Congestive Cardiac Failure With Digoxin Toxicity Essay

Contents (Jump to)

Criterion-1

Causes, Incidences and Risk Factors of Congestive Cardiac Failure with Digoxin Toxicity:

Comprehensive Understanding of the Disease on Patient and Family:

Criterion-2

Signs & Symptoms

Pathophysiology

Criterion-3

Drug Class

Physiological Effect

Criterion-4

Interventions-Rationales:

Comprehensive Treatment of the Identified Condition:

Supportive care

Electrolyte abnormality management

Bradycardia management

Hemodynamic compromise management

Ongoing monitoring and change of medicine Congestive Cardiac Failure With Digoxin Toxicity Essay

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CASE STUDY ON CONGESTIVE CARDIAC FAILURE WITH DIGOXIN TOXICITY

Criterion-1
Causes, Incidences and Risk Factors of Congestive Cardiac Failure with Digoxin Toxicity:
Digoxin toxicity caused by high levels of digitalis in the body. As in our case study Mrs. Sharon McKenzie, a 77 year old woman, used to take daily 250 mcg of digoxin, which is a very high dose for adult patients. Especially those, who are suffering from congestive cardiac failure, like our patient Mrs. Sharon McKenzie (Neo, et al, 2010). Body receives the therapeutic effect when it stores of 8 to 12 mcg/kg generally with minimum risk of toxicity in most patients with failure of heart and normal sinus or breathing rhythm (Mangoni, 2010).
People withheart failurewho have this digoxin are commonly prescribed medications called diuretics that remove excess fluid from the part of body. This is also happens that many diuretics can cause potassium loss from the body (Johnson, Inder, Nagle & Wiggers, 2010). Though ultimately it increases the risk of digitalis toxicity. Again, our patient, Mrs. Sharon McKenzie’s potassium level is low; 2.5 mmol/l. whereas a normal potassium level ranges from 3.5-5.0 mmol/l.
You are more likely to fall into that condition if you take digoxin, digitoxin, or other digitalismedicinesalong with the higher effective drugs that interact withit such as flecainide, quinidine, amiodarone, verapamil, and others. Similarly, Mrs. Sharon McKenzie’s was also taking medication with digoxin like furosemide, warfarin, and enalapril (Siabani, Leeder & Davidson, 2013).Congestive Cardiac Failure With Digoxin Toxicity Essay
In recent years the incidence of digoxin toxicity has dropped among patients in hospitals. A study has been done on 183 outpatients, who are receiving on going treatment of digoxin toxicity at 10 urban and rural Department of Veterans Affairs Medical Centers in the Rocky Mountain region, to evaluate whether a similar decline of digoxin toxicity has occurred or not. The statistics over 1-year period, of that study is like that:
Out of the 183 patients:

50 (27.3%) had one or more risk factors for digoxin toxicity.
Serum digoxin levels were elevated in 13.6% of patients.
Hypokalemia in 14.3%.
Elevated creatinine levels in 17.9%.
And possible drug interactions in 5.5% of patients.
The most common risk factor of digoxin toxicity is the patient’s elderly age. Like in our case study, Mrs. Sharon McKenzie is also 77-year old woman. However there are other risk factors too, which render the elderly more vulnerable to digoxin toxicity. These contain an age-related decline in renal function and a decrease in volume of digoxin distribution. There is also an increase in the number of comorbid conditions, including cardiovascular and chronic obstructive pulmonary disease, which heightens vulnerability to digoxin toxicity.
Comprehensive Understanding of the Disease on Patient and Family:Congestive Cardiac Failure With Digoxin Toxicity Essay
Digoxin toxicity is a life-threatening condition, and when a serious disease like congestive cardiac failure caused by digoxin toxicity then it can impact severely in a bad way on a patient as well as his/her family (Betihavas, 2011). Due to which his/her family also suffer by seeing their loved one mentally disturbed. Often the patients with CHF who are depressed or who lack social support, the higher the support from the social side the higher the rate of healing as the family and the patient both in complex and double trouble.

