You are on page 1of 3

Joy Li

Biology 473 Section 2

TA: Javier Solivan and Mary Chen
Vignesh Murali, Jessica Abbondola, and Katelyn Johnson
Respiratory Volumes, Lung Mechanics, and pH Regulation
Table 1 summarizes the measurements of lung volumes and capacities taken for unobstructed lung
function and simulated obstructed lung function. The subject breathed into a pneumotachometer to obtain
the measurements for the unobstructed lung through spirometry. To simulate lungs with obstructive
disease, a "filter", consisting of duct tape covering the opening with a hole poked through, was placed
onto the pneumotachometer to simulate partially blocked airways. The tidal volume was measured to
decrease significantly by 27.6% from 0.98 liters to 0.71 liters from the unobstructed lung test to the
obstructed lung test. For vital capacity, a significant decrease of 16.8% was measured from 4.24 liters to
3.53 liters. The residual volume was determined to have no significant change from the unobstructed test
to the obstructed test with a value of 1.50 liters from both, for a 0% change. Forced vital capacity resulted
in a significant decrease of 44.7% from 3.20 liters to 1.77 liters and the percent forced vital capacity in
one second significantly decreased 16.7% from 48% to 40%. For each of the measured values, except for
residual volume, the simulated obstructive disease resulted in a significant decrease.
Table 1: Measured Lung Volumes and Capacities of Unobstructed Lung Versus
Simulated Obstructive Disease Lung
Unobstructed Lung Obstructed Lung
Percent Change
Tidal Volume (L)
Vital Capacity (L)
Residual Volume
No Change
Forced Vital
Capacity (L)
% FVC in 1 Second
Different lung volumes and capacities were measured through spirometry for unobstructed lungs and lungs with
simulated obstructive disease, first by breathing into the pneumotachometer normally, and then by breathing into it
with a special cover to simulate partially blocked airways.
*significant values with percent changes greater than +/- 10% compared to baseline. This was calculated with the
formula % change= 100% *(baseline-new value)/baseline. s=(baseline*0.1)*100%.

The data suggested that tidal volume, vital capacity, forced vital capacity, and percent forced vital
capacity in one second all decreased significantly as a result of the simulated obstructive disease on the
lung. However, this is not consistent with the concept of airway resistance of obstructive lung
functioning. An obstructed airway is not completely blocked, and the individual still has the ability to fill
their lungs, but has a difficult time moving air in and out. With unlimited time to breath, they theoretically
can fill their lungs to the same capacity as normal (Wiggs, 1992). This means that tidal volume, vital
capacity, and residual volume are not affected by the obstruction. The same reasoning can be applied to
forced vital capacity. When you breath, your chest wall and lungs move together, driven by the
diaphragm. Contraction of the diaphragm moves it downward, increasing the volume of the chest and
causing the lungs to expand (Silverthorn, 2015). With obstructive lung disease, the ability of the
chest/lung/diaphragm to do this is not affected by the airway obstruction. Therefore, the value of forced
vital capacity across the airway types should not be affected either. This was not consistent with the
experimental values obtained for the measurements of TV, VC, and FVC, which all decreased.
Typically for residual volume, airway obstruction, like the bronchial restriction of asthma, makes
it difficult for the individual to exhale all the air out of the lungs. This results in a greater residual volume,
total lung capacity and functional residual capacity, since more air is left in the lungs after exhalation due
to over-inflation of the lungs (Waters, 2016). The normal residual volume required to keep the lung from
collapsing is left in the lung, along with the addition of any leftover air that was not breathed out. The
measurement of the residual volume for the two airway types indicated no significant change, which was
expected for this particular experiment due to the nature of the obstruction simulation. For percent forced
vital capacity in a second, time was an important consideration, as airway obstruction hinders the
individual's ability to take in as much air as normal during a certain extent of time. This suggests a lower
value for FEV1, resulting in a lower percent FEV1/FVC. This was consistent with the data measured.
The changes in tidal volume, vital capacity, and forced vital capacity were not consistent with the
expected, but changes for forced vital capacity in one second and residual volume were consistent,

suggesting weak data. Sources of error that may have caused these differences in data include the
pneumotachometer not being perfectly flat for maximum consistency from measurement to measurement,
potentially skewing the numbers. Also, the nose clip was not used consistently, allowing for air exchange
through the nose during measurements. In future attempts, the pneumotachometer would be set on a flat
surface and multiple subjects would be tested for general trend lines.
Silverthorn, Dee U. Human Physiology. 7th Ed. Pearson, 2015. Print.
Waters, John R., and Nanette J. Tomicek. Physiology Laboratory Manual. 3rd Ed. Plymouth:
Hayden-McNeil, 2016. Print.
Wiggs, B.R., C. Bosken, P. D. Par, A. James, and J. C. Hogg. A Model of Airway Narrowing in Asthma
and in Chronic Obstructive Pulmonary Disease. American Review of Respiratory Disease.
Vol. 145, No. 6, 1992.