Pulmonary Embolism

Chapter 59

Pulmonary Embolism Kurt R. Daniel and Jeffrey A. Kline

Clinical Features The annual incidence of pulmonary embolism (PE) in the United States ranges from 100,000 to over 600,000 cases, resulting in at least 50,000 deaths each year. The classic clinical description of acute PE includes sudden onset of pleuritic chest pain accompanied by dyspnea in a patient with a risk factor for thrombosis (hypercoagulability, venous stasis, or vascular injury). However, PE rarely presents in such a classic manner and, furthermore, commonly imitates and is imitated by other disorders. In addition, PE produces a highly variable degree of cardiopulmonary stress, ranging from undetectable effects (normal vital signs in a comfortable patient) to proximal pulmonary arterial occlusion and pulseless electrical activity.1 Patients with PE often complain of nonspecific cardiopulmonary symptoms (shortness of breath with variable severity of chest pain) and manifest nonspecific signs (rapid breathing and pulse rate).

systolic pulmonary arterial pressure by approximately 50% will begin to produce ECG changes. In the setting of an acute PE, a completely normal ECG has been reported in 9% to 26% of patients.2 The most important and common ECG abnormalities are described, and the prevalence of these findings is summarized in Table 59-1. Tachycardia. Sinus tachycardia (Fig. 59-1) is probably the most common ECG alteration caused by PE. Significant obstruction of the pulmonary tree, often along with acute tricuspid regurgitation, leads to an acute fall in left ventricular end-diastolic volume. Thus, tachycardia occurs as a reflex response to the resulting reduction in cardiac output and low pressure in the baroreceptor system. However, this finding is

ELECTROCARDIOGRAPHIC HIGHLIGHTS

• Sinus tachycardia—most common finding in pulmonary embolism (PE)

Electrocardiographic Manifestations

• ST segment and T wave abnormalities—also very common in PE

There are no pathognomonic electrocardiographic (ECG) changes that enable the diagnosis of PE or its exclusion. However, the ECG plays an essential role in the evaluation of suspected PE primarily because it can diagnose myocardial injury, and therefore provide rapid, noninvasively obtained evidence of an alternative cause of symptoms. Presence of an alternative diagnosis can substantially lower the likelihood of PE.1 Also, PE that is severe enough acutely to increase the

• S1Q3T3 pattern—occasional finding, but not very helpful • T wave inversion in leads V1 to V4—associated with PE severity

• Incomplete or complete right bundle branch block— associated with mortality

• P pulmonale—uncommon, of little significance • QRS axis deviation

59-1 • FREQUENCY OF COMMON ELECTROCARDIOGRAPHIC FINDINGS IN PULMONARY EMBOLISM

Normal 18%

Tachycardia

Anterior T Wave Inversion

Right Bundle Branch Block*

S1Q3T3 Pattern

P Pulmonale

Right Axis Deviation

44%

34%

18%

20%

9%

16%

Atrial Fibrillation/ Flutter 8%

*Complete or incomplete. These data were compiled from 11 published studies, representing 820 total patients with pulmonary embolism.3,8,9,11–18 Not all criteria were reported in every study. Thus, the data presented represent the available data for each criterion.

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FIGURE 59-1 • S1Q3T3 pattern. This is a tracing from an 82-year-old patient with rapid progression of chest pain and dyspnea.

too nonspecific to be helpful, especially because tachycardia does not develop in some patients with PE. Other Rhythm Disturbances. Other rhythm disturbances reported with PE include first degree atrioventricular block, premature atrial contractions, and premature ventricular contractions. Atrial fibrillation and flutter have been reported to occur in anywhere from 0% to 35% of patients with acute PE.2 Right Bundle Branch Block. The development of complete and incomplete right bundle branch block (RBBB) has been associated with increased mortality in patients with PE (Fig. 59-2). Patients with PE and progressive RBBB are more likely to have severe pulmonary vascular obstruction that causes acute cor pulmonale with refractory shock. In one study of 18 patients with fatal PE who had more than one ECG before death, 11 (61%) had either a new incomplete RBBB or progressed from incomplete RBBB to complete RBBB.3 The clinician should view the development of either incomplete RBBB or RBBB with concern in that such

