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Effect of acute lower respiratory tract infection on pulmonary artery pressure in children with post-tricuspid left-to-right shunt

Published online by Cambridge University Press:  12 January 2021

Sakshi Sachdeva
Affiliation:
Senior Resident, Pediatric Cardiology, Department of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India
Shyam S. Kothari*
Affiliation:
Department of Cardiology, Professor of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India
Saurabh K. Gupta
Affiliation:
Department of Cardiology, Additional Professor of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India
Sivasubramanian Ramakrishnan
Affiliation:
Department of Cardiology, Professor of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India
Anita Saxena
Affiliation:
Department of Cardiology, Professor and Head of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India
*
Author for correspondence: Dr Shyam S. Kothari MD, DM, Department of Cardiology, Professor of Cardiology, 7th Floor, Cardio-Thoracic Science Center, All India Institute of Medical Sciences, Ansari Nagar, New Delhi110029, India. Tel: +91-9868398166; Fax: +91-11-26588641; +91-11-26588663. E-mail: kothariss100@gmail.com

Abstract

We sought to examine the influence of clinically severe lower respiratory tract infection on pulmonary artery pressure in children having CHD with post-tricuspid left-to-right shunt, as it may have physiological and clinical implications. In a prospective single-centre observational study, 45 children with post-tricuspid left-to-right shunt and clinically severe lower respiratory tract infection were evaluated during the illness and 2 weeks after its resolution. Pulmonary artery systolic pressure was estimated non-invasively using shunt gradient by echocardiography and systolic blood pressure measured non-invasively.

Median pulmonary artery systolic pressure during lower respiratory tract infection was only mildly (although statistically significantly) elevated during lower respiratory tract infection [60 (42–74) versus 53 (40–73) mmHg, (p < 0.0001)]. However, clinically significant change in pulmonary artery systolic pressure defined as the increase of >10 mmHg was present in only 9 (20%) patients. In the absence of hypoxia or acidosis, only a small minority (9%, n = 4) showed significant pulmonary artery systolic pressure rise >10 mmHg. In the absence of hypoxia or acidosis, severe lower respiratory tract infection in patients with acyanotic CHD results in only mild elevation of pulmonary artery systolic pressure in most of the patients.

Type
Original Article
Copyright
© The Author(s), 2021. Published by Cambridge University Press

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