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Mary Agnes Ostick DNP, CRNP Villanova University II  to Discuss the Definition and Presentation of Syncope

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Mary Agnes Ostick DNP, CRNP Villanova University II  to Discuss the Definition and Presentation of Syncope Mary Agnes Ostick DNP, CRNP Villanova University II To discuss the definition and presentation of syncope 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 coma. 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 injury 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.,
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