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ELECTROLYTE DISASTERS. POTASSIUM. JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006. COMPOSITION OF BODY FLUID COMPARTMENTS. COMPOSITION OF ECF AND ICF ECFICF Na 141 10 K 4.1 120-150 Cl 113 3 HCO 3 2610 PHOSPHATE 2.0 140 (ORGANIC). GENERATION OF THE RMP. - PowerPoint PPT Presentation

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  • ELECTROLYTE DISASTERSJOSE-MARIE EL-AMMNEPHROLOGY DIVISIONWSU/DMC/HUH AUGUST, 2006POTASSIUM

  • COMPOSITION OF BODY FLUID COMPARTMENTSCOMPOSITION OF ECF AND ICFECFICFNa14110K 4.1120-150Cl1133HCO32610PHOSPHATE2.0140(ORGANIC)

  • GENERATION OF THE RMP

  • THE RESTING MEMBRANE POTENTIAL

  • VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD600-700 mmol70-80%15-20% 3000 mmol60-90 mmolMAJOR SITE OF K+ SECRETIONMid to Late DT and CCD

  • Collecting tubules have selective Na channels in luminal surface (favored movement by Na levels low in cells and intracellular negativity). Pumped out of tubular cells by NaK-ATPase. Tubular lumen negatively charged and favors K movement into lumen by K channels. Aldo when combined with its receptor enhances Na reabsorption & K secretion via # Na channels & # NaK-ATPase pumps.ANP inhibits Na reabsorption by closing Na channels Amiloride & Triamterene close Na channels directly Spironolactone competes w/ aldosterone

  • HYPERKALEMIAPSEUDOHYPERKALEMIASHIFTSIMPAIRED RENAL EXCRETION

  • PSEUDOHYPERKALEMIAMECHANICAL TRAUMAINCREASED WBCINCREASED PLATELETS

  • A 30 YEAR OLD MAN WITH TYPE 1 DIABETES MELLITUS IS COMATOSE.EXAM:BP 110/70 HR 100/MIN LYING 80/50 116 AT 45 TEMP 101 RR 24LABS12894345386.1111.9WHY IS HIS POTASSIUM HIGH?!!!!! INTAKE/SHIFT/OUTPUT !!!!!

  • A 30 YEAR OLD MAN WITH TYPE 1 DIABETES MELLITUS IS COMATOSE.Low serum sodiumCorrected Na= 128 + 7 = 135Low bicarbonate
  • HORMONES THAT SHIFT K INTO CELLS3 Na+2 K+ ELECTROGENICATPADPGLUCOSEG6P2- (CREATES NEW ANIONS)SYNTHESIS OF NEW NaK ATPaseH+Na+ACTIVATED BY INSULINELECTRONEUTRALACTIVATED BY INSULINACTIVATED BY 2ADRENERGICSATPADPK+

  • BUFFERING OF H+ AND THE K+ SHIFTHYPOXIA, NO INSULINL-LACTATE -, -HB -L-LACTATE -, -HB -H+HClCl-BUFFERH-BUFFER+K+BUFFERH-BUFFER+H+H+ K EXCRETION ALTERED BY ALDOSTERONE, RENAL STATUS K SHIFTS OUT OF CELL IN ACIDOSIS WITH HCl-NOT ORGANIC ACIDOSISKIDNEY

  • SHIFTSRhabdomyolysis; tissue breakdownDrugs; Digoxin, succinyl cholineDKA, hyperosmolar state

  • 54 YEAR OLD MAN WITH MILD RENAL FAILURE. C/O DIFFICULTY IN GETTING OUT OF CHAIRS.

    EXAM: SLIGHTLY DECREASED SKIN TURGOR MARKED PROXIMAL MUSCLE WEAKNESSLABS: ECG HAS PEAKED T WAVES, WIDENED QRS

    13098pH=7.329.817CREATININE 2.7(WAS 2.1)

    THE INTERN DRAWS BLOOD TO REPEAT THE LABS (R/O LAB ERROR). THE RESIDENT HAS A SEIZURE. WHY?HE RECENTLY WAS STARTED ON A LOW SODIUM DIET BUT NO NEW MEDICATIONS.mild hemolysis

  • LABORATORY ERROR IS NOT ASSOCIATED WITH SYMPTOMS!

