Gas alkalosis is accompanied by the following symptoms. What is respiratory alkalosis and how to treat it
Alkalosis is rare disease. With this disease, the blood pH increases due to the accumulation of alkaline substances. In this article we will talk about what causes the disease, as well as the symptoms and its treatment.
Types of alkalosis
Based on the origin of alkalosis, several groups are distinguished:
1. Gas alkalosis- occurs due to hyperventilation of the lungs. With gas alkalosis, excessive excretion occurs carbon dioxide from the body, as a result of which the partial tension of carbon dioxide decreases. Hyperventilation of the lungs can be provoked by organic lesions of the brain (tumors, encephalitis, etc.), the effects of various pharmacological and toxic substances on Airways, acute blood loss, as well as elevated body temperature.
2. Non-gas alkalosis is divided into exogenous, excretory and metabolic. Excretory alkalosis occurs with uncontrollable vomiting, with large losses of gastric juice due to gastric fistulas. It can also develop due to long-term use of diuretics, with endocrine disorders, which lead to sodium retention in the body and in some kidney diseases.
Exogenous alkalosis most often occurs due to excessive administration of sodium bicarbonate (this substance is administered to the patient when increased acidity stomach). Sometimes the cause of the development of exogenous alkalosis is prolonged ingestion of food that contains a lot of bases.
Metabolic alkalosis is extremely rare in some pathological conditions that are accompanied by impaired electrolyte metabolism. Doctors can detect it in postoperative period during extensive surgical interventions, as well as in children who suffer from rickets or hereditary disorders regulation of electrolyte metabolism.
3. Mixed alkalosis is a combination of non-gas and gas alkalosis. Mixed alkalosis can occur with brain injuries, which are accompanied by hypocapnia, shortness of breath and vomiting of acidic gastric juice.
What happens during alkalosis?
With this disease, the patient's blood pressure decreases and the heart rate slows down. At the same time, neuromuscular excitability increases and muscle hypertonicity occurs, resulting in cramps. Doctors often observe the appearance of constipation and decreased respiratory activity. With gas alkalosis, mental performance decreases, general weakness appears, dizziness and even fainting states.
Symptoms of alkalosis
With gas alkalosis, disturbances in work appear cerebral arteries, cardiovascular activity is disrupted and cations are excreted from the body in the urine. At an early stage of the disease, the patient develops diffuse cerebral ischemia - the patient is too excited, complains of dizziness and severe fatigue, and paresthesia of the limbs and face often occurs. IN in rare cases fainting conditions are observed. During the examination, the doctor must pay attention to the color of the skin - the skin is pale or has a grayish tint.
Gas alkalosis is caused by breathing disorders - rapid breathing. Rapid breathing can occur due to pulmonary pathology, pulmonary embolism, and even due to hysterical shortness of breath. In addition to these symptoms, doctors note the presence. With prolonged gas alkalosis, the patient becomes dehydrated and has convulsions. As a result, hypocalcemia often develops. If the patient has any pathologies in the central nervous system, this can even provoke epileptic seizure.
Metabolic alkalosis very often occurs due to the use of mercury diuretics, as well as when the patient is given alkaline solutions or nitrate blood. Metabolic alkalosis is usually transitory nature and does not have pronounced clinical manifestations. Swelling and some respiratory depression may occur. Decompensated metabolic alkalosis occurs as a result of prolonged vomiting or with the loss of a large amount of potassium (with massive hemolysis), with the loss of chlorine in the body, in terminal conditions that are accompanied by dehydration of the body.
In patients with metabolic alkalosis, doctors observe progressive weakness, severe fatigue, increased thirst, frequent headaches, minor hyperkinesis of the limbs and facial muscles. Sometimes anorexia occurs. Hypocalcemia causes seizures. The patient's skin is dry and there is severe swelling. Breathing is rare and shallow. Upon examination, tachycardia and embryocardia are often detected. At first, patients become apathetic, and after some time they experience lethargy and drowsiness. If left untreated, symptoms worsen and coma may develop. To accurately confirm the diagnosis, doctors prescribe an ECG and blood tests, as well as a urine test.
Chronic metabolic alkalosis occurs in people suffering from peptic ulcers, which have developed due to long-term intake of milk and alkali-based drugs. Doctors also call it Burnett's syndrome or milk-alkali syndrome. With chronic metabolic alkalosis, patients develop general weakness, decreased appetite, an aversion to dairy foods, and often nausea and vomiting. In advanced states, patients become lethargic and apathetic. Skin itching appears. In severe cases, ataxia and deposition of calcium salts appear in tissues (in the cornea and conjunctiva), in the kidney tubules. This often leads to the development of kidney failure.
Treatment of alkalosis
First of all, doctors eliminate the cause that led to hyperventilation. After this, the gas composition of the blood is normalized by inhaling special mixtures based on carbon dioxide (for example, carbogen). Treatment of non-gas alkalosis depends on its type. For treatment, doctors use solutions of potassium, ammonium chlorides, calcium, insulin, as well as agents that inhibit carbonic anhydrase and promote the release of bicarbonate and sodium ions by the kidneys.
Patients with gas alkalosis, as well as with metabolic alkalosis, which developed against the background of severe diseases (pulmonary embolism) are immediately hospitalized. Gas alkalosis, which arose due to neurogenic hyperventilation, can most often be eliminated at the point of care for the victim. As a rule, the patient is given carbogen-based inhalations - a mixture of oxygen (95%) and carbon dioxide (5%). If the patient begins to have convulsions, calcium chloride is administered intravenously. If necessary, eliminate hyperventilation by administering morphine or seduxen, and if wrong mode artificial ventilation is corrected.
In case of decompensated metabolic alkalosis, the doctor injects the patient intravenously with a solution of calcium chloride and sodium chloride. If the patient has hypokalemia, then he is prescribed intravenous potassium preparations - potassium chloride solution, panangin and potassium-sparing drugs. Doctors may also prescribe ammonium chloride or diacarb (for alkalosis resulting from excessive administration of alkalis). In addition, doctors prescribe treatment that should eliminate the causes of alkalosis (hemolysis, vomiting, diarrhea, etc.).
Alkalosis
What is Alkalosis -
Alkalosis- increasing the pH of the blood (and other tissues of the body) due to the accumulation of alkaline substances.
Alkalosis(Late Lat. alcali alkali, from Arabic al-quali) - a violation of the acid-base balance of the body, characterized by an absolute or relative excess of bases.
What provokes / Causes of Alkalosis:
Based on the origin of alkolosis, the following groups are distinguished.
Gas alkalosis
Occurs as a result of hyperventilation of the lungs, leading to excessive removal of CO 2 from the body and a drop in the partial tension of carbon dioxide in arterial blood below 35 mm Hg. Art., that is, to hypocapnia. Hyperventilation of the lungs can be observed with organic lesions of the brain (encephalitis, tumors, etc.), the effect on the respiratory center of various toxic and pharmacological agents (for example, some microbial toxins, caffeine, corazol), with elevated body temperature, acute blood loss, etc.
