Antipyretics for children are prescribed by a pediatrician. But there are emergency situations for fever when the child needs to be given medicine immediately. Then the parents take responsibility and use antipyretic drugs. What is allowed to be given to infants? How can you lower the temperature in older children? What medications are the safest?
Recently, it has become obvious that the contribution of genetic factors to the occurrence of secondary prolongation of the QT interval cannot be underestimated. In a significant proportion of cases in patients with drug-induced QT prolongation, so-called “silent mutations,” or functional polymorphisms, are identified in the same genes that are responsible for the primary forms of LQTS.
Changes in the structure of ion channels of cardiomyocytes in such cases are minimal and can remain asymptomatic for a long time. Therefore, a person cannot know that some drugs widely available on the pharmaceutical market pose a danger to him. In most people, drug-induced depression of potassium current is mild and is not accompanied by any ECG changes.
However, the combination of genetic features of the structure of potassium channels and drug intake can cause clinically significant arrhythmias, up to the development of polymorphic ventricular tachycardia “Torsade des pointes” and sudden death. Therefore, for patients who have had polymorphic ventricular tachycardia caused by taking any medication at least once, consultation with a geneticist is recommended. In addition, all medications that prolong the QT interval should be avoided throughout your life.
The incidence of the primary form of long QT syndrome is about 1:3000. To date, at least 12 genes are known to be responsible for the development of the disease. A mutation in any of them can lead to the development of the disease.
Genes responsible for the development of long QT syndrome.
Possibilities of DNA diagnostics in Russia
You can apply for a direct DNA diagnosis of long QT syndrome in . Based on the results of DNA diagnostics, a written conclusion from a geneticist is issued with an interpretation of the results obtained. When analyzing all of these genes, it is possible to identify mutations and establish the molecular genetic form of the disease in 70% of probands. Mutations in these genes can also cause idiopathic ventricular fibrillation and sudden infant death syndrome (about 20% of cases).
Why do you need to carry out LQTS DNA diagnostics?
The use of molecular genetic methods for long QT syndrome can be crucial in the following situations:
- The need for confirmatory and / or differential diagnosis (for example, to resolve the issue of the primary or secondary nature of the lengthening of the QT interval).
- Identification of asymptomatic and oligosymptomatic forms of the disease, for example, among relatives of patients with an established diagnosis. According to various authors, up to 30% of individuals with mutations in the genes involved do not have any signs of the disease (including electrocardiographic). At the same time, the risk of developing arrhythmias and sudden cardiac death remains high, especially when exposed to specific risk factors.
- When choosing a treatment strategy for a disease. It has now been shown that patients with different molecular genetic forms of the disease respond differently to treatment. Accurate determination of the molecular genetic variant of the disease allows the patient to choose an adequate drug therapy, taking into account the disruption of the functioning of a particular type of ion channel. Efficiency various methods treatment for various molecular genetic variants of LQTS syndrome. >
ICD - implantable cardioverter-defibrillator, PVT - polymorphic ventricular tachycardia, ECS - pacemaker, +++ - maximum efficiency of the approachLQT1, LQT5 LQT2, LQT6 LQT3 Sensitivity to sympathetic stimulation +++ + - Circumstances under which PVT is often observed Fright At rest/in sleep Specific factor provoking syncope Swimming Sharp sound postpartum period - Limiting physical activity +++ + - b-blockers +++ + - Taking potassium supplements +? +++ +? Class IB antiarrhythmic drugs (sodium channel blockers) + ++ +++ Calcium channel blockers ++ ++ +? Potassium channel openers (nicorandil) + + - THE EX + + +++ ICD ++ ++ +++ - Help with family planning. A serious prognosis of the disease, a high risk of life-threatening arrhythmias in the absence of adequate therapy, determines the relevance of prenatal DNA diagnostics of LQTS. The results of prenatal DNA diagnostics in families with an already established molecular genetic form of long QT syndrome make it possible to most successfully plan the management of pregnancy, childbirth, and drug therapy tactics in the postpartum period.
What to do if a mutation has been identified?
If you or your child has a mutation that confirms the hereditary nature of the disease, you need to remember the following:
- You need to discuss the results of a molecular genetic study with a geneticist, what they mean, and what clinical and prognostic significance they may have.
- Your relatives, even without clinical signs diseases, may be carriers of a similar genetic change, and be at risk of developing life-threatening arrhythmias. It is advisable to discuss with them and/or with a geneticist the possibility of consultation and DNA diagnostics for other members of your family.
