الفهرس 
PHSIOLOGICAL EFFECT OF POTASSIUMOnly 14 pages are availabe for public view
 |  | from | 122 |  |  |
| | | from | 122 | | |
Abstract
potassium plays a major role in the electrophysiology of cell membrane as well as carbohydrate and protein synthesis .The excitability of the cell is proportional to the ratio of intracellular to extracellular potassium concentrations. Intracellular potassium concentration is estimated to be 150 mEq/L while extracellular concentration is about 4 mEq/L. Any variations in this ratio will result in dysfunction of excitable cell membranes and cause the signs and symptoms that are associated with imbalances of potassium concentration .
Dietary potassium is autoregulated principally by the kidney, the fecal excretion of potassium constitutes a second pathway for the elimination of dietary potassium, lastly small amount of potassium is lost in sweat. Potassium excreted in urine is the result of distal tubular secretion . the major determinants of urinary flow rates, mineralocorticoid state ,acid – base state and diuretics intake
Chronic potassium regulation is controlled primarily by the kidney ,while acute potassium homeostasis has a major extrarenal component which is mainly hormonal, the hormones of importance as regard potassium regulation include aldosterone, insulin, catecholamines, glucocorticoids, and antidiuretic hormone.
Hypokalemia may be due to decreased potassium intake, intercompartmental shift of potassium as with insulin administration alkalosis , periodic paralysis , hypothermia and drugs as beta- 2 adrenergic agonists or it may be due to increased potassium losses as with use of diuretics , primary and secondary hyperaldosteronism , hypomagnesemia and increased gastrointestinal losses ( diarrhea, vomiting, fistulae )
Adverse effects of chronic hypokalemia may include skeletal muscle weakness, decreased myocardial contractility, increased automaticity of the atria and ventricles , manifested as cardiac arrhythmias and alteration of cardiac conduction manifested in the ECG as prolongation of P-R interval and Q-T interval, and flattening of T wave .
Treatment of hypokalemia with potassium chloride is recommended when hypokalemia is associated with the appearance of abnormalities on the ECG . Continuous monitoring of ECG and urinary output are mandatory during treatment of hypokalemia
Hyperkalemia may be due to increased potassium intake as with transfusion of old whole blood , intercompartmental shift ( aciodosis, rhabdomyolysis , tissue breakdown , periodic paralysis , drugs as succinyl choline etc) or it may be due to decreased renal potassium excretion ( renal failure , Addison’s disease, drugs etc)
Adverse effects of hyperkalemia are likely to accompany acute increase in serum potassium concentrations . In contrast, chronic hyperkalemia is more likely to be associated with normal gradients between extracellular and intracellular concentrations of potassium. Patients with chronic hyperkalemia are often asymptomatic , this suggests that potassium gradients across cell membranes are more important than absolute serum concentrations of potassium
The most important effects of hyperkalemia are on skeletal and cardiac muscle . Skeletal muscle weakness is generally not seen until plasma potassium is greater than 8 mEq/L . The weakness is due to sustained spontaneous depolarization of the muscle membrane (similar to succinylcholine ) , eventually resulting in ascending paralysis .
Cardiac manifestation of hyperkalemia are usually consistently present when plasma potassium is greater than 7mEq/L. ECG changes characteristically progress in order, from , symmetrically peaked tented shaped T wave, often with a shortened QT interval to widening of ORS. Complex, prolongation of the P.R interval, loss of P. wave, loss of R wave amplitude, ST, segment depression (occasionally) elevation, to an ECG that resemble a sine wave pattern, before final progression into ventricular fibrillation or asystole. Hypocalcemia, hyponatremia , and acidosis accentuate the cardiac effects of hyperkalemia.
Immediate treatment of hyperkalemia is indicated in the presence of electrocardiographic signs of hyperkalemia or in the presence of plasma potassium concentration that exceeds 6.5 mEq/L. Initial treatment of hyperkalemia is directed at antagonizing the adverse effects of potassium on the heart (intravenous calcium) and facilitating the movement of potassium from the plasma into cells (insulin and intravenous glucose) increasing elimination of potassium from the body by diuretics , cation exchange resins and dialysis
The decision to proceed with elective surgery in the presence of hypokalemia is arbitrarily based on lower limits somewhere between 3 and 3.5 mEq/L. The decision , however should be based also on the rate at which hypokalemia developed as well as the presence or absence of secondary organ dysfunction . In general , chronic mild hypokalemia (3- 3.5 mEq/L) without ECG changes does not appear to increase anesthetic risk, but this may not apply to patients receiving digoxin who may be at increased risk of developing digoxin toxicity from hypokalemia plasma potassium values above 3.5 mEq/L are desirable in such patients.
Intraoperative management of hypokalemia requires continuous ECG monitoring . Intravenous potassium should be given if atrial or ventricular arrhythmias develop. Glucose free solutions should be used and hyperventilation is avoided to prevent further decrease in plasma potassium . Increased sensitivity to muscle relaxants may be seen in some patients. Dosage of muscle relaxants should be used to follow the degree of paralysis and the adequacy of reversal .
Elective surgery should not be undertaken in patients with hyperkalemia. Anesthetic management of hyperkalemic surgical patients is directed at both lowering plasma potassium concentration and preventing any further increase. The ECG should be carefully monitored. Succinyl choline is contraindicated as well as the use of any potassium containing intravenous solutions such as, lactated Ringer’s solution. Avoidance of metabolic or respiratory acidosis is critical to prevent further increase in plasma potassium. Ventilation should be controlled under general anesthesia, mild hyperventilation may even be desirable. Lastly neuromuscular function should be monitored closely , since hyperkalemia can accentuate the effects of muscle relaxants.