Books on the topic 'Alveolar process'

Adequate gas exchange in the lungs requires a balance between three key processes: ventilation (V), the flow of gas from the environment to the alveoli; perfusion (Q), the circulation to the pulmonary capillary beds; and diffusion of the gas from the alveolar space into the alveolar capillaries. This chapter discusses the management of diseases of the air space, which include secretions, pneumonia, pulmonary edema, and hemoptysis. Collectively these conditions result in the build-up of fluid in the alveolar space and thickening of the alveolar membrane, leading to a mismatch in ventilation and perfusion (V/Q mismatch). Both anesthesia and disease states can adversely affect gas exchange and the chapter discusses strategies to maximize a patient’s pulmonary status in order to minimize perioperative pulmonary complications.

Ventilation can occur only when the respiratory system expands above and then returns to its resting or equilibrium volume. This is just another way of saying that ventilation depends on our ability to breathe. Although breathing requires very little effort and even less thought, it’s nevertheless a fairly complex process. Respiratory Mechanics reviews the interaction between applied and opposing forces during spontaneous and mechanical ventilation. It discusses elastic recoil, viscous forces, compliance, resistance, and the equation of motion and the time constant of the respiratory system. It also describes how and why pleural, alveolar, lung transmural, intra-abdominal, and airway pressure change during spontaneous and mechanical ventilation, and the effect of applied positive end-expiratory pressure (PEEP).

Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.

Caning (or Shatt), an Eastern Sudanic (Nilo-Saharan) language of Sudan, has bilabial, alveolar, palatal, and velar plosives, but it is not straightforward for which plosives (if any) there is an underlying voicing contrast. Three analyses that can be shown to account reasonably for the data. One analysis proposes a voicing contrast of all plosives in all word positions where plosives occur. Of the three, this analysis posits underlying plosives most closely to the surface forms. A second analysis proposes only a voicing contrast of alveolar and velar plosives in word-initial position, and posits the same alternation processes in roots that are observed across morpheme boundaries. A third analysis proposes no voicing contrast of any plosives in any position by positing a “ghost” consonant before alveolar and velar plosives in word-initial position. There are advantages to each analysis, but none is without certain obstacles. After the noun root and morphological data of plosives is presented as neutrally as possible, the data are analyzed according to each of the three competing analyses, and the evidence for each is summarized. The reader is left to decide which analysis is the best choice.

Mechanical ventilation is indicated when the patient’s ability to ventilate the lung and/or effect gas transport across the alveolar capillary interface is compromised to point that harm is imminent. In practice, this means addressing one or more of three fundamental pathophysiological processes—loss of proper ventilatory control, ventilatory muscle demand-capability imbalances, and/or loss of alveolar patency. A fourth general indication involves providing a positive pressure assistance to allow tolerance of an artificial airway in the patient unable to maintain a patent and protected airway. The decision to initiate mechanical ventilation usually involves an integrated assessment that should include mental status, airway protection capabilities, ventilatory muscle load tolerance, spontaneous ventilatory pattern, and signs of organ dysfunction from either acidosis and/or hypoxaemia. Providing mechanical ventilatory assistance can be life-sustaining, but it is associated with significant risk, including ventilator-induced lung injury, infection, and need for sedatives/paralytics, and must be applied only when indications justify the risk.

Gas Exchange explains how four processes—delivery of oxygen, excretion of carbon dioxide, matching of ventilation and perfusion, and diffusion—allow the respiratory system to maintain normal partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Partial pressure is important because O2 and CO2 molecules diffuse between alveolar gas and pulmonary capillary blood and between systemic capillary blood and the tissues along their partial pressure gradients, and diffusion continues until the partial pressures are equal. Ventilation is an essential part of gas exchange because it delivers O2, eliminates CO2, and determines ventilation–perfusion ratios. This chapter also explains how and why abnormalities in each of these processes may reduce PaO2, increase PaCO2, or both.

The present study sheds light on the phonetic causes of sound change and the intermediate stages of the diachronic pathways by studying the palatalization and assibilation of velar stops (referred to commonly as ‘velar softening’, as exemplified by the replacement of Latin /ˈkɛntʊ/ by Tuscan Italian [ˈtʃɛnto] ‘one hundred’), and of labial stops and labiodental fricatives (also known as’ labial softening’, as in the case of the dialectal variant [ˈtʃatɾə] of /ˈpjatɾə/ ‘stone’ in Romanian dialects). To a lesser extent, it also deals with the palatalization and affrication of dentoalveolar stops. The book supports an articulation-based account of those sound-change processes, and holds that, for the most part, the corresponding affricate and fricative outcomes have been issued from intermediate (alveolo)palatal-stop realizations differing in closure fronting degree. Special attention is given to the one-to-many relationship between the input and output consonantal realizations, to the acoustic cues which contribute to the implementation of these sound changes, and to those positional and contextual conditions in which those changes are prone to operate most feasibly. Different sources of evidence are taken into consideration: descriptive data from, for example, Bantu studies and linguistic atlases of Romanian dialects in the case of labial softening; articulatory and acoustic data for velar and (alveolo)palatal stops and front lingual affricates; perceptual results from phoneme identification tests. The universal character of the claims being made derives from the fact that the dialectal material, and to some extent the experimental material as well, belong to a wide range of languages from not only Europe but also all the other continents.

Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.