Cardiac rhythm disturbance

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Cardiac rhythm disturbance

  1. 1. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 1CARDIAC RHYTHM DISTURBANCE2013MAGDI AWAD SASI
  2. 2. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 2Normal Sinus RhythmImplies normal sequence of conduction, originating in the sinus node andproceeding to the ventricles via the AV node and His-Purkinje system.EKG Characteristics: Regular narrow-complex rhythmRate 60-100 bpmEach QRS complex is proceeded by a P waveP wave is upright in lead II & downgoing in lead AvrP wave should be present, lead 2,v1, positive deflection, single one p followedby one QRS , fixed shape within normal 2.5 width and 2.5 height (2x2), fixedP-R within normal max 0.2 sec.
  3. 3. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 3Rhythm Of The HeartThe Heart is Like an Orchestra.It has a conducting systemthat is directed by aconductor.This conductor is the“Natural Pacemaker” of theHeart.Conducting System:- SA node (PrimaryPacemaker)- AV node- Bundle of His- Purkinje Fibers• Sino-Atrial node (SA Node)-Origination and dissemination of electrical signals to BOTH atria-Causes BOTH atria to contract• Atrioventricular Node (AV Node)-Transmits signal to ventricles by going through interventricular septum-Causes intentional delay, to allow atria to complete pumping• His Purkinje System-Electrical signal flows through the His-Purkinje system and causes theventricles to contract SIMULTANEOUSLY
  4. 4. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 4Normal ECGNormal EKG:1. Regular Rate –-----heart rate of 60-100 bpm2. Regular Rhythm – P – QRS – T – P – QRS – T – P – QRS – T - etc3. The height of the wave – related to the mass of the musclegenerating the wave- The ventricles have more mass than the atria:-large ventricles (ventricular hypertrophy)  more muscle creating astronger signal when the ventricles contract:
  5. 5. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 5ATRIAL FIBRILLATIONAF results from random chaotic depolarization of the atria leading to anirregularly, irregular tachycardia with irregular ventricular response.Atrial rate usually 400-700 beat/minutes but ventricular rate is limited bythe refractory period at the AV node, so ventricular rate ranges from 140-170 beat/minutesIn about one-third of patients with this arrhythmia, the patient is notaware of so-called ‘asymptomatic AF’.The prevalence of AF increases with age, from <0.5% at 40–50 years, to 5–15% at 80 yearsPathophysiology�No organized atrial electrical activity leads to loss of atrial contraction.�Leads to loss of atrial kick with resultant decrease in ventricular filling�This loss of contraction can lead to stagnation of blood in atrium andcan promote thrombus formation�This thrombus can then be dislodged into the systemic circulation whenAF converts to sinus rhythm leading to thromboembolic complications
  6. 6. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 6Mechanisms of atrial fibrillation (AF)–Dynamic interactions between atrial and ventricular function during atrial fibrillation (AF).Iwasaki Y et al. Circulation 2011;124:2264-2274Copyright © American Heart Association
  7. 7. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 7Inducing ectopic firing. A - Enhanced automaticity. B- EADs. C- DADs.EAD indicates early after depolarizations; DAD, delayed after depolarization;RyR, ryanodine receptor; and AP, action potentialEpidemiology� most common arrhythmia encountered in clinical practiceAffects more than 2.3 million Americans�Approximately 15-25% of all strokes in US can be attributed to AF�Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia,occurring in 1–2% of the general population. Over 6 million Europeans sufferfrom this arrhythmia, and its prevalence is estimated to at least double in thenext 50 years as the population ages�The lifetime risk of developing AF is ∼25% in those who have reached the ageof 40year.�AF account for one-third of all admissions for cardiac arrhythmias.�Left ventricular (LV) function is often impaired by the irregular, fastventricular rate and by loss of atrial contractile function and increased end-diastolic LV filling pressure. Both rate control and maintenance of sinus rhythmcan improve LV function in AF patients.Classification��Paroxysmal AFEpisodes that lasts less than 7 daysTerminate spontaneously��Persistent AFEpisodes lasting more than 7 daysRequire either pharmacologic or electrical intervention to terminate��Permanent AFContinuous AF that has failed cardioversion��Lone AFIn individuals without structural or cardiac diseaseLow risk for thromboembolism
  8. 8. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 8Causes:A/Cardiac causes-CardiomyopathyRheumatic heart disease-mitral stenosis/regurgitation, aortic regurgitatonCoronary heart diseaseAtrial septal defectHypertensionB/Non cardiac causesThyrotoxicosisObesity, Diabetes mellitusChronic obstructive pulmonary disease, Sleep apneaPulmonary embolism/ pneumonia/lung cancer.
