34 OSMOSIS ORG Figure 448 chest Lens Crest LEAD? postey Ve Positive VS. VG + LerT veerevcutne v5 py TWwPeeropny a IsoevecTaic, ale -*TRANSITION 2oNE* vB a ve ‘SHIFTS TownRD Vi ve oe 4... Now, let’ switch gears and tak about the chest leads, which essentially view the hea a afferent plane (Figure 4.16). Looking down at the heart we have leads Vv. yy" and V, Normaly, the QRS comple is negative in leads V, and V, isoelectric in iad “4 Vp nth called the vanston zone, and postive in leads V, and V, (Figure 416) no transition zone shits toward V, oF V_ and looks isoelectric instead of negative it sugges that the heart may be rotated tothe persor' right, which can happen ifthe right venti hypesrophved (Figure 4.17) On the other hand, if leads V, oF V, look isoelectric ston pesitve suggests thatthe heart may be otatedto the person's lft which can happen tg left ventricle is hypertrophied (Figure 4.18). ‘SUMMARY Alright, ets qucky recap. A normal hearts axis is between -30 and +90 degrees, Right ventricular hypertrophy ean cause the axis to be between +90 and +180, and can sometings Cause the V, and V, chest leads to appear isoelectric. Left ventricular hypertrophy can cauge the axis to be between -20 and 90, and can sometimes cause the V, and V, chest leads to ‘appear isoelectric (Figure 4.19) : Lert VenTRicuLar 2 HyPeeTRopHY > *VSi.V6 WsoevectPic Figure 419 sto Right venteicuar HYPERTROPHY #vieva ISoevecreicIntervals osmosis.org/learn/ecg_ intervals nen reading an ECG, there are a few key elements to keep in mind: one of them is ooking at the intervals (Figure 5.1). in a typical waveform, there's a P wave, OAS complex. and T wave. In addition, there are certain intervals, including the PR interval, gas complex itself, and the QT interval te igure 54 IR DIOL £(G/EKG ELECTROCARDIOGRAM (£04 EKG) ELeCTRICITY HEART VISUALIZE ts THINGS t KEEP 1 MIND: - /Oasevasioy —— STNTERVALS a JF afte ge ou Foue 52 P-wave cones T-weve, PRUINTERVAL 0 .\2 - 0.20 B-5 bores * NORMALLY ae O1d-0. — Biooves-S bones ou START of Peunve —> START «F ORS Comper pa STAIN COUTERCTION —VEAITRICULAE ConTRACTLON OSMOSISORG 35pasa! epITAgLE thin. cout SANODE CHANGES in PR wteRVAL Lonmin ectopic Focus eFaetHer—> Lovet VENTRICLES: IRRITABLE arma ce CHANGES wn PR wTeRvAL praia ectopic Focus + Fark Lovet 2 chase — Sapte \Lfigst Dearee HearT veuTeicves Brock * CHANGES in PR wteevaL Crrpiat Ectopic Focus + FARTHER —* Lovee ae FIRST DEGREE HEART Block ~ >0.2s VENTRICLES 36 OSMOSIS.ORGChapter § Intervals QRS ComPLex £0105 4 CHANGES in ARS ComPLex (Kvenreioutar ectopic Focus, Ls tower & Depa te Banc Copetneoare soo 010s anno ca L ProtowatD~ 0.12; PR INTERVAL ‘ThePR interval spans from the beginning ofthe P wave to the beginning of 7 venticular depolarization. It's normally 0.12-0.20 seconds, which i tree to fve litle boxes, ‘ince each litle box is 0.04 seconds. Therefore, the PR interval showr'is about four boxes of 0 18 sesonds (Figure 5.2) ‘ary deviation in the normal depotarization pathway from the SA node tothe ventricles can change the PR interval. For exemple, consider if the atria are depolarized by an ectopic atrial foous, such as an iritable atrial cell outside ofthe SA node. if it was farther away from the ‘AVnode it result in a longer PR interval, because the signal has to travel a greater distance (Figure 5:3) Aternatvey fit was really close to the AV node, the PR interval might be super short Another example is frst degree heart block, which is when the electrical signal travels more slowly through the AV node than it normally does, causing the PR interval to lengthen