NUR 631 CLC – Acid-Base Case Study PowerPoint

Sample Answer for NUR 631 CLC – Acid-Base Case Study PowerPoint Included After Question

Assessment Description

This is a Collaborative Learning Community (CLC) assignment.

Working in teams and collaboration is an essential skill that is prevalent in clinical situations. In this
assignment, you will be working in a group to create a PowerPoint to address the “Acid-Base Case Study.” The
PowerPoint should be 10-15 slides and contain speaker notes which expand upon the material in the slides.
You need to include citations identifying resources. Each learner is responsible for participation within the CLC
group. The CLC group is responsible for developing a cohesive presentation that fows smoothly. The
instructor will monitor the CLC Discussion Forum. One member of the group will submit the assignment to the
Research and fll in the normal values for the table in the “Acid-Base Case Study” resource. Include the table in
your PowerPoint presentation.
Address each of the following in the PowerPoint presentation:

  1. What type of acid-base disturbance is Mr. Davis sufering from? Why?
  2. What role does excessive alcohol consumption play in the acid-base disturbance seen?
  3. What type of fuid or electrolyte imbalances does Mr. Davis have and why?
  4. Calculate the anion gap. Is it high or normal? Why is it high or normal? What information does the anion gap
    give the provider?
  5. Are Mr. Davis’s respiratory and renal systems attempting to compensate for his acid-base disturbance? If so,
    how are they compensating and what evidence do you have that they are compensating?
  6. Explain the rationale for the low glucose level and high urine ketones.
  7. Is the protein level seen in the UA abnormal? Provide a rationale. How do the fndings relate to Mr. Davis?
    You are required to cite three to fve sources to complete this assignment. Sources must be published within
    the last 5 years and appropriate for the assignment criteria and nursing content.
    Refer to the resource, “Creating Efective PowerPoint Presentations,” located in the Student Success Center, for
    additional guidance on completing this assignment in the appropriate style.
    While APA style is not required for the body of this assignment, solid academic writing is expected, and in-text
    citations and references should be presented using APA documentation guidelines, which can be found in the
    APA Style Guide, located in the Student Success Center.
    This assignment uses a rubric. Please review the rubric prior to beginning the assignment to become familiar
    with the expectations for successful completion.
    You are not required to submit this assignment to LopesWrite.

A Sample Answer For the Assignment: NUR 631 CLC – Acid-Base Case Study PowerPoint

Title: NUR 631 CLC – Acid-Base Case Study PowerPoint

Assignment Scenario:

Mr. Davis is 56-year-old male who has a past medical history of hypertension.

Every Sunday, he goes to his favorite restaurant to watch sports with his friends.

While making several trips to the restroom in a 1-hour period, Mr. Davis complains of feeling tired and weak.

He starts sweating profusely, his breathing becomes rapid and deep, his speech is slurred, and eventually he passes out.

His friends call 911, and Mr. Davis is transported to the hospital.

-At the hospital, Mr. Davis’s ABG results with a critical pH of 7.15, his PCO2 is 30, and his Bicarbonate is 16. It is fair to assume Mr. Davis is obtunded because he passed out and was not noted to wake. The ABG interpretation is metabolic acidosis with partial respiratory compensation.

-The decision tree shows a low bicarbonate with an acidotic pH is indicative of a primary metabolic acidosis. However, the addition of a low CO2 shows partial compensation. Mr. Davis’s acid-base disturbance is only partially compensated, as the pH has not normalized (McCance et al, 2019).

-Metabolic acidosis results from an accumulation of acid in the body.  Acids are produced in the body as an end product of the cellular metabolism of proteins, carbohydrates, and fats (McCance et al, 2019).  Acids may also accumulate in the body due to a loss of bicarbonate in the stool.  Metabolic acidosis occurs when the body’s compensatory mechanisms are unable to neutralize or excrete the acid, and a drop in pH occurs (McCance et al, 2019).  Conditions that may supersede this acid-base disturbance are diarrhea, acid ingestion, accumulation or overproduction of acid in the blood, or decreased acid secretion by the kidneys (McCance et al, 2019). 

