Potassium from muscle

Ketosis— The most common causes of this condition— which is characterized by an excess of ketones in the blood— are (1) diabetes (2) diets high in fat and protein, but low in carbohydrate (3) fevers and (4) starvation. A mild ketosis in normally healthy people is usually not dangerous, unless it occurs regularly over a long period of time, flien, it may lead to such problems as (1) excessive urinary loss of sodium and water (2) acidosis which provokes the loss of calcium from bone, and potassium from muscle and (3) the accumulation of uric acid (a waste product of protein metabolism) in the blood, and sometimes in the soft tissues where it causes damage and pain (the latter disorder is commonly called gout). Uric acid buildup is usually treated with alkalizers to prevent the formation of kidney stones. However, the alkalizers may cause other alterations in mineral metabolism. 

The catecholamines can play an important role in the short-term regulation of plasma potassium levels. Stimulation of hepatic a-adrenoceptors will result in the release of potassium from the liver. In contrast, stimulation of (32-adrenoceptors, particularly in skeletal muscle, will lead to the uptake of potassium into this tissue. The (32-adrenoceptors are linked to the enzyme Na"", K+ adenosine triphosphatase (ATPase). Excessive stimulation of these (32-adrenoceptors may produce hypokalemia, which in turn can be a cause of cardiac arrhythmias. 

Cantley, L.C., Jr., L. Josephson, R. Warner, M. Yanagisawa, C. Lechene, and G. Guidotti. 1977. Vanadate is a potent (sodium, potassium ion)-dependent ATPase inhibitor found in ATP derived from muscle. J. Biol. Chem. 252 7421-3. 

Several studies of animals exposed to barium by parenteral routes indicate that barium decreases in serum potassium (Foster et al. 1977 Jaklinski et al. 1967 Roza and Berman 1971 Schott and McArdle 1974). In one study, dogs intravenously administered barium chloride demonstrated a decrease in serum potassium accompanied by an increase in red blood cell potassium concentration (Roza and Berman 1971). The authors concluded that the observed hypokalemia was due to a shift of potassium from extracellular to intracellular compartments and not to excretion. Additional intravenous studies have linked the observed hypokalemia to muscle paralysis in rats (Schott and McArdle 1974) and cardiac arrhythmias in dogs (Foster et al. 1977). These experiments in animals strongly support the suggestive human case study evidence indicating hypokalemia is an important effect of acute barium toxicity. 

An arousal pattern can occur on the electroencephalogram, possibly as a result of increased afferent traffic from muscle spindles. This has been speculated as the cause of perioperative dreaming in children in whom an intermit-tent-suxamethonium technique has been used during hght anesthesia (SEDA-13,102) (32). Suxamethonium must be used with caution in neurological disease and is better avoided altogether when there is a risk of a dangerous rise in serum potassium. A transient rise in intracranial pressure has been observed after injection of... 

The primary mechanism of terbutaline is the stimulation of adenylcyclase, which catalyzes cyclic adenosine monophosphate (AMP) from adenosine triphosphate (ATP). In the liver, buildup of cyclic AMP stimulates glycogenolysis and an increase in serum glucose. In skeletal muscle, this process results in increased lactate production. Direct stimulus of sodium/potassium AT-Pase in skeletal muscle produces a shift of potassium from the extracellular space to the intracellular space. Relaxation of smooth muscle produces a dilation of the vasculamre supplying skeletal muscle, which results in a drop in diastolic and mean arterial pressure (MAP). Tachycardia occurs as a reflex to the drop in MAP or as a result of Pi stimulus. )Si-Adrenergic receptors in the locus ceruleus also regulate norepinephrine-induced inhibitory effects, resulting in agitation, restlessness, and tremor. 

Hypokalemic periodic paralysis is a rare complication of hyperthyroidism commonly observed in Asian and Hispanic populations. It presents as recurrent proximal muscle flaccidity ranging from mild weakness to total paralysis. The paralysis may be asymmetric and usually involves muscle groups that are strenuously exercised before the attack. Cognition and sensory perception are spared, whereas deep tendon reflexes are commonly markedly diminished. Hypokalemia results from a shift of potassium from extracellular to intracellular sites. High carbohydrate loads and exercise provoke the attacks. Treatment includes correcting the hyperthyroid state, potassium administration, spironolactone to conserve potassium, and propranolol to minimize intracellular shifts. ... 

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). 

