STUDY - Technical - New Dacian's Medicine
Nervous
system disorders
(2)
Translation Draft
I'll continue with the cardiac syncope. This occurs through a sudden decrease in cardiac output most commonly caused by a cardiac arrhythmia. In normal individuals, low ventricular frequencies, but over 35 to 40 beats per minute, as well as fast ones, but not exceeding 180 beats per minute, do not reduce cerebral blood flow, especially if the person is in clinostatism.
However, variations in heart rate outside these limits may affect brain circulation and function. Orthostatism, cerebrovascular diseases, anemia and coronary, myocardial or valvular diseases all reduce tolerance to frequency variations.
Of these, high-grade atrioventricular block is commonly associated with lipotimia (Stokes-Adams-Morgagnani syndrome). In patients experiencing these seizures, the block may be permanent or intermittent. When the block is high or complete and a lower-block pacemaker does not come into operation or works at too low a frequency, syncope occurs, with seizures occurring suddenly, usually without premonitoring symptoms.
If a cardiac stop persists for more than 8 to 10 seconds, the patient becomes pale, unconscious and may experience several clonic contractions. In a prolonged asystole appear cyanosis, irregular breathing, fixed pupils, incontinence, and bilateral Babinski signs (extension of the thumb outwards, or all fingers in the fan - bilaterally, in both hands) may be present.
While returning after a Stokes-Adams seizure is usually rapid and complete, sometimes prolonged confusion and neurological signs due to cerebral ischemia may sometimes occur, occasionally resulting in permanent impairment of mental functions, although neurological signs of outbreak are rare.
Patients usually don't remind you of presincopal symptoms. Cardiac syncopes of this type can be repeated several times over the course of a day. The period of asystole may be followed by tachycardia or ventricular fibrillation, causing prolonged coma or sudden death.
Another cause is disorders of sinus node automatism or synoatrial conduction that can cause asystole or bradycardia of sufficient severity to cause a presincope or syncope.
These disorders are most commonly detected by ECG monitoring. Data to suggest diagnosis of sinus node disease include symptomatic sinus breaks (more than 3 seconds) resulting from sinus stops or synoatrial block and unexplained severe sinus bradycardia (less than 40 beats per minute).
Bradycardia-tachycardia syndrome is a common form of sinus node dysfunction, in which syncope generally occurs as a result of prolonged sinus breaks, following the end of ventricular paroxysmal tachycardia. In patients with syncope and suspicion of sinus node disease, where diagnosis is not established by ECG monitoring, electrophysiological tests may be useful in highlighting diagnostic abnormalities.
I'm going to tackle tachyarrhythmias now. Paroxysmal tachyarrhythmias can also cause presincope and syncope as a result of sudden reduction in heart rate. The importance of tachycardia-induced hypotension depends on the interaction of several variables, including the frequency and mechanism of tachycardia, the type and severity of the patient's underlying heart disease, the position and level of activity of the patient at the onset of tachycardia, the sensitivity of tachycardia to endogenous catecholamines and the integrity of the autonomic compensatory reflexes.
Supraventricular tachyarrhythmias are not commonly associated with syncope. However, even in the absence of structural heart disease, extremely high heart frequencies can affect filling and heart rate, enough to cause loss of consciousness.
These tachycardias are most commonly represented by the appearance of paroxysmal atrial flutter, atrial fibrillation or re-entry to the atrioventricular node (AV) or accessory pathways that short-circuit part or all of the atrioventricular conduction system (AV).
Patients with Wolff-Parkinson-White syndrome are at increased risk for several forms of supraventricular tachycardia, the most dangerous of which is atrial fibrillation with rapid anterograde conduction to the ventricles through an accessory atrioventricular conduction pathway and which can lead to syncope or, more rarely, sudden death.
When it is suspected that abnormal driving through an AV accessor shunt or a modal AV reentry rate is the cause of syncope, the electrophysiological study is indicated to define the mechanism and pathway of tachycardia and to facilitate the choice of an effective therapeutic intervention.
