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Fig. 46. Mechanism of urine concentration and dilution

K⁺ is reabsorbed only in the proximal portion of convoluted tubule, its release occurs in the distal portion, therefore, even in hyperkalemia K⁺ content is stable.

Glucose concentration in blood is normally, on the average, 5.5 mmol/1 its reabsorption makes up 350 mg/min. If a level of glucose achieves 9-10 mmol/1 ("glucose threshold"), it appears in the urine.

A regulation of renal function is performed by means of:

— hypophysis: ADH decreases diuresis at the expense of diminution of water excretion — a reabsorption of water in the distal portion of convoluted tubule is increased;

— adrenals: glucocorticoids cause a retention of water and Na⁺, and hereinafter increase a water excretion. Mineralocorticoids exert a direct effect on balance of electrolytes — retain Na⁺ and water.

Mineralocorticoids, DOCSA and DOC intensify Na⁺ reabsorption in the proximal portion with subsequent passive reabsorption of water. They increase activity of renin thereby causing a vascular spasm and, consequently, decrease filtration of the primary urine.

Aldosterone acts somewhat otherwise: it retains 25-30 times more actively Na⁺ and increases K⁺ excretion, but it exerts a little effect on water retention. Here, sodium is retained in saliva, intestine, sweat glands and so on.

Na¹" retention leads to the increase of osmotic pressure of interstitial space and blood, and hyperosmolarity causes intense ADH secretion, it acts contrary to aldosterone.

In this regulation a great role is played not only by osmotic component, but a volemic one as well.

Volemic shifts are regulated by means of volemic receptors located in the region of common carotid artery bifurcation, that response to hypovolemia. Elevation of VCB is the stimulator of receptors in the opening of caval veins. Impulses, from here, inhibit mineralocorticoids' secretion, Na⁺ and water are ejected. Besides, the arising hypoosmolarity inhibits ADH secretion and, as a result, the volume of urine increases, so VCB drops that acts on the receptors of sinocarotid node. A decrease of VCB intensifies a secretion of mineralocorticoids with corresponding effect.

EXCHANGE OF IONS CALCIUM

Normally, common calcium concentration in blood plasma makes up 2.1-2.5 mmol/1 and ionized calcium — 1.1-1.3 mmol/1. In percentage it looks like that:

— 50% — physiologically inactive calcium bound with proteins (albumin);

— 5-10% — in complex with anions, bicarbonate in particular, lactate, citrate, phosphate;

— 40% — in ionized form. An ionized C⁺⁺ is just physiologically active, but all 3 fractions are determined in laboratory.

Taking into account that 80% of physiologically inactive Ca⁺⁺ are bound with albumin, in a decrease of albumin concentration by 1 mg/1 a comrron Ca⁺⁺ concentration increases by 8 mg/1.

In acidosis, Ca"*"¹" binding with proteins is diminished and thereby a quantity of ionized calcium is increased.

In alkalosis, a content of ionized calcium decreases under the effect of heparin and in hyponatremia, and in hypernatremia — it increases.

H ypocalcemia is encountered in 2/3 of patients needed in IC (sepsis, hypomagnesiemia, ARF, alkalosis, acute pancreatitis).

Cause: intensive Ca⁺⁺ excretion with the urine as a result of parathormone effect.

Ca⁺⁺ deficit was always accompanied by Mg⁺⁺ deficit, therefore, a correction of Ca⁺⁺ is impossible without a preliminary Mg⁺⁺ correction.

Alkalosis intensifies calcium binding with proteins, therefore, a correction of albumin content remains the main task in elimination of alkalosis.

Sepsis is accompanied by Ca⁺⁺ release through a disturbed system of microcirculation, here a respiratory alkalosis develops.

Renal insufficiency leads to a retention of phosphates in the organism causing a formation of insoluble phosphocalcium crystals, therefore, it is necessary to prescribe antacids blocking the absorption of phosphates from the intestine.

Pancreatitis causes a decrease of parathormone secretion.

In massive hemotransfusions sodium citrate is bound with Ca⁺⁺ with formation of calcium citrate.

Clinical picture: tetany, convulsions, cardiovascular disorders: a decrease of cardiac output, vasodilatation, arterial hypotension, elongation of ST.

Treatment of hypocalcemia:

CaCl,, 10% Ca gluconate — 10 ml i/v, slowly. A maintenance dose is 1-2 mg/kg/hour drop-by-drop in the form of solution in 100 ml 5% glucose.