- It is necessary to discuss with a geneticist the features of this genetic variant of the disease, specific factors risks, and ways to best avoid them.
- A number of medications must be avoided throughout your life.
- You need an early consultation and long-term, usually lifelong, observation by an arrhythmologist. Our Center has a program for monitoring families with hereditary heart rhythm disorders
The QT interval doesn't tell the average person much, but it can tell a doctor a lot about the patient's heart condition. Compliance with the norm of the specified interval is determined based on the analysis of the electrocardiogram (ECG).
Basic elements of an electrical cardiogram
An electrocardiogram is a recording of the electrical activity of the heart. This method of assessing the condition of the heart muscle has been known for a long time and is widespread due to its safety, accessibility, and information content.
The electrocardiograph records the cardiogram on special paper, divided into cells 1 mm wide and 1 mm high. At a paper speed of 25 mm/s, the side of each square corresponds to 0.04 seconds. A paper speed of 50 mm/s is also often found.
An electrical cardiogram consists of three basic elements:
- teeth;
- segments;
- intervals.
A spike is a kind of peak that goes either up or down on a line graph. The ECG records six waves (P, Q, R, S, T, U). The first wave refers to the contraction of the atria, the last wave is not always present on the ECG, so it is called intermittent. The Q, R, S waves show how the heart ventricles contract. The T wave characterizes their relaxation.
A segment is a straight line segment between adjacent teeth. The intervals are a tooth with a segment.
To characterize the electrical activity of the heart, the PQ and QT intervals are of greatest importance.
- The first interval is the time it takes for excitation to travel through the atria and the atrioventricular node (the conduction system of the heart located in the interatrial septum) to the ventricular myocardium.
- The QT interval reflects the combination of processes of electrical excitation of cells (depolarization) and return to a resting state (repolarization). Therefore, the QT interval is called electrical ventricular systole.
Why is the length of the QT interval so significant in ECG analysis? Deviation from the norm of this interval indicates a disruption in the processes of repolarization of the ventricles of the heart, which in turn can result in serious disturbances of the heart rhythm, for example, polymorphic ventricular tachycardia. This is the name for malignant ventricular arrhythmia, which can lead to sudden death of the patient.
Normal interval durationQTis within 0.35-0.44 seconds.
The length of the QT interval can vary depending on many factors. The main ones:
- age;
- heart rate;
- state nervous system;
- electrolyte balance in the body;
- Times of Day;
- the presence of certain medications in the blood.
If the duration of the electrical systole of the ventricles goes beyond 0.35-0.44 seconds, the doctor has reason to talk about the occurrence of pathological processes in the heart.
Long QT syndrome
There are two forms of the disease: congenital and acquired.
ECG for paroxysmal ventricular tachycardia Congenital form of pathology
It is inherited in an autosomal dominant manner (one of the parents passes the defective gene to the child) and an autosomal recessive type (both parents have the defective gene). Defective genes disrupt the functioning of ion channels. Experts classify four types of this congenital pathology.
- Romano-Ward syndrome. The most common occurrence is approximately one child in 2000 births. It is characterized by frequent attacks of torsades de pointes with an unpredictable rate of ventricular contraction.
The paroxysm may go away on its own, or it may develop into ventricular fibrillation with sudden death.
The following symptoms are typical for an attack:
- pale skin;
- rapid breathing;
- convulsions;
- loss of consciousness.
Physical activity is contraindicated for the patient. For example, children are exempt from physical education lessons.
Romano-Ward syndrome is treated with medication and surgery. With the medication method, the doctor prescribes the maximum acceptable dose of beta-blockers. Surgical intervention performed to correct the conduction system of the heart or install a cardioverter-defibrillator.
- Jervell-Lange-Nielsen syndrome. Not as common as the previous syndrome. In this case we observe:
- more noticeable prolongation of the QT interval;
- increased frequency of attacks of ventricular tachycardia, which can lead to death;
- congenital deafness.
Mainly used surgical methods treatment.
- Andersen-Tawil syndrome. This is a rare form of a genetic, inherited disease. The patient is susceptible to attacks of polymorphic ventricular tachycardia and bidirectional ventricular tachycardia. Pathology clearly makes itself known appearance patients:
- short stature;
- rachiocampsis;
- low position of the ears;
- abnormally large distance between the eyes;
- underdevelopment of the upper jaw;
- deviations in the development of fingers.
