POTASSIUM

Bernadette D. Hiñola BSN 3 Nightingale

 Significance of K

Major intracellular


electrolyte
Intracellular-98%
Extracellular-2%
Influences both the skeletal


and neuromuscular function

Ex:alterations in its
concentration change
myocardial irritability and
rhythm
 Normal level: 3.5 to 5.5 mEq/L (3.5
to 5.5 mmol/L)
 K imbalance: commonly

associated w/ varoius diseases,

injuries, medications (diuretics,
laxatives, antibiotics), and special
treatments such as parenteral
nutrition and chemotherapy
Maintenance of K Balance
 Kidneys- primary regulators of
K balance
 80% of K is excreted daily from

the body through the kidneys

 20% is lost through bowel and

sweat
 Concentration gradient- favors
the movement of K into the
renal tubule with the loss of K
in the urine.
 Aldosterone also increases the

excretion of K by the kidneys

 Note:
Kidneys do not conserve K
as well as they conserve
Na, that’s why K may still
be lost in urine in the
presence of hypokalemia.
HYPOKALEMIA
 K-deficit (Hypokalemia)
 GI Loss- most common cause of K
depletion
 Ex. Vomiting and gastric suction, diarrhea
 Intestinal fluid may contain as much as
30mEq/L
 Potassium deficit: ex, prolonged intestinal
suctioning, recent ileostomy, and villous
adenoma (a tumor of the intestinal tract characterized by excretion of potassium-
rich mucus)
 Hypokalemia can cause alkalosis
and in turn, alkalosis can cause
hypokalemia.
Ex. H ions moves out of the cells in
alkalotic states to help correct the
high pH, and K ions move in to
maintain an electrically neutral states
 Hyperaldosteronism increase renal k
wasting and can lead to severe K depletion
 K-losing diuretics, such as the thiazides

(eg. Chlorothiazide [Diuril], and Polythiazide

[Renese]), can induce hypokalemia
 Otherdrugs that may cause potassium
depletion: corticosteroid, sodium penicillin,
carbenicillin, and amphotericin B.
Patients with persistent


insulin hypersecretion may

experience hypokalemia.
Insulinpromotes the entry of
potassium into skeletal
muscle and hepatic cells
Patients who are unable or


unwilling to eat a normal diet

for a prolonged period are at
risk for hypokalemia
Elderly, alcoholics, anorexia
nervosa, bulimia
Magnesium depletion


should be corrected to
prevent renal loss of K
 Clinical Manifestations
 Fatigue  Decreased
 Anorexia bowel motility
 N&V  Paresthesia

 Muscle  Dysrhythmia

weakness  Increased

 Leg cramps sensitivity to

digitalis
 Prolonged hypokalemia can lead
to an inability of the kidneys to
concentrate urine, causing diluted
urine and excessive thirst
 Potassium depletion depresses

the release of insulin and results in

glucose intolerance
Assessment & Dx Findings
 ECG-flat T waves and/or inverted
T waves, suggesting ischemia,
and depressed ST segments.
ElevatedU wave- specific to
hypokalemia
 Hypokalemia- increased sensitivity
to Digitalis
 Metabolic alkalosis
 24-hour urinary k excretion test

K excretion exceeding
20mEq/L with hypokalemia
suggests that renal K loss is
the cause
 Medical Management
Oral or IV Replacement Therapy
 Administer 40-80 mEq/day for
an adult
 For patients at risk for
hypokalemia- K-rich diet
50-100 mEq/Day
If dietary intake is


inadequate- oral or IV K
supplements
Many salt substitutes
contain 50-60 mEq of K per
teaspoon
 Nursing Management
Monitor presence in patients


at risk (fatigue, anorexia,

muscle weakness,
decreased bowel motility,
paresthesias, and
dysrhythmias
In patients receiving digitalis,


monitor signs of digitalis

toxicity (N&V, Anorexia,
blurred vision, diarrhea,
headache, excessive
slowing of the pulse, etc)
Keep serum K level


above 3.5 mEq/L in

patient receiving digitalis
(Digoxin)
 Prevention
 Encourage intake of K-rich foods
 Assess abuse of laxatives or

