Electrolyte Balance: Part II
QUICK LOOK AT THE CHAPTER AHEADElectrolytes are essential for normal cellular functioning and help to maintain normal fluid balance in tissues and cells. Certain electrolytes are needed for conduction of nerve impulses and muscle contraction. Any increase or decrease in the concentration of electrolytes can lead to acidosis or alkalosis. Imbalances can occur as a result of poor diet or fluid intake, vomiting, diarrhea, or certain drugs.
 Figure 3-1 Isotonic intravenous solutions. |
ALTERATIONS IN POTASSIUM, CALCIUM, AND PHOSPHATEPotassium
Potassium (K+) is the major intracellular electrolyte (cation). The balance between intracellular and extracellular K+ levels is maintained by an active transport system. The primary role of K+ is maintaining the resting potential of cell membranes, which allows for transmission and conduction of nerve impulses, maintenance of cardiac rhythm, and
skeletal and smooth muscle contraction. It also plays a role in glycogenesis. Most K+ is located in the small intestine, with a moderate amount found in gastric secretions and lesser amounts in other body fluids. Diet provides the source of potassium.
skeletal and smooth muscle contraction. It also plays a role in glycogenesis. Most K+ is located in the small intestine, with a moderate amount found in gastric secretions and lesser amounts in other body fluids. Diet provides the source of potassium.
The primary role of K+ is maintaining the resting potential of cell membranes, which allows for transmission and conduction of nerve impulses, maintenance of cardiac rhythm, and skeletal and smooth muscle contraction.The kidneys regulate the balance of potassium in the body, and K+ is excreted via passive transport. This occurs as Na+ is reabsorbed and is related to the concentration gradient between the plasma and the distal tubular cells. Therefore any mechanism or condition that influences this gradient influences K+ excretion such as renal blood flow, dietary intake, and changes in pH. Mechanisms for tubular conservation of K+ are weak.
Any mechanism or condition that influences this gradient influences K+ excretion such as renal blood flow, dietary intake, and changes in pH.During states of acid-base imbalance, K+ and hydrogen (H+) shift back and forth, in an inverse relationship, across the cell membrane to maintain a healthy balance of these cations. In other words, when there is excess H+ in the extracellular fluid during states of acidosis, H+ crosses into the cell, causing K+ to leave, which results in hyperkalemia. Conversely, when there is a deficit of H+ in the extracellular fluid during states of alkalosis, H+ leaves the cell, causing K+ to enter the cell, which results in hypokalemia. Renal excretion is affected in these conditions to either conserve or eliminate K+ as necessary.
Aldosterone also plays a role in K+ balance because it is released when K+ levels are high. This causes renal conservation of Na+ and excretion of K+. Insulin facilitates the passage of K+ into liver and muscle cells. This fact should be recalled when patients are receiving insulin for management of diabetes, particularly if they have other disorders that might be influenced by this mechanism.
Insulin facilitates the passage of K+ into liver and muscle cells.Hypokalemia
Serum hypokalemia, a potassium deficiency that develops when serum potassium falls below 3.5 mEq/L, can result from either loss of K+ from the body or shifts of K+ into the cell from alkalosis or insulin
administration. This can occur due to inadequate oral intake of at least 10-30 mEq/day, transcellular shifts that redistribute K+ from extracellular to intracellular compartments, or through diuresis. The loss of K+ through the gastrointestinal tract is usually minimal but can become excessive in the presence of vomiting and diarrhea. Diarrhea can cause the loss of 100 to 200 mEq K+/day. Vomiting or nasogastric tube drainage can result in hypokalemia primarily due to the kidneys’ response to blood volume depletion and metabolic alkalosis.
administration. This can occur due to inadequate oral intake of at least 10-30 mEq/day, transcellular shifts that redistribute K+ from extracellular to intracellular compartments, or through diuresis. The loss of K+ through the gastrointestinal tract is usually minimal but can become excessive in the presence of vomiting and diarrhea. Diarrhea can cause the loss of 100 to 200 mEq K+/day. Vomiting or nasogastric tube drainage can result in hypokalemia primarily due to the kidneys’ response to blood volume depletion and metabolic alkalosis.
Vomiting or nasogastric tube drainage can result in hypokalemia primarily due to the kidneys’ response to blood volume depletion and metabolic alkalosis.It is difficult to measure the amount of total body K+ because only serum K+ is available for such determinations. Total body losses may be present yet not reflected in the serum level due to the body’s maintenance of the balance between extracellular fluid and intracellular fluid levels and its passive excretion by the kidneys. Therefore, extreme care must be taken by all health care providers to monitor patient status in regard to this electrolyte. Dietary deficiencies are rare under normal circumstances but may become important if intake is severely restricted or occurs in the presence of certain comorbidities or medication use (most diuretics). Because K+ is not stored in the body, daily intake is essential. This becomes important if patients are to take nothing by mouth for longer than a few days. Other causes of hypokalemia include renal disease and certain antibiotics.
Serum hypokalemia can occur due to inadequate oral intake of at least 10-30 mEq/day, transcellular shifts that redistribute K+ from extracellular to intracellular compartments, or through diuresis.
It is difficult to measure the amount of total body K+ because only serum K+ is available for such determinations.Hypokalemia affects carbohydrate metabolism and renal function as well as neuromuscular and cardiac function. The latter two are most obvious with a decrease in neuromuscular excitability (due to hyperpolarization of the cell membrane), which manifests as skeletal and smooth muscle atony such as ileus, abdominal distention, nausea and vomiting, and weakness as well as cardiac dysrhythmias due to delayed ventricular repolarization (bradyrhythmias, reflecting delayed repolarization).
Other causes of hypokalemia include diuretic therapy (not K+-sparing), nasogastric tube suction, vomiting and diarrhea, and primary hyperaldosteronism. Alcoholism also contributes to this state. Hypokalemia increases the risk of digitalis toxicity. Acute losses create more symptoms than gradual losses.
Other causes of hypokalemia include diuretic therapy (not K+-sparing), nasogastric tube suction, vomiting and diarrhea, and primary hyperaldosteronism. Alcoholism also contributes to this state. Hypokalemia increases the risk of digitalis toxicity. Acute losses create more symptoms than gradual losses.
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