The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays

The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays

Module 1: Discussion 2

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Mr. B, a 70-year-old man, experienced chest pain radiating down his left arm at home. He was transported to the ER by ambulance, exhibiting labored breathing, rapid and weak pulses, and cold, clammy skin. An ECG revealed significant “Q” waves in most leads, with an elevated troponin level. Arterial blood analysis yielded the following results:

– pH: 7.22
– PCO2: 30 mm Hg
– pO2: 70 mm Hg
– O2 saturation: 88%
– HCO3: 22 meq/liter

Apart from the clear diagnosis of MI, what is Mr. B’s acid-base status, and what caused this disturbance?

Please submit your initial response by Wednesday at midnight. Respond to one student by Sunday at midnight. Both responses should be a minimum of 150 words, scholarly written, APA formatted, and referenced. A minimum of 2 references (other than the text) is required. Refer to the grading rubric for the online discussion on The Cell, Inflammation, Repair, Regeneration, and Fibrosis Discussion Essays.

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Sheryl Dixon posted Jan 20, 2021 11:39 PM

Mr. B’s acid-base status suggests respiratory acidosis. Examining his arterial blood results, the pH is low, and HCO3 is elevated. Respiratory acidosis can be acute or chronic, given his age and fluid distribution in the body. According to Huether, McCance & Brashers (2010), respiratory acidosis occurs due to alveolar hypoventilation, causing excessive carbon dioxide in the blood. With physiological aging, the regulation of pH depends on the kidneys and lungs, both of which deteriorate with age (Nabata T et al., 1992).

NSG-533-Advanced Pharmacology Module III – Men’s and Women’s Health Discussion

Treatment for respiratory acidosis, as stated by Epstein & Singh (2011), may include invasive or noninvasive ventilator support and specific medical therapies addressing the underlying pathophysiology.

References:

Huether, S.E., McCance, K.L., & Brashers, V.L. (2010). Understanding Pathophysiology (7th ed.). Elsevier.

Epstein SK, Singh N. (2001). Respiratory acidosis. Respir Care, 46(4), 366-83. PMID: 11262556.

Nabata T, et al. (1992). Abnormalities in acid-base balance in the elderly. Nihon Rinsho, 50(9), 2249-53. Japanese. PMID: 1434020.

Beth Certain’s last post: January 24 at 11:48 PM.

Working in long-term care, elderly diagnoses are sometimes oversimplified by focusing solely on lab results. It’s crucial to consider the individual’s body composition. Acid-base balance is often overlooked in the elderly because there’s no specific scale for different age groups, and pH levels remain consistent across age groups (The Cell, Inflammation, Repair, Regeneration, and Fibrosis Discussion Essays).

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Hilary Szpara posted Jan 20, 2021 5:08 PM

I believe Mr. B’s acid-base status is metabolic acidosis with compensatory respiratory alkalosis through hyperventilation. When analyzing his arterial blood gases (ABGs), his pH of 7.22 falls below the normal range of 7.35-7.45, indicating acidosis. However, his PCO2 at 30 mmHg and HCO3 at 22 mEq/L initially create confusion. HCO3, within the normal range of 22-26 mEq/L (Verma & Roach, 2010), makes it challenging to determine acid-base status since HCO3 is key in assessing metabolic events.

However, further research suggests a correlation between myocardial infarction (MI) and metabolic acidosis. During an MI, cardiac output decreases, causing arterial hypoxemia and subsequent tissue hypoxia, leading to an increase in lactic acid and metabolic acidosis (Gandhi & Akholkar, 2015). The rise in lactic acid results from decreased systemic blood flow due to the MI (Weil & Tang, 2011).

References:

Gandhi, A. A., & Akholkar, P. J. (2015). Metabolic acidosis in acute myocardial infarction. International Journal of Advancement in Medicine, 2(3), 260-263. http://dx.doi.org/10.18203/2349-3933.ijam20150556

Weil, M.H., Tang, W. (2011). Clinical correlates of arterial lactate levels in STEMI patients. Critical Care, 15(1), 113. http://doi.org/10.1186/cc9383
Verma, A. K., & Roach, P. (2010). The interpretation of arterial blood gases. Australian Prescriber, 33(4), 124-129.

