B P7 C71 Hypotension and Syncope Flashcards

1
Q

Syncope is a symptom that presents with _____.

A

(1) Abrupt, transient, complete loss of consciousness (LOC)
(2) Associated with the inability to maintain postural tone
(3) With rapid and spontaneous recovery

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2
Q

The presumed mechanism of syncope is _____.

A

Cerebral hypoperfusion

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3
Q

It is important to recognize that syncope, as previously defined, represents a subset of a much wider spectrum of conditions that can result in transient LOC, including conditions such as cerebrovascular accident (stroke) and epileptic seizures.Nonsynco- pal causes of transient LOC differ in their mechanism and duration.

A
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4
Q

The metabolism of the brain, in contrast to that of many other organs, is exquisitely dependent on perfusion. Consequently, cessation of cerebral blood flow leads to LOC______. Restoration of appropriate behavior and orientation after a syncopal episode is usually immediate. Retrograde amnesia, although uncommon, can be present in older adults.

A

within approximately 10 seconds

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5
Q

The prognosis of patients with syncope varies greatly with the diag- nosis. Patients with syncope in the setting of structural heart disease or primary electrical disease have an increased incidence of SCD and overall mortality.Syncope caused by orthostatic hypotension is associated with two fold increase in mortality,which reflects the presence of multiple comorbid conditions in this patient group. In contrast, young patients with neurally mediated syncope (NMS) have an excellent prognosis.

A
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6
Q

_____, are by far the most common causes and account for at least one third of all syncopal episodes.

A

Vascular causes of syncope, particularly reflex-mediated syncope and orthostatic hypotension

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7
Q

Standing upright displaces _____ of blood to the abdomen and lower extremities, thereby resulting in an abrupt drop in venous return. to the heart. This drop leads to a decrease in cardiac output and stim- ulation of aortic, carotid, and cardiopulmonary baroreceptors, which triggers a reflex increase in sympathetic outflow. As a result, _____, ______, _______ to maintain stable systemic blood pressure (BP) on standing.

A

500 to 800 mL

Heart rate, cardiac contractility, and vascular resistance increase

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8
Q

This is a term used to refer to the signs and symptoms of an abnormality in any portion of this BP control system

A

Orthostatic intolerance

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9
Q

Orthostatic hypotension is defined as a ______ of standing.

Orthostatic hypotension can be asymptomatic or associated with syncope, lightheadedness/ presyncope, tremulousness, weakness, fatigue, palpitations, diaphoresis, and blurred or tunnel vision.

Many patients with orthostatic hypotension are asymptomatic despite substantial falls in systolic BP and low upright BPs.

These symptoms are often worse immediately on arising in the morning or after meals or exercise.

A

20-mm Hg drop in systolic BP or a 10-mm Hg drop in diastolic BP within 3 minutes

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10
Q

Initial orthostatic hypotension is defined as less _____ immediately on standing with rapid (<30 seconds) return to normal. In contrast, delayed progressive orthostatic hypotension is characterized by a slow progressive decrease in systolic BP on standing.

A

Less than a 40-mm Hg decrease in BP

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11
Q

Syncope that occurs after meals,particularly in older adults,can result from a redistribution of blood to the gut. A _____ has been reported in up to one third of older adult nursing home residents. Although usually asymptomatic, it can result in lightheadedness or syncope.

A

Decline in systolic BP of approximately 20 mm Hg approximately 1 hour after eating

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12
Q

Drugs that either cause ____ or ______ are the most common causes of orthostatic hypotension (Table 71.3).

Older adult patients are particularly susceptible to the hypotensive effects of drugs because of reduced baroreceptor sensitivity,decreased cerebral blood flow, renal sodium wasting, and an impaired thirst mechanism that develops with aging

A

Volume depletion or result in vasodilation

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13
Q

There are three types of primary autonomic failure.

______ is an idiopathic sporadic disorder characterized by orthostatic hypotension, usually in conjunction with evidence of more widespread autonomic failure, such as disturbances in bowel, bladder, thermoregulatory, and sexual function. Patients with pure autonomic failure have reduced supine plasma norepinephrine levels.

______ is a sporadic, progressive, adult-onset disorder characterized by autonomic dysfunction,parkinsonism,and ataxia in any combination.

The third type of primary autonomic failure is ____. A small subset of patients with Parkinson disease may also experience autonomic failure, including orthostatic hypotension.

