severe vomiting, diarrhea, intestinal fistula

diuretic use

Mineralocorticoid excess

Various kidney diseases

renal tubular acidosis

Magnesium deficiency (supplement magnesium first before supplementing potassium)

H escapes from the cell and K from outside the cell enters the cell

This ion transfer also occurs in renal tubular epithelial cells, resulting in weakened H-Na exchange and enhanced K-Na exchange → increased urinary potassium

Activates Na-K-ATPase, increasing extracellular potassium transfer into cells

Promote cellular glycogen synthesis, allowing extracellular potassium to be transferred into cells along with glucose

Activate Na-K pump

Potassium channels are blocked and K outflow is reduced

parts

mechanism

changes in physiological characteristics

EKG changes

Impairment of myocardial function

Potassium deficiency → disappearance of vasodilatory response → tissue ischemia and hypoxia → muscle degeneration and necrosis

Potassium deficiency → reduced glycogen synthesis and reduced energy reserves

Urinary concentrating dysfunction, polyuria

Decrease of extracellular fluid K → Egress of intracellular fluid K and inward movement of extracellular fluid H → Extracellular fluid alkalosis

K in the renal tubular epithelial cells decreases and H increases → K-Na exchange is weak and H-Na exchange is high → Urinary excretion of K decreases and H excretion increases → aggravation of metabolic alkalosis and urine becomes acidic

Too much, too fast, too concentrated, too early (see urinary potassium administration)

During acidosis, extracellular fluid H increases, H enters the cell and is buffered, and K enters the outside of the cell to maintain charge balance.

This ion transfer also occurs inside and outside the renal tubular epithelial cells, resulting in enhanced H-Na exchange, weakened Na-K exchange, and reduced urinary potassium excretion.

Insulin deficiency prevents potassium from entering cells, and hyperglycemia causes blood potassium to rise.

mechanism

mechanism

Excitability

conductivity

self-discipline

Contractibility

QRS—widened, narrowed

T—high tip

P—low level

Arrhythmia

Hyperkalemia → K moves inward, H moves outward → acid substitution

K in the renal tubular epithelial cells increases, H decreases → H-Na exchange weakens, K-Na exchange increases → Urinary potassium excretion increases and becomes alkaline