Gisselle Mustiga’s last post: January 24 at 11:20 PM.

Huether, S.E., McCance, K.L., Brashers, V.L. (2020). Understanding Pathophysiology. Elsevier.
References

Lois Chappell’s last post: January 24 at 7:41 PM.

In evaluating Mr. B’s acid-base balance, it is evident that he is in metabolic acidosis with compensation. Metabolic acidosis can occur rapidly in cases like lactic acidosis or slowly in conditions like renal failure, diabetic ketoacidosis, or starvation (Heuther, McCance, and Brashers, 2020). To understand specific types of acidosis, we can examine the anion gap.

References:

Heuther, S.E., McCance, K.L., & Brashers, V.L. (2020). Understanding Pathophysiology. Elsevier.

Sheryl Dixon’s last post: January 24 at 7:41 PM.

Heuther, S., McCance, K., and Brashers, V. (2020). Understanding Pathophysiology (7th ed.). Elsevier.
References

Caroline Otto’s last post: January 24 at 4:25 PM.

Metabolic acidosis with compensated respiratory alkalosis: Mr. B’s acid-base status indicates metabolic acidosis due to myocardial ischemia, which leads to lactic acidosis from poor myocardial perfusion during the myocardial infarction (MI). A pH below 7.40 indicates an increase in hydrogen ions, reflecting the metabolic environment regulated by buffers inside cells. Mr. B’s low pH and low HCO3 indicate metabolic acidosis. However, his low PaCO2 suggests

respiratory compensation for metabolic acidosis (Castro & Keenaghan, 2020).

References:

Castro, D., & Keenaghan, M. (2020). Arterial Blood Gas. In StatPearls. StatPearls Publishing.
Mechanic OJ, Grossman SA. Acute Myocardial Infarction. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459269/

Eleany Yasein’s last post: January 24 at 4:25 PM.

Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding Pathophysiology 7th ed. Elsevier Mosby.
References

Dennies Jones’s last post: January 24 at 1:22 PM.

Mr. B was experiencing metabolic acidosis based on his lab values. According to Gandhi & Alkholkar (2015), metabolic acidosis occurs in the early stages of acute myocardial infarction (MI). Gandhi & Alkholkar (2015) noted that “a fall in cardiac output and arterial hypoxemia leads to tissue hypoxia, metabolic acidosis, and a decrease in plasma bicarbonate due to a rise in lactic acid. Metabolic acidosis is compensated by hyperventilation” (p.260). In Mr. B’s case, he exhibited labored breathing to compensate for the low blood pH.

References:

Gandhi, A.A. & Akholkar, P.J. (2015). Metabolic acidosis in acute myocardial infarction. International Journal of Advances in Medicine 2(3), 260-263. Doi: http://dx.doi.org/10.18203/2349-3933.ijam20150556

Huether, S.E. (2020. Fluid and electrolytes, acid and base. In S.E. Huether & K.L. McCance (Eds.), Understanding Pathophysiology (114-133). St. Louis, MO: Elsevier Mosby.

Eleany Yasein’s last post: January 24 at 1:22 PM.

Module 1: Discussion 2

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3. 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:

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?

Post your initial response by Wednesday at midnight. Respond to one student by Sunday at midnight. Both responses must be a minimum of 150 words, scholarly written, APA formatted, and referenced. A minimum of 2 references are required (other than text). Refer to grading rubric for online discussion The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays.

