Safe use of PEEP in patients with severe head injury

1985 ◽  
Vol 63 (4) ◽  
pp. 552-555 ◽  
Author(s):  
Kevin R. Cooper ◽  
Peter A. Boswell ◽  
Sung C. Choi
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Venous Pressure ◽  
Peak Inspiratory Pressure ◽  
Inspiratory Pressure ◽  
Content Type ◽  
Physiological Variables ◽  
Residual Capacity ◽  
Pressure Peak ◽  
Fine Print

✓ Thirty-three patients with severe head trauma were studied to determine whether the use of positive end-expiratory pressure (PEEP) would cause an increase in intracranial pressure (ICP). Changes in ICP induced by PEEP were then correlated with a panel of physiological variables to try to explain these changes. Mean ICP increased from 13.2 ± 7.7 mm Hg (± standard deviation) to 14.5 ± 7.5 mm Hg (p < 0.005) due to 10 cm H2O PEEP, but the eight patients with elevated baseline ICP experienced no significant increase. Cardiac output and venous admixture (Qs/Qt) declined significantly, while central venous pressure, peak inspiratory pressure, functional residual capacity, and arterial pCO2 increased significantly due to PEEP. Blood pressure and cerebral perfusion pressure were unchanged. The change in ICP due to PEEP correlated significantly with a combination of cardiac output, peak inspiratory pressure, Qs/Qt, and changes in blood pressure and arterial pCO2 due to PEEP, indicating that the effect of PEEP on ICP could be largely explained by its effect on hemodynamic and respiratory variables. No patient deteriorated clinically due to PEEP. It is concluded that 10 cm H2O PEEP increases ICP slightly via its effect on other physiological variables, but that this small increase in ICP is clinically inconsequential.

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004 ◽  
Vol 101 (4) ◽  
pp. 594-599 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
John M. Abrahams ◽  
Stephanie Bloom ◽  
Michelle J. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Oxygenation ◽  
Content Type ◽  
Poor Grade ◽  
Physiological Variables ◽  
Arterial Blood ◽  
End Tidal ◽  
Fine Print

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor

1989 ◽  
Vol 71 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Jeffrey V. Rosenfeld ◽  
Gene H. Barnett ◽  
Cathy A. Sila ◽  
John R. Little ◽  
Emmanuel L. Bravo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Serum Sodium ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Sodium Concentration ◽  
Control Group ◽  
Central Venous ◽  
Content Type ◽  
Fine Print

✓ Atrial natriuretic factor (ANF) is a diuretic natriuretic peptide hormone produced by both the heart and brain which has been postulated to play a role in the hemodynamic and sodium instability that frequently follows subarachnoid hemorrhage (SAH). Levels of ANF were measured in 12 patients with nontraumatic SAH and nine control patients with unruptured cerebral aneurysms. At surgery, the mean plasma ANF level (± standard deviation) of the SAH group was significantly higher than that of the control group (158.1 ± 83.8 vs. 57.8 ± 45.3 pg/ml, respectively; p = 0.01). There was no significant difference in serum sodium concentration, blood pressure, or central venous pressure between these groups. Nine patients with SAH due to aneurysm rupture had plasma ANF levels similar to those in three patients with SAH due to other causes. Four patients with moderate to severe SAH had significantly higher mean cerebrospinal fluid (CSF) ANF values (17.7 ± 12.8 pg/ml) than five patients with minimal SAH (0.6 ± 0.9 pg/ml) or the control group of nine patients (3.7 ± 1.3 pg/ml) (p < 0.05). Five patients with moderate to severe SAH had significantly higher plasma ANF values (202.6 ± 72.2 pg/ml) than five with minimal SAH (86.8 ± 29.2 pg/ml) or the control group (57.8 ± 45.3 pg/ml) (p < 0.05). Plasma ANF values were substantially higher than CSF ANF content in the SAH group (p < 0.01) and in the control group (p = 0.05). From these data it is concluded that: 1) plasma ANF is elevated significantly after SAH; 2) this rise appears unrelated to the cause of hemorrhage, serum sodium concentration, blood pressure, or central venous pressure, but is related to the extent of the hemorrhage; 3) ANF concentrations in the CSF are significantly lower than in plasma, and are elevated after moderate to severe SAH; and 4) the source of CSF ANF is probably the plasma, and the source of plasma ANF is likely the heart.

Experimental effect of intracranial hypertension upon intraocular pressure

1972 ◽  
Vol 36 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Ralph A. W. Lehman ◽  
Theodore Krupin ◽  
Steven M. Podos
Keyword(s):  
Blood Pressure ◽  
Intraocular Pressure ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Systemic Arterial Pressure ◽  
Content Type ◽  
Experimental Effect ◽  
Fine Print

✓ Intracranial pressure was elevated acutely by inflation of an epidural balloon inside one side of the skull of monkeys. In most of the animals, intraocular pressure rose, beginning only after intracranial pressure had been elevated well above normal and continuing until the pressure in the expanding epidural balloon approached the level of the blood pressure. Thereafter intraocular pressure stabilized until it fell as vasomotor collapse ensued. The role of systemic arterial pressure elevations in the rising phase of intraocular pressure is thought to be less important than increases of ophthalmic venous pressure.

