ArrhythmiasArrhythmiasThe termThe term arrhythmiaarrhythmia refers to any disturbance in the rate, regularity, siterefers to any disturbance in the rate, regularity, siteof 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
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 impulsereaches 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 isburied in the QRS complex).
Normal Sinus Rhythm Sinus node is the pacemaker, firing at a regular rate of 60 - 100 bpm. Each beat isconducted 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
Sinus Bradycardia Sinus node is the pacemaker, firing regularly at a rate of less than 60 times perminute. 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 constantQRS: QRS is less than .12
Sinus Tachycardia Sinus node is the pacemaker, firing regularly at a rate of greater than 100 timesper 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
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 AVnode 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 nodeconducts impulses through in a consistent pattern. If the pattern varies, the ventricularrate will be irregular Rate: Atrial rate is between 250-350 beats per minute. Ventricular rate will depend onthe ratio of impulses conducted through to the ventricles. P Wave: When the atria flutter they produce a series of well defined P waves. Whenseen together, these "Flutter" waves have a sawtooth appearance. PRI: Because of the unusual "Flutter" configuration of the P wave and the proximity ofthe wave to the QRS comples, it is often impossible to determine a PRI in thearrhythmia. Therefore, the PRI is not measured in Atrial Flutter. QRS: QRS is less than .12 seconds; measurement can be difficult if one or moreflutter waves is concealed within the QRS complex.
Atrial Fibrillation The atria are so irritable that a multitude of foci initiate impulses, causing the atria todepolarize repeatedly in a fibrillatory manner. The AV node blocks most of theimpulses, allowing only a limited number through to the ventricles. Regularity: Atrial rhythm is unmeasurable; all atrial activity is chaotic. The ventricularrhythm is grossly irregular, having no pattern to its irregularity. Rate: Atrial rate cannot be measured because it is so chaotic; research indicates thatit exceeds 350 beats per minute. The ventricular rate is significantly slower becausethe AV node blocks most of the impulses. If the ventricular rate is below 100 beatsper minute, the rhythm is said to be "controlled"; if it is over 100 bpm, it is consideredto 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
Ventricular Tachycardia An irritable focus in the ventricles fires regularly at a rate of 150-250 beats per minuteto 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 beatsper minute. If the rate is below 150 bpm, it is considered a slow VT. If the rateexceeds 250 bpm, its called Ventricular Flutter. P Wave: None of the QRS complexes will be preceded by P waves; you may seedissociated 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.
Ventricular Fibrillation Multiple foci in the ventricles become irritable and generate uncoordinated, chaoticimpulses that cause the heart to fibrillate rather than contract. Regularity: There are no waves or complexes that can be analyzed to determineregularity. The baseline is totally chaotic. Rate: The rate cannot be determined since there are no discernible waves orcomplexes to measure. P Wave: There are no discernible P waves. PRI: There is no PRI. QRS: There are no discernible QRS complexes.
II.. Impulse generation disordersImpulse generation disorders145.5 -145.5 - Sinus ArrestSinus Arrestoccurs when the sinus node stops firing. If nothing elseoccurs when the sinus node stops firing. If nothing elsewere to happen, the ECG would show a flat line withoutwere to happen, the ECG would show a flat line withoutany 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..
II.. Impulse generation disordersImpulse generation disorders145.5 -145.5 - Escape BeatsEscape BeatsAtrialAtrialFrom AV nodeFrom AV nodeVentricularVentricularSlowSlowFastFast
Premature beatsPremature beats ((early depolarisationearly depolarisation ))149.1149.1 atrialatrial;;149.2149.2 from AV nodefrom AV node;;149.3149.3 ventricularventricular
147.1147.1 -- tachicardiatachicardia::•• reciprocalreciprocal •• chronicchronic•• focalfocal •• paroxysmalparoxysmal((ectopicectopic))-- supraventricularsupraventricular ::•• from SA nodefrom SA node;;•• atrialatrial;;•• from AV nodefrom AV node::
147.1147.1 -- tachicardiatachicardia::•• from AV nodefrom AV node::nodal • regular type• irregular typeWith additional pathways:• orthodromic• antidromic
-ventricular:147.2 unstable (from 3 complexes to 30 sec);147.2 stable (more then 30 sec);147.0 ever-reccurent.• monomorphic• polymorphic
