SYNCOPE Suggestions for Lecturer -1-hour lecture

SYNCOPE Suggestions for Lecturer -1-hour lecture
-Use GRS slides alone or to supplement your own teaching materials. -Refer to GRS for further content and refer to Geriatrics at Your Fingertips for updated information. -For strength of evidence (SOE) levels, please see the GRS Teaching Slides site or the GRS inside front cover. -See GRS9 questions 52, 101, 130, 139, 223 and 245 for additional case vignettes on syncope.

OBJECTIVES Know and understand: Factors that may lead to syncope in older adults Elements of evaluation (history, physical examination, testing) of older adults with syncope Treatment options for syncope

TOPICS COVERED Natural History: Diagnosis and Prognosis Pathophysiology Evaluation: History, Physical Exam, Diagnostic Testing Treatment

SYNCOPE: INTRODUCTION (1 of 2)
A symptom complex composed of a sudden and transient loss of consciousness resulting from a temporary interruption of global cerebral perfusion A common reason for evaluation in both outpatient clinics and emergency departments, and for hospital admission Annually it accounts for approximately 3% of emergency department visits and 2%–6% of hospital admissions

SYNCOPE: INTRODUCTION (2 of 2)
Incidence of syncope increases with age Incidence doubles in those ≥70 years old, and the rate among those ≥80 years old is three to four times that seen among younger people Approximately 80% of patients hospitalized for syncope are ≥65 years old Potential causes range from those that are benign and self-limiting to those that are life threatening In older adults, the cause of syncope can often be multifactorial, adding to the diagnostic difficulty

SYNCOPE: NATURAL HISTORY
Decreases in Cardiac Output or Peripheral Vascular Resistance, or both Decreased Systemic Blood Pressure and Reduced Cerebral Perfusion Syncope Causes may be benign or life-threatening Causes may be multifactorial Must consider adverse effects of drugs as a cause

COMMON CAUSES OF SYNCOPE
Neurally mediated Cardiac rhythm disturbances Decreased intravascular volume due to blood loss or dehydration Alterations in the peripheral vasculature due to arterial vasodilation or increased venous pooling Medication related Localized atherosclerotic diseases, such as vertebral basilar insufficiency and subclavian steal, can result in syncope without alteration in systemic blood pressure. These causes are uncommon. Epileptic seizure, a common cause of transient loss of consciousness, is no longer categorized as a cause of syncope, because seizure is not mediated by a decrease in cerebral perfusion It is important to differentiate a seizure from syncope as a cause of transient loss of consciousness

DISTINGUISHING CHARACTERISTICS OF SEIZURE AND SYNCOPE
Phase Sign/Symptom Seizure Cardiac Syncope Due to Arrhythmia Vasovagal Syncope Before Position Any Upright; aborted by lying flat Warning/prodrome None <5 seconds Seconds to minutes Precipitant Usually absent Absent Present Palpitations Sometimes Nausea/diaphoresis Rare Common Visual changes During Tone Rigid Flaccid Motionless, relaxed Pulse Rapid Absent or faint Slow, faint Color Pale or normal Blue, ashen Pale Incontinence Very rare Eye findings Tonic eye deviation Variable pupils Dilated, reactive pupils Oral frothing After Type of recovery Slow, incomplete Rapid, complete Fatigue common Mental status Disorientation No retrograde amnesia Focal neurologic findings See Table 28.2 in GRS 9 for more details Characteristics most distinctive in determining the cause of syncope are highlighted in bold.

