Metabolic acidosis is a disorder of acid–base balance, which is characterized by a decrease in the concentration of bicarbonates against the background of normal or elevated acid content in plasma. The main signs are a decrease in the pH of arterial blood to the level of 7.35 and below, a deficiency of alkaline bases of more than -2 mmol / liter, normal or increased partial pressure of carbon dioxide. Clinically manifested by myocardial depression, respiratory center, decreased sensitivity to catecholamines. It is diagnosed on the basis of the results of laboratory examination of the indicators of ABB. Specific treatment is infusion of buffer solutions.
ICD 10
E87.2 P74.0
General information
Metabolic acidosis (MA) or acidemia is a condition associated with a change in the activity of biologically significant proteins against the background of a shift in the acidic side of the ABB. It develops with a severe course of somatic diseases, some poisoning, shocks of any origin. Moderate acidemia is not accompanied by clinical symptoms. When the cause of the failure is eliminated, the normal state of the internal environment is restored without medical intervention. Severe acidosis requires treatment in the ICU due to the high risk of respiratory and cardiovascular disasters. Patients need constant hardware monitoring of vital signs, daily and sometimes hourly blood sampling for laboratory tests.
Causes
The cause of acidemia is hyperproduction or reduced excretion of acids, as well as increased excretion of alkaline components of the blood. Metabolic acidosis occurs in all cases of shock, clinical death and post-resuscitation illness. In addition, pathology can develop with a variety of pathological processes of therapeutic and surgical profile. Depending on the underlying disorder, acidification may occur due to lactate or ketone bodies. There are the following types of this condition:
- Lactic acidosis. They occur when the processes of anaerobic glycolysis in the muscles are intensified. Severe forms of lactic acidosis occur in patients with severe tissue hypoxia, respiratory insufficiency, a decrease in systolic blood pressure below the level of 70 mm Hg. They are observed with sepsis, hypovolemia, synthesis of a large amount of D-lactate by intestinal microflora. Active physical work, including weightlifting, is considered to be the physiological reason for the shifts in CSCS. Acidification does not require correction and takes place on its own shortly after muscle relaxation.
- Ketoacidosis. They are a symptom of somatic diseases. They occur in diabetes mellitus, chronic and acute renal failure, alcohol poisoning, methyl alcohol, ethylene glycol, salicylates, violation of the excretory function of the liver. In addition, the concentration of ketone bodies increases at the terminal stage of shock, with the development of multiple organ failure.
- Loss of grounds. It occurs in a number of diseases of the gastrointestinal tract: prolonged diarrhea, intestinal fistulas, intestinal urine derivation. The latter is the result of a surgical operation, during which the ureters are removed into the intestine with the failure of the bladder. Urine has a hydrogen index at the level of 5-7, that is, it is an acidic medium. When it enters the intestine, it neutralizes the intestinal alkaline environment.
Pathogenesis
Metabolic acidosis leads to a decrease in the concentration of HCO3 and an increase in the amount of Cl-. Potassium ions in cells are actively replaced by sodium and hydrogen, there is an increase in the volume of K+ in plasma. In the absence of renal insufficiency, excess potassium is removed with urine. At the same time, its blood level remains close to normal, intracellular hypokalemia is formed. In acute renal failure, plasma contains an increased amount of K+ ions. Small shifts are compensated by buffer systems: bicarbonate, phosphate, hemoglobin, protein. They reversibly bind protons, maintaining homeostasis, but the action of these systems is insufficient in massive acidosis. There is a decrease in pH, which is reflected in the conformation of amphoteric compounds. The activity of hormones, neurotransmitters changes, the functions of receptor devices are disrupted.
Classification
There are several classifications of alkalemia. One of the most common criteria for fission is the anionic difference – the difference in the concentration of K+, Na+ and CL-, HCO3-. Normally, it is 8-12 mmol / liter. If this indicator is maintained, they speak of alkalosis with a normal anion hole, the excess indicates a decrease in the concentration of unmeasurable Mg+, Ca+ cations or an increase in the level of phosphates, albumins, organic acids. For clinical practice, classifications are used according to the level of compensation of MA:
- Compensated. It proceeds asymptomatically, maintaining homeostasis occurs due to the active work of compensatory mechanisms. The pH is maintained at 7.4, the base deficiency is zero, the partial pressure of CO2 is maintained at 40 mm Hg. It is detected during prolonged work of a large volume of muscle tissue, as well as at the initial stage of internal diseases. No medical correction is required.
- Subcompensated. The hydrogen index remains within the normal range or decreases slightly (7.35-7.29). There is a slight deficiency of bases (up to -9). pCO2 decreases due to compensatory hyperventilation, but does not overcome the value of 28 mm Hg. There is a nonspecific weakly expressed clinical picture. There is no need to use buffer fluids.
- Decompensated. The pH drops below 7.29, the BE deficiency overcomes the mark of -9 mmol/liter. It is not compensated by pulmonary hyperventilation. The partial pressure drops to 27 mmHg or lower. There is a detailed symptomatology, a sharp deterioration in the patient’s well-being. Urgent care is required with the use of buffer solutions.
