NRS 433V Introduction To Nursing Research
Questions
Test Result Normal levels
pH 7.5 7.35 – 7.45
PaCO2 40 mm Hg 35-45 mm Hg
PaO2 95 mm Hg 80-100 mm Hg
SaO2 97% 95-100%
HCO3- 32 meq/liter 22-26 meq/liter
2. Given the case study, what are the possible factors causing this acid-base disturbance? Explain the pathophysiology created by these factors.
3. How would the renal and respiratory systems try to compensate for this acid-base disturbance?
4. What pharmacologic intervention is commonly used to correct this acid-base disturbance? Describe the pharmacological actions.
5. Describe the educational needs for this patient and what your approach will be.
Answers
1. The acid-base disturbance in the patient suggests that she is suffering from metabolic alkalosis. This is evident as there is an increase in the arterial blood pH in combination with the normal levels of the arterial pCO2. The arterial blood gas test also showed that there is an increase in the concentration of arterial HCO3 which shows that it is a condition of metabolic alkalosis (Mæhle et al., 2014). The alkaline levels are high in the patient due to increased bicarbonate or decreased level of carbon dioxide. The HCO3 that is bicarbonate levels has increased where there is loss of hydrogen ions from the body or gain of bicarbonate ions. This manifests the blood pH to rise above the normal level that is more than 7.35. The elevation of bicarbonate concentration is the first clue for metabolic acidosis that is greater than 35mEq/L that is an obvious cause manifested due to metabolic alkalosis.
2. Excessive vomiting might be a reason for the acid-base imbalance in the patient. The gastric secretions in the stomach are very acidic in nature where the pH can be as low as 1.0. In the given case study, the patient is vomiting a lot. This results in loss of hydrogen ions from the lumen of the stomach and also from the blood stream. This leads to an increase in the arterial blood pH levels resulting in the metabolic acidosis. Due to the loss of excessive electrolytes and fluids from the body affects the kidney’s ability to maintain the acid-base balance in the blood. This loss of gastric HCl results in loss of the fixed hydrogen that generates the metabolic alkalosis due to vomiting. This loss causes the contraction of the extracellular fluid volume (ECF) volume that in turn, decreases the renal perfusion pressure. When the Angiotensin II levels increase, sodium-hydrogen exchange pump also increases with an increase in bicarbonate re-absorption resulting in metabolic alkalosis (Mandal, 2014).
3. Renal compensation is less effective than respiratory compensation in metabolic alkalosis. There is an increase in the excretion of bicarbonate ions as there is an increase in the bicarbonate filtered load exceeding beyond the ability of the renal tubules for re-absorption. In this compensation, the kidneys regulate the pH levels in the plasma and is slow than the respiratory compensation (Gierth, Banas & Burger, 2014).
Respiratory compensation mainly occurs in the lungs where carbon dioxide is retained through slow breathing or by the process of hypoventilation. There is consumption of carbon dioxide that is directed towards the carbonic acid intermediate formation and thus, the pH is decreased. Hypoventilation is the leading mechanism for pH correction. This would lead to elevation of the partial pressure of carbon dioxide and restoration of arterial pH in normal range (Liu & Bhalla, 2017).
4. The pharmacologic interventions for metabolic alkalosis include the replacement of bicarbonates. The hydrogen blockers can be used to prevent the further loss of the hydrogen ions. As the patient is having severe vomiting, administration of antiemetics can be used. The expansion of extracellular fluid volume is done with sodium saline. Acetazolamide (carbonic anhydrase inhibitor) or hydrochloric acid is used to balance the acid-base disturbance in metabolic alkalosis. In case of excess mineralocorticoid,, source removal along with potassium replacement, sodium restriction and amiloride or spironolactone is used as alternatives. The mechanism of action of acetazolamide is the reversible inhibition of carbonic anhydrase enzyme that results in hydrogen ion secretion reduction at the renal tubule and an increase in the renal excretion of potassium, sodium, water and bicarbonates. In metabolic alkalosis, it decreases the re-absorption of bicarbonates at the proximal convulated tubules by 80% via carbonic anhydrase inhibition in the luminal borders of PCT cells. It is a common treatment for metabolic alkalosis (Fontana et al., 2016).
5. Patient education is important as to help to get adhered to the treatment, medications and in order to get successful health outcomes and in the prevention of further complications. The patient needs to know the pathophysiology of the fluid and electrolyte loss and adherence to the medications as prescribed. The patient should also be educated to keep an account of the vital parameters like difficulty in breathing, dizziness or weakness that might indicate fluid and electrolyte imbalance. The patient needs to be informed about the side-effects of acetazolamide like dizziness or increased urine amount. She also needs to be taught about the side-effects of overuse of antacids in order to calm the nausea (Dee, 2015).
The approach to successful patient education includes the effective communication that is required to enhance the patient’s satisfaction towards treatment and adherence to medications. The healthcare professionals have to build a long-term, strong and trusting relationship wi8ht the patient that is necessary to improve the compliance.
References
Dee, C. M. (2015). Renal tubular dysfunction, metabolic acidosis, metabolic alkalosis and respiratory alkalosis: 9 case reports. Reactions, 1553, 114-30.
Fontana, V., Santinelli, S., Internullo, M., Marinelli, P., Sardo, L., Alessandrini, G., … & Palange, P. (2016). Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients. Eur Rev Med Pharmacol Sci, 20(1), 37-43.
Gierth, M., Banas, B., & Burger, M. (2014). Metabolic Alkalosis. In Urology at a Glance (pp. 77-80). Springer Berlin Heidelberg.
Liu, G. S., & Bhalla, V. (2017). Explaining the Coincidence Rule for Estimating Respiratory Compensation in Metabolic Acid–Base Disorders. Annals of Internal Medicine.
Mæhle, K., Haug, B., Flaatten, H., & Nielsen, E. W. (2014). Metabolic alkalosis is the most common acid–base disorder in ICU patients. Critical Care, 18(2), 420.
Mandal, A. K. (2014). 8 Metabolic Alkalosis: Pathophysiology and Management. Textbook of Nephrology, 81.
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