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BPK 205 Study Guide - Final Guide: External Intercostal Muscles, Alveolar Pressure, Intrapleural Pressure

Biomedical Physio & Kines
Course Code
BPK 205
Parveen Bawa
Study Guide

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Oxygen molecule traveling through the human body:
I’m at the mouth where there are others just like me. 21% of the air is filled with
other oxygen molecules. The PO2 is around 150 mm Hg
Diaphragm muscle pulls downwards (start of inspiration) increasing superior-
inferior volume of the lungs, and external intercostal muscles pull the outwards
increasing anterior-posterior volume
This causes intrapleural pressure in the pleural cavity to drop from -5 cm H2O to
get more negative, creating a vacuum that pulls on the alveoli increasing alveolar
volume. Increase in alveolar volume will reduce alveolar pressure (boyle’s law);
creating a pressure gradient where lowest pressure is in the alveoli, and highest
total air pressure is outside the mouth
The reduced air pressure creates a vacuum that sucks me into the mouth. I first
travel through the conducting zone where there is no diffusion, only conduction of
air. I see that at the trachea there is much connective tissue such as collagen, but
not as much smooth muscle. There is much turbulence in the first six bifurcations
due to the high velocity that I and other gas molecules are traveling at. As I
continue through the bifurcations, I notice that the bronchioles decrease in
connective tissue and increase in smooth muscle. There has been humidification
on the journey so far. Now there is a greater concentration of myself and other O2
Midway through inspiration phase, I enter an alveolus at bifurcation 20. The PO2
has decreased from 150 mm Hg to around 100 mm Hg here in the alveolus. There
is CO2 molecules being diffused into the alveolus where the PCO2 is 40 mm Hg.
These CO2 molecules come from the capillaries surrounding the alveolus where
the PCO2 is 45 mm Hg
As blood flows through the capillaries I finally get diffused into the capillaries
across the alveolar wall. This wall is only one layer thick making my transition
easy. When I enter the capillary, the PaO2 is constantly changing from the arterial
end to the venous end. PO2 at the arterial end is 40 mm Hg, and at the venous end
it becomes about 95 mm Hg.
In the blood, I get stored in a Hb molecule. There are 3 others just like me on
board this molecule. Some O2 molecules get stored simply in the blood plasma
where they contribute to the O2 partial pressure
We exit the capillaries, and leave the lung via a vein. We are then transported to
the heart by the pulmonary vein.
We first enter the left atrium. The mitral valve is closed. Then atrial systole
occurs. The walls contract and we are pushed through the mitral valve into the left
ventricle. Here the walls are thicker (8-9 mm) and more muscular.
Now ventricular systole takes place, and we are pushed through the aortic valve
into the aorta. When this happens, the blood pressure rises to 120 mm Hg. During
diastole, we continue to travel via elastic forces of the blood vessels, but the blood
pressure drops to around 80.
Traveling farther away from the heart via artery, I notice the increase of smooth
muscle, and decrease in vessel diameter. We travel in a constant rather than
pulsatile flow because the human has good compliance
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