SYNCOPE Module #2 Ed Vandenberg, MD, CMD Geriatric Section OVAMC & Section of Geriatrics 981320 UNMC Omaha, NE 68198-1320 evandenb@unmc.edu Web: geriatrics.unmc.edu 402-559-7512 Welcome to “Syncope” module 2. Over the next slides we will attempt to complete the review of etiologies of syncope in the elderly. Please stay with us and stay conscious.

PROCESS Series of 3 modules and questions on Etiologies, Evaluation, & Management Step #1 Power point module with voice overlay Step #2 Case-based question and answer Step #3 Proceed to additional modules or take a break Our process will be for you to complete the second in a series of 3 modules and questions on syncope. If you have not completed the first module, please do so at this time and then return to this module. These modules will utilize power point with voice overlay. Each module will be followed by case-based questions with answers that will explain the right and wrong responses. Then you will have the option to continue with the next module or take a break at that time. The computerized system will keep track of the modules you have completed so that in the future you may pick up where you left off.

Etiologies P-A-S-S O-U-T (mnemonic) P ressure (hypotensive causes) A rrhythmias S eizures S ugar (hypo/hyperglycemia) O utput (cardiac)/O2 (hypoxia) U nusual causes T ransient Ischemic Attacks & Strokes It the last module, we began a review of common etiologies of syncope following the mnemonic PASS OUT. We will continue with the next cause, arrhythmias.

B) A rrhythmias TYPES: HISTORY: DIAGNOSIS Bradyarrhythmias Tachyarrhythmia’s SVT, NSVT, A.F., pacemaker malfunctions HISTORY: sudden onset associated with known heart disease, quick post event recovery of consciousness DIAGNOSIS 1st step: EKG Continuous cardiac monitor (Inpatient vs. Holter) or —>Event Monitor or Stress Testing (Exercise vs DSE)  Electro-physiologic study ( EPS) Arrhythmia is one of the more lethal causes of syncope. Here listed is a vast array of types of arrhythmias - both brady and tachy alike. The history is sometimes helpful to elicit if arrhythmia is a cause. Indicators of arrhythmia are if the syncope had a sudden onset, without prodrome or warning and had a quick recovery of consciousness post the event. It is more common in patients with known heart disease. Some of the diagnostic steps are first, of course, an EKG, then looking at continuous cardiac monitoring, either inpatient or perhaps outpatient with a Holter. If this doesn’t provide a diagnosis, then we move to an event monitor or stress testing. Stress testing is indicated in patients with risk factors or known coronary artery disease. It is used to elicit an arrhythmia due to ischemia. Lastly, if all else fails, a cardiology consult for possible electrophysiologic study may be indicated.

C) Seizures1 “The Gold Standard”: HISTORY----is the key to diagnosis Compared to young patients; Many more occur with out warning Many more have atypical prodrome POST-ICTAL sx’s: -longer than any other cause of syncope (second only to death: JOKE!) DIAGNOSIS: “The Gold Standard”: EEG positive and appropriate symptoms witnessed The “Fall-Back Position” EEG negative and appropriate symptoms witnessed Gave dx in: < 2 % An infrequent cause of loss of consciousness is seizure. Many times history is key. Compared to young patients; many more occur with out warning or prodrome and those that have a prodrome are more often atypical ( e.g. dizziness). The post-ictal or post event history is helpful as it takes much longer to recover full consciousness than in true syncope. Actually, it’s only second place to death in length of time for it to recover - THAT’s A JOKE! The “gold standard” to make the diagnosis of seizure as cause of episodic loss of consciousness is an EEG that is positive and appropriate symptoms or witness. A “fall-back position” is EEG negative but with a witness still giving you the description of seizure activity. However, it is found to be an establish cause in less than 2% of cases.

Question:2 Can decreased CNS perfusion causes seizures ? Decrease CNS perfusion by 35% SYNCOPE Decrease in CNS perfusion for: >10 secs------>SYNCOPE >15 secs.----->Seizure (possible) PEARL: EEG —>of no use in ABSENCE OF SEIZURE ACTIVITY by history If you decrease CNS perfusion by > 35% and hold it for > 10 seconds,you will get a syncopal episode. If you hold it longer, you can possibly get seizure activity. This is important to remember when you’re working up a first time seizure. The important pearl here is that an EEG is of no use in the absence of any seizure activity by history. Thus, if you have a witness who sees no seizure activity, then an EEG is a fruitless test.

D) Sugar (hypo/hyperglycemia) hypoglycemia from D.M. with hypoglcemic therapy ONLY hyperglycemia from DM and not enough therapy Tips: Don’t look for hypoglycemia in the NON-Diabetic GTT doesn’t add diagnostic information Hypoglycemia of course can cause this event. Hyperglycemia through dehydration and hypotension can also cause syncope. Here are some key tips: do not consider hypoglycemia as a cause in non-diabetic patients, and glucose tolerance test do not add much diagnostic information over a blood sugar draw at the time of the event

E) Output (cardiac)/O2 (hypoxia) History: usually sudden onset (exception in CHF), Associated cardiac sx’s: -dyspnea -chest pain -tachypnea Causes: CARDIAC PULMONARY (O 2) Output problems or O2 problems usually have a sudden onset, except for heart failure. They usually have associated cardiac symptoms that we would expect such as dyspnea, chest pain, tachypnea.

E) Output (cardiac)/O2 Causes: Name some causes of impaired cardiac output: Please name some causes in your mind and move to the next slide for the answer.

