Transcript potassium homeostasis

POTASSIUM
HOMEOSTASIS
Mohammed Almeziny BsPharm R,Ph.
Msc PhD
Clinical Pharmacist
Introduction
POTASSIUM is required for neuromuscular
tissues.
intracellularly (98%).
approximately 3500 mmol.
50 mmol is located in extracellular.
(Hak & Dunham, 1983; Scribner et al, 1956).
Protective effect of potassium
An antihypertensive effect.
Inhibitory effect on free radical formation.
Reduce the relative risk of stroke mortality.
Offer a protective effect on renal arterioles
Daily requirement
1-2 mmol/kg. (1mmol =1mEq 39.1 mg)
HYPOKALEMIA
DEFINITION
Hypokalemia is defined as a serum
potassium concentration less than 3.5
mmol/L. Normal levels range from 3.5 to 5
mmol/L
(Young & Koda-Kimble, 1988)
CAUSES
The most common cause of
hypokalemia is drug therapy.
Shifting of potassium from
extracellular to intracellular.
Reduction in potassium intake
(Lindman, 1976; Lawson et al, 1979; Nardone et al, 1978;
AMA, 1983)
Blood pH effect
0.1 unit potassium of approximately
0.6 mmol/L;
0.1 unit corresponds to slightly less
0.6mmol/L.
Clinical presentation
Usually are asymptomatic between 3.5-3
mmol/l
Malaise, weakness, fatigue and myalgia.
Renal tubular disorders, myocardial
excitability, and metabolic abnormalities
(AMA, 1983; Stanaszek & Romankiewicz, 1985)
Calculate
adult K deficit in hypokalemia
1 mmol/L fall in serum potassium from 4 to 3
mmol/L =200 mmol.
< 3mmol/L, = 200 to 400 mmol for each 1
mmol/L
*After
correct acid-base status of measured serum level.
June 1, 1998, Volume 55, Issue 11
Most hospitals removing KCl concentrate from patient units
, ISMP reports
Institute for Safe Medication Practices (ISMP).
JAMA / volume:280 (page: 1444)
Promoting Patient Safety by Preventing Medical Error
Lucian L. Leape, MD; et al October 28, 1998
Treatment and Prevention
Correct coexisting magnesium depletion.
Give potassium salts, primarily by the oral
route.
POTASSIUM CHLORIDE is the
supplement of choice
(Stanaszek & Romankiewicz, 1985; Beck et al, 1982).
Intravenous indication
Intravenous potassium chloride is
indicated primarily when oral therapy is
not feasible.
Also indicated for the treatment of
DIGITALIS-induced arrhythmias.
(Cohen, 1979; McCarron, 1975).
INTRAVENOUS.
POTASSIUM CHLORIDE MUST BE
DILUTED BEFORE INFUSION.
If serum potassium is > 2.5 mmol/L and
neuromuscular and cardiac abnormalities
are minimal (and renal function is not
impaired),
concentrations not exceeding 40 mmol/L
and at a rate of 10 to 15 mmol/hour. Doses
should not exceed 100 to 300 mmol/day
(AMA, 1983).
INTRAVENOUS. Cont’d
If serum potassium is < 2 mmol/L and
muscle paralysis or cardiac abnormalities
are present.
Concentrations not exceeding 60 mmol/L at
a rate of 40 mmol/hour. Doses should not
exceed 400 mmol/day (AMA, 1983).
Administration of potassium in high
concentration should be given after strict
evaluation.
Intravenous Rate of Administration
Should be kept within 10 to 20
mmol/hour.
Frequent biochemical and ECG
monitoring is necessary when rates
>10 mmol/hour.
The faster rates should be continued
for only short periods of time
(Lawson, 1976; Lawson & Henry, 1977; van der Linde et al, 1977;
Porter, 1976; Beeson et al, 1958; Schwartz, 1976; Dipiro et al,
1989).
Potassium infusion I.V. order
I.V fluid
Rout of
infusion
Ward
Concentration
Peripheral Infusion rate
/ Central
ECG monitoring
mmol/L
mmol/h
Yes/no
ORAL
Liquid, enteric-coated, and slow release
preparation.
