Syncope

ESC guidelines

Karina Wierzbowska-Drabik

Definition

• Syncope (s.) is a T-LOC (transient

loss of consciousness) due to

transient global cerebral

hypoperfusion

• rapid onset

• short duration

• spontaneuos recovery

Definition

• Syncope did not encompass LOC caused

by e.g. epilepsy or stroke

• In some forms of s. there may be a

prodromal period

• Often LOC occurs without warning

• Typical syncope is brief with complete

LOC, in reflex s. no longer than 20 sec

rarely few minutes

Definition • Syncope- prodromal period with

lightheadedness, dizzines, nausea, sweating,

weakness and visual disturbances

Definition

• Recovery from syncope usually is complete

• With immediate restoration of behaviour and

orientation

• But not always retrograde amnesia or

fatigue may take place especially in older

people

• The term „pre-syncope” or „near-syncope”

describes a state that resembles the prodrome

of syncope but which is not folowed by LOC

Classification and pathophysiology

• T-LOC is divided into traumatic and

non-traumatic forms (concussion

usually LOC + posttraumatic amnesia)

• Non-traumatic are divided into:

– Syncope

– Epileptic seizures

– Psychogenic pseudosyncope

– miscellaneous causes (cataplexy,

excessive daytime sleepiness)

Classification and pathophysiology

Several

disorders

may

resemble

syncope

Classification and pathophysiology

• A sudden cessation of cerebral blood flow for

as short as 6 - 8 s is sufficient to cause

COMPLETE LOC

• we know from tilt-test experiences that ↓ of

SBP ≤60 mm Hg is associated with syncope

• Systemic BP is determined by:

Cardiac output

Peripheral vascular resistance

Often these both factors are decreasing and leading

to syncope

Classification of syncope

• There are three main groups of syncope:

REFLEX (neurally-mediated) SYNCOPE

SYNCOPE due to ORTHOSTATIC

HYPOTENSION

CARDIAC SYNCOPE (cardiovascular)

REFLEX (neurally-mediated)

SYNCOPE

Group of conditions in which

CARDIOVASCULAR REFLEXES

controlling the circulation BECOME

INTERMITTENTLY INAPPROPRIATE in

response to trigger

Emotional stress

Orthostatic stress

VASOVAGAL

SYNCOPE

REFLEX (neurally-mediated)

SYNCOPE

weightlifting

SITUATIONAL

REFLEX (neurally-mediated)

SYNCOPE

• Pathomechanism:

– Knowing the various triggers is clinically

important – may have a key role in

DIAGNOSING SYNCOPE

– In most cases the efferent pathway does

not depend on the nature of the trigger

– E.g. both micturition syncope and vasovagal

syncope (VVS) may present as

cardioinhibitory or vasodepresor syncope

REFLEX (neurally-mediated)

SYNCOPE • Triggers:

– VVS + common faint – mediated by emotion, pain,

instrumentation, blood phobia/orthostatic stress –

usually preceded by prodromal syndromes of

autonomic activation (sweating, pallor, nausea)

– Situational syncope- reflex syncope associated

with some specific circumstances

– Post-exercise syncope in young athletes and in

middle-aged or elderly sujects as an EARLY

MANIFESTATION of ANF before more advanced

stadium of orthostatic hypotension (OH)

REFLEX (neurally-mediated)

SYNCOPE

• Triggers:

• Carotid sinus syncope – is triggered by

mechanical manipulation of the carotid sinuses -

it is diagnosed by carotid sinus massage (CSM)

• „atypical form” of RS- syncope occurs with

uncertain or even absent triggers –

DIAGNOSIS rests more on exclusion of other

causes of syncope (absence of structural heart

disease) and on reproducing similar symptoms

with tilt-testing

REFLEX (neurally-mediated)

SYNCOPE - CASE

• 19 year-old male patient, active - sport 3

times a week- football

• Medical history- without DM, HA,

medication

• A few epizodes of near-syncope,

dizzines after blood-taking

• Some presyncope after rapid pionisation

REFLEX (neurally-mediated)

SYNCOPE- CASE

• Cause of hospitalisation: LOC two-days before, during reading- without evident triggers

