Q Waves V4-v6

[Bowie Maur]

Wellens syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with/following ischaemic sounding chest pain) that is highly specific for critical stenosis of the left anterior descending artery.

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner

Pathologic Q waves are a sign of previous myocardial infarction. They are the result of absence of electrical activity. A myocardial infarction can be thought of as an elecrical 'hole' as scar tissue is electrically dead and therefore results in pathologic Q waves. Pathologic Q waves are not an early sign of myocardial infarction, but generally take several hours to days to develop. Once pathologic Q waves have developed they rarely go away. However, if the myocardial infarction is reperfused early (e.g. as a result of percutaneous coronary intervention) stunned myocardial tissue can recover and pathologic Q waves disappear. In all other situations they usually persist indefinitely.

Besides the stethoscope, the electrocardiogram (ECG) is the oldest and most enduring tool of the cardiologist. A basic knowledge of the ECG will enhance the understanding of cardiology (not to mention this book).

At every beat, the heart is depolarized to trigger its contraction. This electrical activity is transmitted throughout the body and can be picked up on the skin. This is the principle behind the ECG. An ECG machine records this activity via electrodes on the skin and displays it graphically. An ECG involves attaching 10 electrical cables to the body: one to each limb and six across the chest.

The standard ECG uses 10 cables to obtain 12 electrical views of the heart. The different views reflect the angles at which electrodes "look" at the heart and the direction of the heart's electrical depolarization.

Three bipolar leads and three unipolar leads are obtained from three electrodes attached to the left arm, the right arm, and the left leg, respectively. (An electrode is also attached to the right leg, but this is an earth electrode.) The bipolar limb leads reflect the potential difference between two of the three limb electrodes:

The limb leads look at the heart in a vertical plane (see Figure 2), whereas the chest leads look at the heart in a horizontal plane. In this way, a three-dimensional electrical picture of the heart is built up (see Table 1).

The route that the depolarization wave takes across the heart is outlined in Figure 3. The sinoatrial node (SAN) is the heart's pacemaker. From the SAN, the wave of depolarization spreads across the atria to the atrioventricular node (AVN). The impulse is delayed briefly at the AVN and atrial contraction is completed.

The wave of depolarization then proceeds rapidly to the bundle of His where it splits into two pathways and travels along the right and left bundle branches. The impulse travels the length of the bundles along the interventricular septum to the base of the heart, where the bundles divide into the Purkinje system. From here, the wave of depolarization is distributed to the ventricular walls and initiates ventricular contraction.

The ECG machine processes the signals picked up from the skin by electrodes and produces a graphic representation of the electrical activity of the patient's heart. The basic pattern of the ECG is logical:

The three waves of the QRS complex represent ventricular depolarization. For the inexperienced, one of the most confusing aspects of ECG reading is the labeling of these waves. The rule is: if the wave immediately after the P wave is an upward deflection, it is an R wave; if it is a downward deflection, it is a Q wave:

The ST segment, which is also known as the ST interval, is the time between the end of the QRS complex and the start of the T wave. It reflects the period of zero potential between ventricular depolarization and repolarization.

Since the direction of a deflection, upward or downward, is dependent on whether the electrical activity is going towards or away from a lead, it differs according to the orientation of the lead with respect to the heart (see Figure 5).

The ECG trace reflects the net electrical activity at a given moment. Consequently, activity in one direction is masked if there is more activity, eg, by a larger mass, in the other direction. For example, the left ventricle muscle mass is much greater than the right, and therefore its depolarization accounts for the direction of the biggest wave.

P waves are the key to determining whether a patient is in sinus rhythm or not. If P waves are not clearly visible in the chest leads, look for them in the other leads. The presence of P waves immediately before every QRS complex indicates sinus rhythm. If there are no P waves, note whether the QRS complexes are wide or narrow, regular or irregular.

This is the hallmark of atrial fibrillation (see Figure 7). Sometimes the baseline appears "noisy" and sometimes it appears entirely flat. However, if there are no P waves and the QRS complexes appear at randomly irregular intervals, the diagnosis is atrial fibrillation.

