Explain The Four Stages Of Hypoxia

A low partial pressure of oxygen (PaO2) suggests that a person is not getting enough oxygen; Metabolic acidosis->Kidney failure, shock, diabetic ketoacidosis

because the higher someone goes there more spaced out the oxygen molecules are. Dalton’s Law states “The human body is affected by the pressure of gases available, meaning as someone is acceding the percent of oxygen remains constant but there are fewer molecules the higher someone is” (Reinhart). Since there are fewer molecules the body becomes starved of oxygen and then the effects of hypoxia begin to develop and the first symptoms will begin to develop. This is where machines will come in to help the human body survive. However, the human body is great at adapting to environments below 10,000 feet. It can handle the oxygen differences well enough on a nonsmoking person and during the day to not need a machine to avoid hypoxia. However above 10,000 feet the human body reaches a point where it can no longer adapt to the lack of oxygen. When hypoxia begins to take over the brain, it is an urgent matter. If someone is suffering from hypoxia it is important to notice the symptoms rather quickly, especially if they are navigating the aircraft. Some of the first warning signs that can be seen are confusion, slurred speech, headache, lightheaded sensation, dizziness and incomplete sentences. An air traffic controller would have to pay attention to these signs if they suspect

Both rapid, shallow breathing patterns and hypoventilation effect gas exchange. Arterial blood gases will be monitored and changes discussed with provider. Alteration in PaCO2 and PaO2 levels are signs of respiratory failure. Patient’s body position will be properly aligned for optimum respiratory excursion, this promotes lung expansion and improved air exchange. Patient will be suctioned as needed to clear secretions and maintain patent airways. The expected outcome is that the patient’s airway and gas exchange will be maintained as evidence by normal arterial blood gases (Herdman,

The Ventilatory threshold was reached at 5 minutes or stage 3 for patient 92 C. The ventilatory threshold is important because it indicates the point at which the blood lactate acid increases non-linearly. It indicates that there is an increase in the lactate acid level in the blood as well as the excess carbon dioxide (Kenny et al., 2015). The increase in carbon dioxide will stimulate chemoreceptors to increase ventilation. The ventilatory threshold is related to the anaerobic threshold which refers to the increase in carbon dioxide and indicates that the body has shifted towards anaerobic metabolism (Kenny et al., 2015).

8. Some people may be in one stage for such a short time that it seems as if they skipped that stage. Some times the person returns to a previous stage. According to Kubler- Ross, the five stages of dying are:

Another follow up ABG at 0100 shows a small improvement on the Ph to 7.18, the Pco2 became more acidotic moved to 53, the Po2 improved to 77 which shows he is oxygenating better but still hypoxic, his Hco3 acidosis is improving at a change to 19.8, and sating 91% now. The Pt is now breathing at a rate has come down to 10 BPM on his own above and beyond the vent. After consulting with the physician we changed the Vt to 600 and the pressure support to 20 and Cpap to 15. The Pt continued on these settings till 0415. The physician then made the change to Bi-level with the settings of a rate of 14 pressure support of 25, and an H/L pressure of 35/15. The Pt at this time is pulling a Vt of 745 and a spontaneous rate of 17 and still at 100% Fio2 and sating 92%. This is the point when the Pt makes the turn. The Bi-level or APRV was the proper setting for this Pt. He continued to improve over the next several days with his peek pressure climbing to 40. The Pt continues these settings and slowly improves and eventually weaned from the ventilator till the Pt no longer needs support.

Assessment: the patient 's vital signs are 108/68, 125 beats per minute, respirations, even and non-labored at 14 breaths per minute, 92% on 2 liters of oxygen via nasal cannula, afebrile 98.5 F.

Hypoxaemia can result when there is inequality in alveolar ventilation and pulmonary perfusion (V/Q mismatch). V/Q mismatch is the most common cause of hypoxia in critically ill patients. It is caused by intrapulmonary shunting of blood resulting from airspace filling or collapse. Findings include dyspnea and tachypnea. Diagnosis is by ABGs and chest x-ray. Treatment usually requires mechanical ventilation.

