Adrenaline is a stress hormone produced in the adrenal medulla. During a stressful situation, its production increases significantly and can reach a critical level. The body sends certain impulses to create a certain reaction. The hormone plays an important role for humans and affects the normal functioning of organs and systems.
When faced with a stressful situation, stress hormones guide actions and prompt certain reactions. For example, if it is necessary to carry out an action that is unpleasant for a person, the stomach may begin to ache, and when speaking in public, the voice may suddenly disappear.
The cause of PA is the release of adrenaline into the blood
It is because of the strong release that a state of adrenaline overdose occurs and a vegetative crisis appears. Therefore, treatment of panic attacks in the initial stages is aimed at reducing and regulating the amount of adrenaline in the blood. Then symptomatic treatment is carried out and work with fear of a recurrence of panic.
How adrenaline affect the human body? This is a substance that is secreted by the adrenal glands and provokes a stressful state in humans. When released into the blood, adrenaline is quickly destroyed, entering into various biochemical reactions. Therefore, as soon as the adrenal glands stop producing adrenaline, the state of stress goes away. However, a person himself can cause relapses of this condition, being under the influence of an experienced event.
Sympathoadrenergic activity and fat metabolism[edit | edit code]
Intravenous administration of epinephrine at rest causes an increase in lipolytic activity, assessed by microdialysis of subcutaneous adipose tissue samples, and this effect is gradually weakened by repeated injections of epinephrine (Stallknecht, 2003). In patients with spinal cord injury, while performing exercise on an arm ergometer using microdialysis, the level of lipolysis was determined in samples of subcutaneous adipose tissue taken in areas above and below the border separating the area of the body with sympathetic innervation (within the clavicle) from the area of the sepsis. deprived (above the buttocks) (Stallknecht et al., 2001). In both areas, an increase in the intensity of lipolysis was observed during physical exercise, which suggests that direct sympathetic innervation is not particularly important for lipolysis processes during muscle work. However, adrenaline circulating in the circulatory system may be the most likely candidate for the role of activator of lillolytic processes. Exercise training leads to a decrease in adipose tissue volume and adipocyte size, and it appears that the sympathoadrenergic system is very important in mediating this adaptation.
Adrenaline is able to stimulate the breakdown of fats not only in adipose tissue, but also in muscles, and lipoprotein lipase (LPL) and hormone dependent lipase (HSL) play an important role in this regulation. Activation of HSL can occur both under the influence of muscle contractile activity and increased levels of adrenaline (Donsmark, 2002), and it has recently been shown that in individuals with removed adrenal glands, there is a parallel activation of HSL and glycogen phosphorylase after adrenaline injections during exercise (Kjaer et al., 2000). This may mean that adrenergic activity leads to the simultaneous mobilization of intramuscular stores of glycogen and triglycerides, and further selection of the substrate for energy supply processes is carried out at a different level.
Symptoms
The symptoms of a panic attack can vary from person to person. This is due to the fact that symptoms are the results of the human body’s struggle with unexpected chemical processes, and exactly how this struggle will manifest itself depends on the individual characteristics of the person. During a panic attack, you may experience difficulty breathing (a feeling that your throat is swelling), rapid heartbeat, and pulsating blood in your temples. A person may feel sick, feel either hot or cold, or feel uncontrollable trembling. But in the end, the most difficult feeling is a feeling of sudden and overwhelming fear or panic.
Adrenaline addiction
What is this term and how can adrenaline be a drug? Indeed, the effect of adrenaline on the body can be called narcotic. When it enters the blood in large quantities, it causes euphoria, which is what those who like to tickle their nerves like.
It is believed that addiction is formed in adolescence, which is why teenagers are so drawn to adventure. Usually by the age of 18, the love for extreme sports fades away. But there are also exceptions. If an adult is prone to reckless actions, then there must be good reasons for this:
- a person has already experienced the powerful mechanism of action of the hormone several times and can no longer live without it;
- low self-esteem and complexes;
- work is associated with a constant release of adrenaline;
- genetic predisposition.
