Question

Patient Profile

E.G. is a 73-year-old woman whose daughter brings her to see the health care provider because she has had a case of the “stomach flu,” with vomiting and diarrhea for the past three to four days and is now experiencing occasional light-headedness and dizziness. Her past medical history includes hypertension, hypercholesterolemia, and mild heart failure. She is taking:

Digoxin 0.125 mg po daily.

Captopril 25 mg po BID.

Furosemide 40 mg po daily.

Potassium chloride 20 mEq po daily.

Atorvastatin 20 mg po at bedtime.

Subjective Data

Has been following a low sodium diet

States her abdomen feels bloated and she has been constipated since the onset of the “flu”

Has been taking her medications except for the potassium chloride pill because it upsets her stomach.

Occasionally takes an extra “water pill” when her ankles are swollen

Objective Data

Physical Examination

Temperature 98.2° F, pulse 88, respirations 20, BP 138/86

Lungs clear to auscultation, breathing regular and unlabored

+1 edema bilaterally in ankles

Muscle strength in upper extremities normal and equal and in lower extremities weak

Sensation to all extremities normal

Abdomen distended with hypoactive bowel sounds

Diagnostic Studies

Lab values

Sodium 139.0mEq/L

Potassium 3.0mEq/L

HCO₃^- 25.4mEq/L

Chloride 99.5 mEq/L

Discussion Questions

1. What a possible pathophysiologic cause is of E.G.’s muscle weakness and dizziness? What other symptom does E.G. have that may be related to this problem?
2. What factors contributed to the development of this electrolyte imbalance?
3. What should you be on an alert for in a patient who is on furosemide and digoxin and why?
4. What additional signs and symptoms should you assess E.G. for?

Answer 1

1.Disruption of normal gastrointestinal function as a result of infection, uncovers its important role in acid base homeostasis. Metabolic acidosis or alkalosis may occur depending on the nature and volume of the unregulated loss that occurAcid -base disorders vary from acidosis to alkalosis depending on the site along the GI tract affected. These disruptions in acid base equilibrium are associated with disorders of potassium balance leading to hyperkalaemia or hypokalaemia.Hypokalemia alters the resting membrane potential and most commonly associated with hyperpolarization. The most serious problems are cardiac. Skeletal muscle weakness and paralysis may occur may occur with hypokalaemia. Severe hypokalaemia can cause weakness or paralysis of respiratory muscles. Smooth muscle function is also impsired by hypokalaemia. The patient may experience decreased GI motility, decreased airway responsiveness and impaired regulation of arteriolar blood flow, possibly contributing to smooth muscle cell breakdown. Finally they can impair function in non muscle tissue. Release of insulin is impaired, leading to hyperglycemia. With prolonged hypokalaemia ,the kidneys are unable to concentrate urine and fiuresis occurs.

2The most common cause of hypokalaemia can result from abnormal losses, via either kidneys or the GItract. GI tract losses of potassium secretion to diarrhea, laxative abuse, vomiting can cause hypokalaemia.

3.Serum electrolytes should be checked and notify the physician if the patient develops digitalis toxicity due to hypokalaemia. Furosemide is given in patients who require

Immediate removal of body fluid as in heart failure. The interaction of Furosemide cause hypokalaemia. Therefore patients are advused to take potassium supplements.

4The incidence of potentially lethal ventricular dysrythmias is increased in hypokalaemia. Patients are at risk for hypokalaemia and those who are critically ill should have cardiac monitoring to detect cardiac changes related to potassium imbalances.