Induced Hypertension Research Articles

The effect of induced hypertension in aneurysmal subarachnoid hemorrhage: A narrative review.

Aneurysmal subarachnoid hemorrhage ‎(aSAH) ‎accounts for 2-5% of all strokes, and 10%-15% of ‎aSAH patients will not survive until hospital admission. Induced hypertension (IH) is an emerging therapeutic option being used for the treatment of vasospasm in ‎aSAH. For patients with cerebral vasospasm (CVS) consequent to SAH, IH is implemented to increase systolic blood pressure (SBP) in order to optimize cerebral blood flow (CBF) and prevent delayed cerebral ischemia (DCI). Prophylactic use of IH has been associated with the development of vasospasm and cerebral ischemia in SAH patients. Various trials have defined several different parameters to help clinicians decide when to initiate IH in a SAH patient. However, there is insufficient evidence to recommend therapeutic IH in aSAH due to the possible serious complications like myocardial ischemia, development of posterior reversible encephalopathy syndrome (PRES), pulmonary edema, and even rupture of another unsecured aneurysm. This narrative review showed the favorable impact of IH therapy on aSAH patients; however, it is crucial to conduct further clinical and molecular experiments to shed more light on the effects of IH in aSAH.

Posterior reversible encephalopathy syndrome after induced hypertension therapy for delayed cerebral ischemia after subarachnoid hemorrhage: A case-control study

Posterior reversible encephalopathy syndrome (PRES) is associated with arterial hypertension. Our aim was to investigate whether induced hypertension (IH) as therapy for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is associated with PRES and to identify risk factors for PRES. We retrospectively searched our database for patients with SAH and IH in our institution between 2009 and 2018 and identified additional cases of PRES after SAH with IH from the literature. We then analyzed demographic findings and clinical features of these patients. 172 patients with acute SAH received IH. PRES was diagnosed in 3/172 (1.7%) patients. Our literature search revealed 17 additional cases. The pooled PRES group (n=20) was non-significantly older than the non-PRES group (n=169) (median, 62.5years vs. 52years, p=0.06). No significant differences were found between both groups with regard to sex (p=0.73), Hunt & Hess-Score (p=0.9), aneurysm treatment (p=0.13), and time from diagnosis of SAH to the start of IH (p=0.14). PRES after IH in SAH patients occurred in 1.7% of our patients. Our results imply that it is important to be aware of a possible development of a PRES in older SAH patients with IH, irrespective of sex, initial clinical status, and treatment modality.

Posterior Reversible Encephalopathy Syndrome Caused by Induced Hypertension to Treat Cerebral Vasospasm Secondary to Aneurysmal Subarachnoid Hemorrhage

The aim of the present study was to describe the case of a patient who had presented to a university hospital with induced-hypertension (IH) posterior reversible encephalopathy syndrome (PRES). We also reviewed all other reports of such patients. We have described the clinical course of a patient who had presented to the university hospital neurosurgical department. We also performed a systematic review of studies related to the incidence of PRES caused by the use of IH in the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. The patient had presented with an acute-onset headache and found to have a subarachnoid hemorrhage due to anterior communicating artery aneurysm rupture. She underwent coiling the next day. During the subsequent days, she demonstrated fluctuating clinical examination findings, aphasia, and decreased levels of arousal. Digital subtraction angiography was performed, and the findings were concerning for mild vasospasm of the anterior and middle cerebral arteries. The systolic blood pressure goal was increased to 180-220 mm Hg for an IH trial, which had initially resulted in some transient clinical improvements in her level of arousal. However, the improvement was not sustained. During the next 36 hours, the patient worsened, and she developed left middle cerebral artery syndrome. Given the concern for a possible ischemic event, magnetic resonance imaging was performed, which demonstrated interval development of multiple areas of cortical-based fluid-attenuated inversion recovery hyperintensity consistent with PRES. The systolic blood pressure goal was relaxed to normotension, and ~48 hours later, the patient's clinical status had significantly improved. IH-PRES is a rare complication that should be remembered in the differential diagnosis for at-risk patients.

