Dr Hala Ezzat Eid Professor of Anesthesia and Intensive care Ain Shams University Potassium...
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Dr Hala Ezzat EidProfessor of Anesthesia and Intensive care
Ain Shams University
Potassium Disorders
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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 .
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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
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Understanding Role of K in membrane potential
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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). .
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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).
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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.
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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
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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
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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)
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Understanding diabetic ketoacidosis:
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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
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Understanding ACEIs
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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.
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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
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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
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Hyperkalemia
Tall, peaked T waves
Flattened P waves
Prolonged PR interval
Widened QRS
Arrhythmias, cardiac arrest
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N.B.
T wave represents ventricular repolarization
High serum K >> High T wave
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Treatment of hyperkalaemia
There are three key treatments for hyperkalaemia5:
1. cardiac protection;
2. shifting potassium into cells;
3. removing potassium from the body.
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CALL FOR HELP
Treatment of hyperkalaemia
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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
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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
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Promote potassium excretion:
1. Diuresis: furosemide 40 to 80 mg IV
2. Potassium exchange resins
3. Dialysis
Treatment of hyperkalaemia
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Hypokalaemia
Serum potassium < 3.5mmoll−1.
Severe hypokalaemia is defined as a K+ < 2.5mmoll−1
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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
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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
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Hypokalemia
U waves
T wave flattening
ST-segment changes
Arrhythmias, cardiac arrest
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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.
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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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