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![ III. Inadequate excretion
A. Inhibition of the renin-angiotensin-
aldosterone axis;
(↑ risk of hyperkalemia when these drugs are
used in
combination)
Angiotensin-converting enzyme (ACE) inhibitors
Renin inhibitors; aliskiren
(in combination with ACE inhibitors or angiotensin
receptor blockers [ARBs])](https://image.slidesharecdn.com/hyperkalemia-160108171542/75/Hyperkalemia-10-2048.jpg)
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Hyperkalemia
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
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Hyperkalemia
- 1.
- 2. PHYSIOLOGY Potassium isa major intracellular cation Total body K+ content in a normal adult -3000- 4000mEq 98% Intracellular , 2% in ECF Normal homeostatic mechanisms maintain the serum K level within a narrow range (3.5-5.0 mEq/L).
- 3. The primarymechanisms maintaining this balance are the buffering of ECF potassium against a large ICF potassium pool (via the Na-K pump) Na-K ATPase pump actively transports Na+ out of the cell and K+ into the cell in a 3:2 ratio Renal excretion – Major route of excess K+ elimination Approx 90% of K+ excretion occurs in the urine, less than 10% excreted through sweat or stool.
- 4. Within thekidneys, K+ excretion occurs mostly in the principal cells of the cortical collecting duct (CCD). Urinary K+ excretion depends on : 1. luminal Na+ delivery to the DCT and the CCD, 2. effect of Aldosterone and other adrenal corticosteroids with mineralocorticoid activity.
- 6. Factor Effect onPlasma K+ Mechanism Aldosterone Decrease Increases sodium resorption, and increases K+ excretion Insulin Decrease Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process) Beta-adrenergic agents Decrease Increases skeletal muscle uptake of K+ Alpha-adrenergic agents Increase Impairs cellular K+ uptake Acidosis (decreased pH) Increase Impairs cellular K+ uptake Alkalosis (increased pH) Decrease Enhances cellular K+ uptake Cell damage Increase Intracellular K+ release Succinylcholine Increase Cell membrane
- 7. HYPERKALEMIA Defined asa plasma potassium level of >5.5 mEq/L Causes of Hyperkalemia I. Pseudohyperkalemia Artifactual increase in K+- Venepuncture, clenching Cellular efflux; thrombocytosis, erythrocytosis, leukocytosis, in vitro hemolysis Hereditary defects in red cell membrane
- 8. II. Intra- toextracellular shift Acidosis – Uptake of H+, efflux of K+ NAGMA Hyperosmolality; hypertonic dextrose, mannitol, - Solvent Drag effect β2-Adrenergic antagonists (noncardioselective agents) Suppresses catecholamine stimulated renin release- in turn aldosterone synthesis Digoxin and related glycosides (yellow oleander,
- 9. Hyperkalemic periodicparalysis- Episodic attack of muscle weakness asso with Hyper k+. Na Muscle channelopathy Lysine, arginine, and ε-aminocaproic acid (structurally similar, positively charged) Succinylcholine; depolarises Muscle cells, Efflux of K+ through AChRs . Contraindicated in thermal trauma, neuromuscular injury, disuse atrophy, mucositis, or prolonged immobilization- upregulated AChRs Rapid tumor lysis / Rhabdomyolysis
- 10. III. Inadequateexcretion A. Inhibition of the renin-angiotensin- aldosterone axis; (↑ risk of hyperkalemia when these drugs are used in combination) Angiotensin-converting enzyme (ACE) inhibitors Renin inhibitors; aliskiren (in combination with ACE inhibitors or angiotensin receptor blockers [ARBs])
- 11. Angiotensin receptorblockers (ARBs) Blockade of the mineralocorticoid receptor: - spironolactone, eplerenone, Blockade of the epithelial sodium channel (ENaC): amiloride, triamterene, trimethoprim, pentamidine, nafamostat B. Decreased distal delivery Congestive heart failure Volume depletion
- 12. C. Hyporeninemic hypoaldosteronism Tubulointerstitial diseases: SLE, sickle cell anemia, obstructive uropathy Diabetes, diabetic nephropathy Drugs: nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase 2 (COX2) inhibitors, β- blockers, cyclosporine, tacrolimus
- 13. Chronic kidneydisease, advanced age Pseudohypoaldosteronism type II: defects in WNK1 or WNK4 kinases, Kelch-like 3 (KLHL3), or Cullin 3 (CUL3) In The above said conditions –most Pt will be volume expanded- secondary increse in circulating ANP that inhibit both Renal renin release and adrenal aldosterone release
- 14. D. Renal resistanceto mineralocorticoid Tubulointerstitial diseases: SLE, amyloidosis, sickle cell anemia, obstructive uropathy, post–acute tubular necrosis Hereditary: pseudohypoaldosteronism type I; defects in the mineralocorticoid receptor or the epithelial sodium channel (ENaC) E. Advanced renal insufficiency Chronic kidney disease End-stage renal disease Acute oliguric kidney injury
- 15. F. Primary adrenalinsufficiency Autoimmune: Addison’s disease, polyglandular endocrinopathy Infectious: HIV, cytomegalovirus, tuberculosis, disseminated fungal infection Infiltrative: amyloidosis, malignancy, metastatic cancer Drug-associated: heparin, low-molecular-weight heparin Hereditary: adrenal hypoplasia congenita, congenital lipoid adrenal hyperplasia, aldosterone synthase deficiency Adrenal hemorrhage or infarction, including in antiphospholipid syndrome
- 16. Clinical Features Most of Hyperkalemic individuals are asymptomatic. If present - symptoms are nonspecific and predominantly related to muscular or cardiac functions. The most common - weakness and fatigue. Occasionally, frank muscle paralysis or shortness of breath. Patients also may complain of palpitations or chest pain. Arrythmias occur- Sinus Brady, Sinus arrest, VT, VF, Asystole Patients may report nausea, vomiting, and paresthesias
- 17. ECG Changes ECG findings generally correlate with the potassium level, Potentially life-threatening arrhythmias - occur without warning at almost any level of hyperkalemia. In patients with organic heart disease and an abnormal baseline ECG, bradycardia may be the only new ECG abnormality.