Changes in Cerebral Perfusion with Induced Hypertension in Aneurysmal Subarachnoid Hemorrhage: A Pilot and Feasibility Study.

The effects of induced hypertension (IH) on cerebral perfusion after subarachnoid hemorrhage (SAH) are unclear. The objectives of this investigation are to: (1) determine whether there are differences in cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) measured with computed tomography perfusion (CTP) before and after IH; (2) evaluate differences in the presence of infarction and clinical outcome between patients with and without IH. We performed a retrospective cohort analysis of 25 aneurysmal SAH patients. IH was initiated as per the standard institutional protocol when patients showed clinical symptoms of delayed cerebral ischemia (DCI). Differences in CBF, CBV, and MTT between early (<72h after aneurysm rupture) and late (7-10days after aneurysm rupture) CTP were quantified in patients with (n=13) and without IH (n=12). Outcome measures included cerebral infarction and clinical outcome at 3months. Early MTT was significantly greater in the IH group compared to the no-IH group. There was no difference in early or late CBV or CBF between the two groups. In patients that received IH, there was a significant decrease in MTT between the early (7.0±1.2s) and late scans (5.8±1.6s; p=0.005). There was no difference in the incidence of infarction (5/13 vs. 2/11) or poor outcome (3/11 vs. 6/13) between the IH and no-IH groups, respectively (p>0.05). Elevated MTT is a significant factor for the development of DCI in patients eventually requiring IH therapy and is improved by IH treatment. Therapies to prevent DCI and improve clinical outcome may need to be initiated earlier, when cerebral perfusion abnormalities are first identified.

Posterior reversible encephalopathy syndrome with thalamic involvement during vasopressor treatment of vertebrobasilar vasospasm after subarachnoid hemorrhage

Hemodynamic augmentation is the primary medical intervention employed to reverse neurological deficits associated with vasospasm and delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage. Failure to improve despite induced hypertension (IH)...

Effect of moderate hyperventilation and induced hypertension on cerebral tissue oxygenation after cardiac arrest and therapeutic hypothermia

AimImproving cerebral perfusion is an essential component of post-resuscitation care after cardiac arrest (CA), however precise recommendations in this setting are limited. We aimed to examine the effect of moderate hyperventilation (HV) and induced hypertension (IH) on non-invasive cerebral tissue oxygenation (SctO2) in patients with coma after CA monitored with near-infrared spectroscopy (NIRS) during therapeutic hypothermia (TH). MethodsProspective pilot study including comatose patients successfully resuscitated from out-of-hospital CA treated with TH, monitored with NIRS. Dynamic changes of SctO2 upon HV and IH were analyzed during the stable TH maintenance phase. HV was induced by decreasing PaCO2 from ∼40 to ∼30mmHg, at stable mean arterial blood pressure (MAP∼70mmHg). IH was obtained by increasing MAP from ∼70 to ∼90mmHg with noradrenaline. ResultsTen patients (mean age 69 years; mean time to ROSC 19min) were studied. Following HV, a significant reduction of SctO2 was observed (baseline 74.7±4.3% vs. 69.0±4.2% at the end of HV test, p<0.001, paired t-test). In contrast, IH was not associated with changes in SctO2 (baseline 73.6±3.5% vs. 74.1±3.8% at the end of IH test, p=0.24). ConclusionsModerate hyperventilation was associated with a significant reduction in SctO2, while increasing MAP to supra-normal levels with vasopressors had no effect on cerebral tissue oxygenation. Our study suggests that maintenance of strictly normal PaCO2 levels and MAP targets of 70mmHg may provide optimal cerebral perfusion during TH in comatose CA patients.