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• • Discussion 2
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  • Sheryl Dixon posted Jan 20, 2021 11:39 PM
  • Mr. B’s acid base status would suggest respiratory acidosis .Looking at his arterial blood result the PH is low and his HCO3 is elevated. Respiratory acidosis can be chronic and acute due to his age and the body distribution of body fluid. “Respiratory acidosis occurs when the alveolar hypoventilation, causing Hypercapnia which is excessive carbon dioxide in the blood” Huether, McCance & Brashers (2010).     With physiological aging regulation of the PH depends on the kidney and lung and these two organs is deceased with physiological aging (Nabata T, et al, 1992) The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays.  According to Epstein &Singh (2011) treatment for respiratory acidosis may include invasive or noninvasive ventilator support and specific medical therapies directed at the underlying pathophysiologyEpstein SK, Singh N. Respiratory acidosis. Respir Care. 2001 Apr; 46 (4):366-83. PMID: 11262556.Nabata T, et al. Abnormalities in acid –base balance in the elderly. Nihon Rinsho.1992 Sep; 50(9) 2249-53. Japanese .PMID1434020 less0 UnreadUnread
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  • Last post January 24 at 11:48 PM by Beth Certain
  • Huether, S.E., McCance, K.L., & Brashers, V.L. (2010).Understanding Pathophysiology (7th ed.).Elsevier
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  •     Working in a long-term care the elderly diagnosis are somewhat overlooked by just checking the labs, I believe some doctors treat the lab and not the person, some don’t take into consideration the body composition. A lot of times in the elderly the acid base is overlooked because there is not a different scale for pediatrician, adult versus the elderly so the PH remained the same despite which age group The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays.
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  • Hilary Szpara posted Jan 20, 2021 5:08 PM
  • I believe that Mr. B’s acid base status is metabolic acidosis with respiratory compensation in the form of hyperventilation. When determining his acid base status, I looked at his levels of certain arterial blood gases (ABGs). To determine acidosis or alkalosis, I looked at what his arterial pH was, 7.22. With the normal range for pH being 7.35-7.45, Mr. B appears to be in acidosis. However, when I continued to analyze the numbers, noting that his PCO2 was 30 mmHg and HC03 was 22, I was somewhat confused. Since HCO3 is within normal limits of 22-26 mEq/L (Verma & Roach, 2010), it became harder for me to determine acid base status, since HCO3 is what helps determine whether or not it is a metabolic event. However, after continuing my research, I was able to find multiple sources that discussed the correlation between myocardial infarction (MI) and metabolic acidosis. I was able to find that during an MI, due to decrease in cardiac output and arterial hypoxemia, tissue hypoxia occurs, which leads to a rise in lactic acid and metabolic acidosis (Gandhi & Akholkar, 2015). The levels of lactic acid rise due to the decrease in systemic blood flow caused by the MI (Weil & Tang, 2011).Gandhi, A. A., & Akholkar, P. J. (2015). Metabolic acidosis in acute myocardial infarction. International Journal of Advancement in Medicine, 2(3), 260-263. http://dx.doi.org/10.18203/2349-3933.ijam20150556  Huether, S.E., McCance, K.L., Brashers, V.L. (2020). Understanding Pathophysiology. Elsevier. less0 UnreadUnread
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  • Last post January 24 at 11:20 PM by Gisselle Mustiga
  • Weil, M.H., Tang, W. (2011). Clinical correlates of arterial lactate levels in STEMI patients. Critical Care, 15(1), 113. http://doi.org/10.1186/cc9383
  • Verma, A. K., & Roach, P. (2010). The interpretation of arterial blood gases. Australian Prescriber, 33(4), 124-129.
  • However, Mr. B’s situation is not just that simple because his PCO2 level is low, which at first glance would be characteristic of alkalosis (Huether, McCance, & Brashers, 2020). Since in the description of Mr. B’s symptoms it was noted that he is having labored breathing, he could be compensating for the metabolic acidosis by hyperventilating in an attempt to blow off CO2 and raise his arterial pH.
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  • Lois Chappell posted Jan 22, 2021 6:19 AM
