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      <title>NURS7105 WEEK 7 PADLET by Jianmin Tan</title>
      <link>https://padlet.com/jianmintantan/f9xmduh4sqkr</link>
      <description></description>
      <language>en-us</language>
      <pubDate>2018-08-27 23:10:58 UTC</pubDate>
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      <webMaster>hello@padlet.com</webMaster>
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         <title>Clinical Skill Textbook Unit 11 (by Jianmin)</title>
         <author>jianmintantan</author>
         <link>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/275741425</link>
         <description><![CDATA[]]></description>
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         <pubDate>2018-08-28 01:59:21 UTC</pubDate>
         <guid>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/275741425</guid>
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         <title>Cardiac Biomarkers and the Diagnosis of Myocardial Infarction in Women  (Tim)</title>
         <author></author>
         <link>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/277854798</link>
         <description><![CDATA[<div><strong>Female Coronary Heart Disease Outcomes</strong><br>-          Women with suspected acute coronary syndrome are less likely to undergo investigation or receive treatment than men, and women consistently have poorer outcomes. </div><div>-          Globally, coronary heart disease remains the major cause of death in women in both high-and low- or middle-income nations. </div><div>-          Gender differences remain in diagnosis, access to investigation and treatment and outcomes. </div><div>-          Women consistently have higher case fatality rates compared to men, and these differences exist despite adjusting for age and comorbid conditions. <br><br></div><div><strong>Cardiac Troponin<br></strong>-          Troponin is a 3-piece regulatory protein complex present in cardiac and skeletal muscle and is integral to muscle contraction.</div><div>-          Both cardiac troponin T and troponin I are derived from genes specific to the myocardium, whereas troponin C is present in both cardiac and skeletal muscles. </div><div>-          Given the high specificity of cardiac troponin T and troponin I to the myocardium, quantification of these biomarkers has now become integral to the diagnosis of myocardial infarction. </div><div>-          Over the last decade, troponin assays have become increasingly sensitive which has allowed quantification of circulating troponin in the majority of individuals in a normal healthy reference population.</div><div>-          The mechanisms through which cardiac troponin is released into the circulation in the apparent ‘healthy’ state is unclear, but may reflect cardiomyocyte apoptosis and cell turnover, hypertrophy or sub-clinical myocardial fibrosis. <br><br></div><div><strong>Sex Specific Cardiac Troponin</strong><br>-          Sex differences in cardiac troponin concentrations are not widely recognised in clinical practice and may contribute to under-diagnosis of myocardial infarction in women and discrepancies in patient care and outcomes. </div><div>-          An explanation gaining increasing attention, is under-diagnosing myocardial infarction in women by not recognising that there are important differences in the reference range and diagnostic threshold of cardiac biomarkers between men and women. </div><div>-          In acute coronary syndrome, women have lower cardiac troponin concentrations than men.<br><br></div><div><strong>Cardiovascular Studies</strong><br>-          In cardiovascular medicine large randomised control trials include a majority of men. As such, the evidence on interventions in acute myocardial infarction are limited in women with data largely derived from their male counterparts. </div><div>-          Women are less likely to be recruited as they are thought to present with less typical symptoms and are older and more likely to have comorbid conditions. </div><div>-          As such, selection bias will influence the generalisability of the findings from diagnostic accuracy studies.<br><br></div><div><strong> Suggested Causes for Sex Differences in Cardiac Troponin Ranges</strong></div><div>-          Changes in reproductive hormones during the menstrual cycle, pregnancy and menopause influence both vasomotor function and endogenous fibrinolysis. </div><div>-          Oestrogen induced attenuation of ventricular hypertrophy</div><div>-          Difference in release and clearance kinetics</div><div>-          Greater left ventricle mass in men</div><div>-          Age adjusted higher BP in men</div><div>-          Greater sympathetic nervous activity in men<br><br></div><div><strong>Summary</strong><br>There are three main arguments in favour of adopting sex-specific thresholds:</div><div><br>1<sup>st</sup> Cardiac troponin concentrations are consistently lower in women than men, across multiple populations from different ethnic backgrounds. </div><div><br></div><div>2<sup>nd</sup> Cardiac troponin concentrations in stable populations infer different prognostic information in men and women with stronger associations noticed in women when uniform thresholds are applied.<br><br></div><div>3<sup>rd</sup> In suspected acute coronary syndrome, sex-specific thresholds for cardiac troponin I identify women at high risk of future myocardial infarction and death. </div>]]></description>
