Appendix 5: Blood Flow Heart and Vasculature Podcast Transcript
Hello everyone and welcome back to the Heart and Vasculature edition of the Human Physiology Podcast. Its me Erica and with me today is Santana. In this episode we’re going to dive deeper into the anatomy of the heart and vasculature, cardiac action potentials and cardiac regulation. The circulatory system is divided into many sections and compartments and each of these play important roles and are interconnected. This tells us that a change in one compartment will then cause a change in another compartment. This relationship can go either way, A can change B and B can change A, therefore we call this bidirectional relationship. Lets just quickly break down the way we compartmentalize the vasculature. So blood moves from the heart through the aorta, then this travels to the arteries, followed by the arterioles into the systemic capillaries. Oxygen diffuses to the tissues, which leads to deoxygenated blood to travel back to the heart via the venules. We see these venules combine into veins ultimately draining back into the superior and inferior vena cava and back to the heart. Now when we think about the pathway of the blood this can often be tricky for students to memorize but its key to understanding the system as a whole. Blood flows from the left ventricle, through the body, and back to the left atrium. A tip from us is to always pay attention to the oxygenation status of RBCs, red blood cells, and the sites of gas and nutrient exchange as these are key players in determining oxygen and carbon dioxide levels in the blood stream.
So we’re going to move on now to Cardiac Action Potentials. When we look at the action potential diagrams of nodal cells and cardiac myocytes, we can see that there are some distinct differences. What are some key features that we can see Santana? Some of the big features we can see are that nodal cells do not have a resting membrane potential and spontaneously depolarize. This is the concept of automaticity – it is due to a leaky sodium channel.
Cardiac myocytes on the other hand have a long plateau phase where the influx of calcium ions through voltage-gated calcium channels equals the transient efflux of potassium ions from potassium channels. Both have effective and relative refractory periods, but cardiac myocytes have an extended refractory period to prevent premature contraction.
So another tough concept for many students is understanding the connections between the electrical and contractile systems of the heart. One of the key things to know about the cardiac cycle is that action potentials are propagated to different regions of the heart to cause the independent contraction of atria and the ventricles. Discussing the difference between cardiac muscle and skeletal muscle is a good way to highlight the physiological features of cardiac muscle. There is a descriptive Venn diagram in this section of the eBook that we highly suggest looking at to really nail down the differences between these 2 muscle types!
Moving on the forever intimidating Pressure Volume Loop, we see many students get overwhelmed by this loop. It can be intimidating to figure out how to relate the pressure changes that occur during the cardiac cycle to their corresponding changes in blood volume in the heart. Our best advice is to practice walking through both of the pressure volume loops. If you understand and are comfortable with the even just one of the two alternative graphs, then you will likely have a good grasp of the material. Practice, practice, practice these graphs and make sure you understand the loop, not simply memorize it. Again, these loops can easily be found in the physiology eBook resource.
Next, were going to quickly go through some important terms that relate to the heart. Its really important to understand the differences in each of these terms as they can sound slightly similar if you’re not paying attention. End diastolic volume also known as EDV or preload – is the volume of blood in the ventricles following passive diastolic filling, this is often at very high volume. Now let’s compare this with end systolic volume or ESV – we see this term as the volume of left-over blood in ventricles following contraction and is typically very low in volume. Afterload on the other hand is the opposing pressure working against end diastolic volume to eject blood from the left ventricle. These terms can be tricky, but when we relate them back to the pressure volume loops, we can see where each of these terms come into play!
This subsection also sets the stage for the more mathematical aspects of cardiology. Mean arterial pressure or MAP and cardiac output or CO are our regulated variables. In this chapter we are presented with some key equations such as cardiac output is equal to stroke volume times heart rate. Here stroke volume is really just the difference in end diastolic volume minus end systolic volume to help simplify the equation. We also have mean arterial pressure equal to cardiac output times total peripheral resistance. You will have to know how to manipulate each of these equations for examinations, so focus on practicing with them and see how an increase in one variable might changes the others.
Cardiac Regulation is an important mechanism that reappears many times in human physiology, this system can be acted on and act on other systems itself. In this subchapter you will largely be investigating how end diastolic volume, end systolic volume and heart rate can be regulated to understand how we control our overall cardiac output. Our body must regulate cardiac output in order to maintain mean arterial pressure and homeostasis.
