Syncope

Hypertension and Syncope. Syncope is transient loss of consciousness due to temporary generalized cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery. Loss of consciousness results from reduced blood flow in the activation system reticular, located in the brain stem and does not require an electrical or chemical treatment for resolution. The metabolism of the brain, unlike that of many other organs, depends largely on its perfusion. Therefore, the interruption of cerebral blood flow causes loss of consciousness in a few 10s. Recovery from proper behavior and orientation after a syncopal episode is usually immediate. Retrograde amnesia, although rare, can be seen in the elderly. Syncope, defined in the terms cited here, it represents a type of situation within a much broader spectrum that causes transient loss of consciousness, including stroke and epileptic seizures. The causes of transient loss of consciousness other than syncope differ in terms of mechanism and duration.

Summary

[ hide ]

  • 1 Classification
  • 2 Reflex mechanism syncope
  • 3 Vasovagal syncope
  • 4 Carotid sinus hypersensitivity
    • 1 Cardiac causes of syncope
      • 1.1 Echocardiography
      • 1.2 Electrocardiography
      • 1.3 Treatment of patients
    • 2 Syncope of metabolic causes
  • 5 Sources

Classification

Syncope summarizes a differential diagnostic strategy for transient unconsciousness. Syncope can be differentiated from most other causes of transient unconsciousness by checking whether the unconsciousness was transient, rapid onset, short-lived, and followed by spontaneous recovery. If the answer to each of these questions is yes and the transient loss of consciousness was not caused by a head injury, diagnostic considerations include true syncope, in which case transient loss of consciousness is considered to be due to global cerebral hypoperfusion, seizures. epileptic, psychogenic syncope and other rare causes. When evaluating a patient with transient unconsciousness,

Reflex mechanism syncope

The causes of reflex mechanism syncope These are a group of conditions in which the cardiovascular reflexes that control circulation are inadequate to respond to a triggering factor that causes vasodilation with or without bradycardia and a drop in blood pressure and generalized cerebral hypoperfusion. In each case, the reflex is made up of a trigger (afferent branch) and a response (efferent branch). This group of reflex syncope syndromes has in common the reflex response pathway, which consists of an increase in vagal tone and the withdrawal of peripheral sympathetic tone that causes bradycardia, vasodilation, and, finally, hypotension, presyncope, or syncope. If hypotension due to peripheral vasodilation predominates, it is classified as a vasodepressor-type reflex response; if bradycardia or asystole predominates, it is classified as a cardioinhibitory response, and when both vasodilation and bradycardia play a role in the process, it is classified as a mixed response. Specific triggers help distinguish these causes of syncope. For example, voiding syncope occurs as a consequence of activation of mechanoreceptors in the urinary bladder; defecation syncope is caused by nerve impulses from tension receptors in the intestinal wall, and swallowing syncope is caused by afferent nerve impulses originating in the upper digestive system. The two most frequent types of reflex syncope, carotid sinus hypersensitivity and neurological mechanism hypotension will be explained later.

