Congestive Cardiac Failure With Digoxin Toxicity

Congestive Cardiac nonstarter With Digoxin Toxicitytable of contents (Jump to)Criterion-1Causes, Incidences and Risk Factors of Congestive Cardiac Failure with Digoxin Toxicity super Understanding of the ailment on Patient and FamilyCriterion-2Signs SymptomsPathophysiologyCriterion-3Drug straighten out physiological EffectCriterion-4Interventions-RationalesComprehensive discourse of the Identified Condition positive tradeElectrolyte abnormality prudenceBradycardia vigilanceHemodynamic compromise managementOngoing supervise and change of medicineCASE STUDY ON CONGESTIVE cardiac FAILURE WITH DIGOXIN TOXICITYCriterion-1Causes, Incidences and Risk Factors of Congestive Cardiac Failure with Digoxin ToxicityDigoxin toxicity ca utilize by high levels of tire outitalin 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 long-suffering roles. Especi ally those, who atomic number 18 vile from congestive cardiac chastisement, like our patient Mrs. Sharon McKenzie (Neo, et al, 2010). Body receives the therapeutic inwardness when it stores of 8 to 12 mcg/kg generally with minimum hazard of toxicity in roughly patients with failure of heart and normal fistula or breathing rhythm (Mangoni, 2010).People withheart failurewho project this digoxin ar commonly prescribed musics called diuretics that remove excess fluid from the part of body. This is overly happens that many diuretics can cause potassium way out from the body (Johnson, Inder, Nagle Wiggers, 2010). though ultimately it increases the risk of digitalis toxicity. Again, our patient, Mrs. Sharon McKenzies potassium level is first 2.5 mmol/l. whereas a normal potassium level ranges from 3.5-5.0 mmol/l.You argon more in all likelihood to fall into that condition if you take digoxin, digitoxin, or other digitalismedicinesalong with the higher(prenominal)(prenominal) stiff medicates that intera ct withit such as flecainide, quinidine, amiodarone, verapamil, and others. Similarly, Mrs. Sharon McKenzies was similarly taking medicinal drug with digoxin like furosemide, warfarin, and enalapril (Siabani, Leeder Davidson, 2013).In recent years the relative 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 non. The statistics over 1-year period, of that study is like thatOut of the 183 patients50 (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 inter set up in 5.5% of patients.The most common risk factor of digoxin toxicity is the patients elderly a ge. Like in our case study, Mrs. Sharon McKenzie is overly 77-year old woman. However there are other risk factors too, which attempt the elderly more vulnerable to digoxin toxicity. These contain an age- relate decline in renal function and a decrease in volume of digoxin distribution. There is to a fault an increase in the number of comorbid conditions, including cardiovascular and continuing obstructive pulmonary disease, which heightens vulnerability to digoxin toxicity.Comprehensive Understanding of the Disease on Patient and FamilyDigoxin toxicity is a life-threatening condition, and when a serious disease like congestive cardiac failure caused by digoxin toxicity then it can impact distastefully in a bad way on a patient as well as his/her family (Betihavas, 2011). Due to which his/her family also suffer by beholding 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 th e higher the rate of healing as the family and the patient both in composite plant and double trouble.Criterion-2Signs SymptomsPathophysiologySevere ventricular arrhythmiasSudden 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, dressing table discomfort, quivering, shortness of breath, and forceful or painful fast beats are commonly addressed with arrhythmias patients. Often, patients notice arrhythmias only afterwards checking their peripheral pulses (Mudge, et al, 2010).The pathogenesis of the arrhythmias go 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 eight-fold depolarization, precipitating ventricular arrhythmias (Johnson, Inder, Nagle Wiggers, 2010).Arrhythmogenesis is probably the most common procedure and impressions from re-entry. It causes the change of state of mind and biliousness too.2) HyperkalemiaHigher potassium rate in your blood can incite how your heart works. Symptoms of hyperkalemia can includeAbnormal heart rhythm arrhythmia that can be life-threateningSlowheart rateWeakness (Neo, et al, 2010)Hyperkalemia may run from an increase in total body potassium secondary to dissymmetry of intake vs. excretion or from misdistribution between intra- and extracellular lieu (Nanda, 2009).3) Hypokalemia commonly symptoms of low potassium are mildWeakness, tiredness, or pain in arms or legs muscles, sometimes this might be so severe to cause inability and disability to move arms or legs receivable to weakness of muscles (much like a paralysis) (Hughes Crowe, 2010)Tingling or numbness sickness or vomitingAbdominal cramping, bloatingConstipationPalpitations (feeling your heart beat irregularly) peeing passing rate is too high simultaneous ly feeling hungry(p) 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 atriums degradeed membrane capability 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) neurological SymptomsIn the identified condition, the patient may also go through with(predicate) with neurologic symptoms which are Visual disturbances, disorientation, and confusion.You might sense confusion. Although rare, you might also see bright spots, have blurry vision, or experience wile spots. In addition, you might urinate much more or slight than usual (Betihavas, 2011). Your body could also become swollen.The physiologies of ne urological symptoms are not easy to judge and too complex and our getting of them are sketchy mostly. From an evolutionary perspective it is easy to judge the neurological symptoms. Though it makes ace that the genuine physiologies of neurological symptoms are intricate and interrelated (Courtney, et al, 2009).5) Sinus guest DysfunctionSinus node dysfunction refers to a number of conditions create 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 followingFatigueAngina asphyxiaDizzinessFallConfusionHeart failure symptoms and palpitationsCriterion-3Drug ClassPhysiological EffectAngiotensin-converting enzyme ( protagonist) inhibitorsACE inhibitors cause blood vessels broadness, further melodic phrase the amount of work the heart has to do they may also have direct beneficial loads on the heart. These drugs are reducing the symptoms and the hire for hospitalization moreover they are helpful to prolong life (Mudge, et al, 2010).Beta-blockersBeta-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 s ystolic 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 whipping 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-4As 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-RationalesI realize that I would hold the medication Due to chess opening of toxicityWait 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 digMonitor I O monitoring for renal functionMonitor for edema and auscultator the lungsMonitor symptoms, VS S/E of dig toxicityCall the gear up. To get orders to carry out interventions and inform doctorStart an IV. For administration of medications (Mudge, et al, 2010).Comprehensive Treatment of the Identified ConditionThe chief(prenominal) 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 includesGeneral support ive careDiscontinuation of digoxin therapy and taproom of further exposureAdministration of digoxin-specific antibody fragments (digoxin immune Fab)Treatment of specific complications for example, dysrhythmias and electrolyte abnormalities (Jeon, Kraus, Jowsey Glasgow, 2010).Supportive careGeneral 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 surfeit of electrolytes in patients with electrolyte abnormalities (Mudge, et al, 2010).Electrolyte abnormality managementIn case of Mrs. Sharon McKenzie, hyperkalemia is only turn (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 promptly 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 managementAs Mrs. Sharon McKenzies ECG report showed sinus bradycardia, this will be treated with atropine. Atropine can be given every 3 to 5 minutes until there is a repartee or the 3 mg maximum dose is reached (San Miguel, et al, 2013).Hemodynamic compromise managementAs 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).Ongoing monitoring and change of medicineIdeally, digoxin is discontinued and a distinguishable 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 patients medication profile (Edgley, Krum Kelly, 2012).ReferencingJeon, Y. H., Kraus, S. G., Jowsey, T., Glasgow, N. J. (2010). The experience of living with inveterate heart failure a narrative review of soft studies. BMC health services research, 10(1), 77.Hughes, J., Crowe, A. (2010). 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