Hello, I'm Dr Eric Fung. I’m the Assistant Professor in the division of Cardiology. Today we'll talk about the Essential Cardiovascular Anatomy and Physiology for Sports Science and Medicine Learners. Learning objectives for today are that after today you should be able to discuss the structures, functions, and contents of the chest, discuss the structures and functions of the heart, explain how they changed during exercise, understand the cardiopulmonary circulation and functions, and lastly, be able to explain how cardiovascular anatomy and physiology change in response to exercise. Now we talk about the basic anatomy of the thorax or the chest. The major structures of the thorax include the thoracic wall and cavity, the organs within including the heart, lungs, and thymus, and the great vessels, muscles, ribs, bones, and cartilage. There are other internal organs, including the trachea, esophagus, nerves and lymphatic ducts. Here's a diagram showing the chest and its contents. As you can see, it's a very crowded space there. Now we'll talk about the pericardium, heart muscle, heart valves and cardiac conduction system. The pericardium is a pericardial sac, and it is comprised of two layers - the fibrous pericardium and the serous pericardium. It is an important structure because it protects and isolates the heart from other thoracic structures and potential infections and other pathogens, possibly, but it also translates pressure and forces during respiration. Between the heart and the pericardium is a space called the pericardial cavity or pericardial space. This is an important space because normally it can contain 30 to 50 milliliters of pericardial fluid, which acts as a lubricant between the heart and the pericardium. In certain pathologic states, including cardiac tamponade, the accumulation of fluid can lead to an emergency. Now we look at the different layers of heart muscles. The epicardium is the outermost layer and is in continuity with the parietal serous pericardium. It's also known as the visceral serous pericardium. It is important because it's the location of the coronary arteries. The middle layer is the myocardium and it's the bulk of the ventricular muscles. During contraction of the heart during systole, you would see thickening of the muscles and in patients with the disease, whether there's a blockage of the artery or previous heart disease, there may be reduced thickening and or thinning of this muscle layer. The innermost layer is also called the endocardium and is susceptible to ischemia and infarction. What you see here is a surgeon’s view at the level of the aortic valve. Anteriorly you have the pulmonary valve, in posterior which is the aortic valve, most posterior is the mitral valve, and laterally to the right is the tricuspid valve. As you can see here, they sit on a similar plane. The heart has four main chambers. They are separated by four different sets of valves. Here, at the root of the aorta is the aortic valve, which comprises a valve with three leaflets. Between the left atrium and the left ventricle is a pair of valves called the mitral valve. In the right heart separating the right atrium and the right ventricle is your tricuspid valve. Lastly, separating the pulmonary trunk and your right ventricular outflow tract is the pulmonary valve. The major vessels of the chest can be divided into arterial or venous depending on their origins and their distribution. The aortic root sits just above the aortic valve, leading to the ascending aorta, the aortic arch and subsequently, as it turns around it becomes the descending aorta. Coronary arteries arise from the aortic root and supply the heart muscles. The two main coronary arteries are the left coronary artery and the right coronary artery. In your venous system, you have this superior venous cava (SVC) that drains the oxygenated blood from above your neck level, much of which comes from the intracranial venous system. Whereas inferiorly you have the inferior vena cava (IVC) coming into this area of the right atrium, transporting blood from the portal system as well as from areas below the diaphragm. There's also a large vein that drains the left ventricle, called the coronary sinus. The heart functions as a pump, but the system also has mechanical sensors and is an important neuroendocrine organ. It has dual circulation because the left side of the heart supplies the systemic circuit. Whereas the right side of the heart pumps blood into the pulmonary circulation for gaseous exchange to occur. What drives the mechanical function of the heart? It can be traced back to the electrical activities of the heart. Here you can see that the action potential underlies the basic electrical activity of the heart. You have the resting membrane potential followed by depolarization and subsequently returning to the resting membrane potential through repolarization. There are five phases of the action potential, phase 0, phase 1, phase 2, and phase 3, followed by phase 4 and each phase represents a different opening and closing of different ion channels. And at the bottom, you see the electrocardiogram which represents the summation of different action potentials of different cells in the heart. What we show here is that there is a hierarchy in terms of the pace-making ability of different conduction tissues of the heart. For example, the