Lectures on increase and decrease the blood Potassium

2021-08-12 05:16 PM

If ECG shows changes of hyperkalemia, life-threatening arrhythmias can occur at any time during treatment

Whole-body potassium: 30 mEq/l, the predominant intracellular cation, only 2% in the extracellular area.

The daily intake of potassium is 50-100 mEq.

Potassium is excreted through feces and sweat 10 mEq/day, the rest is mainly excreted by the kidneys, so the kidneys play an important role in potassium balance.

Normal blood potassium is: 3.5 - 5 mEq/l.

Regulating potassium in the blood:

Due to the kidney.

Due to blood pH.

Due to insulin levels in the blood.

Do Aldosteron.

Hypokalemia 

When blood K + < 3 - 3.5 mEq/l, severe when < 2.5 mEq/l.

Cause

Gastrointestinal loss: diarrhea, enema, intestinal fistula, bile leak, ileostomy, vomiting, gastric aspiration, alkalosis.

Urinary loss: diuretics, antibiotics (Carbenicilline, Amphotericin, Aminoglycosides), osmotic diuretics, renal tubular acidosis, hyperaldosteronism, Fanconi's syndrome, excessive corticosteroid use, Bartter's syndrome.

Insufficient K+ intake: with daily potassium intake <10-20mEq for 1-2 weeks leading to hypokalemia.

K+ from extracellular to intracellular: by alkalizing the extracellular environment or using hypertonic Glucose + Insulin.

Clinical

Occurs when the concentration is < 3 – 3.5 mEq/l.

Signs of neuromuscular disorders: paresthesias, muscle weakness, decreased tendon reflexes, intestinal paralysis, constipation.

Postural hypotension.

Heart rhythm disturbances.

Increased sensitivity to digitalis.

Electrocardiographic changes: T wave is low, then flattened, U wave appears, T wave is negative, U wave is high, PR lengthens, ST low, AV block.

Glucose intolerance.

Metabolic alkalosis makes cirrhotic patients prone to hepatic coma.

Treatment

Eat a diet rich in potassium (fruits, vegetables).

Supplement potassium with pills.

Intravenous potassium type: suitable for patients with severe hypokalemia who cannot drink.

Potassium in the blood > 2.5 mEq/l: Infuse potassium at a rate < 10 mEq / 1 hour and concentration < 30 mEq / l do not use more than 100-200 mEq within 24 hours.

Blood potassium < 2.5 mEq/l with electrocardiographic changes and severe neuromuscular disorders, used at a velocity < 40 mEq/hour (mean 20 mEq/h) and concentration < 60 mEq/l, monitor Continuous ECG and serum potassium every 4-6 hours.

Potassium tablets commonly used: Kaleoride, Slow K.

Potassium tube type commonly used in the form: KCl 15% 30ml = 60mEq, KCl 10% 10ml = 13mEq.

Hyperkalemia 

Serum potassium > 5.5 mEq/l and weight > 6.5 mEq/l.

When blood potassium increases, it leads to interference with nerve conduction (Acetylcholine) leading to muscle paralysis, decreased tendon reflexes, cell edema, bradycardia, cardiac arrest (ventricular fibrillation or asystole).

Cause

Decreased renal excretion:

Acute renal failure, chronic renal failure, Addison's syndrome, Renin deficiency syndrome, Aldosterone, potassium-sparing diuretics, obstructive nephropathy.

Redistribution of potassium from intracellular fluid to extracellular fluid in cases of:

Acid blood.

Digitalis overdose, insulin deficiency, rapid increase in extracellular fluid osmolality (due to high use of hypertonic Glucose, Mannitol).

Potassium increased from exogenous sources:

Oral, potassium infusion, blood transfusion, high dose PNC K+ infusion (1 million PNCs contain 1.7 mEq Potassium).

Endogenous potassium is increased by tissue damage (hemolysis, rhabdomyolysis, major surgery, gastrointestinal bleeding, compression trauma).

False Potassium Boost:

Potassium released from coagulated blood samples with leukocytosis, thrombocytosis.

