Chapter 27 - Syncope Flashcards
How does one define syncope?
“Syncope is a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood flow. The onset is rapid, duration brief, and recovery spontaneous and complete.”
Vertebrobasilar ischemia might be considered a cause of syncope.
True or False?
False.
Vertebrobasilar ischemia will lead to hypoperfusion of the posterior cerebral cortex, cerebellum and medulla. Since syncope is considered a transient global ischemia, localized hypoperfusion due to involvement of selected brain vessels with loss of counsciounsness, while sharing some similarities to syncope, is not seen as a cause of one.
Name the differential diagnosis for syncope.
Seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia.
A syncopal prodrome (presyncope) is common, although loss of consciousness may ocur without any warning symptoms. Which symptoms should one expect in presyncope?
“Typical presyncopal symptoms include dizziness, lightheadedness or faintness, weakness, fatigue, and visual and auditory disturbances.”
Categorize the causes of syncope.
(1) neurally mediated syncope (also called reflex or vasovagal syncope);
(2) orthostatic hypotension;
(3) cardiac syncope.
Summarize the different pathophysiology of the three categories of syncope.
“Neurally mediated syncope comprises a heterogeneous group of functional disorders that are characterized by a transiet change in the reflexes responsible for maintaining cardiovascular homeostasis. Episodic vasodilation (or loss of vasoconstrictor tone) and bradycardia occur in varying combinations, resulting in temporary failure of blood pressure control. In contrast, in patients with orthostatic hypotension due to autonomic failure, these cardiovascular homeostatic reflexes are chronically impaired. Cardiac syncope may be due to arrhythmias or structural cardiac diseases that cause a decrease in cardiac output. The clinical features, underlying pathophysiologic mechanisms, therapeutic interventions, and prognoses differ markedly among these three causes.”
Summarize the Epidemiology regarding syncope as a cause of emergency room visits, annual cost due to hospitalization, cumulative incidence during lifetime, and differences in its features related to the patient’s age and sex.
“Syncope is a common presenting problem, accounting for approximately 3% of all emergency room visits and 1% of all hospital admissions. The annual cost for syncope-related hospitalization in the United States is ~$2,4 billion. Syncope has a lifetime cumulative incidence of up to 35% in the general population. The peak incidence occurs between ages 10 and 30 years, with a median peak around 15 years. Neurally mediated syncope is the etiology in the vast majority of these cases. In elderly adults, there is a sharp rise in the incidence of syncope after 70 years.”
What is the most common cause of syncope?
Neurally-mediated syncope.
The elderly are at increased risk for syncope. How can one explain this finding?
“Orthostatic hypotension also increases in prevalence with age because of the baroreflex responsiveness, decreased cardiac compliance, and attenuation of the vestibulosympathetic reflex associated with aging. In the elderly, orthostatic hgypotension is substantially more common in institutionalized (54-68%) than community-dwelling (6%) individuals, an observation most likely explainted by the greater prevalence of predisposing neurologic disorders, physiologic impairment, and vasoactive medication use among institutionalized patients.”
After a syncopal episode, the prognosis includes an increased mortality rate compared to the general population.
True or False?
False: “The prognosis after a single syncopal event for all age groups is generally benign. In particular, syncope of noncardiac and unexplained origin in younger individuals has an excellent prognosis; life expectancy is unaffected.
True: “By contrast, syncope due to a cardiac cause, either structural heart disease or primary arrhythmic disease, is associated with an increased risk of sudden cardiac death and mortality from other causes. Similarly, mortality rate is increased in individuals with syncope due to orthostatic hypotension related to age and the associated comorbid conditions.”
Summarize the pathophysiology of syncope. Make a correlation between the pooling of blood and the reduced cerebral blood flow.
“The upright posture imposes a unique physiologic stress upon humans; most, although not all, syncopal episodes occur from a standing position. Standing results in pooling of 500-1000mL of blood in the lower extremities and splanchnic circulation. There is a decrease in venous return to the heart and reduced ventricular filling that result in diminished cardiac output and blood pressure. These hemodynamic changes provoke a compensatory reflex response, initiated by the baroreceptors in the carotid sinus and aortic arch, resulting in increased sympathetic outflow and decreased vagal nerve activity. The reflex increases peripheral resistance, venous return to the heart, and cardiac output and thus limits the fall in blood pressure. If this response falls, as is the case chronically in orthostatic hypotension and transiently in neurally mediated syncope, cerebral hypoperfusion occurs.”
