Electrolyte Disorders Flashcards
1
Q
Laboratory Electrolyte Tests
A
- Chem 7: Na, Cl, BUN, K, HCO3, K, Creatinine, Glucose
- Chem 10: Above + Calcium, magnesium, and phosphorous
- Need to order ionized calcium separately
2
Q
Electrolyte Abnormality Treatment Considerations
A
- Symptom severity is related to the acuteness of the electrolyte abnormality
- Slow/chronic onsets tend to be less aggressive and can be gradually corrected
- Acute onsets tend to be more aggressive and need to be more aggressively treated
3
Q
Electrolyte Abnormality Treatment Goals
A
- Treat or prevent severe life-threatening signs and symptoms
- Improve or correct serum [electrolyte]
- Do not overcorrect
- Avoid undesirable side effects of treatment
- Correct underlying cause for abnormality
4
Q
Potassium
A
- Main intracellular cation, only small amount in ECF (maintained by Na/K ATPase)
- Normal: 3.5-5
- Intracellular ~150 mEq/L
- Functions in regulation of osmotic equilibrium, acid/base balance, transmission of nerve impulses, muscle contraction, glycogen, and protein synthesis
5
Q
Potassium ADME
A
- Abundant in diet and well absorbed via small intestine
- Distribution primarily intracellular
- Excretion: mainly renal (influenced by aldosterone), small amounts lost in feces and sweat
6
Q
Etiologies of Hypokalemia
A
- Redistribution: insulin, Beta-agonists, metabolic alkalosis (K decreases 0.6 for each 0.1 increase in blood pH)
- Loss of potassium: GI losses (N/V, diarrhea, etc) or renal losses (mineralcorticoid excess
- Poor intake/re-feeding syndrome
- Drug induced: diuretics, insulin, glucocorticoids, amphotericin B
7
Q
Hypokalemia
A
- Decreases resting potential with no change in threshold, delayed repolarization
- Muscle abnormalities: weakness, cramps, paralysis
- Metabolic: hyperglycemia (decreased B-cell response to glucose) or metabolic alkalosis (increased HCO3 synthesis)
- Cardiac Abnormalities: Bradycardia, heart block, PVCs, V tachycardia, V. fib, atrial flutters
ECG readings: ST depression, Flat t-waves, U-waves, widen PR and QRS interval
8
Q
Treating Hypokalemia
A
- Remove underlying cause if possible
- Replacement therapy in specific scenarios
- Evaluate and replace magnesium losses if present
9
Q
Hypokalemia Replacement Therapy Scenarios
A
- Symptomatic patients
- Underlying cardiac risk factors
- On digitalis glycoside
- Severe (K < 3)
- Ongoing loss of potassium
10
Q
Non-Pharm + Hypokalemia
A
- Potassium containing salt substitutes
- Dietary sources: fresh fruits, vegetables, meat
- Treat precipitating factor: diuretic therapy, vomiting, diarrhea
11
Q
Pharm Therapy + Hypokalemia
A
- Administer orally if possible
- Divided doses better tolerated and safer
- Continue replacement for several days to replete total body stores
- Each 1 mEq under 3.5 represents a deficit of 100-400 mEq
- KCl is most common replacement (Cl often loss in these patients too)
- Caution in renally insufficient patients and those with redistribution to avoid hyperkalemia precipitation
- Use Kacetate or Kcitrate in metabolic acidosis
12
Q
Hypokalemia Pharm Dosing
A
- Preventing Hypokalemia: start with 20 mEq/day
- Treating Mild Hypokalemia: 40-100 mEq/day in divided doses
- Treat severe deficiency: 120 mEq total dose
- Doses >20mEq should be divided to minimize GI toxicity
13
Q
Hypokalemia IV Treatments
A
- Usually 10-20 mEq diluted in 100 mL sterile water or NS
- Central line preferred, but can use the above [] in peripheral lines as well
- 10mEq/hr max without ECG, 20mEq/hr max rate with ECG
- *Can give 20 mEq/hr with closely monitored patients experiencing ECG changes from hypokalemia**
- NO DEXTROSE SOLUTIONS: promotes insulin release which shifts K intracellularly
14
Q
Measuring Serum K
A
- Measure [serum] after each 30-40mEq increment for adults
- Wait at least 30 minutes after K IV to re-measure K
- Max [] for continuous peripheral IV replacement fluids is 80 mEq/L
15
Q
Hyperkalemia Presentation
A
- Cardiac abnormalities (life threatening): V fib., asystole
- ECG: peaked T waves, widened QRS, increased PR interval
- Muscle abnormalities similar to hypokalemia: weakness, paralysis
16
Q
Hyperkalemia Etiologies
A
- Renal Failure
- Acidosis: metabolic acidosis, K increases 0.6 mEq for each 0.1 unit decrease in blood pH
- Rhabdomyolysis
- Mineralcorticoid deficiency
- Drug Induced: K-sparing diuretics, ACE-I/ARBs, Heparin, NSAIDs, salt substitutes
17
Q
Hyperkalemia Treatment Goals
A
- Antagonize adverse cardiac effects, if present
- Reverse other symptoms
- Return [serum] to normal
18
Q
Hyperkalemia Treatment Options
A
- Antagonism of K if cardiac abnormalities exist
- Promote intracellular redistribution
- Remove K from body
19
Q
Hyperkalemia Treatment + Cardiac Effects
A
- IV calcium gluconate or chloride
- Restores normal conduction of heart but doesn’t reduce or redistribute K
- Repeat doses if symptoms return
- Only use calcium chloride for life threatening symptoms (1g IV push)
- Gluconate: 1g IV over 2-3 minutes, repeating every 5 minutes until ECG normalizes
- DON’T administer calcium if digoxin toxicity occuring
20
Q
Hyperkalemia Treatment + Intracellular Redistribution
A
- Regular insulin is first line to reduce K, NOT if patient has acidosis
- 5-10 U IV or SQ
- If glucose <250, give dextrose
- Insulin promotes cellular uptake of K
- Glucose enhances endogenous insulin release and prevents hypoglycemia
- Albuterol is second line, use if unresponsive to insulin/glucose after 30-60 minutes
- Nebulize 10 mg over 10 minutes
21
Q
Hyperkalemia Treatment + Acidosis
A
- Sodium bicarbonate, only used in hyperkalemic patients from metabolic acidosis
- 50-100 mEq IV over 2-5 minutes
- Don’t infuse on same line as parenteral nutrition or other Ca/Phos solutions
22
Q
Hyperkalemia Treatment + Remove K
A
- Loop diuretic if no severe renal impairment
- Furosemide 20-40 mg IV (can repeat) or Bumetanide 0.5-1 mg IV
- Sodium polystyrene sulfonate (Kayexalate)
- Exchanges Na for K
- 15-60 g orally, can administer rectally but less effective (sorbitol enhances elimination, associated with necrosis of large intestine)
-Hemodialysis
23
Q
Hyperkalemia New Drugs
A
- Patiromer (Veltassa): binds to K in exchanges for calcium, 8.4-25.2 gm PO QD
- Sodium Zirconium cyclosilicate (Zs-9 Lokelma): polymer that exchanges K for Na, only for CHRONIC hyperkalemia
- 10 gm PO TID x 2 days initially, 5-15 gm PO QD maintenance
- All binding agents have potential significantly decrease the absorption of other oral medications, separate by other oral meds at least 6 hours if possible