SYNCOPE: PROGNOSIS (1 of 2)
Depends on the underlying cause Cardiac causes have the worst prognosis 1-year mortality is 18%–33%, with deaths chiefly due to underlying disease, not syncope Noncardiac causes 1-year mortality of approximately 6%

SYNCOPE: PROGNOSIS (2 of 2)
Neurally mediated or vasovagal syncope Vasovagal mechanisms as the cause of syncope in approximately 30%–50% of patients >65 years old Some suggestion that vasovagal syncope in older adults is often associated with comorbid illness that can increase overall mortality No cause found In approximately 10%–20% of syncopal patients Prognosis for these patients is no worse or better than that of the general population Neurally mediated or vasovagal syncope, which has a benign prognosis in the young, was once thought to be an unusual cause of syncope in older adults. However, reports from syncope evaluation centers have found vasovagal mechanisms as the cause of syncope in approximately 30%–50% of patients >65 years old (SOE=A). It has not been established that vasovagal syncope in older adults has the same benign prognosis as it does in younger individuals, because there has been some suggestion that vasovagal syncope in older adults is often associated with comorbid illness that can increase overall mortality (SOE=B).

PATHOPHYSIOLOGY: MECHANISMS THAT PREVENT SYNCOPE
The integrity of a number of control mechanisms is crucial for maintaining adequate perfusion of the brain and cerebral oxygen delivery after sudden changes in blood pressure Carotid and aortic baroreceptors Sympathetic renal stimulation of the renin-angiotensin system Arteriolar autoregulation

PATHOPHYSIOLOGY OF SYNCOPE: EFFECTS OF AGING
Reflex mechanisms are less responsive with aging Decreased ability to increase heart rate in response to sympathetic stimulation Increased sensitivity to effects of dehydration, diuretics and vasodilator medications Comorbidities that affect postural responses are common (eg, diabetes mellitus, Parkinson disease) Medications may further impair postural reflexes (eg, vasodilators, calcium channel blockers, ACE inhibitors, -blockers, -blockers, tricyclic antidepressants)

PATHOPHYSIOLOGY: ADDRESSING CAUSES
Age-related decline in adaptive reflexes, comorbid conditions, and medications can all have a role in older adults presenting with syncope Address these issues by: Increasing caution with postural change, physical counter-pressure maneuvers (eg, leg crossing) and compression stockings to increase venous return Adequate hydration Simplification of the patient’s medication regimen to eliminate excessive medications

SYNCOPE EVALUATION: HISTORY (1 of 2)
An accurate recall of the syncopal event is frequently inadequate because of the high prevalence of cognitive dysfunction in the older population. The medical history, if possible, should be obtained from a witness to the event. Precipitants? Eating Urinating Coughing Medication Emotional stress Physical exertion Turning head Prodromal symptoms? Chest pain Palpitations Dyspnea Diaphoresis Presyncope Nausea Vomiting Syncope occurring while sitting or supine suggests a profound hemodynamic disturbance and should raise a concern about a significant cardiac arrhythmia. Syncope occurring during physical exertion should raise the possibility of myocardial ischemia or aortic stenosis. A history of syncope after turning motions of the head should raise the possibility of carotid sinus hypersensitivity. Chest pain, palpitations, or shortness of breath suggests a cardiac or pulmonary cause. Diaphoresis, presyncope, and GI symptoms, such as nausea or vomiting, can be associated with vasovagal syncope. Sudden onset of syncope with <5 sec of warning is characteristic of syncope due to a cardiac arrhythmia and should be evaluated as such. However, in older adults, vasovagal syncope can present with short or no prodrome because of inability to precisely recall the event. Thus, if the initial evaluation for arrhythmia in an older adult with syncope without a prodrome is unrevealing, a vasovagal mechanism should also be considered.