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
149.0 - fibrillation and flutter of ventricles
II. CONDUCTION BLOCKS:145.5 - SA block;144.0 • І degree.144.1 • II degree. Type ІType II144.2 • III degree – full .
AV Block 2 First Degree The AV node selectively conducts some beats while blocking others. Those that arenot blocked are conducted through to the ventricles, although they may encounter aslight 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, andthe 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, theventricular rate will usually be in the bradycardia range, often one-half, one-third, orone-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
AV Block 2 Second Degree As the sinus node initiates impulses, each one is delayed in the AV node a littlelonger 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
Third Degree Heart Block The block at the AV node is complete. The sinus beats cannot penetrate the nodeand thus are not conducted through to the ventricles. An escape mechanism fromeither the junction or the ventricles will take over to pace the ventricles. The atria andventricles function in a totally dissociated fashion. Regularity: Regular Rate: Atrial rate is usually normal (60-100bpm); ventricular rate: 40-60 if the focus isjunctional, 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 canoccasionally be found superimposed on the QRS complex. QRS: Less than .12 seconds if the focus in junctional, .12 seconds or greater if thefocus is ventricular.
Asystole The heart has lost its electrical activity. There is no electrical pacemaker to initiateelectrical 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.
II. CONDUCTION BLOCKS:- AV block:144.0 • І degree.144.1 • II degree. Type ІType II144.2 • III degree.
II. CONDUCTION BLOCKS:-Bundle branch block-Single branch: 145.0 - RBBBLeft anterior hemi block LAHB- Left posterior hemi block LPHB
II. CONDUCTION BLOCKS:-Intraventricular blockTwo branch block:LBBBRBBB+LAHB- RBBB+ LPHB (same as LPHB and angle alpha >120)
II. CONDUCTION BLOCKS:-Intraventricular blockLBBBRBBB145.3 Trifascicular
III.III. COMBINED DISORDERSCOMBINED DISORDERSparasystoleparasystole1) atrial1) atrial2) From AV node2) From AV node3) ventricular3) ventricular
Frederic syndrome:1) AV block III degree;2) Atrial fibrillation.
Quiz Yourself Name the Rhythm # 1:
Answer: Atrial Flutter
Name the Rhythm #2:
Name the Rhythm #3:
Third Degree Heart Block
Name the rhythm # 4:
Name the rhythm #5:
Name the rhythm #6:
AV Block 2 First Degree
Name the rhythm # 7:
Name the rhythm # 8:
Name the rhythm # 9:
Name the rhythm # 10:
AV Block 2 Second degree
Name the rhythm # 11:
A female patient, aged 43, complains of palpitation,that suddenly appeared after physical exertion,dyspnea and dull pain in the heart area. Over the 12years she is under a follow-up care because ofrheumatism and mitral stenosis without anyessential 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 disorderis the most probable?
Patient F., aged 42, suddenly developedpalpitation attack attended by generalweakness, dyspnea, HR - 170 per min.ЕCG: number of heart beats – 180 permin, rhythm regular, QRS - 0,10 s. Aftermassage of carotid sinus area decrease ofheart beats to 75 beats per min wasobserved. What rhythm disorder wasregistered in the patient?
Patient, 35 of age, on strenuous exercisefell suddenly unconscious; is ailing withhypertrophic cardiomyopathy. On anexamination: breath aperiodic,stentorious, Pulse and heart tones cannotbe detected. АP 50/20 mm Hg. On ECG –chaotic contractions. What has thepatient?
Woman, 64 of age, complains of intermittency inthe heart activity, palpitation, performancedecrement, general weakness. Over the fewmonths she remarks recrudescence. After ashort-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. PQinterval — 0,20 s., QRS— 0,08 s. Slowlydecreasing of R—R interval with followingРQRSТ-fallout. What is the most probablecause of this condition?
Sinoatrial block; Atrioventricular block І degree;Atrioventricular block, II degree; Atrioventricular block; III degree;Trifascicular heart block.