patients not infrequently suffer significant morbidity and mortality. S1Q3T3 Pattern. First reported by McGinn and White in 1935, this is still considered the classic ECG finding4 (Fig. 59-1). The classic S1Q3T3 pattern, mistakenly considered pathognomonic for acute PE by many clinicians, is seen less frequently; 2% to 25% of patients ultimately diagnosed with PE have this pattern. In fact, this pattern can also be seen in many patients who do not have a PE and is neither sensitive nor specific for the diagnosis of PE.5 The clinician must realize that its presence neither confirms nor negates the diagnosis of PE. Few experimental data exist to verify the mechanism for this pattern. One frequently proposed mechanism for the S1 and the Q3 is clockwise rotation of the heart in response to right ventricular dilation. As a result, when the septum depolarizes during the initial phase of the QRS complex, the electrical impulse travels away from lead III, producing a Q wave.

FIGURE 59-2 • Incomplete right bundle branch block. A subtle RSR′ pattern developed in leads V1 and V2 in a patient with a PE whose condition worsened.

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SECTION III: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE

FIGURE 59-3 • Anterior T wave inversions. Note the deeply inverted T waves throughout leads V1 to V4 in this patient who was found to have profoundly elevated pulmonary artery pressures.

Similarly, the right ventricular dilatation and the resulting rotation pushes the terminal portion of the QRS vector toward the right and away from lead I, producing an S wave. Others propose the S1Q3T3 pattern results from acute left posterior hemiblock.6 T wave inversion may be caused by subendocardial ischemia in the right ventricle and inferior septal wall in the presence of high right-sided pressures.7 Axis Deviation. As noted previously, the S1Q3T3 pattern may be in part due to a change to the QRS axis. Although right axis deviation is described as the classic axis change associated with PE, left axis deviation as well as indeterminate QRS axis changes have been reported with variable frequency.2 Part of this variability may be related to the specific definitions of right, left, and indeterminate axis deviations. Preexisting cardiopulmonary disease may affect axis changes as well.8 Anterior T Wave Inversions. Inversion of the T waves in leads V1 to V4 has been reported to be closely related to the severity of PE (Figs. 59-3 through 59-5). Ferrari and colleagues demonstrate a relationship between T wave inversion

in the anterior leads and both the Miller index (a measure of vascular blockage derived from the ventilation–perfusion scan) and the degree of pulmonary hypertension.9 Thus, it may be useful in risk-stratifying patients with PE (see later). The morphology of the inverted T waves is typically symmetric, and may be found in a wider anatomic range and with deeper inversion, depending on the severity of PE. An isolated inverted T wave in lead V1 can be normal. Several mechanisms have been proposed to explain this phenomenon, including ischemia in the setting of preexisting right coronary artery stenosis, neurohumorally mediated changes in myocardial repolarization, and myocardial shear injury from increased intramural tension and microvascular compression. Regardless of mechanism, the finding of symmetrically inverted T waves in the precordial leads often signifies profound right ventricular strain and the potential for clinical deterioration in a patient with respiratory distress and hypoxia. Global T wave inversion (Fig. 59-4) in acute PE has been reported in a case report from the literature. Although the differential diagnosis for global

Global T Wave Inversion.

FIGURE 59-4 • Global T wave inversion. This patient was thought to have had a non–Q wave myocardial infarction because of the presence of this pattern along with elevated troponin levels. Pulmonary embolism turned out to be the lone culprit.

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T wave inversion is quite broad, it is a rare finding in pulmonary embolism.

ST depression or elevation has been reported in up to half of all patients with PE.2

In addition to the abnormalities noted previously, other nonspecific ST segment and T wave changes are frequent in PE. For example, nonspecific

P Pulmonale.

ST Segment and T Wave Changes.

