Effect of Alveolar Ventilation on Breath Hold Duration, O2 and Co2 Concentration - Research Paper Example

Table of Contents TITLE: 1 Introduction 1 Method 2 Results 4 Discussion 5 Conclusion 7 Appendix 1. 8 Table1: 8 Descriptive Statistics of table 1 10 Table 1 Graph a. GRAPH OF THE DATA ANALYSED OF TABLE 1 10 Appendix 2: 12 Table 1:TABLE SHOWING THE EXPERIMENT ON BREATHING OXYGEN UNDER DIFFERENT ENVIRONMENT 12 Descriptive Statistics of table 2 13 Table 2 Graph I: 14 Table 2 Graph II. 14 Appendix 3 15 DIAGRAM 18 References: 19 TITLE: EFFECT OF ALVEOLAR VENTILATION ON BREATH HOLD DURATION, O2 AND CO2 CONCENTRATION Introduction During inspiration, the first gas that goes into the alveoli is alveolar gas from the previous breath which is usually in the dead space. This dead space maybe the bronchi and trachea. This is the followed by a room air. In a normal inspiration, the air in the alveoli has equilibrated with the gases in the blood vessels and the composition of alveolar air and almost looks like the one in the arterial blood as far as gas partial pressure is concerned. During expiration, the gas breathed out is dead space gas followed by a mixture of dead space gas and alveolar gas. At the end of expiration therefore, the composition of the gas from the alveoli is a reflection of the blood gas composition. This therefore means that, through an experiment, alveolar gas can be sampled only at the end of expiration. This experiment was out to depict how alveolar ventilation affects alveolar gas composition and oxygen saturation and the duration of breath hold. However, the effect of ventilation gas composition is very complicated bearing in mind that, only a portion of the atmospheric air in each tidal expiration gets to the alveoli and air from the alveoli makes up only a part of the tidal expiration (Cahalin 2002). This therefore entails that the effective ventilation, which is commonly referred to as the alveolar ventilation is the difference between the total amount of gas moved during ventilation and the gas that only ventilates the dead space (Thomas, McKinley & Foy 2001).The experiment therefore aims at determining the effect of alveolar ventilation on O2 concentration, CO2 concentration and the duration of breath hold after a disturbance of ventilation. It is hypothesized that the longer the duration of breath hold, oxygen concentration reduces Method The samples sizes are well indicated in the appendices The subject sat in a chair not facing the computer screen and a mouth piece was labeled with their names An Oximeter was placed on a finger tip and the subject was advised not to make any hand movement. The oximeter measured the oxygen saturation of hemoglobin in the blood. To get the tidal volume sample, subjects we instructed to breathe through the mouthpiece over a tube which was connected to a gas analyzer that was measuring the amount of carbon dioxide and oxygen present in a breath sample. The measurements were continuous The gas values were then read from the trace at the appropriate time and the partial pressure of CO2 (PCO2) and PO2 appeared on the monitor measured in mm Hg. The subject was the advised to hold breathe at the end of a normal inspiration. This was to ensure that O2 stores are not over filled, and hold the same as long as they can as the breath hold is being timed. The onset of the breathe hold were marked on the computer and then the duration can be read off the monitor. The subject were advised to take note of the amount of air the breathed in and how they were feeling when they had to take a breath. Over breathing- the subject was asked to breathe deeply for like 1-2 minutes until they begin to feel light headed. The gas composition was analyzed at the end of a normal expiration. Any