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
other considerations in hyperK treatment (think of causes)
dietary review
control diabetes
stop the meds (ACEi, K-sparing diuretics, NSAIDs, etc.)
does IV bicarb decrease K levels? what’s the basis for that
no. (but would think yes because H (out) K (in) exchanger in alpha intercalated cells would work less and keep more K out)
if you’re on ACEi or ARB or NSAID, how much aldo secretion after K intake
some secretion bc adrenals react to K level
channels stimulated by aldo (or synthesized to its effects)
- ENac, ROMK and Na-K ATPase of principal
- H (out) K (in) ATPase exchanger in alpha int.
ECG changes in hypoK
U wave formation, T wave flattening, arrhythmia but less than hyperK
effect of hypoK on muscles
muscle weakness, cramping and pain (myalgias)
rhabdomyolysis and paralysis if severe
most common cause of hypoK + other causes
- diuretics (distal flow of Na increases K secretion)
- high aldo
- chemo (Fanconi Syndrome: less PCT reabso)
- GI losses
- black licorice (acts like aldo)
hypoK symptoms
weakness or brady arrhythmia
3 conditions or states where hypoK is caused by urinary loss (and increased distal Na flow)
- primary hyperaldo
- RAS
- diuretics
most common GI tract loss cause of hypoK and why
diarrhea (bc GI secretion with highest K)
does alkalosis cause hypoK. (this question is different from ‘‘does bicarb reduce K’’) if yes how
yes. alkalosis: bicarbonaturia. bicarb enters the CCD cells and H (out) K (in) ATPase works less so that H stays inside with bicarb
history in hypoK
hyperaldo? diuretics? diarrhea?
how to differentiate between renal vs extra-renal K loss
- if renal (urine K spot>15 and 24hr>30)
- if extra-renal (diarrhea): low urine K
hypoK treatment
IV or oral replacement
very important rule in K administration
for a serum deficit of 1 mM, there is a K deficit of 100-150 mM (in the body). (K conc in the ICW is 140 mM)