A

Pure autonomic failure (Bradbury-Eggleston syndrome)

Multisystem atrophy (Shy-Drager syndrome)

Parkinson disease with autonomic failure

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14
Q

In addition to these forms of chronic autonomic failure is a rare, ______. This neuropathy generally occurs in young people and results in severe, widespread sympathetic and parasympa- thetic failure with orthostatic hypotension, loss of sweating, disruption of bladder and bowel function,fixed heart rate,and fixed dilated pupils.

A

Acute panautonomic neuropathy

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15
Q

____ is a clinical syndrome characterized by frequent symptoms that occur with standing (e.g., lightheadedness, palpitations, tremulousness, generalized weakness, blurred vision, exercise intolerance, fatigue), an increase in heart rate of _____ (or 40 beats/min in those 12 to 19 years of age), and _______

A

Postural orthostatic tachycardia syndrome (POTS)

Increase in HR of 30 beats/min or more on standing

Absence of a more than 20-mm Hg reduction in systolic BP

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16
Q

In this group of conditions, the cardiovascular reflexes that control the circulation become inappropriate in response to a trigger, which results in vasodilation with or without bradycardia and a drop in BP and global cerebral hypoperfusion. In each case the reflex is composed of a trigger (the afferent limb) and a response (the efferent limb).

A

Reflex-mediated syncope/Situational syncope

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17
Q

If hypotension secondary to peripheral vasodilation predominates, it is classified as a _____ response; if bradycardia or asystole predominates, it is classified as a _____; and when both vasodilation and bradycardia play a role, it is classi- fied as a mixed response

A

Vasodepressor response - peripheral vasodilation

Cardioinhibitory response - bradycardia or asystole

Mixed - mixed response

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17
Q

The two most common types of reflex-mediated syncope are _____.

A

Carotid sinus hypersensitivity
Neurally mediated hypotension

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18
Q

The term neurally mediated hypotension or syncope (also known as neurocardiogenic, vasodepressor, and vasovagal syncope and “faint- ing”) has been used to describe a common abnormality in regulation of BP characterized by an abrupt onset of hypotension with or without bradycardia

A
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19
Q

Triggers associated with the development of NMS include orthostatic stress, such as can occur with prolonged standing or a hot shower, and emotional stress, such as can result from the sight of blood.1

A
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20
Q

It has been speculated that the fall in BP seen during neurally mediated hypotension mimics a “fictitious hemorrhage.” To protect against this fictitious hemorrhage, the brainstem triggers cardioinhibition as pro- tection against the hypothetical loss of blood simulated by the reduc- tion in venous return.

A
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21
Q

Syncope caused by ____ results from stimu- lation of carotid sinus baroreceptors located in the internal carotid artery above the bifurcation of the common carotid artery.

It is diag- nosed by the reproduction of clinical syncope during carotid sinus massage, with a cardioinhibitory response if asystole is longer than 3 seconds or AV block occurs; or a significant vasodepressor response if there is a more than 50-mm Hg drop in systolic BP; or a mixed cardioinhibitory and vasodepressor response

A

Carotid sinus hypersensitivity

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22
Q

Thus the diagnosis of carotid sinus hypersensitivity should be approached cautiously after excluding alternative causes of the syncope. Once diagnosed, dual-chamber pacemaker implantation is recommended for patients with recurrent syncope or falls resulting from carotid sinus hypersensitivity that is cardioinhibitory or mixed (class 2A/IIa,level of evidence [LOE] B-R)

A
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23
Q

Cardiac causes of syncope, particularly tachyarrhythmias and bradyarrhythmias, are the second most common cause of syncope and account for 10% to 20% of syncopal episodes (see Table 71.2 and Chapters 65 and 67).

_____ is the most common tachyarrhythmia that can cause syncope.

A

VT

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24
Q

Neurologic causes of transient LOC, including migraines, seizures, Arnold-Chiari malformations, and transient ischemic attacks, are surprisingly uncommon and account for less than 10% of all cases of syncope.

Most patients in whom a “neurologic” cause of transient LOC is established are in fact found to have had a ______ rather than true syncope.

A

Seizure

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25
Q

Metabolic causes of transient LOC are rare and account for less than 5% of syncopal episodes.

