2. • The presence of potassium in
the blood
• Normal range: 3.5 – 5 mEq/L
= low levels of
potassium, deficient potassium
= high levels of
potassium, excess potassium
6. •Increased entry of K+ into cells
• Reduced intake of K+ in diet & increased losses of K+ from body
• Diuretics / Diuretic effects
•Decreased gastric fluid in GI from vomiting/diarrhea results in
increased renal compensation
Decreased fluid and Na+ stimulates aldosterone =
loss of renal K+ (Na+/K+ pump)
• K+ shifts from ECF -> ICF in exchange for H+ to maintain plasma acid-
base balance (pH) during respiratory or metabolic alkalosis
K+ in the ICF -> hypokalemia
7.
8. 1. Actual total body K+ loss
a. excessive use of medications, such as diuretics and corticosteroids
b. increased secretion of aldosterone
c. vomiting, diarrhea
d. wound drainage
e. prolonged nasogastric suction
f. excessive diaphoresis
g. kidney disease
2. Inadequate K+ intake
3. Movement of potassium from the extracellular fluid to the intracellular fluid
a. Alkalosis
b. Hyperinsulinism
4. Dilution of serum potassium
a. water intoxication
b. IV therapy with potassium-deficient solutions
9. •Certain antibiotics (carbenicillin, gentamicin, amphotericin B)
•Certain drugs, called diuretics, that can cause excess urination
•Diarrhea and vomiting (including the use of too many laxatives, which
can cause diarrhea)
•Diseases that affect the kidney's ability to retain potassium
(Liddle syndrome, Cushing syndrome, hyperaldosteronism, Bartter
syndrome, Fanconi syndrome)
•Eating disorders (such as bulimia)
•Eating large amounts of licorice or using products, such as herbal teas
and chewing tobaccos that contain licorice made with glycyrrhetinic
acid (no longer used in licorice made in the United States)
•Sweating
10. 1. ECG
- Early: Flat or inverted T wave, Prominent U wave, DT segment depression,
prolonged QU interval.
- Late: Prolonged PR interval, decreased voltage and widening of QRS
interval, increased risk of ventricular dysrhythmias.
11. 2. Assess: LOC and orientation (Patient may be confused, apathetic,
anxious, irritable, or in severe cases, even comatose.)
3. Rate and depth of respirations, color of nail beds and mucous
membranes
4. Possible weak and thready pulses, heart rate variability
(Apical pulse may be excessively slow or excessively rapid,
depending on the type of dysrhythmia present.)
5. Presence of skeletal muscle weakness (AEB bilateral weak hand
grasps, inability to stand, hyporeflexia, and profound flaccid
paralysis in advanced stages of hypokalemia.)
6. Abdominal distention and hypoactive bowel sounds
12. 7. Patient’s blood pressure when she or he is lying down, sitting, and
standing (postural hypotension)
13. Balance of potassium is needed on the intracellular and extracellular
levels for muscle contraction, nerve impulses, metabolism, and
homeostasis.
Change in levels of potassium change neuromuscular control (nerve
and muscle)
Potassium works in the cell to let the muscle know when to relax and
contract (Na+/K+ pump). Too much or too little potassium changes
muscle control and causes them to weaken.
14. When there’s too little K+
Arrhythmias: The cardiac heart muscles are affected by the low K+
and cannot contract.
Cardiac Arrest…Death: Decreasing levels of K+ will eventually stop
the cardiac heart muscles leading to cardiac arrest and possibly
death.
Paralysis: Muscles can continually weaken and damage to paralysis
15.
16.
17.
18. • Mnemonic = AIDS
• Acidosis – Metabolic acidosis: bicarbonate is low, pH become acidic
low blood pH causes H+ to go into the cell and cause lysis so that it releases
its potassium content into the blood stream
K+ leaking out to ECF -> hyperkalemia
• Insulin Deficiency – normally insulin binds to the Na+ / K+ pump that causes K+
to flow into the cell and Na+ out of the cell.