P pulmonale, defined as a P wave in lead II greater than 2.5 mm in height, does occur with PE, but is also observed frequently in patients with other, more chronic

A

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

V1

B FIGURE 59-5 • Massive pulmonary embolism (PE). A, This patient had overt circulatory shock secondary to proximal, bilateral PEs. Note the S1Q3T3 pattern, anterior precordial T wave, and the incomplete right bundle branch block pattern. B, After the infusion of tissue plasminogen activator (5 hours later), the patient reported feeling much better, his blood pressure stabilized, and his hypoxia improved. Note the resolution of the RSR′ pattern in lead V1 and anterior T wave inversions.

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SECTION III: ELECTROCARDIOGRAPHIC MANIFESTATIONS OF DISEASE 59-2 • THE DANIEL ELECTROCARDIOGRAM SCORING SYSTEM TO GRADE SEVERITY OF PULMONARY EMBOLISM*

Characteristic Tachycardia? Incomplete right bundle branch block? Complete right bundle branch block? T wave inversion in all leads V1 through V4? T wave inversion in lead V1? If absent, leave blank.

T wave inversion in lead V2? If absent, leave blank.

T wave inversion in lead V3? If absent, leave blank.

Present

Absent

Score

䊐 䊐 䊐 䊐

䊐 䊐 䊐 䊐

2 2 3 4

< 1 mm 1–2 mm > 2 mm

䊐 䊐 䊐

䊐 䊐 䊐

0 1 2

<1 mm 1–2 mm > 2 mm

䊐 䊐 䊐

䊐 䊐 䊐

1 2 3

< 1 mm 1–2 mm > 2 mm

䊐 䊐 䊐 䊐 䊐 䊐

䊐 䊐 䊐 䊐 䊐 䊐

S wave in lead I? Q wave in lead III? Inverted T wave in lead III? If all of S1Q3T3 is present, add a score of 2

1 2 3 0 1 1 2 Max = 21

*A score greater than 10 is 23.5% sensitive and 97.7% specific for a pulmonary embolism causing severe pulmonary hypertension.3

pulmonary diseases that increase right heart pressures. Because this finding is thought to be related to right atrial abnormality, rather than acute stretching, P pulmonale may not occur even with massive acute PE. QRS Complex Abnormalities. Low voltage in the QRS complex in limb leads has been reported in up to 29% of patients with PE.9 Other changes reported include a late R wave in lead aVR and slurred S wave in lead V1 or V2.18

ELECTROCARDIOGRAPHIC PEARLS

• A completely normal ECG is common in acute pulmonary embolism (PE).

• The ECG can neither diagnose nor exclude the diagnosis of PE.

• The ECG is essential in the work-up of the patient in whom PE is being considered in the differential diagnosis, primarily to exclude other causes (such as acute coronary syndrome) for the clinical presentation.

Clinical relevance of electrocardiographic findings Several studies have suggested a role for the ECG as a prognostic indicator in PE. Daniel et al. compiled these findings into a scoring system10 (Table 59-2). The Daniel score was found to relate closely to the degree of pulmonary hypertension (a commonly used measure of severity) in patients with PE. In particular, a score of 10 or greater was shown to be 97.7% specific for severe pulmonary hypertension (systolic pulmonary artery pressure >50 mm Hg). As the PE resolves after clot lysis, the ECG findings of right ventricular strain (Fig. 59-5) also resolve. Ferrari et al. reported that resolution of the anterior T wave inversion after thrombolysis is associated with an improved Miller index and lower pulmonary artery pressure at 6 days after the PE. Therefore, resolution of T wave inversion may be useful as a measure of reperfusion after thrombolysis of PE.

References 1. Courtney DM, Sasser HC, Pincus CL, Kline JA: Pulseless electrical activity with witnessed arrest as a predictor of sudden death from massive pulmonary embolism in outpatients. Resuscitation 2001;49:265.

