This brief review attempts to describe the present understanding of the pathogenesis of venous thrombosis in general with special reference to venous thromboembolism in spinal cord injury patients with paralysis. The component parts of Virchow's triad are examined. Most venous thrombi seem to originate in regions of slow blood flow, ie, the large venous sinuses of the calf and thigh or in valve cusp pockets. Decreased blood flow or even stasis due to lack of the pumping action of the large muscle packages in paralyzed patients is undoubtedly one of the major factors. As blood pools, activation products of the coagulation system accumulate locally leading potentially to local hypercoagulability. Activation products of clotting and fibrinolysis can induce endothelial damage which in turn leads to further activation of the hemostasis system. Endothelial damage may also result from distension of the vessel walls by the pooling blood. Blood flow is further decreased by hyperviscosity due to elevated fibrinogen levels and dehydration. Some spinal cord injury patients may sustain direct trauma to the legs; others may encounter vessel wall damage by the immobilized limbs. Shortly after injury, certain changes develop in the clotting system, especially increases in components of the von Willebrand factor macromolecular complex and increased platelet aggregability which could further contribute to hypercoagulability. Recently, an inhibition of the fibrinolytic system was suggested which also could add to a prothrombotic state. All of these interrelated processes clearly explain the high risk of venous thromboembolism in spinal cord injury patients with paralysis which has been clearly demonstrated by many investigators. It is hoped that intense thrombosis prophylaxis will reduce the incidence of this potentially devastating complication.

A 46-year-old man underwent cosmetic facial surgery under general anesthesia. He was ventilated by mask with an oxygen-enriched gas mixture for 4 to 6 h and monitored by pulse oximetry. Despite adequate arterial saturation (SaO2 > 90 percent) throughout the procedure, he remained in a deep coma after termination of anesthesia. Initial arterial blood gas analysis revealed a pH of 6.60 and a PaCO2 of 375 mm Hg. The patient was intubated and placed on mechanical ventilation. As his respiratory acidosis resolved, he regained consciousness quickly and recovered without any neurologic deficits. This case of record extreme hypercapnia and review of the literature demonstrates that survival is possible in acute severe respiratory acidosis as long as tissue anoxia and ischemia are prevented. We discuss the tissue effects of acute hypercapnia and newer aspects of the nature of intracellular pH regulation in critical tissues that afford considerable tolerance to acidosis. The dependence of these mechanisms upon active ion transport underscores the importance of adequate tissue oxygenation and perfusion.

Patients with acute heart failure or cardiogenic shock following myocardial infarction have a high mortality. The first priority is to salvage any remaining viable myocardium, either by thrombolytic agents or, if necessary, by coronary angioplasty. A mechanical cause for the heart failure or shock needs to be excluded. Thereafter, the optimal therapeutic regimen needs to be chosen on the basis of each patient's hemodynamic profile. Patients can be broadly classified into three groups: (1) patients with a high left ventricular filling pressure (> 18 mm Hg) and a cardiac index < 2.2 L/min/m2 but systolic arterial pressure > 100 mm Hg; (2) patients with a systolic arterial pressure < 90 mm Hg, left ventricular filling pressure > 18 mm Hg, and cardiac index < 2.2 L/min/m2; and (3) patients with an elevated right ventricular filling pressure (> 10 mm Hg) and cardiac index < 2.2 L/min/m2 and a systolic arterial pressure < 100 mm Hg. Patients in the first subset usually require the use of vasodilator therapy and/or dobutamine. The choice of inotropic agent in patients in the second hemodynamic subset depends on the degree of systemic hypotension; dopamine is usually preferred initially because it increases arterial pressure in addition to improving cardiac output. Once the systemic blood pressure has been stabilized, dobutamine can be substituted for superior augmentation of cardiac output and its additional beneficial effects on the left ventricular filling pressure. Norepinephrine may be indicated in cases of severe systemic hypotension. Patients in hemodynamic subset 3, ie, right ventricular infarction, are treated with volume expansion and dobutamine. Use of nonpharmacologic means of circulatory support, eg, intra-aortic balloon pump or left ventricular assist device may also be required in any of these subsets.

We describe a two-month-old infant with early congestive heart failure due to anomalous origin of the right coronary artery from the pulmonary artery. The diagnosis was made by two-dimensional and color flow Doppler echocardiography, confirmed by angiocardiography, and the case was successfully corrected at surgery. As opposed to the more frequent anomalous origin of the left coronary artery from the pulmonary trunk, this anomaly generally does not cause any typical clinical finding, often becoming an autoptic or surgical surprise after infancy or in adult age.