Patient K., aged 50, with large-focalmyocardial infarction of the anteroseptalarea suddenly felt sharp weakness andstaggers. АP 160/90 mm Hg. Heart tonessharply muffeled. Pulse rhythmic 32 permin. On ECG dissociation between atrialand ventricular activity. Call the mostprobable clinical setting:
Solve each case, the extent to which theSolve each case, the extent to which therisk of treatment outweighs the risk of therisk of treatment outweighs the risk of theexistence of the arrhythmiaexistence of the arrhythmia Introducing antiarrhythmic drugs inIntroducing antiarrhythmic drugs insufficient therapeutic dosessufficient therapeutic doses Monitoring for complicationsMonitoring for complicationsPrinciples of antiarrhythmicPrinciples of antiarrhythmictherapytherapy
Factors that determine theFactors that determine thetreatment programtreatment programarrhythmiasarrhythmias hemodynamic status at the time ofhemodynamic status at the time oftermination 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 thepast or the method that was used to treatpast or the method that was used to treat..
The degree of severity of structural heart diseaseThe degree of severity of structural heart diseaseand its potential impact on risk and effectivenessand its potential impact on risk and effectivenessof antiarrhythmic therapyof antiarrhythmic therapyDegrees Characteristics of heart disease Risk Efficiency1 Structural pathology without affecting theventricle: mitral valve prolapse withoutregurgitation or violations of repolarization,additional AV conduction paths, moderatemitral stenosis+++++ +2 Minimum left ventricular dysfunction,moderate hypertrophy or overloadcapacity without severe LV dilatation++++ ++3 Myocardial damages without stagnantphenomena or severe LV systolicdysfunction+++ +++4 Severe left ventricular hypertrophy ++ ++++5 Congestive heart failure, severe leftventricular systolic dysfunction, severeischemia+ +++++
I. Membrane stabilizers, oppress quick Na + channels, blockingNa + entry into the cell during the 0-phase of the action potential---> reduce speed of conducting:IА - moderate repressor 0-phase, extending QRS, prolongation ofaction 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 - impracticalventricular tachycardia and fibrillation - + in 35% of casesatrial fibrillation +++reciprocal supraventricular tachyarrhythmias +++Additional conduction pathways +++Classification AAD (E.Vaughan Williams1979) with additions D.Harrison (1985)
IB - weak repressor 0-phase, less than Ia, affecting theQRS and conductivity, accelerate repolyaryzation,shortening QT, greatly increase the threshold ofventricular fibrillation (lidocaine, trimecaine, meksytylen(meksytyl), tocainide, diphenyl (phenytoin, diphenine,dylantyn)ventricular extrasystoles +++ventricular tachycardia and fibrillation +++IC - strong repressors 0-phase, extending QRS isuppress conduction in small concentrations, little effecton rate of repolarization, duration QT i refractory period(flekainid, morytsyzyn (etmozyn) Etacizin, alapinin,propafenone (rytmonorm) tsybenzolin) ventricular extrasystoles +++Classification AAD
IА – moderate slowdown in the rate ofdepolarization and repolarization;IB - minimum deceleration depolarization andrepolarization accelerated;IC - maximum deceleration rate of depolarizationand minimal impact on repolarization.Classification AAD
II. Beta-blockers with blocking effects of catecholamines,decreased atrial and ventricle automaticity, decreasedAV-and / ventricular conduction, increase refractoryperiod, the effect in cases of oppression andsuppression of automaticity reciprocal tachycardias if thecircuit 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
III. Drugs with primary antyadrenergic effect - blockersof K + channels also prolong action potential andrepolarization, QT interval , increases duration ofrefractory period (amiodarone (CORDARONE,amiokordyn), sotalol (hilukor) bretilium (ornid),dofetilide, ibutylid, sematylid, azymilid, nibentan).atrial extrasystole +++ventricular extrasystoles +++automatic and reciprocal supraventriculartachyarrhythmias +++atrial fibrillation +++ventricular tachycardia and fibrillation +++additional pathways +++Classification AAD
