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Myocardial Infarction Mimics Q Waves

Carol Jacobson, MN, RN

Myocardial Infarction Mimics: Q WavesFundamental concepts in understanding electrocardiography and the origin ofQ waves include the following:

1. The QRS complex represents ventricular depolarization: a Q wave is an ini-tial negative deflection from the baseline, an R wave is a positive deflectionfrom the baseline, and an S wave is a negative deflection that follows an Rwave.

2. The positive electrode in any lead is the recording electrode (ie, the camerataking the picture of depolarization).

3. When the positive electrode sees depolarization traveling toward it, it recordsan upright deflection (ie, ventricular depolarization traveling toward a posi-tive electrode results in an upright deflection, or R wave). If the positive elec-trode sees depolarization traveling away from it, it records a negative deflec-tion (ie, ventricular depolarization traveling away from a positive electroderesults in a negative deflection: a Q wave or an S wave).

4. Leads with a positive electrode facing the left side of the heart (lateral wall)are I, aVL, V5, and V6. Leads with a positive electrode facing the inferior wallor bottom of the heart are II, III, and aVF. Leads with a positive electrode onthe front of the chest with the best view of the right ventricle are V1 and V2,although these leads are also considered anterior leads that face the anteriorwall of the left ventricle (LV).

Normal and Abnormal Q WavesA normal Q wave is an initial negative deflection from the baseline that isless than 0.03 sec in width and less than 25% the height of the R wave inmost ECG leads.1–3 Q waves are recorded in leads where the initial electricalforce is directed away from the positive electrode of that lead. Normal ven-tricular activation begins with septal depolarization in a left to right direc-tion; therefore, leads with positive electrodes on the left side of the body (ie,I, aVL, and V6) usually record normal Q waves caused by septal depolariza-tion. This same septal depolarization is recorded as a small R wave in leadsV1 and V2 facing the front of the heart. The presence of a Q wave up to 0.05sec wide in lead III can be a normal variant,1,2 and a negative QS complex is

Carol Jacobson, MN, RNDepartment Editor

Carol Jacobson is Director, Quality Education Services, 3324 SW 172nd St, Burien, WA 98166

(qeskrit@aol.com).

ECGChallenges

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© 2007, AACN

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normal for lead aVR. The only leads inwhich any Q wave is considered abnormalare V1, V2, and V3.2,3

Normal depolarization of the ventricularfree wall proceeds from the endocardium tothe epicardium; therefore, leads facing normalmyocardium record R waves as electricalforces travel toward the positive electrode ofthe lead. The presence of abnormal Q waves(wider and deeper than normal) is a criterionfor the diagnosis of myocardial infarction(MI) because infarcted myocardium does notdepolarize; therefore, leads facing an area ofinfarction do not record any forces travelingtoward the positive electrode. These leadsusually record a Q wave that reflects normalendocardial to epicardial depolarization ofthe ventricular wall on the opposite side of theheart, proceeding away from the positive elec-trode of the recording lead. However, thepresence of an abnormal Q wave is notspecific for infarction, and several other con-ditions can also cause abnormal Q waves that

can mimic infarction. Some of the causes ofnoninfarction Q waves are listed in Table 1.1–9

Ventricular Hypertrophy/CardiomyopathyIn hypertrophic cardiomyopathy, the right orleft ventricular free walls or both become thickbecause of chronic pressure overload. The in-terventricular septum can also become hyper-trophied and can lead to LV outflow tractobstruction. When the septum hypertrophies,normal septal forces that travel left to rightthrough the septum are exaggerated on theECG because of the enlarged septal mass. Septalhypertrophy can produce larger-than-normalQ waves in lateral leads I, aVL, V5, and V6that can mimic lateral wall MI and can resultin larger-than-normal R waves in V1 and V2that mimic posterior wall MI (Figure 1). If theLV free wall is hypertrophied, a QS complexcan be recorded in V1, V2, and sometimes V3,which can mimic anteroseptal MI (Figure 2). Ifthe ST segment is not elevated or shows an

Table 1: Noninfarction Causes of Abnormal Q Waves1–8

Condition Can cause abnormally large Q waves in these leads

Normal variants

Vertical electrical axis aVL

Horizontal electrical axis III, aVF

Acute pulmonary embolism III, aVF

Emphysema or cor pulmonale

Ventricular hypertrophy

Right ventricular hypertrophy V1 (Q sometimes precedes very tall R wave in right

precordial leads)

Left ventricular hypertrophy V1, V2, V3 (QS complex)

Septal hypertrophy I, aVL, V6; sometimes II, III, aVF

Conduction abnormalities

Left bundle branch block or right V1,V2 (causes a QS complex most often)

ventricular paced rhythm

Left anterior hemiblock V1,V2 (may cause small Q waves in anterior leads)

Wolff-Parkinson-White syndrome I, aVL, V6 if left lateral accessory pathway II, III, aVF

if posteroseptal or right lateral accessory

pathway

Replacement of myocardial tissue by Any lead, depending on location of abnormal tissue

electrically silent material: sarcoid,

amyloid, and tumor

Chest electrode misplacement V1, V2 if electrodes placed too high on chest

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upward concave elevation and the T wave isupright in the presence of a QS complex in V1or V2, this favors LV hypertrophy. If the STsegment shows convex elevation with an in-verted T wave, anteroseptal MI is morelikely.2,8

Wolff-Parkinson-White SyndromeIn Wolff-Parkinson-White syndrome, the pres-ence of an accessory pathway connecting theatria to the ventricles provides a conductionpathway through which a supraventricular im-pulse can enter the ventricle directly, bypassingthe normal delay in the atrioventricular nodeand causing abnormal initial depolarization ofthe ventricular wall. This “pre-excitation” of theventricle produces a slurring of the initial por-tion of the QRS complex called a delta wave.The direction of the delta wave depends on thelocation of the accessory pathway. Left-sidedaccessory pathways can produce negative deltawaves that look like Q waves in left lateral leads(I, aVL, V6) and can mimic lateral wall MI.

