B4.074 Prework 2: Systemic Hyperkalemia vs Local Hyperkalemia Flashcards
what is the resting Na+ channel
activation gate closed
inactivation gate opened
normal resting potential -70 to -80 mV
discuss the logistics pf the voltage gated sodium channel
both gates must be open for Na+ ions to flow
when both gates are open gNa is increased, so INa will increase
this causes V to move toward ENa
this is the basis for the upstroke in action potential
inactivation gates open and close
slowly
activations gates open and close
rapidly
sequence of gates during action potential
activation gates open at threshold potential
inactivation gates begin to close when activation gates open
at +60 mV, inactivation gates are all closed and activation gates begin to close
as V declines back to normal resting, activation gates stay closed and inactivation gates all reopen to prepare for next impulse
what is the consequence of moving resting potential more positive?
closer to original threshold BUT excitability will decrease
number of resting Na+ channels will be decreased because there will be an incomplete repolarization
decreased number of channels will decrease current
threshold will move more positive and amplitude and rate of AP and conduction will be reduced
what is meant by incomplete repolariazation
repolarization stops at “new” resting potential before all inactivation gates have a chance to open back up
what happens when Na+ current is decreased
- threshold potential more positive (decreased excitability)
- rate of rise of AP decreased
- amplitude of AP decreased (diminished height of QRS)
- decreased conduction velocity (wide P wave, wide QRS)
what is the effect of hyperkalemia on resting membrane potential
resting membrane potential must be more positive than potassium Nernst and more negative than sodium Nernst
hyperkalemia shifts potassium Nernst more positive
shifts resting membrane potential more positive
normal Ki conc
150 mM
what is the effect of extracellular K on Nernst
as Ko increases, becomes more similar to Ki
reduces electrical driving force
Ek becomes less negative and moves toward 0
normal Ko conc
5 mM
what happens if you double Ko
Ek goes up 18 mV
normal Ek
-80ish
normal resting potential
-70 mV
what is flaccid paralysis
reduced voltage gated Na+ current in nerve and skeletal muscle will result in difficulty in a person contracting their limbs
what can cause flaccid paralysis
hyper or hypokalemia
hyperkalemia effects on K current
increased gK > increased IK > shorter AP duration
increased amplitude, short duration T wave, spiked T wave
hypokalemia effects on K current
decreased gK > decreased IK > longer AP duration
low amplitude, long duration flat T wave
methods to reverse hyperkalemia
calcium gluconate
NaHCO3
glucose & insulin
lasix
mechanism of calcium
recovers resting sodium channels by shifting sodium channel inactivation curve toward more positive potentials
doesn’t actually get rid of K
mechanism of sodium bicarb
indirectly enhanced Na-K pump by increasing Na influx via Na-H exchanger
mechanism of insulin
stimulated Na-K pump, which moves extracellular K into cell
mechanism of lasix
diuretic
enhanced K excretion by the kidney
effect of hypercalcemia
depolarizing shift of Na+ inactivation curve
depolarizing shift in the Na+ activation gate curve, makes threshold more positive
benefit of increasing # of resting sodium channels outweighs the more positive threshold
overall benefit of calcium
recovers more resting Na+ channels to increase Na+ current towards normal in nerves and muscles
treatment plan of hyperkalemia
recover excitability w calcium
THEN
correct underlying hyperkalemia
what is a U wave
follows a T wave
becomes more prominent as hypokalemia becomes more severe
treatment of hypokalemia
slow IV infusion of K
how does myocardial ischemia shift the ST segment
away from isoelectric line
due to hyperkalemia
why does the ST elevation arise?
insufficient blood flow to area causes extracellular K+ to rise
resting membrane potential in this area is more positive than in rest of ventricle
different in resting potentials results in current flow even before depol
shifts apparent isoelectric point
“injury current”