Critical flow restoration

The lower velocity in the throat does not affect the jet s performance, as long as the velocity remains above the speed of sound. If the velocity in the throat falls below the speed of sound, we say that the jet has been forced out of critical flow. The sonic pressure boost is lost. As soon as the sonic boost is lost, the pressure in the vacuum tower suddenly increases. This partly suppresses vapor flow from the vacuum tower. The reduced vapor flow slightly unloads condenser 1 and jet 2 shown in Fig. 16.2. This briefly draws down the discharge pressure from jet 1. The pressure in the diffuser throat declines. The diffuser throat velocity increases back to, or above, sonic velocity. Critical flow is restored, and so is the sonic boost. The compression ratio of the jet is restored, and the vacuum tower pressure is pulled down. This sucks more vapor out of the vacuum tower, and increases the loads on condenser 1 and... 

Recently, on a job in Arkansas City, I was able to force a jet to surge and lose its sonic boost, simply by raising the condensate level in its downstream condenser by just 6 in. Lowering the level drew down the jet s discharge pressure by a few millimeters of mercury and restored it to critical flow. 

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

When drug therapy fails or if extensive coronary atherosclerosis is present, PCI is often performed to restore coronary blood flow, relieve symptoms, and prevent major adverse cardiac events. Patients with one or more critical coronary stenoses (i.e., greater than 70% occlusion of the coronary lumen) detected during coronary angiography may be candidates for PCI. Several catheter-based interventions maybe used during PCI, including ... 

In the model of Agarwal and Khakhar [57] the polymer molecules are taken to be bead-rod chains with the hydrodynamic forces concentrated at the beads. The chains may bend about a bead, and a spring force acts to restore the chain to is equilibrium conformation, which is a straight chain. The connecting rods are inextensible. The system is confined to a plane, and the chains diffuse due to Brownian forces resisted by hydrodynamic forces. Hydrodynamic forces resulting from an imposed shear flow deform and orient the molecules. Two chains may react and combine to form a longer chain if the chain ends approach to within the capture radius (a) and if the angle between the chains is less than the critical value (0 ). The reaction is assumed to be very fast (kfj k j ) so that every collision that satisfies the above criteria results in... 

The GUSTO trial demonstrated that treatment of patients within 6 hours after onset of symptoms with the combination of a clot-selective thrombolytic agent [recombinant tissue type plasminogen activator (t-PA)] plus conjunctive treatment with aspirin and intravenous unfractionated heparin resulted in 30-day mortality of 6.3% (6). An angiographic substudy demonstrated that patency of the infarct-related artery was not the sole determinant of outcome. Restoration of normal coronary flow after thrombolysis was found to be critical in lowering mortality (7). Thus, angiographic analysis demonstrated that both induction of culprit artery patency and the extent of restoration of flow were determinants of outcome. 

Milavetz and colleagues found that reperfusion was a critical determinant of benefit during the first 2 hours after onset of symptoms and that the restoration of normal blood flow remained a key determinant even when symptoms had begun more than 2 hours earlier (15). Unfortunately, most patients with an acute STEMI will seek medical attention only after more than 2 hours after onset of symptoms. Accordingly, the lack of clinical benefit associated with a combined approach used in the early trials is Ukely to have been a function of then contemporary limitations of pharmacological therapy, limitations of coronary intervention, and cultural and system limitations precluding prompt initiation of treatment. 

First Critical Velocity and Particle Rebound. Let us start examining the reasons for the appearance of the first critical velocity (see Fig. IX. 1). When the air-flow velocity is equal to or less than the first critical velocity, the contact zone is elastically deformed by particle impact (Fig. IX.2, item 1). After the detachment of such a particle, the shape of the surface in the contact zone is restored. We will now return to the condition (IX. 1) and examine it in relation to low velocities of the air stream, i.e., to velocities no greater than the first critical velocity. 

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