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Electrocardiogram voltage attenuation and shortening of the duration of P-waves, QRS complexes, and QT intervals
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/ihj
Case Report
Electrocardiogram voltage attenuation and shortening of the duration of P-waves, QRS complexes, and QT intervals John E. Madias a,b,* a b
The Icahn School of Medicine at Mount Sinai of the New York University, NY, USA The Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, USA
article info
abstract
Article history:
Multiple pathologies in concert may lead to attenuation of the electrocardiogram (ECG)
Received 1 March 2013
voltage. A case of a patient illustrating the above is presented, who showed marked
Accepted 10 August 2013
attenuation of the ECG voltage. Automated values of the amplitude of the ECG QRS com-
Available online 4 September 2013
plexes, P-waves, and T-waves (in mm), duration of the QRS complexes, P-waves, and QT intervals (in ms), in 2 ECGs were compared. The patient was a 64-year-old woman who
Keywords:
developed in the setting of a fatal illness, pleural and pericardial effusions, pneumo-
Electrocardiogram
mediastinum, pneumoperitoneum, subcutaneous emphysema in the neck and chest, pe-
ECG voltage attenuation
ripheral edema with weight gain of 43.4 lbs, marked hypoalbuminemia, abnormal liver
P-wave duration
tests, and renal failure. All the above pathologies led to a marked attenuation of the ECG
QRS duration
voltage, and shortening of the mean P-wave, QRS complexes, and QTc interval durations.
QTc interval duration
The postulated mechanism of the observed ECG phenomena is discussed. Copyright ª 2013, Cardiological Society of India. All rights reserved.
1.
Introduction
There are many factors which singly, on in concert, can influence the electrocardiogram (ECG) voltage and lead to attenuation of the P-waves, QRS complexes, and T-waves. The resultant effects are extracardiac in nature. What is not appreciated is the resultant shortening of the P-wave, QRS complex and QT intervals. The case of a patient presented herein illustrates all the above ECG changes resulting from multiple intrathoracic and systemic pathologies, which the patient suffered.
2.
Case presentation
A 64-year-old woman, with a history of hypertension, failure to thrive, weight loss of undefined etiology worked up at another hospital, was admitted to our facility with dyspnea, hypoxemia, and lung infiltrates, for which she was intubated, and placed on broad spectrum antibiotics and vasopressors. She abruptly decompensated, and was found to have pleural and pericardial effusions, pneumomediastinum, pneumoperitoneum, subcutaneous emphysema in the neck and chest, and peripheral edema with weight gain of 43.4 lbs (Fig. 1).
* Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, USA. Tel.: þ1 718 334 5005; fax: þ1 718 334 5990. E-mail address: [email protected]. 0019-4832/$ e see front matter Copyright ª 2013, Cardiological Society of India. All rights reserved. http://dx.doi.org/10.1016/j.ihj.2013.08.014
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
615
Fig. 1 e Portable chest X-ray on admission (A) reveals right lower lobe infiltrate and probably mild pleural effusion; portable chest X-ray on day 7 of hospitalization (B) reveals extensive subcutaneous emphysema, increasing consolidating changes of both lungs, and the tip of an endotracheal tube is seen proximal to the carina; a short axis parasternal view of the echocardiogram (C) on day 6 of hospitalization showed normal left ventricular size and thickness, with a large pericardial space which contained a large amount of “organized” echo-dense material, adherent to the epicardium and a pericardial effusion; an axial view of the thoracic computerized tomographic angiography (D) on day 2 of hospitalization revealed a prominent right pleural effusion, no parenchymal mass lesions, mediastinal and subcutaneous emphysema, right lower lobe infiltrate/atelectasis, pericardial effusion, suggestion of possible pneumopericardium, but no pleural effusion. Abbreviations: X [ subcutaneous emphysema; P [ pericardial effusion; M [ pneumomediastinum.
