The Human Respiratory System Yuki Yang Aug.14, 2012

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1 The Human Respiratory System Yuki Yang Aug.14, 2012

2 Introduction The human respiratory system is responsible for gas exchange between the environment and body tissues.(sherwood,461) The organs involved in the system are the nose, trachea, lungs (including airway passages, gas exchange surface, and alveoli), and diaphragm. Respiration includes two types: internal and external. Internal respiration refers to the metabolic processes of the mitochondria as the cells respire. External respiration is the whole process of exchanging O 2 and CO 2 between the external environment and the body cells. The act of ventilation is performed when the air goes in and out of the lungs. Many factors can influence and regulate the rate of ventilation according to the body s needs for O 2 uptake and CO 2 removal. The pressure gradient between the lung capacity (alveolar and intrapleural) and the atmosphere allows for breathing or ventilation. Air flows from the region of high pressure to low pressure. Inhalation occurs when the intra-alveolar pressure is lower than the atmospheric pressure. During inhalation, the rib cage expands, lung muscles stretch, and the diaphragm contracts (goes down), allowing air to move in the lungs. During exhalation, the muscles and the diaphragm relax, the elastic recoil property of the lungs raises the alveolar pressure above the atmosphere, and the air moves out of the lungs. The airway branches into bronchi that enter the left and right lungs. (Sherwood, 464) Within the lungs, they continue to branch into bronchioles, and the clusters of end terminals are called the alveoli. The first sixteen generations, which are called the dead space of the branching airway, do not participate in air exchange. Several kinds of volumes are investigated in lab. The tidal volume (TV) is the volume during normal breathing. (Sherwood, 480) The inspiratory reserve volume (IRV) is the

3 volume above the TV that can be breathed in during a forced inhalation. The expiratory reserve volume (ERV) is the volume beyond the TV that can be expelled during a forced exhalation. The residual volume (RV) is the minimum volume that the lungs can hold to prevent collapse. The total lung capacity (TLC) is the total volume of air that the lungs can hold. Therefore, TLC=RV+ERV+TV+IRV. The functional residual capacity (FRC) is the volume remained in the lung after a normal expiration. FRC=ERV+RV. The vital capacity (VC) is the volume of air after a maximum inspiration and expiration. VC=ERV+TV+IRV. The goals of this experiment are to measure the static lung volume of a subject; to examine the effects of gas composition on respiratory mechanics and length of breath-holds; and to examine of effects of exercise workloads on ventilation. In part 2 of this experiment, the percent CO 2 is expected to increase after breath-hold. The re-breathing CO 2 content is expected to be higher than for normal breathing, and the hyperventilation CO 2 content is expected to be lower. The shorter breath-hold the higher the percent CO 2 is expected to be. Breath-hold duration is expected to decrease for respiration types in this order: forced inhalation, normal inspiration, normal expiration, and forced exhalation. In part 3 of this experiment, TV, RR (Respiration Rate), V E (minute ventilation), and Minute CO 2 production are expected to increase with increasing workload in comparison to the at-rest condition. The end-tidal CO 2 is expected to be constant. However, these responses can vary to match O 2 consumption and CO 2 removal needs. Materials and Methods The subject of this experiment was a 20-year-old male. We measured the static lung volumes using the spirometry station with the subject s nose clipped. (Bautista et al., 2009)

4 Normal breathing gave us the TV, inhaling deeply gave the IRV, and exhaling deeply gave the ERV. For normal breathing, we measured the CO 2 content of normal breathing before and after a normal deep breath was held for as long as possible. For re-breathing, we measured the CO 2 content before and after a deep breath was held after breathing into a plastic bag for a 3-minute period. CO 2 measurements for the hyperventilation condition were taken before and after a deep breath were held after a deep breathing period (at normal rate) of 2-4 minutes. The length of breath-hold was also recorded for these three ventilation conditions. We also measured the duration of breath-hold for four types of ventilation: normal expiration, normal inspiration, forced inhalation, and forced exhalation. For the last part of the experiment, we increased the subject s workload from at-rest, to 0.0, 0.5, 1.0, 1.5, and 2kPa by adjusting the workload on a stationary bicycle. We recorded TV, RR, and CO 2 content using the Biopac software on the computer. Details about the materials/methods can be found in Experiment 6 in the lab manual. Results The static lung volumes of a 20-year-old male with a normal breathing TV of 0.46L. A volume of L was inhaled during a deep inhalation, and 0.19L was exhaled during a forced exhalation. Volume IRV ERV 0.19 TV 0.46

