Article, Cardiology

Electrocardiographic findings in left-sided pneumothorax

Likely related to sodium channel blockade, alterations in the QRS complex configuration, or morphology, were seen in the study group as well–namely, the observation of the deep S wave in lead I and prominent R? wave in Lead aVR. In particular, these findings have been reported in patients with tricyclic antidepressant poisoning, but can also be seen after other Sodium channel blocker poisonings [4,7].

The QT interval was prolonged in a significant number of patients seen in this study. Antagonism of the outward potassium currents, or potassium efflux channel blockade, delays the termination of phase 4 of depolarization [7]. This prolongation of repolarization causes the myocardial cell to reduce the charge differential across its membrane; this alteration can result in the activation of the inward depolarization current (early after-depolarization) which can promote triggered activity. The electrocardiographic mani- festation of this cascade is prolongation of the QT interval– and, ultimately, Polymorphic ventricular tachycardia.

Lastly, the sodium-potassium-adenosine triphosphate (Na-K-ATPase) pump inhibitors, such as digoxin, can produce both morphological and rhythm abnormality. When the Na-K-ATPase pump is inhibited, there is an increase in extracellular potassium and intracellular sodium which reduces the transmembrane sodium gradient; this electrocardiographic findings in left-si”>reduction causes an increase in the sodium-calcium exchan- ger, ultimately producing an increase in Intracellular calcium concentration. A number of findings which could have been caused by the Na-K-ATPase pump inhibitors were seen. The study population demonstrated frequent ST-segment and T- wave changes. At therapeutic–that is, nontoxic–levels, digoxin can certainly produce such findings–the so-called digitalis effect with ST-segment depression with T-wave inversion. Regarding toxic manifestations, both increased automaticity and slowed conduction explain the range of dysrhythmias seen in the digoxin-poisoned patient, including premature ventricular contraction, bradycardia, atrioventri- cular and intraventricular blocks, and tachyarrhythmia. Also, with the production of hyperkalemia, a range of electro- cardiographic findings can be seen, including PR interval prolongation and QRS complex widening.

The actual clinical impact of these ECG abnormalities is unknown. What can be definitively drawn from this study is that an association exists. The consequences of the presence of certain abnormalities for future management of the patient need to be further studied. A multitude of further questions are provoked. Which patients should receive the ECG? Should all patients after poisonings receive an ECG, or only patients after exposure to potential cardiovascular toxins? Usually, other clinical signs and symptoms are considered when assessing the need for obtaining an ECG, such as altered mental status or Abnormal vital signs. What is the association of these other diagnostic clues with the ECG findings? What does the ECG abnormality say about end- organ toxicity and direct management? One might hope that the findings of this study will spur further inquiry about the use of the ECG in diagnosis and management of the

undifferentiated poisoned patient. Further work is needed in this area, considering the use of the ECG in the generic ED poisoned patient.

Kathryn Wells

School of Medicine, University of Virginia

Charlottesville, VA, USA

Margaret Williamson MD

Department of Emergency Medicine

Northwestern University Chicago, IL, USA

Christopher P. Holstege MD Andrew B. Bear MD William J. Brady MD

Department of Emergency Medicine

University of Virginia Charlottesville, VA, USA

E-mail address: [email protected]

doi:10.1016/j.ajem.2008.03.008

References

  1. McCaig LF, Nawar EN. National Hospital Ambulatory Medical Care Survey: 2004 emergency department summary. Advance data from vital and health statistics; no 372. Hyattsville, MD: National Center for Health Statistics; 2006.
  2. Lai MW, Klein-Schwartz W, Rodgers GC, et al. 2005 Annual Report of the American Association of Poison control centers‘ national poisoning and exposure database. Clin Toxicol (Phila) 2006;44: 803-932.
  3. Watson WA, Litovitz TL, Klein-Schwartz W, et al. 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2004;22:335-404.
  4. Holstege CP, Eldridge DL, Rowden AK. ECG Manifestations: the poisoned patient. Emerg Med Clin N Am 2006;24:159-77.
  5. Chan TC, Brady WJ, Harrigan RA, Ornato J, Rosen P, editors. The ECG in Emergency Medicine and Acute Care. Philadelphia (Pa): Elsevier Mosby; 2005.
  6. Delk C, Holstege CP, Brady WJ. electrocardiographic abnormalities associated with poisoning. Am J Emerg Med 2008;26:221-8.
  7. Anderson ME, Al-Khatib SM, Roden DM, et al. Cardiac repolarization: current knowledge, critical gaps, and new approaches to drug development and patient management. Am Heart J 2002;144:769-81.