Safety of Induced Hypertension Therapy in Patients With Acute Ischemic Stroke

The management of blood pressure in acute stroke is controversial. Small pilot studies have suggested that blood pressure augmentation improves short-term neurological function, but the rate of adverse events with induced hypertension (IH) therapy is unknown. We reviewed 100 consecutive patients who underwent perfusion magnetic resonance imaging for acute ischemic stroke. IH therapy was employed in 46 patients and standard therapy (ST) in 54. The two groups had similar baseline characteristics, but more patients in the IH group had significant large-artery stenoses. The IH group achieved significantly higher mean arterial pressure (MAP) than the ST group within 3 days of initiation of therapy with a variety of vasopressor agents. Only 35% of patients in the IH group actually achieved the target MAP augmentation of 10-20% above baseline, however. All patients survived to discharge. Four patients experienced major adverse events in each group. Two patients in the IH group experienced intra cerebral hemorrhage compared to none in the ST group. Two patients in the ST group experienced myocardial ischemia, compared to none in the IH group. The National Institutes of Health Stroke Scale during the hospitalization and place of discharge were similar in both groups. Patients in the IH group were more likely to be admitted to the intensive care unit and had a longer hospital stay by nearly 4 days compared to the ST group. These data demonstrate the relative safety of IH therapy in acute stroke patients. Given the greater use of resources, however, the role of IH in improving clinical outcomes requires a prospective, randomized trial.

Efeitos da hipertensão arterial induzida sobre a complacência e pressão de perfusão encefálica em hipertensão intracraniana experimental: comparação entre lesão encefálica criogênica e balão subdural

JUSTIFICATIVA E OBJETIVOS: O trauma cranioencefálico (TCE) pode elevar a pressão intracraniana (PIC) e reduzir a complacência encefálica (CE). Diferentes lesões são aplicadas em modelos de TCE que estudam as mesmas variáveis. Como são usadas indistintamente, o objetivo é comparar a PIC e a CE em dois modelos de TCE. MÉTODO: Dezoito cães machos, anestesiados, ventilados e distribuídos aleatoriamente em dois grupos: BS - balão subdural (n = 9) e LC - lesão criogênica (n = 9). Análise da PIC, CE e pressão de perfusão encefálica (PPE) em cinco momentos: fim da preparação (M0), encéfalo normal (M1), início da lesão (M2), término da lesão (M3) e lesão estabelecida (M4). CE é a variação da PIC durante hipertensão arterial induzida (HAI) em 50 mmHg em M1 e M4. PPE = pressão arterial média (PAM) - PIC. Teste t de Student pareado para o mesmo grupo em momentos diferentes e t de Student para duas amostras distintas para o mesmo momento entre os grupos. RESULTADOS: A PAM foi semelhante nos grupos nos momentos estudados (p = 0,31 em M0; p = 0,25 em M1; p = 0,31 em M2; p = 0,19 em M3; p = 0,05 em M4). A PIC foi semelhante nos grupos em M0 (p = 0,27) e M1 (p = 0,21), mas diferente em M2 (p < 0,001). A PIC tornou-se semelhante nos grupos em M3 (p = 0,39) e M4 (p = 0,98), elevou-se no BS em M1 (p = 0,04) e M2 (p = 0,01), mas não em M3 (p = 0,36) nem M4 (p = 0,12). No LC a PIC aumentou em M1 (p < 0,01), M3 (p < 0,001) e M4 (p < 0,001), mas não em M2 (p = 0,18). Houve aumento da PPE em M1 (p < 0,001) e M4 (p < 0,001), semelhante nos grupos (p = 0,16 em M1 e p = 0,21 em M4). Em M2 houve redução da PPE nos grupos (p < 0,001), mais intensa em LC (p < 0,001). Em M3 houve aumento da PPE no BS (p = 0,02) e redução no LC (p = 0,01), o que tornou a PPE semelhante nos grupos (p = 0,43). Em M4 houve aumento da PPE semelhante nos grupos (p = 0,16). CONCLUSÕES: O efeito da hipertensão arterial induzida no modelo de LC é comparável ao observado no modelo de BS. Esse tipo de lesão deve ser melhor estudado para estabelecer precisão na proporção entre a sua extensão e a redução da CE, aparentemente, um processo gradual e evolutivo cujos limites ainda não são totalmente conhecidos.