Sudden Cardiac Death Case Study

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Introduction Sudden cardiac death (SCD) is a world wide health problem resulting in one-fifth of unexpected deaths in the western world. Ventricular fibrillation (VF) is one of the life-threatening arrhythmias contributing to the increasing number of individuals needing urgent medical assistance (Wellens, Gorgels & Munter, 2013). The following case study will explore a complex critically ill patient who has suffered from a ventricular tachycardia (VT) and VF due to dilated left ventricle (LV) with severe segmental systolic function. The case study will review the pathophysiology of the patient’s current health problem and will further investigate the primary interventions in relationship to evidence based practice.
Sudden Cardiac Death SCD
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Patient X experienced VF for the reason that he previously had experienced acute myocardial infarct (AMI). Myocardial scar tissue occurs with AMIs and comprises a combination of fibrosis and surviving myocytes to provide a path of re-entry for VT which can cause SCD (Stevenson & John, 2011).
Pathophysiology of poor LV function HF is an intricate clinical syndrome that is caused by any systemic or functional impairment of ventricular filling or blood discharge (Yancy et al., pp. 246, 2013), for instance, from injury to the myocardium causing decreased CO. Patient X’s HF is due to IHD, hypertension and smoking. Valvular disease, cardiomyopathy, infections and diabetes can also cause HF. As CO decreases, dyspnoea, peripheral oedema, ascites and fatigue may occur. There are several compensatory mechanisms which occur due to decreased CO (Kemp & Conte, 2012). The first compensatory mechanism is the Frank Starling mechanism which commences as stroke volume (SV) decreases. Higher muscle contraction/stretch and SV intensifies left ventricular end-diastole pressure (LVEDP) hence increasing CO. Patient X’s CA showed a high LVEDP of 28 and a dilated LV with severe global dysfunction (Holubarsch et al.,
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Beta-blockers also minimize risks of arrhythmias that generally results in SCD, as an in the case of the patient X who experienced the reduction of cardiac remodeling through beta-1 receptors blockage (Fletcher, 2000). Bradycardia is considered to be the most regular side effect coupled with hypotension and dizziness (Ko, et al., 2004). Patient X initiated with Nebivolol, regarded as beta-1 selective adrenergic agonist that HF individuals rarely practice. Nevertheless, various trials show its favourable results on LVEDP function and afterload reduction, e.g. Edes et al., trial which resulted in a 6.51% amelioration in LVEDP in comparison with the group who had placepo. Nebivolol reduces BP as well as afterload even so it enhances LV volumes and exercise capacities amongst senior individuals (Ko, et al., 2004). Taking based practice into consideration, Patient X initiated with Perindopril, an ACE inhibitor and Nebivolol with the intended effect of his quality of life improvement, symptoms relief that was produced by HF and the heart work load

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