Arrhythmia. Irregular Heartbeat

1. ArrhythmiaArrhythmia

2. 1. branch Bachmann
2. branch Venkebah
3. branch Torely
4. Total trunk bundle branch
5. Right bundle branch
6. Forward-branching upper left leg
Hiss
7. Posterolateral branch of the left
lower branching Hiss
8. Tree branching system of His-
Purkinje
SCHEME pathways HEART
1
2
3
СА – центр І порядку
60-90/хв
АV – центр ІІ порядку
30-45
4
5
6
7
8
ПГ – центр ІІІ порядку
15-25
ВП – центр ІV порядку
5-10

4. ArrhythmiaArrhythmia oror
irregular heartbeatirregular heartbeat
 is any of a large and heterogeneous group ofis any of a large and heterogeneous group of
conditions in which there is abnormalconditions in which there is abnormal
electrical activityelectrical activity in thein the heartheart..
In adults the normal resting heart rate ranges
from 60 to 90( 100) beats per minute.
BradycardiaBradycardia < 60 to 90( 100) > Tachycardiachycardia

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6.  ≥≥ 90-150/hv -90-150/hv - sinus tachycardiasinus tachycardia,,
 150-220/hv -150-220/hv - paroxysmal tachycardia:paroxysmal tachycardia:
supraventricular / ventricularsupraventricular / ventricular
 220-350/hv -220-350/hv - Flutter: Atrial / VentricularFlutter: Atrial / Ventricular
 350-500-1000/hv -350-500-1000/hv - fibrillationfibrillation
atria / ventricles.atria / ventricles.
TachyarrhythmiaTachyarrhythmia

7. classificationclassification
 AtrialAtrial
 Premature Atrial Contractions (PACs)Premature Atrial Contractions (PACs)
 Wandering Atrial PacemakerWandering Atrial Pacemaker
 Multifocal atrial tachycardiaMultifocal atrial tachycardia
 Atrial flutterAtrial flutter
 Atrial fibrillation (Afib)Atrial fibrillation (Afib)
Junctional arrhythmiasJunctional arrhythmias
 Supraventricular tachycardia (SVT)Supraventricular tachycardia (SVT)
 AV nodal reentrant tachycardiaAV nodal reentrant tachycardia is theis the
most common cause of Paroxysmalmost common cause of Paroxysmal
Supra-ventricular Tachycardia (PSVT)Supra-ventricular Tachycardia (PSVT)
 Junctional rhythmJunctional rhythm
 Junctional tachycardiaJunctional tachycardia
 Premature junctional contractionPremature junctional contraction
 VentricularVentricular
 Premature Ventricular Contractions (PVCPremature Ventricular Contractions (PVC
sometimes called Ventricular Extrasometimes called Ventricular Extra
Beats (VEBs)Beats (VEBs)
 Premature Ventricular beatsPremature Ventricular beats
occurring after every normaloccurring after every normal
beat are termed "beat are termed "
ventricular bigeminyventricular bigeminy""
 PVCs that occur at intervals of 2PVCs that occur at intervals of 2
normal beats to 1 PVC arenormal beats to 1 PVC are
termed "PVCs in trigeminy"termed "PVCs in trigeminy"
 Three premature ventricularThree premature ventricular
grouped together is termed agrouped together is termed a
"run of PVCs"; runs lasting"run of PVCs"; runs lasting
longer than three beats arelonger than three beats are
generally referred to asgenerally referred to as
ventricular tachycardiaventricular tachycardia
 Accelerated idioventricular rhythmAccelerated idioventricular rhythm
 Monomorphic Ventricular tachycardiaMonomorphic Ventricular tachycardia
 Polymorphic ventricular tachycardiaPolymorphic ventricular tachycardia
 Ventricular fibrillationVentricular fibrillation

