SYNCOPE Module #3 Ed Vandenberg, MD, CMD Geriatric Section OVAMC &

1 SYNCOPE Module #3 Ed Vandenberg, MD, CMD Geriatric Sect...
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1 SYNCOPE Module #3 Ed Vandenberg, MD, CMD Geriatric Section OVAMC &Section of Geriatrics UNMC Omaha, NE Web: geriatrics.unmc.edu Welcome to “Syncope” module 3. Over the next slides we will attempt to complete the review of evaluation of syncope in the elderly. Please stay with us thru the next 20 slides.

2 PROCESS Series of 3 modules and questions onEtiologies, 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 third in a series of 3 modules and questions on syncope. If you have not completed the first and second modules, 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 1-3 case-based questions with answers to 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.

3 EVALUATION Etiologies: The evaluation requires: Comprehensive approachStep-wise progression to first rule out the most lethal causes (i.e. cardiac) and then next progressing to the other etiologies as indicated Evaluation should not only be comprehensive, but should first begin with ruling out the lethal cardiac etiologies, then moving on to the other etiologies as indicated.

4 EVALUATION First Step First step: History What to ask? H &P*, EKG,Labs Suggested (CBC, electrolytes, glucose, BUN/Cr. Ca+ and SaO2, cardiac enzymes) History What to ask? Precipitant Activities Prodrome Medications Witnesses Comorbid conditions The basic evaluation would include an H&P, EKG and labs. For labs, it is suggested to do a CBC, basic metabolic profile, cardiac enzymes and a SaO2 to evaluate for anemia, infection, electrolyte disturbance, glucose abnormalities, renal dysfunction, MI and hypoxia. In the history you want to know what precipitated it, what was patient doing at the time, was there a prodrome, what are their current and new medications, do we have a witness who can assist with this evaluation, and, lastly, knowing the comorbid conditions that might give us a clue.

5 Characteristics of the Three Classes of SyncopePhase Cardiac arrhythmia Vasovagal Seizure Prior to event -Any position < 5 secs warning -Precipt. absent -Palpitations rare -Aborted with lying flat -Precipt. present -Nausea -Visual changes -May have a warning or prodrome During event -Flaccid -Absent pulse -Blue, ashen skin -Incontinence rare -Motionless, relaxed tone -Slow, faint pulse -Pale, color skin - Pupils dilated, reactive -Rigid tone -Pulse: rapid  BP -Tonic eye deviation -Frothing Recovery -Rapid, complete -Fatigue after event -No retrograde amnesia -Diaphoresis & nausea -Slow recovery -Disorientation -Focal neuro. findings Here we try to categorize some of the symptomatology that would assist you in differentiating between cardiac arrhythmia, vasovagal and seizure. The prodrome for cardiac arrhythmias can happen in any position, with virtually no warning, no precipitant, and palpitations are rare. In vasovagal it will go away if lying down. It will have some precipitating event, as previously described, often associated with nausea or visual changes. In seizures it can happen in any position, and many times there may be a warning or prodrome. During the event in cardiac arrhythmias, the person is virtually pulseless and flaccid, whereas in vasovagal they may have a faint pulse but otherwise look relatively the same but with better perfusion. Seizure, of course, has a whole different presentation in tonic clonic activity. For the arrhythmias recovery is rapid and complete. In vasovagal there may be some post event fatigue, diaphoresis and nausea. Seizure, of course, has a slow prolonged recovery of the post ictal state.

6 EVALUATION First Step1 Physical-orthostatic BP & pulse (lying, sitting & standing 1 & 3 min.) -pulmonary -cardiac -neurologic exams History (from patient and witness) will give diagnosis 50% of the time Physical will give diagnosis 20% of the time The physical evaluation should include orthostatic blood pressures, a heart and lung exam, and a neurologic exam. Up to half of the time, you will have the diagnoses with history from the patient or witness. Physical exam adds an additional 20% of the time. So there is still hope for us old clinicians to beat out the machines.