A true adrenaline junkie is a person who, in everyday life, feels truly unhappy and frustrated if he is not given the opportunity to perform wild and extreme antics. Such a person tries something new every day, because the hormone adrenaline is produced less and less often, and one day he goes beyond all limits of what is permitted. And he is no longer stopped by rules, laws, moral principles, or the persuasion of loved ones. Unfortunately, sometimes the end of this adrenaline rush is death.
How to win over addiction?
First you need to find out what a person really lacks. Maybe the reason is so banal that you just need to carefully analyze your mental state. Most often, all problems come from childhood. Then you should learn to switch from one type of activity to another - this helps not to get hung up on an uninteresting and boring activity, after which you want to feel adrenaline excitement. And, in the end, new hobbies, knowledge and skills, and quiet travel to unusual places help a lot.
Treatment
Treatment of panic attacks is currently very successful and effective. When treating phobias and panic attacks, treatment is initially aimed at the root cause of the state of panic - the release of adrenaline, and therefore adrenergic blockers are used. However, before therapy it is necessary to exclude diseases with similar symptoms, among which sympathoadrenal crisis can be distinguished. In one case, a vegetative crisis may occur due to an adrenal adenoma - this is a benign tumor, due to which excess adrenaline can be released into the blood. In another case, a symptomatic adrenal crisis may occur against the background of neurosis, and disturbances of the autonomic nervous system may also be observed. The crisis is triggered by an incorrect command from the human brain addressed to the adrenal glands, as a result of which they mistakenly release adrenaline. However, a modern psychiatric clinic has a sufficient range of equipment, and thanks to the work of highly qualified specialists, it will not be difficult to confirm or refute this diagnosis. Psychotherapy plays an important role in the treatment of panic attacks, since drug treatment alone cannot eliminate the underlying cause of the disease. Drug therapy will help temporarily eliminate or mitigate the symptoms of the disease, but intensive psychotherapy can find and eradicate the true causes of panic attacks.
Anatomy of Human Adrenaline – information:
Adrenaline (epinephrine) (L-1(3,4-Dioxyphenyl)-2-methylaminoethanol) is the main hormone of the adrenal medulla, as well as a neurotransmitter. Its chemical structure is a catecholamine. Adrenaline is found in various organs and tissues and is produced in significant quantities in chromaffin tissue, especially in the adrenal medulla. Synthetic adrenaline is used as a medicine under the name Epinephrine (INN).
Physiological role
The effect of adrenaline is associated with the effect on α- and β-adrenergic receptors and largely coincides with the effects of excitation of sympathetic nerve fibers. Adrenaline is involved in the implementation of “fight or flight” reactions; its secretion increases sharply during stressful conditions, borderline situations, a sense of danger, anxiety, fear, injuries, burns and shock. It causes vasoconstriction of the abdominal organs, skin and mucous membranes; to a lesser extent constricts the blood vessels of skeletal muscles. Blood pressure increases under the influence of adrenaline. However, the pressor effect of adrenaline due to the stimulation of β-adrenergic receptors is less constant than the effect of norepinephrine. Changes in cardiac activity are complex: by stimulating the adrenergic receptors of the heart, adrenaline contributes to a significant increase and increase in heart rate; at the same time, however, due to reflex changes due to increased blood pressure, the center of the vagus nerves is excited, which has an inhibitory effect on the heart; As a result, cardiac activity may slow down. Cardiac arrhythmias may occur, especially under hypoxic conditions.
Adrenaline causes relaxation of the smooth muscles of the bronchi and intestines, dilation of the pupils (due to contraction of the radial muscles of the iris, which have adrenergic innervation). Under the influence of adrenaline, the blood glucose level increases and tissue metabolism increases. Adrenaline enhances gluconeogenesis and glycogenolysis, inhibits glycogen synthesis in the liver and skeletal muscles, enhances the uptake and utilization of glucose by tissues, increasing the activity of glycolytic enzymes. Adrenaline also enhances lipolysis (fat breakdown) and inhibits fat synthesis. At high concentrations, adrenaline enhances protein catabolism.
