Tissue oxygenation - an overview (2023)

oxygenation of tissues

Arterial and venous O₂Saturations are measures of DO₂and absorption throughout the body. Although useful, these global measures do not provide any organ oroxygenation of tissues, which is the important local equilibrium between O₂Supply and demand. Regional O₂The balance can differ both between organs and within regions of the same organ.¹¹⁸Current non-invasive methods for assessing microcirculatory oxygenation use reflectance spectroscopy with light in either the visible spectrum (VLS) or near infrared spectrum (NIRS). A recent technique based on the lifetime of the triplet state of protoporphyrin IX aims at the determination of mitochondrial O₂voltage in vivo, and opens up the prospect of future clinical monitoring (cfAbb. 41.1).¹¹⁹

Reflectance spectroscopy probes have light emitters and receivers arranged in series (Abb. 41.8). When placed on a tissue surface, light transmission through tissue is affected by reflection, absorption, and scattering. Reflectance depends on the angle of incidence of the light beam and the wavelength of the light, while scattering depends on the number and type of tissue interfaces. As previously outlined, the Beer-Lambert law relates light absorption by tissue to the concentration of tissue chromophores, their respective extinction coefficients, and the path length of light through tissue.¹²⁰The predominant tissue chromophore is hemoglobin. The path length of light is affected by both reflection and scattering, so it cannot be measured directly, but rather must be estimated. Most of the detected photons move in an arc between the two detectors (cfAbb. 41.8). The depth of penetration of the arc into the tissue is proportional to the wavelength of the light and the distance between the emitter and the detector.^120.121

VLS uses white light with wavelengths from 500 to 800 nm, while NIRS uses light in the 700 to 1100 nm range.¹²²In general, the penetration depth of VLS is less than that of NIRS, allowing surface measurements of up to 16 mm and making it suitable for measurements of small underground volumes. NIRS can penetrate tissue to a depth of several centimeters and allows a larger volume of tissue to be sampled.¹²³The O₂the saturation indicated is that of one volume of tissue. This volume includes arteries, capillaries and veins and has a predominantly venous weighting.¹²⁴

Tissue oxygen saturation distortion

StO₂, similar to OI (see above), cannot be directly compared to any other measurement as it represents the findings in a blood mixture in the arteries, capillaries and veins. Interestingly, however, StO₂was recently validated in the head of infants with cardiac disease during cardiac catheterization.²⁴In this study of a StO₂In the range of 40-80%, the mean value was almost identical to the oxygen saturation in jugular venous blood measured by co-oximetry. This indicates a clearly negative bias, since in addition to venous blood, the StO₂also represents arterial and capillary blood. This distortion is likely to vary between different types of instruments. In addition StO₂was not compared to other measurements of venous saturation in preterm or term newborns; not even internal consistency of the StO₂with SvÖ₂measured by NIRS during obstruction of venous outflow has been reported.

Ischemia and tissue oxygenation

Vascular complications commonly associated with problematic wounds are primarily responsible for wound ischemia. Limitations in the vasculature's ability to deliver O₂-Rich blood flow to the wound tissue lead, among other things, to hypoxia. Hypoxia is a reduction in oxygen delivery below tissue requirements, while ischemia is a lack of blood flow characterized not only by hypoxia but also by inadequate nutrient supply.¹⁰³By definition, hypoxia is a relative term. It is defined by a lower tissue partial pressure of oxygen (pO₂) compared to the pO₂to which the tissue element in question is adapted under healthy conditionslive. Depending on the magnitude, cells exposed to a hypoxic challenge either induce an adaptive response involving an increase in glycolysis rates, energy conservation, or progression to cell death. In general, acute mild to moderate hypoxia supports adaptation and survival. In contrast, chronic, extreme hypoxia leads to tissue loss.

While tumor tissue is metabolically designed to thrive under hypoxic conditions, wound hypoxia, caused primarily by vascular constriction, is exacerbated by concomitant conditions (e.g., infection, pain, anxiety, and hyperthermia) and leads to poor healing outcomes. Oxygen and its reactive derivatives (Abb. 13.12) are required for energy synthesis from oxidative metabolism, protein synthesis and maturation (hydroxylation) of extracellular matrices such as collagen. Molecular oxygen is also required for nitric oxide (NO) synthesis, which in turn plays a key role in the regulation of vascular tone as well as in angiogenesis. In a wound environment, large amounts of molecular oxygen are partially reduced to form reactive oxygen species (ROS). ROS include oxygen-free radicals such as the superoxide anion and its non-radical derivative hydrogen peroxide (H₂Ö₂). The superoxide anion radical is the one-electron reduction product of oxygen. NADPH oxidases are a major source of superoxide anion radicals at the wound site. NADPH oxidases in phagocytes help fight infections. The superoxide anion also controls endothelial cell signaling as required during angiogenesis. In biological tissues, the superoxide anion radical dismutes rapidly to hydrogen peroxide, either spontaneously or facilitated by enzymes termed superoxide dismutases. Endogenous hydrogen peroxide drives redox signaling, a molecular signaling network that supports key aspects of wound healing such as cell migration, proliferation and angiogenesis. Neutrophil-derived hydrogen peroxide can be used by MPO to mediate the peroxidation of chloride ions, resulting in the formation of hypochlorous acid (HOCl), a potent disinfectant (seeAbb. 13.12).