8. Cause arrhythmiasCause arrhythmias
 Functional cardiac arrhythmias
in a healthy heart (tea, coffee,
alcohol, drugs, exercise,
emotions, the effect of physical
factors - heat, cold,
electromagnetic field, ionizing
radiation).
 Functional cardiomyopathy: a
syndrome of mitral valve
prolapse, abnormal chordae,
neuro-circulatory dystonia of the
cardiac type.
 Organic diseases infarction:
coronary heart disease,
myocarditis, hypertensive heart
 Hemodynamic arrhythmias:
congenital and acquired heart
diseases, hypertension, heart
failure
 Hormonal fibrillationHormonal fibrillation::
pheochromocytoma,pheochromocytoma,
thyrotoxicosis, hypothyroidism.thyrotoxicosis, hypothyroidism.
 Yatrogenic arrhythmia:Yatrogenic arrhythmia:
due to manipulation of the heartdue to manipulation of the heart
(coronary angiography,(coronary angiography,
arrhythmogenic effect of drugsarrhythmogenic effect of drugs
-quinidine, novokainamid, β--quinidine, novokainamid, β-
blockersblockers
 Congenital conditionsCongenital conditions::
 WPW, CLC, Romano-Word (L-WPW, CLC, Romano-Word (L-
QT) mukomatoz degenerationQT) mukomatoz degeneration
endocardium, Bruhadaendocardium, Bruhada
syndrome.syndrome.
 Poison:Poison: cardiac glycosides,cardiac glycosides,
agonists purine derivativesagonists purine derivatives
(aminophylline).(aminophylline).

9. 1. Violation of the integrity of cell membranes:
excessive entry of sodium ions into the cell and potassium ions
out of the cell
2. Shortening of the refractory period.
3. Activation of spontaneous diastolic depolarization
1) the mechanism re-entry, i. e. reciprocal tachycardias;
2) the pathologic automatism — as a result of high trigger activity;
3) the combination of impulse formation and impulse conduction
disorders.
Pathogenetic bases arrhythmia
According to American and European Cargiologists Association (2003), doctors
should remember basic tachyarrhythmia mechanisms:

10. SADSSADS (sudden arrhythmic death(sudden arrhythmic death
syndrome)syndrome)is a term used to describe suddenis a term used to describe sudden
deathdeath due todue to cardiac arrestcardiac arrest
brought on by an arrhythmia in thebrought on by an arrhythmia in the
absence of any stracture changesabsence of any stracture changes
Causes of SADS in
young people
include
 viral myocarditisviral myocarditis,,
 long QT syndromelong QT syndrome,,
 Brugada syndromeBrugada syndrome,,
 Catecholaminergic polymorphicCatecholaminergic polymorphic
ventricular tachycardia,ventricular tachycardia,
 Hypertrophic cardiomyopathyHypertrophic cardiomyopathy
 Arrhythmogenic right ventricularArrhythmogenic right ventricular
dysplasia.dysplasia.
 Among all causes of death, 13% is
sudden death, the structure of
which 88% is sudden cardiac death
 Approximately 180,000 to 250,000
people die suddenly of this cause
every year in the US

11. ventricular fibrillation,
asystole,
electromechanical dissociation
(specify if possible);
With the
restoration of
cardiac activity
Mechanisms ofMechanisms of SADSSADS
ventricular fibrillation,
asystole,
electromechanical dissociation
(specify if possible);
Irreversible
cardiac arrest,
fatal

12. Diseases and syndromes in which most
observed sudden cardiac death
Acute coronary syndromes (Q-myocardial infarction, not-Q-Acute coronary syndromes (Q-myocardial infarction, not-Q-
myocardial infarction, unstable angina)myocardial infarction, unstable angina)
Ischemic cardiomyopathy (postinfarction cardio)
Heart failure
Dilated cardiomyopathy
Myocarditis
Aortic stenosis
Mitral valve prolapse
CA-, AV-block II-III degree
Syndrome Wolff-Parkinson-White
Syndrome of prolonged QT (Romano-Ward)
Syndrome Bruhada 11
Arrhythmogenic right ventricular dysplasia
Abnormal development of coronary artery
Myocardial bridges
"Athletic Heart"
І
ІІ
ІІ
І
ІV