Exploratory laparotomy did not reveal any intestinal perforation in the abdomen, upper airways laryngoscopy and bronchoscopy by the Otorynolaryngolology service were negative for perforation, and evaluation via esophagogastroduodenoscopy by the Gastroenterology service did not disclose evidence of esophageal perforation. The echocardiogram on day #6 of hospitalization revealed a normal sized right and left atria, and right and left ventricles, normal left ventricular thickness, suboptimal visualization of the anterior and inferior left ventricular walls, preserved function of the left ventricular base, and severely reduced overall left ventricular ejection fraction; there was trace mitral and aortic regurgitation, moderate tricuspid regurgitation, and an estimated pulmonary artery systolic pressure of 34 mmHg; also there was a large pericardial space with a pericardial effusion and a large amount of “organized” echo-dense material adherent to the epicardium. Subcutaneous emphysema in the neck resolved but her respiratory failure worsened and she developed adult respiratory distress syndrome, shock with hypotension, tachycardia and peripheral hypoperfusion, marked hypoalbuminemia, abnormal liver tests, and renal failure. The family opted for extubation and no resuscitation, and the patient succumbed on day 7 of hospitalization. Comparison of the 2 ECGs recorded 7 days apart (Fig. 2) (Table 1), revealed minor changes in heart rate (118e119 beats/min),
P-wave frontal axis (55 e53 ), QRS frontal axis (14 to 5 ), and T-wave frontal axis (96 e73 ), while sums of peak-to-peak QRS complexes of all 12 leads decreased by 75% (81.68e20.44 mm), sums of peak-to-peak P-waves by 55.0% (11.0e4.95 mm), and sums of peak-to-peak T-waves by 58% (17.48e7.28 mm). This was associated with shortening of the mean P-wave duration by 26.5% (90e66.18 ms), QRS duration by 19.4% (72e58 ms), QT interval by 8.5% (328e300 ms), and QTc by 8% (460e423 ms).
3.
Discussion
What precipitated the ECG amplitude changes was the combination of pneumonia, acute respiratory distress syndrome, pericardial effusion, pleural effusion, mediastinal and subcutaneous emphysema, hypoalbuminemia, and peripheral edema.1e4 All these pathologies either enhance the water content (thereby resulting in reduction of electrical impedance) or produce marked disparities in the boundary of layers of the passive volume conductor (e.g., emphysema) leading to attenuation of all components of the ECG curve (extracardiac phenomenon). What is not as much appreciated is that such attenuation results in shortening of the durations of P-waves, QRS complexes and T-waves.5,6 The postulated mechanism for
616
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
Fig. 2 e Electrocardiograms on day 1 (A) and day 7 (B) of hospitalization.
Table 1 e Quantitative automated measurements of electrocardiogram variables. Date
HR
P-axis
QRS-axis
T-axis
SQRS
SP
ST
QRSd
QT
QTc
Pd
8/3/12 810/12 D%
118 119
55 53
14 5
96 73
81.68 20.44 75.0
11.0 4.95 55.0
17.48 7.28 58.4
72 58 19.4
328 300 8.5
460 423 8.0
90 66.18 26.5
Abbreviations: SQRS ¼ sum of peak-to-peak QRS complexes of all 12 ECG leads; SP ¼ sum of peak-to-peak P-waves of all 12 ECG leads; ST ¼ sum of peak-to-peak T-waves of all 12 ECG leads; QT ¼ QT interval; QTc ¼ QTc interval; QRSd ¼ global QRS duration; Pd ¼ mean P-wave duration.
this shortening is that the overall decrease in the amplitude of the P-waves, QRS complexes and T-waves introduces a measurement error of a portion after the onset and before the offset of these components of the ECG curve, which become as low as the underlying noise amplitude, and thus they are lost in the automated ECG measurement.5,6 All the above have significant diagnostic, monitoring, and prognostic implications in the setting of lung infections, lung congestion, pericardial and pleural effusions, emphysema in any location, hypoalbuminemia, and peripheral edematous states, encountered in clinical practice or research. Consequently knowledge about the association of these pathologies and ECG amplitudes of complexes, waves, and durations of intervals, for all clinicians caring for patients, is contributory to correct ECG-based diagnosis. However the above should be considered with caution when interpreting changes in the P-wave duration and dispersion (i.e., difference between the longest and the shortest Pwave duration among the 12 ECG leads, in ms) in the setting of development and amelioration of increased water content in any extracardiac body compartment. Indeed, mean P-wave duration P-wave dispersion did not change in patients who developed peripheral edema during a variety of critical illnesses, and their stability was attributed to the offsetting of the
electrophysiologically-mediated real changes (due to hemodynamic perturbations), by opposite apparent changes, imparted by the effect of the peripheral edema, as described above.7 Another matter of practical importance is that such changes in voltages/duration of ECG QRS complexes, exerted by extracardiac influences, may carry special bearing in patients with ischemic and nonischemic cardiomyopathies and heart failure, who are being considered for implantable cardioverterdefibrillation implantation, or cardiac resynchronization therapy, since such decisions often are based, among other parameters, on the duration of the QRS complexes.8
Conflicts of interest The author has none to declare.
