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
