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Hypokalemia
Hypokalemia, or low potassium levels, can have significant effects on muscles, the cardiovascular and nervous systems. It is defined as a potassium level below 3.5 mEq/L. The majority of potassium is found inside cells and is essential for various cellular functions through membrane pumps and channels. Causes of hypokalemia include reduced intake, redistribution into cells, and increased losses through the kidneys or gastrointestinal tract. Treatment focuses on replacing potassium stores through oral or intravenous supplementation, addressing the underlying cause, and preventing further losses and complications like cardiac arrhythmias.
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Hypokalemia
- 1. HYPOKALEMIA Dr. Nisheeth M.Patel M. D (Medicine), FCCCM Consultant Physician & Intensivist
- 2. Normal rangeof potassium is 3.5 to 5 mEq/L Potassium is essential for Muscles, cardiovascular system, Central nervous system, respiratory system. Maintain osmolarity of ECF and ICF and hence cellular volume Regulation of acid base balance along with cellular growth, protein synthesis and hormonal secretion Vital for cell excitability and muscle contraction Maintainance of transmembrane electric potential.
- 3. PHYSIOLOGICAL HEMOSTASIS: 98%of total body K+ is intracellular and chiefly in muscles. In a healthy individual steady state K+ excreted 90% in urine and 10% in feces. K+ absorbs from small intestine; through duodenum, jejunum and ileum. K+ mainly required for the below mentioned channels: Na+K+ ATPase: almost all cells contains this pump; required for maintenance of ICF and ECF through electromechanical gradient (3 Na+ out & 2 K+ in) H+K+ATPase: In GI cells and renal tubules (H+ out and K+ in) Na+K+Cl- co transport: in salivary gland, GI tract and Renal tubules; brings 1 Na+, 1 K+ & 2 Cl- inside cell K+Cl- Co transport: plays role in maintaining volume of erythrocytes.
- 4. RENAL HANDLING OFPOTASSIUM: Proximal convoluated tubules: 60% of K+ reabsorbption occurs through paracellualr K+ channels. In ascending thick part of Loop of henle K+ is reabsorbed by Na+K+Cl- co transport channel. Distal convoluted tubules and collecting duct: major determinants of urinary K+ levels as K+ is secreted by principle cells. Potassium secretion occurs in ‘principal cells’ by active uptake across the basolateral membrane by Na+/K+-ATPase and passive diffusion into the lumen across the apical membrane by K+ channels or using a K+ Cl_ cotransport. Increased concentration of Na+ makes K+ to secrete in lumen because increase in Na+ concentration potential difference across cell membrane and that makes K+ drive out of the cells.
- 5. Reabsoption ofK+ occurs through H+K+ATPase and Na+K+Cl- co transport through intercalated cells. Potassium homesostatsis is mainly done by renal system. In case of hypokalemia it reabsorbs the filtered K+ and in hyperkalemia it promotes secretion of K+ by principle cells. Pottasium rich diet: Bananaas, Kiwi, Mango, Oranges, Papaya, coconut water, fruit juice, spinach, sweet potato, tomato, pickles, beet, dry fruits, chocolate coffee.
- 6. Serum level <3.5 mEq/L defined as a hypokalemia Causes: Psuedohypokalemia: Drip arm sample Reduced intake: starvation and dietary deficiency Magnesium deficiency: treatment resistance hypoK+ Redistributive hypokalemia: Acid base disorder Metabolic alkalosis
- 7. REDISTRIBUTIVE HYPOKALEMIA Increasedcellular uptake through Na+K+ ATPase ↓ K+ insulin Beta 2 agonist Thyroid hormone Refeeding syndrome
- 8. ALTERATION IN SYMPATHETICACTIVITY Alcohol withdrawl Thyrotoxic periodic paralysis Acute MI Head injury Sympathomimetic drugs: Ephedrine pseudoephedrine Rarely theophylline and caffine can cause downregulation of beta 2 receptor (Na+K+ATPase) causing hypokalemia Hypothermia, Familial Hypokalemic Periodic Paralysis, barium toxicity (inhibition of leak K+ channel) as in cough syrup
- 9. INCREASED POTASSIUM LOSS Renal loss: Increased distal Na delivery: Diuretics Osmotic diuretics Salt wasting nephropathies Antibiotics: penicillin related, aminoglycosides, AMP B, cisplatin, ifofosphomide Non renal loss: Infectious: Diarrhoea and vomiting Non infectious: Celiac disease Ileostomy Villous adenoma VIPoma Chronic laxative abuse Colonic pseudo- obstruction
- 10. INCREASED SECRETION OFK+ HYPERALDOSTERONISM Genetic : Congenital adrenal hyperplasia Acquired: Aldosterone producing adenomas Adrenal hyperplasia Idiopathic Malignant hypertension Renal artery stenosis Renin secreting tumour Mineralocoticoid excess: Cushings syndrome Barters syndrome Liddle’s syndrome Gitelman’s syndrome. Primary Secondary
- 11. CLINICAL FEATURES: Maybe asymptomatic Fatigue, myalgia, LL weakness with depressed DTR Paralytic ileus, constipation Respiratory muscle weakness and complete paralysis Increased risk of arrythmia and heart failure; esp patients on digitalis treatment. No neurological presentation
