Seminars in respiratory and critical care medicine
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Semin Respir Crit Care Med · Oct 2023
Blood Gas Transport: Carriage of Oxygen and Carbon Dioxide in Blood.
The ways in which oxygen (O2) and carbon dioxide (CO2) are carried in the blood are well known and well understood, with a plethora of textbooks, both general and lung specific, all presenting the topic in a very similar manner. This first of two companion chapters similarly summarizes this information. ⋯ However, what available texts have not emphasized is why knowing how gases are carried in blood matters, and the second, companion, chapter specifically addresses that critical aspect of gas exchange physiology. In fact, each of the chapters in this volume describes physiological behavior that depends more or less directly on the dissociation curves of O2 and CO2.
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Semin Respir Crit Care Med · Oct 2023
Tissue Perfusion and Diffusion and Cellular Respiration: Transport and Utilization of Oxygen.
This article provides an overview of the journey of inspired oxygen after its uptake across the alveolar-capillary interface, and the interplay among tissue perfusion, diffusion, and cellular respiration in the transport and utilization of oxygen. The critical interactions between oxygen and its facilitative carriers (hemoglobin in red blood cells and myoglobin in muscle cells), and with other respiratory and vasoactive molecules (carbon dioxide, nitric oxide, and carbon monoxide), are emphasized to illustrate how this versatile system dynamically optimizes regional convective transport and diffusive gas exchange. The rates of reciprocal gas exchange in the lung and the periphery must be well-matched and sufficient for meeting the range of energy demands from rest to maximal stress but not excessive as to become toxic. ⋯ Intracellular oxygen diffusion and facilitation via myoglobin into the mitochondria, and utilization via electron transport chain and oxidative phosphorylation, are summarized. Physiological and pathophysiological adaptations are briefly described. Dysfunction of any component across this integrated system affects all other components and elicits corresponding structural and functional adaptation aimed at matching the capacities across the entire system and restoring equilibrium under normal and pathological conditions.
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Substantial advances have been made recently into the discovery of fundamental mechanisms underlying the neural control of breathing and even some inroads into translating these findings to treating breathing disorders. Here, we review several of these advances, starting with an appreciation of the importance of V̇A:V̇CO2:PaCO2 relationships, then summarizing our current understanding of the mechanisms and neural pathways for central rhythm generation, chemoreception, exercise hyperpnea, plasticity, and sleep-state effects on ventilatory control. We apply these fundamental principles to consider the pathophysiology of ventilatory control attending hypersensitized chemoreception in select cardiorespiratory diseases, the pathogenesis of sleep-disordered breathing, and the exertional hyperventilation and dyspnea associated with aging and chronic diseases. These examples underscore the critical importance that many ventilatory control issues play in disease pathogenesis, diagnosis, and treatment.
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The pulmonary circulation is a low-pressure, low-resistance circuit whose primary function is to deliver deoxygenated blood to, and oxygenated blood from, the pulmonary capillary bed enabling gas exchange. The distribution of pulmonary blood flow is regulated by several factors including effects of vascular branching structure, large-scale forces related to gravity, and finer scale factors related to local control. Hypoxic pulmonary vasoconstriction is one such important regulatory mechanism. ⋯ Pulmonary vascular resistance describes the flow-resistive properties of the pulmonary circulation and arises from both precapillary and postcapillary resistances. The pulmonary circulation is also distensible in response to an increase in transmural pressure and this distention, in addition to recruitment, moderates pulmonary arterial pressure and vascular resistance. This article reviews the physiology of the pulmonary vasculature and briefly discusses how this physiology is altered by common circumstances.
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With ascent to high altitude, barometric pressure declines, leading to a reduction in the partial pressure of oxygen at every point along the oxygen transport chain from the ambient air to tissue mitochondria. This leads, in turn, to a series of changes over varying time frames across multiple organ systems that serve to maintain tissue oxygen delivery at levels sufficient to prevent acute altitude illness and preserve cognitive and locomotor function. ⋯ Because other organ systems, including the cardiovascular, hematologic and renal systems, contribute to acclimatization, the responses seen in these systems, as well as changes in common activities such as sleep and exercise, are also addressed. While the pattern of the responses highlighted in this review are similar across individuals, the magnitude of such responses often demonstrates significant interindividual variability which accounts for subsequent differences in tolerance of the low oxygen conditions in this environment.