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From the moment that consciousness is regained, there is a correct perception of the environment Confusion, headache, and drowsiness, the common sequelae of a convulsive seizure, do not follow a syncopal attack Nevertheless, the patient often feels weak and groggy after a vasodepressor faint and, by arising too soon, may precipitate another faint The clinical features of cardiac and carotid sinus syncope are much the same as those described above except that the onset of these forms of syncope may be absolutely abrupt, without any warning symptoms, and is much less dependent upon the patient being in an upright posture The clinical particulars of these and other forms of syncope are described further on

From a clinical and pathophysiologic perspective, syncope is essentially of three main types, each of which may lead to a temporary reduction in the ow of blood to the brain: 1 Re ex loss of vascular sympathetic tone (vasodepressor effect), triggered by centrally mediated inhibition of the normal tonic sympathetic in uences, often associated with excessive vagal effect and bradycardia (vasovagal effect) These are referred to generally as vasovagal syncopes, a special form of the neurogenic, or neurocardiogenic syncopes, by which is meant the withdrawal of sympathetic tone through a re ex neural mechanism Neurocardiogenic syncope signi es that the inciting stimulus originates in neural receptors within the heart A failure of sympathetic innervation of blood vessels and of autonomically activated compensatory responses (re ex tachycardia and vasoconstriction), which occurs with assumption of the upright body position and leads to pooling of blood in the lower parts of the body causing orthostatic hypotension and syncope Typically, in individuals with these rst two forms of syncope, there is no evidence of underlying cardiac disease Diminished cardiac output due to disease of the heart itself (as in the Stokes-Adams bradyarrhythmia attack or in severe aortic stenosis) or to greatly reduced blood volume from dehydration or blood loss

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As a rough guide to the relative frequency of the various causes of syncope, the large amount of information from the Framingham Heart Study accumulated by Soteriades and colleagues can be taken as representative; the leading cause was vasovagal, 21 percent, a cardiac cause was established in 9 percent, and orthostatic hypotension in 9 percent; fully 40 percent could not be categorized Also notably, 7 percent of cases were attributed to medications, mainly those that interfered with sympathetic tone The three main types of syncope and several others that cannot readily be included within these categories can be further subdivided by their pathophysiologic mechanism, as follows: I Neurogenic vasodepressor reactions A Elicited by extrinsic signals to the medulla from baroreceptors 1 Vasodepressor (vasovagal) 2 Neurocardiogenic 3 Carotid sinus hypersensitivity

4 Vagoglossopharyngeal 5 Severe pain, especially if arising in a viscera (bowel, ovary, testicle, etc) B Coupled with diminished venous return to the heart 1 Micturitional 2 Tussive 3 Valsalva, straining, breath-holding, weight lifting 4 Postprandial C Intrinsic psychic stimuli 1 Fear, anxiety (presyncope more common) 2 Sight of blood 3 Hysterical II Failure of sympathetic nervous system innervation (postural-orthostatic hypotension) A Peripheral nervous system autonomic failure 1 Diabetes 2 Pandysautonomia 3 Guillain-Barre syndrome 4 Amyloid neuropathy 5 Surgical sympathectomy 6 Antihypertensive medications and other blockers of vascular innervation B Central nervous system (CNS) autonomic failure 1 Primary autonomic failure (idiopathic orthostatic hypotension) 2 Multiple system atrophy (parkinsonism, ataxia, orthostatic hypotension) 3 Spinal cord trauma, infarction, and necrosis 4 Centrally acting antihypertensive and other medications III Reduced cardiac output or inadequate intravascular volume (hypovolemia) A Reduced cardiac output 1 Cardiac arrhythmias a Bradyarrhythmias a Atrioventricular (AV) block (second and third degree) with Stokes-Adams attacks b Ventricular asystole c Sinus bradycardia, sinoatrial block, sinus arrest, sick sinus syndrome b Tachyarrhythmias a Episodic ventricular tachycardia b Supraventricular tachycardia (infrequently causes syncope) 2 Myocardial: infarction or severe congestive heart failure 3 Obstruction to left ventricular or aortic out ow: aortic stenosis, hypertrophic subaortic stenosis, Takayasu arteritis 4 Obstruction to pulmonary ow: pulmonic stenosis, tetralogy of Fallot, primary pulmonary hypertension, pulmonary embolism 5 Pericardial tamponade B Inadequate intravascular volume (hemorrhage); dehydration IV Other causes of episodic faintness and syncope A Hypoxia B Anemia C Diminished CO2 due to hyperventilation (faintness common, syncope rare) D Hypoglycemia (faintness frequent, syncope rare) E Anxiety (panic) attacks F Environmental overheating

Long butter y spreads are created by purchasing a premium close to the current market while selling a ratio to that premium on an out-of-the-money strike price, creating a ratio spread of one long to two short To nish the butter y, the ratio is covered by another purchased option that is an equal distance from the short strike prices The long butter y creates a window of pro t potential with limited risk and low premium exposure Let s look at an example to help you understand the construction of the butter y spread Using the option chain shown in Figure 81, let s assume a hypothetical purchase of ve of the July IBM 100 call options at 944 along with the sale of ten July IBM 110 call options for 475 and nally the purchase of ve July 120 call options for 193, giving us a total combined option premium of 187 The combined delta of the position is approximately 12 percent long, very near neutral delta Calculating breakeven on a long call butter y spread is accomplished by taking the total premium of the spread and adding it to the closer-to-the-market long call strike price: 100 strike price 193 premium 10193 underlying breakeven