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ECG: Hypokalemia
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  • 1. PROF.DR. G.SUNDARAMURTHY’S UNIT – M5
  • 2.
    • ECG OF THE WEEK
    • Prof. G Sundaramurthy’s Unit
    • P.Vanjinathan
  • 3.
    • 52 yrs old male,
    • C/o Loose stools X 4 days
      • 8-10 episodes/day, watery
      • assc. vomiting +
      • No blood/mucus/tenesmus
    • H/o Vomiting +
      • 4 – 5 episodes/day
      • Colourless, watery, non-bilious, no blood
      • H/o Fatiguability +
      • H/o Cramps +
  • 4.
    • ON EXAMINATION:
    • Pulse– 76 per min
    • BP---100/70mmHg
    • RR---16per min
  • 5. ECG
  • 6.  
  • 7.
    • HR - 70/min
    • Rhythm - Normal sinus rhythm
    • PR interval - 0.12 sec
    • P wave - Normal morphology
    • QRS interval - 0.08 sec
    • QT interval - Prolonged
    • QRS Voltage - Normal
    • QRS axis - Normal axis
    • R wave progression - Normal
  • 8.
    • Abnormal Q wave - No abnormal Q wave
    • ST segment - Depression in V 3 -V 6
    • T wave - Amplitude decreased
    • U wave - Seen in L Ӏ I , L Ӏ II ,aVF,V 2 -V 6
  • 9. INVESTIGATIONS
    • CBC--- NORMAL
    • URINE ROUTINE---NORMAL
    • RFT---UREA- 30mgs/dl
    • CREAT-0.9mgs/dl
    • ELECTROLYTES---Na---128meq
    • K----2.7meq
  • 10. ECG Changes in Hypokalemia
    • Early changes :
      • Flattening or inversion of T waves
      • Prominent U waves
      • ST segment depression
      • Prolonged QT interval
    • Severe Potassium depletion:
      • Prolonged PR interval
      • Decreased voltage of QRS
      • Widening of QRS complex
      • Ventricular arrhythmia
  • 11. Causes of Hypokalemia
    • Decreased intake
    • Redistribution into cells
      • Acid base - Metabolic acidosis
      • Hormonal – Insulin, β 2 agonist, α -Antagonist.
      • Anabolic state – B 12 / Folic acid supplements
      • Others – Pseudohypokalemia, Hypothermia, Hypokalemic periodic paralysis
  • 12.
    • Increased Loss
      • Non renal - GI loss, Integumentary loss (sweat)
      • Renal -
        • Increased distal flow : diuretics, osmotic diuresis, salt-wasting nephropathies
        • Increased secretion of potassium:
          • Mineralocorticoid excess : Primary hyperaldosteronism, Secondary hyperaldosteronism (malignant hypertension, Renin-secreting tumors, Renal artery stenosis, Hypovolemia), Congenital adrenal hyperplasia, Cushing's syndrome, Bartter's syndrome
          • Distal delivery of non-reabsorbed anions : vomiting, NG suction, proximal (type 2) RTA, DKA, penicillin derivatives
          • Others: Amphotericin B, Liddle's syndrome, Hypomagnesemia
  • 13. CLINICAL FEATURES
    • Neuromuscular : Fatigue, myalgia, and muscular weakness of the lower extremities.
      • Smooth muscle involvement – Constipation, ileus, urinary retention
      • progressive weakness, hypoventilation (due to respiratory muscle involvement), and eventually complete paralysis
    • Impaired ability of kidneys to concentrate urine – Polyuria, urine with low osmolality, polydipsia
    • GI manifestations :
      • Anorexia, nausea, vomiting
      • Constipation, Abdominal distension, paralytic ileus
    • CVS – Arrhythmias
    • Metabolic alkalosis
  • 14. Treatment
    • Correct volume depletion & Rx of underlying etiology
    • Estimate the K + deficit
      • 1 mEq/L = Total body K + deficit of 200 to 400 mEq
    • If no ECG changes - start oral K + supplementation
    • If ECG changes present – Start I.V K + repletion
      • Rate of < 20 mEq/hr
      • In peripheral vein < 40 mEq/L
      • In central vein < 60 mEq/L
    • Monitor K + during therapy
    • Search for & Rx hypomagnesemia
  • 15. Treatment Contd...
    • Preparations Available
      • Various salts of K + : Cl - , HCO 3 - , Phosphate & Gluconate salts
      • KCl : More effective in hypokalemia with metabolic alkalosis . (e.g. Diuretic usage, Diarrhea)
      • KHCO 3 / K Citrate : Hypokalemia & metabolic acidosis (e.g. RTA)
  • 16. THANK YOU