Non-gas alkalosis
The main forms of non-gas alkalosis are: excretory, exogenous and metabolic. Excretory alkalosis can occur, for example, due to big losses acidic gastric juice with gastric fistulas, uncontrollable vomiting, etc. Excretory alkalosis can develop with long-term use of diuretics, certain kidney diseases, as well as with endocrine disorders leading to excessive delay sodium in the body. In some cases, excretory alkalosis is associated with increased sweating.
Exogenous alkalosis is most often observed with excessive administration of sodium bicarbonate to correct metabolic acidosis or neutralize increased gastric acidity. Moderate compensated alkalosis can be caused by prolonged consumption of food containing many bases.
Metabolic alkalosis occurs in some pathol. conditions accompanied by disturbances in electrolyte metabolism. Thus, it is observed during hemolysis, in the postoperative period after some extensive surgical interventions, in children suffering from rickets, hereditary disorders of the regulation of electrolyte metabolism.
Mixed alkalosis
Mixed alkalosis - (a combination of gas and non-gas alkalosis) can be observed, for example, with brain injuries accompanied by shortness of breath, hypocapnia and vomiting of acidic gastric juice.
Pathogenesis (what happens?) during Alkalosis:
With alkalosis (especially associated with hypocapnia), general and regional hemodynamic disturbances occur: cerebral and coronary blood flow, blood pressure and cardiac output decrease. Neuromuscular excitability increases, muscle hypertonicity occurs, up to the development of convulsions and tetany. Suppression of intestinal motility and the development of constipation are often observed; activity decreases respiratory center. Gas alkalosis is characterized by a decrease mental performance, dizziness, fainting may occur.
Alkalosis symptoms:
Symptoms of gas alkalosis reflect the main disorders caused by hypocapnia - hypertension of the cerebral arteries, hypotension of the peripheral veins with a secondary decrease in cardiac output and blood pressure, loss of cations and water in the urine. The earliest and leading signs are diffuse cerebral ischemia - patients are often excited, anxious, may complain of dizziness, paresthesia on the face and limbs, quickly get tired of contact with others, concentration and memory are weakened. In some cases, fainting occurs. The skin is pale, gray diffuse cyanosis is possible (with concomitant hypoxemia). Upon examination, the cause of gas alkalosis is usually determined - hyperventilation due to rapid breathing(up to 40-60 respiratory cycles in 1 min), for example: with thromboembolism of the pulmonary arteries; lung pathology, hysterical shortness of breath (the so-called dog breath) or due to the mode of artificial ventilation of the lungs above 10 l/min. As a rule, there is tachycardia, sometimes a pendulum-like rhythm of heart sounds; pulse is small. Systolic and pulse blood pressure are slightly reduced with horizontal position patient, when transferring him to a sitting position, it is possible orthostatic collapse. Diuresis is increased. With prolonged and severe gas alkalosis (pCO2 less than 25 mmHg st.) dehydration and seizures may occur as a result of developing hypocalcemia. In patients with organic pathology Central nervous system and “epileptic readiness”, gas alkalosis can provoke an epileptic seizure. The EEG reveals an increase in amplitude and a decrease in the frequency of the main rhythm, bilateral synchronous discharges of slow waves. ECG often shows diffuse changes myocardial repolarization.
Metabolic alkalosis, which often appears with the use of mercury diuretics and with massive infusions of alkaline solutions or nitrate blood into the patient, is usually compensated, is transient in nature and does not have pronounced clinical manifestations (some respiratory depression and the appearance of swelling are possible). Decompensated metabolic alkalosis usually develops as a result of primary (with prolonged vomiting) or secondary (from potassium loss during massive hemolysis, diarrhea) loss of chlorine by the body, as well as in terminal conditions, especially accompanied by dehydration. Progressive weakness, fatigue, thirst are noted, anorexia, headache, and minor hyperkinesis of the muscles of the face and limbs appear. Convulsions due to hypocalcemia are possible. The skin is usually dry, tissue turgor is reduced (swelling is possible with excessive fluid infusion). Breathing is shallow, rare (unless pneumonia or heart failure is associated). As a rule, tachycardia, sometimes embryocardia, is detected. Patients first become apathetic, then lethargic, drowsy; subsequently, disorders of consciousness worsen until the development of coma. The ECG often reveals low T wave voltage and signs of hypokalemia. Hypochloremia, hypokalemia, and hypocalcemia are detected in the blood. The reaction of urine in most cases is alkaline (in A., due to primary losses of potassium, it is acidic).
Chronic metabolic alkalosis, developing in patients peptic ulcer due to long-term use large quantities alkalis and milk, is known as Burnett's syndrome, or milk-alkali syndrome. It manifests itself general weakness, decreased appetite with aversion to dairy foods, nausea and vomiting, lethargy, apathy, itching, in severe cases - ataxia, deposition of calcium salts in tissues (often in the conjunctiva and cornea), as well as in the kidney tubules, which leads to the gradual development renal failure.
Treatment of Alkalosis:
Therapy for gas alkalosis consists of eliminating the cause that caused hyperventilation, as well as direct normalization gas composition blood by inhaling mixtures containing carbon dioxide (for example, carbogen). Therapy for non-gas alkalosis depends on its type. Solutions of ammonium, potassium, calcium chlorides, insulin, and agents that inhibit carbonic anhydrase and promote the excretion of sodium and bicarbonate ions by the kidneys are used.
Patients with metabolic alkalosis, as well as with gas alkalosis that developed against the background of serious diseases, such as pulmonary embolism, are hospitalized. Gas alkalosis due to neurogenic hyperventilation can in most cases be eliminated at the point of care for the patient. With significant hypocapnia, inhalation of carbogen is indicated - a mixture of oxygen (92-95%) and carbon dioxide (8-5%). For convulsions, calcium chloride is administered intravenously. If possible, eliminate hyperventilation, for example, by administering seduxen, morphine, and if the mode of artificial ventilation is incorrect, by correcting it.
In case of decompensated metabolic alkalosis, solutions of sodium chloride and calcium chloride are administered intravenously to the patient. For hypokalemia, intravenous potassium preparations are prescribed - panangin, potassium chloride solution (preferably simultaneous administration of glucose with insulin), as well as potassium-sparing drugs (spironolactone). In all cases, ammonium chloride can be prescribed internally, and for alkalosis caused by excessive administration of alkalis, diacarb can be prescribed. Treatment of the underlying disease is carried out, aimed at eliminating the cause of alkalosis (vomiting, diarrhea, hemolysis, etc.).
Which doctors should you contact if you have Alkalosis:
Is something bothering you? Do you want to know more detailed information about Alkalosis, its causes, symptoms, methods of treatment and prevention, the course of the disease and diet after it? Or do you need an inspection? You can make an appointment with a doctor– clinic Eurolab always at your service! The best doctors will examine you, study external signs and help you identify the disease by symptoms, advise you and provide necessary help and make a diagnosis. you also can call a doctor at home. Clinic Eurolab open for you around the clock.
