China
Africa
Explore chapters and articles related to this topic
Unusual Inherited Pulmonary Diseases Which Provide Clues to Pulmonary Physiology and Function
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Thomas Κ. C. King, Robert A. Norum
Chest x ray characteristically shows an increase in size in the pulmonary artery and its main branches with rapid peripheral tapering. There is increase in the heart size with encroachment on the retrosternal clear space in the lateral projection due to right ventricular hypertrophy. The electrocardiogram invariably shows evidence of right ventricular hypertrophy.
Chronic Obstructive Pulmonary Disease
Published in Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 2, 2017
Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod
Target investigations to define the extent of the disease, establish pre-operative baseline respiratory function and enable respiratory optimisation. Bloods – FBC may reveal polycythaemia from chronic hypoxaemia.ECG – may show right ventricular hypertrophy.CXR – look for hyperexpanded lung fields or the presence of bullae.ABG – on air, as a baseline.Pulmonary function tests – spirometry (reduced FEV1: FVC ratio) and flow–volume loops.Indicators of the requirement for likely post-operative ventilation include: FEV1 <1 LFEV1: FVC ratio <50%Baseline type 2 respiratory failure
Valvular Heart Disease
Published in P. Chopra, R. Ray, A. Saxena, Illustrated Textbook of Cardiovascular Pathology, 2013
Pulmonary valve stenosis It is almost always congenital in nature. Involvement of this valve has also been reported in carcinoid syndrome, rheumatic heart disease and infective endocarditis. Clinically, effects of right ventricular hypertrophy result.
Fixed and dynamic obstruction in double-chambered right ventricle
Published in Acta Cardiologica, 2021
Avinash Mani, Arun Gopalakrishnan, Kavassery Mahadevan Krishnamoorthy
A 4-year-old intelligent boy was referred for evaluation of an incidentally detected cardiac murmur. The arterial pulses were normal, blood pressure was 88/54 mmHg and oxygen saturation was 99%. Prominent ‘a’ waves were noted in the neck veins. Epigastric pulsations were prominent. A harsh pan-systolic murmur was noted at the left lower-sternal border and a grade 3 long late-peaking mid-systolic murmur was noted along the left upper-sternal border. Electrocardiography revealed right axis deviation of the QRS and right ventricular hypertrophy. Transthoracic echocardiography showed a hypertrophic muscle bundle in the mid-part of the right ventricle causing severe outflow tract obstruction, consistent with double-chambered right ventricle (DCRV) (Figure 1(a)). A restrictive perimembranous ventricular septal defect was noted opening to the proximal high pressure chamber. The interventricular gradient was 10 mmHg. In addition, the pulmonary valve was thickened and doming (annulus z-score: −2.3) with moderate – severe valvar pulmonary stenosis (video 1). Continuous-wave doppler confirmed the two levels of obstruction with a maximal right ventricle-to-pulmonary artery gradient of 75 mmHg (Figure 1(b)). The dagger-shaped relatively late peaking jet suggested severe dynamic subinfundibular obstruction and the parabolic jet confirmed severe valvar pulmonary stenosis. There was no tricuspid regurgitation. The inferior vena cava dimension was normal with >50% respiratory variation.
Elevated lipoprotein A in acute on chronic CTEPH with cardiogenic shock: a case report
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Kyaw Kyaw, Shakya Sabnam, Melanie Cheing, Fidencio Davalos, Michael Gramuglia
The admission laboratory was significant for D-dimer 2,518 ng/ml (normal 0–243 ng/ml), troponin 0.031 (normal ≤0.010 ng/ml), BUN 21 mg/dl (normal 7–18 mg/dl), Creatinine 1.3 mg/dl (normal 0.7–1.2 mg/dl), ESR 10 (normal 0–22 mm/h), CRP 1 (normal <4 mg/l) and ferritin 113 (normal 15–150 ng/ml). Chest X ray was unremarkable. The EKG reported T wave inversion in V2 to V5. CT angiogram chest showed bilateral subsegmental pulmonary embolism and mild right-heart strain (Figure 1). The echocardiogram revealed no obvious valvular abnormalities, normal left-ventricle systolic function, mild right-ventricular hypertrophy, pulmonary arterial pressure 50–55 mmHg, severe right ventricular dilatation and dysfunction (Figure 2). The hypercoagulability work-up was remarkable for elevated lipoprotein A 461.7 nmol/L (normal <75 nmol/L) and elevated homocysteine level 28.7 umol/L (normal <15 umol/L).
Overview and surgical aspects of Uhls anomaly
Published in Expert Opinion on Orphan Drugs, 2020
Kotturathu Mammen Cherian, Lydia Jeris W, Mohamed Thayub
Earlier, diagnosis of Uhls anomaly was made only at autopsy but currently non-invasive imaging modalities like ECHO, MRI would aid in the diagnosis of Uhls anomaly. X-ray shows marked cardiomegaly with increased pulmonary vascular network. Electrocardiogram (ECG) shows right atrial and right ventricular hypertrophy. ECHO usually reveals a symmetrical thinning of right ventricular free wall and abnormally enlarged right ventricle [35,36]. Doppler ECHO reveals tricuspid insufficiency and hypokinesia of right ventricle. Radio nucleotide angioventriculography shows decreased right ventricular ejection fraction. MRI shows thin-walled right ventricle with absence of right ventricular myocardium. Apical trabeculation is also lost with dilated right atrium. Cardiac catheterization reveals markedly dilated right atrium and right ventricle. Transillumination test can also be done revealing thinning of right ventricular wall. Histopathological examination would reveal loss or lack of myocardium, poorly developed cardiac myocytes with fibrosis and direct apposition of endocardium to epicardium with absence of myocardial layer in between [37,38].