Electrolytes Flashcards
Isotonic contraction
Equal sodium and water loss Vomiting. diarrhea Kidney disease, diuretics Cholera Replace with NS
Normal Na+ and osmolality
135-145 mEq/L
280-300 mOsm/kg
Hypertonic contraction
More water than Na+ loss.
Extracellular hypertonicity draws water out of cells, partially compensating for loss of volume
Sweating, excessively concentrated baby food, burns, unable to respond to thirst
Hypertonic contraction tx with hypotonic saline
Replace 50% of volume in first few hours, rest over 1-2 days
Hypotonic contraction
More Na+ than water loss
Volume and osmolality of ECF are reduced, which moves ECF into cells.
Usually from excess Na+ lost through kidneys from insufficiency, hypoaldosteronism, diuretics.
Hypervolemic hyponatremic volume expansion
Vasopressin antagonist (conivaptan, tolvaptan)
Acid-base status regulation
Bicarb-carbonic acid buffer
Respiratory system
Kidneys
Acid base
CO2 represents volatile carbonic acid, exhalation of CO2 tends to elevate pH (reduce acidity)
Kidneys raise pH by retaining bicarb or lower by excreting
Respiratory alkalosis
Hyperventilation blows off too much Co2 which lowers pCO2 and increases pH.
Tx by rebreathing CO2, giving 5% CO2 or giving a sedative
Respiratory acidosis
CO2 retention from hypoventilation which raises pCO2 causing pH to fall. Hypoventilation or air trapping.
Metabolic Alkalosis
Increase in pH and bicarb. Vomiting, suctioning, alkalinizing salts.
Body corrects with hypoventilation and increased renal bicarb excretion.
Sodium chloride plus potassium chloride facilitates renal excretion of bicarb and promotes normalization of plasma pH.
Metabolic Acidosis
Chronic renal failure, diarrhea, lactic acidosis or ketoacidosis. Methanol, ASA.
Bicarb
Intracellular K+
150mEq/L.
Most abundant intracellular cation.
Extracellular 4-5mEq/L
Nerve impulses and acid/base balance
Potassium regulation
Excretion increased by aldosterone which increases Na+ reabsorption
Hypokalemia
Less than 3.5 mEq/L
Thiazide or loop diuretic
Insufficient intake, alkalosis, excessive insulin, excess aldosterone, vomiting, diarrhea and laxatives can all cause hypokalemia.
Weakness, paralysis, dysrhythmias, intestinal dilation and ileus.
Principal cause of dig tox
Risk of HTN and stroke
HypoK+ TX
Potassium Chloride preferred as chloride deficiency goes with hypoK
Oral may upset GI tract
Take with meals to decrease chance of localized hyper K resulting in severe intestinal injury.
Potassium IV dilution
40mEq/L or less
Monitor ECG changes
HyperK+ causes
Severe tissue trauma, addison’s disease, acute acidosis, acute renal failure, misuses of K+ sparing diuretics, OD with IV K+
Kayexalate, kionex
An exchange resin that absorbs potassium
Mag needed for
Activity of many enzymes and binding of mRNA to ribosomes.
Also neurochemical transmission and muscle excitability
40 mEq/L intracellularly
2mEq/L extra
Hypomag causes and consequence
Diarrhea, hemodialysis, kidney disease, prolonged IV feeding with mag free solutions, ETOH abuse, diabetes, pancreatitis.
Often goes with hypocalcemia and hypokalemia
Hypomag symptoms
Ach at NMJ is enhances, increasing muscle excitability to the point of tetany.
Increases excitability of neurons causing disorentation, psychoses and seizures
May cause calcium stones in nephrons
Excess mag
Neuromuscular blockade resulting in paralysis of resp muscles (12-15 mEq/L, at 25 cardiac arrest).
Can intensify effects of NMBAs and can be countered with calcium
Contraindicated with heart blocks as it may suppres AV impulse conduction
Symptoms of excess mag
Muscle weakness from inhibition of Ach, hypotension, sedation, ECG changes.
