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ORIGINAL ARTICLE
Year : 2013  |  Volume : 27  |  Issue : 1  |  Page : 19-24

Electrocardiographic changes in obstructive airway disease


1 Department of Respiratory Medicine, Regional Institute of Medical Sciences, Imphal, Manipur, India
2 Department of Physiology, Jawaharlal Nehru Institute of Medical Sciences, Imphal, Manipur, India
3 Department of Physiology, Regional Institute of Medical Sciences, Imphal, Manipur, India

Date of Web Publication17-Aug-2013

Correspondence Address:
Irom Ibungo Singh
Department of Respiratory Medicine, Regional Institute of Medical Sciences, Imphal, Manipur
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4958.116627

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  Abstract 

Objectives: To grade the severity of airway obstruction in the cases of obstructive airway disease (OAD) selected for the study and to observe for any electrocardiographic changes and correlate it with the severity of airway obstruction. Materials and Methods: 50 cases of OAD, 37 of chronic obstructive pulmonary disease (COPD) and 13 of Bronchial Asthma, attending the out patient department (OPD) of Respiratory Medicine, Regional Institute of Medical Sciences (RIMS), Imphal were included in the study. Spirometry was performed and electrocardiogram (ECG) was recorded for the cases in the Department of Physiology, RIMS, Imphal. For analytical purposes, well known statistical techniques like mean, standard deviation, X2 -test and F-test are used whenever found suitable and necessary through SPSS software and accordingly interpretations are made. Results: The cases were found to have mild to moderate to severe to very severe degree of airway obstruction. The ECGs showed normal to varied findings. Conclusion: Electrocardiographic changes are found to be observed more with those who have higher grade or degree of airway obstruction. Relationship between ECG findings and degree of airway obstruction is found to be highly significant.

Keywords: Chronic obstructive pulmonary disease, Electrocardiogram, Obstructive airway disease, Spirometry


How to cite this article:
Singh II, Susie K, Ningthoujam S, Lalvarmawi F, Kanan W, Singh W A. Electrocardiographic changes in obstructive airway disease. J Med Soc 2013;27:19-24

How to cite this URL:
Singh II, Susie K, Ningthoujam S, Lalvarmawi F, Kanan W, Singh W A. Electrocardiographic changes in obstructive airway disease. J Med Soc [serial online] 2013 [cited 2020 Oct 30];27:19-24. Available from: https://www.jmedsoc.org/text.asp?2013/27/1/19/116627


  Introduction Top


Obstructive diseases of the airways are a diverse group. In general, they have a common airway narrowing, with the consequent increase in the work of breathing and the sites of obstruction vary from the upper airways to the most peripheral bronchioles. Obstructive airway diseases include, asthma, chronic bronchitis, and emphysema, bronchiectasis, cystic fibrosis, disease of the extrathoracic airways and other disorders of the intrathoracic airways. [1] The National Heart, Lung and Blood Institute/World Health Organization Global initiative for chronic obstructive lung disease defined airflow obstruction as forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC) ratio of < 0.70 of predicted. Severity of airflow obstruction were graded as Stage 1 or Mild, Stage 2a or Moderate, Stage 2b or Severe and Stage 3 or Very Severe when FEV 1 is >80% of predicted, 50-80% of predicted, 30-50% and <30% of predicted respectively. [2] Electrocardiographic changes accompanying increasing airway obstruction and arterial blood gases in chronic bronchitis and emphysema are due to several mechanisms: (a) Hyperinflation of lungs, which changes the conditions of transmission or cardiac action currents (b) Depression of the diaphragm, which alters the anatomic relationship of the heart to the electrode positions (c) Hypoxia and changes in body chemistry, which alter cardiac metabolism, and (d) Pulmonary hypertension resulting from vasoconstriction and reduced pulmonary vascular bed as a result of destructive parenchymal changes. [3] American thoracic society in 1987 defined asthma as "A clinical syndrome characterized by increased responsiveness of the tracheobronchial tree to a variety of stimuli." That basic definition is expanded to include, major symptoms (variable paroxysms of dyspnea, wheezing, and cough), primary physiologic abnormalities (airway obstruction), and histological changes. [4] In severe bronchial asthma, reversible electrocardiographic abnormalities are not rare. It is usually sinus tachycardia, right axis deviation, atrial enlargement and right bundle branch block (RBBB). Transient ST segment depression or elevation in inferior leads in severe acute asthma has been observed since long and severity of electrocardiogram (ECG) signs correlate with the degree of airway obstruction. [5]