By simulating the effects of stimulation of “trophic” sympathetic nerve fibers, adrenaline in moderate concentrations that do not have an excessive catabolic effect has a trophic effect on the myocardium and skeletal muscles. With prolonged exposure to moderate concentrations of adrenaline, an increase in the size (functional hypertrophy) of the myocardium and skeletal muscles is noted. Presumably this effect is one of the body’s adaptation mechanisms to long-term chronic stress and increased physical activity. However, prolonged exposure to high concentrations of adrenaline leads to increased protein catabolism, decreased muscle mass and strength, weight loss and exhaustion. This explains emaciation and exhaustion during distress (stress that exceeds the body's adaptive capabilities). Adrenaline improves the functional ability of skeletal muscles (especially during fatigue). Its action is similar in this respect to the effect of excitation of sympathetic nerve fibers.
Adrenaline has a stimulating effect on the central nervous system, although it poorly penetrates the blood-brain barrier. It increases the level of wakefulness, mental energy and activity, causes mental mobilization, orientation reaction and a feeling of anxiety, restlessness or tension, generated in borderline situations. Adrenaline also has a pronounced anti-allergic and anti-inflammatory effect, inhibits the release of histamine, serotonin, kinins and other mediators of allergy and inflammation from mast cells, and reduces the sensitivity of tissues to these substances.
Adrenaline causes an increase in the number of leukocytes in the blood, partly due to the release of leukocytes from the depot in the spleen, partly due to the redistribution of blood cells during vasospasm, partly due to the release of incompletely mature leukocytes from the bone marrow depot. One of the physiological mechanisms for limiting inflammatory and allergic reactions is an increase in the secretion of adrenaline by the adrenal medulla, which occurs during many acute infections, inflammatory processes, and allergic reactions. Adrenaline also causes an increase in the number and functional activity of platelets, which, along with spasm of small capillaries, causes the hemostatic (hemostatic) effect of adrenaline. One of the physiological mechanisms promoting hemostasis is an increase in the concentration of adrenaline in the blood during blood loss.
pharmachologic effect
Alpha and beta adrenergic stimulant. At the cellular level, the effect is due to the activation of adenylate cyclase on the inner surface of the cell membrane, an increase in the intracellular concentration of cAMP and Ca2+. In very low doses, at a rate of administration less than 0.01 mcg/kg/min, it can reduce blood pressure due to vasodilation of skeletal muscles. At an injection rate of 0.04-0.1 mcg/kg/min, it increases heart rate and force of heart contractions, SV and IOC, and reduces OPSS; above 0.02 mcg/kg/min constricts blood vessels, increases blood pressure (mainly systolic) and peripheral vascular resistance. The pressor effect can cause a short-term reflex slowdown in heart rate. Relaxes the smooth muscles of the bronchi. Doses above 0.3 mcg/kg/min reduce renal blood flow, blood supply to internal organs, tone and motility of the gastrointestinal tract. Dilates the pupils, helps reduce the production of intraocular fluid and intraocular pressure. Causes hyperglycemia (increases glycogenolysis and gluconeogenesis) and increases plasma levels of free fatty acids. Increases conductivity, excitability and automatism of the myocardium. Increases myocardial oxygen demand. Inhibits the release of histamine and leukotrienes induced by antigens, eliminates spasm of bronchioles, and prevents the development of edema of their mucosa.
Acting on alpha-adrenergic receptors located in the skin, mucous membranes and internal organs, it causes vasoconstriction, reduces the rate of absorption of local anesthetics, increases the duration and reduces the toxic effect of local anesthesia. Stimulation of beta2-adrenergic receptors is accompanied by increased removal of K+ from the cell and can lead to hypokalemia. When administered intracavernosally, it reduces the blood supply to the cavernous bodies. The therapeutic effect develops almost instantly with intravenous administration (duration of action - 1-2 minutes), after 5-10 minutes. after subcutaneous administration (maximum effect - after 20 minutes), with intramuscular administration - the onset of the effect is variable.