E) Output (cardiac)/O2 Causes: Aortic or Mitral or Pulmonic Stenosis Hypertrophic Cardiomyopathy Cardiomyopathies: (Restrictive or Dilated) Atrial Myxoma Cardiac Tamponade Aortic Dissection MYOCARDIAL INFARCT CHF PULMONARY (O 2 Related) Pulmonary embolii Pulmonary Hypertension Carbon monoxide COPD exacerbation ( add  PCO2) The list here is fairly long. Some of the common factors are aortic stenosis, myocardial infarct, heart failure, pulmonary emboli, and COPD exacerbations.

E) Output (cardiac)/O2 The DIAGNOSIS: Tests: SaO2 +/- ABG’s EKG CXR Echo? CT chest? NOTE: ECHO: helpful in 5 % of all syncopes Therefore: use Echo in: structural heart dz, heart murmurs hx of : impaired cardiac output symptoms Evaluation would include O2 sats, ABG’s, EKG, and chest x-ray. What about echocardiograms? Echos are probably helpful in only 5% of all syncopes, but they are a critical test in ruling out structural heart disease, evaluation of murmurs, and evaluation of any symptomatology that is consistent with cardiac output impairment.

F) U nusual causes Causes: Anxiety Panic disorder Somatizations disorder Major Depressive disorder Hyperventilation syndrome History Psychiatric history Symptoms don’t fit Diagnosis -sometimes by exclusion “The Good News” infrequent in the elderly The unusual causes are mostly psychiatric, and these are mediated through a reduction in CNS perfusion through vasoconstriction. Diagnosis often can be one of exclusion or with a clear psychiatric history. But the good news here is that this is an infrequent cause in elders.

G) Transient Ischemic Attacks & Strokes (and other CNS causes) CVAs TIAs (vertebro-basilar) Subarachnoid hemorrhage Subdural hematoma Basilar artery migraine Subclavian steal CNS mass effect: tumor, edema, AVM Diagnosis; Neuroimaging (“Aren’t you glad you live in the New Millennium?”) Transient Ischemic Attacks ( TIA’s) as part of the mnemonic includes CVA’s, vertebro-basilar TIA’s, hemorrhages, and subdural. But the good news is that we live in an era of neuro-imaging. This helps us a great deal in looking for these types of lesions, first by establishing the CNS anatomy with a CT or MRI and then if needed evaluating further with an MRA if the history is suspect for vertebro-basilar insufficiency.

The End of Module two on Evaluation of Syncope3 This completes our second module on causes, we have more to do but lets review with a question and answer. Then, if you have enough energy, proceed to module 3 where we will work on the evaluation of syncope. Add question #189

Post Test4 A 72-year-old man is hospitalized following a syncopal episode that occurred while he was walking to the library. Cardiac monitoring reveals sick sinus syndrome with short periods of paroxysmal atrial fibrillation and prolonged episodes of sinus bradycardia with occasional sinus pauses of up to 3.2 seconds. The patient takes no medications and has been well except for an episode of dizziness that occurred while he was walking down the hall at home. Cardiac telemetry at that time revealed a 3.0-second sinus pause. The patient tells you that he is not concerned about dying but does want to remain alert, functional, and able to walk to the library. Which of the following should you recommend?

Which of the following should you recommend? A. Exercise stress test B. Electrophysiologic study (EPS) C. Dual-chamber pacemaker D. Ventricular pacemaker E. Ventricular pacemaker and amiodarone therapy

Answer: C. Dual-chamber pacemaker This patient clearly meets the criteria for sick sinus syndrome; further diagnostic testing is not needed. The symptomatic sinus pause is an indication for pacemaker therapy. Although coronary artery disease can cause sick sinus syndrome in elderly patients, it most often is caused by degeneration and fibrosis of the sinus node. Several large, randomized, controlled trials have investigated the best pacing mode for elderly patients with symptomatic bradycardias. This patient is less concerned about mortality than quality of life; therefore, a pacing mode that will eliminate his symptoms, permit continued social function, and prevent stroke and recurrent atrial fibrillation is most desirable. In the Pacemaker Selection in the Elderly (PASE) study, both ventricular and dual-chamber pacing were found to improve overall quality of life in patients with sinus bradycardia, but nearly one quarter of those assigned to ventricular pacing developed pacemaker syndrome and eventually required dual-chamber pacing.

During the 18-month follow-up period, dual-chamber pacing was found to result in moderately better quality of life and cardiovascular function. Studies have shown no effect of pacing mode on overall survival. In another study, 1474 elderly patients (average age 73 ± 10 years) with symptomatic bradycardia were randomly assigned to either ventricular or dual-chamber pacing. No overall effect of pacing mode on stroke or death from cardiovascular causes was reported. However, in a subgroup of patients aged 74 and under, a significant reduction in both outcomes was seen with dual-chamber pacing. The study also showed an 18% reduction in the risk of atrial fibrillation. Treatment with amiodarone is not indicated at this time. End

REFERENCES 1. Ramsay ER, Rowan JA, Pryor FM. Special considerations in treating the elderly patient with epilepsy. Neurology 2004; 62:S24-S29 2. Davis TL, Freemon FR. Electroencephalography should not be routine in the evaluation of syncope in adults. Arch Int Med 1990; 73:593-598 3. Bush D. Syncope. In: Geriatric Review Syllabus: A Core Curriculum in Geriatric Medicine, 5th Edition (Cobbs EL, Duthie EH, Murphy JB, eds.), Blackwell Publishing for the American Geriatrics Society, Malden, MA, Chapter 24, pp 165-169, 2002 4. Used with permission from Murphy JB, et. al. Case Based Geriatrics Review: 500 Questions and Critiques from the Geriatric Review Syllabus, AGS 2002, New York, NY