There are at least three common “shortness of breath emergencies” – pulmonary thromboembolism, pericardial effusion and myocarditis – where the ECG often provides the first diagnostic information. While the ECG is not the definitive test for any of these conditions, the ECG is often the first test performed. In many cases, the ECG provides unmistakable clues that can guide initial treatment and further diagnostic testing.
Pulmonary embolism (PE) is a common cause of dyspnea. The most common ECG abnormalities are sinus tachycardia; T-wave inversions in leads V1, V2 and V3; a rightward QRS axis (or an axis that is more rightward than normal for the patient’s age); the S1-Q3-T3 pattern; and an rSR’ pattern in lead V1. Atrial flutter and atrial fibrillation occur less commonly.
Concurrent T-wave inversions in the anterior and inferior leads are a vital clue to the presence of acute PE; however, these T-wave inversions are often misinterpreted by clinicians and computer algorithms as “possible anterior ischemia, possible inferior ischemia.”
In patients with acute PE, anterior T-wave inversions, an rSR’ complex in V1 and acute right axis deviation are markers of acute pulmonary hypertension and right heart strain. They are associated with more severe pulmonary hypertension, right ventricular dysfunction, extensive pulmonary vascular obstruction (clot burden) and mortality.
Myocarditis often presents with dyspnea as well as chest pain, palpitations and, frequently, signs of congestive heart failure. Classically, a viral prodrome is present. The combination of low voltage in the limb or precordial leads and sinus tachycardia should raise the suspicion of acute myocarditis. The ECG may also demonstrate diffuse ST- and T-wave changes, including ST-segment elevations, ST-segment depressions, T-wave inversions, premature atrial or ventricular beats and conduction abnormalities. Echocardiography is frequently the key test that defines the global wall motion abnormalities that are characteristic of diffuse myocarditis.
Some patients develop a focal myocarditis; here, the ECG may show ST-segment elevations in a regional pattern (for example, suggesting inferior wall STEMI). Acute myocarditis is a “don’t-miss” diagnosis because patients may develop fulminant congestive heart failure or malignant ventricular arrhythmias.
Shortness of breath is the most common symptom in patients with cardiac tamponade. The characteristic ECG findings include sinus tachycardia, low-voltage QRS complexes and, frequently, electrical alternans.
Chronic emphysema also presents characteristic ECG changes. The most common are abnormal right axis deviation and other features of right ventricular enlargement, right atrial enlargement (p-pulmonale), low QRS voltage in the limb or precordial leads, the “Lead I sign,” and poor R-wave progression. Tachycardias, including multifocal atrial tachycardia, also occur commonly in patients with severe emphysema, especially during hypoxic respiratory emergencies.
The Electrocardiography of Shortness of Breath
There are dozens of causes of shortness of breath; in most cases, the diagnosis does not depend on the electrocardiogram. Pneumonia, asthma, emphysema, congestive heart failure, upper airway obstruction and other common conditions are usually evident after performing a careful history and physical examination.
At the same time, there are at least three common “shortness of breath emergencies” – pulmonary thromboembolism, pericardial effusion and myocarditis – where the ECG often provides the first diagnostic information. The ECG is not the definitive test for any of these conditions; in terms of “diagnostic test characteristics” (sensitivity and specificity), the ECG may perform poorly. However, the ECG is often the first test performed. In many cases, the ECG provides unmistakable clues to these critical conditions.
The ECG in Pulmonary Embolism
Pulmonary embolism (PE) is a common cause of dyspnea. Even though the ECG is not a sensitive or specific test for acute pulmonary embolism and even though the exact contribution of the ECG to other clinical decision tools (for example, Wells, Geneva, PERC, the d-dimer or other cardiac biomarkers) is unknown, the ECG often presents early clues to this diagnosis (Digby et al., 2015). In addition, PE typically presents with chest pain, dyspnea, dizziness or syncope. Since virtually every patient with one of these symptoms receives an ECG, it will always be important to recognize the telltale electrocardiographic features of PE (Digby et al., 2015).