Pharmacokinetics
When administered intramuscularly or subcutaneously, it is well absorbed. When administered parenterally, it is quickly destroyed. It is also absorbed after endotracheal and conjunctival administration. TCmax with subcutaneous and intramuscular administration - 3-10 minutes. Penetrates through the placenta, into breast milk, does not penetrate the BBB. Metabolized mainly by MAO and COMT in the endings of sympathetic nerves and other tissues, as well as in the liver with the formation of inactive metabolites. T1/2 with intravenous administration - 1-2 minutes. Excreted by the kidneys in the main form of metabolites: vanillylmandelic acid, metanephrine, sulfates, glucuronides; and also in small quantities - unchanged.
Indications
- immediate allergic reactions (including urticaria, angioedema, anaphylactic shock) that develop when using drugs, serums, blood transfusions, eating food, insect bites or the introduction of other allergens;
- bronchial asthma (relief of attack), bronchospasm during anesthesia;
- asystole (including against the background of acutely developed stage III AV block);
- bleeding from superficial vessels of the skin and mucous membranes (including from the gums), arterial hypotension that is not amenable to adequate volumes of replacement fluids (including shock, trauma, bacteremia, open heart surgery, renal failure, CHF, drug overdose) , the need to prolong the action of local anesthetics;
- hypoglycemia (due to insulin overdose);
- open-angle glaucoma, during eye surgery
- swelling of the conjunctiva (treatment), to dilate the pupil, intraocular hypertension, stop bleeding; priapism (treatment).
Contraindications
Hypersensitivity, Hypertrophic cardiomyopathy (HOCM), pheochromocytoma, arterial hypertension, tachyarrhythmia, coronary heart disease (CHD), ventricular fibrillation, pregnancy, lactation.
Carefully
Metabolic acidosis, hypercapnia, hypoxia, atrial fibrillation, ventricular arrhythmia, pulmonary hypertension, hypovolemia, myocardial infarction, shock of non-allergic origin (including cardiogenic, traumatic, hemorrhagic), thyrotoxicosis, occlusive vascular diseases (including a history of arterial embolism, atherosclerosis, Buerger's disease, cold injury, diabetic endarteritis, Raynaud's disease), cerebral atherosclerosis, angle-closure glaucoma, diabetes mellitus, Parkinson's disease, convulsive syndrome, prostate hypertrophy; simultaneous use of inhalation agents for general anesthesia (fluorothane, cyclopropane, chloroform), elderly age, children.
Dosage regimen
- SC, IM, sometimes IV drip.
- Anaphylactic shock: IV slowly 0.1-0.25 mg diluted in 10 ml of 0.9% NaCl solution, if necessary continue IV drip administration at a concentration of 0.1 m/ml. When the patient's condition allows a slow action (3-5 minutes), it is preferable to administer 0.3-0.5 mg intramuscularly (or subcutaneously) in diluted or undiluted form, if necessary, repeat administration after 10-20 minutes (up to 3 times).
- Bronchial asthma: subcutaneously 0.3-0.5 mg in diluted or undiluted form, if necessary, repeated doses can be administered every 20 minutes (up to 3 times), or intravenously 0.1-0.25 mg diluted in a concentration of 0.1 mg/ml.
- As a vasoconstrictor, it is administered intravenously at a rate of 1 mcg/min (with a possible increase to 2-10 mcg/min).
- To prolong the effect of local anesthetics: at a concentration of 5 mcg/ml (the dose depends on the type of anesthetic used), for spinal anesthesia - 0.2-0.4 mg.
- For asystole: intracardial 0.5 mg (diluted with 10 ml of 0.9% NaCl solution or other solution); during resuscitation measures - 1 mg (diluted) IV every 3-5 minutes. If the patient is intubated, endotracheal instillation is possible - the optimal doses have not been established; they should be 2-2.5 times higher than the dose for intravenous administration.
- Newborns (asystole): IV, 10-30 mcg/kg every 3-5 minutes, slowly. Children over 1 month: IV, 10 mcg/kg (subsequently, if necessary, 100 mcg/kg is administered every 3-5 minutes (after administration of at least 2 standard doses, higher doses of 200 mcg can be used every 5 minutes /kg) It is possible to use endotracheal administration.
