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Cerebral perfusion pressure

Georgiadis D, Schwarz S, Kollmar R, Baumgartner RW, Schwab S. Influence of inspiration expiration ratio on intracranial and cerebral perfusion pressure in acute stroke patients. Intensive Care Med 2002 28(8) 1089-1093. [Pg.189]

Rosner MJ, Coley IB. Cerebral perfusion pressure, intracranial pressure, and head elevation. J Neurosurg 1986 65(5) 636-641. [Pg.189]

Fan JY. Effect of backrest position on intracranial pressure and cerebral perfusion pressure in individuals with brain injury a systematic review. J Neurosci Nurs 2004 36(5) 278-288. [Pg.189]

Meixensberger J, Baunach S, Amschler J, Dings J, Roosen K. Influence of body position on tissue-po2> cerebral perfusion pressure and intracranial pressure in patients with acute brain injury. Neurol Res 1997 19(3) 249-253. [Pg.189]

Chan K-H, Miller JD, Dearden NM, Andrews PJ, Midgley S. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg 1992 77(1) 55-61. [Pg.195]

Maintain cerebral perfusion pressure (CPP) between 60-80 mmHg... [Pg.62]

The goal of sympathomimetic therapy is to augment both coronary and cerebral perfusion pressures during the low-flow state associated with CPR. These agents increase systemic arteriolar vasoconstriction, thereby improving coronary and cerebral perfusion pressure. They also maintain vascular tone, decrease arteriolar collapse, and shunt blood to the heart and brain. [Pg.92]

Nordstrom CH. 2003. Assessment of critical thresholds for cerebral perfusion pressure performing bedside monitoring of cerebral energy metabolism. Neurosurg Focus... [Pg.251]

Nordstrom CH, Reinstrup P, Xu W, Gardenfors A, Ungerstedt U. 2003. Assessment of the lower limit for cerebral perfusion pressure in severe head injuries by bedside monitoring of regional energy metabolism. Anesthesiology 98(4) 809-814. [Pg.251]

Stahl N, Ungerstedt U, Nordstrom CH. 2001b. Brain energy metabolism during controlled reduction of cerebral perfusion pressure in severe head injuries. Intensive Care Med 27(7) 1215-1223. [Pg.254]

At rest, the brain consumes 20% of the total oxygen that the whole body consumes. Global brain ischemia occurs when the arterial blood pressure cannot maintain a sufficient cerebral perfusion pressure. This happens with cardiac dysfunction, shock, and critical increase in intracranial pressure. Cerebral hypoxia is the deprivation of oxygen with a maintained cerebral blood flow. Pure hypoxia will occur in rare instances such as reduced atmospheric oxygen, which is an extremely rare cause of brain hypoxia, or as a result of drowning. Most cases occur in a combination of hypoxia and ischemia since pure hypoxia very often causes cardiac arrest and, thus, interruption of cerebral blood flow. The combination of both hypoxia and ischemia leads to more serious neuronal damage than hypoxia alone. [Pg.239]

Soukup J., Zauner A., Doppenberg E. M., et al. (2002) The importance of brain temperature in patients after severe head injury relationship to intracranial pressure, cerebral perfusion pressure, cerebral blood flow, and outcome. 7. Neurotrauma 19,559-571. [Pg.75]

Kahveci et al. (13) compared the cerebral protective effects of two known protective anesthetics, isoflurane and propofol, in combination with hypothermia (33-34°C) after traumatic brain injury (TBI). In that study, the authors found that propofol anesthesia plus hypothermia following TBI was better than the isoflurane-hypothermia combination because it reduced intracranial pressure and increased cerebral perfusion pressure under those conditions. [Pg.98]

CBF, Cerebral blood flow CMR02, cerebral metabolic rate for oxygen ICP, intracranial pressure CPP, cerebral perfusion pressure. [Pg.123]