Slow release:
1) Sugar-coated (slow-K) or film coated (K-Tab)
tablets;
2) KCL incorporated into wax matrix, controlled
release tablets (K-Dur)
3) A gelatin capsule containing microencapsulated
KCL crystals that are coated with a water
polymer
Food, Standard Amount
Potassium
(mg)
Calories
Sweetpotato, baked, 1 potato (146 g)
694
131
Tomato paste, ¼ cup
664
54
Beet greens, cooked, ½ cup
655
19
Potato, baked, flesh, 1 potato (156 g)
610
145
White beans, canned, ½ cup
595
153
Yogurt, plain, non-fat, 8-oz container 579
127
Tomato puree, ½ cup
549
48
Clams, canned, 3 oz
534
126
Yogurt, plain, low-fat, 8-oz container 531
143
Prune juice, ¾ cup
136
530
Food, Standard Amount
Potassium (mg)
Calories
Carrot juice, ¾ cup
517
71
Blackstrap molasses, 1 Tbsp
498
47
Halibut, cooked, 3 oz
490
119
Soybeans, green, cooked, ½ cup
485
127
Tuna, yellowfin, cooked, 3 oz
484
118
Lima beans, cooked, ½ cup
484
104
Winter squash, cooked, ½ cup
448
40
Soybeans, mature, cooked, ½ cup
443
149
Rockfish, Pacific, cooked, 3 oz
442
103
Cod, Pacific, cooked, 3 oz
439
89
Bananas, 1 medium
422
105
Food, Standard Amount
Potassium (mg)
Calories
Spinach, cooked, ½ cup
419
21
Tomato juice, ¾ cup
417
31
Tomato sauce, ½ cup
405
39
Prunes, stewed, ½ cup
398
133
Peaches, dried, uncooked, ¼ cup
398
96
Pork chop, center loin, cooked, 3 oz
382
197
Milk, non-fat, 1 cup
382
83
Apricots, dried, uncooked, ¼ cup
378
78
Rainbow trout, farmed, cooked, 3 oz
375
144
Pork loin, center rib (roasts), lean,
roasted, 3 oz
371
190
Food, Standard Amount
Potassium (mg)
Calories
Buttermilk, cultured, low-fat, 1 cup
370
98
Cantaloupe, ¼ medium
368
47
1%-2% milk, 1 cup
366
102-122
Lentils, cooked, ½ cup
365
115
Honeydew melon, 1/8 medium
365
58
Kidney beans, cooked, ½ cup
358
112
Plantains, cooked, ½ cup slices
358
90
Split peas, cooked, ½ cup
355
116
Orange juice, ¾ cup
355
85
Yogurt, plain, whole milk, 8 oz
container
352
138
Continuous Subcutaneous Infusion
Effective in elderly patients who do not need
acute potassium repletion.
Monitoring Parameters
Should be monitored at least every two
weeks in ambulatory patients with mild
deficiencies and in patients requiring
prophylactic.
After a pattern is established, monitoring
every 3 to 6 months is adequate (Stanaszek &
Romankiewicz, 1985).
HYPERKALEMIA
Introduction
Hyperkalemia is a potentially lifethreatening illness, which can be
difficult to diagnose clinically because
of paucity of reliable signs and
symptoms.
Definition
Hyperkalemia is defined as a serum
potassium concentration greater than
5.5 mmol/L
Some hospitals > 5mmol/L
(Cox, 1981).
Clinical Manifestation
cardiac excitability, possibly
progressing to ventricular fibrillation
and asystole.
Mortality/Morbidity
Reported death rates rate range up to 67% if
severe hyperkalemia is untreated.
Gender: Male = Female
Causes
Decreased or impaired potassium
excretion.
Acute or chronic renal failure (most
common).
Potassium sparing diuretics.
Urinary obstruction.
 Sickle cell disease.
 Addison disease.
Systemic lupus erythematosus (SLE).
Causes cont’d
Additions of potassium into extracellular
space:
potassium supplements (eg, PO/IV
rhabdomyolysis,
hemolysis (eg, venipuncture, blood transfusions,
burns, tumor lysis).
