pump. Sodium and Potassium are moved across the cell membrane via active transport. This inhibits this action, thereby inhibiting the electrical impulses in the atrioventricular node in the upper portion of the heart. In turn, the medication is utilized to control the rate in RVR (Rapid Ventricular Rate) Atrial Fibrillation, most commonly. The hypokalemia that you see by checking electrolyte levels of the K+ (Potassium) is most frequently caused prior to the digoxin toxicity and is many times a key element to causing the digoxin toxicity. Here's what happens most often with this combination: a patient has an underlying need for K+ secondary to a reduction of intake and or excess excretion. This leads to a rapid reduction of the remainder of potassium ions available for the "pump" action we mentioned above. As a result, this is known as hypo- (lacking) kalemia (potassium). Diuretics commonly used in associated illnesses such as the first-line treatment of HTN (hypertension) & CHF (congestive heart failure), will result in increased secretion of K+ through the renal system (kidneys). This reduction of K+ from the diuretic will enhance and speed the toxic serum levels of the digitalis/digoxin. Hyperkalemia is generally defined as the inability of the kidneys to excrete adequate levels of potassium from the body. When digoxin's mechanism kicks-in, then it decreases the use of K+ ions in the sodium-potassium pump by decreasing the NA-K ATPase activity. This reduction leads to a build-up of potassium in the body. Dehydration and various illnesses often are also contributing factors to the change to K+ levels and hyperkalemia. Creatinine, urine K+, and Osmolarity labs would be the first step in determination of the reason for the hyperkalemia. Treatments for digoxin toxicity includes GI decontamination and control of arrythmias & electrolyte imbalance. I do hope this brief explanation will assist you in knowing more about the process. All my best! For more information, talk with your local physician. They will be able to provide an up-close and personal explanation inclusive of some drawings and texts that you can read. Also, Wikipedia is usually a fair source of basic to moderate level information on a subject. You might want to search these key words: hypokalemia, hyperkalemia, digoxin toxicity, ATPase, and cardiac glucosides. These will lead you to a better definition of the keywords in my response. Good luck! Sincerely, Nathaniel - Paramedic Answered by Kyle Rotermund 1 month ago.
This Site Might Help You. RE: how does digoxin toxicity cause both hyper and hypokalemia? Answered by Jenee Gleen 1 month ago.
Digoxin blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear however is perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin resulting in increased inotropy (contractility). Digoxin toxicity causes hyperkalemia (high potassium). The sodium/potassium ATPase pump normally causes sodium to leave cells and potassium to enter cells. Blocking this mechanism results in higher serum potassium levels. Digoxin toxicity is worsened in states of hypokalemia (low potassium) since digoxin normally binds to the ATPase pump on the same site as potassium. When potassium levels are low, digoxin can more easily bind to the ATPase pump exerting the inhibitory effects. The end-point of digoxin’s effect is to open membrane calcium channels resulting in increase calcium influx into cells. When the calcium levels are high, in the setting of digoxin toxicity, the result is an increase in calcium influx and enhanced toxicity. As mentioned above digoxin toxicity can cause hyperkalemia. Recall that the treatment for hyperkalemia causing ECG changes is usually intravenous calcium administration. In the setting of digoxin toxicity and hyperkalemia, giving IV calcium may be potentially fatal. The massive influx of calcium into myocytes after the IV calcium is given has been theorized to induce a non-contractile state and has been termed "Stone Heart". There is no evidence to validate this theory and some reports have shown safe administration of calcium during digoxin toxicity in isolated cases. Answered by Ngoc Kotarski 1 month ago.
Digoxin And Potassium Answered by Jacinda Boettner 1 month ago.
Azithromycin with digoxin what is problem?
Asked by Sharell Aranjo 1 month ago.
