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Aritm eng
1. ArrhythmiasArrhythmias
The termThe term arrhythmiaarrhythmia refers to any disturbance in the rate, regularity, siterefers to any disturbance in the rate, regularity, site
of origin, or conduction of the cardiac electrical impulse.of origin, or conduction of the cardiac electrical impulse.
Why Arrhythmias HappenWhy Arrhythmias Happen ::
•HypoxiaHypoxia
•Ischemia and Irritability:Ischemia and Irritability:
•Sympathetic StimulationSympathetic Stimulation
•DrugsDrugs
•Electrolyte DisturbancesElectrolyte Disturbances
•BradycardiaBradycardia
•StretchStretch
3. Cardiac Cycle
P Wave-Atrial Depolarization
PR Segment-Indicative of the delay in the AV node
PR Interval-Refers to all electrical activity in the heart before the impulse
reaches the ventricles
Q Wave-First negative deflection after the P wave but before the R wave
R Wave-First positive deflection following the P wave
S Wave-First negative deflection after the R wave
QRS Complex-Signifies ventricual depolarization
T Wave-Indicates ventricular repolarization (Note: Atrial repolarization wave is
buried in the QRS complex).
5. Normal Sinus Rhythm
Sinus node is the pacemaker, firing at a regular rate of 60 - 100 bpm. Each beat is
conducted normally through to the ventricles
Regularity: regular
Rate: 60-100 beats per minute
P Wave: uniform shape; one P wave for each QRS
PRI: .12-.20 seconds and constant
QRS: .04 to .1 seconds
6. Sinus Bradycardia
Sinus node is the pacemaker, firing regularly at a rate of less than 60 times per
minute. Each impulse is conducted normally through to the ventricles
Regularity: The R-R intervals are constant; Rhythm is regular
Rate: Atrial and Ventricular rates are equal; heart rate less than 60
P Wave: Uniform P wave in front of every QRS
PRI: PRI is between .12 -.20 and constant
QRS: QRS is less than .12
7. Sinus Tachycardia
Sinus node is the pacemaker, firing regularly at a rate of greater than 100 times
per minute. Each impulse is conducted normally through to the ventricles .
Regularity: The R-R intervals are constant; Rhythm is regular
Rate: Atrial and Ventricular rates are equal; heart rate greater than 100
P Wave: Uniform P wave in front of every QRS
PRI: PRI is between .12 -.20 and constant
QRS:QRS is than .12
8. Atrial Flutter
A single irritable focus within the atria issues an impulse that is conducted in a rapid,
repetitive fashion. To protect the ventricles from receiving too many impulses, the AV
node blocks some of the impulses from being conducted through to the ventricles.
Regularity: Atrial rhythm is regular. Ventricular rhythm will be regular if the AV node
conducts impulses through in a consistent pattern. If the pattern varies, the ventricular
rate will be irregular
Rate: Atrial rate is between 250-350 beats per minute. Ventricular rate will depend on
the ratio of impulses conducted through to the ventricles.
P Wave: When the atria flutter they produce a series of well defined P waves. When
seen together, these "Flutter" waves have a sawtooth appearance.
PRI: Because of the unusual "Flutter" configuration of the P wave and the proximity of
the wave to the QRS comples, it is often impossible to determine a PRI in the
arrhythmia. Therefore, the PRI is not measured in Atrial Flutter.
QRS: QRS is less than .12 seconds; measurement can be difficult if one or more
flutter waves is concealed within the QRS complex.
9. Atrial Fibrillation
The atria are so irritable that a multitude of foci initiate impulses, causing the atria to
depolarize repeatedly in a fibrillatory manner. The AV node blocks most of the
impulses, allowing only a limited number through to the ventricles.
Regularity: Atrial rhythm is unmeasurable; all atrial activity is chaotic. The ventricular
rhythm is grossly irregular, having no pattern to its irregularity.
Rate: Atrial rate cannot be measured because it is so chaotic; research indicates that
it exceeds 350 beats per minute. The ventricular rate is significantly slower because
the AV node blocks most of the impulses. If the ventricular rate is below 100 beats
per minute, the rhythm is said to be "controlled"; if it is over 100 bpm, it is considered
to have a "rapid ventricular response."
P Wave: In this arrhythmia the atria are not depolarizing in an effective way; instead,
they are fibrillating. Thus, no P wave is produced. All atrial activity is depicted as
"fibrillatory" waves, or grossly chaotic undulations of the baseline.
PRI: Since no P waves are visible, no PRI can be measured.
QRS: QRS is less than .12
10. Ventricular Tachycardia
An irritable focus in the ventricles fires regularly at a rate of 150-250 beats per minute
to override higher sites for control of the heart.
Regularity: This rhythm is usually regular, although it can be slightly irregular.
Rate: Atrial rate cannot be determined. The ventricular rate range is 150-250 beats
per minute. If the rate is below 150 bpm, it is considered a slow VT. If the rate
exceeds 250 bpm, its called Ventricular Flutter.
P Wave: None of the QRS complexes will be preceded by P waves; you may see
dissociated P waves intermittently across the strip.
PRI: Since the rhythm originates in the ventricles, there will be no PRI.
QRS: The QRS complexes will be wide and bizarre, measuring at least .12 seconds.