The most common metabolic causes of syncope are _______. Establishing hypoglycemia as the cause of apparent LOC requires demonstration of hypoglycemia during the syncopal episode. Although hyperventilation-induced syncope has generally been considered to result from a reduction in cerebral blood flow, one study demonstrated that hyperventilation alone was not sufficient to cause syncope.

A

Hypoglycemia, hypoxia, and hyperventilation

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26
Q

The 2017 ACC/AHA/HRS syncope guidelines provide a class I (LOE B-NR) recommendation for performing a detailed history and physical examination in patients with syncope.

A
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27
Q

Initial evaluation should begin by determining whether the patient did in fact experience a syncopal epi- sode by asking the following: (1) Did the patient experience complete LOC? (2) Was the LOC transient with a rapid onset and short duration? (3) Did the patient recover spontaneously, completely, and without sequelae? and (4) Did the patient lose postural tone?

f the answer to one or more of these questions is negative, other nonsyncopal causes of transient LOC should be suspected.

A
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28
Q

When evaluating a patient with syncope,particular attention should then be focused on (1) determining whether the patient has a _____ (i.e., diabetes) or a family history of cardiac disease, syncope, or sudden death; (2) identifying medications that may have played a role in syncope, especially those that may cause hypo- tension, bradycardia/heart block, or a proarrhythmic response (anti- arrhythmics); (3) quantifying the number and chronicity of previous syncopal and presyncopal episodes; (4) identifying precipitating fac- tors,including body position and activity immediately before syncope; and (5) quantifying the type and duration of prodromal and recovery symptoms.

A

History of cardiac disease or metabolic disease
Family history - CD, Syncope, SCD
Medications
Number/chronicity
Precipitating factors
Type and duration

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29
Q

The clinical histories obtained from patients with syncope related to AV block and VT are similar. In each case, syncope typically occurs with less than 5 seconds of warning and few if any prodromal and recovery symptoms. .Demographic features suggesting that the syncope results from an arrhythmia such as VT or AV block include male sex, fewer than three previous episodes of syncope, and increased age

A
30
Q

Features of the clinical history that point toward a diagnosis of NMS include palpitations, blurred vision, nausea, warmth, diaphoresis, or lightheadedness before syncope and the presence of nausea, warmth, diaphoresis,or fatigue after syncope.

A
31
Q

Features of the clinical history useful in distinguishing seizures from syncope include orientation following an event, a blue face or not becoming pale during the event, frothing at the mouth, aching muscles, feeling sleepy after the event, time of seizure relative to onset of syncope—early points to neurologic whereas late suggests arrhyth- mic cause—and a duration of unconsciousness of longer than 5 minutes

A

Early seizure - neurologic
Late - cardiac/arrhythmic

32
Q

Tongue biting strongly points toward a seizure rather than syncope as the cause of LOC. One recent study reported that a his- tory of tongue biting during an episode of LOC had 33% sensitivity and 96% specificity in predicting a seizure as the cause of the LOC

A
33
Q

Other findings suggestive of a seizure as a cause of the syncopal episode include (1) an aura before the episode, (2) horizontal eye deviation during the episode, (3) elevated BP and pulse during the episode, and (4) a headache following the even

A
34
Q

Urinary or fecal incontinence can be observed with either a seizure or a syncopal episode but occurs more often with a seizure.

A
35
Q

Grand mal seizures are usually associated with tonic-clonic movements.It is important to note that syncope caused by cerebral ischemia can result in decorti- cate rigidity with clonic movements of the arms.

A
36
Q

Akinetic or petit mal seizures can be recognized by the patient’s lack of responsiveness in the absence of loss of postural tone

A
37
Q

Temporal lobe seizures last sev- eral minutes and are characterized by confusion, changes in level of consciousness, and autonomic signs such as flushing.

A
38
Q

Vertebral bas- ilar insufficiency should be considered as the cause of the syncope if it occurs in association with other symptoms of brainstem isch- emia (i.e., diplopia, tinnitus, focal weakness or sensory loss, vertigo, or dysarthria).

A
39
Q

Migraine-mediated syncope is often associated with a throbbing unilateral headache, scintillating scotomata, and nausea.

