Arterial Carbon Dioxide Levels Research Articles

Exercise and Cystic Fibrosis: A Review.

Cystic fibrosis (CF) results in chronic obstructive pulmonary disease with progressive increases in areas of the lung with poor gas exchange (dead space). The pulmonary response to exercise is characterized by a higher than expected minute ventilation (V̇E). In some patients the elevated V̇Eis inadequate to overcome the large dead space, resulting in decreases in arterial oxygen and/or increases in arterial carbon dioxide levels during exercise. Chronic lung hyperinflation in patients with severe disease limits the ability to increase tidal volume, and therefore V̇E, during exercise. Most patients can exercise without decreases in arterial oxygen and should be encouraged to participate in regular activity. Oxygen supplementation during exercise allows many patients with severe lung dysfunction to participate in some form of activity. Regular exercise has been shown to be of some benefit and should be encouraged on an individual basis in patients with CF.

Carbon dioxide elimination during spontaneous ventilation with a modified mapleson D system: Studies in a lung model

A lung model was used to simulate gas exchange for a 70 kg adult under anaesthesia. It was demonstrated that the modified Mapleson D circuit (Bain) with low fresh gas flows determined according to body weight is a partial rebreathing system. With controlled ventilation this can be compensated for by increasing minute ventilation above the predicted and the arterial carbon dioxide level can then be regulated by adjusting the fresh gas flow. During spontaneous ventilation this compensation is critically dependent on the patient's ability to increase minute ventilation. Therefore in any particular case the arterial carbon dioxide is unpredictable and totally dependent on carbon dioxide responsiveness, carbon dioxide production, physiological dead-space, respiratory wave form, and apparatus dead-space. Although normocarbia can be achieved by certain ideal patients despite low fresh gas flows it can be done only if minute ventilation is markedly increased. This enforced hyperpnoea will significantly encroach on the respiratory reserve of these patients and may well be unattainable in some. We conclude that any decrease in respiratory drive, increase in carbon dioxide production, increase in physiological or apparatus dead-space (i.e. a mask) will produce potentially dangerous hypercarbia using a Bain circuit with a fresh gas flow of 100 ml/kg/minute. This hazard is not easily recognized. The only way to minimize these factors during spontaneous ventilation is by the use of a non-rebreathing circuit. To do this with a T-piece or Bain circuit the fresh gas flow must be between 200 and 300 ml/kg/min for an average adult, with this requirement being highly dependent on all the variables outlined. One must decide whether the low economy and high level of operating room pollution with this wide range of flow outweigh the advantages of trying to make the Mapleson D a universal circuit.

Ventilation and Cardiovascular Studies during Mechanical Control of Ventilation in Horses

Eleven out of 12 horses were underventilating while breathing spontaneously during halothane anaesthesia with high arterial carbon dioxide tensions. In addition, large alveolar to arterial oxygen tension gradients were found to be present. Mechanically, controlled ventilation with an intermittent positive pressure of 20-30 cm H2O reduced arterial carbon dioxide levels to normal. The alveolar to arterial oxygen gradients did not increase and in some cases decreased. These (A - a) Po2 gradients were due mainly to true shunt of the order of 30 per cent and not to ventilation perfusion inequality.

Cardiovascular effects of centrally administered ketamine in goats.

The cardiovascular effects of centrally and peripherally administered ketamine were evaluated in unanesthetized goats and in goats anesthetized with pentobarbital. Small doses of ketamine (0.1 to 4 mg.) were injected directly into the central nervous system (CNS) of the unanesthetized goats via a temporal artery catheter, while cerebral blood flow (CBF), cardiac output (C.O.), systemic blood pressure (B.P.), and heart rate (H.R.) were continuously monitored. Administered by this route, ketamine produced an immediate increase in mean systemic B.P., C.O., and H.R. Changes in CBF were variable, increasing on some occasions and decreasing on others. Cardiovascular changes were not the result of alterations in blood gases, since these remained unchanged. When ketamine, 0.1 to 4 mg., was injected into the temporal artery of goats anesthetized with pentobarbital, no changes were observed in B.P., C.O., H.R. or CBF. Ketamine (2 mg./kg.) intravenously administered to unanesthetized goats produced anesthesia and an increase in B.P., C.O., H.R., CBF, and arterial carbon dioxide (Paco2) levels. Administered by the same route and dosage in mechanically ventilated goats previously anesthetized with sodium pentobarbital, ketamine did not produce any changes in cardiovascular or blood-gas measurements. It was therefore concluded that ketamine produces peripheral sympathomimetic effects primarily by direct stimulation of CNS structures, and that when these structures are depressed by pentobarbital, the peripheral effects of ketamine are ameliorated.

Disposable membrane oxygenator support during emergency coronary angiography and during surgery for acute myocardial infarction or chronic myocardial ischemia.

Forty-two patients received successful total cardiopulmonary support with the effective, easy to use, completely disposable, Lande-Edwards Membrane Oxygenator.In 4 patients, partial cardiopulmonary support was provided with the Membrane Oxygenator and/or intra-aortic baloon pump during emergency coronary arteriography and corrective cardiac surgery for shock, following myocardial infarction.Two Lande—Edwards membrane oxygenators, 3 m2, were connected in parallel and joined in either a recirculation circuit or, more recently, a simplified gravity circuit. Three oxygenators were used for patients 80 kg to 103 kg body weight.Effective gas exchange was documented by the normal range of arterial and venous oxygen and carbon dioxide levels during flow rates of 50 cc/kg/min at 30°C. Safety of perfusion was demonstrated by 25 of 26 patients being discharged improved after complex aortocoronary artery by-pass graft operations. Minimal side effects were observed including plasma hemoglobin under 100 mg%, platelet c...

INSTRUMENTATION AND MONITORING DURING OPEN-HEART SURGERY

The necessity for following certain physiological functions of a patient undergoing heart-lung surgery is well known. 1-3 At Stanford University Hospital we have, over the past several years, evolved certain techniques for accomplishing this which we feel will be of interest to other workers in this and similar fields. Figure 1 is a diagrammatic representation of the floor plan and the personnel involved. Functions which are usually monitored include the EKG, arterial pressure, inferior vena caval pressure (via the long saphenous vein), and superior vena caval pressure. In addition, when hypothermia is employed, blood temperature and body temperature are also followed. These functions are deemed to be an irreducible minimum consistent with the welfare of the patient undergoing open-heart surgery. Other functions, such as venous and arterial oxygen saturation, blood pH, 4 respiratory and pump-oxygenator carbon dioxide levels, and atrial and ventricular pressures, are sometimes determined when indicated but are

Electroencephalographic and Biochemical Changes in Acute Hypoxia and Hypercapnia

Introduction Serum potassium alterations have been demonstrated in hyper- and hypocapnic states. 1-6 It has been postulated that these changes, in part, may represent physiologic buffering mechanisms, 6 but their relationship to the maintenance of normal cerebral function has not been investigated with controlled experiments. In chronic pulmonary failure a significant increase of serum potassium has been observed in patients who were both chronically hypoxic and hypercapnic. 7 It was suggested that the elevation of serum potassium might serve as a buffering mechanism whereby normal cerebral function was maintained in spite of markedly elevated arterial blood carbon dioxide levels. If this theory were correct, prevention of increase in serum potassium by glucose infusion as previously used in the studies of the early hyperkalemia of hyperventilation 8 should result in increased sensitivity of cerebral electroactivity to carbon dioxide. However, it is possible that the increase in serum potassium seen in the