Criterion-2
Signs & Symptoms
Pathophysiology
Severe ventricular arrhythmias:
Sudden cardiac death and loss of consciousness are the basic signs and symptoms of the cardiac arrhythmias. Complaints such as dizziness, lightheadedness, fluttering, dizziness, and pounding, chest discomfort, quivering, shortness of breath, and forceful or painful fast beats are commonly reported with arrhythmias patients. Often, patients notice arrhythmias only after checking their peripheral pulses (Mudge, et al, 2010).

The pathogenesis of the arrhythmias falls into one of two basic mechanisms: increased or covered up automaticity, triggered activity, or re-entry.Congestive Cardiac Failure With Digoxin Toxicity Essay

Triggered activity occurs when early after depolarization and delayed after depolarization initiate spontaneous multiple depolarization, precipitating ventricular arrhythmias (Johnson, Inder, Nagle & Wiggers, 2010).
Arrhythmogenesis is probably the most common procedure and results from re-entry. It causes the change of state of mind and mood too.
2) Hyperkalemia:

Higher potassium rate in your blood can affect how your heart works. Symptoms of hyperkalemia can include:

Abnormal heart rhythm –arrhythmia– that can be life-threatening
Slowheart rate
Weakness (Neo, et al, 2010)
Hyperkalemia may result from an increase in total body potassium secondary to imbalance of intake vs. excretion or from misdistribution between intra- and extracellular space (Nanda, 2009).

3) Hypokalemia:

Usually symptoms of low potassium are mild

Weakness, tiredness, or pain in arms or legs muscles, sometimes this might be so severe to cause inability and disability to move arms or legs due to weakness of muscles (much like a paralysis) (Hughes & Crowe, 2010)Congestive Cardiac Failure With Digoxin Toxicity Essay

Tingling or numbness
Nausea or vomiting
Abdominal cramping, bloating
Constipation
Palpitations (feeling your heart beat irregularly)
Urine passing rate is too high simultaneously feeling thirsty mostly (Neo, et al, 2010).
In the heart, low potassium levels make the myositis hypo-polarized or hyper excitable. Thus, arrhythmia occurs as a result of the atrium’s lowered membrane potential due to recovery from inactivation of the Na channel, which may trigger an action potential. In addition to this, reduced potassium in the extracellular space inhibits the IKr potassium current activity, and ventricular depolarization is delayed, which thereby promotes reentrant arrhythmias (Jeon, Kraus, Jowsey & Glasgow, 2010).

4) Neurologic Symptoms:

In the identified condition, the patient may also go through with neurologic symptoms which are: Visual disturbances, disorientation, and confusion.You might experience confusion. Although rare, you might also see bright spots, have blurry vision, or experience blind spots. In addition, you might urinate much more or less than usual (Betihavas, 2011). Your body could also become swollen.Congestive Cardiac Failure With Digoxin Toxicity Essay

The physiologies of neurological symptoms are not easy to judge and too complex and our getting of them are incomplete mostly. From an evolutionary perspective it is easy to judge the neurological symptoms. Though it makes sense that the genuine physiologies of neurological symptoms are intricate and interrelated (Courtney, et al, 2009).

5) Sinus Node Dysfunction:

Sinus node dysfunction refers to a number of conditions causing physiologically inappropriate atrial rates. Symptoms may be minimal or include weakness, effort intolerance, palpitations, and syncope. Diagnosis is by ECG. Symptomatic patients require a pacemaker.

Sinus node dysfunction includes inappropriate and misbalancing the sinus bradycardia, alternating bradycardia and atrial tachyarrhythmia, sinus pause or arrest, and sinoatrial exit block (Jeon, Kraus, Jowsey & Glasgow, 2010).

SND also causes the abnormalities in SN impulse formation and propagation that also causes abnormalities in the atrium and in the conduction system of the heart (Higgins, et al, 2013). Slow ventricular rates and pauses at the time of stress is the general causes, furthermore, it includes following:

Fatigue
Angina
Syncope
Dizziness
Fall
Confusion
Heart failure symptoms and palpitations
Criterion-3
Drug Class
Physiological Effect
Angiotensin-converting enzyme (ACE) inhibitors:
ACE inhibitors cause blood vessels broadness, further descent the amount of work the heart has to do they may also have direct beneficial effects on the heart. These drugs are reducing the symptoms and the need for hospitalization moreover they are helpful to prolong life (Mudge, et al, 2010).