13. EMD
ventricular fibrillation,
asystole
electromechanical dissociation
electrocardiographic signs of cardiac arrest – sudden cardiac
death

14. mV
+20
0
-30
-60
-90
30
1
2
4 4
Detection
potential
potential
alone
absolute
refractory
period
overshut
Na+
Ca2+
K+
К+
К+Na+
Na+ Ca++
Na+
transmembrane potentialtransmembrane potential
The relative
refractory
period
0 - phase depolarization
1 - phase of early rapid repolarization
2 - Plateau - an early phase of slow repolarization
3 - the final phase of rapid repolarization
4 - phase of spontaneous diastolic depolarization

15. Unidirectional
Block
Recovery of
Excitability
& Reentry
Bidirectional
Conduction
Mechanism of Re-entry

16. sinus tachycardia
Inappropriate ST
Sustained increase in heart rate at rest, not associated with the level of physical,
emotional, pathological or pharmacological stress. Treatment: β-AB.
Physiological ST
Increased frequency generation sinus impulses to over 100/hv.
according to the physical, emotional, pathological or pharmacological
stress.
ST by type of re-entry (ST-RE).
Circuit re-entry through SN generates paroxysm of tachycardia (≥ 150-
220/hv.). P is similar, but not identical synusuvomu rhythm. Starts and ends
with supraventricular extrasystoles. Treatment: vagal tests, adenosine

17. Supraventricular tachycardia (SVT)
 Two common types of SVT are
- atrioventricular reciprocating tachycardia (AVRT)
- AV nodal reentrant tachycardia (AVNRT).
 SVT is generally not life threatening, though it may
cause worsening heart function if it is sustained for
hours.

18. SymptomsSymptoms (SVT)
 Symptoms can come on suddenly and may go away without treatment.
Stress, exercise, and emotion can all result in a normal or physiological
increase in heart rate, but can also, though more rarely, precipitate
SVT.
 Episodes can last a few minutes or as long as 1 or 2 days, sometimes
persisting until treated. The rapid beating of the heart during SVT can
make the heart a less-effective pump, decreasing cardiac output and
blood pressure. The following symptoms are typical with a rapid pulse
of 150–270 or more beats per minute:
 Pounding heartPounding heart
 Shortness of breathShortness of breath
 Chest painChest pain
 Rapid breathingRapid breathing
 DizzinessDizziness
 Loss of consciousness (in serious cases)Loss of consciousness (in serious cases)

19. Congenital conditions
CLC Syndrome:
interval PQ ≤ 0,1
- 0,1 сек
Лівий пучок Паладіно-Кента
Пучок Бахмана
Пучок Венкебаха
Пучок Тореля
Правий пучок Паладіно-Кента
Пучок Джеймса
Пучок Махейма
ДЕЛЬТА-
ХВИЛЯ
WPW- синдром:
WPW syndrome
1.PQ ≤ 0,1
2. Delta - wave
3. Deformation of QRS,
4. Discordant R ↔ T

20. SА SА
АVNАVN
Лівий
пучок
Кента
Правий
пучок
Кента
ORTODROMIC antidromic
P is present
to the QRS
QRS -
narrow
P is present
after the QRS
QRS wide
deformed
Atrioventricular reciprocating tachycardia (AVRT) with the
participation of additional pathways
Left bundle Paladin-Kent
Пучок Бахмана
Пучок Венкебаха
Пучок Тореля
ATP, verapamil, novokainamid,
aymalin (hilurytmal)
cardioversion, defibrillation
CORDARONE
cardioversion, defibrillation
Right bundle Paladin-Kent
Пучок Джеймса
Пучок Махейма

