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Transcript of EKG Extravaganza!
EKG Extravaganza!Michele Ritter, M.D.Argy Resident Feb. 2007
Normal Conduction of the HeartSA nodeLeft/Right atriumAtrial ContractionAV nodeBundle of HisPurkinjie fibersEndocardiumEpicardiumVentricular contraction
Generation of EKG
Generation of EKGP wave:= depolarization/contraction of both atriaQRS complex: = depolarization/contraction of ventriclesT wave= rapid phase of ventricular repolarizationST segment= plateau phase of ventricular repolarizationQT interval = ventricular systole
ECG LeadsLimb LeadsBipolarLead I left arm (+) and right arm (-) Lead II left leg (+) and right arm (-)Lead III left leg (+) and right leg (-) UnipolaraVR - right arm potentialsaVL left arm potentialsaVF left leg potentials
Large Box = 0.2 secondsSmall Box = 0.04 seconds
Rate300-150-100-75-60-50 RuleIf one box between R-waves, then rate is 300; If two boxes between, then rate 150, etc.Rate = 1500/(mm between R waves)
What is the rate?
RhythmIs the rhythm regular (distance between QRS complexes equal)?Is there a P-wave before every QRS complex?Is the PR interval normal?0.12 sec - 0.20 sec Is the QRS duration normal?0.04 sec to 0.12 sec
Irregular RhythmsUsually caused by multiple, active automaticity sites that causes irregular atrial and ventricular activityInclude:Wandering PacemakerMultifocal Atrial TachycardiaAtrial Fibrillation
Irregular RhythmsWandering PacemakerHave P waves (not true P waves because pacemaker activity is wandering from SA node to a nearby atrial automaticity foci)Atrial Rate less than 100Irregular shape to P waves and irregular ventricular rhythm.
Irregular Rhythms (cont.)Multifocal Atrial TachycardiaThink of it as tachycardic wandering pacemakerP waves againAtrial rate excees 100Irregular ventricular rhythmIrregular morphology of P wavesOccurs in:COPDHeart Disease
Irregular Rhythm (cont.)Atrial Fibrillation No P waves (because there are multiple atrial automaticity foci sending impulses no single impulse depolarizes atria completely)Irregular ventricular rhythmCaused by:Heart disease (CAD, CHF)Thyroid diseasePericardial effusion Alcohol
Tachy-arrhythmiasRapid rhythms originating in a very irritable foci that paces rapidly.Includes:
Atrial TachyarhythmiasSupraventricular tachycardiaIncludes paroxysmal junctional tachycardias Paroxysmal Atrial Tachycardia and Paroxysmal Junctional TachycardiaCaused by very irritable automaticity foci that originate above the ventricles.Narrow QRS complex tachycardiaHave P waves often get lost in QRS.
Atrial Tachyarrhythmias (cont.)Torsades de PointesRate is usually 250 to 350 beats/min.The amplitude of each successive complex gradually increases and then gradually decreases party streamerCaused by:Severe hypokalemiaMedications that block potassium channelsCongenital abnormality (Long QT syndrome)
Atrial TacchyarrhythmiaAtrial FibrillationRapid Ventricular Response = increased heart rate, putting patient at risk for hypotension.
Atrial Tachyarrhythmias (cont.)Atrial FlutterExtremely irritable atrial focus produces a rapid series of atrial depolarizations (250-350 beats/min.)
Ventricular tacchyarrythmias (cont.)Paroxysmal Ventricular TachycardiaIs like a run of PVCsIrritable (hypoxic) ventricular focus results in rapid rate that is too fast for heart to function effectively.WIDE QRS COMPLEX tachycardia
Ventricular Tacchyarhythmia (cont.)Ventricular FibrillationCaused by rapid-rate discharges from many irritable, parasystolic entricular automaticity foci.An erratic, rapid twitching of the ventricles, with ventricular rate reaching 350 to 450 beats/min.Tracing is totally erratic, without identifiable waves.
TacchyarrhythmiaWolff-Parkinson-White syndrome A ventricular pre-excitation arrhythmiaAn abnormal, accessory AV conduction pathway, the bundle of Kent, can short circuit the usual delay of ventricular conduction in the AV node.Results in Shortened PR interval (< 0.12 sec)Widened QRS (> 0.12 sec)Delta wavesCan result in several tachyarrhythmias including supraventricular tachycardia, atrial flutter, atrial fibrillation
BlocksSinus BlockAV BlockBundle Branch Block
Sinus BlockSA node fails to pace for at least complete cycle.Occurs in:Sick Sinus Syndrome (SSS)SA node dysfunction resulting recurrent episodes of sinus block or sinus arrestFrequently occurs in elderly patients with heart disease.Bradycardia-Tachycardia SyndromePatients with SSS who develop episodes of supraventricular tachycardia mingled with sinus bradycradia.
AV Block1 (first degree) AV BlockProlongs AV node conductionProlonged PR interval (>0.2 sec one big box)The PR interval is consistently prolonged the same amount in every cycleP-QRS-T sequence is normal in every cycle.
