Dr Sajeer K T Senior Resident Dept. of Cardiology MCH, Kozhikode 1

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Dr Sajeer K TSenior ResidentDept. of Cardiology MCH, Kozhikode

Syncope- initial approach, diagnosis and management of neurocardiogenic

syncope

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Definition: Syncope is a transient loss of consciousness due to transient global cerebral hypo perfusion characterized by rapid onset, short duration, and spontaneous complete recovery - ESC 2009

Mechanism: Transient global cerebral

hypoperfusion.

Brignole et al. Europace. 6:467-537;2004

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Impact of Syncope 40% will experience syncope

at least once in a lifetime

Major morbidity reported in 6%(e g: fractures, motor vehicle accidents)

Minor injury in 29%(e g: lacerations, bruises)

common medical problem ≈ 3% of ER visits ≈1-6 % of hospital admissions

Brignole M, et al. Europace. 2003;5:293-298

Impact of Syncope

1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.

0%

20%

40%

60%

80%

100%

Anxiety/Depression

Alter DailyActivities

RestrictedDriving

ChangeEmployment

73% 171% 2

60% 2

37% 2

Pro

port

ion

of P

atie

nts

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Syncope – A Symptom, Not a Diagnosis

Self-limited loss of consciousness and postural tone Relatively rapid onset Variable warning symptoms Spontaneous, complete, and usually prompt recovery

without medical or surgical intervention

Brignole M, et al. Europace, 2004;6:467-537.

Complete loss of consciousness in vasovagal syncope is usually no longer than 20 s in duration

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Pre-syncope or near-syncope indicate symptoms and signs that occur before

unconsciousness in syncope

- Patients feels syncope is imminent

- Symptoms associated with pre-syncope may be non-specific (e.g. dizziness)

- tend to overlap the premonitory phase of true syncope ( light-headedness, nausea, sweating, weakness, and visual disturbances)

- True Syncope should be differentiated from Nonsyncopal

events a/w real or apparent transient LOCCauses of non-syncopal attacks (commonly misdiagnosed as syncope)

European Heart Journal (2009) 30, 2631–2671

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Syncope Evaluation

- Two main reasons to evaluate patients with syncope: 1. To determine the etiology of syncope

2. To stratify the risk of future adverse outcomes

ESC

syncope

Neurally mediated

Orthostatic

Cardiac arrhythmia related

Structural heart disease related

Cerebrovascular syncopeBrignole et al. Europace. 6:467-537;2004

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Classification and Etiology of Syncope

Orthostatic (11%)

CardiacArrhythmia

(14%)

StructuralCardio-

Pulmonary (4%

1• VVS• CSS• Situational

CoughPost- Micturition

2• Drug-Induced• Vol. Depletion• ANS FailurePrimarySecondary

3• Brady

SN Dysfunction

AV Block

• TachyVTSVT

• L QT S• Brugada

Neurally-Mediated

(24%)

Unexplained Causes = Approximately 1/3 (34%)

Cerebro- Vascular

(12%)

5 • Vascular steal synd.

• VBA disease

• Carotid .A disease

4 • Acute

Myocardial Ischemia

• Aortic Stenosis

• HCM• Pulmonary

Hypertension• Aortic

Dissection


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Classification of Syncope According to Etiology (Modified by ESC Guidelines )Versus Classification According to Mechanism (Modified by ISSUE Classification

J Am Coll Cardiol 2012;59:1583–91

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Causes of syncope & Prevalence

Linzer et al. Ann Intern Med 1997;126:989-96

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Frequency of the causes of syncope in general population, Emergency Department and specialized clinical settings from some recent studies


14 BMJ 2010;340:c880

Causes of syncope by age

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Frequency of the causes of syncope according to age


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Clinical Features Suggestive of Specific Causes of Syncope

Episodes occur after sudden unexpected pain, fear, or unpleasant sight, sound, or smell Episodes occur after prolonged standing at attention

Episodes occur in a well-trained athlete without heart disease after exertion

Vasovagal attack

Kapoor. NEJM, 1857 -1862; 2000

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Episodes occur during or immediately after micturition, cough, swallowing,or defecation - Situational syncope

