Hypokalemia & Hyperkalemia PPT (2)
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This document discusses potassium levels in the blood and factors that can cause hypokalemia (low potassium) or hyperkalemia (high potassium). It begins by stating the normal range for potassium in blood is 3.5-5 mEq/L. It then provides multiple potential causes for abnormal potassium levels including medications, diet, vomiting/diarrhea, kidney disease, and cellular shifts of potassium between extracellular and intracellular fluid. Mnemonics are also presented to help remember key points. Assessment findings and complications associated with hypo- and hyperkalemia like arrhythmias and muscle weakness are described.
Hypokalemia & Hyperkalemia PPT (2)
- 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
- 3. Helpful mnemonic = think of the pump as a fishing boat Sea water (Na+) out / Fish (K+) in
- 4. Helpful mnemonic = Drink milk after spicy (and salty) food!
- 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
- 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
- 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.
- 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.
Editor's Notes
- #22: 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.
- #26: 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