Focused Assessment v Complete Assessment


This case study presents a patient with acid-base disturbance. The patient has been vomiting, having difficulties maintaining fluids and liquids down, is dehydrated, and experiencing nausea. The patient fainted and on being taken to the hospital, the arterial blood gas indicated the following: high pH, 7.5; high PaCO2, 40 mm Hg; PaO2, 95 mm Hg; SaO2, 97%; and lastly high HCO3-, 32. For this patient, a focused assessment was performed because it involved a detailed nursing assessment of the patient’s specific body system relating to the presenting problem.

Classification of Acid-Base Disturbance for the Patient

The acid-base disturbance for this patient can be categorized as metabolic alkalosis as evidenced by the increased PH, increased HCO3-, and normal pCO2 (Adamczak et al, 2018, p. 960). The increased PH is due to reduced hydrogen ion concentration, which leads to elevated bicarbonate concentrations. On the other hand, the increased HCO3- is as a result of the body losing hydrogen ions from the body. As a result, metabolic alkalosis is a compensatory mechanism that results to alveolar hypoventilation with an increase in PaCO2, which reduces the change in PH that would if not, occur (Adamczak et al, 2018, p. 961)Focused Assessment v Complete Assessment.

Probable Reasons for the Acid-Base Disturbance

From the case study, the patient is vomiting various times a day and has difficulty in keeping liquid. Excessive vomiting is causing fluid imbalances for the patient (Raphael, 2016, p. 698). Normally, gastric secretions are normally very acidic where the PH can even be below 1.0. Accordingly, because there was a lot of vomiting for this patient, there was a net loss of hydrogen ions from the stomach lumen, and in due course loss of hydrogen ions fro, the bloodstream. This, therefore, increased the patient’s arterial PH and caused metabolic alkalosis. In addition, the patient has been taking antacids which are an alkalotic agent and administration of excess alkalotic agents can result to alkalosis (Raphael, 2016). Finally, the case study indicates that the patient is dehydrated, which caused water loss within the extracellular space. Reduced extracellular volume activates renin-angiotensin-aldosterone system, as well as aldosterone, which consequently rouses re-absorption of sodium and hence water in the kidney’s nephron. In addition, aldosterone stimulates renal system to excrete H+ and retains bicarbonate, and therefore the loss of H+ increases the PH of the blood (Adamczak et al, 2018, p. 960).

Renal/Respiratory Compensatory Mechanisms

The respiratory compensatory mechanism for metabolic alkalosis takes place within the lungs, where the lungs retain CO2 via reduced breathing or inadequate ventilation. As a result, there is consumption of carbon dioxide in order to form the carbonic acid intermediate, therefore reducing the PH level. The reduced PH level indicated reduced hydrogen ions (Adamczak et al, 2018, p.962). The reduced level of hydrogen ions holds back the peripheral chemo-receptors; they have high sensitivity to PH; however, since the respiration is slow, there is an elevation in pCO2, and this stimulates depression counteract due to central chemo-receptors responsive to the CO2’s partial pressure within the cerebral spinal fluid act. Accordingly, the central chemo-receptors cause the respiratory rate to increase (Wiseman & Linas, 2015, p.943).

For the renal compensatory mechanism for metabolic alkalosis, the kidney excretes hydrogen ions in exchange for potassium ions. In addition, there is increased excretion of HCO3− because the filtered HCO3− load surpasses the capacity of the renal tube to reabsorb HCO3−.

Pharmacological Interventions for the Acid-Base Disturbance

Normal saline administration: This will lower the HCO3− through reversal of the stimulus to retention of renal Na+, and this allows NaHCO3 to be excreted and increases delivery of chlorine delivery, promoting secretion of HCO3−.

Sodium chloride PO: The rationale for this is to provide chloride that is required for the kidney to absorb sodium with chloride, improving bicarbonate excretion (Wiseman & Linas, 2015, p.942).
Acetazolamide (Diamox): This medication is a carbonic anhydrase inhibitor that stimulates renal system to excrete bicarbonate
Encourage the patient to take fluids IV/PO: This will replace the extracellular fluids that were lost during vomiting. Sufficient hydration will facilitate pulmonary secretions to be removed in order to enhance ventilation (Raphael, 2016).
Administration of supplemental oxygen: This will improve the patient’s ventilation. This is because respiratory compensation in metabolic alkalosis is characterized by hypoventilation, which can lead to hypoxia or reduced levels of Pao2 (Wiseman & Linas, 2015, p.942)Focused Assessment v Complete Assessment.
Educational Needs for the Patient

Nutritional needs: The patient will be encouraged to take food high in potassium and calcium such as grapefruit and apple juice, bananas, figs and This will be helpful in replacement of potassium losses (Raphael, 2016, p. 700).
Medication educational needs: The patient has been overdosing antacids which may be a contributing factor to metabolic alkalosis. Accordingly, the patient will be educated on the risks of taking excessive alkaline antacids and instructed to avoid this.
Fluid intake needs: The patient will be encouraged to increase the intake of water and fluids to avoid dehydration
Healthcare needs: The patient will be educated on the importance of visiting a healthcare facility in case of any ailment. The patient was unwell for the past 8 days but did not visit any healthcare facility until she was taken after fainting.
The patient presented showing signs and symptoms of acid-base disturbance and a focused assessment was performed. The assessment outcome indicated metabolic alkalosis as evidenced by the increased PH, increased HCO3-, and normal pCO2. Factors contributing to the metabolic alkalosis included excessive vomiting as well as excessive intake of antacids. The renal and respiratory systems compensatory mechanisms for the acid-base disturbance have been described. The recommended pharmacological interventions for the patient include; normal saline administration, sodium chloride PO, Acetazolamide (Diamox), and administration of supplemental oxygen. Finally, the patient needs to be educated on the risks associated with taking excessive antacids, the appropriate nutritional intake, and fluid intake Focused Assessment v Complete Assessment.


Adamczak M, Masajtis-Zagajewska A, Mazanowska O, Madziarska K & Stompór T. (2018). Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease – Position Statement of the Working Group of the Polish Society of Nephrology. Kidney Blood Press Res. 1(43), pp: 959–969.

Raphael K. (2016). Approach to the Treatment of Chronic Metabolic Acidosis in CKD. American Journal of Kidney Diseases. 67(4), pp: 696–702.

Wiseman A & Linas S. (2015). Disorders of Potassium and Acid-Base Balance. American Journal of Kidney Diseases. 45(5), pp: 941–949.



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