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Report
ELECTROLYTE DISASTERS
POTASSIUM
JOSE-MARIE EL-AMM
NEPHROLOGY DIVISION
WSU/DMC/HUH
AUGUST, 2006
COMPOSITION OF BODY FLUID
COMPARTMENTS
COMPOSITION OF ECF AND ICF
ECF
ICF
Na
K
Cl
HCO3
PHOSPHATE
141
4.1
113
26
2.0
10
120-150
3
10
140(ORGANIC)
GENERATION OF THE RMP
THE RESTING MEMBRANE
POTENTIAL
VIRTUALLY ALL K
EXCRETION OCCURS IN
THE CCD
MAJOR SITE
OF K+
SECRETION
70-80%
600-700
mmol
Mid to Late DT
and CCD
15-20%
3000
mmol
60-90 mmol
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
HYPERKALEMIA
PSEUDOHYPERKALEMIA
SHIFTS
IMPAIRED RENAL EXCRETION
PSEUDOHYPERKALEMIA
MECHANICAL TRAUMA
INCREASED WBC
INCREASED 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
LABS
128
94
6.1
11
34
538
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
ACTIVATED BY
3 Na+
2 K+
2ADRENERGICS
ELECTROGENIC
ATP
ADP
Na+
K+
ATP
H+
ACTIVATED BY
ADP
ACTIVATED BY SYNTHESIS OF NEW
NaK ATPase
G6P2(CREATES
ELECTRONEUTRAL
NEW ANIONS)
INSULIN
GLUCOSE
INSULIN
BUFFERING OF H+ AND
THE K+ SHIFT
H+
HCl
ClH+
H-BUFFER+ BUFFER
K+
KIDNEY
HYPOXIA, NO INSULIN
L-LACTATE -, -HB
-
L-LACTATE H+ , -HB H-BUFFER+
BUFFER
K SHIFTS OUT OF CELL IN
ACIDOSIS WITH HCl-NOT
ORGANIC ACIDOSIS
K EXCRETION ALTERED BY
ALDOSTERONE, RENAL STATUS
SHIFTS
Rhabdomyolysis; tissue breakdown
Drugs; Digoxin, succinyl choline
DKA, hyperosmolar state
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
9.8
98
17
“mild hemolysis”
pH=7.32
CREATININE 2.7
(WAS 2.1)
THE INTERN DRAWS BLOOD TO REPEAT THE
LABS (R/O “LAB ERROR”).
THE RESIDENT HAS A SEIZURE. WHY?
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 RATES
2. 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
Na+
Na+
H2O + CO2
H2CO3
K+
H+
K+
ALDO
NONALDO
HCO3+ +
H+
TREATMENT OF
HYPERKALEMIA
1.CALCIUM
2.INSULIN
3.ALBUTEROL
4.KAYEXALATE
5.HEMODIALYSIS
10mL OF 10% Ca
GLUCONATE OVER 10
MINUTES
10 U IVP (REGULAR)
WITH 50mL 50%
DEXTROSE
10 mg NEBULIZED 0.5 mg
IV
30-60 G PO OR 60 G
AS ENEMA
TREATMENT OF
HYPERKALEMIA
1.CALCIUM
2.INSULIN
3.ALBUTEROL
4.KAYEXALATE
5.HEMODIALYSIS
10mL OF 10% Ca
GLUCONATE OVER 10
MINUTES
10 U IVP (REGULAR)
WITH 50mL 50%
DEXTROSE
10 mg NEBULIZED 0.5 mg
IV
30-60 G PO OR 60 G
AS ENEMA
Emergency Treatment of
Hyperkalemia
medication
Mechanism
effect
Calcium
Gluconate
Antagonism of
Membrane effect
ACTION
Onset
1-2 Min
Peak
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
Kayexalate
Removal of
excess
K+ from the body
Hemodialysis
Removal of
excess
K+ from the body
30 Min
30-60 Min
60 Min
2-4 hours
Removes 25-30
meq
hourly
Continous, most
Efficient 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:
WHAT TEST(S)
135 85
2.1
UNa=80
UK=70
45
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 OUT
MINERALOCORTICOID OR
MINERALOCORTICOID-LIKE
EXCESS HORMONES
LABS:
135
85
2.1
45
UNa=80
UK=70
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 INCREASE
URINARY POTASSIUM LOSSES
1.
2.
3.
4.
5.
HIGH URINE FLOW RATES
INCREASED Na DELIVERY TO
DISTAL TUBULE
INCREASED
MINERALOCORTICOID ACTIVITY
ALKALOSIS
POORLY REABSORBED LUMINAL
ANION
VIRTUALLY ALL K EXCRETION
OCCURS IN THE CCD
MAJOR SITE
OF K+
SECRETION
480 mmol
720
mmol
60-90
mmol
3000
mmol
60 mmol
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
6.8
20
28
90
1.0
UNa=50
UK=48
Uosm=450
!!!!! INTAKE/SHIFT/OUTPUT !!!!!
TESTS USED TO MONITOR K
EXCRETION
TEST
TTKG
STRENGTHS
PHYSIOLOGIC
BASIS
TRANSLATES
URINE TO
CCD
SEPARATES
+
 K  FROM
URINE FLOW
RATE
WEAKNESSES EXPECTED EXPECTED
VALUE K VALUE K
MANY
UNVERIFIED
ASSUMPTIONS
<2
>10
TTKG: TRANSTUBULAR
POTASSIUM GRADIENT
ASSUME A TTKG OF 3.3
10 mmol/L
3 mmol/L K+
CORTEX
CCD
300 mOsm/L
1 LITER LEAVES CCD
MEDULLA
MCD
1 L=10mmol/L
URINE
UOSM=300
0L
10
mmol/L
OSM=300
OSM 
0.75 L
0.25 L=40mmol/L
UOSM=1200
TTKG
TTKG=
[ K+ ]urine /(urine/plasma)osm / [ K+ ]plasma
ASSUMPTIONS:
1. OSMOLALITY IS KNOWN IN CCD. TTKG CANNOT BE
USED IF UOSM< 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
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
6.8
20
28
90
1.0
UNa=50
UK=48
Uosm=450
137
106
6.8
20
28
90
1.0
UNa=50
UK=48
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.
ADDISON’S DISEASE
A LACK OF ALDOSTERONE LEADS TO:
INCREASED URINARY SODIUM LOSSES
HYPERKALEMIA
METABOLIC ACIDOSIS

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