Mr. Davis is likely suffering from alcoholic ketoacidosis. Alcoholic ketoacidosis is diagnosed by history and the presence of ketoacidosis (observed by the ketones in his urine) without hyperglycemia (Mr. Davis is hypoglycemic with a BG of 52). Chronic alcohol consumption can lead to depleted protein and carbohydrate stores. In most cases, dietary intake is reduced, and although some caloric intake is received from ethanol, the result is starvation and depleted hepatic glycogen stores. The metabolism of alcohol further impairs gluconeogenesis, and this can manifest in hypoglycemia (McGuire, Cruickshank, & Munro, 2006).

Various abnormalities can be linked to alcohol abuse, including acid-base disorders, dehydration, and electrolyte imbalances. In patients who abuse alcohol, it is the production of lactic acid and ketone bodies that result in an acidotic state. In alcohol metabolism, the ratio of elevated hepatic nicotinamide adenine dinucleotide + hydrogen (NADH) and reduced nicotinamide adenine dinucleotide (NAD+) is the first step in developing acidosis. This increased ratio of NADH to NAD+ has an inhibitory effect on hepatic gluconeogenesis, which can lead to severe, life-threatening hypoglycemia. With the excess of NADH, lactate is produced from pyruvate. Acetic acid, an oxidative product of alcohol, is converted in the liver to acetyl CoA and is used as a substrate for fatty acid synthesis. This process leads to the formation of ketones such as acetoacetate, B-hydroxybutyric acid, or acetone (Alabi, et. al, 2020).  In addition to this process, the reduced oral intake causes reduced insulin release that in turn triggers an increase in glucagon, norepinephrine, and cortisol. This results in the formation of additional ketones from the breakdown of fatty acids leading to severe ketoacidosis (Alabi, et., al 2020).

Q: What type of fluid or electrolyte imbalances does Mr. Davis have and why?

Mr. Davis is suffering from hypernatremia, hyperkalemia, hyperchloremia, and hypoglycemia. Ingesting large amounts of alcohol induces diuresis due to increased vasopressin levels, leading to dehydration (Baj et. Al, 2020). Within 20 minutes of consumption, alcohol begins to produce an increase in urine flow leading to urinary fluid losses and an increase in the concentration of serum electrolyte concentrations. Mr. Davis’s history states he made multiple trips to the bathroom in a one-hour period suggesting this may be the reason behind his hypernatremia, hyperkalemia, and hyperchloremia. (Epstein, 1997). Mr. Davis’s hypoglycemia is likely due to decreased oral intake, decreased glycogen stores, and alcohol metabolism’s effect on gluconeogenesis.


-The anion gap represents the difference between positive (cations) and negative (anions) particles not accounted for by a chloride or bicarbonate molecule.

-Anions become elevated when byproducts of abnormal body acid (H+) breakdown occur, or accumulation of acid occurs faster than can be neutralized. These abnormal acids (i.e. ketoacid, lactic acid, toxins, or uremic acids) contribute to the presence of unmeasured anions and increase the anion gap.

-In other words, the difference between the sodium and the sum of chloride and serum bicarbonate represents all the other negatively charged molecules not bonded with a neutral or positive ion. The normal range of 10-12 is optimal for gas exchange and other cellular functions (Seifter & Chang, 2017). An anion gap over 12 indicates acid accumulation and cellular dysfunction and can be used to monitor response to treatment.

-Included on the slide is the anion gap formula Na+ – [Cl+ HCO3]. Mr. Davis’s anion gap is calculated to be 19 mEq/L using the available ABG and chemistry values.

-Elevated anion gap metabolic acidosis is caused by a select number of reasons, including glycols, oxoproline, L-lactate, D-Lactate, methanol, aspirin, renal failure, rhabdomyolysis, and diabetic, alcoholic, or starvation ketoacidosis (Seifter & Chang, 2017).  The presence of an anion gap helps narrow the differential diagnosis for the patient. Metabolic acidosis with a normal anion gap points toward loss of bicarbonate as the primary reason for the acidosis. An example of this is diarrhea causing metabolic acidosis. Mr. Davis does not have manifestations that result in loss of acid. However, he does have indications that the accumulation of acid is occurring with an inability to excrete the acid. In addition, the consequences of biological compensation mechanisms put Mr. Davis at risk for further decompensation.