- Children with anaphylactic shock: subcutaneously or intramuscularly - 10 mcg/kg (maximum - up to 0.3 mg), if necessary, these doses are repeated every 15 minutes (up to 3 times).
- Children with bronchospasm: subcutaneously 10 mcg/kg (maximum - up to 0.3 mg), doses, if necessary, repeated every 15 minutes (up to 3-4 times) or every 4 hours.
- Locally: to stop bleeding in the form of tampons moistened with a solution of the drug.
- For open-angle glaucoma - 1 drop of 1-2% solution 2 times a day.
Overdose
Symptoms: - excessive increase in blood pressure - tachycardia alternating with bradycardia - rhythm disturbances (including atrial and ventricular fibrillation) - coldness and pallor of the skin - vomiting - headache - metabolic acidosis - myocardial infarction - cranial hemorrhage (especially in elderly patients ) - pulmonary edema - death
Treatment: - stop administration - symptomatic therapy - to lower blood pressure - alpha-blockers (phentolamine) - for arrhythmia - beta-blockers (propranolol)
Side effect
Cardiovascular system: - less often - angina pectoris, bradycardia or tachycardia, palpitations, increased or decreased blood pressure, at high doses - ventricular arrhythmias; - rarely - arrhythmia, chest pain.
Nervous system:
- more often: headache - anxiety - tremor - less often: - dizziness, nervousness - fatigue - impaired thermoregulation (coldness or heat) - psychoneurotic disorders: psychomotor agitation - disorientation - memory impairment - aggressive or panic behavior - schizophrenia-like disorders - paranoia - sleep disturbance - muscle twitching
Digestive system: - often - nausea, vomiting
Urinary system: - rarely - difficult and painful urination (with prostatic hyperplasia).
Local reactions: - pain or burning at the site of intramuscular injection.
Allergic reactions: - angioedema - bronchospasm - skin rash - erythema multiforme
Other: - rarely: hypokalemia - less often: increased sweating - strong erection, making urination difficult
Interaction
Epinephrine antagonists are alpha- and beta-adrenergic receptor blockers. Weakens the effects of narcotic analgesics and sleeping pills. When used simultaneously with cardiac glycosides, quinidine, tricyclic antidepressants, dopamine, inhalation anesthetics (chloroform, enflurane, halothane, isoflurane, methoxyflurane), cocaine, the risk of developing arrhythmias increases (they should be used together with extreme caution or not at all); with other sympathomimetic drugs - increased severity of side effects from the cardiovascular system; with antihypertensive drugs (including diuretics) - a decrease in their effectiveness.
Co-administration with MAO inhibitors (including furazolidone, procarbazine, selegiline) can cause a sudden and pronounced increase in blood pressure, hyperpyretic crisis, headache, cardiac arrhythmias, vomiting; with nitrates - weakening of their therapeutic effect; with phenoxybenzamine - increased hypotensive effect and tachycardia; with phenytoin - a sudden decrease in blood pressure and bradycardia (depending on the dose and rate of administration); with thyroid hormone preparations - mutual enhancement of action; with drugs that prolong the QT interval (including astemizole, cisapride, terfenadine) - prolongation of the QT interval; with diatrizoates, iothalamic or ioxaglic acids - increased neurological effects; with ergot alkaloids - increased vasoconstrictor effect (up to severe ischemia and the development of gangrene). Reduces the effect of insulin and other hypoglycemic drugs
Special instructions During infusion, you should use a device with a measuring device to regulate the rate of infusion. Infusions should be carried out into a large (preferably central) vein. It is administered intracardially during asystole if other methods are not available, as there is a risk of cardiac tamponade and pneumothorax. During the treatment period, it is recommended to determine the concentration of K+ in the blood serum, measure blood pressure, diuresis, IOC, ECG, central venous pressure, pressure in the pulmonary artery and wedge pressure in the pulmonary capillaries.
Excessive doses during myocardial infarction may increase ischemia by increasing myocardial oxygen demand. Increases glycemia, and therefore diabetes mellitus requires higher doses of insulin and sulfonylurea derivatives. When administered endotracheally, absorption and final plasma concentrations of the drug may be unpredictable. The administration of epinephrine during shock does not replace transfusions of blood, plasma, blood substitute fluids and/or saline solutions. Epinephrine is not advisable for long-term use (constriction of peripheral blood vessels, leading to the possible development of necrosis or gangrene).
