ASHP Fluids/ Electrolytes Review Flashcards
(35 cards)
Q: What are crystalloids, and what are some examples?
A: Crystalloids are balanced salt/electrolyte solutions that contain water, sodium, and chloride. They can be isotonic, hypertonic, or hypotonic. Examples include:
Normal Saline (0.9% NaCl) – isotonic
Hypertonic Saline (3%, 5%, 7.5% NaCl)
Lactated Ringers – contains NaCl, lactate, potassium (K⁺), and calcium (Ca²⁺)
Q: What are free water solutions, and what is an example?
A: Free water solutions are isosmotic fluids that are metabolized into water and carbon dioxide. An example is 5% Dextrose in Water (D5W). It distributes evenly in total body water (TBW) and can cross any membrane in the body.
Q: What are colloids, and what are some examples?
A: Colloids are large molecules that are too big to cross capillary membranes, so they primarily remain in the intravascular space. Examples include:
- Packed red blood cells
- Pooled human plasma (5% albumin, 25% albumin, 5% plasma protein fraction)
- Semisynthetic glucose polymers (dextran)
- Semisynthetic hydroxyethyl starch (hetastarch)
Q: What is normal plasma osmolality, how is it regulated, and what affects fluid shifts between compartments?
A:
- Normal plasma osmolality: 275–290 mOsm/kg
- Regulation: Maintained by thirst and secretion of arginine vasopressin (ADH) from the posterior pituitary
- Primary determinant: Sodium salts
- Effect on fluid shifts:
- ↑ Osmolality → fluid shifts into plasma → cellular shrinkage
- ↓ Osmolality → fluid shifts into cells → cellular swelling
Hyponatremia
Q: What are the classifications and common causes of hyponatremia?
A:
Three classifications of hyponatremia:
1. Hypovolemic Hyponatremia
2. Euvolemic Hyponatremia
3. Hypervolemic Hyponatremia
Common causes:
- Loss of isotonic fluid (e.g., vomiting, diarrhea)
- Post-operative administration of hypotonic fluids
- Excessive ADH (antidiuretic hormone - vasopressin) secretion due to:
* Volume depletion
* Organ hypoperfusion
* SIADH
* Cortisol deficiency
- Certain medications
- Renal failure
Q: Which medications commonly cause hyponatremia?
A: Medications that can cause hyponatremia, particularly in older adults, include:
- Thiazide diuretics
- Antiepileptic drugs:
* Carbamazepine
* Oxcarbazepine
- Antidepressants:
* Selective serotonin reuptake inhibitors (SSRIs)
* Tricyclic antidepressants (TCAs)
Q: What causes symptoms of hyponatremia, and what are the common symptoms?
A: Symptoms of hyponatremia are caused by hypoosmolality, which leads to water shifting into brain cells, causing cerebral swelling and potential CNS damage.
Common symptoms include:
- Nausea
- Malaise
- Headache
- Lethargy
- Confusion
- Delirium
- Seizures
- Respiratory arrest
Q: What are the goals of treatment for hyponatremia, and when should treatment be initiated?
A:
Goals of treatment:
- Raise plasma sodium concentration by restricting water intake and promoting water loss
- Raise serum sodium at a safe rate (no greater than 10–12 mEq/L in 24 hours) to avoid Central Pontine Myelinolysis
- Correct the underlying disorder
When to treat:
- Symptomatic with sodium <120 mEq/L
- Asymptomatic with sodium <110 mEq/L
HYPONATREMIA: TREATMENT
Q: What are the causes of hypernatremia?
A:
Causes of hypernatremia include:
- Loss of water:
* Fever
* Burns
* Infection
* Renal loss (e.g., diabetes insipidus)
* Gastrointestinal losses
- Retention of sodium secondary to the administration of hypertonic saline
Q: How is hypernatremia treated?
A:
Treatment includes:
- Correcting underlying causes such as medications, hyperglycemia, hypercalcemia, hypokalemia, or diarrhea
- Administering free water orally or intravenously (e.g., D5W)
* Plasma sodium should be lowered no more than 0.5 mEq/hr or 12 mEq/L in 24 hours
- If the patient is hypotensive (volume depletion), restore intravascular volume with 0.9% sodium chloride first to improve tissue perfusion
- For severe central diabetes insipidus, treat with Desmopressin (DDAVP), a synthetic ADH
Q: What factors impact potassium balance, and what are the normal ranges for plasma potassium?
A:
Factors affecting potassium balance:
- β2-Adrenergic stimulation: promotes cellular uptake of potassium
- Insulin: promotes cellular uptake of potassium
- Potassium intake or losses
Normal plasma potassium range:
- 3.5–5 mEq/L
Conditions:
- Hypokalemia: K⁺ < 3.5 mEq/L
- Hyperkalemia: K⁺ > 5 mEq/L
Q: What are the causes of hypokalemia?
A:
Causes of hypokalemia include:
- Gastrointestinal losses:
* Vomiting
* Diarrhea
* Medications (mainly laxative overuse)
- Increased urinary losses:
* Mineralocorticoid excess (aldosterone)
* Medications (loop/thiazide diuretics, aminoglycosides, amphotericin-B)
- Increased shift of potassium into cells:
* Alkalosis
* Insulin elevation
* β2 receptor stimulation (e.g., albuterol, dobutamine)
- Hypomagnesemia: Increases renal losses of potassium
Q: What are the signs and symptoms of hypokalemia?
