K Flashcards
potassium
-Most abundant intracellular cation
-Intracellular:Extracellular ~ 38:1
-Plasma concentration: 3.5-5mmol/L
-Intracellular concentraion: 150mmol/L
-Total body potassium: 3500-4500mmol
-Total Extracellular K+: 30-70 mmol
-Na+K+ATPase pump sets up membrane potentials and is key to neuromuscular function
-Increased by: higher intracellular Na
-Decreased by: Digoxin toxicity, CHF, CRF
basics of lab medicine involved with hyperkalemia
-sources of specimens:
-venous blood
-arterial blood
-urine
-“The result is only as good as the specimen provided”
-Location of the draw
-Avoid drawing from a limb with an IV
-If necessary, stop IV for 30 mins and draw venous blood distal to IV site
-Decrease risk of hemolysis!!
-Use as large bore needle as possible- Limitations
-Recognizing a suboptimal blood draw
potassium: GI
-10% of K excretion
-Average Western diet 40-120mmol/day
-90% of K+ consumed is absorbed
-GI loss of potassium(10%) increased in:
-renal failure -> up to 50-60%
-diarrhea with large volume
-oral intake -> GI absorp -> extra-renal adaption -> renal loss = K balance
potassium: muscle
-muscles hold a large amount of K
-rhabdomyolysis -> huge release of K
-crush injury trauma -> release K
potassium: renal excretion
-90% of K is excreted via kidney (10% colon)
-Assuming a typical 100mmol intake and normal renal function:
-Filtered K+ = GFR x [K+serum] = 100 x 4 = 400mmol
-Passive reabsorption in the proximal convoluted tubule and Loop of Henle = 90%
-Active secretion in distal convoluted tubule and the cortical collecting duct by Principal cells
-Secretion/reabsorption is increased or decreased based on potassium concentrations and aldosterone!
potassium balance: renal
-aldosterone - increase K secretion
-hyperkalemia - increase K secretion
-distal urinary flow - enhance K excretion
-hypokalemia - reabsorption K increased
hyperkalemia causes
-sample error- asymptomatic pt -> redraw
-potassium shift
-decreased excretion
-excessive K intake
hyperkalemia: etiology K shift
-Rhabdomyolysis- crush injury
-Hemolysis
-Burns
-Strenuous exercise
-Sepsis
-Hypertonicity-K follows the flow
-Insulin deficiency
-Metabolic acidosis-Will be covered in acid-base lecture
-Pharmaceuticals:
-Digoxin
-Beta-antagonists
-Succinylcholine
-arginine
effects of exercise on K
-easy walking pace- +0.4 plasma elevation
-moderate exercise- +0.7
-strenuous exercise- + 2.0
-with beta blocker- + up to 4
-exercise effect will decrease with training
-dont memorize numbers
-beta blocker increases K by blocking it from going back into the cell
-cardiac rehab is needed for pts with prior MI and taking a beta blocker
hyperkalemia: decreased excretion
-Renal failure
-Interstitial nephritis
-Sickle cell disease
-Hypoaldosteronism
-Type IV RTA
-Diabetic nephropathy
-Heparin
-End stage AIDS
-Adrenal insufficency
-Pharmaceuticals
-ACE inhibitors
-Trimethoprim
-NSAIDs
-Spironolactone
-Triamterene
-pentamadine
hyperkalemia: etiology excessive intake
-ingestion
-iatrogenic*- most dangerous tool you will have may often be ur pen
-accidently overprescribe K
hyperkalemia symptoms
-None
-Weakness
-Palpitations
-Constipation
-Normal exam
-Pulse Irregular rhythm
-Decreased/absent bowel sounds
-Muscle weakness
hyperkalemia dx and labs
-Hyperkalemia is made by getting the result from the lab = >5mmol/L
-Associated labs/tests:
-BUN/Creatinine
-Serum glucose
-EKG!!!!!
-Urine: Potassium and creatinine
hyperkalemia EKG
-peaked T waves
hyperkalemia fraction
-Fractional excretion of potassium(FEK)
urine K/serum K
—————————- x 100%
urine cre/serum cre
-FEK < 10% = renal cause
-FEK > 10% = extrarenal cause
transtubular potassium gradient
-Trans-tubular potassium gradient
Urine potassium x serum osmolarity —————————————————-
Serum potassium x urine osmolarity
-Gradient < 6-8 indicates renal cause
-Gradient > 8 indicates extrarenal cause
-Caveat: Chronic renal failure can have > 8
hyperkalemia tx
-Ultimately, finding the cause and correcting the cause or compensating for it is the long term goal!