• Echo examination: normal morphology and function of the heart,

• Holter monitoring without arrhythmias

• SUSPICION of „atypical form” of RS

Tilt-test examination

REFLEX (neurally-mediated)

SYNCOPE

• Natural history of VVS:

– Usually starts in young subjects as an isolated episode

– Frequently with an atypical presentation

– When starts in older age is often associated with cardiovascular or neurological disorders displaying ORTHOSTATIC or POST-PRANDIAL HYPOTENSION

– In these latter forms there is an overlap with ANF

ORTHOSTATIC HYPOTENSION and

orthostatic intolerance syndromes

• OH is defined as an abnormal decrease

in systolic BP upon standing

• In contrast to RS in these patients there is

ANF- sympathetic efferent activity is

chronically impaired and

VASOCONSTRICTION is DEFICIENT

• Upon standing BP falls and syncope or

pre-syncope occurs

ORTHOSTATIC HYPOTENSION and

orthostatic intolerance syndromes

• From a pathophysiological point of view OH is

caused by autonomic nervous failure (ANF)

and VVS and situational s. are only non-

adequate reflexes

• but clinical manifestation frequently overlap

• Orthostatic intolerance – symptoms and signs

in the upright position due to circulatory

abnormality

– Dizzines, weakness, palpitations, sweating, visual and

hearing disturbances (blurring, brightness), (crackles,

tinnitus), neck, back or precordial pain

ORTHOSTATIC HYPOTENSION -

classification

Diabetic neuropathy-

sores of the foot

Amyloidosis-

involvement of blood

vessel wall

Syndromes of orthostatic

intolerance

Syndromes of orthostatic

intolerance • INITIAL OH

Diagnosis: lying-to-standing testSBP

TIME from standing to symptoms: 0-30 s

Pathophysiology: mismatch between CO and SVR

Symptoms: dizziness and visual disturbances a few seconds after standing up

PATIENTS:

young asthenic subjects

old age

drug induced (alfa blockers)

CSS (carotid sinus syndrome)

Syndromes of orthostatic

intolerance • Classical OH (classical autonomic failure)

Diagnosis: lying-to-standing test or tilt table SBP

TIME from standing to symptoms: 30 s- 3 min

Pathophysiology: impaired increase in SVR in autonomic failure POOLING OF BLOOD/VOLUME DEPLETION

Symptoms: dizzines, presyncope, fatigue, palpitations, visual and hearing disturbances

PATIENTS:

old age

drug induced (any vasoactive drugs and diuretics, NTG…)

Syndromes of orthostatic

intolerance • Delayed OH (progressive)

Diagnosis: lying-to-standing test or tilt table SBP

TIME from standing to symptoms: 3 min- 30 min !

Pathophysiology: PROGRESSIVE FALL IN VENOUS RETURN: low CO, diminished vasoconstriction capacity, no reflex bradycardia

Symptoms: PROLONGED PRODROME: dizzines, fatigue, palpitations, visual and hearing disturbances, hyperhydrosis, neck, low back, precordial pain ALWAYS FOLLOWED BY RAPID SYNCOPE

PATIENTS:

old age

autonomic failure

drug induced (any vasoactive drugs and diuretics, NTG…)

comorbities

Syndromes of orthostatic

intolerance • Delayed (progressive) OH + reflex syncope

• Diagnosis: tilt table

TIME from standing to symptoms: 3 min- 45 min !

Pathophysiology: PROGRESSIVE FALL IN VENOUS RETURN (as above) followed by vasovagal reaction (active reflex including reflex bradycardia and vasodilation)

Symptoms: PROLONGED PRODROME: dizzines, fatigue, palpitations, visual and hearing disturbances, hyperhydrosis, neck, low back, precordial pain ALWAYS FOLLOWED BY RAPID SYNCOPE

PATIENTS:

old age

autonomic failure

drug induced (any vasoactive drugs and diuretics, NTG…)

comorbities

Syndromes of orthostatic

intolerance • Reflex syncope (VVS) triggered by standing

• Diagnosis: tilt table

TIME from standing to symptoms: 3 min- 45 min !