beyond 0.2 seconds (Figure 5.4) QRS COMPLEX ‘The QRS complex represents depolarization of the ventricles; i's normally less than 100 mrillseconds or two and a half litle boxes. Just lke the PR interval, the QRS duration can differ inits path from the AV node to the ventricles (Figure 5.8) For example, if an ectopic ventricular focus, such as an initated ventricular cell, ies off, the resulting depolarization wave will move slowly from muscle cell to muscle cel instead of traveling quickly through the electrical conduction system. Therefore it takes a longer time to depolarize the ventricles, and the QRS is wider. I's considered intermediate fits 100 to 120 miliseconds, and proionged if i's aver 120 miliseconds, or three litte boxes (Figure 5.6) QSMOSISORG 37Figure 57 QT wresva _— NORMAL ~ Less THAN (pee) HALF » CARDIAC CYCLE + ABNORMALLY LONG | 2 Gomm Gs > aHo ms (es) (= en La peo ms (omen!) VENTRICULAR SYSTOLE = DEPOLARIZATION bwoagh RePoLAeIeATION Le conaiges wets RaTEl Figure 58 QT wrervat * ABNORMALLY LONG C Gown > 440 ms (oes) La 240 ms (woner’) C40 Bem - G doors = a nL 440 ms Qaen)) Ly 2 Yo0 os (wonen)) @ 90 Bem doors (ar) Connected OT weevaL (ar.) ——\¥Nes (ax) p Home # Bazerrs FORMULA ; At. = BTL _ Hom _ YOOms Lona! oe opie ae 7 38 OSMOSIS.ORG ane eat)Chapter § Intervals. 10 Fa PROLONGED QT INTERVAL PROLONGED: CITA INTERVAL: MEDICATIONS LpwiopaPone ~ arrects tow CHANNELS »* IuneriTep Crutations « L071, Lore, tors Aft Towa OT ToRSADES o¢ Pontes iL at INTERVAL The QF terval spans from the beginning of the QRS complex to the end of the T wave. i represents ventricular systole, which is the entire span from depolarization through repolarization, Normally, the QT interval should be less than half ofa cardiac oyele Infact: fey aear rate of 60 beats per minute the QT intervals generally considered to be abnormally! long when ifs greater than 440 miliseconds!in men, or 460 milliseconds in women, IF yon measure someone's QT interval ata different rate, say 90 beats per minute, and t was 200 millseeonds you might think that that'd be considered normal however you cant really use these values to compare to the normal QT interval at 60 beats per minute or bpm, becance the OT interval changes depending on the rate (Figure 5.7). As rate increases, the QT interval decreases; thus, at 60 440 ms, whereas at 90 bpm. it's likely something lower. So, what we have to do is fou the coected QT interval, or QT. atthe different rate. Then, you can compare it to the OT intervalnc 60 beats per minute. Even though there are several formulas you can use, Bazet's formula is Brobably the simplest. where the corrected QT interval equals the GT interval in miliseconds, Aided by the square root of the R to R interval.in seconds, divided by one second. As a side, note, this formula is usually expressed without the “divide by T Second" part, but the astute observer will notice that the units won't work out if you leave it out (Figure 8.8) {et use our 90 bom and 400 milliseconds QT interval from before, and imagine the person 'smale.f we plug in 400 for GT and 90\peats per minute, or 66 seconds per beat. we have 207 of 400 miliseconds divided by the square root of 0.66 seconds over 1 second, which is 400 miliseconds divided by 0.81, which is unless, and we get a corrected QT interval of 488 miliseconds_ Now we can compare this sum to the value at {60 bpm) We see that the doected QTc actually greater than 440 ms, which means that this measured QT interval of 4001ms at 90 bpm is indeed abnormally long (Figure 5.9)! all ai ‘bpm, the abnormal cutoff might be The