It is often difficult to differentiate between the QRS and the T wave.
11. Ventricular Fibrillation
Multiple foci in the ventricles become irritable and generate uncoordinated, chaotic
impulses that cause the heart to fibrillate rather than contract.
Regularity: There are no waves or complexes that can be analyzed to determine
regularity. The baseline is totally chaotic.
Rate: The rate cannot be determined since there are no discernible waves or
complexes to measure.
P Wave: There are no discernible P waves.
PRI: There is no PRI.
QRS: There are no discernible QRS complexes.
12. II.. Impulse generation disordersImpulse generation disorders
145.5 -145.5 - Sinus ArrestSinus Arrest
occurs when the sinus node stops firing. If nothing elseoccurs when the sinus node stops firing. If nothing else
were to happen, the ECG would show a flat line withoutwere to happen, the ECG would show a flat line without
any electrical activity, and the patient would die.any electrical activity, and the patient would die.
Prolonged electrical inactivity is calledProlonged electrical inactivity is called asystoleasystole..
17. 147.1147.1 -- tachicardiatachicardia::
•• reciprocalreciprocal •• chronicchronic
•• focalfocal •• paroxysmalparoxysmal
((ectopicectopic))
-- supraventricularsupraventricular ::
•• from SA nodefrom SA node;;
•• atrialatrial;;
•• from AV nodefrom AV node::
20. 148.0 - fibrillation and flutter of atrium
• paroxysmal (rhythm back to normal independently for 48 h);
• persistent (rhythm back to normal after medical intervention);
• constant (sinus rhythm not restore or inappropriate to restore);
•bradisystolic (HR < 60 /min);
• tachisystolic (HR > 90 /min).
Atrial flutter Atrial fibrillation
22. II. CONDUCTION BLOCKS:
145.5 - SA block;
144.0 • І degree.
144.1 • II degree. Type І
Type II
144.2 • III degree – full .
23. AV Block 2 First Degree
The AV node selectively conducts some beats while blocking others. Those that are
not blocked are conducted through to the ventricles, although they may encounter a
slight delay in the node. Once in the ventricles, conduction proceeds normally.
Regularity: If the conduction ratio is consistent, the R-R interval will be constant, and
the rhythm will be regular. If the conduction ratio varies, the R-R will be irregular.
Rate: Atrial rate is usually normal; since many of the atrial impulses are blocked, the
ventricular rate will usually be in the bradycardia range, often one-half, one-third, or
one-fourth of the atrial rate.
P Wave: Upright and uniform; there are always more P waves than QRS complexes.
PRI: PRI on conducted beats will be constant across the strip
QRS: QRS is less than .12
24. AV Block 2 Second Degree
As the sinus node initiates impulses, each one is delayed in the AV node a little
longer than the preceding one, until one impulse is eventually blocked completely.
Those impulses that are conducted travel normally through the ventricles.
Regularity: Irregular; the R-R interval gets shorter as the PRI gets longer.
Rate: Usually slightly slower than normal
P Wave: Upright and uniform; some P waves are followed by QRS complexes.
PRI: Progressively lengthens until one P wave is blocked
QRS: QRS is less than .12
25. Third Degree Heart Block
The block at the AV node is complete. The sinus beats cannot penetrate the node
and thus are not conducted through to the ventricles. An escape mechanism from
either the junction or the ventricles will take over to pace the ventricles. The atria and
ventricles function in a totally dissociated fashion.
Regularity: Regular
Rate: Atrial rate is usually normal (60-100bpm); ventricular rate: 40-60 if the focus is
junctional, 20-40 if the focus in ventricular.
P Wave: Upright and uniform; more p waves than QRS complexes.
PRI: No relationship between p waves and QRS complexes; p waves can
occasionally be found superimposed on the QRS complex.
QRS: Less than .12 seconds if the focus in junctional, .12 seconds or greater if the
focus is ventricular.
26. Asystole
The heart has lost its electrical activity. There is no electrical pacemaker to initiate
electrical flow.
Regularity: Not measurable; there is no electrical activity.
Rate: Not measurable; there is no electrical activity.
P Waves: Not measurable; there is no electrical activity.
PRI: Not measurable; there is no electrical activity.
QRS: Not measurable; there is no electrical activity.
27. II. CONDUCTION BLOCKS:
- AV block:
144.0 • І degree.
144.1 • II degree. Type І
Type II
144.2 • III degree.
28. II. CONDUCTION BLOCKS:
-Bundle branch block
-Single branch: 145.0 - RBBB
Left anterior hemi block LAHB
- Left posterior hemi block LPHB
31. III.III. COMBINED DISORDERSCOMBINED DISORDERS
parasystoleparasystole
1) atrial1) atrial
2) From AV node2) From AV node
3) ventricular3) ventricular
56. A female patient, aged 43, complains of palpitation,
that suddenly appeared after physical exertion,
dyspnea and dull pain in the heart area. Over the 12
years she is under a follow-up care because of
rheumatism and mitral stenosis without any
essential circulatory embarrassment. Objectively:
pallor of skin integuments, HR 140/min, PS –
100/min., АP 130/85 mm Hg, ЕCG: instead of Рw.
waves, dissimilar R-R interval. What rhythm disorder
is the most probable?