when insulin can’t bind, K+ can’t flow into the cell, and stays outside
K+ in the ECF -> hyperkalemia
19. • Drugs
1. Digitalis or Digoxin: competes with K+ at the Na+ / K+ pump
Takes the place of K+,
decreasing cellular K+ and making it stay outside of the cell
K+ in the ECF -> hyperkalemia
20. • Drugs
2. Succinylcholine: causes up-regulation of nicotinic
acetylcholine receptors on the muscle membrane
up-regulation causes the amount of receptors to increase,
resulting in K+ efflux into the plasma
3. Beta blockers: take the place of beta agonists
stop activation of cyclicAMP, then protein kinase, and then phosphorylation
of the the sodium potassium ATPase pump
Can’t pump out K+, so K+ stays outside of the cell
K+ in the ECF -> hyperkalemia
21. 1. The body experiences decreased K+ excretion…
• Renal failure - impaired renal function causes electrolyte retention
• Potassium - sparing diuretics (given for HF)cause loss of Na+ & Ca2+ while
saving K+
•Adrenal insufficiency - imbalance of K+ when adrenal glands don’t
produce the right amount of aldosterone
22. 2. The body experiences a cellular shift of K+ from cells to ECF…
• Tumor lysis syndrome: massive release of K+ from cells
• Rhabdomyolysis: damaged skeletal muscle releases toxic intracellular
constituents into circulation
• Metaboic acidosis: acid-base balance disorder causing electrolyte
imbalance
• Diabetic ketoacidosis: severe electrolyte imbalance with dehydration
• Drug-induced diuresis: loss of too much K+ from polyuria
(adverse effects of ACE inhibitors)
23. 1. ECG
- Early: Increased T wave amplitude or peaked T waves. Middle: Prolonged PR
interval and QRS duration, atrioventricular conduction delay, loss of P waves.
- Late: Progressive widening on QRS complex and merging with T wave to
produce sine wave pattern.
24. 2. Assess: Heart rate (may be slowed with or without irregular or extra beats)
3. Significant muscle weakness that progresses upward from legs to trunk
4. Paresthesia of the face, feet, hands, and tongue may occur
5. General anxiety and irritability
6. Low urinary output
7. Nausea and vomiting (due to hyperactivity of GI smooth muscle)
25. When there’s too much K+
Arrhythmias: The cardiac heart muscles cannot efficiently contract and
relax. This alters the rate or rhythm of the heartbeat. Ventricular fibrillation
can occur in which the ventricles flutter rapidly instead of pumping blood.
Cardiac Arrest… Death: Imbalance of potassium causes muscles to
decrease in efficiency (cramping, fatigue) eventually causing the heart to
fail.
26.
27. Dugdale, D. C., & (2013, Oct 31). High potassium levels. (2 Feb. 2014) Retrieved from,
http://www.nlm.nih.gov/medlineplus/ency/article/001179.htm
Huether, S. (2012). Understanding pathophysiology, 5th edition. St.
Louis: Elsevier Inc.
MyOptumHealth. Hypokalemia. N.p., n.d. (5 Feb. 2014). Retrieved from,
<https://client.myoptumhealth.com/myoptumhealth/guest/page.esync?view=prelogin.learn.learnLanding&com
mand=DiseasesAndConditions&article=7876d666b1259110VgnVCM1000005220720a>.
Potter, Patricia, Anne Perry, Patricia Stockert, Amy Hall (2013). Fundamentals of Nursing, 8th Edition. Mosby Inc.
Schambelan, M., Sebastian, A., Biglieri, E.G. (1979). Prevalence, pathogenesis, and functional significance of
aldosterone deficiency in hyperkalemic patients with chronic renal insufficiency. Kidney International, 17, 89-101.
Silvestri, Linda. Saunders Comprehensive Review for the NCLEX-RN Examination. 6th ed. N.p.: Saunders, an imprint of
Elsevier Inc., 2014. 92. Print.
Notas del editor
Drug succinylcholine given to paralyze patients to intubate them in ER- causes up regulation of nicotinic acetylcholine receptors on the muscle membrane But patients with increased risk of developing hyperkalemia are those with injuries, burns, and trauma because the cells are crushed or broken and will leak out a lot of K.
Drugs Digitalis or Digoxin: competes with K at Na K ATPase pump; digoxin comes and takes place so K coming into the cell decreases and stays outside of the cell. It also inhibits cardiac muscle sodium calcium channels on the cell membrane potential. Because Na can’t be pumped out from the ATPase pump, Na won’t come into the cell and Ca2+ can’t be pumped out of the cell from the sodium calcium channel. (Ca2+ comes out each time Na+ comes in)So digitalis causes you to retain more calcium in the heart muscle cell and that extra calcium allows for more contractility because the actin myosin filaments can form cross bridges that allow them to move- resulting in more active myocardiac contraction. (Digitalisis given to patients with congestive heart failure so the heart will pump) COMPLICATIONS