Digoxin is originated from the foxglove plant. It is usually given to patients who suffer from arrhythmias. Arrhythmia is a condition in which the myocardium beings to either beat too fast (tachycardia) or beat too slow (bradycardia). Antiarrhythmic drugs are given to the patient to correct these non-synchronous contractions and bring the myocardium back into a normal rhythm. Pharmacodynamics Digoxin is a cardiac glycoside; its pharmacological properties are related to its ability to inhibit the sodium-potassium ATPase. Digoxin upon administration causes the intracellular levels of sodium to increase, above normal physiological concentrations. This increase in sodium levels causes the sodium-calcium exchanger to be active. This then exchanges the intracellular sodium for extracellular calcium. This extracellular calcium upon entry into the myocardium induces intracellular calcium to be released due to calcium induced calcium release (CIRC). Digoxin has a negative chronotropic and positive inotropic effect on the myocardium; these can be explained by the electro-physiochemical changes which take place across the myocardium upon the application of digoxin. The negative chronotropy is due to the sodium-potassium ATPase being inhibited, this then leads to a less number of action potentials (APs) being generated and as a result if less APs are being generated this will have a negative effect on the rate at which the myocardium contracts (negative chronotropic effect). The positive inotropic effects are linked with the activation of the sodium-calcium exchanger, upon activation it introduces extracellular calcium into the myocardium, this extracellular calcium along with the intracellular calcium (CIRC) causes an increase in the forc... ... middle of paper ... ...). Stockley's Drug Interactions - Digoxin. [ONLINE] Available at: [Accessed 2 February 2012]. The Digitalis Investigation Group, (1997). The Effect of Digoxin on Mortality and Morbidity in Patients with Heart Failure. New England Journal Medicine, (issue 336). pp 525-533 The electronic Medicines Compendium (eMC), (2011). Capoten Tablets - Patient Information Leaflet (PIL). [ONLINE] Available at: [Accessed 15 February 2012]. The electronic Medicines Compendium (eMC), (2012). Digoxin Tablets BP 250 micrograms - Summary of Product Characteristics (SPC). [ONLINE] Available at: [Accessed 2 February 2012].
Corlanor use is indicated to reduce the risk of hospitalization for worsening heart failure in patients with stable, symptomatic chronic heart failure with left ventricular ejection fraction ≤ 35%, who are in sinus rhythm with resting heart rate ≥ 70 beats per minute and either are on maximally tolerated doses of betablockers or have a contraindication to beta-blocker use.
Digoxin (Lanoxin) 250 mcg daily: In heart failure, increases contractility by inhibiting sodium/potassium ATPase pump in myocardial cells promoting calcium influx via sodium –calcium exchange pump ("Digoxin," 2015, p. 6).
Dealing with alcohol withdrawal, Atenolol can be used as an addition to tradition alcohol withdrawal treatment to help make the results more effective. In relation to anxiety disorders, atenolol is usually used in small stress reactions, minor panic disorders, and generalized anxiety syndrome. Results are most easily obtainable in patients who have bodily anxiety, as opposed to the mind, and helps reduce trembling and rapid heart beat. Atenolol also had a large affect on cardiac illnesses. In the most common, angina pectoris, atenolol is used to decrease the amount of repeated attacks and to prevent any immediate death. Atenolol is best effective on middle-aged or teenagers, and to those with high blood pressure and heart rate as a result of exercise. The other major heart sickness is congestive heart failure. Giving Atnolol to a person with congestive heart failure must be taken with much care and precauution. One should start with low doses at first, and as time passes, increase the intake gradually. Overall, it affects the heart and circulatory system to either lessen the effect of or prevent any type of cardiovascular illness that may cause serious and/or permanent damage to the body. But how exactly does the medication work?
(14) Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, Wang S, Alings M, Xavier D, Zhu J, Diaz R, Lewis BS, Darius H, Diener HC, Joyner CD.. (2009). Dabigatran versus warfarin in patients with atrial fibrillation.. New England Journal Of Medicine. 361 (12), 1139-51.
Cooke GA, Williams S, Marshall P, Al-Timman J, Shelbourne J. (2002) [cited 2011 Oct 22]. A mechanistic investigation of ACE inhibitor dose effects on aerobic exercise capacity in heart failure patients. EUR HEART J [Internet]; 23(17): 1360-1368.
