Pulsatile flow

About: Pulsatile flow is a research topic. Over the lifetime, 6278 publications have been published within this topic receiving 149638 citations.

Noninvasive continuous cardiac output monitor

Abstract: The invention provides apparatus and methods for using the electrical bioimpedance measurements to monitor parameters associated with blood flow in a segment of body tissue. The invention eliminates the effect of respiration from the thoracic impedance as a function of time to provide a signal indicative of pulsatile thoracic impedance changes continuously. The pulsatile thoracic impedance signal is processed to produce signals indicative of the ventricular ejection time and the maximum rate of change of pulsatile thoracic impedance which are used in a microprocessor to calculate the volume of blood pumped per stroke according to an improved systolic upstroke equation.

Alteration of hemodynamics in aneurysm models by stenting: Influence of stent porosity

Abstract: Recent developments in minimally invasive approach to cerebrovascular diseases include the placement of stents in arteries for treatment of aneurysms. Preliminary clinical observations and experimental studies have shown that intravascular stents traversing the orifice may lead to thrombosis and subsequent occlusion of the aneurysm. The alterations in vessel local hemodynamics due to the introduction of a stent are not yet well understood. We investigated changes in local hemodynamics resulting from stent implantation. Pulsatile flow patterns in an experimental flow apparatus were visualized using laser-induced fluorescence of rhodamine dye. The test cells were constructed in a rectangular shape to facilitate an undisturbed longitudinal view of flow patterns in parent vessel and aneurysm models with and without porous stents. Woven nitinol stents of various porosities (76%, 80%, 82%, and 85%) were investigated. The selected fluid dynamic similarity parameters (Reynolds and Womersley numbers) represented conditions usually found in high-flow, larger arteries in humans (such as the carotid artery) and low-flow, smaller arteries (such as the vertebral artery). The mean Reynolds number for the larger arteries was 180, with maximum/minimum values of 490/-30 and the Womersley number was 5.3. The mean Reynolds number for the smaller arteries was 90, with maximum/minimum values of 230/2, and the Womersley number was 2.7. For the larger arteries modeled, placement of a stent of the lowest porosity across the aneurysm orifice resulted in reduction of aneurysmal vortex speed and decreased interaction with parent vessel flow. For smaller arteries, a stent of the same porosity led to a substantial reduction of parent vessel/aneurysmal flow interaction and the appearance of a nonrecirculating crescent of fluid rich in rhodamine dye in the aneurysm dome. Our results can help explain in vivo thrombus formation within an aneurysm after placement of a stent that is compatible with local hemodynamics.

Cerebrospinal fluid circulation and associated intracranial dynamics. A radiologic investigation using MR imaging and radionuclide cisternography.

Abstract: UNLABELLED AIMS OF THE PRESENT INVESTIGATION: Observations made in a preliminary study of pulsatile cerebrospinal fluid (CSF) and brain motions using MR imaging called for a reconsideration of the CSF flow model currently accepted. The following questions were addressed: 1) The nature of the CSF-circulation, e.g., the magnitude and pattern of pulsatile and bulk flow; 2) The driving forces of the CSF circulation and assessment of the role of associated hemodynamics and brain motions; 3) The major routes for the absorption of CSF. MATERIAL AND METHODS CSF flow and associated hemodynamics were studied using gated MR imaging, in 26 healthy volunteers, 5 patients with communicating hydrocephalus and 10 with benign intracranial hypertension. Radionuclide cisternography was performed in 10 individuals with venous vasculitis. RESULTS AND CONCLUSIONS 1) The CSF-circulation is propelled by a pulsating flow, which causes an effective mixing. This flow is produced by the alternating pressure gradient, which is a consequence of the systolic expansion of the intracranial arteries causing expulsion of CSF into the compliant and contractable spinal subarachnoid space. 2) No bulk flow is necessary to explain the transport of tracers in the subarachnoid space. 3) The main absorption of the CSF is not through the Pacchionian granulations, but a major part of the CSF transportation to the blood-stream is likely to occur via the paravascular and extracellular spaces of the central nervous system. 4) The intracranial dynamics may be regarded as the result of an interplay between the demands for space by the four components of the intracranial content, i.e. the arterial blood, brain volume, venous blood and the CSF. This interaction is shown to have a time offset within the cerebral hemispheres in a fronto-occipital direction during the cardiac cycle (the fronto-occipital "volume wave"). 5) The outflow from the cranial cavity to the cervical subarachnoid space (SAS) is dependent in size and timing on the intracranial arterial expansion during systole. Similarly, the outflow from the aqueduct mirrors the brain expansion. The brain expansion is typically very small as evident from the minute aqueductal flow observed in healthy individuals. This expansion occurs simultaneously with an inflow of CSF and will be directed inwards towards the ventricular system. The brain expansion is of decisive importance for the formation of the normal transcerebral pressure gradient. 6) The instantaneous increase of flow in the superior sagittal sinus at the beginning of the systole reflects a direct pressure transmission via the SAS from the expanding arteries to the cerebral veins. It is contended that this early increase in venous pressure together with the volume wave is most likely an important prerequisite for sustaining normal intracranial pressure (ICP) and normal cerebral blood flow. This counter pressure should be reduced in hydrocephalus due to the decreased arterial expansion and could explain the reduced blood flow as well as an increased transmantle pressure gradient causing the ventricular dilatation. An increased pressure in the venous system is likely to be the cause of increases in ICP, including the increased pressure observed in benign intracranial hypertension (BIH).

Menopausal flushes: a neuroendocrine link with pulsatile luteninizing hormone secreation

Abstract: Menopausal flush episodes were found to be invariably associated with the initiation of pulsatile pituitary release of luteinizing hormone. This was not accompanied by a significant change in circulating catecholamine or prolactin concentrations. Since pulsatile luteinizing hormone release results from episodic secretion of luteinizing hormone releasing factor by the hypothalamus, these findings suggest a link between the neuroendocrine mechanisms that initiate such episodic secretion and those responsible for the onset of flush episodes.