Endogenous arterial blood pressure increase after aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 190 ◽  
pp. 105639
Author(s):  
Arthur Hosmann ◽  
Sarah Klenk ◽  
Wei-te Wang ◽  
Johannes Koren ◽  
Samir Sljivic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Pressure Increase ◽  
Blood Pressure Increase ◽  
Arterial Blood

scholarly journals Bioreactance-Based Noninvasive Fluid Responsiveness and Cardiac Output Monitoring: A Pilot Study in Patients with Aneurysmal Subarachnoid Hemorrhage and Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Sanjeev Sivakumar ◽  
Christos Lazaridis
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Subarachnoid Hemorrhage ◽  
Pulmonary Edema ◽  
Fluid Responsiveness ◽  
Arterial Blood Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cardiac Output Monitoring ◽  
Arterial Blood ◽  
Pulmonary Manifestations

Management of volume status, arterial blood pressure, and cardiac output are core elements in approaching the patients with aneurysmal subarachnoid hemorrhage (SAH). For the prevention and treatment of delayed cerebral ischemia (DCI), euvolemia is advocated and caution is made towards the avoidance of hypervolemia. Induced hypertension and cardiac output augmentation are the mainstays of medical management during active DCI, whereas the older triple-H paradigm has fallen out of favor due to lack of demonstrable physiological or clinical benefits and serious concern for adverse effects such as pulmonary edema and multiorgan system dysfunction. Furthermore, insight into clinical hemodynamics of patients with SAH becomes salient when one considers the frequently associated cardiac and pulmonary manifestations of the disease such as SAH-associated cardiomyopathy and neurogenic pulmonary edema. In terms of fluid and volume targets, less attention has been paid to dynamic markers of fluid responsiveness despite the well-established, in the general critical care literature, superiority of these as compared to traditionally used static markers such as central venous pressure (CVP). Based on this literature and sound pathophysiologic reasoning, reliance on static markers (such as CVP) is unjustified when one attempts to assess strategies augmenting stroke volume (SV), arterial blood pressure, and oxygen delivery. There are several options for continuous bedside cardiorespiratory monitoring and optimization of SAH patients. We, here, review a noninvasive monitoring technique based on thoracic bioreactance and focusing on continuous cardiac output and fluid responsiveness markers.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

scholarly journals Intracranial and Blood Pressure Variability and Long-Term Outcome After Aneurysmal Sub-arachnoid Hemorrhage

2009 ◽  
Vol 18 (3) ◽  
pp. 241-251 ◽  
Author(s):  
Catherine J. Kirkness ◽  
Robert L. Burr ◽  
Pamela H. Mitchell
Keyword(s):  
Blood Pressure ◽  
Intensive Care ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Functional Outcome ◽  
Adaptive Capacity ◽  
Arterial Blood Pressure ◽  
Long Term Outcome ◽  
Arterial Blood

Background Care of brain-injured patients in intensive care units has focused on maintaining arterial blood pressure and intracranial pressure within prescribed ranges. Research suggests, however, that the dynamic variability of these pressure signals provides additional information about physiological functioning and may reflect adaptive capacity.Objectives To see if long-term outcomes can be predicted from variability of arterial blood pressure and intracranial pressure in patients with aneurysmal subarachnoid hemorrhage.Methods Arterial blood pressure and intracranial pressure were monitored continuously for 4 days in 90 patients (74% women; mean age, 53 years) in an intensive care unit after subarachnoid hemorrhage. Variability of arterial blood pressure and intracranial pressure signals was calculated on 4 timescales: 24 hours, 1 hour, 5 minutes, and the difference of sequential 5-second means. The Extended Glasgow Outcome Scale was used to assess functional outcome 6 months after subarachnoid hemorrhage.Results Pressure variability was better than mean pressure levels for predicting 6-month functional outcome. When initial neurological condition was controlled for, greater faster variability (particularly 5-second) was associated with better outcomes (typical P&lt;.001), whereas greater 24-hour variability was associated with poorer outcomes (typical P&lt;.001).Conclusions The relationship between long-term functional outcome and variability of arterial blood pressure and intracranial pressure levels depends on the timescale at which the variability is measured. Because it is associated with better outcome, greater faster variability may reflect better physiological adaptive capacity.

scholarly journals Functional relationship of arterial blood pressure, central venous pressure and intracranial pressure in the early phase after subarachnoid hemorrhage

2021 ◽  
pp. 1-14
Author(s):  
Gabriela Maissen ◽  
Gagan Narula ◽  
Christian Strässle ◽  
Jan Willms ◽  
Carl Muroi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Functional Relationship ◽  
Venous Pressure ◽  
Correlation Coefficients ◽  
Central Venous ◽  
Arterial Blood

BACKGROUND: Intracranial pressure (ICP) and arterial blood pressure (ABP) are related to each other through cerebral autoregulation. Central venous pressure (CVP) is often measured to estimate cardiac filling pressures as an approximate measure for the volume status of a patient. Prior modelling efforts have formalized the functional relationship between CVP, ICP and ABP. However, these models were used to explain short segments of data during controlled experiments and have not yet been used to explain the slowly evolving ICP increase that occurs typically in patients after aneurysmal subarachnoid hemorrhage (SAH). OBJECTIVE: To analyze the functional relationship between ICP, ABP and CVP recorded from SAH patients in the first five days after aneurysm. METHODS: Two methods were used to elucidate this relationship on the running average of the signals: First, using Spearman correlation coefficients calculated over 30 min segments Second, for each patient, linear state space models of ICP as the output and ABP and CVP as inputs were estimated. RESULTS: The mean and variance of the data and the correlation coefficients between ICP-ABP and ICP-CVP vary over time as the patient progresses through their stay in the ICU. On average, after an SAH event, the models show that a) ABP is the bigger driver of changes in ICP than CVP and that increasing ABP leads to reduction in ICP and (b) increasing CVP leads to an increase in ICP. CONCLUSIONS: Finding a) agrees with the hypothesis that patients with subarachnoid hemorrhage have defective autoregulation, and b) agrees with the positive correlation observed between central venous pressure and intracranial pressure in the literature.