How to contact the clinic:
Phone number of our clinic in Kyiv: (+38 044) 206-20-00 (multi-channel). The clinic secretary will select a convenient day and time for you to visit the doctor. Our coordinates and directions are indicated. Look in more detail about all the clinic’s services on it.
(+38 044) 206-20-00
If you have previously performed any research, Be sure to take their results to a doctor for consultation. If the studies have not been performed, we will do everything necessary in our clinic or with our colleagues in other clinics.
You? It is necessary to take a very careful approach to your overall health. People don't pay enough attention symptoms of diseases and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific symptoms, characteristic external manifestations- so called symptoms of the disease. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to do it several times a year. be examined by a doctor to not only prevent terrible disease, but also support healthy mind in the body and the organism as a whole.
If you want to ask a doctor a question, use the online consultation section, perhaps you will find answers to your questions there and read self care tips. If you are interested in reviews about clinics and doctors, try to find the information you need in the section. Also register on medical portal Eurolab to stay up to date latest news and information updates on the website, which will be automatically sent to you by email.
Other diseases from the group Diseases of the endocrine system, nutritional disorders and metabolic disorders:
| Addisonian crisis (acute adrenal insufficiency) |
| Breast adenoma |
| Adiposogenital dystrophy (Perchkranz-Babinski-Fröhlich disease) |
| Adrenogenital syndrome |
| Acromegaly |
| Nutritional insanity (nutritional dystrophy) |
| Alkaptonuria |
| Amyloidosis (amyloid dystrophy) |
| Amyloidosis of the stomach |
| Intestinal amyloidosis |
| Pancreatic islet amyloidosis |
| Liver amyloidosis |
| Amyloidosis of the esophagus |
| Acidosis |
| Protein-energy malnutrition |
| I-cell disease (mucolipidosis type II) |
| Wilson-Konovalov disease (hepatocerebral dystrophy) |
| Gaucher disease (glucocerebroside lipidosis, glucocerebrosidosis) |
| Itsenko-Cushing's disease |
| Krabbe disease (globoid cell leukodystrophy) |
| Niemann-Pick disease (sphingomyelinosis) |
| Fabry disease |
| Gangliosidosis GM1 type I |
| Gangliosidosis GM1 type II |
| Gangliosidosis GM1 type III |
| Gangliosidosis GM2 |
| Gangliosidosis GM2 type I (amaurotic idiocy of Tay-Sachs, Tay-Sachs disease) |
| GM2 gangliosidosis type II (Sandhoff's disease, Sandhoff's amaurotic idiocy) |
| Gangliosidosis GM2 juvenile |
| Gigantism |
| Hyperaldosteronism |
| Hyperaldosteronism secondary |
| Primary hyperaldosteronism (Conn's syndrome) |
| Hypervitaminosis D |
| Hypervitaminosis A |
| Hypervitaminosis E |
| Hypervolemia |
| Hyperglycemic (diabetic) coma |
| Hyperkalemia |
| Hypercalcemia |
| Hyperlipoproteinemia type I |
| Hyperlipoproteinemia type II |
| Hyperlipoproteinemia type III |
| Hyperlipoproteinemia type IV |
| Hyperlipoproteinemia type V |
| Hyperosmolar coma |
| Hyperparathyroidism secondary |
| Primary hyperparathyroidism |
| Hyperplasia of the thymus (thymus gland) |
| Hyperprolactinemia |
| Testicular hyperfunction |
| Hypercholesterolemia |
| Hypovolemia |
| Hypoglycemic coma |
| Hypogonadism |
| Hypogonadism hyperprolactinemic |
| Hypogonadism isolated (idiopathic) |
| Primary congenital hypogonadism (anorchism) |
| Primary acquired hypogonadism |
| Hypokalemia |
| Hypoparathyroidism |
| Hypopituitarism |
| Hypothyroidism |
| Glycogenosis type 0 (aglycogenosis) |
| Glycogenosis type I (Gierke's disease) |
| Glycogenosis type II (Pompe disease) |
| Glycogenosis type III (Measles disease, Forbes disease, limit dextrinosis) |
| Glycogenosis type IV (Andersen's disease, amylopectinosis, diffuse glycogenosis with liver cirrhosis) |
| Glycogenosis type IX (Haga's disease) |
| Glycogenosis type V (McArdle disease, myophosphorylase deficiency) |
| Glycogenosis type VI (Hers disease, hepatophosphorylase deficiency) |
| Glycogenosis type VII (Tarui disease, myophosphofructokinase deficiency) |
| Glycogenosis type VIII (Thomson's disease) |
| Glycogenosis type XI |
| Glycogenosis type X |
| Deficiency (insufficiency) of vanadium |
| Magnesium deficiency (insufficiency) |
| Manganese deficiency (insufficiency) |
| Copper deficiency (insufficiency) |
| Deficiency (insufficiency) of molybdenum |
| Deficiency (insufficiency) of chromium |
| Iron deficiency |
| Calcium deficiency (nutritional calcium deficiency) |
| Zinc deficiency (dietary zinc deficiency) |
| Diabetic ketoacidotic coma |
| Ovarian dysfunction |
| Diffuse (endemic) goiter |
| Delayed puberty |
| Excess estrogen |
| Involution of the mammary glands |
| Dwarfism (short stature) |
| Kwashiorkor |
| Cystic mastopathy |
| Xanthinuria |
| Lactic acidemic coma |
| Leucinosis (maple syrup disease) |
| Lipidoses |
| Farber lipogranulomatosis |
| Lipodystrophy (fatty degeneration) |
| Congenital generalized lipodystrophy (Seyp-Lawrence syndrome) |
| Hypermuscular lipodystrophy |
| Post-injection lipodystrophy |
| Progressive segmental lipodystrophy |
| Lipomatosis |
| Lipomatosis is painful |
| Metachromatic leukodystrophy |
| Myxedema coma |
| Cystic fibrosis (cystic fibrosis) |
Alkalosis- increasing the pH of the blood (and other tissues of the body) due to the accumulation of alkaline substances.
Alkalosis(Late Lat. alcali alkali, from Arabic al-quali) - a violation of the acid-base balance of the body, characterized by an absolute or relative excess of bases.
What provokes / Causes of Alkalosis:
Based on the origin of alkolosis, the following groups are distinguished.
Gas alkalosis
It occurs as a result of hyperventilation of the lungs, leading to excessive removal of CO 2 from the body and a drop in the partial tension of carbon dioxide in the arterial blood below 35 mm Hg. Art., that is, to hypocapnia. Hyperventilation of the lungs can be observed with organic lesions of the brain (encephalitis, tumors, etc.), the effect on the respiratory center of various toxic and pharmacological agents (for example, some microbial toxins, caffeine, corazol), with elevated body temperature, acute blood loss, etc.
Non-gas alkalosis
The main forms of non-gas alkalosis are: excretory, exogenous and metabolic. Excretory alkalosis can occur, for example, due to large losses of acidic gastric juice due to gastric fistulas, uncontrollable vomiting, etc. Excretory alkalosis can develop with long-term use of diuretics, certain kidney diseases, as well as endocrine disorders leading to excessive sodium retention in the body. In some cases, excretory alkalosis is associated with increased sweating.
