Congestive Cardiac Failure With Digoxin Toxicity Essay
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:Congestive Cardiac Failure With Digoxin Toxicity Essay
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Supportive care
Electrolyte abnormality management
Bradycardia management
Hemodynamic compromise management
Ongoing monitoring and change of medicine
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).Congestive Cardiac Failure With Digoxin Toxicity Essay
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).Congestive Cardiac Failure With Digoxin Toxicity Essay
The pathogenesis of the arrhythmias falls into one of two basic mechanisms: increased or covered up automaticity, triggered activity, or re-entry.
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).Congestive Cardiac Failure With Digoxin Toxicity Essay
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.
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.Congestive Cardiac Failure With Digoxin Toxicity Essay
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:Congestive Cardiac Failure With Digoxin Toxicity Essay
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).
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).Congestive Cardiac Failure With Digoxin Toxicity Essay
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).
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)Congestive Cardiac Failure With Digoxin Toxicity Essay
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
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).Congestive Cardiac Failure With Digoxin Toxicity Essay
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).
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.Congestive Cardiac Failure With Digoxin Toxicity Essay
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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).
General Pharmacology
Cardiac glycosides represent a family of compounds that are derived from the foxglove plant (Digitalis purpurea). The therapeutic benefits of digitalis were first described by William Withering in 1785. Initially, digitalis was used to treat dropsy, which is an old term for edema. Subsequent investigations found that digitalis was most useful for edema that was caused by a weakened heart (i.e., heart failure).Congestive Cardiac Failure With Digoxin Toxicity Essay
Mechanisms of action
Digitalis compounds are potent inhibitors of cellular Na+/K+-ATPase. This ion transport system moves sodium ions out of the cell and brings potassium ions into the cell. This transport function is necessary for cell survival because sodium diffusion into the cell and potassium diffusion out of the cell down their concentration gradients would reduce their concentration differences (gradients) across the cell membrane over time. Loss of these ion gradients would lead to cellular depolarization and loss of the negative membrane potential that is required for normal cell function. The Na+/K+-ATPase also plays an active role in the membrane potential. this pump is electrogenic because it transports 3 sodium ions out of the cell for every 2 potassium ions that enter the cell. This can add several negative millivolts to the membrane potential depending on the activity of the pump.Congestive Cardiac Failure With Digoxin Toxicity Essay
cellular mechanism by which digitalis stimulates the heart
Cardiac myocytes, as well as many other cells, have a Na+-Ca++ exchanger (not an active energy-requiring pump) that is essential for maintaining sodium and calcium homeostasis. The exact mechanism by which this exchanger works is unclear. It is known that calcium and sodium can move in either direction across the sarcolemma. Furthermore, three sodium ions are exchanged for each calcium, therefore an electrogenic potential is generated by this exchanger. The direction of movement of these ions (either inward or outward) depends upon the membrane potential and the chemical gradient for the ions. We also know that an increase in intracellular sodium concentration competes for calcium through this exchange mechanism leading to an increase in intracellular calcium concentration. As intracellular sodium increases, the concentration gradient driving sodium into the cell across the exchanger is reduced, thereby reducing the activity of the exchanger, which decreases the movement of calcium out of the cell. Therefore, mechanisms that lead to an accumulation of intracellular sodium cause a subsequent accumulation of intracellular calcium because of decreased exchange pump activity.Congestive Cardiac Failure With Digoxin Toxicity Essay
By inhibiting the Na+/K+-ATPase, cardiac glycosides cause intracellular sodium concentration to increase. This then leads to an accumulation of intracellular calcium via the Na+-Ca++ exchange system. In the heart, increased intracellular calcium causes more calcium to be released by the sarcoplasmic reticulum, thereby making more calcium available to bind to troponin-C, which increases contractility (inotropy). Inhibition of the Na+/K+-ATPase in vascular smooth muscle causes depolarization, which causes smooth muscle contraction and vasoconstriction.Congestive Cardiac Failure With Digoxin Toxicity Essay
By mechanisms that are not fully understood, digitalis compounds also increase vagal efferent activity to the heart. This parasympathomimetic action of digitalis reduces sinoatrial firing rate (decreases heart rate; negative chronotropy) and reduces conduction velocity of electrical impulses through the atrioventricular node (negative dromotropy).