Beta-blockers:
Beta-blockers drugs lower down the heart rate and block excessive blockage in the heart. They also helpful in the heart disease. These drugs are usually used with ACE inhibitors and provide an added benefit. They may temporarily worsen symptoms but result in long-term improvement in heart function (Betihavas, 2011).Congestive Cardiac Failure With Digoxin Toxicity Essay

Although ACE inhibitors improve outcome in patients with systolic dysfunction, many patients with hypertension experience congestive heart failure due to diastolic dysfunction related to left ventricular hypertrophy. ACE inhibitors have been shown to reverse left ventricular hypertrophy in patients with hypertension.A meta-analysis of the effects of several antihypertensive agents suggested that ACE inhibitors were the most effective agent in reducing left ventricular hypertrophy (Katz & Konstam, 2012).

Beta blocker is helpful in improving the function of the failing LV and need to prevent or reverse progressive LV dilation, sphericity, chamber and hypertrophy. Beta blockers also lower down the heart beating rate and LV wall stress. According to recent studies from laboratories have also proven that beta blockers can satisfy cardiomyocyte apoptosis in HF. These are the basic advantages and benefit of beta-blocker for the patient of heart at any higher stage (Katz & Konstam, 2012).Congestive Cardiac Failure With Digoxin Toxicity Essay

Criterion-4
As a registered nurse, my care plan for a patient suffering from Congestive Cardiac Failure with digoxin toxicity would be like, (Driscoll, et al, 2009)

Interventions-Rationales:
I realize that I would hold the medication – Due to possibility of toxicity

Wait for Electrolytes and digoxin test, as these tests were already ordered for our patient – electrolytes can affect the action of dig and cause dysthymias and to find out the level of dig

Monitor I & O – monitoring for renal function

Monitor for edema and auscultator the lungs

Monitor symptoms, VS – S/E of dig toxicity Congestive Cardiac Failure With Digoxin Toxicity Essay

Call the doctor. – To get orders to carry out interventions and inform doctor

Start an IV. – For administration of medications (Mudge, et al, 2010).

Comprehensive Treatment of the Identified Condition:
The main goal of treatment is to correct cardiac toxicity.If the person has stopped breathing, as our patient Mrs.Sharon McKenzie confronting with shortness of breath, startCPRand get emergency medical help (Betihavas, 2011).

Initial treatment includes:

General supportive care
Discontinuation of digoxin therapy and prevention of further exposure
Administration of digoxin-specific antibody fragments (digoxin immune Fab)
Treatment of specific complications: for example, dysrhythmias and electrolyte abnormalities (Jeon, Kraus, Jowsey & Glasgow, 2010).
Supportive care
General supportive care includes attaching patients to a cardiac monitor, providing IV fluids in patients with hypotension or volume depletion (with caution for patients with CHF), supplemental oxygen, and/or repletion of electrolytes in patients with electrolyte abnormalities (Mudge, et al, 2010).Congestive Cardiac Failure With Digoxin Toxicity Essay

Electrolyte abnormality management
In case of Mrs. Sharon McKenzie, hyperkalemia is only corrected (e.g., with insulin/glucose) if it is considered life-threatening, because of the risk of producing hypokalemia, because her potassium level is low i.e. 2.5 mmol/l. One study showed that insulin interacts directly with Na(+)/K(+) ATPase pump and alters the effect of digoxin (Betihavas, 2011). This supports the finding that for patients with diabetes, insulin has been shown to have cardio protective effects after digoxin intoxication. Calcium is not used to treat hyperkalemia in patients with suspected digoxin toxicity as it may induce arrhythmia or cardiac arrest.

Bradycardia management
As Mrs. Sharon McKenzie’s ECG report showed sinus bradycardia, this will be treated with atropine. Atropine can be given every 3 to 5 minutes until there is a response or the 3 mg maximum dose is reached (San Miguel, et al, 2013).