The disease can progress with varying degrees gravity. The most effective method of therapy is the installation of a cardioverter-defibrillator.
- Timothy syndrome. It is extremely rare. In this disease, there is a maximum lengthening of the QT interval. Six out of ten patients with Timothy syndrome have different birth defects heart (tetralogy of Fallot, patent ductus arteriosus, ventricular septal defects). There are a variety of physical and mental anomalies. The average life expectancy is two and a half years.
Clinical picture similar in manifestations to those observed in the congenital form. In particular, attacks of ventricular tachycardia and fainting are characteristic.
Acquired long QT interval on an ECG can be recorded for various reasons.
- Taking antiarrhythmic drugs: quinidine, sotalol, ajmaline and others.
- Electrolyte imbalance in the body.
- Alcohol abuse often causes paroxysm of ventricular tachycardia.
- A number of cardiovascular diseases cause prolongation of the electrical systole of the ventricles.
Treatment of the acquired form primarily comes down to eliminating the causes that caused it.
Short QT syndrome
It can also be either congenital or acquired.
Congenital form of pathology
It is caused by a rather rare genetic disease that is transmitted in an autosomal dominant manner. Shortening of the QT interval is caused by mutations in the genes of potassium channels, which ensure the flow of potassium ions through cell membranes.
Symptoms of the disease:
- attacks of atrial fibrillation;
- attacks of ventricular tachycardia.
Study of families of patients with short interval syndromeQTshows that sudden deaths of relatives at a young and even infancy occurred in them due to atrial and ventricular fibrillation.
The most effective treatment for congenital short QT syndrome is the installation of a cardioverter-defibrillator.
Acquired form of pathology
- The cardiograph may reflect on the ECG a shortening of the QT interval during treatment with cardiac glycosides in case of overdose.
- Short QT syndrome can be caused by hypercalcemia (increased calcium levels in the blood), hyperkalemia (increased potassium levels in the blood), acidosis (a shift in the acid-base balance towards acidity) and some other diseases.
Therapy in both cases comes down to eliminating the causes of the short QT interval.
More:
How to decipher an ECG analysis, norms and deviations, pathologies and diagnostic principles
Lengthened syndrome QT interval attracts close attention as a factor in sudden cardiovascular death, first described by the French cardiologist Dessertin in 1966. It has been established that both congenital and acquired forms of Q-T interval prolongation are harbingers of fatal heart rhythm disturbances, which, in turn, lead to sudden death.
Long QT syndrome is a combination of a long QT interval on a standard ECG with life-threatening ventricular tachycardias (torsade de pointes - French pirouette). Paroxysms of ventricular tachycardia of the “pirouette” type are clinically manifested by episodes of dizziness, loss of consciousness and can result in ventricular fibrillation and sudden death.
The Q-T interval is the distance from the beginning of the QRS complex to the end of the T wave on the ECG curve. From the point of view of electrophysiology, it reflects the sum of the processes of depolarization (electrical excitation with a change in cell charge) and subsequent repolarization (restoration of electrical charge) of the ventricular myocardium. The duration of the QT interval depends on the heart rate and gender of the person. Normally, women have an average O-T interval slightly longer than men of the same age. U healthy people at rest there is only a slight variability in the repolarization processes, so the change in the Q-T interval is minimal. Prolongation of the Q-T interval is diagnosed if the average QT duration exceeds 0.44 s.
There are two most studied mechanisms of arrhythmias in long QT interval syndrome.
- The first is intracardiac disorders of myocardial repolarization, namely, increased sensitivity of the myocardium to the arrhythmogenic effect of adrenaline, norepinephrine and other synthetic adrenergic agonists. For example, it is a well-known fact Q-T extensions in acute myocardial ischemia and myocardial infarction.
- The second pathophysiological mechanism is an imbalance of sympathetic innervation (decreased right-sided sympathetic innervation due to weakness or underdevelopment of the right stellate ganglion) and other genetic abnormalities, especially against the background of congenital deafness. The most dangerous thing is that a person may not realize the existence of such a pathology for a long time and use drugs and their combinations that affect the Q-T interval.