7 EVALUATION First Step2,3 LAB: BMP CBCGave diagnosis for what % of patients? 2-3% of patients EKG Gave diagnosis for 5% of patients BUT Often gave clue to dx: e.g. (old MI, BBB, arrhythmias) Labs, though necessary, only give the diagnosis in 2-3 % of cases. EKG, even though it establishes diagnosis in only 5%, often gives clues to the next step by noticing old arrhythmias, MI’s, etc.

8 EVALUATION additional steps4Echocardiography yields unsuspected findings in----- < 10% of patients (should be performed pre stress test, if patient has exertional syncope to r/o cardiac obstruction; eg septal hypertrophy) Echocardiogram will yield unsuspected findings in < 10% of patients; however, if you’re going to do any stress testing syncope, you will need to do an echo first to rule out obstructive diseases such as aortic stenosis or septal hypertrophy.

9 EVALUATION additional steps5FOR Patients with Structural cardiac abnormalities* * structural heart. Dz: (CAD, CHF, Valve dz, cong. hrt dz) or EKG abnormalities (old MI, BBB, arrhythmias, conduction syst. dz) who have: Ischemic symptoms Perform: Exercise or Pharmacologic Stress Testing If your syncopal patient has structural abnormalities - defined here as any kind of coronary disease, heart failure, valvular disease or congenital heart disease - or if they have an EKG abnormality as listed here and have ischemic symptoms then you should add an exercise or pharmacologic stress test to the evaluation.

10 EVALUATION additional steps6If added: Ambulatory ECG (Holter) gave: correlation of arrhythmia with symptoms 4% of the time absence of arrhythmia with symptoms 17% of the time (79% of pts. had no arrhythmia or brief arrhythmia) Note: 72 hr ambulatory monitoring did not increase yield for symptomatic arrhythmias over 24 hr monitoring If there are no structural abnormalities but you are still suspect of a cardiac source of syncope, an ambulatory Holter monitor may assist you. How it is helpful is that it demonstrates the absence of arrhythmia with symptoms in up to 17% of the time, whereas correlates the arrhythmia with symptoms would happen in only 4%. If your 24 hour Holter did not show any abnormalities, longer monitors will not add additional diagnostic power. You should then move to event monitors.

11 EVALUATION additional stepsAmbulatory loop recorders or Event monitors (“King of Hearts”): (11) in patients able to operate recorder gave diagnosis 25% of time in patients unable to operate recorder consider implantable loop recorder An ambulatory loop recorder, or event monitor, is helpful if your patient is able to operate the recorder. It gave a diagnosis 25% of the time. If your patient is unable to operate the recorder and you feel that you need to establish a diagnosis with electrocardiographic monitoring, then using an implantable loop recorder would be your next step; however, some may move at this point to electrophysiologic studies.

12 EPS: Electrophysiologic studies7Indications High yield patients: structural heart disease with unexplained syncope detection of arrhythmias in ischemic heart disease Detect arrhythmias by: via by EKG, cardiac monitoring or Holter or Event monitoring Significant findings: NSVT, Sinus Brady, 3 degree Heart Block, BiFasicular BBB EP studies have high yield in patients with structural heart disease who despite an evaluation as we’ve described up to this point, still have unexplained syncope. Another indicator of high yield is their detection of arrhythmia in patients with no ischemic disease. Significant findings that may lead you in any type of monitoring situation to use of EPS studies are: non-sustained ventricular tachycardia, sinus bradycardia, third degree heart block or bifasicular bundle branch block.

