Fainting is caused by a temporary loss of blood supply to the brain and may be a sign of a more serious condition...
Fainting is a temporary loss of consciousness.
Fainting is caused by a temporary loss of blood supply to the brain and may be a sign of a more serious condition.
People of any age can faint, but older people may have more serious causes.
The most common causes of fainting are vasovagal (sharp decrease in heart rate and blood pressure) and heart disease.
In most cases, the cause of fainting is unknown.
Vasovagal syncope also known as "general weakness". This is the most common cause of syncope and is caused by an abnormal vascular reflex.
The heart pumps more intensely, the blood vessels relax, but the heart rate does not compensate quickly enough to maintain blood flow to the brain.
1) environmental factors (happens more often when it’s hot);
2) emotional factors (stress);
3) physical factors (loads);
4) illness (fatigue, dehydration, etc.).
Situational fainting only occurs in certain situations.
1) cough (some people faint when coughing too hard);
2) when swallowing (in some people, loss of consciousness is associated with illness in the throat or esophagus);
3) when urinating (when a susceptible person loses consciousness with a full bladder);
4) hypersensitivity of the carotid sinus (in some people when turning the neck, shaving or wearing a tight collar);
5) postprandial syncope can occur in older people when they blood pressure falls about an hour after eating.
Orthostatic syncope occurs when a person feels great in supine position, but when he gets up, he may suddenly faint. Blood flow to the brain decreases when a person stands due to a temporary decrease in blood pressure.
This fainting sometimes occurs in people who have recently started taking (or have been changed to) certain heart medications.
1) low circulating blood volume caused by blood loss (external or internal blood loss), dehydration or heat exhaustion;
2) impaired circulatory reflexes caused by medications, diseases of the nervous system, or congenital problems. Cardiac syncope occurs when a person loses consciousness due to cardiovascular disease.
1) abnormal heart rhythm - arrhythmia. Electrical problems in the heart impair its pumping function. This leads to decreased blood flow. Your heart rate may be too fast or too slow. This condition usually causes fainting without any warning.
2) cardiac obstructions. Blood flow may be obstructed in the blood vessels in the chest. Cardiac obstruction can cause loss of consciousness during exercise. Various diseases can lead to obstruction (heart attacks, diseased heart valves during pulmonary embolism, cardiomyopathy, pulmonary hypertension, cardiac and aortic tamponade).
3) heart failure: the pumping ability of the heart is impaired. This reduces the force with which blood circulates through the body, which can reduce blood flow to the brain.
Neurological syncope may be associated with neurological conditions.
1) a stroke (bleeding in the brain) can cause fainting associated with headache;
2) a transient ischemic attack (or mini-stroke) can cause loss of consciousness. In this case, fainting is usually preceded by double vision, loss of balance, slurred speech or dizziness;
3) in rare cases, migraine can cause fainting. Psychogenic fainting. Hyperventilation due to anxiety can lead to fainting. The diagnosis of psychogenic syncope should only be considered after all other causes have been excluded.
Losing consciousness is an obvious sign of fainting.
Vasovagal syncope. Before fainting, a person may feel light-headed; blurred vision will be noted. A person may see “spots before the eyes.”
The patient experiences pallor, dilated pupils, and sweating.
While unconscious, a person may have a low heart rate (less than 60 beats per minute).
The person must quickly regain consciousness. Many people do not have any warning signs before fainting.
Situational fainting. Consciousness returns very quickly when the situation passes.
Orthostatic syncope. Before an episode of fainting, a person may notice blood loss (black stools, heavy periods) or fluid loss (vomiting, diarrhea, fever). The person may also experience delusions. Observers may also note paleness, sweating, or signs of dehydration (dry lips and tongue).
Cardiac syncope. The person may report palpitations, chest pain, or shortness of breath. Observers may note the patient's weakness, irregular pulse, pallor, or sweating. Fainting often occurs without warning or after exertion.
Neurological syncope. The person may have a headache, loss of balance, slurred speech, double vision, or dizziness (the feeling that the room is spinning). Observers note strong pulse during the unconscious period and normal color skin.
Because fainting can be caused serious condition, All episodes of loss of consciousness should be taken seriously.
Anyone, even after the first episode of loss of consciousness, should consult a doctor as soon as possible.
Depending on what was shown medical examination, the doctor may require tests.
