1. What is the patient’s acid-base abnormality? Justify your answer.

Metabolic alkalosis is the patient’s acid-base balance abnormality. This is supported by her high pH since
a high pH indicates alkalosis and her high pCO2 which points to an ongoing respiratory compensatory
mechanism seen in metabolic alkalosis.

Persistent vomiting of the patient results in the loss of hypochloric acid with the stomach contents. The
loss of fluid and NaCl in vomitus results in contraction of ECF and increased secretion of renin nd
aldosterone. Severe vomiting also causes loss of potassium, chloride and sodium. The kidneys
compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ion by
the action of aldosterone, leading to metabolic alkalosis.

Results seen in the four primary acid-base disorders:

The patient’s signs and symptoms of having an acid-base abnormality of metabolic acidosis:

Patient’s profile Metabolic acidosis

Persistent vomiting
Tachycardia
Mild fever
Hypertension
Sunken eyes and poor skin turgor
Dryness of skin and mucous membranes
Lethargic with proximal muscle weakness
Increased hematocrit and BUN
Hypokalemia and Hypochloremia
Proteinuria and high specific gravity
High pH and pCO2
Prolonged vomiting and severe dehydration
- GI origin
Arrhythmia
Fever
High renin and aldosterone -> hypertension
Sunken eyes and decreased skin turgor
Dryness of skin and mucous membranes due to
dehydration
Seizures, muscle cramps and weakness are
symptoms of hypokalemia
Kidney failure (increased hematocrit and BUN)
Loss of potassium, sodium and chloride
Increased urine chloride
High pH and pCO2

2. Outline the treatment for the patient’s acid-base abnormality.

 a. Saline-responsive metabolic alkalosis
Therapy is aimed at restoring intravascular volume depletion through the administration of
intravenous sodium chloride until hemodynamic stability is achieved. Concomitant hypokalemia
may be treated with intravenous or oral potassium supplementation. In patients with metabolic
alkalosis in the setting of diuretic therapy, repletion with potassium chloride aids in resolving the
alkalosis. Alternatively, in patients with significant edema, consider the use of the carbonic
anhydrase inhibitor acetazolamide to effect enhanced renal bicarbonate wasting. Proton pump
inhibitors or H2blockers may mitigate the loss of acidic gastric contents in patients requiring long-
term nasogastric suctioning.

b. Saline-resistant metabolic alkalosis

Management will depend upon the underlying cause. Patients with primary hyperaldosteronism
may be treated with surgical resection of the adrenal adenoma, or medical therapy with
aldosterone antagonists, such as spironolactone or eplerenone. Glucocorticoid-remediable
aldosteronism responds to oral steroid therapy. Inhibition of the constitutively active epithelial
sodium channel (ENaC) with amiloride in patients with Liddle syndrome is the most effective
treatment.

c. Exogenous alkali

Recognition of the exogenous source of alkali and prompt discontinuation or dose adjustment
should alleviate the alkalosis. In patients on chronic total parenteral nutrition, adjustment of
acetate levels is necessary. In patients with milk-alkali or calcium-alkali syndrome, therapy is
aimed at reversing the renal failure with aggressive fluid resuscitation and treating hypercalcemia.
Furosemide may be used to enhance calciuresis.

Metabolic Alkalosis Clinical Presentation. (2018, November 01). Retrieved from

https://emedicine.medscape.com/article/243160-clinical