HyperK causes
K+ sparing diuretics ACE inhibitors NSAIDS Renal Rhabdo Acidosis (renal, diarrhea, DKA, ASA) Hemolysis Diet ADdisons
Hyper K presentation
Cardiac N/V Diarrhea Muscular weakness Dysrhythmias
Tented T waves
5.5-6
Normal K+
3.5-5
PR/QT prolongation K+
6-6.5
6.5-7 K+
Flat P/ST segment
7-7.5 K+
QRS widening
ST merging K+
7.5-8 mEq
Sine wave/IVR K+
8-10
> 10 K+
VT/VF
TX for mild hyper K (5-6mEq)
Lasix 1mg/kg SIVP
Kayexalate
Dialysis
Moderate hyper K TX (6-7)
Bicarb 50mEq over 5 minutes
Glucose + slin 50g D50 plus 10 IU regular insulin over 15-30 minutes
Ventol 15mg over 15 minutes
K+ TX over 7 (severe)
10mL of 10% solution over 10 minutes (1g)
8-16mg/kg no faster than 100mg/min
Bicarb
Plasma buffering bicarb formulation
HCO3+ + H+ = H2CO3 = H2O + CO2
Pharmacokinetics of bicarb
8.4 solution (4.2 in Peds)
1mmol Na+ and 1mmol HCO3 per mL
pH = 7.8
Bicarb uses
Prolonged cardiac arrest
Hyper K
Metabolic acidosis
Cocaine, TCA, ASA OD
Adverse effects/contras of bicarb
Alkalosis, hypernatremia, extravasation causes significant damage
Contras are arrest without a tube, hypernatremia, alkalosis
Precautions of bicarb
Monitor labs Hypocalcemia (tetany) Excessive chloride loss from vomiting or GI suction Hypokalemia Renal or heart failure
Bicarb doses
Arrest and OD 1mEq/kg SIVP
Repeat the dose once for OD
HyperK 50 mEq
Kayexolate
Sodium Polystyrene Sulfonate
Class is cation-exchange resin
Kayexolate MOA
Cation exchange system in GI tract is utilized, it donates Na+ ion which causes K+ excretion in GI tract where kayexolate binds to K+ to remove through GI
Adverse effects of kayexolate
Fecal impaction constipation
N/V
Lyte issues
Colonic necrosis
Kayexolate dose
15G PO 1-4X daily, can be given rectally
Manifestations of hypoK
Muscle fatigue, flaccid paralysis, mental confusion, increased urinary output, shallow resps, dysrhytmias
HypoK ECG
U waves
T wave flattening
ST segment changes
PEA/asystole
KCl dose
10-20 mEq/hr in non emergent
2 mEq/min for 10 minutes in emerg
Causes of hyper Na+
Sweating, osmotic diuresis, DI, burns, CNS disorders (thirst) dehydration, diet, hypertonic saline
Manifestations of hyperNa
Thirst, HTN, edema, agitation, convulsions
TX hyperNA
Hypotonic fluids (D5W) Do gradually
Total body water =
Half of weight in KG
Water deficit (L)
((Plasma Na+conc-140)/140) X TBW
Causes of hypoNa
Thiazide diuretics Renal failure Vomiting/diarrhea with water intake Addison CHF Cirrhosis Diet
Manifestations of hypoNa
Muscle weakness
Dizzy, confusion, stupor coma, headache
Hypotension, tachycardia
Tx hypoNa
Hypertonic saline (3%) slowly to prevent pontine myelinolysis
Na+ deficit =
(desired Na+ - current Na+) X 0.6 X bodyweight (kg)
Divide Na deficit by concentration of Na (513 mEq/L) to determine amount delivered
Normal mag
1.5-2. >2 is hypermag
ECG changes in ghyper mag
Increased PR/QT intervals Increased QRS duration Decreased P wave voltage Peaked Ts AV blocks Asystole
Manifestations of hyper mag
Hypotension, muscle weakness and paralysis
Decreased reflexes
N/V
Altered LOC
TX of hyper mag
Calcium as serum levels are controlled by same mechanisms as Mag
Calcium antagonizes effect of mag and K+ at cell membrane
Dialysis, saline and lasix also
Calcium dose hyper mag
10mL of 10% solution of 10 minutes
Hypomag
GI loss, malnutrtion Renal disease Diuretics, dig, ETOH Hypothermia Hypercalcemia DKA Thyroid either way Hypophostate Burns, sepsis, lactation
Hypomag manifestations
Weakness, irritability, tetany, paresthesia, delirium, confusion, convulsions, anorexia, N/V, dysrhythmias
ECG of hypo mag
Prolonged QT/PR intervals ST depression T wave inversion P wave flattening or inversion Wide QRS torsades, v-fib
TX of hypo mag
Mag 2g in 50mL of 10 minutes
CaCl may be used as hypocalcemia is common in hypo mag, or KCl as hypokalemia is common with hypomag
Hypercalcemia
Normal range is 2.1-2.6 mmol/L
Total 9-10.5 mg/dL
Causes of hypercalc
Hyperparathyroid
Malignancy
Vit D disorders
Bone disorders
Hypercalc ECG
Short QT Long PR/QRS with increases QRS voltage T wave flattening/widening QRS notching AV block
Manifestations of hypercalc
Lethargy, weakness, anorexia, N/V, polyuria, pruritis, bone pain, depression, confusion stupid coma
Paresthesia
TX hypercalcemia
IV NS for diuresis
Dialysis for CHF/renal
Agents that reduce bone reabsorption (calcitonon, glucocorticoids)
Hypocalcemia
Below 2.1mmol/L
Hypocalc causes
Hypoparathyroid Hypomag Hypermag Vit D deficit Alkalosis
ECG changes hypocalc
QT prolongation
T wave inversion
Heart blocks
V fib
Manifestations of hypocalc
Increased reflexes Muscle cramps, spasms Paresthesia Tetany Bone fracture
TC of hypocalc
CaCl 10mL 10% over 10 minutes
Mag, K+ and pH must be treated too
Calcium chloride
Electrolyte
MOA contraction of muscle via actin myosin
Depol of slow channels via influx during stage 0
regulation of neuronal transmission
Pharmacokinetics of CaCl
Half bound to albumin
Half ionized (active)
Alkalosis increases albumin binding
CaCl uses
Hypocalc
Hypermag
HyperK
BB or CCB OD
Contras to CaCl
Hypercalcemia
Dig tox
Precautions
Dedicated line (preciptate formation) IV only, extravastion will fuck your shit up
Dose of CaCl
Arrest 1g SIVP Q 10 one time
OD 500mg in 50mL over 10 minutes repeat X1