QT interval can be prolonged by medications, sraraithmic that affects cardiomyocyte ion channels, or caused by inherited long OT! Qindromes; where there are mutations in genes, including LOT, LAT2, or LAT3. One of rast feared complications of having a prolonged QI interval is a type of ventricular etvearcia called torsades de pointes, which can lead to ‘sudden cardiac death; here, the ‘shows a “twisting of the Ponts (Figure 5.10), Such as amiodarone! which is an OSMOSIS.ORG 3940 OSMOSISORG Figure 5.11 PR WTERVAL~120-200-1 QRS COMPLEX ~ 100-5 QT wwreaval ar, - ot Cede (8 2440 #8 (on) Barzert Formuta: = C404 (oomee) SUMMARY Al right, let's quickly recap, An ECG waveform has a PR interval that's usually {hiliseconds, a QRS complex that’ less than 100 milliseconds, and a QT interval that’s less {han 440 millseconds in men and 460 millseconds in women: these values arc rates at coPom.Bazet’ formula can be used to find the corrected OT interval which yourse, use to ‘Compare rates other than 60 bpm to the normal rate (Figure 5.11). 12010 209 |QRS Transition osmosis.org/learn/ecg_qrs__tran ion jan ECG, there are a few key elements to keep (23 | In mind: one is to figure out the ston (Figure 6.1).The chest leads (Figure 6:2) wil hose» mostly positive Ts san. i'a depolarization wave is moving renee oo eon ps VECTOR & TRANSITION ZONE. a ion zone refers to where the QAS complex switches ff The OFS Lan positive, ftom the pamntot view ore ain speartthrough the horizontaplane The URS teat, Usually happens inlesdV. ot ‘ve ting on fct0fs Such as chest lead placement Vv, de and the exact anatomy of a person's 6.3). So the QRS transition tls us when the overall ORS vector oslanceeon neat arte chest leads it's a way of Understanding whats happening to the OAS axis recor ‘he horizontal plane. ‘OM being mostly fe chest leads, V, through V, which Figure 64 TROCARDIOGRAM (ECG /EkG) ELECTROCARDIO —— ELECTRICITY HenRT — VisuaLie THINGS t KEEP 1 MIND: ° THBAGs © FER. HAND Duvowerason QRS TRANSITION 12 Janie 7 speek dee ou Fque 6.2 Chest Leap QSMOSISORG 41Figure 63 = ‘Crest LeaDs f ORS TRANSITION 20NE mosey \T 4 QRS COMPLEX Soreness Necarive { + USUALLY Vy Wy - Depounnsteion «Depends,» LEAD AWAY jon E.2cTRODE PLACEMENT | ANATOMY Figure 64 QRS TRANSITION ZONE SHIFTS Scar Tissue RIGHT (Toonro viv2) MYOCARDIAL INFARCTION | seat Tissue err Se 9 HEART HL, ter corcummtex i L : me oe hs TuFARCTION of Posteo? wat QRS TRANSITION ZONE SHIFTS RIGHT (Fouse0 vive) MYOCARDIAL INFARCTION sere tasve Ceerr soe nese ‘*# CARDIAC HYPERTROPHY. Lotwever muscue RicHT sive o HenRe 42 OSMOSIS.ORGChapter 6 OAS Transition Figure 6S QRS TRANSITION ZONE SHIFTS, LEFT Couto visu) “PAYOCARDIAL JpROCAPDIAL WFARLTON Cseas tissue RIGHT S106 5 Hener 4 CARDIAC HYPERTROPHY Letwover Musee Leer swe of Hemet oar If something alters the heart's overall ORS vector, then the QRS transition zone can shift to the right, towards V, and V,,or to the left, towards V, and V,, For example, a myocardial infarction leads to the formation of scar tissue that can't depolarize. Generally speaking, the ORS ‘rensition zone will sift away from a region of scar tissue, because it no longer contributes to the overall QRS vector. Consider the following: a blockage in the left circumflex artery can cause infarction of the posterior wall of the left ventricle, which would lead to a rightward rotation of the QRS transition zone, toward V, and V, (Figure 6.4). Another example would be cardiac hypertrophy, because a thicker muscular wall contributes more to the overall QRS vector (Figure 6.5). If i's right ventricular