- 18. K+ 5.5-6.5mEq/L - Early changes include tall, peaked T waves with a narrow base, best seen in precordial leads; shortened QT interval; and ST-segment depression. K+ level of 6.5-8.0 mEq/L, in addition to peaked T waves, Widening of the QRS Prolonged PR interval Decreased or disappearing P wave Amplified R wave
- 19. • Tall, symmetricallypeaked T waves. This patient had a serum K+ of 7.0.
- 20. K+ levelhigher than 8.0 mEq/L, The ECG shows absence of P wave, progressive QRS widening, and intraventricular/fascicular/bundle-branch blocks. The progressively widened QRS eventually merges with the T wave, forming a sine wave pattern. Ventricular fibrillation or asystole follows.
- 21. Sine wave appearancewith severe hyperkalaemia (K+ 9.9 mEq/L).
- 22.
- 23. Tests InEvaluation of Hyperkalemia RFT Serum Electrolytes- including Mg, Ca Urine potassium, sodium, and osmolality Complete blood count (CBC) Metabolic profile ECG
- 24. Trans-tubular potassium gradient(TTKG) TTKG is an index reflecting the conservation of potassium in the cortical collecting ducts (CCD) of the kidneys. It is useful in diagnosing the causes of hyperkalemia or hypokalemia. TTKG estimates the ratio of potassium in the lumen of the CCD to that in the peritubular capillaries. TTKG= Urine K/ Serum K x serum Osm/Urine osm
- 27. TREATMENT 3 mainapproaches to the treatment of hyperkalemia : ●Antagonizing the membrane effects of potassium with calcium ●Driving extracellular potassium into the cells ●Removing excess potassium from the body
- 28. ECG manifestationsof hyperkalemia- a medical emergency and treated urgently. Patients with significant hyperkalemia (K+≥6.5 mM) in the absence of ECG changes should also be aggressively managed Immediate antagonism of the cardiac effects of hyperkalemia IV calcium serves to protect the heart, recommended dose is 10 mL of 10% calcium gluconate, infused intravenously over 2–3 min with cardiac monitoring.
- 29. Rapid reductionin plasma K+ concentration by redistribution into cells. Insulin lowers plasma K+ concentration by shifting K+ into cells - GI Bolus β2-agonists, most commonly albuterol, are effective but underused agents for the acute management of hyperkalemia. – Salbutamol Nebulisations
- 30. Removal ofpotassium. use of cation exchange resins, Diuretics, and/or Hemodialysis. Cation Exchange Resins sodium polystyrene sulfonate (SPS) exchanges Na+ for K+in the gastrointestinal tract and increases the fecal excretion of K+ Dose of SPS is 15–30 g of powder, almost always given in a premade suspension with 33% sorbitol. The effect of SPS on plasma K+ concentration is slow; the full effect may take up to 24 h and usually requires repeated doses every 4–6 h.
- 31. Therapy withintravenous saline may be beneficial in hypovolemic patients with oliguria and decreased distal delivery of Na+, with the associated reductions in renal K+ excretion. Loop and Thiazide diuretics can be used to reduce plasma K+ concentration in volume-replete or hypervolemic patients with sufficient renal function usually combined with iv saline or isotonic bicarbonate to achieve or maintain euvolemia
- 32. Sodium Bicarbonatemay be given for the treatment of significant metabolic acidosis . Reversible causes of impaired renal function asso with hyperkalemia. Includes hypovolemia, NSAIDs, urinary tract obstruction, and inhibitors of the renin-angiotensin- aldosterone system (RAAS), which can also directly cause hyperkalemia RX- Removal of offending agent & Hydration
- 33. Hemodialysis isthe most effective and reliable method to reduce plasma K+ . The amount of K+ removed during hemodialysis depends on The relative distribution of K+ between ICF and ECF The type and surface area of the dialyzer used, dialysate and blood flow rates, dialysate flow rate, dialysis duration, and the plasma-to- dialysate K+ gradient.