Systemic-to-pulmonary shunting in growing pigs has been proposed as an experimental model of high-flow pulmonary hypertension associated with congenital heart defects. We investigated multipoint pulmonary arterial pressure (Ppa) vs. cardiac output (Q) plots and pulmonary vascular impedance spectra in 13 piglets aged approximately 4 mo and ventilated alternatively in hyperoxia (inspired O2 fraction 0.4) and in hypoxia (inspired O2 fraction 0.12). The measurements were done 8 wk after either an anastomosis between the thoracic aorta and the pulmonary trunk (n = 7 piglets) or a sham operation (n = 6). Cardiac output was altered by a manipulation of venous return. In the sham-operated piglets, hypoxia increased Ppa by an average of 12 mmHg over the entire range of Q studied, from 60 to 120 ml/kg, and increased both 0 Hz (Z0) and characteristic (Zc) pulmonary vascular impedance. In the shunted piglets compared with the sham-operated piglets in hyperoxia, Ppa was increased by an average of 5-6 mmHg at all levels of Q studied, from 60 to 120 ml/kg (P < 0.01), and Zc was also increased (P < 0.01), whereas Z0 was unchanged. In the shunted piglets, hypoxia increased Ppa at all levels of Q studied only to an average of 3 mmHg, and neither Z0 nor Zc was altered by hypoxia. We conclude that an aortopulmonary shunt of 2-mo duration in growing pigs increases both pulmonary vascular resistance and impedance and is associated with a blunting of pulmonary vascular reactivity to hypoxia.
Because of the large interindividual variability in the difference between SvO2 and ScvO2, the measure of ScvO2 should not replace the measure of SvO2 with a pulmonary artery catheter for the management of patients undergoing cardiac surgery with cardiopulmonary bypass.
The pulmonary vascular effects of inhaled anesthetics have been reported variably. We compared the effects of intravenous anesthesia (propofol) and inhalational anesthesia (isoflurane) on multipoint mean [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (PpaO)]/cardiac output (Q) plots and on pulmonary vascular impedance (PVZ) spectra in eight dogs alternatively ventilated in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). Q was altered by a manipulation of venous return. During propofol, hypoxia increased (Ppa-PpaO) by an average of 2-3 mmHg over the entire range of Q studied, from 1 to 2.5 l.min-1 x m-2. This hypoxic pulmonary vasoconstriction (HPV) was associated with insignificant changes in PVZ. Decreasing Q in hypoxia and hyperoxia did not affect PVZ. Compared with propofol, isoflurane decreased (Ppa-PpaO) by an average of 2-5 mmHg at all levels of Q studied in both hypoxia and hyperoxia but did not affect HPV. During isoflurane anesthesia, 0 Hz PVZ was lower (P < 0.01) in hypoxia, but otherwise the PVZ spectrum was not different from that recorded during propofol anesthesia. We conclude that, in dogs, 1 degree general anesthesia with isoflurane alone decreases pulmonary vascular tone without inhibition of HPV and that 2 degrees pressure/Q plots in the time domain are more sensitive than those in the frequency domain to subtle hemodynamic changes induced by hypoxia or isoflurane at the periphery of the pulmonary vasculature.
We describe a rare case of a 21-year-old man presenting with hereditary multiple exostosis and a pseudoaneurysm of the popliteal artery caused by femoral osteochondroma. Principles of management and surgical technique are discussed.
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