Right-sided or posteroseptal pathways can pro-duce negative delta waves in leads II, III, andaVF that mimic inferior infarction (Figure 3),and anteroseptal pathways can produce negativedelta waves in V1 and V2 that mimic anteriorMI.

Left Bundle Branch BlockThe first part of the ventricles to depolarize isthe septum in a left to right direction becauseof Purkinje fibers originating high on the leftbundle branch that carry the electrical im-pulse to the left side of the septum and acti-vate it before the rest of the ventricular my-ocardium depolarizes. When the left bundlebranch is blocked, these Purkinje fibers arealso blocked, and the septum depolarizesfrom right to left instead of from left to right.This causes the loss of the normal R wavesseen in the right to middle chest leads (V1–V3)and sometimes in one or more of the inferiorleads (II, III, aVF). This loss of the initial Rwave creates a Q wave that can mimic MI

Figure 1: Recorded from a patient with hypertrophic obstructive cardiomyopathy. Noteabnormally deep Q waves in leads II, III, AFV, V3–V6, and tall R waves caused by septalhypertrophy in V1, V2.

Figure 2: From a patient with left ventricular hypertrophy. Note Q waves in V1–V3 with normal STsegment and upright T wave. Left anterior fascicular block is also present.

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(Figure 4). In left bundle branch block, theQRS is 0.12 sec wide or wider, which is notthe case in MI unless bundle branch block ispresent.

Cor PulmonaleCor pulmonale is acute or chronic right-sidedheart overload caused by pulmonary patho-physiology such as pulmonary embolism,chronic obstructive pulmonary disease, orprimary pulmonary hypertension. Chronic

right-sided heart overload results in rightventricular hypertrophy. Acute right-sidedheart overload due to pulmonary embolismcan cause a large Q wave in lead III that canmimic inferior wall MI (Figure 5). Othercommon ECG changes in pulmonary em-bolism are right axis deviation, a deep S wavein lead I, and T wave inversion in lead III (theSI, Q3, T3 pattern of acute pulmonary em-bolism). Unlike inferior MI, leads II and aVFare rarely involved.

Figure 3: (A): From a 16-year-old boy with Wolff-Parkinson-White syndrome. Note prominent Qwaves in II, III, and aVF mimicking inferior wall MI. (B): Recorded from the same patient a few hourslater. The accessory pathway is not being used for conduction at this time, and the “abnormal Qwaves” have disappeared. The “Q waves” in the first tracing were actually negative delta waves dueto pre-excitation of the ventricle through an accessory pathway. (Tracings courtesy of Dr WilliamNelson, Denver, CO.)

(A)

(B)

Figure 4: Left bundle branch block creating a QS complex in leads III and aVF, mimicking inferior infarction,and in V1–V3, mimicking anterior infarction.

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Chest Electrode MisplacementChest electrodes for leads V1 and V2 placedone interspace too high can cause the R wavenormally recorded in these leads to disappear,which creates a QS complex and can mimicanteroseptal MI (Figure 6).9 These same chestelectrodes placed one interspace too low canexaggerate the size of the R wave in V1 and V2,simulating posterior MI.

References

1. Conover MB. Understanding Electrocardiography. 8thed. St Louis, MO: Mosby; 2003.

2. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P.ECG in Emergency Medicine and Acute Care. Philadel-phia: Elsevier/Mosby; 2005.

3. Wagner GS. Marriott’s Practical Electrocardiography. 10thed. Philadelphia: Lippincott Williams & Wilkins; 2001.

4. Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braun-wald’s Heart Disease: A Textbook of CardiovascularMedicine. 7th ed. Philadelphia: Elsevier Saunders; 2005.

5. Sreeram N, Cheriex EC, Smeets JL, Gorgels AP, WellensHJ. Value of the 12-lead electrocardiogram at hospitaladmission in the diagnosis of pulmonary embolism. AmJ Cardiol. 1994;73:298–303.

6. Geibel A, Zehender M, Kasper W, Olschewski M, KlimaC, Konstantinides SV. Prognostic value of the ECG onadmission in patients with acute major pulmonary em-bolism. Eur Respir J. 2005;25:843–848.

7. Goldberger AL. Pathogenesis and Diagnosis of Q Waveson the Electrocardiogram. In: Rose BD, ed. UpToDate.Waltham, MA; 2006. www.uptodate.com.

8. Marriott HJL. Pearls and Pitfalls in Electrocardiography.Philadelphia: Lea & Febiger; 1990.

9. Marafioti V, Variola A. Pseudoinfarction pattern by mis-placement of electrocardiographic precordial leads. AmJ Emerg Med. 2004;22:62.

Figure 5: Recorded from a 28-year-old woman with acute pulmonary embolism. Note the deep Q wave inlead III that can mimic inferior wall MI. This electrocardiogram also illustrates the S1, Q3, T3 pattern of acutecor pulmonale. (Tracing courtesy of Dr William Nelson, Denver, CO.)

Figure 6: Leads V1–V3 in the left panel recorded one interspace too high and cause Q waves that mimicanterior MI. The right panel shows the same leads recorded at the correct interspace, showing normal R waves in V1–V3.

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