March 25 Lecture - Dr, Valenzuela

Valenzuela

Potassium changes are confusing.  Hyperkalemia according to the Nernst equation causes hypopolarization.  However, the significant effect on the heart is due to the effect on Na channels (decreases conductance) and potassium channels (increases conductance).  These effects are summarized in the figure below:

Illustration of a normal action potential (solid line) and the action potential as seen in the setting of hyperkalemia (interrupted line). The phases of the action potential are labeled on the normal action potential. Note the decrease in both the resting membrane potential and the rate of phase 0 of the action potential (V_max) seen in hyperkalemia. Phase 2 and 3 of the action potential have a greater slope in the setting of hyperkalemia compared with the normal action potential due to hyperkalemia induced increase in K conductance (I kr).
reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/
The membrane potential at the onset of phase 0 determines the number of Na channels that are activated during phase 0, so with hypopolarization there are fewer activated Na channels and a reduced rate of depolarization. This decrease in V_max causes a slowing of impulse conduction through the myocardium and a prolongation of membrane depolarization; as a result, the QRS duration is prolonged.

Beta blockers reduce sympathetic NS stimulation of renin production from juxtaglomerular cells of the afferent arteriole in the kidney, but decreased pressure will still trigger renin release from these cells.

Combo pill - ACEinhibitor + thiazide diuretic stabilizes K levels (blocked aldosterone increases plasma K - thiazide diuretic reduces plasma K)