Episodes occur with head rotation or pressure on carotid sinus (due to tumors, shaving, or tight collars) - Carotid-sinus syncope

Episodes occur immediately on standing - Orthostatic hypotension

Patient takes medications that may lead to a long QT interval or orthostasisand bradycardia - Drug-induced syncope

Patient is confused after episode, or loss of consciousness lasts >5 minutes - Seizure

Patient has a brief loss of consciousness with no prodrome and has heart disease - Arrhythmias

Syncope occurs with exertion - AS, Pul.HTN, MS,HCM CADPatient has frequent syncope with somatic symptoms but no heart disease - Psychiatric illness

Kapoor. NEJM, 1857 -1862; 2000

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Reflex syncope (neurally mediated syncope)Neurocardiogenic, Vasodepressor, Vasovagal syncope ,Fainting

Cardiovascular reflexes controlling the circulation become intermittently inappropriate

(In response to a trigger)

Resulting in vasodilatation and/ or bradycardia

Fall in arterial BP and global cerebral perfusion


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Reflex syncope (neurally mediated syncope)Neurocardiogenic, Vasodepressor, Vasovagal syncope ,Fainting

- Common abnormality of blood pressure regulation characterized by the abrupt onset of hypotension with or without bradycardia

- Triggers: - orthostatic stress ( prolonged standing )- hot shower- emotional stress ( sight of blood)

- Neurally mediated syncope results from a paradoxical reflex - initiated when ventricular preload is reduced by venous pooling

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Venous pooling→ reduced ventricular preload

↓ in COP and BP sensed by arterial baroreceptors

↑catecholamine levels Vigorously contracting vol-depleted ventricle

Mechanoreceptors or C fibers (atria, ventricles, pulmonary artery)

Afferent C fibers → dorsal vagal nucleus of the medulla

Paradoxical withdrawal of peripheral sympathetic tone Increase in vagal toneVasodilatation bradycardia

syncope or presyncope

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Vasodepressor type

Reflex syncope-3 types ( based on efferent pathway) sympathetic or parasympathetic

Cardioinhibitory type Mixed type

Vasodilatation (↓BP)

hypotension

Bradycardia(↓HR)

or

Asystole( predominate)

Vasodilatation (↓BP)

+ Bradycardia (↓HR)

- ESC 2009

Etiology of CSS

Sensory nerve endings in the carotid sinus walls respond to deformation

“Deafferentation” of neck muscles may contribute

Increased afferent signals tobrain stem

Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation

Carotid Sinus

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Orthostatic hypotension and orthostaticintolerance syndromes

OH is defined as an abnormal decrease in systolic BP upon standing.

1.Classical OH : - a decrease in systolic BP ≥ 20 mmHg and in diastolic BP ≥10

mmHg within 3 min of standing

- in patients with pure ANF, hypovolemia, or other forms of ANF

2.Initial OH: - Characterized by a BP decrease immediately on standing of

> 40 mmHg, BP then spontaneously and rapidly returns to normal

- period of hypotension and symptoms is short (< 30 s)J Neurol Sci 1996;144:218–219

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J Neurol Sci 1996;144:218–219

(L) panel - healthy 17-year-old teenager with complaints of severe transient light headedness upon active standing, a pronounced initial fall in BP is observed. The nadir is at 7–10 s and followed by recovery of BP.

(R) panel- 47-year-old male with pure ANF : BP starts to fall immediately after standing to very low levels after 1 min upright with little increase in HR despite the hypotension.

Initial orthostatic hypotension ( L)

V/S

Classical orthostatic

hypotension (R).

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3.Delayed (progressive) OH : - slow progressive decrease in systolic blood pressure on standing

- absence of a bradycardiac reflex (vagal) differentiates delayed OH from reflex syncope

Reflex syncope (mixed form) induced by tilt testing : 1. 31-year-old patient (upper panel)

And

2. 69-year-old patient (lower panel).

Note the typical age differences with a much steeper fall in BP in the younger subject compared with the older subject

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Syndromes of orthostatic intolerance which may cause syncope

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Initial evaluation- Careful history- Physical examination (including orthostatic BP measurements)- ECG

Initial evaluation should answer three key questions (1) Is it a syncopal episode or not?(2) Has the etiological diagnosis been determined?