58. Patient F., aged 42, suddenly developed
palpitation attack attended by general
weakness, dyspnea, HR - 170 per min.
ЕCG: number of heart beats – 180 per
min, rhythm regular, QRS - 0,10 s. After
massage of carotid sinus area decrease of
heart beats to 75 beats per min was
observed. What rhythm disorder was
registered in the patient?
60. Patient, 35 of age, on strenuous exercise
fell suddenly unconscious; is ailing with
hypertrophic cardiomyopathy. On an
examination: breath aperiodic,
stentorious, Pulse and heart tones cannot
be detected. АP 50/20 mm Hg. On ECG –
chaotic contractions. What has the
patient?
62. Woman, 64 of age, complains of intermittency in
the heart activity, palpitation, performance
decrement, general weakness. Over the few
months she remarks recrudescence. After a
short-term fainting episode consulted a doctor.
Objectively: Pulse — 52 per 1 min, arrhythmic.
On cardiophony no murmurs were registered.
revealed. On ECG: sinus rhythm , irregular. PQ
interval — 0,20 s., QRS— 0,08 s. Slowly
decreasing of R—R interval with following
РQRSТ-fallout. What is the most probable
cause of this condition?
63. Sinoatrial block;
Atrioventricular block І degree;
Atrioventricular block, II degree;
Atrioventricular block; III degree;
Trifascicular heart block.
64. Patient K., aged 50, with large-focal
myocardial infarction of the anteroseptal
area suddenly felt sharp weakness and
staggers. АP 160/90 mm Hg. Heart tones
sharply muffeled. Pulse rhythmic 32 per
min. On ECG dissociation between atrial
and ventricular activity. Call the most
probable clinical setting:
66. Solve each case, the extent to which theSolve each case, the extent to which the
risk of treatment outweighs the risk of therisk of treatment outweighs the risk of the
existence of the arrhythmiaexistence of the arrhythmia
Introducing antiarrhythmic drugs inIntroducing antiarrhythmic drugs in
sufficient therapeutic dosessufficient therapeutic doses
Monitoring for complicationsMonitoring for complications
Principles of antiarrhythmicPrinciples of antiarrhythmic
therapytherapy
67. Factors that determine theFactors that determine the
treatment programtreatment program
arrhythmiasarrhythmias
hemodynamic status at the time ofhemodynamic status at the time of
termination of arrhythmiastermination of arrhythmias;;
impact of arrhythmias on hemodynamicsimpact of arrhythmias on hemodynamics;;
directly, the preceding therapydirectly, the preceding therapy;;
efficacy and tolerability of the drug in theefficacy and tolerability of the drug in the
past or the method that was used to treatpast or the method that was used to treat..
68. The degree of severity of structural heart diseaseThe degree of severity of structural heart disease
and its potential impact on risk and effectivenessand its potential impact on risk and effectiveness
of antiarrhythmic therapyof antiarrhythmic therapy
Degrees Characteristics of heart disease Risk Efficiency
1 Structural pathology without affecting the
ventricle: mitral valve prolapse without
regurgitation or violations of repolarization,
additional AV conduction paths, moderate
mitral stenosis
+++++ +
2 Minimum left ventricular dysfunction,
moderate hypertrophy or overload
capacity without severe LV dilatation
++++ ++
3 Myocardial damages without stagnant
phenomena or severe LV systolic
dysfunction
+++ +++
4 Severe left ventricular hypertrophy ++ ++++
5 Congestive heart failure, severe left
ventricular systolic dysfunction, severe
ischemia
+ +++++
69. I. Membrane stabilizers, oppress quick Na + channels, blocking
Na + entry into the cell during the 0-phase of the action potential
---> reduce speed of conducting:
IА - moderate repressor 0-phase, extending QRS, prolongation of
action potential and QT, inhibit conduction and slow repolarization
(quinidine (kinelentyn), procainamide (novokainamid),
disopyramide (rytmilen, norpase) aymalin (hilurytmal) praymalin
(neo-hilurytmal) imipramine, pirmenol.
atrial extrasystole +++
asymptomatic ventricular extrasystoles - impractical
ventricular tachycardia and fibrillation - + in 35% of cases
atrial fibrillation +++
reciprocal supraventricular tachyarrhythmias +++
Additional conduction pathways +++
Classification AAD (E.Vaughan Williams
1979) with additions D.Harrison (1985)
70. IB - weak repressor 0-phase, less than Ia, affecting the
QRS and conductivity, accelerate repolyaryzation,
shortening QT, greatly increase the threshold of
ventricular fibrillation (lidocaine, trimecaine, meksytylen
(meksytyl), tocainide, diphenyl (phenytoin, diphenine,
dylantyn)
ventricular extrasystoles +++
ventricular tachycardia and fibrillation +++
IC - strong repressors 0-phase, extending QRS i
suppress conduction in small concentrations, little effect
on rate of repolarization, duration QT i refractory period
(flekainid, morytsyzyn (etmozyn) Etacizin, alapinin,
propafenone (rytmonorm) tsybenzolin)
ventricular extrasystoles +++
Classification AAD
71. IА – moderate slowdown in the rate of
depolarization and repolarization;
IB - minimum deceleration depolarization and
repolarization accelerated;
IC - maximum deceleration rate of depolarization
and minimal impact on repolarization.