These tests may include: blood tests; ECG, daily monitoring, echocardiography, functional stress test. Table tilt test. This test checks how your body reacts to changes in position. Tests to detect nervous system problems (head CT scan, brain MRI or EEG).
If the person next to you faints, help him.
Treatment for fainting depends on the diagnosis.
Vasovagal syncope. Drink plenty of water, increase your salt intake (under medical supervision), and avoid standing for long periods of time.
Orthostatic syncope. Change your lifestyle: sit down, bend over calf muscles for a few minutes before getting out of bed. Stay hydrated.
Elderly people with low blood pressure Large meals should be avoided after meals or you should plan to lie down for several hours after eating. In most cases, you should stop taking the medications that cause fainting (or change them).
Cardiac fainting. To treat cardiac syncope, the underlying condition must be treated.
Valvular heart disease often requires surgery, while arrhythmia can be treated with medications.
Medications and lifestyle changes.
These procedures are designed to optimize cardiac performance and monitoring is necessary. high pressure blood; in some cases, antiarrhythmic drugs may be prescribed.
Surgery: bypass surgery or angioplasty are used to treat coronary disease hearts; in some cases the valves may need to be replaced. A pacemaker may be implanted to normalize the heart rate (slows the heart for fast arrhythmias or speeds up the heart for slow arrhythmias). Implanted defibrillators are used to control life threatening fast arrhythmia.
Preventative measures depend on the cause and severity of the fainting problem.
Fainting can sometimes be prevented by taking simple precautions.
In other cases, the causes of fainting may be subtle. That's why Consult your doctor to determine the cause of fainting.
Once the cause is determined, treatment for the underlying disease should begin.
Cardiac syncope: because of high risk death from cardiac syncope, people who experience it must be treated for the underlying illness.
Periodic fainting. Consult a doctor to determine the reasons for frequent loss of consciousness.
The prognosis for a person who has fainted depends largely on the cause, the patient's age, and available treatments.
Checking the pulse in the neck area. The pulse can be clearly felt only near the throat (trachea).
If the pulse is felt, note whether it is regular and count the number of beats in 15 seconds.
To determine your heart rate (beats per minute), multiply this number by 4.
The normal heart rate for adults is between 60 and 100 beats per minute.
If fainting happened just once, then you don’t have to worry about it.
It is important to see a doctor because fainting can have serious causes.
1) it often occurs over a short period of time.
2) it occurs during physical exercise or vigorous activity.
3) fainting occurs without warning or in a supine position. When fainting is not serious, the person often knows it is about to happen and vomits or feels sick.
4) a person loses a lot of blood. This may include internal bleeding.
5) shortness of breath is noted.
6) chest pain is noted.
7) a person feels that his heart is pounding (palpitations).
8) Fainting occurs along with numbness or tingling in one side of the face or body. published .
If you have any questions, please ask
The materials are for informational purposes only. Remember, self-medication is life-threatening; consult a doctor for advice on the use of any medications and treatment methods.
P.S. And remember, just by changing your consumption, we are changing the world together! © econet
The most common cause of sudden loss of consciousness is fainting of various types. Often, not only does the patient fall (acute postural insufficiency), but also loss of consciousness for a period measured in seconds. Prolonged loss of consciousness during fainting is rare. The most common types of syncope: vasovagal (vasodepressor, vasomotor) syncope; hyperventilation syncope; fainting associated with hypersensitivity of the carotid sinus (GCS syndrome); cough syncope; nocturic; hypoglycemic; orthostatic fainting of various origins. With all fainting, the patient notes a lipothymic (pre-fainting) state: a feeling of lightheadedness, unsystematic dizziness and a premonition of loss of consciousness.
The most common type of fainting is vasodepressor (simple) syncope, usually provoked by certain stressful influences (anticipation of pain, the sight of blood, fear, stuffiness, etc.). Hyperventilation syncope is caused by hyperventilation, which is usually accompanied by dizziness, mild headache, numbness and tingling in the limbs and face, visual disturbances, muscle spasms(tetanic spasms), palpitations.
Nocturic syncope is characterized by a typical clinical picture: usually these are nocturnal episodes of loss of consciousness that occur during or (more often) immediately after urination, due to the need for which the patient is forced to get up at night. They sometimes have to be differentiated from epileptic seizures using a traditional EEG study.