Paroxysmal ventricular tachycardia is a relatively common cause of syncopes, especially patients with organic heart disease. Typically, tachycardias are rapid and associated with sudden loss of consciousness, without premonitoring symptoms.
Usually, the patient does not accuse palpitations and the return after an episode is rapid and complete, without residual cardiac or neurological sequelae. The appearance of an unexplained syncope in a patient with organic heart disease is an episode with potential for severe prognosis and deserves careful evaluation. The presence on ECG of pathological Q-waves indicating a previous transmural myocardial infarction is commonly associated with ventricular tachycardia as the etiology of syncopes in patients with ischemic heart disease.
Other forms of heart disease, such as hypertrophic or dilatative cardiomyopathy, right ventricle dysplasia and QT interval syndrome, are also commonly associated with paroxysmal ventricular tachycardia and syncope.
The reflex heart block is given by irritation of the vagus nerve and is present in the forms of cardiac syncope. Examples of this phenomenon have been observed in some patients with esophageal diverticules, mediastinal tumors, cholecyst damage, carotid sinus disease, glosopharyngeal neuralgia and pleural and pulmonary irritation. In these circumstances, reflex bradycardia is more commonly of the synoatrial type than atrioventricular.
Other causes of syncope would be acute myocardial infarction, especially if associated with cardiogenic shock. Aortic stenosis frequently causes syncope at exertion, most often by limiting cardiac flow under conditions of peripheral vasodilation, with resulting myocardial and cerebral ischemia and sometimes arrhythmias. Idiopathic hypertrophic subaortic stenosis can also cause ssyncopine of exertion by accentuating obstruction or by ventricular arrhythmias or both.
In primary pulmonary hypertension, a relatively fixed cardiac output and bouts of right ventricular failure may be associated with syncope. However, vagal reflexes may be involved in this situation, as well as in syncopes that occur in the pulmonary embolism.
Spherical valvular trombiins in the left atrium, left atrial mixoma, thrombosis or dysfunction of valvular prostheses can cause sudden mechanical circulatory obstruction and syncope. The congenital heart defect most commonly responsible for syncope is tetralogy of Fallot, a condition in which systemic vasodilation, probably associated with infundibular spasm, greatly increases the risk of right-left shunt and produces arterial hypoxia that can lead to syncope.
The next syncope is that of the carotid sinus. The carotid sinus is normally sensitive to mechanical stimuli and gives rise to sensory impulses transmitted through the Herring nerve, a branch of the glossopharynx nerve, to the brain stem.
Massage of one or both carotid sinuses, especially in the elderly, produces a reflex slowdown in heart rate (sinus bradycardia, sinus stop or even atrioventricular block), the so-called vagal response and a decrease in blood pressure without a decrease in heart rate, the so-called depressive type response.
Both carotid responses can coexist. Syncope due to the sensitivity of the carotid sinus is extremely unusual and is said to be triggered by turning the head to one side, by a tight collar or by shaving in the sinus area. In the case of a patient with lipotimia at the compression of a carotid sinus, it is important to make a differential diagnosis between a benign damage (hypersensitivity of the carotid sinus) and one with much more serious consequences such as contralateral carotid artery stenosis. Thus, carotid compression is a risky manoeuvre that can lead to cerebral ischemia.
Next comes the glosopharyngeal neuralgia. This painful condition can induce reflex lipotimia. The sequence is always of pain followed by syncope. Pain is localized to the jaw, at the base of the tongue, in the pharynx or larynx, the tonsil area and the ear.
Cardiovascular effects are attribution of stimulation of the dorsal motor nucleus of the vagus through collateral fibers from the nucleus of the solitary tract. Treatment of neuralgia (with carbamazepine) is commonly effective for syncope as well as for pain.
There's also syncope through coughing. It is a rare situation that follows a paroxysm of cough, usually in chronic bronchitis. After a strong cough, the patient suddenly has weakness and temporarily loses consciousness. Cough increases intraoracic pressure and increased pressure is transmitted through the large veins to the intracranial compartment, causing increased intracranial pressure and secondary decreasein brain flow. Syncope occurs at a low critical blood flow.