A
40
Q

The patient’s BP and heart rate should be deter- mined while supine and then repeated each minute for approximately 3 minutes while standing.The two abnormalities that should be sought are (1) early orthostatic hypotension, defined as a 20-mm Hg drop in systolic BP or a 10-mm Hg drop in diastolic BP within 3 minutes of standing, and (2) POTS, an increase in heart rate of 30 beats/min or more on standing (or >/=40 beats/min in those 12 to 19 years of age), and absence of a more than 20-mm Hg reduction in systolic BP.

A
41
Q

Carotid sinus massage should be performed after checking for bruits by applying gentle pressure over the carotid pulsation, first one side and then the other, just below the angle of the jaw where the carotid bifurcation is located. Pressure should be applied for 5 to 10 seconds in both the supine and the upright position because an abnormal response to carotid sinus massage is present only in the upright position in up to one third of patients.

A
42
Q

Since the main complications associated with performing carotid sinus massage are neurologic, it should be avoided in patients with ________, except if significant stenosis has been excluded by carotid Doppler studies

A

Previous transient ischemic attacks, strokes within the past 3 months, and carotid bruits

43
Q

A normal response to carotid sinus massage is a _____. Carotid sinus hypersensitivity is diagnosed by the ____ and the responses previously noted.

A

Transient decrease in the sinus rate, prolongation of AV conduction, or both

CSH - reproduction of clinical syncope during carotid sinus massage

Diagnosis of carotid sinus hypersensitivity as the cause of the syn- cope requires reproduction of the patient’s symptoms during carotid sinus massage.

44
Q

The tilt-table test is a valuable diagnostic test for evaluating patients with syncope,1,2,13 with a positive response indicating susceptibility to NMS. The 2017 ACC/AHA/HRS syncope guidelines state that tilt-table testing can be useful for patients with suspected vasovagal syncope if the diagnosis is unclear after initial evaluation (class IIa, LOE B-NR).1

A
45
Q

Upright tilt testing is generally performed for 30 to 45 minutes fol- lowing a 20-minute horizontal pretilt stabilization phase at an angle between 60 and 80 degrees (with 70 degrees being most common). The sensitivity of the test can be increased, along with an associated fall in specificity, by the use of longer tilt durations, steeper tilt angles, and provocative agents such as isoproterenol or nitroglycerin.When isoproterenol is used, it is recommended that the infusion rate be increased incrementally from 1 to 3 μg/min to increase the heart rate 25% greater than baseline. When nitroglycerin is used, a fixed dose of 300 to 400 μg of nitroglycerin spray should be administered sublin- gually after a 20-minute unmedicated phase with the patient in the upright position.These two provocative approaches are equivalent in diagnostic accuracy. In the absence of pharmacologic provocation, the specificity of the test has been estimated to be 90%; when provocative agents are used,specificity decreases significantly.

A
46
Q

The main indication for upright tilt testing is to confirm a diagnosis of NMS when the initial evaluation was insufficient to establish this diagnosis.Tilt-table testing is also of value in diagnosing psychogenic pseudosyncope.

A
47
Q

The 2017 ACC/AHA/HRS syncope guidelines state that echocardiography can be useful in selected patients present- ing with syncope if structural heart disease is suspected (class IIa,LOE B-NR).1

A
48
Q

The guidelines also state that routine cardiac imaging is not useful in the evaluation of patients with syncope unless cardiac etiol- ogy is suspected on the basis of an initial evaluation including history, physical examination, or ECG (class 3/III, LOE B-NR).

A
49
Q

These guidelines also recommend that computed tomography (CT) or magnetic reso- nance imaging (MRI) may be useful in selected patients presenting with syncope of suspected cardiac etiology (class IIb, LOE B-NR

A
50
Q

Echocardiographic findings considered diagnostic of the cause of syncope include severe aortic stenosis, pericardial tamponade, aortic dissection, congenital abnormalities of the coronary arteries, and obstructive atrial myxo- mas or thrombi. Findings of impaired right or left ventricular function, evidence of right ventricular overload or pulmonary hypertension (pulmonary emboli),or the presence of hypertrophic cardiomyopathy (see Chapter 54) are of prognostic importance and justify additional diagnostic testing.

A
51
Q

Myocardial ischemia is an unlikely cause of syncope and, when pres- ent, is usually accompanied by angina (see Chapters 35 and 40). The use of stress tests (see Chapter 15) is best reserved for patients in whom syncope or presyncope occurred during or immediately after exertion in association with chest pain or in a patient at high risk for coronary artery disease.

