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![3. Inadequate excretion
A. Inhibition of the renin-angiotensin-aldosterone axis; I risk of hyperkalemia
when used in combination
1. Angiotensin- converting enzyme (ACE) inhibitors
2. Renin inhibitors, aliskiren (in combination with ACE inhibitors or angiotensin
receptor blockers ARBs])
3. ARBs
4. Blockade of the mineralocorticoid receptor: spironolactone, eplerenone,
drospirenone
5. Blockade of the epithelial sodium channel (ENaC): amiloride, triamterene,
trimethoprim, pentamidine, nafamostat
B. Decreased distal delivery
1. Congestive heart failureINSPIOBO
2. Volume depletion](https://image.slidesharecdn.com/potassiumimbalance-250728171511-452e5424/75/Presentation-About-Potassium-Imbalance-with-Causes-Management-Types-19-2048.jpg)
![Treatment: Treatment of hyperkalaemia depends on the severity and the rate of development
1. In the absence of neuromuscular symptoms or ECG changes, reduction of potassium intake and correction of
underlying abnormalities may be sufficient.
2. Acute &/or severe hyperkalaemia more urgent measures must be taken:
Mechanism Therapy
Stabilization of the cell
membrane potential
• I/V calcium gluconate (10 ml of 10% solution) is to be given very
slowly over 10-20 minutes.
To shift into K+
cells • Inhaled ß2 agonist: Nebulization with Salbutamol.
• Glucose with Insulin: 50 ml of 50% glucose with 5-10 IU Insulin-R
[or 100 ml 25% glucose + Inj. Insulin-R 10 IU in Bangladesh].
• Correction of acidosis: I/V sodium bicarbonate (100ml of 8.4%
solution)
To remove K+
from
body
• Intravenous furosemide and normal saline.
• Ion-exchange resin (e.g. Resonium) orally or rectally.
• Newer Cation Exchange resin (Ex. Sodium zirconium cyclosilicate)
• Dialysis.](https://image.slidesharecdn.com/potassiumimbalance-250728171511-452e5424/75/Presentation-About-Potassium-Imbalance-with-Causes-Management-Types-29-2048.jpg)
Presentation About Potassium Imbalance with Causes,Management, Types
- 1. Potassium Imbalance Speakers : Dr.FariaJahan Mumu Dr.Ashraful Alam Intern Doctor Dept. of Medicine Central Medical College
- 2. POTASSIUM • Normal serumlevel of K+ : 3.5- 5.0 mmol/L • 98% of body potassium is intracellular whereas only 2% of it is extracellular
- 5. HYPOKALAEMIA Defination: When K+ levelgo below 3.5 mmol/L
- 6. Causes of Hypokalemia 1.Decreased intake A. Starvation B. Clay ingestion 2. Redistribution into cells C. Acid-base I. Metabolic alkalosis B. Hormonal 1. Insulin 2. Increased By-adrenergic sympathetic activity: post-myocardialinfarction, head injurv 3. B, Adrenergic agonists -bronchodilators, tocolytics 4. a-Adrenergic antagonists 5. Thyrotoxic periodic paralysis 6. Downstream stimulation of Na-/K+-ATPase: theophylline, caffeine
- 7. C. Anabolic state a)Vitamin B, or folic acid administration (red blood cell production) b) Granulocyte-macrophage colony-stimulating factor (white blood cellproduction) c) Total parenteral nutrition d) Other 1. Pseudohypokalemia 2. Hypothermia 3. Familial hypokalemic periodic paralvsis 4. Barium toxicity: systemic inhibition of "leak" K* channel
- 8. 3. Increased loss A.Nonrenal 1. Gastrointestinal loss (diarrhea) 2. Integumentary loss (sweat) B. Renal 1.Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis, salt- wasting nephropathies 2. Increased secretion of potassium a. Mineralocorticoid excess: primary hyperaldosteronism ,Aldosterone-producing adenomas, primary or unilateral adrenal hyperplasia, idiopathic hyperaldosteronism due to bilateral adrenal hyperplasia, and adrenal carcinoma), genetic hyperaldosteronism (familial hyperaldosteronism types V/I/II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), Cushing's syndrome, Barter's syndrome, Gielman’s syndrome b. Apparent mineralocorticoid excess: genetic deficiency of11-dehydrogenase-2 (syndrome of apparent mineralocoricoid excess c. Distal delivery of nonreabsorbed anions vomting, nasogastric suction proximal renal tubular acidosis, DKA, penicilin derivatives 3. Magnesium deficiency
- 9. Clinical Features 1. Muscularweakness. 2. Tiredness 3. Fatigue 4. Myalgia 5. Abdominal distention due to paralytic ileus 6. Features of arrhythmia: Palpitation, irregular pulse, hypotension
- 11. Investigations: 1. Measurement ofplasma electrolytes 2. Plasma bicarbonate 3. Arterial Blood Gas (ABG) Analysis 4. Urine potassium and sometimes calcium and magnesium 5. ECG.
