A specialist tells how to interpret subtle changes on the ECG, including those caused by two life-threatening syndromes you might otherwise miss.
Reading ECGs is like learning to appreciate art—it is a skill acquired over time. The more ECGs you read, the easier it becomes to interpret and recognize diagnostic variants. Subtle irregularities can rule in or rule out a probable cause or condition. Comparing a patient’s serial ECGs can be of added value and help determine significant changes over time.
There are two types of ECGs: the single rhythm strip or the 12-lead ECG. The rhythm strip is limited because it provides only one view or a single lead. The 12-lead ECG reveals the pattern by which electrical activity travels through the heart and thus can assist in recognizing conduction abnormalities and the source of conduction problems. An analysis of the waveform and the subsequent depolarization and repolarization yields valuable information.
An ECG has other uses as well. It shows the effects of cardiovascular drugs such as beta blockers, which lower the heart rate. It reveals the location of heart blocks and traces the efficiency of electronic devices, such as permanent pacemakers and automated implantable cardioverter defibrillators (AICDs). It can also reveal electrolyte imbalances.
Several heart diseases or conditions also show up as abnormal tracings. These include ongoing MIs, prior MIs, coronary artery disease or stenosis, ectopic beats, enlargement of the heart, enlargement of different chambers of the heart, rate disturbances, myocarditis, and pericarditis. Correlating ECG tracings with the patient’s history and physical examination can help you determine the treatment for these conditions—whether medical, pharmacologic, or surgical.
There are different approaches to interpreting a tracing. Depending on what you are looking for, the approach may vary. Each arrhythmia has a unique pattern or different morphology that can help make a diagnosis. I have a particular method or a mental checklist for reviewing, interpreting, and evaluating the ECG. Below is the method I follow.
Determining the heart rate
First observe the ECG in its entirety. Take a step back and assess it from a foot away. Instead of counting the tiny squares (each representing 0.04 second), look at the overall appearance.
You should be able to recognize immediately whether the heart rate is fast or slow and simultaneously observe whether there is an irregular rhythm. Using the standard paper speed and size, the minute rate can be determined by counting blocks. Five small blocks equal one large block translating into 0.20 seconds. There are five large, bold blocks per second. Every sixth large block is marked or has a hatch mark. Multiply the number of beats counted within the six large blocks by 10 to determine the heart rate per minute. An alternative method is to count down from 300, 150, 100, 75, and 60 from each of the dark vertical lines between the QRS complexes. It is easiest to start with a QRS point that lies directly on a darkened line. Either method is acceptable for calculating the heart rate per minute. A normal rate ranges from 60-100.
It is important to observe the regularity and the source of the heart’s rhythm. The source can be the sinus or an ectopic beat. Evaluate the relationship of the P wave (if a P wave is present) to the QRS complex. Is there a one-to-one relationship? If not (an ominous sign), the beats are not synchronized. Assess the quality and shape of the P wave, which should be gently rounded, not peaked or sharp. A P wave that is inverted and larger than anticipated could indicate left-atrial hypertrophy. In atrial fibrillation, however, the quivering of the atrium makes it impossible to accurately count the P waves, which appear irregular in relation to the QRS complex.
Heart blocks have different presentations with the relationship of the P wave to the QRS complex. The P and QRS relationship can be prolonged, skipped, or completely disassociated. The ECG of a patient with a permanent pacemaker may exhibit “pacer spikes,” depending on the mode the device is set on and the patient’s intrinsic heart rate. A dual-chamber pacemaker can have two spikes if it is set in the fully automatic pacing (DDD) mode. A pacemaker can be set to initiate when the heart rate goes below a certain number of beats per minute.
A single-chamber pacemaker can be set to commence from the atrial or from the ventricular position, depending on the precipitating condition—bradycardia, heart block, junctional rhythm, or sick sinus syndrome.
Understanding anatomically how the heart is positioned and the distribution of the corresponding coronary arteries makes it easier to determine whether and where an MI is evolving or whether ischemia is present. An ECG can present with Q waves illustrating whether an MI has already occurred. This is when a baseline ECG for comparison is particularly helpful. The location of the abnormal tracing on the ECG will allow you to assess the extent of heart function or dysfunction. Knowing the clinical lead groups (Table 1) can enable you to quickly determine the location of an MI or ischemia.
