22: Electrocardiography

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CHAPTER 22 Electrocardiography

William A. Baker, MD, Christopher M. Lowery, MD

1 Are all abnormal ECGs indicative of heart disease?

No. Just as some individuals are very tall, some individuals without real cardiac pathology have electrocardiogram (ECG) findings that deviate enough from the population mean to raise the question of heart disease. Careful history and physical examination may help identify individuals who truly have cardiac pathology. Noninvasive techniques such as echocardiography and cardiac magnetic resonance imaging may aid in separating patients with true structural heart disease from those with unusual variations who are abnormal only in a statistical sense.

Other findings such as right bundle-branch block (RBBB), are present in patients with heart disease but also occur frequently in patients who have no evidence of heart disease by history, physical examination, or echocardiography.

2 What is the differential diagnosis for low voltage?

Chronic obstructive pulmonary disease, hypothyroidism, pericardial effusion, anasarca, amyloidosis, ischemic cardiomyopathy, and obesity are included in the differential diagnosis.

3 Is electrocardiography sensitive or insensitive for detecting chamber enlargement and hypertrophy?

It is insensitive. When echocardiography or autopsy is used as the gold standard, ECG misses many patients with real chamber enlargement or hypertrophy. This is particularly true with patients who have less severe (yet still potentially meaningful) degrees of these findings. Although useful because of low cost and ease of application, electrocardiography certainly has its limitations.

4 Which clues suggest that a patient may have left ventricular hypertrophy?

High QRS voltage is the hallmark of left ventricular hypertrophy (LVH), although many young patients have high QRS voltage without real LVH. Other associated hints (albeit nonspecific) are left axis deviation, left atrial enlargement, widening of the QRS, and strain (associated ST-T abnormalities).

Patients with left bundle-branch block (LBBB) cannot be diagnosed with LVH from the ECG, but it is important to remember that many patients with LBBB actually have LVH by echocardiography. There are a number of scoring systems to decide whether a patient meets ECG criteria for LVH, and all of them are insensitive.

5 An adult has a large R wave in V1. What is the differential diagnosis?

image Right ventricular hypertrophy (look for associated right axis deviation, right atrial enlargement, and right ventricular (RV) strain with ST-T abnormalities)
image Posterior myocardial infarction
image Wolff-Parkinson-White (WPW) syndrome
image Muscular dystrophy
image Normal early transition

6 What leads are most helpful when looking for a bundle-branch block?

image V1, V6, I, and to some extent II
image The QRS duration should be more than 120 ms to identify a bundle-branch block. Not every wide QRS is a bundle-branch block; the differential diagnosis also includes a ventricular beat, intraventricular conduction delay, hyperkalemia, drug effect, and WPW with conduction through an accessory pathway.

7 What are the characteristics of a right bundle-branch block?

Patients with RBBB typically have an rSR′ pattern in V1 and a broad terminal S wave in I and V6 (Figure 22-1).

image

Figure 22-1 Typical appearance of a right bundle-branch block in V1, with rSR′.

8 What is an intraventricular conduction delay? When is it seen?

An intraventricular conduction delay is a wide QRS that arises from supraventricular conduction that is neither a typical RBBB nor a typical LBBB. It is often noted in patients with a cardiomyopathy.

9 What are the characteristics of a left bundle-branch block?

In V1 there is a broad, deep S wave (or QS wave), with ST segment elevation, that may be preceded by a very narrow R wave (Figure 22-2). In lead I there is a broad R wave (sometimes notched) without a Q or S wave.

image

Figure 22-2 Typical appearance of a left bundle-branch block in V1. In some cases a narrow R wave precedes the large monomorphic S wave.

10 What is a hemiblock?

The left bundle bifurcates into two fascicles (anterior and posterior), and either one may be blocked. With a hemiblock the QRS duration is generally less than 120 milliseconds unless there is an associated RBBB (commonly termed a bifascicular block).