  Materials and Methods Top


Fifty subjects were selected for the study, out of which 13 cases are of bronchial asthma and 37 of chronic obstructive pulmonary disease (COPD) cases. Age ranging from 13 years and above attending the out patient department (OPD) and indoor wards of the Departments of Respiratory Medicine were included in the study. Patients with associated diseases such as hypertension, cardiac diseases (not secondary to pulmonary conditions), pulmonary fibrosis, neuromuscular diseases, and with ascites were excluded. A12 lead ECG was recorded by means of Cardiart108T/MK, BPL Limited in the Department of Physiology, Regional Institute of Medical Sciences (RIMS), Imphal. The results were analyzed for abnormality in the duration, voltage, and wave forms in all the leads. Spirometric studies were conducted by means of a computerized medspiror with built-in electronic pneumotach transducer (Recorders and Medicare Systems, Chandigarh) in the Respiratory Physiology Laboratory of Department of Physiology, RIMS. The procedures were explained to the patients followed by a demonstration. Three consecutive tests were taken with a rest of 10-15 min between two spirometric sessions and the results among the three tests were recorded. The following parameters were recorded by the medspiror- (i) FVC (ii) FEV 1 (iii) Peak expiratory flow rate (iv) Maximum voluntary ventilation.


  Results Top


[Table 1] shows the patient as an adult (age more than 18 years) or a child (age less than 18 years), male or female and selects the suitable set of equations for computation of predicted parameter values by using clinical prediction equations in medspiror. [Table 2] shows that there is a significant variation of FEV 1 (%) among the patients under study. The highest percentage of patients (34%) have their FEV 1 (%) within the range of 45-60 and thereafter tapering both sides. Besides, average FEV 1 (%) is found to be 56.00 with a standard deviation (SD) of 14.86. [Table 3] shows distribution of patients according to the stage of obstruction of airway disease. The highest percentage i.e., 56% of the patients belongs to Stage 2a which is followed by 32% of Stage 2b, 6% of Stage 1 and stage 3. In other words, 10% of the cases have mild airway obstruction while 56% have moderate and the remaining 34% have severe airway obstruction. The variation of percentages of patients in the study sample over the stages is found to be very highly significant even at 0.1% level of significance. Here, in [Table 4], there is a fluctuation of mean age of patients over the four stages of patients. Besides, test value shows significant result (P = 0.049) showing that age of the patient is related to the stage of the disease i.e., as age advances, severity of airway obstruction also increases. [Table 5] shows a very high significant F-value (2.675) with P value of 0.000 and as the stage advances, the ratio value tends to reduce. The ratios for mild and moderate are alike at around 62 while severe has sudden low ratio i.e., Stage 2b has mean ratio of 53.57 and Stage 3, the ratio of 48.00. [Table 6], analysis is made in 73 parameters instead of 50 cases. It is because of the fact that we counted the number of appearances of a particular type of ECG findings in the sample and therefore, its numbers exceed the number of patients. Regarding the ECG changes (i.e., excluding normal ECG), analysis is made in 53 parameters. Of all the ECG findings, normal ECG has the highest percentage (27.4) of occurrence. Among the ECG changes observed, sinus tachycardia accounts for 32.1%, right axis deviation (13.2%), P-pulmonale (11.3%), [Figure 1] low-voltage QRS and ventricular conduction defect (9.4% each), [Figure 2] left axis deviation and myocardial ischemic changes (7.5% each), right axis deviation [Figure 3] with right ventricular hypertrophy (RVH) and lead I sign (3.7% each) and lowest percentage (1.8%) belongs to left axis deviation with left ventricular hypertrophy (LVH) [Figure 4]. Again, when we consider the ECG findings excluding the normal ECG, the electrocardiographic changes thus observed in our cases are distributed in the different stages of airway obstruction as follows - cases belonging to stage 1 has no ECG changes, 33.96% of the ECG changes observed is found in stage 2a, 52.83% in stage 2b, and 9.6% in stage 3. The relationship between ECG findings and stage of airway obstruction is found to be highly significant (P < 0.001). [Table 7] highlights the distribution of patients with respect to ECG record (appearances) and type of OAD. Due to absence of electrocardiographic findings in most of the cases of bronchial asthma, most of the cell frequencies are found to be either nil or very less and it is not feasible to use statistical technique. However, χ2 -test is used with "Yate" correction and found to be significant at 5% probability level.
Table 1: Clinical prediction equations used in medspiror


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Table 2: Forced expiratory volume in 1 s (percentage)-wise distribution of cases


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Table 3: Stage - wise distribution of cases


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Table 4: Distribution of mean±SD of age with respect to stage


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Table 5: Distribution of mean±SD of ratio of forced expiratory volume in 1 s/forced vital capacity with respect to stage