Electrocardiographic findings in left-sided pneumothorax

To the Editor,

Left-sided pneumothorax and myocardial infarction (MI) are common diseases exhibiting chest symptoms. Electro- cardiogram (ECG) is a routine examination in patients with

Fig. 1 Representative ECGs in patients with left-sided pneumothorax and prior anterior MI. Both ECGs showed poor precordial R-wave progression. However, QRS vector in aVL was negative in left-sided pneumothorax and positive in prior anterior MI. QRS voltage ratio (aVF/ I) value was 11 in left-sided pneumothorax and 0.67 in prior anterior MI.

chest symptoms, and previous studies have shown that poor precordial R wave progression is often found in both disorders [1-8]. In this study, we assessed ECG differentia- tion between the 2 disorders.

A total of 10 patients with left-sided pneumothorax and 20 patients with prior anterior MI were studied. Left-sided pneumothorax was confirmed by the collapse of the left lung on chest radiograph. Prior anterior MI was confirmed by an increase in the serum creatine kinase concentration by more than 2-fold the normal value and the angiographic occlusion of left anterior descending artery during early phase. We measured R-wave amplitude and QRS voltage in each ECG and compared those between the 2 disorders. QRS voltage was defined as the sum of positive and negative forces in each lead. We also assessed the ECG findings previously shown to be associated with left-sided pneumothorax such as rightward shift in mean frontal QRS axis, poor precordial R- wave progression, precordial T-wave inversion, and phasic QRS voltage variation [1-6]. Rightward shift in mean frontal QRS axis was evaluated by QRS vector in leads I and aVL. Poor precordial R-wave progression was defined as R-wave amplitude less than 3 mm in V3 lead. Precordial T-wave

inversion was defined as T waves with a negative amplitude 2 mm or greater in 2 or more contiguous ECG leads. Phasic QRS voltage variation depending on respiration was considered present if the difference in QRS voltage between inspiration and expiration was more than 5 mm in any lead on ECG. R-wave amplitude and QRS voltage were measured during expiration when the phasic QRS voltage variation was present.

Statistical analysis was performed with ?2 and Student t tests. Differences were considered significant if the P value was less than .05. All data are expressed as mean +- SD.

There was no significant difference in baseline character- istics between the 2 disorders except for lower body weight in patients with left-sided pneumothorax (Table 1). Electro- cardiogram was obtained within 2 days after the onset in patients with left-sided pneumothorax and 166 +- 89 days after the onset in patients with prior anterior MI. R-wave amplitude and QRS voltage in each lead were shown in Table 1. QRS voltage was significantly lower in leads I, V5, and V6 in patients with left-sided pneumothorax than in those with prior anterior MI, whereas it was significantly higher in leads II, III, and aVF. As a result, incidence of QRS

Pneumothorax (n = 10)

Prior anterior MI (n = 20)

P

Age (y)

50 (26)

61 (11)

NS

Male sex

9 (90)

18 (90)

NS

Height (cm)

165 (9)

165 (9)

NS

Weight (kg)

53 (12)

64 (9)

b.01

Smoking

9 (90)

12 (60)

NS

R wave amplitude (mm)

I

1.5 (1.2)

5.2 (2.2)

b.01

II

9.7 (4.4)

4.6 (2.1)

b.01

III

8.3 (4.2)

2.1 (1.7)

b.01

aVR

1.8 (1.4)

0.9 (0.9)

NS

aVL

0.7 (0.9)

3.7 (2.1)

b.01

aVF

9.0 (4.3)

2.8 (1.9)

b.01

V1

1.7 (2.3)

0.1 (0.2)

b.01

V2

2.0 (2.1)

0 (0.1)

b.01

V3

3.9 (5.2)

0.7 (1.1)

b.05

V4

3.7 (3.4)

4.0 (3.4)

NS

V5

3.5 (2.4)

7.5 (3.3)

b.01

V6

3.4 (2.1)

8.1 (2.6)

b.01

QRS voltage (mm)

I

2.4 (0.9)

6.0 (2.3)

b.01

II

12.4 (4.6)

6.2 (2.4)

b.01

III

10.4 (4.2)

5.7 (2.5)

b.01

aVR

7.2 (2.6)

5.8 (1.9)

NS

aVL

4.0 (1.9)

5.1 (2.4)

