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Pulse Oximetry , Plethysmography , Capnography , and Respiratory Monitoring
| Content Provider | Semantic Scholar |
|---|---|
| Author | Poler, S. Mark |
| Copyright Year | 2017 |
| Abstract | Pulse oximetry and capnography are mainstays of physiologic monitoring, evaluating oxyhemoglobin saturation as a proxy for tissue availability of oxygen, and concentration of carbon dioxide being eliminated, respectively. Both technologies can provide additional information to the sophisticated clinician, as analysis of the shape and characteristics of continuous waveforms shows changing physiologic information. This large literature can only be superficially represented in the space of this general chapter. Ehrenfeld and Cannesson (1) have recently produced Monitoring Technologies in Acute Care Environments, an excellent resource for these and other monitoring technologies relevant to critical care. Oxygen provides the essential metabolic oxidizer that must flow down a partial pressure gradient from alveolar gas to end-organ tissue. As the quantity of dissolved O2 in blood is small relative to the quantity of the gas bound to hemoglobin, O2 even at high partial pressures decreases rapidly to less than 100 torr as it diffuses from blood to tissue. This physiology must be kept in mind, even though not directly observed, for the oximetric assessment of hemoglobin in precapillary blood, this being where gas exchange with tissue occurs. In the reverse direction, the primary metabolic waste product, CO2, must have a partial pressure gradient from tissue to exhaled gas in order to be eliminated at the rate of production; this is typically from a venous tension of about 46 torr to a normal of 40 torr in arterial blood (or equilibrated alveolar gas) (2). Pulse oximetry is a ubiquitous de facto standard of care in ambulatory and inpatient facilities, emergency medical services (EMS), and lowand high-acuity patient care. Quickly and noninvasively obtaining oxygen saturation by pulse oximetry is often the first step in the decision-making process of caring for a patient. Continuous monitoring can detect acute or longterm deterioration of delivery of O2 (DO2) to tissue. It provides a measure of the essential supply of O2 for oxidative metabolism, and can provide insight into pulmonary and cardiovascular function, metabolism, and dyshemoglobinemias. While conceptually convenient that the saturation of hemoglobin typically reaches 100% near a PaO2 of 100 torr (2), this also exposes one of the principal shortcomings of pulse oximetry. Above about 100 torr, the increase of PaO2 is not accompanied by a proportional increase in saturation. Below 100 torr, the nonlinearity of the sigmoid oxygen–hemoglobin binding relationship confounds easy conversion of saturation to the PaO2 that provides the driving gradient for diffusion of O2 into tissue and intracellular mitochondria. So, large changes in PaO2 in blood do not have a simple relationship to hemoglobin saturation. Until recently, tissue and mitochondrial PO2 could not be easily assessed in clinical settings, except where tissue surfaces were accessible. These limitations are yielding to near-infrared spectroscopy (NIRS), new applications of pulse oximetry and, now, mitochondrial oximetry. Formerly tissue and mitochondrial PO2 (PmO2) tension could not be easily characterized because of technological limitations, though it was understood that at PmO2 below 2 torr, oxidative metabolism is impaired, becoming anaerobic below 1 torr (3). More recently, methods including positron emission tomography (PET) and magnetic resonance imaging (MRI) have provided surveys of PO2 in various tissues, and are largely consistent with the earlier data (4). These newer technologies are yielding new data dramatically changing the assessment of PO2 sensitivity of oxidative metabolism in mitochondria at the end of the O2 delivery pathway. Both O2 tension and consumption can be characterized by O2-dependent quenching of protoporphyrin fluorescence. This technique reports typical PmO2 of 50–60 torr, and reveals metabolic adaptation below 70 torr (5). An endotoxin-induced model of sepsis in rats reports PmO2 near 60 torr initially, decreasing to as low as 30 torr without fluid resuscitation (6). Capnography assesses the elimination of CO2, the principle end-product of oxidative metabolism (water not needing to be eliminated). While providing a snapshot of the steady elimination of CO2 via the lungs, the shape of the capnogram can provide insight into the mechanics of ventilation, matching of cardiovascular and pulmonary function to metabolism. Attention to the ratio of partial pressures and content of O2 and CO2 in blood and exhaled gases contribute to evaluation of lung function or injury. Capnography and other monitors of respiratory function will be discussed in the second part of this chapter. |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://examdev.theaba.org/E-Library/texts/2/25.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