Pathophysiology: INITIAL NORMAL ADAPTATION (!) followed by rapid fall in venous return and vasovagal reaction (active reflex bradycardia and vasodilatation)

Symptoms: CLEAR PRODROME and triggers ALWAYS FOLLOWED BY SYNCOPE

PATIENTS:

Young healthy

Female dominance

Syndromes of orthostatic

intolerance • POTS -postural orthostatic tachycardia

syndrome

• Diagnosis: tilt table

TIME from standing to symptoms: variable

Pathophysiology: uncertain: severe deconditioning, inadequate venous return or excessive blood venous pooling

Symptoms: Symptomatic, marked heart rate increases and instability of blood pressure. NO SYNCOPE

PATIENTS:

Young female

Comparison of initial and classical

OH INITIAL OH –

decrease immediately on standing

>40 mmHg, than return to normal-

period of hypotension short <30 s

CLASSICAL OH –

decrease in systolic BP ≥20 mmHg in

diastolic ≥10 mmHg within 3 min of

standing

ANF, hypovolaemia

Reflex syncope induced by tilt test comparison between young and old patient

• Steeper fall in BP in

younger subject

Upper panel

POTS syndrome

• Young women

• HR increase >30 beats/min or >120

bpm

• Instability of BP

• Severe complaints of orthostatic

intolerance

• Often associated with chronic fatigue

syndrome

Cardiac syncope (cardiovascular)

Cardiac syncope (cardiovascular)

• Arrhytmias – the most comon cardiac causes of syncope

• Severe arrhytmia hemodynamic impairment critical decrease in CO and cerebral blood flow

• Sick sinus syndrome – sinoatrial node is damaged abnormal automaticity or sinoatrial conduction

Cardiac syncope (cardiovascular)

• Sick sinus syndrome – SYNCOPE due to

long pauses caused by sinus arrest or

sinoatrial block and a failure of ESCAPE

mechanism

• Pauses are most often when an atrial

tachyarrhytmia suddenly stops brady-

tachy syndrome

Cardiac syncope (cardiovascular)

• telemetry strips show the tachy-brady syndrome manifested by cascade of

arrhythmic events. There is a baseline first degree AV block at approximately

260 ms.

Top strip: After 4 cycles of

sinus bradycardia (43

bpm), atrial flutter occurs.

The atrial rate is

approximately 260 bpm,

and 2:1 AV conduction

occurs,

resulting in a ventricular

rate of 130 bpm.

There are F waves (flutter

waves) superimposed on

each T wave.

Middle strip: It shows the atrial

flutter persisting with the same

AV ratio for several seconds.

Bottom strip: After a while, 4:1

conduction occurs for one

cycle. The next cycle is

interrupted by a PVC triplet, or

a short run of ventricular

tachycardia (VT). After the

ventricular triplet, the AV node

alternates with 2:1 and 3:1

conduction.

Cardiac syncope (cardiovascular)

Cardiac syncope (cardiovascular)

• As a rule, the more severe forms of acquired AV block (Mobitz II, „high grade” and complete – are most closely related to SYNCOPE

• Cardiac rhythm may become dependent on escape pacemaker sites

• The delay before these pacemakers begin to „fire” is long

• They have also slow rates (25-40 bpm)

• BRADYCARDIA also prolongs repolarization and predisposes to polymorphic VT- especially TdP

Adams-Stokes / Complete (Third

Degree) Atrioventricular Block

• Patient: 75 y/o male. Experienced several Adams-Stokes episodes and

his wife called EMS. This is a prehospital 12 lead ECG :

• No P-QRS relationship. Independent pacemakers.

• Atrial rate is 125 bpm. Ventricular rate is close to zero.

• No escape rhythm present

• This is ventricular standstill. The underlying rhythm is sinus tachycardia

at 125 bpm, but there is complete failure of the impulses to reach the

ventricles. The first QRS complex is of junctional origin, the second is

probably the right ventricle.

Cardiac syncope – onset of

tachycardia/ but …

dangerous tachyarrhytmiasno

longer syncope BUT cardiac arrest

– needs treatment !!!