21. Atrioventricular reciprocating tachycardia - AVRT involving
additional way of
Paladin-Kent - 210 beats / min

22. Orthodromic AV Reentrant Tachycardia
SVT with
P(+) to
QRS
SVT:
P(-)
After QRS
Retrograde P waves
in the ST segment
Anterogade
conduction
via normal
pathway
Retrograde
conduction
via accessory
pathway (AP)

23. , CLC, Махайма.
Delta Wave
Atrioventricular reciprocating tachycardia involving
additional ways of
The resulting syndrome WPW, CLC, Mahayma

24. Accessory Pathway with
Ventricular Preexcitation
(Wolff-Parkinson-White Syndrome)
Fusion activation
of the ventricles
“Delta” Wave
AP
PR < .12 s
QRS ≥ .12 s
Sinus
beat
Hybrid
QRS shape

25. Syndrome Wolff-Parkinson-White
Type A. Functions left
b.Paladino-Kent.
Type B. Functions right
b.Paladino-Kent.

26. АВ-
вузол
АВ
шлуночки
передсердя
α β
1
2
3
4
5
6
7
Atrioventricular nodal
reciprocating tachycardia - AVNRT
Dissociation AV node zone α (slow) and
β (fast) with different refractory
АВ-
вузол
АВ
шлуночки
передсердя
α β
1
2
3
4
5
6
7
Conducting:
I.) antegrad - via α-zone and retrohrpdno through β-zone? ("Slow-fast" - "slow-
fast" tachycardia);
II). Antegrad - through β-zone, and retrograde through α-zone? ("Fast-slow" -
"fast-slow" tachycardia).
1 - sinus node, 2 - bundle Bachmann, 3 - bundle Venkebaha,
4 - bundle Torrelya, 5 - anterior upper branch bundle branch block, 6 - anterior
lower branch bundle branch block, 7 - posterior branch bundle branch block.
І
Slow-
fast
ІІ
Fast-
slow

27. AV Nodal Reentrant Tachycardia
F = fast AV
nodal pathway
S = slow AV
nodal pathway
(His Bundle)
Atrioventricular (ortodrom) nodal reciprocating
tachycardia - AVNRT - 205 beats / min

28. Monomorphic
Ventricular
tachycardia

29. Ventricular paroxysmal
tachycardia - 200 beats / min
Ventricular paroxysmal tachycardia with
Ventricular fibrillation - 300 beats / min

30. Polymorphic ventricular tachycardiaPolymorphic ventricular tachycardia
((Torsades de Pointes)Torsades de Pointes)

31. Treatment of arrhythmiasTreatment of arrhythmias
Classification of antiarrhythmicClassification of antiarrhythmic
drugs bydrugs by
Vaughan WilliamsVaughan Williams
There are five main classes in the Singh Vaughan WilliamsThere are five main classes in the Singh Vaughan Williams
classification of antiarrhythmic agents:classification of antiarrhythmic agents:
Class IClass I agents interfere with the sodium (Na+) channelagents interfere with the sodium (Na+) channel..
Class IIClass II agents are anti-sympathetic nervous system agents areagents are anti-sympathetic nervous system agents are
beta blockers.beta blockers.
Class IIIClass III agents affect potassium (K+) efflux.agents affect potassium (K+) efflux.
Class IVClass IV agents affect calcium channels and the AV node.agents affect calcium channels and the AV node.
Class VClass V agents work by other or unknown mechanisms.agents work by other or unknown mechanisms.