Exogenous alkalosis is most often observed with excessive administration of sodium bicarbonate to correct metabolic acidosis or neutralize increased gastric acidity. Moderate compensated alkalosis can be caused by prolonged consumption of food containing many bases.
Metabolic alkalosis occurs in some pathol. conditions accompanied by disturbances in electrolyte metabolism. Thus, it is observed during hemolysis, in the postoperative period after some extensive surgical interventions, in children suffering from rickets, hereditary disorders of the regulation of electrolyte metabolism.
Mixed alkalosis
Mixed alkalosis - (a combination of gas and non-gas alkalosis) can be observed, for example, with brain injuries accompanied by shortness of breath, hypocapnia and vomiting of acidic gastric juice.
Pathogenesis (what happens?) during Alkalosis:
With alkalosis (especially associated with hypocapnia), general and regional hemodynamic disturbances occur: cerebral and coronary blood flow decreases, blood pressure and cardiac output decrease. Neuromuscular excitability increases, muscle hypertonicity occurs, up to the development of convulsions and tetany. Suppression of intestinal motility and the development of constipation are often observed; the activity of the respiratory center decreases. Gas alkalosis is characterized by decreased mental performance, dizziness, and fainting may occur.
Alkalosis symptoms:
Symptoms of gas alkalosis reflect the main disorders caused by hypocapnia - hypertension of the cerebral arteries, hypotension of the peripheral veins with a secondary decrease in cardiac output and blood pressure, loss of cations and water in the urine. The earliest and leading signs are diffuse cerebral ischemia - patients are often excited, anxious, may complain of dizziness, paresthesia on the face and limbs, quickly get tired of contact with others, concentration and memory are weakened. In some cases, fainting occurs. The skin is pale, gray diffuse cyanosis is possible (with concomitant hypoxemia). Upon examination, the cause of gas alkalosis is usually determined - hyperventilation due to rapid breathing (up to 40-60 respiratory cycles per 1 min), for example: with thromboembolism of the pulmonary arteries; lung pathology, hysterical shortness of breath (so-called dog breathing) or due to a mode of artificial ventilation of the lungs above 10 l/min. As a rule, there is tachycardia, sometimes a pendulum-like rhythm of heart sounds; pulse is small. Systolic and pulse blood pressure are slightly reduced when the patient is in a horizontal position; when he is transferred to a sitting position, orthostatic collapse is possible. Diuresis is increased. With prolonged and severe gas alkalosis (pCO2 less than 25 mmHg st.) dehydration and seizures may occur as a result of developing hypocalcemia. In patients with organic pathology of the central nervous system and “epileptic readiness,” gas alkalosis can provoke an epileptic seizure. The EEG reveals an increase in amplitude and a decrease in the frequency of the main rhythm, bilateral synchronous discharges of slow waves. ECG often reveals diffuse changes in myocardial repolarization.
Metabolic alkalosis, which often appears with the use of mercury diuretics and with massive infusions of alkaline solutions or nitrate blood into the patient, is usually compensated, is transient in nature and does not have pronounced clinical manifestations (some respiratory depression and the appearance of swelling are possible). Decompensated metabolic alkalosis usually develops as a result of primary (with prolonged vomiting) or secondary (from potassium loss during massive hemolysis, diarrhea) loss of chlorine by the body, as well as in terminal conditions, especially accompanied by dehydration. Progressive weakness, fatigue, thirst are noted, anorexia, headache, and minor hyperkinesis of the muscles of the face and limbs appear. Convulsions due to hypocalcemia are possible. The skin is usually dry, tissue turgor is reduced (swelling is possible with excessive fluid infusion). Breathing is shallow, rare (unless pneumonia or heart failure is associated). As a rule, tachycardia, sometimes embryocardia, is detected. Patients first become apathetic, then lethargic, drowsy; subsequently, disorders of consciousness worsen until the development of coma. The ECG often reveals low T wave voltage and signs of hypokalemia. Hypochloremia, hypokalemia, and hypocalcemia are detected in the blood. The reaction of urine in most cases is alkaline (in A., due to primary losses of potassium, it is acidic).
Chronic metabolic alkalosis, which develops in patients with peptic ulcers due to long-term intake of large quantities of alkalis and milk, is known as Burnett's syndrome, or milk-alkali syndrome. It is manifested by general weakness, loss of appetite with aversion to dairy foods, nausea and vomiting, lethargy, apathy, itching, in severe cases - ataxia, deposition of calcium salts in tissues (often in the conjunctiva and cornea), as well as in the kidney tubules, which leads to the gradual development of renal failure.
Treatment of Alkalosis:
Therapy for gas alkalosis consists of eliminating the cause that caused hyperventilation, as well as directly normalizing the gas composition of the blood by inhaling mixtures containing carbon dioxide (for example, carbogen). Therapy for non-gas alkalosis depends on its type. Solutions of ammonium, potassium, calcium chlorides, insulin, and agents that inhibit carbonic anhydrase and promote the excretion of sodium and bicarbonate ions by the kidneys are used.
Patients with metabolic alkalosis, as well as with gas alkalosis that developed against the background of serious diseases, such as pulmonary embolism, are hospitalized. Gas alkalosis due to neurogenic hyperventilation can in most cases be eliminated at the point of care for the patient. With significant hypocapnia, inhalation of carbogen is indicated - a mixture of oxygen (92-95%) and carbon dioxide (8-5%). For convulsions, calcium chloride is administered intravenously. If possible, eliminate hyperventilation, for example, by administering seduxen, morphine, and if the mode of artificial ventilation is incorrect, by correcting it.
In case of decompensated metabolic alkalosis, solutions of sodium chloride and calcium chloride are administered intravenously to the patient. For hypokalemia, intravenous potassium preparations are prescribed - panangin, potassium chloride solution (preferably simultaneous administration of glucose with insulin), as well as potassium-sparing drugs (spironolactone). In all cases, ammonium chloride can be prescribed internally, and for alkalosis caused by excessive administration of alkalis, diacarb can be prescribed. Treatment of the underlying disease is carried out, aimed at eliminating the cause of alkalosis (vomiting, diarrhea, hemolysis, etc.).
Which doctors should you contact if you have Alkalosis:
Is something bothering you? Do you want to know more detailed information about Alkalosis, its causes, symptoms, methods of treatment and prevention, the course of the disease and diet after it? Or do you need an inspection? You can make an appointment with a doctor– clinic Eurolab always at your service! The best doctors will examine you, study external signs and help you identify the disease by symptoms, advise you and provide the necessary assistance and make a diagnosis. you also can call a doctor at home. Clinic Eurolab open for you around the clock.
How to contact the clinic:
Phone number of our clinic in Kyiv: (+38 044) 206-20-00 (multi-channel). The clinic secretary will select a convenient day and time for you to visit the doctor. Our coordinates and directions are indicated. Look in more detail about all the clinic’s services on it.
(+38 044) 206-20-00
If you have previously performed any research, Be sure to take their results to a doctor for consultation. If the studies have not been performed, we will do everything necessary in our clinic or with our colleagues in other clinics.