Symptoms
Compensated or subcompensated varieties are asymptomatic. With a deficiency of hydrocarbonates of more than -10, a hydrogen index below 7.2, compensatory hyperventilation occurs. It manifests itself in the form of deep slow breathing. As the patient decompensates, Kussmaul’s breathing develops. Chronic acidosis in children leads to growth and development delays. Other clinical signs depend on the underlying pathology. There may be diarrhea, itchy skin, polyuria, visual disturbances, dizziness. There is a history of prolonged fasting, taking high doses of salicylates, ethylene glycol, methanol or ethanol, the presence of diabetes mellitus, intestinal disorders, chronic kidney failure.
Severe metabolic disorders potentiate hypotension. The reaction to the introduction of pressor amines is reduced or absent. There is a decrease in myocardial contractility, compensatory tachyarrhythmia. Plasma hyperkalemia on the background of renal insufficiency causes atrial fibrillation (atrial fibrillation). There are signs of impaired atrioventricular conduction. Patients complain of chest pain, palpitations, lack of air. On objective examination, the skin is pale or cyanotic, cold to the touch, the pulse is arrhythmic, weak filling and tension, breathing is deep, heavy, noisy. Encephalopathy may develop.
Complications
Severe metabolic acidosis at the terminal stage causes depression of the respiratory center. Hyperventilation is replaced by weak shallow breathing. Hypoxia of the brain develops, leading to loss of consciousness and coma. The activity of the kidneys and liver is disrupted, multiple organ failure occurs. The neuromuscular conduction disorder progresses, which causes a disorder of the activity of all body systems. Initially, atrial arrhythmias spread to the ventricles. Fibrillation of the latter is observed, clinical death is diagnosed.
Diagnostics
The diagnosis of MA in ICU patients is carried out by an anesthesiologist-resuscitator. In the presence of chronic somatic diseases, it is necessary to consult narrow specialists: an endocrinologist, a surgeon, a nephrologist, a hepatologist. Chronic metabolic acidosis can be detected by a general practitioner at an outpatient appointment. The diagnosis is established on the basis of data from the following studies:
- Physical. It does not allow to accurately determine the presence of changes, since the signs of the violation are too nonspecific and can occur with a variety of other pathological processes. However, the corresponding clinical picture gives grounds for the appointment of an analysis of ABB and plasma electrolytes.
- Laboratory. It is the basis of diagnostic search. Acidemia is diagnosed with a moderate or significant decrease in pH, a deficiency of bicarbonates, a decrease in the partial pressure of carbon dioxide. To determine the type of acidosis, an anionic difference is evaluated. To clarify the mechanism of base loss, it may be necessary to study the anion hole not only in plasma, but also in urine.
- Hardware. It is carried out to identify the underlying disease, as well as to diagnose emerging changes. The ECG shows the sharpening of the T wave, the expansion of the QRS complex, the disappearance of the P wave, large-wave or small-wave atrial fibrillation, uneven intervals between ventricular complexes. If stagnation occurs in a large circle, ultrasound may be noted-signs of enlargement of the liver, spleen, accumulation of fluid in the abdominal cavity.
Treatment
Therapy of MA without eliminating its causes is impractical, it is based on the detection and treatment of the underlying disease. With diabetic ketoacidosis, correction of blood sugar levels is necessary, with lactic acidosis – relief of tissue ischemia and hypoxia. In case of shock, the patient is shown appropriate resuscitation measures. The treatment of the root cause of acidemia is carried out in parallel with the normalization of the acid-base composition of the internal environment. To do this, the following methods are used:
- Medication. In decompensated forms of the disease, correction is carried out by intravenous infusion of sodium bicarbonate. In other cases, buffer solutions are not used. It is possible to transfuse lactasol, which is metabolized in the liver to form HCO3. The electrolyte balance is restored with the infusion of disol, acesol, trisol. With hypoproteinemia, protein transfusion is indicated. Normalization of oxidative processes in tissues is carried out by the appointment of multivitamin complexes, pantothenic and pangamic acid.
- Hardware. They are necessary for the complicated course of the process for the correction of vital functions. Respiratory insufficiency is an indication for transferring the patient to artificial ventilation of the lungs, a decrease in kidney function requires hemodialysis. With a decrease in blood pressure, a hardware (through an injection machine) infusion of vasopressors is performed. In case of ventricular fibrillation, electro-pulse treatment, indirect heart massage are used.
Prognosis and prevention
The course of the disorder directly depends on the underlying pathological process and the possibility of its complete elimination. After the elimination of the causes of acidemia, ABB disorders can be easily corrected even at the stage of decompensation. Medicamental replenishment of the deficiency of hydrocarbonates while maintaining the etiological factor of acidification does not allow for stable normalization of the hydrogen index and BE (excess/ deficiency indicator of HCO3). Prevention consists in the timely treatment of processes that can cause acidosis, regulation of blood sugar levels, undergoing hemodialysis in CRF. In the ICU, metabolic acidosis is detected and corrected at an early stage with daily study of acid-base balance indicators.