Arterial Oxygen Saturation

Hypoxia is one of the major problems associated with this increase in altitude. This is due to the fact that the partial pressure of oxygen decreases proportionately with increases in altitude. Carbon dioxide that is continually excreted from the pulmonary blood to the alveoli along with water vaporizing in the inspired air from the respiratory surfaces dilute the oxygen in the alveoli which cause the oxygen concentration to decrease.

Because the PCO2 levels are too high the body is not getting the adequate amount of oxygen. This means the oxygen-carrying hemoglobin is not working properly do to the excessive amounts carbon dioxide causing respiratory acidosis.

*Yes, air pressure changes with altidue. The rate of pressure is not constant, air pressure decreases at a decreasing rate with an increase in altitude.

The altitude that this stage could happen in is between 5000 to 11400 ft.(3) "The body generally has the ability to stave off further effects of hypoxia by increasing the rate and depth of ventilation and cardiac output ".(1) The respiration rate, blood pressure, and the heart rate can rise up in this stage.(2) the arterial oxygen saturations in this stage is between 80 and 90 percent.(1)

Oxygen deficit occurs when the ATP production increases. It also occurs during the beginning of exercise. Anytime an individual changes the intensity of a workout, there will be an oxygen deficit. Oxygen deficit uses aerobic metabolism during an exercise bout.

This choice represents a situation of acute respiratory alkalosis, which can be seen in hyperventilation, and high altitudes. The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase. This causes decreased circulating hydrogen ion concentration, and increased pH

At higher altitudes, the amount of air pressure is reduced. If there is less air pressure this means there is a lesser amount of oxygen present. With the oxygen levels decreased, you have to breathe faster and deeper to get the amount of oxygen you would normally have at surface level.

Hypoxia affects more than just the blood and hemoglobin; a prolonged hypoxia causes a low rise in the red blood cell count (polycythaemia). This increase in the rate of red blood cell production is produced by hypoxia s effect on the kidney. It causes the kidney to secrete a substance known as enythrogenin into the blood stream. There, it acts upon a plasma protein called erythropoietinogen, which produces erythropoietin, stimulating the red bone marrow to make more red blood cells. Hypoxia also affects the brain-especially the respiratory center of the brain. Even a brief lack of oxygen has effects on this area in the brain, such as a loss of consciousness. When hypoxia causes a shortage of oxygen it affects the respiratory center of the brain because the brain struggles to recover from the shortage of oxygen by causing the breathing rate to increase. If one becomes so starved of oxygen that he/she loses consciousness this causes him/her to lose many of his/her brain cells.

Chronic Pathophysiology effects the alveolar ventilation due to limited chest wall expansion, structural changes in the lungs, and the air being obstructed. PaCO2 rises over time

Figure 1 shows the responses of alveolar gas composition and haemoglobin-oxygen (Hb-O2) saturation to various ventilation conditions. All comparisons between various ventilation patterns were found to be statistically significant. The p-values, raw experimental data (n=44), and absolute and relative changes can be found in the Appendix. The mean baseline values, indicating normal breathing, for PO2 were approximately three times the mean PCO2. The values were 108.75  9.56 mmHg and 42.04  5.75 mmHg respectively. The mean baseline value for %O2 saturation was 97.93  1.64 % (Figure 1). For breath-holding following hypoventilation, mean PO2 and %O2 decreased and PCO2 increased when compared to normal ventilation. The values were 79.19

Acute altitude sickness can last days and although it is not life threatening the symptoms can be incapacitating (Kenney, 2012). Symptoms can be seen anywhere from 6-48 hours after arriving at the high altitude and can range from headaches, vomiting, dyspnea (difficulty breathing), and nausea (Kenney, 2012). There are not many ways to avoid acute altitude sickness; however, ascending gradually to higher altitudes can help minimize the risks (Kenney, 2012). There is also a drug called acetazolamide that if started the day before ascent can be very effective. However, it must be used under medical supervision. On the more severe end of things, high altitude pulmonary edema (HAPE) is a very serious complication associated with high altitudes. HAPE is likely a result of pulmonary vasoconstriction resulting from hypoxia and causing blood clots to form in the lungs (Kenney, 2012). This mostly occurs in acclimated individuals who ascend to quickly above 2,500m (Kenney, 2012). Some symptoms include, shortness of breath, persistent cough, chest tightness, and excessive fatigue (Kenney, 2012). The risks for this can only be minimized through ensuring acclimation before ascending to higher altitudes. If a person does develop this they must be treated with oxygen and moved to a lower altitude to

The practice of administering inhaled high concentration oxygen to patients suffering chest pain is widespread, has been followed for about a century, and is advised in major textbooks of emergency care, general medicine, and cardiology. There remains an expectation amongst the general public and medical practitioners that oxygen simply forms part of the standard treatment of a ‘sick’ patient (Nicholson, 2004). A review of the evolution of supplemental oxygen therapy reveals that it is not evidence-based, and there is uncertainty about the benefits and safety. This paper will discuss the different approaches of the use of high concentration oxygen therapy for the client with acute chest pain, including previously conducted trials. The physiological benefits and harms, the variation in international guidelines and the need for future research will also be analysed.

Recent research shows that oxygen administration in higher concentration are not always necessary and can actually be damaging. It oxygen therapy is not deter mind properly, too much oxygen level causing hypoxemia and increase in reactive oxygen sepsis. At the same way too little o2 may cause tissue that hypoxia that can lead to some abnormalities such as lactic acidosis, confusion

This resulted in an “increase in CO2 elimination, respiratory acidosis, haemodynamic instability.” To control this the “ventilatory settings were adjusted to achieve a tidal volume of 480 ml, positive end-expiratory pressure of 5mmHg and respiratory rate of 14/min.” BP,

Oxygen saturation and pH levels are lowered during breath holding, while CO2 levels are increased. pH is lowered because carbon dioxide is the primary way that the body regulates blood pH, and when CO2 levels are high, there is an increase in carbonic acid in blood (Skow). Voluntary breath holding is affected by many factors such as practice, respiratory chemoreflexes, lung stretch, and psychology (Skow). All factors are processed by the respiratory center in the brain stem. These factors can either increase or decrease ventilation. Volitional control of higher brain centers and lung stretch will signal the respiratory center to decrease ventilation (Skow). Furthermore, decreased O2 levels and lower pH will signal the respiratory centers to