And, I'm going to finish the syncopes with the mechanical presentation, which is rare and occurs in otherwise normal teenagers. The challenge maneuver is the simultaneous extension of the neck and the stretching of the upper limb, the mechanism appears to be compression of the vertebral arteries in the neck.
Differential diagnosis is made in relation to several manifestations. The most appropriate is the one achieved against anxiety attacks and hyperventilation syndrome. Anxiety, as it occurs in panic attacks, is commonly interpreted as a feeling of lowblood or dizziness, without loss of consciousness. These symptoms are not accompanied by facial pallor and are not improved by clinostatism.
Diagnosis is made on the basis of associated symptoms and the attack can be reproduced by hyperventilation. Hyperventilation leads to hypocapnia, alkalosis, increased cerebrovascular resistance and decreased cerebral blood flow. The release of epinephrine in anxiety states also contributes to symptoms.
Another landmark is hypoglycaemia. Severe hypoglycaemia is usually the result of a serious condition, such as a tumor of the Langerhans Islands, advanced adrenal disease, pituitary gland or liver disease, including excessive insulin administration (this leads to confusion or even loss of consciousness). Mild hypoglycaemia is often reactive, occurring 2 to 5 hours after eating and is not usually associated with a disorder of consciousness.
Acute bleeding, usually in the gastrointestinal tract, is an occasional cause of syncope. In the absence of pain and hematemesis, the cause of weakness, liptomy or even loss of consciousness may remain obscure until the appearance of melena.
Transient cerebral ischemic attack (AIT) occurs in patients with atherosclerotic stenosis, occlusions or embolisms of the large arteries of the brain. Symptoms are varied and sudden fall seizures can mimic syncope. Isolated loss of consciousness is rare.
And in the end, we shouldn't forget hysterical lypothymia. The attack is not usually preceded by any outward manifestation for anxiety. the absence of any change in the pulse, blood pressure or color of the skin and mucous membranes differentiates it from vasopressor lypotimia.
For tomorrow I think I'll complete the syncopes and be able to tackle dizziness and vertigo.
I'll continue with the cardiac syncope. This occurs through a sudden decrease in cardiac output most commonly caused by a cardiac arrhythmia. In normal individuals, low ventricular frequencies, but over 35 to 40 beats per minute, as well as fast ones, but not exceeding 180 beats per minute, do not reduce cerebral blood flow, especially if the person is in clinostatism.
However, variations in heart rate outside these limits may affect brain circulation and function. Orthostatism, cerebrovascular diseases, anemia and coronary, myocardial or valvular diseases all reduce tolerance to frequency variations.
Of these, high-grade atrioventricular block is commonly associated with lipotimia (Stokes-Adams-Morgagnani syndrome). In patients experiencing these seizures, the block may be permanent or intermittent. When the block is high or complete and a lower-block pacemaker does not come into operation or works at too low a frequency, syncope occurs, with seizures occurring suddenly, usually without premonitoring symptoms.
If a cardiac stop persists for more than 8 to 10 seconds, the patient becomes pale, unconscious and may experience several clonic contractions. In a prolonged asystole appear cyanosis, irregular breathing, fixed pupils, incontinence, and bilateral Babinski signs (extension of the thumb outwards, or all fingers in the fan - bilaterally, in both hands) may be present.
While returning after a Stokes-Adams seizure is usually rapid and complete, sometimes prolonged confusion and neurological signs due to cerebral ischemia may sometimes occur, occasionally resulting in permanent impairment of mental functions, although neurological signs of outbreak are rare.
Patients usually don't remind you of presincopal symptoms. Cardiac syncopes of this type can be repeated several times over the course of a day. The period of asystole may be followed by tachycardia or ventricular fibrillation, causing prolonged coma or sudden death.
Another cause is disorders of sinus node automatism or synoatrial conduction that can cause asystole or bradycardia of sufficient severity to cause a presincope or syncope.
These disorders are most commonly detected by ECG monitoring. Data to suggest diagnosis of sinus node disease include symptomatic sinus breaks (more than 3 seconds) resulting from sinus stops or synoatrial block and unexplained severe sinus bradycardia (less than 40 beats per minute).