Carotid sinus massage helps identify carotid sinus hypersensitivity. Such patients often have a history of poor tolerance to tight collars and ties. Compression of the carotid sinus area by the doctor’s hand in such patients can provoke dizziness and even fainting with a decrease in blood pressure and other vegetative manifestations.
Orthostatic hypotension and fainting can have both neurogenic (in the picture of primary peripheral autonomic failure) and somatogenic origin (secondary peripheral failure). The first variant of peripheral autonomic failure (PVF) is also called progressive autonomic failure. It has chronic course and is represented by such diseases as idiopathic orthostatic hypotension, strio-nigral degeneration, Shy-Drager syndrome (variants of multiple system atrophy). Secondary PVN has an acute course and develops against the background somatic diseases(amyloidosis, diabetes mellitus, alcoholism, chronic renal failure, porphyria, bronchial carcinoma, leprosy and other diseases). Dizziness in the picture of PVN is always accompanied by other characteristic manifestations of PVN: anhidrosis, fixed heart rate, etc.
In the diagnosis of any variants of orthostatic hypotension and fainting, in addition to special cardiovascular tests, it is important to take into account the orthostatic factor in their occurrence.
Deficiency of adrenergic influences and, therefore, clinical manifestations orthostatic hypotension are possible in the picture of Addison's disease, in some cases of use pharmacological agents(gpnglioblockers, antihypertensive drugs, dopaminomimetics such as Nakoma, Madopar and some dopamine receptor agonists).
Orthostatic circulatory disorders also occur with organic pathology of the heart and blood vessels. Thus, syncope can be a frequent manifestation of obstructed aortic flow with aortic stenosis, ventricular arrhythmia, tachycardia, fibrillation, weakness syndrome sinus node, bradycardia, atrioventricular block, myocardial infarction, syndrome extended interval QT, etc. Almost every patient with significant aortic stenosis has a systolic murmur and a “cat’s purr” (easier to hear in a standing position or in the “a la your” position).
Sympathectomy can lead to insufficient venous return and, as a result, to orthostatic circulatory disorders. The same mechanism for the development of orthostatic hypotension and fainting occurs when using ganglion blockers, some tranquilizers, antidepressants and anti-adrenergic agents.
When blood pressure drops against the background of current cerebrovascular disease, ischemia often develops in the brain stem (cerebrovascular syncope), manifested by characteristic brain stem phenomena, non-systemic dizziness and fainting (Unterharnscheidt syndrome). Drop attacks are not accompanied by lipothymia and fainting. Such patients require careful examination to exclude cardiogenic syncope (cardiac arrhythmias), epilepsy and other diseases.
Predisposing factors to lipothymia and orthostatic syncope are somatic disorders associated with a decrease in circulating blood volume: anemia, acute blood loss, hypoproteinemia and low plasma volume, dehydration. In patients with suspected or existing blood volume deficiency (hypovolemic syncope), unusual tachycardia while sitting in bed is of important diagnostic value. Hypoglycemia is another important predisposing factor to fainting.
Orthostatic syncope often requires differential diagnosis with epilepsy. Fainting is extremely rare in a horizontal position and never occurs during sleep (at the same time, they are possible when getting out of bed at night). Orthostatic hypotension can be easily detected on a rotary table (passive repositioning). Postural hypotension is considered established when systolic blood pressure drops by at least 30 mmHg. column when moving from a horizontal to a vertical position. A cardiac examination is necessary to exclude the cardiogenic nature of these disorders. The Aschner test has a certain diagnostic value (a slowdown of the pulse by more than 10 - 12 per minute during the Aschner test indicates increased reactivity of the vagus nerve, which often occurs in patients with vasomotor syncope), as well as such techniques as compression of the carotid sinus, performing the Valsalva maneuver, a 30-minute standing test with periodic measurement of blood pressure and heart rate.
The Valsalva test is most informative in patients with nocturic, cough syncope and other conditions accompanied by a short-term increase in intrathoracic pressure.
At first glance, diagnosing the postictal state should not cause any difficulties. In fact, the situation is often complicated by the fact that the convulsions themselves during an epileptic seizure may go unnoticed, or the seizure may be non-convulsive. Characteristic symptoms such as biting the tongue or lips may be absent. Involuntary urination can occur for many reasons. Post-attack hemiparesis can mislead the doctor if we are talking about a young patient. Useful diagnostic information is provided by an increase in blood creatine phosphokinase levels. Post-attack drowsiness epileptic activity EEG (spontaneous or provoked by increased hyperventilation or sleep deprivation) and observation of an attack help in correct diagnosis.