IV. Calcium channel blockers - inhibittransmembrane flow of calcium ions in the areas ofSA- and AV-node, reduce the spontaneous activityof SA-node affect the mechanism of re-stimulation,inhibit 4-th phase of depolarization, reduces thetransmembrane resting potential, prolong therefractory period of these zones (verapamil(finoptyn) hallopamil (prokorum), diltiazem (dylzem,dyltysan, kardil) bepredyl (kordium).supraventricular arrhythmias +++Classification AAD
Classification AADThe Task Force of the Working Group on Arrhythmias of the European Society of Cardiology: TheSicilian Gambit (Circulation 1991; 84: 1831-1851. )
Ventricular arrhytmiasVentricular arrhytmias Ventricular fibrillationVentricular fibrillation;; Resistant ventricular paroxysmal tachycardiaResistant ventricular paroxysmal tachycardia ((monomonoand polymorphic)and polymorphic);; ventricular paroxysmal tachycardia in patients withventricular paroxysmal tachycardia in patients withMIMI;; Often, doublet, polymorphic premature ventricularOften, doublet, polymorphic premature ventricularbeats in patients with MIbeats in patients with MI..Rhythm disturbances requiredemergency care
Rhythm disturbances requiredRhythm disturbances requiredemergency careemergency care SA blockadeSA blockade,, SA node weak syndromeSA node weak syndrome withwithsyncopesyncope,, 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..
Supraventricular paroxysmalSupraventricular paroxysmaltachicardiastachicardias ReciprocalReciprocal tachycardia from AV nodetachycardia from AV node,, working onworking on„re-entry”„re-entry” mechanismmechanism ((Retrograde P waves often areRetrograde P waves often arenot detected, or placed over QRS, or seen after QRSnot detected, or placed over QRS, or seen after QRSwith short intervals RP (RP <50% RR). Impulse passeswith short intervals RP (RP <50% RR). Impulse passesthrough anterograde in slow path and retrograde inthrough anterograde in slow path and retrograde inquick path , atrium and ventricle simultaneouslyquick path , atrium and ventricle simultaneouslyexcited.excited.
Supraventricular paroxysmalSupraventricular paroxysmaltachicardiastachicardias orthodromicorthodromic supravenrticular tachycardia arises withsupravenrticular tachycardia arises withthe existence of additional path (syndrome WPW) withthe existence of additional path (syndrome WPW) withconduction through the AV anterograde on theconduction through the AV anterograde on theventricles and then retrograde back through anventricles and then retrograde back through anadditional way in atrium, recorded retrograde P wavesadditional way in atrium, recorded retrograde P waveswith short intervals RP (RP <50% RR), negative P in Iwith short intervals RP (RP <50% RR), negative P in Ilead, the delta wave is absent because the ventricleslead, the delta wave is absent because the ventriclesare activated via AV-zoneare activated via AV-zone..
Supraventricular paroxysmalSupraventricular paroxysmaltachicardiastachicardias Antidromic supraventricular tachycardia rarely occurAntidromic supraventricular tachycardia rarely occurand 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 throughan additional path to the ventricles, followed by thean additional path to the ventricles, followed by thereturn 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 activationoccurs through an additional path is similar to anoccurs through an additional path is similar to anelectrocardiogram of ventricular tachycardiaelectrocardiogram of ventricular tachycardia ..
AdenosinAdenosin AdenosinAdenosin 66 mgmg,, ATFATF 10-2010-20 mgmg ii//vv duringduring5-105-10 secsec;; Quick effectQuick effect,, short half-lifeshort half-life Do not changeDo not change blood pressureblood pressure andandcontractilitycontractility Caution in patients with SA node weakCaution in patients with SA node weaksyndromesyndrome
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 activityof atriumsof atriums;; Prolongs PQ intervalProlongs PQ interval,, decrease refractory of additional pathwaydecrease refractory of additional pathway,, forforWPW syndrome lead to fibrillationWPW syndrome lead to fibrillation..
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 2-3times per daytimes per day):): reduces automaticity, increases arousal threshold, increasesreduces automaticity, increases arousal threshold, increaseseffective 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 WPWsyndromesyndrome;; 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, renalfailure (decrease output novokainamide)failure (decrease output novokainamide)..