The axis is the net direction of electrical activity during depolarization. It is altered by left ventricular or right ventricular hypertrophy or by bundle branch blocks. It is a very straightforward measurement that, once it has been grasped, can be calculated instantaneously:

The first electrical resuscitation of a human took place (almost certainly) in 1872. The resuscitation of a drowned girl with electricity is described by Guillaume Benjamin Amand Duchenne de Boulogne, a pioneering neurophysiologist, in the third edition of his textbook on the medical uses of electricity. Although it is sometimes described as the first artificial pacing, the stimulation was of the phrenic nerve and not the myocardium.

A distance of more than five small squares from the start of the P wave to the start of the R wave (or Q wave if there is one) constitutes first-degree heart block (see Figure 10). It rarely requires action, but in the presence of other abnormalities might be a sign of hyperkalemia, digoxin toxicity, or cardiomyopathy.

A normal ECG has only very small Q waves. A downward deflection immediately following a P wave that is wider than two small squares or greater in height than a third of the subsequent R wave is significant: such Q waves can represent previous infarction (see Figure 11, previous page).

The ST segment extends from the end of the S wave to the start of the T wave. It should be flat or slightly upsloping and level with the baseline. Elevation of more than two small squares in the chest leads or one small square in the limb leads, combined with a characteristic history, indicates the possibility of MI (see Figure 15, previous page). ST depression is diagnostic of ischemia (see Figure 16). It is worth noting that although ST elevation can localize the lesion (eg, anterior MI, inferior MI), ST depression cannot. Concave upwards ST elevation in all 12 leads is diagnostic of pericarditis.

In a normal ECG, T waves are upright in every lead except aVR. T-wave inversion can represent current ischemia or previous infarction (see Figure 17). In combination with LVH and ST depression, it can represent "strain". This form of LVH carries a poor prognosis.

Sinus tachycardia is seen in many patients with pulmonary embolism. New right bundle branch block (RBBB) or right axis deviation with "strain" can also indicate PE. The classic SIQIIITIII is less common.

Nobody knows for sure why these letters became standard. Certainly, mathematicians used to start lettering systems from the middle of the alphabet to avoid confusion with the frequently used letters at the beginning. Einthoven used the letters O to X to mark the timeline on his ECG diagrams and, of course, P is the letter that follows O. If the image of the PQRST diagram was striking enough to be adopted by researchers as a true representation of the underlying form, it would have been logical to continue the same naming convention when the more advanced string galvanometer started creating ECGs a few years later.

On the other hand, old anterior QS waves with persisting ST elevation (LV aneurysm morphology) are the most frequently misdiagnosed form of ST elevation in ED patients presenting with chest pain, and can lead to unnecessary cath lab activation [10]. ECG machines and STEMI criteria can not tell the difference, but past medical history, symptom duration, prior ECG and other ECG criteria can help with this distinction. Acute ischemia produces hyperacute T waves (relative to the preceding QRS complex) that can help differentiate new STE from old STE. If the differential is LV aneurysm vs anterior STE (i.e. not STE from LBBB or LVH), then a single lead in V1-4 with a T wave amplitude to QRS amplitude ratio > 0.36 identifies STEMI with a sensitivity of 92% and specificity of 81%. False negatives arise when the symptoms have been present for more than 6 hours, because hyperacute T waves diminish and can become inverted [11-12].

Impression: In contrast to LBBB that reverses septal depolarization and produces anterior Q-waves and discordant ST elevation, RBBB does not disturb septal depolarization, so there should be no Q-waves and discordant ST depression. But here there are new Q-waves and concordant ST elevation, a sign of RBBB with occlusion MI (a high risk infarct). Initially missed by computer and physician and treated with puffers for presumed COPD. First Troponin I = 15,000, cath lab activated: 100% LAD occlusion. Peak troponin 42,000 and cardiac arrest.

Impression: Multiple signs of proximal LAD occlusion. Cath lab activated: 95% proximal LAD occlusion, first Trop I of 2,000, peak at 50,000. Next day ECG had persisting anterior QS waves but reduction of hyperacute T waves.

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