references
1. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarca-mediated attenuation of the amplitude of
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
electrocardiogram complexes: a description of a heretofore unrecognized phenomenon. J Am Coll Cardiol. 2001;38: 756e764. 2. Madias JE. P waves in patients with changing edematous states: implications on interpreting repeat P wave measurements in patients developing anasarca or undergoing hemodialysis. Pacing Clin Electrophysiol. 2004;27:749e756. 3. Madias JE. T-wave amplitude attenuation/augmentation in patients with changing edematous states: implications for patients with congestive heart failure. Congest Heart Fail. 2007;13:257e261. 4. Madias JE. Effect of changes in body weight and serum albumin levels on electrocardiographic QRS amplitudes. Am J Cardiol. 2002;89:1233e1235.
617
5. Madias JE. Significance of shortening of the mean QRS duration of the standard electrocardiogram in patients developing peripheral edema. Am J Cardiol. 2002;89:1444e1446. 6. Madias JE. QTc interval in patients with changing edematous states: implications on interpreting repeat QTc interval measurements in patients with anasarca of varying etiology and those undergoing hemodialysis. Pacing Clin Electrophysiol. 2005;28:54e61. 7. Madias JE. P-wave duration and dispersion in patients with peripheral edema and its amelioration. Indian Pacing Electrophysiol J. 2007;7:7e18. 8. Madias JE. The impact of changing oedematous states on the QRS duration: implications for cardiac resynchronization therapy and implantable cardioverter/defibrillator implantation. Europace. 2005;7:158e164.
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/ihj
Case Report
Electrocardiogram voltage attenuation and shortening of the duration of P-waves, QRS complexes, and QT intervals John E. Madias a,b,* a b
The Icahn School of Medicine at Mount Sinai of the New York University, NY, USA The Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, USA
article info
abstract
Article history:
Multiple pathologies in concert may lead to attenuation of the electrocardiogram (ECG)
Received 1 March 2013
voltage. A case of a patient illustrating the above is presented, who showed marked
Accepted 10 August 2013
attenuation of the ECG voltage. Automated values of the amplitude of the ECG QRS com-
Available online 4 September 2013
plexes, P-waves, and T-waves (in mm), duration of the QRS complexes, P-waves, and QT intervals (in ms), in 2 ECGs were compared. The patient was a 64-year-old woman who
Keywords:
developed in the setting of a fatal illness, pleural and pericardial effusions, pneumo-
Electrocardiogram
mediastinum, pneumoperitoneum, subcutaneous emphysema in the neck and chest, pe-
ECG voltage attenuation
ripheral edema with weight gain of 43.4 lbs, marked hypoalbuminemia, abnormal liver
P-wave duration
tests, and renal failure. All the above pathologies led to a marked attenuation of the ECG
QRS duration
voltage, and shortening of the mean P-wave, QRS complexes, and QTc interval durations.
QTc interval duration
The postulated mechanism of the observed ECG phenomena is discussed. Copyright ª 2013, Cardiological Society of India. All rights reserved.
1.
Introduction
There are many factors which singly, on in concert, can influence the electrocardiogram (ECG) voltage and lead to attenuation of the P-waves, QRS complexes, and T-waves. The resultant effects are extracardiac in nature. What is not appreciated is the resultant shortening of the P-wave, QRS complex and QT intervals. The case of a patient presented herein illustrates all the above ECG changes resulting from multiple intrathoracic and systemic pathologies, which the patient suffered.
2.