32.  IA-class - intermediate
 Chinidin Quinidine, kinelentyn,
kinitard; Dizopiramid, rytmodan,
rytmilen,
 Novokainamid, procainamide
Digoxin
 Class IB - fast
Lidocaine, Mexeti, lDiphenine
Class IC - - slow
Flekainid, Propafenone,
rytmonorm, propanorm;
Etacizin.
Class ID- combined
Etmozyn (moritsyzyn)
ClassI E - (not officially recognized)
Aymalin (hilurytmal, neohilurytmal
 Class IIClass II:: ββ-blockers-blockers
Propranolol, atenolol, metoprololPropranolol, atenolol, metoprolol
succinate, bisoprolol.succinate, bisoprolol.
 Class III: repolarizationClass III: repolarization
processes continueprocesses continue
CORDARONECORDARONE sotalol bretyliyasotalol bretyliya
tozilat.tozilat.
 Class IV: calcium channelClass IV: calcium channel
blockers:blockers:
VerapamilVerapamil (izoptyn, finoptyn);(izoptyn, finoptyn);
Class IClass I sodium channel blockers

33. Канали Рецептори Пом-
пи
Клінічні
ефекти
ЕКГ
ефекти
Na+
Препарат
ш с п
Ca
2+
K+
Lf α β М2 А1
Na+-
K+-
АТФ-
аза
ЛШ
ЧСС
ЕК
PR QRS QT
Лідокаїн  → → ∅ ↓
Мекселітин  → → ∅ ↓
Токаїнід  → → ↓
Етмозин ↓ →  ↑
Прокаїнамід ∅ ↓ → ↑ ↑ ↑
Дізопірамід ∅  ↓ → ∅ ↑↓ ↑ ↑
Хінідин ∅   → ↑ ∅ ↑↓ ↑ ↑
Пропафенон ∅ ↓ ↓  ↑ ↑
Флекаїнід  ↓ →  ↑ ↑
Енкаїнід ↓ →  ↑ ↑
Верапаміл  ∅ ↓ ↓  ↑
Ділтіазем ∅ ↓ ↓  ↑
Бретіліум → ↓  ↑
Соталол ↓ ↓  ↑ ↑
Аміодарон   ∅ ∅ → ↓ ↑ ↑
Пропранолол  ↓ ↓  ↑
Атропін → ↑ ∅ ↓
Аденозин  ? ↓  ↑
Дігоксин  ↑ ↓ ↑ ↓
Відносна здатність до блокування:  - низька ∅ середня висока
 Агоніст Агоніст/Антагоніст

34. Sicilian Gambit-1
AVNRT HR - 150-220 per min., QRS correct shape, not warped.
methods of stimulation of the vagus
ATP, iv jet 10-20 mg.
Verapamil (finoptyn, izoptyn) iv 10 mg.
Novokainamid 1 g (10 ml of 10% solution) iv.
Consists of digoxin 0.5 mg iv.
Cardioversion. Defibrillation. PECS.
Sicilian Gambit-2
AVRT involving additional pathways (Paladin-Kent, James Mahayma) QRS
irregular shape
1. CORDARONE - 300-450 mg iv + 600 mg / day po.
2. Etmozyn (moritsyzyn) - 2.5% 2-4 ml iv.
3. Etacizin 50-100 mg iv.
4. Aymalin (hiluritmal, tahimalin) 2.5% 2-4 ml iv.

35. Sicilian Gambit-3
Ventricular paroxysmal tachycardia
When stable hemodynamics
● Lidocaine: First bolus of 80-120 mg i.v. ↔ 3-4 min, i.v. 2 mg / min. (80-120 mg / h)
over 10 min. i.v. second bolus of 50% (40-60 mg) i.v. jet / m every 3-4 hours to 200
mg total dose of 3 mg / kg body weight
SEU:
 Meksytylen (meksetyl): 125-500 mg i.v. Inkjet 5-10 min.
 CORDARONE: 150-300-450 mg i.v. ↔ 10-30 min.
Novokainamid - 10-20 ml of 10% solution in 10 ml 0,9% NaCl, i.v. Inkjet, 5 min.
Obzidan: 1 ml 0.1% in 10 ml 0,9% NaCl, i.v. spray every 5 minutes. to 5-10 mg.
If no effect or in the presence of hypotension,
HF, ACS, DCMP - cardioversion, defibrillation.
After each EIT: i.v. 80-120 mg of lidocaine spray, 10-20 ml Panangin or 30-60 ml of
3% potassium chloride, 50 mg / min. Magnesium sulfate.
In establishing normal sinus rhythm: the drug, which filmed attack VPT:
Lidocaine - / m 200 mg every 4 h (at least 2 days)
Novokainamid - RO 500 mg every 6 hours. (at least 2 days)
CORDARONE - 200 mg 3 t / d, 1 month
Obzidan 20 mg 4h /d, 1 month