DRUGS THAT PROLONGE THE QT INTERVAL
Prolongation of the QT interval may occur with such electrolyte disturbances, such as hypokalemia, hypocalcemia, hypomagnesemia. Such conditions occur under the influence of many factors, for example, with long-term use of diuretics, especially loop diuretics (furosemide), as well as strong laxatives. The development of ventricular tachycardia of the “pirouette” type is described against the background of prolongation of the Q-T interval with a fatal outcome in women who were on a low-protein diet for the purpose of losing weight and taking furosemide. The QT interval can also be lengthened when therapeutic doses of a number of drugs are used, in particular quinidine, procainamide, phenothiazine derivatives, etc. (see table). Prolongation of the electrical systole of the ventricles can be observed in case of poisoning with drugs and substances that have a cardiotoxic effect and slow down the processes of repolarization. For example, pachycarpine in toxic doses, a number of alkaloids that block the active transport of ions (K +, Mg 2+)
HEART AND MEDICINES
Recently, pharmacovigilance authorities in various countries, including the FDA (USA), Australia and Canada, as well as the domestic State Expert Center, have been drawing the attention of doctors and pharmacists to the danger of developing arrhythmias associated with taking well-known drugs, especially when they are prescribed in combination with other drugs. drugs that prolong the QT interval in the myocardial cell and have a ganglion-blocking effect. There are also cases of prolonged QT interval and fatal arrhythmias due to poisoning with barbiturates, organophosphate insecticides and mercury, and scorpion stings.
In case of arrhythmias or their threat, all drugs that can prolong the QT interval should be discontinued. Correction of serum electrolytes is necessary, especially potassium, calcium and magnesium. In some cases, this is sufficient to normalize the size and dispersion of the Q-T interval and prevent ventricular arrhythmias.
DOMPERIDONE AND SUDDEN CARDIAC DEATH
In December 2012, the Australian TGA published the results of pharmacoepidemiological studies indicating that the use of domperidone may be associated with a risk of serious ventricular premature beats or sudden cardiac death, particularly in patients taking the drug in daily doses. above 30 mg, and persons over 60 years of age. These findings confirmed the warnings issued by Canadian pharmacovigilance authorities in 2007. Therefore, domperidone should be avoided in the presence of cardiac arrhythmias, heart failure, coronary disease heart disease, myocardial infarction, heart defects, and in the absence of contraindications, start with the lowest dose. Domperidone, despite its over-the-counter status, should not be used in children. It is necessary to avoid joint use with CYP3A47 inhibitors that may increase its plasma level, such as itraconazole, amprenavir, atazanavir, fosamprenavir, indinavir, nelfinavir, ritonavir, saquinavir, diltiazem, verapamil, aprepitant, etc. In addition, domperidone is contraindicated for simultaneous use use with other drugs that prolong the QT interval.
AZITHROMYCIN AND OTHER MACROLIDE ANTIBIOTICS
Also, special care should be taken when prescribing macrolides, in particular azithromycin preparations, available in the form of tablets, capsules, powders for the preparation of oral suspensions and lyophilisate for injection solutions. The fact is that with regard to azithromycin, back in March 2013, the FDA informed about the risk of developing pathological changes electrical conduction of the heart, which can lead to potentially fatal arrhythmias. It must be remembered that the risk group consists of patients with a history of QT interval prolongation, hypokalemia or hypomagnesemia, bradycardia, as well as patients using class IA (quinidine, procainamide) and class III antiarrhythmic drugs (dofetilide, amiodarone, sotalol). Therefore, it is necessary to avoid the combined use of these drugs with azithromycin and other macrolides in order to avoid the development of potentially dangerous arrhythmias. When choosing an alternative antibacterial therapy For such patients, it should be remembered that other macrolide drugs, as well as fluoroquinolones, can cause prolongation of the QT interval.
Thus, when prescribing these drugs, it is necessary to determine the presence of contraindications and drug incompatibility. Patients taking these medications should stop taking all medications and seek immediate medical attention if they experience heart failure or abnormal heart rate or rhythm (especially palpitations - tachycardia), dizziness, loss of consciousness, or seizures. .