hypertrophy, it would lead to a rightward rotation of the QRS transition zone, towards V, and V,, similar to the result of an infarction of the posterior wall of the left ventricle. In contrast, aright ventricular infarction ora left ventricular hypertrophy would lead to a leftward rotation of the QRS transition zone, towards V, and V, (Figure 6.6) SUMMARY ‘Alright, les quickly recap, The QRS transition zone, in the horizontal plane, is where the QRS. complex switches from being mostly negative to mostly positive; it normally happens in lead ¥, or V, The QRS transition zone rotates away from previous myocardial infarctions, and toward hypertrophied tissue (Figure 6.7). Figure 67 QRS TRANSITION ZONE Positive Rotates... Away FeOM | (MYacAROIAL INFARCTIONS Towne a HrpeRrRopmien Tissue “ Mass ahs ate Neartwe OSMOSISORG 43Cardiac Hypertrophy & Enlargement ee eee 19 figurin ure 7.1), Hy ickness. Dilation r is generally us PENS in the atria In igure 7.2). An ECG can tet here are lots of things to look for when reading an ECG, incluing ae of the heart has undergone hypertrophy or enlargement (Fig Par Means that a heart's muscular wall has increased in thic increase in the volume of the chamber. The term enlargement hypertrophy and dilation occur together; this is what typically ha the ventricles often undergo hypertrophy without dilation (Fi fridence of hypertrophy and enlargement inallof the heart's four chambers Lere them one by one, 9 efers to a) ed when bout CaN sho 90 through ATRIAL ENLARGEMENT ‘can be a stenotic, or narrowed, tricuspid val ive that makes it mi blood into the ventricles. in response, the ‘re dificult fort right atrium enlarge es (Figure 7.3; he atria tog} Figure 7.4), ELECTROCARDIOGRAM (cca le€k@) eevee ELECTRICITY HeaRT —visunLize. THINGS & Look FoR Deroxnsieni Leno i fee * HYPERTROPHY 3 pe ENLARGEMENT ou. 44 OSMOsIS.oRG,| Chapter 7 Cardiac Hypertiophy & ena gement nent 12 po? HYPERTROPHY OFTEN SEEN ws VENTRICLES TMCREASED THICKNESS, pent ome . or DicaTion, TWAS Vou got 73 BIGHT ATRIAL ENLARGEMENT 14 LEFT ATRIAL ENLARGEMENT Yom 2110s = | rey Chuse : steworic (MITRAL VALVE Soules QsMOSISORG 45Figure 75, LEFT ATRIAL ENLARGEMENT Nw pteno i >110rs Toman mat LeaD vi. Cause: STenorTic Sf 7 (MITRAL VALVE >o- Figure 76 RIGHT VENTRICULAR HYPERTROPHY Leno v1, ) a Caio Neate VENTRICULAR HYPERTROPHY Normally, the QRS complex is mostly negative in ead V,, because the large left ventricle, which caries the greatest amount of muscle tissue, is oriented down and away from this electrode (Figure 7.6) In right ventricular hypertrophy, the thicker right ventricle helps to counterbalance the left ventricle and makes lead V, more positive. Specifically, it makes the(@wave bigger, which is the upward deflection of the QRS complex. In fact, a dominant R wave in V, is a classic sign of right ventricular hypertrophy; i's defined as an R wave that is over 7 mm tall,or7 ite boxes, and is larger than the S wave, making the A/S ratio > 1. Another classic sign of right ventricular hypertrophy is a dominant S wave in V, or V,, meaning that it's over 7 mm deep, (7 litle bores, and bigger than the R wave, making the R/S ratio < 1. Typically, theres also right axis deviation in right ventricular hypertrophy that results in an axis of 110 degrees or ‘more (Figure 7.7). In ight ventricular hypertrophy the QRS complex is «120 ms, meaning that it’s not longer than normal. This is important because it means that the changes cant bbe the result of something like a right bundle branch block, which would cause a prolonged QRS complex. Right ventricular hypertrophy can develop for'a number of reasons. Acommon cause is pulmonary hypertension, which makes sense because the right ventricle has to build ‘up muscle to push blood into the lungs (Figure 7.8). 