Syncope & blackout

Ludovit Paulis

ludo@lfuk.sk

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)

• Migraine*

• Acute hypoxemia*

• Hyperventilation*

• Somatization disorder (psychogenic syncope)

• Acute Intoxication (e.g., alcohol)

• Seizures (epileptic)

• Hypoglycemia

• Sleep disorders

* may cause ‘true’ syncope

Differential diagnosis

• 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.

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

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

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

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...

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

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)

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

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

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

Investigation of syncope:

ambulatory ECG (holter) monitoring

AV block

Value of

Event

Recorder in

Syncope

Linzer M. Am J Cardiol. 1990;66:214-219.

*Asterisk denotes

event marker

Head-up Tilt Test (HUT)

• Unmasks VVS susceptibility

• Reproduces symptoms

• Patient learns VVS warning

symptoms

• Physician is better able to

give prognostic / treatment

advice

Tilt testing - outcomes

Electroencephalogram

• Not a first line of testing

• Syncope from Seizures

• Abnormal in the interval between two

attacks – Epilepsy

• Normal – Syncope

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

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

NMS: Neurological basis

• 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

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

DG Benditt, UM Cardiac Arrhythmia Center

16.3

sec

Continuous Tracing1 sec

Spontaneous VVS

Kaplan-Meier Survival Curves

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

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

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

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

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

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

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)

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

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.

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

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

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

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.

VVS Pacing Trials Conclusions

DDD pacing reduces the risk of syncope

in patients with recurrent, refractory,

highly-symptomatic, cardioinhibitory

vasovagal syncope.

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

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

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

CS: Subclavian Steal Syndrome

• Abnormal narrowing of the subclavian

artery proximal to the origin of the

vertebral artery

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

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%

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?

AS: Torsades

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.

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

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

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

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