SYNCOPE EVALUATION: HISTORY (2 of 2)
Medications? How, when taken, what doses Relationship to meals and activities Recent changes Any witnesses? Duration of event Appearance of patient during event (flaccid tone and motionless or increased tone and motion?) Comorbid conditions? For example, CAD, Diabetes Mellitus Many antiarrhythmic medications and other commonly used medications can increase the propensity for ventricular arrhythmias by prolonging the QT interval (for a full current list, see

PREDICTING CARDIAC SYNCOPE: EGSYS SCORE
Variable Score Palpitations preceding syncope 4 Heart disease or abnormal ECG 3 Syncope during effort Syncope while supine 2 Precipitating or predisposing factors, or both (warm or crowded place, prolonged orthostasis, fear, pain or emotional distress) –1 Autonomic prodromes (nausea/vomiting) EGSYS = Evaluation of Guidelines in Syncope Study Scores ≥3 are associated with higher rates of cardiac syncope and higher mortality. SOURCE: Data from Del Rosso A, Ungar A, Maggi R, et al. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to a general hospital: the EGSYS score. Heart ;94(12):1620–1626.

CARDIAC SYNCOPE DUE TO ARRHYTHMIA
Prior to event Occurs in any position, <5 sec warning No precipitant; palpitations are sometimes present No nausea, diaphoresis or visual changes During event Flaccid tone; pulse faint or absent Blue, ashen skin Incontinence (rare) Variable pupils, no oral frothing Recovery Rapid and complete For more information, see Table 28.2 in GRS 9

VASOVAGAL SYNCOPE Prior to event Aborted if person lies flat
Seconds to minutes of warning Precipitant present; nausea/diaphoresis common Visual changes are common During event Motionless; relaxed tone; slow, faint pulse Pale color; dilated, reactive pupils Recovery Fatigue, nausea, and diaphoresis common No retrograde amnesia For more information, see Table 28.2 in GRS 9

SYNCOPE CAUSED BY SEIZURE
Prior to event Occurs in any position No warning or prodrome During event Rigid tone; rapid pulse Tonic eye deviation common Frothing at mouth Recovery Slow, incomplete Disorientation; focal neurologic findings For more information, see Table 28.2 in GRS 9

SYNCOPE EVALUATION: PHYSICAL EXAMINATION (1 of 2)
Should focus on elements raised by the history Pulse in supine and standing positions Orthostatic vital signs: Measure BP in both arms, 1 min after standing and again after standing for 3 min Carotid pulse examination Delayed upstroke and low volume may identify aortic stenosis Perform carotid massage only with continuous ECG and resuscitation equipment available Contraindicated with carotid bruit, CVD, recent MI

SYNCOPE EVALUATION: PHYSICAL EXAMINATION (2 of 2)
Cardiac examination for murmurs, extra heart sounds Stool for occult blood Neurologic examination for focal deficits

SYNCOPE EVALUATION: DIAGNOSTIC TESTING (1 of 4 )
The following slides review the various diagnostic tests that are available for the evaluation of syncope It is important to remember that not every test is required; the history and physical are used to determine appropriate testing In all patients, an assessment of orthostatic vital signs, gait, laboratory tests, and ECG are reasonable first steps

SYNCOPE EVALUATION: DIAGNOSTIC TESTING (2 of 4)
ECG for all syncopal older adults; assess for: Acute or remote MI Conduction abnormalities and pre-excitation, such as Wolff-Parkinson-White Sinus bradycardia Prolonged QT interval Ambulatory ECG Among patients able and willing to operate loop recorders, diagnostic yield is ~25% Implantable loop recorders Consider using in patients when an arrhythmic cause of syncope is suspected but not sufficiently proved Although an ECG establishes a diagnosis in only 5% of those with syncope, approximately 50% have an abnormal ECG. Abnormalities on an ECG can provide clues for further cardiovascular evaluation; a normal ECG is associated with a more favorable prognosis. An ambulatory ECG recording can establish or exclude many causes of syncope if the patient experiences syncopal or presyncopal symptoms during the recording. Unfortunately, the occurrence of symptoms during ambulatory ECG monitoring is relatively infrequent in most patients with syncope that remains unexplained after a history, physical examination, and ECG.

