Blood respiratory control

Stage IV. Medullary Paralysis. This stage is marked by the cessation of spontaneous respiration because respiratory control centers located in the medulla oblongata are inhibited by excessive anesthesia. The ability of the medullary vasomotor center to regulate blood pressure is also affected, and cardiovascular collapse ensues. If this stage is inadvertently reached during anesthesia, respiratory and circulatory support must be provided or the patient will die.39... 

Conversely, dmgs that indnce P450 enzymes increase theophylline clearance and lower blood concentrations. These inclnde the barbitnrates, phenjdoin, carbamaze-pine, and rifampicin. Increased clearance also occnrs with a high-protein diet, marijnana, and tobacco. With phenytoin the interaction is two-sided the plasma concentrations of both dmgs fall. This can resnlt in poor seiznre and respiratory control and in dmg toxicity. 

Table I summarizes the important existing respiratory control models. Each model is made up of certain structural elements (1) lungs, (2) body tissues, (3) blood-gas relations, (4) ventilatory control law, and (5) blood flow and blood flow distribution control laws. The models differ mainly in the treatment of the last four elements.

The control of the blood respiratory chemistry the process by which for any given metabolic exchange requirement of oxygen and carbon dioxide the level of ventilation is kept at a minimum. 

Like any closed-loop system, the behavior of the respiratory control system is defined by the continual interaction of the controller and the peripheral processes being controlled. The latter include the respiratory mechanical system and the pulmonary gas exchange process. These peripheral processes have been extensively studied, and their quantitative relationships have been described in detail in previous reviews. Less well understood is the behavior of the respiratory controller and the way in which it processes afferent inputs. A confounding factor is that the controller may manifest itself in many different ways, depending on the modeling and experimental approaches being taken. Traditionally, the respiratory control system has been modeled as a closed-loop feedback/feedforward regulator whereby homeostasis of arterial blood gas and pH is maintained. Alternatively, the respiratory controller may be viewed as a... 

Bacterial catabolism of oral food residue is probably responsible for a higher [NHj] in the oral cavity than in the rest of the respiratory tract.Ammonia, the by-product of oral bacterial protein catabolism and subsequent ureolysis, desorbs from the fluid lining the oral cavity to the airstream.. Saliva, gingival crevicular fluids, and dental plaque supply urea to oral bacteria and may themselves be sites of bacterial NH3 production, based on the presence of urease in each of these materials.Consequently, oral cavity fNTi3)4 is controlled by factors that influence bacterial protein catabolism and ureolysis. Such factors may include the pH of the surface lining fluid, bacterial nutrient sources (food residue on teeth or on buccal surfaces), saliva production, saliva pH, and the effects of oral surface temperature on bacterial metabolism and wall blood flow. The role of teeth, as structures that facilitate bacterial colonization and food entrapment, in augmenting [NH3J4 is unknown. 

Respiratory alkalosis is the rise in pH associated with excessive respiration. Hyperventilation, which can result from anxiety or high fever, is a common cause. The body may control blood pH during hyperventilation by fainting, which results in slower respiration. An intervention that may prevent fainting is to have a hyperventilating person breathe into a paper bag, which allows much of the respired CX)2 to be taken up again. 

Voriconazole is started in the patient along with 1 mg/kg per day of methylprednisolone to control the graft-versus-host disease. Her tacrolimus dose was also decreased by 70% with the addition of voriconazole and a recent tacrolimus blood level of 1 0 ng/mL. Unfortunately, the patient remains febrile with worsening respiratory pain. A repeat CT scan of the lung demonstrates new nodules, and pleural effusion in the right lung. 

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