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PROF.DR. G.SUNDARAMURTHY’S UNIT – M5

ECG: Hypokalemia

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Page 1: ECG: Hypokalemia

PROF.DR. G.SUNDARAMURTHY’S UNIT – M5

Page 2: ECG: Hypokalemia

ECG OF THE WEEK Prof. G Sundaramurthy’s Unit

P.Vanjinathan

Page 3: ECG: Hypokalemia

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 +

Page 4: ECG: Hypokalemia

• ON EXAMINATION:

Pulse– 76 per min

BP---100/70mmHg

RR---16per min

Page 5: ECG: Hypokalemia

ECG

Page 6: ECG: Hypokalemia
Page 7: ECG: Hypokalemia

• 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

Page 8: ECG: Hypokalemia

• Abnormal Q wave - No abnormal Q wave

• ST segment - Depression in V3-V6

• T wave - Amplitude decreased

• U wave - Seen in LӀI, LӀII,aVF,V2-V6

Page 9: ECG: Hypokalemia

INVESTIGATIONS

• CBC--- NORMAL

• URINE ROUTINE---NORMAL

• RFT---UREA- 30mgs/dl

CREAT-0.9mgs/dl

ELECTROLYTES---Na---128meq

K----2.7meq

Page 10: ECG: Hypokalemia

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

Page 11: ECG: Hypokalemia

Causes of Hypokalemia

1. Decreased intake

2. Redistribution into cells

a. Acid base - Metabolic acidosis

b. Hormonal – Insulin, β2 agonist, α-Antagonist.

c. Anabolic state – B12 / Folic acid supplements

d. Others – Pseudohypokalemia, Hypothermia, Hypokalemic periodic paralysis

Page 12: ECG: Hypokalemia

3. Increased Loss

A. Non renal - GI loss, Integumentary loss (sweat)

B. Renal -

i. Increased distal flow: diuretics, osmotic diuresis, salt-wasting nephropathies

ii. Increased secretion of potassium:a. Mineralocorticoid excess: Primary hyperaldosteronism,

Secondary hyperaldosteronism (malignant hypertension, Renin-secreting tumors, Renal artery stenosis, Hypovolemia), Congenital adrenal hyperplasia, Cushing's syndrome, Bartter's syndrome

b. Distal delivery of non-reabsorbed anions: vomiting, NG suction, proximal (type 2) RTA, DKA, penicillin derivatives

c. Others: Amphotericin B, Liddle's syndrome, Hypomagnesemia

Page 13: ECG: Hypokalemia

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

Page 14: ECG: Hypokalemia

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

Page 15: ECG: Hypokalemia

Treatment Contd...

• Preparations Available

– Various salts of K+ : Cl-, HCO3-, Phosphate & Gluconate salts

– KCl : More effective in hypokalemia with metabolic alkalosis . (e.g. Diuretic usage, Diarrhea)

– KHCO3 / K Citrate : Hypokalemia & metabolic acidosis (e.g. RTA)

Page 16: ECG: Hypokalemia

THANK YOU