You? It is necessary to take a very careful approach to your overall health. People don't pay enough attention symptoms of diseases and do not realize that these diseases can be life-threatening. There are many diseases that at first do not manifest themselves in our body, but in the end it turns out that, unfortunately, it is too late to treat them. Each disease has its own specific signs, characteristic external manifestations - the so-called symptoms of the disease. Identifying symptoms is the first step in diagnosing diseases in general. To do this, you just need to do it several times a year. be examined by a doctor, in order not only to prevent a terrible disease, but also to maintain a healthy spirit in the body and the organism as a whole.
If you want to ask a doctor a question, use the online consultation section, perhaps you will find answers to your questions there and read self care tips. If you are interested in reviews about clinics and doctors, try to find the information you need in the section. Also register on the medical portal Eurolab to keep abreast of the latest news and information updates on the site, which will be automatically sent to you by email.
Other diseases from the group Diseases of the endocrine system, nutritional disorders and metabolic disorders:
| Addisonian crisis (acute adrenal insufficiency) |
| Breast adenoma |
| Adiposogenital dystrophy (Perchkranz-Babinski-Fröhlich disease) |
| Adrenogenital syndrome |
| Acromegaly |
| Nutritional insanity (nutritional dystrophy) |
| Alkaptonuria |
| Amyloidosis (amyloid dystrophy) |
| Amyloidosis of the stomach |
| Intestinal amyloidosis |
| Pancreatic islet amyloidosis |
| Liver amyloidosis |
| Amyloidosis of the esophagus |
| Acidosis |
| Protein-energy malnutrition |
| I-cell disease (mucolipidosis type II) |
| Wilson-Konovalov disease (hepatocerebral dystrophy) |
| Gaucher disease (glucocerebroside lipidosis, glucocerebrosidosis) |
| Itsenko-Cushing's disease |
| Krabbe disease (globoid cell leukodystrophy) |
| Niemann-Pick disease (sphingomyelinosis) |
| Fabry disease |
| Gangliosidosis GM1 type I |
| Gangliosidosis GM1 type II |
| Gangliosidosis GM1 type III |
| Gangliosidosis GM2 |
| Gangliosidosis GM2 type I (amaurotic idiocy of Tay-Sachs, Tay-Sachs disease) |
| GM2 gangliosidosis type II (Sandhoff's disease, Sandhoff's amaurotic idiocy) |
| Gangliosidosis GM2 juvenile |
| Gigantism |
| Hyperaldosteronism |
| Hyperaldosteronism secondary |
| Primary hyperaldosteronism (Conn's syndrome) |
| Hypervitaminosis D |
| Hypervitaminosis A |
| Hypervitaminosis E |
| Hypervolemia |
| Hyperglycemic (diabetic) coma |
| Hyperkalemia |
| Hypercalcemia |
| Hyperlipoproteinemia type I |
| Hyperlipoproteinemia type II |
| Hyperlipoproteinemia type III |
| Hyperlipoproteinemia type IV |
| Hyperlipoproteinemia type V |
| Hyperosmolar coma |
| Hyperparathyroidism secondary |
| Primary hyperparathyroidism |
| Hyperplasia of the thymus (thymus gland) |
| Hyperprolactinemia |
| Testicular hyperfunction |
| Hypercholesterolemia |
| Hypovolemia |
| Hypoglycemic coma |
| Hypogonadism |
| Hypogonadism hyperprolactinemic |
| Hypogonadism isolated (idiopathic) |
| Primary congenital hypogonadism (anorchism) |
| Primary acquired hypogonadism |
| Hypokalemia |
| Hypoparathyroidism |
| Hypopituitarism |
| Hypothyroidism |
| Glycogenosis type 0 (aglycogenosis) |
| Glycogenosis type I (Gierke's disease) |
| Glycogenosis type II (Pompe disease) |
| Glycogenosis type III (Measles disease, Forbes disease, limit dextrinosis) |
| Glycogenosis type IV (Andersen's disease, amylopectinosis, diffuse glycogenosis with liver cirrhosis) |
| Glycogenosis type IX (Haga's disease) |
| Glycogenosis type V (McArdle disease, myophosphorylase deficiency) |
| Glycogenosis type VI (Hers disease, hepatophosphorylase deficiency) |
| Glycogenosis type VII (Tarui disease, myophosphofructokinase deficiency) |
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Respiratory alkalosis (gas) is pathological condition body, caused by excessive concentration in the blood and in all biological fluids alkaline compounds. This is actually a violation acid-base balance in the body in the direction of reducing acidity and increasing the alkaline environment. The development of the disease is provoked by a pair of substances that have an alkaline base and are very volatile in open and closed conditions.
Violation of the acid-base balance in the direction of increasing alkali concentration is no less dangerous than an excess of organic acids. For vital important organs and systems, such an altered blood composition poses a threat and destruction of their tissues. Let's try to understand in more detail why there is an increase in alkali levels in the body, what the symptoms of the pathology look like, and also what they are modern methods treatment of respiratory alkalosis.
The development of respiratory alkalosis is characteristic of certain categories of people who are employed at facilities chemical industry, or suffer from a number of chronic diseases. In general, there are following reasons occurrence of respiratory alkalosis:
Classification
Gas oversaturation of the body with alkali has its own medical classification type clinical picture and the severity of the development of pathology. This information helps to put more accurate diagnosis and determine which therapies will be most effective in a particular case.
Gas alkalosis is divided into the following groups:
Quite often, respiratory alkalosis develops in adults and children after severe traumatic brain injury with damage to the cerebral cortex, which is accompanied by shortness of breath, vomiting with acidic gastric juice, and hypocapnia.
What happens?
In patients with respiratory alkalosis, indicators rapidly decrease blood pressure and the intensity of contraction of the heart muscle slows down to a minimum value. In this regard, patients are often misdiagnosed and the first signs of respiratory alkalosis are confused with this disease. of cardio-vascular system like bradycardia. Against this background, the excitability of the receptors of the central nervous system increases increasingly.
Muscles throughout the body become hypertonic, after which the patient begins to experience cramps in the lower and upper limbs. Developing acute constipation and respiratory activity decreases to superficial ventilation of the lungs. The patient cannot concentrate and complains of headache and dizziness. It is not uncommon for patients with respiratory alkalosis to experience presyncope, including loss of consciousness.
Symptoms of respiratory alkalosis
When a person has respiratory alkalosis, all elements of the cardiovascular system are the first to suffer. Systemic disturbances occur in the functioning of the cerebral arteries. As a result of the disturbed acid-base balance, cations begin to be excreted from the blood along with the urine, without which it is impossible for the blood to carry out its previous functions.
Signs of respiratory alkalosis in adults and children are as follows::
- Excitation of the central nervous system. It becomes so pronounced that the patient experiences confusion. He can laugh, cry, show aggression, fall into a stupor. All these emotions occur with a minimum interval of time. A person actually ceases to control his psycho-emotional reactions and reacts very sharply to all external stimuli.