  9. 9. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 9CLINICAL FEATURES:Asymptomatic, discover that they have atrial fibrillation at a doctor’sappointment. Even without symptoms, atrial fibrillation is a serious medicalcondition.Others present with acute left ventricular failure symptoms if the atrialcontraction is mandatory for cardiac cycle in conditions with high endintraventricular diastolic pressure i.e. aortic stenosis, HOCM, hypertension ormitral stenosis.Others present with dyspnea, palpitation, syncopy, chest pain or according tounderlying cause symptomatic presentation.Chest discomfort or painFainting or light-headednessFatigue, shortness of breath, or weaknessAtrial Fibrillation: Screening Procedures All patients– History– Physical examination– ECG– Echocardiogram– CBC, Thyroid function Many/most patients– Exercise stress test– Holter monitor Selected patients– Chest x-ray– Invasive procedures
  10. 10. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 10Risk FactorsTo help prevent atrial fibrillation, some risk factors may be controlled or modified.Controllable Risk FactorsHigh cholesterolHigh blood pressureHeart diseaseSmokingExcess weightCaffeineAlcohol abuseLack of exerciseSome medicationsSleep apneaNon-controllable Risk FactorsFamily historyAdvancing ageHeart disorders from birthAtrial Fibrillation: Clinical ProblemsEmbolism and stroke (presumably due to LA clot)Acute hospitalization with onset of symptomsAnticoagulation, especially in older patients (> 75 yr.)Congestive heart failureo Loss of AV synchronyo Loss of atrial “kick”o Rate-related cardiomyopathy due to rapid ventricular responseRate-related atrial myopathy and dilatationChronic symptoms and reduced sense of well-beingECG��Results from random chaotic depolarization of the atria��No organized electrical activity��No real P waves��Irregular ventricular rhythm��Ventricular rate may be fast or slow
  11. 11. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 11The Major Goals in treating Atrial Fibrillation are:Relieve AF symptoms and improve patient’s quality of lifePrevent blood clots to decrease the risk of strokeControl the heart rate to allow the ventricles enough time to fill withbloodRestore the heart rhythm to allow the atria and ventricles to worktogether more efficientlyTREATMENT:stableRate controlAnticoagulationConversion to and maintenance of sinus rhythm.IF A PATIENT PRESENTS WITH A.F.,ANSWER 4 QS:1. Is he/she haemodynamically stable?2. Weather to control the rate or rhythm ?3. What is the underlying cause ?4. Is there an indication for anticoagulation ?Urgent cardioversion W/ defibrillator: if hemodynamic instability, hypotension,angina, heart failure , confusion due to low cardiac output ,no urine.If cardioverting, ensure R-wave synchronization with electrical cardioversion toprevent “R-on-T” shock which can induce Ventricular fibrillation.
  12. 12. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 12There is also a role in the management of recent or new onset AF for electivecardioversion when the patient is hemodynamically stable and one wishes totry to bring them out of the arrhythmia if AF IS ACUTE AND LESS THAN 72 HRS,OR TO BE ON WARFARIN FOR 4 WEEKS TO RAISE INR 2 TIMES NORMAL AND TODO CARDIOVERSION.RHYTHM COTROL- Synchronized DC cardioversion and pharmacologic cardioversion > 48 hours, or <48 hrs with mitral stenosis or history of emboli – you mustanticoagulate 3-4 weeks of INR at 2-3 Unless – TEE has excluded thrombi If unstable –DC cardioversion If stable and correction of underlying problem does not help – eitherchoiceA. DC cardioversion – 75-93% successfulDepends on atrial size and duration of AFB. Drugs – 30-60% successful<7 days – dofetilide, flecainide, ibutilide, propafenone>7 days – dofetilide AGENT: III: Amiodarone, Ibutilide, Dofetilide, Sotalol IC: Flecainide, Propafenone IA: Procainamide RHYTHM CONTROLADVANTAGES Avoids electrical and anatomical remodeling Improves hemodynamics Enhanced exercise capacity Symptom relief Improves Quality Of Life Restores atrial transport Reduces thromboembolic events?
