ELECTROLYTE DISASTERS

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ELECTROLYTE DISASTERS
POTASSIUM

• JOSE-MARIE EL-AMM
• NEPHROLOGY DIVISION
• WSU/DMC/HUH
• AUGUST, 2006

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COMPOSITION OF BODY FLUID COMPARTMENTS

• COMPOSITION OF ECF AND ICF
• ECF ICF
• Na 141 10
• K 4.1 120-150
• Cl 113 3
• HCO3 26 10
• PHOSPHATE 2.0 140(ORGANIC)

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GENERATION OF THE RMP
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THE RESTING MEMBRANE POTENTIAL
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VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD
MAJOR SITE OF K SECRETION Mid to Late DT and CCD
70-80
600-700 mmol
15-20
3000 mmol
60-90 mmol
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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.
Amiloride Triamterene close Na channels
directly
Spironolactone competes w/ aldosterone
ANP inhibits Na reabsorption by closing Na
channels
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HYPERKALEMIA

• PSEUDOHYPERKALEMIA
• SHIFTS
• IMPAIRED RENAL EXCRETION

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PSEUDOHYPERKALEMIA

• MECHANICAL TRAUMA
• INCREASED WBC
• INCREASED PLATELETS

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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 24
LABS 128 94 34 538 6.1 11 1.9
WHY IS HIS POTASSIUM HIGH? !!!!!
INTAKE/SHIFT/OUTPUT !!!!!
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A 30 YEAR OLD MAN WITH TYPE 1 DIABETES MELLITUS
IS COMATOSE.

• Low serum sodium
• Corrected Na 128 7 135
• Low bicarbonate
• lt14 so metabolic acidosis AG 23
• Corrected bicarb 24
• Elevated BUN/creatinine
• ARF vs. CRF vs. Acute on Chronic
• Hyperkalemia

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HORMONES THAT SHIFT K INTO CELLS
ACTIVATED BY ?2ADRENERGICS
3 Na
2 K ELECTROGENIC
ATP
ADP
Na
K
GLUCOSE
ATP
H
ACTIVATED BY INSULIN
ADP
SYNTHESIS OF NEW NaK ATPase
ACTIVATED BY INSULIN ELECTRONEUTRAL
G6P2- (CREATES NEW ANIONS)
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BUFFERING OF H AND THE K SHIFT
H
HYPOXIA, NO INSULIN
HCl Cl-
L-LACTATE -, ?-HB -
L-LACTATE -, ?-HB -
H
H
H-BUFFER
H-BUFFER
BUFFER
BUFFER
K SHIFTS OUT OF CELL IN ACIDOSIS WITH HCl-NOT
ORGANIC ACIDOSIS
K
K EXCRETION ALTERED BY ALDOSTERONE, RENAL STATUS
KIDNEY
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SHIFTS

• Rhabdomyolysis tissue breakdown
• Drugs Digoxin, succinyl choline
• DKA, hyperosmolar state

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54 YEAR OLD MAN WITH MILD RENAL FAILURE. C/O
DIFFICULTY IN GETTING OUT OF CHAIRS.
HE RECENTLY WAS STARTED ON A LOW SODIUM DIET BUT
NO NEW MEDICATIONS.
EXAM SLIGHTLY DECREASED SKIN TURGOR
MARKED PROXIMAL MUSCLE WEAKNESS
LABS ECG HAS PEAKED T WAVES, WIDENED
QRS 130 98 pH7.32 9.8 17 CREATININE
2.7 (WAS 2.1)
mild hemolysis
THE INTERN DRAWS BLOOD TO REPEAT THE LABS (R/O
LAB ERROR). THE RESIDENT HAS A SEIZURE. WHY?
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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 !!!!!
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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 !!!!!
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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)

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VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD
MAJOR SITE OF K SECRETION
K H
ALDO
Na
NONALDO
Na
K
H2O CO2 H2CO3 HCO3
H
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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 30-60 G PO OR 60 G AS ENEMA
• 5.HEMODIALYSIS