- Dizziness and fatigue. This painful condition caused by cerebral vascular ischemia, as they are greatly reduced functionality cerebral arteries. As the acid-base balance changes towards alkali, dizziness only intensifies.
- Pallor skin. Violation of the act of breathing leads to a failure in the gas exchange process. Less and less air enters the blood, and carbon dioxide is released in an increased volume. As a result, the patient develops oxygen starvation.
- Epileptic seizures. This is the most severe consequences respiratory alkalosis, when the level of alkali in the body is exceeded to a critical value and the brain is not able to fully cope with its tasks.
The clinical picture of gas alkalosis is quite blurred and doctors cannot always make an accurate diagnosis based only on the above symptoms.
Therefore, when a patient arrives with these complaints, it is very important that the doctor is interested in the conditions environment, in which the patient was located before he felt dizziness, weakness and attacks of nervous excitability.
Treatment of gas alkalosis
Therapy for a pathological condition begins with doctors eliminating the source that provokes a change in the acid-base balance. Then the patient is prescribed gas inhalations with drugs that contain substances based on carbon dioxide. Most often in medical practice Carbogen is used. In parallel with this, the patient undergoes a course intravenous drips solutions of calcium, ammonium chloride, insulin, potassium.
In especially severe cases, when there is a violation of the respiratory rhythm, it is possible to connect the patient to a ventilator with a supply of a gas mixture in a ratio of 95% pure oxygen and 5% carbon dioxide. Each case of respiratory alkalosis is individual, so the specifics of treatment also depend on the clinical picture of the development of the disease.
Alkalosis– this is a type of imbalance between acids and alkalis, which is characterized by a total or partial excess of substances that add hydrogen in comparison with the acids that remove them. Depending on the pH of the blood, the disease can be compensated or decompensated. If alkalosis is compensated, pH value fluctuates within normal values for the human body (from 7.35 to 7.45), some shifts and disturbances may be in buffers and physiological mechanisms regulation. Uncompensated alkalosis is accompanied by a high pH value - more than 7.45. The reason for this is a serious excess of bases and poor regulation of the balance of acids and alkalis.
Alkalosis and acidosis
Acidosis is an imbalance in the body accompanied by excessive amounts of acids in the blood. Alkalosis – a large number of grounds. Acidosis and compensated alkalosis are a state of the body in which the absolute numbers of H2CO3 and NaHCO3 change, but, despite this, their ratio remains normal (one to twenty). If the ratios indicated above are maintained, the pH varies within normal limits.
Failures in the regulation of CBS occur in some extreme conditions for the body, in certain diseases. Buffers of the blood, excretory, and respiratory systems do not cope with the system of maintaining the required pH level. Because of this, either acids or bases accumulate in the blood, which leads to acidosis or alkalosis.
Both types of equilibrium changes are divided into varieties, which are distinguished depending on what caused the change in the water indicator. One of the reasons is changes in the ventilation system. Thus, increased ventilation (hyperventilation) will lead to a decrease in CO2 tension. High blood carbon dioxide tension is quite common when various diseases lungs. A change in the normal balance of bases and acids, caused by dysfunction in the pulmonary ventilation system, is called respiratory alkalosis (acidosis). For problems related to metabolism (for example), in bloodstream Non-volatile acids accumulate. When the body loses HCl (through vomiting), reverse processes are observed - a decrease in the concentration of non-volatile acids. Such changes are called metabolic acidosis, alkalosis.
Non-respiratory acidosis and alkalosis occur due to changes not associated with respiratory disorders (for example,). Respiratory and non-respiratory acidosis and alkalosis can be distinguished by the ratio of PCO2 voltage and the level of buffer bases. The starting point is considered to be a concentration level of buffer bases equal to forty-eight millimoles per liter. This is a conditional zero. If the level differs significantly from the original figure, it is called kurtosis of the bases. If the deviation from the norm occurs in the direction of decrease, this is called reduction (deficit).
For violations respiratory cause characterized by a change in PCO2 towards a decrease or, conversely, an increase, without a prior change in the level of buffer bases. In non-respiratory disorders, a decrease or increase in PCO2 is preceded by an excess of bases. Both acidosis and alkalosis are divided into types. Types of alkalosis: excretory, metabolic, respiratory, non-gas, gas alkalosis.
Metabolic alkalosis
Metabolic alkalosis is expressed in a decrease in hydrogen and chlorine in the extracellular space. It is characterized by high pH numbers and bicarbonate concentration. In severe cases, metabolic alkalosis makes itself felt with intense headaches, tetany, etc. In this case, it is necessary to act on the original cause that led to alkalosis. Sometimes the patient has to be given HCl or Acetazolamide.
The main factors in the appearance of metabolic alkalosis are the loss of positively charged hydrogen by the body and bicarbonate load. Loss of H+, accompanied by this type of acidosis, often occurs in patients with pathological changes kidneys, gastrointestinal tract. In this case, hydrogen ions leave the body along with chlorine. Chloride-sensitive alkalosis often occurs due to vomiting (repeated), during gastric drainage, and therapy with diuretics. Chloride-resistant alkalosis accompanies Conn's syndrome, adrenogenital syndrome, Barter syndrome, and potassium starvation. It also occurs in renovascular hypertension during glucocorticoid therapy.
Metabolic alkalosis sometimes accompanies large blood transfusions and bicarbonate treatment. With such alkalosis, a person loses potassium, which can also lead to increased sensitivity of the heart to certain medications (usually cardiac glycosides). In this state, calcium is excreted. This entails increased neuromuscular excitability, development convulsive syndrome. A serious complication is a failure in enzymatic systems.
Respiratory alkalosis
This type of alkalosis is caused by chronic or acute hyperventilation, due to which CO2 pressure is significantly reduced. It is divided into acute and chronic.
Chronic respiratory alkalosis occurs when a person has moderate hypercapnia for a long time. Acute alkalosis occurs with pronounced hypercapnia.
With respiratory alkalosis, blood begins to flow to the brain in smaller volumes due to a rapid decrease in PCO2. This can lead to lightheadedness, convulsions, and a state of stupor. If patients have heart disease, arrhythmias may occur due to decreased oxygen delivery. Respiratory alkalosis causes K, Na+, and phosphates to migrate through membranes, Ca2+ binds to cell proteins and decreases in concentration. Due to hypocapnia, slight hypokalemia appears.
Respiratory alkalosis occurs very often in severely bedridden patients. Mild alkalosis can often be seen in the first stages of cardiovascular diseases, respiratory system, and if hyperventilation is combined with normal pressure CO2 and hypoxemia, this indicates the beginning of decompensation. In this case, it is necessary to urgently examine the patient and prescribe therapy.
Often, alkalosis of this type develops during mechanical ventilation. It may entail long-term consequences, as numbness of the lips, the appearance of paresthesia, nausea, a feeling of squeezing chest remain for a long time and appear periodically. Any damage to the nervous system can lead to persistent hyperventilation.
