Appendix 7: Blood Gases Podcast Transcript

Ok, hi everyone and welcome to the Blood Gas Chapter of the Physiology podcast. My name is Erica. And I’m Santana, and we are both 4th year students at the University of Guelph who have taken physiology 1 and 2. To start us off, we’re going to introducing the basics of pulmonary mechanics and the anatomy of respiration. It is important to have a good grasp of the anatomy contributing to the mechanism of breathing. So during inspiration we see a contraction of muscle and movement of our diaphragm. So I ask you to like take a deep breath in and exhale out, as you’re doing this look in a mirror and observe the way your body accommodates for this increase in air volume. The process is actually very simple when broken down!

So, when we breathe in, we inspire and cause 2 things to happen. We will see the diaphragm contract and move down; this creates additional space in the thoracic cavity. And we also contract our external intercostal muscles, which are the muscles that line the ribcage, um the contracting of these muscles pull the ribcage up and out again creating more space. And you can see this um increase in chest volume when you take a deep breath in. Once we inhale, we must then exhale. Here we want to think about causing the reverse of what our body just did. So since we just contracted our diaphragm, now we will relax it and it will move up to its original position. Following the external intercostal muscles that were contracted when we inhaled will now relax and cause the volume of the thoracic cavity to become smaller. This is a key process to remember as you will relate back to it a lot throughout the course.

By now you are probably so tired of seeing the equation for flow or Q equals P1 minus P2 all over R. This equation has been occurring in many parts of human physiology and will continue to throughout this unit as well. The relationship flow has with pressure is so key to understanding the way the human body regulates systems. In this unit we must now relate this equation to respiratory flow instead so our P1 and P2 will be different from pervious units. When we discuss respiratory flow, we see that P1 will represent the atmospheric pressure at 760 millimeters of mercury, we almost always set this to zero. We commonly relate other lung pressure to atmospheric pressure to make things simpler this way! P2 will then represent the pressure in the alveoli, or alveolar pressure. Though this equation may seem easy, uh, the biggest tip that we have for you guys is to know how to manipulate this equation to get flow as its key for understanding pressure changes. One of the big hints is that alveolar pressure must be negative to get flow during inspiration, so look out for this is practice questions and exams!

Next, a common thing for students to get tripped up on is the idea of surfactant. In physiology you’re just quickly introduced to surfactant and students often know what it is, but not why we need it. In your lung you have so many different sizes of alveoli, from large to small, each one is different. If we were to try to breathe in air without surfactant, we would see all the air rush to the larger alveoli. Think about why this is! So pressure gradients and relationships again are in play…uh, the air would rush to the largest alveoli only due to the lowest pressure there. We have millions of alveoli, so its not efficient for all the air to only go into one. Surfactant is that cool middle player that swoops in and makes the pressure gradient the same in every alveoli so air is distributed equally to each one. Hopefully this helps to give you an easier background understanding of why we need surfactant to connect with your knowledge of what it is.

So much of the pulmonary mechanics and respiration subchapter is based on basic anatomy and how this anatomy contributes to inspiration and expiration. Our best advice is to nail down the anatomy before continuing to the next subchapter as the anatomy continually comes into play throughout the Blood Gas unit as well as our good old friend Q equals P1 minus P2 all over R. If you ever get tripped up in a question, take a deep breath and think about the process. The great part is your body becomes a great study tool to use as you can see your chest move in relationship to your breathing!

Who would’ve thought we’d see another subchapter focused on flow? When we learn about pulmonary blood flow, we can see a lot of it connects right back to concepts learned earlier in the course and makes it a great place to stop and review for many students. Many of you already know that blood vessels contain smooth muscle that allows us to constrict or dilate the vessel. Let’s think about what factors can cause a change in the smooth muscle of blood vessels. We’ve got nervous control, endocrine control, paracrine control that, uh, we have learned about previously! Each of these can vasodilate or vasoconstrict our blood vessels. If you don’t remember the mechanisms behind each of the regulators, we highly suggest pausing the podcast here and jumping back a few units to quickly review the concepts again.

So moving into transmural pressure it’s often a tough concept for students. We find it best to really visualize where in the body we are looking at first. In the case of alveolar vessels we’re zooming in specifically onto a singular alveolus and imagining the alveolar vessels also known as a capillaries, tightly wrapping itself around and around this alveolus. Now since the capillary is in such direct contact with the alveolus, we would see oxygen passing from the alveoli into the blood. Now that we can imagine this tight knit relationship, we can start to label pressures. The transmural pressure which is sometimes labeled as the environmental pressure is the pressure in the alveolus. Because the capillary is so tightly wrapped, we can appreciate how changes in the shape/size and pressure of the alveolus will directly affect the capillary! The eBook goes into much more depth discussing the ultimate pressure relationships to allow for flow and is a great resource to look at for further information to nail down the concepts of transmural pressure. But a single tip from us is to remember back to when we talked about the heart. In order to get flow, we must have a larger pressure on the pulmonary artery side compared to the pulmonary vein side of the capillary, that still stands true in the case of the alveolar vessels.

