THE CARDIOVASCULAR RESPONSE of the patient with acute spinal cord injury (SCI) is known to be altered secondary to the cord injury. Our current protocol of managing the acute phase of patients with SCI includes invasive hemodynamic monitoring (with arterial line and Swan-Ganz catheter) and support with fluids and dopamine and/or dobutamine, titrated to maintain a hemodynamic profile with adequate cardiac output (to be determined by oxygen consumption and delivery) and a mean blood pressure of >90 mm Hg. We feel that this protocol provides two benefits: 1) maintaining the mean blood pressure improves the morbidity of these patients by deterring ischemia and accompanying secondary insults; 2) aggressive monitoring and hemodynamic intervention help stabilize the hemodynamic status of these patients and make it possible to consider early surgery in selected cases. Our hypothesis is that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI. We analyzed the demographic, neurologic, and hemodynamic data of 50 consecutive patients during their first week postinjury. All had signs of myelopathy; 31 (62%) were considered clinically complete. Of the 50 patients, 9 (18%) died, 20 did not improve functionally, and 21 improved. The mean heart rate (82.1 ± 13.3), blood pressure (94.4 ± 9.4), pulmonary artery pressure (22 ± 5) and wedge (12.7 ± 3.4), cardiac index (4.5 ± 0.9), systemic vascular resistance index (SVRI) (1637 ± 399), pulmonary vascular resistance index (PVRI) (181 ± 80), and oxygen transport (694 ± 156) showed good response to the treatment. Because the measurements were obtained during treatment, they differ from the expected “classic sympathectomized” response, but they provide a database for further analysis of hemodynamic manipulation in SCI. An analysis of the hemodynamic parameters did not differentiate between complete and incomplete lesions or between patients with functional improvement. We determined, on the basis of the initial hemodynamic measurements, that no patient with a clinically complete motor deficit (Frankel Grade A+B) improved of the 10 who had measurements compatible with either: 1) PVRI < 100 with SVRI < 1200; or 2) PVRI < 115 with SVRI < 1300 or PVR/SVR ratio of <0.08 when SVRI was <1600. These patients could not have other measurements that showed low SVRI < 1350 with PVRI > 139. At odds with this unique group, 13 of 29 patients with the same clinical picture and without the above physiological criteria of severe hemodynamic deficit eventually improved (P < 0.05). This method of aggressive monitoring and hemodynamic intervention is feasible and safe, and we recommend its use. The potential prognostic implications are important during the first hours. Our theory that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI is strengthened by these data, mainly on the basis of the poor prognosis of patients who had persistent severe reduction of their PVRI versus a less marked reduction of the SVRI, even with the use of inotropic drugs.