Case presentation
A 64-year-old woman, with a history of hypertension, failure to thrive, weight loss of undefined etiology worked up at another hospital, was admitted to our facility with dyspnea, hypoxemia, and lung infiltrates, for which she was intubated, and placed on broad spectrum antibiotics and vasopressors. She abruptly decompensated, and was found to have pleural and pericardial effusions, pneumomediastinum, pneumoperitoneum, subcutaneous emphysema in the neck and chest, and peripheral edema with weight gain of 43.4 lbs (Fig. 1).
* Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, USA. Tel.: þ1 718 334 5005; fax: þ1 718 334 5990. E-mail address: [email protected]. 0019-4832/$ e see front matter Copyright ª 2013, Cardiological Society of India. All rights reserved. http://dx.doi.org/10.1016/j.ihj.2013.08.014
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
615
Fig. 1 e Portable chest X-ray on admission (A) reveals right lower lobe infiltrate and probably mild pleural effusion; portable chest X-ray on day 7 of hospitalization (B) reveals extensive subcutaneous emphysema, increasing consolidating changes of both lungs, and the tip of an endotracheal tube is seen proximal to the carina; a short axis parasternal view of the echocardiogram (C) on day 6 of hospitalization showed normal left ventricular size and thickness, with a large pericardial space which contained a large amount of “organized” echo-dense material, adherent to the epicardium and a pericardial effusion; an axial view of the thoracic computerized tomographic angiography (D) on day 2 of hospitalization revealed a prominent right pleural effusion, no parenchymal mass lesions, mediastinal and subcutaneous emphysema, right lower lobe infiltrate/atelectasis, pericardial effusion, suggestion of possible pneumopericardium, but no pleural effusion. Abbreviations: X [ subcutaneous emphysema; P [ pericardial effusion; M [ pneumomediastinum.
Exploratory laparotomy did not reveal any intestinal perforation in the abdomen, upper airways laryngoscopy and bronchoscopy by the Otorynolaryngolology service were negative for perforation, and evaluation via esophagogastroduodenoscopy by the Gastroenterology service did not disclose evidence of esophageal perforation. The echocardiogram on day #6 of hospitalization revealed a normal sized right and left atria, and right and left ventricles, normal left ventricular thickness, suboptimal visualization of the anterior and inferior left ventricular walls, preserved function of the left ventricular base, and severely reduced overall left ventricular ejection fraction; there was trace mitral and aortic regurgitation, moderate tricuspid regurgitation, and an estimated pulmonary artery systolic pressure of 34 mmHg; also there was a large pericardial space with a pericardial effusion and a large amount of “organized” echo-dense material adherent to the epicardium. Subcutaneous emphysema in the neck resolved but her respiratory failure worsened and she developed adult respiratory distress syndrome, shock with hypotension, tachycardia and peripheral hypoperfusion, marked hypoalbuminemia, abnormal liver tests, and renal failure. The family opted for extubation and no resuscitation, and the patient succumbed on day 7 of hospitalization. Comparison of the 2 ECGs recorded 7 days apart (Fig. 2) (Table 1), revealed minor changes in heart rate (118e119 beats/min),
P-wave frontal axis (55 e53 ), QRS frontal axis (14 to 5 ), and T-wave frontal axis (96 e73 ), while sums of peak-to-peak QRS complexes of all 12 leads decreased by 75% (81.68e20.44 mm), sums of peak-to-peak P-waves by 55.0% (11.0e4.95 mm), and sums of peak-to-peak T-waves by 58% (17.48e7.28 mm). This was associated with shortening of the mean P-wave duration by 26.5% (90e66.18 ms), QRS duration by 19.4% (72e58 ms), QT interval by 8.5% (328e300 ms), and QTc by 8% (460e423 ms).
3.
Discussion
What precipitated the ECG amplitude changes was the combination of pneumonia, acute respiratory distress syndrome, pericardial effusion, pleural effusion, mediastinal and subcutaneous emphysema, hypoalbuminemia, and peripheral edema.1e4 All these pathologies either enhance the water content (thereby resulting in reduction of electrical impedance) or produce marked disparities in the boundary of layers of the passive volume conductor (e.g., emphysema) leading to attenuation of all components of the ECG curve (extracardiac phenomenon). What is not as much appreciated is that such attenuation results in shortening of the durations of P-waves, QRS complexes and T-waves.5,6 The postulated mechanism for
616
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
Fig. 2 e Electrocardiograms on day 1 (A) and day 7 (B) of hospitalization.