Hemodynamic compromise management
As Mrs. Sharon McKenzie has signs of hemodynamic insufficiency and/or compromise (e.g., hypotension, altered consciousness or dizziness), digoxin immune Fab is given as primary management (Mudge, et al, 2010).Congestive Cardiac Failure With Digoxin Toxicity Essay

Ongoing monitoring and change of medicine
Ideally, digoxin is discontinued and a different medicine for rate control or a different inotrope prescribed (for AF, atrial flutter or CHF, respectively). If the patient has to remain on digoxin for some reason, then the dose of digoxin is adjusted for the patient’s medication profile (Edgley, Krum & Kelly, 2012).

The original description by Withering of the use of digitalis for “dropsy” was published in 1785.1 Even allowing for the fact that Withering’s observations were uncontrolled, the dramatic diuresis and relief of dyspnoea with the use of foxglove in patients with “dropsy” left him in little doubt about its efficacy.Congestive Cardiac Failure With Digoxin Toxicity Essay

Two hundred years later, digoxin was regarded as one of the cornerstones of therapy for heart failure,2 but controversy persisted about its efficacy, particularly in patients in sinus rhythm. More recently, the advent of neurohormonal antagonists (angiotensin-converting enzyme [ACE] inhibitors, β-blockers and spironolactone) that both produce improvements in survival and reduce symptoms has relegated digoxin down the list of therapeutic options for heart failure. Questions have been raised about the incremental benefit of adding digoxin to these newer agents, and there are concerns about the hazards of using digoxin in patients with heart failure. Two studies in the 1980s reported that digoxin use was associated with increased mortality in survivors of myocardial infarction.3,4 In addition, other drugs with positive inotropic properties were found to increase mortality in patients with heart failure.5

Atrial fibrillation and flutter are the only arrhythmias for which there is widespread support for the use of digoxin, and the use of digitalis preparations in these conditions predates their recognition as specific arrhythmias. There is no doubt that some of Withering’s original patients had atrial fibrillation.1 In 1836, Bouillaud described digitalis as the “opium of the heart” in the treatment of a patient with severe mitral stenosis and a rapid irregular pulse which, despite remaining irregular, was slowed dramatically by digitalis.6 Bouillaud was undoubtedly referring to the ability of digitalis to slow the ventricular rate in atrial fibrillation. Early in the 20th century, James McKenzie and Thomas Lewis firmly established the place of digitalis as the treatment of choice for chronic atrial fibrillation.Congestive Cardiac Failure With Digoxin Toxicity Essay

Thus, in the early years of the 21st century, digitalis, usually in the form of digoxin, is still widely prescribed to control the ventricular response rate in patients with chronic atrial fibrillation.

How does digoxin work?
Although digoxin has traditionally been considered to be a positive inotropic agent (via inhibition of Na+–K+-ATPase and secondary activation of the Na+–Ca2+ membrane exchange pump), there is considerable evidence that its primary benefit is mediated via neurohormonal modulation.7,8 Several investigators have reported that digoxin enhances vagotonic responses and inhibits sympathetic activity. Furthermore, these neurohormonal modulatory effects are seen with lower doses of digoxin (< 0.25 mg/day), whereas the positive inotropic actions are seen when doses in excess of 0.25 mg per day are used.7

Hypokalaemia and hypomagnesaemia, usually a consequence of diuretic use, lower the threshold for digoxin toxicity. The use of spironolactone or other potassium-sparing diuretics in combination with digoxin is likely to limit this problem. Patients taking digoxin in combination with diuretics (including spironolactone) should have their serum electrolytes and renal function monitored regularly.Congestive Cardiac Failure With Digoxin Toxicity Essay

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Information on the pharmacology of digoxin is provided in Box 1.
Box 1
Pharmacology of digoxin

