THE CELL, INFLAMMATION, REPAIR, REGENERATION, AND FIBROSIS DISCUSSION ESSAYS

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

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 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
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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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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View profile card for Beth Certain
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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View profile card for Gisselle Mustiga
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.
Mr. B
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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 (9th ed).   Elsevier.  less0 UnreadUnread
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View profile card for Sheryl Dixon
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 (7th ed.).  Elsevier.
References
                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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View profile card for Eleany Yasein
Last post January 24 at 4:25 PM by Eleany Yasein
Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding Pathophysiology 7th ed. Elsevier Mosby.
References
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
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View profile card for Melissa Morgan
Last post January 24 at 4:24 PM by Melissa Morgan
Howarth, A. T. (1970). Acid-Base Changes and Hypoxia following Myocardial Infarction. Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, 7(2), 38-40 The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays. doi:10.1177/000456327000700204
References
       Since the blood PH is low and the PCO2 is also low, it is understood that the acidosis was not caused by any respiratory factors but by metabolic processes within the body. According to Huether et al. (2020), an instance of primary metabolic acidosis is an individual experiencing DKA (diabetic ketoacidosis acidosis) from lack of insulin secretion or administration. Mr. B may have issues where he lacks insulin, or he cannot metabolize glucose. Mr. B’s body metabolizes store fat and, as a result, creating acid as a byproduct. According to A.T Howarth (1970), metabolic acidosis appears to be due to the increase of lactic acid. The lungs attempt to compensate by Kussmaul respiration.
Aina Oluwo’s discussion 2Subscribe
Aina Oluwo posted Jan 19, 2021 11:14 PM
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View profile card for Dennies Jones
Last post January 22 at 5:35 PM by Dennies Jones
Worse? Cellular Physiology and Biochemistry, 51:949-960. /doi:10.1159/000495397
Pang, B., Zhao, F., Zhou, Y., He, B., Huang, W., Zhang, F., . . . Jiang, Y. (2018). Systematic
Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding 
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Module I: Discussion Post #2Subscribed
Gisselle Mustiga posted Jan 20, 2021 8:38 PM
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Huether et al. (2020) affirm that pathophysiology is essential in grasping disease mechanisms and examining how a modification to one’s body structure may impact their functionality and reveal the signs and symptoms of an ailment. Mr B’s case is an example of a patient that could have multiple diagnoses despite similarities in the disease indications. Mr B likely has respiratory acidosis in which the blood ends up acidic since not all the carbon dioxide is eliminated from the lungs. The condition occurs due to various reasons such as the diseases in one’s airways, pulmonary fibrosis, scoliosis, incompatible medications, obesity, and obstructive sleep apnea among others. In Mr B’s case, the remaining CO2 caused a reduction in the pH. levels of the body fluids and thus the acidity. The patient has metabolic acidosis due to the pH level of 7.22 and the bicarbonate level of at 22 mEq/liter The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays. The former may be normal but the difference between the HCO3 and the PCO2 levels makes the illness to be respiratory due to elimination of normalcy. The oxygen reduction also results in the patient being hypoxemic as blood will not be sufficiently supplying oxygen to the body tissues.References     Pathophysiology 7th ed.  Elsevier Mosby.Surat, P. (2018, August 24). PH in the Human Body. https://www.news-medical.net/health/pH-in-the-HumanBodyless1 UnreadUnread15 ViewsViews
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View profile card for Candice Russell
Last post January 22 at 4:52 PM by Candice Russell
Schück, O., & Matoušovic, K. (2015). Relation between pH and the strong ion difference (SID) in body fluids. Biomedical Papers, 149(1), 69-73.
Huether, S. E., McCance, K. L. & Brashers, V. L. (2020). Understanding  
His situation was likely linked to his myocardial infarction that caused the labored breathing, weak yet rapid pulses, and the chest pains. In a normal setting, the body fluid’s pH levels should be about 7.35 to 7.45, the pCO2 should be between 35-45, and the HCO3 should be at about 22-26 (P, 2018). Again, the Hg PO2 ought to be at 80-100mm and the oxygen pressure at 90-100%. Evaluating these components is critical in maintaining the acid-base status of body fluids (Schück & Matoušovic, 2015). Mr B should treat his condition by opting for bronchodilator drugs to curb the effects of the obstruction in his airways. Secondly, he should consider a breathing machine or a Continuous Positive Airway Pressure (CPAP) therapy. Also, he should have an adequate oxygen supply especially when there is a reduction of the oxygen levels in his blood.