symptoms that the subject felt were recorded, and asked to note the degree of light headedness. Over breathing and breath holding – subjects hyperventilated as before, to the same degree of symptoms and then hold their breath at the end of a normal inspiration. Same breath as had earlier taken. Held the breath for as long as they can, then the gas composition was analyzed at the end of the first expiration. Results The results of the experiment are indicated in the appendices. Table 1 showed the relation of the airway obstruction and breathing duration over a maximum PCO2. Table 2 showed the relation of breathing room air with the mask put on over breathing pure oxygen without the mask. Table 3 showed the relation in normal breathing and over breathing with the duration of holding the breath. The Sample size was 48 study subjects. The mean scores are indicated in appendix in the descriptive statistics of table 1. Also the standard deviation is also provided for all the variables in the same table as the mean. The p- value is also provided with comparison of the level of significance where the level of confidence ranges at a confidence of 95 percent. The Sample size of the population was taken to be a total of 38 people who were the study subjects in the experiment. All the means are in the appendices table 2 in the descriptive statistics table 2. Table3 shows the results of the ventilation pattern when individuals were made to breathe normally and overbeating. Discussion The results were consistent with the hypothesis that we provided at the start of our experiment, different ventilation modification caused changes in alveolar gas composition. The PO2 result for normal breathing was higher than the PO2 when the breath was held. During breath-hold, metabolisms occurred and the amount of oxygen reduced and these made it lower the concentration of oxygen in the tidal gas. After over-breathing, PO2 was increased to higher volume since the more air was breath into the alveoli’s and the oxygen in the dead space was forced towards the bronchioles. The airway obstruction was kept constant. When breath was held after over breathing this brought an effective change in the pressure difference was detected as shown in the tables and graphs in the appendix. We understood that carbon dioxide has a high level of solubility than oxygen and this makes it oxygen to require a higher concentration gradient to provide adequate oxygen to the blood. Ventilation maintains alveolar airflow that is proportional to the pulmonary capillary blood flow (Meuret 2008). When there was kind of obstruction in the bronchioles and the trachea as when the mucus blocks the air, this results to low PO2 in the alveoli and causes the local arterioles to vasoconstriction. On the contrary the resulting high PO2 causes vasodilatation of arteries and more blood is brought closer to the alveoli for the pickup of oxygen which is in plenty. Also the bronchioles responded to the partial pressure of carbon dioxide which was in the alveoli. Excess carbon dioxide is exhaled by the effect of the dilating bronchioles (Raupach 2008). When the air flow is high in the trachea than the blood supply the partial pressure of Carbon dioxide dropped. From the results it’s a clear indication that change in pressure changes composition of the end tidal gas i.e. oxygen and carbon dioxide. There pressure difference also had a significance effect on the duration of breath hold (Nagler 2008). The potential errors we encountered were identified in the recording of the airway resistance column. There was an outlier which altered the consistency of the results. The problem could have been solved by having an accurate instrument to measure the airway resistance. This will enable