Exacerbation of hypoxic injury after restoration of oxygenation (reoxygenation) is an important mechanism of cellular injury in transplantation and in myocardial, hepatic, intestinal, cerebral, ren...

Reactive species mechanisms of cellular hypoxia-reoxygenation injury.

T hroughout medical history, unusual patient groups have often provided vital clues to the pathogenesis of disease. For example, the discovery of a small group of patients with a1proteinase inhibitor deficiency provided critical insights into the pathogenesis of emphysema. The study of hemophiliacs opened exciting new avenues of research and clinical intervention that are still being fruitfully explored. And chronic major-vessel thromboembolic pulmonary hypertension (C T-E PH) promises to be an instance in which a relatively small, unusual group of patients may provide much information about both thromboembolism and pulmonary vascular disease. C T-E PH is the result of single or recurrent pulmonary emboli arising from sites of venous thrombosis. The natural history of most emboli is to undergo total resolution, or resolution leaving minimal residua, with restoration of normal pulmonary hemodynamics.1-5 For reasons still unclear, the emboli in C T-E PH patients do not resolve completely; rather, they follow an aberrant path of organization and recanalization, leaving endothelialized residua that obstruct or significantly narrow major (main, lobar, or segmental) pulmonary arteries. From the reports of others6-1"2141 and our own experience with more than 250 C T-E PH patients, it is clear that there is a wide spectrum of residual embolic obstruction and therefore the degree to which pulmonary vascular resistance is increased. Some patients with chronic obstruction of one or more segmental or lobar arteries are nearly asymptomatic. At the other extreme are those who have major obstructions in multiple central pulmonary arteries and develop severe pulmonary hypertension and progressive right ventricular failure. This disorder is quite distinct from so-called "primary" pulmonary hypertension in which the obstructing lesions appear in the small, distal pulmonary arteries. While in primary pulmonary hypertension there may be thrombotic lesions in these small arter-

Chronic major-vessel thromboembolic pulmonary hypertension.

https://www.thelancet.com/pdfs/journals/lanres/PIIS2213-2600(14)70089-X.pdf

Chronic thromboembolic pulmonary hypertension

It is likely that chronic thromboembolic pulmonary hypertension (CTEPH) is more prevalent than currently recognised. Imaging studies are fundamental to decision making with respect to operability. All patients with suspected CTEPH should be referred to an experienced surgical centre. Currently, there is no risk scoring stratification system to guide operability assessment and it is predominantly based on surgical experience. The aim of pulmonary endarterectomy (PEA) is the removal of obstructive material to immediately reduce pulmonary vascular resistance. PEA affords the best chance of cure, but is difficult to perfect. Recognition and clearance of distal segmental and subsegmental disease is the main problem. The basic surgical techniques include: median sternotomy incision, cardiopulmonary bypass, arteriotomy incisions within pericardium, and a true endarterectomy with meticulous full distal dissection. Deep hypothermic circulatory arrest is recommended as the best means of reducing blood flow in the pulmonary artery to allow a clear field for dissection. In the recent PEACOG (PEA and COGnition) trial there was no evidence of cognitive impairment post-PEA. Reperfusion pulmonary oedema and residual pulmonary hypertension are unique post-operative complications post-PEA and are associated with increased mortality. However, in-hospital mortality is now <5% in experienced centres.

https://erj.ersjournals.com/content/erj/41/3/735.full.pdf

Surgical treatment of chronic thromboembolic pulmonary hypertension

Pulmonary artery thromboendarterectomy (PAT) is a potentially curative procedure in chronic, major vessel thromboembolic pulmonary hypertension. However, postoperative reperfusion pulmonary edema (RPE) has been a serious complication, often requiring prolonged mechanical ventilation. This entity has been described only anecdotally in the past. To characterize it more fully, we retrospectively analyzed the course and potential determinants of RPE after thromboendarterectomy in 22 patients who had PAT at our institution from 1969 through 1984. Particular attention was directed to clinical data, thrombus location, areas operated, postoperative roentgenograms, and preoperative and postoperative hemodynamic data. In all patients but 1, RPE developed within 72 h after surgery, corresponding to anatomic locations distal to vessels subjected to PAT. Regions of lung not reperfused at surgery were uniformly spared. Pulmonary capillary wedge and/or left atrial pressures preoperatively and postoperatively were not elevated. None of the preoperative data predicted which patients would develop more persistent RPE. These observations suggest that the phenomenon of RPE is a peculiar, focal form of pulmonary edema, the basis for which remains to be defined.

Reperfusion pulmonary edema after pulmonary artery thromboendarterectomy.

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Reperfusion pulmonary edema after pulmonary artery thromboendarterectomy.