Presentation on theme: "Professor of Anesthesia and Intensive care"— Presentation transcript:
1 Professor of Anesthesia and Intensive care Potassium DisordersProfessional Diploma in ResuscitationDr Hala Ezzat EidProfessor of Anesthesia and Intensive careAin 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/hypokalemiaDiscuss 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+, HCO31mmol = 2 mEq for divalent ions e.g. Ca++, Mg++So always use mmols
5 Understanding Role of K in membrane potential Sodium is predominantly an extracellular cation while potassium is predominantly an intracellular cationCell 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 intakeShift from ICF.Insulin enhances potassium entry into cellsBeta-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)
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 LUnderstanding body fluid compartmentTotal body water (TBW) constitutes 60% of total body weight. For a 70 kg man, TBW = 0.6 x 70 = 42 L
14 HyperkalaemiaThis is the most common electrolyte disorder associated with cardiopulmonary arrest.Serum K concentration higher than 5.5mmoll−1Severe hyperkalaemia serum K > 6.5mmoll−1.
15 Causes of hyperkalemia: GITIC compartmentRenalAldosteronDietTissue breakdown (rhabdomyolysis, tumour lysis, haemolysis),Stored Packed red blood cellsMetabolic acidosis,beta-blockers,Insulin deficiencyRenal failureAddisonsACE-INSAIDsK sparing diureticsN.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 tendonreflexesSk MusclesWeakness, paralysis, respiratory failureCardiac msECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death
17 Arrhythmias, cardiac arrest HyperkalemiaTall, peaked T wavesFlattened P wavesProlonged PR intervalWidened QRSArrhythmias, cardiac arrest
18 N.B.T wave represents ventricular repolarizationHigh 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.
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 IVPotassium exchange resinsDialysis
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 therapyRenal losses (DI) DialysisDiuretics-Cushing’s Syndrome -Hyperaldosteronism-Steroids
26 C/P hypokalemia Excitable Tissues Effect Sk Muscles weakness, cramps rhabdomyolysis, respiratory failure.Smooth msconstipation.Cardiac msECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death
27 Hypokalemia U waves T wave flattening ST-segment changes Arrhythmias, cardiac arrestDue 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 HypokalemiaN.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 HypokalemiaN.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.