There are no strictly controlled studies of the use of epinephrine in pregnant women. A statistically consistent relationship has been established between the appearance of deformities and inguinal hernia in children whose mothers used epinephrine during the first trimester or throughout pregnancy; it was also reported in one case that anoxia occurred in the fetus after intravenous administration of epinephrine to the mother. Epinephrine should not be used in pregnant women with blood pressure above 130/80 mmHg. Experiments on animals have shown that when administered in doses 25 times higher than the recommended dose for humans, it causes a teratogenic effect. When used during breastfeeding, the risks and benefits should be assessed due to the high likelihood of side effects in the child.
Use to correct hypotension during labor is not recommended as it may delay the second stage of labor; when administered in large doses to weaken uterine contractions, it can cause prolonged uterine atony with bleeding. Can be used in children with cardiac arrest, but caution should be exercised as the dosing regimen requires 2 different concentrations of epinephrine. When discontinuing treatment, doses should be reduced gradually, as sudden discontinuation of therapy can lead to severe hypotension. Easily destroyed by alkalis and oxidizing agents. If the solution has turned pinkish or brown in color or contains sediment, it should not be administered. The unused portion should be destroyed.
Panic attacks and willpower
There are a number of common points in the treatment of panic attacks and neuroses - their therapy involves searching for the internal cause of the attacks. Usually these reasons are psychological trauma and severe stress. However, if a person with a strong will was able to suppress them and displace the strongest experiences into the subconscious, then deeply hidden emotions will make themselves felt. Since a person has not allowed himself to fully experience a strong emotion - joy, grief, excitement, etc., this feeling will find a way out for the realization of nervous excitement. As a result, a panic attack may develop. But having found out the true cause of the disease, the psychotherapist can, using the patient’s volitional qualities, eliminate the source of the panic state. Therefore, treating panic attacks through psychotherapy is quite successful and effective, as it combats the underlying cause of the disease.
How to normalize adrenaline levels
You can normalize the level of adrenaline in the body yourself, but if the condition is not critical. Simple rules will help control the hormone.
How to lower stress hormones without medications? Follow the established rules:
- restore mode;
- eat a balanced diet;
- exercise regularly;
- learn to control emotions;
- find a relaxing activity;
- receive positive emotions;
- interact more with animals.
But these are just recommendations. If the hormone content is high, which negatively affects the general condition and poses a clear threat, it is necessary to seek professional help.
Outpatient and inpatient treatment
The Mental Health Clinic successfully combines the treatment of panic attacks both with medication and through psychotherapy. Most often, treatment for panic attacks is carried out on an outpatient basis, but there are also options for inpatient placement. The attending physician will select an antidepressant that will help relieve acute symptoms and draw up a treatment plan, including the prevention and relief of possible recurrences of panic attacks. Patients who clearly know how to help themselves when the disease manifests itself experience significantly less fear of the manifestation of a crisis, which reduces general anxiety and raises the emotional background in general. However, the most important psychiatric help for panic attacks is to conduct active psychotherapeutic work with the patient. This will allow you to find the root cause of the disease and, by completely eliminating it, get rid of the disease forever.
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What are the dangers of excess adrenaline?
When stress hormones are elevated, the body may react negatively. It is noteworthy that in some cases, excessive adrenaline production may not be caused by stress. An increased amount of the hormone is accompanied by dizziness, weakness, and also:
- rapid heartbeat;
- tachycardia;
- general anxiety;
- headache;
- tremor of the limbs;
- hypertension.
In severe situations, acute pulmonary edema cannot be ruled out. With a constant overabundance of the hormone, constant anxiety and irritability are observed. If these symptoms appear, it is advisable to seek help from specialists. Altimed Medical Center specializes in the treatment of abnormalities in the body using innovative equipment. Modern devices accurately determine the weak point. Based on the diagnosis, the optimal treatment regimen is determined.
