Pulmonary vein stenosis of ex-premature infants is a complex problem with poor survival, delayed diagnosis, and unsatisfactory treatment. The lack of concordance in twins suggests epigenetic or environmental factors may play a role in the development of pulmonary vein stenosis. In ex-premature infants with pulmonary hypertension and bronchopulmonary dysplasia a focused echocardiographic assessment of the pulmonary veins is required with further imaging if the echocardiogram is inconclusive.

We hypothesized that an automated speech- recognition-inspired classification algorithm could differentiate between the heart sounds in subjects with and without pulmonary hypertension (PH) and outperform physicians. Heart sounds, electrocardiograms, and mean pulmonary artery pressures (mPAp) were recorded simultaneously. Heart sound recordings were digitized to train and test speech-recognition-inspired classification algorithms. We used mel-frequency cepstral coefficients to extract features from the heart sounds. Gaussian-mixture models classified the features as PH (mPAp ≥ 25 mmHg) or normal (mPAp < 25 mmHg). Physicians blinded to patient data listened to the same heart sound recordings and attempted a diagnosis. We studied 164 subjects: 86 with mPAp ≥ 25 mmHg (mPAp 41 ± 12 mmHg) and 78 with mPAp < 25 mmHg (mPAp 17 ± 5 mmHg) (p  < 0.005). The correct diagnostic rate of the automated speech-recognition-inspired algorithm was 74% compared to 56% by physicians (p = 0.005). The false positive rate for the algorithm was 34% versus 50% (p = 0.04) for clinicians. The false negative rate for the algorithm was 23% and 68% (p = 0.0002) for physicians. We developed an automated speech-recognition-inspired classification algorithm for the acoustic diagnosis of PH that outperforms physicians that could be used to screen for PH and encourage earlier specialist referral.

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High inspired oxygen concentration (FiO > 0.85) is administered to test pulmonary vascular reactivity in children with pulmonary hypertension (PH). It is difficult to measure oxygen consumption (VO) if the subject is breathing a hyperoxic gas mixture so the assumption is made that baseline VO does not change. We hypothesized that hyperoxia changes VO. We sought to compare the VO measured by a thermodilution catheter in room air and hyperoxia. A retrospective review of the hemodynamic data obtained in children with PH who underwent cardiac catheterization was conducted between 2009 and 2014. Cardiac index (CI) was measured by a thermodilution catheter in room air and hyperoxia. VO was calculated using the equation CI = VO/arterial-venous oxygen content difference. Data were available in 24 subjects (males = 10), with median age 8.3 years (0.8-17.6 years), weight 23.3 kg (7.5-95 kg), and body surface area 0.9 m (0.4-2.0 m). In hyperoxia compared with room air, we measured decreased VO (154 ± 38 to 136 ± 34 ml/min/m, p = 0.007), heart rate (91 [Formula: see text] 20 to 83 [Formula: see text] 21 beats/minute, p=0.005), mean pulmonary artery pressure (41 [Formula: see text] 16 to 35 [Formula: see text] 14 mmHg, p=0.024), CI (3.6 [Formula: see text] 0.8 to 3.3 [Formula: see text] 0.9 L/min/m, p = 0.03), pulmonary vascular resistance (9 [Formula: see text] 6 to 7 [Formula: see text] 3 WU m, p = 0.029), increased mean aortic (61 [Formula: see text] 11 to 67 [Formula: see text] 11 mmHg, p = 0.005), pulmonary artery wedge pressures (11 [Formula: see text] 8 to 13 [Formula: see text] 9 mmHg, p = 0.006), and systemic vascular resistance (12 [Formula: see text] 6 to 20 [Formula: see text] 7 WU m, p=0.001). Hyperoxia decreased VO and CI and caused pulmonary vasodilation and systemic vasoconstriction in children with PH. The assumption that VO remains unchanged in hyperoxia may be incorrect and, if the Fick equation is used, may lead to an overestimation of pulmonary blood flow and underestimation of PVRI.