Cardiac syncope – drugs

• DRUGS can cause brady- and tachyarrhytmias (B-adrenolitics, calcium antagonists, digoxin)

• SYNCOPE due to TdP torsade de pointes may be caused by drugs prolonging QT interval (antiarrhytmics, vasodilators, psychotropics, antimicrobials, antihistamines) www.qtdrugs.org

• Inherited long-QT syndromes

Cardiac syncope –

structural disease • Conditions in which there is fixed or dynamic

obstruction to left ventricular outflow

• Beyond the result of restricted CO (cardiac output) SYNCOPE may be in part due to an inappropriate reflex or OH

• E.g. in aortic stenosis (AS) S. may be due to: – restricted CO

– inappropriate reflex vasodilation

– cardiac arrhytmia

– mechanism may be MULTIFACTORIAL

Cardiac syncope –

structural disease

• Conditions in

which there

is fixed or

dynamic

obstruction to

left

ventricular

outflow

(HCM, AS)

Cardiac syncope –

structural disease

• Conditions in

which there

is fixed or

dynamic

obstruction to

left

ventricular

outflow

(HCM, AS)

Prevalence of syncope

• Syncope is common in the general

population, and the first episode presents

at characteristic ages

high prevalence of first faints

in pts between 10 and 30 ys

only 5 % of adults have a first

syncope over the age of 40

finally, there appears to be a

peak

above the age of 65 years

ABOUT 1 % of all attendances of ED

(emergency)

Prevalence of syncope

• Reflex syncope is the most frequent cause

• S. secondary to cardiovascular disease is the second most common cause (higher especially in older patients)

• <40 years OH is a rare cause of S. OH is frequent in very old patients

• The high unexplained syncope rate justifies new strategies for evaluation and diagnosis

Prognosis

• Risk of death/life-threatening events

– Structural and primary electrical heart disease are major risk factors for SCD and overal mortality in pts with syncope

– OH (often connected with old age and comorbities) 2 x higher risk than general population

– RS – excellent prognosis

THE MOST IMPORTANT: severity of underlying disease…

Primary electrical heart disease

Precordial leads of the electrocardiogram (ECG) of a patient with the Brugada syndrome with recurrences (A), a Brugada-type ECG (B), and a control case (C)

Castro Hevia, J. et al. J Am Coll Cardiol 2006;47:1828-1834

VF

Prognosis

• Impact on quality of life

– Reccurent syncope has serious effect on QoL comparable with chronic illnesses (artritis, reccurent depressive disorders)

– While syncope occurs intermittently, its threat of recurrence CONTINUOUSLY impairs QoL

– female gender,

– high level of co-morbidity,

– number of S.,

– presence of pre-syncope seemed to be associated with poorer quality of life

Initial evaluation

• Patient with T-LOC

–Careful history

–Physical examination with orthostatic BP measurement

–ECG • It is a syncopal episode or not ?

• Has the aetiological diagnosis been determined ?

• Are there data suggestive of a high risk of cardiovascular events or death ?

Additional evaluation

• CSM in pts > 40 years

• Echocardiogram – where there are data

suggestive of structural heart disease

• ECG monitoring when there is a suspicion of

arrhytmic syncope

• Orthostatic challenge (lying-to-standing

orthostatic test/head – up tilt testing) when

syncope is related to the standing position or

there is a suspicion of a reflex mechanism

• Neurological evaluation or blood tests – when

there is suspicion of non-syncopal T-LOC

Diagnosis of SYNCOPE

DETAILED CLINICAL HISTORY

Was LOC complete ?

Was with rapid onset and short duration ?

Did the patient recover spontaneously, completely

and without sequelae ?

Did the patient lose postural tone ?

Positive answers on all these questions the

episode has high likehood of being SYNCOPE

Diagnosis of SYNCOPE

DETAILED CLINICAL HISTORY- initial evaluation

is able to define the cause of syncope in 23-

50% of patients

1. History from patient

Diagnosis of SYNCOPE

• history from eyewitness

Diagnosis of SYNCOPE

• history about the background

Diagnosis of SYNCOPE

Diagnosis of SYNCOPE

Diagnosis of SYNCOPE Arrhythmogenic

right ventricular

cardiomyopathy

(ARVC),

biventricular,

autopsy heart,

young man who

died suddenly

playing basketball.