Digoxin is a heart medication that increase heart contractility (makes the heart pump harder) but it also decreases your heart rate. People who are taking Digoxin must check their heart rate every morning before they take it. Typically, if their heart rate is less than 60 they skip that dose. The problem is when azithromycin is taken with Digoxin is that it can increase how well Digoxin works... way too much. It can lead to unstable conditions or even digoxin toxicity. Only take these two medications under strict MD control. Also, it is always a great idea to keep a current list of medications, doses, and times you take these meds with you. For example, many people see more than one doctor. If you are going to have your medications changed, having this list can help he or she decide the best options for you. Don't forget to tell them about herbals and over the counter meds to, as these can interact with each other. Answered by Leslie Dittemore 1 month ago.
What is the status of digoxin now in treatment of heart failure?
is digoxin the drug number one in human usage of drugs?
Asked by Freddie Lashutva 1 month ago.
The main pharmacological effects of digoxin are on the heart. Extracardiac effects are responsible for many of the adverse effects which are below Its main cardiac effects are * A decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter. * An increase of force of contraction via inhibition of the Na+/K+ ATPase pump Mechanism of action Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na+/K+ pump leads to increased Na+ levels, which in turn slows down the extrusion of Ca2+ via the Na+/Ca2+ exchange pump. Increased amounts of Ca2+ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This is a different mechanism from that of catecholamines. Digoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias. Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response. High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling. The use of digoxin in congestive heart failure during sinus rhythm is controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and digoxin is no longer the first choice for congestive heart failure. However, it can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment. Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125 μg or 250 μg dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (such as digitoxin which although having a much longer elimination half-life of around 7 days, is mainly eliminated from the body via the liver, and thus not affected by changes in renal function). Effective plasma levels are fairly well defined, 1-2.6 nmol/l. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled. The occurrence of adverse drug reactions is common, owing to its narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are concentration-dependent, and are rare when plasma digoxin concentration is <0.8 μg/L. They are also more common in patients with low potassium levels (hypokalemia), since digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump. Common adverse effects (≥1% of patients) include: loss of appetite, nausea, vomiting, diarrhoea, blurred vision, visual disturbances (yellow-green halos), confusion, drowsiness, dizziness, nightmares, agitation, and/or depression. Less frequent adverse effects (0.1%–1%) include: acute psychosis, delirium, amnesia, shortened QRS complex, atrial or ventricular extrasystoles, paroxysmal atrial tachycardia with AV block, ventricular tachycardia or fibrillation, heart block but when sytematically sought, the evidence for this is equivocal. The pharmacological actions of digoxin usually results in electrocardiogram (ECG) changes, including ST depression or T wave inversion, which do not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Additionally, increased intracellular Ca2+ may cause a type of arrhythmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. The combination of increased (atrial) arrhythmogenesis and inhibited atrio-ventricular conduction (for example paroxysmal atrial tachycardia with A-V block - so-called "PAT with block") is said to be pathognomonic (i.e. diagnostic) of digoxin toxicity. An often described but rarely seen adverse effect of digoxin is a disturbance of colour vision (mostly yellow and green colour) called xanthopsia. Digoxin has an interaction with the antimalarial medication Hydroxychloroquine. Other informationDigoxin has potentially dangerous interaction with verapamil, amiodarone and erythromycin. In overdose, the usual supportive measures are needed. If arrhythmias prove troublesome, or malignant hyperkalaemia occurs (inexorably rising potassium level due to paralysis of the cell membrane bound ATPase-dependant Na/K pumps), the specific antidote is antidigoxin (antibody fragments against digoxin, trade name Digibind®). Digoxin is not usefully removed by hemodialysis.Some physical properties of digoxin are water solubility of 64.8 mg/L at 25 °C and melting point at 249.3 °C. Answered by Nita Whitney 1 month ago.
Why do patients who are on chronic digoxin therapy present with hypokalemia when they have digoxin toxicity?
I'm a pharmacy student so you can use medical jargon on me.