Intracerebral hemorrhage occurs, as a rule, in patients with chronic arterial hypertension. The reason is the rupture of an aneurysm of a small-caliber sclerotically modified vessel; the most common locations are the basal ganglia, pons, and cerebellum. The patient is in a doubtful or unconscious state. The most likely presence is hemiplegia, which can be detected in a comatose patient by a unilateral decrease in muscle tone. Deep reflexes on the side of the paralysis may be reduced, but the Babinski sign is often positive. With hemispheric hemorrhage, it can often be detected concomitant abduction of the eyeballs towards the lesion. With hemorrhage in the area of the bridge, tetraplegia with bilateral extensor reflexes and various oculomotor disorders is observed. With concomitant eye abduction, gaze is directed in the direction opposite to the side of the pontine lesion, in contrast to hemispheric hemorrhage, when gaze is directed towards the lesion (the intact hemispheric oculomotor system “repels” eyeballs to the opposite side). “Floating” friendly or unfriendly eye movements are often observed and do not represent diagnostic value in the sense of determining the localization of the lesion within the brain stem. Spontaneous nystagmus more often it is horizontal in case of a pontine lesion and vertical in case of localization of the lesion in the midbrain region.
Ocular bobbing most often observed with compression of the lower parts of the brain stem by a cerebellar space-occupying process. This symptom is often (but not absolutely) a sign of irreversible brainstem dysfunction. The extinction of the oculocephalic reflex corresponds to the deepening of the coma.
Often available pupillary disorders. Bilateral miosis with intact photoreactions indicates damage at the level of the bridge, and sometimes the integrity of photoreactions can only be verified with the help of a magnifying glass. Unilateral mydriasis is observed with damage to the nucleus of the third cranial nerve or its autonomic efferent fibers in the tegmentum of the midbrain. Bilateral mydriasis is a formidable, prognostically unfavorable sign.
The cerebrospinal fluid is in most cases colored with blood. Neuroimaging studies clearly determine the location and size of the hemorrhage and its effect on the brain tissue, and decide on the need for neurosurgical intervention.
Note that some patients are found unconscious after subarachnoid hemorrhage. Rigidity of the neck muscles is almost always detected, and when lumbar puncture blood-stained cerebrospinal fluid is obtained. Centrifugation of the cerebrospinal fluid is necessary, since during a puncture the needle may enter a blood vessel, and the cerebrospinal fluid will contain blood. Neuroimaging reveals subarachnoid hemorrhage, the volume and location of which can sometimes even determine the prognosis. With a large volume of bleeding, arterial spasm should be expected to develop over the next few days. Neuroimaging also allows early detection of communicating hydrocephalus.
Basilar artery thrombosis without previous symptoms is rare. Such symptoms usually exist for several days before illness; this is slurred speech, double vision, ataxia or paresthesia in the limbs. The severity of these warning symptoms usually fluctuates until sudden or rapid loss of consciousness occurs. Taking an anamnesis in such cases is very important. The neurological status is similar to that of hemorrhage into the pons. In such cases, it is most valuable Doppler ultrasound, since it allows us to identify a characteristic pattern of blood flow disturbances in large vessels. The diagnosis of basilar artery thrombosis is especially likely when recording high resistance in the vertebral arteries, which is found even with occlusion of the basilar artery. Transcranial Doppler ultrasound allows direct measurement of blood flow in the basilar artery and is extremely useful diagnostic procedure for patients who require angiographic examination.
Angiography of the vessels of the vertebrobasilar system reveals stenosis or occlusion in this basin, in particular, “occlusion of the apex of the basilar artery,” which has an embolic origin.
In case of acute massive stenosis or occlusion of the vertebrobasilar vessel, the patient can be helped by urgent measures - either intravenous infusion therapy heparin or intra-arterial thrombolytic therapy.
Information about the injury itself may be missing (there may be no witnesses). The patient is found in a coma with the symptoms described above, presented in various combinations. Each patient in a comatose state should be examined and examined to identify possible damage to the soft tissues of the head and bones of the skull. In case of possible development of epi- or subdural hematoma. These complications should be suspected if the coma deepens and hemiplegia develops.
