electrolytes Flashcards
Hypernatremia
Na > 145 mEq/L
Causes
- excess sodium intake
- not enough water intake
- too much water loss
- 66666Disease: diabetes insipidus, primary hyperaldosteronism, Cushing, diabetes666666
Manifestations
-With low ECF: symptoms of low ECF as well as thirst,
changes in mental status
possible seizures and coma
-With normal or high ECF: twitching, weight gain, edema, flushed skin
Hyponatremia
NA <136 mEq/L
Causes:
- sodium loss due to GI, Renal losees, or skin losses
- not enogh sodium intake
- too much water
- 6666Disease: SIADH, heart failure, primary hypoaldosteronism, cirrhosis6666
Manifestations
- mild: headache, irritability, difficulty concentrating
- severe: confusion, vomitting, seizures, coma
How to deal with hyponatremia from fluid loss
replace fluid with isotonic sodium solution
encourage oral intake
withold diuretics
how to deal with hyponatremia from water excess
fluid restriction
possibly loop diuretics and demeclocycline
acute hyponatremia allows for small amts of IV hypertonic saline solution
vasopressor receptor antagonists if can’t deal with fluid restriction (vaprisol from water excess and samsca for SIADH or heart failure)
IMportant not to corret faster than 6-12 mEq/l per hour during first day to avoid demyelination syndrome
how to deal with hypernatremia in primary water defecit
replace fluid orally or with isotonic IV
how to deal with hypernatremia from excess sodium
how fast?
dilute with sodium free IVS (5% dextrose in water)
diuretics
restrict sodium intake
Should not decrease by more than 8-15 mEq/L in 8 hrs to avoid cerebral edema
Potassium -where is it? why is it important? -where do we get it? -how do we lose it?
- 98% of body potassium is in cells (sodium potassium pump)
- regulates membrane potential of nerve and muscle cells. Also regulates osmolality and cell growth. Also needed for glycogen deposit. Also acid-base balance
- diet (also IVs, transfusions, meds)
- kidneys lose 90% of K intake (inverse relationship bt Na and K reabsorption)
Hyperkalemia causes
K > 5 mEq/L
Excess K intake
Shift of potassium out of cells
- acidosis
- tissue catabolism
- intense exercise
- tumor lysis syndrome
Failure to eliminate K
- renal disease ——————-> most common
- adrenal insufficiency
- Meds: Angio II blockers, ACE inhibitors, heparin, K sparing diuretics, NSAIDs
Hyperkalemia manifestations
Dysrhythmias Fatigue, confusion Tetany, muscle cramps Weak or paralyzed skeletal muscles Abdominal cramping or diarrhea
Hyperkalemia ECG changes
- Tall peaked T wave
- prolonged PR interval
- ST segment depression
- widening QRS
- loss of P wave
- Ventricular fibrillation
- ventricular standstill
How to deal with hyperkalemia (Don’t really need to know this slide)
-stop potassium intake
Increase secretions
-loop or thiazide diuretics, dialysis, patiromer (Veltassa), Kayexalate
Force K from ECF to ICF
- use IV with dextrose insulin and B-adrenergic agonists (stimulates Na/K pump)
- can use IV sodium bicarb if patient is acidotic
Stabilize cardiac membranes
-IV CaCl2 or calcium gluconate (doesn’t lower K but reverses toxic effects on heart cell membrane –> protects from dysrhthmias
Monitor ECG and BP (Ca causes decrease)
Monitor for hypoglycemia if giving insulin
Veltassa and Kayexalate
Kayexalate binds K in bowel –> each gram removes 1 mEq of K
Veltassa does same thing, but takes hours to days and is used in chronic cases –> careful! It also binds to other drugs
Hypokalemia causes
K <3.5 mEq/L
K loss
-GI, Renal (hyperaldosteronism), skin (diaphoresis), dialysis
Shift of K into cells
- increased insulin release
- insulin therapy
- alkalosis
- increased epinephrine from stress
Lack of K intake
Renal loss from diuresis
Hypokalemia clinical manifestations
-Cardiac most serious Skeletal muscle weakness (legs) Weakness of respiratory muscles Decreased GI motility Hyperglycemia
-hyperglycemia (from impaired insulin secretion)
Hypokalemia ECG changes
- flattened T wave
- U wave
- ST segment depression
- prolonged QRS
- peaked P
- ventricular dysrhythmias
- first and second degree heart block
How to deal with Hypokalemia
-increase K intake via food, oral KCl supplements, or IV KCl
IV infusion shouldn’t be more than 10 mEq/hr unless critical and constant ECG monitor –> USE infusion pump –> careful! it irritates skin!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
only give KCL if urine is 0.5 ml/kg body weight per hr
Monitor for digitalis toxisity (confusion, lazy, GI issues, nausea, bad appetite, blurry vision)
don’t eat a bunch of licorish
Calcium
- why’s it important?
- what is needed for its absorbance?
- where is it?
- serum Ca levels reflect what?
- hormones that affect serum Ca levels?