So finally, we’re going to quickly go over an example that students tend to struggle with and break it down into easier steps! If a question asks you to explain the difference of blood flow between the different regions of the lung when doing a handstand, the first thing we’re going to think about is what is the normal blood flow distribution of a person when standing normally? Its important to think back to where we see the most amount of blood flow. Is it at the top of the lung, or the bottom of the lung or somewhere in the middle? We see it at the bottom of the lung! So in a typical person standing upright we would see a negative 10 centimeters of water at the top of the lung, negative 4 centimeters of water in the middle of the lung and negative 2 centimeters water at the bottom of the lung. Now, let’s flip this, think about doing a handstand, what direction would our lung be in now. The top of our lung closest to our head would now be positioned at the bottom relative to the rest of the lung. Essentially we are flipping the lung upside down! We know that distribution of flow across the lung is largely dependent on gravity so with an upside-down lung in our handstand position we are going to see gravity affecting it. So the top of the lung in upside down position now has the pressure that the bottom of the lung had before. We would simple flip the distribution! If you are struggling to visualize these distribution changes, we highly suggest taking 5 minutes and checking out the diagrams that can help you learn the distribution relationships in the eBook Pulmonary Blood Flow subunit.

Moving on, we’re going to talk about a super important relationship called the VA Q ratio, or the ventilation perfusion ratio. The equation is quite simple but so helpful in predicting blood gas levels and becomes a great tool if you are able to manipulate the equation. We always want this ratio to equal 1, this means we are getting a good level of air flow in proximity to the blood. When its off balance we can have not enough air for the level of blood, or not enough blood for the level of air coming in. The most important thing about the VAQ ratio is that we can connect it to predict the concentration of blood gases, which is what this entire chapter is really about! The best way to understand the VAQ ratio is to practice it, increase and decrease different variables in this equation and see what happens. Practicing this ratio will make you ready for any situation that comes at you in future questions including ones with real life examples!

A really helpful tool for many students to understand the VAQ ratio and how it relates to the PaO2 and PACO2 is the diagram shown in the eBook Ventilation Perfusion subchapter. This helps integrate both ideas into one visual diagram that can easily be manipulated for different scenarios! If this diagrams works for you it can be such a helpful thing to have up your sleeve for real life questions and examples. If you’re not sure what diagram we are talking about pause the podcast now and go take a look now!

So we’re going to dive deeper into an example now connecting the VAQ ratio to Blood gas concentrations to a real life scenario as well as connecting ideas from previous chapters. I’m sure we have all been feeling nervous for a big test or exam, imagine you are keeping your breathing normal but your heart rate is through the roof causing an increase in cardiac output. How will this affect the gas levels of oxygen and carbon dioxide? So the key thing here is understanding that increased cardiac output really just means that we are increasing the blood flow across the body even around the alveoli! If we remember we already talked about these vessels. These blood vessels around the alveoli are called the alveolar vessels. So we have increased blood flow and can add that to our equation. An increase in blood flow is going to change the rate at which we remove carbon dioxide and add oxygen to the body. The increase in blood flow is going to cause an increase in the perfusion and allow more carbon dioxide to be added by flow than removed by ventilation from the alveolar space. So as a result, we see an increase in PACO2. When we think about the oxygen levels, we know that an increased perfusion would cause more oxygen to be removed from the alveolar space by flow than what can be added by ventilation which would cause a decrease in PAO2. This is only one example of how our VAQ ratio can be manipulated by our body and external sources but we encourage you to think and come up with your own scenarios that might affect the VAQ ratio and the affects that would have on blood gas levels.

We’re going to move on now to the Gas Exchange and Transport unit. This unit quite often ends up being a hurdle in the course for students. The information can often feel non-intuitive and sort of complex, and if you’re feeling this way, don’t worry, you’re not alone. The information we go over in this podcast is designed to help you get past this hurdle, and paired with the e-textbook, we have no doubt that you’ll get a handle on gas exchange and transport in no time. So first, let’s talk about a unique phenomenon that we see when looking at partial pressures. As you guys know by now, the atmospheric partial pressure of oxygen and carbon dioxide are 150 millimeters of mercury and 0 millimeters of mercury respectively. But, you guys also know that by the time the air reaches the alveoli, these partial pressures have changed to be 100 millimeters of mercury and 40 millimeters of mercrury respectively. How did that happen? How does the partial pressures of oxygen and carbon dioxide change from outside the body to the lung? Well, there are 4 mechanisms driving this that you need to know. First, the idea that gas exchange is always occurring, so oxygen is constantly being taken out of air we inspire and carbon dioxide being put into it at lungs. Next, the concept of residual volume. Residual volume is air remaining in the lungs from prior inspiration that is already equilibrated, mixes in with the air of the next breath. We also have to think about dead space, which is the air remaining in the respiratory tract after expiration. This dead space air is the first air that enters your lungs when you inspire, and is the same equilibrated air that was in the trachea from your last breath. Finally, air is being warmed and hydrated as we inspired. Partnered with our other mechanisms, all of these factors lead to this change of partial pressures.