-ex. hyperaldosteronism state -> no cure -> try to compensate
-However, QUICK correction of potassium abnormality is needed due to its importance in action potentiation (cardiac)
-If hyperkalemia is suspected, do not delay treatment to find the cause
acute treatment hyperkalemia
-1st option- calcium gluconate- does not fix K at all…it stabilizes membranes and prevents cardiac affect -> immediate to 2 hours
-now that it is stable -> you want to move K out of blood so you can use:
-glucose and insulin- shift K into cell -> mins- 3-4 hours
-albuterol nebulized (beta 2 agonist)- shift K into cell -> mins-1-2 hours
-albuterol is going to increase HR -> give benzo with it to calm the pt
-now we want to get rid of K:
-diuretics (furosemide)- removal renal - lasts 6 hours
-kayexalate (sodium polystyrene sulfonate)- GI tract loss (via fluid loss) -> several hours
-if pt is in renal failure/acid base disorder/tx didnt work:
-hemodialysis- remove through artificial filtration -> as needed
hyperkalemia chronic tx
-Dietary restriction
-Removal of iatrogenic causes
-Loop diuretics
-Treatment of the route cause
-Fludrocortisone in hyporeninemic hypoaldosteronism
hypokalemia
-Renal potassium loss
-Potassium shift favoring intracellular
-Decreased potassium intake
-Typically coupled with another cause
-Extrarenal potassium loss
-Sample error
hypokalemia- etiology renal potassium loss
-Inc. aldosterone effect*
-Hyperaldosteronism
-Renovascular HTN
-Cushing’s syndrome
-german Licorice
-Congenital anomaly
-11beta or 17alpha hydroxylase deficiency
-Inc. flow at distal nephron
-Diuretics(furosemide or thiazide diuretics)
-Hypomagnesemia
-Renal Tubular Acidosis
-Fanconi syndrome
-Interstitial nephritis
-Metabolic alkalosis
-Genetic Disorders (study this)
-Bartter’s syndrome
-Liddle’s syndrome
hypokalemia- etiology K shift into cells
-Insulin excess (maybe during DKA tx)
-Postprandial
-Iatrogenic cause
-Alkalosis(Respiratory or Metabolic)
-Beta-adrenergic excesses
-Hypokalemic periodic paralysis
hypokalemia- etiology extrarenal loss
-Vomiting and/or diarrhea
-Villous adenoma
-Zollinger-Ellison syndrome
hypokalemia S&S
-Symptoms
-None
-Muscle cramps
-Fatigue
-Weakness
-Constipation
-Blood pressure
-Inc with aldosteronism
-Dec with Gitelmans
-Dec with diuretic abuse
-Irregular heart rates
-Paralysis
-Decreased bowel sounds
hypokalemia dx and lab
-Diagnosis is made by obtaining a lab result finding of K <3.5 mmol/L
-Other tests to aid in dx and tx
-BUN/Creatinine
-Glucose
-Magnesium
-EKG
-ABG
-24 hour urine potassium
hypokalemia ekg
-can cause cardiac arrest
hypokalemia- urinalysis
-24 hour urine
-<30 mmol = extrarenal cause
->30 mmol = renal cause
-Using Transtubular potassium gradient
-<2 = nonrenal cause
->3 = renal cause
bartter’s syndrome
-Hypokalemia
-Increased urine output
-Normal renal function
-Increased urine ions:
-Calcium
-Potassium
-Sodium
-Magnesium
-Chloride
gitelmans syndrome
-Hypokalemia
-Normal urine output
-Normal renal function
-Increased urine ions:
-Potassium
-Sodium
-Magnesium
-Chloride
-Dec’d urine calcium
hypokalemia tx
-If patient is stable, focus on treating the underlying cause
-Evaluate diet for intake
-Evaluate medications that waste K
-Potassium replacement
-if pt not improving and Mg is low! -> magnesium replacement !
hypokalemia tx K replacement
-Candidate for potassium replacement
-Hypokalemia
-Patient unable or unwilling to eat low Na diet
-Patient with nausea, vomiting, diarrhea
-Patient unable to stop diuretic or laxative
-Patient with drug-related hypokalemia
hypokalemia tx potassium replacement
-Regardless of deficit, 40-100mmol/day is typically effective
-Oral replacement is preferred if an option (avoids overshooting)
-If IV is only option (vomiting):
-Rate and site of IV is most important
-Potassium should be suspended in saline (if you give with dextrose…stimulates insulin…pushing K into cell)
-Cannot give faster than 40mmol/hr (faster causes arrest)
-20-40mmol/hr requires cardiac monitoring
-K is irritating to venous structures
hypokalemia tx Mg replacement
-Consider magnesium deficiency in cases of hypokalemia refractive to treatment and:
-CHF
-Digoxin toxicity
-Chemo:Cisplatin
-Loop Diuretics
hypokalemia tx follow up
-In emergency situations:
-Check the electrolytes every 1-2 hours or as conditions change
-In stable situations:
-Check 4-6 hours after treatment as conditions change
-Then check daily, or if conditions change
-In Outpatient setting:
-Often will check weekly until stable then monthly or quarterly depending on patient compliance