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         <pubDate>2018-09-05 06:50:44 UTC</pubDate>
         <guid>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/277854798</guid>
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         <title>Pharm chp 27 - Cardiac stimulants and depressants (Jas)</title>
         <author>jasmine_knight1</author>
         <link>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/278643502</link>
         <description><![CDATA[]]></description>
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         <pubDate>2018-09-06 20:26:51 UTC</pubDate>
         <guid>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/278643502</guid>
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      <item>
         <title>Altered mental status predicts mortality in cardiogenic shock–results from the CardShock study (Char)</title>
         <author></author>
         <link>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/279060751</link>
         <description><![CDATA[<div><strong>Background and objective:</strong></div><div>·      Altered mental status is among the signs of hypoperfusion in cardiogenic shock, the most severe form of acute heart failure  </div><div>·      The purpose of the study was to investigate the prevalence of altered mental status</div><div>·      Identify factors associating with it and to assess the prognostic significance of altered mental status in cardiogenic shock   </div><div><strong>Methods:</strong></div><div>·      Mental status were assessed as presentation of shock in 215 adult cardiogenic shock patients in a multinational, prospective, observational study</div><div>·      Clinical picture, biochemical variables and short-term mortality were compared between patients presenting with altered and normal mental status </div><div><strong>Results:</strong></div><div>·       Altered mental status was detected in 147 (68%) patients, whereas 68 (32%) patients had normal mental status</div><div>·       Patients with altered mental status were older (68 <em>vs</em>. 64 years, <em>p</em>=0.04) and more likely to have an acute coronary syndrome than those with normal mental status (85% <em>vs</em>. 74%, <em>p</em>=0.04)</div><div>·       Altered mental status was associated with lower systolic blood pressure (76 <em>vs</em>. 80 mmHg, <em>p</em>=0.03) and lower arterial pH (7.27 <em>vs</em>. 7.35, <em>p</em>&lt;0.001) as well as higher levels of blood lactate (3.4 <em>vs</em>. 2.3 mmol/l, <em>p</em>&lt;0.001) and blood glucose (11.4 <em>vs</em>. 9.0 mmol/l, <em>p</em>=0.01)</div><div>·       Low arterial pH (adjusted odds ratio 1.6 (1.1–2.2), <em>p</em>=0.02) was the only factor independently associated with altered mental status</div><div>·       Ninety-day mortality was significantly higher (51% <em>vs</em>. 22%, <em>p</em>&lt;0.001) among patients with altered mental status.</div><div> </div><div><strong>Conclusion:</strong></div><div>·      Altered mental status is common clinical sign of systemic hypoperfusion in cardiogenic shock and is associated with poor outcome</div><div>·      It is also associated with several biochemical findings that reflect inadequate tissue perfusion, of which low arterial pH is independently associated with altered mental status   </div><div> </div><div> </div>]]></description>
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         <pubDate>2018-09-08 07:20:35 UTC</pubDate>
         <guid>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/279060751</guid>
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         <title>Oxygen therapy for acute myocardial infarction: A systematic review and meta-analysis (Salika)</title>
         <author></author>
         <link>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/279298157</link>
         <description><![CDATA[<div>- O2 therapy for pt with acute MI are inconclusive - some studies indicate that O2 therapy may increase O2 delivery to ischemic myocardium and therefore benefit and other studies found that O2 therapy was actually harmful<br>- this study was a meta-analysis with the following criteria: <br>      1. design: randomised and quasiradomised controlled clinical trials<br>      2. population: pt with acute MI &lt;24 hours<br>      3.  intervention: O2 at normal pressure, regardless of O2 flow rate<br>      4. data: 95% confidence interval<br>- 5 studies were included in the meta-analysis<br>RESULTS<br>- O2 could not reduce in-hospital mortality, arrhythmia incidence or pain incidence<br>- O2 may increase recurrent MI - may be due to O2 promoting leukocyte chemotaxis and inflammatory processes = increase number of myocardial cell death<br>- European Society of Cardiology recommends pt with normal O2 saturation (O2 &gt;90%) not receive O therapy but pt with acute MI with hypoxemia are to receive O2 therapy<br>- <strong>bottom line - O2 inhalation did not benefit pt with acute MI</strong><br><br></div>]]></description>
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         <pubDate>2018-09-10 08:23:04 UTC</pubDate>
         <guid>https://padlet.com/jianmintantan/f9xmduh4sqkr/wish/279298157</guid>
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