ELECTROLYTE DISASTERS

JOSE-MARIE EL-AMMNEPHROLOGY DIVISION

WSU/DMC/HUH AUGUST, 2006

POTASSIUM

COMPOSITION OF BODY FLUID COMPARTMENTS

COMPOSITION OF ECF AND ICFECFECF ICFICF

Na 141 10K 4.1 120-150Cl 113 3HCO3 26 10PHOSPHATE 2.0 140(ORGANIC)

GENERATION OF THE RMP

THE RESTING MEMBRANE POTENTIAL

VIRTUALLY ALL K EXCRETION OCCURS IN THE CCD

600-700 mmol

70-80%

15-20%

3000 mmol

60-90 mmol

MAJOR 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 24

LABS128 94 34

5386.1 11 1.9

WHY IS HIS POTASSIUM HIGH?!!!!! INTAKE/SHIFT/OUTPUT !!!!!

A 30 YEAR OLD MAN WITH TYPE 1 DIABETES MELLITUS IS COMATOSE.

Low serum sodium Corrected Na= 128 + 7 = 135

Low bicarbonate <14 so metabolic acidosis AG= 23 Corrected bicarb 24

Elevated BUN/creatinine ARF vs. CRF vs. Acute on Chronic

Hyperkalemia

HORMONES THAT SHIFT K INTO CELLS

3 Na+

2 K+

ELECTROGENIC

ATP ADP

GLUCOSE

G6P2- (CREATES NEW ANIONS)

SYNTHESIS OF NEW NaK ATPase

H+

Na+

ACTIVATED BY INSULINELECTRONEUTRAL

ACTIVATED BY INSULIN

ACTIVATED BY 2ADRENERGICS

ATP

ADP

K+

BUFFERING OF H+ AND THE K+ SHIFT

HYPOXIA, 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 ACIDOSIS

KIDNEY

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

130 98 pH=7.329.8 17 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”

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 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 !!!!!

FACTORS THAT DECREASE URINARY POTASSIUM EXCRETION

1. 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 CCD

MAJOR SITE OF K+ SECRETION

ALDO

NONALDO

K+

H+Na+

Na+ K+

H2O + CO2 H2CO3 HCO3+ +

H+

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 IV4.KAYEXALATE 30-60 G PO OR 60 G AS ENEMA5.HEMODIALYSIS

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 IV4.KAYEXALATE 30-60 G PO OR 60 G AS ENEMA5.HEMODIALYSIS

Emergency Treatment of Hyperkalemia

medication ACTIONMechanism Onset Peak effect

Calcium Gluconate

Antagonism of Membrane effect

1-2 Min 5 Min

Insulin and glucose

Increased K+ entryInto the cells 5-10 Min 30-60 Min

Sodium Bicarbonate

Increased K+ entryInto the cells 15-30 Min 30-60 Min

AlbuterolIncreased K+ entry into the cells 30 Min 30-60 Min

KayexalateRemoval of excessK+ from the body

60 Min 2-4 hours

HemodialysisRemoval of excessK+ from the body

Removes 25-30 meq hourly

Continous, mostEfficient 1st hour

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 45UNa=80UK=70

WHAT TEST(S) WILL HELP YOU MAKE THE DIAGNOSIS?

WHY IS HIS POTASSIUM LOW?!!!!! INTAKE/SHIFT/OUTPUT !!!!!

METABOLIC ALKALOSIS AND HYPOKALEMIA

1. VOMITING

2. DIURETIC USE

3. BARTTER’S/GITELMAN’S

THE LACK OF HYPERTENSION RULES OUTMINERALOCORTICOID OR

MINERALOCORTICOID-LIKEEXCESS HORMONES

LABS: 135 85 UNa=80UK=70

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 BARTTER’S SYNDROME (or GITELMAN’S SYNDROME)

FACTORS THAT INCREASEURINARY POTASSIUM LOSSES

1. 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 CCD

720 mmol

480 mmol

60-90 mmol

3000 mmol

60 mmol

MAJOR SITE OF K+ SECRETION

HYPOKALEMIA HAS DRAMATIC EFFECTS ON MUSCLE ACTION

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).

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

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

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.

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 UNa=50

90 UK=486.8 20 1.0 Uosm=450

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

TESTS USED TO MONITOR K EXCRETION

TEST

STRENGTHS WEAKNESSES EXPECTED VALUE K

EXPECTED VALUE K

TTKG PHYSI OLOGI C BASI S

MANY UNVERI FI ED

ASSUMPTI ONS

<2 >10

TRANSLATES URI NE TO

CCD

SEPARATES K+ FROM

URI NE FLOW RATE

TTKG: TRANSTUBULAR POTASSIUM GRADIENT

CORTEX

MEDULLA

URINE

3 mmol/L K+300 mOsm/LCCD

MCD

ASSUME A TTKG OF 3.3

10 mmol/L

10 mmol/L

1 LITER LEAVES CCD

0 L 0.75 L

1 L=10mmol/L UOSM=300

0.25 L=40mmol/L UOSM=1200

OSM=300

OSM

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 K

4. 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 EDEMA

LABS:137 106 28 UNa=50

90 UK=486.8 20 1.0 Uosm=450

137 106 28 UNa=5090 UK=48

6.8 20 1.0 Uosm=450

TTKG={48 (450 289)} 6.8= 4.5HYPERKALEMIA STIMULATES ALDOSTERONE

RELEASE. IN HYPERKALEMIA THE TTKG SHOULD BE 10 OR ABOVE. THIS FELLOW LACKS SUFFICIENTMINERALOCORTICOID ACTIVITY.

ADDISON’S DISEASE

A LACK OF ALDOSTERONE LEADS TO:

INCREASED URINARY SODIUM LOSSES

HYPERKALEMIA

METABOLIC ACIDOSIS