  13. 13. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 13DISADVANTAGESVentricular proarrhythmiaIncreased mortality?Drug-induced bradyarrhythmiasAdverse effectsRecurrences are likelyAF Antiarrhythmic Therapy• Treatment goals– ↓ frequency of recurrences– ↓ duration of recurrences– ↓ severity of recurrences– Not to abolish every episode• Safety is primary concern• Minimize risk of proarrhythmiaAfter cardioversion;Only 20-30 percent of patients stay in sinus for >1 year.When to Consider Antiarrythmics ? Don’t in patients with AF less than 1 year, no atrial enlargement,reversible cause Consider it in patients with high risk of recurrence Risks generally outweigh benefits. Amiodirone – good, but high toxicity profile, used in patients withbad heart disease (significant systolic dysfunction, hypertensionwith LVH) Toxicity – pulmonary, photosensitivity, thyroid dysfxn,corneal deposits, ECG changes, Liver dysfunction.RATE CONTROLo Essential in all patients.o Persistent tachycardic rates can induce cardiomyopathy and heart failure.o Occasional follow-up holter monitor to ascertain rate control.o Achieved by slowing AV conduction (beta blockers, CCB, dig, amiodarone)o Digoxin only in hypotension and Heart Failureo Amiodirone – rarely but effective
  14. 14. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 14Agents: Beta Blocker: Metoprolol and Propranolol (ICU=esmolol ) Non-dihydropyridine CA blockers: verapamil & Diltiazem (ICU=diltiazem ) Digoxin Goal: Rest 60-80 bpm and Activity 80-110 IV Amiodarone (in the ICU setting) Electrical ablationRATE CONTROL; Which Agent to choose? Estimated risk of stroke is determined with a CHADS2 score and therapydetermined with this scale of 1-6. (CHF, HTN, Age, DM, Secondaryprevention) 0 get ASA because of 0.5%/year w/o coumadin 1-2 intermediate risk > or = 3 warfarin P.S. – ASA usually added to warfarinAnticoagulation during reversion to NSR AF >48 hrs or unknown Anticoagulate for >3 weeks, INR 2-3
  15. 15. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 15 Or, TEE to evaluate for clots in LA Appendage – if no clots – convert. After, anticoagulate for 4 weeks with warfarin – “stunned atrium”Consider chronic anticoagulation for those with high risk for reversion
  16. 16. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 16Multifocal Atrial Tachycardia (MAT):• Multiple ectopic focuses fire in the atria, all of which are conductednormally to the ventricles• QRS complexes are almost identical to the sinus beats• Rate is usually between 100 and 200 beats per minute• The rhythm is always IRREGULAR• P-waves of different morphologies (shapes) may be seen if the rhythm isslow• If the rate < 100 bpm, the rhythm may be referred to as“wandering pacemaker”• Commonly seen in pulmonary disease, acute cardiorespiratory problems,and CHF.• Treatments:1. Ca++channel blockers2. B blockers3. potassium4.magnesium,• supportive therapy for underlying causes (antiarrhythmic drugs areoften ineffective)
  17. 17. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 17Atrial Flutter:• A single ectopic macroreentrant focuses fire in the atria causing the“fluttering” baseline Classic inverted ,“sawtooth” ,flutter waves.• AV node cannot transmit all impulses (atrial rate: 250 –350 per minute)• ventricular rhythm may be regular or irregular and range from 150–170 beats / minute• A-fibrillation and A-flutter rhythm may alternate – these rhythms mayalso alternate with SVT’s• May be seen in CAD (especially following surgery), VHD, history ofhypertension, LVH, CHF• Treatment:• DC cardioversion if patient is unstable• Drugs: (goal: rate control) Ca++channelblockers to delay AVconduction• Amiodarone to delay AV conduction + prolong myocardial AP(refractoriness of myocardium)• The danger of thromboembolic events is also high in A-flutter.
