Oxygen Therapy PDF

11/27/23, 4:37 AM Realizeit for Student Oxygen Therapy Oxygen therapy is the administration of oxygen at a concentration greater than that found in the environmental atmosphere. At sea level, the concentration of oxygen in room air is 21%. The goal of oxygen therapy is to provide adequate transpor...

11/27/23, 4:37 AM Realizeit for Student Oxygen Therapy Oxygen therapy is the administration of oxygen at a concentration greater than that found in the environmental atmosphere. At sea level, the concentration of oxygen in room air is 21%. The goal of oxygen therapy is to provide adequate transport of oxygen in the blood while decreasing the work of breathing and reducing stress on the myocardium. Oxygen transport to tissues depends on factors such as cardiac output, arterial oxygen content, concentration of hemoglobin, and metabolic requirements. These factors must be kept in mind when oxygen therapy is considered for use in all patients, regardless of underlying disorders. Indications A change in the patient’s respiratory rate or pattern may be one of the earliest indicators of the need for oxygen therapy. These changes may result from hypoxemia or hypoxia. Hypoxemia, a decrease in the arterial oxygen tension in the blood, is manifested by changes in mental status (progressing through impaired judgment, agitation, disorientation, confusion, lethargy, and coma), dyspnea, increase in blood pressure, changes in heart rate, arrhythmias, central cyanosis (late sign), diaphoresis, and cool extremities. Hypoxemia usually leads to hypoxia, a decrease in oxygen supply to the tissues and cells that can also be caused by problems outside the respiratory system. Severe hypoxia can be life-threatening. The signs and symptoms signaling the need for supplemental oxygen may depend on how suddenly this need develops. With rapidly developing hypoxia, changes occur in the central nervous system because the neurologic centers are very sensitive to oxygen deprivation. The clinical picture may resemble that of alcohol intoxication, with the patient exhibiting lack of coordination and impaired judgment. With long-standing hypoxia (as seen in patients with COPD as well as in patients with chronic heart failure), fatigue, drowsiness, apathy, inattentiveness, and delayed reaction time may occur. The need for oxygen is assessed by arterial blood gas analysis, pulse oximetry, and clinical evaluation. Arterial Blood Gas Studies Arterial blood gas (ABG) studies aid in assessing the ability of the lungs to provide adequate oxygen and remove carbon dioxide, which reflects ventilation, and the ability of the kidneys to reabsorb or excrete bicarbonate ions to maintain normal body pH, which reflects metabolic states. ABG levels are obtained through an arterial puncture at the radial, brachial, or femoral artery or through an indwelling arterial catheter. Pain (related to nerve injury or noxious stimulation), infection, hematoma, and hemorrhage are potential complications that may be associated with obtaining ABGs (Pagana et al., 2017). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IZsc2gfB3djkaGXwQ9ctgb2A3gz%2bCKrCW4cKwIi8CIqb… 1/3 11/27/23, 4:37 AM Realizeit for Student Venous Blood Gas Studies Venous blood gas (VBG) studies provide additional data on oxygen delivery and consumption. VBG levels reflect the balance between the amount of oxygen used by tissues and organs and the amount of oxygen returning to the right side of the heart in the blood. VBG levels can be obtained by drawing blood from the venous circulation; this test is performed to provide an estimation of this balance when the ability to draw ABGs is not feasible. Mixed venous oxygen saturation (SO2) levels, the most accurate indicator of this balance, can be obtained only from blood samples drawn from a pulmonary artery catheter. However, central venous oxygen saturation (ScO2) levels, which are measured using blood drawn from a central venous catheter placed in the superior vena cava, closely approximate SO2 levels and are, therefore, useful as an alternative measure in patients without pulmonary artery catheters (Morton, Reck, & Headly, 2018). Regulation of Acid–Base Balance The normal serum pH is about 7.35 to 7.45 and must be maintained within this narrow range for optimal physiologic function (Norris, 2019). The kidney performs major functions to assist in this balance. One function is to reabsorb and return to the body’s circulation any bicarbonate from the urinary filtrate; other functions are to excrete or reabsorb acid, synthesize ammonia, and excrete ammonium chloride (Fischbach & Fischbach, 2018). Because bicarbonate is a small ion, it is freely filtered at the glomerulus. The renal tubules actively reabsorb most of the bicarbonate in the urinary filtrate. To replace any lost bicarbonate, the renal tubular cells generate new bicarbonate through a variety of chemical reactions. This newly generated bicarbonate is then reabsorbed by the tubules and returned to the body. The body’s acid production is the result of catabolism, or breakdown, of proteins, which produces acid compounds, particularly phosphoric and sulfuric acids. The normal daily diet also includes a certain amount of acid materials. Unlike carbon dioxide (CO2), phosphoric and sulfuric acids cannot be eliminated by the lungs. Because accumulation of these acids in the blood lowers pH (making the blood more acidic) and inhibits cell function, they must be excreted in the urine. However, if the hydrogen ions are low, they will be reabsorbed. A person with normal kidney function excretes about 70 mEq of acid each day. The kidney is able to excrete some of this acid directly into the urine until the urine pH reaches 4.5, which is 1000 times more acidic than blood (Norris, 2019). However, more acid usually needs to be eliminated from the body than can be secreted directly as free acid in the urine. These excess acids are bound to chemical buffers so that they can be excreted in the urine. Two important chemical buffers are phosphate ions and ammonia (NH3). When buffered with acid, ammonia becomes ammonium (NH4). Phosphate is present in the https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IZsc2gfB3djkaGXwQ9ctgb2A3gz%2bCKrCW4cKwIi8CIqb… 2/3 11/27/23, 4:37 AM Realizeit for Student glomerular filtrate, and ammonia is produced by the cells of the renal tubules and secreted into the tubular fluid. Through the buffering process, the kidney is able to excrete large quantities of acid in a bound form without further lowering the pH of the urine. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=0Dn26kXyU%2f6F5gOCz4%2f2IZsc2gfB3djkaGXwQ9ctgb2A3gz%2bCKrCW4cKwIi8CIqb… 3/3