1. SYNCOPE Module #1 Ed Vandenberg, MD, CMD Geriatric Section OVAMC &
Section of Geriatrics
UNMC
Omaha, NE
Web: geriatrics.unmc.edu
Welcome to the “Syncope” modules. Over the next many slides we will attempt to review the causes and evaluation of syncope in the elderly. We hope that you will enjoy this module and just PASS OUT with joy over it.

2. 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
Our process will be for you to complete a series of 3 modules and questions on the topics Etiologies and Evaluation of syncope.
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.

3. 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
What we hope you get out of these modules is a good definition of syncope and to know a little bit about the it’s epidemiology. Most important is understanding the aging physiology that predisposes the elder to syncope. In future modules we’ll look at the causes more closely and describe the evaluation of syncope.

4. SYNCOPE
DEFINITION:
The sudden, transient loss of consciousness and postural tone that is followed by spontaneous recovery
Clearly, the important feature here is the transient loss of consciousness and postural tone followed by spontaneous recovery. This differentiates it from “near syncope”, lightheadedness and some of the other dizzy etiologies you can review in the “dizzy” modules.

5. EPIDEMIOLOGY1 80% of hospitalized for syncope are >65 y.o.
Incidence: Community: age > % 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)
Syncope has a 2-6% annual incidence in those over age 80. Almost half of all elders will have an episode of syncope in their lifetime. It accounts for up to 6% of all ED visits, and many ED physicians are very interested in this etiology. For the folks in nursing homes, the incidence is about 6% per year with recurrence rate of about 30%. If you have been hospitalized for syncope, very likely you are over age 65. But this does not reflect how many episodes there are, as up to 44% of elderly probably don’t report their syncopal event.
This next slide is a question. Please note your response to yourself and proceed to the next slide for the answer.

6. MORTALITY What cause of Syncope has the highest mortality? Vasovagal
Cardiac
Orthostatic hypotension
CVA

7. What cause of Syncope has the highest mortality?2-4
ANSWER Year Mortality
Cardiac cause %-30 %
All others with known etiologies----6 %
Unknown etiology after w/u %
The most lethal of all causes of syncope is, of course, cardiac. With a cardiac cause, if left untreated, up to 30% can die within the ensuing year. The good news here, is that all of the other etiologies besides cardiac have only about a 6% per year mortality. This number is close to those cases of syncope in which we are unable to make a diagnosis after adequate workup. So, this reassures the clinician that if you are able to do a good workup, you’ve lowered the mortality risk to probably as low as you can get despite not always finding the cause. We are unable to find causes in up to % of syncopal causes.

8. ETIOLOGIES most common causes
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
GENERAL CATEGORIES
 Vascular resistance & venous return + bradycardia
Arrhythmia
Obstruction (cardiac or pulmonary)
Cerebral blood flow impairment
General categories of physiologic causes include a drop in the vascular resistance associated with bradycardia, arrhythmia, cardiac or pulmonary obstruction, and any cerebral blood flow impairment. What is the common pathophysiologic mechanism of these causes? Please note your response to yourself and proceed to the next slide for the answer.

9. TRANSIENT CEREBRAL HYPOPERFUSION
From either:
Alteration is systemic blood pressure or
Increase cerebral vascular resistance
Transient cerebral hypoperfusion is the common pathophysiologic mechanism. It’s caused either by alteration in systemic blood pressure, such as in orthostatic hypotension or changes in cardiac output or an increase in cerebral vascular resistance such as might be seen in hyperventilation, panic attacks or cerebral vascular vasoconstriction.

10. ETIOLOGIES Less 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
The less common etiologies, of course, include hypoxia, hypoglycemia and seizures. By now you’re probably saying “How can I remember all of these causes?” What you need is a mnemonic, and we propose the “P-A-S-S O-U-T” mnemonic that will assist you.