2. Chan TC, Vilke GM, Pollack M, Brady WJ: Electrocardiographic manifestations: Pulmonary embolism. J Emerg Med 2001;21:263. 3. Cutforth R, Oram S: The electrocardiogram in pulmonary embolism. Br Heart J 1958;20:41. 4. McGinn S, White PD: Acute cor pulmonale resulting from pulmonary embolism: Its clinical recognition. JAMA 1935;104:1473. 5. Panos RJ, Barish RA, Depriest WW, Groleau G: The electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988;6:301. 6. Scott RC: The s1q3 (McGinn-White) pattern in acute cor pulmonale: A form of transient left posterior hemiblock? Am Heart J 1971;82:135. 7. Gold FL, Bache RJ: Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Circ Res 1982; 51:196. 8. Petruzzelli S, Palla A, Pieraccini F, et al: Routine electrocardiography in screening for pulmonary embolism. Respiration 1986;50:233. 9. Ferrari E, Imbert A, Chevalier T, et al: The ECG in pulmonary embolism: Predictive value of negative T waves in precordial leads—80 case reports. Chest 1997;111:537. 10. Daniel KR, Courtney DM, Kline JA: Assessment of cardiac stress from massive pulmonary embolism with 12-lead ECG. Chest 2001; 120:474.

CHAPTER 60: Chronic Obstructive Pulmonary Disease 11. Weber DM, Phillips JH Jr: A re-evaluation of electrocardiographic changes accompanying acute pulmonary embolism. Am J Med Sci 1966;251:381. 12. Smith M, Ray CT: Electrocardiographic signs of early right ventricular enlargement in acute pulmonary embolism. Chest 1970;58:205. 13. Szucs MM Jr, Brooks HL, Grossman W, et al: Diagnostic sensitivity of laboratory findings in acute pulmonary embolism. Ann Intern Med 1971;74:161. 14. Sasahara AA, Hyers TM, Cole CM, et al: The Urokinase-Pulmonary Embolism Trial (UPET): A national cooperative study. Circulation 1973;47/48(Suppl 2):II60. 15. Stein PD, Dalen JE, McIntyre KM, et al: The electrocardiogram in acute pulmonary embolism. Prog Cardiovasc Dis 1975;17:247.

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16. Stein PD, Terrin ML, Hales CA, et al: Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest 1991;100:598. 17. Sreeram N, Cheriex EC, Smeets JL, et al: Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol 1994;73:298. 18. Rodger M, Makropoulos D, Turek M, et al: Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol 2000;86:807.

Chapter 60

Chronic Obstructive Pulmonary Disease Chris A. Ghaemmaghami

Clinical Features The term chronic obstructive pulmonary disease (COPD) is used to describe the spectrum of pulmonary diseases that are characterized by chronic airway obstruction caused primarily by emphysema, chronic bronchitis, or, most commonly, components of both. COPD affects over 52 million individuals worldwide and is the fourth leading cause of mortality in the United States. Emphysematous changes are the result of chronic inflammatory processes in the lung leading to irreversible destruction of the normal architecture of the terminal bronchi. As the disease process progresses, an overall decrease in lung compliance, prolonged expiratory flow times, and chronic lung hyperinflation are observed. Coalescence of damaged areas can lead to bullae formation and increased anatomic dead space in the lung. Hyperinflation of the lungs results in an increased anterior–posterior diameter of the thorax and flattening and downward displacement of the diaphragm. These changes allow the anatomic position of the heart to become more vertical. In addition, because of its attachments with the great vessels, the heart makes a clockwise rotation, resulting in posterior rotation of the left ventricle and anterior rotation of the

right ventricle. The pulmonary vascular bed is affected both directly and indirectly by COPD. The active destruction of lung tissue directly damages pulmonary capillaries. Chronic vasoconstriction of pulmonary arterioles and arteries occurs in response to the low alveolar oxygen tensions present throughout alveoli in the injured tissue. Over time, muscular hyperplasia in these vessels results in a further decrease in the total pulmonary vascular cross-section. The combination of the loss of capillaries and increased resistance through the medium and large pulmonary arteries results in chronic pulmonary hypertension and a pressure-overloaded state for the right atrium and ventricle. These changes can lead to right heart failure and cor pulmonale. Most of the electrocardiographic (ECG) findings related to COPD can be attributed to the chamber-altering effects of this pulmonary hypertension.

Electrocardiographic Manifestations The greater the extent of secondary cardiac disease from COPD and cor pulmonale, the more pronounced the ECG findings. In fact, although COPD has several associated ECG abnormalities, once right ventricular hypertrophy (RVH) is