13 EPS meta-analysis Ann Intern Med 1997;127:76-86Patients with: EPS yield: history of Structural heart Disease (N=406) 21% demonstrated ventricular tachycardia (VT) 34% demonstrated bradycardia*  Total diagnostic yield: 50% in patients with OHD (14% patients had both VT and bradycardia)  Abn EKG (i.e. conduction abnormalities) 3% demonstrated VT 19% demonstrated bradycardia* *EPS has low sensitivity and specificity for bradycardia with “normal hearts” (i.e. absence of structural heart disease) (N= 219) 1% VT 10% bradycardia  Total diagnostic yield: 10% in patients without OHD This meta-analysis demonstrates when to consult a cardiologist for EPS study. In structural heart disease, up to 21% demonstrated ventricular tachycardia. 34% demonstrated bradycardia with a pretty good total diagnostic yield of up to 50% in patients with organic heart disease. Note that some patients had both ventricular tachycardia and bradycardia. However, if you have an abnormal EKG without any other structural heart disease, only 3% demonstrated v tach and 19% demonstrated bradycardia. Lastly, if you have a normal heart, that is, no structural heart disease whatsoever, a very low yield was found with EPS studies in patients without organic heart disease. So, the implementation of EPS studies really is for the patient with structural heart disease and unexplained syncope, and even in some cases abnormal EKG as described on a previous slide and unexplained syncope.

14 EVALUATION additional stepsIf added: CT(head) or EEG yielded diagnosis in only---- 4% of pts (12) (these tests are rarely helpful unless neurologic signs or symptoms are present) all patients with positive scans had focal neurologic signs or witnessed seizure) CT or EEG yields a diagnosis in only 4% of patients unless the patient has neurologic signs or symptoms, and all patients who had positive scans were predicted by the fact that they had focal neurologic signs or witnessed seizures. A good neurologic exam will tell you whether or not to use neuroimaging, and a good history will help you to decide whether or not EEG will be helpful.

15 EVALUATION additional steps8when added to above evaluation, these tests gave diagnostic yield to total of .60-76% of patients Specificity 90% Sensitivity 66% Caveat What is false positive rate? Can have false positives: positive tilt table in 10% of the elderly population If added: Head-up tilt table test (HUTT): Indications: -suspect vasovagal or -unexplained syncope in those not suspect or ruled out for cardiac cause When is the use of a tilt table test useful? Two areas: if you suspect vasovagal but you cannot prove it and the patient has recurrences. Or you have done a thorough evaluation for unexplained syncope and cannot find any cardiac cause. Do tilt tables help? In folks who had a very complete evaluation it was helpful in up to 70% of patients. It has a very good specificity at 90%, but it has a false positive rate that can be up to 10% in the elderly population - just to confuse the issue.

16 * Tilt table testing The Technique1st Passive testing: Technique fasting serial BP’s in various tilt positions up to 60 degrees with patient standing still 2nd Isoproteronol infusion: Technique: as above plus infusion of isoproteronol Positive: demonstrates drop in BP> 20 mm Hg and symptom reproduction How do you perform a tilt table test? First, the patient is strapped onto a board so they do not have to contract their legs to hold themselves up, then they are tilted up to approximately 60 degrees. Heart rate and blood pressures are followed to see if there is any significant drop. If this fails to show anything in the way of symptomatology or signs, then isoproteronol is added in appropriate subjects since this can trigger the vasovagal effect. A positive test is a drop of blood pressure or symptom reproduction.

17 This brings us to the end of our sequence on evaluation.Summary of the evaluation: This slide (this card is available through our Geriatric Education Center) summarizes the evaluation that we just went through. The first thin rectagular box at the top indicates the initial evaluation, the larger rectangular box on the left shows the indications for inpatient management which are structural heart disease, cardiac signs or symptoms, abnormal EKG, insecure home environment, seizures, acute neurologic symptoms, or significant injury. In the right-hand column for an inpatient, you would rule out an MI, cardiac monitorand evaluate orthostatic BP’s. If a seizure was described, then an EEG would be important. If structural heart disease exists or cardiac symptoms, then you would move on to get an echo. If there are neuro symptoms or signs, then performance of the CT would be indicated. If that workup fails to provide a diagnosis and if you still have any kind of cardiac risk, you would move on to a stress test. If that is negative and you are still suspicious of cardiac etiology, a cardiology consult for possible EPS would be indicated. However, if after their inpatient evaluation the patient has none of the negative workup and no structural heart disease or other cardiac symptoms, and you have no suspicion for arrhythmia, then moving to complete the rest of the etiologies of syncope described in the P-A-S-S O-U-T mnemonic would be in order. Occasionally you may end up using the tilt table in this portion of the evaluation. We feel that this algorithm will provide a good basic guideline for you to proceed in any syncopal evaluation in the elderly.