11 You are attempting to pass a Swan-Ganz catheter into the pulmonary artery in a patient with LBBB. When the hemodynamic tracing suggests that the catheter tip is in the right ventricle, the patient suddenly becomes bradycardic, with a heart rate of 25. What happened?

The patient is probably in complete heart block as a result of a catheter-induced RBBB (together with a preexisting LBBB). Fortunately the injury to the right bundle branch is often brief, but temporary pacing may be required.

For patients with LBBB, consider the value of a pulmonary artery catheter carefully before proceeding. In addition, you should have emergency pacing equipment readily available to respond properly if this complication develops. Transient stunning of the right bundle may occur in as many as 5% to 10% of cases.

12 Does a normal ECG exclude the possibility of severe coronary artery disease?

No, although an ECG done during ischemic chest pain is usually abnormal. It is common for patients with severe coronary artery disease (CAD) to have an ECG with only nonspecific abnormalities.

For an example of ECG findings noted in a patient with exertional angina, see Figure 22-3.

image

Figure 22-3 This 12-lead ECG shows deep relatively symmetric T wave inversions, meeting ECG criteria for ischemia. Coronary insufficiency is generally the most common life-threatening cause of this pattern. Not uncommonly patients with chest pain at rest from coronary insufficiency (an acute coronary syndrome) may present with an ECG like this. They might also present with ST segment depression, nonspecific ST-T abnormalities, or even a normal ECG. Although deep symmetric T inversions should generally provoke a clinical evaluation for coronary disease, other causes should be considered, including pulmonary embolus, acute central nervous system pathology (classically a subarachnoid bleed), a cardiomyopathy, abnormal repolarization from ventricular hypertrophy, or significant electrolyte disturbances. This patient was a 42-year-old woman with history of smoking who presented with progressive angina, occurring with only minimal exertion. Catheterization showed severe multivessel disease for which she underwent coronary artery bypass surgery.

13 How are patients with myocardial infarction subdivided on the basis of ECG changes during infarction?

Myocardial infarctions (MIs) are often divided into two types: ST segment elevation MI and non-ST segment elevation MI. Patients with ST segment elevation should be considered for immediate percutaneous coronary intervention (PCI), or thrombolytic therapy if PCI is unavailable. Q waves usually develop over time in the leads where there is elevation. Q waves may diminish in size or go away over time. Patients with acute MI without ST elevation often have ST-segment depression (which may be dynamic) and/or T-wave inversions. Patients with non-ST-elevation MI can usually be made pain-free with medical therapy, and cardiac catheterization is often performed within several days. However, ongoing symptoms and ECG changes refractory to medical therapy can prompt emergent invasive evaluation.

For an example of ECG changes associated with a non-ST segment elevation MI, see Figures 22-4 and 22-5.

image image

Figures 22-4 and 22-5 These ECGs are from the same patient, a vigorous 78-year-old with new chest pain that began after moderate exertion. Figure 22-4 was obtained while the patient was in an emergency room with persistent chest pain. The main finding is significant ST segment depression in the anterolateral precordial leads. The chest pain and ST segment changes resolved over the next 30 minutes (see Figure 22-5). Troponin I serum levels were mildly elevated. Because the pain was provoked by minimal exertion, with significant ECG abnormalities and abnormal troponin I, coronary angiography was performed instead of stress testing. Significant left main and multivessel coronary artery disease (CAD) was found, and the patient underwent successful coronary artery bypass surgery. In this example the suspicion of CAD was very strong, based on the ECG changes and clinical characteristics. However, more modest degrees of ST depression are less specific for coronary insufficiency, particularly when differences are subtle and when there is a potential alternative explanation (electrolyte imbalance, digoxin effect, or repolarization abnormality from left ventricular hypertrophy).

14 Does ST-segment elevation always indicate a myocardial infarction?

No. Other causes of ST-segment elevation are listed in Table 22-1.