Examples of high-risk causes of LOC

1.Pre-excited

QRS complex-

WPW syndrome

2.Ventricular

tachycardia

3.Acute

myocardial

infarction

Diagnostic tests

• Carotid sinus massage

• produce slowing HR and fall in BP

• contraindicated in patients after stroke or TIA

within the past 3 months

• contraindicated in patients with carotid bruits

or stenosis

• pause > 3 sek oraz ↓ sBP > 50 mmHg

defines carotid sinus hypersensitivity (CHS)

• + SYNCOPE defines CSS

Diagnostic tests

• Carotid sinus massage • 10 s massage

• sequential right and left CSM

• performed supine and erect

• under continuous monitoring of HR and periodic measurement of BP

• Up to 30% of pts an abnormal reflex is present only in the upright position

• CSH common in older male

• CSS exceptional <40 years old

Diagnostic tests

Diagnostic tests

• Orthostatic challenge

Changing from supine to upright position produced displacement of blood from the thorax to the lower limbs that leads to a decrease in venous return and CO

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

Diagnostic tests

SYMPTOMATIC FALL

SBP≥20; DBP ≥10

OR DECREASE SBP<90

Diagnostic tests –tilt testing

• Tilt test enables the reproduction of neurally mediated reflex in laboratory setting

• BLOOD POOLING

• DECREASE IN VENOUS RETURN

• IMMOBILIZATION • Clinical situation corresponding

to tilt test: REFLEX SYNCOPE triggered by prolonged standing

Trigger the reflex

Diagnostic tests –tilt testing

Final effect of tilt

test hypotension and

HR slowing is related

to IMPAIRED

VASOCONSTRICTOR

CAPABILITY followed

by sympathetic

withdrawal and vagal

overactivity

Parasympathetic

innervation

Slows heart rate

Pathway

Reticular

formation in

medulla

Cardioinhib

itory center

Vagus nerve

(CN X)

To SA & AV

nodes

ACh

Diagnostic tests –tilt testing

Introduced into clinical evaluation of patients with SYNCOPE of unknown origin by Kenny in 1986

Patients should be fasted for 4 h prior to the test

TT is not usually nedeed when reflex syncope is already diagnosed by clinical history

In patients with T-LOC associated with jerking movements tilt test has been demonstrated to be helpful in discriminating syncope from epilepsy

Diagnostic tests –tilt testing

POSITIVE CARDIOINHIBITORY (ASYSTOLE) RESPONSE to TILT TEST predicts with a high probability an asystolic spontaneous syncope

POSITIVE VASODEPRESOR or MIXED RESPONSE or even NEGATIVE RESPONSE does not exclude the presence of asystole during spontaneous syncope

Diagnostic tests –tilt testing

Diagnostic tests –tilt testing

Diagnostic tests –tilt testing

THERE WERE some life-threatening arrhytmias reported,

other contraindications: uncontrolled HA, LVOTO, SA

Diagnostic tests –tilt testing

Diagnostic tests- ECG monitoring

• Gold standard correlation between symptoms

and a documented arrhytmia

• Significant is also the presence of such severe

arrhytmias as:

– Prolonged asystole ≥3 sek

– Rapid SVT ≥160/min for> 32 beats

– VT

Patients>40 years with reccurent syncope, without

structural heart disease an arrhytmia USUALLY

ASYSTOLE is present during syncope in up to 50%.

Diagnostic tests- ECG HOLTER

monitoring

• Usually undertaken with 24-48 h or 7 days

recordings

• True yield in syncope may be as low as 1-2

% in an unselected population

• May be of more value if symptoms are very

frequent daily single or multiple episodes

• Very frequent episodes suggests

psychogenic syncope

Diagnostic tests- external loop

recorders

• 5-15 min of pre-activation ECG is

stored and can be retrieved for analysis

• Documentation of syncope in up to

25% for 1 month monitoring

• Increased diagnostic yield when

compared with Holter

Diagnostic tests- implantable loop

recorders (ILR) • Implanted under local

anaesthesia, battery life up to 36 months

• In small series of highly selected patients (at the end of negative work-up) symptom-ECG correlation was achieved in 88% in 5 months monitoring

• Automatically activated memory- predefined arrhytmias

The mechanism of syncope detected by ILR-

according to ISSUE 2 study

Experience from ILR showed that the mechanism of syncope is

heterogeneous with bradycardia or asystole accounting for

approximately one-half of the syncope events

In ISSUE 2 among 106 ILR documented episodes:

A long asystolic pause (median 11.5 sec duration)

was present in 54% of cases

Bradycardia < 40 bpm was present in 4%

No rhythm variation were present in 27%

Progressive sinus tachycardia was present in 7%

Primary tachyarrhythmia was present in 8% of

cases

Diagnostic tests –ILR

• Int J Med Sci 2009; 6:296-300

• Differentiation of convulsive syncope from epilepsy with an implantable loop recorder

• Khalil Kanjwal, Beverly Karabin, Yousuf Kanjwal, Blair P Grubb

• Introduction: Not all convulsive episodes are due to epilepsy and a number of these have a cardiovascular cause.

• Failure to identify these patients delays the provision of adequate therapy and exposes the individual to the risk of injury or death.

Diagnostic tests –ILR

• Int J Med Sci 2009; 6:296-300

• Schott et al (8) found that 20% of patients diagnosed with idiopathic epilepsy actually had a cardiac arrhythmia as a cause of their convulsive events.

• the majority of patients suffering from “seizure like” episodes are diagnosed as having epilepsy purely on clinical grounds, often without extensive cardiovascular investigations

• We report on three patients who were initially diagnosed with recurrent seizures due to epilepsy

Diagnostic tests –ILR • Int J Med Sci 2009; 6:296-300 –CASE 1

• A 10 year-old young boy recurrent idiopathic “seizures” since 1 year of age

• During episodes he suddenly turned pale then abruptly falled to the floor followed by convulsive activity that would last from 30 seconds to one minute.

• He would often be incontinent of urine and have a postictal period of confusion and disorientation from ten to twenty minutes, followed by confusion and fatigue

• The patient experienced 5-7 major episodes each year, as well as less severe episodes every one to two months.

• He had undergone extensive neurologic and cardiovascular evaluation at the several medical centers but an etiology for these events could not be found.

Diagnostic tests –ILR

• The EKG, ECHO, baseline and sleep deprived electroencephalogram (EEG), and MRI of the brain were normal (repeated multiple times)

• A tilt table test was normal as was an exercise stress test. He was tried on multiple seizure medications. External event recorders were unable to capture an episode.

• An ILR (Medtronic Reveal XT) was inserted and one month later, the patient experienced a witnessed “mild” convulsive episode while sitting at the table. The download of the ILR showed the patient had experienced > 20 seconds of cardiac asystole coincident with the episode

• Afterward he underwent dual chamber pacemaker placement and over 10 m follow-up no further events.

CASE 2. A 41-year-old woman was referred for evaluation of recurrent convulsive episodes. At the age of 29 years, she began to experience episodes of sudden loss of consciousness associated with convulsive activity.

She would experience a prodrome of ringing in her ears followed by an abrupt loss of consciousness.

Diagnostic tests –ILR

She would become pale “her eyes would roll back” and she would collapse to the floor. She would then experience convulsive activity that would last between 10 seconds and 15 minutes.

During episodes, she would experience urinary incontinence and on two episodes had fecal incontinence. She also suffered from multiple traumatic injuries to her face head and arms during these episodes.

Diagnostic tests –ILR

She underwent ILR implantation

This demonstrated that her witnessed convulsive events were associated with prolonged episodes of cardiac asystole and complete heart block

Since pacemaker implantation, she has had no further

convulsive episodes over a 17-month follow up period.

Diagnostic tests –ILR

In some individuals, global cerebral hypoxia may result not only in loss of consciousness but in convulsive activity as well (6, 7, 8).

These episodes of “convulsive syncope” may at times be difficult to distinguish from seizures resulting from epilepsy.

Indeed, some studies have reported that anywhere between 30 -42% of patients initially thought to have epileptic seizures were later found to have convulsive syncope due to cardiovascular cause (3, 4).

From studies with ILR –presyncope were MUCH LESS LIKELY associated with an arrhytmia than SYNCOPE… ? Other

mechanisms .

Diagnostic tests –ILR

Pts with features

suggesting

arrhytmic syncope

Holter

syncope/presyncope

≥1/week

Reccurent syncope

of uncertain origin and

absence of high risk

criteria

High risk patients in

whom

comprehensive

evaluation

did not demonstrate

a cause of syncope

The heart rate usually

slows down in athletes.