Bradycardia-tachycardia syndrome is a common form of sinus node dysfunction, in which syncope generally occurs as a result of prolonged sinus breaks, following the end of ventricular paroxysmal tachycardia. In patients with syncope and suspicion of sinus node disease, where diagnosis is not established by ECG monitoring, electrophysiological tests may be useful in highlighting diagnostic abnormalities.
I'm going to tackle tachyarrhythmias now. Paroxysmal tachyarrhythmias can also cause presincope and syncope as a result of sudden reduction in heart rate. The importance of tachycardia-induced hypotension depends on the interaction of several variables, including the frequency and mechanism of tachycardia, the type and severity of the patient's underlying heart disease, the position and level of activity of the patient at the onset of tachycardia, the sensitivity of tachycardia to endogenous catecholamines and the integrity of the autonomic compensatory reflexes.
Supraventricular tachyarrhythmias are not commonly associated with syncope. However, even in the absence of structural heart disease, extremely high heart frequencies can affect filling and heart rate, enough to cause loss of consciousness.
These tachycardias are most commonly represented by the appearance of paroxysmal atrial flutter, atrial fibrillation or re-entry to the atrioventricular node (AV) or accessory pathways that short-circuit part or all of the atrioventricular conduction system (AV).
Patients with Wolff-Parkinson-White syndrome are at increased risk for several forms of supraventricular tachycardia, the most dangerous of which is atrial fibrillation with rapid anterograde conduction to the ventricles through an accessory atrioventricular conduction pathway and which can lead to syncope or, more rarely, sudden death.
When it is suspected that abnormal driving through an AV accessor shunt or a modal AV reentry rate is the cause of syncope, the electrophysiological study is indicated to define the mechanism and pathway of tachycardia and to facilitate the choice of an effective therapeutic intervention.
Paroxysmal ventricular tachycardia is a relatively common cause of syncopes, especially patients with organic heart disease. Typically, tachycardias are rapid and associated with sudden loss of consciousness, without premonitoring symptoms.
Usually, the patient does not accuse palpitations and the return after an episode is rapid and complete, without residual cardiac or neurological sequelae. The appearance of an unexplained syncope in a patient with organic heart disease is an episode with potential for severe prognosis and deserves careful evaluation. The presence on ECG of pathological Q-waves indicating a previous transmural myocardial infarction is commonly associated with ventricular tachycardia as the etiology of syncopes in patients with ischemic heart disease.
Other forms of heart disease, such as hypertrophic or dilatative cardiomyopathy, right ventricle dysplasia and QT interval syndrome, are also commonly associated with paroxysmal ventricular tachycardia and syncope.
The reflex heart block is given by irritation of the vagus nerve and is present in the forms of cardiac syncope. Examples of this phenomenon have been observed in some patients with esophageal diverticules, mediastinal tumors, cholecyst damage, carotid sinus disease, glosopharyngeal neuralgia and pleural and pulmonary irritation. In these circumstances, reflex bradycardia is more commonly of the synoatrial type than atrioventricular.
Other causes of syncope would be acute myocardial infarction, especially if associated with cardiogenic shock. Aortic stenosis frequently causes syncope at exertion, most often by limiting cardiac flow under conditions of peripheral vasodilation, with resulting myocardial and cerebral ischemia and sometimes arrhythmias. Idiopathic hypertrophic subaortic stenosis can also cause ssyncopine of exertion by accentuating obstruction or by ventricular arrhythmias or both.
In primary pulmonary hypertension, a relatively fixed cardiac output and bouts of right ventricular failure may be associated with syncope. However, vagal reflexes may be involved in this situation, as well as in syncopes that occur in the pulmonary embolism.
Spherical valvular trombiins in the left atrium, left atrial mixoma, thrombosis or dysfunction of valvular prostheses can cause sudden mechanical circulatory obstruction and syncope. The congenital heart defect most commonly responsible for syncope is tetralogy of Fallot, a condition in which systemic vasodilation, probably associated with infundibular spasm, greatly increases the risk of right-left shunt and produces arterial hypoxia that can lead to syncope.