11. 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
First, we must look for correctable causes.
The mnemonic here gives you a basic list of causes.
Orthostatic hypotension is perhaps one of the areas where we have the most potential to benefit our patients. If you’ve reviewed this in the “Dizziness” module, you may proceed ahead in the slides. Otherwise, review the next slides that delve into each of the causes Pressure related causes in detail.

12. P ressure (Hypotensive induced causes)
Elderly are predisposed to pressure problems
I want to pause over the next few slides to discuss elders and why they are predisposed to orthostatic hypotension. This is important knowledge to prepare us to reduce this problem in the elderly.

13. Mechanisms of compensation for gravitational effects of standing
Autonomic
Endocrine
Carotid/aortic baroreceptors
 renin release
 angiotensin II
 aldosterone
sympathetic tone
To maintain blood pressure, whether we are elders or not, we need an intact autonomic nervous system that is driven by our carotid/aortic baroreceptors. When the baroreceptors sense a decline in pressure, they send stimuli to the brain to increase sympathetic tone, which then causes increased peripheral vasoconstriction and heart rate.
On the other side, our endocrine system must release renin that increases angiotensin II and aldosterone leading to vasoconstriction and sodium retention, respectively. Another thing that we ask our endocrine system to do is to reduce atrial natriurectic factor which reduces vasodilatation and increases the renin-angiotensin system.
 vasoconstriction
 sodium retention
peripheral vasoconstriction
&  heart rate
Atrial
Natriurectic
factor
 vasodilator
 renin-angiotensin

14. Aging, Physiology and Blood Pressure
Physiology of Pressure maintenance
Aging Physiologic changes
Baroreceptors sensitivity
Decreased sensitivity
Volume (fluid)
Decreased reserve
Vascular tone
Decreased tone
B-receptor responsiveness
Decreased B-receptor responsiveness
Muscle tone and therefore venous return
What happens to this system as we age?
Elder’s baroreceptors become less sensitive and are less quick to respond to dropping blood pressure. They keep less fluid reserve in their bodies due to reduced muscle mass and, hence, have less margin of error. Elders can quickly get hypo-tensive if they do start to drop in their fluid intake or experience increased fluid loss.
Elder’s vascular tone decreases and, perhaps most important, their beta responsiveness in cardiac output declines and they cannot reach the same maximum heart rate or cardiac output they might have had as younger people. Lastly, muscle tone is decreased and, therefore, our venous return is decreased. All of these set the stage for an increased incidence of hypotensive events.

15. Disease changes that predispose Incidence increased
Physiology of Pressure maintenance
Aging Physiologic changes
Disease changes that predispose
Incidence
Autonomic Nervous System dysfunction (e.g.DM)
increased
Cerebrovascular auto-regulatory dysfunction (HTN)*
Medications
*(20-30% of HTN pop. Age > 65 can have orthostatic hypotension (O.H.))
( 7% of Normotensive pop. age > 65 can have orthostatic hypotension)5
Then along come diseases that affect the system even more profoundly.
Diseases that affect the autonomic nervous system, such as diabetic neuropathy. Another cause is cerebrovascular auto regulatory changes such as in chronic hypertension.
Of course lastly is medications.
As noted here, up to 30% of patients with hypertension over age 65 will demonstrate orthostatic changes of significance, whereas only 7% of the normotensive population will do the same.
Lastly, medications are a significant factor in the incidence of orthostatic hypotension.

16. General Causes of Pressure Problems:1
1)Vasovagal
1-29 % of all causes syncope.
2) Orthostatic Hypotension
5-29 % of all causes syncope
General causes of pressure problems overall include vasovagal and orthostatic hypotension as the dominant mediators.
Both Vasovagal and orthostatic hypotension can account for up to 29% of the causes each.

