Mary Agnes Ostick DNP, CRNP Villanova University II  To discuss the definition and presentation of

 To present the classifications of syncope

 To discuss the necessary history and physical for syncope

 To discuss clinical practice guidelines of syncope  Syncope is an abrupt and transient loss of consciousness caused by cerebral hypoperfusion which results in lost of postural tone

 Cerebral blood flow falls below half normal value

 Duration short  Trigger affects parasympathetic system which affects vagal tone-relaxation

 While withdraw of sympathetic-loss of compensatory mechanisms

 Vasodilation and bradycardia

 Fainting occurs

Studies report as much as 41% of US population will have episode

Recurrent syncope 13.5%

Females 22%, males 15%

In teens, incidence of >1 syncopal episode is 40% by age 21 1-1.5% of all ED visits/year

250,000 annual admissions

Median hospital cost $2,500 /day Mortality is low 0.7% at 10 days 1.6% at 30 days 8.4% at 1 year (1/3 of deaths are cardiac) h ot o b y U n k n o w n A ut h or is li c e ns e d u n d er C C B Y- N C - N D Lightheadedness Palpitations Weakness Dimming or blurred vision Nausea, epigastric distress Feeling warm or cold Facial pallor May manifest similar symptoms of prodrome

Lasts few seconds: nearly “blackout”

 Younger age with fewer comorbidities Seizures

Sleep disturbances

Metabolic disorders

Psychogenic disorders

Acute intoxication Neurally mediated

Orthostatic hypotension

Cardiac Vasovagal

Situational

Carotid sinus syndrome Most common form, 45%

Benign

 Prodrome symptoms

 TLOC (30 seconds) with full recovery

Normal vital signs

No hypoxia

No signs anemia

No EKG abnormalities No further testing needed

Avoid triggers

Good hydration Micturation or post micturation syncope

Defecation, cough, swallow

“Sitcom syncope”  1% of all syncope, affects older patients

 Pressure on carotid sinus baroreceptor, vagus nerve mediated bradycardia

 Diagnosis by carotid sinus massage

“Minister's disease” 15% of ED fainting cases

Normal response to gravitational stress ( cardiac output and cerebral perfusion ) becomes inadequate  Medication induced most common cause

 Volume depletion

 Postural tachycardia syndrome (POTS)

 Primary and secondary autonomic failure

 Post prandial hypotension Orthostatic vital signs (OVS)

Drop in systolic BP >= 20 mm Hg or diastolic > or =10 mm Hg with position change

A 50% decrease will lead to presyncope or syncope  Orthostatic hypotension is common in ED patients with syncope 12-24% of ED visits

 OVS alone cannot be the only measurement to determine cause of syncope because some cardiac patients will show OH ( 2018 Journal of Emergency Medicine )  POTS : form of orthostatic intolerance characterized by increase in HR, without hypotension that occurs on standing

 500,000 Americans

 Common in young :15-45 years old

 Women > men 4.5:1  Cause? Number of abnormalities

 Symptoms : dizziness , lightheadedness, blurred vision, fatigue with standing , GI symptoms

 Hallmark is exaggerated heart rate in response to postural changes Diagnosis: Tilt Table

Sustained HR greater than 130 beats/ min or increase to 120 beats/min within 10 minutes of tilt

No orthostatic hypotension  Optimal treatment is uncertain

 Non- pharmacologic: Exercise ,high salt diet and oral volume expansion

 Medications Fludrocortisone combined with diet and volume

20 % of all syncope cases are cardiac

 Decreased cardiac output and diminished cerebral perfusion

6 month mortality with proven cardiac syncope is 10%or greater

Framingham study :those with syncope 2x as likely to die during the 17 year study Arrhythmia

Structural cardiac disease

Obstructive cardiomyopathy Onset during exertion Palpitations at onset

History cardiac disease Chest pain

EKG Changes Occurs while supine

Lack of prodrome Family history of sudden death

>60 years old Bradycardia VT , SVT’s Sick sinus syndrome Wolf Parkinson White Atrial arrhythmias 2nd and 3rd degree heart blocks Brugada syndrome Pacemaker dysfunction  Brugada syndrome: pattern on EKG pseudo- Rt bundle branch block and ST elevation in V1-V3