Hypoglycemia (insulinoma, nutritional hypoglycemia, condition after gasterectomy, severe damage to the liver parenchyma, insulin overdose in patients with diabetes mellitus, hypofunction of the adrenal cortex, hypofunction and atrophy of the anterior pituitary gland) with its rapid development can contribute to neurogenic syncope in persons predisposed to it or lead to stuporous and comatose states. Another common metabolic cause is uremia. But it leads to a gradual deterioration in the state of consciousness. In the absence of anamnesis, a state of stupor and stupor is sometimes visible. Decisive in diagnosis metabolic reasons sudden loss consciousness are laboratory blood tests to screen for metabolic disorders.
More often it leads to subacute deterioration of consciousness (psychotropic drugs, alcohol, drugs, etc.), but sometimes it can create the impression of a sudden loss of consciousness. In the case of coma, this cause of loss of consciousness should be considered to the exclusion of other possible causes. etiological factors sudden onset of unconsciousness.
Typical signs of a psychogenic “coma” are: forced closing of the eyes when the doctor tries to open them for examination oculomotor functions and pupillary disorders, friendly upward movement of the eyes when the doctor opens the patient’s closed eyelids (rolling of the eyes), the patient’s non-response to painful stimuli while intact blink reflex when touching eyelashes. A description of all possible behavioral markers of the presence of a psychogenic seizure in a patient is beyond the scope of this chapter. Let us only note that the doctor must develop a certain intuition that allows him to detect some “absurdities” in the neurological status of a patient demonstrating an unconscious state. An EEG, as a rule, clarifies the situation if the doctor is able to distinguish a non-reactive EEG during alpha coma from a waking EEG with easily detectable activation reactions on it. Autonomic activation in terms of GSR, heart rate and blood pressure is also characteristic.
0 6 630 0
Fainting (or syncope) is a short-term loss of consciousness that occurs when blood flow to the brain is disrupted.
There are many reasons for fainting. In the article we will look in detail at the mechanisms of the development of fainting, and we will tell you how to notice a person in a pre-fainting state in time in order to protect him from dangerous consequences.
Fainting occurs due to a decrease in blood supply to the brain, where oxygen does not reach, and the person suddenly feels weak, dizzy and has an increased heart rate. There is a fever, as if there was a fever, and dry mouth. This state does not last long (up to half a minute). A person is most often conscious, but cannot always help himself. Coordination of movement at this moment is weak, the legs cannot hold up, and you can fall.
People around you should help you sit down or lie down, support you, and give you water. After all, during a fall a person can get seriously injured.
Fainting always indicates the presence of a disease or a predisposition to it. There are exceptions in which fainting occurs due to poisoning or due to starvation.
Neurogenic
Caused by disorder cardiovascular system. It occurs as a result of a vasodepressor state (due to strong stressful emotions). Occurs most often.
Cardiogenic
People with heart disease who have suffered or are susceptible to diseases such as ischemia or myocardial infarction suffer.
Hyperventilation
Triggered when under stress. At such a moment, a person’s breathing becomes uncontrollable. He begins to choke.
Reflex
It is caused by disruption of the heart. It doesn't last long, but it's hard.
In medicine, there are forms of fainting.
The fainting state lasts about thirty seconds. And outwardly it can appear like this:
Loss of consciousness is a condition in which the functioning of the central nervous activity. A person falls, is motionless (with the exception of convulsions during epileptic seizures), does not perceive the environment, does not answer questions, does not react to external stimuli(loud voice, clapping, light slaps, splinters, cold, warmth).
A short-term loss of consciousness from several minutes to half an hour is called “syncope” in medicine.
More severe and prolonged conditions are divided according to severity into comas of various degrees.
1. Insufficient blood flow to the brain.
2. Lack of oxygen in the blood
3. metabolic disorder, that is, brain nutrition.
4. disruption for any reason of the transmission of impulses along the axons of the brain or the occurrence of pathological discharges in the neurons of the brain.
Now let's look at it in order.
1. As a result increased reaction of the autonomic nervous system to various psychological situations such as excitement, fear, fatigue, a sharp expansion of peripheral vessels occurs, blood rushes down due to a decrease in resistance, a lack of blood and, consequently, oxygen in the brain is formed.