diuretics
 I&O monitoring: 40mEq of k is lost
for every L of urine output
 ECG

 ABG
 Administering IV K
Should be administered only


after adequate urine flow has

been established
If urine vol. is <20mL for 2
consecutive hours, stop the IV
infusion
 IV K should not be
administered faster than
20mEq/h or in concentration
>30-40 mEq/L unless
hypokalemia is severe because
this can cause life threatening
DYSRHYTMIAS.
 If administered on peripheral
vein, administer at a slow rate
to prevent irritating the vein and
causing a burning sensation
HYPERKALEMIA
 Often iatrogenic (treatment-
induced)
 Usually more dangerous

because CARDIAC ARREST is

more frequently associated with
high serum K levels
 PSEUDOHYPERKALEMIA

CAUSES
 Use of tight torniquet around an
exercising extremity while
drawing a blood sample
 hemolysis of the sample before

analysis
Other causes
 Familial pseudohyperkalemia

 Leukocytosis

 Thrombocytosis

 Drawing blood from an IV site

where K is infusing
 Elevated K should be verified
 Major cause of HYPERKALEMIA

Decreased renal excretion of K

 Other cause: hypoaldosteronism
and Addison’s Dse (Na loss and K
retention)
 60% of hyperkalemic episodes are
caused by medications (eg. KCl,
heparin, captopril, potassium-sparing
diuretics )
 In acidosis, K moves out of the cell
into the ECF
 Increased extracellular K level- burns,
crushing injuries, severe infections
 Clinical Manifestations
 Most important consequence is the
effect of hyperkalemia in myocardium
 Effects of increased serum K level is

not significant below a concentration of

7 mEq/L
 As serum K increases, disturbance in

cardiac conduction occur

 Earliest changes occuring at a
serum K level >6mEq/L are
peaked, narrow T waves; ST
segment depression, and a
shortened QT interval
 Continuous rise in serum K level-
prolonged PR interval followed by
disappearance of P wave. Finally
there is a decomposition and
prolongation of QRS complex
 Ventricular dysrhytmias and
cardiac arrest may occur at any
point in this progression
 Severe hyperkalemia causes skeletal
muscle weakness and even paralysis,
related to depolarization block in
muscle
 Paralysis of respiratory and speech
muscles
 Nausea, intermittent intestinal colic, &
diarrhea
Assessment and Dx Findings

Electrocardiogram (ECG)
Arterial blood gases

(ABG)- metabolic
acidosis
 Medical management
Immediate ECG should be
obtained
Obtain a repeat serum

potassium level from a vein

w/o IV infusion containing
potassium to verify results
NON-ACUTE SITUATIONS
 Restriction of dietary K and K-

containing medications
PREVENTION OF SERIOUS
HYPERKALEMIA
 Administer either orally or by retention

enema of cation exchange resins (eg

Kayexalate)
 EMERGENCY PHARMACOLOGIC
THERAPY

 IV calcium gluconate
Within minute of administration,
calcium antagonizes the action of
hyperkalemia in the heart
Does not reduce the serum
potassium concentration but
immediately antagonizes the adverse
cardiac conduction abnormalities
 Calcium gluconate and calcium
chloride are not interchageable
 Calcium gluconate- 4.5mEq of Ca
 Calcium Chloride- 13.6mEq of Ca

 Monitor BP to detect hypotension

 Resultsfrom rapid IV administration of
calcium gluconate
 Monitor ECG
 IV administration of sodium
bicarbonate may be necessary to
alkalinize the plasma and cause a
temporary shift of potassium into
cells
 Sodium bicarbonate furnishes
sodium to antagonize the cardiac
effects of potassium
IV administration of regular


insulin and hypertonic

dextrose solution causes a
temporary shift of potassium
into cells
Onsetof 3 mins and lasts for
several hours
Beta-2 agonists also move K


into the cells and may be

used in the absence of
ischemic cardiac disease
 Nursing Management
 Identify clients at risk for potassium excess
 Observe signs of muscle weakness and
dysrhytmias, paresthesia, nausea, intestinal
colic
 Monitor serum K levels periodically

 Verify abnormally elevated K levels

 Deliver blood samples as soon as

possible
Preventing Hyperkalemia
 Potassium-rich food should be
avoided