sinoatrial (SA) node, which is known as your native pacemaker, has an intrinsic frequency of about 70 beats per minute. Whereas the atrioventricular (AV) node, which is at the junction between the atrium and the ventricle, has an intrinsic frequency of about 40 beats per minute. The bundle of His has a frequency of 20 to 40/min followed by Purkinje fibers in the ventricles with an intrinsic frequency of 20 to 40/min as well. This is important because, particularly in older people, when the cardiac conduction system starts to fail, different parts of your conduction system or your pacemaker structure may take over the pacemaker activity. Also in athletes, because of the state of the parasympathetic nervous system, sometimes we may see different kinds of what appear to be atrioventricular blocks in the electrocardiogram. At a lower level, you can see that the sinoatrial node can discharge and produce this action potential here whereas the areas that are surrounding the sinoatrial node may have slightly different action potential profiles depending on the function of the heart. Going a little bit, even a little bit deeper is the biochemistry that goes on in the cell. What is critical to the discharge or the depolarization, is calcium binding to troponin. Upon depolarization, you have the actin filaments exposed, leading to myosin binding to actin, and through the use of ATP, the myosin moves actin along. And then when ATP is converted into ADP and inorganic phosphate (Pi), you have myosin releasing actin and myosin head which is “cocked”. The myosin is finally ready to bind another actin-binding site. This happens in a cyclical function as shown here. How does the heart generate an impulse and a contraction? The key elements are calcium and ATP. Initially, you have a leakage of calcium into the cell and subsequently when it reaches a threshold you have, it triggers the inward release of calcium leading to the calcium that causes binding of the mechanisms as described in the last slide. Now, the anatomy of the cardiac conduction system has been discussed earlier, but again it can be divided into the sinoatrial node, the atrioventricular node, the bundle of His, and then splitting subsequently into the right and left bundle branches. The Left bundle branch can also be divided into the anterior and posterior fascicles. While different parts of the heart and conductive tissues may have pace-making activities. The sympathetic and parasympathetic nervous systems play important roles in influencing heart rate, blood pressure and blood flow to skeletal muscles. One of the most important systems is your sympathetic nervous system, as it represents your fight or flight response, or when someone is faced with danger or is nervous, this response is activated. The sympathetic nervous system is also activated or increased during exercise. This may lead to the release of noradrenaline or norepinephrine from neurons, and with prolonged activation, adrenaline may also be released from the adrenal glands. The parasympathetic nervous system on the other hand normally slows the heart and reduces blood pressure. It's the parasympathetic nervous system has a higher activity during sleep relative to the sympathetic nervous system and after exercise. Release from the main nerve supplying the heart and playing an important part in the peripheral nervous system is the neurotransmitter called acetylcholine or citicoline. This substance is what is chiefly responsible for the reduction in heart rate and blood pressure. This slide summarizes the electromechanical coupling from action potential to cardiac contraction via calcium. As mentioned earlier, there's the electrical component of the heart that comes from the pace-making activity which leads to the spreading of an electrical front throughout the heart. It's through calcium where actin and myosin binding and lead to a mechanical component of the cardiac contraction as shown here. They can be displayed using a heat map of how it occurs. This is a diagram showing the cardiac muscle fibers and their orientation. You can see that it's not simply organized in one dimension, but it's very complex. There are circular arrangements, longitudinal as well as radial and other oblique arrangements of the muscles. The movements can be described as radial, longitudinal as well as torsion, twist, and other movements. The actual mechanical movements of the heart are very complicated, very complex. One way to characterize the cardiac cycle is by using the so-called pressure-volume loop. Because the heart is a mechanical structure, therefore it can generate different pressures depending on different parts of the cardiac cycle. Here you can see that when the mitral valve opens, the left ventricular volume is at its lowest as the heart fills. Then it reaches a certain point here where the mitral valve closes because the left ventricle begins contraction. This contraction is known as isovolumetric contraction. This is where the pressure increases tremendously. Up to a certain point when the mitral valve opens, releasing the blood into the aorta. When the systolic blood pressure reaches a certain level where the aortic pressure is similar to or above the left ventricle, the aortic valve would close, and this is when suddenly you have a drop in the left ventricular pressure. This pressure-volume loop