Objective:
The purpose of this study is to classify and describe the clinically distinct metabolic and hemodynamic phases post-ASAH.
Methods:
224 patients who suffered an ASAH (mean age 55±14; 74% female, 26% male) were examined. Patients underwent daily transcranial Doppler (TCD) and cerebral blood flow (CBF) studies (using
133
Xe clearance). Due to the paucity of data on post-hemorrhage day (PHD) 0, the internal carotid artery end-diastolic (ICA
ED
) velocity, a surrogate for CBF, was used for the first 24 hours. The brain arteriovenous oxygen difference (AVDO
2
) was recorded for each patient and the cerebral metabolic rate of oxygen (CMRO
2
) was calculated. Clinical outcome was evaluated based on the Glasgow Outcome Scale (GOS) 6 months after rupture.
Results:
Following ASAH, 3 distinct hemodynamic phases arose for the entire study population. Phase I (hypoperfusion phase), occurs on the day of rupture (PHD 0) and is defined by a low ICA
ED
velocity (mean 17.8±1.1 cm/s), normal middle cerebral artery (MCA) velocity (mean V
MCA
58.0±23.4 cm/s), and normal Lindegaard Ratio ([LR], mean 1.66±0.50). Phase II (relative hyperemia), (PHD 1–3), is characterized by an increasing ICA
ED
(mean 35.4±1.0 cm/s, p<0.0001), a relative hyperemia (mean CBF
15
40.1±1.5 ml/100g/minute, CMRO
2
1.17±0.41 ml/100g/min), a rising V
MCA
(mean 71.5±5.8 cm/sec, p<0.0001), and a rising but normal LR (mean 2.21±0.19, p<0.0001). During phase III (vasospasm phase, PHD 4–21), both the ICA
ED
and CBF decrease (mean ICA
ED
19.9±0.9 cm/s, p<0.0001; mean CBF
15
36.8±0.7 ml/100g/minute, p=0.04), V
MCA
continues to rise (mean 107.6±2.9cm/sec, p<0.0001), and the LR is further increased (mean 3.25±0.08, p<0.0001). The CMRO
2
remains low (mean 1.17±0.40 ml/100g/min, p=1). Based on the GOS up to 90% of patients who experienced either a relative or absolute hyperemia had good outcomes.
Conclusions:
After an ASAH, 3 discrete metabolic and hemodynamic phases arise each with the potential for its own unique phase-specific management and therapy. Relative hyperemia, or “luxury perfusion,” during Phase II in the setting of non-elevated ICPs may provide some type of benefit for patients.