36. First detected AF /
AFL
Paroxysmal (lasting no
longer than 7 days and
stops independently)
Persistent
(does not stop)
constant
De- novo
Classification of atrial fibrillation / flutter
tahysystolic
The frequency of ventricular
reductions over 90 per
minute
Bradysystolic
The frequency of ventricular
rate less than 60 per
minute

38. Atrial flutter

39. V1
V3
f f
Atrial fibrillation tahysystolic form. Ventricular rate - from
78 to 100 in 1 minute on average - about 80 bpm. / Min.;
Wave f.
60:f-f=600/хв.
=0,1 c.
R R0,8 с.
60:R-R=75/хв.
f f f f f f f f

40. Features vagal and adrenergic
atrial fibrillation
Вагусна:
vagal
Адренергіч
на:
adrenergic
•Male, age 30-50 years, often idiopathic AF
Paroxysms weekly, over night
Triggers: eating, alcohol
The combination of atrial fibrillation
Often - bradysystoliya
No trends in persistent AF
Sensitive to vahotropnyh drugs (IA, amiodarone)
• Usually there is structural heart disease
Patients older
Emergence paroxysms morning, afternoon, at
physical and emotional stress
The dependence on heart rate
Effective β-blockers, propafenone

41. I
II
III
F F
Atrial fibrillation, an irregular shape. Waves F-F.
60:F-F=300/хв.
=0,2 c.F F F F F F

42. Treatment of atrium FIBRILLATION
 Restoration of sinus rhythm by the use of
antiarrhythmic drugs, electric pulse therapy,
pacing.
 Prophylactic administration of antiarrhythmic
agents to prevent recurrences of AF.
 Catheter radiofrequency ablation for radical
removal of the anatomical substrate systems.

43. Antiarrhythmic drugs, which are often used to restore sinus rhythm
in patients with atrial fibrillation
drug is saturating dose Maintenance dose side effects
Cordaron
Propahpenon
Novocainamid
Chinsdin
sulfat
150-450 мг for
10-30 min. iv
1 mg / min. duration
6 h. v / v, then
0.5 mg / min.
Hypotension,
Bradycardia
interaction with
drugs warfarin, consists
of digoxin, novokainamid,
150-300 мг 3 td
Or
2 mg/kg for 10 min. iv
5-15 мg/kg iv or 0,2-0,4
mg/kgminупродовж
10-15 min.
(to 1000 мg)
450-900 mg d
in three divided
doses
Gastrointestinal
side effects
arrhythmogenic
action
6.2 mg / kg / in, then
i/ m 4-6 times a day Hypotension,
300-600 мг iv 200-400 mg every 6 hours
(20 mg / kg per day)
Gastrointestinal
side effects (diarrhea)
interaction with drugs
(digoxin, warfarin,
amiodarone, cimetidine)
pirouette-tachycardia

44. anticoagulation
 Direct anticoagulants for 3-5 days to restore heart rhythm and indirect anticoagulants
(warfarin controlled MNI-2-3, PI-55-60%) 3 weeks before and 4 weeks after
cardioversion.
 Permanent anticoagulant therapy is prescribed for chronic forms of TP when there is
risk factors for thromboembolism.
 Warfarin 1 tab = 2.5, 3, 5 mg dose is determined by the International
Normalization Index( MNI)
 MNI = prothrombin time patient: prothrombin time control •
sensitivity index . Normally MNI = 2-3.
 When MNI <2 - hypercoagulation,> 3 hypocoagulation (risk of bleeding)
V1
V3
f f