 Pre-excitation syndrome: Wolff- Parkinson White

 Ventricular tachycardia  Ventricular repolarization disorder characterized by long Qt interval that can lead to ventricular arrhythmias or sudden cardiac death

 Symptoms: syncope, seizures, cardiac arrest

 Can be congenital or acquired

 Acquired : drug therapy (fluoroquinolones and CP450 inhibitors) electrolyte imbalance (eating disorders) anti psychotics

 Diagnosis : presenting symptom of syncope personal and family history

 Due to decrease cardiac output secondary to structural defect

 In young : hypertrophic cardiomyopathy predisposing to tachycardia arrhythmias

 In elderly : chest pain & SOB, R/O aortic stenosis Hypertrophic MI or ischemia obstructive cardiomyopathy Acute aortic dissection

Saddle pulmonary Pulmonary embolus hypertension

Valvular diseases

 Genetic heart muscle disease caused by mutation in genes are rare < 200,000/year

 Affects young

Characterized by LVH causing • LV outflow obstruction • Diastolic and systolic dysfunction • Myocardial ischemia • Mitral regurgitation  Symptoms : • Presyncope or syncope • Fatigue • Dyspnea • Chest pain • Palpitations Prone to atrial and ventricular arrhythmias can be asymptomatic and can lead to sudden cardiac death( SCD) Treatment: cardio-defibrillator  Most will be neurally mediated

 Syncope during exertion deserves a cardiology workup: HOCM, ion channel disorders or arrhythmias  Heat illness (exercise associated collapse) occurs after running a race or workout due to abrupt decrease in venous return causing athlete to collapse

 Heat stroke: collapse with altered mental status , seizure or . Different from syncope by elevated core temp tachycardia, hypotension, nausea vomiting  Conversion disorder

 Can be associated with anxiety or depression

 Females more frequently

 Can report syncope and falls without and lasting longer than a typical syncopal event  Seizures , metabolic, intoxication, subclavian steal syndrome

 Syncope: Can cause a transient hypoxia that causes myoclonic jerking involuntary, brief, mimics seizures

 No post-ictal obtundation in syncope

2017 Clinical practice guidelines American College of Cardiology American Heart Association Heart Rhythm Society

2018 (ESC) European Society of Cardiology  Recommendations

EKG

Complete history and physical

Orthostatic vital signs  Prodrome  Setting: trigger? Hydration?  Syncope without warning : cardiac  Past history : structural heart disease?  Metabolic diseases  Medications  Family history sudden death  Circumstances at time of syncope

 Witnessed?

 Neurally mediated • Vasovagal: Precipitated by fear with prodrome of pallor, sweating, nausea

• Situational : urinating, coughing defecating

• Carotid sinus hypersensitivity - turning neck Orthostatic hypotension • After or prolonged standing • Change or start of medication

Cardiac • During exertion or supine • Sudden palpitations followed by syncope  True syncope lasts 1-2 minutes • Can have persistent nausea post syncopal episode

 Prolonged LOC • seizure or conversion reaction

 Arrhythmias may recover quickly

 Confusion or neurological changes during recovery may be attributed to seizure or stroke  Vital signs Heart rate; check for arrhythmia Hypoxia or tachypnea, consider PE Orthostatic BP’s

 Cardiovascular exam

 Neuro exam Vertigo, nystagmus, ataxia

 If anemia suspected; rectal exam  EKG

 Labs only if indicated by history Pregnancy, CBC, comprehensive panel Glucose

 D- dimer or CT angiography for PE

 Cardiac Echo if structural heart condition

 Only if head trauma or CVA ->CT head  Tilt table for postural or recurrent neurally mediated syncope  If cardiac arrhythmias suspected

Holter monitor 24-48 hour Event monitor Implantable loop recorder

Implantable loop recorder

 POTS and Neurocardiogenic syncope 450 charts reviewed 39 -4 episodes of syncope past 6 months 33 women (20-46)