Three main factors may contribute to wound tissue hypoxia: (1) peripheral vascular disease affecting O₂delivery; (2) elevated O₂stress on healing tissue; and (3) generation of ROS by respiratory burst and for redox signaling.¹³⁷Other related factors, such as B. Arterial hypoxia (eg, pulmonary fibrosis or pneumonia, sympathetic response to pain, hypothermia, anemia caused by large blood loss, cyanotic heart disease, high altitude), may also contribute to wound hypoxia. Depending on such factors, it is important to recognize that wound hypoxia can range from near-anoxia to mild to moderate hypoxia. In this context, it is also important to understand that point measurements taken in wound tissue may not provide a complete picture of wound tissue biology, as it is likely that the extent of wound hypoxia is not evenly distributed across the affected tissue, particularly in large wounds. This is most likely the case with chronic wounds that present clinically as opposed to experimental wounds that are more controlled and homogeneous. Any single problem wound presented to the clinic is likely to have both nests of anoxia and hypoxia of varying degrees (Abb. 13.13). As the weakest link in the chain, the tissues at the near-anoxic pockets are susceptible to necrosis, which in turn can propagate secondary tissue damage and infection. Pockets of extreme hypoxia may be swamped with hypoxia-inducible angiogenic factors but would not functionally vascularize due to insufficient O₂this is necessary to drive the repair process. In fact, uncontrolled expression of VEGF and its receptors leads to insufficient angiogenesis in the skin.¹³⁸Whether cells in the pockets of extreme hypoxia O₂-responsive is another concern. Even if such cells have passed the point of no return in the survival curve, a correction ofoxygenation of tissueswill likely help clear out the dead or dying tissue and replace the cavity with proliferating adjacent cells. Pockets of moderate or mild hypoxia are likely to be the starting point of a successful angiogenic response as long as other barriers such as infection and epigenetic changes are kept to a minimum.

Tissue oxygen saturation distortion

oxygenation of tissuescannot be compared directly with any other measurement, since it represents the findings in a blood mixture in the arteries, capillaries and veins. Interestingly, however, StO₂was validated on the head of infants with cardiac disease during cardiac catheterization.³⁵In this study of a StO₂range of 40%up to 80% the mean was almost identical to the oxygen saturation in the jugular venous blood measured by co-oximetry. This indicates a clearly negative bias, since in addition to venous blood, the StO₂also represents arterial and capillary blood. This distortion is likely to vary between different types of instruments.^36–38

oxygenation of tissues

Measurements of transcutaneous oxygen pressure (TcPO₂)^223–225and transcutaneous carbon dioxide pressure were studied to monitor compromised lobes. In experimental studies, TcPO₂was found to be more sensitive to lobe ischemia; However, in clinical studies, it has been difficult to differentiate between lobe ischemia and congestion based on TcPO₂alone. Instead a TcPO₂more than 90 mm Hg in an obstructed lobe proved to be a more useful guide in justifying further treatment.²²⁶Monitoring with partial oxygen tension (PtO₂) sensor placed in the subcutaneous fat of a series of breast free lobes has shown promise to identify and salvage defective free lobes based on the rapid rate of decline of PtO₂.²²⁷

Metabolic Acidosis

oxygenation of tissuesmay be affected by either low arterial oxygen saturation, as in congenital cyanotic heart disease, or decreased blood flow, as occurs in myocardial insufficiency or left heart obstruction (aortic atresia). Anaerobic metabolism leads to the accumulation of lactic acid in tissues. The kidneys partially compensate for this by excreting hydrogen ions, but especially in the first few weeks of life with poor tubular function, this is usually not sufficiently compensated and progressive metabolic acidosis develops. This can be demonstrated by measuring the pH and bicarbonate levels of the blood. The pH can drop below 7.0 and the bicarbonate below 10 mmol/L. A pH below 7.20 indicates a poor prognosis unless palliative surgery is performed.

The depressant effect of acidemia on the myocardium is initially masked by stimulation of the sympathoadrenal system with release of catecholamines, which increase the force of contraction of the ventricle. Eventually, however, high levels of catecholamines result in cardiovascular failure. In the presence of acidemia, the ventricular fibrillation threshold decreases.

The reduction in pH causes depression of the myocardium and central nervous system. The former is indicated by poor peripheral pulses and cold, splotchy extremities with poor return of capillary fill after pressure. A depression of the central nervous system manifests itself as missing or reduced spontaneous movements and diminished reflexes. Below pH 7.20, the respiratory center is depressed, so a respiratory element is added to acidosis and respiratory effort is reduced and eventually ceases.