So, let’s circle back to our first point and discuss how gas exchange occurs at the lungs. Concentration gradients play a huge role in gas exchange- both oxygen and carbon dioxide want to leave high concentration areas for lower concentration areas. In the case of oxygen, we see this as oxygen in the alveoli will follow a concentration gradient and enter the arteries. With carbon dioxide, we see it travel along its concentration gradient as it leaves an area of high concentration in the veins and enters an area of low concentration in the alveoli where it can then be exhaled. Once in the blood, oxygen and carbon dioxide are transported by a number of ways. The majority of oxygen is transported bound to hemoglobin in a compound called carbaminohemoglobin. The remaining oxygen is transported dissolved in the blood plasma. The majority of carbon dioxide is transported and stored in bicarbonate, while the rest is either bound to plasma proteins or carried in the blood plasma like oxygen.

There are four equations for gas exchange that you have to know for this unit, and this is usually where students get tripped up. We won’t be going through each individual equation in this podcast, but you can reference these equations in the e-textbook. Our best suggestion is to focus more on understanding the equations than on memorizing them. This way, when working through a question you can work through the components of the equation from the process itself, if you’ve forgotten them. Furthermore, this allows you to study the process and the equations at the same time!

So, once gas exchange occurs in the lung, it’s time to look at the tissue. What occurs at the tissue is essentially inverse of what occurs at the lung; we want to drop off oxygen and pick-up carbon dioxide. Both still follow concentration gradients and both travel using the same methods! Best yet, the equations at the tissue are the exact same, just with reversed direction. Which is an absolute relief, considering by this point in the unit I remember questioning if my brain could hold more information. This emphasizes the need to understand the steps instead of just memorizing the equations, so you can better differentiate whether something is occurring at the lungs or the tissues. There’s a great video featured in the e-book that better demonstrates the events occurring in each equation and can help visualize these for students still having difficulties.

Moving forward, we start to look at the oxygen dissociation curve. The oxygen dissociation curve is a tool we can use to relate a percentage saturation of hemoglobin to the partial pressure of oxygen. On the x axis of this curve you’ll have the partial pressure of oxygen and on the y axis you’ll have a percent hemoglobin saturation, which just represents how much oxygen is bound to hemoglobin. This curve is a sigmoid shape, which plateaus around a partial pressure of oxygen of 75 millimeters of mercury. We live just past this point, well within the plateau, at 100 millimeters of mercury of oxygen and approximately 98 percent hemoglobin saturation. What does this tell us, Erica? So, let me break it down for you Santana, first this tells us that in a healthy lung under normal conditions, our hemoglobin’s are nearly 100 percent saturated with oxygen. So this then tells us that small changes in the partial pressure of oxygen will have little to no effect on hemoglobin saturation. In fact, it would take a huge drop in the partial pressure of oxygen to influence hemoglobin saturation. In contrast, due to the sigmoidal shape of the curve, which kind of looks like you’re travelling up a ski hill, small changes to the partial pressure of oxygen will have large impacts on hemoglobin saturation. Once we leave that plateau, we’re in for some real trouble!

Thanks Erica! Let’s dive deeper, as with everything in physiology, there are conditions that affect this curve and that can shift it either right or left. These conditions are pH, temperature, and 2,3 DPG, which from now on we’re going to refer as BPG. When the curve shifts to the right, this means that hemoglobin’s affinity for oxygen is reduced, so hemoglobin is more likely to be off-loading oxygen. This shift to the right can be caused by decrease in pH, due to increases in CO2, increases in temperature, and increases in BPG. This is seen in places like the muscle or in a pregnant woman’s placenta, where we want to off-load oxygen. In contrast, when the curve shifts to the left, this means hemoglobin’s affinity for oxygen is increased, so hemoglobin is more likely to be on-loading oxygen. This shift to the left can be caused by the opposite so an increase in pH due to decrease CO2, decreased temperature, and decrease BPG. Luckily for you and for Erica and I when we were taking this course, these phenomena mirror each other, which make them much simpler to understand.

