Respiratory alkalosis is an increase in blood pH of more than 7.45 against the background of an absolute decrease in the partial voltage of carbon dioxide (pCO2) of less than 35 mm Hg. The condition occurs against the background of hyperventilation in cerebral pathology, bronchopulmonary diseases, negative iatrogenic factors. Symptoms of alkalosis include impaired consciousness, dehydration, muscle weakness and a tendency to hypotension. Diagnosis of pathology requires analysis of the biochemical and gas composition of blood, registration of an electrocardiogram. Treatment includes correction of the root cause of ABB disorders, adequate respiratory and medical support of vital functions.
ICD 10
E87.3 Alkalosis
General information
In anesthesiology and emergency therapy, respiratory alkalosis occurs with approximately the same frequency as other forms of violation of the acid-base index of the blood. It is a clinical syndrome that develops secondary to the underlying pathology, accompanied by electrolyte disorders of the blood composition. In practice, there is often a mixed form of alkalosis and a complication of the syndrome with metabolic acidosis. Given the wide variety and non-specificity of pH disorders, the true frequency of pathology has not been established.
Causes
The respiratory variant of alkalosis is associated with disorders of the respiratory system and increased pulmonary ventilation. Physiologically, this condition is observed in conditions of high altitude and rarefied air, when the excitation of the respiratory center is caused by oxygen starvation of tissues. Shortness of breath is a natural manifestation of fever in infectious and other diseases. Pathological hyperventilation of the lungs develops under the influence of the following reasons:
- Diseases of the central nervous system. Shortness of breath occurs with various forms of damage to the respiratory center and violations of the central regulation of the function of external respiration. The condition is diagnosed with TBI, stroke, brain tumor or encephalitis involving the medulla oblongata.
- Respiratory diseases. In severe bronchopulmonary diseases, excessive stimulation of intra-pulmonary receptors occurs, resulting in an increase in the frequency of respiratory movements. This is observed in pneumonia, interstitial lung diseases, bronchial asthma and all types of pulmonary edema.
- Mental illness. Hyperventilation and alkalosis develop against the background of an attack of hysterical neurosis, which is manifested by sudden laughter or crying, excitement, and various vegetative reactions. The condition is short-lived, after the end of the paroxysm, blood counts recover quickly.
- Taking medications. Violation of respiratory function is observed in the treatment of salicylates, catecholamines, narcotic analgesics. In women, signs of respiratory alkalosis are possible against the background of taking medroxyprogesterone and progestins. Hyperventilation develops with an overdose of L-thyroxine in the treatment of hypothyroidism.
For the above reasons, shortness of breath is limited in time, since a decrease in the level of carbon dioxide in the blood causes depression of the respiratory center in the medulla oblongata. Prolonged loss of carbon dioxide with respiration is observed in patients on a ventilator if ventilation parameters are selected incorrectly or blood gases are not monitored. As a result, severe respiratory alkalosis develops with deep depression of respiratory function.
Pathogenesis
Acid-base equilibrium is the regulation of the concentration of hydrogen ions in body fluids. 3 systems take part in the maintenance of ABB: lungs, kidneys, buffer connections. The most significant of them is the bicarbonate buffer system, which ensures the dissociation of carbonic acid and the production of positively charged H+ ions. The lungs are responsible for regulating the acidic component of the bicarbonate buffer, the alkaline component is controlled by the kidneys.
In the case of pulmonary hyperventilation, the volume of exhaled carbon dioxide per unit of time exceeds the amount of CO2 produced in the body as a result of metabolic reactions. Since the diffusion of carbon dioxide through the alveolar wall is much easier compared to the oxygen molecule, significant CO2 losses develop quite quickly.
With respiratory alkalosis, the level of HCO3-anions increases and the number of H+ decreases. In such a situation, the renal component of the regulation of CSR is activated: the secretion of hydrogen ions into the urine decreases, the reabsorption of bicarbonate is inhibited. Compensatory mechanisms can restrain moderate manifestations of alkalosis, however, with a sharp drop in the level of carbon dioxide, sub- and decompensated alkalosis occurs with vivid clinical symptoms.
Symptoms
The initial stages of CSR disorders have no clinical manifestations, since buffer systems successfully perform a compensatory function. As the amount of CO2 decreases and the hydrogen index increases, the patient’s condition progressively worsens. The defeat of the central nervous system manifests delirium, confusion, impaired attention and speech function. There may be a narrowing of the fields of vision, the appearance of photopsies.