Many factors can change our heart rate including hormones, autonomic innervation and atrial reflex. Both hormonal and autonomic innervation should be review for many of you and is a great way to test your knowledge from previous units. Take a minute now and think about the different ways hormones and autonomic innervation can have on our heart rate. So atrial reflex might be a new concept for some of you, so we will explain it quick. Atrial reflex occurs when our heart rate increases in response to a rise in atrial pressure. This mechanism often works as a compensatory one. Why is this Santana? Well, this is because increased right atrial pressures often result from elevated left heart pressure from a decreased cardiac output. Increased blood volume is detected by our stretch receptors located in the atria and causes this atrial reflex. Overall, the main outcome is an increase in our heart rate.
Our stroke volume or end diastolic volume minus end systolic volume can also be regulated by lots of factors including preload, afterload, contractility, hormones, venous return, autonomic innervation, as well as by vasoconstriction & vasodilation.
Let’s look an example of an increased Stroke volume and how some factors contribute to this. Preload can increase the end diastolic volume when we have fast filling time and increased venous return, ultimately increasing the stroke volume! Another factor here is contractility, when we have increased sympathetic stimulation or high blood calcium causes a decrease in end systolic volume. When we think about a decrease in end systolic volume, we would see that it would increase our stroke volume as well as stroke volume equals end diastolic volume minus end systolic volume. Afterload can also help contribute to this. When we have decreased vascular resistance, we see a lowered afterload which decreases end systolic volume and therefore an increase in stroke volume. These are just a few ways we can increase our stroke volume, for more examples check out the cardiac regulation subsection in the physiology eBook.
When we look at controlling end diastolic volume and heart rate, we see that they are very similar, their only difference is their site of epinephrine and norepinephrine release from sympathetic neurons and adrenal glands, respectively. We can see that neuronal control is faster than hormonal control, but hormonal control is far more prolonged as these hormones can circulate in the body for much longer than a single neuronal signal that is fast in nature. This allows the body to match its physiological response with the duration of the stimulus that it encounters. Pretty neat stuff ay!
Another tricky concept for students can often be the Frank-starling mechanism and the staircase phenomenon. Both of these are intrinsic cardiac mechanisms used to control end systolic volume. Due to the staircase phenomenon, we see that with an increase in heart rate, we will increase the contractility of the heart. You’ll just have to trust us on this one, as we don’t know the mechanism of this yet. When we compare this to the frank-starling mechanism we see that Frank-starlings mechanism describes the nonlinear relationship between stroke volume and end diastolic volume.
Vasculature radius plays a huge role in physiology of the heart! We can have vasoconstriction which is the contraction of smooth muscle cells in the vasculature which causes a tightening of the vessels and allows for less blood to flow through. Vasodilation on the other hand is the relaxation of smooth muscle which causes a widening of the blood vessel and allows for more blood flow through the vasculature. So when we want to compare how much a vessel will stretch when under a force, we compare the compliancy of the vessel. The compliance of blood vessels and their resistance are the two factors that are going to influence blood volume in the vessel.
When we want to calculate flow, we must use the flow equation which is Q equals P1 minus P2 all over R. This equation is going to come up a lot in the next few chapters, so make sure you get a good grasp of it and know how to manipulate it in different scenarios. For example, let’s look at how we could use the flow equation when we have a decreased cardiac output, but the resistance, or R, of the arterioles stay the same.
The first thing we need to do is identify what P1 and P2 are and how they change depending on the situation. Since cardiac output is decreased, this means that there is less blood entering the vessel, so P1 will represent the heart and P2 will represent the aorta. Since we have less blood entering the aorta, its pressure is decreasing, therefore we have a decrease in P2 that we can throw into our equation. Since resistance is staying the same, we will have an overall increase in flow due to a larger numerator compared to before. This is only one example of how we can affect the flow in different compartments, so we encourage you to think of more ways that we can change flow by manipulating P1, P2 and R! One thing that students get confused about is how vasodilation and vasoconstriction contribute to this equation for flow. Some students think that it will affect P1 or P2 but this is not the case. Instead, vasodilation and constriction directly affects the resistance or R in the denominator of the equation. During vasodilation we see an increase in the radius of the vessel, while during vasoconstriction we see the arteriole vessels decrease in radius. Make sure to keep an eye out for changes in radius in questions that ask you about the relationship it has with flow!
Moving on now to fluid flux and sensors. It can be hard for some students to see the connection between the lymphatics system and the circulatory system, but we can see this connection when we look at filtration and absorption. Filtration is when we move fluid from the blood to the interstitial space. In contrast to absorption, when we move fluid from the interstitial space to the blood. Both really affect the pressure of each space. When we increase fluid in a compartment, we increase pressure, and we all know that pressure gradients are the main drivers for flow! The eBook goes into much more detail on what happens when each force is dominant and goes into depth on the specific pressures we experience along the capillary, so we highly suggest you go and take a look at this.