-A high anion gap in the presence of metabolic acidosis guides the treatment plan to close the anion gap and correct the acid-base disturbance.

Respiratory compensation Evidence

Mr. Davis’s deep and rapid respiratory pattern is known as Kussmaul Respiration Pattern

 Kussmaul Respirations are the body’s attempt to compensate for acidemia (evidenced by abnormal pH of 7.15)

 Increased rate and depth of respirations to “blow off” carbon dioxide and reduce overall acid concentration in the body (McCance et al, 2019).

-With respiratory compensation, the respiratory system regulates acid-base balance by controlling the rate of ventilation when there is metabolic acidosis or alkalosis. Central respiratory chemoreceptors (CRCs) sense increases or decreases in pH and PaCO2. When acidemia exists, the respiratory rate increases, eliminating CO2 and reducing carbonic acid concentration (McCance et al, 2019).

-This triggers the almost immediate physiological compensation mechanism for normalizing pH due to immediate feedback from chemoreceptors and subsequent parasympathetic changes in respiratory depth and rate(McCance et al, 2019).

.-Mr. Davis’s ABG indicates a partially compensated metabolic acidosis. The partial compensation is evidenced in a low CO2, indicating that the lungs are attempting to blow off the acid while other buffering systems are impaired in his acute state. Metabolic buffering can occur both quickly and over days, weeks, and years. However, the metabolic functions  (primarily by the kidneys) to excrete acid takes longer to respond to correction. Therefore, peripheral and central respiratory receptor actions prompt increased breathing to attempt to achieve homeostasis or at least maintain a pH compatible with life processes.

The metabolic buffers discussed in the following slides take longer to regulate pH. Therefore, manipulation of the respiratory system is the first-line defense for correcting acid-base disturbances. Without intervention, Mr. Davis’s ability to maintain this compensation is going eventually fail as his other buffering systems have been acutely compromised.


These images from the course textbook, Pathophysiology: The Biological Basis for Disease in Adults and Children, provide a visual aid to the balance required to maintain the optimal pH range of 7.35-7.45 (McCance et al, 2019).

Metabolic Acid-base Buffers

-In renal compensation, the distal tubule of the kidney regulates acid-base balance by secreting excess hydrogen into the urine with a maximum urine acidity of a pH of about 4.4 to 4.7. Urine is more alkaline under normal conditions (5-8pH).

-Buffer processes in the tubular fluid combine with hydrogen ions, allowing more to be secreted before the limiting pH value is reached. The renal system compensates by producing more acidic or more alkaline urine, which may take hours to days.

Dibasic phosphate and ammonia (NH3) are two important renal buffers:

•They can attach hydrogen ions and be secreted into the urine.

•Dibasic phosphate is filtered at the glomerulus.

•75% is reabsorbed, and the remainder is available for buffering H+.

•Monobasic phosphate is formed.

•The remaining negative charge on the molecule makes it lipid insoluble, preventing it from diffusing back across the tubular cells and into the blood.

•Thus the monobasic phosphate containing the secreted H+ is excreted in the urine (McCance et al, 2019).

Urine Ketones

Explain the rationale for the low glucose level and high urine ketones.

-As stated previously, alcohol consumption may lead to depleted protein and carbohydrate stores. Combined with decreased meaningful dietary intake, the body can go into starvation mode with depleted hepatic glycogen stores.  Furthermore, alcohol metabolism also impairs gluconeogenesis due to the metabolism of lactate, glycerol, and amino acids, which can result in hypoglycemia (McGuire, Cruickshank, & Munro, 2006).  The resulting hypoglycemia causes a decrease in insulin production (McGuire, Cruickshank, & Munro, 2006).

Decreased insulin production, paired with catecholamine release, increases the release of free fatty acids from triglycerides.  In addition, alcohol consumption may also promote lipolysis, further increasing the amount of fatty acids available to the liver (McGuire, Cruickshank, & Munro, 2006). 