5 Duration of Breath-Hold(sec) % CO2 VC Table 1. Static lung volumes of a 20-year-old male. Measured TV during sedentary normal breathing. IRV was measured during a deep inhalation. ERV was measured during a deep exhalation. VC was measured from the peak of maximum inhalation to the trough of maximum exhalation. RR of 14 breaths/min was recorded. Percent CO 2 and breath-hold durations of a 20-year-old male subject under 3 ventilation types. The CO 2 content is greater after the breath-hold for all types of ventilation. Re-breathing has the highest CO 2 content (5.65%) and shortest breath-hold (24 seconds) while hyperventilation has the lowest CO 2 content (2.98%) and longest breath-hold (48 sec). The higher the CO 2 content, the shorter the breath holds. 6 Ventilation Type vs. %CO Normal Re-Breathing Hyper 1 0 %CO2 before %CO2 after Ventilation Type vs. Breath-Hold Normal Re-Breathing Hyper Ventilation Type Figure 1. Percent CO 2 and breath-hold durations of a 20-year-old male subject under 3

6 Duration of Breath-Hold(sec) ventilation types. CO 2 content was measured before and after breath-hold for 3 types of ventilation, and duration of breath-hold was recorded. The breath-hold duration of a 20-year-old male for 4 types of lung volume. Inhalation breath-hold is longer than that for exhalation. The highest duration (54.1 sec) was recorded for forced inhalation. The lowest (12.9 sec) was recorded for forced exhalation Static Lung Volume vs. Breath-Hold 10 Normal Inspiration Normal Expiration Forced Inhalation Forced Exhalation Lung Volume Type Figure 2. A graph of breath-hold duration (in sec) of a 20-year-old male subject for 4 types of lung volume. The ventilation response for a 20-year-old male subject under different exercise conditions. The TV, RR, V E, and Minute CO 2 increased as the workload increased. FE CO2 fluctuated from around 4.7% to 6.5%. An unexpected increase of 1.46% in FE CO2 was measured at workload 0.5kPa.

7 Minute CO2 VE(L/min) FE CO2 TV(L) RR(breath/min) Workload vs. TV Workload(kPa) Workload vs. RR Workload(kPa) Workload vs. VE Workload(kPa) Workload vs. FECO Workload(kPa) Workload vs. Minute CO Workload(kPa) Figure 3. Parameters of a 20 years old male subject at workloads of rest (-0.5), 0, 0.5, 1, 1.5, 2 kpa. Subject exercised at each for 2 min. A. TV B. RR C. VE D. FE CO2 E. Minute CO 2 Discussion In Part 1 of this lab, minute ventilation was calculated as TV (tidal volume) times RR (respiration rate), and it indicates the volume of air that moves in and out of the lungs per minute. However, to better estimate the volume of air that actually participates in the

8 exchange (alveolar ventilation, V A ), the volume of dead space needs to be considered. To calculate the V A, the volume of dead space needs to be subtracted from the minute ventilation. (Sinha et al, 2011) Detailed calculations of the subject s static lung volume can be found in the section titled Calculation. Figure 1 shows that the percent CO 2 after breath-hold for all types of ventilation is higher than before breath-hold. This is consistent because while the breath was held, the CO 2 had more time to build up in the body, and therefore the CO 2 content was higher for after. Re-breathing had the highest CO 2 content because the subject had breathed the same air in a bag for 3 minutes. When there was no fresh air to breathe in, the subject was only taking up the O 2 from the air in the bag, and with each breath the CO 2 content built up. The bag contained a high concentration of CO 2, explaining the results for re-breathing whether before or after the breath-hold. With hyperventilation, since the subject breathed in more O 2 than needed, the body content of CO 2 was relatively lower than for normal breathing. The CO 2 content for re-breathing and normal ventilation after breath-hold was considered to be similar (~0.8% difference) because of the concept of CO 2 threshold, which refers to the % CO 2 that the body can hold before inhalation is initiated. So once the CO 2 threshold was reached, the subject couldn t hold the breath anymore and started to inhale. Hyperventilation had the lowest %CO2 to start off with; it takes longer for CO 2 to accumulate and therefore it has a longer breath-hold than normal breathing (48 sec). In contrast, re-breathing had the highest %CO 2 at the beginning; it took less time (24 sec) to build up the CO 2 content and therefore it had a shorter breath-hold than for normal breathing. Another explanation was presented by Michael J. Parkes in the article The Limits of Breath Holding.