correct recording of data and help in having a proper random sample to avoid bias. From the results, an increase in P02 can be said to be enhanced by low pulmonary oxygen diffusing capacity, and limited capacity to increase diffusion capacity when there is an activity. This is evident especially when the participants were told to hold their breath. Form the results, it is clear that, PCO2 and PO2 decreases on breath holding (Rassler& Kohl 2000) . This is attributed to the fact that, there was the lack of air or even oxygen. Hyperventilation reduces the carbon dioxide concentration in the blood below the level it is supposed to go because more carbon dioxide is expiring that it is being produced in the body. This on the other hand causes constriction of the blood vessels which supply the brain and prevents the transportation of oxygen. This therefore entails that, breath withdrawing causes the supply of oxygen in the body. In the same case, hypomania causes an escalation of the affinity of oxygen to hemoglobin reducing the oxygen which is of great importance in the brain causing light-headiness. This is exonerated in the graphs given below When Alveolar ventilation is reduced as a result of a reduction in total ventilation, the PCO2 increases because the gas in the alveolus is not being exchanged at the normal rate. This is depicted in the results of the experiment. From the results, it is clear that the PCO2 increase causes the PO2 to decrease (Moser 2006). This therefore connotes that, a decrease in alveolar ventilation leads to decrease in alveolar oxygen for the oxygen present in the alveolus is diffusing in the blood but the replacement is minimal. It is very clear that, from the results when alveolar ventilation is reduced and carbon dioxide production remains constant, then PCO2 must increase (Gashev 2002). Conclusion In conclusion the alveolar gas composition is composed of the oxygen and carbon dioxide. The alveolar ventilation affects the dropping of oxygen and increase of carbon dioxide. The results show that not all of the inhaled gases are taken to the alveoli. The trapped air mixes with the tracheal air and during clinical test the estimation is made to measure the mean alveolar gas concentration. From the hypothesis this explains the relationship between partial pressure and the concentration of gases and ventilation maintains the airflow in proper proportions due to changing atmospheric pressures. Hyperventilation reduces the carbon dioxide concentration in the blood below the level it is supposed to go because more carbon dioxide is expiring that it is being produced in the body. This on the other hand causes constriction of the blood vessels which supply the brain and prevents the transportation of oxygen. This therefore entails that, breath withdrawing causes the supply of oxygen in the body. Appendix 1. Table1: RESULTS OF EFFECT OF INCREASED PCO2, AIRWAY OBSTRUCTION ON BREATH DURATION Volume (L) Breath duration (sec) PCO2 maxium (mmHg) Airway Resistance (Low/High) Time (sec) 0.8 4 42.2 Low 0 high refers to airway obstruction 0.57 3.8 43.5 Low 4.1 0.58 3.8 44.6 Low 8 0.6 3.8 45.6 Low 11.9 0.75 4.1 46.4 Low 15.8 0.69 4.3 47.5 Low 19.8 0.87 4.5 47.8 Low 24.1 0.75 4.2 48 High 28.7 0.75 3.9 48.6 High 32.9 0.74 3.2 48.4 Low 36.9 0.71 3.4 48.9 Low 40.1 0.71 3 48.8 Low 43.5 0.78 3.5 48.9 Low 46.6 0.85 3.3 49.4 Low 50.2 0.85 3.6 49.5 Low 53.6 0.89 3.3 49.9 Low 57.3 0.9 3.3 49.9 Low 60.7 0.89 3.3 50.2 Low 64.2 0.99 3.4 50.1 Low 67.6 0.99 3.2 50.6 Low 71.1 1.03 3.6 50.4 Low 74.4 0.97 3.6 50.8 Low 78.1 1.07 3.6 51 Low 81.7 1 3.4 51.1 Low 85.3 1.08 3.6 51.6 Low 88.8 1.08 3.8 51.9 Low 92.4 1.04 3.6 52.1 Low 96.3 1.07 3.5 52.5 Low 100 1.07 3.5 52.8 Low 103.5 1.17 3.6 53.3 Low 107.1 1.05 3.4 53.3 Low 110.8 1.14 