- 12. Figure-2: ECG changesin Hypokalaemia ECG changes in hypokalaemia: Flattened T wave ST-depression Appearance of U wave
- 13. Complications of hypokalaemia 1.Cardiac arrhythmia (most dangerous) 2. Cardiac arrest 3. Paralytic ileus 4. Metabolic alkalosis 5. Muscular weakness, depression, myopathy etc. 6. Acute confusional state / delirium 7. Constipation 8. Nephrogenic diabetes incipidus
- 16. Type of HypokalaemiaSerum level of K+ Correction of K+ Mild Hypokalaemia 3-3.5 mmol/L Oral Correction by- • Green coconut water • Fruit and fruit juice • Banana • Orange • Pineapple • Potato • Bean etc. Moderate Hypokalaemia 2.5- 3.0 mmol/L Oral K+ Supplementation by potassium tablet (must be with half glass of water and in full stomach) and syrup (in full stomach) Severe Hypokalaemia 2.5 mmol/L ˂ I/V correction • Intravenous potassium diluted in normal saline • Not more than 10 mmol/hour • 1 ampoule contains 20 mmol of potassium • 1 litre of normal saline should not be mixed with more than 40 mmol (i.e. 2 ampoules) Treatment Note: Never Administer Potassium Directly via IV Route Direct IV push can cause severe cardiac complications
- 17. HYPERKALAEMIA Definition: When potassiumlevel exceed 5 mmol/L
- 18. Causes of HYPERKALAEMIA 1.Pseudohyperkalemia A. Cellular efflux, thrombocytosis, erythrocytosis, leukocytosis, in vitrohemolysis B. Hereditary defects in red cell membrane transport 2. Intra- to extracellular shift A. Acidosis B. Hyperosmolality; radiocontrast, hypertonic dextrose, mannitol C. B2,- Adrenergic antagonists (noncardioselective agents) D. Digoxin and related glycosides (yellow oleander, foxglove, bufadienolide) E. Hyperkalemic periodic paralysis F. Lvsine, arginine, and e-aminocaproic acid (structurally similar, positivelycharged) G. Succinylcholine; thermal trauma, neuromuscular injury, disuse atrophy. mucositis, or prolonged immobilization si H. Rapid tumor lysisII.
- 19. 3. Inadequate excretion A.Inhibition of the renin-angiotensin-aldosterone axis; I risk of hyperkalemia when used in combination 1. Angiotensin- converting enzyme (ACE) inhibitors 2. Renin inhibitors, aliskiren (in combination with ACE inhibitors or angiotensin receptor blockers ARBs]) 3. ARBs 4. Blockade of the mineralocorticoid receptor: spironolactone, eplerenone, drospirenone 5. Blockade of the epithelial sodium channel (ENaC): amiloride, triamterene, trimethoprim, pentamidine, nafamostat B. Decreased distal delivery 1. Congestive heart failureINSPIOBO 2. Volume depletion
- 20. C. Hyporeninemic hypoaldosteronism 1.Tubulointerstitial diseases: systemic lupus ervthematosus (SLE), sickle cell anemia, obstructive uropathy 2. Diabetes, diabetic nephropathy 3. Drugs: nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase2 (COX2) inhibitors, ß blockers, cyclosporine, tacrolimus 4. Chronic kidney disease, advanced age D. Renal resistance to mineralocorticoid 1. Tubulointerstitial diseases: SLE, amyloidosis, sickle cell anemia, obstructive uropathy, post-acute tubular necrosis
- 21. E. Advanced renalinsufficiency 1. Chronic kidney disease 2. End-stage renal disease 3. Acute oliguric kidney injury F. Primary adrenal insufficiency 4. Autoimmune: Addison's disease, polyglandular endocrinopathy 5. Infectious: HIV, cytomegalovirus, tuberculosis, disseminated fungal infection 6. Infiltrative: amyloidosis, malignancy, metastatic cancer 7. Drug-associated: heparin, low-molecular-weight heparin 8. Hereditary: adrenal hypoplasia congenita, congenital lipoid adrenal hyperplasia, aldosterone synthase deficiency 9. Adrenal hemorrhage or infarction, including in antiphospholipid Syndrome
- 22. Clinical Features Mainly cardiacand central nervous system depression, such as – Progressive muscular weakness Mental confusion Bradycardia Cardiac arrhythmia Cardiac arrest
- 24. Investigations: Plasma electrolytes Plasma creatinine Plasma bicarbonate Arterial Blood Gas (ABG) Analysis ECG findings: Tall T wave in ECG with widening of QRS complex.
- 25. Figure-1: ECG changesin Hyperkalaemia
- 26. Complication • Cardiac arrhythmia(VT, VF), • Cardiac arrest • Death
- 27. Management Approach History: Historyof potassium containing drug intake History of intake of drugs that can increase serum potassium e.g. spironolactone, ACE inhibitors etc. History of CKD History of any condition that can cause renal impairment Any condition that can cause metabolic acidosis History of crush injury or soft tissue damage Massive blood transfusion.
- 29. Treatment: Treatment ofhyperkalaemia depends on the severity and the rate of development 1. In the absence of neuromuscular symptoms or ECG changes, reduction of potassium intake and correction of underlying abnormalities may be sufficient. 2. Acute &/or severe hyperkalaemia more urgent measures must be taken: Mechanism Therapy Stabilization of the cell membrane potential • I/V calcium gluconate (10 ml of 10% solution) is to be given very slowly over 10-20 minutes. To shift into K+ cells • Inhaled ß2 agonist: Nebulization with Salbutamol. • Glucose with Insulin: 50 ml of 50% glucose with 5-10 IU Insulin-R [or 100 ml 25% glucose + Inj. Insulin-R 10 IU in Bangladesh]. • Correction of acidosis: I/V sodium bicarbonate (100ml of 8.4% solution) To remove K+ from body • Intravenous furosemide and normal saline. • Ion-exchange resin (e.g. Resonium) orally or rectally. • Newer Cation Exchange resin (Ex. Sodium zirconium cyclosilicate) • Dialysis.
- 30.