Classification AAD
72. II. Beta-blockers with blocking effects of catecholamines,
decreased atrial and ventricle automaticity, decreased
AV-and / ventricular conduction, increase refractory
period, the effect in cases of oppression and
suppression of automaticity reciprocal tachycardias if the
circuit re-entry associated with the AV-node (propranolol
(Inderal), nadolol, metoprolol, atenolol, esmolol,
betaxolol (lokren), bisoprolol (Concor).
ventricular extrasystoles with catecholamine genesis +++
atrial fibrillation +
automatic and reciprocal supra/ventricular tachyarrhythmias +
ventricular tachycardia and fibrillation +++
additional pathways ++
Classification AAD
73. III. Drugs with primary antyadrenergic effect - blockers
of K + channels also prolong action potential and
repolarization, QT interval , increases duration of
refractory period (amiodarone (CORDARONE,
amiokordyn), sotalol (hilukor) bretilium (ornid),
dofetilide, ibutylid, sematylid, azymilid, nibentan).
atrial extrasystole +++
ventricular extrasystoles +++
automatic and reciprocal supraventricular
tachyarrhythmias +++
atrial fibrillation +++
ventricular tachycardia and fibrillation +++
additional pathways +++
Classification AAD
74. IV. Calcium channel blockers - inhibit
transmembrane flow of calcium ions in the areas of
SA- and AV-node, reduce the spontaneous activity
of SA-node affect the mechanism of re-stimulation,
inhibit 4-th phase of depolarization, reduces the
transmembrane resting potential, prolong the
refractory period of these zones (verapamil
(finoptyn) hallopamil (prokorum), diltiazem (dylzem,
dyltysan, kardil) bepredyl (kordium).
supraventricular arrhythmias +++
Classification AAD
75. Classification AAD
The Task Force of the Working Group on Arrhythmias of the European Society of Cardiology: The
Sicilian Gambit (Circulation 1991; 84: 1831-1851. )
77. Ventricular arrhytmiasVentricular arrhytmias
Ventricular fibrillationVentricular fibrillation;;
Resistant ventricular paroxysmal tachycardiaResistant ventricular paroxysmal tachycardia ((monomono
and polymorphic)and polymorphic);;
ventricular paroxysmal tachycardia in patients withventricular paroxysmal tachycardia in patients with
MIMI;;
Often, doublet, polymorphic premature ventricularOften, doublet, polymorphic premature ventricular
beats in patients with MIbeats in patients with MI..
Rhythm disturbances required
emergency care
78. Rhythm disturbances requiredRhythm disturbances required
emergency careemergency care
SA blockadeSA blockade,, SA node weak syndromeSA node weak syndrome withwith
syncopesyncope,, periods of asystoleperiods of asystole,, HR<HR<4040/min/min;;
AV blockadeAV blockade (ІІ, ІІІ(ІІ, ІІІ degreedegree)) with syncopewith syncope,,
periods of asystoleperiods of asystole,, HR<HR<4040/min/min..
79. Supraventricular paroxysmalSupraventricular paroxysmal
tachicardiastachicardias
ReciprocalReciprocal tachycardia from AV nodetachycardia from AV node,, working onworking on
„re-entry”„re-entry” mechanismmechanism ((Retrograde P waves often areRetrograde P waves often are
not detected, or placed over QRS, or seen after QRSnot detected, or placed over QRS, or seen after QRS
with short intervals RP (RP <50% RR). Impulse passeswith short intervals RP (RP <50% RR). Impulse passes
through anterograde in slow path and retrograde inthrough anterograde in slow path and retrograde in
quick path , atrium and ventricle simultaneouslyquick path , atrium and ventricle simultaneously
excited.excited.
80. Supraventricular paroxysmalSupraventricular paroxysmal
tachicardiastachicardias
orthodromicorthodromic supravenrticular tachycardia arises withsupravenrticular tachycardia arises with
the existence of additional path (syndrome WPW) withthe existence of additional path (syndrome WPW) with
conduction through the AV anterograde on theconduction through the AV anterograde on the
ventricles and then retrograde back through anventricles and then retrograde back through an
additional way in atrium, recorded retrograde P wavesadditional way in atrium, recorded retrograde P waves
with short intervals RP (RP <50% RR), negative P in Iwith short intervals RP (RP <50% RR), negative P in I
lead, the delta wave is absent because the ventricleslead, the delta wave is absent because the ventricles
are activated via AV-zoneare activated via AV-zone..
81. Supraventricular paroxysmalSupraventricular paroxysmal
tachicardiastachicardias
Antidromic supraventricular tachycardia rarely occurAntidromic supraventricular tachycardia rarely occur
and where there are substantial additional way ofand where there are substantial additional way of
(syndrome WPW) holding pulse anterograde through(syndrome WPW) holding pulse anterograde through
an additional path to the ventricles, followed by thean additional path to the ventricles, followed by the
return of retrograde AV-node in the atrium,return of retrograde AV-node in the atrium,
occasionally recorded anterograde P waves,occasionally recorded anterograde P waves,
necessarily delta wave, so as ventricular activationnecessarily delta wave, so as ventricular activation
occurs through an additional path is similar to anoccurs through an additional path is similar to an
electrocardiogram of ventricular tachycardiaelectrocardiogram of ventricular tachycardia
..