2. Due to cardiac reasons, when the cardiac ejection fraction, that is, the amount of blood pushed into systole by the left ventricle of the heart, sharply decreases. This condition is typical for acute myocardial infarction. Heart rhythm disturbances, such as atrial fibrillation (chaotic contraction of the atria, independent of the ventricles of the heart), atrioventricular conduction blocks nerve impulses between the atrium and the ventricle, sick sinus syndrome (the central nerve connection that regulates the rhythm of the heart). As a result of these pathologies, interruptions occur, entire sets of heart contractions disappear, the flow of blood becomes irregular, which also leads to brain hypoxia. With significant stenosis aortic valve heart, syncope is also possible due to difficulty in releasing blood into the aorta.
Right away in this section I want to make a reservation that incomplete blocks of the Hiss bundle branches (nerve fibers in the ventricles of the heart), which are often found on cardiograms, do not lead to attacks with loss of consciousness and in general in most cases do not have any symptoms and diagnostic value, if they exist for a long time.
3. Orthostatic syncope, occurs in people with low blood pressure when taking inadequate doses antihypertensive drugs hypertensive patients, as well as in elderly people. It occurs when there is a sudden change in body position (suddenly getting up from a bed or chair). The reason for its occurrence is a delay in the vascular reaction lower limbs, they do not have time to narrow in time and as a result there is a decrease in blood pressure, a decrease in cardiac output and, again, a lack of blood supply to the brain.
4. With atherosclerotic changes in large vessels supplying the brain, and these are the carotid and vertebral arteries. Atherosclerosis as it is known cholesterol plaques tightly fused with the wall of the vessel and narrowing its lumen.
5. Loss of consciousness is possible when a blood clot appears that completely covers the vessel; the risk of thrombosis exists in postoperative period any surgical interventions, especially when replacing heart valves with artificial ones, after bypass surgery coronary arteries, in the last two cases, since in the body foreign body, the risk of thrombosis exists throughout life and requires constant use of indirect anticoagulants. Heart rhythm disturbances such as constant or periodic atrial fibrillation ( atrial fibrillation) also has a high risk of thrombosis and also requires the use of antiplatelet agents or indirect anticoagulants.
6. When anaphylactic shock(severe manifestation allergic reaction on any medicinal product), as well as infectious-toxic shock (with severe infectious diseases), loss of consciousness is also caused by the expansion of peripheral vessels and the outflow of blood from the heart, but due to the release into the blood of a vasodilating (vasodilating) mediator of inflammatory and allergic processes - histamine and other intracellular elements that appear during the destruction of cellular structures, they not only have a vasodilatory effect property, but also increase the permeability of small capillaries, due to which blood rushes to the skin, the circulating volume of blood decreases, and again, decreases cardiac output, the result is a violation of the blood supply to the brain and syncope.
1. Consultation with a neurologist to exclude neuro-vegetative-vascular dystonia.
2. Consultation with a therapist to exclude hypotension (low blood pressure, below the figures of 100\60 mm RT), as well as the prescription of adequate doses of antihypertensive therapy in the presence of hypertension.
3. ECHO KG (ultrasound of the heart), electrocardiogram, Holter ECG (daily ECG), all this to clarify the existence of heart defects, the presence of arrhythmias in the heart.
4. Doppler ultrasound examination of the vessels of the neck and brain reveals atherosclerotic or other pathology in these vessels.
1. Lack of oxygen in the inhaled air, that is, prolonged exposure to stuffy room.
2. Possible loss of consciousness when serious illnesses lungs, primarily with exacerbation of bronchial asthma, the appearance of status asthmaticus, with high degrees of chronic obstructive pulmonary disease (obstructive bronchitis).
During paroxysm of prolonged cough in patients with obstructive pulmonary disease, the mechanism of occurrence is double, firstly directly due to a lack of oxygen in the blood and secondly increases with prolonged cough intrathoracic pressure, which interferes with venous return, as a result of which cardiac output also decreases.
3. For anemia with low hemoglobin high degree (below 70-80g/l) fainting is possible under any conditions. With higher hemoglobin numbers, the likelihood of loss of consciousness increases when you are in a stuffy room.