So let’s round out this unit by talking about what might happen when Santana begins to exercise. Let’s talk about how it affects oxygen levels in the veins and capillaries, our drive for diffusion, carbon dioxide levels. After reading this question, the first thing you should focus on is that Santana is exercising. This means that she is going from a state of rest to a state of exercise that will increase her level of tissue metabolism. Due to an increase in activity you would expect a decrease in capillary and venous partial pressure of oxygen, or PO2. This is because oxygen would be used for cellular respiration and the production of energy at the tissue, so we that lowering of PO2. Due to the decrease in tissue PO2, there would be an increase in the drive for diffusion between the systemic arterial blood and the tissue. Instead of having a concentration gradient with a difference of 60 millimeters of mercury, partial pressure of arterial oxygen of 100 mmHg and partial pressure of venous oxygen of 40 millimeters of mercury, you’re going to see a greater difference due to the PO2 decreasing below 40 millimeters of mercury at the tissue and venous side. So at the onset of exercise, we would anticipate an increase in PCO2 at the tissue, because carbon dioxide is a by-product of tissue metabolism. So, the more Santana works, the more carbon dioxide her working tissues produce. Due to an increased concentration of carbon dioxide in the tissue and a low concentration of carbon dioxide in the systemic blood passing by, the drive for diffusion into the blood is going to increase.

Our final unit looks at how we breathe, from our brain to our muscles and all the in-between that helps us breathe in deep. First, we’re going to talk about chemoreceptors, what they are, and what they do. To begin, there are two types of chemoreceptors that we’re going to talk about, peripheral and central. Peripheral chemoreceptors are located in the carotid and aortic bodies and detect chemical changes in blood. Specifically, they detect changes in oxygen, pH, and CO2. For example, reductions in oxygen, reductions in pH, and increases in carbon dioxide would all be detected by the peripheral chemoreceptors, which would then signal back to the respiratory centre to increase ventilation. So our central chemoreceptors are located in the medulla and detect changes in pH and CO2, but not O2. Again, here we would see an example where if there’s a reduction in pH or an increase in CO2, the central chemoreceptors would signal back to the respiratory centre to increase ventilation. Other important receptors in the body that play a role in respiration are, muscle receptors, irritant receptors, and stretch receptors. Respectively these receptors act to increasing respiration during exercise, protect the respiratory system by decreasing respiration when something has entered the respiratory tract, and protect against overinflation of the lungs.

Now let’s talk about these respiratory centres that we’ve been referring to, or more specifically, involuntary and voluntary control of respiration. Starting with involuntary respiration, we define this as any type of respiration that occurs without voluntary control. This type of respiration is controlled at the coordinating centre, or the brainstem, which contains our central chemoreceptors. These chemoreceptors, as previously mentioned, send signals to the coordinating centre to adjust the ventilation rate to control acidity by increasing or decreasing the removal of CO2. Following this, the coordinating centre signals to the effectors, which are the diaphragm and external intercostal muscles to contract and adjust ventilation. Voluntary respiration is respiration that is under conscious control. We voluntarily breathe all the time, interrupting our involuntary normal breathing to perform actions like talking, singing, and blowing out a candle. This voluntary respiration is controlled by the cerebral cortex. Neither of these methods of respiration are superior inputs to the other, as both can be overridden by one or the other.  This is why we can stop breathing to talk but can’t hold our breath until we die!  Isn’t that convenient? There’s a fantastic diagram in the e-textbook that dives deeper into the complete pathway of controlling our breathing. I would highly suggest referencing this diagram for the clearest understanding of this process, as it appropriately outlines the roles and relationships of the coordinating centre, effectors, override system, and receptors discussed in this podcast.

Now let’s go over this information by looking at an example of hyperventilation. During hyperventilation, arterial partial pressure of oxygen increases and arterial partial pressure of carbon dioxide decreases. How do you think, Erica, given what we’ve just learned, the body would compensate for these changes in blood gases during hyperventilation? So, the first thing that we should think about is what is happening at the level of the sensors. Here, we would see an increase in PaO2 that will the cause a decrease the action potential frequency from sensors to the coordinating centre. Similarly, at the sensor level, a decrease in PaCO2 will result in a decrease the action potential frequency from sensors to the coordinating centre as well. Overall we are going to get a decrease our ventilation by decreasing the frequency of breathing and our depth of breathing.

Now we hope that you guys enjoyed this student-student learning experience and gained some friendly knowledge and advice from fellow students. Physiology can be a tough subject to learn but stick to it and make sure you review some of the learning strategies we presented in the How to use Book page as these are great strategies used by past students. We thank you for listening to Erica and I break down some of the sticky spots of the Human Physiology the Blood Gases Unit. Goodluck and don’t forget to breathe!