1. Professor of Anesthesia and Intensive care
Potassium Disorders
Professional Diploma in Resuscitation
Dr Hala Ezzat Eid
Professor of Anesthesia and Intensive care
Ain Shams University

2. Objectives:
By the end of this lecture and reviewing ERC guidelines you should be able to:
Define normal serum K, hyper/hypokalemia.
Enumerate causes of hyper/hypokalemia.
Recognize hyper/hypokalemia
Discuss management of hyper/hypokalemia and if any modifications to BLS/AlS .

3. 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

4. Understanding Role of K in membrane potential

5. 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). .

6. 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).

7. 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.

8. Where does potassium in blood come from?
GIT intake
Shift from ICF.
Insulin enhances potassium entry into cells
Beta-adrenergic agonists enhance potassium entry into cells.
Alkalosis enhances potassium entry into cells

9. 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

10. 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)

11. Understanding diabetic ketoacidosis:

12. 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
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

13. Understanding ACEIs

14. 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.

15. Causes 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
Addisons
ACE-I
NSAIDs
K sparing diuretics
N.B. Hemolysis of blood sample can cause Pseudohyperkalemia, because of the use of torniquet >> recheck in stable patients without a risk of hyperkalemia.

16. Hyperkalemia Excitable Tissues Effect Nerve
paraesthesia, depressed deep tendon
reflexes
Sk Muscles
Weakness, paralysis, respiratory failure
Cardiac ms
ECG abnormalities,
arrhythmias, cardiopulmonary arrest or sudden death

17. Arrhythmias, cardiac arrest
Hyperkalemia
Tall, peaked T waves
Flattened P waves
Prolonged PR interval
Widened QRS
Arrhythmias, cardiac arrest

18. N.B.
T wave represents ventricular repolarization
High serum K >> High T wave

19. Treatment of hyperkalaemia
There are three key treatments for hyperkalaemia5:
1. cardiac protection;
2. shifting potassium into cells;
3. removing potassium from the body.

20. Treatment of hyperkalaemia
CALL FOR HELP

21. 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.

22. Treatment of hyperkalaemia
Shifting potassium into cells:
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)
Salbutamol 5mg nebulised. Several doses (10–20 mg) may be required (onset 15–30 min)
Sodium bicarbonate: 50 mmol IV over 5 minutes if metabolic acidosis present (onset 15–30 min).

23. Treatment of hyperkalaemia
Promote potassium excretion:
Diuresis: furosemide 40 to 80 mg IV
Potassium exchange resins
Dialysis

24. Hypokalaemia Serum potassium < 3.5mmoll−1.
Severe hypokalaemia is defined as a K+ < 2.5mmoll−1

25. Causes of hypokalemia GIT IC compartment Renal Aldosteron
-Poor dietary intake
-GIT loss (diarrhoea)
laxatives
-Metabolic alkalosis
-Beta-agonists
-Insulin therapy
Renal losses (DI) Dialysis
Diuretics
-Cushing’s Syndrome -Hyperaldosteronism
-Steroids

26. 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

27. Hypokalemia U waves T wave flattening ST-segment changes
Arrhythmias, cardiac arrest
Due to prolonged repolarization of ventricular Purkinje fibers, a prominent U wave occurs, that is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval.

28. 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.

29. 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.

30. ?

31. Thank You