blood pressure regulation and arterial hypertension ... · • acute intoxication (e.g., alcohol)...
TRANSCRIPT
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Definition
Syncope is a medical SYMPTOM characterized by:
►transient loss of consciousness and postural tone
►relatively rapid, sudden onset
►±variable prodromal warning signs
►spontaneous complete recovery
►absence of prolonged confusion (post-ictal period)
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• Migraine*
• Acute hypoxemia*
• Hyperventilation*
• Somatization disorder (psychogenic syncope)
• Acute Intoxication (e.g., alcohol)
• Seizures (epileptic)
• Hypoglycemia
• Sleep disorders
* may cause ‘true’ syncope
Differential diagnosis
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• Individuals <18 yrs
• Military Population 17- 46 yrs
• Individuals 40-59 yrs*
• Individuals >70 yrs*
15%
20-25%
16-19%
23%
Syncope:Reported Frequency
*during a 10-year periodBrignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22: 1256-1306.
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Etiology
OrthostaticCardiac
Arrhythmia
Structural
Cardio-
Pulmonary
*
1
Vasovagal
Carotid Sinus
Situational➢Cough
➢Post-
micturition
2
Drug-induced
ANS Failure➢Primary
➢Secondary
3
Bradycardic➢Sick sinus
➢AV block
Tachycardic➢VT
➢SVT
Long QT
Syndrome
4
Aortic
Stenosis
HOCM
Pulmonary
Hypertension
5
Psychogenic
Metabolic
e.g. hyper-
ventilation
Neurological
Non-
Cardio-
vascular
Neurally-
Mediated
Unknown Cause = 34%
24% 11% 14% 4% 12%
DG Benditt, UM Cardiac Arrhythmia Center
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Impact of Syncope
1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.
0%
20%
40%
60%
80%
100%
Anxiety/
Depression
Alter Daily
Activities
Restricted
Driving
Change
Employment
73% 1 71% 2
60% 2
37% 2
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1 Day SC, et al. Am J of Med 1982;73:15-23.2 Kapoor W. Medicine 1990;69:160-175.3 Silverstein M, Sager D, Mulley A. JAMA. 1982;248:1185-1189.4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:499-504.
• Some causes of syncope are potentially fatal• Cardiac causes of syncope have the highest mortality rates
The Significance of Syncope
0%
5%
10%
15%
20%
25%
Sy
nc
op
e M
ort
ality
Overall Due to Cardiac Causes
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Syncope: Basic Diagnostic Steps
• Detailed History & Physical– Document details of events
– Assess frequency, severity
– Obtain careful family history
• Heart disease present? – Physical exam
– ECG: long QT, WPW, conduction system disease
– Echo: LV function, valve status, HCM
• Follow a diagnostic plan...
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Syncope: Evaluation and Differential Diagnosis
• Complete Description
– From patient and observers
• Type of Onset
• Duration of Attacks
• Posture
• Associated Symptoms
• Sequelae
History – What to Look for
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12-Lead ECG
• Normal or Abnormal?
– Acute MI
– Severe Sinus Bradycardia/pause
– AV Block
– Tachyarrhythmia (SVT, VT)
– Preexcitation (WPW), Long QT, Brugada
• Short sampling window (approx. 12 sec)
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Carotid Sinus Massage
• Site:
– Carotid arterial pulse just below thyroid cartilage
• Method:
– Right followed by left, pause between
– Massage, NOT occlusion
– Duration: 5-10 sec
– Posture – supine & erect
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Carotid Sinus Massage
• Outcome:– 3 sec asystole and/or 50 mmHg fall in systolic blood pressure with
reproduction of symptoms =
Carotid Sinus Syndrome (CSS)• Contraindications
– Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
• Risks– 1 in 5000 massages complicated by TIA
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Method Comments
Holter (24-48 hours) Useful for frequent events
Event Recorder •Useful for infrequent events
•Limited value in sudden LOC
Loop Recorder •Useful for infrequent events
•Implantable type more convenient (ILR)
Wireless (internet) Event Monitoring
In development
Ambulatory ECG
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Investigation of syncope:
ambulatory ECG (holter) monitoring
AV block
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Value of
Event
Recorder in
Syncope
Linzer M. Am J Cardiol. 1990;66:214-219.
*Asterisk denotes
event marker
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Head-up Tilt Test (HUT)
• Unmasks VVS susceptibility
• Reproduces symptoms
• Patient learns VVS warning
symptoms
• Physician is better able to
give prognostic / treatment
advice
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Tilt testing - outcomes
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Electroencephalogram
• Not a first line of testing
• Syncope from Seizures
• Abnormal in the interval between two
attacks – Epilepsy
• Normal – Syncope
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Neurally-Mediated Reflex Syncope (NMS)
• Vasovagal syncope (VVS)
• Carotid sinus syndrome
(CSS)
• Situational syncope
– post-micturition
– cough
– swallow
– defecation
– blood drawing
– etc.