3) Are there data s/o of a high risk CVS events or death?

Diagnosis of syncope

The following questions should be answered:1. Was LOC complete?2. Was LOC transient with rapid onset and short duration?3. Did the patient recover spontaneously, completely and without sequelae?4. Did the patient lose postural tone?

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Risk stratification

When cause of syncope remains uncertain after

initial evaluation

Assess the risk of major CVS

events or SCD.

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Risk stratification at initial evaluation in prospective population studies

Table shows several different studies that have analysed the impact of different clinical data on the follow-up of patients presenting with syncope. ( presence of abnormal ECG, increased age, or data suggestive of heart disease imply a worse prognosis at 1–2 year follow-up)

CHESS acronym Patients with syncope are at 25% risk for serious outcomes if they present with one of these five clinical conditions:

1. Congestive heart failure (CHF), 2.Hematocrit <30%3. ECG abnormalities4. Shortness of breath5. Systolic blood pressure <90 mm Hg

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Diagnostic Tests

Ambulatory ECGHolter monitoringEvent recorder

○ Intermittent vs. Loop○ Implantable Loop Recorder (ILR)

Head-Up Tilt (HUT)Includes drug provocation (NTG, isoproterenol)Carotid Sinus Massage (CSM)

Adenosine Triphosphate Test (ATP)


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Diagnostic tests

1. Carotid sinus massage

- Pressure at CCA bifurcation site produces a reflex slowing in heart rate and fall in blood pressure

- Carotid sinus hypersensitivity (CSH): - a ventricular pause lasting > 3 s

and/or - a fall in systolic BP of >50 mmHg

- When CSH associated with spontaneous syncope → CSS.

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Afferent limb arising from the mechanoreceptors of the carotid. A

Carotid sinus reflex arc

Midbrain centres ( vagal nucleus and the vasomotor centre)

Efferent limb is via the vagal nerve and the parasympathetic ganglia to the sinus and atrioventricular nodes

via the sympathetic nervous system to the heart and the blood vessels

Carotid Sinus Massage (CSM)

MethodMassage, 5-10 secondsDon’t occludeSupine and upright

posture (on tilt table)

Outcome>3 second asystole

and/or > 50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome

Absolute contraindicationsCarotid bruit, known

significant carotid arterial disease, previous CVA( last 3 months )

Complications Primarily neurologicalLess than 0.2%Usually transient

Kenny RA. Heart. 2000;83:564.Linzer M. Ann Intern Med. 1997;126:989.

Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.

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Tests for orthostatic challenge

Changing from supine to upright position →displacement of blood from the thorax to the lower limbs → ↓ in venous return and CO

In the absence of compensatory mechanisms→ a fall in BP may lead to syncope

2 methods: 1. Active standing: (in which patients arise actively from

supine to erect) 2. Tilt table test :


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Recommendations: active standing

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Head-up tilt test (HUTT)

Kenny et al (1986) : reported usefulness of HUTT in the investigation of patients with vasovagal syncope

Protocols: - Patients should be fasted for 4 h prior to the test- Passive phase (20 min) + Sensitization phase (20 min)

1. low-dose intravenous isoproterenol test : incremental doses in order to increase average HR by 20–25% over baseline (usually ≤3 µg/min)2. Sublingual nitro-glycerine protocol 300–400 µg of NTG after a 20 min unmedicated phase.

- Both protocols have a similar rate of positive responses (61– 69%)- Specificity (92–94%)

Arq Bras Cardiol 2011;96(3):246-254

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40

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HUTT-Class I recommendation1. Young patients without obvious or suspected heart disease with recurrent syncope of unexplained origin, in which the history is not typical enough for the diagnosis NMS.

2. In cases of a single episode of unexplained syncope, which occurred in situation where there is high risk of physical injury

or with occupational implications

HUTT- Class II recommendation1. In the differentiation between convulsive syncope and epilepsy.2. In diagnosis to differentiate between reflex syncope and OH3. For the evaluation of patients unexplained recurrent falls.4. When dealing with patients with presyncope or recurrent dizziness.5. In the evaluation of patients with recurrent syncope and psychiatric illnesses.

