[NURSING/AUSTRALIA][CASE STUDY]

[Nursing/Australia][Case Study]

QUESTION 1:

Identify four (4) key pieces of assessment data that support a diagnosis of acute myocardial infarction

Troponins in Cardiology Routine

Since their first introduction in the early nineties, troponin assays have been implemented in most emergency facilities as point-of-care tests or are offered on stat basis by the hospital central laboratories. Initially, there has been some confusion with regard to the correct cut-off values. Particularly irritating to many clinicians was the fact that the results with different troponin I assays were not comparable. This relates to the fact that the antibodies employed in assays of different manufacturers are directed against different epitopes of troponin I. Because circulating troponin I is unstable, some epitopes are lost as a result of degradation, whereas others still remain unaltered, resulting in different recoveries by different assays.6 In contrast, there is, because of patent reasons, only one troponin T assay available that has been repeatedly refined, resulting in a lowering of the analytical detection limit.7,8 The consensus document of the ESC and the ACC, therefore, recommended that each laboratory should determine its cut-offs individually at the 99th percentiles of normals with a <10% variance(Gulianick, 2003).2

Non-Coronary-Related Troponin Elevations

Unexplained elevations of troponins are extremely rare but may sometimes cause confusion. A rise of troponins reflects irreversible myocardial cell necrosis. Accordingly, abnormal values have been described in various conditions not related to acute coronary disease, like myocarditis, pulmonary embolism, acute heart failure, septic shock, and as a result of cardiotoxic drugs as well as after therapeutic procedures like coronary angioplasty, electrophysiological ablations, or electrical cardioversions.

In Mrs. Wyatt's with severe renal dysfunction troponin T as well as troponin I, elevations are found that cannot be linked to myocardial injury. The reasons for these elevations are not yet convincingly explained. Reexpression of cardiac isoforms in skeletal muscles has been excluded by different analyses and investigators. Loss of membrane integrity and constant outflow from the free cytosolic troponin pool as well as amplified elevation of normal low levels because of impaired renal excretion are more likely. The higher unbound cytosolic pool and higher molecular weight may explain why troponin T is more frequently found elevated than troponin I.

The fraction of troponin-positive Mrs. Wyatt's with end-stage renal disease naturally depends on the assay technology and on the chosen discriminator value. Because of the higher analytical precision of newer troponin T assays, the discriminator level could be lowered stepwise, and abnormal values in Mrs. Wyatt's with renal dysfunction have become less frequent.

Troponins in Nephrology

In asymptomatic Mrs. Wyatt's with renal dysfunction, troponins are not presently part of the routine diagnostic work-up because results with regard to their predictive value based on small series was controversely discussed. Accordingly, the prospective study by Apple et al in 733 Mrs. Wyatt's represents a landmark in support of the clinical role of troponin T in this setting.19 The documented 2- to 5-fold increase in all-cause mortality is a finding that deserves clinical attention. Of particular interest is the gradual rise in risk with increasing ...