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Digoxin in heart failure
Randomised controlled trials
The role of digoxin in the management of heart failure was clarified by a number of well-designed randomised placebo-controlled clinical trials in the 1990s (Box 2). The largest and most important of these was conducted by the Digitalis Investigation Group (DIG),9 which involved 7788 patients with heart failure, all of whom were in sinus rhythm on entry into the trial. The large majority were maintained on therapy with diuretics and ACE inhibitors. β-Blocker use was not reported in the trial, but was probably very low. Trial participants comprised 6800 patients with systolic heart failure (left ventricular ejection fraction, < 45%), and 988 patients with preserved systolic function. The average maintenance dose of digoxin was 0.25 mg daily, and patients were followed up for 3–5 years. Digoxin therapy had no effect on mortality (the primary endpoint of the study), but did reduce the need for hospital admission, mainly because of reduced hospitalisations for worsening heart failure (E2).Congestive Cardiac Failure With Digoxin Toxicity Essay (See Box 3 for an explanation of levels of evidence). The benefit of digoxin appeared to be greater among patients with more severe heart failure (ie, those with lower ejection fraction, greater cardiomegaly, and higher NYHA [New York Heart Association] class [E2]). However, the benefit was also observed in those with milder systolic heart failure and in those with preserved systolic function.

Box 2
Randomised placebo-controlled trials of digoxin in heart failure

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Box 3
Level-of-evidence codes

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The DIG study9 did not report the impact of digoxin on symptomatic status and quality of life. However, the benefit of digoxin in reducing hospitalisation for heart failure suggests that digoxin helped to maintain a stable clinical condition. Similar conclusions were drawn from two smaller and shorter studies of digoxin withdrawal in patients with stable heart failure: the PROVED10 and RADIANCE11 trials. In both studies, withdrawal of digoxin was associated with a decline in exercise capacity, deterioration in left ventricular systolic function, and significantly increased risk of hospitalisation for worsening heart failure (E2).

A recent retrospective analysis of the DIG study reported that digoxin therapy was associated with a significantly increased risk of death in women, but not in men.14 However, this finding should be interpreted with extreme caution, as the analysis according to sex was not pre-specified and women comprised only a small proportion (up to 22%) of the study population. Thus, this mortality difference could simply be a chance finding. Alternatively, the increased mortality could be explained by a higher rate of digoxin toxicity in women, as digoxin levels at 1 month were significantly higher in women than in men.Congestive Cardiac Failure With Digoxin Toxicity Essay

β-Blocker use was very low in the randomised controlled clinical trials of digoxin described above. The subsequent demonstration that β-blockers have a marked benefit when given with ACE inhibitors has raised the question of whether β-blockers have rendered digoxin redundant in the management of patients with heart failure. One study tested this hypothesis in 47 patients with heart failure and atrial fibrillation, and found that the average 24-hour heart rate was lower, and the mean left ventricular ejection fraction higher, in patients receiving both carvedilol and digoxin than either drug alone (CAFE study; see Box 2).12 The authors concluded that patients with atrial fibrillation and heart failure should be treated with the combination of a β-blocker and digoxin.

What is the optimal dose of digoxin?
The median maintenance dose of digoxin in the DIG Study was 0.25 mg per day — 70% of patients were maintained on this dose. The steady-state serum digoxin level in patients receiving this dose (available in a subset of patients) averaged between 0.8 ng/mL and 0.9 ng/mL (therapeutic range 0.5–2.0 ng/mL). Higher maintenance doses of digoxin (0.375 mg per day) were used in the PROVED10 and RADIANCE trials,11 but there was no evidence that increasing the dose in the range 0.2–0.39 mg per day resulted in any symptomatic improvement.15 There are several lines of evidence showing that the risk of digoxin toxicity (including death) rises rapidly when the average daily digoxin dose exceeds 0.25 mg per day or when trough serum digoxin levels are above 1.0 ng/mL.Congestive Cardiac Failure With Digoxin Toxicity Essay