The posterior wall is typically read by flipping the 12-lead ECG over and looking at reciprocal changes in V1 and V2. The left anterior descending (LAD) coronary artery distribution is reflected in the pattern of the T wave in V2 and V3. (LAD stenosis will be discussed below.) The circumflex coronary artery can supply the lateral and the inferior walls. The right coronary-artery supply distribution is reflected in the inferior wall leads.
Bundle branch blocks
The normal transmission of electrical impulse from the atrial sinus node to the interventricular septum is simultaneously through both ventricles. Bundle branch blocks (BBBs) can either be right (RBBB) (Figure 2) or left (LBBB) (Figure 3). The electrical conduction through the ventricles of a BBB is reflected on the ECG because it is delayed on its way through either the left or the right ventricle.
Typically, an LBBB is an indication of underlying disease, whereas the RBBB often occurs in normal individuals. However, in Brugada’s syndrome, an ECG tracing similar to the tracing of an RBBB can be a sign of danger. A helpful hint for recalling an RBBB is “rabbit ears.” The QRS complex can resemble rabbit ears in V1 and V2. There are two peaks of the R wave (R and R’).
In an LBBB, the QRS complex has a recognizable morphology. The delayed impulse through the ventricle makes the complex wider than normal. Reading ECGs for MIs, infarctions, and bundle branch blocks is a topic for another article. The illustration here is to review at the surface level and prepare for a better understanding of the two cardiac syndromes — Brugada and Wellens.
The morphology depicted in the ECG of a patient with Brugada syndrome is similar to an RBBB but indicates a potentially fatal condition (an arrhythmia that can lead to ventricular tachycardia). It was first described with clinically based evidence about 15 years ago. The incidence is higher in Asians and healthy adults in their 30s and 40s.1 In fact, Brugada syndrome is responsible for approximately one half of sudden deaths in young persons without structural heart disease.1 There is little warning of impending crisis. An otherwise healthy patient may present with a syncopal episode and then suddenly be in ventricular tachycardia or ventricular fibrillation. Unfortunately, no medication exists to treat the condition.
With Brugada syndrome, the ECG tracings in V1, V2, and V3 have a distinct pattern. The QRS is widened and has two upward peaks. This resembles the pattern in an RBBB. Although it is not a true physiologic RBBB, it is a function of the unusual repolarization abnormality (Figure 4). The ST segment begins at the second peak of the widened QRS, then slopes gradually downward.2 However, the QT segment length is not prolonged (i.e., not >0.40 seconds).
Approximately 60% of patients who suffer sudden death (or aborted sudden death) who have the typical Brugada syndrome ECG have a family history of sudden death or have family members with the same ECG abnormalities.1 The condition is autosomal dominant and predominates in men. Genetic mutations occur in the SCN5A gene, which encodes the cardiac sodium channel.1 The altered function of the sodium current leads to altered refractory periods and a suitable substrate for phase 2 re-entry-based arrhythmias. Brugada syndrome can be referred to as a channelopathy.
In conjunction with a thorough history, physical examination, and implantation of an AICD, knowing what to look for can help prevent a Brugada syndrome death.
There is also usually little warning when a patient is having an MI. Wellens syndrome, discernible on an ECG, is a precursor. Typically the T wave in a normal ECG is upright or somewhat flattened in V2 and V3, but in Wellens syndrome the T wave in V2 and V3 is inverted, indicating stenosis or narrowing of the LAD coronary artery (Figure 5).
Identifying LAD coronary artery stenosis can be lifesaving. A patient with Wellens syndrome should be scheduled for an immediate cardiac workup, including a stress test, an echocardiogram, and a diagnostic cardiac catheterization. If a stenosed artery is confirmed, it can be treated with angioplasty, stenting, or coronary artery bypass grafting surgery. In addition, the patient should be started on a cardioprotective medication regimen at once.
ECGs are vital tools in the differential diagnosis of heart-related conditions. The knowledge and understanding of subtle differences and changes over time can alter a treatment plan and make for a better outcome. Brugada and Wellens are two life-threatening syndromes that are revealed on tracings and call for quick diagnostic workups.
Dr. Kleinschmidt practices at St. Vincent’s Hospital, Department of Cardiothoracic Surgery, in New York City, and is a contributing editor to The Clinical Advisor.
1. Brugada J, Brugada R, Brugada P. Determinants of sudden cardiac death in individuals with the electrocardiographic pattern of Brugada syndrome and no previous cardiac arrest. Circulation. 2003;108:3092-3096.
2. Dubin DB. Rapid Interpretation of EKG’s. 6th ed. Tampa, Fla.: Cover Publishing; 2007:251.