The spontaneous arterial blood pressure rise after aneurysmal subarachnoid hemorrhage – A biphasic phenomenon

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.

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

Journal of Neurosurgery ◽

10.3171/jns.1994.80.5.0857 ◽

1994 ◽

Vol 80 (5) ◽

pp. 857-864 ◽

Cited By ~ 90

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.

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Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: The phase relationship between arterial blood pressure and cerebral blood flow velocity

Critical Care Medicine ◽

10.1097/00003246-200101000-00031 ◽

2001 ◽

Vol 29 (1) ◽

pp. 158-163 ◽

Cited By ~ 126

Author(s):

Erhard W. Lang ◽

Rolf R. Diehl ◽

H. Maximilian Mehdorn

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Subarachnoid Hemorrhage ◽

Blood Flow Velocity ◽

Cerebral Autoregulation ◽

Cerebral Blood Flow Velocity ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Phase Relationship ◽

Arterial Blood

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

American Journal of Critical Care ◽

10.4037/ajcc2009743 ◽

2009 ◽

Vol 18 (3) ◽

pp. 241-251 ◽

Cited By ~ 10

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<.001), whereas greater 24-hour variability was associated with poorer outcomes (typical P<.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.

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Some effects of apneic underwater diving on blood gases, lactate, and pressure in man

Journal of Applied Physiology ◽

10.1152/jappl.1962.17.6.938 ◽

1962 ◽

Vol 17 (6) ◽

pp. 938-942 ◽

Cited By ~ 28

Author(s):

C. Robert Olsen ◽

Darrell D. Fanestil ◽

Per F. Scholander

Keyword(s):

Carbon Dioxide ◽

Blood Pressure ◽

Heart Rate ◽

Pressure Rise ◽

Blood Gases ◽

Breath Holding ◽

Blood Oxygen ◽

Arterial Blood ◽

Blood Pressure Rise ◽

Arterial Blood Oxygen

Five men of outstanding diving ability performed apneic underwater dives in a specially fitted tank. The divers hyperventilated to extreme degrees of hypocapnia before submerging, and their arterial blood carbon dioxide tensions rarely rose above normal levels during a dive. Arterial blood oxygen content was 15.5 vol % or above at the end of two 3-min resting dives and of three 1.5-min exercise dives. Blood lactate concentrations increased during the latter half of exercise dives and reached peak values after surfacing. A rise in arterial blood pressure began by 10 sec in each dive and persisted, coincident with a falling heart rate, to the end of the dive. The rate of blood pressure rise was greater during a dive in water of 26 C than with breath holding by the same subject out of water. Some differences between the adaptations of diving men and of other diving mammals are briefly discussed. Submitted on April 2, 196

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Blood Pressure Over-Shoot Due to Acute Clonidine (Catapres) Withdrawal: Studies on Arterial and Urinary Catecholamines and Suggestions for Management of the Crisis

Clinical Science ◽

10.1042/cs045181s ◽

1973 ◽

Vol 45 (s1) ◽

pp. 181s-183s

Author(s):

Lennart Hansson ◽

Stephen N. Hunyor

Keyword(s):

Blood Pressure ◽

Pressure Rise ◽

Withdrawal Symptoms ◽

Adrenergic Blockade ◽

Urinary Catecholamines ◽

Hypertensive Patients ◽

Arterial Blood ◽

Blood Pressure Rise ◽

Catecholamines In Urine ◽

Cessation Of Treatment

1. Clonidine was withdrawn acutely in five hypertensive patients with a documented blood pressure over-shoot after previous temporary cessation of treatment. 2. In all patients a severe rise of systolic and diastolic blood pressure was seen (average 67/58 mmHg). This was accompanied by a number of ‘withdrawal symptoms’, e.g. restlessness, tremor, headaches and nausea. 3. Catecholamines in urine rose from 32 μg/l to 112 μg/l (001 < P < 0.02) and in arterial blood from 0.52 μg/l to 1.0 μg/l (not significant). 4. The crisis could be reversed acutely by α- and β-adrenergic blockade. 5. Catecholamine depletion with reserpine before the withdrawal of clonidine seemed to reduce the blood pressure rise and the withdrawal symptoms.

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

Technology and Health Care ◽

10.3233/thc-212956 ◽

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.

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

Journal of Neurosurgery ◽

10.3171/jns.1997.87.5.0746 ◽

1997 ◽

Vol 87 (5) ◽

pp. 746-751 ◽

Cited By ~ 123

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.

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