Brugada Syndrome Case Study

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Brugada Syndrome is a hereditary illness that is categorized by irregular electrocardiogram (ECG) results (Refer to Appendix 1) and an augmented danger of unexpected cardiac arrest. It is titled after the Spanish cardiologists Josep and Pedro Brugada. It is counted amongst one of the key (Nademanee, 1997) reasons for "Sudden Unexplained Death Syndrome" (SUDS), and is the most regularly occurring reason of unexpected expiration amongst young men without knowing the fundamental cardiac ailment. This holds particularly true for Laos and Thailand.

The purpose of this research essay is to talk about the Brugada Syndrome by focusing on its epidemiology, pathophysiology, pharmacology and implications for advanced nursing techniques. It also discusses the disease itself in tremendous detail and makes thorough used of secondary research to validate statements wherever required.

Even though, if the ECG results of Brugada Syndrome were initially found amongst survivors of cardiac arrest in the year 1989 (Martini, 1989). Furthermore, it was in the year 1992 that the Brugada brothers acknowledged it as a separate clinical object; instigating abrupt death by triggering ventricular fibrillation in the heart (Brugada, 1992).

Brugada Syndrome characteristically becomes observable during maturity. While a large segment of the total patients are in later leg of their lives (30's to 40's), the Syndrome has been seen in patients as small as 2 years in age. On the other end, an individual of 84 years was also suffering from the disease. It has also been established that males are impacted more frequently than their female counterparts. Research has claimed this to be a ratio of 8/9:1 (Matsuo, 2001). The cause for these statistics in terms of males in the population is conceivably associated to fundamental dissimilarities in the hormonal position. It is assessed that the Brugada Syndrome is accountable for at minimum, 4% of all abrupt bereavements and at the smallest, 20% of all unexpected deaths befalling patients who did not have a serious physical heart malady (Brugada, 2005). The condition transpires most regularly in the Southeast Asian region, with the main occurrence taking place in the population of Northern Thailand (Tunsunga, 1993).

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Nearly 20% of the cases of Brugada Syndrome have been seen to be connected with alterations in the DNA segment that encrypts the sodium ion channel in the cell-membranes of the muscles present in the cardiac region. The inheritable factor, called SCN5A, is situated on the tiny arm of the third chromosome (3p21). Alterations reslting in a loss of control in this genetic factor result in a forfeiture of the possible action dome of some epicardial regions of the right ventricle. These consequences in the transfer of and epicardial diffusion of repolarization. The transmural scattering motivates the raising of the ST-segment and the expansion of a susceptible window diagonal to the ventricular partition, although the epicardial spreading out of repolarization enables the easy progress of phase 2 reentries, which creates an additional applicant action systole that seizes the defenseless window to precipitate the fibrillation that repeatedly is the outcome in unexpected cardiac arrest cases. But, presently, all of the documented patients who expired owing to the sickness and were surrendered to a comprehensive post-mortem examination have displayed a structural right ventricular pathology pertaining to the disease.

In excess of 160 transmutations in the SCN5A gene have been revealed to this day. With each having fluctuating instruments and impacts on the utility, hence, elucidating the changing degrees of infiltration and manifestation of this syndrome (Hedley, 2009).

An instance of one of the contrivances in which damage to the purpose of the sodium channel takes place can be a transformation of the gene that disturbs the sodium channel's capacity to bind appropriately to ankyrin-G, a significant protein arbitrating contact concerning both cytoskeletal elements and ion channels. In recent times, such a metamorphosis in an additional gene, Glycerol-3-phosphate dehydrogenase 1-like (GPD1L) gene has been seen to consequence in the Brugada Syndrome in a huge number of multi-generational families. This genetic factor performs as an ion channel modulator in….....

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