STUDY - Technical - New Dacian's Medicine
Syncope
Translation Draft
Even though I have treated syncopa predominantly, so far, I have changed the title of the post only now, at the end, because I think it is only now that it matters to stress that this is what I will "talk" about. So...
The first "delimitation" of syncopes is done according to the type of onset. Time localization and onset type can help determine the cause. The syncope that begins in seconds is very likely due to orthostatic tension, suddenly installed atrioventricular block, asistola or ventricular tachycardia.
When symptoms appear progressively within a period of several minutes, hyperventilation or hypoglycaemia should be taken into account. Installation of syncope during or immediately after exertion, suggests aortic stenosis, idiopathic hypertrophic subaortic stenosis or extreme bradycardia and, in elderly patients, orthostatic hypotension.
Effort syncope is occasionally found in people with aortic insufficiency. In patients with cardiac arrest or ventricular fibrillation, loss of consciousness occurs 8 to 10 seconds later and is frequently followed by short clonic muscle contractions.
Important is also the position at the start of the attack. Epilepsy and syncopal attacks due to hypoglycaemia, hyperventilation or cardiac block are likely positional independent. Lipotimia associated with a decrease in blood pressure and ectopic tachycardia usually occurs only in a sitting or orthostatic position, while loss of consciousness resulting from orthostatic hypotension occurs rapidly after changing position from clinostatism to orthostatism.
Let's see now what the associated symptoms are! Symptoms like palpitations may be present when attacks are due to anxiety or hyperventilation, ectopic tachycardia or hypoglycaemia. Feelings of numbness and tingling in the hands and face frequently accompany hyperventilation.
True seizures during an attack may occasionally occur in the heart block, asystole or ventricular tachycardia. In patients with recurrent syncope trying to reproduce an attack is useful for diagnosis.
Symptoms induced by hyperventilation can be easily reproduced, asking the subject to breathe quickly and deeply for 2 to 3 minutes. Anxiety attacks induced by hyperventilation tend to be reduced when the patient learns that symptoms can be reproduced or removed voluntarily, simply, only by breathing control.
Other situations in which the diagnosis is frequently clarified by the reproduction of the attack are orthostatic hypotension and orthostatic tachycardia (observation of the frequency of the pulse, blood pressure and symptoms in the clino and orthostatic position) and syncope by cough (pri induction of the Valsalva maneuver).
In all these situations, the main element is not the production of symptoms (the procedures mentioned frequently induce symptoms in healthy people) but if the exact characters of the symptoms that occur in the spontaneous attack are reproduced by the artificially induced one. Continuous ECG monitoring is essential in identifying an arrhythmia responsible for syncopal episodes, especially in patients with recurrent recurrent symptoms. Monitoring is diagnostic if it shows episodes of asystole, extreme bradycardia or tachyarrhythmia.
In the case of recurrent syncopes of unknown origin, in which ECG monitoring is equivocal and there is a underlying heart disease, especially ischemic and myocardial infarction in the past, the use of electrophysiological intracardiac techniques with programmed stimulation may be useful in detecting heart rhythm disorders and in establishing effective treatment.
During stimulation, up to two-thirds of these patients may experience fast-paced ventricular tachycardia. Sometimes electrophysiological studies help to identify significant driving delays of the His beam or sinus node disease.
The diagnostic area of intracardiac electrophysiological testing is lower in patients with non-ischemic heart disease and in patients with structurally normal hearts than in patients with ischemic heart disease. Recently, the medium signal electrocardiogram has proven useful in identifying patients with unexplained syncopes where there is a risk of ventricular tachycardia induced in electrophysiological testing.
The upside-down table test is a useful challenge technique for the diagnosis of vasodrepressor syncope. Vertical inclination at a maximum of 60 to 70 degrees usually precipitates symptomatic hypotension or syncope in 10 to 30 minutes in patients with this syndrome.
In normal subjects, passive inclination at 60 degrees produces a slight decrease in systolic blood pressure and an increase in diastolic blood pressure and heart rate. Recently, the tilted table test has been used in conjunction with electrophysiological testing to assess the efficacy of prophylactic pacing in selected patients with vasodrepressor syncope and to assess the influence of the position on the hemodynamic consequences of tachyarrhythmias. Nitroglycerin administered sublingually during the tilted table test may expose certain causes of vasovagal-induced syncope.
Syncopa should be distinguished from disorders of brain function caused by seizures. A seizure can occur day or night, regardless of the patient's position while syncope rarely occurs when the patient is in clinostatism, the only common exception being the Stokes-Adams crisis.
The patient's color may not change into seizures, although cyanosis may occur, pallor being an early and invariable feature in all types of syncope, with the exception of chronic orthostatic hypotension and hysteria and precedes loss of consciousness.