Hypercalcemia > 3.2 mmol/1. Changes of psychic status, ileus and renal failure are observed, AP decreases.

Treatment:

NaCl 0.9% + saluretics (furosemid) 40-100 mg every 2 hours. A rate of administration of 0.9% NaCl is equal to the rate of diuresis.

Calcitoninum — 4 U/kg i/m or 8 U/kg p/c in 12 hours. It inhibits a process of decalcification of bones.

Mitramycin — 25 mg/kg i/v (antitumoral agent) are administered once in 2-3 days.

Hemodialysis.

PHOSPHORUS is the main intracellular anion. An extracellular fluid contains less than 1% of the total phosphorus. A normal level of phosphorus in blood serum is 3-5mmol/l. Almost all phosphorus in the organism is in the

form of phosphates (P0₄---) and the terms of "phosphate" and "phosphorus"

are used as equivalents.

Hypophosphatemia

Causes: i/v infused glucose, aluminium-containing antacids, respiratory alkalosis, ketoacidosis, parenteral feeding.

In treatment with glucose the number of phosphorus ions decreases that is due to the use of insulin contributing to the transport of glucose and phosphate through cell membranes.

The increase of pH (alkalosis) contributes to stimulation of glycolysis and intensification of glucose phosphorylation contributes to a transfer of phosphorus through membranes. Such state is observed in the patients being on APV in the regimen of hyperventilation.

Sepsis is accompanied by increased metabolism requiring raising a consumption of phosphates that leads to a decrease of phosphorus.

A groundless decrease of phosphorus blood concentration must direct to a search of infection.

Diabetic ketoacidosis: glucosuria leads to the increase of phosphates' excretion with the urine that is accompanied by a decrease of phosphorus level in plasma. Besides, application of insulin in diabetes mellitus contributes to a rapid migration of phosphorus from plasma into the cell.

Aluminium-containing antacids bind phosphorus in the intestine that is accompanied by a decrease of its level in blood.

In decrease of phosphorus content a supply of oxygen to the tissues worsens, an oxygen affinity to hemoglobin intensifies and it does not go into the cell.

A muscular weakness in decrease of phosphorus content is explained by a diminution of ATP production. When a phosphorus content in blood serum is <0.8 mmol/1 (<25 mg/1) a weakness of respiratory muscles is noted.

Treatment of hypophosphatemia:

When phosphatemia is <0.17 mmol/1 (<5 mg/1) a dose of phosphorus 15 mg/kg in 4 hours should be administered, and in phosphorus content 0.36 mmcl/1 (10 mg/1), doses of phosphorus are 7.7 mg/kg in 4 hours.

A normal phophorus content is achieved in 3 days of treatment.

Hyperphosphatemia

Causes: renal failure and destruction of cells, increase of phosphorus consumption, respiratory acidosis and diabetic ketoacidosis. Treatment of hyperphosphatemia:

— removal of the main cause;

— binding phosphorus by means of aluminum, magnesium and calcium gels and antacids;

— diet with reduced phosphorus content;

— hemodialysis.

MAGNESIUM — an intracellular cation Mg⁺⁺ is an activator of enzymes, it also participates in reactions with ATPand Na⁺ transport from the cell and K⁺ into the cell. Its content in blood plasma is 0.7-1.2 mmol/1.

Hypomagnesemia

Causes:

— Mg²⁺ losses with the urine (in application of diuretics);

— decrease of Mg entry (in intensive therapy, application of amino­glycosides with simultaneous increase of Mg excretion through the kidneys;

— absorption disorders in the intestine.

It is usually combined with a decrease of K⁺ and Ca²⁺.

riinir.al picture: arrhythmias, muscular weakness, tremor, mental disorders, convulsions and neuromuscular excitation.

Treatment:

MgS0₄ — 0.5 mmol/l in the first 24 hours, then 0.25 mmol/l a day for 3-5 days, (1 ml 25% MgS0₄ contains 1 mmol Mg).

In life-threatening arrhythmias as a result of Mg²⁺ decrease:

— i/v MgS0₄ 25% — 8 ml in the course of 1-2 min as a bolus;

— i/v MgS0₄ 25% — 20.0 per 500 ml physiologic solution for subsequent 6 hours;

— continue to introduce this solution i/v every 12 hours for 5 days.

