Tins lyte abnormalaties Flashcards
Substances that contribute most to osmotic pressure in ECG
Na+, HCO3-, CL- and glucose
Formulation to calculate effective osmolality (tonicity)
2XNA+ + glucose/18 (range 275-290mOsm/L)
Fluid percentages
TBW 60%
ICF 40%
ECF 20% of which 15% IF and 5% IVF
IF = interstitial fluid (extravascular) and IVF is intravascular
Hyponatremia definition
Serum Na+ <138 mEq/L
Symptomatic at 135
Epidemiology of hyponatremia
Mild is common (15-30%) but only 4% have sodium below 130mEq/L
50% of cases are iatrogenic
Hyperosmolar hyponatremia
> 295 mOsm/kg H2O
common in hyperglycemia, each 100mg/dL in plasma glucose above normal (100mg/dL) drops serum Na+ by 1.6 mEq
Iso-osmolar hyponatremia
275-295 mOsm/kg
Severe hyperproteinemia or hyperlipidemia causes displacement of serum water (some labs use instruments to avoid this lab error)
MDMA hyponatremia
Induces inappropriate secretion of ADH and causes increased gut water reabsorption
Clinical features of hyponatremia
Moderately severe start at 130mEq/L
Headache, nausea, disorientation, confusion, agitation, ataxia and areflexia
Severe ate 120mEq/L Intractable vomiting, seizures, coma, resp arrest from brainstem herniation
Post exercise hyponatremia
From too much solute free fluid. Check for bloating, nausea, vomiting and edema at wrists and fingers
Osmotic Demyelination Syndrome
Rapid correction of hyponatremia (<12 mEq/L/24h) as water moves from cells to ECF (intracellular dehydration)
Symptoms are dysarthia, dysphagia, lethargy, parapereis or quadriparesis, seizurescomadeath
Hypernatremia definition
Na+ > 145mEq/L AND hyperosmolality (>295 mOsm/L)
Patho hypernatremia
Deficit in TBW or less commonly net gain of Na+
Needs a limit of sense of thirst, availability of water, kindeys ability to concentrate urine
May cause intracranial hemorrhage if too quick
Severity of symptoms based on onset (fast onset = worse symptoms like hyponatremia)
Hypovolemic hypernatremia
Decreased TBW and total body Na+ with a relatively greater decrease in TBW)
Hypervolemic hypernatremia
Increased total Na+ with normal or increased TBW
Normovolemic hypernatremia
Normal sodium with decreased TBW
Clinical features of hypernatremia
Nausea, vomiting, lethargy, weakness, increased thirst, low water intake, salt intake, polyuria (greater than 3000mL/hr of urine/24h)
Hypernatremia predisposing risk factors
Beeties, hypercalcemia hypokalemia, lactulose, loop diuretics, lithium, demeclocycline or NSAIDS (interstitial nephritis)
Hypernatremia physical exam
Hypotension, tachycardia, orthostatic pressure, sunken eyes, dry mucous membranes, altered mental status, poor skin turgor, edema in hypervolemic hypernatremia
Cushings syndrome - moon face, fatty deposits
TX hypernatremia
Tx volume deficits first then cause (diabetes insipidus) vomiting diarrhea fever then free water deficit
Diabetes insipidus
Ability of kidney to reabsorb free water is compromised
Neurogenic due to inadequate ADH
Nephrogenic from renal causes (v2R receptors don’t respond properly to ADH)
Diabetes insipidus characterized by
polyuria, polydipsia, increased volume of hypo-osmolar urine
Normal K+
98% intracellular, 75% in muscles
150mEq/L intracellular
3.5-5 mEq/L extracellular
K+ in the kidneys
Filtered freely through renal glomerulus then reabsorbed in proximal and ascending tubules, secreted in distal tubule in exchange for Na+
Things that cause K+ shift
Surgical stress, trauma, burns, acid-base imbalance, catabolic states, increased extracellular osmolality, insulin deficiency
(possible to have hyperk+ with reduced TB K+ and other way around)
K+ and pH
K+ rises 0.6mEq/L for every 0.1 decrease in PH and vice versa through H+ and K+ exchange
HypoK+ definition
Serum <3.5mEq/L
Common are fasting, eating disorders, ETOH abuse, alkolosis, insulin, B2-agonists, hypokalemia periodic paralysis
Vomiting, nasogastric suction, diarrhea
Diuretics, hyperaldosteronism, osmotic diuresis, toxins
HypoK+ manifestations
Effect every system
Makes resting membrane more electronegative, enhancing depol and delays repol
Prolonged QT, flattened T waves, appearance of U waves
Starts at <2.5mEq/L usually
Arrythmias of hypoK+
A fib, torsades, v tach and v fib
HyperK definition
> 5.5 mEq/L
Diuretics that cause hypoK
Carbonic anhydrase inhibitors, loop diuretics, thiazide-like diuretics)
Alkalosis is another common cause
Excessive Chaw, licorice, hyperaldosteronism can also cause it
Same with heavy sweat, heat stroke, fever, hypomagensia, leukemia, hypothermia
Causes of pseudo hyperK
Tourniquet use, hemolysis, leukocytosis, thrombocytosis
Intra to extracellular shifts causing hyperK
Acidosis, exercise, B-blockade, insulin deficiency, dig
HyperK diuretics
Renal failure is a common cause of hyper K+
Potassium-sparing diuretics, b-blockade, NSAIDS, ACE inhibitors and Angio II blockers
Aldosterone deficiency
HyperK in da heart
Less electronegative resting membrane, partial depol which reduces activation of voltage-dependent sodium channels. Slower and reduced amplitude of action potential
Calcium antagonizes effects of hyperK by raising threshold potential and restoring membrane potential
ECG changes in hyper K
Long PRI, peaked T waves, short QT, flattening of P wave, QRS widening and eventuall QRS degradation into sinusoidal pattern
Three tx modalities for hyper K
Membrane stabilization
Intracellular shift of K+
Removal/excretion
All three sequentially in rapid succession as they have different onset and duration
Treat pH if acidy, if not acidy the shift won’t work as well
Dougs that block renal excretion of K+
ACE inhibitors, Angio II receptor blockers, K+sparing diuretics and NSAIDS
Magnesium
total body 24 grams or 2000 mEq
50-70% fixed in bone and only slowly exchangable, rest is mostly ICF (second most abundant intracellular cation)
Normal Mg2+
1.5-2.5mEq/L
Major causes of hypomagnesia
ETOH, malnutrition, cirrhosis, pancreatitis, excessive GI fluid losses
TX of DKA w/o mag (especially if malnourished) can cause this
Hypomagnesia presentation
If normal calcium, hyperreflxia, tremor, tetany or convulsions
Tetany
Intermittent muscular spasms
Hyperalimentation
IV nutrients
Chvostek sign
Hypocalcemia typically, but possible in respiratory alkalosis or hypomagnesemia
Tapping infront of tragus or at angle of jaw will illicit a facial spasm (stimulating facial nerve cause a facial nerve spasm)
Trousseau sign
Flexion of the wrist and fingers after a BP cuff is inflated past systolic and remains there for 3 mins. Indicates hypocalcemia (sensitivity 94%) also could be hypomagnesia
ECG changes in hypomagnesemia
Similar to hypokalemia and or hypocalcemia
Hypomagensemia may be secondary to hypoalbuminemia