It is particularly important to use lower maintenance doses of digoxin (0.125–0.25 mg/day) in the elderly because of the age-related decline in renal function. This issue is likely to arise frequently in clinical practice, as the elderly constitute the bulk of the population with heart failure. Furthermore, digoxin toxicity may be difficult to recognise in the elderly.17 Taking concomitant medications that increase serum digoxin concentrations (eg, amiodarone, quinidine, verapamil) may also necessitate a reduction in the maintenance dose. Cautions also apply to the use of a number of herbal preparations and so-called complementary medicines in patients taking digoxin. For example, squill, strophanthus and oleander contain cardiac glycosides and can trigger toxicity, while senna and cascara may augment potassium loss, leading to toxicity, and St John’s wort reduces serum digoxin levels by about 25%.Congestive Cardiac Failure With Digoxin Toxicity Essay

Digoxin in diastolic heart failure
Diastolic heart failure has been increasingly recognised as a clinical entity, particularly in the elderly and in women.18 There is little information about the use of any drug therapy in diastolic heart failure. However, the DIG study included a large subgroup of almost 1000 patients with diastolic heart failure.9 The benefit of digoxin in this subgroup was similar to that observed in the main trial.Congestive Cardiac Failure With Digoxin Toxicity Essay

Digoxin is an appropriate drug for controlling the ventricular response rate to atrial fibrillation in association with diastolic heart failure, as the onset of this arrhythmia may cause marked symptomatic deterioration.

Recommendations
Digoxin is indicated for the management of heart failure. Its primary indication is to maintain clinical stability and exercise capacity in patients with symptomatic heart failure (NYHA class II-IV). For patients in sinus rhythm, it should be used as a second-line drug after diuretics, ACE inhibitors and β-blockers (E4). For those in atrial fibrillation, it should be used as a first-line drug (E2). Maintenance doses of digoxin should not exceed 0.25 mg per day, and may need to be lower in women and the elderly.

Important messages for patients are shown in Box 4.
Box 4
Important messages for patients

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Digoxin for arrhythmia
While there is little doubt that appropriate doses of digoxin (see above) will slow the resting ventricular rate in most patients with chronic atrial fibrillation (E1), it has been known for many years that digoxin is far less successful in controlling exercise-induced or stress-induced tachycardia in atrial fibrillation in many patients, even when plasma drug concentrations are near the upper end of the accepted therapeutic range.19 A study of 12 patients with chronic atrial fibrillation confirmed that medium-dose diltiazem was comparable, in terms of rate control at rest, to a therapeutic dose of digoxin and superior to digoxin during exercise.20 High-dose diltiazem (360 mg/day) was superior to digoxin, both at rest and during exercise.Congestive Cardiac Failure With Digoxin Toxicity Essay

Atrial fibrillation
Very recently, the results of the AFFIRM trial, involving 4060 patients with atrial fibrillation randomly allocated to a “rhythm control” versus a “rate control” strategy, were published.21 This benchmark trial showed no difference in mortality and other important secondary endpoints, including quality of life, between the two strategies. A substudy of 1968 patients from the rate-control arm of AFFIRM found that both β-blockers and calcium-channel blocking agents were effective as first-line agents in about 50%–70% of patients, and that digoxin (which was allowed to be added as a second-line agent) appeared to increase the rate control efficacy of these agents modestly.Congestive Cardiac Failure With Digoxin Toxicity Essay

The use of digoxin in paroxysmal atrial fibrillation, either to revert the arrhythmia to sinus rhythm or to suppress further paroxysms, was widespread in the second half of the 20th century and remains a popular strategy. However, contrary to common belief, there is no evidence from controlled trials to suggest that digitalis increases the likelihood of reversion to sinus rhythm in patients with recent onset atrial fibrillation. Indeed, there is no electrophysiological reason to suppose such an effect. Digoxin shortens the effective refractive period of the atrial myocardium and, if anything, would be expected to make atrial fibrillation more likely to occur and persist.

