Abstract
A higher rate of pulmonary embolism has been associated with pulmonary artery (PA) catheters; however, no mechanism has been described. Conventional tests of coagulation reveal no changes related to PA catheterization. The purpose of this study was to determine whether PA catheterization resulted in a hypercoagulable state detectable by thrombelastography (TEG).
Healthy, anesthetized, swine (n = 19) underwent PA catheterization. Samples were drawn from 7F femoral arterial catheters before and two hours after PA catheterization, at 5 mL/min, and analyzed (native whole blood, n = 15, kaolin activated blood, n = 4) by TEG (Hemoscope, Niles, IL) at precisely two minutes. Human: An IRB-approved prospective, observational trial was conducted in critically ill patients (n = 19). Samples were drawn from 22-gauge radial artery catheters, before and three hours after PA catheterization. Kaolin-activated TEG samples were analyzed at precisely five minutes. Data are mean +/- SE; Groups were compared with analysis of variance and significance was assessed at the 95% confidence interval.
In both animals and patients, PA catheterization truncated R times (time to initial fibrin formation). In swine, the R times were 17.6 +/- 1.3 minutes (native) and 3.8 +/- 0.4 (kaolin) before PA catheterization, and decreased to 6.3 +/- 1.0 minutes (p = 0.002) and 1.9 +/- 0.5 minutes (p = 0.010) afterward. There were no changes in pH or temperature during the experiment. In patients, 4 of 19 were excluded for protocol violations. The R time was 6.3 +/- 1.0 minutes (kaolin) before and 3.0 +/- 0.3 minutes after catheterization (p = 0.003). No changes were observed in conventional coagulation parameters, temperature or pH.
In healthy swine, and critically ill patients, PA catheters may enhance thrombin formation and fibrin polymerization, indicating a systemic hypercoagulable state. This may explain why PA catheters are associated with an increased risk of pulmonary emboli.