9 He says that the diaphragm plays an important in how long a breath can be held. By synthesizing several studies about breath holding, he concludes the best hypothesis is that the diaphragm sends signals to the brain about the level of discomfort as the breath is being held and the fatigue of the diaphragm (indicated biochemically by the level of O 2 and CO 2 ; a rising O 2 level and a lowering CO 2 level can reduce the biochemical indicators of fatigue). When the brain receives the signals to an intolerant level, breathing starts again. (Parkes, 2012) In the human body, there are chemoreceptors that control breathing. Peripheral chemoreceptors mainly sense the arterial P O2. When they sense the P O2 has severely dropped (like 60%), they are activated and cause an increase in the ventilation rate to let the P O2 go back to normal. Central chemoreceptors are located in the brain and sense the cerebral P CO2 and ph. The CO 2 is able to cross the brain barrier to the extracellular fluid. With the bicarbonate reaction CO 2 +H 2 O <-> H 2 CO 3 <-> H + +HCO - 3, the H + ion increases in the fluid as the CO 2 content increases, and the ph drops. When the central chemoreceptors sense the drop in ph, they are activated to increase the ventilation rate in order to decrease the concentration of CO 2. In Figure 1, the hyperventilation after breath-hold is less than for re-breath. It could be that the peripheral chemoreceptors have been activated since hyperventilation has driven the O 2 content to be so high, and the sudden drop in O2 (breath-hold) is sensed by the peripheral chemoreceptors and the body functions to breathe in. When the breath is held, normal and re-breathing ventilations are regulated by central chemoreceptors. Since the CO 2 content is building up in the cerebral fluid, the concentration of H + increases and ph decreases. The central chemoreceptors sense the decrease in ph and

10 initiate inhalation. In the study Intracellular Acidosis and ph Regulation in Central Respiratory Chemoreceptors by C.R. Marutha Ravindran et al. investigated the importance of central chemoreceptions in respiration by studying the brainstem of tadpoles with different conditions of CO 2. They concluded that the dysfunction of the central chemoreceptors can lead to sudden death since they are quick to detect acidification of the blood (decrease in ph), and drive inspiration. A failure to respond to the high CO 2 content could lead to low O 2 concentration and result in death. (Ravindran et al., 2011)[3] There are stretch receptors in the lungs which sense the stretch of lung muscles. When increased stretch is sensed, the Hering Breuer Reflex is activated. The receptors inhibit the inspiratory neurons and reduce the drive to inhale. At that moment, the breath can be held longer. In Figure 2, the most stretched lung volume is forced inhalation. IRV amount of air is inhaled and the stretchiness leads to the longest breath-hold (54.1 sec) in the experiment. In contrast, forced expiration has no stretch on the lungs since ERV of air is exhaled and all the muscles are relaxed. Because of no stretch, inspiratory neurons are not inhibited and body wants to inhale. Therefore, breathes cannot be held for a long time. The function of stretch receptors has been confirmed since 1933 by E.D. Adrian in the study Afferent Impulses in the Vagus and Their Effect on Respiration by studying the cat s vagus nerve and central nervous system. Recent study Madoulation of the Hering-Breuer Reflex by raphe pallidus in rabbits by YanChun Li et al. suggests that the raphe pallidus (RP, one of the subnuclei of raphe nuclei complex) has some respiratory effects by adjusting the strength of HB reflex. They investigate this by comparing the strength of HB reflex on anesthetized rabbits before and after the stimulation of RP. The conclusion is that activations of RP can weaken HB reflex;