It is certainly possible that, in patients with concomitant heart failure, the beneficial effects of digitalis on the myocardium may improve haemodynamic variables enough to produce spontaneous reversion to sinus rhythm. However, it must be remembered that spontaneous reversion is quite common in recent onset atrial fibrillation, and that restoration of normal rhythm during treatment with digoxin does not prove cause and effect.Congestive Cardiac Failure With Digoxin Toxicity Essay

A small, but well designed randomised double-blind placebo-controlled trial in 36 patients with recent onset atrial fibrillation, and without heart failure, who were given either 1.4 mg digoxin orally over 14 hours or placebo capsules, reported reversion to sinus rhythm in eight out of 18 patients taking placebo and nine out of 18 patients taking digoxin.23 This, of course, was not statistically significant. The mean time to conversion in those patients who returned to sinus rhythm during the observation period was 5.1 hours in the digoxin group compared with 3.3 hours in the placebo group. A number of similar studies have produced very similar results, including a much larger (239 patients), multicentre Swedish study.24 These are referenced in the latest guidelines for the management of atrial fibrillation, published jointly by the American Heart Association, the American College of Cardiology and the European Society of Cardiology (AHA/ACC/ESC).25 These guidelines state very clearly that “digitalis glycosides are generally no more effective than placebo for conversion of recent onset AF [atrial fibrillation] to sinus rhythm. Digoxin may prolong the duration of episodes of paroxysmal AF in some patients” (E1).Congestive Cardiac Failure With Digoxin Toxicity Essay

What of the widespread practice of using digitalis as prophylactic therapy in patients with paroxysmal atrial fibrillation? There are no comparable randomised placebo-controlled studies of this strategy, but a study of 139 episodes of atrial fibrillation during ambulatory monitoring in 72 patients did not support it.26 Thirty-one of the patients were taking digoxin, and there was no difference between those taking and those not taking digoxin, either in the frequency of attacks or in the ventricular rate during attacks (140/minute v 134/minute). Furthermore, digoxin therapy was associated with a significantly greater number of prolonged attacks of atrial fibrillation (defined as those lasting more than 30 minutes). In keeping with this and other observations, the AHA/ACC/ESC guidelines state that “the evidence available does not support a role for digitalis in suppressing recurrent AF in most patients”.25

Atrial flutter
Most studies of digoxin in atrial fibrillation or flutter have either enrolled patients with atrial fibrillation only, or have combined patients with atrial fibrillation and atrial flutter. There is certainly no reason to believe that digoxin has any role for either pharmacological cardioversion or prophylaxis for atrial flutter (any more than it does for atrial fibrillation), and common observation supports the widely-held belief that digoxin is less effective at rate control in patients with atrial flutter than it is in those with atrial fibrillation (E4).Congestive Cardiac Failure With Digoxin Toxicity Essay

In 2003, there is little or no role for digoxin in managing arrhythmias other than atrial fibrillation or flutter. It has been widely used in the past to treat re-entrant supraventricular tachycardia in adults and children, but newer agents have superseded it for treating these arrhythmias. It has occasionally been recommended for use in multifocal atrial tachycardia, and there are occasional observational reports of efficacy for this, but its use for this indication is limited by the fact that these patients commonly have pulmonary hypertension and hypoxia, which renders them more liable to digitalis toxicity. Other agents, such as β-blockers and verapamil, are probably best used in this situation. There is no evidence for efficacy of digoxin in suppressing ventricular arrhythmias and every reason to suspect that the agent should be avoided in this situation. (It is of course occasionally observed that patients treated with digoxin for left ventricular dysfunction show reduced ventricular ectopy concomitant with improvement in their underlying condition.)Congestive Cardiac Failure With Digoxin Toxicity Essay

Recommendations
Digoxin has a limited but useful role, either alone or in combination with other agents such as β-blockers, diltiazem or verapamil, in achieving satisfactory resting ventricular rate control in patients with chronic atrial fibrillation (E1). In patients who lead a predominantly sedentary lifestyle, particularly the elderly, digoxin alone may be the agent of choice for chronic atrial fibrillation (E4). Certainly, digoxin carries a potential advantage over the other agents in that it is very unlikely to precipitate worsening ventricular function in patients whose ventricular function is either depressed or unknown. Other than this, there is no role for digoxin in pharmacological reversion of atrial fibrillation, and little or no support for the use of digoxin in the management of other arrhythmias. Congestive Cardiac Failure With Digoxin Toxicity Essay