Seizures are often announced by an aura, which is determined by a focal discharge of the convulsion and therefore has the significance of localization in the brain. Aura is usually followed by a rapid return to normal or loss of consciousness while the onset of syncope is usually slow and without aura. Falling hitting is common in a seizure and rare for syncope for the reason that only in convulsions the protective reflexes are instantly abolished.
Tonic-convulsive movements are a characteristic of seizures and usually do not occur in syncope although episodes of lipotimia may be accompanied by a brief tonic-clonic convulsional activity. The upward deflection of the eyeballs occurs under both conditions.
The period of unconsciousness tends to be longer in convulsions than in syncope and urinary incontinence is common in seizures and rare in syncope. Regaining consciousness is prompt in syncope and slow after convulsion. mental confusion, headache and drowsiness are frequent sequelae of seizures and physical weakness with preserved sensors characterizes the presincopal state.
Repeated ranges of loss of consciousness in a young person, with a frequency of several pores per day or per month, are more suggestive for epilepsy than for syncope. Electroencephalogram (EEG) may be useful in differentiating syncopes from epileptic seizures. In the intervals between epileptic seizures, it can show abnormalities of varying degrees up to 80% of patients. In the interval between syncopal attacks, the EEG must be normal.
The possibility of intervention by treatment is the end of this post. Most of the time, loss of consciousness is relatively benign. In addressing these patients who have fainted, it is necessary first to identify which causes fainting as a therapeutic emergency, between them being massive internal bleeding and myocardial infarction, which can be painless, and cardiac arrhythmias.
In the elderly, a sudden lipotimia, without obvious causes, must raise the suspicion of a complete cardiac block or tachyartimia, despite negative data obtained when examining the patient.
Patients caught in the early stages of a loss of consciousness or after its loss should be placed in a position that allows maximum brain flow, i.e. with their heads bent between the knees if they are in a sitting position, or preferably in clinostatism. Tight clothing and other constrictions should be undone and the head turned to one side so that the tongue is not swallowed, blocking the airways.
Peripheral stimulation, such as splashing or moistening the face and neck with cold water or applying cold, moist towels, is useful. If the temperature is subnormal, the body should be covered with a warm blanket. Because vomiting is common, aspiration should be prevented. The head should be turned to one side and nothing will be administered orally until the patient has regained consciousness. The patient will not be allowed to stand up until the feeling of physical weakness has passed and will be watched closely for a few minutes after lifting.
Due to the critical role of beta-adrenergic stimulation and hypercontractility in a vasovagal syncopal syndrome, effective prophylaxis can usually be achieved by using beta-adrenergic receptor blockers or with dysopiramide.
Because vasovagal syncope usually occurs in patients with normal left ventricular systolic function, the use of these agents is usually well tolerated. other pharmacological agents that have been used to treat this type of syncope include theophylline, scopolamine and ephedrine.
The pacemaker alone is rarely indicated or effective in preventing this type of syncope, but may be necessary for a small majority of patients in whom deep bradycardia or asistola predominates over peripheral vasodilation as the primary mechanism of syncope.
Prevention of loss of consciousness depends on the mechanisms involved. In the usual vasovagal syncope of adolescents, which tends to occur during periods of emotional stimulation, fatigue, hunger, etc. it is sufficient for the patient to be advised to avoid such situations. In orthostatic hypotension, the patient should be prevented from suddenly getting out of bed.
Instead, they need to move your legs for a few seconds and then stand at the edge of the bed and make sure they don't feel mild or vertigo before they start walking. It is often useful to put on foot at the head of the bed using pieces of wood with a height of 20 to 30 cm and to wear a comfortable elastic abdominal belt and elastic stockings. The distinction made between the different types of orthostatic hypotension has therapeutic significance (with special reference to the drugs administered).
Treatment of carotid sinus syncope involves, above all, training the patient on measures that reduce the risk of a fall. The collars must be wide and the patient must be taught to turn around with the whole body, rather than just with the head, when looking to the side. Drugs of the class of atropine or ephedrine should be used during attacks. Similarly, the treatment of various cardiac arrhythmias that may induce syncope, the treatment of hypoglycaemia, etc. should be considered.
The major risk of loss of consciousness in most elderly people is not background disease, but a fracture or other type of trauma caused by the fall. Therefore, patients with recurrent syncopes should cover the bathroom floor and bathtub with soft, rubbery materials, and should carpet as much as possible in their dwelling. Very important is the space between the bed and the bathroom, because syncopes are common in older people who go from bed to toilet.
Outdoor walks should be made on softer ground rather than hard surfaces and the patient should avoid standing for a long time, a situation that is more likely to induce an attack than walking.
And, that's enough! I'll move on to dizziness and vertigo!