Hypovolemic shock is the result of whole blood loss, and plasma or interstitial fluid loss in large amounts. Moreover, hypovolemic shock begins when the intravascular volume decreases by approximately fifteen percent. The pathophysiology of hypovolemic shock includes both the heart rate and SVR increasing. As a result cardiac output and tissue perfusion pressures are boosted and interstitial fluid moves into the vascular compartment. Also, both the liver and spleen boost the body’s blood volume by disgorging the stored red blood cells and plasma. In the kidneys, renin prompts the release of aldosterone and also the retention of sodium. Whereas, ADH that is from the posterior pituitary gland surges water retention. In addition, if the initial

At extreme altitudes, sleeping becomes very difficult, digesting food is near-impossible, and the risk of HAPE or HACE increases greatly. HACE may include profoundly inhibited mental function, hallucinations, loss of muscle coordination, impaired speech, severe headache, nausea or vomiting and coma. HAPE may include extreme difficulty breathing, very rapid breathing rate, exhaustion, lack of motivation, pale complexion, constant coughing and gurgling sounds coming from chest. The death zone, refers to altitudes above a certain point where the amount of oxygen is insufficient to sustain human life. This point is generally tagged as 8,000 m (26,000 ft). Any time that the temperature is below -4°C (25°F), skin's freezing point, people are at risk

Respiratory rate may increase with the presence of interstitial pulmonary process or chest wall restriction, but tidal volume typically remains unchanged. The presence of slow, gasping ventilatory maneuvers is an ominous sign suggesting cerebral hypoxemia.

With this person I feel he has the symptoms of what is called decompression sickness (DCS) this being a result from when he went scuba diving and then getting on a flight. For starters the person from being so deep in the reef, and where a good amount of gases went into his bloodstream when he was diving. After returning above the water his body did not have time to decompress the gases from his lungs. Meanwhile once the person boarded the plane and with the different altitudes within a short period of time. Taken in consideration of comparing to the sea level and the plan where the pressure was different. From the two different oxygen level places and then being on the plane with realizing there will be a decrease of pressure. With a

It is interested that you chose to highlight Altitude Sickness, a condition that is rarely discussed. Symptoms occur in three stages that range from mild to severe. Altitude sickness can affect anyone who goes to high altitudes without giving the body time to adjust to the changes in air pressure and oxygen level. The more rapidly a climb to high altitude, the more likely that altitude sickness will develop. Altitude sickness also is more likely to develop when climbs are more difficult and take more energy, compared with a slow and easy climb ( Cleveland Clinic Foundation, 2013). Patients presenting with severe symptoms related to Altitude Sickness are predisposed to respiratory acidosis due to the increased elimination of hydrogen ions and

Hypoxia tolerance usually depends on individual basis varying with physical fitness, fatigue, lack of sleep, lack of exercise, history of smoking or any active or recent illness. Airplane cabins are routinely pressurized at 5,000 to 8,000 feet leading to an ambient environment of hypocarbic hypoxia [5-7]. This exposure increases rate of ventilation due to sensing by peripheral receptors, leading to a reduction in partial pressure of carbon dioxide. This in turn, can have an inhibitory role on ventilation leading to development of hypoxia. Hypobaric hypoxia also stimulates vasodilation and subsequent hemodynamic adjustments cause increased sympathetic activity [8, 9]. In normal healthy individuals, this increased sympathetic activity is associated with parasympathetic withdrawal. However, in individuals experiencing airline syncope, there is abnormal parasympathetic activation with reflex bradycardia likely mediated by Bezold-Jarisch reflex [4,10] which is further compounded by hypocapnia, cerebral vasoconstriction and reduced cerebral blood flow [11]. Other factors loosely associated in promotion of hypoxia in these individuals include immobility, drowsiness, gastrointestinal distention and a high cabin temperature

It is known that as altitude increases, atmospheric pressure decreases, as does the partial pressure of oxygen (Hall Table 44-1). That same table demonstrates that the partial pressures of both oxygen and carbon dioxide in the alveoli decrease as well. However, the alveolar water vapor pressure remains unchanged—constant at 47mmHg no matter the altitude (Hall 561). The most deleterious result of these factors is that less oxygen is being delivered to the tissues. Fortunately for me, Guyton and Hall says that altitude has a relatively insignificant effect on arterial oxygen saturation at 9,000ft (Hall Figure 44-1). It is not until 10,000ft that arterial oxygen saturation begins to steeply decline. The physical affects of acute hypoxia according to Hall are “drowsiness, lassitude, mental and muscle fatigue, sometimes headache, occasionally nausea, and sometimes euphoria. These effects progress to a stage of twitchings or seizures above 18,000 feet and end,