Effect of naloxone on cerebral perfusion and cardiac performance during experimental cerebral ischemia

1986 ◽  
Vol 64 (5) ◽  
pp. 780-786 ◽  
Author(s):  
Robert J. Hariri ◽  
Elizabeth L. Supra ◽  
John Paul Roberts ◽  
Michael H. Lavyne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Perfusion ◽  
Blood Gases ◽  
Experimental Stroke ◽  
Arterial Blood Gases ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ Transient global cerebral ischemia (TGI) was induced in awake rats using the “four-vessel” occlusion model of Pulsinelli and Brierley. Blood pressure, arterial blood gases, cerebral blood flow, and cardiac output were measured during the acute (up to 2 hours) and chronic (2 to 72 hours) postischemic time periods. Coincident with the onset of TGI, cardiac output and caudate blood flow were depressed. The former returned to baseline within 30 minutes after the conclusion of TGI, and the latter progressed to hyperemia at 12 hours (81.8 ± 4.9 vs 68.6 ± 3.9 ml/min/100 gm tissue (mean ± standard error of the mean)) and oligemia at 72 hours (45.5 ± 4.8 ml/min/100 gm tissue) post-TGI in the untreated control rats. Arterial blood gases and blood pressure were unchanged. Naloxone (1 mg/kg) given at the time of TGI or as late as 60 minutes post-TGI and every 2 hours thereafter for 24 hours or bilateral cervical vagotomy prevented the depression in cardiac output and blocked the hyperemic-oligemic cerebral blood flow pattern that was predictive of stroke in this rat model. Changes in cardiac output after TGI in this model appear to be mediated by parasympathetic pathways to the heart from the brain stem. Opiate receptor blockade probably blocks endogenous opioid peptide stimulation of these brain-stem circulatory centers, which results in inhibition of parasympathetic activity and improvement in cardiac output. The usefulness of naloxone in the treatment of experimental stroke may be a function of its ability to improve cerebral perfusion in pressure-passive cerebrovascular territories. Variations in cardiac output during experimental stroke may explain the dissimilar responses to naloxone treatment reported by other investigators of experimental stroke.

Surgical experiences with giant intracranial aneurysms

1984 ◽  
Vol 61 (6) ◽  
pp. 1009-1028 ◽  
Author(s):  
Lindsay Symon ◽  
Janos Vajda
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Intracranial Aneurysms ◽  
Visual Loss ◽  
Considerable Improvement ◽  
Brain Circulation ◽  
Content Type ◽  
Space Occupying Lesion ◽  
Fine Print

✓ A series of 35 patients with 36 giant aneurysms is presented. Thirteen patients presented following subarachnoid hemorrhage (SAH) and 22 with evidence of a space-occupying lesion without recent SAH. The preferred technique of temporary trapping of the aneurysm, evacuation of the contained thrombus, and occlusion of the neck by a suitable clip is described. The danger of attempted ligation in atheromatous vessels is stressed. Intraoperatively, blood pressure was adjusted to keep the general brain circulation within autoregulatory limits. Direct occlusion of the aneurysm was possible in over 80% of the cases. The mortality rate was 8% in 36 operations. Six percent of patients had a poor result. Considerable improvement in visual loss was evident in six of seven patients in whom this was a presenting feature, and in four of seven with disturbed eye movements.

Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neurosurgical Procedures ◽  
Shr Rats ◽  
Mr Microscopy ◽  
Content Type ◽  
Wky Rats ◽  
Arterial Blood ◽  
Fine Print

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

Cerebral oxygen and microdialysis monitoring during aneurysm surgery: effects of blood pressure, cerebrospinal fluid drainage, and temporary clipping on infarction

2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Brain Tissue ◽  
Total Duration ◽  
Wilcoxon Test ◽  
Fisher Exact Test ◽  
Content Type ◽  
The Impact ◽  
Temporary Clipping ◽  
Fine Print

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Laser-sealed arteriotomy: a reliable aneurysm model

1987 ◽  
Vol 67 (2) ◽  
pp. 284-287 ◽  
Author(s):  
Matthew R. Quigley ◽  
Kenneth Heiferman ◽  
Hau C. Kwaan ◽  
Danko Vidovich ◽  
Peter Nora ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Carotid Artery ◽  
Systolic Blood Pressure ◽  
Systemic Hypertension ◽  
Chi Square ◽  
Content Type ◽  
Small Arteries ◽  
Rigid Supports ◽  
Aneurysm Model ◽  
Fine Print

✓ Laser-assisted vascular anastomosis (LAVA) is associated with a significant aneurysm problem when it is applied to small arteries. The etiology of this phenomenon was investigated by creating arteriotomies of different lengths and orientation in the rat carotid artery and sealing them with the milliwatt CO2 laser. It was found that increasing the arteriotomy length from 0.5 to 1.0 mm significantly raised aneurysm occurrence (4/17 vs. 25/28, chi-square: p < 0.001) regardless of orientation. Systemic hypertension (systolic blood pressure ≥ 170 mm Hg) also significantly affected the aneurysm rate among the 0.5-mm arteriotomy group, raising aneurysm occurrence from 23.5% (4/17) to 100% (14/14) (p < 0.001). Assuming that the stay-sutures used for LAVA's act as rigid supports, the rate of aneurysm occurrence must be related to the distance between sutures. This phenomenon has been exploited to create a reliable aneurysm model.

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