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      <title>DEMONSTRATION 2: Pulmonary Embolism by Pauline Wong</title>
      <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8</link>
      <description>NUR5923 Respiratory Pathiphysiology</description>
      <language>en-us</language>
      <pubDate>2022-03-10 02:30:25 UTC</pubDate>
      <lastBuildDate>2025-10-25 23:07:29 UTC</lastBuildDate>
      <webMaster>hello@padlet.com</webMaster>
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      <item>
         <title>Instructions</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087363794</link>
         <description><![CDATA[<ol><li>Choose a spokesperson</li><li>All students in the group are to work on all of the following questions/sections included in the Padlet</li><li>When we come back to the whole class, the spokesperson will feedback findings</li><li>You can use diagrams/images other visual resources to explain each respiratory condition.</li></ol>]]></description>
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         <pubDate>2022-03-10 02:31:27 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087363794</guid>
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      <item>
         <title>Brief definition</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087363984</link>
         <description><![CDATA[<div><br>Pulmonary embolism is<strong>&nbsp; blockage in one of the pulmonary arteries in your lungs.</strong> Most often, pulmonary embolism is caused by blood clots that travel to the lungs from deep veins in the legs or, rarely, from veins in other parts of the body.<br>Risk factors for PE include conditions and disorders that promote blood clotting as a result of venous stasis (immobilization, heart failure), hypercoagulability (inherited coagulation disorders, malignancy, hormone replacement&nbsp;<br>https://radiopaedia.org/articles/pulmonary-embolism </div>]]></description>
         <enclosure url="https://radiopaedia.org/articles/pulmonary-embolism" />
         <pubDate>2022-03-10 02:31:33 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087363984</guid>
      </item>
      <item>
         <title>Is it obstructive or restrictive? Why?</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364132</link>
         <description><![CDATA[<div>Neither<br>(but is it either? Doesn't this refer to lung conditions, and PE isn't a lung condition but a perfusion issue? Like you get obstructive shock but that's not obstructive lung disease)</div>]]></description>
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         <pubDate>2022-03-10 02:31:39 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364132</guid>
      </item>
      <item>
         <title>How does the condition effect lung compliance and/or airway resistance?</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364280</link>
         <description><![CDATA[<div>PE's themselves should not affect lung compliance or airway resistance as it is purely a perfusion issue (that is, the lungs still ventilate in the same manner as normal but the reduced blood flow causes decreased perfusion). This in and of itself creates dead space, as there are ventilated areas with little to no perfusion, however this is not a defect of the lungs but of the perfusion mechanism.<br><br>In some forms of decompensated PEs, you can see elements of both due to complications such as APO</div>]]></description>
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         <pubDate>2022-03-10 02:31:44 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364280</guid>
      </item>
      <item>
         <title>How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation </title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364412</link>
         <description><![CDATA[<div>Reduced pulmonary perfusion leads to hypoxia as less haemaglobin is being oxygenated, as dead space is formed. The dead space will result in an increase in CO2 due to less gas exchange. Decrease in SPO2 due to less O2 being carried on Hb.&nbsp;<br>An elevated A-a gradient: because the partial pressure of O2 is higher in the alveoli than in arterial blood.<br><br>Patients experience SOB and compensate by hyperventilating to get rid of excess CO2. Therefore, administering supplemental O2 to maintain SPO2 &gt;94%&nbsp; is ideal treatment.</div>]]></description>
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         <pubDate>2022-03-10 02:31:49 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364412</guid>
      </item>
      <item>
         <title>Explain the role of V/Q mismatch in this condition.</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364590</link>
         <description><![CDATA[<div>The VQ mismatch occurs due to redistribution of blood from occluded pulmonary arteries to the nonoccluded vessels.<br>Increased Dead Space.<br>This will cause a raised V/Q due to underperfusion in the presence of normal ventilation.</div>]]></description>
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         <pubDate>2022-03-10 02:31:55 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364590</guid>
      </item>
      <item>
         <title>What type of respiratory failure would this condition lead to?</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364793</link>
         <description><![CDATA[<div>T1RF can lead to T2RF once compensating</div>]]></description>
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         <pubDate>2022-03-10 02:32:02 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364793</guid>
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      <item>
         <title>What are the typical ABGs and why?</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364971</link>
         <description><![CDATA[<div>Initially - low PaO2, Low/Normal CO2, Respiratory alkalosis most often.&nbsp;<br>initially - CO2 is low/normal. then once compensating, can remain normal or can rise to compensate for lactic acidosis.<br>Lactate Rise which can cause metabolic acidosis due to anaerobic respiration.&nbsp;<br><br>(low co2 = alkalosis, high = acidosis)</div>]]></description>
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         <pubDate>2022-03-10 02:32:07 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087364971</guid>
      </item>
      <item>
         <title>What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087365140</link>
         <description><![CDATA[<div>Increased pulmonary artery pressure, can lead to right ventricular dilation and increase afterload. Decrease in surfactant production, the overall affect is atelectasis. Which further contributes to hypoxemia.&nbsp; Increased JVP<br>Pulmonary oedema, hypoxic vasoconstriction , dysrhythmias , decreased cardiac output, shock&nbsp;<br>https://litfl.com/ecg-changes-in-pulmonary-embolism/&nbsp;</div>]]></description>
         <enclosure url="https://litfl.com/ecg-changes-in-pulmonary-embolism/" />
         <pubDate>2022-03-10 02:32:13 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087365140</guid>
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      <item>
         <title>OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))</title>
         <author>paulinewong1</author>
         <link>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087365309</link>
         <description><![CDATA[<div> <br><br></div>]]></description>
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         <pubDate>2022-03-10 02:32:19 UTC</pubDate>
         <guid>https://padlet.com/paulinewong1/lt6fi639dsr64kn8/wish/2087365309</guid>
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