Asked by Janeen Bolay 1 month ago.
Digoxin toxicity can occur with any condition that increases total body levels of Digoxin or modifies the cardiac sensitivity to Digoxin. Digoxin toxicity can occur with hyperkalemia, hypokalemia or normokalemia. Hypokalemia potentiates the toxicity from Digoxin and Digoxin toxicity can occur with lower serum concentrations of Digoxin in the presence of hypokalemia. Severe acute Digoxin toxicity will frequently produce a hyperkalemia. Digoxin inhibits the Sodium/Potassium ATPase, which leads to increased intracellular Sodium concentrations. This results in a decreased transmembrane Sodium gradient, which is the driving force for the Sodium/Calcium transport. This results in increased concentration of Calcium in the cell, which increases the strength of cardiac contractions. Potassium competes with Digoxin for the alpha subunit of the Na-K-ATPase enzyme. Hypokalemia results in less potassium available to compete with Digoxin, which results in more Digoxin binding to the enzyme therefore more toxicity. Hypokalemia decreases Na-K-ATPase activity, thereby exacerbating the principal cellular derangement of cardiac glycoside toxicity. Acute severe Digoxin toxicity usually produces hyperkalemia, because of the inhibition of Na-K ATPase pump resulting in increased extracellular potassium. The severity of acute Digoxin toxicity is positively correlated with the degree of hyperkalemia. I hope I answered your question, but if not let me know. It can be confusing. Good luck with your school. Answered by Rosy Widlak 1 month ago.
Digoxin interferes with the Na+/K+ pumps. Digoxin competes with K+ for use of the pumps. If they have enough K+, then there is equal comptetition for use of the pumps. However, if a person does not have enough K+, then too many Digoxin molecules will bind to the pumps, causing toxicity. "It is important to note that although hypokalemia predisposes to digoxin toxicity, a massive overdose can lead to hyperkalemia." I'm also thinking that hypokalemia could result from renal failure, when the kidneys stop reabsorbing larger molecules, which could lead to dig toxicity. Answered by Siu Pein 1 month ago.
Can digoxin cause insomnia?
I really hope to get some answers here, from someone who knows what they're talking about... So: I have a heart condition, I take this drug, digoxin, every day, 0.25 mg. In the last 4 nights it's been really hard for me to fall asleep, only happens late in the morning around 2 or 3 am. I should say I never...
Asked by Joe Fauver 1 month ago.
I really hope to get some answers here, from someone who knows what they're talking about... So: I have a heart condition, I take this drug, digoxin, every day, 0.25 mg. In the last 4 nights it's been really hard for me to fall asleep, only happens late in the morning around 2 or 3 am. I should say I never before had trouble sleeping, always slept well and rested well after 7-8 hours of sleep. So I'm really confused. I also take a cumarinic blood thinner and water pills for my condition. I would be so grateful if someone could help me. A heart patient really needs sleep. Thank you. Answered by Marianela Dexter 1 month ago.
The generic drug digoxin is mainly prescribed for heart problems like irregular rhythms (arrhythmias) and heart failure. It comes in the form of capsules, liquid, and tablets, and common brand names for it are Lanoxin Elixir Pediatric, Lanoxicaps, Lanoxin, and Digitek. Recognizing the side effects of digoxin and understanding what to do when they occur is simple with proper background information. Difficulty: Moderately Easy Instructions 1 Consult a doctor if your breasts become larger after taking digoxin and the symptom doesn't go away or becomes uncomfortable. This is a common side effect that both men and women experience. 2 Note that moderate side effects of digoxin require medical intervention if they grow worse or persevere for a period of time. Such symptoms include dizziness, drowsiness, and lightheadedness. 3 Seek immediate medical attention if you experience symptoms like abnormal eyesight or heartbeat, breathing difficulty, confusion, diarrhea, fatigue, hives, itching, lack of appetite, nausea, rash, swollen body parts like the hands or face, unusual bleeding or bruising, upset stomach, vomiting, and weight gain. All of these side effects are considered severe and shouldn't be ignored. 4 Avoid eating too much bran fiber while taking digoxin. People who eat a lot of food with large amounts of bran fiber may absorb less of the drug into the bloodstream through the stomach, which may reduce its effectiveness. 5 See a doctor first for advice if medication for allergies, colds, or coughs is required while taking digoxin. Some drugs used to treat those conditions may react adversely with digoxin and increase both the risk and the severity of side effects. Answered by Delores Wagatsuma 1 month ago.
