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GRADED DISCUSSION - Half-life and drug dosing Gayle - Case Study Example

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Heart failure is a physiological condition where the heart beat is insufficient to maintain the regular circulation of blood necessary to meet the needs of the body (Ansari & Massie, 2003)…
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GRADED DISCUSSION - Half-life and drug dosing Gayle
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? Graded Discussion Half-Life and Drug Dosing Gayle Graded Discussion Half-Life and Drug Dosing Gayle Heart failure is a physiological condition where the heart beat is insufficient to maintain the regular circulation of blood necessary to meet the needs of the body (Ansari & Massie, 2003). The disease has varied clinical symptoms such as exercise intolerance, tachycardia and oedema. Renal failure, on the other hand, is a reduction in renal efficiency leading to accumulation of toxic metabolic products in the blood. This medical condition is associated with increased body fluids, hyperkalaemia, diminished calcium levels and increased phosphate levels. Persistent kidney failure is a potential risk factor for cardiovascular diseases; however there are a couple of other possible underlying causes. Gayle, who is 80years old, presents with the two medical conditions and the proposed intervention, is to increase digoxin dose, a drug that she is on long term use. Digoxin is a cardiac glycoside that is indicated for the management of all degrees of cardiac failure. This medication has a positive inotropic effect that improves the cardiac output, which in turn alleviates hemodynamic insufficiency symptoms. Although digoxin stands out as the primary drug of choice for Gayle’s disease, its side effects could be fatal to her putting into account her present age and the other medical condition (Alexander & Biswas, 2003). When a new (increased) dose of digoxin is administered to her it would take approximately five times the half-life of the drug to reach a steady state, which in this case is about 150 hours (7days). However, in renal failure patients such as Gayle, the half-life of digoxin is considerably prolonged and can take more than 10days to reach a stable plasma state. The steady state is an equilibrium of the drug’s intake and elimination. This steady state is dependent on the elimination half-life, and it is also affected by a change in dosage of the drug as well as co-administered drugs (Ahmed, 2003). The main route of elimination of the drug is through renal excretion and involves the P-glycoprotein. Therefore, renal insufficiency in Gayle’s condition will negatively affect the time to steady state; therefore, increasing the dosage could easily lead to toxicity. For geriatrics such as Gayle, there is age related decline in renal function, which also potentially reduces the rate of digoxin elimination (Ansari & Massie, 2003). A co-founding factor that can elevate serum digoxin levels in her case is reduction in lean muscle mass due to old age, which corresponds to the volume of distribution of the drug in the tissues. Another significant challenge in Gayle’s case is gender related impaired clearance of digoxin in female compared to male patients (Rudinger, Harjola, & Muller et al. 2005). Digoxin has narrow therapeutic window with recommended 0.5 and 1.0ng/ml plasma levels for congestive heart failure (Rudinger, Harjola, & Muller et al. 2005). The above conditions significantly affect the therapeutic plasma levels of the drug in this patient and require close monitoring. Digoxin toxicity is common in patients who are on long term therapy with a prevalence rate of about 10% to20% (Kerzner, Gage, & Freedland et al.2003). Cardio toxicity is one of the most severe side effects, and it is manifested as ventricular arrhythmias with a high prevalence of cardiac death due pump failure. Scientific researches on digoxin have reported contradicting outcomes and in a recent study on retrospective analysis of the drug, there was associated increase in mortality, in women. Apart from cardiac toxicity other effects include nausea, vomiting, and visual effects, however, these are not life threatening. There are several drugs that interact with digoxin; they include; verapamil, a calcium channel blocker effective in the management of angina due to spasms of coronary arteries. Other drugs are quinidine, spironolactone and itraconazole. These drugs can significantly increase plasma digoxin levels and increase the risk of toxicity. Drugs that can be co administered with digoxin such as beta-channel blockers and calcium channel blockers, and which reduce the overall heart rate, can increase the risk of mortality to the patient. Furosemide can lower plasma potassium and magnesium levels, which is a predisposing factor for abnormal heart rhythms. Other drugs that interact with digoxin include protease inhibitors such as saquinavir, nelfinavir and ritonavir. These drugs affect the active excretion of digoxin in the kidney resulting in increased plasma levels. Potassium sparing diuretic such as Aldactone that inhibits the action of aldosterone in cardiac failure can potentially increase serum levels of digoxin. Majority of the drugs that interact with digoxin positively affect its concentration in plasma hence poses a risk of toxicity. In Gayle’s case, there are low survival chances due to digoxin toxicity potentiated by the aforementioned factors that alter the overall pharmacokinetics and pharmacodynamics interactions of the drug. In managing her case proper evaluation and identification of the aetiology and underlying cause is critical, equally is the use of effective intervention and prognosis (Ahmed, 2003). While congestive heart failure is common in the elderly, it often has varying manifestation and severity. It is, therefore, essential to pinpoint the exact cause of heart failure in the patient. The following risk factors such as hypertension, reno-vascular and valvular heart diseases are likely the underlying aetiology in Gayle and are worth screening. This patient (Gayle) requires an initial clinical evaluation and the presentation of symptoms such as dyspnoea and orthopnoea can be suggestive of congestive heart failure. Another critical symptom in this initial assessment is presence