Dabigatran is a direct reversible thrombin inhibitor that has been approved for treatment of nonvalvular atrial fibrillation (AF) based on results of the Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) study, but its use for other indications remains untested. It works by inhibiting both free and clot-bound thrombin, which enables the conversion of fibrinogen into fibrin. Dabigatran is eliminated primarily by the kidneys and it’s dosed orally.5
These causes will change the heart significantly. The pathophysiology of heart failure is described differently as: (1) an oedematous disorder, by means of which the deviations in renal hemodynamics and excretory ability lead to salt and water holding; (2) a hemodynamic disorder, considered by peripheral vasoconstriction and decreased cardiac output; (3) a neurohormonal disorder, mainly by stimulation of the renin-angiotensin-aldosterone system and adrenergic nervous system; (4) an inflammatory syndrome, related with amplified local and circulation pro-inflammatory cytokines; (5) a myocardial disease, started with an damage to the heart trailed by pathological ventricular transformation. In heart failure, the heart sustains either a sudden or longstanding structural injury. When damage occurs, sequences of firstly compensatory but consequently maladaptive mechanisms follow (Henry & Abraham, ).
Digoxin is primarily used to treat heart failure, by increasing the physical strength and force of heart’s contractions. In turn increases the output of blood from the heart, this increase is done by inhibiting the enzyme ATPase (the release of energy to make chemical reactions occur within the cells) which controls circulation of calcium, sodium, and potassium into the heart muscle. Inhibiting ATPase brings a rise in intercellular calcium which increases the force of heart contractions and the contracture of smooth vascular muscle, the sodium pump moves the sodium ions out of and the potassium ions into the cells.
In 1976 a pharmaceutical beta blocker named Atenolol (a synthetic derivative of isopropylamino-propanol) was discovered and developed by the Imperial Chemical Industries (ICI) to treat common cardiovascular disorders (6). To fully understand Atenolol one must first recognize that it is specifically a beta-1 adrenoceptors antagonist. This is crucial because beta blockers follow strict classification guidelines in regards to the specific receptors they will interact with. These receptors are known as β1 adrenoceptors and β2 adrenoceptors, and when a drug (like Atenolol) is found to interact with only β1 adrenoceptors it is called cardioselective while drugs affecting both β1 adrenoceptors and β2 adrenoceptors are known as non-cardioselective. This differentiation between cardioselective versus non-cardioselective allows Atenolol to treat a variety of cardiovascular disorders such as antihypertensive, hypotensive and antiarrhythmic by interacting specifically with the beta-1 adrenergic receptors (7). Atenolol is special when talking about β1 adrenoceptors antagonists because it has the lowest lipid solubility without affecting intrinsic sympathomimetic activity aka ISA (8).
Mcmurray, J. "Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: Putting guidelines into practice." HUG - Service de pharmacologie et toxicologie cliniques - Genève. The European Journal of Heart Failure, 5 July 2005. Web. 20 Mar. 2014.
Frisinghelli, A., & Mafrici, A. (2007). Regression or Reduction in Progression of Atherosclerosis, and Avoidance of Coronary Events, With Lovastatin in Patients With or at High Risk of Cardiovascular Disease: AÂ Review. Clinical Drug Investigation, 27(9), 591-604.
Antiarrhythmic agents are used to suppress abnormal rhythms of the heart. Many attempts have been made to classify antiarrhythmic agents. There is a problem from the fact that many of the antiarrhythmic agents have multiple actions, making any classification accurate. Betapace (sotalol) comes in tablets and solution for oral a...
... patients with heart failure: Impact on patients. American Journal of Critical Care, 20(6), 431-442.
...blood and increase the absorption and concentration of digoxin in the blood. This may reduce the effectiveness of ketoconazole or increase digoxin toxicity. Through unknown mechanisms, omeprazole may increase blood levels of saquinavir and reduce blood levels of nelfinavir and atazanavir, drugs that are used for treating patients with infection caused by the human immunodeficiency virus (HIV). Omeprazole can be contraindicated in patient with hepatic impairment thus doctors are advised not to prescribe more than 20mg daily of omeprazole for such patients. [1] [3] [4]
The second part of this lab was a computer simulation program to illustrate a frog’s electrocardiogram using various drugs in an isolated setting. The computer program entitled “Effects of Drugs on the Frog Heart” allowed experimental conditions to be set for specific drugs. The different drugs used were calcium, digitalis, pilocarpine, atropine, potassium, epinephrine, caffeine, and nicotine. Each of these drugs caused a different electrocardiogram and beats per minute reading. The calcium-magnesium ration affects “the permeability of the cell membrane”(Fox). When calcium is placed directly on the heart it results in three physiological functions. The force of the heart increases while the cardiac rate decreases. It also causes the appearance of “ectopic pacemakers in the ventricles, producing abnormal rhythms” (Fox). Digitalis’ affect on the heart is very similar to that of calcium. It inhibits the sodium-potassium pump activated by ATP that promotes the uptake of extracellular calcium by the heart. This in return strengthens myocardial contraction (Springhouse). Pilocarpine on the other hand