18 Review Definition List the consequencesDescribe the aging physiology that predisposes to syncope List the causes Describe the evaluation Sudden LOC Mortality high in cardiac Baroreceptor,  B receptors, Volume  MM tone P-A-S-S O-U-T R/o cardiac first H &P, EKG, Labs Let’s review. Syncope is a sudden loss of consciousness and has a high mortality in cardiac causes. The physiology is reduction in baroreceptors, B-responsiveness, volume, and muscle tone. The etiologies can be remembered by the P-A-S-S O-U-T mnemonic, and always remember to rule out cardiac etiologies first.

19 How to remember the causes? “Mnemonics”P-A-S-S O-U-T The following mnemonic reviews the etiologies of syncope, and pertinent data on each: P ressure (hypotensive causes) O utput (cardiac)/O2 (hypoxia) A rrhythmias U nusual causes S eizures T ransient Ischemic Attacks S ugar (hypo/hyperglycemia) & Strokes, CNS dz’s The etiologies of syncope can be remembered by low pressure causes, arrhythmia causes, seizures, hypoglycemia, cardiac output or hypoxia, unusual causes and, of course, TIA’s.

20 One last glimpse of the evaluation to lock it into your brainOne last glimpse of the evaluation to lock it into your brain. If your brain won’t hold it, then see the next slide.

21 The End of Module three on Evaluation of Syncope9Request “Syncope Pearls” summary card from or This completes our final module on syncope, please complete the question and answer session. If you would like a copy of the summary “Syncope Pearls” card please contact our office at the number shown. Proceed to the final question of this module. Add question #193 and 194

22 Post Test (10) A 75-year-old woman has chronic congestive heart failure with normal systolic function. Current medications are furosemide and an angiotensin-converting enzyme (ACE) inhibitor. While sitting in a chair approximately 1 hour after eating breakfast and taking her medications, she suddenly loses consciousness and falls to the floor. On examination at the hospital, her pulse rate is 68 per minute and blood pressure is 160/72 mm Hg. A grade 3/6 midsystolic murmur is heard at the left sternal border and radiates to the carotid arteries. There are good carotid upstrokes and no carotid bruits. Complete blood cell count, serum electrolytes, cardiac enzymes, electrocardiogram, and chest radiograph are normal. One day later, blood pressure is 104/70 mm Hg 1 hour after breakfast. Which of the following is the most appropriate next step?

23 Which of the following is the most appropriate next step?A. Order Doppler echocardiography. B. Encourage the patient to drink two cups of coffee (250 mg of caffeine) each morning. C. Discontinue furosemide. D. Discontinue the ACE inhibitor. E. Prescribe fludrocortisone, 0.1 mg orally every morning.

24 Answer: C Discontinue furosemide.This patient has postprandial hypotension, which could be exacerbated by hypotensive medications taken with breakfast. Diuretics have been shown to exacerbate postprandial and orthostatic hypotension, probably because of their preload-reducing effects. In one study, furosemide withdrawal improved postprandial hypotension in elderly patients with heart failure and preserved systolic function.

25 Doppler echocardiography probably would confirm reduced early diastolic ventricular filling and normal left ventricular function, which are characteristic of diastolic heart failure. This will not change the treatment approach, however. It is possible but unlikely that the systolic murmur represents aortic stenosis or hypertrophic cardiomyopathy. Even if present, these probably are not hemodynamically significant, given the normal physical findings and electrocardiogram. Caffeine has been effective in ameliorating postprandial hypotension in some patients, but tolerance develops rapidly. ACE inhibitors may improve postprandial regulation of blood pressure. Fludrocortisone is useful for chronic orthostatic or postprandial hypotension, but it is relatively contraindicated in patients with heart failure because it causes sodium retention.