TABLE 22-1 Causes of St-Segment Elevation

Acute subepicardial injury (i.e., acute ST-segment elevation myocardial infarction) HypercalcemiaLeft ventricular hypertrophy
Early repolarization pattern Left bundle-branch block
Pericarditis Brugada syndrome
Hyperkalemia Normal variant

15 For patients with ST-segment elevation myocardial infarction, how is the location identified?

image Patients with inferior MI generally have ST elevation in II, III, and aVF
image Patients with lateral MI have ST elevation in I, aVL, V5, and V6
image Patients with anterolateral MI have ST elevation in I, aVL, and V3-V6
image Patients with septal MI have ST elevation in V1-V2
image Patients with anteroseptal MI have ST elevation in V1-V4
image Patients with anterior MI have ST elevation in V3-V4

For an example of an ST segment elevation MI, see Figure 22-6.

image

Figure 22-6 This 12-lead ECG was obtained from a 60-year-old woman with chest pain. Massive ST segment elevation (subepicardial injury) accompanied by Q waves in V1-3 and reciprocal inferior ST depression, is noted in this florid example of an anterior ST elevation myocardial infarction, or STEMI. The prominent rectangular-shaped ST elevation is sometimes referred to as a tombstone. The infarct vessel was the left anterior descending (LAD) coronary artery. Patients with a STEMI should receive some form of emergent reperfusion therapy (percutaneous coronary intervention, if readily available, or thrombolytic therapy when not contraindicated).

16 A patient has evidence on ECG of an acute inferior myocardial infarction. What associated findings should you look for?

image Evidence of right ventricular involvement. Since V1 is really a right-sided lead, ST elevation in V1 accompanying an inferior MI suggests right ventricular involvement. Alternatively you may check right-sided leads over the right precordium. ST elevation of 1 mm in right-sided V4 or V5 indicates RV infarction.
image Evidence of lateral wall involvement, usually suggested by ST elevation in V5-V6.
image Evidence of posterior wall involvement, as suggested by an R wave in V1 that is broad and/or tall, particularly in comparison with prior ECGs. Patients with posterior MI often have ST depression in V1-V2.
image Evidence of bradycardia caused by sinoatrial (SA) or atrioventricular (AV) nodal block. Patients with inferior MI may require atropine and/or temporary pacing (Figure 22-7).
image

Figure 22-7 Limb leads from a patient with inferior myocardial infarction and complete heart block (see Chapter 30). The patient has ST segment elevation in II, III, and aVF, along with ST segment depression in I and aVL (reciprocal change). Complete heart block is indicated by atrioventricular dissociation with the atrial rate (≈110) greater than the ventricular rate (≈40/min) with a regular RR interval.

17 What is reciprocal change? Why is it important?

Reciprocal change is ST-segment depression that occurs in patients with an ST-elevation MI. For example, a patient with an inferior MI may have ST elevation in II, III, and aVF, with ST depression (reciprocal change) in I and aVL. Not all patients with ST-elevation MI have reciprocal change, but when it is seen, it generally confirms the diagnosis of acute MI (see Figure 22-7).

18 What ECG findings suggest hypothyroidism?

Low QRS voltage, bradycardia, and QT interval prolongation. There may also be associated T-wave abnormalities and AV block.

19 An elderly patient presents with fatigue, confusion, and atrial fibrillation with a slow ventricular response (heart rate = 40). The ECG demonstrates ST depression that is concave upward. The family states that the patient is on an unknown medication that is locked in his apartment. What laboratory test should you order to confirm your suspicion?

Serum digoxin level.

20 An ECG recorded when the operating room nurse is scrubbing the patient’s chest demonstrates wide complex electrical activity. The patient is asymptomatic. What do you suspect? How can you prove that you are correct when you analyze the ECG tracing?

Artifact is common in this scenario, and in other situations in which there is to-and-fro activity such as tooth brushing. With artifact the heart rate is generally about the same before and immediately after the wide complex signal. With calipers, QRS complexes marching through the artifact at the baseline heart rate can often be seen. If simultaneous pulse oximetry waveforms are available, it is possible to confirm that the heart rate is relatively constant throughout the “arrhythmia.”