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.
Strategy for the treatment ofStrategy for the treatment ofpatients with atrial fibrillationpatients with atrial fibrillationTasksTasks reduction of clinical symptomsreduction of clinical symptoms;; prevent complications (stroke, heart failure, myocardial infarction), whichprevent complications (stroke, heart failure, myocardial infarction), whichcan 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..
Patient with AFRestoration of heartrhythm (Cardioversion):•Drug Cardioversion•Electrical CardioversionTherapies aimed atpreventing therecurrence of AFPrevention ofthrombo-embolicdisordersRhythmcontrolCatheterablationStrategy for the treatment of patients withatrial fibrillation
Benefits of restoration andBenefits of restoration andpreservation of sinus rhythmpreservation of sinus rhythm reduction of clinical symptoms caused byreduction of clinical symptoms caused byarrhythmiaarrhythmia;; 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 thromboemboliccomplicationscomplications..
Problems restoring andProblems restoring andmaintaining sinus rhythmmaintaining sinus rhythm low efficiency of most antiarrhythmic drugs, and thelow efficiency of most antiarrhythmic drugs, and thenecessity 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, mostpronounced 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 manyelderly patientselderly patients;; high cost of antiarrhythmic drugshigh cost of antiarrhythmic drugs..
Diseases and conditions under which theDiseases and conditions under which therecovery rate at a constant atrialrecovery rate at a constant atrialfibrillation 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 ofcommissurotomycommissurotomy.. 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 forpatients with IHDpatients with IHD.. Duration of atrial fibrillation over 3 yearsDuration of atrial fibrillation over 3 years..
Control of heart rate withoutControl of heart rate withoutrestoring sinus rhythmrestoring sinus rhythmBenefitsBenefits 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 sinusrhythmrhythm 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 withinadequate rate controlinadequate rate control;; incomplete elimination of clinical symptomsincomplete elimination of clinical symptoms;; reduced quality of lifereduced quality of life
Pharmacological therapy ofPharmacological therapy ofpatients with firs time AFpatients with firs time AFFirst time Atrial FibrillationParoxysmalPersistentTherapy no neededif no hypotension,heart failure, anginaAnticoagulanttherapy if riskfactors of embolismpresentConsider apermanent form ofatrial fibrillationAnticoagulanttherapy and ratecontrolAnticoagulanttherapy and ratecontrol if neededConsider drugtherapyCardioversionNo need for long-term drug therapy
Drug CardioversionCardioversionDrugDrug ClassClassLevelLevelDosageDosageDrugs with recognized efficacyDrugs with recognized efficacyDofetilideDofetilide I / AI / A 125-500125-500 mcgmcg 22 dailydailyFlecainideFlecainide I / AI / A 200-300200-300 mgmg oraloral; 1,5-3,0; 1,5-3,0 mgmg//kgkg ii//vvIbutilideIbutilide I /AI /A ii//vv 11 mgmg perper 1010 minmin,, if necessary againif necessary again 11mgmgPropafenonePropafenone ** I / AI / A OralOral 600600mgmg;; ii//vv 1,5-21,5-2mgmg//kgkg perper 10-2010-20minminAmiodaroneAmiodarone ** IIa/AIIa/A ii//vv:: 5-75-7 mgmg//kgkg perper 30-6030-60 minmin,, thenthen toto 1,2-1,81,2-1,8gg//dayday ii//vv or oral up toor oral up to 1010 gg,, thenthen 200-400200-400mgmg//dayday –– support dosagesupport dosageLess efficacyLess efficacy //insufficiently studiedinsufficiently studiedDisopiramideDisopiramide IIb /BIIb /B OralOral toto 300300 mgmgProkainamideProkainamide IIb /BIIb /B OralOral toto 3,0-4,03,0-4,0 ggQuinidineQuinidine IIb /IIb /ВВ OralOral 0,75-1,50,75-1,5 gg perper 6-126-12 hhDo not useDo not useDigoxin SotalolDigoxin Sotalol* - can used ambulatory, after safety control in hospital
Electrical CardioversionCardioversion•Synchronized discharges (QRS on ECG)•General anesthesia•Fasting•Output power level 200 joules, then 360 joules•In early relapse after EC maybe a re-EC at background drugtherapy (amiodarone, sotalol)