  18. 18. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 18Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT):• A single reentrant ectopic focuses fires in and around the AV node, all ofwhich are conducted normally to the ventricles (usually initiated by aPAC)• QRS complexes are almost identical to the sinus beats• Rate is usually between 150 and 250 beats per minute• The rhythm is always REGULAR• Possible symptoms:palpitations, angina, anxiety, polyuruia, syncope .• Prolonged runs of PSVT may result in atrial fibrillation or atrial flutter• May be terminated by carotid massage• carotid pressure - baroreceptor firing rate –to increase vagal toneby valsalva maneuver ,gag reflex, eye ball massage.Treatment:Ablation of focus, Adenosine (delay AV conduction), Ca++Channel blockersAV nodal reentrant tachycardia (AVNRT)AV reentrant tachycardia (AVRT)– Orthodromic– Antidromic
  19. 19. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 19PVCA premature ventricular contraction (PVC), also known as a prematureventricular complex, ventricular premature contraction (or complex orcomplexes) (VPC), ventricular premature beat (VPB), or extrasystole, is arelatively common event where the heartbeat is initiated by the heart ventriclesrather than by the sinoatrial node, the normal heartbeat initiator. The electricalevents of the heart detected by the electrocardiogram allow a PVC to be easilydistinguished from a normal heart beat.PVC- bizarre , wide , not preceded by P wave, QRS reverse T waveCausesIschemiaCertain medicines such as digoxin, whichincreases heart contractionMyocarditisCardiomyopathy, hypertrophic or dilatedMyocardial contusionHypoxiaHypercapnia (CO2 poisoning)Sarcoidosis[citation neededMitral valve prolapseSmokingAlcoholDrugs such as cocaineCaffeineTheobromine[citation neededTricyclic antidepressantsMagnesium and potassium deficiencyCalcium excessThyroid problemsChemical (electrolyte) problems in the bloodHeart attackAdrenaline excessLack of sleep/exhaustionStress
  20. 20. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 20PVCs may be unifocal , multifocal or multiformed. Multifocal PVCs havedifferent sites of origin, which means their coupling intervals (measured fromthe previous QRS complexes) are usually different. Multiformed PVCs arecommon in digitalis intoxication.PVCs may occur as isolated single events or as couplets, triplets, and salvos (4-6PVCs in a row), also called brief ventricular tachycardia’s.
  21. 21. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 21PVCs may occur early in the cycle (R-on-T phenomenon), after the T wave , orlate in the cycle - often fusing with the next QRS (fusion beat). R-on-T PVCs maybe especially dangerous in an acute ischemic situation, because the ventriclesmay be more vulnerable to ventricular tachycardia or fibrillation."Late" (end-diastolic) PVCs are illustrated with varying degrees of fusion. Forfusion to occur the sinus P wave must have made it to the ventricles to start theactivation sequence, but before ventricular activation is completed the "late"PVC occurs. The resultant QRS looks a bit like the normal QRS, and a bit like thePVC; i.e., a fusion QRS.What is the risk of VPCS?It depends on:a. Frequency of VPCSb. Form of VPCS_ uniform, multiform, salvosVPCS IN ACUTE SYNDROMES:1. Myocarditis/percarditis2. Myocardial reperfusion-PRINZEMATALS ANGINATHROMBOLYSIS IN MI, BALLON DEFLATION IN PTCAc. Transient ischemic events
  22. 22. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 22Ventricular tachycardia(V-Tach or VT) is a tachycardia, or fast heart rhythm, that originates in one ofthe ventricles of the heart. This is a potentially life-threatening arrhythmiabecause it may lead to ventricular fibrillation, a systoles, and sudden death.VT is defined as three or more consecutive ventricular ectopic impulses at arate 120/minutes or greater.By ECG, rapid broad often bizarre QRS complexes with T waves usually oppositein direction to the main QRS deflection and with rate /min or more.VT can be defined by duration or ECG pattern.Ventricular tachycardia can be classified based on its morphology:A. Monomorphic ventricular tachycardia means that the appearance of all thebeats match each other in each lead of a surface electrocardiogram (ECG).
  23. 23. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 23B. Polymorphic ventricular tachycardia, on the other hand, has beat-to-beatvariations in morphology. This most commonly appears as a cyclical progressivechange in cardiac axis, previously referred to by its French name torsades depointes ("twisting of the points"). However, currently the term torsades depointes is reserved for polymorphic VT occurring in the context of a prolongedresting QT interval.