The next syncope is that of the carotid sinus. The carotid sinus is normally sensitive to mechanical stimuli and gives rise to sensory impulses transmitted through the Herring nerve, a branch of the glossopharynx nerve, to the brain stem.
Massage of one or both carotid sinuses, especially in the elderly, produces a reflex slowdown in heart rate (sinus bradycardia, sinus stop or even atrioventricular block), the so-called vagal response and a decrease in blood pressure without a decrease in heart rate, the so-called depressive type response.
Both carotid responses can coexist. Syncope due to the sensitivity of the carotid sinus is extremely unusual and is said to be triggered by turning the head to one side, by a tight collar or by shaving in the sinus area. In the case of a patient with lipotimia at the compression of a carotid sinus, it is important to make a differential diagnosis between a benign damage (hypersensitivity of the carotid sinus) and one with much more serious consequences such as contralateral carotid artery stenosis. Thus, carotid compression is a risky manoeuvre that can lead to cerebral ischemia.
Next comes the glosopharyngeal neuralgia. This painful condition can induce reflex lipotimia. The sequence is always of pain followed by syncope. Pain is localized to the jaw, at the base of the tongue, in the pharynx or larynx, the tonsil area and the ear.
Cardiovascular effects are attribution of stimulation of the dorsal motor nucleus of the vagus through collateral fibers from the nucleus of the solitary tract. Treatment of neuralgia (with carbamazepine) is commonly effective for syncope as well as for pain.
There's also syncope through coughing. It is a rare situation that follows a paroxysm of cough, usually in chronic bronchitis. After a strong cough, the patient suddenly has weakness and temporarily loses consciousness. Cough increases intraoracic pressure and increased pressure is transmitted through the large veins to the intracranial compartment, causing increased intracranial pressure and secondary decreasein brain flow. Syncope occurs at a low critical blood flow.
And, I'm going to finish the syncopes with the mechanical presentation, which is rare and occurs in otherwise normal teenagers. The challenge maneuver is the simultaneous extension of the neck and the stretching of the upper limb, the mechanism appears to be compression of the vertebral arteries in the neck.
Differential diagnosis is made in relation to several manifestations. The most appropriate is the one achieved against anxiety attacks and hyperventilation syndrome. Anxiety, as it occurs in panic attacks, is commonly interpreted as a feeling of lowblood or dizziness, without loss of consciousness. These symptoms are not accompanied by facial pallor and are not improved by clinostatism.
Diagnosis is made on the basis of associated symptoms and the attack can be reproduced by hyperventilation. Hyperventilation leads to hypocapnia, alkalosis, increased cerebrovascular resistance and decreased cerebral blood flow. The release of epinephrine in anxiety states also contributes to symptoms.
Another landmark is hypoglycaemia. Severe hypoglycaemia is usually the result of a serious condition, such as a tumor of the Langerhans Islands, advanced adrenal disease, pituitary gland or liver disease, including excessive insulin administration (this leads to confusion or even loss of consciousness). Mild hypoglycaemia is often reactive, occurring 2 to 5 hours after eating and is not usually associated with a disorder of consciousness.
Acute bleeding, usually in the gastrointestinal tract, is an occasional cause of syncope. In the absence of pain and hematemesis, the cause of weakness, liptomy or even loss of consciousness may remain obscure until the appearance of melena.
Transient cerebral ischemic attack (AIT) occurs in patients with atherosclerotic stenosis, occlusions or embolisms of the large arteries of the brain. Symptoms are varied and sudden fall seizures can mimic syncope. Isolated loss of consciousness is rare.
And in the end, we shouldn't forget hysterical lypothymia. The attack is not usually preceded by any outward manifestation for anxiety. the absence of any change in the pulse, blood pressure or color of the skin and mucous membranes differentiates it from vasopressor lypotimia.
For tomorrow I think I'll complete the syncopes and be able to tackle dizziness and vertigo.
A
pleasant, soothing and restful weekend!
Dorin, Merticaru