happens with every heartbeat, and it can change with different preload or venous filling and different afterload depending on the arterial blood pressure as well as the intrinsic myocardial contractility. This is the Frank-Starling curve that governs cardiac output. What does this tell us? For the heart to squeeze, you need to have the filling of the heart and the venous return of the filling determines how much the left ventricle would squeeze. After we've talked about the Frank-Starling curve, here we summarized the Frank-Starling relationship, which is a result of intrinsic forces. These forces are also variable during exercise. The Frank-Starling relationship is also dependent on the magnitude of myocardial fiber stretch in diastole or during the relaxation of the heart, which governs the contractile force and the stroke volume (SV). As I mentioned earlier, venous return is very important during exercise. With increased venous return leading to increased ventricular volume loading and increased diastolic filling pressure (LVEDP). There is also intrinsic regulation of myocardial contractile forces that allow automatic adjustment of stroke volume to match the venous return. As mentioned earlier, there are extrinsic forces that can impact this, which include circulating adrenaline and noradrenaline from the sympathetic nervous system. In this slide, what we're trying to tell you is that depending on where about in the circulation, whether in the systemic circuit or the pulmonary circuit, there is a very variable change in blood pressure. Depending on which vessel you're in, in the arteries or arterioles, the pressure is normally high by the time you reach the capillaries. Much of this historic pressure has been attenuated by the arterials, and by the time you reach the venules. The pressure in the vessels is usually very low until you return to the heart. Again, the blood pressure itself is dictated by various factors and is a balance between vasoconstrictor and vasorelaxant. What regulates blood pressure are several very complex receptors in the receptors or sensors in the blood vessels. These sensors are in arteries as well as in veins. Much of what's in the arteries are mechanical sensors, also called baroreceptors. They are pressure sensors and with an increase or decrease in pressure, they would activate different nervous systems and alter the heart rate, blood pressure and other neurohormonal systems. A lot of that may be dependent on the brainstem, as well as the spinal cord. There are other receptors in the cardiopulmonary circuit, including chemoreceptors that sense pH, the partial pressure of CO2 (PCO2), partial pressure of oxygen (PO2) … etc. In the carotid arteries, there are even chemoreceptors that project from the brain to the several cerebral cortexes and may induce something called air hunger, which sometimes may occur in athletes when they're undergoing very intensive exercise. They're also metaboreceptors and skeletal muscles as well as vagal receptors that we've talked about earlier which originate in the brain. Other kinds of receptors determine what is called shortness of breath. This is an important symptom displayed by athletes or patients. They may be slowly adapting receptors (SARs) and rapidly adapting receptors (RARs) that sense different kinds of chemical substances in your circulation. There are also C-fibre receptors that work closely with the alveolar in the lungs. It's very complex. Then activation of respiratory muscles has recently been shown that is not essential for the perception of dyspnoea or shortness of breath. More importantly are the vagal receptors including C-fibre and other chemoreceptors that lead to the sensation of dyspnoea. As mentioned earlier, the sensation of dyspnoea is very complex. How does one perceive shortness of breath? Do you know that air hunger sensation? It's a very complex neurosensory balance showing here. (Part 2) Now we talk about cardiopulmonary interactions. It is a complicated relationship between the heart, pericardium, pleura and lungs, as respiration and cardiac function interact. There's the transmission of respirophasic changes and translation of this intrathoracic pressure with every breath. The basic physiology of the heart can be summarized by what goes on in the cardiac cycle. You have systole, which is when your cardiac muscles contract; in your diastole when cardiac muscles undergo relaxation and ventricular filling. Diastole represents 2/3 of the time in the cardiac cycle. The complexity of the cardiac cycle can be best represented by the Wiggers diagram, which is a simultaneous display of your electrocardiogram, heart sounds, ventricular pressure, and atrial pressure. So as you can envisage the electrocardiogram or electrical signal is almost like you're conductor then followed by different instruments that can play. Here you have atrial depolarization represented by the P wave and as you can see in their atrial systole here you have depolarization of the atrial tissues, eventually leading to your QRS and your ventricular systole. All this follows the electrical signals and below here you see heart sounds. S1 represents the closure of mitral and tricuspid valves whereas S2 represents the closure of aortic and pulmonary valves. So, all these can be represented simultaneously in a Wiggers diagram. The primary function of the