46 OSMOSIS ORGChapter 7 Cardiac Hypertrophy & Enlargement RIGHT AXIS DEVIATION * >+110° lean vi Tea 0ms |“ MORMAL *NoT REE waeneaa # Rls Ren10 > 1 Cause: PuLmonarY HYPERTENSION “Figure 78 LEFT VENTRICULAR HYPERTROPHY Leap VS (sve) LONG v >S0ms «S$ (vi) + R(VS) 235m T-WAVE INVERSION CAUSE: SYSTEMIC HYPERTENSION OSMOSIS.ORG 4748 OSMOSIS.ORG In left ventricular hypertrophy, the pattern is almost the opposite of what happen, eicuar hypertrophy Lead V, has even more positive charge traveling away a ght Usual making the S wave really deep. Meanwhile, lead V, and V, are located on the eal” Haicventncle and therefore have an enormous R wave. The most commonly useg Side of ore ana toentify lft ventricular hypertrophy is thatthe sum ofthe S wavein V, and th volt wave nV, or V, has to be over 35 millimeters, or 35 Ile boxes. Adtional ontei nates Fairy an Rave that goes on for longer than usual typically over 80 ms, and ST elude reser segment depression, and T wave inversion in V, or V,, These ae signs ‘heen Tee dentrclers straining during muscle contraction. Left ventricular hypertrophy comm the evelops due to systemic hypertension, or elevated systemic blood pressure, because theo dee te needs more muscle so that itcan eject blood against higher pressures (Figure 73 SUMMARY Al right, let's quickly recap. Right atrial enlargement show's a big P wave in lead Il and v, nhereas left atrial enlargement has a biphasic P wave in lead V, and a double-humped P wave vrcoe I Right ventricular hypertrophy shows 2 big R wave in V, and a big S wave in V, ang rtrophy shows the opposite an enormous S wave in V, and a VV, whereas left ventricular hyps latge A wave in V, and V, that add up to over 35 mm (Figure 7.10). Figure 740 RiHT areal Lee uci) ENLARGEMENT Pr wu KEEP ny MIND: Deroapiennion —-#ISCHENAIA er INFARCTION eo ‘ane : oper oot ou Foure 82 ISCHEMIA or INFARCTION . 20 mares, so ——, = Bioop Flow oa (eee) | Relies Necrosis onaae + ceuweae Dent OSMOSIS.ORG 49Figure 8.3 TRANSMURAL “CRTIRE THICKNESS oF MYOCARDIUM wre _evonsoun “SuBENDOCARDIAL WNeRMosT LAYER CPIAOCARDIHA on 6LG Sr LEFT VENTRICLE Figure 8.4 SUBENDOCARDIAL ISCHEMIA + TucomPLeTe BLocKAGe (-70'2) » CORONARY ARTERY opr ResT—> Enovah pee. ANGINA “Suton » Gest Cccepeise > NOT eMoUEH feuioum s ost BRANCHES » CORONARY peieey ie ae Broop SUBENDOCARDIAL IScHEMIR *ST DePRession = Cg:poust Dou! 65 20S nm OSMOSIS.ORGChapter 8 Cardiac infarc, gue 98 SUBENDOCARDIAL IscHEMin POSER VIAL CHEN *ST DePRession « LFPonIT BOW 45 20.5 um -$L0PING Dowrwaro-* pened 1WA20-SLoPIN Gosessriee. 4 OFTEN AFFECTS LEADS 1,11,VU,VS,Ve Covercve + eretame patepy nuied SUBENDOCARDIAL ISCHEMIA subendocardial ischemia might happen when there's incomp : coronary artery In this situation, there's enough blood Towing traoghtore belie athe myocardium when the person is at rest, but during exercise there's Ameo eet fhe increased demand of the myocardium. Therefore the subendacardal tssve becomes ir ic because isthe last bit of tissue to recive blood fram the tiny branches of te isepeiy arteries as they make their way through the ventricular wall from outside to ine cna ion ig caled stable angina, because thet’ ischemia that causes chest in wth perise, and the pain disappears with rest (Figure 8.4). ain wi When there's subendocardial ischemia in a region, it causes ST depressions in the toresponding lead on the ECG. An ST depression