Vasovagal syncope

Also known as neurocardiogenic, vasodepressor, and vasovagal syncope, and “lipothymia” has been used to describe a frequent abnormality in blood pressure regulation, characterized by the sudden onset of hypotension with or without bradycardia. Triggers associated with neurological mechanism syncope include orthostatic stress, such as that which can be caused by prolonged standing or a hot shower, and emotional stress, caused, for example, by blood vision.1,2, 10 Recently, it has been recognized that a large number of patients who manifest syncope of the neurological mechanism have mild psychiatric disorders.21, 22 It has been proposed that the syncope of the neurological mechanism originates from a paradoxical reflex that begins when the ventricular preload decreases due to venous accumulation. This reduction causes a decrease in cardiac output and blood pressure, a circumstance detected by arterial baroreceptors. The consequent increase in the concentration of catecholamines, in combination with the decrease in venous filling, causes the energetic contraction of an almost empty ventricle. The heart itself participates in this reflex through the mechanoreceptors, or C fibers, which consist of unmyelinated fibers present in the atria, ventricles, and pulmonary artery. Energetic contraction of a nearly empty ventricle has been proposed to cause activation of these receptors in susceptible individuals. These afferent C fibers project centrally to the dorsal vagal nucleus of the medulla oblongata, causing a “paradoxical” withdrawal of peripheral sympathetic tone and an increase in vagal tone, which in turn causes vasodilation and bradycardia. The last clinical consequence is syncope or presyncope. Not all syncopes of the neurological mechanism are produced by the activation of the mechanoreceptors. In humans, blood vision or extreme emotion can trigger syncope, indicating that higher neural centers may also be involved in the pathophysiological process of vasovagal syncope. Furthermore, central mechanisms may contribute to the production of neurological mechanism syncope. causing a “paradoxical” withdrawal of peripheral sympathetic tone and an increase in vagal tone, which in turn causes vasodilation and bradycardia. The last clinical consequence is syncope or presyncope. Not all syncopes of the neurological mechanism are produced by the activation of the mechanoreceptors. In humans, blood vision or extreme emotion can trigger syncope, indicating that higher neural centers may also be involved in the pathophysiological process of vasovagal syncope. Furthermore, central mechanisms may contribute to the production of neurological mechanism syncope. causing a “paradoxical” withdrawal of peripheral sympathetic tone and an increase in vagal tone, which in turn causes vasodilation and bradycardia. The last clinical consequence is syncope or presyncope. Not all syncopes of the neurological mechanism are produced by the activation of the mechanoreceptors. In humans, blood vision or extreme emotion can trigger syncope, indicating that higher neural centers may also be involved in the pathophysiological process of vasovagal syncope. Furthermore, central mechanisms may contribute to the production of syncope of the neurological mechanism. Not all syncopes of the neurological mechanism are produced by the activation of the mechanoreceptors. In humans, blood vision or extreme emotion can trigger syncope, indicating that higher neural centers may also be involved in the pathophysiological process of vasovagal syncope. Furthermore, central mechanisms may contribute to the production of neurological mechanism syncope. Not all syncopes of the neurological mechanism are produced by the activation of the mechanoreceptors. In humans, blood vision or extreme emotion can trigger syncope, indicating that higher neural centers may also be involved in the pathophysiological process of vasovagal syncope. Furthermore, central mechanisms may contribute to the production of neurological mechanism syncope.

Carotid sinus hypersensitivity

Syncope caused by hypersensitivity of the carotid sinus is caused by stimulation of the carotid sinus baroreceptors, located in the internal carotid artery, above the bifurcation of the common carotid artery. Carotid sinus hypersensitivity is detected in almost a third of elderly patients with syncope or falls. However, this disorder is also frequently observed in asymptomatic elderly patients. Therefore, the diagnosis of carotid sinus hypersensitivity should be rigorously addressed, after excluding other alternative causes of syncope. Once diagnosed, the implantation of a dual-chamber pacemaker is recommended, in patients who manifest recurrent syncope or falls due to hypersensitivity of the carotid sinus. according to a large number of randomized and non-randomized clinical studies. The AHA / ACC / HRS guidelines for implantation of a device consider this situation a Class I indication for pacemaker placement. If the diagnosis of carotid sinus hypersensitivity is based on a sinus pause> 3s with massage to the carotid sinus, without clear episodes of provocation of syncope, the recommendation to implant a pacemaker is less important (class lia).

 

Cardiac causes of syncope

Cardiac causes of syncope, especially tachyarrhythmias and bradyarrhythmias, are the second most frequent group of causes of syncope, accounting for between 10 and 20% of syncopal episodes Ventricular tachycardia (VT) is the most common tachyarrhythmia

Echocardiography

Echocardiography is commonly used to evaluate patients with syncope, but current guidelines recommend that only patients suspected of presenting with structural heart disease be performed. For example, echocardiography will be obtained in% of patients whose clinical picture is indicative of syncope. of cardiac origin, such as exertional or supine syncope, 8 family history of sudden death or sudden onset syncope. Echocardiographic features that are considered diagnostic of the cause of syncope include severe aortic stenosis, pericardial tamponade, or aortic dissection, congenital abnormalities of the coronary arteries, and obstructive atrial myromas or thrombi. Observations of impaired left or right ventricular function,

