Metabolic alkalosis is a change in the acid–base balance of the internal environment associated with the accumulation of hydroxyl anions OH- and “alkalinization” of blood. It manifests itself in the form of severe respiratory and vasomotor disorders. When the pH (hydrogen index) is shifted by more than 0.2-0.3, a comatose state occurs, by 0.4 – the patient dies. The condition is diagnosed on the basis of the results of the analysis on the ABB. Specific treatment – hydrochloric acid before normalization of the ratio of OH- and H+ ions, restoration of electrolyte balance, correction of diseases that caused metabolic failure.
Metabolic (non–gas) alkalosis is a disorder that occurs when hydrogen, chlorine, and potassium ions are lost against the background of a preserved or increased number of hydroxyl molecules in the blood. It occurs in a variety of pathological conditions. It is more often detected in resuscitation patients who have undergone a forced diuresis procedure with a violation of manipulation techniques. It can occur in compensated and decompensated forms, the nature of the flow is determined by the pH level. Decompensated varieties are observed with insufficiency of compensatory and adaptive mechanisms. Pathology requires correction at the compensation stage, otherwise the chances of treatment success decrease.
A change in the concentration of ions involved in the regulation of ABB occurs under the action of external or internal etiofactors. The loss of H+ as a result of their mechanical removal from the body leads to the formation of a chlorine-sensitive form of the disease. Chlororesistant varieties are the result of internal pathological processes. The most common reasons are:
- External factors. MA develops with hypovolemia, formed due to improper use of diuretics, blood loss, loss of gastric contents on the background of vomiting, gastric lavage through a probe, the presence of gastrostomy. This group also includes conditions that occur during attempts to medically correct acidosis, and a compensatory metabolic type of disorder.
- Internal factors. MA is one of the symptoms of diseases such as renal artery stenosis, renin-producing tumors, and malignant arterial hypertension. Pathology is detected with hormonal disorders – an increase in the production of adrenocorticotropin, glucocorticosteroids. In some cases, metabolic alkalosis results from hypercorrection of ketoacidosis and lactic acidosis.
When the hydrogen index deviates to the alkaline side, a number of negative changes occur in the body. There is a redistribution of electrolytes between the cell and the intercellular fluid, which disrupts the processes of polarization and depolarization. There is an inhibition of enzyme systems, hypoventilation of the compensatory type. The ability of hemoglobin to bind to oxygen increases, at the same time the ability of blood to remove carbon dioxide decreases, the dissociation curve of oxyhemoglobin shifts.
The described process leads to the accumulation of CO2 in tissues, respiratory disorders, tissue hypoxia. Against the background of deterioration of oxygenation of cells, a lesion of the brain, including its vasomotor center, is formed. This causes changes in vascular tone, fluctuations in blood pressure. Initially, the blood pressure level rises, later decreases to shock or undetectable figures. In the final stages, the activity of the cerebral cortex is suppressed, coma develops.
Metabolic alkalosis is classified according to the level of the hydrogen index and sensitivity to therapy with chlorine-containing drugs. With a preserved hydrogen index, the pathology is considered compensated, not accompanied by severe disorders. If the displacement of pondus Hydrogenii is more than 0.1, there is a violation of vital functions of the body. Alkalemia occurs in a chlorine-sensitive or chlorine-resistant form:
- Chloro-sensitive. Occurs when the body loses a large amount of chlorine ions. It is relatively easily corrected by the introduction of a saline solution of sodium chloride. Usually provoked by external causes. With a prolonged course, it is accompanied by a compensatory delay of sodium and chlorides, the excretion of which in the urine decreases to 10 mmol / liter.
- Chlororesistant. It occurs in somatic diseases with an increase in the concentration of corticosteroid hormones. There is an increased urinary excretion of chlorides associated with potassium and sodium. Hypokalemia develops. A distinctive feature of chlorine-resistant varieties is the lack of effect from the introduction of NaCl 0.9%.
Compensated varieties of alkalemia in patients with Burnett syndrome, gastric pathology can last for a long time without noticeable manifestations. Over time, patients develop edema, skin turgor decreases, appetite worsens, generalized itching occurs. Aversion to milk and dairy products is possible. Due to the deposition of calcium salts in the renal tubules, the excretory ability of the kidneys worsens. The clinical picture is formed a few months or years after the onset of the disease.
Mild alkalosis is accompanied by headache, drowsiness and fatigue, increased neuromuscular excitability. In some patients, convulsive contractions of individual muscle fibers are detected, blood pressure decreases. Partial blockade of intracardiac conduction, extrasystole is possible. In moderate and severe forms, tachyarrhythmia is noted. Patients complain of palpitations, chest pains. There are clonic-tonic convulsions, delirium, disorders of consciousness.