26 Post Test #2 (10) You are called to see an 80-year-old nursing-home resident with Alzheimer’s disease, reflux esophagitis, and glaucoma who suddenly lost consciousness and fell to the floor at 9:00 am while sitting in the dining room beginning his breakfast. He was noted by his nurse during morning rounds to be more lethargic than usual, not engaging in his usual pacing behavior before breakfast. At 8:00 am he received docusate, omeprazole, and timolol eye drops. After his collapse the patient spontaneously regained consciousness while lying on the floor and was diaphoretic. There were no other symptoms. On examination by the nurse, his supine blood pressure was found to be 168/92 mm Hg, heart rate was regular at 96 per minute, respiration rate was 28 per minute, and axillary temperature was 37.7°C (99.8°F). What is the most likely diagnosis?

27 What is the most likely diagnosis?A. Postprandial hypotension B. Arrhythmia C. Pneumonia D. Neurally mediated syncope E. Acute myocardial infarction

28 Answer; C. Pneumonia Syncope in the elderly patient is often the atypical manifestation of diseases or situations that may not be expected to result in loss of consciousness. Pneumonia is a common cause of syncope in the elderly patient, possibly as a result of hypoxemia, dehydration, or altered cardiovascular reflexes. In this case there are several signs consistent with this diagnosis. First, the patient was lethargic during morning rounds, suggesting that there was an occult illness. Also, during the nurse’s examination he had a relatively high heart rate and respiration rate, suggesting the presence of an acute respiratory illness. His axillary temperature of 37.7°C (99.8°F) corresponds to an oral temperature of 38.2°C (100.8°F).

29 Although the patient was eating a breakfast meal, postprandial hypotension usually does not occur until 30 to 45 minutes after the meal. The fact that he was receiving ophthalmic timolol drops might predispose him to a bradyarrhythmia; however, his heart rate was 96 per minute following the event. Certainly an arrhythmia is possible, but this would present acutely and would not be associated with lethargy earlier in the morning. The diagnosis of neurally mediated syncope is less common in the elderly patient but does occur; usually this is preceded by a prodrome of nausea, abdominal discomfort, diaphoresis, or a stressful situation. Finally, it is possible that an acute myocardial infarction precipitated syncope; however, in the setting of lethargy, fever, and tachypnea in a nursing-home patient without prior cardiovascular disease, this diagnosis is less likely than pneumonia. End

30 References Bush D. Syncope. In: Geriatric Review Syllabus: A Core Curriculum in Geriatric Medicine, 6th Edition (Pompei P, Murphy JB, eds.), New York: American Geriatrics Society, Chapter 23, pp , 2006. 2. Kapoor WN. Current evaluation and management of syncope. Circulation 2002 Sep ;106(13): 3. Linzer M, Yang EG, Estes NA, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Int Med 1997; 126: 4. Recchia D, Barzilai B. Echocardiography in the evaluation of patients with syncope. J Gen Intern Med 1995 Dec;10(12): 5. Kapoor WN. Syncope. N Engl J Med 2000 Dec 21; 343(25): 6. Bass EB, Curtiss EL, ArenVC, et al. The duration of holter monitoring in patients with syncope. Is twenty-four hours enough? Arch Int Med 1990;150(5): 7. Menozzi C, Brignole M, Garcia-Civera R, et.al. Mechanism of syncope in patients with heart disease and negative electrophysiologic test. Circulation 2002 Jun 11; 105(23): 8. Natale A. Akhtar M, Jazayeri M, et.al. Provocation of hypotension during head-up tilt testing in subjects with no history of syncope or presyncope. Circulation 1995 Jul 11;92(1):54-8. Bush D. Syncope. In: Geriatric Review Syllabus: A Core Curriculum in Geriatric Medicine, 5th Edition (Cobbs EL, Duthie EH, Murphy JB, eds.), Malden, MA: Blackwell Publishing for the American Geriatrics Society, Chapter 24, pp , 2002 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. Bush D. Syncope. Geriatric Review Syllabus, sixth edition,, chapter 23, page 171 Linzer M., Yang EH. Et. al. Diagnosing syncope; part one: value of history, physical exam, a nation and electrocardiography. Annals Int Med, June 15, 1997; 126:99-996