    THIS MAN HAS BOTH SKELETAL MUSCLE AND CARDIAC MUSCLE SYMPTOMS OF HYPERKALEMIA.

    WHY DID HE SUDDENLY BECOME HYPERKALEMIC?WHY IS HIS POTASSIUM HIGH?!!!!! INTAKE/SHIFT/OUTPUT !!!!!

  • IS HE TAKING A SALT SUBSTITUTE????

    CRF: RENAL DISEASE CONTRIBUTES BUT DIDNT CAUSE HIS K PROBLEMS. PEOPLE WITH CRF CAN HAVE TROUBLE WITH SODIUM CONSERVATION IF THERE ARE SUDDEN CHANGES IN THEIR INTAKE. DECREASED TOTAL BODY SODIUM LEADS TO DECREASED RENAL BLOOD FLOW, DECREASED Na PAST THE DISTAL TUBULE AND HENCE DECREASED K EXCRETION.

    !!!!! INTAKE/SHIFT/OUTPUT !!!!!

  • FACTORS THAT DECREASE URINARY POTASSIUM EXCRETION1. LOW URINE FLOW RATES2. DECREASED Na DELIVERY TO DISTAL TUBULE (ARF, AGN, ESLD) 3. DECREASED MINERALOCORTICOID ACTIVITY (Renin-Ag system)

  • VIRTUALLY ALL K EXCRETION OCCURS IN THE CCDMAJOR SITE OF K+ SECRETIONALDONONALDOK+H+Na+Na+K+H2O + CO2 H2CO3 HCO3+ + H+

  • TREATMENT OF HYPERKALEMIA1.CALCIUM 10mL OF 10% Ca GLUCONATE OVER 10 MINUTES2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV4.KAYEXALATE30-60 G PO OR 60 G AS ENEMA5.HEMODIALYSIS

  • TREATMENT OF HYPERKALEMIA1.CALCIUM 10mL OF 10% Ca GLUCONATE OVER 10 MINUTES2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV4.KAYEXALATE30-60 G PO OR 60 G AS ENEMA5.HEMODIALYSIS

  • Emergency Treatment of Hyperkalemia

    medication ACTIONMechanism Onset Peak effectCalcium GluconateAntagonism of Membrane effect 1-2 Min 5 MinInsulin and glucoseIncreased K+ entryInto the cells 5-10 Min 30-60 MinSodium BicarbonateIncreased K+ entryInto the cells 15-30 Min 30-60 MinAlbuterolIncreased K+ entry into the cells 30 Min 30-60 MinKayexalateRemoval of excessK+ from the body 60 Min 2-4 hoursHemodialysisRemoval of excessK+ from the bodyRemoves 25-30 meq hourlyContinous, mostEfficient 1st hour

  • A 22 YEAR OLD COMPLAINS OF FATIGABILITY AND WEAKNESS. PHYSICAL EXAM: BP 122/68 HR 72/MIN NO ORTHOSTATIC CHANGES NO EDEMALABS:135852.145UNa=80UK=70WHAT TEST(S) WILL HELP YOU MAKE THE DIAGNOSIS?WHY IS HIS POTASSIUM LOW?!!!!! INTAKE/SHIFT/OUTPUT !!!!!

  • METABOLIC ALKALOSIS AND HYPOKALEMIA1.VOMITING

    2.DIURETIC USE

    3.BARTTERS/GITELMANSTHE LACK OF HYPERTENSION RULES OUTMINERALOCORTICOID ORMINERALOCORTICOID-LIKEEXCESS HORMONES

  • LABS: 13585UNa=80UK=702.145URINE CHLORIDE = 6 DIAGNOSIS IS VOMITING WITH URINARY K LOSSES FROM THE OSMOTIC DIURESIS AND SECONDARY HYPERALDOSTERONISM

    URINE CHLORIDE = 60 DIAGNOSIS IS RECENT USE OF DIURETICS OR BARTTERS SYNDROME (or GITELMANS SYNDROME)

  • FACTORS THAT INCREASEURINARY POTASSIUM LOSSES1.HIGH URINE FLOW RATES2.INCREASED Na DELIVERY TO DISTAL TUBULE3.INCREASED MINERALOCORTICOID ACTIVITY4.ALKALOSIS5.POORLY REABSORBED LUMINAL ANION

  • VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD720 mmol480 mmol60-90 mmol3000 mmol60 mmolMAJOR SITE OF K+ SECRETION

  • HYPOKALEMIA HAS DRAMATIC EFFECTS ON MUSCLE ACTION

  • TREATMENT OF HYPOKALEMIAThe safest route of replacement is PO.KCl is the preparation of choice for K w/ECF volume contraction, diuretic use metabolic alkalosis.Potassium bicarbonate (or citrate) for K w/ RTA diarrhea associated K losses. K phosphate for K w/ anabolism (TPN) phosphate depletion (recovering DKA).

  • TREATMENT OF HYPOKALEMIAThe goal of emergency therapy should be to get the patient out of danger rapidly but replacing the entire potassium deficit quickly is not desirable. During chronic hypokalemia, renal mechanisms develop to minimize aldosterone-induced K losses. These may persist for 1 to 2 days after correction. Aggressive, rapid replacement of potassium may lead to hyperkalemia

  • EVER HEAR THE SAYING ABOUT TOO MUCH OF A GOOD THING?

  • TREATMENT OF HYPOKALEMIAPeripheral IV potassium infusions should be less than 60mEq/L to avoid vascular spasm or sclerosis. Rates should be less than 20mEq/hr unless done in a monitored setting.20mEq of KCl in 1 liter of D5W can lead to a further drop in serum potassium.Concentrated potassium solutions through a central line can lead to dangerous cardiac sequelae.

  • A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY COMPLAINS OF CHRONIC FATIGUE.EXAM: BP 100/60 WITHOUT ORTHOSTATIC CHANGE.NO EDEMALABS:13710628UNa=5090UK=486.8201.0Uosm=450!!!!! INTAKE/SHIFT/OUTPUT !!!!!

  • TESTS USED TO MONITOR K EXCRETION

    TEST

    STRENGTHS

    WEAKNESSES

    EXPECTED VALUE (K

    EXPECTED VALUE (K

    TTKG

    PHYSIOLOGIC BASIS

    MANY UNVERIFIED ASSUMPTIONS

    10

    TRANSLATES URINE TO CCD

    SEPARATES

    ( K+ ( FROM URINE FLOW RATE

  • TTKG: TRANSTUBULAR POTASSIUM GRADIENTCORTEXMEDULLAURINE3 mmol/L K+300 mOsm/LCCDMCDASSUME A TTKG OF 3.3 10 mmol/L10 mmol/L1 LITER LEAVES CCD0 L0.75 L1 L=10mmol/L UOSM=3000.25 L=40mmol/L UOSM=1200OSM=300OSM

  • TTKGTTKG= [ K+ ]urine /(urine/plasma)osm / [ K+ ]plasma

    ASSUMPTIONS:1.OSMOLALITY IS KNOWN IN CCD. TTKG CANNOT BE USED IF UOSM< POSM2. WATER REABSORPTION IN MCD CAN BE ESTIMATED, BUT IF ANP IS COMPLETELY SHUT OFF THERE IS Na REABSORPTION IN THE MCD AND TTKG IS AN OVERESTIMATE.3. K+ IS NOT REABSORBED OR SECRETED IN MCD. THIS IS TRUE UNLESS PROFOUND K DEPLETION OR TAKING INDUSTRIAL DOSES OF K4.THE K IN PLASMA REFLECTS THE PERITUBULAR K

  • A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY COMPLAINS OF CHRONIC FATIGUE.EXAM: BP 100/60 WITHOUT ORTHOSTATIC CHANGE.NO EDEMALABS:13710628UNa=5090UK=486.8201.0Uosm=450

  • 13710628UNa=5090UK=486.8201.0Uosm=450TTKG={48 (450 289)} 6.8= 4.5HYPERKALEMIA STIMULATES ALDOSTERONERELEASE. IN HYPERKALEMIA THE TTKG SHOULD BE 10 OR ABOVE. THIS FELLOW LACKS SUFFICIENTMINERALOCORTICOID ACTIVITY.

  • ADDISONS DISEASEA LACK OF ALDOSTERONE LEADS TO:

    INCREASED URINARY SODIUM LOSSES

    HYPERKALEMIA

    METABOLIC ACIDOSIS