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
symptoms for mild, moderate, severe hyperkalemia?
• Generally related to cardiac, neuromuscular, and smooth muscle cell function
• Mild (5.1-5.9 mmol/L)
– May be asymptomatic
• Moderate (6.0-7.0 mmol/L)
– Cardiac arrhythmias (patient may sense heart palpitations)
• Severe (>7 mmol/L)
– Cardiac arrhythmias, weakness, ascending paralysis, respiratory failure
what ECG changes are seen in hyperkalemia
- Narrowing in wavelength, peaking of T wave
- P wave separated from QRS complex, widening interval
- loss of P wave
- widening of QRS complex
- QRS complex and t wave merge, greating sine wave
goals of theapy for hyperkalemia
- Evaluate severity of hyperkalemia, rate of onset, and patient’s clinical condition
- Identify any diet or drug-related contributions to elevated potassium levels
• Goals of therapy:
– Minimize cardiac conduction effects
• Administer intravenous calcium to antagonize cardiac membrane actions of hyperkalemia
– Return serum and total-body stores of potassium to normal levels
Management of Mild to Moderate Hyperkalemia
• Asymptomatic patients with [K+]<6 mmol/L and normal or mildly impaired renal function usually respond well to:
– Dietary changes (reduce potassium intake)
– Drug therapy changes (discontinue or ↓dose of potassium-sparing diuretic, potassium supplement, NSAID, ACE inhibitor, ARB)
– Furosemide (loop diuretic) to promote urinary potassium excretion
– Close follow-up of [K+], fluid volume status, and other electrolyte conc
Management of Severe Hyperkalemia
6 things
• Calcium raises threshold for the cardiac action potential
– Reverses electrocardiographic effects
• Furosemide inhibits sodium reabsorption from the ascending loop of Henle (loop diuretic)
– Increases urinary potassium loss
• Insulin stimulates intracellular uptake of potassium
– May require concurrent administration of dextrose
• Sodium bicarbonate raises serum pH (promotes intracellular shift of potassium)
• Sodium polystyrene sulfonate (Kayexalate®) cation-exchange resin
• Hemodialysis will remove potassium from serum
Magnesium (Mg2+)
fxn?
• Daily magnesium intake 420 mg/day (men) and 320 mg/day (women)
• Predominantly an intracellular cation
– Second most abundant after potassium
• Plays a central role in cellular function
– Cofactor in biochemical reactions – especially those dependent on
adenosine triphosphate
– Mitochondrial function, protein synthesis, glucose metabolism
Magnesium Concentration
• Normal serum magnesium concentration
– 0.7-1.0 mmol/L (1.4 to 1.8 mEq/L)
___% of filtered magneisum is reabsorbed?
what can cause magnesium loss in kidneys?
~95% of filtered magnesium is reabsorbed
• 20% in the proximal tubule
• 70% in thick ascending limb of loop of Henle
⟹Loop diuretics can often cause profound magnesium loss through the kidneys
• 10% in distal convoluted tubule
Hypomagnesemia causes (2)
• Gastrointestinal
– Reduced intake: malnutrition, alcoholism
– Reduced absorption: celiac disease, chronic proton pump inhibitor (PPI) use
– Increased loss: excessive vomiting, excessive laxative use, prolonged diarrhea
• Renal
– Glomerulonephritis, pyelonephritis
– Drug-induced: aminoglycosides, diuretics
Hypomagnesemia goals of therapy
– Resolve signs and symptoms of hypomagnesemia
– Return serum and total-body stores of magnesium to normal levels
– Correct concurrent electrolyte imbalances
• Hypokalemia and Hypocalcemia are common
– Identify and correct the underlying cause
Hypomagnesemia Management
• Serum [Mg2+] >0.5 mmol/L and asymptomatic
– Oral supplementation is preferred
– Common sources include oxide, hydroxide, chloride, citrate, and gluconate salts
• Most have small amounts of elemental magnesium
⟹multiple daily doses required
– Most common dose-limiting side effect is diarrhea
• Serum [Mg2+] <0.5 mmol/L or symptoms present
– IV magnesium sulfate should be administered
Hypermagnesemia causes
Serum magnesium concentration >1.0 mmol/L
• Rare condition, generally occurs in patients with advanced chronic kidney disease when magnesium intake exceeds renal clearance
• Drug-Induced: antacids and laxatives that contain magnesium, lithium
Hypermagnesemia symtons and goals of therapy
• Symptoms
– Usually asymptomatic if [Mg2+]<2.0 mmol/L
– Lethargy, confusion, muscle weakness, dysrhythmias
• Treatment goals
– Reverse the neuromuscular and cardiovascular symptoms of hypermagnesemia
– Normalize the [Mg2+]
– Identify and correct the underlying cause
Hypermagnesemia management
• Management
– Reduce magnesium intake
• Stop or reduce use of antacids and laxatives
– Enhance elimination of magnesium
• Furosemide 40 mg IV
• Forced diuresis (0.45% NaCl + loop diuretic)
– Antagonize the physiologic effects of magnesium
• Calcium IV
other electrolytes
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• Calcium (Ca2+) intracellular cation
– Approximately 99% stored in bone
• Phosphate (PO3-4) intracellular anion
– Significant roles in metabolism and bone formation
Bicarbonate (HCO3)
– Major role in regulating pH
– Normal concentration is 24-30 mmol/L