- 12. ECG CHANGES INHYPOKALEMIA (DO NOT CORRELATE WITH S. K+ LEVEL) Early changes: T wave inversion or flattening U wave ST segment depression Prolong QT interval Severe K+ depletion Prolong PR Low voltage ECG Wide QRS comples Ventricular arrythmia
- 13. DIAGNOSTIC APPROACH TO HYPOKALEMIA HYPOKAEMIA PSUEDOHYOKALEMIA TRUEK+ DEPLETION REDISTRIBUTIVE •Drip arm sample •No treatment required •Confirmed with repeat lab Find out the cause for redistribution and treat accordingly
- 14. True hypokalemia Measure urinary K+ URK+ < 20mEq/L/day extra renal loss UR K+ >30mEq/L/day Renal loss Metabolic Acidosis Metabolic Alkalosis Diarrhea Fistula Ileostomy Laxative abuse Villous adenoma VIPoma Celiac disease Vomiting Diuretic use of recent origin Metabolic Acidosis Metabolic Alkalosis Variable RTA I/II DKA AMP B ACETAZOLMIDE ADR INFUSION HYPO MAGNESEMIA HYPERTENSION
- 15. Low Cortisol S. Aldosterone High Renin High RAS RST Malignant HTN Primary Hyperaldosteronism Mineralocorticoid Excess Low High Cushing’s syndrome SAME Liddle’ssyndrome Low HYPERTENSION NO YES BARTTER’S SYND Current Diuretic use Essential Hypertension on diuretics
- 16. THERAPEUTIC GOALS FOR TREATINGHYPOKALEMIA Prevent life threatening complications like arrhythmia and respiratory failure Correction of underlying etiology Correct K+ deficiet Minimize ongoing losses Prevention of hypokalemia
- 17. PREVENTION OF HYPOKALEMIA Normal daily intke: 60 mEq/L Prophylactic K+ Supplements in patients taking Digitalis Long term use of diuretics Larger doses of Steroids Prevention of hypokalemia required in: Digitalis therapy Hepatic failure Prev MI or IHD DM Post op on TPN or IV fluid: Give 40-50 mEq/ day of K+
- 18. TREATMENT GUIDELINES: K+level 3 to 3.5 mEq/L: Treat in special high risk groups: Risk of arrhythmia Hepatic failure/ Congestive Cardiac Failure Digitalis therapy IHD/DM K+ level below 3 mEq/L: Definitive treatment thorugh IV route
- 19. PRECAUTIONS: Never giveK+ In oligouric or anuric patient Cautious use of K+: pt on K+ sparing diuretics, ACEi, pt with renal failure Pt on digitalis therapy IV K+ infusion rate shoud be < 20 mEq/hr If rate > 20 mEq/hr, every pt needs to have continouos ECG monitoring and frequent S. K+ Level.
- 20. Roughly fallof 1 mEq/L of S. K+ = 200 – 400 mEq body deficit When deficit of K+ about 200 to 400 mEq; 50 to 100 mEq/day of K+ slowly but adequately corrects deficit. KCl (potassium chloride) salts are the preapartion of choice for treating hypokalemia. It will correct hypokalemia and also metabolic alkalosis. Potassium bicarb and citrate will alkalize the patients and more appropriate for hypokalemia asso with chronic diarrhoea and RTA Oral potassium therapy safer than IV as it carries less risk of hyperkalemia
- 21. IV POTASSIUM Ivroute carries high risk for hyperkalemia Reserved only for severe symptomatic hypokalemia or for the patients who can’t take oral feeds. Always monitor IV therapy with cont EC monitoring and frequent K measurements Avoid IV till U/O is established Don’t Give > 10-20 mEqL/hr > 40 mEq/Litre >240 mEq/day
- 22. Never give: Direct Inj. KCL IV; can cause sudden cardiac arrest Add KCL to Isolyte M Rapid IV correction can cause dangerous hyperkalemia; hypo is better than hyper Avoid treating Meta. Acidosis; asso with Hypokalemia; with IV NaHCO3 as it may aggravate hypokalemia In severe hypoK, add KCl in isotonic saline; not in D5% as diluent.
- 23. DKA andnon ketotic hyperosmolar hypergylcemia are the commenest indication for IV potassium therapy. 100 mEq of K+ mixed in 1 litre of isotonic saline at rate of 100 ml/hour (25 macro or 100 micro drops ) will deliver 10 mEq KCl per hour. IV potassium max rate of infusion: Central line 60 mEq/L and peripheral line 40 mEq/L. > 40 mEq/L can cause thrombophlebitis Avg rise in S. K+ level ins 0.25 mEq/L when 20 mEq/l given in one hour. As soon as cardiac rhythm returns to normal or respiratory muscle strength is restored to normal; IV potassium drip is to be tapered and switch to oral potassium therapy.
- 24. ASSO MAGNESIUM DEFICIENCY Always suspect if: Malnutrition/ alcoholic Diarrhoea Diuretics Not responding to replacement of hypokalemia even with adequate doses Associated hypocalcemia DM Aminoglycoside use
- 25. ORAL K+ SALTS: Oral salts are safer as having minimal risk of hyperkalemia Mild to mod hypo K+ ( 3 to 3.5 mEq/L): avg dose is 20 mEq 3 to 4 times a day along with treatment of underlying disorder Potassium chloride solution contains 20 mEq per 15 ml solution. KCl Tab contains 8 mEq per tab. May cause frequent GI Irritation; so advised to take solution with proper dilution with water and after food Oesophageal or small bowel erosion or stricture are uncommon side effects.
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