The acute renal failure is typical for acute tubular necrosis and is characterized by a urine sediment with granular pigmented casts, and benzidine positive urine often in the absence of significant hematuria. With rhabdomyolytic acute tubular necrosis the urinary sodium concentration and fractional excretion of sodium are not always increased as in classic acute tubular necrosis [99]. One half to two-thirds of patients have ohguria, which may last from hours to many weeks. During this phase of the acute renal failure, there is a very rapid rise in the serum creatinine (often > 2.0 mg/ dl/ day), and profound increases in the serum levels of a variety of solutes normally foimd in muscle or produced from muscle derived precursors. Thus, fhe levels of potassium, phosphate, and uric acid all rise dra-... 

F. Hyperkalemia and hypokalemia. A variety of drugs and toxins can cause serious alterations in the semm potassium level (Table 1-27). Potassium levels are dependent on potassium intake and release (eg, from muscles), diuretic use, proper functioning of the ATPase pump, serum pH, and beta-adrenergic activity. Changes in serum potassium levels do not always reflect overall body... 

Excessive uptake of potassium by muscles from fluids in the immediate environment... 

A reversible reaction catalyzes the conversion of pyruvate to phosphopyruvate, and the enzyme involved is pyruvic kinase. The equilibrium of that reaction is on the side of the formation of ATP. Thus, pyruvate kinase is the enzyme responsible for the conversion of phosphoenolpyruvate to pyruvate. The enzyme has been crystallized from muscle it requires ADP, potassium, and magnesium and is noncompetitively inhibited by some estrogenic steroids. Steroids alter the enzyme s viscosity and electrophoretic properties. From this observation, it was assumed that steroids act by modifying the protein molecule. 

Potassium, Adequate potassium may lower blood pressure, which, in turn, will lessen the risk of heart attack. Also, depletion of potassium from the heart muscle renders it more susceptible to nonrhythmic beating, particularly when digitalis is used to treat heart failure. 

Goiter—People with goiter may be overly susceptible to the toxic effects of excess iodine because their thyroid glands have become extra efficient in the utilization of this mineral. Therefore, they may develop oversecretion of thyroid hormones (hyperthyroidism) when given extra iodine. This toxic condition may sometimes be accompanied by the loss of calcium from the bones, and of potassium from the muscles. 

The uptake of potassium by muscle exposed to insulin is amenable to interpretation since Zierler (1959) has demonstrated hyperpolarization of the cell membrane under such circumstances, whether or not glucose was present during incubation the Mine was observed with adipocytes (Beigelman and Hollander, 1963). Hyperpolarization of cell membrane induced by insulin might in turn result from enhanced active sodium transport from the cytoplasm outward, as has been shown by Moore (1965) to occur in the case of frog sartorius. 

It is established that suxamethonium may liberate potassium from skeletal muscles. An excessive rise in extracellular potassium levels which may lead to cardiac arrest will frequently occur in patients with traumatic or bum injuries of muscle, in neuropathies, myopathies and in patients with renal insufficiency (SED VIII, p. 281), In a clinical study Kohlschutter et al. (9 ) found that patients with severe and prolonged intraabdominal infections represent an additional group of individuals susceptible to suxa-methonium-induced hyperkalaemia. 

Other Potassium and Sodium Disorders. Potassium and/or sodium deficiency can lead to muscle weakness and sodium deficiency to nausea. Hyperkalemia resulting in cardiac arrest is possible from 18 g/d of potassium combined with inadequate kidney function. Faulty utilisation of K" and/or Na" can lead to Addison s or Cushing s disease. 

Burgen, A. S. V., and Spero, L. (1968). The action of acetylcholine and other drugs on the efflux of potassium and rubidium from smooth muscle of the guinea-pig intestine. Br. J. Pharmacol., 34 99—115. 

Hyperkalemia is defined as a serum potassium concentration greater than 5 mEq/L (5 mmol/L). Manifestations of hyperkalemia include muscle weakness, paresthesias, hypotension, ECG changes (e.g., peaked T waves, shortened QT intervals, and wide QRS complexes), cardiac arrhythmias, and a decreased pH. Causes of hyperkalemia fall into three broad categories (1) increased potassium intake (2) decreased potassium excretion and (3) potassium release from the intracellular space. 

With active transport, energy is expended to move a substance against its concentration gradient from an area of low concentration to an area of high concentration. This process is used to accumulate a substance on one side of the plasma membrane or the other. The most common example of active transport is the sodium-potassium pump that involves the activity of Na+-K+ ATPase, an intrinsic membrane protein. For each ATP molecule hydrolyzed by Na+-K+ ATPase, this pump moves three Na+ ions out of the cell and two K+ ions into it. As will be discussed further in the next chapter, the activity of this pump contributes to the difference in composition of the extracellular and intracellular fluids necessary for nerve and muscle cells to function. 

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