The Cell Inflammation Repair Regeneration and Fibrosis discussion

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The Cell Inflammation Repair Regeneration and Fibrosis discussion

Mr. B suffered a myocardial infarction as noted by Q waves on ECG as well as elevated troponins in the ED.  His acid-base status is indicative of metabolic acidosis’s as evident by his labs with a pH of 7.22, PCO2 of 30mm and HCO3 of 22meq (Huether et al., 2020, p.127).
Burger & Schaller (2020), defines metabolic acidosis as the arterial blood pH’s that is lower than 7.35.  Also a bicarbonate concentration of less than 22 mEq per liter is indicative of metabolic acidosis.  A normal range of bicarbonate concentration is 22-26 mEq per liter.  The etiology of acidosis can be further elicited by history and physical examination as well as laboratory values.  The CO2 and HCO3 elaborate if the acidosis is metabolic versus respiratory.  In our case study, metabolic acidosis is seen with a PCO2 of 30 mm which is below the normal range of 35-45 mm (Castro & Keenaghan, 2020).  According to the case study, the patient also presented with labored breathing, rapid and weak pulse which is highly likely suspect for Kussmaul’s respiration (Huether et al., 2020, p.129).  This is the body’s attempt at respiratory compensation.  Mr. B’s PO2 is 70mm and O2 sat is 88%, which is also below normal. The Cell Inflammation Repair Regeneration and Fibrosis discussion   Considering that the pH, PaCO2 and HCO3 are low, the patient’s is highly suspicious for metabolic acidosis.  This can be caused by a decrease in the patient’s cardiac output given his initial presentation and diagnosis of myocardial infarction.  Additionally with his PO2 dictated at 70, patient is also suffering from hypoxia.  With the presentation of myocardial infarction, the heart can suffer an extensive damage leading to decrease in the effective pumping requirements of the heart.  According to literature, metabolic acidosis can be known to occur in the early stages of acute myocardial infarction and can lead to cardiogenic shock which increases mortality.  Several correlations were found between metabolic acidosis and mortality.  These correlations stipulates as blood pH decreases, mortality increases (Gandhi & Akholkar, 2017).ReferencesCenter for Biotechnology Information. https://www.ncbi.nlm.nih.gov/books/NBK482146/Castro, D., & Keenaghan, M. (2020). Arterial blood gas. StatPearls. Retrieved January 19, 2021Gandhi, A., & Akholkar, P. (2017). Metabolic acidosis in acute myocardial infarction. International Elsevier Canada.less1 UnreadUnread6 ViewsViews The Cell Inflammation Repair Regeneration and Fibrosis discussion The Cell Inflammation Repair Regeneration and Fibrosis discussion

 

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    • View profile card for Caroline Otto
    • Last post January 24 at 5:20 AM by Caroline Otto
    • Huether, S. E., McCance, K. L., & Brashers, V. L. (2020). Understanding pathophysiology (7th ed.).
    • Journal of Advances in Medicine, 2(3), 260-263. doi:http://dx.doi.org/10.18203/2349-3933.ijam20150556
    • Burger, M., & Schaller, D. (2020, July 25). Metabolic acidosis – StatPearls – NCBI bookshelf. National
    • Joanne Hogan Module 1Subscribe
    • Joanne Hogan posted Jan 19, 2021 3:49 PM
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    •             In addition to acute myocardial infarction, Mr. B. is also suffering from metabolic acidosis. Metabolic acidosis occurs when a low pH is matched with a low PaCO2 level during ABG analysis. Metabolic acidosis is usually caused by lactic acid build up due to poor perfusion and/or hypoxemia (Huether et al., 2020). If the lactic acid level is high, often times the anion gap will also be elevated (Brubaker et al., 2020). Mr. B is partially compensating for his metabolic acidosis as evidence by a normal HCO3-, as well as his clinical presentation. Mr. B’s respirations are labored which could be in an effort to expel CO2, in an effort to compensate for the metabolic acidosis.ReferencesHuether, S. E., & McCance, K. L. (2020). Understanding pathophysiology (pp. 128-129). St. Louis, MO: Elsevier.less1 UnreadUnread11 ViewsViews The Cell Inflammation Repair Regeneration and Fibrosis discussion
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    • View profile card for Alfonsina Perez
    • Last post January 23 at 8:54 PM by Alfonsina Perez
    • Wu, M., Yiang, G., Liao, W., Tsai, A., Cheng, Y., Cheng, P., . . . Li, C. (2018, April 20). Current Mechanistic Concepts in Ischemia and Reperfusion Injury. Retrieved January 19, 2021, from https://www.karger.com/Article/FullText/489241
    • Brubaker, R. (2020, August 10). High Anion Gap Metabolic Acidosis. Retrieved January 19, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK448090/
    • Clinical presentation supports that Mr. B is suffering from possible cardiogenic shock. Common symptoms of cardiogenic shock include hyperventilation, clammy skin, and tachycardia. When cardiac output is diminished, poor perfusion occurs resulting in vasoconstriction and anaerobic metabolism which leads to decreased production of ATP (Wu et al., 2018). This then leads to fluid leakage into the interstitial spaces which will cause clotting and a rise in lactic acid, further decreasing cardiac output (Wu et al., 2018). The Cell Inflammation Repair Regeneration and Fibrosis discussion
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    • Alfonsina Perez posted Jan  20, 2021 4:30 PM
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    • Based on Mr. B’s arterial blood gas results, apart from experiencing an MI, Mr. B is also experiencing metabolic acidosis. Mr. B’s PH result is 7.22, making the result acidotic. A normal PH is 7.4 (Huether et al., 2020). Additionally, Mr. B’s PCO2 of 30 mm, is indicative of a metabolic imbalance due to the low PCO2. Mr. B’s metabolic acidosis could be a result of the current cardiac dysfunction he is experiencing. According to Jamme et al. (2018), metabolic acidosis can result as a product of cardiac ischemia and it has been associated with patients who have experienced cardiac arrest. Additionally, Mr. B is also exhibiting symptoms of hypoxemia as indicative by the 02 saturation of 88% as well as the labored breathing and rapid pulse he is experiencing. Hypoxemia can be a direct result of the myocardial infarctions as it has been documented that thirty to seventy percent of patients experiencing an MI will experience hypoxemia (Pang et al., 2018).              Pathophysiology 7th ed.  Elsevier Mosby.Jamme, M., Ben Hadj Salem, O., Guillemet, L., Dupland, P., Bougouin, W., Charpentier, J. &Geri, G. (2018). Severe metabolic acidosis after out-of-hospital cardiac arrest: Riskfactors and association with outcome. Annals of Intensive Care, 8(1), 1-8.doi:10.1186/s13613-018-0409-3Review and Meta-Analysis of the Impact of Hypoxia on Infarcted Myocardium:

 

  1. Mr. B is a 70-year-old man who developed sub sternal chest pains radiating down his left arm while at home. He was taken to the ER via ambulance. His breathing was labored, pulses rapid and weak, and his skin was cold and clammy.An ECG was done which revealed significant “Q” waves in most leads. Troponin level was elevated. Arterial blood was draw with the following results: The Cell Inflammation Repair Regeneration and Fibrosis discussion The Cell Inflammation Repair Regeneration and Fibrosis discussion

Ph 7.22

PCO2 30 mm

Hg pO2 70 mm

Hg O2 sat 88%

HCO3 22 meq/liter

  1. Aside from the obvious diagnosis of MI, what is Mr. B’s acid base status and what caused this disturbance?

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