A
52
Q

The 2017 ACC/AHA/HRS syncope guidelines state exercise stress testing can be useful to establish the cause of syncope in selected patients who experience syncope or presyncope during exertion (class IIa, LOE C-LD

A
53
Q

_____ is suggestive of a cardiac cause. In contrast, syncope following exercise is usually caused by NMS

A

Syncope occurring during exercise

54
Q

The 2017 ACC/AHA/HRS syn- cope guidelines provide a class I (LOE B-NR) recommendation for performing an ECG in patients with syncope.1 The initial ECG results in establishment of a diagnosis in approximately 5% of patients and sug- gests a diagnosis in another 5% of patients. Specific findings that can identify the probable cause of the syncope include QT prolongation (long-QT syndrome), the presence of a short PR interval and a delta wave (Wolff-Parkinson-White syndrome),the presence of a right bundle branch block pattern with ST-segment elevation (Brugada syndrome), or evidence of acute myocardial infarction, high-grade AV block, or T wave inversion in the right precordial leads (arrhythmogenic right ven- tricular dysplasia)

A
55
Q

Most patients with syncope have normal findings on ECGs, which is useful because it suggests a low likelihood of a cardiac cause of the syncope and is associated with an excellent prognosis,particularly when observed in a young patient with syncope. Despite the low diagnostic yield of electrocardiography,the test is inex- pensive and risk free and is considered a standard part of the evalua- tion of virtually all patients with syncope.1

A
56
Q

Class I Indications for Electrophysiologic Testing in Evaluation of Patients with Syncope

A

In patients with ischemic heart disease when the initial evaluation suggests an arrhythmic cause and there is no established indication for an ICD. (IB)

57
Q

Diagnostic Findings of Electrophysiologic Testing in Evaluation of Patients with Syncope (IB recommendations)

A

(1) Sinus bradycardia and a prolonged CSNRT (>525 msec)
(2) BBB and either a baseline H-V interval >/=100 msec or second- or third-degree His-Purkinje block during incremental atrial pacing or with pharmacologic challenge
(3) Induction of sustained monomorphic VT in patients with a previous myocardial infarction
(4) Induction of SVT with reproduction of the hypotensive or spontaneous symptoms

58
Q

The 2017 ACC/AHA/HRS syncope guidelines state that the choice of a specific cardiac monitor should be determined on the basis of the frequency and nature of the syncope events (class I, LOE C-EO)

A
59
Q

EP testing is no longer indicated for patients with a severely depressed ejection fraction, because in this setting an implantable cardioverter-defibrillator (ICD) is indi- cated regardless of the presence or mechanism of the syncope.1,2

A
60
Q

Sinus node function is evaluated during EP testing primarily by determining the SNRT. Identification of sinus node dysfunction as the cause of syncope is uncommon during EP tests (<5%).The sensitivity of an abnormal SNRT or corrected SNRT (CSNRT) is approximately 50% to 80%.The specificity of an abnormal SNRT or CSNRT is less than 95%.It is important to note that the absence of evidence of sinus node dysfunction during EP testing does not exclude a bradyarrhythmia as the cause of the syncope

A
61
Q

VT is the most common abnormality uncovered during EP testing in patients with syncope and was identified as the probable cause in approximately 20% of patients

A

AV block was identified as the probable cause of syncope in approximately 10% to 15% of patients.

Identification of sinus node dysfunction as the cause of syncope is uncommon during EP tests (<5%)

62
Q

The 2017 ACC/AHA/HRS syncope guidelines state that MRI and CT of the head are not recommended in the routine evaluation of patients with syncope in the absence of focal neurologic findings or

A
63
Q

Treatment of a patient with syncope has three goals:(1) prolong survival, (2) prevent traumatic injuries,and (3) prevent recurrences of syncope.

A
64
Q

However, ICD implanta- tion may not be required for patients with VT/VF occurring within 48 hours of an acute myocardial infarctio

A
65
Q

Factors that should be considered when making a recommendation for a particular patient include: (1) the potential for recurrent syncope, (2) the presence and duration of warning symp- toms,(3) whether syncope occurs while seated or only when standing, (4) how often and in what capacity the patient drives,and (5) whether any state laws may be applicable.