NS

aVF

11.1 (4.3)

5.0 (2.3)

b.01

V1

13.6 (4.2)

9.7 (4.7)

b.05

V2

14.6 (6.3)

14.5 (5.4)

NS

V3

15.9 (10.6)

12.5 (4.9)

NS

V4

11.6 (6.1)

10.8 (4.7)

NS

V5

7.1 (1.7)

11.5 (4.0)

b.01

V6

5.1 (2.0)

9.6 (2.7)

b.01

QRS voltage ratio

10 (100)

2 (10)

b.01

(aVF/I) N2

QRS vector in I

NS

Positive

5 (50)

19 (95)

Isometric

3 (30)

1 (5)

Negative

2 (20)

0 (0)

QRS vector in aVL

b.01

Positive

1 (10)

17 (85)

Isometric

2 (20)

2 (10)

Negative

7 (70)

1 (5)

Poor precordial R-wave

5 (50)

18 (90)

b.05

progression

Precordial T-wave

0 (0)

9 (45)

b.05

inversion

Phasic voltage variation

4 (40)

0 (0)

b.05

Data are shown as the mean value (SD). NS indicates not significant.

voltage ratio (aVF/I) greater than 2 was significantly higher in patients with left-sided pneumothorax (100% vs 10%; P b

Table 1 Baseline characteristics and ECG findings

Table 2 Sensitivity, specificity, positive predictive value, and negative predictive value of electrocardiographic variables for the diagnosis of left-sided pneumothorax

.01). Incidence of isometric or negative QRS vector in leads I or aVL was significantly higher in patients with left-sided pneumothorax, suggesting higher incidence of rightward shift in mean frontal QRS axis. This rightward shift in the mean frontal QRS axis disappeared in 7 patients whose ECG

was obtained after the treatment of left-sided pneumothorax. Poor precordial R-wave progression (50% vs 90%; P b .05) and precordial T wave inversion (0% vs 45%; P b .05) were seen less frequently, and phasic QRS voltage variation (40% vs 0%; P b .05) was seen more frequently in patients with left-sided pneumothorax. Representative ECGs in patients with both disorders are shown in Fig. 1. Table 2 lists the sensitivity, specificity, and predictive accuracy of ECG findings for the diagnosis of left-sided pneumothorax. QRS voltage in I 5 mm or less, QRS voltage in V6 10 mm or less, and isometric or negative QRS vector in aVL were very sensitive for left-sided pneumothorax. QRS voltage in aVF 10 mm or greater, QRS voltage in V6 5 mm or less, isometric or negative QRS vector in I, and phasic QRS voltage variation were very specific for left-sided pneumothorax. Furthermore, QRS voltage ratio (aVF/I) greater than 2 predicted left-sided pneumothorax with high sensitivity (100%) and specificity (90%).

This study demonstrated that poor precordial R-wave progression was often found in both disorders, but QRS voltage ratio (aVF/I) greater than 2 accurately differentiated left-sided pneumothorax from prior anterior MI. Possible mechanisms of increased QRS voltage ratio (aVF/I) and decreased QRS voltage in lead V6 include clockwise rotation on the longitudinal axis, right ventricular dilatation due to a sudden increase in pulmonary resistance, posterior displace- ment of the mediastinum, and insulating effect of intrathor- acic air. Precordial T-wave inversion has been ascribed to

Sensitivity (%)

Specificity (%)

PPV (%)

NPV (%)

QRS voltage in

100

50

50

100

I <=5 mm

QRS voltage in

70

90

88

86

aVF >=10 mm

QRS voltage ratio

100

90

83

100

(aVF/I) N2

QRS voltage in

60

95

86

83

V6 <=5 mm

QRS voltage in

100

40

45

100

V6 <=10 mm

Isometric or negative

50

95

83

79

QRS vector in I

Isometric or negative

90

85

75

94

QRS vector in aVL

Poor precordial R-wave

50

10

22

29

progression

Precordial T-wave

0

55

0

52

inversion

Phasic QRS voltage

40

100

100

77

variation

PPV indicates positive predictive value; NPV, negative predictive value.

hypoxemia or change in Coronary blood flow. However, it was neither sensitive nor specific for left-sided pneu- mothorax in this study. Phasic QRS voltage variation was probably due to the intrathoracic air adjacent to the heart that underwent phasic alteration in size with respiration. It was very specific for left-sided pneumothorax, but the specificity was only 40% in this study.