45. Catheter radiofrequency ablation

46. Права нижня
Права верхня
Ліва нижня
Ліва верхня
легенева артерія
ПраваЛіва
Клінічна анатомія легеневих венКлінічна анатомія легеневих вен
Radiofrequency ablation

47. ExtrasystolesExtrasystoles
 SupraventricularSupraventricular
P wave to the QRSP wave to the QRS
QRS-complex narrowQRS-complex narrow
compensatory pause iscompensatory pause is
not completenot complete
 VentricularVentricular
hdylya P absent beforehdylya P absent before
QRSQRS
Wide QRS P and TWide QRS P and T
discordantdiscordant
Compensatory pause fullCompensatory pause full

48. Classification of ventricular extrasystoles according
to Lown
I - singles extrasystoles to 5 for 1 minute or until 30 for 1 hour;
II - frequents> 5 for 1 minute or> 30 for 1 hour;
III - polytopics (polymorphic) beats (2 or more ectopic foci);
IV a - allorithmics bisystoliya, even nomotop extrasystoles;
IV b - group 3-5 consecutive extrasystoles,
short "jog" ventricular paroxysmal tachycardia;
V - earlyes extrasystoles type "R-on-T"

49. Ventricular extrasystoles
Bihemeniya - II class
group beats - IV B class
bisystoliya - IV A class
0,10 с 0,10 с
0,16 с 0,16 с

51. left ventricle ЕS right ventricular ЕS
ЕS ЕS

52. Fatal arrhythmiaFatal arrhythmia
syndromessyndromes
WPWWPW
CLCCLC
Romano-WordRomano-Word
Jervel-Lange-NilsenJervel-Lange-Nilsen
shortened Q-Tshortened Q-T
Bruhad syndromeBruhad syndrome
Frederic syndromeFrederic syndrome
Lenegre LevLenegre Lev
SSSNSSSN

53. The prolonged Q-T interval (The prolonged Q-T interval (is more than 48 sis more than 48 s ))
syndromesyndrome
 can be observed in two variants:can be observed in two variants:
with deaf-and-blindness -with deaf-and-blindness - Jervel-Lange-Nilsen syndromeJervel-Lange-Nilsen syndrome
is characterized by a triad:is characterized by a triad:
 congenitalcongenital deaf-and-blindness,deaf-and-blindness,
 loss of consciousness episodes 3-5 minloss of consciousness episodes 3-5 min
 and changes on the ECG.and changes on the ECG.
Romano-Word syndrome.Romano-Word syndrome.
 loss of consciousness episodes 3-5 minloss of consciousness episodes 3-5 min
 and changes on the ECG.and changes on the ECG.
The appearance of ventricular tachycardia attacks, increase risk ofThe appearance of ventricular tachycardia attacks, increase risk of
sudden death. The acquired prolonged Q-T interval syndrome issudden death. The acquired prolonged Q-T interval syndrome is
clinically shown at the age of 40-50 years.clinically shown at the age of 40-50 years.
 Treatment: β-blockers, potassium, magnesium, implantation ofTreatment: β-blockers, potassium, magnesium, implantation of
cardioverter-defibrillatorcardioverter-defibrillator

54. Romano-Word syndromeRomano-Word syndrome
ventricular paroxysmal tachycardia
ventricular fibrillation
elongate QT=0,50

