Hyperkalemia

Question 1

___ should be considered in patients with no symptoms, no EKG changes, and preserved kidney function

Answer 1

Pseudohyperkalemia should be considered in patients with no symptoms, no EKG changes, and preserved kidney function

Question 2

CBC findings of someone with pseudohyperkalemia

Answer 2

Leukocytosis (>100,000/cc)

Thrombocytosis (>500,000/cc)

Hemolysis, fist clenching

K+ is leaking from cells cause theres just so many, cell trauma is going on due to crowding– K+ leaks out and serum levels seem high

Question 3

after pseudohyperkalemia exclusion, there are three broad factors that could be contributing to hyperkalemia

1. transcellular shift due to ____ release or ___ entry
2. increased intake (usually IV)
3. Reduced excrestion due to a principle cell problem (TTKG<7), reduced ___, or decreased distal flow with urine sodium being

Answer 3

1. transcellular shift due to INCREASED release or DECREASED entry
2. increased intake (usually IV)
3. Reduced excrestion due to a principle cell problem (TTKG<7), reduced GFR, or decreased distal flow with urine sodium being <20mmol

Question 4

Is the principle cell causing this hyperkalemia?

Answer 4

looking at his labs, he has ECG findings. we can EXCLUDE PSEUDOhyperkalemia.

• he has a reduced GFR – going down the reduced excretion scheme route. His sodium is not under 20 , thus this reduced excretion is NOT being caused by reduced EABV.
• his TTKG is 8.3. recall that if TTKG is <7 and he is hyperkalemia, then the PC is causing it. HOWEVER IN THIS CASE TTKG IS OVER 7, THUS PC IS NOT CAUSING HYPERKALEMIA.

-

Question 6

note: hyperkalemia
1. Pseudohyperkalemia should be considered in patients with no symptoms, no EKG changes, and preserved kidney function
2. Approach to hyperkalemia begins with interpretation of renal handling
3. …then looking for circumstantial evidence of shift

Question 7

ECG changes in hyperkalemia

Answer 7

1. increase in T wave amplitude with “peaking”
2. prolongation of PR interval
3. Flattening or absence of P wave
4. Prolongation of QRS +/- ventricular arrythmias
5. QRST “sine wave” – classic– bad out come

Question 8

Answer 8

Prolongation of QRS +/- ventricular arrythmias

Question 9

3 ways pf treating hyperkalemia with life-threatening ECH changes

Answer 9

1. IV calcium– NOT DONE ANYMORE
2. addrses the intracellular shift with insulin (maybe a bit of glucose), beta agonists, and bicarbonate
3. increase elimination via diuretics

Question 10

2 ways of treatning non-life threatening hyperkalemia (no ECG changes)

1. reduce intake
2. increase elimination
   - increase renal excretion by increaseing the __ flow rate, or incresing __ using flurocortisone, CCN __+, or __.
   - incease GI excretion using __
   - using __ hemodialysis

Answer 10

2 ways of treatning non-life threatening hyperkalemia (no ECG changes)

1. reduce intake
2. increase elimination
   - increase renal excretion by increaseing the CCD flow rate, or incresing TTKG using flurocortisone, CCN Na+, or bicarbonate.
   - incease GI excretion using resins
   - using RRT hemodialysis

Question 11

how can osmole in ECF affect K+ loss?

Answer 11

if there are osmoles in the ECF, water follows (osmotic diuresis), leaving less water in the cell. Less water in the cell causes K+ concentration to increase in the cell, making K+ efflux out of the cell trhoguh their channles. this is called SOLVENT DRAG

Question 12

how does insulin concentration affect K+? How does H+ affect K+?

Answer 12

recall that there is an Na+/H+ exchanger. Insulin activates the Na+/H+ exchanger, bringin Na+ inand H+ out. when Na+ comes in, the Na+/K+ ATPase pump turns out, inuslin pumps K+ INTO THE CELL (leaving serum K+ LOWER)

H+ in serum (metabolic acidosis normal anion gap) affects the H+NA+ exchanger.