In conclusion, QRS voltage ratio (aVF/I) greater than 2 was a simple and accurate ECG finding to differentiate left- sided pneumothorax from prior anterior MI.

Satoshi Kurisu MD Ichiro Inoue MD Takuji Kawagoe MD Masaharu Ishihara MD Yuji Shimatani MD Yasuharu Nakama MD

Department of Cardiology, Hiroshima City Hospital

Hiroshima 730-8518, Japan E-mail address: [email protected]

doi:10.1016/j.ajem.2008.03.032

References

  1. Walston A, Brewer DL, Kitchens CS, Krook JE. The electrocardio- graphic manifestations of spontaneous left pneumothorax. Ann Intern Med 1974;80:375-9.
  2. Copeland R, Omenn GS. Electrocardiographic changes suggestive of coronary artery disease in pneumothorax. Arch Intern Med 1970;125: 151-3.
  3. Werne CS, Sands MJ. Left Tension pneumothorax masquerading as anterior myocardial infarction. Ann Emerg Med 1985;164:166.
  4. Ruo W, Rupani G. Left tension pneumothorax mimicking myocardial ischemia after percutaneous central venous cannulation. Anesthesiology 1992;76:306-8.
  5. Dimitar R. A case of spontaneous left-sided pneumothorax with ECG changes resembling acute myocardial infarction. Int J Cardiol 1996;56: 197-9.
  6. Kozelj M, Rakovec P, Sok M. Unusual ECG variations in left-sided pneumothorax. J Electrocardiol 1997;30:109-11.
  7. DePace NL, Colby J, Hakki AH, et al. Poor R wave progression in the precordial leads: clinical implications for the diagnosis of myocardial infarction. J Am Coll Cardiol 1983;2:1073-9.
  8. Gami AS, Holly TA, Rosenthal JE. Electrocardiographic poor R-wave progression: analysis of multiple criteria reveals little usefulness. Am Heart J 2004;148:80-5.

Clinical questions in the ED

To the Editor,

We read with great interest the article by Graber et al [1]. Capturing clinical questions in the emergency department (ED) is an important area of research, fundamental to developing resources that better meet the information needs of ED physicians. Earlier research has demonstrated broadly

similar findings to those of Graber et al in relation to number of questions asked, sought, answered, and sources used. How- ever, it additionally examined such factors as motivation and, crucially, impact on present and future patient management [2]. This earlier study was conducted in 3 phases and examined the information behavior (ie, information needs, seeking, and use) of 13 ED physicians in a Canadian tertiary care-level pediatric ED. During the first phase, physicians completed an initial questionnaire designed to describe their current information management (including an estimate of the number of questions they anticipated asking during each shift). Secondly, using a microcassette recorder, each physician recorded questions arising over three 8-hour shifts and indicated how quickly answers were needed. Finally, a follow-up questionnaire solicited responses relating to several issues, including whether or not answers were sought and found, if answers were found within specified time frames, which sources were used, and present and future

impact on patient management.

Physicians estimated that they would ask an average of

4.8 questions per shift, but in actual practice raised 3 questions per shift. Most questions were treatment-related and drawn from the specialty topic areas of infectious disease and orthopedics. Participants pursued answers to 66% of their questions and found answers to 58% of pursued questions. Urgent questions were more likely to be pursued. Print and human sources were consulted most frequently, with physical accessibility and credibility the major determinants of source selection. In seeking answers, physicians were motivated by a variety of factors including the needs of patient care, for confirmation, curiosity, uncertainty, and generalizability. Reasons for not seeking an answer were similar to those in the study of Graber et al, including lack of time and the answer not immediately applicable to patient care. Factors resulting in questions remaining unanswered included lack of time and problems experienced in retrieving answers.

This earlier study confirms the findings of Graber et al that ED physicians ask fewer questions but pursue a higher proportion of them than in other clinical specialties. However, Talbot’s study determined additionally that the information retrieved changed both present and future patient management in approximately 50% of cases. In both present and future management, the most common categories identified were drug treatment, “other” (such as expanding the differential diagnosis), and choice of tests. These findings underscore the significance of the supposition of Graber et al that, “it is possible, although unlikely, that cognitive gaps have no impact on patient outcome (p 147). Talbot’s study further showed that questions are raised not just for immediate patient management, suggesting that patient care episodes may prompt questions that are indicative of general learning need (a “want to know” as opposed to a “need to know”). A more detailed exploration of these questions is likely to enhance future disease management, educational benefit, and quality improvement.

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