heart is to maintain blood circulation and haemodynamics properties of your circulation. As mentioned in the last slide, closure of the S1 and S2 results from the closure of mitral and tricuspid valves, and aortic and pulmonary valves. The S2 heart sound can also be heard in normal individuals by a very rapid splitting. Now, other cardiac signs may or may not be normal. Flow murmur is considered normal, whereas S3, which is usually a lower frequency sound associated with heart failure, is abnormal. There are also other kinds of flow or flow murmurs that are abnormal, such as in individuals with atrial septal defects, or when there is a hole in the interatrial septum. Then there are also shunts that may be heard, depending on the defect or the abnormality. In patients with stiff ventricles, the blood hitting the ventricle can be heard as S4 and impaired in individuals with pericardial fluid. Sometimes a pericardial rub may be heard, so heart sounds can often be very informative to the experienced physicians. The heart also is an important endocrine organ that is underappreciated. It can release different types of peptide hormones that may also cause vasodilation, or also cause the kidneys to release fluid and sodium. There are other peptides and other substances that are increasingly being studied. The left ventricular function can best be analyzed by echocardiogram and typically to the right here you can see that what the sonographer or cardiologist has outlined is the endocardial border in diastole or end-diastolic diameter (EDD) in the apical four-chamber view. Then 90 degrees from this view is your apical two chambers view. Again, once you've outlined it, the echo machine can automatically create 20 slides, and then you do the same when the heart is in systole in different views. Through these four different views and with the endocardial border outlined, the computer can automatically generate an ejection fraction or percentage of your cardiac function. So, this is the most common method of analysis of LV systolic function. Studies have shown that the use of echo contrast may improve the accuracy of this assessment. And more recently, 3D echo is accurate as well, but the gold standard currently is cardiac MRI, which we'll see in a moment. There are other methods, including nuclear imaging and fluoroscopy which have been used, but they are not standard methods of quantification of LV systolic function. There's another less commonly used but more advanced imaging analysis called LV deformation or LV strain analysis, which uses tracking of different features on your echo image to obtain values. These values can represent subclinical or early changes in LV systolic dysfunction. Here to the left you can see a beating heart on a cardiac MRI, and the computer can help us to assess the LV systolic function by calculating the ejection fraction. This can also be done for the right heart, as will be discussed later. On the right, you have four panels showing the tracking of different parts of your ventricular wall and afterward it generates a 17-segment map or six 17-segment maps with different numbers to indicate how well different parts of the wall and how well the walls are moving. For the right heart, one could also use ejection fraction, but it turns out that echo has limitations for estimation of right ventricular function. So the best still is through the use of cardiac MRI. Now we come to a bit more physics to describe the different properties and behavior of the circulation as relevant to cardiac function. So often we go back to high school or secondary school physics. Ohm’s Law defines voltage as a product of the current and the resistance, so V equals IR. This can comprehensively describe the different pressures of the heart and different chambers and different parts of the circulation. Using Ohm’s law, the voltage would represent the pressure, whereas the current is represented by cardiac output which is the stroke volume times the heart rate and then lastly the resistance represents the resistance from the vessel wall. These are values that frequently define the different characteristics of the human dynamics. Here is a bit more detailed that's a little more advanced. Basically, all the R's represent resistance, so whether it's pulmonary vascular resistance, systemic vascular resistance…etc. These represent different parts of the circuit. For those interested in greater details, I encourage you to look them up in textbooks for further information. Now schematically we can show that the cardiac cycle depends on where you are in the pulmonary circulation here and depends on which phase of the cardiac cycle or rather the ECG cardiac cycle. You can see the pressure can change depending on where you are in circulation. This looks complicated but this is just to show you that all this can be mapped out because of the relationship that we know between the electrical signal, the anatomy, and then now the physiology represented by haemodynamics or pressure values depending on where they are in the pulmonary circulation. And then here is the cardiac cycle for the left heart in what is called the Wright table. You can also see that depending on whether it's the P wave, QRS complex, or the T wave on the ECG, it tracks with different pressures and in different parts of the heart depending on where the blood is.
