Syncope. ESC guidelines Karina Wierzbowska-Drabik

Transcription

1 Syncope ESC guidelines Karina Wierzbowska-Drabik

2 Definition Syncope (s.) is a T-LOC (transient loss of consciousness) due to transient global cerebral hypoperfusion rapid onset short duration spontaneuos recovery

3 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

4 Definition Syncope- prodromal period with lightheadedness, dizzines, nausea, sweating, weakness and visual disturbances

5 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

6 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)

7 Classification and pathophysiology Several disorders may resemble syncope

8 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

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10 Classification of syncope There are three main groups of syncope: REFLEX (neurally-mediated) SYNCOPE SYNCOPE due to ORTHOSTATIC HYPOTENSION CARDIAC SYNCOPE (cardiovascular)

11 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

12 REFLEX (neurally-mediated) SYNCOPE weightlifting SITUATIONAL

13 REFLEX (neurally-mediated) Pathomechanism: SYNCOPE 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

14 Triggers: REFLEX (neurally-mediated) SYNCOPE 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)

15 REFLEX (neurally-mediated) Triggers: SYNCOPE 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

16 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

17 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

18 Tilt-test examination

19 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

20 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

21 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 nonadequate 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

22 ORTHOSTATIC HYPOTENSION - classification Diabetic neuropathysores of the foot Amyloidosisinvolvement of blood vessel wall

23 Syndromes of orthostatic intolerance

24 Syndromes of orthostatic intolerance INITIAL OH Diagnosis: lying-to-standing test SBP 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)

25 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 )

26 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

27 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

28 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

29 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

30 Comparison of initial and classical INITIAL OH decrease immediately on standing >40 mmhg, than return to normalperiod of hypotension short <30 s OH CLASSICAL OH decrease in systolic BP 20 mmhg in diastolic 10 mmhg within 3 min of standing ANF, hypovolaemia

31 Reflex syncope induced by tilt test comparison between young and old patient Steeper fall in BP in younger subject Upper panel

32 Young women POTS syndrome HR increase >30 beats/min or >120 bpm Instability of BP Severe complaints of orthostatic intolerance Often associated with chronic fatigue syndrome

33 Cardiac syncope (cardiovascular)

34 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

35 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 bradytachy syndrome

36 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.

37 Cardiac syncope (cardiovascular) 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.

38 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

39 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.

40 Cardiac syncope onset of tachycardia/ but dangerous tachyarrhytmias no longer syncope BUT cardiac arrest needs treatment!!!

41 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) Inherited long-qt syndromes

42 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

43 Conditions in which there is fixed or dynamic obstruction to left ventricular outflow (HCM, AS) Cardiac syncope structural disease

44 Conditions in which there is fixed or dynamic obstruction to left ventricular outflow (HCM, AS) Cardiac syncope structural disease

45 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)

46 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

47 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

48 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: VF

49 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

50 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?

51 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

52 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

53 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

54 Diagnosis of SYNCOPE history from eyewitness

55 Diagnosis of SYNCOPE history about the background

56 Diagnosis of SYNCOPE

57 Diagnosis of SYNCOPE

58 Diagnosis of SYNCOPE Arrhythmogenic right ventricular cardiomyopathy (ARVC), biventricular, autopsy heart, young man who died suddenly playing basketball.

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61 Examples of high-risk causes of LOC 1.Pre-excited QRS complex- WPW syndrome 2.Ventricular tachycardia 3.Acute myocardial infarction

62 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

63 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

64 Diagnostic tests

65 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

66 SYMPTOMATIC FALL SBP 20; DBP 10 OR DECREASE SBP<90 Diagnostic tests

67 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

68 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

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70 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

71 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

72 Diagnostic tests tilt testing

73 Diagnostic tests tilt testing

74 Diagnostic tests tilt testing THERE WERE some life-threatening arrhytmias reported, other contraindications: uncontrolled HA, LVOTO, SA

75 Diagnostic tests tilt testing

76 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%.

77 Diagnostic tests- ECG HOLTER monitoring Usually undertaken with 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

78 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

79 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

80 The mechanism of syncope detected by ILRaccording 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

81 Diagnostic tests ILR Int J Med Sci 2009; 6: 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.

82 Diagnostic tests ILR Int J Med Sci 2009; 6: 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

83 Diagnostic tests ILR Int J Med Sci 2009; 6: 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.

84 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.

85 Diagnostic tests ILR 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.

86 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.

87 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.

88 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.

89 Pts with features suggesting arrhytmic syncope Holter syncope/presyncope 1/week

90 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

91 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.

92 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

93 ILR TRENDS ISSUE study International Study of Syncope of Unknown Etiology

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95 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

96 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%,

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99 Diagnostic tests ECHOCARDIOGRAPHY Key technique to diagnose the presence of structural cardiac disease Risk stratification according to EF Diagnosis in: SA, myxoma, tamponade

100 Diagnostic tests exercise testing

101 Diagnostic tests psychiatric evaluation Pseudosyncope usually lasts longerpts may lie on the floor for many minutes Numerous attacks a day Lack of recognizable trigger

102 Part 2- Treatment

103 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

104 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

105 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

106 Treatment of reflex syncope and orthostatic intolerance Education/reassurance and physical counterpressure manoeuvres (PCMs) have I class of recommendation

107 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

108 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

109 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 selfadministered single dose 1 h before prolonged standing- pill in the pocket strategy in addition to LIFESTYLE MEASURES and PCMs

110 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 tilttest- AFTER ALTERNATIVE THERAPY HAS FAILED-IIb class of recommendation

111 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

112 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

113 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

114 Treatment of orthostatic intolerance

115 Treatment of cardiac arrhythmias

116 Treatment of cardiac arrhythmias

117 Treatment of cardiac arrhythmias

118 Treatment of cardiac arrhythmias

119 Treatment of pts with high risk of SCD

120 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

121 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

122 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

123 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

124 Syncope in paediatric pts Most common: reflex syncope, but may be manifestation of life-threatening cardiac arrhythmias or structural abnormalities

125 Syncope and driving

126 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

127 TEST 1. Transient global cerebral hypoperfusion is a key feature of: A) epilepsy B) hypoglicaemia C) syncope D) all listed clinical situations

128 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

129 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

130 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

131 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