Pharmacokinetics and toxicity
The long half-life of digitalis compounds necessitates special considerations when dosing. With a half-life of 40 hours, digoxin would require several days of constant dosing to reach steady-state, therapeutic plasma levels (digitoxin with a half-life of 160 hours, would require almost a month!). Therefore, when initiating treatment, a special dosing regimen involving “loading doses” is used to rapidly increase digoxin plasma levels. This process is termed “digitalization.” For digoxin, the therapeutic plasma concentration range is 0.5 – 1.5 ng/ml. It is very important that therapeutic plasma levels are not exceeded because digitalis compounds have a relatively narrow therapeutic safety window. Plasma concentrations above 2.0 ng/ml can lead to digitalis toxicity, which is manifested as arrhythmias, some of which may be life-threatening. If toxicity occurs with digoxin, it may take several days for the plasma concentrations to fall to safe levels because of the long half-life. There is available for digoxin toxicity an immune Fab (Digibind) that can be used to rapidly reduce plasma digoxin levels. Potassium supplementation can also reverse the toxic effects of digoxin if the toxicity is related to hypokalemia Congestive Cardiac Failure With Digoxin Toxicity Essay
Drug Interactions
Many commonly used drugs interact with digitalis compounds. The Class IA antiarrhythmic, quinidine, competes with digoxin for binding sites and depresses renal clearance of digoxin. These effects increase digoxin levels and can produce toxicity. Similar interactions occur with calcium-channel blockers and nonsteroidal anti-inflammatory drugs. Other drugs that interact with digitalis compounds are amiodarone (Class III antiarrhythmic) and beta-blockers. Diuretics can indirectly interact with digoxin because of their potential for decreasing plasma potassium levels (i.e., producing hypokalemia). Hypokalemia results in increased digoxin binding to the Na+/K+-ATPase (possibly through increased phosphorylation of the enzyme) and thereby enhances digoxin’s therapeutic and toxic effects. Hypercalcemia enhances digitalis-induced increases in intracellular calcium, which can lead to calcium overload and increased susceptibility to digitalis-induced arrhythmias. Hypomagnesemia also sensitizes the heart to digitalis-induced arrhythmias.Congestive Cardiac Failure With Digoxin Toxicity Essay
Therapeutic Uses
Therapeutic Uses of
Digitalis Compounds
Heart Failure
↑ inotropy
↑ ejection fraction
↓ preload
↓ pulmonary congestion/edema
Arrhythmias
↓ AV nodal conduction
(parasympathomimetic effect)
↓ ventricular rate in atrial flutter
and fibrillation
Heart failure
Digitalis compounds have historically been used in the treatment of chronic heart failure owing to their cardiotonic effect. Although newer and more efficacious treatments for heart failure are available, digitalis compounds are still widely used. Clinical studies in heart failure patients have shown that digoxin, when used in conjunction with diuretics and vasodilators, improves cardiac output and ejection fraction, and reduces filling pressures and pulmonary capillary wedge pressure (this reduces pulmonary congestion and edema); heart rate changes very little. These effects are to be expected for a drug that increases inotropy. Although the direct effect of digoxin on blood vessels is vasoconstriction, when given to patients in heart failure, the systemic vascular resistance falls. This most likely results from the improvement in cardiac output, which leads to withdrawal of compensatory vasoconstrictor mechanisms (e.g., sympathetic adrenergic activity and angiotensin II influences). Digitalis compounds have a small direct diuretic effect on the kidneys, which is beneficial in heart failure patients.Congestive Cardiac Failure With Digoxin Toxicity Essay
Atrial fibrillation and flutter
Atrial fibrillation and flutter lead to a rapid ventricular rate that can impair ventricular filling (due to decreased filling time) and reduce cardiac output. Furthermore, chronic ventricular tachycardia can lead to heart failure. Digitalis compounds, such as digoxin, are useful for reducing ventricular rate when it is being driven by a high atrial rate. The mechanism of this beneficial effect of digoxin is its ability to activate vagal efferent nerves to the heart (parasympathomimetic effect). Vagal activation can reduce the conduction of electrical impulses within the atrioventricular node to the point where some of the impulses will be blocked. When this occurs, fewer impulses reach the ventricles and ventricular rate falls. Digoxin also increases the effective refractory period within the atrioventricular node.Congestive Cardiac Failure With Digoxin Toxicity Essay
Specific Drugs
Three different digitalis compounds (cardiac glycosides) are listed in the table below. The compound most commonly used in the U.S. is digoxin. Ouabain is used primarily as a research tool. (See www.rxlist.com for more details on digoxin).
Drug Oral Availability* Half-life (hours) Elimination
Digoxin 75% 40 kidneys
Digitoxin >90% 160 liver
Ouabain 0% 20 kidneys
* percent absorption Congestive Cardiac Failure With Digoxin Toxicity Essay
Side Effects, Contraindications and Warnings
The major side effect of digitalis compounds is cardiac arrhythmia, especially atrial tachycardias and atrioventricular block. Digitalis compounds are contraindicated in patients who are hypokalemic, or who have atrioventricular block or Wolff-Parkinson-White (WPW) syndrome. Impaired renal function leads to enhanced plasma levels of digoxin because digoxin is eliminated by the kidneys. Lean, elderly patients are more susceptible to digitalis toxicity because they often have reduced renal function, and their reduced muscle mass increases plasma digoxin levels at a given dose because muscle Na+/K+-ATPase acts as a large binding reservoir for digitalis. A 2012 analysis of the AFFIRM trial determined that digoxin significantly increased all-cause mortality in patients with atrial fibrillation. This calls into question the practice of using digoxin for lowering ventricular rate in patients with atrial fibrillation. Congestive Cardiac Failure With Digoxin Toxicity Essay
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