You are on page 1of 10

CASE STUDY

Genevieve Frias Jib Sinsuat Patient : Gallo, Ramon

HYPOKALEMIA
color meaning = looks like milk, its malabo because hypokalemia means low in potassium (banana).

INTRODUCTION What is hypokalemia?


Hypokalemia abnormally low level of potassium in the circulating blood leading to weakness and heart abnormalities.

Abnormally low potassium concentration in the blood; it may result from potassium loss by renal secretion or via the gastrointestinal tract, as in vomiting and diarrhea. Other causes include uncontrolled diabetes mellitus and attendant polyuria, increased adrenocortical secretion, steroid therapy, diuretic therapy, and burns or other injuries that result in loss of potassium. A special circumstance in which hypokalemia occurs is dilatation and displacement of the abomasum in which large quantities of potassium accumulate. The clinical syndrome of hypokalemia includes muscle weakness, lethargy, recumbency and terminal coma. Called also hypopotassemia.

WHAT IS POTASSIUM
Small chemicals in the body known as electrolytes are crucial for cells to function. Potassium is one of the main electrolytes, and is concentrated within the cells of the body. Only 2% of the body's total potassium is available in the serum (the fluid part of the bloodstream that is not red or white blood cells or platelets). Small changes in the serum levels of potassium can affect body function. One of the important functions of potassium is maintenance of the cell electrical potential. The serum bathes the cells, and if the serum potassium level falls, cells with high electrical activity (for example, muscles and nerves) are particularly affected. Normal potassium levels measured in the serum range from 3.5 to 5.0 mEq/liter. Normal daily intake of potassium is 70-100 mEq

(270 to 390 mg/dl), and requires the kidneys to remove that same amount each day. If more is removed, the body's total potassium store will be decreased, and the result is hypokalemia (hypo=low + kal=potassium +emia= in the blood) occurs. Potassium enters the body through dietary intake. Examples of potassium rich foods include: Fresh fruits: bananas, cantaloupe, oranges, strawberries, kiwi, avocados, apricots Fresh vegetables: greens, mushrooms, peas, beets, tomatoes Meats: beef, fish, turkey, Juices: Orange, prune, apricot, grapefruit

CAUSES OF HYPOKALEMIA
Hypokalemia is not commonly caused by poor dietary intake. Excessive loss is the most common reason that potassium levels are low. Loss of potassium may occur from both the gastrointestinal (GI) tract and from the kidney. Potassium loss from the intestines may be caused by:

Vomiting Diarrhea

Ileostomy: In some patients who have had bowel surgery and an ileotomy formed, significant potassium loss can occur. Villous adenoma (a type of colon polyp that can cause the colon to leak potassium)

Laxative use

Causes of potassium loss from the kidney:

Diuretic medications (water like hydrochlorothiazide (HCTZ) or furosemide (Lasix)

pills)

Elevated corticosteroid levels, either like prednisone or from Cushing's Syndrome


from

medication

Elevated levels of aldosterone, a hormone that can increase with renal artery stenosis or adrenal tumors

Renal tubular acidosis Low body magnesium levels

Low potassium levels may result from side effects of some medications: Aminoglycosides or tobramycin (Nebcin)

like gentamicin

(Garamycin)

Amphotericin B Prednisone

PATHOPHYSIOLOGY
Potassium is essential for many body functions, including muscle and nerve activity. Potassium is the principal intracellular cation, with a concentration of about 145 mEq/L, as compared with a normal value of about 4 mEq/L in extracellular fluid, including blood. More than 98% of the body''s potassium is intracellular; measuring it from a blood sample is relatively insensitive, with small fluctuations in the blood corresponding to very large changes in the total bodily reservoir of potassium. The osmotic gradient of potassium between intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of

the resting membrane potential. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. Potassium is also essential to the normal muscular function, in both voluntary muscle (e.g. the arms and hands) and involuntary muscle (e.g. the heart and intestines). Severe abnormalities in potassium levels can seriously disrupt cardiac function, even to the point of causing cardiac arrest and death.