Starlings Law is another common sticky point along with the equation for it. This concepts often gets forgotten by students during their studying, so make sure you spend some extra time reviewing starling’s law. The basis of the law is that stroke volume in the left ventricle is going to increase if we see an increase in left ventricular volume. Why is this Santana? Great question Erica, this increase in stroke volume is due to the increased volume causing an increase in myocyte stretch which then causes a stronger systolic contraction. The more volume in the ventricle, the stronger the contraction! Starlings’ equation looks at many factors including the capillary hydrostatic pressure, the plasma oncotic pressure, the interstitial hydrostatic pressure and the interstitial oncotic pressure. Each of these forces cause either a push or a pull of fluid in or out of the capillary or interstitial space. Though we can’t go over all these forces in this podcast, we suggest you review by thinking about what each force does individually to fluid flow and then what the overall net effect of the combined forces would do! For more material, check out the fluid flux and lymphatic system chapter in the eBook now.
We’re going to quickly touch on some sensors which we see come up in many other units after this one, so if you don’t fully understand it now, you’ll get much more practice with it as you continue through this course. The key here is to understand how chemoreceptors and baroreceptors, work together with all of the tools you know regulate cardiac output and mean arterial pressure. Let’s just compare two types of receptors quick! Baroreceptors are sensors that are typically found with close relation to the heart, including the aorta, carotid arteries, vena cava and the atria’s. For chemoreceptors we instead find these mainly in the central nervous system as well as in close proximity to the baroreceptors. Baroreceptors are really sensitive to increased stretch, so when the heart is stretched, the baroreceptors will react and cause changes to parasympathetic stimulation to decrease the blood flow and pressure to the heart and cause hemostasis to be restored. Chemoreceptors on the other hand are sensitive to increasing oxygen and decreasing carbon dioxide, this causes the sympathetic stimulation to be suppressed which will also decrease blood flow and pressure to the heart and contribute to restoring hemostasis as well. So, we can see that we have two totally different receptors sensitive to different stimuli, but they both help to contribute to the same overall effect. Neat isn’t it?
Now we think it’s a great time to go through some examples with you to practice! A frequently asked question by students is “how do paramedics use automatic external defibrillators, or AEDs to effectively restart the heart?” This clinical example illustrates many important points Erica. AEDs deliver an electrical stimulus to the heart that is very large – so large, that it instantly depolarizes all of our cells. Even cells in their relative refractory period are depolarized by this shock because the stimulus that is generated is large enough to overcome the hyperpolarized state. All cells experience an action potential, then reach their effective refractory periods. If the nodal cell pathways are intact, the SA node will fire first, since it has the fastest conduction velocity. The signal will propagate from the SA node to atrial pathways, to the AV node, to the bundle of His, to Purkinje fibers, and finally, to ventricular myocytes. Contraction will resume at a rate of 70-80 beats per minute. In this way, AEDs effectively restart the heart. They are useful in treating ventricular fibrillation or ventricular tachycardia. Now the next time you’re watching a medical show you’ll know exactly how the AED works when reviving someone!
Another question we should think about is what molecular mechanisms occur within cardiac myocytes to increase the heart rate during stress? To answer this question we need to think about what occurs during stress. Epinephrine and norepinephrine will be released from adrenal glands upon SNS stimulation. These hormones bind to beta-adrenergic membrane receptors on ventricular myocytes. This triggers an intracellular signalling cascade. Stimulatory G-proteins activate the enzyme adenylate cyclase, which produces a potent second messenger called cAMP. cAMP activates protein kinases, which phosphorylate two types of calcium channels: L-type and voltage-dependent calcium channels and Ca2+ pumps on the sarcoplasmic reticulum. More trigger calcium is present in the cell to stimulate sarcomere shortening, so contractility increases. So overall we see that the net effect is increasing the speed and force of contraction.
Ok, lets cover one more question Santana! Let’s think about how a drop in mean arterial pressure or MAP influences the pressure in arterioles, venules and systemic capillary beds. Ok, imagine a single capillary bed. In this example, we’ll consider a change in MAP on the arteriole side. Since there is no change in the resistance of arterioles, a decrease in the pressure of the blood entering the capillary will result in a decrease in the blood volume entering the capillary bed. This is because, according to the helpful equation Q equals P1 minus P2 over R, bet you guys don’t miss seeing that, decreasing P1 will decrease blood flow into the capillary bed. This makes intuitive sense! With less flow into the space, the pressure in that space will drop. We call this pressure capillary hydrostatic pressure, or Pc for short.
And that concludes our Heart and Vasculature edition of the Physiology Podcast brought to you by students for students. Thanks for listening everyone and enjoy learning physiology.