- bones, blood clotting, nerve impulses, muscle contraction
- vit D
- 99% in bones –> of the rest, 50% bound to plasma prots, 40% free, and the rest is bound to ions
- all forms of plasma ca (including bound to albumin)
- PTH moves Ca out of bones, causes GI and kidneys to retain it
- calcitonin does the exact opposite
Hypercalcemia causes
Ca> 10.5 mg/dL (2.62 mmol/L)
hyperparathyroidism
cancer
Acidosis
Hypercalcemia manifestations
Fatigue, lethargy, weakness, confusion Hallucinations, seizures, coma Dysrhythmias Bone pain, fractures, nephrolithiasis Polyuria, dehydration
Hypercalcemia ECG (IGNORE)
short ST
short QT
ventricular dysrhythmias
increased digitalis effect
How to deal with Hypercalcemia (Only kinda relevant)
- stop taking meds related to hypercalcemia
- lower Ca intake
- weight bearing exercise
- maintain hydration 3000-4000 mL fluid per day (esp cranberry or prune juice) to avoid kidney stones
If severe:
- IV isotonic saline (beware fluid overload if kidneys cant excrete Na)
- bisphosphonate (interfere with osteoclasts, but takes 2-4 days
- calcitonin (quick Ca excretion, but temporary and risks tachycardia)
- denosumab (Prolia)
Hypocalcemia causes
Ca < 9 mg/dL (2.25 mmol/L)
Low serum Ca levels caused by Decreased production of PTH Multiple blood transfusions - discuss Alkalosis Increased calcium loss
tumor lysis syndrome
chronic alcohol use
Alkalosis
Excess citrated blood
Hypocalcemia manifestations
Positive Trousseau’s or Chvostek’s sign Laryngeal stridor Dysphagia Numbness and tingling around the mouth or in the extremities Dysrhythmias
hypocalcemia ECG (IGNORE)
elongation of ST
prolonged QT interval
ventricular tachycardia
How to deal with hypocalcemia
- eat more calcium and vit D and/or have supplements
- IV calcium glutonate
- breathe into paper bag to retain CO2 for muscle spasms or tetany
- quit loop diuretics –> change to thiazide diuretics
- make sure parathyroid gland isn’t damaged
- make sure they’re not anxious
Phosphorus
where?
what’s it for?
what regulates it?
- most in bones as CaPO4; the rest metabollically active as salts
- helps muscles, RBCs, and nerv syst to func –> acid-base buffer, ATP formation, glucose uptake, carb/prot/fat metabolism
- PTH and kidneys –> if PTH low, kidneys reabsorb more —> reciprocal relationship bt phosphate and calcium
Hyperphosphatemia causes
PO4 > 4.5 mg/dl (1.45 mmol/L)
Acute kidney injury or chronic kidney disease
Excess intake of phosphate or vitamin D
Hypoparathyroidism
Hyperphosphatemia manifestations
Tetany, muscle cramps, paresthesias, hypotension, dysrhythmias, seizures (hypocalcemia)
Calcified deposition in soft tissue such as joints, arteries, skin, kidneys, and corneas (cause organ dysfunction)
How to deal with hyperphosphatemia
restrict phosphorus foods
phosphate binding agents (CaCo3) limits abosorbtion and increases secretion
If serious
-hemodialysis
loop diuretics to increase secretion
Almost always happens with low Ca, so watch out for that
Hypophosphotemia causes
PO4 < 3 mg/dL (0.97 mmol/L)
Malnourishment/malabsorption
Diarrhea
Use of phosphate-binding antacids
Inadequate replacement during parenteral nutrition
Hypophosphatemia manifestations
CNS depression
Muscle weakness and pain
Respiratory and heart failure
Rickets and osteomalacia
Most of these due to low cellular energy and O2 delivery
Chronic hypophosphatemia alters bone metabolism
How to deal with hypophosphatemia
eat more phosphorus and dairy or take supplements
-dairy supplements are better bc they won’t fuck up GI
If serious
- IV sodium phosphate or potassium phosphate
- watch for hypocalcemia, hyperkalemia, hypotension, dysrhythmias
Monitor serum calcium and phosphorus levels every 6 to 12 hours
Magensium abundance? what's it for? where's it stored? what regulates it?
- 2nd most abundant intracellular cation
- cofactor in enzyme systs (carb metabolism, DNA snth, blood glucose contr, BP regulation) —> ATP production, muscle contraction, neurologic func
- 50-60% in muscle/bone; 30% in cells; 1% ECF
- Kidneys and GI syst regulate through ascending loop and distal tubules
Hypermagnesemia causes
Mg > 2.1 mEq/L (1.05 mmol/L)
Increased intake of products containing magnesium when renal insufficiency or failure is present
Excess IV magnesium administration
Hypermagnesemia manifestations
Inhibits acytylcholine at myoneural junc and Ca movement into cells
Hypotension, facial flushing Lethargy Nausea and vomiting Impaired deep tendon reflexes Muscle paralysis Respiratory and cardiac arrest
super severe: paralysis, coma, respiratory/cardiac arrest
How to deal with Hypermagnesemia
- avoid Mg drugs and limit intake
- more fluids and diuretics if kidneys are ok
- dialysis if kidneys aren’t ok
If serious
-IV calcium gluconate or CaCl to help cardiac muscles
Hypomagnesemia causes
Mg <1.3 mEq/L (0.65 mmol/L)
Prolonged fasting or starvation Chronic alcoholism Fluid loss from GI tract Prolonged parenteral nutrition without supplementation Diuretics, proton-pump inhibitors Hyperglycemic osmotic diuresis
Hypomagnesemia manifestations
Resembles hypocalcemia
Muscle cramps, tremors Hyperactive deep tendon reflexes Chvostek’s and Trousseau’s signs Confusion, vertigo, seizures Dysrhythmias
How to deal with Hypomagnesemia
oral supplements and increased dietary intake
If severe or hypocalcemia
- IV magnesium
- CAREFUL: rapid infusion can lead to hypotension or cardiac/respiratory arrest
