Overview of hyperventilation syndrome
Hyperventilation syndrome (HVS) is a group of syndromes caused by abnormal regulation of the respiratory center and hyperventilation exceeding physiological metabolic needs. It is often characterized by dyspnea, numbness of the limbs, dizziness, and in severe cases, fainting and convulsions. During the attack, the patient will feel rapid heartbeat, palpitation, sweating, and speed up breathing because he/she can not feel the breathing, which leads to the carbon dioxide in the body is constantly being discharged and the concentration is too low, causing secondary respiratory alkalosis and other symptoms, which is also known as respiratory alkalosis syndrome, respiratory neurological syndrome, hyperventilation syndrome.
Causes
1. Psychogenic hyperventilation
This is a common cause of respiratory alkalosis, but generally not serious. In severe cases, there may be dizziness, abnormal sensation and occasionally convulsions. It is common in patients with hysterical attacks.
2. Abnormal metabolic processes
In hyperthyroidism and fever, ventilation may increase markedly beyond the amount of carbon dioxide (CO2) that should be expelled. This can lead to respiratory alkalosis, but it is usually not serious. This indicates that ventilation does not depend solely on the [H+] and partial pressure of carbon dioxide (PCO2) in the body fluids, but is also related to the intensity of metabolism and oxygen demand. Hyperventilation at this point may be caused by increased pulmonary blood flow through a reflex response.
3. Hypoxic hypoxia
Hyperventilation in hypoxic hypoxia is a compensation for the lack of oxygen, but at the same time can cause excessive CO2 excretion and respiratory alkalosis. Commonly into the plateau, high mountains or high altitude people; thoracic and lung lesions such as pneumonia, pulmonary embolism, pneumothorax, pulmonary stasis, etc. caused by thoracic, pulmonary vascular or pulmonary tissue afferent nerve stimulation and reflex ventilation increases in patients; in addition, some patients with congenital heart disease, due to the increase in the right-to-left shunt and lead to hypoxia hypotonic hypoxemia can also be hyperventilation. These all cause plasma carbonic acid (HCO3-) drop and respiratory alkalosis.
4. Central nervous system disorders
Encephalitis, meningitis, brain tumors, cerebrovascular accidents and craniocerebral injury patients in the respiratory center is stimulated and excited, hyperventilation.
5. Salicylic acid poisoning
Salicylic acid can directly stimulate the respiratory center so that its excitability is elevated and its sensitivity to normal stimuli is also elevated. As a result, hyperventilation occurs.
6. Gram-negative bacillus sepsis
In patients in whom gram-negative bacilli enter the blood circulation and multiply, marked hyperventilation can occur before changes in body temperature and blood pressure occur. pCO2 can be as low as 17 mmHg. This change is very helpful in the diagnosis. The mechanism is unclear, as the phenomenon has not been successfully replicated in animal studies.
7. Excessive artificial respiration
Hyperventilation can be caused by too rapid a rate or too large a tidal volume during artificial respiration.
8. Cirrhosis
Hyperventilation may occur in cirrhosis with ascites and elevated blood ammonia (NH3). It may be caused by the stimulating effect of NH3 on the respiratory center. Of course, ascites elevates the diaphragm and also stimulates respiration, but non-cirrhotic patients with ascites do not have hyperventilation.
9. Sudden correction of metabolic acidosis
If sodium bicarbonate (NaHCO3) is used to correct metabolic acidosis, the extracellular fluid [HCO3-] concentration rises rapidly to normal, but it passes the plasma-brain barrier very slowly, for about 12-24 hours, at which time the brain is still metabolically acidotic, and so hyperventilation persists. This results in respiratory alkalosis with low HCO3-.
10. Pregnancy
There is a moderate increase in ventilation over CO2 production, which is now thought to be due to the stimulatory effect of progesterone on the respiratory center, and is also found in some synthetic progesterone preparations. Ketoacidosis may occur during the reaction period of pregnancy due to vomiting and dietary deficiencies, while respiratory alkalosis may occur after the reaction period of pregnancy, sometimes causing tetany.
11. Other
About 14% of patients with dyspnea have no organic pathologic changes on systematic examination, which is called “medically unexplained dyspnea”.
Symptoms
During the onset of dyspnea, respiration deepens and accelerates, and the patient complains of labored breathing; chest tightness, oppression or suffocation, chest pain, palpitations, tachycardia, etc. The patient also complains that he/she is unable to breathe. Numbness of the ends of the limbs and face, twitching of the hands and feet, muscle spasm or even ankylosis, headache, dizziness, and impaired consciousness may also be present. There are no positive signs on physical examination.
Examination
1. Blood gas analysis with decreased PaCO2 and increased pH.
2. In case of tachycardia, ECG may reveal abnormalities.
Diagnosis
1. Under the premise of excluding other organic diseases, clinical diagnosis is made on the basis of the presence of cardiac factors prior to the onset of the disease, typical symptoms, confirmation of respiratory alkalosis by arterial blood gas analysis, and partial or complete induction of the main symptoms by hyperventilation provocation test. It is common in females.
2. Hyperventilation provocation test uses an end-tidal carbon dioxide analyzer to induce instability in the patient’s respiratory regulation by allowing the patient to spontaneously hyperventilate for 3 minutes (60 breaths/minute), which causes hyperventilation resulting in respiratory alkalosis, and reproduces the major symptoms in whole or in part.
3. Experimental treatment:A trial of carbon dioxide-containing gas for inhalation can stop the onset of symptoms.
Treatment
1. If it is caused by infection, cirrhosis or other diseases, actively prevent and treat the original disease;
2. Explain to the patient the relationship between symptoms and hyperventilation, reduce the patient’s mental burden and eliminate fear;
3. learning abdominal breathing and slow breathing to reduce or eliminate the tendency of hyperventilation by slowing down the respiratory rate;
4. using mask to restrict ventilation, repeated inhalation of carbon dioxide in the mask to correct hypocapnia;
5. sedation may be appropriate for patients with more pronounced symptoms of anxiety;
6. in order to increase the blood PCO2 can be used paper bag or long tube bag cover the mouth and nose, in order to increase the dead space of the airway, reduce the exhalation and loss of CO2. Oxygen containing 5% CO2 can also be inhaled to achieve symptomatic treatment.
7. For tachycardia, calcium can be given intravenously to increase the plasma calcium ion ([Ca2+]) (slow injection of 10% calcium gluconate 10 ml).