In moderate deficit of magnesium they use MgS0₄ 25% — 24 ml per 500ml physiologic solution for 3 hours, then for subsequent 6 hours. Continue a daily i/v drop-by-drop administration of MgS0₄ every 12 hours up to 6 days.

Hypermagnesemia

Causes:

— excessive entry of Mg (magnesium-containing preparations — laxatives);

— diabetic ketoacidosis — Mg release from the cells;

— pheochromocytoma.

Clinical picture: AP decrease in Mg⁺⁺ = 1.5-2.5 mmol/l, a complete A-V block in Mg⁺⁺ = 3.75 mmol/l, respiratory depression and coma in 5 mmol/l.

Treatment: hemodialysis, 10% CaCl₂ solution — 20 ml i/v (for elimination of hypotension), without hemodialysis — diuretics (furosemid).

POTASSIUM K ⁺

Human organism contains 3150 mmol K⁺, 98% of them are in the tissues and 2% — in plasma. In plasma and interstice K⁺ is in a mobile ionized form. A normal level of K⁺ in plasma is 3.5-5 mmol/l and its intracellular concentration is 150 mmol/l.

In the tissues a small portion of K⁺ is free and the remaining part is bound with proteins, glucose, creatinine and phosphorus. Its tissue compounds are instable.

Passing K⁺ through a cell membrane takes place in presence of sodium-potassium-dependent ATP-ase and depends on its activity. In its turn, the latter's activity is influenced by insulin, and catecholamines. Glucose and insulin increase the ability of K⁺ penetration into the cell. K⁺ penetration into the cell occurs in parallel with Na⁺ transfer from the cell (sodium pump).

A role of JC in metabolism:

— plastic in binding with proteins,

— metabolism of carbohydrates,

— takes part in synthesis of ATP and phosphocreatinine,

— influences a contraction of muscular fibers,

— participates in synthesis of Ach,

— participates in degradation of cholinesterase,

— influences a transmission of nerve impulses in the synapse, dilates vessels by exerting its effect on chemoreceptors of carotid zone.

K⁺ delivery to the organism with foodstuffs makes up 3-4 g/day (76-120 mmol).

Up to 90% of K⁺ are excreted through the kidneys.

Regulation of K⁺ exchange in the organism occurs at the expense of AAB and endocrine influences. Aldosterone increases K⁺ elimination 5 times and retains Na⁺ excretion 25 times.

Hypokalemia in (K⁺ <3.5 mmol/l).

Causes: increase of K⁺ entry into the cell, losses of K⁺ and decrease of its delivery from the outside, losses of K⁺ in application of diuretics and corticosteroids, in prolonged use of gastric and intestinal tube, vomiting, hyperventilation and cirrhosis of the liver, in diarrhea.

Clinical picture:

Muscular weakness and changes of mental status are noted. A weakening of reflexes, decrease of mental and psychic activities, enteroparesis, meteori.'.m, repeated vomiting, increased sensitivity to myorelaxants, a late recovery from general anesthesia are observed. There is an elevation of P wave, elongatior of ST interval, not steep T, enlargement of U wave on the ECG. Hypokalemia is able to potentiate arrhythmias in which antiarrhythmic agents are not effective!

A binding of cardiac glycosides with Na⁺/K⁺ — ATP-ase of the myocardial cells membrane increases. Consequently, K⁺ concentration inside the cells reduces and Na⁺ increases with development of transmineralization syndrome. Therefore, it is necessary to normalize K⁺ content in blood.

Treatment: 's^<Y«i

— KC1 solutions are prescribed i/v — in metabolic alkalosis, and potassium hydrocarbonate — in metabolic acidosis with concentrated glucose and insulin;

— if GIT function is not disturbed a diet rich in potassium is prescribed: potatoes, fruits, peaches and apricots, in particular.

A calculation of K⁺, needed for correction, is made by formula:

Deficit of K⁺xVICF;

Deficit K⁺ = K⁺_N — K⁺_fact (by laboratory findings);

VICF (volume of intracellular fluid) = m_k x 0.2 1.

It should be rejnembered that a decrease of K⁺ in plasma by 1 mmol/l is equal to the decrease of total supplies of K⁺ by 10%.

For example:

In a patient with a body weight of 80 kg, K⁺_fact = 2.5 mmol/l. Deficit of K⁺ = K⁺_N — K⁺_fact = 4.5 — 2.5 = 2mmol/l.