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- Table tilted at an angle of 70 degrees, with footrest and rest for the upper limb in which the BP will be measured. - The Velcro straps allow securing the patient in case of loss of postural tone. - The necessary equipment:

- Device for non-invasive monitoring of BP (beat to beat)- BP curve - ECG monitoring devices Arq Bras Cardiol 2011;96(3):246-254

Head-up tilt test (HUTT)

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A modified classification of VASIS (Vasovagal Syncope International Study)


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Complications and contraindications

- Tilt testing is safe- life-threatening ventricular arrhythmias with isoproterenol in the presence of IHD or sick sinus syndrome

-No complications have been published with the use of NTG

- Minor side effects are common- - Palpitations with isoproterenol - Headache with nitro glycerine

Contraindications to the administration of isoproterenol : - IHD

- uncontrolled HTN-left ventricular outflow tract obstruction- significant aortic stenosis

Method CommentsHolter (24-48 hours) Not Useful for infrequent events

Event Recorder Useful for infrequent eventsLimited value in sudden LOC

Loop Recorder Useful for infrequent eventsImplantable type more convenient (ILR)

Ambulatory ECG

The recording device is worn by the patient using a shoulder strap or belt loop, attaching to 3-5 skin electrodes for continuous monitoring.

An event button (not shown) at the top of the housing of the device is pressed in the event of symptoms to mark the recording

Holter Monitor

Continuous ECG monitoring ispossible for a maximum of 48 hours

Current Cardiology Reviews, 2008, 4, 41-48

Patient Activator Reveal® Plus ILR 9790 Programmer

Reveal

Plus Insertable Loop Recorder

World J Cardiol 2010 ; 26 : 2(10): 308-315

Am J Cardiol, 1998;82:117-119.

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Time-Dependent Cumulative Diagnostic Yield of ILRJ Am Coll Cardiol 2012;59:1583–91

Diagnostic Assessment: Yields (N=341)

Yield (%)

Initial Evaluation

History, Physical Exam, ECG 38-40

Other Tests/Procedures

Head-Up Tilt 27

External Cardiac Monitoring 5-13

Insertable Loop Recorder (ILR) 43-88

EP Study <2-5

J Am Coll Cardiol. 2001;37:1921-1928. Circulation. 2001;104:46-51

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Treatment of Neurocardiogenic syncope

Management Strategies for VVS

Optimal management strategies for VVS are a source of debatePatient education, reassurance, instructionFluids, saltsTilt Training

Drug therapies

Pacing Class IIb indication for VVS patients with positive HUT

and cardioinhibitory or mixed reflex

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Goals of treatment: - Prevention of symptom recurrence and associated injuries - improved quality of life

General principles of treatment of syncope:

Initial treatment:

1.Education regarding avoidance of triggering events(hot crowded environments, volume depletion, effects of

cough, tight collars) 2. Recognition of premonitory symptoms

3. Manoeuvres to abort the episode (e.g. supine posture, physical Counter pressure manoeuvres (PCMs))4.Careful avoidance of agents lowering BP:

: alpha-blockers, diuretics, alcohol

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Additional treatment may be necessary in high risk or high frequency settings when:

syncope is very frequent (e.g. alters the quality of life )

syncope is recurrent and unpredictable (absence of premonitory symptoms) and exposes patients at high risk of trauma

syncope occurs during the prosecution of a high risk activity(e.g., driving, machine operator, flying, competitive athletics).

Treatment is not necessary in patients who have sustained a single syncope and are not having syncope in a high risk setting.

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Physical counter pressure manoeuvres

Isometric PCMs - induce a significant increase in BP- leg crossing- hand grip and arm tensing

- Mediated largely by sympathetic nerve discharge - Vascular resistance increase during manoeuvres - Mechanical compression of the venous vascular bed in the legs and abdomen

J Am Coll Cardiol 2006;48:1652–7

VVS - Tilt Training Protocol Objectives

Enhance orthostatic toleranceDiminish excessive autonomic

reflex activityReduce syncope

susceptibility/recurrences Technique

Prescribed periods of upright posture against a wall

Start with 3-5 min BIDIncrease by 5 min each

week until a duration of 30 min is achieved

Reybrouck T, et al. PACE. 2000;23:493-498.

