Acute Orthostatic Intolerance and Syncope

 

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Up ] Physiology of Orthostasis ] Patterns of Orthostatic Intolerance ] [ Acute Orthostatic Intolerance and Syncope ] Chronic Orthostatic Intolerance ]

Splanchnic pooling in syncope ] Hyperpnea and Biphasic Peripheral Resistance Changes Characterize Vasovagal Syncope in the Young ] Decreased Cerebral Autoregulation during Syncope in the Young ]

While neurologic disease may produce acute orthostatic intolerance, most acute OI is produced by syncope (literally "to chop off" in Greek) in which there is a sudden transient loss of consciousness produced by decreased cerebral blood flow. Mostly this is caused by a sudden fall of blood pressure below the range where cerebral autoregulation can maintain consciousness. It may be due to medication, cardiac disease, most commonly arrhythmic disease, or severe impairment of cardiac output by mechanical failure or obstruction. It may be due to transient impairment of central nervous system function as in a transient ischemic attack but this is less common. However, although convulsive-like movements may occur during syncope, it is almost always distinct from a seizure disorder, and is distinct from coma in which loss of consciousness is not transient at all.

Cardiac syncope is often quite serious and should be regarded as life-threatening. Although cardiac syncope is not often closely associated with orthostasis it may be. Causes of cardiac syncope include the long QT syndrome, arrhythmogenic right ventricular dysplasia, cardiomyopathies, left ventricular outflow obstruction, myocardial infarction, primary pulmonary hypertension, and most commonly ventricular tachycardia, bradyarrhythmias and related arrhythmic events. The first job in evaluating syncope is to evaluate the patient for possible cardiac syncope. When specific cardiac disease is found, it is treated specifically. Thus, for example, ventricular tachycardia is treated with antiarrhythmics, bradyarrhythmias causing syncope are treated with a pacemaker, long QT syndrome with medication and a defibrillator, and aortic stenosis with surgery. Cardiac syncope may first manifest during exercise, which is the best and most physiologic stressor of the myocardial circulation and overall cardiac function. Exercise related syncope should raise a "red flag" for underlying heart disease. Nevertheless, despite flag-waving, the large majority of exercise related syncope cases are non-cardiogenic in origin, at least for children and adolescents. Cardiogenic syncope has been well described in numerous texts including those already referenced and is not the central topic for discussion here because it accounts for a small percentage of syncope in children and of those many have previously known cardiac conditions.

Approximately 90% of syncope in children is either "neurocardiogenic" or "unexplained". Often the unexplained variety is reclassified as neurocardiogenic once tilt table testing has been performed. Neurocardiogenic is the current term (at least for today) for fainting mediated through a combination of inappropriate vascular and heart rate control. It is rarely fatal although it can be under certain unique circumstances but it can be injurious. There little compelling evidence for a primary role for the heart in neurocardiogenic syncope, once cardiogenic syncope has been ruled out. The term is thus somewhat misleading. Synonyms for neurocardiogenic include neurally mediated syncope and vasovagal syncope. Almost all of neurocardiogenic syncope in children can be deemed vasovagal, an appropriate descriptive designation coined by Sir. Thomas Lewis. On the other hand adult syncope is much more likely to be cardiogenic about a 50/50 split with neurocardiogenic syncope. Vasovagal syncope almost always occurs in the upright position, which may sometimes include sitting. Therefore it is regarded as a form of orthostatic intolerance.

Other forms of simple faint may involve either an isolated fall in heart rate (so-called cardioinhibitory syncope), or an isolated fall in blood pressure (so-called vasomotor or dysautonomic syncope). In addition some simple faints aren't so simple and may be associated with prolonged asystole and personal injury. Often this occurs with so-called "convulsive syncope" which may be mistaken for a seizure. These forms of syncope are denoted by many other terms which seem to change from year to year and include neurally mediated hypotension, neurocardiogenic syncope and many others. The nomenclature is confusing.

Simple faint with a near simultaneous fall in heart rate and blood pressure at the time of loss of consciousness. Data indicates that there is always vasodilation associated with the bradycardia  - thus "vasovagal"

In a smaller percentage of children but in a larger fraction of adults syncope may be provoked by more pernicious disease. This is most often cardiovascular disease and is often associated with arrhythmia, most commonly ventricular tachycardia. In addition "sick sinus syndrome" with bradycardia, Wolf-Parkinson White syndrome, long QT syndrome (Torsades-de-Pointe), Brugada syndrome, other brady or tachyarrhythmias and acute cardiac pump failure as in myopathic disease (also associated with arrhythmia), myocardial infarction, pulmonary infarction, pulmonary hypertension, and many more may result in syncope with potentially fatal sequelae. The first job of the cardiologist is to rule out these more dangerous disease states. 

However, in children the most common problems relate to simple faint and its close relations.

 


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Physiology of Orthostasis
Patterns of Orthostatic Intolerance
Acute Orthostatic Intolerance and Syncope
Chronic Orthostatic Intolerance