describes when the J point, which s where the QRS complex meets the ST segment, goes down by at least 0. mm ors of a small box (Figure 85). The ST depression can be upward sloping, downward sloping, or horizontal. n Subendocardial ischemia, ST depressions are usually widespread, and often affect leads | ihandV, to V, With such widespread involvement its dificult to determine which coronary artery caused the ST depression (Figure 8.6). As aside note, the ST segment is depressed and curved, it may be due to the digitalis fect, which happens when the patient takes the tredication digoxin, rather than being due to subendocardial ischemia (Figure 8.7) TRANSMURAL ISCHEMIA Net there's transmuralischemia. When a coronary artery is narrowed froman atherosclerote pleaue buildup overtime, there are two parts tothe plaque: a hard flrous cap an the sof erctee ike interior As blood flows past the plaque, the flrous cap can sometimes rip That heesy interior is considered thrombogenic, meaning that blood cots form on t ery quickly these Can quickly stop blood flow! This means that none ofthat wall ets aeoauert blood Tow Ithappens during unstable angina or during a non ST elevation myocardial infarction, OrNSTEMI for short. The key diference is that in an NSTEMM, the ischemia So St that damaged heart cells leak out certain enzymes, such as troponin and CKMB| (Figure 8.8). ion & Ischemia OsMOSISORG 51Figure 87 Diaitaus EFrectT Figure 88 TRANSMURAL ISCHEMIA UNSTABLE ANGINA Now ST ELEVATION Moun DIAL INFARCTION Chen cauts Lea ATHeROScLEROTIC PLAQUE“ Hetel cls bene Lyneo Fibrous CAP Contesy ivresion = THROMEOREME Figure 8.9 U TRANSMURAL ISCHEMIA, ST Depression T-WAVE INVERSION $2 mm DEEP Most NOTICEABLE 9 CHEST Leaps Two Cowtiauous Leaos eg.V2 evs 90 DOMINANT R-WAVE, T-wave INVERSION NORMAL «Ill, avR,c VI A ABNORMAL 0 V2-Ve 52 OSMOSISORGChapter 8 Cardiac Infarction & Is, rt? oS yBeNDOCARDIAL ‘INFARCTION pe ENDOCRRDIBEXTNFRECTION “4 CORONARY ARTERY BLocKeD Tor 920 ranvures CeLLs NECROSE. op NSTEMI 5 Reease TRoPonans. bce #57 DePRESsION + TWAVE INVERSION Fue 811 TRANSMURAL INFARCTION (220 mimates) pn Figure 812 TRANSMURAL INFARCTION Fwave version HvPepacure Twine Two Couriauous LeA0s ona iS = ST ELEVATION 2 2tem + ST ELeURTION PAOCARDIAL INFARCTION (ste) cchernia QSMOSIS.ORG 5354 OSMOSIS.ORG fs may show ST depressions and 1 stable angina and NSTEMIS may 8 | frersene, Theses dapessons ek sii othe oes insubendocadl sheria, They " jeal, and are at least 1 mm, oF 1 little box deep, wave inversions are usually symmetti eae eo ae one Taye most noticeable in the chest leads, but can al \, and, are not contiguous. They also occur with a dominant R save which means hat the ‘wave hi ‘Now, it turns out that a little bit of T way wave has a higher amplitude than the S wave. me i: inversion eanbe formal min leads Il, aVR, and V, but any sign of T wave inversion in leads to, is abnormal (Figure 8.9) SUBENDOCARDIAL INFARCTION : 3rtery remains blocked for around Next let's look at subendocartial infarction. I the coronary af 20 minutes, the subendocardial cells begin to die, which results in Necrosis. Just tke in ‘subendocardial and transmural ischemia, there's ST depression. Given that there's necrosis, weld expect there to be leakage of troponin and CK-MB, so this would be an infarction without ST elevation, an NSTEMIL which can again show ST depression and T wave inversion (Figure 8.10) TRANSMURAL INFARCTION The final box is for transmural infarction. This occurs when a coronary artery becomes completely blocked for greater than about 20 minutes, which causes transmural