 ALL had prior Holter or event monitors with INCONCLUSIVE results

 Implantable loop recorders placed  All subjects had >6 sec asystole or bradycardia <30/min

 15 subjects >10 sec asystole with prolonged and convulsive syncope San Francisco syncope rule

 Consider admission if 1 or more present

Abnormal EKG CHF history Hematocrit < 30% Dyspnea Systolic BP <90  High risk • Arrhythmias : syncope during exercise; • with palpitations; without prodrome • Comorbidities; anemia, electrolyte imbalance • EKG changes • Family hx of sudden death • Hypotension ( less than 90 systolic) • Older age • Structural heart disease , CHF, or CAD  Disposition after evaluation

 Additional evaluations

 Cardiac monitoring and EPS testing

 Neurological testing

 Arrhythmias

 Driving after syncope

 Athletes

Benditt, D. (2016). Syncope in adults: Clinical manifestations and diagnostic evaluation. U: UpToDate, Hockberger S Robert, Kowey P ur. UpToDate [Internet]. Waltham, MA: UpToDate.

Brignole, M., Moya, A., de Lange, F. J., Deharo, J. C., Elliott, P. M., Fanciulli, A., ... & Probst, V. (2018). 2018 ESC Guidelines for the diagnosis and management of syncope. European heart journal, 39(21), 1883-1948.

Edwards, F. ,Syncope. (2018)Emergency Medicine Reports; 39(19), 1-22. Gass, M., Apitz, C., Salehi-Gilani, S., Ziemer, G., & Hofbeck, M. (2006). Use of the implantable loop recorder in children and adolescents. Cardiology in the young, 16(6), 572-578.

Kanjwal, K., Qadir, R., Ruzieh, M., & Grubb, B. P. (2018). Role of implantable loop recorders in patients with postural orthostatic tachycardia syndrome. Pacing and Clinical Electrophysiology, 41(9), 1201-1203. Kaufmann,H., Freeman,R., (2015) Postural tachycardiasyndrome. In M.J.Aminoff (Ed.)Up to Date. Retrieved May 21,2019 from https://www.uptodate.com/contents/postural-tachycardia- syndrome Krediet, C. P., van Dijk, N., Linzer, M., Van Lieshout, J. J., & Wieling, W. (2002). Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing. Circulation, 106(13), 1684-1689.

Providência, R., Silva, J., Mota, P., Nascimento, J., & Leitão- Marques, A. (2011). Transient loss of consciousness in young adults. International journal of cardiology, 152(1), 139-143. Runser, L. A., Gauer, R. L., & Houser, A. (2017). Syncope: Evaluation and Differential Diagnosis. American family physician, 95(5).

Schaffer, J. T., Keim, S. M., Hunter, B. R., Kirschner, J. M., & De Lorenzo, R. A. (2018). Do Orthostatic Vital Signs Have Utility in the Evaluation of Syncope?. The Journal of emergency medicine, 55(6), 780-787.

Thiruganasambandamoorthy, V., Taljaard, M., Stiell, I. G., Sivilotti, M. L., Murray, H., Vaidyanathan, A., ... & Sheldon, R. (2015). Emergency department management of syncope: need for standardization and improved risk stratification. Internal and emergency medicine, 10(5), 619-627. Salerno,J., (2017)Causes of syncope in children and adolescents. In J. F. Wiley (Ed.) UptoDate. Retrieved May 21,2019, from https://www.uptodate.com/contents/causes-of-syncope-in- children-and-adolescents

Shen, W. K., Sheldon, R. S., Benditt, D. G., Cohen, M. I., Forman, D. E., Goldberger, Z. D., ... & Olshansky, B. (2017 ) . ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm S syncope in children and adolescents.ociety Journal of the American College of Cardiology, 70(5), e39-e110. Providência, R., Silva, J., Mota, P., Nascimento, J., & Leitão-Marques, A. (2011). Transient loss of consciousness in young adults. International journal of cardiology, 152(1), 139-143.

Wieling, W., Ganzeboom, K. S., & Saul, J. P. (2004). in children and adolescents. Heart, 90(9), 1094-1100.