Metabolic alkalosis

Metabolic alkalosis - a violation of the acid-base state, manifested by a decrease in hydrogen and chlorine ions in the extracellular fluid, high blood pH values and high concentration of bicarbonate in the blood. To maintain alkalosis, there must be a violation of renal excretion of HCO3 ~. Symptoms and signs in severe cases include headache, lethargy and tetany. Diagnosis is based on clinical data and the determination of the gas composition of arterial blood and the level of plasma electrolytes. Correction of the original cause is sometimes indicated intravenous or oral administration of acetazolamide or HCI.

[1], [2], [3],

Causes of the metabolic alkalosis

The main causes of the development of metabolic alkalosis - loss of body H ⁺, exogenous bicarbonate load.

Losses of H ^{+ by the}  body with the development of metabolic alkalosis are observed, as a rule, with lesions of the gastrointestinal tract and kidney pathology. In these situations, along with the loss of hydrogen ions, the chlorides are also lost. The response of the body, aimed at replenishing chloride losses, depends on the type of pathology, which is reflected in the classification of metabolic alkalosis.

Loss of H ⁺  through the gastrointestinal tract

This is the most common cause of the development of metabolic alkalosis in the clinic of internal diseases.

Classification and causes of metabolic alkalosis

Classification	Cause
Lesions of the gastrointestinal tract
Chloride-resistant alkalosis
Chloride-sensitive alkalosis	Vomiting, drainage of the stomach, adrenal adenoma of the rectum or large intestine
Renal damage
Chloride-sensitive alkalosis	Diuretic therapy, post-hypercapnic alcalosis
Chlorinated-resistant alkalosis with arterial hypertension	Konna's syndromes, Itenko-Cushing's disease, adrenogenital, renovascular hypertension, drugs with mineralocorticoid properties (carbenoksolon, licorice root), treatment with glucocorticoids
Chloride-resistant alkalosis with normal pressure	Bartter's syndrome, severe potassium depletion
Bicarbonate loading	Massive bicarbonate therapy, massive blood transfusion, treatment with alkaline-exchange resins

In gastric juice in high concentrations contain sodium chloride and hydrochloric acid, in lower concentrations - potassium chloride. Secretion in the lumen of the stomach 1 mmol / L H ^{+ is}  accompanied by the formation of 1 mmol / L bicarbonate in the extracellular fluid. Therefore, the loss of hydrogen and chlorine ions during vomiting or aspiration of gastric juice through the probe is compensated by an increase in the blood concentration of bicarbonates. At the same time, a loss of potassium occurs, which leads to the release of K ⁺  from the cell with its replacement by H ⁺ ions  (development of intracellular acidosis) and stimulation of reabsorption of bicarbonates. The developed intracellular acidosis is an additional factor contributing to the loss of hydrogen ions due to the compensatory reaction, manifested in the enhancement of their secretion by cells, including the kidney tubules, which leads to acidification of urine. This complex mechanism explains the so-called "paradoxical acid urine" (low urinary pH values under metabolic alkalosis) with prolonged vomiting.

Thus, the development of metabolic alkalosis caused by the loss of gastric juice is due to the accumulation of bicarbonates in the blood in response to several factors: direct loss of H ⁺  with the contents of the stomach, the development of intracellular acidosis in response to hypokalemia, and the loss of hydrogen ions by the kidneys, as a compensatory reaction on intracellular acidosis. For this reason, the correction of alkalosis requires the introduction of solutions of sodium chloride, potassium chloride or HCL.

[4], [5], [6]

Loss of H ⁺  through the kidneys

In this case, alkalosis usually develops with the use of powerful diuretics (thiazide and loop), which remove sodium and potassium in a chlorine-related form. In this case, a large amount of fluid is lost and hypovolemia develops, a sharp increase in the total excretion of acids and chlorine, resulting in metabolic alkalosis.

However, with prolonged use of diuretics against the background of developed hypovolemia and persistent metabolic alkalosis, compensatory retention of sodium and chlorides occurs, and urinary excretion decreases to values below 10 mmol / l. This indicator is important in the differential diagnosis of chloride-sensitive and chloride-resistant variants of metabolic alkalosis. With a chloride concentration of less than 10 mmol / l, alkalosis is regarded as hypovolemic, chloride-sensitive, and it can be corrected by the introduction of solutions of sodium chloride.

Symptoms of the metabolic alkalosis

Symptoms and signs of mild alkalosis are usually associated with an etiological factor. More severe metabolic alkalosis increases the binding of ionized calcium to proteins, leading to  hypocalcemia  and the development of symptoms of headache, lethargy and neuromuscular excitability, sometimes with  delirium, tetany and convulsions. Alkalemia also reduces the threshold for the onset of symptoms of angina and arrhythmias. Concomitant hypokalemia can cause weakness.

Forms

Post-hypercapnichesky alkalosis

Post-hypercapnia alkalosis usually develops after elimination of respiratory failure. The development of post-hypercapnia alkalosis is associated with the restoration of the acid-base state after respiratory acidosis. In the genesis of post-hypercapnia alkalosis, the main role is played by increased renal reabsorption of bicarbonates on the background of respiratory acidosis. Rapid recovery of P _and CO ₂  via ventilator to norm does not reduce reabsorption of bicarbonate and replaced development alkalosis. This mechanism of the development of disorders of the acid-base state requires a cautious and slow decrease in P _and CO 2  in the blood in patients with chronic hypercapnia.

