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ELECTROLYTE DISASTERS JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006 POTASSIUM.

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Presentation on theme: "ELECTROLYTE DISASTERS JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006 POTASSIUM."— Presentation transcript:

1 ELECTROLYTE DISASTERS JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006 POTASSIUM

2 COMPOSITION OF BODY FLUID COMPARTMENTS COMPOSITION OF ECF AND ICF ECFICF Na14110 K Cl1133 HCO PHOSPHATE2.0140(ORGANIC)

3 GENERATION OF THE RMP

4 THE RESTING MEMBRANE POTENTIAL

5 VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD mmol 70-80% 15-20% 3000 mmol mmol MAJOR SITE OF K + SECRETION Mid to Late DT and CCD

6 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

7 HYPERKALEMIA zPSEUDOHYPERKALEMIA zSHIFTS zIMPAIRED RENAL EXCRETION

8 PSEUDOHYPERKALEMIA zMECHANICAL TRAUMA zINCREASED WBC zINCREASED PLATELETS

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

10 A 30 YEAR OLD MAN WITH TYPE 1 DIABETES MELLITUS IS COMATOSE. zLow serum sodium yCorrected Na= = 135 zLow bicarbonate y<14 so metabolic acidosis AG= 23 yCorrected bicarb 24 zElevated BUN/creatinine yARF vs. CRF vs. Acute on Chronic zHyperkalemia

11

12 HORMONES THAT SHIFT K INTO CELLS 3 Na + 2 K + ELECTROGENIC ATP ADP GLUCOSE G6P 2- (CREATES NEW ANIONS) SYNTHESIS OF NEW NaK ATPase H+H+ Na + ACTIVATED BY INSULIN ELECTRONEUTRAL ACTIVATED BY INSULIN ACTIVATED BY  2 ADRENERGICS ATP ADP K+K+

13 BUFFERING OF H + AND THE K + SHIFT HYPOXIA, NO INSULIN L-LACTATE -,  -HB - H+H+ HCl Cl - BUFFER H-BUFFER + K+K+ BUFFER H-BUFFER + H+H+ H+H+ K EXCRETION ALTERED BY ALDOSTERONE, RENAL STATUS K SHIFTS OUT OF CELL IN ACIDOSIS WITH HCl-NOT ORGANIC ACIDOSIS KIDNEY

14 SHIFTS zRhabdomyolysis; tissue breakdown zDrugs; Digoxin, succinyl choline zDKA, hyperosmolar state

15 54 YEAR OLD MAN WITH MILD RENAL FAILURE. C/O DIFFICULTY IN GETTING OUT OF CHAIRS. EXAM: SLIGHTLY DECREASED SKIN TURGOR MARKED PROXIMAL MUSCLE WEAKNESS LABS: ECG HAS PEAKED T WAVES, WIDENED QRS 13098pH= CREATININE 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”

16 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 !!!!!

17 IS HE TAKING A SALT SUBSTITUTE???? CRF : RENAL DISEASE CONTRIBUTES BUT DIDN’T 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 !!!!!

18 FACTORS THAT DECREASE URINARY POTASSIUM EXCRETION 1. LOW URINE FLOW RATES 2. DECREASED Na DELIVERY TO DISTAL TUBULE (ARF, AGN, ESLD) 3. DECREASED MINERALOCORTICOID ACTIVITY (Renin-Ag system)

19 VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD MAJOR SITE OF K + SECRETION ALDO NONALDO K+H+K+H+ Na + K+K+ H 2 O + CO 2 H 2 CO 3 HCO H +

20

21 TREATMENT OF HYPERKALEMIA 1.CALCIUM 10mL OF 10% Ca GLUCONATE OVER 10 MINUTES 2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE 3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV 4.KAYEXALATE G PO OR 60 G AS ENEMA 5.HEMODIALYSIS

22

23 TREATMENT OF HYPERKALEMIA 1.CALCIUM 10mL OF 10% Ca GLUCONATE OVER 10 MINUTES 2.INSULIN 10 U IVP (REGULAR) WITH 50mL 50% DEXTROSE 3.ALBUTEROL 10 mg NEBULIZED 0.5 mg IV 4.KAYEXALATE G PO OR 60 G AS ENEMA 5.HEMODIALYSIS