  24. 24. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 24Another way to classify ventricular tachycardias is the duration of the episodes:1. Non-sustained V. T__ the fast rhythm self-terminates within 30 seconds.2. Sustained V.T. the rhythm lasts more than 30 seconds, (even if it terminateson its own after 30 seconds).VT CAN BE:d. Bigiminy, trigiminy.e. Couplet , triplet.f. Salvos-uniform morphology VT-3 to 5 v.ectopics.Descriptors to consider when considering ventricular tachycardia:Sustained (lasting >30 sec) vs. nonsustainedMonomorphic (uniform morphology) vs. polymorphic vs. Torsade-d.p.
  25. 25. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 25Torsade-de-pointes: a polymorphic ventricular tachycardia associatedwith the long-QT syndromes characterized by phasic variations in thepolarity of the QRS complexes around the baseline. Ventricular rate isoften >200bpm and ventricular fibrillation is a consequence.Presence of AV dissociation (independent atrial activity) vs. retrogradeatrial capturePresence of fusion QRS complexes (Dressler beats) which occur whensupraventricular beats (usually sinus) get into the ventricles during theectopic activation sequence.What is the risk?Depends oni. Structural heart diseaseii. Ejection fractureSymptoms:palpitation, SOB, chest, syncopeD/D OF WIDE QRS TACCHYCARDIA:SVT with LBBBSVT with RBBBWolf Parkinson white syndromeHyperkalemiaAF with preexcitationPacemaker mediated tachycardiaSVT with aberrant conduction
  26. 26. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 26Ventricular fibrillation is life-threatening.Ventricular fibrillation (v-fib for short) is the most serious cardiac rhythmdisturbance. The lower chambers quiver and the heart cant pump any blood,causing cardiac arrest.How it worksThe hearts electrical activity becomes disordered. When this happens, thehearts lower (pumping) chambers contract in a rapid, unsynchronized way. (Theventricles "flutter" rather than beat.) The heart pumps little or no blood.Collapse and sudden cardiac arrest follows -- this is a medical emergency!Signs of cardiac arrestSudden loss of responsiveness (no response to tapping on shoulders)No normal breathing (the victim does not take a normal breath when youtilt the head up and check for at least five seconds)Pulse less, Apnea , Centrally cyanosed, convulsion .This is sudden cardiac arrest (SCA) -- which requires immediate medicalhelp (CPR and defibrillation)!Treatment :Ventricular fibrillation can be stopped with a defibrillator, which gives anelectrical shock to the heart.
  27. 27. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 27HEART BLOCK------------------------First-degree AV block• First-degree (AV) block is defined as a fixed prolonged PR intervalexceeding 0.21 seconds with all atrial impulses conducted.CAUSESE:1. Athletic training2. Vascular--Acute MI3. Drugs:• Calcium channel blockers,• Beta-blockers,• Digoxin,• Amiodarone4. Valvular-- Mitral or aortic valve annulus calcification , Rheumatic fever5. Infectious disease:• Infective endocarditis,• Diphtheria,• Chagas disease,• Lyme disease,• Tuberculosis6.Collagen vascular disease:• Rheumatoid arthritis• systemic lupus erythematous• scleroderma7.Fetuses of pregnant women who are anti-SSA/Ro positive.8.Infiltrative diseases such as amyloidosis or sarcoidosis9.Myotonic dystrophy
  28. 28. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 28SYMPTOMS:• Asymptomatic at rest.• Markedly prolonged PR interval may reduce exercise tolerance inpatients with left ventricular systolic dysfunction.• Syncope may result from transient high-degree AV block and inthose with infranodal block and wide QRS complexSIGNS:• The intensity of the first heart sound (S1) is decreased in patientswith first-degree AV block.• Patients with first-degree AV block may have a short, soft, blowing,diastolic murmur heard at the cardiac apex. The diastolic murmur isthought to be related to antegrade flow through closing mitralvalve leaflets that are stiffer than normal.TREATMENT:• Patients with asymptomatic first-degree AV block----no treatment• In patients with symptomatic first-degree AV block medications withpotential for AV block must be discontinued if possible.• Permanent electronic pacemakers may be indicated in those withthe following:1. Severe bradycardia2. Syncope associated with infranodal block3. Left ventricular systolic dysfunction, when a shorter AVdelay has been shown to improve hemodynamic condition• Medications
  29. 29. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 29COMPLCATIONS:• Progression to higher degrees of AV block• Reduction in left ventricular stroke volume and cardiac output• Pseudo-pacemaker syndromePROGNOSIS:• Isolated first-degree AV block carries no increased risk of mortality.• Patients with first-degree AV block and infranodal blocks haveincreased risk of progression to complete AV block
  30. 30. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 30Second-degree block:Mobitz type I (Wenckebach) AV blockMobitz type II AV blockMobiz type 1It is a progressive prolongation of P-Rinterval, with the RR interval shortening,before the blocked beat; this phenomenon is almost always due to abnormalconduction within the AV node. (one P in ECG except in one place B/W 2QRSs).CAUSES:
  31. 31. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 31It may occur in normal individuals with heightened vagal tone.1. Drug effect (especially digitalis, calcium channel blockers, β-blockers, or other sympatholytic agents), often superimposed onorganic disease.2. These disturbances also occur transiently or chronically due toA. IschemiaB. InfarctionC. Inflammatory processesD. fibrosisE. CalcificationF. Infiltration.The prognosis is usually good, since reliable alternative pacemakers arise fromthe AV junction below the level of block if higher degrees of block occur.THE MOST IMPORTANT AETIOLOGY TO BE R/O IS STEMI (INFERIOR WALL).