You may experience

sinus bradycardia

during sleep or

vagally-induced during

the Valsalva maneuver.

Lone sinus

bradycardia in a

normal heart usually

does not require any

type of intervention.

ILR may be indicated

• Epilepsy suspected…(treatment non-effective)

• Reccurent reflex syncope suspected

• Bundle branch block (BBB) in whom

paroxysmal A-V block is likely

• Structural heart disease and nsVT in whom

tachyarrhytmia is likely …(negative EPS)

• Unexplained falls

ILR TRENDS

ISSUE study – International Study of Syncope

of Unknown Etiology

Diagnostic tests –EPS

• Reserved for specific situations

• Data from registries show that about 2% pts with unexplained syncope undergo EPS

• BBB are at higher risk of developing high degree AV block, prognostic factors are:

– History of syncope

– Prolonged H-V interval

(<55 ms normal, ≥70 ms, ≥100 ms

Diagnostic tests –EPS

Pts with severely

depressed LVEF

should have ICD

implanted

LVEDV=183mL, LVESV=136mL,

end-diastolic diameter [DTD]=7.46cm,

end-systolic diameter [DTS]=5.64cm,

ejection fraction 31.7%,

Diagnostic tests –

ECHOCARDIOGRAPHY

Key technique to diagnose the presence

of structural cardiac disease

Risk stratification according to EF

Diagnosis in: SA, myxoma, tamponade

Diagnostic tests –exercise testing

Diagnostic tests –psychiatric

evaluation

Pseudosyncope

usually lasts longer-

pts may lie on the floor

for many minutes

Numerous attacks a day

Lack of recognizable trigger

Part 2- Treatment

Treatment of reflex syncope and

orthostatic intolerance

• The goal: prevention of reccurence and injuries/ improvement of QoL

• education according to AVOIDANCE of triggers (crowded places, agents lowering BP, alcohol) , RECOGNITION of prodromal symptoms and PERFORMING manoeuvers to abort the episode

• reassurance regarding the benign nature of the contition

Treatment of reflex syncope and

orthostatic intolerance

• PERFORMING manoeuvers to abort the

episode

• supine posture

• physical counterpressure manoeuvres

(PCMs): leg crossing, hand grip, arm

tensing are able to cause significant BP

increase during the phase of impending

reflex syncope

Treatment of reflex syncope and

orthostatic intolerance

• Physical counterpressure manoeuvres

(PCMs) – have its PC-Trial- it is EBM

• 51% of conventionally treated experienced

recurrence of syncope

• 32% pts trained in PCMs; p<0,004

Treatment of reflex syncope and

orthostatic intolerance

• Education/reassurance and physical

counterpressure manoeuvres (PCMs) –

have I class of recommendation

Treatment of reflex syncope and

orthostatic intolerance

• Role of PCM IMPLANTATION

– In pts with dominant CARDIOINHIBITORY

CSS

– Pts with frequent symptoms, age>40 and

CARDIOINHIBITORY RESPONSE during

monitoring- class IIa recommendation

Treatment of reflex syncope and

orthostatic intolerance

• So called „tilt training” is more difficult (low compliance)

• Progressively prolonged periods of enforced upright posture

• Possible in HIGHLY MOTIVATED young pts with recurrent VVS

• Four trials failed to confirm short-term effectiveness in reducing positive response of tilt testing

Treatment of reflex syncope and

orthostatic intolerance

• Medical treatment- since failure to achieve proper vasoconstriction of the peripheral vessels is comon in reflex syncope alfa-agonist vasoconstrictors- etilefrine and midodrine have been used

• Etilefrine 25 md twice daily did not show advantage over placebo in one trial

• Midodrine – can be usefull e.g. as a self-administered single dose 1 h before prolonged standing- pill in the pocket strategy in addition to LIFESTYLE MEASURES and PCMs