Causes cont’d
Transmembrane shifts
Acidosis.
Medication effects (eg, acute digitalis
toxicity, beta-blockers, succinylcholine).
Causes cont’d
Pseudohyperkalemia:
Improper blood collection (eg, ischemic
blood draw from venipuncture technique)
Laboratory error
Leukocytosis
Thrombocytosis.
Classification of Hyperkalemia
Serum sodium is usually decreased, and
acidosis is usually present.
The relationship between serum potassium
and symptoms is not consistent.
Classification of Hyperkalemia cont’d
MINIMAL TOXICITY - < 6.5 mmol/L.
MODERATE TOXICITY - 6.5-8 mmol/L
give lassitude, fatigue, and weakness.
SEVERE TOXICITY - >8 mmol/L,
complete neuromuscular paralysis may
dominate the clinical picture.
Death from cardiac arrest occurs usually at
10 to 12 mmol/L. It may occur at lower
levels if cellular potassium is severely
depleted.
Treatment
Urgency of therapy depends on EKG
findings and level of serum potassium.
 If serum K is greater than 8 mmol/L.
 If the EKG shows the changes of
hyperkalemia.
If the patient is extremely symptomatic.
Goal of therapy
stabilizing the myocardium
Shifting potassium from the
extracellular to the intracellular
compartment.
Promoting the renal excretion and GI
loss of potassium.
CALCIUM
The first drug to be used for severe hyperkalemia
(> 7.0 mmol/L) when the ECG also manifests
significant abnormalities.
Antagonizes cardiac toxicity.
onset < 5 min and lasts 30-60 min.
Calcium chloride is the preferred salt.
Calcium chloride is very irritating, and should
only be given via a central venous catheter.
Enhance the effects of the cardiac glycoside by
causing arrhythmias
SODIUM BICARBONATE
Shift potassium intracellularly.
Onset of action is within minutes and lasts
approximately 15-30 min.
Blood pH should be monitored to avoid
excess alkalosis.
INSULIN/DEXTROSE
Enhances intracellular potassium shift.
This regimen will lower serum potassium
by 1 to 2 mmol/L within 30 to 60 minutes
with the decrease lasting for several hours
(Saxena, 1989).
ADULT DOSE
Administer 25 g of dextrose (250 ml of a 10%
solution) I.V + 10 units of regular insulin over
30 minutes, and then continue the infusion at a
slower rate. (Saxena, 1989).
Or, 50 ml of a 50% dextrose solution with 5 to
10 units of regular insulin may be
administered I.V over 5 minutes.
PEDIATRIC DOSE
0.5 to 1 g/kg/dose followed by 1 unit of
regular insulin intravenously for every 4
grams of glucose infused; may repeat every
10 to 30 minutes (Barkin, 1986).
HYPEROSMOLARITY
It must be remembered that 50% dextrose
(2525 mOsm/L) , and even 25% dextrose
(1330 mOsm/L) , are very hyperosmolar
and may be sclerosing to peripheral veins
(Chameides, 1988).
Peripheral veins can tolerate up to (900
mOsm/L).
Administration of hypertonic solutions via
central lines is preferred, if possible.
SODIUM POLYSTYRENE
SULFONATE
SPS is a cation exchange resin.
Onset 2-12 h, (longer when administered
rectally).
SORBITOL is added to combat the
constipating effect of the cation-exchange
resin (Gilman et al, 1990)
Multiple doses of SPS are usually necessary.
BETA-2-AGONIST
Appears to be a safe and reasonably
effective means of treatment while
waiting for dialysis or other potassium
removing therapies to be initiated.
Use with caution in hyperthyroidism,
diabetes mellitus, or cardiovascular
disorders.
Diuretics
Effects of diuretics are slow and frequently
take an hour to begin.
Avoid use in patients with anuria
HEMODIALYSIS
Peritoneal and hemodialysis are
effective methods.
Slow to be practical in treatment of
acute poisoning.
Patients who cannot tolerate fluids or
have kidney dysfunction may benefit
from dialysis (Ellenhorn & Barceloux, 1988).
Summary
Chronic
Vs
Acute
Symptomatic Vs Asymptomatic
Level
Questions?