  •      Understanding clinical presentations due to changes at the cellular level will enable you to skillfully care for your patients in diverse practice settings.  In evaluating Mr. B’s acid base balance, we see that Mr. B is in metabolic acidosis with compensation.  Metabolic acidosis can occur rapidly in the case of lactic acidosis or slowly in the case of renal failure, diabetic ketoacidosis, or starvation (Heuther, McCance and Brashers, 2020).  To understand specific types of acidosis, we can look at the anion gap.  Goldberger, AL. Goldberger ZD, Shvilkin, AS.  (2017).  Goldberger’s Clinical Electrocardiography: A Simplified Approach (9^th ed).   Elsevier.  less0 UnreadUnread
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  • Last post January 24 at 7:41 PM by Sheryl Dixon The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays
  • Heuther, S., McCance, K., and Brashers, V.  (2020).  Understanding Pathophysiology (7^th ed.).  Elsevier.
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  •                 This week’s case study is one we see often in acute care but imagine if this patient entered your family practice.  Would you look at him and be able to triage him appropriately?  What are the signs and symptoms of a cardiac event, what if chest pain was not present?  Please follow an algorithm, like the one on page 128 of your text to determine acid base status.
  •      In our case study, we are told Mr. B is having a myocardial infarct (MI); the cause of his acid base disturbance is most likely lactic acidosis from tissue hypoxia due to arterial occlusion from a blood clot.  His hyperventilation is a compensatory response to rising acidosis; the body’s intrinsic balancing act is to blow off acid through an increased respiratory rate.  The q wave in his ECG seen in “most leads” may be an indication of a previous myocardial infarction (MI), but we need more information about the q wave presentation including which leads the q wave is present, and the height and width of the q wave in order to make a diagnosis (Goldberger, 2017).  Treatment for Mr. B will initially be aimed at saving myocardial tissue and quickly reversing acidosis before decompensation and organ damage occurs The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays.
  • Arterial Blood Gas interpretation in the MI Client.Subscribe
  • Caroline Otto posted Jan 20, 2021 10:10 PM
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  • Metabolic Acidosis with compensated Respiratory alkalosisMyocardial ischemia undoubtedly causing lactic acidosis secondary to poor myocardial perfusion from the myocardial infarction which induces metabolic acidosis.A Ph balance less than 7.40 indicates an increase in hydrogen ions, and the Ph reflects the metabolic environment which is protected by buffers which work to maintain the Ph level inside the cells.Mr. B’s Ph is low, and his HCO3 is low indicating metabolic, however Mr. B also has a low PaCO2 indicating respiratory compensation for his metabolic acidosis.Castro, D., & Keenaghan, M. (2020). Arterial Blood Gas. In StatPearls. StatPearls Publishing.Mechanic OJ, Grossman SA. Acute Myocardial Infarction. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459269/less3 UnreadUnread20 ViewsViews
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  • Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding Pathophysiology 7^th ed. Elsevier Mosby.
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  • In this situation the lungs attempt to compensate by increasing ventilation which causes alkalosis.
  • A state of cell injury creates an abruption in the physiologic functioning inside the homeostatic cell environment disturbing the acid-base balance.
  • Coronary artery disease in the individual may cause a thrombus to form which will occlude a coronary artery. This phenomenon causes a state of hypoxia which will lead to
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  • Dennies Jones posted Jan 20, 2021 1:22 PM
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  •          Mr. B was experiencing Metabolic acidosis due to the lab values. According to Gandhi & Alkholkar (2015), Metabolic acidosis occurs in the primeval stages of acute myocardial infarction. Gandhi & Alkholkar (2015) also said that the “combination of a fall in cardiac output and arterial hypoxemia leads to tissue hypoxia, metabolic acidosis, and fall in-plasma bicarbonate due to rise in lactic acid. Metabolic acidosis is compensated by hyperventilation” (p.260). In Mr. B’s case, he was having labored breathing to compensate for the blood’s low PH level.   Gandhi, A.A. & Akholkar, P.J. (2015). Metabolic acidosis in acute myocardial infarction. International Journal of Advances in Medicine 2(3), 260-263. Doi: http://dx.doi.org/10.18203/2349-3933.ijam20150556Huether, S.E. (2020. Fluid and electrolytes, acid and base. In S.E. Huether & K.L. McCance (Eds.), Understanding Pathophysiology (114-133). St. Louis, MO: Elsevier Mosby.less1 UnreadUnread2 ViewsViews