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Table 6: Electrocardiogram record - wise distribution with respect to stage


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Table 7: Electrocardiogram record - wise distribution with respect to type of obstructive airway disease


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Figure 1: Electrocardiogram of a chronic obstructive pulmonary disease patient showing P-pulmonale, right axis deviation, sinus tachycardia and right ventricular hypertrophy

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Figure 2: Electrocardiogram of a chronic obstructive pulmonary disease patient showing lead 1 sign and ventricular conduction defect

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Figure 3: Electrocardiogram of a patient showing right axis deviation, sinus tachycardia and myocardial ischemic changes

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Figure 4: Electrocardiogram of a patient showing left axis deviation with left ventricular hypertrophy

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  Discussion Top


In our study, we have taken 50 cases of OAD who's spirometric and electrocardiographic assessments were carried out and made relevant observations. The highest percentage of patients (34%) has their FEV 1 % predicted within the range of 45-60 with an average FEV 1 % of 56.00 with a S.D. of 14.86. Based on FEV 1 % predicted, severity of airway obstruction is graded. The highest percentage (56%) belongs to Stage 2a, which is followed by 32% of Stage 2b, 6% of Stage 1 and Stage 3. In other words, 6% of the cases have mild airway obstruction while 56% have moderate, 32% severe and the remaining 6% have severe airway obstruction [Table 2] and [Table 3]. [Table 4] shows a fluctuation of mean age of patients over the four stages of patients. Besides, test value shows significant result (P = 0.049) showing that age of the patient is related to the stage of the disease i.e., as age advances, severity of airway obstruction also increases. [Table 5] shows a very high significant F value (2.675) with P value of 0.000 and as the stage advances, the ratio value tends to reduce. The ratios for mild and moderate are alike at around 62 while severe has sudden low ratio i.e., Stage 2b has mean ratio of 53.57 and Stage 3, the ratio of 48.00.In the present study [Table 6], it is observed that there is an increase of mean age of patients over the four stages of severity of airway obstruction i.e., mean age of patient increases with progressing stage of the severity of airway obstruction. Besides, test value shows significant result showing that age of the patient is related to his/her disease stage. Lindberg et al. (2007) reported that higher age was a significant risk factor in men and decline in FEV 1 was associated with age. [6] As the stage of disease advances, the ratio value of FEV 1 /FVC with respect to stage tends to reduce [Table 7]. The ratios of mild and moderate are alike at around 62 while severe has sudden low ratio i.e., Stage 2b has mean ratio of 53.57 and Stage 3, the ratio of 48.00. Schaeffer and Pryor (1977) also found that patients with severe degree of airway obstruction had reduction in FEV 1 /FVC% below 45%. [7] Of all the ECG findings, normal ECG has the highest percentage (27.4) of occurrence. Among the ECG changes observed, sinus tachycardia accounts for 32.1%, right axis deviation (13.2%), P-pulmonale (11.3%), low voltage QRS and ventricular conduction defect (9.4% each), left axis deviation and myocardial ischemic changes (7.5% each), right axis deviation with RVH and lead 1 sign (3.7% each) and lowest percentage (1.8%) belongs to left axis deviation with LVH. Irrespective of type of ECG findings, cases belonging to stage 1 have no ECG changes, 33.96% of the ECG changes observed is found in stage 2a, 52.83% in stage 2b and 9.6% in stage 3. The relationship between ECG findings and stage of airway obstruction is found to be highly significant (P < 0.001). Bazuave et al. also concluded that ECG findings correlate with the spirometric assessments of FEV 1 and clinical severity. [8] In our study, 94.3% of ECG changes observed are in COPD patients while 5.7% are observed in patients of bronchial asthma which may be attributed to the fact that most of the patients of bronchial asthma were not in severe acute phases and lacked ECG changes. Acute electrocardiographic changes accompanying asthma include, sinus tachycardia, right axis deviation, clockwise rotation, and signs of RVH. Electrocardiographic changes caused by asthma resolved within hours of response to therapy. [9] Normal ECG is found in highest percentage (27.4%) of all the ECG findings in our study. This may be probably because, most of our cases belongs to mild to moderate grades of severity of airway obstruction with FEV 1 % predicted between 50 to > 80% i.e., belonging to stage 1 and 2a. Sinus tachycardia (32.1%) may be explained by the well-known fact that acute hypoxia induces sinus tachycardia. Recent evidence suggests that when stimulated with hypoxic blood aortic and carotid bodies elicit a directionally opposite response. Although, the reflex effect of stimulation of the carotid bodies is primarily inhibitory (bradycardia), stimulation of aortic bodies causes an increase in heart rate and ventricular function. Perfusion of aortic bodies with hypoxic and hypercapnic blood produces the same degree of vasoconstriction as perfusion of the carotid bodies. There are also direct effects of hypoxia on the brain and spinal