AV Block (cont.)2 (second degree) AV BlockWenckebach (Mobitz Type I)Gradually prolongs the PR interval , until the final P wave fails to produce a QRS response.This cycle then repeats itself.Usually non-pathologicMobitz (Mobitz Type II)Totally blocks a number of paced atrial depolarizations (P waves) before conduction to the ventricles is successful.Can be:2:1 two P waves to every QRS3:1 three P waves to every QRSUsually permanent, and can progress to complete heart block
2 AV Block Wenckebach
2 AV Block - Mobitz2:13:1
AV Block - 2 AV block (cont.)If see 2:1 AV block and uncertain if Wenckebach or MobitzDo vagal maneuverIf Wenckebach, there is an increase the number of cycles/series (increasing to 2:3 or 4:3)If Mobitz (Type II), it becomes a 1:1 AV conduction.
AV Block (cont.)3 (third degree) AV block:Complete Heart BlockComplete block of the conduction to the ventricles, so atrial depolarizations are not conducted to the ventricles. See a sinus-paced atrial (P wave) rate and a totally independent, focus-pased, slow ventricular (QRS rate) AV dissociation.Can have:Junctional FocusNormal (narrow) QRSVentricular rate: 40-60/min.Ventricular FocusPVC-like QRSsVentricular rate: 20-40/min.
AV Block (cont.)3 (third degree) AV Block
Bundle Branch Block
Bundle Branch BlocksCaused by block of conduction in the right or left bundle branch. The bundle branch delays depolarization to the ventricles that it supplies.Left Bundle Branch Block (LBBB)Associated with cardiovascular disease!Incidence increases greatly with age.Think V5, V6!!Right Bundle Branch Block (RBBB)Associated with structural heart disease, increased age, sometimes iatrogenic (cardiac cath.)Think V1, V2!!
Bundle Branch Block
Left Bundle Branch BlockWidened QRS (> 0.12 sec, or 3 small squares)Two R waves appear R and R in V5 and V6, and sometimes Lead I, AVL.Have predominately negative QRS in V1, V2, V3 (reciprocal changes).
Right Bundle Branch BlockWidened QRS (> 0.12 sec or 3 small squares)R and R in V1 and V2, often with ST depression and T wave inversion.Reciprocal changes (big negative S) in V5,V6, I and AVL.
Right Bundle Branch Block
Bundle Branch BlockFinal Note:If you have the above changes with R and R, but a normal (not widened) QRS, it is referred to as an incomplete bundle branch block.
AxisThe direction of depolarization as it passes through the heart.A vector towards a lead results in a positive deflection on the ECG, while a deflection away from a lead results in a negative deflection.If hypertrophy is present, the overall vector (axis) points towards the hypertrophied part.
AxisFrontal PlaneHorizontal Plane
AxisNormal Axis: QRS vector pointed downard and to the patients left, in the 0 to 90 Range.Right axis Deviation: > 100Left axis Deviation: < 0
Axis the nitty grittyQRS net positive in Lead I and AVF: normal axisQRS net positive in Lead I and net negative in AVF: Left axis DeviationQRS net negative in Lead I and net positive in AVF: Right axis DeviationAVF
AxisLeft Axis Deviation:Can occur in:Left Ventricular Hypertrophy (hypertension!)Inferior myocardial infarctionRight Axis Deviation:Can occur in:Right ventricular overload (cor pulmonale)Left pneumothoraxLateral myocardial infarction.
Hypertrophy were going to essentials only.Left Ventricular HypertrophyImportant because it is often a sign of long- standing hypertension!Calculation:mm of S in V1 +mm of R in V5If sum is more than 35 mm, you have LVH!!!
Remember, you usually see Left axis deviation with LVH.
Now the most important.MYOCARDIALINFARCTION !!!!
EKG in Myocardial InfarctionGives information about:Duration hyperacute/acute versus evolving/chronic Extent transmural versus subendocardial Size amount of myocardium affected Localization (which area of heart affected)Difficult to use EKG in certain situations:Left bundle branch blockPaced rhythm
EKG in myocardial infarctionIschemia: T wavesInjury: ST changesNecrosis: Q waves
Myocardial IschemiaRepresented by inverted T waves.Should be symmetrically inverted.Can be marker of OLD infarctionWellens syndrome: Marked T wave inversion in V2 and V3, which alerts to stenosis of the left anterior descending coronary artery (LAD)
Myocardial InjuryInjury = acute or recent ischemia.ST changes show that the episode is acute.Transmural injuryST Elevation Subendocardial injuryST Depression
Myocardial NecrosisQ wave:Diagnostic for myocardial infarction.Can have MI in its absence (non Q-wave MI)Can be acute or old! (Use ST changes to determine if acute)Is significant if at least one small square (1 mm or 0.4 seconds in duration)Is usually at least 1/3 of the QRS amplitude
Location of InfarctionPosteriorRight Coronary ArteryLarge R, ST depressions in V1, V2, V3InferiorR or L coronary arteryST changes/Q waves in II, III, AVFMay have reciprocal ST depressions in I and AVLLateralCircumflex arteryST changes/Q waves in I and AVL, V5, V6May have reciprocal ST depressions in II, III, AVF.AnteriorLeft Anterior Descending arteryST changes/Q wave in V1, V2, V3, V4
Wheres the MI?
Wheres the MI?
Wheres the MI?
EKG - ConclusionRateRhythmRegular, irregular, irregularly irregular?P waves? PR interval? QRS duration?AxisHypertrophyIschemic Changes T wave changes?ST changes?Q waves