ANATOMY and PATHOPHYSIOLOGY


Potassium homeostasis Potassium, the most abundant intracellular cation, is essential for the life of the organism. Potassium is obtained through the diet, and common potassium-rich foods include meats, beans, fruits, and potatoes. Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present. Excretion is increased by (1) aldosterone, (2) high sodium delivery to the collecting duct (eg, diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level, and (5) delivery of negatively charged ions to the collecting duct (eg, bicarbonate). Excretion is decreased by (1) absence or relative deficiency of aldosterone, (2) low sodium delivery to the collecting duct, (3) low urine flow, (4) low serum potassium level, and (5) renal failure. Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, obligatory renal losses are 10-15 mEq/d. Thus, chronic

losses occur in the absence of any ingested potassium. The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load. Serum potassium level Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis. Mechanisms for sensing extracellular potassium concentration are not well understood. Evidence suggests that adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium sensing, resulting in alterations in aldosterone and insulin secretion.[1, 2] As both of these hormonal systems play important roles in potassium homeostasis, these new findings are no surprise; however, the molecular mechanisms by which these potassium channels signal changes in hormone secretion and activity have still not been determined. Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Insulin stimulated by potassium ingestion increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of

changes in muscle cell sodium pump expression. However, long term potassium deprivation results in a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium.[3, 4, 5] Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for long-term potassium homeostasis. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion. Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows: Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells, and (2) glucagon impairs potassium entry into cells. Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry into cells, and (2) alpha-adrenergic stimuli impair potassium entry into cells. pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells. An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space.

PATHOPHYSIOLOGY Hypokalemia mechanisms. can occur due to 1 of 3 pathogenetic

The first is deficient intake. Poor potassium intake alone is an uncommon cause of hypokalemia but occasionally can be seen in very elderly individuals unable to cook for themselves or unable

to chew or swallow well. Over time, such individuals can accumulate a significant potassium deficit. Another clinical situation where hypokalemia may occur due to poor intake is in patients receiving total parenteral nutrition (TPN), where potassium supplementation may be inadequate for a prolonged period of time. The second is increased excretion. Increased excretion of potassium, especially coupled with poor intake, is the most common cause of hypokalemia. The most common mechanisms leading to increased renal potassium losses include enhanced sodium delivery to the collecting duct, as with diuretics; mineralocorticoid excess, as with primary or secondary hyperaldosteronism; or increased urine flow, as with an osmotic diuresis. Gastrointestinal losses, most commonly from diarrhea, also are common causes of hypokalemia. Vomiting is a common cause of hypokalemia, but the pathogenesis of the hypokalemia is complex. Gastric fluid itself contains little potassium, approximately 10 mEq/L. However, vomiting produces volume depletion and metabolic alkalosis. These 2 processes are accompanied by increased renal potassium excretion. Volume depletion leads to secondary hyperaldosteronism, which, in turn, leads to enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption. Metabolic alkalosis also increases collecting tubule potassium secretion due to the decreased availability of hydrogen ions for secretion in response to sodium reabsorption. The third is due to a shift from extracellular to intracellular space. This pathogenetic mechanism also often accompanies increased excretion, leading to a potentiation of the hypokalemic effect of excessive loss. Intracellular shifts of potassium often are episodic and frequently are self-limited, for example, with acute insulin therapy for hyperglycemia. Regardless of the cause, hypokalemia produces similar signs and symptoms. Because potassium is overwhelmingly an intracellular cation and because a variety of factors can regulate the actual serum potassium concentration, an individual can incur very

substantial potassium losses without exhibiting frank hypokalemia. Conversely, hypokalemia does not always reflect a true deficit in total body potassium stores.

NURSING MANAGEMENT
- Electrolyte management: Hypokalemia - Dysrhythmias management - Acid-base management: Metabolic alkalosis - Administer potassium replacement therapy as ordered. * oral potassium should be diluted in 4-8 oz of water or juice (decreased gastric mucosa irritation) * dilute IV potassium 20-40 mEq in 1L of IV fluids (irritating to blood vessels and myocardium) * Never administer bolus IV potassium - Monitor IV site for phlebitis and infiltration - Protect form injury - Monitor I&O hourly - Monitior vital signs - Monitor heart rate and rhythm - Monitor patient closely for signs of digitalis toxicity (premature atrial and ventricular beats). - Teach patient about potassium-rich fods and how to prevent excessive loss (abuse of laxative and diuretics)

EVALUATION (PROGNOSIS)
The prognosis for correcting hypokalemia is excellent. However, in emergency situations, where potassium is administered intravenously, the physician must be careful not to give too much potassium. The administration of potassium at high levels, or at a high rate, can lead to abnormally high levels of serum potassium.