Even though I have treated syncopa predominantly, so far, I have changed the title of the post only now, at the end, because I think it is only now that it matters to stress that this is what I will "talk" about. So...
The first "delimitation" of syncopes is done according to the type of onset. Time localization and onset type can help determine the cause. The syncope that begins in seconds is very likely due to orthostatic tension, suddenly installed atrioventricular block, asistola or ventricular tachycardia.
When symptoms appear progressively within a period of several minutes, hyperventilation or hypoglycaemia should be taken into account. Installation of syncope during or immediately after exertion, suggests aortic stenosis, idiopathic hypertrophic subaortic stenosis or extreme bradycardia and, in elderly patients, orthostatic hypotension.
Effort syncope is occasionally found in people with aortic insufficiency. In patients with cardiac arrest or ventricular fibrillation, loss of consciousness occurs 8 to 10 seconds later and is frequently followed by short clonic muscle contractions.
Important is also the position at the start of the attack. Epilepsy and syncopal attacks due to hypoglycaemia, hyperventilation or cardiac block are likely positional independent. Lipotimia associated with a decrease in blood pressure and ectopic tachycardia usually occurs only in a sitting or orthostatic position, while loss of consciousness resulting from orthostatic hypotension occurs rapidly after changing position from clinostatism to orthostatism.
Let's see now what the associated symptoms are! Symptoms like palpitations may be present when attacks are due to anxiety or hyperventilation, ectopic tachycardia or hypoglycaemia. Feelings of numbness and tingling in the hands and face frequently accompany hyperventilation.
True seizures during an attack may occasionally occur in the heart block, asystole or ventricular tachycardia. In patients with recurrent syncope trying to reproduce an attack is useful for diagnosis.
Symptoms induced by hyperventilation can be easily reproduced, asking the subject to breathe quickly and deeply for 2 to 3 minutes. Anxiety attacks induced by hyperventilation tend to be reduced when the patient learns that symptoms can be reproduced or removed voluntarily, simply, only by breathing control.
Other situations in which the diagnosis is frequently clarified by the reproduction of the attack are orthostatic hypotension and orthostatic tachycardia (observation of the frequency of the pulse, blood pressure and symptoms in the clino and orthostatic position) and syncope by cough (pri induction of the Valsalva maneuver).
In all these situations, the main element is not the production of symptoms (the procedures mentioned frequently induce symptoms in healthy people) but if the exact characters of the symptoms that occur in the spontaneous attack are reproduced by the artificially induced one. Continuous ECG monitoring is essential in identifying an arrhythmia responsible for syncopal episodes, especially in patients with recurrent recurrent symptoms. Monitoring is diagnostic if it shows episodes of asystole, extreme bradycardia or tachyarrhythmia.
In the case of recurrent syncopes of unknown origin, in which ECG monitoring is equivocal and there is a underlying heart disease, especially ischemic and myocardial infarction in the past, the use of electrophysiological intracardiac techniques with programmed stimulation may be useful in detecting heart rhythm disorders and in establishing effective treatment.
During stimulation, up to two-thirds of these patients may experience fast-paced ventricular tachycardia. Sometimes electrophysiological studies help to identify significant driving delays of the His beam or sinus node disease.
The diagnostic area of intracardiac electrophysiological testing is lower in patients with non-ischemic heart disease and in patients with structurally normal hearts than in patients with ischemic heart disease. Recently, the medium signal electrocardiogram has proven useful in identifying patients with unexplained syncopes where there is a risk of ventricular tachycardia induced in electrophysiological testing.
The upside-down table test is a useful challenge technique for the diagnosis of vasodrepressor syncope. Vertical inclination at a maximum of 60 to 70 degrees usually precipitates symptomatic hypotension or syncope in 10 to 30 minutes in patients with this syndrome.
In normal subjects, passive inclination at 60 degrees produces a slight decrease in systolic blood pressure and an increase in diastolic blood pressure and heart rate. Recently, the tilted table test has been used in conjunction with electrophysiological testing to assess the efficacy of prophylactic pacing in selected patients with vasodrepressor syncope and to assess the influence of the position on the hemodynamic consequences of tachyarrhythmias. Nitroglycerin administered sublingually during the tilted table test may expose certain causes of vasovagal-induced syncope.
Syncopa should be distinguished from disorders of brain function caused by seizures. A seizure can occur day or night, regardless of the patient's position while syncope rarely occurs when the patient is in clinostatism, the only common exception being the Stokes-Adams crisis.
The patient's color may not change into seizures, although cyanosis may occur, pallor being an early and invariable feature in all types of syncope, with the exception of chronic orthostatic hypotension and hysteria and precedes loss of consciousness.