Echocardiography and Exercise Stress Testing Most useful in confirming a specific diagnosis suspected by other assessment, otherwise it is low yield Tilt-table testing Useful for patients suspected of having vasovagal syncope and those with unexplained syncope who are not suspected of having a cardiac cause. Electrophysiologic studies Not recommended for patients with a normal ECG or those without a history of heart disease or symptoms of palpitations Echocardiography: In the absence of features suggestive of heart disease by history, physical examination, or ECG, two-dimensional echocardiography has a low yield. It is most useful in confirming a specific diagnosis suspected by other assessment. Occult coronary artery disease is also relevant among older adults, and stress testing is often used for screening. In some patients, particularly those with the suggestion of structural cardiac abnormalities and ischemia by history, physical examination, or ECG, it is efficient to perform stress echocardiography as a single procedure. Tilt-Table Testing: Head-up tilt-table testing results in pooling of blood in the legs, and in susceptible individuals it can trigger syncope mediated by neurocardiogenic mechanisms or confirm postural hypotension. Tilt-table testing is useful for patients suspected of having vasovagal syncope and those with unexplained syncope who are not suspected of having a cardiac cause. Responses to tilt testing performed for evaluation of syncope tend to differ by age among adults without significant structural heart disease. Those ≥65 years old tend to have far higher rates of symptoms due to pure vasodilatation without significant change in heart rate than individuals ≤35 years old. In contrast, individuals ≤35 years old tend to have more profound cardioinhibitory responses, characterized by profound bradycardia or asystole induced by tilt testing. The different patterns of responses suggest that different mechanisms for neurocardiogenic syncope predominate at different ages. Electrophysiologic Study (EPS): The development of effective noninvasive methods, such as prolonged rhythm monitoring, has decreased the importance of EPS as a diagnostic test. Nevertheless, this test is still useful for diagnosis in suspected intermittent bradycardia, tachyarrhythmia, or in patients with bundle-branch block (suggestive of impending high-grade AV block). EPS is not recommended for patients with a normal ECG or those without a history of heart disease or symptoms of palpitations.

Neurologic testing (CT or MRI, and/or EEG) Not generally required Appropriate in situations when focal neurologic signs or symptoms are present or when the history suggests seizure or trauma Consider autonomic evaluation if signs and symptoms of autonomic dysfunction are present

SYNCOPE: IS HOSPITAL ADMISSION REQUIRED?
Older patients are frequently hospitalized for evaluation because they are presumed to be higher risk However, patients with no risk factors for adverse events were found to have no significant increase in adverse events regardless of age A specialized syncope observational unit in the hospital setting has been shown to reduce hospital admission and expedite the diagnosis of potential causes of syncope

RISK FACTORS FOR ADVERSE PROGNOSIS IN SYNCOPE
Symptoms Chest pain Shortness of breath Palpitations or rapid heart beat GI bleeding Cardiac history Coronary artery disease Heart failure Hypertrophic cardiomyopathy Pacemaker or defibrillator Antiarrhythmic medications Ventricular tachycardia or ventricular fibrillation Syncope characteristics Syncope during exercise >1 episode within 6 months Family history First-degree relative with sudden death, hypertrophic cardiomyopathy, Brugada syndrome, or long QT syndrome Physical examination Tachypnea Hypoxia (O2 saturation <90%) Sinus heart rate <50 beats/min or >100 beats/min Systolic blood pressure <90 mmHg Heart murmur Volume depletion Neurologic deficits ECG abnormalities Q waves Ischemic ST segment or T wave changes Ventricular or supraventricular arrhythmias, including rapid atrial fibrillation Second- or third-degree AV block Corrected QT interval >500 ms Laboratory abnormalities Hematocrit <30% Occult blood in feces SOURCE: Data from Grossman SA, Chiu D, Lipsitz L, et al. Can elderly patients without risk factors be discharged home when presenting to the emergency department with syncope? Arch Gerontol Geriatr. 2014;58:110–114. Note: Patients with no risk factors for adverse prognosis can likely be safely dismissed from the emergency department without hospitalization.