[7]

Chloride-resistant alkalosis

The main cause of chloridereal resistant developmental alkalosis is an excess of mineralocorticoids that stimulate the reabsorption of potassium and H ⁺  in the distal sections of the nephron and the maximum reabsorption of bicarbonates by the kidneys.

These variants of alkalosis may be accompanied by an increase in arterial pressure with increased production of aldosterone primary (Conn's syndrome) or due to activation of renin-RAAS (renovascular hypertension), increased production (or content) of cortisol or its precursors (Isenko-Cushing syndrome, corticosteroids, medication with mineralocorticoid properties: carbenoksolona, licorice root).

The normal level of blood pressure is detected with a disease such as Bartter's syndrome and severe hypokalemia. In Bartter's syndrome, hyperaldosteronism also develops in response to RAAS activation, but the extremely high production of prostaglandins that occurs with this syndrome inhibits the development of hypertension.

The reason for metabolic alkalosis is the violation of the reabsorption of chlorides in the ascending knee of the Henle loop, which leads to an increase in urinary excretion of chlorides associated with H ⁺, sodium, and potassium. Chloride-resistant variants of metabolic alkalosis are characterized by a high concentration of chloride in the urine (more than 20 mmol / l) and resistance of alkalosis to the introduction of chlorides and replenishment of the circulating blood volume.

The next reason for the development of metabolic alkalosis may be a load of bicarbonate, which occurs with the constant introduction of bicarbonates, massive blood transfusion and treatment with alkaline-exchange resins, when the alkaline load exceeds the ability of the kidneys to excrete them.

[8], [9], [10]

Diagnostics of the metabolic alkalosis

To recognize metabolic alkalosis and the adequacy of respiratory compensation, it is necessary to determine the gas composition of arterial blood and plasma electrolyte levels (including calcium and magnesium).

Often the cause can be determined from the history and physical examination data. For an unknown reason and normal kidney function, it is necessary to measure the concentrations of K and Cl ~ in the urine (the values are not diagnostic for renal failure). The level of chlorine in the urine is less than 20 meq / l indicates significant renal reabsorption and suggests an Cl-dependent cause. The level of chlorine in the urine more than 20 meq / l assumes a Cl-independent form.

The level of potassium in the urine and the presence or absence of hypertension help differentiate Cl-independent metabolic alkalosis.

The level of potassium in urine less than 30 meq / day indicates hypokalemia or misuse of laxatives. The level of potassium in the urine of more than 30 meq / day without hypertension suggests excessive use of diuretics or the syndromes of Barter or Gitelman. A potassium level of more than 30 meq / day in the presence of hypertension requires an assessment of the likelihood of hyperaldosteronism, an excess of mineralocorticoids, and renovascular diseases; Studies usually include the determination of plasma renin activity and levels of aldosterone and cortisol.

[11], [12], [13], [14], [15]

Treatment of the metabolic alkalosis

Treatment of metabolic alkalosis is closely related to the immediate cause, which determines the development of this disturbance of the acid-base state. It is necessary to treat the initial causes with correction of hypovolemia and hypokalemia.

Patients with Cl-dependent metabolic alkalosis intravenously administered 0.9% saline; the rate of administration is usually 50-100 ml / hr higher than urinary and other fluid losses, until the level of chlorine in the urine is more than 25 meq / l and the urinary pH is normalized after the initial rise due to bicarbonate. In patients with O-independent metabolic alkalosis, the effect of rehydration is usually not observed.

In patients with severe metabolic alkalosis (eg, pH> 7.6), more urgent correction of plasma pH is sometimes necessary. It is possible to use hemofiltration or hemodialysis, especially with hypervolemia. Assignment of acetazolamide 250-375 mg orally or intravenously 1 or 2 times a day increases the excretion of HCO3-, but can also increase the loss of K + or PO4 in the urine; the greatest efficacy can be observed in patients with hypervolemia and metabolic alkalosis caused by diuretics, as well as in patients with post-hypercapnic metabolic alkalosis.

Intravenous introduction of hydrochloric acid in 0.1-0.2 normal solution is safe and effective, but can be carried out only through the central catheter in connection with hyperosmosis and sclerosis of peripheral veins. The dose is 0.1-0.2 mmol / (kghh) with the need for frequent monitoring of the arterial blood gas composition and plasma electrolyte levels.

With an intensive loss of chlorides and H ⁺  through the gastrointestinal tract, it is necessary to introduce chlorine-containing solutions (sodium chloride, potassium chloride, HCl); with a simultaneous decrease in the volume of circulating blood - replenishment of its volume.

When the hypokalemia is severe against the background of excess mineralocorticoids in the body (Conn's syndrome, Itenko-Cushing's syndrome, Bartter's syndrome, adrenogenital syndrome), it is necessary to use low-salt diet, to perform operative treatment of a tumor that caused excess production of mineralocorticoids; use mineralocorticoid antagonists (diuretics: amiloride, triamterene, spironolactone); to introduce solutions of potassium chloride, to use indomethacin, antihypertensive drugs.

In addition, in order to eliminate metabolic alkalosis with pronounced hypokalemia, developed as a result of the long-term administration of diuretics, it is necessary to stop using them; at exogenous introduction of bicarbonates - to stop infusions of alkaline solutions, blood.