cord, causing an increase in sympathetic efferent discharge with hypertension and tachycardia. [10] Chronic corpulmonale or pulmonary heart disease is defined as hypertrophy of right ventricle (RV) resulting from diseases affecting the function and/or the structure of the lung, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart or congenital heart diseases. Chronic pulmonary hypertension with a corresponding increase in right ventricular work results in a uniform hypertrophy of the RV in COPD. The pulmonary hypertension that leads to corpulmonale and right heart failure in COPD is the result of several mechanisms including hypoxic vasoconstriction, a loss of pulmonary capillary bed, a decrease in pulmonary vascular compliance and vascular wall remodeling. [11] P-pulmonale and electrocardiographic evidence of RVH are uncommon until the FEV 1 is less than 45% of predicted in patients of COPD. [12] Controversy has existed over the years as to whether the left ventricle eventually fails when Right Ventricular failure results from chronic corpulmonale. Although, Left Ventricular catheterization studies have revealed abnormal Left Ventricular end-diastolic function that correlated with the severity of pulmonary hypertension, it is likely that this results in large part, from the bulging of interventricular septum from the hypertrophied and dilated RV into the cavity of Left Ventricle. As a result, Left Ventricular diastolic geometry becomes distorted and filling characteristics may be altered such that a higher filling pressure is required to accomplish the same end-diastolic fiber stress needed for stroke work in accordance with the Starling's law of the heart. Thus, our observation of left axis deviation (LAD) and LVH is also not unexpected. Chappell [13] concluded that LAD may be the sole electrocardiographic abnormality in patients with COPD. Electrocardiographic changes associated with emphysema in the absence of disabling chronic airway obstruction and pulmonary hypertension are limited to low voltage and pseudo left axis deviation. [14] We found low voltage QRS in 9.4% of our patients. Severe COPD patients have been shown to have elevated circulating levels of C-reactive protein (CRP) and other systemic inflammatory markers. Presence of systemic inflammation even in moderate COPD (FEV 1 50-80%) have been demonstrated. Airflow obstruction is an important risk factor for cardiac injury, the risk increases almost 2-fold in the presence of elevated CRP, which suggest an important interplay of systemic inflammation with airflow obstruction in the development of ischemic heart disease. Moderate to severe (but not mild) COPD is strongly associated with systemic low-grade inflammation and ECG evidence of ischemic heart disease. [15] In our study, we observed features of myocardial ischemic changes in the ECG of 4 cases of COPD belonging to moderate to severe degrees of airway obstruction. "Lead 1 sign" was observed in two cases of COPD, one of moderate degree and another of severe degree. "The lead 1 sign" is a highly specific ECG marker of COPD. It has not been described in COPD patients with coexisting cardiac disease. In patients with COPD, the frontal plane P, QRS and T-wave axis are not infrequently all directed at around + 90°. These three vectors are therefore directed either precisely or almost perpendicular to the standard lead 1 axis. As a result of this, lead 1 reflects either absent or very low amplitude P, QRS, T-wave complexes giving the appearance of a minimally disturbed baseline. This ECG phenomenon is known as the "lead 1 sign."Schamroth described the "lead 1 sign" as being reflected by "absent or very low amplitude P, QRS, T-wave complexes giving the appearance of a minimally disturbed baseline" without any specification of the cut-off values for the amplitude of these three waveforms. [16] A very strict arbitrary criteria for the diagnosis of the "lead 1 sign" consists of isoelectric P-wave in lead 1 combined with a very small QRS complex of less than 1.5 mm total deflection and a T-wave of less than 0.5 mm in lead 1 [17] .Ventricular conduction defect accounts for 9.4% of the ECG changes observed in our study. It is not conforming to be typically ascribed as RBBB or Left Bundle Branch Block and was observed in patients belonging to moderate to severe degrees of airway obstruction of both COPD and bronchial asthma. Carilli et al. [18] opined that ECG may serve as a means for estimating the degree of pulmonary impairment in patients with COPD.


  Conclusion Top


Functional lung impairment in patients of OAD like COPD and Bronchial Asthma can be identified by computerized spirometry and further, the degree of impairment in terms of severity of airflow obstruction can be graded based on FEV 1 /FVC ratio percentage of predicted and FEV 1 percentage of predicted, respectively. Electrocardiographic assessment of these patients shows certain abnormalities or changes while some have normal ECG. Electrocardiographic changes are found to be observed more with those patients who have higher grade or degree of severity of airflow obstruction with no electrocardiographic changes seen in case of mild or Stage 1 airway obstruction. Electrocardiographic changes observed in our cases under study are mostly those suggestive of hypoxia, right ventricular hypertrophy or failure secondary to chronic pulmonary hypertension, alteration in anatomical relationship of the heart to the electrode positions and changes in conditions of transmission or cardiac action currents.

