Dr Hala Ezzat EidProfessor of Anesthesia and Intensive care

Ain Shams University

Potassium Disorders

Objectives:

By the end of this lecture and reviewing ERC guidelines you should be able to:

1. Define normal serum K, hyper/hypokalemia.

2. Enumerate causes of hyper/hypokalemia.

3. Recognize hyper/hypokalemia

4. Discuss management of hyper/hypokalemia and if any modifications to BLS/AlS .

Normal serum potassium

Extracellular potassium concentration 3.5 and 5.0 mmoll−1 (mmol/L).

N.B. 1mmol = 1mEq for univalent ions e.g. Na+, K+, HCO3

1mmol = 2 mEq for divalent ions e.g. Ca++, Mg++

So always use mmols

Understanding Role of K in membrane potential

Understanding Role of K in membrane potential

Sodium is predominantly an extracellular cation while potassium is predominantly an intracellular cation

Cell membrane is permeable to K but much less to Na, hence K+ diffuses down its concentration gradient out of the cell leaving behind negatively charged proteins. This leads to a potential difference across the membrane (a negative voltage on the inside relative to outside). .

Understanding Role of K in membrane potential

If K+ continued to leak out of the cell, its chemical gradient would be lost over time; however, a Na+/K+-ATPase pump brings the K+ back into the cell and thereby maintains the K+ chemical gradient (the pump moves three sodium ions out of the cell for every two potassium ions it puts in).

Understanding Role of K in membrane potential

During action potential Na+ channels open > Na+ enters the cells with reversal of membrane potential (positive IC)

Repolarization takes place mainly by potassium leaving the cells. Thus K+ has an important role in repolarization.

Where does potassium in blood come from?

GIT intake

Shift from ICF.(1) Insulin enhances potassium entry into cells(2) Beta-adrenergic agonists enhance potassium

entry into cells.(3) Alkalosis enhances potassium entry into cells

How does the body get rid of potassium?

1. Mainly RENAL excretion.

Aldosterone stimulates potassium secretion and sodium and water retention .

2. GIT losses.

3. Shift into ICF

N.B.

In acidosis H+ increase in ECF, so H+ move into the cell and K+ move out of the cell in order to decrease the acidity.

Beta-adrenergic agonists enhance potassium entry into cells (stimulates Na+-K= ATPase)

Understanding diabetic ketoacidosis:

Understanding body fluid compartment

Total body water (TBW) constitutes 60% of total body weight. For a 70 kg man, TBW = 0.6 x 70 = 42 L

 

Total body water (TBW) constitutes 60% of total body weight. For a 70 kg man, TBW = 0.6 x 70 = 42 L

Understanding ACEIs

Hyperkalaemia

This is the most common electrolyte disorder associated with cardiopulmonary arrest.

Serum K concentration higher than 5.5mmoll−1

Severe hyperkalaemia serum K > 6.5mmoll−1.

Causes of hyperkalemia:

N.B. Hemolysis of blood sample can cause Pseudohyperkalemia, because of the use of torniquet >> recheck in stable patients without a risk of hyperkalemia.

GIT IC compartment Renal Aldosteron

Diet Tissue breakdown (rhabdomyolysis, tumour lysis, haemolysis),Stored Packed red blood cells

Metabolic acidosis,beta-blockers, Insulin deficiency

Renal failure AddisonsACE-INSAIDsK sparing diuretics

Hyperkalemia

Excitable Tissues Effect

Nerve paraesthesia, depressed deep tendonreflexes

Sk Muscles Weakness, paralysis, respiratory failure

Cardiac ms ECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death

Hyperkalemia

Tall, peaked T waves

Flattened P waves

Prolonged PR interval

Widened QRS

Arrhythmias, cardiac arrest

N.B.

T wave represents ventricular repolarization

High serum K >> High T wave

Treatment of hyperkalaemia

There are three key treatments for hyperkalaemia5:

1. cardiac protection;

2. shifting potassium into cells;

3. removing potassium from the body.

CALL FOR HELP

Treatment of hyperkalaemia

Cardiac protection (In presence of ECG changes)

Calcium chloride (10%): 10 ml IV over 2 to 5 minutes.

It reduces the effects of potassium at the myocardial cell membrane and lowers risk of VF.

Treatment of hyperkalaemia

Shifting potassium into cells:

1. Glucose / insulin: 25 g glucose (50 mL of D50 or 100 ml D25) and 10 U regular insulin given IV over 15 to 30 minutes (onset 15–30 min)

2. Salbutamol 5mg nebulised. Several doses (10–20 mg) may be required (onset 15–30 min)

3. Sodium bicarbonate: 50 mmol IV over 5 minutes if metabolic acidosis present (onset 15–30 min).

Treatment of hyperkalaemia

Promote potassium excretion:

1. Diuresis: furosemide 40 to 80 mg IV

2. Potassium exchange resins

3. Dialysis

Treatment of hyperkalaemia

Hypokalaemia

Serum potassium < 3.5mmoll−1.

Severe hypokalaemia is defined as a K+ < 2.5mmoll−1

Causes of hypokalemia

GITIC compartment Renal Aldosteron

-Poor dietary intake-GIT loss (diarrhoea)laxatives

-Metabolic alkalosis-Beta-agonists -Insulin therapy

Renal losses (DI) DialysisDiuretics

-Cushing’s Syndrome -Hyperaldosteronism-Steroids

C/P hypokalemia

Excitable Tissues Effect

Sk Muscles weakness, cramps rhabdomyolysis, respiratory failure.

Smooth ms constipation.

Cardiac ms ECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death

Hypokalemia

U waves

T wave flattening

ST-segment changes

Arrhythmias, cardiac arrest

Hypokalemia

N.B.

The maximum recommended IV dose of potassium is 20 mmol per hour in an adult with continuous ECG monitoring during infusion.

Better via a central line. If using a peripheral line dilute in 500 ml ringer.

Reassess by measuring serum K. In severe hypokalemia >> give magnesium 4 mmol

(2 gm ) over 15 minutes i.v.i.

Hypokalemia

N.B>

Rapid infusion (10 mmol over 5 minutes and repeat once if needed, followed by 10mmol 10min if needed) is indicated for unstable arrhythmias when cardiac arrest is imminent.

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