Table 1 e Quantitative automated measurements of electrocardiogram variables. Date
HR
P-axis
QRS-axis
T-axis
SQRS
SP
ST
QRSd
QT
QTc
Pd
8/3/12 810/12 D%
118 119
55 53
14 5
96 73
81.68 20.44 75.0
11.0 4.95 55.0
17.48 7.28 58.4
72 58 19.4
328 300 8.5
460 423 8.0
90 66.18 26.5
Abbreviations: SQRS ¼ sum of peak-to-peak QRS complexes of all 12 ECG leads; SP ¼ sum of peak-to-peak P-waves of all 12 ECG leads; ST ¼ sum of peak-to-peak T-waves of all 12 ECG leads; QT ¼ QT interval; QTc ¼ QTc interval; QRSd ¼ global QRS duration; Pd ¼ mean P-wave duration.
this shortening is that the overall decrease in the amplitude of the P-waves, QRS complexes and T-waves introduces a measurement error of a portion after the onset and before the offset of these components of the ECG curve, which become as low as the underlying noise amplitude, and thus they are lost in the automated ECG measurement.5,6 All the above have significant diagnostic, monitoring, and prognostic implications in the setting of lung infections, lung congestion, pericardial and pleural effusions, emphysema in any location, hypoalbuminemia, and peripheral edematous states, encountered in clinical practice or research. Consequently knowledge about the association of these pathologies and ECG amplitudes of complexes, waves, and durations of intervals, for all clinicians caring for patients, is contributory to correct ECG-based diagnosis. However the above should be considered with caution when interpreting changes in the P-wave duration and dispersion (i.e., difference between the longest and the shortest Pwave duration among the 12 ECG leads, in ms) in the setting of development and amelioration of increased water content in any extracardiac body compartment. Indeed, mean P-wave duration P-wave dispersion did not change in patients who developed peripheral edema during a variety of critical illnesses, and their stability was attributed to the offsetting of the
electrophysiologically-mediated real changes (due to hemodynamic perturbations), by opposite apparent changes, imparted by the effect of the peripheral edema, as described above.7 Another matter of practical importance is that such changes in voltages/duration of ECG QRS complexes, exerted by extracardiac influences, may carry special bearing in patients with ischemic and nonischemic cardiomyopathies and heart failure, who are being considered for implantable cardioverterdefibrillation implantation, or cardiac resynchronization therapy, since such decisions often are based, among other parameters, on the duration of the QRS complexes.8
Conflicts of interest The author has none to declare.
references
1. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarca-mediated attenuation of the amplitude of
i n d i a n h e a r t j o u r n a l 6 5 ( 2 0 1 3 ) 6 1 4 e6 1 7
electrocardiogram complexes: a description of a heretofore unrecognized phenomenon. J Am Coll Cardiol. 2001;38: 756e764. 2. Madias JE. P waves in patients with changing edematous states: implications on interpreting repeat P wave measurements in patients developing anasarca or undergoing hemodialysis. Pacing Clin Electrophysiol. 2004;27:749e756. 3. Madias JE. T-wave amplitude attenuation/augmentation in patients with changing edematous states: implications for patients with congestive heart failure. Congest Heart Fail. 2007;13:257e261. 4. Madias JE. Effect of changes in body weight and serum albumin levels on electrocardiographic QRS amplitudes. Am J Cardiol. 2002;89:1233e1235.
617
5. Madias JE. Significance of shortening of the mean QRS duration of the standard electrocardiogram in patients developing peripheral edema. Am J Cardiol. 2002;89:1444e1446. 6. Madias JE. QTc interval in patients with changing edematous states: implications on interpreting repeat QTc interval measurements in patients with anasarca of varying etiology and those undergoing hemodialysis. Pacing Clin Electrophysiol. 2005;28:54e61. 7. Madias JE. P-wave duration and dispersion in patients with peripheral edema and its amelioration. Indian Pacing Electrophysiol J. 2007;7:7e18. 8. Madias JE. The impact of changing oedematous states on the QRS duration: implications for cardiac resynchronization therapy and implantable cardioverter/defibrillator implantation. Europace. 2005;7:158e164.