Alkalosis is a symptom of poisoning with salicylates that stimulate central chemoreceptors. Taking certain medications enhances the response of the respiratory center and ventilation. These include Aminophylline and Theophylline (Methylxanthine group). In pregnant women, serum progesterone increases significantly, which causes hyperventilation and alkalosis, not life-threatening. In liver failure, respiratory alkalosis is a common occurrence. Moreover, the brighter it is, the more serious the liver pathology. Respiratory alkalosis may be the first sign of the onset of sepsis, since it develops even before the full picture of the disease ( heat, hypoxemia).
Alkalosis causes
Each type of alkalosis has its own causes. Thus, metabolic alkalosis appears due to the massive loss of hydrogen ions by the body. The reason for the loss of necessary vital ions can be repeated vomiting, which loses a lot of hydrochloric acid from the stomach, treatment with drugs that significantly increase diuresis, drainage in the stomach, long-term use GCS or drugs with strong mineralocorticoid properties.
A special place is occupied by syndromes and metabolic diseases (S-M Itsenko-Cushing, Barter, Conn, adrenogenital syndrome). Massive infusions of blood, components and substitutes can also provoke the disease. This condition is extremely rare, but may have unpleasant consequences. Most often it is found in postoperative time after major operations, as well as in young children with rickets.
Exogenous alkalosis occurs in patients who are given too high a dose of sodium bicarbonate (it is administered when high acidity in the stomach). This usually happens by accident or when long-term treatment serious doses. In rare cases, alkalosis of this type is possible due to prolonged consumption of foods with high content bases in its composition (same type of food, poor diet).
Decompensated alkalosis of a metabolic nature most often occurs due to the body’s loss of chlorine (primary or secondary). Fever external environment, accompanied by a lack of water in the body, can also lead to alkalosis. At the same time, unbearable thirst increases, severe fatigue with the most ordinary exertion, as well as weakness, causing a desire to lie down. It begins to worry, hyperkinesis occurs in small muscles (usually the face, hands), appetite worsens.
Mixed alkalosis is a non-gas alkalosis combined with gas alkalosis. It appears with brain injuries, which develop shortness of breath, hypercapnia, and sour vomiting. In this pathological condition, a person’s blood pressure drops and the heart rate decreases, neuromuscular excitation increases, and hypertonicity appears, which leads to seizures. Quite often, alkalosis is accompanied by deterioration in respiratory activity. Also diagnosed general symptoms: deterioration in performance, constant weakness, reluctance to do anything, up to stupefaction or even loss of consciousness.
Alkalosis symptoms
Symptoms of the gas form of alkalosis consist of disorders that are caused by hypocapnia. These include high pressure cerebral arteries, hypotension of veins located on the periphery, drop in pressure and cardiac output, loss of cations along with urine.
The very first significant signs Alkalosis becomes a phenomenon of diffuse cerebral ischemia. Because of this, the patient is anxious, excited, dizzy, paresthesia of the limbs and face appears, he gets tired of communication very quickly, memory and attention are deteriorated.
The skin in this condition has a pale tint, and may appear gray due to hypoxemia. During the examination, you can easily detect the cause of alkalosis - breathing forty to sixty cycles per minute. Such breathing can be accompanied by pulmonary embolism, hysterical shortness of breath, with mechanical ventilation of more than ten liters per minute, and with other pathologies. Often such alkalosis is accompanied by a small pulse and a pendulum-like rhythm of tones. When the patient lies down, blood pressure drops significantly, and upon transition to a vertical state, orthostatic collapse often develops. Diuresis increases, and with prolonged alkalosis, the risk of dehydration increases. Hypocalcemia develops, which causes seizures.
If the patient has a history of organic lesion NS or epileptic readiness of the brain is increased, doctors need to be prepared for the fact that an epileptic attack may suddenly begin. On electroencephalography, fluctuations in the basic rhythm are increased and the frequency is decreased; synchronous bilateral discharges of slow waves are diagnosed. Electrocardiography shows extensive changes in the repolarization of the heart muscle. Sometimes the cause of gas alkalosis can be chronic course. The pathophysiology of this phenomenon is not yet clear. Such alkalosis is completely uncharacteristic of any clinic. In this case, the manifestations will only be those that are related to the underlying disease (hepatitis).
Metabolic alkalosis in most reported cases is compensated in nature and does not have significant symptoms and manifestations. Sometimes such alkalosis is accompanied by swelling or pastiness, signs of respiratory depression. Decompensated alkalosis occurs after vomiting, often multiple times, when hemolysis occurs in the body with loss of potassium and chlorine. It often occurs during terminal conditions that are accompanied by dehydration.
Decompensated alkalosis makes itself felt by weakness, thirst, slight hyperkinesis, lack of appetite, headaches, constant desire drink liquid. The skin is dry with significantly reduced turgor. If there is no heart failure, pneumonia, breathing is superficial and rare. Tachycardia is a characteristic sign of this type of alkalosis. At the first stages, patients are apathetic, later some confusion in consciousness and severe drowsiness appear. If help is not provided at these stages, the condition may worsen, even to the point of coma. An ECG helps confirm hypokalemia; the T wave voltage is very low. A blood test indicates low levels of calcium, potassium, and chlorine in the plasma. The urine reaction is alkaline (in the case of alkalosis with primary loss of potassium, it is acidic).
Burnett's syndrome (milk-alkali syndrome) is a chronic metabolic alkalosis. The disease often appears in people with diabetes who need to constantly take alkaline drugs or milk orally. Alkalosis is expressed in the fact that an aversion to dairy products develops, appetite decreases, weakness with apathy increases, and the skin begins to itch. Often salt accumulations (calcium) appear in the conjunctiva, cornea, and kidney tubules. This may lead to kidney failure.
Metabolic alkalosis is a companion to Barter syndrome. The pathology consists of a congenital disorder in the movement of chlorine into renal tubules. The disease manifests itself in the first months of life and begins with vomiting and developmental delay. Polyuria and also polydipsia are later diagnosed. In the blood - hypochloremia, renin activity and the amount of aldosterone are increased, hypokalemia.
Alkalosis in children
Alkalosis in children develops according to the same principles as in adults, but due to the fact that the child’s metabolism is more labile, it occurs much more often in many pathological conditions.
Metabolic alkalosis often occurs in children if the child has suffered from birth trauma, he has pyloric stenosis, a violation of intestinal patency.
Constant alkalosis from childhood can be observed with certain diseases that are inherited by the baby. Certain hereditary diseases accompanied by poor transport of chlorine in the gastrointestinal tract. In this case, the child undergoes a stool test, which detects a lot of chlorine. There will be no chlorine in the urine at all.
Toxic syndrome in a child entails a state of hyperventilation, which leads to gas-type alkalosis. This condition can develop during respiratory diseases of viral origin, pneumonia, fever, skull injuries, brain tumors, and encephalitis.
Artificial ventilation of the lungs during resuscitation measures or surgical manipulations can serve as an impetus for the appearance of a compensated type of gas alkalosis in the child. This condition is transitory. The disease can also occur, for example, in case of poisoning with sulfonamide drugs or salicylates. This is why it is so necessary to hide all medications away from the child.
