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This module provides an overview of syncope, including its definition, epidemiology, and causes. It also covers the aging physiology that predisposes to syncope.
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SYNCOPEModule #1 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
PROCESS Series of 3 modules and questions on Etiologies and Evaluation 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
Objectives Upon completion of the module the learner will be able to: Define syncope Describe the epidemiology of syncope Describe the aging physiology that predisposes to syncope List the causes of syncope
SYNCOPE DEFINITION: The sudden, transient loss of consciousness and postural tone that is followed by spontaneous recovery
Incidence:Community:age > 80 2-6% annual 48 % lifetime incidence 1-6 % of all ED visits Institutionalized: 6 % per year, with a reoccurrence rate of 30 % 80% of hospitalized for syncope are >65 y.o. (this number underestimates the problem as……up to 44% don’t report for evaluation) EPIDEMIOLOGY1
MORTALITY What cause of Syncope has the highest mortality? • Vasovagal • Cardiac • Orthostatic hypotension • CVA
What cause of Syncope has the highest mortality?2-4 ANSWER1 Year Mortality Cardiac cause---------------------18%-30 % All others with known etiologies----6 % Unknown etiology after w/u----------6 %
GENERAL CATEGORIES Vascular resistance & venous return + bradycardia Arrhythmia Obstruction (cardiac or pulmonary) Cerebral blood flow impairment What is The Common pathophysiologic mechanism of the previously mentioned causes ? a) Transient cerebral hypoperfusion b) Hypoglycemia Post hypoxic cerebral edema Reduced acetylcholine production in the CNS ETIOLOGIESmost common causes
TRANSIENT CEREBRAL HYPOPERFUSION From either: • Alteration is systemic blood pressure or • Increase cerebral vascular resistance
ETIOLOGIESLess common causes • hypoxia • hypoglycemia • seizures HOW CAN I REMEMBER ALL THOSE CAUSES ? The Answer is: You need a mnemonic • P-A-S-S O-U-T
EtiologiesP-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
P ressure (Hypotensive induced causes) Elderly are predisposed to pressure problems
Mechanisms of compensation for gravitational effects of standing Autonomic Endocrine Carotid/aortic baroreceptors renin release angiotensin II aldosterone sympathetic tone vasoconstriction sodium retention peripheral vasoconstriction & heart rate Atrial Natriurectic factor vasodilator renin-angiotensin
General Causes of Pressure Problems:1 1)Vasovagal 1-29 % of all causes syncope. 2) Orthostatic Hypotension 5-29 % of all causes syncope
Physiology: LV Sensorsrespond to: forceful contractions and increased heart rate ( also stimuli can come from esophagus, bladder, carotid sinus, resp. tract) Medullaresponds via increase in vagal efferent activity sympathetic activity (vasodilation) parasympathetic activity (bradycardia) History: the setting: emotion, hunger, heat, PAIN, upright posture Pressure 1)Vasovagal
Definition: A decline in systolic BP > 20 mm Hg with supine to standing &/or increase in heart rate > 20 beats/min Technique: measure BP & pulse in each position lying for > 5 minutes then–> sitting then–> standing for 1 and 3 minutes. 2)Orthostatic Hypotensiondefinition Pressure
Aging changes in physiology that predispose to orthostatic hypotension: • decrease in B-adrenergic responsiveness • decrease in baroreflex: (B-adrenergic responsiveness and baroreflex: would in younger patients cause an increase heart rate and vasoconstrict and thus compensate for postural BP decline)
Causes: a) Volume loss b) Medications c) Situational d) Primary Autonomic Disease e) Secondary Autonomic Disease f) Adrenal Insufficiency a) Volume Loss blood loss fluid loss (diarrhea, sweating, diuresis, dehydration) b) Medications: antihypertensives B-blockers alcohol anticholinergics antianginals vasodilators antiparkinsonian 2) Orthostatic HypotensionCAUSES Pressure
c)Situational (many of these involve Vasovagal) micturition postprandial* cough carotid sinus sensitivity defecation laughing postprandial* “36 % elderly NH pop. had orthostatic hypotension postprandially” BUT: only 2 % had symptoms from it 2)Orthostatic HypotensionCAUSES5continued Pressure
d) Primary Autonomic Disease: Idiopathic Multi-System Atrophy (e.g.Shy-Dragger) Parkinson’s disease e) Secondary autonomic disease: Neuropathic e.g.DM, amyloid, alcoholism, auto-immune Cancer, B12 def., porphyria CNS e.g. CVA’S, MS, Tumors, Wernickes, spinal cord lesions Renal failure 2)Orthostatic Hypotension CAUSEScontinued Pressure
The “Gold Standard” a) Proven orthostatic hypotension and symptoms reproduced via: clinically demonstrated decline in BP with symptoms or Tilt table testing* with provocation of symptoms The “Fall-Back Position” a) Proven orthostatic hypotension and strong suspicions based on: consistent history 2) Orthostatic Hypotension“The Diagnosis” Pressure
Post Test7 • After rising from bed in the morning, an elderly nursing-home resident with a history of recurrent falls is found to have a 30–mm Hg decline in systolic blood pressure. Which of the following statements is correct?
Which of the following statements is correct? A. The orthostatic change will persist throughout the day. B. Postprandial hypotension also is likely to be present. C. The patient probably does not have a history of hypertension. D. The patient’s falls are probably related to orthostatic hypotension E. The patient is at increased risk for rapid cognitive deterioration in the next 2 years.
Answer: D. The patient’s falls are probably related to orthostatic hypotension. Nearly 50% of elderly nursing-home residents experience orthostatic hypotension (OH) one or more times per day. At any given time, approximately 20% to 30% of residents experience OH. In the nursing home, it is associated with falls only in residents who have a history of falling in the past 6 months. The condition is highly variable, occurring most often before breakfast or after 1 minute of standing. It is more common in patients with hypertension. Although OH may occur after a meal and in patients with postprandial hypotension, these two abnormalities in blood-pressure regulation rarely occur together in the same patient.
Longitudinal studies examining long-term outcomes have shown a relationship between OH and cardiovascular mortality in community-dwelling populations. Although transient hypotension might be expected to result in decreased cerebral perfusion and cause cognitive dysfunction, a Finnish study of community-dwelling and institutionalized elderly persons showed no association with cognitive deterioration during a 2-year follow-up period. End
REFERENCES 1. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347:878-885 2. Junaid A, Dubinsy IL. Establishing an approach to syncope in the emergency department. J Emer Med 1997;15:593-599 3. Eagle KA, Black HR, Cook EF, et al. Evaluation of prognostic classifications for patients with syncope. Am J Med 1985;79:455-460 4. Gilman JK. Syncope in the emergency department. Emer Med Clinic North Am 1995;13:955-971 5. Lipsitz LA. Altered blood pressure homeostasis in advanced age: Clinical and research implications. J Gerontol 1989; 44:M179-183 6. 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 7. 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