  32. 32. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 32Mobitz type II AV blockThere are intermittently nonconducted atrial beats not preceded bylengthening AV conduction. It is usually due to block within the His bundlesystem.The distance of P waves from QRS complexes is fixed but only one P wave passthrough AV node and result in QRS .It is called 2:1 block- 2 P waves, or 3:1block 3 P waves.
  33. 33. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 33Mobitz type II block is almost always due to organic disease involving theinfranodal conduction system.In the event of progression to complete heart block, alternative pacemakers arenot reliable.Thus, prophylactic ventricular pacing is required.SUMMARY:FIRST DEGREE- ONE P /FIXED PROLONGED PR INTERVAL MORE THAN 5 SQSECOND DEGREEMOBIZ 1 - PROGRESSIVE PROLONGATION OF PR INTERVALONE P / EXCEPT IN ONE PLACE 2 P WITH ONE QRSREVERSIBLE/ BENIGN CONDITIONACUTE INFERIOR MIMOBIZ 2 - MANY FIXED P WAVES /FIXED NUMBER AND DISTANCES3:1 BLOCK, 4:1 BLOCK ONE P ONLY PRODUCE ONE QRSPACEMAKER IS THE TREATMENT.ACUTE STEMI CAN CAUSE ALL TYPES OF BLOCK.ANY PATIENT PRESENTED WITH HEART BLOCK SHOULD ALARM US TO LOOKFOR DRUGS AND POSSIBILITY OF ACUTE CORONARY SYNDROMES.
  34. 34. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 34Complete heart block:Complete (third-degree) heart block is a more advanced form of block often dueto a lesion distal to the His bundle and associated with bilateral bundle branchblock. The QRS is wide and the ventricular rate is slower, usually less than50 beats/min. Transmission of atrial impulses through the AV node iscompletely blocked, and a ventricular pacemaker maintains a slow, regularventricular rate, usually less than 45 beats/min. Exercise does not increase therate.(( LBBB + RBBB+ 1STDEGREE HAERT BLOCK=CHB ))SYMPTOMS:Patients may be asymptomatic or may complain of low cardiac outputsymptoms- fatigue, sweating, dizziness, lose of effort, weakness or dyspnea ifthe rate is less than 35 beats/min; symptoms may occur at higher rates if theleft ventricle cannot increase its stroke output.The patient may be in shock if it is caused by acute myocardial infarction.During periods of transition from partial to complete heart block, some patientshave ventricular asystole that lasts several seconds to minutes. Syncope occursabruptly.SIGNS:The first heart sound varies in intensityWide pulse pressureChanging systolic BP levelCannon venous pulsations in the neck are also present.
  35. 35. MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013 35TreatmentThe indications for permanent pacing have been discussed:Symptomatic bradyarrhythmias,asymptomatic Mobitz II AV block, or complete heart blockCAUSES OF AV BLOCKSREVERSIBLE PERMANENTPHYSIOLOGIC; CAD;CAD; MATERNAL SLE;INF. ENDOCARDITIS; CMP;MYOCARDITIS; INFILTRATIVE;METABOLIC; TRAUMATIC;TRAUMATIC; TUMOURS;DRUG INDUCED; NM DISORDERS;IDIOPATHIC;

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