necrosis (Figure 8.11). Within minutes, a transmural infarction leads to ECG changes. The most common change is T wave inversions, but there might also be hyperacute T waves, which are large asymmetric T waves that appear in at least two contiguous Teads. The classic sign of transmural infarction is ST elevation; when this i calledan eae mej infarction, or STEMI. On ECG, the ST elevation at the (J Bpint must be over any two contiguous leads, except V, or V,, where it has to be ove 2 mm (Figure 8.12): ST elevation can also be caused by other conditions, such as coronary artery vasospasm, left ventricular hypertrophy, and pericarditis. For example, a physically fit 20-year-old with a viral illness, who gradually develops chest pain and is found to have ST-elevation on ECG, is more likely to have pericarditis than an ST-elevation myocardial infarction (Figure 8.13) Transmural infarction can also cause pathologic Q waves to appear on the ECG. Normally, depolarization in the ventricle spreads from the endocardium to the epicardium; most of this wave ends up pointing toward the positive electrode, which means a positive deflection However, infarcted tissue doesn't conduct electricity, which means that the electrode essentially sees through the infarcted tissue, as if it was a hole, to the other ventricular wall Therefore, the electrode sees the depolarization wave that moves through the healthy wall ‘on the opposite side of the heart. Because those waves are mostly moving away from the positive electrode, you end up with a big, negative pathologic Q wave. So, pathologic Q waves are waves that are longer than .04 secands, or one small box, and over 2 mm, or two small boxes deep (Figure 8.14) cece ~ The location ofthe transmuralinfarction can beidentified based on the lead thathas pathologic Q waves. Septal wall infarctions show changes in leads V, and V,, whereas anterior wall infarctions show changes in leads V, and V,. Anterolateral wall infarctions show up in leads |,V, through V, and aVL. Small subendocardial infarctions don't cause pathologic Q waves because some of the affected wall still conducts electricity. Also, the aVR lead is oriented in a way that normally produces Q waves, so it's not a reliable lead to look for pathologic Q waves. Finally, pathologic Q waves can also result from things other than transmural infarction, ike a left bundle branch block or Wolff-Parkinson-White syndrome (Chapter 8 Cardiac. Infarction & Ischemia ye ee 7é LeVATION woe CRISES: t oes ATE | YASOCPRSM ] Lert VENTRICULAR A Lt atbontt | PERICARDITIS a ee Exnaoner 29 gor Pr Ls Pericaroins v ee ais bate TRANSMUBAL INFARCTION «PATHOLOGIC Q-waves >o.04s gure 815 TRANSMURAL INFARCTION = PATHOLOGIC Q-waves, ‘Tureect Leap) wate ‘Locations —_Patwotoaic Guinve SerTaL war ——V1N2 farTetiog wai — V3, V4 IAL NENG, oN | ‘Sueeupocapoin. ——NONE — >2-~ ZI * OR NoT RELIABLE * OTHER CAUSES: BunDLe BRANCH 0.04ms Block, WoLrF-PARKINSON-WHITE SYNDROME OSMOSIS.ORG 55Figure 816 TRANSMURAL INFARCTION Davs wens str! Moras, sete gee version | eStroy Parise an Gunes After transmural myocardialinfarction, the ECG: the first two days there might be T wave inversi ‘months, the T wave inversion may start to improve as we ‘ll but pathologic Q waves can linger for much longer That's why its always important to compare ECGs to proven ‘ones to look for new changes (Figure 8.16) SUMMARY Figure 817 IScHemia INFARCTION E ~Snie mann | ~omste monn ; a re oerBssans | Seco ~ONSTARLE RWANR | STEAL Temsmurn, | 30 a Terceneateteesious ‘ST eLevaTiON fame woicasons | nce Quaves, 56 OSMOSIS.ORG