Once the aneurysm has been secured by clipping or coiling, BP management is directed to optimizing CBF in the setting of vasospasm. In the presence of large artery vasospasm, autoregulation is impaired in the majority of patients (31,32). Yundt et al. (25) used positron-emission tomography to study CBV in response to global or regional reductions in CPP and found that in patients with aneurysmal SAH without vasospasm, CBF, cerebral metabolic rate of oxygen (CMRO2), and CBV were reduced with normal oxygen extraction fraction. In patients with arteriographic vasospasm, CBF and CBV were decreased, with minimal change in CMRO2 and with increased oxygen extraction fraction. This pattern is consistent with misery perfusion and suggests that parenchymal vessels distal to arteries with vasospasm are not capable of normal autoregulatory vasodilation (25). More practically, cerebral autoregulation can be assessed clinically with tests, such as the cuff deflation test (33) and transient hyperemic response test (34), or by continuously using transcranial Doppler methods (35 ).
BP management in the presence of clinical vasospasm has largely been incorporated as part of triple-H therapy, which also includes hypervolemia and permissive hemodilution. The evidence for resolution of ischemic deficits that result from this therapy is based on uncontrolled, nonrandomized studies (4,36). In one series of 58 patients with progressive neurologic deterioration from angiographically confirmed cerebral vasospasm, induced arterial hypertension reversed neurologic deficits transiently in 47 patients, with permanent improvement in 43 cases (36). Reversal of ischemia by increasing CBF is the main goal of triple-H therapy. In another study, increases in cortical CBF of 34% (mean CBF increased 21%) were recorded in 43 SAH patients over the first 24 hr of triple-H therapy (37). However, values for CBF were within the normal range, and a control group was not evaluated in this study. Still unknown are the optimal levels of BP and volume status, as well as which component of triple-H therapy is the most important. Pharmacologically induced hypertension has been shown to improve
CBF in ischemic regions in patients with symptomatic vasospasm (31,38). Raising MABP from 90 ± 11 mmHg to 111 ± 13 mmHg with dopamine infusion in 13 SAH patients with suspected clinical vasospasm increased CBF to above the ischemic range (defined as 25 mL/100 gm /min) in more than 90% of uninfarcted ischemic territories (identified by using xenon-enhanced CT) and decreased local CBF in one-third of the nonischemic territories (31 ) . The increase may be explained by passive perfusion-dependent flow in areas with impaired autoregulation, by mechanical vasodilation, by increased collateral flow, or by direct vasodilatory response to dopamine, mediated by dopaminergic receptors at low doses (31).
The case against prophylactic use of triple-H therapy to prevent vasospasm was made by another randomized, controlled study in 32 patients who presented within 72 hr of SAH. Half of the patients were treated with triple-H therapy, and half with normovolemic fluid therapy (39). No statistical differences were found between groups regarding the frequency or severity of clinical or transcranial Doppler-defined vasospasm, regional CBF evaluated by Single Photon Emission CT (SPECT), or 1-year outcome assessed by Glasgow coma scale (GCS) and neuropsychologic tests (39). In addition, additional costs and more complications were involved in the hyperdynamically treated group. The results of this study are consistent with findings that only a proportion of patients with vasospasm respond to triple-H therapy, which may also reflect the realization that the causes of delayed ischemic neurologic deficits in the SAH population are probably multifactorial, including vasospasm, as well as embolization, thrombosis, reperfusion injury, and cerebral edema.
Kim et al. demonstrated in humans with vasospasm after SAH that raising cardiac output (4.1-6.0 L/min/m2) with dobutamine was equally as efficacious as raising MABP (102-132 mmHg) with phenylephrine in producing significant elevation of CBF, measured by xenon CT (40). Studies comparing clinical benefits of a cardiac output strategy versus a MABP strategy for clinical vasospasm are not available. However, patients with unsecured aneurysms or neurogenic-stunned myocardium and clinical vasospasm may be more safely managed with CO rather than MABP optimization. In the setting of an unsecured aneurysm, the risk of rerupture must be carefully weighed against the risk of cerebral ischemia secondary to vasospasm. In one series, 3 out of 16 patients with unclipped ruptured aneurysms rebled, all with arterial pressures greater than 160 mmHg (36). Although it cannot be proven that hypertension was the cause of rebleeding, the potential stress of increased arterial pressure in this setting suggests that BP should be carefully controlled and that alternative treatments for vasospasm should be considered.
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