Metabolic acidosis can be temporarily corrected by administration of sodium bicarbonate. In mild cases, it can be administered orally, but if the pH is below 7.2, intravenous therapy is indicated. Sodium bicarbonate is a hyperosmolar solution and its administration to acidotic and hypoxic neonates induces extensive vasodilation and blood pooling in skeletal muscle, resulting in severe hypotension. A solution containing 5 mmol/10 mL (0.42 g/10 mL) sodium bicarbonate should be used in neonates and 50 mmol/50 mL (4.2 g/50 mL) in the elderlyChildren. Two mmol/kg body weight should be administered slowly and the pH remeasured. Excessive administration of sodium bicarbonate leads to hypernatremia and intraventricular cerebral hemorrhage in the sick newborn. Calcium should be measured and associated hypocalcaemia treated with calcium gluconate. In hypoglycemia, Dextrose 5% should be administered.

The child's general condition improves after acidosis is corrected, but acidosis recurs if no action is taken to correct the underlying situation. Correcting acidosis is just a time saver for cardiac catheterization or surgery.

Variables that determine tissue oxygenation

CO is the product of stroke volume (amount of blood ejected per beat) and heart rate, and SAP is determined by CO and systemic vascular resistance (SVR). The four main determinants of cardiac function are preload (which determines the pre-contractile lengths of myofibrils), end-systolic wall tension (a function of systemic blood pressure and physical properties of the arterial system, ventricular wall thickness and chamber dimension), myocardial contractility, and heart rate. These determinants of ventricular function can be altered by many factors in critical care medicine. Preload, or end-diastolic volume, is affected by ventricular compliance (rate and extent of cardiomyocyte relaxation and cardiac connective tissue), intravascular volume, and intrathoracic pressure. The expansion of the heart resulting from the transmural inflation pressure, and not the LA pressure itself, determines the force of contraction. Therefore, intrathoracic (or intrapericardial) pressure is a key determinant of preload. Ventricular hypertrophy, vasodilator and diuretic therapies, and positive pressure mechanical ventilation all adversely affect preload. Similarly, cardiac function is inversely related to afterload, or end-systolic wall stress. Anatomical obstructions and systemic or pulmonary hypertension can adversely affect ventricular systolic and diastolic function. Excessively fast or slow heart rates and improperly timed atrial contractions (relative to ventricular systole) can adversely affect ventricular function. Finally, myocardial contractility is often negatively affected by the following factors: hypoxemia, acidosis, hypomagnesemia, hypocalcemia, hypoglycemia, hyperkalemia, cardiac surgery, sepsis, and cardiomyopathies.

oxygenation

Since most of the oxygen content in the blood is bound to hemoglobin, the oxygen delivery rate (DO₂) is therefore directly proportional to CO, hemoglobin concentration (Hb) and hemoglobin oxygen saturation (SaO₂). Therefore, optimizing the CO and oxygen transport capacity of the blood is just as essential as increasing the SaO₂or PaO₂in critically ill patients. It is also crucial to consider the interactions between these factors. In some patients, changes in mechanical ventilation to improve SaO₂could result in a decrease in CO, which would have an overall adverse effect on tissue oxygenation.

Oxygenation of brain tissue (PbO₂)

Brainoxygenation of tissues(PbO₂) can be measured directly with a combined electrode-fiber optic device originally developed for continuous intra-arterial blood gas monitoring. The PbO₂Unlike less invasive alternatives that can only measure regionally and globally, the probe is able to assess oxygenation at a specific site. A study byValadka and colleagues (1998)examined the prognostic utility of PbO₂in 43 severely injured TBI patients and found that the 3-month survival rate was inversely proportional to the total time in which PbO₂was < 15 mmHg. Likewise any PbO₂A value < 6 mmHg put the patient at increased risk of death within 3 months. Direct PbO₂The measurement has the advantage of allowing data to be collected at a specific location in the brain. However, it is invasive and requires probe placement directly in the brain parenchyma. In patients with multiple injury sites, or where the site of interest is not known, the benefit of direct PbO₂Measurement may be limited.

Abstract

Generally,oxygenation of tissuesrefers to oxygen saturation, which is a relative measure of the percentage of dissolved oxygen in tissues. Tissue oxygenation occurs when oxygen molecules enter the tissues of humans, as occurs when blood becomes oxygenated in the lungs via oxygen molecules migrating from the air into the blood. Blood, the body fluid responsible for transport and waste products, consists of cells and plasma. More than 99% of the cells in the blood are erythrocytes, which carry oxygen to and carbon dioxide from the lungs. The cardiovascular system is responsible for proper blood flow throughout the body, and oxygenation ability plays an important role in vital signs monitoring, especially in cardiovascular insufficiency assessment in critical patients with heart failure, septic shock and cerebral ischemia.