24 Emergency Treatment of Hyperkalemia medication ACTION Mechanism Onset Peak effect Calcium Gluconate Antagonism of Membrane effect 1-2 Min 5 Min Insulin and glucose Increased K + entry Into the cells 5-10 Min Min Sodium Bicarbonate Increased K + entry Into the cells Min Min Albuterol Increased K + entry into the cells 30 Min Min Kayexalate Removal of excess K + from the body 60 Min 2-4 hours Hemodialysis Removal of excess K + from the body Removes meq hourly Continous, most Efficient 1 st hour

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

26 METABOLIC ALKALOSIS AND HYPOKALEMIA 1.VOMITING 2.DIURETIC USE 3.BARTTER’S/GITELMAN’S THE LACK OF HYPERTENSION RULES OUT MINERALOCORTICOID OR MINERALOCORTICOID-LIKE EXCESS HORMONES

27 LABS: 13585U Na =80 U K = URINE 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 BARTTER’S SYNDROME (or GITELMAN’S SYNDROME)

28 FACTORS THAT INCREASE URINARY POTASSIUM LOSSES 1.HIGH URINE FLOW RATES 2.INCREASED Na DELIVERY TO DISTAL TUBULE 3.INCREASED MINERALOCORTICOID ACTIVITY 4.ALKALOSIS 5.POORLY REABSORBED LUMINAL ANION

29 VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD 720 mmol 480 mmol mmol 3000 mmol 60 mmol MAJOR SITE OF K + SECRETION

30

31 HYPOKALEMIA HAS DRAMATIC EFFECTS ON MUSCLE ACTION

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

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

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

35 TREATMENT OF HYPOKALEMIA z Peripheral IV potassium infusions should be less than 60mEq/L to avoid vascular spasm or sclerosis. z Rates should be less than 20mEq/hr unless done in a monitored setting. z 20mEq of KCl in 1 liter of D 5 W can lead to a further drop in serum potassium. z Concentrated potassium solutions through a central line can lead to dangerous cardiac sequelae.

36 A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY COMPLAINS OF CHRONIC FATIGUE. EXAM: BP 100/60 WITHOUT ORTHOSTATIC CHANGE.NO EDEMA LABS: U Na =50 90U K = Uosm=450 !!!!! INTAKE/SHIFT/OUTPUT !!!!!

37 TESTS USED TO MONITOR K EXCRETION

38 TTKG: TRANSTUBULAR POTASSIUM GRADIENT CORTEX MEDULLA URINE 3 mmol/L K mOsm/L CCD MCD ASSUME A TTKG OF mmol/L 1 LITER LEAVES CCD 0 L 0.75 L 1 L=10mmol/L U OSM = L=40mmol/L U OSM =1200 OSM=300 OSM 

39 TTKG TTKG= [ K+ ] urine /(urine/plasma) osm / [ K+ ] plasma ASSUMPTIONS: 1.OSMOLALITY IS KNOWN IN CCD. TTKG CANNOT BE USED IF U OSM < P OSM 2. 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 K 4.THE K IN PLASMA REFLECTS THE PERITUBULAR K

40 A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY COMPLAINS OF CHRONIC FATIGUE. EXAM: BP 100/60 WITHOUT ORTHOSTATIC CHANGE.NO EDEMA LABS: U Na =50 90U K = Uosm=450

41 U Na =50 90U K = Uosm=450 TTKG={48  (450  289)}  6.8= 4.5 HYPERKALEMIA STIMULATES ALDOSTERONE RELEASE. IN HYPERKALEMIA THE TTKG SHOULD BE 10 OR ABOVE. THIS FELLOW LACKS SUFFICIENT MINERALOCORTICOID ACTIVITY.

42 ADDISON’S DISEASE A LACK OF ALDOSTERONE LEADS TO: INCREASED URINARY SODIUM LOSSES HYPERKALEMIA METABOLIC ACIDOSIS


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