“Syncope is a consequence of global cerebral hyopperfusion and thus represents a failure of cerebral blood flow autoregulatory mechanisms. Myogenic factors, local metabolites, and to a lesser extent autonomic neurovascular control are responsible for the autoregulation of cerebral blood flow. The latency of the autoregulatory response is 5-10 s. Typically cerebral blood flow ranges from 50 to 60 mL/min per 100 g brain tissue and remains relatively constant over perfusion pressures ranging from 50 to 150 mmHg. Cessation of blood flow for 6-8 s will result in loss of consciousness, while impairment of consciousness ensues when blood flow decreases to 25mL/min per 100 g brain tissue.”
Name the causes of reduced cardiac output related to syncope.
Decreased effective circulating blood volume; increased thoracic pressure; massive pulmonary embolus; cardiac brady- and tachyarrhythmias; valvular heart disease; and myocardial dysfunction.”
Name the causes of reduced systemic vascular resistance.
Central and peripheral autonomic nervous system diseases, sympatholytic medications, and transiently during neurally mediated syncope.
Name the causes of increased cerebral vascular resistance.
“Increased cerebral vascular resistance, most frequently due to hypocarbia induced by hyperventilation, may also contribute to the pathophysiology of syncope.”
Which patterns of electroencephalographic (EEG) might one observe during a syncopal event?
“Two patterns of electroencephalographic (EEG) changes occur in syncopal subjects. The first is a “slow-flat-slow” pattern in which normal backgroud activity is replaced with high-amplitude slow delta waves. This is followed by sudden flattening of the EEG - a cessation or attenuation of cortical activity - followed by the return of slow waves, and then normal activity. A second pattern, the “slow pattern”, is characterized by increasing and decrasing slow wave activity only. The EEG flattening that occurs in the slow-flat-slow pattern is a marker of more severe cerebral hypoperfusion. Despite the presence of myoclonic movements and other motor activity during some syncopal events, EEG sizure discharges are not detected.”
In order to elitic neurally mediated syncope, a functioning autonomic nervous system is necessary, in contrast to syncope resulting from autonomic failure.
True or False?
True.
Neurally mediated syncope might be subdivided. Explan this subclassification and its pathophysiological mechanisms.
“Neurally mediated syncope may be subdivided based on the afferent pathway and provocative trigger. Vasovagal syncope (the common faint) is provoked by intense emotin, pain, and/or orthostatic stress, whereas the situational reflex syncopes have specificed localized stimuli that provoke the reflex vasodilation and bradycardia that leads to syncope. The underlying mechanisms have been identified and pathophysiology delineated for most of these situational reflex syncopes. The afferent trigger may originate in the pulmonary system, gastrointestinal system, urogenital system, heart, and carotid artery. Hyperventilation leading to hypocarbia and cerebral vasoconstriction, and raised intrathoracic pressure that impairs venous return to the heart, play a central role in many of the situation reflex syncopes. The afferent pathways of the reflex arc differs among these disorders, but the efferent response via the vagus and sympathetic pathways is similar.”
Summarize the features of neurally mediated syncope, as well as the differences between a syncopal episode and seizure.
“In addition to symptoms of orthostatic intolerance such as dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present in patients with neurally mediated syncope. These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning. During the syncopal event, proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy. The eys typically remain open and usually deviate upward. Pupils are usually dilated. Roving eye movements may occur. Grunting, moaning, snorting, and stertorous breathing may bepresent. Urinary incontinence may occur. Fecal incontinence is very rare. Postictal confusion is also rare, although visual and auditory hallucinations and near death and out-of-body experiences are sometimes reported.”
Give examples of known predisposing factors and provocative stimuli for neurally mediated syncope.
Motioless upright posture, warm ambient temperature, intravascular volume depletion, alcohol ingestion, hypoxemia, anemia, pain, the sight of blood, venipuncture, and intense emotion.
Are there any maneuvers that avoid or delay syncope? Is there any available evidence for these?
Yes. “Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing) may raise blood pressure by increasing central blood volume and cardiac output by increasing central blood volume and cardiac output. By maintaining pressure in the autoregulatory zone, these maneuvers avoid or delay the onset of syncope. Randomized controlled trials support this intervention.”
Which pharmacotherapies might be used in neurally mediated syncope? Is there any avaible evidence for their use?
“Fludrocortisone, vasoconstricting agents, and beta-adrenoreceptor antagonists are widely used by experts to treat refractory patients, although there is no consistent evidence from randomized controlled trials for any pharmacotherapy to treat neurally mediated syncope.”
Are there any patients with neurally mediated syncope who might benefit from pacemaker implantation?
“Because vasodilation is the dominant pathophysiologic syncopal mechanism in most patients, use of a cardiac pacemaker is rarely beneficial. Possible exceptions are older patients (>40 years) in whom syncope is associated with asystole or severe bradycardia and patients with prominent cardioinhibition due to carotid sinus syndrome. In these patients, dual-chamber pacing may be helpful.”