TREATMENT OF SYNCOPE (1 of 5)
Goals of treatment: Improve quality of life and prevent physical injuries Focus on treating the underlying disorder In older patients, treatment of multiple possible causes is often necessary Discontinuation of medications that increase the risk of syncope is always an early step Polypharmacy is increasingly identified as a risk of syncope because of the actual number of medications and risk of interaction and adverse effects, and potentially because of the number of comorbid conditions requiring complex pharmacotherapy. Before any new medication is added, the medication list must be reviewed for potential culprits (in particular, α-antagonists, clonidine, vasodilators, and excessive diuretics). Timing of medication administration should also be reviewed, and shifting antihypertensive medications to evening administration may reduce daytime orthostatic symptoms.

Reflex Syncope and Postural Hypotension Nonpharmacologic measures with physical counter-pressure maneuvers Leg crossing, arm tensing, hand grip, and buttock clenching are able to induce a significant blood pressure increase during the phase of impending reflex syncope so that the patient can avoid or delay losing consciousness Compression stockings and abdominal binders Smaller and frequent meals can be effective in patients with postprandial hypotension

TREATMENT OF SYNCOPE (3 of 5 )
Medical Management Midodrine Increases vasoconstriction, may help with persistent postural hypotension Use with caution: May cause supine hypertension in those with decreased vascular compliance Monitor blood pressure response and symptoms Pyridostigmine Increases both standing blood pressure and peripheral resistance, attenuating orthostatic blood pressure Adverse effects: Abdominal cramps, diarrhea, urinary urgency Use with close supervision, older adults may not tolerate adverse effects

TREATMENT OF SYNCOPE (4 of 5 )
Medical Management Volume expansion with added salt Fludrocortisone Both increase renal sodium retention and intravascular volume May be effective in patients with persistent postural hypotension

Role of Pacemakers Mainstay of treatment for sinus node dysfunction or high grade AV block Permanent pacing is indicated when syncope or near syncope is correlated with bradycardia after ensuring that medications that may be causing bradycardia have been discontinued, if indicated after a risk vs benefit analysis Not recommended in patients with unexplained syncope or falls without documentation of bradycardia Although the recommendation to avoid pacemaker placement but rather discontinue medications causing bradycardia in patients taking them makes sense, often these medications are treatment for a significant cardiac condition (ie, β- blockers) or dementia (acetylcholinesterase inhibitors). Acetylcholinesterase inhibitors are associated with a significant risk of bradycardia, and bradycardic patients have a significant risk of syncope. Although recommendations for when it is appropriate or necessary to discontinue acetylcholinesterase inhibitors are needed, the risk of these medications in patients with bradycardia may outweigh the benefits.

SUMMARY (1 of 2) In older adults the cause of syncope is often multifactorial Important to review the medication list of each patient, as medications are commonly implicated as a source of syncope Most diagnostic procedures for syncope are expensive and have a low yield unless findings from the history and physical suggest a particular cause

SUMMARY (2 of 2) Important to rule out cardiac conditions as a cause of syncope as they are associated with worse prognosis Treatment of syncope focuses on treating the underlying disorder

CHOOSING WISELY Recommendations for GRS9 Syncope, based on the American Board of Internal Medicine Foundation’s Choosing Wisely® Campaign: Do not perform imaging of the carotid arteries for simple syncope without other neurologic symptoms. In the evaluation of simple syncope and a normal neurologic examination, do not obtain brain imaging studies (CT or MRI).