Seizures are often announced by an aura, which is determined by a focal discharge of the convulsion and therefore has the significance of localization in the brain. Aura is usually followed by a rapid return to normal or loss of consciousness while the onset of syncope is usually slow and without aura. Falling hitting is common in a seizure and rare for syncope for the reason that only in convulsions the protective reflexes are instantly abolished.
Tonic-convulsive movements are a characteristic of seizures and usually do not occur in syncope although episodes of lipotimia may be accompanied by a brief tonic-clonic convulsional activity. The upward deflection of the eyeballs occurs under both conditions.
The period of unconsciousness tends to be longer in convulsions than in syncope and urinary incontinence is common in seizures and rare in syncope. Regaining consciousness is prompt in syncope and slow after convulsion. mental confusion, headache and drowsiness are frequent sequelae of seizures and physical weakness with preserved sensors characterizes the presincopal state.
Repeated ranges of loss of consciousness in a young person, with a frequency of several pores per day or per month, are more suggestive for epilepsy than for syncope. Electroencephalogram (EEG) may be useful in differentiating syncopes from epileptic seizures. In the intervals between epileptic seizures, it can show abnormalities of varying degrees up to 80% of patients. In the interval between syncopal attacks, the EEG must be normal.
The possibility of intervention by treatment is the end of this post. Most of the time, loss of consciousness is relatively benign. In addressing these patients who have fainted, it is necessary first to identify which causes fainting as a therapeutic emergency, between them being massive internal bleeding and myocardial infarction, which can be painless, and cardiac arrhythmias.
In the elderly, a sudden lipotimia, without obvious causes, must raise the suspicion of a complete cardiac block or tachyartimia, despite negative data obtained when examining the patient.
Patients caught in the early stages of a loss of consciousness or after its loss should be placed in a position that allows maximum brain flow, i.e. with their heads bent between the knees if they are in a sitting position, or preferably in clinostatism. Tight clothing and other constrictions should be undone and the head turned to one side so that the tongue is not swallowed, blocking the airways.
Peripheral stimulation, such as splashing or moistening the face and neck with cold water or applying cold, moist towels, is useful. If the temperature is subnormal, the body should be covered with a warm blanket. Because vomiting is common, aspiration should be prevented. The head should be turned to one side and nothing will be administered orally until the patient has regained consciousness. The patient will not be allowed to stand up until the feeling of physical weakness has passed and will be watched closely for a few minutes after lifting.
Due to the critical role of beta-adrenergic stimulation and hypercontractility in a vasovagal syncopal syndrome, effective prophylaxis can usually be achieved by using beta-adrenergic receptor blockers or with dysopiramide.
Because vasovagal syncope usually occurs in patients with normal left ventricular systolic function, the use of these agents is usually well tolerated. other pharmacological agents that have been used to treat this type of syncope include theophylline, scopolamine and ephedrine.
The pacemaker alone is rarely indicated or effective in preventing this type of syncope, but may be necessary for a small majority of patients in whom deep bradycardia or asistola predominates over peripheral vasodilation as the primary mechanism of syncope.
Prevention of loss of consciousness depends on the mechanisms involved. In the usual vasovagal syncope of adolescents, which tends to occur during periods of emotional stimulation, fatigue, hunger, etc. it is sufficient for the patient to be advised to avoid such situations. In orthostatic hypotension, the patient should be prevented from suddenly getting out of bed.
Instead, they need to move your legs for a few seconds and then stand at the edge of the bed and make sure they don't feel mild or vertigo before they start walking. It is often useful to put on foot at the head of the bed using pieces of wood with a height of 20 to 30 cm and to wear a comfortable elastic abdominal belt and elastic stockings. The distinction made between the different types of orthostatic hypotension has therapeutic significance (with special reference to the drugs administered).
Treatment of carotid sinus syncope involves, above all, training the patient on measures that reduce the risk of a fall. The collars must be wide and the patient must be taught to turn around with the whole body, rather than just with the head, when looking to the side. Drugs of the class of atropine or ephedrine should be used during attacks. Similarly, the treatment of various cardiac arrhythmias that may induce syncope, the treatment of hypoglycaemia, etc. should be considered.
The major risk of loss of consciousness in most elderly people is not background disease, but a fracture or other type of trauma caused by the fall. Therefore, patients with recurrent syncopes should cover the bathroom floor and bathtub with soft, rubbery materials, and should carpet as much as possible in their dwelling. Very important is the space between the bed and the bathroom, because syncopes are common in older people who go from bed to toilet.
Outdoor walks should be made on softer ground rather than hard surfaces and the patient should avoid standing for a long time, a situation that is more likely to induce an attack than walking.
And, that's enough! I'll move on to dizziness and vertigo!
A
soothing Sunday, full of faith, love and gratitude!
Dorin, Merticaru