A
66
Q

The 2017 ACC/AHA/HRS guidelines on man- agement of syncope identify the following physical measures as class IIA treatments of NMS.1 It has been reported that 2 minutes of an iso- metric handgrip maneuver initiated at the onset of symptoms during tilt testing rendered two thirds of patients asymptomatic. Other studies have demonstrated that tilt (standing) training is effective in the treatment of NMS.Standing training involves leaning against a wall with the heel 10 inches (25 cm) from the wall for progressively longer periods for 2 to 3 months.Standing time should initially be 5 minutes two times per day with a progressive increase to 40 minutes twice daily.

A
67
Q

Medications that are generally relied on to treat NMS include beta blockers,fludrocortisone,serotonin reuptake inhibitors, and midodrine.

A
68
Q

Even though beta blockers were previ- ously considered by many to be first-line therapy, recent studies have reported that the beta blockers metoprolol, propranolol, and nadolol are no more effective than placebo.13 A recent subanalysis of data from a randomized prospective study evaluating the effectiveness of fludro- cortisone (Florinef) reported weak evidence that fludrocortisone may be of therapeutic value despite missing its primary endpoint.

A
69
Q

Clinical Variables for Identification of High-Risk Syncope Patients Who May Benefit from Hospitalization or an Accelerated Outpatient Evaluation

A

Severe structural heart disease (low ejection fraction, previous myocardial infarction, heart failure)

Clinical or ECG features suggesting arrhythmic syncope :
Syncope during exertion or while supine
Palpitations at the time of syncope
Family history of sudden death
Nonsustained ventricular tachycardia
Bifascicular block or QRS >120 msec
Severe sinus bradycardia (<50 beats/min) in the absence of medication or physical training
Preexcitation
Prolonged or very short QT interval
Brugada ECG pattern (right bundle branch block with ST elevation in leads V1–V3)
Arrhythmogenic right ventricular dysplasia ECG pattern (T wave inversion
in leads V1–V3 with or without epsilon waves)
ECG suggestive of hypertrophic dilated cardiomyopathy
Clinical evidence or suspicion of a pulmonary embolus (clinical setting, sinus tachycardia, shortness of breath)
Severe anemia

Important comorbid conditions
Significant electrolyte abnormalities
Severe anemia

70
Q

Characteristics of neurally mediated hypotension

A

Demographics and clinical setting:
Female > male sex
Younger age (<55 years)
More episodes (>2)
Standing, warm room, emotional upset

Premonitory symptoms:
Longer duration (>5 sec)
Palpitations
Blurred vision
Nausea
Warmth
Diaphoresis
Lightheadedness

Other observations:
Pallor
Diaphoresis
Dilated pupils
Slow pulse, low BP
Incontinence may occur
Brief clonic movements may occur

Residual symptoms:
Residual symptoms common
Prolonged fatigue common (>90%) Oriented

71
Q

Characteristics of Arrhythmias

A

Demographics and clinical setting:
Male > female sex
Older age (>54 years)
Fewer episodes (<3)
During exertion or supine
Family history of sudden death

Premonitory symptoms:
Shorter duration (<6 sec)
Palpitations less common

Other observations:
Blue, not pale
Incontinence may occur
Brief clonic movements may occur

Residual symptoms:
Residual symptoms uncommon (unless prolonged unconsciousness)
Oriented

71
Q

Characteristics of Seizures

A

Demographics and clinical setting:
Younger age (<45 years)
Any setting

Premonitory symptoms:
Sudden onset or brief aura (déjà vu, olfactory, gustatory, visual)

Other observations:
Blue face, no pallor
Frothing at the mouth
Prolonged syncope (duration > 5 min)
Tongue biting
Horizontal eye deviation
Elevated pulse and BP
Incontinence more likely*
Tonic-clonic movements if grand mal

Residual symptoms:
Residual symptoms common Aching muscles
Disoriented
Fatigue
Headache Slow recovery

71
Q

Characteristics of Psychogenic syncope

A

Demographics and clinical setting:
Female > male sex
Occurs in presence of others
Younger age (<40 years)
Many episodes (often many episodes in a day)
No identifiable trigger

Premonitory symptoms:
Usually absent

Other observations:
Normal color
Not diaphoretic
Eyes closed
Normal pulse and BP No incontinence
Prolonged duration (minutes) common

Residual symptoms:
Residual symptoms uncommon
Oriented