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Fundamental concepts in understanding electrocardiography and the origin of Q waves include the following:
1. The QRS complex represents ventricular depolarization: a Q wave is an initial negative deflection from the baseline, an R wave is a positive deflection from the baseline, and an S wave is a negative deflection that follows an R wave.
2. The positive electrode in any lead is the recording electrode (ie, the camera taking the picture of depolarization).
3. When the positive electrode sees depolarization traveling toward it, it records an upright deflection (ie, ventricular depolarization traveling toward a positive electrode results in an upright deflection, or R wave). If the positive electrode sees depolarization traveling away from it, it records a negative deflection (ie, ventricular depolarization traveling away from a positive electrode results 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 wall or bottom of the heart are II, III, and aVF. Leads with a positive electrode on the 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 anterior wall of the left ventricle (LV).
A normal Q wave is an initial negative deflection from the baseline that is less than 0.03 sec in width and less than 25% the height of the R wave in most ECG leads.1-3 Q waves are recorded in leads where the initial electrical force is directed away from the positive electrode of that lead. Normal ventricular activation begins with septal depolarization in a left to right direction; 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 depolarization. This same septal depolarization is recorded as a small R wave in leads V1 and V2 facing the front of the heart. The presence of a Q wave up to 0.05 sec wide in lead III can be a normal variant,1,2 and a negative QS complex is normal for lead aVR. The only leads in which any Q wave is considered abnormal are V1, V2, and V3.2,3
Normal depolarization of the ventricular free wall proceeds from the endocardium to the epicardium; therefore, leads facing normal myocardium record R waves as electrical forces travel toward the positive electrode of the lead. The presence of abnormal Q waves (wider and deeper than normal) is a criterion for the diagnosis of myocardial infarction (MI) because infarcted myocardium does not depolarize; therefore, leads facing an area of infarction do not record any forces traveling toward the positive electrode. These leads usually record a Q wave that reflects normal endocardial to epicardial depolarization of the ventricular wall on the opposite side of the heart, proceeding away from the positive electrode of the recording lead. However, the presence of an abnormal Q wave is not specific for infarction, and several other conditions can also cause abnormal Q waves that can mimic infarction. Some of the causes of noninfarction Q waves are listed in Table 1.1-9
In hypertrophic cardiomyopathy, the right or left ventricular free walls or both become thick because of chronic pressure overload. The interventricular septum can also become hypertrophied and can lead to LV outflow tract obstruction. When the septum hypertrophies, normal septal forces that travel left to right through the septum are exaggerated on the ECG because of the enlarged septal mass. Septal hypertrophy can produce larger-than-normal Q waves in lateral leads I, aVL, V5, and V6 that can mimic lateral wall MI and can result in larger-than-normal R waves in V1 and V2 that mimic posterior wall MI (Figure 1). If the LV free wall is hypertrophied, a QS complex can be recorded in V1, V2, and sometimes V3, which can mimic anteroseptal MI (Figure 2). If the ST segment is not elevated or shows an upward concave elevation and the T wave is upright in the presence of a QS complex in V1 or V2, this favors LV hypertrophy. If the ST segment shows convex elevation with an inverted T wave, anteroseptal MI is more likely.2,8
In Wolff-Parkinson-White syndrome, the presence of an accessory pathway connecting the atria to the ventricles provides a conduction pathway through which a supraventricular impulse can enter the ventricle directly, bypassing the normal delay in the atrioventricular node and causing abnormal initial depolarization of the ventricular wall. This "pre-excitation" of the ventricle produces a slurring of the initial portion of the QRS complex called a delta wave. The direction of the delta wave depends on the location of the accessory pathway. Left-sided accessory pathways can produce negative delta waves that look like Q waves in left lateral leads (I, aVL, V6) and can mimic lateral wall MI. Right-sided or posteroseptal pathways can produce negative delta waves in leads II, III, and aVF that mimic inferior infarction (Figure 3), and anteroseptal pathways can produce negative delta waves in V1 and V2 that mimic anterior MI.
The first part of the ventricles to depolarize is the septum in a left to right direction because of Purkinje fibers originating high on the left bundle branch that carry the electrical impulse to the left side of the septum and activate it before the rest of the ventricular myocardium depolarizes. When the left bundle branch is blocked, these Purkinje fibers are also blocked, and the septum depolarizes from right to left instead of from left to right. This causes the loss of the normal R waves seen in the right to middle chest leads (V1-V3) and sometimes in one or more of the inferior leads (II, III, aVF). This loss of the initial R wave creates a Q wave that can mimic MI (Figure 4). In left bundle branch block, the QRS is 0.12 sec wide or wider, which is not the case in MI unless bundle branch block is present.
Cor pulmonale is acute or chronic right-sided heart overload caused by pulmonary pathophysiology such as pulmonary embolism, chronic obstructive pulmonary disease, or primary pulmonary hypertension. Chronic right-sided heart overload results in right ventricular hypertrophy. Acute right-sided heart overload due to pulmonary embolism can cause a large Q wave in lead III that can mimic inferior wall MI (Figure 5). Other common ECG changes in pulmonary embolism are right axis deviation, a deep S wave in lead I, and T wave inversion in lead III (the SI, Q3, T3 pattern of acute pulmonary embolism). Unlike inferior MI, leads II and aVF are rarely involved.
Chest electrodes for leads V1 and V2 placed one interspace too high can cause the R wave normally recorded in these leads to disappear, which creates a QS complex and can mimic anteroseptal MI (Figure 6).9 These same chest electrodes placed one interspace too low can exaggerate the size of the R wave in V1 and V2, simulating posterior MI.
1. Conover MB. Understanding Electrocardiography. 8th ed. St Louis, MO: Mosby; 2003. [Context Link]
2. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Philadelphia: Elsevier/Mosby; 2005. [Context Link]
3. Wagner GS. Marriott's Practical Electrocardiography. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2001. [Context Link]
4. Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. Philadelphia: Elsevier Saunders; 2005. [Context Link]
5. Sreeram N, Cheriex EC, Smeets JL, Gorgels AP, Wellens HJ. Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol. 1994;73:298-303. [Context Link]
6. Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV. Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. Eur Respir J. 2005;25:843-848. [Context Link]
7. Goldberger AL. Pathogenesis and Diagnosis of Q Waves on the Electrocardiogram. In: Rose BD, ed. UpToDate. Waltham, MA; 2006. http://www.uptodate.com. [Context Link]
8. Marriott HJL. Pearls and Pitfalls in Electrocardiography. Philadelphia: Lea & Febiger; 1990. [Context Link]
9. Marafioti V, Variola A. Pseudoinfarction pattern by misplacement of electrocardiographic precordial leads. Am J Emerg Med. 2004;22:62. [Context Link]
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