83. AdenosinAdenosin
AdenosinAdenosin 66 mgmg,, ATFATF 10-2010-20 mgmg ii//vv duringduring
5-105-10 secsec;;
Quick effectQuick effect,, short half-lifeshort half-life
Do not changeDo not change blood pressureblood pressure andand
contractilitycontractility
Caution in patients with SA node weakCaution in patients with SA node weak
syndromesyndrome
84. VerapamilVerapamil
((tabtab. 40-80-120-240. 40-80-120-240 mgmg,, ampamp. 0,25%. 0,25% solutionsolution 22 mlml.. Target -Target -
supraventricular arrhytmiassupraventricular arrhytmias):):
decreasedecrease slow transmembrane flowslow transmembrane flow of calcium in cellof calcium in cell;;
Not change repolarization and depolarization speedNot change repolarization and depolarization speed;;
Decrease activity of AV nodeDecrease activity of AV node;;
InhibitsInhibits «re-entry»«re-entry» mechanismmechanism;;
Decrease speed of AV conductionDecrease speed of AV conduction and abnormally increased activityand abnormally increased activity
of atriumsof atriums;;
Prolongs PQ intervalProlongs PQ interval,, decrease refractory of additional pathwaydecrease refractory of additional pathway,, forfor
WPW syndrome lead to fibrillationWPW syndrome lead to fibrillation..
85. NovokainamideNovokainamide
((tabtab. 250. 250 mgmg,, ampamp.10%.10% solutionsolution -10-10 mlml i/vi/v 500-1000500-1000 mgmg 2-42-4 daily,daily,
after transition to intramuscular administration, support tablets 2-3after transition to intramuscular administration, support tablets 2-3
times per daytimes per day):):
reduces automaticity, increases arousal threshold, increasesreduces automaticity, increases arousal threshold, increases
effective refractory period, inhibits conduction in the atriums, AV-effective refractory period, inhibits conduction in the atriums, AV-
node, ventriclesnode, ventricles;;
reduces contractility, reduces blood pressurereduces contractility, reduces blood pressure;;
increases the action potentialincreases the action potential;;
increasesincreases QRS, QTQRS, QT intervalsintervals;;
increases refractoriness in additional conduction way at WPWincreases refractoriness in additional conduction way at WPW
syndromesyndrome;;
negative effects: anorexia, vomiting, diarrheanegative effects: anorexia, vomiting, diarrhea;;
contraindicated in AV block, heart failure, cardiogenic shock, renalcontraindicated in AV block, heart failure, cardiogenic shock, renal
failure (decrease output novokainamide)failure (decrease output novokainamide)..
86. ECG at Atrial FibrillationECG at Atrial Fibrillation
High frequency fibrillation (450-600 per min.) prevents register sinus rhythmHigh frequency fibrillation (450-600 per min.) prevents register sinus rhythm
(frequency - 60 - 90 per min.), so on the ECG not register P - wave(frequency - 60 - 90 per min.), so on the ECG not register P - wave.
Instead P wave recorded flutter waves (fibrillation waves), denoted by the letters F (f),Instead P wave recorded flutter waves (fibrillation waves), denoted by the letters F (f),
which are best visualized in leads VI and V2which are best visualized in leads VI and V2.
Fibrillation wave frequency - 450-600 per minuteFibrillation wave frequency - 450-600 per minute.
Ventricular QRS complex registered irregular (arrhythmia), RR interval differentVentricular QRS complex registered irregular (arrhythmia), RR interval different.
Form of ventricular complex QRS is usual, width not exceeding 0.12 sForm of ventricular complex QRS is usual, width not exceeding 0.12 s.
87. Strategy for the treatment ofStrategy for the treatment of
patients with atrial fibrillationpatients with atrial fibrillation
TasksTasks
reduction of clinical symptomsreduction of clinical symptoms;;
prevent complications (stroke, heart failure, myocardial infarction), whichprevent complications (stroke, heart failure, myocardial infarction), which
can reduce morbidity and mortalitycan reduce morbidity and mortality..
Criteria for clinical efficacyCriteria for clinical efficacy
physiological control of heart ratephysiological control of heart rate;;
increasing the length between new paroxysmsincreasing the length between new paroxysms;;
reduce the severity and duration of AF paroxysmsreduce the severity and duration of AF paroxysms;;
facilitate tolerability and termination of AF episodesfacilitate tolerability and termination of AF episodes;;
improving quality of lifeimproving quality of life..
88. Patient with AF
Restoration of heart
rhythm (Cardioversion):
•Drug Cardioversion
•Electrical Cardioversion
Therapies aimed at
preventing the
recurrence of AF
Prevention of
thrombo-embolic
disorders
Rhythm
control
Catheter
ablation
Strategy for the treatment of patients with
atrial fibrillation
89. Benefits of restoration andBenefits of restoration and
preservation of sinus rhythmpreservation of sinus rhythm
reduction of clinical symptoms caused byreduction of clinical symptoms caused by
arrhythmiaarrhythmia;;
improve hemodynamicsimprove hemodynamics;;
increase exercise toleranceincrease exercise tolerance;;
psychological benefits of "normal" rhythm;psychological benefits of "normal" rhythm;
may improve quality of lifemay improve quality of life;;
no need for prolonged anticoagulation therapyno need for prolonged anticoagulation therapy;;
reduce the risk of thromboembolicreduce the risk of thromboembolic
complicationscomplications..