Medicines that can prolong the QT interval
| Pharmacological group | Drugs |
| Antiarrhythmic drugs | Class IA - quinidine, procainamide, disopyramide Class 1C - encainide, flecainide Class III - amiodarone, sotalol, sematilide |
| Psychotropic (psycholeptic) drugs | thioridazine, trifluoperazine, haloperidol, citalopram, escitalopram, etc. |
| Local anesthetics | lidocaine |
| Tricyclic antidepressants | imipramine, amitriptyline, clomipramine, doxepin, etc. |
| Antihistamines | terfenadine, astemizole |
| Antibiotics and chemotherapeutic agents | erythromycin, azithromycin, clarithromycin, spiramycin and other macrolides, pentamidine, sulfamethoxazole (trimethoprim), fluoroquinolones |
| Antifungals (azoles) | ketoconazole, fluconazole, itraconazole, voriconazole |
| Diuretics | thiazide diuretics, loop diuretics (furosemide, torsemide, ethacrynic acid), etc., except for potassium-sparing ones |
| Peristalsis stimulants (propulsants) | domperidone |
Long QT syndrome (LQT) is a congenital or acquired cardiac pathology, which is characterized by prolongation of the corresponding interval by , the presence of repeated syncope and a high risk of sudden death due to the development of malignant arrhythmias. The congenital variant of the syndrome occurs in all ethnic groups with a frequency of 1:2000 to 1:2500. Females suffer from it somewhat more often. The prevalence of the acquired syndrome ranges from 2.5 to 4 cases per 1 million people. In our article we will look at why LQT occurs, what symptoms it causes, why it is dangerous, and how to treat it.
The disease has been known since the end of the 19th century, when the observation of a girl with congenital deafness and frequent fainting that occurs with strong excitement was first described in the medical literature (1856, Meissner). Later, his electrocardiographic picture was revealed (1953, Moller). Currently studying this syndrome and searching for effective methods his treatment is ongoing.
Causes of congenital syndrome
Long QT syndrome is characterized by corresponding changes in the electrocardiogram.The hereditary variant of the syndrome is based on mutations in genes encoding the functions of protein molecules of ion channels in the heart muscle. Currently, more than 180 such mutations are known in 7 genes, which are located on chromosomes 3, 7, 11 and 21. In most cases, they disrupt the functioning of potassium and sodium channels, less often - calcium channels and specific building proteins. This leads to an increase in the duration of the action potential in cardiomyocytes, initiating the appearance of ventricular tachycardia of the “pirouette” type, which can develop into.
The processes of depolarization and repolarization that occur as a result of the movement of electrolytes into the cell from the extracellular space and back are reflected on the ECG by the QT interval, which lengthens with this pathology.
In clinical practice, there are 3 main variants of hereditary syndrome:
- Romano-Ward (characterized by isolated QT prolongation, transmitted from parents with dominant genes);
- Jervell-Lange-Nielsen (inherited in an autosomal recessive manner and combined with congenital deafness);
- autosomal dominant variant with extracardiac manifestations.
The last of them can manifest itself in the form:
- Andersen-Tawil syndrome (QT prolongation combined with pronounced U-wave, ventricular tachycardia, developmental abnormalities skeletal system, hyper- or hypokalemic periodic paralysis);
- Timothy syndrome (syndactyly, congenital cardiac anomalies, various conduction disorders, extremely high risk of sudden death).
Acquired form
Previously, it was believed that the occurrence of acquired LQT syndrome is associated with a disruption in the functioning of ion channels, which is caused not by a mutation, but by the influence of some external or internal factors. This statement is true, but it has been proven that it contributes to the development pathological process genetic defect. At the same time, the acquired syndrome is difficult to distinguish from congenital pathology, since they have much in common. Usually, this pathology goes unnoticed for a long time and manifests itself in adverse conditions, for example, under the influence of stress or physical activity. Factors that contribute to prolongation of the QT interval include:
- taking medications (we’ll look at which ones below);
- electrolyte disturbances (lack of potassium, sodium, magnesium);
- heart rhythm disturbances;
- diseases of the nervous system (trauma, infection, tumor);
- change in hormonal status (pathology thyroid gland or adrenal glands)
- alcoholism;
- starvation, etc.
Of particular danger is the exposure of a susceptible organism to several risk factors.
Groups of drugs that can affect the length of the QT interval
Due to the fact that the LQT syndrome can be caused by the direct effect of drugs, and their cancellation often leads to the normalization of all indicators, we will consider in more detail which medicines can change the length of the QT interval:
- (amiodarone, procainamide, sotalol, propafenone, disopyramide);
- antibiotics (erythromycin, spiramycin, clarithromycin, isoniazid);
- (ebastine, astemizole);
- anesthetics;
- antimycotics (fluconazole, ketoconazole);
- antitumor drugs;
- psychotropic drugs (droperidol, amitriptyline);
- (indapamide), etc.
They should not be prescribed to persons who already have a prolongation of this interval. And with a late debut of the disease, their role as a provoking factor is necessarily excluded.
