NUR 631 Topic 3 DQ 2 A 75-year-old man was admitted with shortness of breath and lower extremity edema

1: Acid-base disorder: Metabolic Acidosis, Respiratory Compensation.

2: Metabolic alkalosis is a condition characterized by an elevated pH above 7.45, which is patient is, indicating alkalemia. It occurs when there is an increase in bicarbonate (HCO3-) concentration in the blood. This can be caused by various factors, but one common cause is the excessive loss of metabolic acids. His respiratory system undergoes compensatory mechanisms. The elevated pH inhibits the respiratory center, which reduces the rate and depth of ventilation. As a result carbon dioxide (CO2) is retained in the body. The retention of CO2 helps to normalize the ratio of bicarbonate (HCO3-) concentration to carbonic acid (H2CO3) concentration.

3: Active compensatory compensation.

4: Respiratory alkalosis is a condition characterized by alveolar hyperventilation, leading to a decrease in the concentration of plasma carbon dioxide (hypocapnia) and an increase in the ratio of H2CO3 (carbonic acid) to PCO2 (partial pressure of carbon dioxide). I’d like to clarify a few points based on the information you provided.

Causes of respiratory alkalosis include (Huether, 2019):

1. Hypoxemia: Low oxygen levels in the blood can stimulate ventilation and lead to hyperventilation.

2. Hypermetabolic states: Conditions such as fever, anemia, and thyrotoxicosis can increase the metabolic rate and result in hyperventilation.

3. Early salicylate intoxication: Salicylate overdose, commonly seen with aspirin ingestion, can cause respiratory alkalosis as a result of direct stimulation of the respiratory center.

4. Anxiety or panic disorder: Psychological factors, including anxiety or panic attacks, can trigger hyperventilation and contribute to respiratory alkalosis.

To diagnose respiratory alkalosis, the arterial pH is typically greater than 7.45, and the PaCO2 is less than 38 mmHg. In acute cases, bicarbonate levels are usually within the normal range. However, in chronic respiratory alkalosis, there is compensatory renal response, leading to a decrease in bicarbonate levels and bringing the pH closer to normal.

Reference:

McCance, K. L., & Huether, S. E. (2018). Pathophysiology (8th ed.). Elsevier Health Sciences.

Use information provided and the “Discussion Forum Sample” to answer the following questions.

Scenario

A 75-year-old man was admitted with shortness of breath and lower extremity edema. He has been unwell for about a week and had multiple bouts of diarrhea over the previous 5 days. He does not take any medications. He was hyperventilating and was very distressed when EMS arrived. Admission arterial blood gas is listed below. He was on high concentration oxygen by mask on arrival to the emergency department.

Chemistry Results

• Na+ = 127
• HCO3- 20
• HCO- = 30meq/L 3
• K+ = 5.2
• BUN 50.5
• Glucose 9.5 mmols/l
• Cl- 79
• Creatinine 0.38
• Anion gap 33 mmols/l

Arterial Blood Gases

• pH 7.58
• pCO2 21 mmHg
• pO2 154 mmHg
• HCO3 19 mmol/l

Questions

Answer the following questions:

1. What is this patient’s acid-base disorder?
2. Discuss why you how you came to that conclusion.
3. Is the patient compensating?
4. What are the pathophysiological responses that the body is attempting to use to compensate?

As a critical care nurse, blood gas interpretation and context are important to daily care. For arterial blood gas (ABG) interpretation, a useful and easy method is the ABG decision-making chart (attached as a photo). It is also used in the book Arterial Blood Gases Made Easy by Hennessey and Japp (2016). This book is recommended by the American Association of Critical Care Nurses (AACN) and is highly referenced in the organization’s publications and nursing resources.

The rules of the chart are that the format is consistent each time and

·      the circled value on the same side as the ph is the cause

·      when the remaining value is on the opposite side of the chart, it is compensating, and pH is abnormal

·      If all three are on the same side, no compensation is occurring

·      If pH is normal and compensating value is normal, total compensation is occurring

·      If all values fall in the middle, ABG is normal.

The 75-year-old man in this scenario has respiratory alkalosis with partial metabolic compensation.

In this case, the arterial pH is high (7.58), indicating alkalosis. The PaCo2 is low (21) and the HCO3 is low (19). Based on the rules above, the patient is in partial compensation with abnormal pH. The abnormal PaCO2 of 21 falls on the same side of the pH and opposite of the HCO3 of 19, indicating respiratory alkalosis. The low bicarbonate and abnormal ph indicate there is partial compensation by the metabolic processes. In alkalemia, the reduction of PaCO2 in normal humans is compensated by buffer and renal responses that diminish plasma bicarbonate concentrations (Uedel et al., 2008). Some important principles in ABG interpretation are that the metabolic system is not a backup to the respiratory compensation mechanisms and that addressing the cause of metabolic-driven pH abnormalities is essential. The patient is hyperventilating and distressed while admitting he did not take his medications. Patients in panicked states can have high lactic acid and anion gaps that can distract from underlying causes. The patient is exhibiting distress and likely anxiety from the circumstances and the shortness of breath he is experiencing.  Though lactic acid is not provided, a notably high anion gap of 33 indicates a state of metabolic impairment. Understanding the metabolic response to respiratory correction can be predicted by understanding renal function (Uedel et al., 2008). The adaptive response in respiratory alkalosis is induced by a renal mechanism, which consists of decreasing the re-absorption of filtered HCO3 and reducing the generation of HCO3. This process takes about 24-48 hours under normal conditions. Therefore, acute respiratory alkalosis is severe compared to chronic. Acute respiratory alkalosis is often prompted by extra or pre-renal conditions such as toxicity and dehydration (Uedel et al., 2008). This patient will likely be acutely dehydrated with low serum protein levels due to nearly a week of malnutrition and diarrhea. Low plasma levels reduce the metabolic buffer capacity due to increases in intracellular lactic acid production, which can be represented in an elevated anion gap.

Reference

Hennessey, I., & Japp, A. (2016). Arterial blood gases made easy. Churchill Livingstone.

Uedel, Y., Aizawa, M., Takahashi, A., Fujii, M., & Isaka, Y. (2008). Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production. Nephrology Dialysis Transplantation. 24 (3) p. 825-828, https://doi.org/10.1093/ndt/gfn585Attachments