If sinus tachycardia and “nonspecific ST-T-wave changes” are included, the ECG is abnormal in most patients with an acute PE (Geibel et al., 2005; Pollack, 2006; Petrov, 2001; Ferrari et al., 1997; Wagner and Strauss, 2014; Surawicz and Knilans, 2008; Chan et al., 2005; Chan et al., 2001). The most common and helpful ECG findings are listed in the table and are described later.
Increasingly, the ECG is recognized for providing valuable prognostic, as well as diagnostic, information in patients with suspected PE (Digby et al., 2015). Many of the ECG abnormalities (for example, right axis deviation, S1Q3T3, right bundle branch block and, especially, right precordial T-wave inversions) are reflections of elevated pulmonary artery pressures and right heart strain. They are associated with more severe pulmonary hypertension and right ventricular dysfunction; they are also associated with more extensive pulmonary vascular obstruction (clot burden) and in-hospital complications, such as cardiogenic shock and mortality (Ferrari et al., 1997; Geibel et al., 2005; Petrov, 2001; Digby et al., 2015). The ECG findings in patients with acute PE are often transient, and they may lessen or disappear after successful lytic therapy (Surawicz and Knilans, 2008; Chan et al., 2001).
In 2015, Digby et al. published a comprehensive review of the prognostic value of the ECG in patients presenting with acute PE (Digby et al., 2015). They summarized decades of evidence regarding sinus tachycardia, right axis deviation, S1Q3T3, right bundle branch block and T-wave inversions in the right precordial and other leads. The review also highlighted several more recently recognized ECG manifestations of PE, including ST-segment elevations in V1, ST-segment elevations in aVR, QT prolongation and low QRS voltage.
Right Axis Deviation
One critical ECG clue to pulmonary embolism is the finding of right axis deviation. The QRS axis must be interpreted in light of the patient’s age. ECG textbooks and computer algorithms often assert that the QRS axis is abnormally rightward only if the measured QRS axis is outside the range between –30 and +105 degrees. However, the clinician has to be more flexible (and more astute). The axis in newborns and children is rightward, reflecting the dominance of the right ventricle and right ventricular outflow tract. However, the axis shifts leftward as people age (Stephen, 1990; Wagner and Strauss, 2014; Surawicz and Knilans, 2008; Rijnbeek et al., 2014). Therefore, any degree of rightward axis – that is, any visible S-wave in lead I – may be abnormal in patients older than age 45–50 years. In older patients with chest pain, dyspnea, syncope or other cardiovascular symptoms, the presence of an S-wave in lead I, signifying a QRS axis that is abnormally rightward for the patient’s age, may be the only clue to acute right heart strain and PE. Examples are provided later in this chapter.
Right axis deviation (including S1-Q3-T3)
T-wave inversions in right precordial leads
T-wave inversions in both anterior precordial and inferior limb leads
Complete or incomplete right bundle branch block (rSR’ in V1)
Atrial fibrillation or atrial flutter
Right atrial enlargement (P-pulmonale)
While sinus tachycardia is the most common ECG abnormality in patients with acute PE, the S1-Q3-T3 pattern is often considered a “classic” or even “pathognomonic” finding (Pollack, 2006). However, the S1-Q3-T3 pattern is uncommon, and it is neither sensitive nor specific for acute PE.
The most important component of the S1-Q3-T3 is probably the right axis deviation (S-wave in lead I), indicating acute right heart strain. The Q3-T3 is harder to explain; it may reflect acute clockwise rotation of the heart due to right ventricular dilatation. This would result in an abnormal direction of septal and ventricular depolarization in a posterior and leftward direction (away from lead III) (Chan et al., 2005).
T-wave inversions in the right precordial leads (V1–V3) are, in some series, the most common ECG abnormality in patients with acute PE, occurring more frequently than sinus tachycardia or the S1Q3T3 pattern (Ferrari et al., 1997). In patients who present with symptoms suggestive of an acute coronary syndrome and T-wave inversions in the right precordial leads, acute PE, as well as anterior wall ischemia, should be considered in the differential diagnosis.