Clinical manifestations
This disease is characterized by attacks sudden loss consciousness. The clinical picture of the syndrome is characterized by polymorphism of symptoms. Their severity can vary from mild dizziness to loss of consciousness and sudden death. Sometimes the latter can act as the first sign of illness. The most typical manifestations of this pathology are:
- bouts of loss of consciousness;
- congenital deafness;
- cases of sudden death in the family;
- changes on the electrocardiogram (QT more than 450 ms, T wave alternation, ventricular tachycardia of the "pirouette" type,).
With congenital variants of the syndrome, other symptoms characteristic only of it can be detected.
It should be noted that syncopal conditions in this pathology have their own characteristics:
- occur against a background of stress, under the influence of strong sound stimuli (alarm clock, phone call), physical activity, sports (swimming, diving), during a sharp awakening from a night's sleep, in women - after childbirth;
- the presence of symptoms preceding loss of consciousness (severe weakness, ringing in the ears, darkening of the eyes, feeling of heaviness in the chest);
- rapid restoration of consciousness with a favorable outcome;
- absence of amnesia and personality changes (as with epilepsy).
Sometimes loss of consciousness may be accompanied by convulsions and involuntary urination. In such cases, differential diagnosis with epileptic seizures is carried out.
The course of the pathological process in each patient may have certain differences. It depends both on the genotype and on living conditions. The following options are considered the most common:
- syncope occurring against the background of prolongation of the QT interval;
- isolated prolongation of this interval;
- syncope in the absence of changes on the ECG;
- complete absence of symptoms (high risk without phenotypic manifestations of the disease).
The most unfavorable course is complicated by the development of ventricular fibrillation and cardiac arrest.
With congenital variants of the disease, fainting appears in childhood(5-15 years). Moreover, their occurrence in children preschool age– a prognostically unfavorable sign. And paroxysm of ventricular tachycardia, which required treatment emergency care, increases the likelihood of a second cardiac arrest in the near future by 10 times.
Patients with asymptomatic long QT syndrome may be unaware of their diagnosis and have a normal life expectancy, but pass the mutation on to their children. This trend is observed very often.
Diagnostic principles
Diagnosis of the syndrome is based on clinical findings and electrocardiography results. Holter monitoring provides additional information to the doctor.
Given that it is not always easy to make a diagnosis, large and small diagnostic criteria. The latter include:
- lack of hearing from birth;
- variability of the T wave in different leads (on the electrocardiogram);
- disruption of the processes of repolarization of the ventricular myocardium;
- low heart rate.
Among the major criteria are:
- prolongation of the corrected QT interval more than 450 ms at rest;
- episodes of loss of consciousness;
- cases of illness in the family.
The diagnosis is considered reliable if two major or one major and two minor criteria are present.
Treatment
If other therapeutic measures are ineffective, the patient needs implantation of a cardioverter-defibrillator. The main focus of treatment for such patients is the prevention of malignant arrhythmias and cardiac arrest.
All persons with prolonged QT interval should avoid:
- stressful situations;
- doing sports;
- heavy physical activity;
- taking medications that increase the length of this interval.
Medications for this syndrome are usually prescribed:
- β-blockers;
- magnesium and potassium preparations;
- mexiletine or flecainide (in low doses).
If ineffective conservative therapy resort to sympathetic denervation or implantation of a cardioverter-defibrillator. The latter is especially important in patients at high risk of sudden cardiac death and undergoing resuscitation.
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QT interval(electrical ventricular systole) - the time from the beginning of the QRT complex to the end of the T wave. The QT interval depends on gender, age (in children the interval is shorter), and heart rate.
Normally, the QT interval is 0.35-0.44 s (17.5-22 cells). The QT interval is a constant value for the rhythm frequency (separately for men and women). There are special tables that present QT standards for a given gender and rhythm frequency. If the result on the ECG exceeds 0.05 seconds (2.5 cells) of the table value, then they speak of prolongation of the electrical systole of the ventricles, which is characteristic feature cardiosclerosis.
Using Bazett's formula, you can determine whether the QT interval in a given patient is normal or pathological (the QT interval is considered pathological if the value exceeds 0.42):
QT = QT(measured by ECG, sec) / √(R-R)(interval, measured by ECG, between two adjacent R waves, sec)
For example, the QT value calculated for the cardiogram presented on the right (calculation using standard lead II:
- The QT interval is 17 cells (0.34 seconds).
- The distance between two R waves is 46 cells (0.92 seconds).
- Square root of 0.92 = 0.96.
- QT = 0.34/0.96 = 0.35