3 53.5 Low 114.4 1.24 3.6 53.8 Low 117.5 1.28 3.3 54.3 Low 121.1 1.23 3.3 54.1 Low 124.4 1.27 3.5 54.6 Low 127.7 1.26 3.2 54.7 Low 131.3 1.26 3.6 55.2 Low 134.5 1.26 3.3 55.3 Low 138.2 1.5 3.6 55.6 Low 141.5 1.12 3.9 56.3 High 145.2 1.09 3.8 56.7 High 149.2 1.46 3.8 56.7 Low 152.9 1.34 3.4 56.8 Low 156.8 1.32 3.1 57.1 Low 160.2 1.51 3.1 57.5 Low 163.3 1.66 3.2 57.5 Low 166.4 1.66 3.5 57.7 Low 169.6 Descriptive Statistics of table 1 N Range Minimum Maximum Mean Std. Deviation Statistic Statistic Statistic Statistic Statistic Std. Error Statistic VOLUME 48 1.0900 .5700 1.6600 1.039375 .0395614 .2740896 DURATION 48 1.500 3.000 4.500 3.54792 .047545 .329403 PCO2 48 15.50 42.20 57.70 51.6042 .55888 3.87205 AO 0 TIME 48 169.600 .000 169.600 86.86875 7.229232 50.085591 Valid N (listwise) 0 The table above shows the mean ,standard deviation ,minimum and maximum values , the range and the sample size . Table 1 Graph a. GRAPH OF THE DATA ANALYSED OF TABLE 1 The x axis represents the duration of holding breath. The y axis represents the partial pressure of CO2 TABLE 1 GRAPH B: EFFECT OF PARTIAL PRESSURE ON VENTILATION X –axis represents time Y –axis represents the partial pressure The graph above shows the relation between the partial pressure of CO2 and the breath duration. Appendix 2: Table 1:TABLE SHOWING THE EXPERIMENT ON BREATHING OXYGEN UNDER DIFFERENT ENVIRONMENT   Breathing Room Air with Mask Breathing Pure O2   Subject's Initials PO2 PCO2 O2 Saturation PO2 PCO2 O2 Saturation nnk 93.44 48.78 97.9 211.06 44.2 99 mmsr 127.47 39.54 99 271.54 42.31 91.7 S.S. 105.3 45.86 99 203.57 39.76 97.6 A.H 110.41 45.17 97.9 211.01 43.8 m.m 117 37.35 100 260.5 36 100 G.W. 110.5 41 99 241 39 100 D.R. 113 33.2 100 215 32.4 100 X.H 107.3 40.4 99 325.2 42 100 A.L. 111 38.4 98 296 41 100 nnk 93.44 48.78 97.9 211.06 44.2 99 mmsr 127.47 39.54 99 271.54 42.31 91.7 S.S. 105.3 45.86 99 203.57 39.76 97.6 A.H 110.41 45.17 97.9 211.01 43.8 m.m 117 37.35 100 260.5 36 100 G.W. 110.5 41 99 241 39 100 D.R. 113 33.2 100 215 32.4 100 X.H 107.3 40.4 99 325.2 42 100 A.L. 111 38.4 98 296 41 100 D.R. 106.68 44.89 100 226.58 40.82 100 A.Y. 98.37 43.8 100 248.49 42.71 100 J.H 97.78 43.97 95.9 241.2 40.24 88.6 A.B 108 43.05 99 181.41 32.87 100 A.X 98.37 45.8 100 248.49 42.71 100   110 41.88 99 209 34.62 100 C.C 105.9 47.57 96.9 285.36 43.68 101.1 G.Y 87.41 47.9 99 195.69 44.68 101.1 K.E. 103.5 36.82 101.1 175.35 29.02 101.1 M.A. 113.65 42.55 99 230.17 38.22 100 C.Y. 63.01 43.68 98 259.29 46.62 101.1 LR 102.99 43.63 99 277.76 36.05 99 SM 117.88 37.96 99 264.28 33.68 100 JL 94.33 45.07 91.7 250.42 41.9 98 RW 118.47 37.74 100 298.57 34.33 100 BP 121.48 32.52 100 215.4 24.94 99 JW 118.45 40.68 99 207.92 34.74 100 CJ 121.4 32.52 100 215.4 24.94 99 AS 119.03 41.97 99 307.32 40.26 100 JE 119.33 36.01 96.99 214.467 25.9 100 Descriptive Statistics of table 2 N Minimum Maximum Mean Std. Deviation Statistic Statistic Statistic Statistic Std. Error Statistic PO2M 38 63.010 127.470 108.33868 1.957491 12.066783 PCO2M 38 32.52 48.78 41.3003 .73388 4.52391 O2M 38 91.7000 101.1000 98.741842 .2545008 1.5688485 PO2 38 175.350 325.200 242.69282 6.365649 39.240498 PCO2 38 24.940 46.620 38.25974 .919613 5.668875 O2 36 88.60 101.10 99.0167 .45276 2.71656 Valid N (listwise) 36 The table above shows the mean ,standard deviation ,minimum and maximum values , the range and the sample size of the experiment. Table 2 Graph I: EFFECT OF PRESSURE ON O2 CONCENTRATION Table 2 Graph II. EFFECT OF PRESSURE ON O2 CONCENTRATION X – axis represents the alteration of ventilation Y – axis represents pressure of the gases The graph above indicates the trend of the oxygen concentration as PO2 and PCO2 varies. Appendix 3 TABLE 3: RESULTS OF THE VENTILLATION PATTERNS   Normal Breathing Breath-holding