conditions of K+ and Mg2+ imbalance Flashcards
what is the most abundant intracellular cation
Daily potassium intake 4700 mg (Adequate Intake)
– Most Canadians do not reach this recommendation
– Foods with a high potassium content: fruits (apricots, bananas, guava, kiwifruit, nectarines), vegetables (broccoli, spinach), potatoes, milk, yogurt, bran cereals
• Potassium is the most abundant intracellular cation
– 98% of total body potassium is located within cells
• Actively transported into cells
– Via the Na+-K+-ATPase pump
fxn of K+
Major determinant of the resting action potential
– Neurons
– Skeletal muscle cells
– Cardiac myocytes
Potassium Concentration
read
Normal serum potassium concentration (represents about 2%
of total body K+)
– 3.5-5.0 mmol/L (mEq/L)
• Serum potassium concentration is affected by
– Dietary intake
– Excretion from the kidneys (90%) and gastrointestinal system (10%)
– Sequestration in muscle and hepatic cells
– Hormone levels (insulin, aldosterone)
– Acid/Base balance
Hypokalemia
- what may cause total body deficit
- what causes shift into intracellular compt
• Serum potassium concentration <3.5 mmol/L
• Total body deficit
– Poor dietary intake
– Excessive loss (e.g., diarrhea, renal, vomit)
• Potassium shift into intracellular compartment
– Metabolic alkalosis
– Insulin (elevated insulin secretion)
– B2 receptor agonists (epinephrine, salmeterol)
what drugs cause hypokalemia?
• Diuretics (loop and thiazide) inhibit sodium reabsorption
⟹↑[Na+] in distal tubule and collecting ducts
⟹Na+ reabsorption in exchange for K+
– Reduction in vascular volume will also stimulate release of aldosterone (mineralocorticoid)
• works in distal tubule and collecting duct to promote Na+ reabsorption in exchange for K+
• Insulin promotes glucose uptake into cells
– ↑K+ transport into liver, muscle, and adipose
– Balanced with glucagon to regulate potassium levels
• Decongestants (pseudoephedrine), Caffeine, �2 receptor agonists
– Promote intracellular shift of potassium
explain how diuretics cause hypokalemia
MOA: inhibit reabs of sodium in the proximal or Loop of Henle
- Increases conc in distal tubule and collecting ducts
- Body wants to preserve sodium, at expense of having K+ exreted into the urine so there may be an excess loss of potassium as body tries to retain soidum
- Sodium and water excretion = low vascular volume = aldosterone promotes sodium reabs at exchange of K+
- Excess sodium in distal tubules, body wants to absorb that
- Combination that leads to further loss
explain how insulin cause hypokalemia
Insulin promotes glucose uptake into cells and also K+ into liver, muscle, adipose
As we get more glucose into cells, that increases metabolism, and K+ is needed to help maintain that
Hypokalemia Symptoms
mild, moderate, severe
Mild (3.0-3.5 mmol/L)
– Usually asymptomatic (may see in lab values)
• Moderate (2.5-3.0 mmol/L)
– Muscle cramping, weakness, malaise, myalgias
• Severe (<2.5 mmol/L)
– ECG changes, arrhythmias (heart block, atrial flutter, paroxysmal atrial tachycardia), cramping, impaired muscle contraction
General Considerations of K+
• Increase dietary potassium intake will reduce risk of developing hypokalemia
• Most dietary sources of potassium are coupled with phosphate
– Will not be effective for treating conditions with chloride loss in addition to potassium loss (e.g., vomiting, diarrhea, diuretic therapy, laxative use)
• Many salt substitutes use KCl instead of NaCl
• Potassium supplementation should be administered in divided doses to minimize GI side effects (w/food)
• Consider patient’s ability to adhere to the therapy
Potassium Supplementation
– General rules:
• for every 1 mmol/L below 3.5 mmol/L, the total body deficit is 100 to 400 mmol
• in an acute care setting, every 10 mmol of potassium supplementation should ↑ serum [K+]
by 0.1 mmol/L
• Monitor [K+] frequently (avoid hyperkalemia), for IV
• Identify underlying medical conditions (e.g., heart failure)
• Identify potential drug interactions
– Medications that alter potassium level (e.g., potassium-sparing diuretics: spironolactone, triamterene, amiloride)
– Medication adverse effects potentiated by hypokalemia (e.g., digoxin)
Oral Potassium Supplementation
3 salts
• Potassium phosphate: use when the patient is both
hypokalemic and hypophosphatemic
• Potassium bicarbonate: use when the patient has metabolic acidosis
• Potassium chloride: most common salt for replacement therapy
Potassium Chloride – Oral Options
what types of formulations available?
• Available strengths: 8 mEq 10 mEq 20 mEq
• Liquid formulations are the cheapest option, but have a strong, unpleasant taste
• Wax-matrix tablets
– Slow-K, generics
• Controlled release microencapsulated
– Micro-K Extendcaps, generics
– Less GI irritation compared to wax-matrix tablet
Potassium Chloride - Intravenous
when can IV K+ be used?
• Limited to the following:
– Severe hypokalemia (<2.5 mmol/L)
– Severe signs and symptoms of hypokalemia (e.g., ECG changes, muscle spasms)
– Patient unable to tolerate oral therapy
Monitor patient closely
– ECG changes
– High risk of over correcting (hyperkalemia)
– Injection site pain and phlebitis
Use saline-containing solutions for administration
– Dextrose-containing solutions will stimulate insulin release and cause intracellular shift of
potassium
Hyperkalemia
causes?
Serum potassium concentration >5.0 mmol/L
• Less common compared to hypokalemia
• Increased potassium intake – Over correction of hypokalemia • Decreased potassium excretion – Acute or chronic renal failure – Adrenal insufficiency • Redistribution of potassium into extracellular space – Metabolic acidosis
what drugs cause hyperkalemia
Decreased potassium excretion – Angiotensin Converting Enzyme (ACE) inhibitors – Angiotensin Receptor Blockers (ARBs) – Direct renin inhibitors – Potassium-sparing diuretics – Nonsteroidal anti-inflammatory drugs (NSAIDs) – Cyclosporine – Tracolimus – Trimethoprim/Sulfamethoxazole
