Pulmonary: Cellular Respiration

Which type of breathing resulted in PCO2 levels closest to the ones we experimented with in this activity – normal breathing, hyperventilation, or rebreathing? Hyperventilation

Respiratory acidosis is a condition closely related to patients with Chronic Obstructive Pulmonary Disease (COPD). According to Ranson & Pierre, respiratory acidosis is characterized by lab values including an increased amount of carbon dioxide (CO2) in the blood and a lower, more acidic pH level (2016). More specifically, a CO2 value greater than 26 mEq/L and a pH level below 7.35 (Ranson & Pierre, 2016). These lab values signify the lungs inability to effectively eliminate the CO2 produced by the body. In turn, this produces “more carbonic acid H2CO3, which then increases the acidity of the blood” (Wasserman, 2017).

These results are due to metabolic rates and the need for homeostasis which is driven by the production of CO2 (Mason, 2015). The results suggest that the values obtained in the normal ventilation condition for PO2, PCO2 and %O2 are consistent with the proposed values 100 mmHg, 40 mmHg and around 98% (Silverthorn, Johnson & Ober, 2013, p. 590). This is due to arterial gas composition being approximately equal to alveolar gas composition (Silverthorn, Johnson & Ober, 2013, p. 590). The breath-hold after hypoventilation condition resulted in an increased CO2 intake into the lungs due to breathing deeply. There was a decrease in PO2 and %O2 and increase in PCO2 as arterial PCO2 rose because metabolic processes continued without a new intake of air into the lungs. This disturbance of respiratory homeostasis hinders the ability to hold one’s breath (Mason, 2015). CO2 decreases pH of extracellular brain fluid, which stimulates central chemoreceptors, causing a break-point in breath-hold (Moreira, Takakura, Colombari & Guyenet, 2006). CO2 is detected very quickly in the blood (respiratory acidosis) by peripheral chemoreceptors (carotid and aortic bodies) (Miller, Cunningham, Lloyd & Young, 1974). The respiratory centre is controlled by chemoreceptor response, which then re-establishes respiratory homeostasis, by inducing a change in ventilation (Haldane & Priestley, 1905). However, the hyperventilation pattern, which involved shallow breathing, caused an increase in PO2 due to greater accumulation rate of O2 and larger O2 store in the lungs. A reduction in arterial PCO2 and increased expiration of CO2, increased %O2, which explains why there was a reduction in PCO2 (Lindholm &

Control centers: the medulla oblongata and neural circuits establish a person’s breathing rhythm that gathers information from the internal environment to coordinate breathing based on the body’s need for oxygen. To accomplish this, the sensors in the medulla monitor the pH of the cerebrospinal fluid to indicate the concentration of carbon dioxide in the body. A normal pH is about ~7.4. When the blood pH falls below this range, the medulla’s sensors detect a low pH in the cerebrospinal fluid and blood. This cause the ribs and diaphragm to increase their rate of rate of ventilation, causing the carbon dioxide level in the blood to fall and raising the blood and cerebrospinal fluid pH once again. The higher the carbon dioxide level, the more hydrogens that are present in a substance, causing its pH to

The PETCO2 is even more useful if its relationship to PaCO2 can be established initially by blood gas analysis. If the gradient between arterial and end tidal carbon dioxide partial pressures, P(a-ET)CO2 is stable with time, changes in treatment and clinical conditions, then PETCO2 can be reliably used to follow respiratory acid-base status and assist in the titration of hyperventilation therapy, at the same time decreases the expense and time involved in frequent ABG sampling.

The overarching goal of this experiment was to measure respiratory volumes and capacities using spirometry (Marieb & Smith, 2016). Spirometry is a technique which makes use of a device known as a spirometer in order to determine values for inspiratory reserve volume, tidal volume, expiratory reserve volume, as well as others, and thus has a practical use in the fields of anatomy and medicine (Marieb & Smith, 2016). Consequently, since this experiment deals extensively with the processes involved in respiration, it is essential to have a sufficient level of background information on the anatomy and physiology of the lungs (Marieb & Smith, 2016). The lungs are an essential part of the respiratory system, since their main purpose is to perform

In this paper I will be discussing the effects of respiratory acidosis on the body. More specifically, I will be discussing these effects in the relation to Asthma. I will describe the anatomical changes and pathophysiology of the disease, explain how it effects elimination of carbon dioxide from the airway, state the physiological compensation mechanisms and relate this condition back to respiratory acidosis and its effect on the body.