CASE 1 (1 of 3) A 67-year-old man is in the emergency department because he fainted. He had accidentally cut his finger with a table knife. He then rose from seated position, at which point he felt dizzy. The dizziness lasted about 10 sec. It was accompanied by nausea, sweating, palpitations, and chest pain. He lost and then regained consciousness within 30 sec, and rapidly returned to baseline cognition. According to witness, patient had sporadic, arrhythmic limb jerking for several seconds during episode. History: hypertension, CAD, benign prostatic hyperplasia Medications: aspirin, simvastatin, doxazosin Normal vital signs and cardiopulmonary examination on arrival at emergency department

CASE 1 (2 of 3) Which one of the following suggests a higher risk of mortality in this patient? Use of doxazosin Nausea and diaphoresis preceding loss of consciousness Injury preceding loss of consciousness Palpitations preceding loss of consciousness Witnessed brief, arrhythmic limb jerks

CASE 1 (3 of 3) Which one of the following suggests a higher risk of mortality in this patient? Use of doxazosin Nausea and diaphoresis preceding loss of consciousness Injury preceding loss of consciousness Palpitations preceding loss of consciousness Witnessed brief, arrhythmic limb jerks ANSWER: D The patient has a history of coronary artery disease, and now he has syncope associated with chest pain and palpitations. This raises concern for cardiogenic syncope, which has been shown to carry higher mortality than other types of syncope. Although aspects of the case might suggest other etiologies of syncope, the patient should be admitted, closely observed, and evaluated with electrocardiography (ECG), telemetry, and echocardiography. Other signs and symptoms that would suggest a cardiogenic etiology are an abnormal ECG, syncope during exertion or while supine, and onset of syncope with <5 seconds of warning (SOE=C). Conversely, a normal ECG is associated with a more favorable prognosis (SOE=C). Doxazosin, a selective α1-blocker used for symptomatic treatment of benign prostatic hyperplasia, causes smooth muscle relaxation in the bladder and prostate. It also works on vascular smooth muscle cells, leading to vasodilation and possibly orthostatic hypotension. Medications such as α- and β-blockers and calcium channel blockers can diminish postural reflexes. In a patient who takes doxazosin, syncope that is precipitated by a postural change from sitting to standing suggests postural hypotension as a possible etiology (SOE=B). Preceding symptoms such as nausea, vomiting, diaphoresis, or lightheadedness can be associated with vasovagal syncope, in this case possibly precipitated by pain from the patient’s minor injury. In contrast, syncope with <5 seconds of warning would be more suggestive of a cardiac etiology. The patient’s injury did not cause the episode of syncope. The patient recovered rapidly after the event and was hemodynamically stable in the emergency department, indicating no profound blood loss. Pain, or even the sight of blood, can in some people induce vasovagal syncope. Brief, arrhythmic limb jerking suggests myoclonic activity. Its presence would not necessarily increase mortality risk. Convulsive syncope is a term that has been used to describe syncope with myoclonus, and the entity is relatively common. The myoclonus is thought to result from reduction in cerebral blood flow and transient cerebral hypoxia. A true epileptic seizure is less likely, because the rest of the history suggests a syncopal episode.

CASE 2 (1 of 3) A 68-year-old man lost consciousness twice in the last several months. His daughter witnessed the second event. Patient was washing dishes when he suddenly felt lightheaded, looked pale and sweaty, and collapsed to the floor. He felt lightheaded for about 30 sec before losing consciousness. He awoke within 30 sec and was back to baseline within 1 minute of the event. History: hyperlipidemia, stroke, Parkinson disease, diabetes mellitus Examination Blood pressure 129/78 mmHg Normal cardiopulmonary and neurologic findings ECG: no significant abnormalities

CASE 2 (2 of 3) Which one of the following would most likely establish the diagnosis? Electroencephalography Tilt table test Magnetic resonance imaging of the brain Doppler ultrasonography of the carotid artery 24-Hour Holter monitoring