Electrocardiograph

The 12-lead ECG is another important element in the study of a patient with syncope. The initial ECG allows a diagnosis to be made in almost 5% of patients and a possible diagnosis to be signaled in another 5%. Specific characteristics that can identify the probable cause of syncope include QT prolongation (long QT H syndrome); a short PR interval and the presence of a wave 8 (^ Wolff-Parkinson-White syndrome); Characteristics of a right bundle branch block in ST bundle with ST segment elevation (Brugada syndrome), and Qv signs of acute myocardial infarction, high-grade AV block, or T-wave inversion in right precordial leads (arrhythmogenic right ventricular dysplasia). Any abnormality on the initial ECG is an independent predictor of cardiac syncope or increased mortality, and indicates the need to continue studying the cardiac causes of syncope.1,2 Most patients with syncope have a Normal ECG. This observation is useful because it makes it possible to assume that the probability of a cardiac cause of syncope is low and is associated with an excellent prognosis, particularly in young patients with syncope. Despite the poor diagnostic performance of electrocardiography, this test is inexpensive and without risk, and is considered a standard element of the evaluation of practically all patients with syncope. 2 Most patients with syncope have a normal ECG. This observation is useful as it makes it possible to assume that the probability of a cardiac cause of syncope is low and is associated with an excellent prognosis, particularly in young patients with syncope. Despite the poor diagnostic performance of electrocardiography, this test is inexpensive and without risk, and is considered a standard element of the evaluation of practically all patients with syncope. 2 Most patients with syncope have a normal ECG. This observation is useful as it makes it possible to assume that the probability of a cardiac cause of syncope is low and is associated with an excellent prognosis, particularly in young patients with syncope. Despite the poor diagnostic performance of electrocardiography, this test is inexpensive and without risk, and is considered a standard element of the evaluation of practically all patients with syncope.

 

Treatment of patients

  • Severe dehydration.

Syncope of metabolic causes

There are three goals of treatment in a patient with syncope: prolong survival; avoid traumatic injuries, and avoid recurrences of syncope. The strategy of treating a patient with syncope depends primarily on the cause and mechanism of syncope. For example, the appropriate treatment of a patient with syncope associated with AV block will be the placement of a pacemaker, in most situations.34 However, a patient with syncope due to heart block, in a context of heart attack The myocardium of the lower wall does not usually require a permanent pacemaker, since heart block usually resolves spontaneously. Similarly, heart block caused by neurological mechanism syncope does not require pacemaker implantation. Treatment of a patient with syncope associated with Wolff-Parkinson-White syndrome generally involves catheter ablation, and treatment of a patient with syncope caused by VT or with a picture of ischemic or non-ischemic cardiomyopathy will likely require DAI placement. However, an ICD may not be necessary in patients with VT / VF when it occurs 48 hours after an acute myocardial infarction. For other types of syncope, optimal treatment may include discontinuation of the triggering drug treatment, increased salt intake, or patient information on the subject. Other issues that need to be considered include the indication for hospitalization of a patient with syncope and the duration of vehicle driving limitations. Current guidelines recommend hospitalizing patients with syncope when they manifest certain or suspected heart disease, electrocardiographic abnormalities indicating arrhythmic syncope, syncope with severe injury or during exercise, and syncope with a family history of sudden death. Syncope often have to address the issue of defining risk from driving vehicles. Patients who present with syncope while driving are at risk, both for themselves and for others. Although some people argue that all syncope patients should never drive due to the possibility of recurrence, it is an unworkable solution that would be ignored by many patients. The factors that should be considered when making recommendations in this regard, for a particular patient they include: 1) the possibility of recurrence of syncope; the presence and duration of warning symptoms the fact that syncope occurs when the patient is sitting or standing; 4) frequency and ability of the patient to drive, and 5) the existence of applicable state laws. When evaluating these aspects, physicians should take into account that acute diseases, such as syncope, do not usually cause traffic accidents. According to a study of 3,877 patients with syncope, it was observed that syncope occurred during driving in 380 cases (9.8%) .35 The most frequent cause was reflex syncope in more than a third of cases. Syncope recurrence during driving occurred only in 10 patients. During 8 years of follow-up, the cumulative probability of recurrence while driving was 7%. An important fact was the observation of a total syncope recurrence rate in all patient groups, regardless of whether syncope occurred while driving. Guidelines on this topic have been published by the American Heart Association and the Canadian Cardiovascular Society. For non-commercial drivers, a driving limitation of several months is usually recommended. If the patient remains asymptomatic for several months, he is allowed to drive again. Guidelines on this topic have been published by the American Heart Association and the Canadian Cardiovascular Society. For non-commercial drivers, a driving limitation of several months is usually recommended. If the patient remains asymptomatic for several months, he is allowed to drive again. Guidelines on this topic have been published by the American Heart Association and the Canadian Cardiovascular Society. For non-commercial drivers, a driving limitation of several months is usually recommended. If the patient remains asymptomatic for several months, he is allowed to drive again.

 

Leave a Comment