Presentation on theme: "Professor of Anesthesia and Intensive care"— Presentation transcript:
1Professor of Anesthesia and Intensive care Potassium DisordersProfessional Diploma in ResuscitationDr Hala Ezzat EidProfessor of Anesthesia and Intensive careAin Shams University
2Objectives: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 .
3Normal 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
5Understanding 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). .
6Understanding 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).
7Understanding 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.
8Where 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
9How 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
10N.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)
12Understanding 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
14HyperkalaemiaThis is the most common electrolyte disorder associated with cardiopulmonary arrest.Serum K concentration higher than 5.5mmoll−1Severe hyperkalaemia serum K > 6.5mmoll−1.
15Causes 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.
16Hyperkalemia Excitable Tissues Effect Nerve paraesthesia, depressed deep tendonreflexesSk MusclesWeakness, paralysis, respiratory failureCardiac msECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death
17Arrhythmias, cardiac arrest HyperkalemiaTall, peaked T wavesFlattened P wavesProlonged PR intervalWidened QRSArrhythmias, cardiac arrest
18N.B.T wave represents ventricular repolarizationHigh serum K >> High T wave
19Treatment of hyperkalaemia There are three key treatments for hyperkalaemia5:1. cardiac protection;2. shifting potassium into cells;3. removing potassium from the body.
21Treatment 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.
22Treatment 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).
23Treatment of hyperkalaemia Promote potassium excretion:Diuresis: furosemide 40 to 80 mg IVPotassium exchange resinsDialysis
24Hypokalaemia Serum potassium < 3.5mmoll−1. Severe hypokalaemia is defined as a K+ < 2.5mmoll−1
25Causes 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
26C/P hypokalemia Excitable Tissues Effect Sk Muscles weakness, cramps rhabdomyolysis, respiratory failure.Smooth msconstipation.Cardiac msECG abnormalities,arrhythmias, cardiopulmonary arrest or sudden death
27Hypokalemia 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.
28HypokalemiaN.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.
29HypokalemiaN.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.