ACUTE MANAGEMENT OF Hyperkalemia
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This document discusses hyperkalemia, or high levels of potassium in the blood. It begins by listing the normal potassium range and then describes some common causes of hyperkalemia, including the release of potassium from cells due to conditions like rhabdomyolysis or tumor lysis syndrome, and decreased renal excretion of potassium due to renal failure or medications. Clinical manifestations of hyperkalemia are then outlined, such as weakness, paralysis, arrhythmias, and ECG changes including peaked T waves. The document concludes by presenting two case histories of patients with hyperkalemia and CKD and recommends treatment approaches starting with calcium gluconate for cardiac instability and then other options to increase potassium excretion or remove it through dialysis if
![ECG changes
All of the illustrations are from lead V3.
A. Serum [K+] = 6.8 mEq/L
note the peaked T waves together with
normal sinus rhythm.
B. Serum [K+] = 8.9 mEq/L
note the peaked T waves and absent P
waves.
C. Serum [K+] = >8.9 mEq/L
note the classic sine wave with absent P
waves, marked prolongation of the QRS
complex, and peaked T waves](https://image.slidesharecdn.com/hyperkalemiafriday-190812150452/85/ACUTE-MANAGEMENT-OF-Hyperkalemia-8-320.jpg)
ACUTE MANAGEMENT OF Hyperkalemia
- 1. HYPERKALEMIA DR ANKIT GAJJAR MD, IDCCM, IFCCM, EDIC CONSULTANT INTENSIVIST
- 2. Potassium •Normal range : 3.5 – 5 mEq/L
- 3. Causes of Hyperkalemia - Potassium release from cells - Decreased renal loss - Iatrogenic
- 4. Potassium release from cells • Intravascular hemolysis • Tumor Lysis Syndrome • Rhabdomyolysis • Metabolic acidosis • Severe Digitalis toxicity • Beta-blockers • Succinylcholine; especially in case massive trauma, burns or neuromuscular disease
- 5. Decreased renal loss • Renal failure • Decreased distal flow • Decreased K+ secretion Impaired Na+ reabsorption adrenal insufficiency drugs: ACEi, NSAIDS, heparin, K+-sparing diuretics, trimethoprim, pentamidine distal type 4 RTA
- 6. Clinical Manifestations • Weakness, which can progress to flaccid paralysis and hypoventilation. Secondary to prolonged partial depolarization from the elevated K+ , which impairs membrane excitability. • Metabolic acidosis, which further increases K+ Secondary to hyperkalemia impairing renal ammoniagenesis and absorption, and thus net acid excretion. • Altered electrical activity of heart, cardiac arrhythmias.
- 7. ECG Changes of Hyperkalemia • Easily Distinguished ECG signs: – peaked T wave. – prolongation of the PR interval – ST changes (which may mimic myocardial infarction) – very wide QRS, which may progress to a sine wave pattern and asystole. • Patients may have severe hyperkalemia with minimal ECG changes, and prominent ECG changes with mild hyperkalemia.
- 8. ECG changes All of the illustrations are from lead V3. A. Serum [K+] = 6.8 mEq/L note the peaked T waves together with normal sinus rhythm. B. Serum [K+] = 8.9 mEq/L note the peaked T waves and absent P waves. C. Serum [K+] = >8.9 mEq/L note the classic sine wave with absent P waves, marked prolongation of the QRS complex, and peaked T waves
- 9. Case history • 55 years old female A. H/O fever CKD On evaluation, S.K+ - 6.5 No ECG changes What next? B. H/O fever CKD On evaluation, S.K+ - 6.5 ECG – peaked T wave What next?
- 10. 1st Line option
- 11. OTHER THERAPIES ● Hypertonic saline, where calcium administration is contraindicated ● NaHCO3 infusion – only in metabolic acidosis (pH < 7.2) pts - Need to consider side effects like volume overload, hypernatremia, hypocalcemia - Dose - ????? K-BIND SACHETS??? • HEMODIALYSIS. . Peritoneal is only 15% as effective as hemodialysis
- 12. ● STEP 1 – Calcium Gluconate, if cardiac instability ● STEP 2 – Discontinue offending agent ● STEP 3 – GI drip (1st choice) - B2 agonist nebulisation - NaHCO3 if Metabolic acidosis (Ph<7.2) ● STEP 4 – Increase potassium excretion - Loop diuretics - K BIND ● STEP 5 – Dialysis
- 13. THANK YOU
Editor's Notes
- #4: Pseudohyperkalemia: exit of K+ from cells at time of venipuncture; tourniquet left too long, hemolysis, marked leucocytosis or thrombocytosis (latter two secondary to release of intracellular K+ after clot formation). Mention blood transfusions with iatrogenic.
- #5: Exer. Induced proportionate to degree exertion. BB mild degree. HyperKalemic PP: autosomal dominant d/o; episodic weakness/paralysis precipitated by stimuli that cause mild hyperkalemia; mutated skeletal musc. Na+ channel. Digitalis secondary inhibition Na/K/ATPase pump.
- #6: This category associated overall with chronic hyperkalemia. Decreased distal flow: excretion = concentration x volume. Seldom the only cause. Hyporeninemia: seen in mild CKD, diabetic nephropathy, chronic tubulointerstitial disease. Gordon’s: hyperkalemia, met acidosis, with normal GFR
- #7: Impaired net acid excretion occurs in the TALH.
- #8: Review: ECG changes of Hyperkalemia, may review back to ECG example in slide 5
- #10: Review: Peaked T-waves (V2-V5), widened QRS and prolonged PR interval resulting in (Sine-wave)- I, AvR, V1-V2 .
- #12: Table of Pharmacological interventions summarized
- #13: Review: ECG changes of Hyperkalemia, may review back to ECG example in slide 5