Prevention of recurrence of paroxysmal or persistent AF)Heart disease?No or mildPropafenonSotalolFlecainideAmiodaroneDofetilideCatheterablationHF CADSotalolDofetilideACC/AHA/ESC 2006 Guidelines for the management… of AF.-EHJ-2006-27-p.1979-2030AmiodaroneDofetilideCatheterablation AmiodaroneCatheterablationAHLVG++ LVG-/+PropafenonSotalolFlecainideAmiodaroneDofetilideCatheterablation
AmiodaroneAmiodarone ((tabtab. 200. 200 mgmg,, ampamp. 150. 150 mgmg daily dose ivdaily dose iv 150-300150-300 mgmg.. The drug isThe drug ismost effective antiarrhythmic, for a long time still means third-linemost effective antiarrhythmic, for a long time still means third-lineantiarrhythmic 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, inAV 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, ventricularfibrillationfibrillation;; Contraindicated in case of increasing of interval QT, thyroidContraindicated in case of increasing of interval QT, thyroiddysfunction, chronic lung diseasesdysfunction, chronic lung diseases..
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 forcumulation)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 ofthe 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 periodan 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, ventriculararrhythmia. 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, acutepsychosispsychosis; 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.
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, tripledcarefully at constant elektrokardiostymulationcarefully at constant elektrokardiostymulation;; may increase the action potential, strengthen themay increase the action potential, strengthen theeffect of beta-blockerseffect of beta-blockers;; with increased action potential leads to decreasewith increased action potential leads to decreasein the rate of (treatment of arrhythmias within the rate of (treatment of arrhythmias withadditional conduction ways)additional conduction ways);; prolong the interval PQ, QRS complexprolong the interval PQ, QRS complex..
Beta - blockersBeta - blockers Propranolol (anaprylin) nonselective beta-blocker withoutPropranolol (anaprylin) nonselective beta-blocker withoutsympathomimetic activity with membrane stabilizing action in dosesympathomimetic activity with membrane stabilizing action in dose10 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 mgper 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 effectspredominate over other beta-blockers, which causedpredominate over other beta-blockers, which causedelectrophysiological effects of antiarrhythmic drugs II and IIIelectrophysiological effects of antiarrhythmic drugs II and IIIclassesclasses..
Paroxysmal tachycardia with WPW syndromeParoxysmal tachycardia with WPW syndromeand wide QRSand wide QRS
Variations paroxysmal VT (A -Variations paroxysmal VT (A -tachycardia "Torsades de pointes",? B -tachycardia "Torsades de pointes",? B -syndromal tachycardia with prolongedsyndromal tachycardia with prolongedQT)QT)
Treatment of VT with antiarrhythmic drugsTreatment of VT with antiarrhythmic drugsН а з в а н и е д и а г р а м м ыA m io d a r o n eN o v o c a in a m id eM o n o f o c a l V TC a r d ia c S t im u la t io nM a g n iu mE le c t r o ly t e sD is c o n t in u in g A A DP r o lo n g e d Q TA m io d a r o n eL id o c a in eB e t a - b lo c k e r sN o r m a lQ TM u lt if o c a l V TA m io d a r o n eA FV e m t r ic u la r a r r h y t m ia s
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 thisintramuscularly)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 ventricularfibrillationfibrillation;; contraindicated in combination with quinidine, sic sinuscontraindicated in combination with quinidine, sic sinussyndrome in old age, blockadessyndrome in old age, blockades..
Big-(A) and small wave (B) ventricularBig-(A) and small wave (B) ventricularfibrillationfibrillation
CPR: initial stageCPR: initial stageА.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 andabove the apex of the heart on the frontabove the apex of the heart on the frontaxillary lineaxillary line))
CPR: Secondary StageCPR: Secondary StageА.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. orvasopressin 40 U oncevasopressin 40 U once 360 Joules defibrillation 360 Joules defibrillation
Ventricular fibrillation and effectiveVentricular fibrillation and effectivedefibrillationdefibrillation