Over-breathing Breath-hold after Over-breathing Subject's Initials PO2 PCO2 O2 Saturation PO2 PCO2 O2 Saturation Length of breath-hold PO2 PCO2 O2 Saturation PO2 PCO2 O2 Saturation Length of breath-hold A.H 101.75 47.69 99 92.67 47.46 99 30.8 140.17 24.99 100 89.25 45.75 96.9 93 S.S 108.65 45.94 95.9 74.64 51.87 97.9 35.9 132.86 26.86 97.9 49.34 42.8 90.7 97 MMSR 111.13 40.65 100 98.23 47.02 97.6 35 144.69 28.38 99 64.89 42.95 88.6 112 JB 109.29 44.77 100 104.23 52.83 101 36.4 134.47 32.64 92.8 52.17 44.13 79.3 164 M.M 109.57 43.3 100 95.5 51 99 19.4 128.52 34.5 100 108 39.49 100 30.5 GW 104 48.3 99 69.5 55.2 99 39 131 37.3 100 80 49 99 83 DR 113 44 99 84 50 100 41 146 27 100 109 30.3 100 47 X.H 107.4 46.2 99 96.4 52.5 99 37.2 130 35 99 91 45 99 63 A.L. 114 41 99 100.1 49 100 27.3 134 34 100 115 42 100 43 J.H. 112 43 100 83.31 52.85 98 30 140.28 26.07 101.1 52.03 41.47 77.2 124 S.G. 118.84 35.56 99 84.7 43.31 98 28 133.56 24.55 96.9 38.97 35.96 75.2 150 J.L. 118.69 35.31 96.9 73.82 46.82 80.4 37.9 136.8 21.08 81.4 41.88 38.7 72.1 146 E.J 91.72 46.29 100 74.38 47.23 99 41 134.22 27.28 100 54.06 37.3 95.9 122 Y.T 109.2 43.3 99 72.25 54.22 92.8 45 136.44 27.24 100 68.73 43.27 91.7 145 C.C 111.67 45.58 99 104.8 49.29 99 23 151.26 22.9 100 127.81 33.61 100 30.3 D.G 109.25 40.6 99 70.37 49.58 95.9 80 135.71 32.11 99 48.66 41.95 82.4 225 GY 87.41 47.9 99 74.97 50.19 100 15 128.08 35.73 101.1 64.65 46.24 100 38 K.E. 111.23 44.65 100 71.81 51.56 99 32 134.76 36.32 100 52084 44.27 93.8 90 M.A 129.69 41.38 100 100.79 49.51 100 22 144.29 33.49 100 70.98 41.53 100 40 C.Y. 96.41 46.25 100 68.83 50.45 99 25 121.94 34.69 101.1 49.88 41.01 87.6 130 CH 100.64 44.27 95.9 68.27 52.94 95.9 30.2s 141.63 25.89 99 107.34 39.84 99 22s VD 104.09 37.76 98 77.66 45 100 20.25 143.09 19.61 100 98.96 26.54 100 39.3 SH 113.95 39.99 100 90.57 48.03 99 50 145.15 21.56 100 69.12 45.73 93.8 2min 20 JM 109.79 40.23 100 83.04 49.07 99 30.9 143.29 20.41 101.1 38.07 42.42 73.1 2m 09s JJ 111.94 41.56 100 67.95 53.89 98 49.6 128.98 33.56 100 46.77 48.93 93.8 2MIN ER 114.12 40.16 99 88.78 49.39 98 34 146.42 20.82 100 105.44 40.29 98 45.6 CJ 114.36 41.44 100 66.04 51.86 96.9 57 128.2 28.34 100 27.21 40.77 70 1min 53 sec JW 116.32 41.53 99 72.3 53.45 97.6 51.1 142.34 24.5 100 33.1 42.39 70 3min 53sec KA 116.46 36.99 100 91.38 38.09 99 45.5 136.22 24.47 100 54.7 36.83 96.9 83 Table 3 Graph1. Graph of the ventilation pattern DIAGRAM The above figure from one of the lecture classes explains what happens during ventilation and how the partial pressure affects composition of gases during normal breathing References: Cahalin L (2002) Efficacy of diaphragmatic breathing in persons with chronic obstructive pulmonary disease: a review of the literature. J Cardiopulm Rehabil;22:7–21. Meuret A, (2009). Changes in respiration mediate changes in fear of bodily sensation in panic disorder. J Psychiatr Res ;43:634–41. Gashev A. (2002) Physiological aspects of lymphatic contractile functions: current perspectives. Ann N Y Acad Sci;979:178–87 Thomas M, McKinley RK, Freeman E, Foy C (2001). Prevalence of dysfunctional breathing in patients treated for asthma in primary care: cross sectional survey. BMJ;322:1098–100. .Moser M, (2006). Why life oscillates-biological rhythms and health. ConfProc IEEE Eng Med BiolSoc ;1:424–8. Nagler J, Krauss B. (2008) Capnography: a valuable tool for airway management. Emerg Med Clin North Am;26:881–97. Meuret A, (2008) Feedback of end-tidal pCO2 as a therapeutic approach for panic disorder. J Psychiatr Res;42:560–8. Rassler B, Kohl J (2000). Coordination-related changes in the rhythms of breathing and walking in humans. Eur J Appl Physiol;82:280–8. Raupach T, (2008) Slow breathing reduces sympathoexcitation in COPD. EurRespir J;32:387– Read More