11 suggesting the respiratory regulation can be influence by many factors.(li, 2005) Figure 3 shows an increase in TV, RR, V E, and minute CO 2 as the workload increases. This is consistent that human s need for O 2 increases when they are exercising. TV and RR match (goes up) to meet the need for O 2 consumption and CO 2 removal. When TV and RR go up, a larger amount of O 2 will be inhaled more rapidly. So O 2 consumption and CO 2 removal (Minute CO 2 ) will go up also. However, the end-tidal CO 2 (FE CO2 ) is expected to be constant since the CO 2 content for every breath will not change. The body is expected to remove the same amount of CO 2 for every breath. To meet up the need of high CO 2 removal, RR would be higher to remove more CO 2. The unexpected increase in FE CO2 at the workload of 0.5 to 1.0 kpa might be explained by the constancy of TV at the same workload range. When TV doesn t increase and RR is almost constant, more CO 2 stays in body and the only way to remove the CO 2 is to increase CO 2 content for each breath. The ventilatory responses to hyperpnea (exercise) remain unclear. Many studies have been done to suggest possibilities about the ventilatory responses. The review Layers of Exercise hyperpnea: Modulation and Plasticity by Gordon S. Mitchell and Tony G. Babb suggests the idea that the modulation and plasticity of bodies contributes to the exercise ventilatory responses. They present evidence from a goat model of hyperpnea in regards to the modulation and plasticity and conclude that the modulation and plasticity work together to let the body adapt the exercise ventilatory response. For example, the physiological conditions may change during exercises; the body has to change ventilatory responses to maintain the regulation of arterial blood gas. However, the researchers still believe there are many layers of mechanism to the ventilatory responses. (Mitchell, 2005)[4] This idea is consistent that bodies will adjust responses to

12 match the conditions changed by exercises. Further study might need to be done to prove that. Citation 1. Sherwood, Lauralee. Human Physiology, From Cells to Systems,Seventh Edition. Canada:Yolanda Cossio, Bautista, Erwin; Korber, Julia. NPB 101L, Physiology Lab Manual. Second Edition. United States of America: Micheal Stranz, Sinha, Pratik; Flower, Oliver; Soni, Neil. Deadspace ventilation: a waste of breath! National Hospital for Neurology and Neurosurgery, Yniversity College London Hospitals NHS Foundation Trust Ravindran, C.R. Marutha; Bayne, James N.; Bravo, Sara C.; Busby, Theo. Intracellular Acidosis and ph Regulation in Central Respiratory Chemoreceptors. Journal of Health Care for the Poor and Underserved, Volume 22, Number 4, November Parkes, Michael J. The Limits of Breath Holding. Scientific American. Apr Adrian, E.D. Afferent Impulses in the Vagus and Their Effect on Respiration. Physiological Laboratory, Cambridge Li, Yanchun; Song, Gang; Cao, Ying; Wang, Hui; Wang, Guimin; Yu, Shuyan; Zhang, Heng. Modulation of the Hering-Breuer Reflex by Raphe Pallidus in Rabbits. Laboratory of Respiratory Neurobiology, Institute of Physiology, School of Medicine, Shandong

13 University Mitchell, Gordon S.; Babb, Tony G. Layers of exercise hyperpnea: Modulation and plasticity. Science Direct Calculation: Part 1: V E =TV x RR 0.46L x 14 breaths/min=6.44l Subject s weight: 175lbs ~ DS: 175mL =0.175L V DS = DS x RR 0.175L x 14 breaths/min=2.45l V A = V E -V DS 6.44L 2.45L = 3.99L Part 3: V E =TV x RR Minute CO 2 =V E x FE Rest: 0.713L x 16 br/min = Rest: L/min x 5.7% = % L/min

Observations of the Properties of the Human Respiratory System. April Ramos Dela Fuente. Bill Keenen; Tommy Kham; Grace Park

P a g e 1 Observations of the Properties of the Human Respiratory System April Ramos Dela Fuente Bill Keenen; Tommy Kham; Grace Park NPB 101L - Section 06 - Ailsa Dalgliesh 11/25/14 P a g e 2 INTRODUCTION