Heavy alkaloses disrupt the work of the pulmonary system. Patients have dyspnea with an increase in the frequency of respiratory movements, acrocyanosis, the inclusion of auxiliary muscles. Hypoxia occurs, which leads to damage to the muscular apparatus and the development of rhabdomyolysis. The resulting myoglobin is excreted in the urine, giving it a dark color. There is a blockage of the renal tubules. Nitrogenous slags accumulate in the body, the degree of violation of acid-base balance increases.
Complications of alkalemia include renal and respiratory insufficiency, ventricular fibrillation of the heart. ARF proceeds according to the secondary type, is more characterized by hypercapnia. AKF occurs due to blockage of the tubules by calcium deposits and myoglobin, manifested by anuria or oliguria. Ventricular fibrillation actually represents cardiac arrest, requires resuscitation. All these processes can be detected in the first hours from the onset of the disease, if there are pronounced metabolic disorders. Compensated forms of MA do not lead to the development of such complications.
The diagnosis of metabolic alkalosis in most cases is made by an anesthesiologist-resuscitator or therapist. Other specialists with higher medical education who are familiar with the normal values of ABB can also determine the condition. Differential diagnosis is carried out with metabolic acidosis, gas alkalosis. In the first case, an increase in H+ ions is detected in the serum, a decrease in pH less than 7.35, in the second, a recent alveolar hyperventilation is determined. MA is diagnosed using the following methods:
- Anamnesis, physical examination. Clinical signs characteristic of a certain degree of alkalinization of the internal environment are revealed. There is a history of multiple vomiting, gastric lavage, adrenal diseases, accompanied by increased production of corticotropic hormones. The signs are non-specific, so it is unacceptable to make a diagnosis only on their basis.
- Blood test. The main way to determine metabolic failures is to analyze arterial blood for ABB and electrolytes. At MA, the pH value exceeds 7.4, the partial pressure of carbon dioxide is more than 40 mmHg, standard bicarbonate is above 25 mmol/liter, the excess of bases is more than 5 mmol/ liter. There is a decrease in the concentration of potassium, magnesium, and serum chlorides. With a compensated flow, laboratory parameters are within the reference values.
- Hardware research. Metabolic alkalosis is not directly diagnosed by hardware methods, so such techniques are of auxiliary importance. An indirect sign is depression of the ST segment and a negative T wave on the ECG, a decrease in saturation according to the results of pulse oximetry. X-ray examination of the kidneys reveals clusters of calcifications in them. During gastroscopy, signs of chronic gastritis and stomach ulcers are often detected.
The therapy is based on the elimination of the primary process that led to the development of metabolic disorders. Patients are referred for consultation to a gastroenterologist, in the presence of ulcerative defects, drugs that promote scarring of the ulcer are prescribed. It is recommended to abandon the absorbed antacids. Treatment of hormonal disorders is carried out by an endocrinologist. With frequent vomiting, drugs that reduce the excitability of the vomiting center are used, the drug of choice is cerucal or metoclopramide. For the direct treatment of alkalemia and its consequences , the following methods are used:
- Medication. The patient is prescribed sodium chloride infusions. With a deficiency of K + ions, a glucose-potassium mixture is introduced, into which, with a lack of magnesium, magnesium sulfate is added. With hyperactivity of adrenal hormones, spironolactone is recommended. The hydrogen index at the level of 7.7 and above requires the introduction of weak hydrochloric acid solutions into the central vein. Ammonium chloride can be used as an alternative to HCL, but it is contraindicated in renal insufficiency.
- Hardware. They are used as a way of maintaining vital activity in cases when metabolic alkalosis leads to severe disorders. Patients suffering from respiratory insufficiency need oxygen therapy or a ventilator. If renal function is impaired, hemodialysis is prescribed to remove nitrogenous compounds. In case of ventricular fibrillation, electropulse therapy is indicated.
In Burnett’s syndrome, caused by the consumption of large amounts of milk or baking soda, medication correction is not required. The condition of patients normalizes within a few days after the elimination of alkaline foods from the diet. The exception is neglected cases in which chronic kidney failure develops. If necessary, the patient is hospitalized for hemodialysis, blood filtration and drug correction of the water-salt balance are carried out.
Prognosis and prevention
The prognosis of MA depends on the course of the underlying disease. Varieties provoked by frequent vomiting, gastric lavage, gastritis are usually easy to correct. Drug modification of pondus Hydrogenii without treatment of the primary process in hyperaldosteronism is irrational, since the pathology will constantly recur. Severe forms of alkalosis, accompanied by complications, have an unfavorable prognosis. There is a high risk of death of the patient against the background of cardiac arrhythmias, intoxication with the products of their own metabolism, hypoxemia.
Prevention consists in the timely treatment of diseases that can lead to metabolic changes. Pathology of the gastrointestinal tract, frequent causeless vomiting require consultation with a gastroenterologist. When a patient is in the ICU, the task of preventing alkalemia falls on the doctor on duty. Patients with a high risk of alkalinization are shown daily tests for the concentration of electrolytes in serum, the study of blood gases and pH. This allows you to identify changes at the initial stage and make the necessary correction.