VVS: Pharmacologic treatment

Salt /VolumeSalt tablets fludrocortisone

Beta-adrenergic blockers

Disopyramide

SSRIs Paroxetine

Vasoconstrictors Midodrine

Etilephrine

The Role of Pacing as Therapy for Syncope

VVS with +HUT and Cardioinhibitory response: - Class IIb indication for

pacing Three randomized, prospective trials reported benefits

of pacing in select VVS patients:VPS IVASISSYDIT

Subsequent study results less clearVPS IISynpace

Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.Sutton R. Circulation. 2000;102:294-299.

Ammirati F. Circ. 2001;104:52-57.

VPS I (North American Vasovagal Pacemaker Study)

Objective: To evaluate pacemaker therapy for severe recurrent vasovagal

syncope Randomized, prospective, single center N=54 patients

27: DDD pacemaker with rate drop response 27: No pacemaker

Inclusion: ≥ 6 lifetime episodes of syncope & +ve HUT Primary outcome: First recurrence of syncope

Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.

100

90

80

70

60

50

40

30

20

10

0

0 3 6 9 12 15Time in Months

No Pacemaker (PM)

2P=0.000022

PacemakerCu

mu

lati

ve R

isk

(%)

Connolly SJ. J Am Coll Cardiol. 1999;33:16-20.

Results: 6/27 (22%) with PM had recurrence vs. 19/27 (70%) without PM 84% RRR (2p=0.000022)

VPS I (North American Vasovagal Pacemaker Study)

VASIS (VAsovagal Syncope International Study)

Objective: To evaluate pacemaker therapy for severe cardioinhibitory tilt-

positive neurally mediated syncope Randomized, prospective, multi-center N=42 patients

19: Dual chamber pacemaker with rate hysteresis23: No pacemaker

Inclusion: Positive cardioinhibitory response Primary outcome: First recurrence of syncope

Sutton R. Circulation. 2000;102:294-299.

Sutton R. Circulation. 2000;102:294-299.

Pacemaker (PM)

No Pacemaker

p=0.0004

Years

% S

ynco

pe-

Fre

e

100

80

60

40

20

0 2 3 4 5 6

Results: 1/19(5%) with PM had recurrence vs. 14/23 (61%) without PM

VASIS (VAsovagal Syncope International Study)

SYDIT (SYncope Diagnosis and Treatment)

Objective: To compare the effects of cardiac pacing with

pharmacological therapy in patients with recurrent vasovagal syncope

Randomized, prospective, multi-center N=93 patients

46: DDD pacemaker with rate drop response47: Atenolol 100 mg/d

Inclusion: Positive HUT with relative bradycardia Primary outcome: First recurrence of syncope

Ammirati F. Circulation. 2001;104:52-57.

SYDIT (SYncope DIagnosis and Treatment)

Ammirati F. Circulation. 2001;104:52-57.

0.6

0.7

0.8

0.9

1.0

0 100 200 300 400 500 600 700 800 900 1000

Drug

Pacemaker (PM)

Time (Days)

% S

ynco

pe-

Fre

e

p=0.0032

Results: 2/46 (4%) with PM had syncope recurrence vs. 12/47 (26%) without PM

VPS II (Vasovagal Pacemaker Study II)

Objective: To determine if pacing therapy reduces the risk of syncope

in patients with vasovagal syncope Randomized, double-blind, prospective, multi-center N=100 patients

52: Only sensing without pacing48: DDD pacemaker with rate drop response

Inclusion: Positive HUT with (HR x BP) < 6000/min x mm Hg Primary outcome: First recurrence of syncope

Connolly S. JAMA. 2003;289:2224-2229.

Dual Chamber Pacing (DDD)

Only Sensing Without Pacing (ODO)

1.0

0.8

0.6

0.4

0.2

0

Months Since Randomization

Cu

mu

lati

ve R

isk

6543210

Connolly S. JAMA. 2003;289:2224–2229.