• Multiple triggers
• Variable contribution
of vasodilatation and
bradycardia
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NMS: Basic Pathophysiology
Cerebral
Cortex
Vascular
Bed Bradycardia/
Hypotension
Baro-
receptors
Heart
Feedback via
Carotid Baroreceptors
Other Mechanoreceptors
Parasympathetic (+)
sympathetic (+) ¯ Heart Rate
¯ AV
Conduction
_
Vasodilatation
Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc
JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996
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NMS: Neurological basis
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• Neurally Mediated Physiologic Reflex Mechanism with two Components:
– Cardioinhibitory (↓HR )
– Vasodepressor (↓BP )
• 3 types:
– Hypersensitive (↓BP )
– Cardioinhibitory (↓HR)
– Central (no change in BP or HR)
NMS: Clinical Pathophysiology
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NMS: Prevalence of VVS
• Prevalence is poorly known
– Various studies report 8% to 37% (mean 18%)
of cases of syncope (Linzer 1997)
• In general:
– VVS patients younger than CSS patients
– Ages range from adolescence to elderly
(median 43 years)
– Pallor, nausea, sweating, palpitations are common
– Amnesia for warning symptoms in older patients
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DG Benditt, UM Cardiac Arrhythmia Center
16.3
sec
Continuous Tracing1 sec
Spontaneous VVS
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Kaplan-Meier Survival Curves
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NMS: Etiology of CSS
• Sensory nerve endings in the carotid sinus
walls respond to deformation
• “Deafferentation” of neck muscles may
contribute
• Increased afferent signals to brain stem
• Reflex increase in efferent vagal activity
and diminution of sympathetic tone results
in bradycardia and vasodilation
Carotid Sinus
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NMS: Carotid Sinus Hypersensitivity(CSH)
• Abnormal response to CSM
• Major symptom and prerequisite for CSS
• Absence of symptoms attributable to CSS
• CSH reported frequent in ‘fallers’ (Kenny)
CSH CSS
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NMS: CSS and Falls in the Elderly
• 30% of people >65 yrs of age fall each year1
– Total is 9,000,000 people in USA
– Approximately 10% of falls in elderly persons are due to syncope2
• 50% of fallers have documented recurrence3
• Prevalence of CSS among frequent and unexplained fallers unknown but…
– CSH present in 23% of >50 yrs fallers presenting at ER 3
1Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, 1995.2 Campbell et al: Age and Aging 1981;10:264-270.3Richardson DA, Bexton RS, et al. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting
to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE 1997
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Management Strategies for VVS
• Optimal management strategies for VVS are a source of debate
– Patient education, reassurance, instruction
– Fluids, salt, diet
– Tilt Training
– Support hose
• Drug therapies
• Pacing
– Class II indication for VVS patients with positive Head-up-tilt testing
and cardioinhibitory or mixed reflex
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VVS: Tilt-Training
• Objectives
– Enhance Orthostatic Tolerance
– Diminish Excessive Autonomic Reflex Activity
– Reduce Syncope Susceptibility / Recurrences
• Technique
– Prescribed Periods of Upright Posture
– Progressive Increased Duration
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NMS: Carotid Sinus Syndrome (CSS)
• Syncope clearly associated with carotid
sinus stimulation is rare (≤1% of syncope)
• CSS may be an important cause of
unexplained syncope / falls in older
individuals
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NMS: Pharmacological treatment for VVS
• Salt /Volume
– Salt tablets, ‘sport’ drinks, fludrocortisone
• Beta-adrenergic blockers
– 1 positive controlled trial (atenolol),
– 1 on-going RCT (POST)
• Disopyramide (Antiarrhytmic Na channel blocker with antimuscarinic
action)
• SSRIs
– 1 controlled trial
• Vasoconstrictors (e.g., midodrine)
– 1 negative controlled trial (etilephrine)
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NMS: Midodrine treatment
Journal of Cardiovascular Electrophysiology Vol. 12, No. 8, Perez-Lugones, et al.
Months
p < 0.001
Sym
pto
m –
Fre
e I
nte
rval
180160140120100806040200
100
80
60
40
20
0
Fluid
Midodrine
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NMS: Status of Pacing in VVS
• Perception of pacing for VVS changing:
– VVS with +HUT and cardioinhibitory response a Class IIb indication1
• Recent clinical studies demonstrated benefits of pacing in select VVS patients:
– VPS I
– VASIS
– SYDIT
– VPS II –Phase I
– ROME VVS Trial
1Gregoratos G, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmic Devices. Circulation. 1998; 97:
1325-1335.
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NMS:
VPS-I (Vasovagal Pacemaker Study I)
Connolly S, et al. J Am Coll Cardiol 1999; 33: 16-20.
Study Design:
– 54 patients randomized, prospective, single center27 DDD pacemaker with rate drop response (RDR)
27 no pacemakerPatient Inclusion Criteria:
– 6 syncopal events ever
– +HUT
– Relative bradycardia*
*a trough heart rate <60/min if no isoproterenol used,
<70/min if up to 2 mcg/min isoproterenol used, or <80/min
if over 2 mcg/min isoproterenol used
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NMS:
VPS- I
Connolly S, et al. J Am Coll Cardiol 1999; 33: 16-20.