Even more diagnostic, if there are concurrent T-wave inversions in the anterior and inferior leads, PE should be strongly considered (Marriott, 1997). All too often, when the T-waves are inverted in the anterior and inferior leads, clinicians and computer algorithms misinterpret this finding. It is common for the computer to suggest, “T-wave abnormality, consider anterior ischemia; T-wave abnormality, consider inferior ischemia.” Of course, simultaneous inferior and anterior ischemia is quite uncommon. Thus, in a patient with dyspnea, chest pain, dizziness, syncope or other cardiovascular symptoms, acute PE should rise to the top of the differential list. T-wave inversions are a critical finding that suggests a greater clot burden and a higher risk of hemodynamic collapse and mortality. T-wave inversions also tend to persist longer on the ECG, even after successful lytic therapy or spontaneous lysis (Surawicz and Knilans, 2008; Ferrari et al., 1997).
Consider the ECG, which is nearly diagnostic of acute PE.
ECG 5.1 A 62-year-old man, with a history of hypertension, presented with a sore throat, cough, fatigue, bilateral lower extremity swelling and periodic bouts of hemoptysis. On presentation, he had severe hypoxemia (pulse oximetry reading of 68 percent on room air).
This ECG demonstrates an array of features that are nearly diagnostic of acute pulmonary embolism. The computer algorithm did not detect any of them, with the exception of sinus tachycardia. All of the following are present: sinus tachycardia; a marked right axis deviation, especially for this patient’s age (including the well-known S1-Q3-T3 pattern); an abnormal rSR’ in lead V1 (an “incomplete RBBB”); and T-wave inversions in both the anterior and inferior leads. These features correlate strongly with ultrasonographic and CT-scan evidence of pulmonary hypertension, right ventricular dysfunction and an extensive clot burden. Obviously, the computer algorithm is completely befuddled, and we must overrule it.
He underwent an emergent CT–pulmonary embolism (CTPE) study, which revealed the following: “Extensive bilateral pulmonary emboli, more extensive on the right, with left lung base pulmonary infarction. Bowing of the intraventricular septum is noted, suggestive of right heart strain.”
He had a markedly elevated BNP (1,484). Point-of-care ultrasound demonstrated severe right heart strain with right ventricular dilatation and reduced RV systolic function. His lower extremity ultrasound studies were positive for extensive, bilateral deep venous thrombosis. He was treated with intravenous heparin, and an IVC filter was placed.
Patients with acute myocarditis often present with shortness of breath, chest pain, palpitations, syncope or other cardiovascular symptoms. Often, signs of congestive heart failure are present.
The combination of low QRS voltage in the limb or precordial leads plus sinus tachycardia should raise the suspicion of acute myocarditis. The ECG may also demonstrate ST-segment elevations, which may be diffuse or regional (Sarda et al., 2001). ST-segment depressions, T-wave inversions, premature atrial and ventricular ectopic beats and conduction abnormalities, including bundle branch blocks, are also common. Q-waves may also develop in patients who have fulminant myocarditis that has resulted in significant myocyte necrosis (Demangone, 2006). Cardiac biomarker elevation is almost always present.
Echocardiography is the most important test in defining the global wall motion abnormalities that are characteristic of diffuse myocarditis. But some patients will present with a focal myocarditis; here, the ECG may show ST-segment elevations in a regional pattern (for example, suggesting inferior or inferolateral STEMI). Reciprocal lead ST-segment depressions may also be present, further suggesting an acute STEMI. In these patients, the echocardiogram may show regional, rather than diffuse, hypokinesis (Sarda et al., 2001; Chan et al., 2005). When an acute STEMI cannot be ruled out, catheterization is usually indicated.
Acute myocarditis is a “don’t-miss” diagnosis. Patients with myocarditis are at risk of developing fulminant heart failure and malignant ventricular arrhythmias leading to sudden cardiac death. The final chapter of this atlas (Critical Cases at 3 A.M.) includes a case where vital clues to acute myocarditis were missed, resulting in sudden cardiac death after discharge from the emergency department.
Pericardial Effusion and Tamponade
Pericardial effusion should always be considered in patients who present with unexplained dyspnea (Blaivas, 2001). Shortness of breath is the most common presenting symptom in patients with pericardial tamponade, but it is often missed, as the diagnostic workup is directed at ruling out pulmonary embolism, heart failure, pneumonia and other causes. While bedside echocardiography is the definitive test for pericardial effusion and pericardial tamponade, the ECG often provides the first clues to the diagnosis.