Treatment of reflex syncope and

orthostatic intolerance

• „tilt training” - more difficult- without good EBM-

• Midodrine- in pts refractory to lifestyle measures-

• PCM- pts with frequent symptoms, age>40 and

CARDIOINHIBITORY RESPONSE during tilt-

test- AFTER ALTERNATIVE THERAPY

HAS FAILED-IIb class of recommendation

Treatment of reflex syncope and

orthostatic intolerance

• PCM (cardiac pacing) in the absence of

CARDIOINHIBITORY REFLEX

• Beta-adrenergic blocking drugs -

CONTRAINDICATION (β-blockers have failed to

be effective in five/six long-term studies)- III

class of recommendation

Treatment of orthostatic intolerance

• In drug-induced ANF – elimination of the offending agent

• Expansion of extracellular volume- in the absence of

hypertension – the salt and water intake 2-3 L per day

and 10 g of NaCl

• Rapid cool water ingestion (in orthostatic intolerance and

post-prandial hypotension)

• Sleeping with the head of the bed elevated 10◦ prevents

nocturial polyuria and ameliorates nocturnal

hypertension !

• Compression stockings in older pts with gravitational

venous pooling

Treatment of orthostatic intolerance

• Medical treatment: MIDODRINE

• The use of alfa-agonist midodrine is a useful addition to the first-line treatment in pts with chronic ANF

• Increases BP in supine and upright position and ameliorates symptoms of OH

• 5-20 mg three times daily – was effective in three randomised trials

• Fludrocortisone 0,1-0,3 mg once daily mineralocorticoid that expands fluid volume

Treatment of orthostatic intolerance

Treatment of cardiac arrhythmias

Treatment of cardiac arrhythmias

Treatment of cardiac arrhythmias

Treatment of cardiac arrhythmias

Treatment of pts with high risk of

SCD

Treatment of pts with high risk of

SCD

• High risk pts with HCM

– Unexplained syncope

– Family history of SCD

– nsVT

– Hypotension during exercise

– Marked hypertrophy

Treatment of pts with high risk of

SCD

• High risk pts with ARVC

– Young age

– Extensive RV dysfunction

– LV involvement

– Polymorphic VT

– Late potentials, epsilon waves

– Family history of SCD

In pts with unexplained syncope appropriate ICD interventions 15% per year

Treatment of pts with high risk of

SCD

• unexplained syncope ominous finding in

pts with inherited ion channel

abnortmalities

• LQTS2/LQTS3 (factors of worse

prognosis)

– The number of cardiac events before 18 year

– Very prolonged QT

– Female gender

Syncope in the elderly

• Most common: OH, from reflex s – CSS, cardiac

arrhythmias

• Main causes of OH:

– 25% „age-related”

– Medication

– Atrial fibrillation

Supine systolic hypertension complicates treatment

OH occurs mainly IN THE MORNING

Differentiation between falls and syncope may be

difficult

Syncope in paediatric pts

• Most common: reflex syncope, but may be

manifestation of life-threatening cardiac

arrhythmias or structural abnormalities

Syncope and driving

Syncope- summary

• The most common VVS

• Active search for alarming symptoms

– Syncope during exertion or lying

– Absence of external factors

– Family history of SCD

– Slow recovery from syncope

Recognise pts with life-threatening

conditions and hospitalised them

TEST

• 1. Transient global cerebral hypoperfusion

is a key feature of:

– A) epilepsy

– B) hypoglicaemia

– C) syncope

– D) all listed clinical situations

TEST

• 2. Situational syncope during

gastrointestinal stimulation (eg.

swallowing) may be classified as:

– A) typical orthostathic intolerance

– B) reflex (neurally mediated) syncope

– C) syncope of cardiac origin

– D) none is true

TEST

• 3. Chose the best answer connecting ILR:

– A) it is small device implanted under local anaesthesia, with long battery life (nowadays up to 36 months) and automatically activated memory

– B) it may be indicated even in an early phase of evaluation in pts with reccurent syncope of uncertain origin and absence of high risk criteria

– C) both sentence are true

– D) none sentence is true

TEST

• 4. Cardiac pacing for treatment of reflex

syncope in the absence of a documented

cardioinhibitory response

– A) is a first-line treatment

– B) depends of the age of patient

– C) is not indicated

– D) none of the answers is true

TEST

• 5. Which drug may be consider as „pill in

the pocket strategy” in prevention of reflex

syncope and for constant use in

prevention of OH

– A) beta-adrenergic agent

– B) etilefrine

– C) midodrine

– D) all of these drugs