Vegetative manifestations of respiratory alkalosis include excessive sweating, dry mouth. Increased excretion of bicarbonate anions by the kidneys is accompanied by polyuria, which, against the background of hyperventilation and sweating, quickly causes symptoms of dehydration. The skin is dry with reduced elasticity, the addition of hypoxemia causes gray cyanosis. The patient is very thirsty, while there is no appetite.
Gas alkalosis is characterized by muscle weakness, intestinal paresis, paralysis of skeletal muscles. Paresthesia of the limbs and face is possible. The heartbeat quickens, the pulse has a weak filling. When trying to move to a vertical position, an orthostatic collapse develops. In severe cases, hyperventilation tetany occurs.
Complications
With respiratory alkalosis, specific circulatory disorders develop: narrowing of cerebral vessels and expansion of arterioles of all other organs. This is accompanied by arterial hypotension, blood deposition in peripheral tissues, and a decrease in CBV. As a result, venous pressure and blood flow to the heart decrease, heart failure develops. Thus, a vicious circle is closed with gas alkalosis.
Hypokalemia is a dangerous consequence of ABB violations, which is caused by the exchange of potassium ions for hydrogen ions to compensate for pH violations. A pattern has been established that with a decrease in pCO2 by 10 mmHg, the potassium level drops by 0.5 mmol/l. Hypokalemia is fraught with extrasystole, atrioventricular blockages, ventricular fibrillation. If the K+ level is less than 2 mmol/l, there is a risk of cardiac arrest in systole.
Diagnostics
Acute symptoms of respiratory alkalosis require urgent therapy, so the patient is examined in the intensive care unit in parallel with comprehensive medical support. Diagnosis of the condition is within the competence of the resuscitator. To confirm the pathological condition, the following research methods are shown:
- Blood test. The main sign of pathology is a pH level of more than 7.45. Blood biochemistry shows a decrease in alkaline reserves, the level of standard bicarbonate is in the range of 15-24 mmol/l, buffer bases are 40-52 mmol/l. Hypokalemia, hypocalcemia, hyperchloremia are also determined.
- Urine analysis. With respiratory alkalosis, an increase in the pH of the liquid to 8 is observed with a simultaneous decrease in the titrated acidity index. Increased potassium losses are detected, the levels of ammonia and chlorides are reduced.
- ECG. When studying a cardiogram, a low voltage of the T teeth and an increase in the U wave are determined, which unmistakably indicates hypokalemia. It is characterized by increased heart rate, single atrial and ventricular extrasystoles. With a further decrease in potassium in the blood, the PQ interval lengthens, signs of AV blockade are detected.
If an increased pH is detected in combination with a reduced amount of carbon dioxide, the diagnosis of respiratory alkalosis is established unmistakably. Difficulties may arise in the differential diagnosis of the root cause of this condition. According to the indications, patients are prescribed a consultation with a neurologist, psychiatrist, endocrinologist. To detect organic lesions of the central nervous system, CT or brain MRI is performed.
Treatment
In most cases, the problem of CSR disorders is solved after the cure or persistent compensation of the underlying disease. The therapy program is selected by a pulmonologist, neurologist or other specialists after examination and clarification of the trigger factor of pulmonary hyperventilation. In the acute period of respiratory alkalosis, a complex of emergency care is required to stabilize the patient’s condition, which includes the following directions:
- correction of the operating mode of the ventilator equipment if the patient continues to need respiratory support;
- use of breathing mixtures with 95% oxygen and 5% carbon dioxide;
- conducting infusion therapy to correct dehydration and normalize the electrolyte composition of the blood;
- the use of medications that reduce the phenomena of tissue hypoxia;
- administration of sedative drugs in hyperventilation on the background of psychomotor agitation.
Prognosis and prevention
The outcome of respiratory alkalosis depends on the degree of pH shift: with an increase in the index within 0.1 of the norm, cardiovascular and respiratory complications develop, 0.2-0.3 – comatose state, 0.3-0.4 there is a high risk of death. Primary preventive measures have not been developed. Secondary prevention consists in early detection and adequate correction of the state of alkalosis in order to prevent the development of complications.