الفهرس 
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Abstract
Bronchial asthma has been accused in causing arrythmias and affecting the cardiac function and anatomy especially during the acute exacerbation attacks.
It is essential to study the role of bronchial asthma in cardiac dysfunction, this will not only help clinicians to assess the risk of death and institute the appropriate level of care, but it will also help to explain the mechanism of death and to guide for other treatment.
This work was done to study the various ECG abnormalities in acute asthma as well as the relation between the ECG abnormalities with severity of airway obstruction and the effect of bronchodilators used on the ECG.
This descriptive prospective study was conducted on 50 asthmatic children with moderate-severe acute asthmatic attack who were divided according to GINA guidelines 2016 into:
1. group I: Included 20 patients with moderate acute attack.
2. group II: Included 30 patients with severe acute attack
Inclusion Criteria:
The present study was conducted on patients ranging 3 to 16 years of age, presenting with moderate to severe asthmatic attack. They received B2 agonist nebulization and IV magnesium and 32 patients took add on theophylline
Exclusion Criteria:
• Congenital or acquired cardiac patients.
• Patients with other system illness that may affect cardiac functions (known chronic obstructive lung disease, hypertensive patient, collagen disease and immunocompromised patients).
Methods:
A) Thorough history taking from all patients
B) Thorough clinical examination laying stress on:
o Vital data: temperature, heart rate, respiratory rate
o Full chest, cardiac and abdominal examination.
C) Investigations
ECG: 12 lead ECG was done on presentation before start of medication, then it was repeated daily till discharge; for assessment of heart rate, P wave changes, ECG voltage, axis, arrhythmias, right ventricular strain and QTc interval.
2D and Tissue doppler echocardiography (TDE) were done during the acute asthmatic attack to all patients.
Our studied children had median age of 7.20 ± 2.63 years (range 3- 14 years) with 34 (68%) males and 16 (32%) females.
All patients (100%) had sinus tachycardia for age (mean 149.16 ± 11.41), 11 patients (22%) had P- pulmonale, 19 patients (38%) had Rt axis deviation, 29 patients (58%) had Rt ventricular strain, 8 patients (16%) had atrial ectopics, 6 patients (12%) had prolonged QTc interval >450msec and 5 patients (10%) had complete RBBB.
All studied patients (100.0%) had sinus tachycardia (mean= 150 +/- 12 bpm) in initial ECGs, which resolved after attack with mean heart rate 126.17±18.0. Also, it was more evident in patients with severe asthmatic attacks (154.33 ± 10.84 bpm) than those with moderate attacks (141.40 ± 7.13).
11 patients (22%) had developed P- pulmonale in our study, of which 3 patients had moderate attack and 8 patients had severe attack. However, it showed significant improvement in which only 2 patients 5% had P-pulmonale on 4th day.
The current study showed 19 of our patients (38%) had right axis deviation in initial ECG of which 4 (20%) had moderate attack and 15 (50%) had severe attack, with significant gradual decrease and disappeared completely on the fourth day.
Our study showed that 28 patients (56%) had right ventricular strain initially which significantly improved with treatment in all patients. Also, there was a highly significant relation between right ventricular strain and severity of the asthmatic attacks; 5 of patients (25%) with moderate asthmatic attacks had RV strain in initial ECGs, where as 23 of patients (76%) with severe attack showed RV strain in their initial ECGs.
Our current study showed no right ventricular enlargement, ST segment changes, nor PVCs in any of the ECGs of the studied patients during the acute asthmatic attack
The present study showed transiently prolonged QTc interval > 450msec in 6 patients (12%) and 5 patients (10%) had transient complete right bundle branch block (RBBB) however, they had no significant relation with acute asthmatic attack or its severity.
As regard atrial ectopic contractions, 16% of patients had atrial ectopic beats of whom 3% persisted on 4th day of acute attack. It was of no significant relation with acute asthmatic attack nor with its severity, yet they were more significantly evident in patients receiving theophylline (20%) than in patients not receiving theophylline 11%.
Regarding Echo findings, 50 patients (100%) had pulmonary hypertension, 6 patients (12%) had increased RV diameter, 1 patient (2%) had increased RV wall thickness, 8 patients (16%) had increased right ventricle Myocardial Performance Index and none had an altered E/A ratio across tricuspid valve.
Pulmonary pressure was elevated >25mmHg in all patients; of whom 5 (10%) had moderate hypertension > 40mmHg, and 45 patients (90%) had mild hypertension (pulmonary pressure between 25- 40 mmHg)
Our study showed no significant increase in RV diameter during diastole between asthmatic children and reference range and normal E/A ratios across tricuspid valve during asthmatic attack; being 1.56 ± 0.31 in moderate cases and 1.75 ± 0.24 in more severe cases; in comparison to reference range (0.8-2),
Our study showed no significant difference in echo parameters in relation with severity of the acute attack.