Why should a patient who suffers from hypothyroidism need to take an increased dose of Digoxin?
Asked by Tanner Tureson 1 month ago.
Digoxin (Lanoxin) is a drug that is used to control heart rate. Individuals with hypothyroidism tend to be more sensitive (respond more) to digoxin, and, conversely, individuals with hyperthyroidism are less responsive to digoxin. Therefore, increasing the level of thyroid hormone in the body may warrant an increase in the dose of digoxin. The mechanism for this interaction is not clear, but it may involve changes in the absorption of digoxin, digoxin metabolism, or the effects of thyroid hormone on the heart. [Digoxin is used to treat congestive heart failure and the associated symptoms of shortness of breath when lying flat, wheezing, and ankle swelling. Digoxin is also used to slow heart rate in rapid atrial rhythm disturbances such as atrial fibrillation and atrial flutter] Answered by Jesusita Karalis 1 month ago.
Because the plasma of your blood (the fuid without the red cells) has a "limit" of saturation, and can carry les thyroxine when you are taking thyroxine, or viceversa. Because digoxin has a very slow limit for toxicity (the maximun dose varies between 0.25 and 0.5 miligrams per day) its safer to increase the Thyroxine by roughly one quarter or one third, to make it available to the tissues of the body. (that is what is called biodisponibility.....sorry, There is another little "word" that will surely keep you busy No big deal in that... Answered by Myrta Shingleur 1 month ago.
I have been diagnosed with hypothyroidism and am currently taking thyroxine, never heard of the other drug...sorry! Answered by Nicolasa Munno 1 month ago.
thyroxine ,not digoxin unless it is to regulate their heartbeat Answered by Augusta Lamkins 1 month ago.
Can Digoxin cause death?
Asked by Morris Rampley 1 month ago.
Digoxin has one of the narrowest therapeutic ranges. That is that there is not a lot of difference in the dose that is therapeutic and the dose that is toxic. Since digoxin is use heart conditions but can cause every kind of arrhythmia there is, it is hard to tell if you need more or have too much. Not trying to scare you, just make sure to treat it with respect. The resent recall is do to some tablets having a DOUBLE dose. Since this drug can build up over time, this is a serious recall. Answered by Sadye Brihon 1 month ago.
Many a drug can cause death in toxic doses, digoxin (one brand name is Lanoxin) is no exception. But in the usual therapeutic doses digoxin is fairly safe, especially in children. Digoxin toxicity occurs more commonly in elderly and those with compromised kidney function as a good portion of the drug is excreted by the kidney. Children metabolise and excrete the drug very fast so that digoxin toxicity is quite rare in children. Answered by Narcisa Wholly 1 month ago.
Yes. Digoxin toxicity leads to complete heart block and death. Answered by Saran Michel 1 month ago.
u scared me...my son was on lanoxin 4 a year after his first SVT.but the second time docs put him on digoxin ,he develloped some reaction(they say it was due to him beiing on Desferal for iron overload/sickle cell) but no one mentionned death to me........ drduet can u please edit ur answer and give me a web address to get more info?thanx... sorry richard,cant help Answered by Wendell Skalla 1 month ago.
any meds can if you are allergic to them and some you have to have blood test for to make sure you dont get a over laod in the blood digoxin is one of them Answered by Bella Fellezs 1 month ago.