90. Problems restoring andProblems restoring and
maintaining sinus rhythmmaintaining sinus rhythm
low efficiency of most antiarrhythmic drugs, and thelow efficiency of most antiarrhythmic drugs, and the
necessity of stopping new paroxysms of AFnecessity of stopping new paroxysms of AF;;
thromboembolism after restoration of sinus rhythmthromboembolism after restoration of sinus rhythm;;
poor tolerance for antiarrhythmic drugspoor tolerance for antiarrhythmic drugs;;
arrhythmogenic effects of antiarrhythmic drugs, mostarrhythmogenic effects of antiarrhythmic drugs, most
pronounced after the restoration of sinus rhythmpronounced after the restoration of sinus rhythm;;
background sick sinus syndrome or bradycardia in manybackground sick sinus syndrome or bradycardia in many
elderly patientselderly patients;;
high cost of antiarrhythmic drugshigh cost of antiarrhythmic drugs..
91. Diseases and conditions under which theDiseases and conditions under which the
recovery rate at a constant atrialrecovery rate at a constant atrial
fibrillation is not appropriatefibrillation is not appropriate
Heart defects, subject to operational correctionHeart defects, subject to operational correction..
Small (less than six months) period from the date ofSmall (less than six months) period from the date of
commissurotomycommissurotomy..
Not removed activity of rheumatism of second and third degreeNot removed activity of rheumatism of second and third degree..
Not treated thyrotoxicosisNot treated thyrotoxicosis..
Arterial HypertensionArterial Hypertension ІІІІІІ degreedegree..
Heart FailureHeart Failure ІІІІІІ degreedegree..
ObesityObesity ІІІІІІ degreedegree..
CardiomegalyCardiomegaly (cor bovinus).(cor bovinus).
Age over 65 years in patients with heart defects and 70 years forAge over 65 years in patients with heart defects and 70 years for
patients with IHDpatients with IHD..
Duration of atrial fibrillation over 3 yearsDuration of atrial fibrillation over 3 years..
92. Control of heart rate withoutControl of heart rate without
restoring sinus rhythmrestoring sinus rhythm
BenefitsBenefits
symptomatic improvement, increased exercise tolerancesymptomatic improvement, increased exercise tolerance;;
safety of treatmentsafety of treatment;;
good tolerability for drugsgood tolerability for drugs;;
relatively low cost of treatmentrelatively low cost of treatment..
Problems of rate control without restoring sinusProblems of rate control without restoring sinus
rhythmrhythm
less adequate compared to the physiological control of heart rateless adequate compared to the physiological control of heart rate;;
the loss of deposit fibrillation in cardiac outputthe loss of deposit fibrillation in cardiac output;;
frequent occurrence of bradycardia syndrome "tachy-bradycardia"frequent occurrence of bradycardia syndrome "tachy-bradycardia";;
often - need lifelong treatment with anticoagulantsoften - need lifelong treatment with anticoagulants;;
formation of left atrial dilatation and left ventricular dysfunction withformation of left atrial dilatation and left ventricular dysfunction with
inadequate rate controlinadequate rate control;;
incomplete elimination of clinical symptomsincomplete elimination of clinical symptoms;;
reduced quality of lifereduced quality of life
93. Pharmacological therapy ofPharmacological therapy of
patients with firs time AFpatients with firs time AF
First time Atrial Fibrillation
Paroxysmal
Persistent
Therapy no needed
if no hypotension,
heart failure, angina
Anticoagulant
therapy if risk
factors of embolism
present
Consider a
permanent form of
atrial fibrillation
Anticoagulant
therapy and rate
control
Anticoagulant
therapy and rate
control if needed
Consider drug
therapy
Cardioversion
No need for long-
term drug therapy
94. Drug CardioversionCardioversion
DrugDrug ClassClass
LevelLevel
DosageDosage
Drugs with recognized efficacyDrugs with recognized efficacy
DofetilideDofetilide I / AI / A 125-500125-500 mcgmcg 22 dailydaily
FlecainideFlecainide I / AI / A 200-300200-300 mgmg oraloral; 1,5-3,0; 1,5-3,0 mgmg//kgkg ii//vv
IbutilideIbutilide I /AI /A ii//vv 11 mgmg perper 1010 minmin,, if necessary againif necessary again 11mgmg
PropafenonePropafenone ** I / AI / A OralOral 600600mgmg;; ii//vv 1,5-21,5-2mgmg//kgkg perper 10-2010-20minmin
AmiodaroneAmiodarone ** IIa/AIIa/A ii//vv:: 5-75-7 mgmg//kgkg perper 30-6030-60 minmin,, thenthen toto 1,2-1,81,2-1,8
gg//dayday ii//vv or oral up toor oral up to 1010 gg,, thenthen 200-400200-400
mgmg//dayday –– support dosagesupport dosage
Less efficacyLess efficacy //insufficiently studiedinsufficiently studied
DisopiramideDisopiramide IIb /BIIb /B OralOral toto 300300 mgmg
ProkainamideProkainamide IIb /BIIb /B OralOral toto 3,0-4,03,0-4,0 gg
QuinidineQuinidine IIb /IIb /ВВ OralOral 0,75-1,50,75-1,5 gg perper 6-126-12 hh
Do not useDo not use
Digoxin SotalolDigoxin Sotalol
* - can used ambulatory, after safety control in hospital
96. Prevention of recurrence of paroxysmal or persistent AF)
Heart disease?
