Jan9 M2-Potassium Pathophysiology Flashcards
hyperK and hypoK effect on resting potential
hyperK: depol (resting potential more positive)
hypoK: hyperpol (resting potential more negative)
electrical effects of hyperK on the heart + ultimate effect (less or more excitable)
- sustained gradual depolarization
- inactivation of Na channels
- *less excitable even though closer to threshold bc Na channels inactivated
hyperK on ECG (step by step)
peaked T wave, widened QRS, loss of P wave, sine wave, V fib
3 causes of hyperkalemia
impaired cell entry, increased cell release, reduced urinary excretion
key points in hyperK
almost all cases involve decreased GFR and are multifactorial
why can have hyperK in heart failure
volume contraction with decreased GFR
hormonal problem that can cause hyperK and 3 causes to that
hypoaldosteronism (1. primary adrenal insufficiency 2. ACEi 3. NSAIDs bc inhibit PGs’ effect on renin release)
drug that can cause hyperK
K sparing diuretics
can high K diet cause hyperK? yes no and why
no bc aldo turned on and K excreted normally
why does high K diet not cause high Na reabso
when euvolemic, RAAS is off (aldo is on because detects K but renin and therefore AT2 are off so AT2 doesn’t promote Na reabso at PCT)
hyperK cause related to not enough cell entry
insulin deficiency in hyperglycemia or uncontrolled diabetes
hyperK cause related to too much excretion from cells
rhabdomyolysis (muscle breakdown so K from these cells is released)
why can have false positive hyperK
when blood sample is hemolyzed (cells in it lysed)
history of patient with hyperK
- ask for CKD!!! (GFR!!), diabetes, adrenal insufficiency
- drugs taken (ACEi, ARB, K-sparing like spironolactone)
labs in hyperK patient
Cr, urea (GFR!!), glucose, electrolytes, bicarb
important test to do in hyperK patient
ECG
drugs that contribute to hyperK (4 types)
- ACEi and ARBs
- NSAIDs
- cyclosporine (reduce renin release)
- all K sparing (ENac blockers or MRAs)
how diabetes affects renin release
reduced renin release
symptoms of hyperK + what kind of arrhythmia
weakness, feeling faint, arrhythmia (brady)
summary of 3 causes to hyperK
low GFR low aldo (drug, adrenals) K shift out (insulin, rhabdo)
3 parts of hyperK treatment
- protect the heart
- shift the K in the cells
- excrete the K
hyperK treatment: how to protect the heart and when
if peaked T waves, give IV Ca gluconate. Ca increases AP threshold
hyperK treatment: how to shift K in the cells (2)
- IV D5W + insulin
- inhaled beta-2 agonist (salbutamol)
hyperK treatment: how to excrete the K + this part of the treatment depends on what
oral K exchange resin (exchanges K with Ca)
loop diuretic if volume overloaded
NS if volume deplete