4. In cases of carbon monoxide poisoning. CO is a colorless, odorless and tasteless gas, which increases the risk of poisoning. Poisoning often occurs in everyday life during the heating of stoves, gas water heaters and the absence of the required exhaust hood and ventilation of the room, when exhaust gases from the car engine enter the driver's cabin (for example, while the driver is sleeping in the car with the engine running with the windows closed or in the garage). Penetrating through the lungs into the blood, carbon monoxide combines with hemoglobin to form carboxyhemoglobin, blocks the transport of oxygen in the blood, causing acute oxygen starvation- hypoxia, in addition, by binding to myoglobin (a protein contained in muscles), CO inhibits the contraction of the myocardial muscle.
To exclude the causes of short-term loss of consciousness due to lack of oxygen in the blood, the following examinations and tests are desirable:
1 A general blood test, which determines the amount of hemoglobin and red blood cells, as well as the number of eosinophils, can determine the presence of bronchial asthma.
2. X-ray of the lungs - exclude chronic bronchitis, cancer and other lung diseases.
3. Spirography (we exhale air with force into a special device) allows us to judge the functions of external respiration.
4. If you suspect bronchial asthma allergic genesis, it is useful to visit an allergist and test for allergens.
1. When an overdose of insulin occurs, a decrease in the amount of sugar in the blood occurs - hypoglycemia, as a result of which the nutrition of the brain is disrupted, which leads to a disruption in the function of transmitting nerve impulses.
2. Diabetic ketoacidotic coma - on the contrary, occurs with a lack of insulin and an increased amount of glucose in the blood (blood sugar above 17-20 mmol/l). characterized by enhanced education ketone bodies(acetone, urea) in the liver and an increase in their content in the blood. As a result of metabolic disturbances in the cells of the brain and, as a consequence, loss of consciousness. The peculiarity of this coma is the smell of acetone emanating from the patient.
Lactic acidosis (lactic acid coma) in diabetes mellitus usually occurs against the background renal failure and hypoxia. There is a large amount of lactic acid in the blood. Unlike ketoacidotic coma, there is no smell of acetone.
To diagnose diabetes mellitus, repeated blood tests for sugar are required from a finger stick on an empty stomach. When glucose in capillary blood increases by more than 6.1 to 7.0 mmol/l, it indicates impaired glucose tolerance (that is, a decrease in insulin sensitivity to glucose), an increase in glucose over 7.0 mmol/l is alarming in terms of diabetes mellitus, and then it is required donating blood after a load with glucose (on an empty stomach, donate blood for sugar, then drink 75 grams of glucose dissolved in a glass of water and two hours later the level of sugar in capillary blood is measured. A glucose level after a load above 11.1 indicates the presence of diabetes mellitus. Also important glucose content in urine (should not be normal). The most accurate method for diagnosing diabetes mellitus is the measurement of glycosylated hemoglobin, which is a time-averaged indicator of the concentration of glucose in the blood for 6-8 weeks preceding observation.
It makes sense to produce ultrasound examination pancreas, in order to exclude diseases leading to diabetes mellitus. As you know, insulin is produced in the cells of the pancreas.
1. First of all, epileptic syndrome - repeated seizures, often with loss of consciousness, arising as a result of hypersynchronous discharge of brain neurons (pathological foci of excitation in the cerebral cortex). Seizures, unlike other cases of loss of consciousness, are characterized by the presence of clonic (muscle twitching) and tonic (increased tone, muscle tension) convulsions.
2. For various cranial brain injuries in which a concussion, bruise, or compression of the brain occurs, resulting in displacement cerebral hemispheres brain, relative to the rigidly fixed brain stem, there is a transient increase intracranial pressure, tension and twisting of long axons (nerve fibers) occurs in depth white matter hemispheres, and brain stem. In mild cases, as a result of this process, the conduction of axons is temporarily disrupted (temporary, short-term loss of consciousness); in severe cases, swelling and rupture of axons and small vessels accompanying them occurs (coma - long-term loss of consciousness of varying degrees).
3.Loss of consciousness may occur when an ischemic or hemorrhagic stroke occurs. The difference between them is that in the first case, a violation of the blood supply to the brain occurs due to blockage of a vessel due to a blood clot, the cause of which may be atherosclerosis or the toxic effects of certain substances (from practice I observe a large number ischemic strokes after consuming alcohol substitutes, including after taking large quantities of alcohol-containing infusions sold in pharmacies.