CASE 2 (3 of 3) Which one of the following would most likely establish the diagnosis? Electroencephalography Tilt table test Magnetic resonance imaging of the brain Doppler ultrasonography of the carotid artery 24-Hour Holter monitoring ANSWER: B A head-up tilt table test is used to identify autonomic dysfunction that can contribute to a syncopal event. This patient had a syncopal event associated with prolonged standing, suggesting autonomic dysfunction. Further, his history of Parkinson disease and diabetes puts him at increased risk of autonomic dysfunction. Orthostatic vital signs should be obtained before testing to evaluate for orthostatic hypotension. Electroencephalography is appropriate if seizure is suspected to evaluate for epileptiform activity. However, this patient had a short syncopal episode preceded by lightheadedness, and with rapid return to baseline. Because there is no evidence of seizure activity, the test would not likely yield a diagnosis. Magnetic resonance imaging of the brain should be obtained if there is suspicion of structural abnormalities, but it has no role in routine evaluation of syncope if there are no focal neurologic signs or symptoms. This patient has normal findings on neurologic examination. Doppler ultrasonography of the carotid artery is not indicated in the routine evaluation of syncope. It can be used to measure blood flow velocities within the cervical carotid arteries, which supply blood to the anterior circulation of the brain. A syncopal episode can in rare cases be caused by decreased perfusion to the posterior circulation (not the anterior circulation) of the brain, specifically to the reticular activating system in the brainstem. In order for carotid disease to lead to syncope, simultaneous compromise of blood flow in both carotid arteries would be required, which is extremely unlikely. Ambulatory external Holter monitoring devices are often used for 1–2 days. Because in most cases symptoms do not recur during the monitoring period, the positive diagnostic yield of Holter monitoring for syncope evaluation is low. However, a Holter monitor or an ambulatory loop recorder might be considered for this patient if evaluation with tilt table test is unrevealing.

CASE 3 (1 of 3) A 73-year-old woman is in the emergency department because she had a syncopal episode at her nursing home. The patient was seated and eating lunch when she suddenly lost consciousness for 30 sec. She returned to baseline rapidly. History: dementia, CAD, hyperlipidemia, diabetes mellitus Medications: glyburide, hydrochlorothiazide, haloperidol, simvastatin Examination Blood pressure 116/68 mmHg, heart rate 58 bpm ECG: mild sinus bradycardia, QTc interval of 540 msec, QRS interval of 60 msec, PR interval of 150 msec Laboratory findings Blood glucose level 110 mg/dL Normal electrolyte levels

CASE 3 (2 of 3) Which one of the following medications should be discontinued at this time? Hydrochlorothiazide Glyburide Haloperidol Simvastatin

CASE 3 (3 of 3) Which one of the following medications should be discontinued at this time? Hydrochlorothiazide Glyburide Haloperidol Simvastatin ANSWER: C This patient has a prolonged QTc interval that can lead to torsades de pointes, a polymorphic ventricular tachycardia that can cause syncope as well as sudden death. Normal values for QTc usually range from 440–460 msec, and values >500 msec are considered highly abnormal for both men and women. The QTc interval is likely prolonged, because the patient recently started haloperidol, which is one of many medications that can lead to QTc prolongation and torsades de pointes (SOE=A). The risk of QTc prolongation increases when the drug is administered intravenously or in doses higher than recommended. Further risk factors for QTc prolongation with haloperidol use include age >65 years, female sex, and bradycardia. In this patient, haloperidol should be discontinued, and she should be admitted and monitored closely for arrhythmia. Hydrochlorothiazide is a thiazide diuretic used in treatment of hypertension. It can lead to hypotension or electrolyte abnormalities, which may in turn lead to syncope. However, it would not cause prolongation of the QTc interval. Glyburide, a sulfonylurea used in treatment of diabetes, is a common cause of medication-induced hypoglycemia, but it is not associated with QTc prolongation. Simvastatin has not been linked to QTc prolongation and would not be expected to lead to syncope.

Copyright © 2016 American Geriatrics Society
GRS9 Slides Editor: Mandi Sehgal, MD GRS9 Chapter Authors: J. William Schleifer, MD Win-Kuang Shen, MD GRS9 Question Writers: Stephen Krieger, MD Asaf Harel, MD Managing Editor: Andrea N. Sherman, MS Copyright © American Geriatrics Society

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