Artificial organs
-
The treatment of cardiogenic shock using inotropic agents and vascular volume expansion places an added burden on the heart. The resultant increase in cardiac work may cause myocardial ischemia and lead to cardiac arrest. Extracorporeal membrane oxygenation (ECMO) may be used to treat cardiogenic shock. ⋯ The rise in blood pressure associated with restoring systemic circulation afterloads the heart and can cause left atrial hypertension and pulmonary edema. ECMO does not automatically reduce cardiac work, especially in the presence of residual shunts. Left atrial drainage or decompression may be essential in certain patients both to avert pulmonary edema and to reduce cardiac work.
-
The hemostatic system poses a major problem in extracorporeal membrane oxygenation (ECMO). The foreign surface in the extracorporeal circuit activates platelets and the clotting system. To avoid loss of platelets and activation of the clotting system, anticoagulation is necessary. ⋯ Most ECMO centers use heparin for anticoagulation and the activated clotting time (ACT) for monitoring. Reduction of problems with hemostasis may be obtained with less thrombogenic surfaces, new anticoagulants with a short half-life, platelet inhibitors, protease inhibitors, or selective anticoagulation in the extracorporeal circuit. While there will probably never be a complete nonthrombogenic surface available and all anticoagulants will have some risk of bleeding, improvement can be obtained by a combination of measures including better surfaces, more sophisticated anticoagulation regimens, and close laboratory monitoring.
-
Congenital heart disease with increased pulmonary blood flow commonly leads to the development of pulmonary hypertension and increased vascular reactivity. These serious sequelae are associated with the following two major categories of congenital heart defects: those resulting in increased pulmonary blood flow and increased pulmonary arterial pressure and those resulting in increased pulmonary venous pressure. Recent evidence that the pulmonary vascular endothelium is an important determinant of vascular tone has led to the hypothesis that endothelial injury, secondary to congenital heart disease with increased pulmonary blood flow, disrupts these regulatory mechanisms and thereby plays a role in the development of pulmonary hypertension and its associated increased vascular reactivity. ⋯ In this model, we found significant physiologic and molecular alternations of both the nitric oxide (NO) and endothelin signaling pathways, two important mechanisms by which the endothelium regulates pulmonary vascular tone. These alterations occur extremely early and precede severe anatomic changes. Early endothelial damage may contribute to the development of pulmonary hypertension and its associated enhanced pulmonary vascular reactivity.