The pH of the blood is normally 7.35 to 7.45 it only takes a small change in the pH of the body to cause severe injury or death. The higher the pH the more alkaline the blood. When the oxygen and carbon dioxide change at high altitudes, the bodies system adjusts to regulate carbon dioxide while maintaining the correct pH in the body. Substances in blood plasma react with the excess carbon dioxide this increases the rate and depth of breathing to speed up the rate at which carbon dioxide is removed from the bloodstream. Breathing exchanges oxygen and carbon dioxide between the body and the environment. Carbon Dioxide is fundamentally a waste product of the body. The level of C02 in the blood is the most significant stimulus on the regulation

Hyperventilation is a rapid breathing, an increased in alveolar ventilation and decrease in metabolism. It occur when greater amount of carbon dioxide are removed from the blood stream than the body can produce, meaning more carbon dioxide been breath out (Bell & Rhoades, 2012). As shown in the result (figure 1, 2 & table 1), hyperventilation compare to normal breathing increase mean PO2 and Hb-O2 saturation, decrease mean PCO2. This is because when alveoli ventilation double, metabolic CO2 decrease, PCO2 will be lower than normal. PO2 have the opposite effect. During hyperventilation, more fresh oxygen is delivered to the alveoli than the blood, as a result this will increase PO2 in the blood (Sherwood, 2013). PO2 had increase rapidly because

CO2 and O2 levels are monitored in the body by central chemoreceptors and peripheral chemoreceptors. These two receptors are sensitive to changes of CO2 and O2 which stimulate ventilation rate and depth. Central chemoreceptors are located in the brainstem, specifically on the ventrolateral areas of the medulla. The central chemoreceptors main function is to maintain levels of arterial CO2 (Pathway). Arterial CO2 is normally 40mm Hg and is kept within a +/-3 range by highly sensitive central chemoreceptors (Marieb and Hoehn 842). The central chemoreceptors are stimulated by changes in the pH of the surrounding cerebrospinal fluid of the brainstem. Central chemoreceptors do not readily respond to changes of arterial pH because of the blood

The point when the subjects breath-hold after hypoventilation and breath-hold after hyperventilation ‘broke’ their breath hold was at pO2; 80mmHg and 60mmHg respectively. This value is significant (p=5.12e-16). It indicates that oxygen levels do not control ventilation, as the results were completely different when the subjects broke breath-hold. Oxygen levels have not decreased to the trigger values so chemoreceptors would not have been a driving force for the subject to breath normally. Hyperventilation greatly increased the length of breath-hold by roughly three times longer, yet the pCO2 did not

Respiration rate is one of the main vital signs used in all clinical settings. An increased respiratory rate is an important predictor for

“Bicarbonate infusion and pH clamp moderately reduce hyperventilation during ramp exercise in humans”, executed and written by Francois Peronnet, Tim Meyer, Bernard Aguilaniu, Carl-Etienne Juneau, Oliver Faude, and Wilfried Kindermann was first published on September 7th, 2006. The purpose of the study was to test and determine if the decrease in plasma pH contributes to the hyperventilation observed in humans in response to high intensity workload. During the experiment, the plasma pH was the vocal point of this experiment where five healthy male subjects preformed a ramp exercise. The experiment was done to see if the reduction in plasma pH and the development of exercise hyperventilation is conclusive data to the hypothesis that says, “...Hyperventilation is a ventilatory compensation of the metabolic acidosis that develops at high workloads and could be triggered, at least in part, by the reduction in plasma pH.” (Journal of Applied Psychology) The plasma pH and the hyperventilation from exercise were the main focuses of the experiment and the end results data suggest that the decrease in plasma pH is one of the factors that contribute to the hyperventilation observed at high workloads. In the conclusion of the experiment, in the control situation, plasma pH decreased greatly below resting value and reached 7.270 at the conclusion opposed to 7.414 at a resting position. However, pH

O B J E C T I V E S 1. To explain how the respiratory and circulatory systems work together to enable gas exchange among the lungs, blood, and body tissues 2. To define respiration, ventilation, alveoli, diaphragm, inspiration, expiration, and partial pressure 3. To explain the differences between tidal volume, inspiratory reserve volume, expiratory reserve volume, vital capacity, residual volume, total lung capacity, forced vital capacity, forced expiratory volume, and minute respiratory volume 4. To list various factors that affect respiration 5. To explain how surfactant works in the lungs to promote respiration 6. To explain what happens in pneumothorax 7. To explain how hyperventilation,

Respiratory Acidosis occurs when the lungs cannot remove all the carbon dioxide that the body makes. In turn this makes fluid in the body become too acidic. The distinctive feature of respiratory acidosis is an abnormally high PCO2, meaning above 45 mmHg. Improper exhalation of oxygen can cause the blood pH to drop.” Any condition that decreases the movement of CO2 from the blood to the alveoli of the lungs to the atmosphere causes a buildup of CO2, H2CO3, and H+ (Tortora, 2014, p.1036)”. Symptoms of this condition may include: confusion, lethargy, fatigue, sleepiness, and shortness of breath. Probable causes are: obesity, disease of the chest, diseases of the lungs and airways, and drugs that suppress breathing (MedlinePLus, 2012). A health care provider will perform a physical exam to see if this is what is happening. He may do so by: arterial blood gas which measures oxygen and carbon dioxide levels in the blood, basic metabolic panel, a chest x-ray, or possibly a pulmonary function test (MedlinePLus, 2012). Treatment is mainly aimed at the underlying cause not at condition itself. It is treated