The characteristic ECG findings in patients with pericardial tamponade include sinus tachycardia, low-voltage QRS complexes and, frequently, electrical alternans (Surawicz and Knilans, 2008; Spodick, 2003; Madias, 2008; Chan et al., 2005; Wagner and Strauss, 2014; Demangone, 2006).
Classically, the low voltage spares the P-wave (Chan et al., 2005; Surawicz and Knilans, 2008). There is, reportedly, a poor correlation between the ECG QRS voltage and the size of the pericardial effusion (Chan et al., 2005; Surawicz and Knilans, 2008).
Low voltage QRS complexes
< 5 mm in all limb leads (refers to total R- and S-wave voltage) OR
< 10 mm in all precordial leads
Cyclic (beat-to-beat) variation in the QRS amplitude or direction
Total electrical alternans (involving the P-wave as well as the QRS complex and T-wave), while rare, may be diagnostic of tamponade and has been associated with malignant effusions
Infiltrative myocardial diseases or cardiomyopathy (e.g., amyloid)
Congestive heart failure
Chronic ischemic heart disease (s/p multiple myocardial infarctions leading to myocardial fibrosis)
Other fluid retention states (nephrotic syndrome, myxedema, anasarca)
Electrical alternans, a cyclic variation in the amplitude or direction of the QRS complexes, has been attributed to a “swinging” or rotation of the heart in the fluid-filled pericardium. Fifty years ago, Littman called it “cardiac nystagmus” (Surawicz and Knilans, 2008). When there is electrical alternans that involves the P-wave, QRS complex and T-wave (“total electrical alternans”), it is said to be highly specific for pericardial tamponade.
Electrical alternans has also been associated with some supraventricular tachycardias, severe left ventricular failure and even extreme respiratory effort.
Low-voltage QRS complexes are not specific for pericardial tamponade (or for acute myocarditis). Other common causes of low-voltage QRS complexes are listed in the table (Chan et al., 2005; Surawicz and Knilans, 2008).
ECG 5.2 A 73-year-old female with recurrent breast cancer presented with sudden shortness of breath.
Not all patients with cancer and shortness of breath have a pulmonary embolism. This ECG has features that are practically pathognomonic for pericardial tamponade – specifically, sinus tachycardia, low-voltage QRS complexes in the limb leads and electrical alternans. Electrical alternans is most obvious in lead II and in precordial leads V1, V2 and V3. Lead V3 shows actual reversal of the polarity of the QRS complexes.
Technically, “low voltage” is present in the limb leads when the QRS complexes (including the R-wave and the S-wave) are less than 5 mm. In the precordial leads, the QRS complexes are said to have “low voltage” if the combined R-wave and S-wave voltage is less than 10 mm.
The echocardiogram showed a large pericardial effusion without clear tamponade physiology. A pericardial window was placed, and an 800 cc pericardial effusion was drained.
The ECG in Chronic Obstructive Pulmonary Disease and Emphysema
While chronic obstructive pulmonary disease (COPD) and emphysema are not acute conditions, many of these patients present with acute dyspnea and chest pain; therefore, it is important to recognize the characteristic ECG features of these common, chronic conditions.
The most common ECG findings in emphysema are abnormal right axis deviation and other features of right ventricular enlargement, right atrial enlargement (P-pulmonale), low QRS voltage in the limb or precordial leads, the “Lead I sign” and poor R-wave progression (Wagner and Strauss, 2014; Surawicz and Knilans, 2008; Rodman et al., 1990; Goudis et al., 2015).
Here are some of the explanations for these ECG abnormalities in patients with emphysema:
Low QRS Voltage (and the “Lead I Sign”)
Low voltage is usually attributed to hyperinflation of the lungs, which impedes the surface electrodes’ ability to record the depolarization currents. The “Lead I sign” includes such low voltage in lead I that the P-wave, QRS complex and T-wave are barely discernible (Surawicz and Knilans, 2008; Goudis et al., 2015).