55. The shortened Q-T interval (< 300The shortened Q-T interval (< 300
ms)ms) syndromesyndrome
 There are two forms of this syndrome:There are two forms of this syndrome:
 permanentpermanent (the frequency of heart contractions doesn’t influence);(the frequency of heart contractions doesn’t influence);
 transitorytransitory (is discovered in connection with the slowing down of heart(is discovered in connection with the slowing down of heart
rhythm),rhythm),
which is stimulated by:which is stimulated by:
 genetic disorders;genetic disorders;
 hyperthermia;hyperthermia;
 increase in calcium content or potassium in the blood plasma;increase in calcium content or potassium in the blood plasma;
 acidosis;acidosis;
 disorder of the autonomic nervous system tone .disorder of the autonomic nervous system tone .
 Assessment of the QT interval based onAssessment of the QT interval based on
a formula P. Rautahrju:a formula P. Rautahrju:
QTr = 656 / (1 + FHB100)QTr = 656 / (1 + FHB100)
where QTr-predictive value of the interval QT.where QTr-predictive value of the interval QT.
left mustache Salvador Dali
QT=0,28QT=0,28

56. syndrome BRUHADA
In 1992, the clinics Belgium,
Spain and the United States to
Bruhad Pedro, Jose and Ramon
described the syndrome of
sudden cardiac death in patients
without structural heart disease.
The mechanism of development:
electrical instability
heart.
syndrome
BRUHADA
Characterized by:
1. Blockade of the right leg
bundle branch block in
combination with
segment elevation ST;
2. attacks ventricular
tachycardia (often fatal);
3. Defects heart gene SCN5A,
localized in chromosome 3 (3p α 1-
23), which controls the sodium
channels.
For demonstration erased and / or atypical forms Bruhada syndrome test is
done with aymalinom (1 mg / kg, intravenously) or flekainid (2 mg / kg intravenously).
These drugs can unmask hidden or intermittent forms Bruhada syndrome by identifying
common ECG abnormalities.

57. •Manifestations of the syndrome is Bruhada episodes fast polymorphic VT /
VF in patients with complete blockade of right bundle branch block and ST
segment elevation in V1 - V3.
When spontaneously ending episode of tachycardia, the patient with the syndrome Bruhada may
lose consciousness.
•
Bruhada syndrome
treatment
Implantation of automatic cardioverter defibrillator.
If not applied CP, 30% of patients die within three years after the first appearance of
symptoms. Developed means of gene therapy to correct the genetic defect and
restore normal electrical activity of the heart.

59. Emergency help in case of theEmergency help in case of the
Morgagni-Adams-Stokes syndromeMorgagni-Adams-Stokes syndrome
 First of all, it is necessary to hit one’s chest energetically several times with aFirst of all, it is necessary to hit one’s chest energetically several times with a
fist (precordial thump) and start the outer massage of one’s heart andfist (precordial thump) and start the outer massage of one’s heart and
breathing.breathing.
 If during 3 minutes the heart activity has not restored, the electroimpulseIf during 3 minutes the heart activity has not restored, the electroimpulse
therapy is conducted. Atrial fibrillation is eliminated by means oftherapy is conducted. Atrial fibrillation is eliminated by means of
defibrillation,defibrillation,
 In case of a diagnosed asystole, the most effective procedure is theIn case of a diagnosed asystole, the most effective procedure is the
introduction of an active electrode in a right ventricle through a subclavianintroduction of an active electrode in a right ventricle through a subclavian
vein and the conduction of electrocardiostimulation.vein and the conduction of electrocardiostimulation.
 If the heart activity is not restored, the medicamental therapy is conducted:If the heart activity is not restored, the medicamental therapy is conducted:
Adrenaline HydrochlorideAdrenaline Hydrochloride is injected iv- 0,5 – 1 mg (0,5 – 1 ml of a 0,1 %is injected iv- 0,5 – 1 mg (0,5 – 1 ml of a 0,1 %
solution) in 5 ml of the isotonic solution of Sodium Chloride.solution) in 5 ml of the isotonic solution of Sodium Chloride.
 AlupentAlupent is injected iv by drops in the dose of 0,5 – 1 mg (1—2 ml of a 0,05 %is injected iv by drops in the dose of 0,5 – 1 mg (1—2 ml of a 0,05 %
solution) in 200 ml of the isotonic solution of Sodium Chloride.solution) in 200 ml of the isotonic solution of Sodium Chloride.