Reversal and prevention of cerebral vasospasm by intracarotid infusions of nitric oxide donors in a primate model of subarachnoid hemorrhage

1997 ◽  
Vol 87 (5) ◽  
pp. 746-751 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Edward H. Oldfield ◽  
Robert J. Boock
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Arterial Blood ◽  
Infusion Experiment ◽  
The Mean ◽  
The Right

✓ Decreased endothelium-derived relaxing factor, nitric oxide (NO), in the arterial wall has been hypothesized to be a potential cause of cerebral vasospasm following subarachnoid hemorrhage (SAH). The authors sought to determine whether intracarotid infusions of newly developed NO-donating compounds (NONOates) could reverse vasospasm or prevent the occurrence of cerebral vasospasm in a primate model of SAH. Twenty-one cynomolgus monkeys were studied in two experimental settings. In an acute infusion experiment, saline or NONOate was infused intracarotidly in four normal monkeys and in four monkeys after onset of SAH. During the infusions regional cerebral blood flow (rCBF) was measured in eight animals and CBF velocity in two. In a chronic infusion experiment, saline (four animals) or NONOate (diethylamine-NO [three animals] or proli-NO [six animals]) was infused intracarotidly in monkeys for 7 days after SAH. In acute infusion experiments, 3-minute intracarotid diethylamine-NO infusions reversed arteriographically confirmed vasospasm of the right middle cerebral artery (MCA) (as viewed on anteroposterior projection, the decrease in area was 8.4 ± 4.3% in the treatment group compared with 35 ± 12% in the control group; p < 0.004), increased rCBF by 31 ± 1.9% (p < 0.002), and decreased the mean systolic CBF velocity in the right MCA. In a long-term infusion experiment, the area of the right MCA in control animals decreased by 63 ± 5%. In animals undergoing a 7-day continuous glucantime-NO intracarotid infusion, the area of the right MCA decreased by 15 ± 6.2%, and in animals undergoing a 7-day proli-NO infusion, the area of the right MCA decreased by 11 ± 2.9% (p < 0.05). The mean arterial blood pressure decreased in the glucantime-NO group from 75 ± 12 mm Hg (during saline infusion) to 57 ± 10 mm Hg (during glucantime-NO infusion; p < 0.05), but it was unchanged in animals undergoing proli-NO infusion (76 ± 12 mm Hg vs. 78 ± 12 mm Hg). Results of these experiments show that cerebral vasospasm is both reversed and completely prevented by NO replacement. However, only the use of regional infusion of the NONOate with an extremely short half-life avoided a concomitant decrease in arterial blood pressure, which could produce cerebral ischemia in patients with impaired autoregulation of CBF after the rupture of an intracranial aneurysm.

Impairment of Cerebral Autoregulation during the Development of Chronic Cerebral Vasospasm after Subarachnoid Hemorrhage in Primates

Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Hiroaki Takeuchi ◽  
Yuji Handa ◽  
Hidenori Kobayashi ◽  
Ilirokazu Kawano ◽  
Minoru Hayashi
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm ◽  
The Brain

Abstract We studied the impairment of autoregulation of cerebral blood flow (CBF) and its effect on the electrical activity of the brain during the development of chronic cerebral vasospasm after subarachnoid hemorrhage, using a vasospasm model in primates. Fourteen animals were divided into two groups: a clot group (8) and a sham-operated group (6). To induce subarachnoid hemorrhage, all the animals underwent craniectomy, and in the clot group, the autologous blood clot was located around the arteries dissected free from the arachnoid membrane. Cerebral angiography was performed before subarachnoid hemorrhage and 7 days after (Day 7). On Day 7, regional CBF in the parietal lobe—measured by the hydrogen clearance method—and central conduction time were studied during either graded hypertension or hypotension. In the clot group, the mean vessel caliber of the cerebral arteries on the right side (clot side) of the circle of Willis showed significant (P&lt;0.01) reduction (more than 40%) as compared with the values on the contralateral, non-clot side. The values for the bilateral parietal CBF in the sham-operated group and the left parietal CBF in the clot group were fairly constant when the mean arterial blood pressure (MABP) was in the range of 60 to 160 mm Hg. In the clot group, right parietal CBF was significantly (P &lt; 0.05) smaller than that on the left side at an MABP level of 40 to 100 mm Hg, and increased at an MABP level of 180 mm Hg. The right parietal CBF increased as the arterial blood pressure increased, showing impairment of autoregulation. The central conduction time on the right side in the clot group was significantly (P&lt;0.05) prolonged at an MABP of 40 mm Hg. It is suggested that impairment of autoregulation is strongly affected by the development of cerebral vasospasm and that, in this state, a decrease in cerebral perfusion pressure easily depresses the electrical function of the brain.

Sign in / Sign up

Export Citation Format

Share Document