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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 30-60 G PO OR 60 G AS ENEMA
• 5.HEMODIALYSIS

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Emergency Treatment of Hyperkalemia
medication ACTION Mechanism Onset Peak effect ACTION Mechanism Onset Peak effect 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 30-60 Min
Sodium Bicarbonate Increased K entry Into the cells 15-30 Min 30-60 Min
Albuterol Increased K entry into the cells 30 Min 30-60 Min
Kayexalate Removal of excess K from the body 60 Min 2-4 hours
Hemodialysis Removal of excess K from the body Removes 25-30 meq hourly Continous, most Efficient 1st hour
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A 22 YEAR OLD COMPLAINS OF FATIGABILITY AND
WEAKNESS.
PHYSICAL EXAM BP 122/68 HR 72/MIN NO
ORTHOSTATIC CHANGES NO EDEMA
LABS 135 85 2.1 45 UNa80 UK70
WHAT TEST(S) WILL HELP YOU MAKE THE DIAGNOSIS?
WHY IS HIS POTASSIUM LOW? !!!!!
INTAKE/SHIFT/OUTPUT !!!!!
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METABOLIC ALKALOSIS AND HYPOKALEMIA
1. VOMITING 2. DIURETIC USE 3. BARTTERS/GITELMA
NS
THE LACK OF HYPERTENSION RULES OUT MINERALOCORTICO
ID OR MINERALOCORTICOID-LIKE EXCESS HORMONES
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LABS 135 85 UNa80 UK70 2.1 45
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 BARTTERS SYNDROME
(or GITELMANS SYNDROME)
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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
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VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD
MAJOR SITE OF K SECRETION
480 mmol
60-90 mmol
720 mmol
3000 mmol
60 mmol
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HYPOKALEMIA HAS DRAMATIC EFFECTS ON MUSCLE ACTION
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TREATMENT OF HYPOKALEMIA

• The 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).

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TREATMENT OF HYPOKALEMIA

• 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.
• 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

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

• Peripheral 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.

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A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY
COMPLAINS OF CHRONIC FATIGUE.
EXAM BP 100/60 WITHOUT ORTHOSTATIC CHANGE. NO
EDEMA
LABS 137 106 28 UNa50 90 UK48 6.8 20 1.0
Uosm450
!!!!! INTAKE/SHIFT/OUTPUT !!!!!
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TESTS USED TO MONITOR K EXCRETION
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TTKG TRANSTUBULAR POTASSIUM GRADIENT
ASSUME A TTKG OF 3.3
10 mmol/L
10 mmol/L
3 mmol/L K
CORTEX
300 mOsm/L
CCD
OSM300
1 LITER LEAVES CCD
OSM ?
MEDULLA
0.75 L
0 L
MCD
0.25 L40mmol/L UOSM1200
1 L10mmol/L UOSM300
URINE
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TTKG

• TTKG
• K urine /(urine/plasma)osm / K plasma
• ASSUMPTIONS
• 1. OSMOLALITY IS KNOWN IN CCD. TTKG CANNOT BE
  USED IF UOSMlt POSM
• 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

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A 54 YEAR OLD MAN WITH NO PRIOR MEDICAL HISTORY
COMPLAINS OF CHRONIC FATIGUE.
EXAM BP 100/60 WITHOUT ORTHOSTATIC CHANGE. NO
EDEMA
LABS 137 106 28 UNa50 90 UK48 6.8 20 1.0
Uosm450
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137 106 28 UNa50 90 UK48 6.8 20 1.0 Uos
m450
TTKG48 ? (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.
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ADDISONS DISEASE
A LACK OF ALDOSTERONE LEADS TO INCREASED
URINARY SODIUM LOSSES HYPERKALEMIA METABOLIC
ACIDOSIS