Background: Blood pressure (BP) parameters for management of tPA treated patients are well known among experienced stroke clinicians, and violation of systolic and diastolic BP limits have previously been shown to be associated with symptomatic intracerebral hemorrhage (sICH) in tPA treated patients. Non-invasive oscillometric BP monitoring measures a “true” mean arterial pressure (MAP), and then algorithmically defines what systolic and diastolic pressure "might" be. Because this form of BP monitoring has become the national standard, we examined the occurrence of MAP BP elevations to determine their association with sICH and treatment outcome in acute ischemic stroke patients that received systemic tPA. Methods: Two-years of consecutive systemic tPA cases were retrieved from our Stroke Center database and arterial blood pressures for the first 24 hours from time of bolus were entered from auto-recordings in our electronic medical records. Protocol violations in MAP were defined as greater than 120 mm Hg at any point in the first 24 hours from time of bolus. Off-label treatment with intravenous tPA beyond 4.5 hours from symptom onset was identified a priori as a potential counfounder to stroke outcome. Symptomatic intracerebral hemorrhage was defined as an increase in the NIHSS of ≥ 4 points. Spearman’s correlation was used to assess the relationship between MAP and post-tPA NIHSS score. Results: 191 tPA cases were identified for inclusion in the analysis with 150 (79%) receiving their tPA at our Comprehensive Stroke Center and another 41 (21%) administered as a telephone-consult supported drip and ship. Patients were 65.5±16 years of age with median admission NIHSS scores of 12 (IQR=7-17). All patients had normal CT scans or minor changes consistent with acute stroke without hypo-attenuation. A total of 77 (40%) patients experienced a MAP violation overall. There were 11 isolated systolic BP violations, 4 isolated diastolic BP violations, and 21 isolated MAP violations that were otherwise not detectable by a violation in systolic or diastolic parameters, averaging 123.3±2 mm Hg. A total of 2 (1%) sICHs occurred in the sample, and of these 1 was associated with on-label peri-treatment BP protocol violations affecting systolic, diastolic and MAP parameters. An increased reduction in post-tPA NIHSS points was significantly associated with higher MAPs (r=.92; p=.008). Conclusions: Evidence-based guidelines are silent on MAP limits, and MAP is rarely monitored clinically in tPA treated patients despite dependence on the MAP for assignment of systolic and diastolic pressures in oscillometric BP monitoring. Our findings suggest that an improved understanding of the contribution of MAP-dependent oscillometric methods to BP monitoring in acute stroke patients is warranted.
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