17. Pressure 1)Vasovagal History: the setting:
Physiology:
LV Sensors respond to:
forceful contractions and increased heart rate
( also stimuli can come from esophagus, bladder, carotid sinus, resp. tract)
Medulla responds via increase in vagal efferent activity
 sympathetic activity (vasodilation)
 parasympathetic activity (bradycardia)
History:
the setting:
emotion, hunger, heat, PAIN,
upright posture
Perhaps one of the more intriguing physiological events is vasovagal syncope. In this, the left ventricular sensors feel both the forceful contractions and the increase heart rate. Stimuli can also come from esophagus such as if we get food stuck, fro the bladder if it gets overstretched and then empties, the carotid sinus and lastly, if we stimulate the respiratory tract (such as foreign body in the laryngeal or trachea areas). These sensors send their message to the medulla that responds by an increase in vagal efferent activity with subsequent decrease in sympathetic activity (vasodilation) and an increase in parasympathetic activity (bradycardia). Some of the situations that are set-ups for this, are times of emotion, hunger, and certainly the most common is pain. You need to almost always be in the upright posture, either sitting or standing, for this to have an effect on the patient.

18. 2)Orthostatic Hypotension definition Pressure
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.
Orthostatic hypotension is defined by a drop in blood pressure > 20 mm supine to standing, or an increase in heart rate > 20 beats/minute. Elders have a poorly responsive beta system so often you will not see the increase in heart rate that you would expect with this kind of drop in blood pressure. The procedure to elicit this response is described in the right hand column.

19. 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)
What also happens in aging, besides the decrease in B-adrenergic response that I just described, is a decline in baroreflex. Certainly in a younger patient a drop in blood pressure would cause an increase in heart rate and vasoconstriction that would compensate for the postural decline in blood pressure, not so with the aged.

20. 2) Orthostatic Hypotension CAUSES Pressure
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
The list of orthostatic causes is quite long. However, the clinician can quickly sort through these.
We will work through each of these in the next slides.
Certainly volume loss is often quite apparent. Medications, which as no surprise, here we see the same list of common offenders that would either affect blood pressure through direct vasodilatation or impaired cardiac output.

21. 2)Orthostatic Hypotension CAUSES5 continued 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
Situational causes, mostly mediated through vasovagal mechanisms will include micturition, postprandial, cough, carotid sinus sensitivity, defecation, and laughing. An interesting note regarding postprandial, is that up to 30-40% of elderly nursing home population will show orthostatic blood pressure changes after meals, but only 2% are symptomatic from it.

22. 2)Orthostatic Hypotension CAUSES continued 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
Additional causes include both the primary autonomic diseases, foremost of which is Parkinson’s disease, and the secondary autonomic diseases, which are more common. Among those, probably the most common are diabetic neuropathies, alcoholic neuropathies, renal failure, and various autonomic disease.

23. 2) Orthostatic Hypotension “The Diagnosis” 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
How do you make a diagnosis of orthostatic hypotension? Certainly, there is “the gold standard” in which you demonstrate orthostatic hypotension in your patient and simultaneously reproduce their symptoms. This can be done during an exam or sometimes using the more sophisticated “tilt table” testing, which we’ll talk about in later modules. The “fall back” position, however, is if you prove that the patient has orthostatic hypotension and you have strong suspicions of it being related to the syncope but cannot reproduce it during the exam. This diagnosis must then be based on a consistent history.

24. The End of Module One on Evaluation of Syncope6
This completes our first module on causes of syncope, to complete the question for credit for this module, please close out this module, and advance to the question in 2 in Blackboard, then answer the question and review the answer. Then, when ready proceed to module #2 where we will continue to work on some more etiologies.
Add question 191

25. 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?

26. 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.

27. 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.

28. 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

29. REFERENCES
1. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347:
2. Junaid A, Dubinsy IL. Establishing an approach to syncope in the emergency department. J Emer Med 1997;15:
3. Eagle KA, Black HR, Cook EF, et al. Evaluation of prognostic classifications for patients with syncope. Am J Med 1985;79:
4. Gilman JK. Syncope in the emergency department. Emer Med Clinic North Am 1995;13:
5. Lipsitz LA. Altered blood pressure homeostasis in advanced age: Clinical and research implications. J Gerontol 1989; 44:M
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 , 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