Mr. B’s acid base statusSubscribe
Tallona Boddy posted Jan 20, 2021 6:03 PM
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As stated in the discussion prompt, Mr. B appears to be experiencing a myocardial infarction, also known outside of the medical community as a heart attack.less1 UnreadUnread9 ViewsViews
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View profile card for Jazmin Jerez-Rivera
Last post January 22 at 11:59 AM by Jazmin Jerez-Rivera
Mayo Clinic (n.d) states that when experiencing a myocardial infarction patients can experience labored breathing, just like Mr. B.  The labored breathing is most likely due to poor perfusion and hypoexmia.  The body’s decreased ability to adequately perfuse and get the adequate amount of oxygen into the blood stream can consequently cause acid to build up, causing metabolic acidosis (Huether et al, 2020).  Metabolic acidosis when defined in its most simplest form is, the build up of acid in a person’s body fluids (Medline Plus, 2021).  Mr. B’s arterial blood gas shows a pH of 7.22, this is considered acidic and lower than the expected range. Mr. B’s PCO2 was 30 mm, this is also below an acceptable standard, and considered to be acidic. When a patient’s pH and PCO2 falls below the acceptable range they are then considered to have an acid-base imbalance, specifically metabolic acidosis.
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Cassie Fritzinger posted Jan 19, 2021 6:49 PM
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Acute myocardial infarction (MI) produces tissue hypoxia resulting in an acid base imbalance secondary to the decrease in cardiac output and arterial hypoxemia (Gandhi & Akholkar, 2015). Mr. B, a 70-year-old gentleman experiencing a sudden MI displays this imbalance given his arterial blood gas (ABG) of pH: 7.22, pCO2: 30mm, and HCO3: 22 mew/L. This ABG shows the patient is in an uncompensated metabolic acidosis. The patient also presented with significant “Q” waves in most leads. According to MacAlpin (2006), a ‘Q’ wave abnormality has an indication of cardiac disease or coronary heart disease with MI and generally this is the chronic stage of an MI. It is also found that Q waves are associated with ventricular hypertrophy. When this patient experiences an MI there is a hypoxic injury to cardiac tissue. The body responds within minutes when there is a mitochondrial compromise. Then there is an insufficient production of Adenosine Triphosphate (ATP) which results in a loss of contractility of the heart, further decreasing the cardiac output. This loss of contractility is a result of the rapid decrease in mitochondrial phosphitylation. When this occurs, anaerobic metabolism generates ATP from glycogen. However, when the glycogen is depleted even anaerobic metabolism ceases as well (Heuther, McCance, & Brashers, 2020)Metabolic Acidosis can be severe, specifically in those with profound cardiogenic shock secondary to an MI (Gandhi & Akholkar, 2015). Gandhi & Akholkar (2015), also found that there was a link between the patient experiencing an MI’s admitting pH level and their mortality rate. They found that those with a pH <7.35 were statistical more likely to die. Similarly they found that these patients who had a HCO3 level of <22 were also more likely to develop ventricular dysrhythmias and more likely to die (Gandhi & Akholkar, 2015). Since acidosis has been shown to have an increased mortality rate, Lazzeri, Valente, Chiostri, Picariello, & Gensini (2010), suggest the use of the anion gap to show more subtle changes in the degree of acidosis to assist with predicting patient outcomes..ReferencesHeuther, S. E., McCance, K. L., & Brashers, V. L. (2020). Understanding Pathophysiology (7th ed.). Elsevier.MacAlpin, R. N. (2006, July). Significance of abnormal Q waves in the electrocardiograms of adults less than 40 years old. Annals of Noninvasive Electrocardiology, 11(3), 203-210. less1 UnreadUnread12 ViewsViews 12 1 1 RepliesReplies 1 View profile card for Steven Bartos Last post January 22 at 3:14 AM by Steven Bartos Lazzeri, C., Valente, S., Chiostri, M., Picariello, C., & Gensini, G. (2010) The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays. Acid-base imbalance in uncomplicated ST-elevation myocardial infarction: the clinical role of tissue acidosis. Internal and Emergency Medicine, 5, 61-66. 