Hemorrhagic stroke (intracerebral hemorrhage) is a rupture of a cerebral vessel, always has more severe course and a higher percentage of deaths.
One of important factors in the development of both types of strokes has an uncontrolled hypertension, for the brain is unfavorable in terms of the development of strokes, both constantly high and spasmodic (from low to high blood pressure).
What to do if you witness another person losing consciousness.
1. If loss of consciousness occurred in a stuffy room during mass events. Fainting is more likely due to lack of oxygen or due to overexcitation autonomic innervation body. The mechanism of occurrence of this condition is sometimes mixed.
Actions in this case:
1. Extend the collar of a shirt or other clothing.
2. Open a window to allow oxygen to enter or take the victim to a well-ventilated area.
3. Apply a cotton swab with ammonia to the nasal passages for up to 1-2 minutes.
4. If after this it does not come to consciousness, place it on your right side, place your right hand along the body, place your head on the back of your left hand. In this position, there is less likelihood of tongue retraction and more free speech. respiratory tract. If you can, check with the index finger of your hand, having first unclenched your jaws, whether the tongue is retracted into the throat. If so, then you need to clear the airways by fixing the tongue to the side surface of the oral cavity (pressing it with the thumb of your hand). Naturally, completely blocking the airways.
5. Check if there is a pulse and breathing (how to do this is described below).
6. If there is no pulse and breathing, you can, if you know how, before the ambulance arrives, begin artificial respiration and chest compressions (the method is given below).
7. Call an ambulance and describe the symptoms of loss of consciousness as accurately as possible.
If you find an unconscious person on the street
1. Find out from witnesses, maybe someone knows what the victim is sick with.
Sometimes chronically ill patients have data about their illness and a record of possible help in their pockets. If you find them or receive data about the patient, follow the recommendations of the note or report all the data to the ambulance.
2. Check by palpation whether there are open injuries and bleeding; if they are detected, try to stop them using available methods until the ambulance arrives.
3. Check if there is a pulse; the best way to feel the pulse is on the carotid artery; to do this, place your index and middle fingers right hand on the thyroid cartilage of the victim, smoothly lower your hand down the neck (with the patient lying down) to a soft depression, here the pulse should be felt.
4. If there is no pulse, there is no breathing (no movement chest, there is no fogging on the glass brought to the nose and mouth of the affected person), and the skin is still warm, we check the reaction of the pupils to light. In a living person, or in clinical death, the reaction of the pupils to light is preserved. We check as follows:
If the patient lies with eyes closed, we open our eyelids, if there are signs of life, we observe the constriction of the pupils to the light. If the victim’s eyes are open, cover them with your hand for 10 seconds, then remove your hand; you should again observe a constriction of the pupils. In the dark, any illumination (flashlight, cell phone). Also, to determine signs of life, the corneal reflex is checked; for this, a handkerchief or cotton wool; if not, then we touch the eyelids with another soft textile - blinking occurs in a living person.
If there are signs of life or clinical death, it is possible, before the arrival of emergency medical services, to begin artificial respiration and indirect (direct for specialists, it is carried out when the chest is opened) cardiac massage. Most often early onset resuscitation measures brings more benefit than an emergency medical team staying after some time. The only thing exception for holding artificial respiration not specialists- this is a suspicion of a spinal fracture in the cervical region.
We place the patient lying on his back, having previously cleared the airways of possible vomit and mucus. We tilt the victim's head back by placing a cushion under the occipital region of the head so that the lower jaw moves forward. When clenching the jaws tightly, you can use the technique of compressing the lateral surfaces of the lower jaw. Next, we perform artificial respiration using the “mouth to mouth” method (used most often), or the “mouth to nose” method (used in cases of inaccessibility oral cavities). To do this, we take 2 breaths into the patient through a handkerchief, having previously pinched the nose or mouth (depending on the type of artificial respiration), then we press with straightened arms folded one above the other in the area of the lower third of the sternum in the amount of 8-10 presses, with reasonable application strength to move the chest, and naturally freeing the airways for air to escape. When performing artificial respiration and indirect massage hearts together, the following technique is proposed: One breathes “mouth to mouth” or “mouth to nose” in the amount of one breath, the other makes 4-5 compressions on the chest.
Cycles of artificial respiration and chest compressions are repeated until emergency medical assistance arrives.