Cumulative
Risk
(%)
100
90
80
70
60
50
40
30
20
10
0
15129630
Control
(No Pacemaker)
2P=0.000022
Pacemaker
Time in Months
Number
At Risk
C 27 9 4 2 1 0
P 27 21 17 12 11 8
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NMS:
VASIS (Vasovagal Syncope International
Study)
Sutton, R, et al. Circulation. 2000; 102:294-299.
Study Design:– 42 patients, randomized, prospective, multicenter
19 DDI pacemaker (80 bpm) with rate hysteresis (45 bpm)
23 no pacemaker
Patient Inclusion Criteria:– > 3 syncopal events in 2 years and last event occurring within 6
months of enrollment and,
– Positive VASIS type 2A or 2B cardioinhibitory response to HUT and,
– Age > 40 years or drug refractory if < 40 years
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NMS:
VASIS
Pacemaker
No-Pacemaker
p=0.0004
Years
% s
yn
co
pe
-fre
e
100
80
60
40
20
0 2 3 4 5 6
7121415233140
# of
pts
Sutton, R, et al. Circulation. 2000; 102:294-299.
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VVS Pacing Trials Conclusions
DDD pacing reduces the risk of syncope
in patients with recurrent, refractory,
highly-symptomatic, cardioinhibitory
vasovagal syncope.
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OS: Principal Causes of Orthostatic Syncope
• Drug-induced (very common)
– diuretics
– vasodilators
• Primary autonomic failure
– multiple system atrophy
– Parkinsonism
• Secondary autonomic failure
– diabetes
– alcohol
– amyloid
• Alcohol
– orthostatic intolerance apart from neuropathy
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AS, CS: General Rules
• Often life-threatening and/or exposes patient to high risk of injury
• May be warning of critical CV disease
– Aortic stenosis, Myocardial ischemia, Pulmonary hypertension
– “Survived sudden cardiac death”
• Assess culprit arrhythmia / structural abnormality aggressively
• Initiate treatment promptly
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CS: Principal Causes
• Acute MI / Ischemia– Acquired coronary artery disease
– Congenital coronary artery anomalies
• HCM
• Acute aortic dissection
• Pericardial disease / tamponade
• Pulmonary embolus / pulmonary hypertension
• Valvular abnormalities– Aortic stenosis, Atrial myxoma
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CS: Subclavian Steal Syndrome
• Abnormal narrowing of the subclavian
artery proximal to the origin of the
vertebral artery
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AS: Causes
• Bradyarrhythmias
– Sinus arrest, exit block
– High grade or acute complete AV block
• Tachyarrhythmias
– Atrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome)
– Paroxysmal SVT or VT
– Torsades de pointes
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AS: Rhythms During Recurrent Syncope
Krahn A, et al. Circulation. 1999; 99: 406-410
Normal Sinus
Rhythm
58%Sinus Rhythm
58%
Bradycardia
36%
Tachyarrhythmia
6%
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AS: Abnormal sinus pause
From the files of DG Benditt, UM Cardiac Arrhythmia Center
Is it the cause for syncopes?
What is the pathophysiological mechanism: NMS or intrinsic disease?
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AS: Torsades
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83 yo woman
Bradycardia: Pacemaker
implanted
28 yo man in the ER multiple
times after falls resulting in
trauma
VT: ablated and medicated
Reveal ® ILR recordings; Medtronic data on file.
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AS: Drug-Induced QT Prolongation
• Antiarrhythmics
– Class IA ...Quinidine, Procainamide, Disopyramide
– Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, (NAPA)
• Antianginal Agents
– (Bepridil)
• Psychoactive Agents
– Phenothiazines, Amitriptyline, Imipramine, Ziprasidone
• Antibiotics
– Erythromycin, Pentamidine, Fluconazole
• Nonsedating antihistamines
– (Terfenadine), Astemizole
• Others
– (Cisapride), Droperidol
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AS: Treatment of Syncope Due to
Bradyarrhythmia
• Class I indication for pacing using dual-
chamber system wherever adequate atrial
rhythm is available
• Ventricular pacing in atrial fibrillation with
slow ventricular response
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AS: Treatment of Syncope Due to
Tachyarrhythmia
• Atrial Tachyarrhythmias;– AVRT due to accessory pathway – ablate pathway– AVNRT – ablate AV nodal slow pathway– Atrial fib– Pacing, linear / focal ablation, ICD selected pts– Atrial flutter – Ablation of reentrant circuit
• Ventricular Tachyarrhythmias;– Ventricular tachycardia – ICD or ablation where appropriate– Torsades de Pointes – withdraw offending Rx or ICD (long-
QT/Brugada)
• Drug therapy may be an alternative in many cases
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Pathophysiology
CNS perfusion
Ascending Reticular Activating System (ARAS)
BP=SV x HR x PR
Autonomous vegetative system
Carotic sinus RA and LV mechanoceptors
Stress
ValsalvFood Cough
Defecation
Cold food
Carotid compression (head turning, shaving)
Hypersensitivity
Overinhibiting Failure
Dysrhythmias
Structural CD
Pulmonary hypertension
Subclavian steal phenomenon