21 What ECG findings suggest hyperkalemia?

QRS widening and/or peaked T waves (Figure 22-8). In the worst cases the ECG looks like a sine wave.

image

Figure 22-8 This ECG was obtained from a patient with hyperkalemia (9.2 mmol/L). Note the sharp peaking of T waves, broadening of the QRS complex, and diminished P wave amplitude.

22 What ECG findings suggest hypokalemia?

U waves (which occur after the T wave) are prominent and may merge with the T wave, creating a broad T wave and a prolonged QT interval. In addition, the P wave may be amplified, and ST depression may occur (Figures 22-9 and 22-10).

image

Figure 22-9 This ECG was obtained from a patient with hypokalemia (2.1 mmol/L). ST-T wave abnormalities in the anterior leads raised concern for myocardial ischemia, but abnormalities were substantially improved after repletion of potassium.

image

Figure 22-10 This ECG was obtained from a patient with hypokalemia (3.2. mmol/L). Note the prominent U wave after the T wave in the precordial leads V2-6. There is often TU fusion with hypokalemia, creating a broad T wave and an increase in the measured QT interval. Polymorphic ventricular tachycardia may result from hypokalemia.

23 What ECG findings suggest hypocalcemia?

The QT interval is prolonged without broadening of the T wave (in contrast to the situation with hypokalemia). The T wave appears to be pushed away from the QRS complex. See Figure 22-11.

image

Figure 22-11 This ECG was obtained from a 34-year-old man with pseudohypoparathyroidism and a dilated cardiomyopathy. Serum calcium was 5.9 mg/dl, with ionized calcium 0.74 mmol/L. The QT was measured at 484 msec, with QTc 586. The QT is pushed away from the QRS complex, merging with the P wave in some leads. This patient’s dilated cardiomyopathy gradually resolved after treatment with calcium.

24 What ECG changes suggest hypercalcemia?

Shortening of the QT interval, with or without ST segment elevation (Figure 22-12).

image

Figure 22-12 This ECG was obtained from a patient with hypercalcemia (serum calcium 12.5 mg/dl). The ST-T complex is pushed up, and the QT is shortened. Hypercalcemia may be a result of malignancy (especially with bone metastasis), hyperparathyroidism, sarcoid, or other conditions.

KEY POINTS: Electrocardiography image

Differential diagnosis of large R wave in V1:

1. Right ventricular hypertrophy
2. Posterior wall myocardial infarction
3. Normal variant (early transition)
4. WPW syndrome
5. Muscular dystrophy

25 What are some of the common causes of a prolonged QT interval?

image Abnormal electrolytes, especially hypokalemia, hypocalcemia, and hypomagnesemia, can contribute to lengthening of the QT.
image Many medications may contribute to QT prolongation, and certain categories are more notorious than others. Psychoactive medications, particularly phenothiazines, tricyclic antidepressants, methadone, and butyrophenones, can prolong the QT.
image Many antiarrhythmics (especially sotalol, amiodarone, and type Ia antiarrhythmics such as procainamide) prolong the QT.
image In other cases introduction of medications (cimetidine, verapamil, ketoconazole, erythromycin) or cirrhosis may interfere with hepatic metabolism of agents that prolong the QT.
image Structural heart disease from a cardiomyopathy or myocardial ischemia may prolong the QT.
image Patients with bradycardia or QRS prolongation (e.g., from a bundle-branch block) may have QT prolongation.
image Systemic illnesses such as hypothyroidism may result in QT prolongation.
image Some patients have a hereditary predisposition to QT prolongation (a congenital long QT syndrome resulting from abnormal ion channels), which can become more evident during pregnancy.

Many patients have QT prolongation from a combination of the above factors. For example, a patient with congenital long QT syndrome may have more extreme prolongation with the addition of a new drug or electrolyte abnormality. In some cases these multifactorial processes can result in life-threatening ventricular arrhythmias such as torsades de pointes (see Chapter 30).