Thus, without enough insulin, the body is unable to make the energy needed. This causes a breakdown of fat as a form of energy. Increased glucagon and free fatty acids stimulate fatty acid oxidation to acetyl CoA.  The acetyl CoA is then diverted to ketogenesis (McGuire, Cruickshank, & Munro, 2006).  When ketones are produced in high enough amounts, the ketones “spill over” into the urine.  This pathophysiology pathway explains Mr. Davis’ low blood glucose while having ketones present in his urine.

Urine Protein

Is the protein level seen in the UA abnormal? Provide a rationale. How do the findings relate to Mr. Davis?

-A small amount of protein in the urine is normal at times, but urine is generally negative for protein and ketones. Protein in the urine (proteinuria) in significant amounts indicates cellular injury and altered cellular function in the glomerular membrane (McCance et al., 2019).  The glomerular membrane becomes more permeable in certain conditions, allowing for the exchange of larger protein molecules to spill into the urine. Proteinuria contributes to tubulointerstitial injury by accumulating in the interstitial space and activating complement proteins and other mediators and cells, such as macrophages, that promote inflammation and progressive fibrosis. (McCance et al., 2019).  Patients with proteinuria may begin to manifest edema due to the leakage of fluid and protein into the interstitial compartment.

-In Mr. Davis’ scenario, his apparent dehydration may have significantly contributed to the positive protein in his urinalysis.  If he has had previous episodes of ketoacidosis, dehydration, and kidney injury, he may have developed a progressive injury to his kidneys.  Kidney injury/kidney disease can further impair his kidney’s ability to filter protein from his urine.   

Recommendations for treatment

-Recommendations for treatment include thiamine infusion to prevent Wernicke’s encephalopathy (Brashir et al., 2021).

-Administer dextrose to correct hypoglycemia and stimulate insulin production and decrease glucagon production (Brashir et al., 2021; Long et al., 2021)

-Fluid administration with a balanced fluid

– As practitioners, providing prompt response to acidemia is vital, as cardiac collapse may result. Prompt and thorough patient assessment and clinical workup, including blood and urine chemistries, ABGs, or venous blood gases, are useful tools for decision-making.

-Appropriate ABG interpretation followed by an appropriate response to catalyze pH neutralization, correct electrolyte abnormalities, and protect tissue perfusion are priority interventions.

-Patients with severe ABG and electrolyte abnormalities require serum studies about every 2-4 hours to evaluate for correction or worsening (Long et al., 2021). Beta-hydroxybutyrate is an additional lab that can indicate resistant acidosis.

-The following slide offers a decision tree for treatment


Alabi, F., Alabi, C., Basso, R., Lakhdar, N., Oderinde, A. (2020). Multiple electrolyte imbalances and acid-base disorder posing a diagnostic dilemma: a case   report.   Journal of Medical Case Reports, 14:15.

Baj, J., Flieger, W., Teresinski, G., Buszewicz, G., Sitarz, R., Forma, A., Karakula, K., Maciejewski, R. (2020). Magnesium, calcium, potassium, sodium, phosphorus,   selenium, zinc, and chromium levels in alcohol use disorder: A review. Journal of Clinical Medicine, 9(6), 1901.

Bashir, B., Fahmy, A. A., Raza, F., & Banerjee, M. (2021). Non-diabetic ketoacidosis: a case series and literature review. Postgraduate Medical Journal, 97(1152),   667-  671.

Epstein,  M. (1997). Alcohol’s impact on kidney function. Alcohol Health and Research World, 21(1), 84-92. Retrieved on May 23, 2023, from

Long, B., Lentz, S., & Gottlieb, M. (2021). Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management. Journal of Emergency Medicine, 61(6), 658–665.

McCance, K. L., Huether, S. E., Brashers, V.L., & Rote, N.S. (2019). Pathophysiology the biological basis for disease in adults and children (8th ed.). Elsevier Health

  Sciences. ISBN-13:9780323402811

McGuire, L, Cruickshank, A., Munro, P. (2006). Alcoholic ketoacidosis. Emergency Medicine Journal 23(6), 417-420.

Seifter, J. L., & Chang, H. Y. (2017). Disorders of Acid-Base Balance: New Perspectives. Kidney diseases (Basel, Switzerland)2(4), 170–186.