Hypokalamia/Hyperkalemia Flashcards
potassium predominantes in what fluid compartment?
- most common cation in the ICF (whereas sodium is the most common cation in the in the ECF)
what is the effect of insulin on [K+] in the ICF/ECF?
insulin directly pumps K+ into cells, maintaining the high intracellular [K+]. this in turn stimulates the Na+/H+ antirpoter, promoting H+ secretion
which patients should regularly have their potassium checked?
- patients with cardiac disease
- both hypo/hyper - kalemia could have significant effects on cardiac conduction
- K+ levels are critically important in patients with an MI, dysthrythmias, or receiving digoxin therapy
- patients receiving drugs that may effect K+ level
- risk of hypokalemia - by loop diuretics
- risk of hyperkalemia, with
- k+ sparing diuretics
- ACE inhibitors
- NSAIDS
- patients with diabetes mellitus
- acute DKA
- type IV renal tubular acidosis
- patients with major fluid/electrolytice imbalances
- those on IV fliuds
- those receiving parenteral nutrition
- tthose w/ severe diarhea
- patients with renal impairments
what serum [K+] levels constitute hyperkalemia?
a serum [K+] > 5.5 mEq/L
what to look out for during a physical exam a possibly hyperkalemic patient?
- exam will usually be negative
- otherwise, you may see
- bradycardia
- weakness, fatigue
- dyspnea
- arrthymias
- parethesias
- nausea and vomitting
- muscle tenderness/weakness/paralysis
- depressed or absent deep tendon reflexes
discuss the pathophsyiology (common causes) of hyperkalemia?
- excessive intake of K+ (rare)
- decreased excretion of K+ (almost all of these causes involved decrease in aldosterone)
- kidney disease (chronic or acute)
-
Addison’s disease:
- characterized by a decrease in aldosterone production: less Na+ absorbed, less K+ secreted at collecting ducts –> K+ retention
-
Type IV RTA (Renal Tubular Acidosis)
- this variation of RTA is due to an aldosterone deficiency.
- K+ retention drives K+ out of the plasma in the cell. this promotes uptake reabsoprtion of H+ in “exchange for” the K+ we’re trying to get rid of
-
drugs:
-
diuretics that lower K+ secretion:
- potassium sparing diruetics
- ACEs/ARBS
- (these lower inhibit Ang II and thus aldosterone production)
-
renin inhibitors
- RAAS decrease –> aldosterone decrease –> K+ retention
-
diuretics that lower K+ secretion:
-
a shift of K+ from intracellular to the extracellular space
- rhabdomyolsis - muscle breakdown
- hemolysis - breakdown of RBCs
- metabolic acidosis
- drugs: beta blockers and alpha antagonists
clinical presentation of rhabdomyolysis
- rhabdomyolysis = muscle breakdown that causes a causes a shift of K+ from the ICF to the ECF
- presentation:
- myalgias
- dark urine
- possible compartment syndrome
discuss the EKG changes seen in hyperkalemia
different EKG changes are seen dependent on the level of hyperkalemia (serum K+ > 5 mEq/L)
how to check renal function for a hyperkalemic patient?
- determine the BUN and Creatinine
- creatinine clearance = used to estimate GFR
- can estimate creatinine clearance using the Cockcroft- Gault Formula (utilizes patient’s age and body weight)
- creatinine clearance = used to estimate GFR
what can urine potassium levels you with regards to hyperkalemia?
how to obtain these urine levels?
- A urine K+ level <20 mEq/L suggests impaired renal excretion
- A urine K+ level > 40 mEq/L suggests intact renal excretory mechanisms
- means that hyperkalemia is likely nonrenal
a spot urine K+ measurement is easiest to obtain
outline the diagnosis of hyperkalemia based on serum [K+], luekocyte/platelet levels, and urine [K+]
general treatment of hyperkalemia?
- Discontinue all drugs causing hyperkalemia (K+ sparing diruetics -spironlactone, eplernone, triamterine, amiloride - and trimethoprim)
- Discontinue any dietary potassium
- If pt on digoxin, check for digitalis toxicity—Hyperkalemia
-
In severe (potassium >7.0 mEq/L) OR if pt is symptomatic
- Start treatment first!
- Then look for underlying cause
-
In severe (potassium >7.0 mEq/L) OR if pt is symptomatic
in pharm, digoxin is contraindicated with loop/thiazide diuretics because it can “worsen hypokalemia” idk what to do about this.
after intitial treatment for hyperkalamia (discotinuing K+ retaining drugs, ect.) what is the next step?
- next step is achieving membrane stabilization
- calcium is key in stabilizing membrane stability (use either calcium chloride or calcium gluconate)
- next, want to drive K+ intracellullary:
- this is often done with insulin, which drives K+ into cells.
- if insulin is give, also administer glucose so pt doesnt beome hypoglycemic.
- this can also be done with:
- bicarbonate (especially if the patient is also acidotic)
- magnesium
- sympathonimetic agents (eg beta-agonists)
- this is often done with insulin, which drives K+ into cells.
- we can also remove K+ from the body entirely:
- hemodialysis
- normal saline
- furosemide (loop diuretic)
- remember that loop diuretics increase the tubular Na+ load that arrives to the collecting ducts, which then drives Na+ reabsorption/K+ secretion
- this promotes excretion of K+
- remember that loop diuretics increase the tubular Na+ load that arrives to the collecting ducts, which then drives Na+ reabsorption/K+ secretion
what blood serum is considered hypokalemia?
serum level < 3.5 mEq/L
general causes of hypokalemia
- inadequate potassium intake
- increased potassium excretion (most common)
- shft of potassium from ECF to ICF
what ECG changes are seen with hypokalemia?
- ST depression
- prominent U wave
outline steps for determining cause of hypokalemia