 
  References Top

1.Nadel JA. Obstructive diseases-general principles and diagnostic approach. In: Murray JF, Nadal JA, editors. Textbook of respiratory medicine. 3 rd ed. Philadelphia: W.B. Saunders Company; 2000. p. 1173-84.  Back to cited text no. 1
    
2.Pauwels RA, Buist AS, Calverley PM, Jenkins CR, Hurd SS, GOLD Scientific Committee. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO global initiative for chronic obstructive lung disease (GOLD) Workshop summary. Am J Respir Crit Care Med 2001;163:1256-76.  Back to cited text no. 2
    
3.Tandon MK. Correlations of electrocardiographic features with airway obstruction in chronic bronchitis. Chest 1973;63:146-8.  Back to cited text no. 3
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4.Moser KM. Definition of asthma. In: Weiss EB, Stein M, editors. Bronchial Asthma: Mechanisms and Therapeutics. 3 rd ed. Boston: Little, Brown and Company; 1985. p. 11-4.  Back to cited text no. 4
    
5.Chazan R, Droszcz W. Electrocardiographic changes in patients with airway obstruction. Pol Arch Med Wewn 1992;87:237-41.  Back to cited text no. 5
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6.Lindberg A, Larsson LG, Rönmark E, Jonsson AC, Larsson K, Lundbäck B. Decline in FEV 1 in relation to incident chronic obstructive pulmonary disease in a cohort with respiratory symptoms. COPD 2007;4:5-13.  Back to cited text no. 6
    
7.Schaeffer JW, Pryor R. Pseudo left axis deviation and the S1S2S3 syndrome in chronic airway obstruction. Chest 1977;71:453-5.  Back to cited text no. 7
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8.Bazuaye EA, Obasohan AO, Jarikre LN, Onadeko BO. Relationship of the ECG with ventilatory function tests in chronic obstructive lung disease (COLD) in Nigerians. Afr J Med MedSci1997;26:111-4.  Back to cited text no. 8
    
9.Rapaport E. CorPulmonale. In: Murray JF, Nadel JA, editors. Textbook of respiratory medicine. 3 rd ed. Philadelphia: W.B. Saunders Company; 2000. p. 1631-48.  Back to cited text no. 9
    
10.Covell JW. Neuromuscular control of the circulation. In: West JB, editor. Best and Taylor's physiological basis of medical practice. 1 st ed. Imphal, India: BI Waverly Pvt. Limited; 1996. p. 276-89.  Back to cited text no. 10
    
11.Fraser RS, Muller NL, Colman N, Pare PD. Chronic obstructive pulmonary disease. In: Fraser RS, Pare PD, editors. Fraser and Pare's diagnosis of diseases of the chest. 4 th ed. Philadelphia: W.B. Saunders Company; 1999. p. 2077-263.  Back to cited text no. 11
    
12.Caird FI, Wilcken DE. The electrocardiogram in chronic bronchitis with generalized obstructive lung disease. Its relation to ventilatory function. Am J Cardiol 1962; 10:5-13.  Back to cited text no. 12
    
13.Chappell AG. The electrocardiogram in chronic bronchitis and emphysema. Br Heart J 1966;28:517-22.  Back to cited text no. 13
    
14.Shmock CL, Mitchell RS, Pomerantz B, Pryor R and Maisel JC. The electrocardiogram in chronic airway obstruction. The role of bronchitis and emphysema. Chest 1971; 60:335-40.  Back to cited text no. 14
    
15.Sin DD, Man SF. Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease. Circulation 2003;107:1514-9.  Back to cited text no. 15
    
16.Yip JW, Chia BL, Tan WC. The ECG "lead I sign" in cardiac disease: An indicator of coexisting obstructive pulmonary disease. Singapore Med J 1999;40:281-3.  Back to cited text no. 16
    
17.Fowler NO, Daniels C, Scott RC, Faustino BS, Gueron M. The electocardiogram in corpulmonale with and without emphysema. Am J Cardiol 1965;16:500-5.  Back to cited text no. 17
    
18.Carilli AD, Denson LJ, Timmapuri N. Electrocardiographic estimation of pulmonary impairment in chronic obstructive lung disease. Chest 1973; 64:483-7.  Back to cited text no. 18
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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