If an acute lack of calcium occurs during alkalosis, the child’s limbs will tremble, convulsions periodically occur, and he will begin to sweat. Older children will complain of noise in their ears, numbness, and tingling hands. If the disturbances have already gone deep, disturbances of a neuropsychic nature may also appear. Such changes occur in children with acutely developed hypercapnia.
Alkalosis treatment
Metabolic, gas, and mixed alkalosis, which has developed against the background of severe illness, requires immediate hospitalization.
If the cause of gas alkalosis lies in neurogenic hyperventilation (nervous shock, hysterical state), then help can be provided on the spot, without being admitted to a hospital. In this case, the person must be protected from the traumatic factor, reassured, and any conditions favorable for calm must be created. Need to give sedatives(a couple of valerian tablets will do), if the patient feels that the heart is beating strongly, feels faint after a shock, you need to give Validol or Corvalol (Corvalol - no more than fifteen drops, Validol - a tablet under the tongue). These medications are in almost every first aid kit, and in this case they will be effective, will help you calm down, come to your senses, normalize the rhythm of your heart and improve your overall condition.
Then, if necessary, you can move on to measures that eliminate alkalosis itself. If hypocapnia has reached significant levels, the patient is given inhalation of carbogen. Carbogen includes ninety-two to ninety-eight percent oxygen and five to eight percent CO2. If convulsions develop, an injection of Calcium Chloride into a vein is necessary. It can be administered intravenously by drip or stream. Five cubes of calcium chloride (10%) are injected into a vein. The product is administered very slowly, at least three minutes! The dropper is set to a rate of six drops per 60 seconds. Before starting the procedure, about ten milliliters of ten percent calcium chloride are added to a solution of sodium chloride (isotonic!), which requires one hundred to two hundred milliliters. Sodium chloride can be replaced with five percent glucose - the effect will be the same. Before introducing calcium chloride into the body, you need to tell the patient that immediately during the administration he will begin to feel heat (first in the mouth, and then throughout the body). This is completely normal; previously, guided by the patient’s sensations during the administration of this drug, blood circulation was examined.
In case of alkalosis, hyperventilation must also be eliminated. For this purpose they give Seduxen. Usually, two and a half to ten milligrams of this drug are prescribed per dose, that is, 0.5-2 tablets. The frequency of administration per day is two to four. In people who are severely weakened by the disease, as well as in the elderly, this medicine may cause unwanted effects, so the dose is halved. Treatment with Seduxen should be carried out especially carefully in children. The initial dose for them is a quarter of a tablet per day, and the “quarter” should be divided into at least three, and preferably four, doses. If the body responded well to this amount of Seduxen, half a tablet is prescribed per day (several times), and this is adjusted, if necessary, to whole tablet, divided into three to four doses. It is important to know that for babies under six months of age this medical drug do not give. If alkalosis was caused by incorrect artificial ventilation, it needs to be adjusted.
If metabolic alkalosis is uncompensated, the person is first injected into a vein with calcium and sodium chloride in solution. The method of administration is described above. When the patient has signs of hypokalemia, Panangin should be injected into a vein, followed by potassium chloride in the form of a solution. It is advisable to give a solution of glucose and insulin at the same time. Spironolactone (a drug that preserves potassium in the body) is also indicated. Panangin is administered by drip: a couple of ampoules are mixed with fifty to one hundred milliliters of a five percent glucose solution. The infusion is carried out every twelve to twenty-four hours. If necessary, the frequency of administration can be increased to four to six. When administering Panangin, you need to constantly monitor the homeostasis of electrolytes so that hyperkalemia does not occur, which in this situation will be extremely difficult to combat. A solution of potassium chloride is also injected into a vein. The number and frequency of infusions depends on the severity of the deficiency of this element. Potassium deficiency is considered as follows: potassium = human weight multiplied by 0.2, then by 2, and then by 4.5. The resulting number is the volume of the drug required for administration (four percent), which is diluted in water for infusion ten times (we get about half a liter ready solution). The infusion rate is no more than thirty drops per minute. Glucose (five percent) can also be used for dissolution.
Spironolactone for alkalosis can be given to the patient orally. The daily dose is three hundred milligrams. It must be divided into several times (usually three doses). As soon as the condition has improved, the dose is reduced and brought to a maintenance dose of twenty-five milligrams. Spironolactone has a mass side effects, about which the patient should be informed in advance. So, if he begins to experience nausea, pain in the intestines, vomiting, colic, the patient should report this, since when these occur side effects the drug is discontinued at urgently. Before including Spironolactone in the treatment regimen for alkalosis, it is necessary to find out whether the patient has any diseases, since this drug is not prescribed to people with diabetes, liver failure, nephropathies, menstrual irregularities, chronic failure kidneys, anuria. The drug is contraindicated for pregnant women due to the fact that it can significantly harm the fetus.
For any type of alkalosis, ammonium chloride can be administered. And if alkalosis has developed due to the fact that a lot of alkalis were introduced into the body, Diacarb is prescribed. The drug Diacarb is used exclusively under the supervision of a physician. Dosing is always individual, depending on the nature of the disease. Usually it is taken in the morning, one to one and a half tablets. To prevent the development mountain sickness and alkalosis, the drug is used one tablet three times a day. It is better to start taking it a day or two before the ascent; if symptoms of the disease appear, treatment should be carried out over the next two days. It is not recommended to drink Diacarb for more than five days, since long-term use This medicine greatly increases the risk of acidosis, the consequences of which will have to be treated for a long time. If the medicine is taken by the patient in high doses(a thousand milligrams or more), it is better to refrain from operating mechanisms, machines and performing any activities that require concentration and constant monitoring, as drowsiness, disorientation, and deterioration of attention may occur.
Besides special treatment It is necessary to simultaneously influence the pathological condition that caused alkalosis with drugs. In other words, existing hemolysis, vomiting, or. It is important to know that alkalosis needs to be corrected only when water indicator blood pH (pH) is 7.50 or greater. If alkalosis appears due to a lack of fluid in the body (dehydration), a variety of saline solutions. In this case, many problems can be dealt with by an ordinary saline- an inexpensive and effective drug in this case.
If hypokalemic alkalosis is accompanied low content chlorine, it can be compensated for with the same potassium chloride in solution. A one percent solution of HCl in drops along with pepsin is also recommended. The dose is selected according to age.
The development of alkalosis in premature babies is stopped by administering a small amount of ascorbic acid inside. The dose will depend on the weight of the baby. Premature babies are usually not treated with other drugs, since the body is not yet ready for them, and often this is not required.
In the event that alkalosis occurs against the background of liver pathologies or increased sodium concentration in the body, medicines based on amino acids. These include arginine and lysine hydrochloride. 4.2% arginine hydrochloride is injected into a vein through an IV. Begin administration at a rate of ten drops, and then slowly increase to thirty drops per minute. The drug is administered once a day in the amount of one hundred milliliters. The introduction of amino acids requires the supervision of a doctor, that is, the patient must be monitored by medical staff throughout the entire procedure. At the slightest deterioration and the appearance of complaints, the infusion of arginine hydrochloride should be stopped.