A:
Signs and symptoms of hypokalemia include:
- Muscle weakness (especially in the lower extremities) and fatigue
* Progressive weakness and hypoventilation as severity increases
- Rhabdomyolysis
- Cardiac arrhythmias:
* Bradycardia
* Heart block
* Ventricular tachycardia
* Ventricular fibrillation
* Orthostatic hypotension
* Decreased cardiac contractility
- ECG changes:
* Flattened T waves
* Elevated U waves
- Digoxin toxicity: Increased arrhythmogenic potential with hypokalemia
Q: Why is it important to monitor potassium, magnesium, and calcium levels in patients on digoxin?
A:
- Potassium: Maintain serum potassium between 4.0 and 5.5 mmol/L to prevent hypokalemia, which increases the risk of digoxin toxicity, even with therapeutic serum digoxin levels.
- Magnesium: Normal serum magnesium levels are important as hypomagnesemia can predispose patients to digoxin toxicity.
- Calcium: Maintain normal serum calcium levels, as hypercalcemia can increase the risk of digitalis toxicity, while hypocalcemia can reduce digoxin efficacy.
Regular monitoring of these electrolytes is essential for preventing imbalances and adjusting digoxin dosage accordingly.
Q: What is the treatment for hypokalemia, and what are some important treatment considerations?
A:
Goals of therapy for hypokalemia:
- Correct potassium deficit
- Minimize ongoing potassium losses
- Prevent life-threatening complications
Treatment pearls:
- Oral potassium correction is safer if clinically appropriate
- Avoid dextrose-containing solutions as they can cause insulin release, leading to intracellular shift of potassium
- Potassium deficit can be estimated as 200–400 mEq of K⁺ for every 1 mEq/L reduction in plasma potassium
- K⁺ replacement is guided by potassium concentrations; recheck every 2–4 hours if K⁺ is < 3 mEq/L
- Hypomagnesemia may contribute to and worsen hypokalemia, so magnesium (Mg²⁺) should be checked and treated accordingly
Q: What are the causes of hyperkalemia?
A:
Causes of hyperkalemia include:
-
Reduced urinary excretion:
- Kidney dysfunction
- Intravascular volume depletion
- Hypoaldosteronism
-
Drugs:
- RAAS inhibitors (e.g., ACE inhibitors, ARBs)
- K⁺-sparing diuretics
- Trimethoprim, tacrolimus, cyclosporine, potassium supplements
-
Shift of K⁺ from ICF to ECF:
- Metabolic acidosis
- Digoxin overdose
- β-adrenergic blockade (including beta blockers)
- Succinylcholine
- Rewarming after hypothermia
Let me know if you’d like to dive into symptoms or treatment!
Q: What is the clinical presentation of hyperkalemia, and what is pseudohyperkalemia?
A:
Clinical presentation of hyperkalemia:
- May be asymptomatic
- Muscle weakness
- Abnormal cardiac conduction:
* Narrowed T waves and widening of the QRS
* Ventricular fibrillation
Pseudohyperkalemia:
- Consider if there is no apparent cause or symptoms of hyperkalemia
- K⁺ release from cells during blood specimen collection (often due to trauma during venipuncture or hemolysis)
- Measurement of serum rather than plasma K⁺ concentration, which can result from K⁺ release during coagulation
- Contamination of the blood specimen with K⁺-containing IV fluids or parenteral nutrition
Q: What are the goals of treatment for hyperkalemia, and how are therapy choices made?
A:
Goals of therapy for hyperkalemia:
- Reverse or prevent adverse cardiac effects
- Return serum and total-body potassium to normal
- Prevent life-threatening complications
Therapy choices are based on the severity of the presentation and the patient’s clinical condition:
- Severe hyperkalemia: K⁺ ≥ 6.5 mEq/L
* With ECG changes: K⁺ ≥ 6 mEq/L
- Moderate hyperkalemia: K⁺ 5–5.9 mEq/L
Immediate treatment is required for either severe or moderate hyperkalemia with ECG changes.
HYPERKALEMIA: TREATMENT
CHOICES
Q: How is calcium gluconate used in the treatment of hyperkalemia, and what are its important considerations?
A:
Calcium Gluconate
- Mechanism of action: Antagonizes the effects of hyperkalemia by affecting the threshold potential and the speed of impulse propagation at the cellular level
- Used to: Prevent hyperkalemia-induced arrhythmias, even in patients with normocalcemia
- Does not decrease plasma potassium levels
- Urgent use: Typically used while waiting for other treatments to lower plasma potassium
- Caution: Avoid in patients receiving digoxin, as hypercalcemia can precipitate digoxin toxicity, with some reports of sudden death
Q: How is insulin used in the treatment of hyperkalemia, and what are the important considerations?
A:
Insulin
- Mechanism of action: Accelerates the intracellular movement of potassium into muscle cells by binding to its receptor on skeletal muscle
- Dose:
* Regular insulin 10 units intravenously
* Plus 25–50 g of glucose as a 50% dextrose intravenous push to prevent hypoglycemia
* If the patient has hyperglycemia (~ >150-180 mg/dL), insulin alone can be administered
- Effect: Typically lowers plasma potassium by 0.5–1.5 mEq/L within 1 hour, and the effect may last for several hours
- Note: Insulin adsorbs to IV tubing, so flush IV tubing with 30 mL of insulin solution before administration to ensure accurate insulin concentration during delivery
Q: How is sodium bicarbonate used in the treatment of hyperkalemia, and what are the key considerations?
A:
Sodium Bicarbonate
- Mechanism of action: Shifts potassium intracellularly
- Dose:
* 50 mEq of intravenous sodium bicarbonate infused slowly over 5 minutes
* Can be repeated after 30 minutes if needed
- Efficacy:
* Debate exists regarding its effectiveness
* Not considered first-line treatment
* Least effective in patients with advanced kidney disease
* May be more effective in patients with underlying metabolic acidosis
- Effect: Can lower plasma potassium within 30–60 minutes, with effects lasting several hours