Results: 16/48 (33% ) with pacing had recurrence vs. 22/52(42% ) with only sensing

(not statistically significant)

VPS II (Vasovagal Pacemaker Study II)

SYNPACE (Vasovagal SYNcope and PACing)

Objective: To determine if pacing therapy will reduce syncope

relapses in patients with recurrent vasovagal syncope, compared to those with a pacemaker programmed to OFF

Randomized, double-blind, prospective, multi-center, placebo-controlled

N=29 patients16: DDD PM with rate drop response programmed ON13: PM programmed OFF (OOO mode)

Inclusion: Recurrent VVS and +HUT with asystolic or mixed response

Primary outcome: First recurrence of syncope

Raviele A, et al. Eur Heart J. 2004;25:1741-1748.

SYNPACE (Vasovagal SYNcope and PACing)

Results: 8/16(50%) with pacing ON had recurrence vs. 5/13 (38%) with pacing OFF

(not statistically significant)

0.6

0.7

0.8

0.9

1.0

0 200 400 600 800 1000

Pacemaker OFF

% S

ynco

pe-

Fre

e

p=0.58

0.5

0.4

0.3

0.2

0.1

0.0

Pacemaker ON

Days Since Randomization

Raviele A, et al. Eur Heart J. 2004;25:1741-1748.

Role of Pacing as Therapy for Syncope: Summary

Pacemaker implantation may modulate reflex syncope and autonomic responses

Study results may differ based on pre-implant selection criteria and tilt-testing techniques

Pacing therapy is effective in some but not all (cardioinhibition vs. vasodepression)

In five pacing studies, syncope recurred in 33/156 (21%) of paced patients, 72/162 (44%) in non-paced patients (p<0.000)

Kapoor W. JAMA. 2003;289:2272-2275.

CSS : Role of Pacing – Syncope Recurrence Rate

Class I indication for pacing (AHA and HRS)

Limit pacing to CSS that is:CardioinhibitoryMixed

DDD/DDI superior to VVI

If the diagnosis of CSH is based on a >3-second pause with carotid sinus massage without clear, provocative events, pacemaker implantation is less strongly recommended (Class IIa).

VVS Pacing Trials Conclusions

DDD pacing reduces the risk of syncope in patientswith recurrent, refractory, highly-symptomatic,

cardioinhibitory vasovagal syncope.

SAFE PACESyncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation

ObjectiveDetermine whether

cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity

Randomized controlled trial (N=175)Adults > 50 years,

non-accidental fall, positive CSM

Pacing (n=87) vs. No Pacing (n=88)

ResultsMore than 1/3 of adults

over 50 years presented to the ER because of a fall

With pacing, falls 70%Syncopal events 53%Injurious events 70%

Kenny RA. J Am Coll Cardiol. 2001;38:1491-1496.

SAFE PACE

ConclusionsStrong association between non-accidental falls and

cardioinhibitory CSHCardiac pacing significantly reduced subsequent fallsCSH should be considered in all older adults who have

non-accidental falls

Kenny RA, J Am Coll Cardiol. 2001; 38:1491-1496.

Conclusion

Syncope is a common symptom with many causes Deserves thorough investigation and appropriate

treatment A disciplined approach is essential ESC guidelines offer current best practices

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1. Guidelines for the diagnosis and management of syncope (version 2009)- The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)-European Heart Journal (2009) 30, 2631–26712. Guidelines on Management (Diagnosis and Treatment) of Syncope Update 2004 Europace (2004) 6,

467e5373. Kapoor- Syncope Review article New Eng J Med 2000, 12; 1856-18674. Steve W Parry, Maw Pin Tan- clinical review- An approach to the evaluation and management of

syncope in adults BMJ 2010;340:c8805. Paula Gonçalves Macedo Tilt Test - from the Necessary to the Indispensable. Arq Bras Cardiol

2011;96(3):246-2546. Rajesh Subbiah Syncope: Review of Monitoring Modalities Current Cardiology Reviews 2008, 4, 41-487. Michele Brignole, New Concepts in the Assessment of Syncope J Am Coll Cardiol 2012;59:1583–918. Kapoor- Current evaluation of syncope Circulation. 2002;106:1606-16099. Paolo Alboni Diagnostic Value of History in Patients With Syncope With or Without Heart Disease J Am Coll Cardiol 2001;37:1921–8 10. Nynke van DijkEffectiveness of Physical Counterpressure Maneuvers in Preventing Vasovagal Syncope The Physical Counterpressure Manoeuvres Trial (PC-Trial) J Am Coll Cardiol 2006;48:1652–711. Nevin T Wijesekera, Arvinder S Kurbaan Pacing for Vasovagal Syncope. Indian Pacing and Electr.