26 A patient has a right bundle-branch block that is new compared to the ECG from 2 years ago. How should I proceed?

Although a RBBB can be caused by CAD (e.g., with a large anterior infarct destroying some of the conduction system in the interventricular septum), this is only true in a minority of RBBB patients. Such patients typically have a qR in V1 instead of an rSR′ prime because the initial r wave is lost as a consequence of the MI.

Occasionally an RBBB may be caused by congenital heart disease (such as tetralogy of Fallot), prior cardiac surgery, a cardiomyopathy, or pulmonary hypertension. History and physical examination can supplement the ECG in theses cases; and, if clinical signs of structural heart disease are noted, echocardiography may be useful.

In a minority of cases RBBB may be present in patients with significant conduction system disease. For example, some patients with coexisting hemiblock, first-degree AV block, and RBBB may be at risk for complete heart block. However, in the absence of symptoms of complete heart block (e.g., syncope or near syncope) or some ECG evidence of higher degree AV block, prophylactic pacing is not indicated.

Patients who have had (at different times) both an RBBB and an LBBB are at significant risk of complete heart block; permanent pacing is generally indicated.

For most patients with RBBB, the prognosis is excellent, and the likelihood of serious underlying heart disease is low. If the history and physical examination do not reveal any evidence of such disease, no further testing or consultation is necessary.

27 A patient has a left bundle-branch block that is new compared to the ECG from 2 years ago. How should I proceed?

In a patient with signs and symptoms of acute myocardial ischemia (e.g. chest pain, new congestive heart failure (CHF), hemodynamic instability), a new LBBB may be a sign of a new, large acute anterior MI. However, in the vast majority of cases a new LBBB is not caused by an acute MI. Sometimes a 12-lead ECG may indicate superimposed subepicardial injury in acute MI cases, but the diagnosis is more difficult than the diagnosis of an ST elevation MI without a bundle-branch block.

Even in the absence of an acute MI, an LBBB may indicate underlying structural heart disease such as a dilated cardiomyopathy or left ventricular hypertrophy. History and physical examination looking for signs and symptoms of angina, heart failure, syncope, hypertension, and valvular heart disease, are important. For elective situations echocardiography is reasonable to look for structural heart disease. Some practitioners obtain stress imaging (such as with adenosine or persantine nuclear perfusion scintigraphy) to exclude chronic ischemic heart disease as a cause of LBBB.

Overall LBBB is a less favorable prognostic sign than RBBB, even in the absence of abnormalities noted on history, physical examination, and noninvasive testing. However, the timing and necessity of any noninvasive testing depends on the patient’s clinical situation and the acuity of the surgical need. For an urgent surgical indication in a patient without other signs and symptoms of CHF or acute myocardial ischemia, it is reasonable to proceed with surgery.

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SUGGESTED READINGS

1. Bowbrick S., Borg A.N. ECG complete. New York: Churchill Livingstone, 2006.

2. Ellis K.M. EKG Plain and simple, ed 2. Prentice Hall: Upper Saddle River, New Jersey, USA, 2007.

3. Kilgfield P., Lauer M.S. Exercise electrocardiogram resting: beyond the ST segment. Circulation. 2006;114:2070-2082.

4. Lanza G.A. The clectrocardiogram as a prognostic tool for predicting major cardiac events. Prog Cardiovasc Dis. 2007;50:87-111.

5. Nelson W.P., Marriott H.J.L., Schocken D.D. Concepts and cautions in electrocardiography, ed 1. MedInfo: Northglenn, Colorado, USA, 2007.

6. Roden D.M. Drug-induced prolongation of the QT interva. N Engl J Med. 2004;350:1013-1022.

7. Sgarbossa E.B., Pinski S.L., Barbagelata A., et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996;334:481-487.

8. Surawicz B., Kailans T.K. Chou’s electrocardiography in clinical practice: adult and pediatric, ed 6. Philadelphia: Saunders, 2008.

9. Wagner G.S. Marriott’s practical electrocardiography, ed 11. Philadelphia: Lippincott, Williams & Wilkins, 2007.

10. Wang K., Asinger R.W., Marriott H.J.L. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med. 2003;349:2128-2135.

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