Total VICF = 80 x 0.2 = 16 1.

Deficit of K⁺ in 16 1 = 32 mmol/l (it is without taking into account K⁺ deficit in the cells).

One should know that 1 ml 7.5% KC1 contains 1 mmol K\ 4% KC1 — 0.53 mmol K⁺ and 3% KG — 0.4 mmol K⁺, 10 ml of panangin contain 2.5 mmol K⁺.

For correction of hypokalemia this patient should be administered i/v 32 ml 7.5% KC1 or 80 ml 3% KC1.

The rate of K intravenous infusion through peripheral veins should be no more than 8 mmol/hour. The rate of K⁺ infusion is allowed within the range of 10-20 mmol/hour, but only through a catheter introduced into a central vein. This is associated with irritating effect of potassium on venous endothelium. A single administration of K⁺ must not exceed 0.7 mmol/kg and at this rate it is recommended to infuse potassium into peripheral veins.

While correcting K⁺ deficit it is necessary to make also a correction for daily losses of K⁺ with the urine up to 40 mmol and data of repeated determination of K⁺ in plasma;

— to discontinue the intake of agents contributing to K⁺ accumulation in
the cells.

Proceeding from all said above, a conclusion may be drawn that a great deficit of K⁺ in plasma should be corrected gradually, in the course of few days.

In metabolic acidosis a deficit of K⁺ does not require replenishment because of a dangerous development of hyperkalemia accompanying acidosis.

If K⁺ concentration does not increase under the effect of IC one should think of Mg²⁺ deficit in that K⁺ is intensively being lost with the urine.

Hyperkalemia (K >5.5 mmol/1). (_ f\V"HC cIL"k.

A threat to life is more serious than in K⁺ decrease.

Causes are as follows: excessive supply of potassium to the organism, hyperproduction of K⁺ because of muscular necrosis (RDS), burns, internal bleeding, insulin deficit (insulin intensifies potassium supply to the cell), intoxications, dyshydrias, acidosis leading to a decrease of K⁺ excretion by the kidneys and increase of K⁺ release from the cell, renal failure, adrenal insufficiency, administration of drugs having potassium-saving properties (verospiron and heparin inhibit synthesis of aldosterone).

Clinical picture:

Weakness of skeletal musculature, paresthesias of the skin of extremities,

flaccid paralyses, adynamia down to coma are observed. Disturbances of

conduction and cardiac rhythm are noted. On the ECG there are changes —

^widening of QRS, gothic T wave, PQ elongation, ST depression and

arrhythmias. In K⁺ > 7 mmol/1 — a cardiac arrest in diastole.

Treatment:

— potassium antagonists: calcium chloride, calcium gluconate 10% — 10-20 ml i/v. In absence of effect — to repeat in 5 minutes. Action of calcium preparations has a temporary character;

— infusion of glucose-insulin mixture (20% glucose — 500 ml, insulin 10 U,

5% soda — 250 ml) i/v in the course of 1 hour allows to transfer potassium into the cell;

— increase of K⁺ excretion by the kidneys — furosemid, ethacrynic acid;

— hemosorption, ion-exchange resins;

— hemodialysis.

SODIUM Na ⁺

It's the main electrolyte that with Cf maintains the osmotic pressure in plasma 300 mosmol/1.

Normal Na-concentration in plasma is 142 mmol/1. A daily entry and excretion of sodium in balanced regimen are 4-5 g. Its absorption occurs in the colon and excretion — by the kidneys, as well as with sweat, saliva and feces. It participates in the origin and transfer of nerve impulse. Relation of sodium effect with other ions upon skeletal musculature and myocardium is given in Table 26.

Table 26 Action of ions on peripheral musculature and myocardium (Moor's formula)

Na⁺ is neither toxic, nor hydrophilic, but retains around it water owing to its great amount in the extracellular space. Its pathology is closely connected with dyshydrias.

Treatment is carried out with 10% and 0.9% NaCl solutions.

Calculation is being made by due (142 mmol/1) and factual Na⁺ content in plasma. Na" deficit in 1 1 = Na_N - Na_fact.

Na deficit in extracellular fluid = Na deficit mmol/1 x body weight x 0.2 Total Na deficit = Na deficit mmol/1 x body weight x 0.6 1 g NaCl contains 17 mmol of Na ions, therefore, the obtained result of Na deficit in mmol is divided by 17 and we obtain Na deficit in grams.

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