or absence of peripheral oedema (Ahmed, 2003). However Clinical examination may not be conclusive and an objective differential diagnosis maybe necessary to provide proof of the disease. Such differential diagnosis include; electrocardiogram (ECG), which is a useful preliminary investigation in congestive heart failure (Fonseca, Mota & Morais et al. 2004). This test will differentiate between symptoms attributed to heart failure and other diseases. Abnormalities in ECG, coupled with past evidence of infarction and arterial fibrillation can be indicative of cardiac failure (Remes, Lansimies & Pyorala, 1991). If, the ECG is abnormal a confirmatory test is recommended, in which case echocardiogram is a primary choice (Fonseca, Mota & Morais et al. 2004). This analysis will provide additional evidence of cardiac valves and ventricular function abnormalities. Echocardiogram can also enable classification of the severity of heart failure. Alternative confirmatory tests apart from echocardiography include; plain chest radiology and blood for B-type natriuretic peptide. These tests can provide valuable information about cardiomegaly, pulmonary congestion and cardiac dysfunction (Torp-Pederson & Kobe, 1999). Other additional tests such as full blood count and serum electrolytes can also be used to improve on the diagnosis. All these tests are needed to conclude on Gayle's heart problem. After a conclusive diagnosis, the appropriate intervention for Gayle can be started. There are many treatment options, which include; diuretic treatment, this would be appropriate since the patient has an imbalance of body fluid attributed to by renal insufficiency. Other interventions include the use of beta-blockers, spironolactone and ACE inhibitor (Torp-Pederson & Kobe, 1999). However, these treatments need particular attention to dosage and tolerability, especially in renal failure. The use of ACE inhibitor has been shown to be effective in managing cardiac failure caused by left ventricular systolic dysfunction (Torp-Pederson & Kober, 1999); though this may not be apparent in Gayle Herbert, therefore, not appropriate. The use of beta-blockers drugs is only suitable for stable patients since its negative inotropic effect remains contentious. Beta-blockers have an agonist effect when co-administered with diuretic and ACE inhibitors in patients with chronic heart failure (Torp-Pederson & Kobe, 1999). Interaction of beta-blockers and digoxin results in reduced elimination of the later, making this combination unsuitable for her. While increasing the dosage of digoxin in managing Gayle’s situation is promising, a slight overdose of the drug can lead to drug toxicity. To reduce this risk a review of all co-interventions and over the counter medication should be done. This information can be obtained both clinically and through laboratory analysis of a blood sample. Based on the above factors digoxin dosage should rather be reduced in order to effectively manage Gayle’s condition. Increasing the dose in this patient raises the risk of plasma accumulation of the drug to toxic levels. Elevated plasma digoxin levels impairs electrolyte imbalance through inhibition of sodium potassium pump, which can result in cardiac arrest. In the absence of interfering medication, a combination of a diuretic and digoxin can efficiently contain the patient’s condition. However, keen monitoring of the plasma levels of these drugs through blood tests and assessment of renal clearance efficiency should be a primary concern. Other useful tests include serum electrolytes and calcium levels in diagnosing possible drug toxicity (Blue, Lang, & McMurray, et al. 2001). It is the right of every patient to know and understand the type of interventions they are receiving (Ekman, Andersson, & Ehnfors, et al.1998). I would, therefore, inform Gayle about the possible benefits of this intervention and the associated risks. Preparing the patient psychologically is essential in effective patient management. References Alexander, K. & Biswas, M. (2003). Heart failure and the elderly: Disease diversity, data, and delivery of care. American Heart Journal, 146:194–6. Ansari, M. & Massie, B. (2003). Heart Failure: How big is the problem? Who are the patients? What does the future hold? American Heart Journal, 146:1–4. Rudinger, A. Harjola, V. P. &Muller, A. et al. (2005). Acute heart failure: clinical presentation, one year mortality and prognostic factors. European Journal of Heart Fail, 7(4):662–70. Kerzner, R. Gage, B. & Freedland, K. et al. (2003). Predictors of mortality in younger and older patients with heart failure and preserved or reduced left ventricular ejection fraction. American Heart Journal, 146:286–90. Ahmed, A. (2003). American College of Cardiology/American Heart Association Chronic Heart Failure Evaluation and Management guidelines: relevance to the geriatric practice. Journal of American Geriatric Society, 51:123–6. Remes, J. Lansimies, E. & Pyorala, K. (1991). Usefulness of M-mode echocardiography in the diagnosis of Heart failure. Cardiology, 78(3):267–77. Fonseca, C. Mota, T. & Morais, H. et al. (2004). EPICA investigators. The value of the electrocardiogram and chest x-ray for confirming or refuting a suspected diagnosis of heart failure in the community. European Journal of Heart Fail, 6(6):793–4. Torp-Pederson, C. & Kober, L. (1999). Effect of ACE inhibitor trandolapril on life expectancy of patients with reduced left ventricular function after acute myocardial infarction. TRACE Study Group. Lancet,354:9–12. Ekman, I. Andersson, B. & Ehnfors, M. et al. (1998). Feasibility of a nurse monitored, outpatient-care programme for elderly patients with moderate-to-severe, chronic heart failure. European Heart Journal, 19:1254–60. Sing, A. Blackwell, J. & Neher, J. (2005). Clinical inquiries. Does furosemide decrease morbidity or mortality for patients with diastolic or systolic dysfunction. Journal of Family Practise,54:370–2. Sin, D.D. & McAlister, F.A. (2002).The effects of B blockers on morbidity and mortality in a population based cohort of 11,942 elderly patients with heart failure. American Journal of Medicine,113:650–6. Blue, L. Lang, E. McMurray, J.J. et al. (2001) Randomised controlled trial of specialist nurse intervention in heart failure. BMJ, 323:715–18. Read More
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