Stroke 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. 

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). 

Andrews BT, Levy ML, Dillon W et al. (1987). Unilateral normal perfusion pressure breakthrough after carotid endarterectomy case report. Neurosurgery 21 568-571 Barnett HJM, Plum F, Walton JN (1984). Carotid endarterectomy an expression of concern. Stroke 15 941-943 Barnett HJM, Taylor DW, Eliasziw M for the North American Symptomatic Carotid Endarterectomy Trial Collaborators (1998). Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. New England Journal of Medicine 339 1415-1425... 

An embolus to the MCA is common and can cause a catastrophic stroke. It is also amenable to rapid therapy. For these reasons, special emphasis is placed here on this stroke subtype. As discussed above, carotid stenosis and occlusion can cause stroke by artery-to-artery embolus to the MCA territory or by causing a low-flow state [17]. Distinguishing features of carotid stenosis include the common occurrence of multiple stereotypic spells of transient ipsilateral hemispheric or monocular dysfunction. In addition, in carotid stenosis multiple emboli may occur over a short period of time. In some cases of embolus to the MCA from a severely stenotic carotid, the embolus may be less well tolerated and the stroke more severe due to the lower perfusion pressure above the carotid lesion [17]. Embolus from the carotid to the MCA can also occur from the stump of a completely occluded carotid [59]. If the occlusion is hyperacute, often the absence of flow in the region fi om the carotid bulb to the distal ICA reflects coUapse of the lumen due to low pressure rather than occlusion of the entire carotid with thrombus. In these cases, it is sometimes possible to dissolve the fresh clot in the extracerebral portion of the carotid and advance a catheter to treat the intracerebral clot. This can be... 

The generic term cerebral perfusion refers to tissue level blood flow in the brain. This flow can be described using a variety of parameters, which primarily include CBF, CBV, and MTT (Table 5.6). Understanding the dynamic relationships between these parameters as cerebral perfusion pressure drops in the setting of acute stroke is crucial to the accurate interpretation of perfusion maps. Definitions of these parameters are as follows ... 

In order to better understand the clinical implications of findings in PWI maps, it will be worthwhile to consider how the parameters that they measure are altered in patients with acute stroke. In response to a regional decrease in cerebral perfusion pressure (CPP), such as that which occurs downstream of embolic occlusion of an artery, blood vessels in the brain dilate, in an attempt... 

In many acnte stroke patients, spontaneons resoln-tion of the arterial lesion(s) before the time of presentation resnlts in spontaneous reperfusion of some or all of the previously ischemic tissue. Various studies have found that spontaneous reperfusion occurs in 16% of patients scanned within 8 h of stroke onset [10], and 33% of patients scanned within 48 h of onset [11], hi this reperfused tissue, vasodilation that persists even after the reduction in perfusion pressure has resolved often results in postischemic hyperperfusion, which is... 

As mentioned earlier, survival of ischemic penumbra is highly dependent on the efficiency of collateral vasculature to provide adequate CBF in the periphery of the ischemic territory. The viability of the penumbra depends on the degree and the duration of ischemia. In animal stroke models the reduction of CBF in the periphery of the ischemic territory is down to about 20% (Jones et al., 1981). Similar levels of diminished CBF are observed in humans (Bandera et al., 2006). In a healthy brain, CBF is maintained between 60 and 150 mmHg by vasoconstriction or vasodilatation in response to changes of perfusion pressure. However, during ischemia this autoregulation is lost, which makes the penumbra highly dependent on systemic blood pressures. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

HilUs AE, Ulatowski JA, Barker PB, Torbey M, Ziai W, Beauchamp NJ, Oh S, Wityk RJ. A pilot randomized trial of induced blood pressure elevation effects on function and focal perfusion in acute and subacute stroke. Cerebrovasc Dis 2003 16 236-246. 

Vasoconstriction Maintain blood pressure and perfusion in the face of reduced cardiac output Increased MV02 Increased afterload decreases stroke volume and further activates the compensatory responses... 

Hypertension is a common and progressive disorder which, if not effectively treated, results in an increased risk of atherosclerosis (see above), haemorrhagic stroke and damage to the kidney. For most cases of hypertension, there is no obvious cause, hence it is known as essential hypertension, so called because it was originally thonght to be essential to maintain tissue perfusion. In order to better nnderstand the regulation of blood pressure, a brief description of the regulation of contraction of smooth mnscle is provided. 

Blood pressure is only a part of the mechanism that controls the perfusion of blood through the various tissues, and elevated blood pressure itself does not cause death rather it is the deleterious effects it has on the smooth muscle of the body, whether the muscle is in the heart or the blood vessels. It is for the latter reason that stroke, representing damage to cerebral blood vessels, heart failure, the inability of the heart muscle to cope with the demand for blood, and kidney failure (uremia), the inability of the kidneys to remove waste products effectively, are the three common, immediate causes of death in the hypertensive population. 

Both LPA and SIP have vaso-regulatory functions, such as regulation of heart rate, blood pressure, platelet aggregation, and smooth muscle contraction (Karliner, 2004 Siess et al., 2000). Atherosclerosis is a type of accelerated vasculitis that reduces blood flow leading to heart attacks and strokes (Siess, 2002). It is well known that HDL level correlates with a reduced risk of cardiovascular disease, such as atherosclerosis (Choi et al., 2006), and it has been recently shown that it is the SIP content of HDL that mediates many of its effects. For example, HDL induces vasodilation and myocardial perfusion by activation of SIP3 (Levkau et al, 2004 Nofer et al., 2004). Furthermore, in an in vivo mouse study, HDL and SIP reduce the infarction size about by 20 and 40% and also inhibit inflammation caused by the recruitment of polymorphonuclear leukocytes and cardiomyocyte apoptosis via the SIP3 receptor eNOS/NO pathway (Theil-meier et al., 2006). 

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