Journal 2002 2(4): 114-11912. Blair P. Grubb, M.D Neurocardiogenic Syncope N Engl J Med 2005;352:1004-10.

REFERENCES

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13. Joanne L.Evaluation and Management of Syncope Clinical Scholars Review, Vol. 2, No. 2, 2009 14. Attilio Del Rosso Relation of Clinical Presentation of Syncope to the Age of Patients Am J Cardiol 2005;96:1431–143515. Chad Kessler The Emergency Department Approach to Syncope: Evidence-based Guidelines and Prediction Emerg Med Clin N Am 28 (2010) 487–5016. STUART J. The North American Vasovagal Pacemaker Study (VPS) A Randomized Trial of Permanent Cardiac Pacing for the Prevention of Vasovagal Syncope J Am Coll Cardiol 1999;33:16–2017. Richard Sutton et al .Dual-Chamber Pacing in the Treatment of Neurally Mediated Tilt-Positive Cardioinhibitory Syncope Pacemaker Versus No Therapy: A Multicenter Randomized Study Circulation. 2000;102:294-29918. Fabrizio Ammirati et al. Permanent Cardiac Pacing Versus Medical Treatment for the Prevention of Recurrent Vasovagal Circulation. 2001;104:52-5719. Rose Anne M. Kenny Carotid Sinus Syndrome: A Modifiable Risk Factor for Non accidental Falls in Older Adults (SAFE PACE) J Am Coll Cardiol 2001;38:1491– 6 20. Ward .Midodrine: a role in the management of neurocardiogenic syncope. Heart 1998;79:45–4921. Peter et al. Fludrocortisone in neurally mediated hypotension chronic fatigue syndrome JAMA 2001; 285: 52-59. 22. Antonio Raviele et al . Effect of Etilefrine in Preventing Syncopal Recurrence in Patients With Vasovagal Syncope -A Double-Blind, Randomized, Placebo-Controlled Trial Circulation. 1999;99:1452-1457. 23. Enrico Di Girolamo et al. Effects of Paroxetine Hydrochloride : A Selective Serotonin Reuptake Inhibitor, on Refractory Vasovagal Syncope: A Randomized, Double-blind, Placebo-controlled Study J Am Coll Cardiol 1999;33:1227–30.

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THANK YOU

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MCQs

1. Drugs proven to be useful in VVS except

A) Midodrine B) Etilefrine C) Fludrocortisone D) Paroxetine E) Atenolol

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2). Carotid sinus hypersensitivity (CSH) : incorrect ?

A) a ventricular pause lasting > 3 s B) a fall in systolic BP of >50 mmHg C) A & B D) BP < 100 mm Hg

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3). Investigation with highest diagnostic yield in evaluation of syncope?

A) Holter B) EP study C) ILR D) TMT

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4) True about HUTT A) Passive phase 40 min+ sensitization

phase 40 min B) isoproterenol contraindicated in IHD C) done in all cases of syncope

evaluation D) gold standard for NMS evaluation

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5) Contraindications to the administration of isoproterenol except? :

a) - IHD b) - hypotension c) -left ventricular outflow tract obstruction -d) significant aortic stenosis

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6. trials showing benefit of pacing in VVS except? VPS IVASISSYDITSynpace

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7. All are CHESS acronym in SFS score except?

1. Congestive heart failure (CHF) 2.Hematocrit <30% 3. ECG abnormalities 4. Angina 5. Systolic blood pressure <90 mm Hg

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8) True about CSS except? a) Sensory nerve endings in the carotid sinus walls

respond to deformation

B) “Deafferentation” of neck muscles may contribute

C) Increased afferent signals to brain stem

Reflex decrease in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation

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9. True about pacing in NMS except? A) class I recommendation in CSS B) Calss II b recommendation In VVS C) DDD with rate drop response is

preferred D) none

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10. All are trials in VVS except? A) VPS 1 B) Issue 3 C) VASIS D) SAFE pace trial

Documents

Dr Sajeer K T Senior Resident Dept. of Cardiology MCH, Kozhikode 1