No or mild
Propafenon
Sotalol
Flecainide
Amiodarone
Dofetilide
Catheter
ablation
HF CAD
Sotalol
Dofetilide
ACC/AHA/ESC 2006 Guidelines for the management… of AF.-EHJ-2006-27-p.1979-2030
Amiodarone
Dofetilide
Catheter
ablation Amiodarone
Catheter
ablation
AH
LVG++ LVG-/+
Propafenon
Sotalol
Flecainide
Amiodarone
Dofetilide
Catheter
ablation
97. AmiodaroneAmiodarone
((tabtab. 200. 200 mgmg,, ampamp. 150. 150 mgmg daily dose ivdaily dose iv 150-300150-300 mgmg.. The drug isThe drug is
most effective antiarrhythmic, for a long time still means third-linemost effective antiarrhythmic, for a long time still means third-line
antiarrhythmic protection affects practically all types of arrhythmias,antiarrhythmic protection affects practically all types of arrhythmias,
is minimal compared to other antiarrhythmics side effects)is minimal compared to other antiarrhythmics side effects);;
anti-adrenergic effectanti-adrenergic effect;;
increase action potential refractory period of an additional path, inincrease action potential refractory period of an additional path, in
AV node, in the system of His-PurkinjeAV node, in the system of His-Purkinje;;
operates with paroxysmal and ventricular arrhythmia, ventricularoperates with paroxysmal and ventricular arrhythmia, ventricular
fibrillationfibrillation;;
Contraindicated in case of increasing of interval QT, thyroidContraindicated in case of increasing of interval QT, thyroid
dysfunction, chronic lung diseasesdysfunction, chronic lung diseases..
98. QuinidineQuinidine
(tab.100 mg daily dose of 1200-2000 mg (no more than 4000 mg within 2-4 hours for(tab.100 mg daily dose of 1200-2000 mg (no more than 4000 mg within 2-4 hours for
cumulation)cumulation):
reduces excitability, contractility, conductivityreduces excitability, contractility, conductivity;
inhibits the function of SA-nodeinhibits the function of SA-node;
bidirectional affect the function of AV conduction (increases the refractory period ofbidirectional affect the function of AV conduction (increases the refractory period of
the AV-node and blocks n.vagus)the AV-node and blocks n.vagus);
increases the refractory period and blocks «re-entry», increases the refractory periodincreases the refractory period and blocks «re-entry», increases the refractory period
an additional way in WPW syndromean additional way in WPW syndrome;
reduces blood pressure by peripheral vasodilatationreduces blood pressure by peripheral vasodilatation;
blocks n.vagus increases heart rate and positive influence on digitalis arrhythmias.blocks n.vagus increases heart rate and positive influence on digitalis arrhythmias.
Digitalis toxicity better treated lidocaine, propranolol, diphenineDigitalis toxicity better treated lidocaine, propranolol, diphenine;
leads to sinus tachycardia, SA-blockade, increasing PQ and QT intervalsleads to sinus tachycardia, SA-blockade, increasing PQ and QT intervals;
used for atrial fibrillation, supraventricular arrhythmia paroxysms, ventricularused for atrial fibrillation, supraventricular arrhythmia paroxysms, ventricular
arrhythmia. In 65-85% restores sinus rhythm in atrial fibrillationarrhythmia. In 65-85% restores sinus rhythm in atrial fibrillation;
contraindicated in AV block, pregnancy, heart failure, low blood pressurecontraindicated in AV block, pregnancy, heart failure, low blood pressure;
negative effects: dyspepsia, headache, blurred vision, thrombocytopenia, acutenegative effects: dyspepsia, headache, blurred vision, thrombocytopenia, acute
psychosispsychosis;
combination with quinidine and cordarone can lead to arrhythmias such ascombination with quinidine and cordarone can lead to arrhythmias such as
"pirouette";"pirouette";
verapamil reduces effect of quinidineverapamil reduces effect of quinidine.
99. PropafenonePropafenone
(Tab. 150-300 mg, 450-900 mg internally daily)(Tab. 150-300 mg, 450-900 mg internally daily)::
increases the threshold of stimulation, tripledincreases the threshold of stimulation, tripled
carefully at constant elektrokardiostymulationcarefully at constant elektrokardiostymulation;;
may increase the action potential, strengthen themay increase the action potential, strengthen the
effect of beta-blockerseffect of beta-blockers;;
with increased action potential leads to decreasewith increased action potential leads to decrease
in the rate of (treatment of arrhythmias within the rate of (treatment of arrhythmias with
additional conduction ways)additional conduction ways);;
prolong the interval PQ, QRS complexprolong the interval PQ, QRS complex..