A significant reduction of the ICP was seen, which was similar to the results of Marion and Shiozaki, who used hypothermic therapy in traumatic brain injuries (37,38). With an unaffected mean arterial blood pressure (MABP) and increased cerebral perfusion pressure (CPP), hypothermic therapy appeared to benefit stroke patients, as uncontrolled intracranial hypertension is the main cause of death in the first week after stroke. However, rewarming the patients consistently led to a secondary rise of ICP, which required additional ICP therapy with mannitol. In some cases it even exaggerated the initial ICP levels (Fig. 3). [Pg.152]

Cerebral blood flow depends on cerebral perfusion pressure and cerebrovascular resistance. The perfusion pressure is the difference between systemic arterial pressure at the base of the brain when in the recumbent position and the venous pressure at exit from the subarachnoid space, the latter being approximated by the intracranial pressure. Cerebral perfusion pressure divided by cerebral blood flow gives the cerebrovascular resistance. In normal humans, cerebral blood flow remains almost constant when the mean systemic blood pressure is between approximately 50 and 170mmHg, which, under normal circumstances when the intracranial venous pressure is negligible, is the same as the cerebral perfusion pressure. This homeostatic mechanism to maintain a constant cerebral blood flow in the face of changes in cerebral perfusion pressure is known as autoregulation (Reed and Devous 1985 Powers 1993). Autoregulation is less effective in the elderly, and so postural hypotension is more likely to be symptomatic (Wollner et al. 1979 Parry et al. 2006). [Pg.45]

If the perfusion pressure rises above the autoregulatory range, where compensatory vasoconstriction and cerebral perfusion pressure are maximal, then hyperemia occurs followed by vasogenic edema, raised intracranial pressure and the clinical syndrome of hypertensive encephalopathy. [Pg.45]

Chronically impaired perfusion reserve tends to occur when one or both internal carotid arteries are stenosed by at least 50% of the luminal diameter (Brice et al. 1964 DeWeese et al. 1970 Schroeder 1988), or are occluded, and the collateral circulation is inadequate (Powers et al. 1987 Kluytmans et al. 1999). In this situation, the brain is vulnerable to any fiirtber fall in cerebral perfusion pressure and cerebral metabolism is begiiming to become impaired, with the appearance of structural abnormalities on MRI (van der Grond et aL 1996 Isaka et al. 1997 Derdeyn et al. 1999). [Pg.45]

Schumann P, Touzani O, Young AR et al. (1998). Evaluation of the ratio of cerebral blood flow to cerebral blood volume as an index of local cerebral perfusion pressure. Brain 121 1369-1379... [Pg.48]

Piper, I.R. Garrioch, M.A. Souter, M.J. Andrews, P.J.D. Thomson, D. Effects of diaspirin cross-linked haemoglobin on past-traumatic cerebral perfusion pressure and blood flow in a rodent model of diffuse brain injury. Brit. J. Anaesthes. 1998, 80, 639-643. [Pg.375]

Despite a fall in mean arterial pressure, with a consequent reduction in cerebral perfusion pressure, sevoflurane should be a suitable agent for neuroanesthesia (14). Even in patients with ischemic cerebrovascular diseases, both the CO2 response and cerebral autoregulation were well maintained during sevoflurane anesthesia (0.88 MAC) (15). [Pg.3124]

Brown MM, Parr MJ, Manara AR. The effect of suxamethonium on intracranial pressure and cerebral perfusion pressure in patients with severe head injuries following blunt trauma. Eur J Anaesthesiol 1996 13(5) 474-7. [Pg.3268]


See other pages where Cerebral perfusion pressure is mentioned: [Pg.16]    [Pg.109]    [Pg.126]    [Pg.164]    [Pg.1554]    [Pg.194]    [Pg.194]    [Pg.85]    [Pg.46]    [Pg.6]    [Pg.120]    [Pg.45]    [Pg.53]    [Pg.124]    [Pg.253]    [Pg.245]    [Pg.366]    [Pg.2624]    [Pg.3257]   
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See also in sourсe #XX -- [ Pg.6 ]

See also in sourсe #XX -- [ Pg.245 ]

See also in sourсe #XX -- [ Pg.183 ]




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