10.1007/s11739-009-0338-0 Gandhi, A., & Akholkar, P. (2015). Metabolic acidosis in acute myocardial infarction. International Journal of Advances in Medicine, 2(3), 260-263. http://dx.doi.org/10.18203/2349-3933.ijam20150556 So, in short review of the case study, Mr. B. developed the chest & left arm pain secondary to the referred pain from his MI. His breathing became labored secondary to two reactions. First the decreased cardiac output increased the oxygen demand of all tissues thus his body began to compensate with increased respirations. Furthermore the labored breathing was also a result of the body’s compensation for the acidosis trying to blow off excess HCO3 (an acid). Mr. B.’s pulses were weak from his decreased cardiac output most likely from the decreased contractility of his heart from the decreased ATP production secondary to hypoxia. The decreased cardiac output further more caused his skin to become cool and clammy from decreased peripheral circulation and most likely hypotension. A failure of the sodium (Na+) potassium (K+) pump and Na+ Calcium (Ca+) exchange occurs with this prolonged hypoxia and resulting mechanisms. This causes Na+ and Ca+ into the cells causing it to swell and K+ out of the cells into the extracellular fluid. Without the sodium/potassium pump, there is free movement of sodium and water. Because of the shifting of electrolytes, the patient enters metabolic acidosis. The treatment for this process is to correct the hypoxia. Without fixing the hypoxia a process known as vacuolation and eventually cell death will occur. Decreased protein synthesis and calcium accumulate within the cell, the cell membrane becomes dysfunctional and the influx of calcium in the cells triggers a pro apoptotic protein causing cell apoptosis (Heuther, S.E., McCance, K.L. & Brashers, V.L., 2020). Module 1: Discussion 2Subscribe Candice Russell posted Jan 21, 2021 11:34 PM Contains unread posts Arterial blood gas (ABG) measurements are collected for the assessment of ventilation, oxygenation, and the acid-base status of the body. The levels of pH, oxygen (O2), carbon dioxide (CO2), and bicarbonate (HCO3) are measured in arterial blood. Interpretation of ABG results allows for assessment of acid-base imbalances. “Slight changes in the amounts of hydrogen and changes in pH can significantly alter biologic processes in cells and tissues” (Brenneman & Huether, 2020, p. 123). Ranges for normal and abnormal lab values can vary based on where the measurements were conducted The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays. Pompey & Abraham-Settles (2019) provide their interpretation of normal ABG values, “four values are used in ABG analysis: pH, PaCO2, HCO3, and PaO2” (p.53). Normal ABG values:  pH: 7.35-7.45, PaCO2: 35-35 mm Hg, HCO3: 22-26 mEq/L, PaO2: 80-100 mm HG.Elevation of PaCO2 with decreased pH, indicates respiratory acidosis. PaCO2 decrease with elevated pH, indicates respiratory alkalosis. HCO3 values are normal with respiratory imbalances. Elevated levels of HCO3 along with increased pH, indicates metabolic alkalosis. Decreased HCO3 along with decreased pH, indicates metabolic acidosis. Hypoxemia may be present if PaCO2 Level is decreased during a metabolic disturbance.The patient’s presentation can provide some background into acid-base imbalance. His cardiac and respiratory distress, signal signs of metabolic acidosis, in form of rapid pulse rate and labored breathing. Hypoxia noted as evidence by the patients’ presentation, as well as, decreased PaCO2 level.I feel the cause of metabolic acidosis is possibly due to ketoacidosis or lactic acidosis. In the case of normal anion gap, unable to be assessed due to unknown values, the possible cause could be gastrointestinal related or renal related. I also thought of mixed acid-base imbalance, respiratory alkalosis. Respiratory alkalosis secondary to metabolic acidosis, in response to hyperventilation, which is seen lactic acidosis  Huether, S. E., McCance, K. L., & Brashers, V. L. (2020). Understanding pathophysiology / Sue E. Huether, Kathryn L. McCance ; section editor, Valentina L. Brashers (7th ed.). Elsevier.less0 UnreadUnread The Cell, Inflammation, Repair, Regeneration, and Fibrosis discussion essays 2 ViewsViews 2 0 0 RepliesReplies 0 Pompey, J. & Abraham-Settles, B. (2019). Clarifying the Confusion of Arterial Blood Gas Analysis. AJN, American Journal of Nursing, 119(3), 52–56. doi: 10.1097/01.NAJ.0000554035.74335.59. References  To find the cause of metabolic acidosis, anion gap needs to be determined. Anion gap is resulted by finding the sum of chloride (Cl) and HCO, which is then subtracted from cation sodium (Na). In this patients’case the Na and Cl are unknown. Normal values for Na 140, Cl 103, known value of HCO3 22. Using the anion gap formula 140 Na – [103 Cl+ 22 HCO3}is approximately 15, suggesting elevated anion gap, with normal values of approximately 10-12 mEq/L. Elevated anion gap in metabolic acidosis is indicative of possible ketoacidosis, lactic acidosis, ingestion of certain substances and renal disorders   ORDER A PLAGIARISM FREE PAPER NOW After assessing the provided lab values, I determined the acid-base imbalance to be metabolic acidosis, demonstrated by abnormal lab values of 7.22 for pH and 30 mm Hg for PCO2. It is noted that the HCO3 value remains in normal range, this is where things became confusing. According to Brenneman & Huether, (2020), when pH is low and PaCO2 is “normal or low, acidosis is not caused by respiratory factors. Instead, it is caused by metabolic processes within the body” (p. 128). However metabolic acidosis is said to be Place your order now for a similar assignment, and have writers from our team of experts write it for you, guaranteeing you an A+

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