100. Beta - blockersBeta - blockers
Propranolol (anaprylin) nonselective beta-blocker withoutPropranolol (anaprylin) nonselective beta-blocker without
sympathomimetic activity with membrane stabilizing action in dosesympathomimetic activity with membrane stabilizing action in dose
10 and 40 mg in tab form and 5 mg solution. On average 40-160 mg10 and 40 mg in tab form and 5 mg solution. On average 40-160 mg
per day before mealsper day before meals..
Metoprolol (korvitol) - 50 and 100 mg per day, 150-400 mgMetoprolol (korvitol) - 50 and 100 mg per day, 150-400 mg..
Atenolol (atenosan) - 50-100 mg 2 times a day (12 hours)Atenolol (atenosan) - 50-100 mg 2 times a day (12 hours)..
Acebutolol (sektral) - 400 mg per day (24 hours)Acebutolol (sektral) - 400 mg per day (24 hours)..
Nebivolol - 5-10 mg once dailyNebivolol - 5-10 mg once daily..
Lokren - 10-20 mgLokren - 10-20 mg..
Sotalol - 80-160 mg 1-2 times a day. Antiarrhythmic effectsSotalol - 80-160 mg 1-2 times a day. Antiarrhythmic effects
predominate over other beta-blockers, which causedpredominate over other beta-blockers, which caused
electrophysiological effects of antiarrhythmic drugs II and IIIelectrophysiological effects of antiarrhythmic drugs II and III
classesclasses..
103. Variations paroxysmal VT (A -Variations paroxysmal VT (A -
tachycardia "Torsades de pointes",? B -tachycardia "Torsades de pointes",? B -
syndromal tachycardia with prolongedsyndromal tachycardia with prolonged
QT)QT)
104. Treatment of VT with antiarrhythmic drugsTreatment of VT with antiarrhythmic drugs
Н а з в а н и е д и а г р а м м ы
A m io d a r o n e
N o v o c a in a m id e
M o n o f o c a l V T
C a r d ia c S t im u la t io n
M a g n iu m
E le c t r o ly t e s
D is c o n t in u in g A A D
P r o lo n g e d Q T
A m io d a r o n e
L id o c a in e
B e t a - b lo c k e r s
N o r m a lQ T
M u lt if o c a l V T
A m io d a r o n e
A F
V e m t r ic u la r a r r h y t m ia s
105. LidocaineLidocaine
Table 250 mg vial. 2% solution - 2 ml (40 mg), 10%Table 250 mg vial. 2% solution - 2 ml (40 mg), 10%
solution - 2 ml (200 mg), intravenous bolus of 80 mg,solution - 2 ml (200 mg), intravenous bolus of 80 mg,
then 120 mg drip through 4-6 hours to 40 mg after thisthen 120 mg drip through 4-6 hours to 40 mg after this
intramuscularly)intramuscularly)::
decreases automaticity of Purkinje fibersdecreases automaticity of Purkinje fibers;;
increases the difference of action potentialincreases the difference of action potential;;
reduces activation of the sympathetic nervous systemreduces activation of the sympathetic nervous system;;
has little effect on atrialhas little effect on atrial;;
does not increase the intervals PQRSTdoes not increase the intervals PQRST;;
effect on ventricular arrhythmias and ventriculareffect on ventricular arrhythmias and ventricular
fibrillationfibrillation;;
contraindicated in combination with quinidine, sic sinuscontraindicated in combination with quinidine, sic sinus
syndrome in old age, blockadessyndrome in old age, blockades..
106. Big-(A) and small wave (B) ventricularBig-(A) and small wave (B) ventricular
fibrillationfibrillation
107. CPR: initial stageCPR: initial stage
А.А. AirwayAirway..
В.В. Breathing 2:15 with circulationBreathing 2:15 with circulation..
С.С. CirculationCirculation 100/100/minmin..
DD.. DefibrillationDefibrillation ((dischargesdischarges 360360 joulejoule;;
electrodes below the right clavicle andelectrodes below the right clavicle and
above the apex of the heart on the frontabove the apex of the heart on the front
axillary lineaxillary line))
108. CPR: Secondary StageCPR: Secondary Stage
А.А. IntubationIntubation..
В.В. Ventilation 2:15 to massageVentilation 2:15 to massage..
С.С. Contact vein 100/minContact vein 100/min..
DD.. Correction return reasons:Correction return reasons:
adrenaline 1 mg / in every 3 minutes. oradrenaline 1 mg / in every 3 minutes. or
vasopressin 40 U oncevasopressin 40 U once
360 Joules defibrillation 360 Joules defibrillation
111. Acute conduction disordersAcute conduction disorders
atropine sulfate - 1 ml of 0.1% solutionatropine sulfate - 1 ml of 0.1% solution
intravenouslyintravenously..
isoproterenol 5 mg sublingually after 2-4 hisoproterenol 5 mg sublingually after 2-4 h,,
alupent 0.5-1.0 ml of 0.05% solution in 10 mlalupent 0.5-1.0 ml of 0.05% solution in 10 ml
0.9% NaCl solution intravenously slowly0.9% NaCl solution intravenously slowly..
Acute AV conduction disorders, occurring withAcute AV conduction disorders, occurring with
MAS syndrome or heart failure requiringMAS syndrome or heart failure requiring
constant elektrokardiostymulyationconstant elektrokardiostymulyation..