Hemolysis in blood samples.

Place the ligature for too long.

Clinical

Occurs when blood potassium concentration > 6.5 mEq/l.

Neuromuscular symptoms: paresthesia, muscle weakness, decreased reflexes, loss of reflexes, muscle paralysis.

Cardiac symptoms: mostly occur when the concentration is > 8 mEq/l and less when the concentration is 6.5 - 8 mEq/l.

Bradycardia, cardiac arrest due to ventricular fibrillation or asystole.

Electrocardiographic disturbances: sharp, large, and high T waves, ST decrease, P and R waves decrease in amplitude, PR prolongation, QRS dilation, QT prolongation. Loss of P wave.

Electrocardiographic changes are evident when blood pH decreases, blood Na+ decreases, and blood calcium decreases.

Emergency treatment

Treatment of hyperkalemia is aimed at:

Well, protect cells from the influence of Kalium (using Calcium).

Push potassium to move from the extracellular fluid into the intracellular fluid (Sodium bicarbonate, Insulin+Glucose, Beta 2 receptor).

Decreases total body potassium (cation exchange resins, dialysis).

Treatment is urgently needed if serum potassium is > 7 mEq/l or if the ECG shows changes to hyperkalemia, life-threatening arrhythmias can occur at any time during treatment. treat. Therefore, continuous monitoring by ECG is required.

Specifically:

K + 5.5 - 6 mmol/l, stop importing potassium into the body.

K > 6 mmol/l causes temporary hypokalemia by:

Calcium administration temporarily antagonizes the cardiac and neuromuscular effects of hyperkalemia:

Calcium gluconate 10% 10cc IV > 2 - 5 minutes, a second dose can be given after 5 minutes if there is no obvious response (ECG monitoring) and the effect is temporary for about 1 hour.

Sodium bicarbonate administration begins within 15 minutes and lasts 1 to 2 hours 8.4% NaHCO3 (50cc = 50mEq) IV > 5 minutes and repeats 15 to 30 minutes if ECG abnormalities persist.

Intravenous Glucose and Insulin:

Regular Insulin 10 UI IV at once with 1 ampoule of Glucose 50% 50 cc (25g) > 5 minutes, the response is seen within 30-60 minutes, lasts for many hours, or

Glucose 20% 250ml + Insulin 20UI IV/30-60' lasting 3-6 hours

Or: 100 mEq NaHCO3 (2 ampoules) + 1000cc Dextrose 10% with the first 300 cc for intravenous infusion > 30 min and the remainder > 3 hrs and 25 UI Regular Insulin S/C at the same time.

Diuretics:

Furosemide 40 mg IV.

Cation exchange resins:

The exchange between Na+ and K+ in the gut.

Sodium poly Styrene sulfonate (Kayexalate). [1g resins expels 1 mEq kalium from the body, and introduces 1.5 mEq Na+] (with caution in congestive heart failure or severe hypertension).

Oral A 15 - 30g combined with 50 - 100 cc Sorbitol 20% (to avoid constipation) / every 3 - 4 hours for a full dose of 4-5 doses/day, until no longer hyperkalemia.

Rectal A when oral intolerance or paralytic ileus, 50g mixed with 200cc Sorbitol 20% or Dextrose 20% can be easily retained for 30-60 minutes every 4-6 hours, for 4 doses/day (effective when pre-washed).

Dialysis (When K+ > 6.5 mEq/l):

Effective expulsion of Kalium from the body is often used for clinical conditions for which conservative methods have failed or are not appropriate.

Treatment of chronic hyperkalemia

Renin aldosterone syndrome (type IV renal tubular acidosis):

Reducing the diet with kalium to 40-60 mEq/day is sufficient if serum K+ is < 5.5 mEq/l.

Treatment with diuretics (Thiazide) does not use Spironolactone, triamterene, Amiloride.

Oral bicarbonate replacement (25-100mEq/day).

Fludrocortisone acetate 0.1 - 0.4 mg/day often causes Na+ retention and hypertension.

Long-term cation exchange resins are beneficial but poorly tolerated