Unit 3 Cardiovascular System PDF

Unit Three The Cardiovascular System S1. Introduction to the Cardiovascular System  Overview of the Cardiovascular System Heart, Vessels, and Blood There are three components to the cardiovascular system 1. Heart: the pum...

Unit Three The Cardiovascular System S1. Introduction to the Cardiovascular System  Overview of the Cardiovascular System Heart, Vessels, and Blood There are three components to the cardiovascular system 1. Heart: the pump that creates pressure to move blood through the rest of the cardiovascular system 2. Vessels: tubes that blood flows through. Including arteries, arterioles, capillaries, venules, and veins. They all have a different structure that relates to their important functions 3. Blood: the fluid that carries important gases, like oxygen, nutrients, hormones, immune cells, proteins, and wastes Organization Pulmonary Circuit (think lungs)- heart sends blood to lungs for pick up of oxygen and deviver Cardiovasuclar Functions: carbon dioxide (a waste product) and send it back to heart through the pulmonary veins 1. distribution of blood to meet metabolic demands Systemic Circuit- blood leaves the heart through aorta to circulate through all the organs and tissue 2. enable exchange/delivery of nutrients, wastes, in the body (except for the lungs); goal is delivery of that oxygen that was picked up at the lungs and hormones to pick up waste to deliver it back to the lungs 3. role in heat regulation (how much blood enters your periphery might be different on a cold day vs. a warm day) Arteries- carry blood AWAY from the heart 4. essential for hemostasis (clotting) arteries become arterioles then capillaries Capillaries is where EXCHANGE occurs capillaries reunite to form venules and then veins Veins- carry blood BACK to the heart The Heart You can think of the heart as having a left side and a right side with a "wall" down the middle. The "wall" is called the septum. There are 4 chamberes: 2 atria (left and right) at the top, and 2 wentricles (left and right) below the atria. · Superior and Inferior Vena Cava 4. Pulmonary Artery Vena cava is the largest vein in your body. Together Blood that enters the pulmonary arteries will head to the the superior vena cava and inferior vena cava lungs, aka pulmonary circuit. We have a left and right 8 deliver blood back to the right side of the heart pulmonary artery to deliver blood to the left and right lung 4 from systemic circulation 4 5 Pulmonary Vein Superior- blood comes from your neck, chest, and. S We have 2 right pulmonary veins and 2 left pulmonary arms 6. 5 veins that collect blood from different areas of the right Inferior- blood come from your legs and feet plus and left lungs. These veins bring blood to the left side of abdominal and pelvic organs 2 A ⑭ ⑪ the heart FROM the pulmonary circuit (back to the heart). Right 2 Atrium. Left Atrium 6 Blood enters the right atrium from the systemic D ⑭ Blood enters the left atrium form the pulmonary circuit through circuit through the vena cava. This will send blood to # the pulmonary veins. It will be sent to left ventricle next your right ventricle next 7 * Left Atrioventricular Valve- prevents blood from flowing * Right Atrioventricular Valve- prevents blood from 3 1 backwards from left ventricle into the left atrium flowing backward from ventricle to atrium 3 Right Ventricle 7. Left Ventricle ⑭ This chamber will fill with blood that was in the left atrium. This chamber will fill w blood that was in the It’ will send blood out of the heart and into the systemic right atrium. It will send blood out of the heart # Left Ventricular Myocardium- notice how the circuit. Blood on this side of the heart has higher oxygen through the pulmonary arteries and into the left ventricular wall is thicker than the right and lower carbon dioxide than the right side bc it has pulmonary circuit, Blood on this side of the heart ventricular wall. The left ventricle has to create a collected blood from your lungs has lower oxygen and higher carbon dioxide than lot of pressure by contracting very forcefully to · Aortic Valve- prevents blood from moving back into the the left side bc it has collected blood from your move blood all the way around your systemic circuit. This is in part due to the effects of gravity. Ex. left ventricle from the aorta systemic organs and tissues where oxygen was dropped off and carbon dioxide was picked up Pushing against gravity when sending blood to the. Aorta 8 legs (more pressure required) whereas gravity is Blood entering the aorta from the left ventricle will head to ⑭ Pulmonary Valve- prevents blood from moving less of an issue when sending blood to the lungs the systemic circuit to be delivered to every organ and tissue back into right ventricle from the pulmonary (less pressure required) hence a thinner right in your body except the lungs. Aorta is the largest artery in arteries ventricular wall your body D Apex of the Heart- bottom of the heart.. When your ventricles contract, M Interventricular Septum- “wall” between your left and right they will contract starting at the apex, and then the “wave” of contraction ventricles, so blood cannot mix between these two chambers will spread upward to the top of the ventricles  How blood moves through the heart: direction matters! venaby , systemilation it is Pulmonary Pulmonary ↳of pulmonary artery r I Porticvalelation Arvaive pulmonary pulmonary value circut Heart Valves Prevent the backflow of blood that tries to enter the wrong chamber The Aortic and Pulmonary Valves The valves that blood must pass to leave the ventricles The pulmonary valve sends blood to the pulmonary arteries and into pulmonary circulation from the right ventricle The aortic valve sends blood to the aorta and into systemic circulation from the left ventricle. When looking from the aorta down into the ventricle, the valve looks like three little pockets. These “pockets” are called cusps. When blood tries to move backward into the ventricle, those cusps fill up with blood, causing them to expand and close The Atrioventricular (AV) Valves These valves have several different names eg. Semilunar valves or mitral and tricuspid valves. To keep things simple for physiology, we will call them the AV valves since they are found between the atria and the ventricles. These valves look different then the aortic or pulmonary valves but still close when blood tries to back up from the ventricle to the atrium Heart Sounds As these valves close, it changes the dynamics of blood flow which creates sound. When listening with a stethoscope, a normal heart has two dominant sounds, a “lub” and a “dub”. The first sound (lub) is created by the AV valves closing, which happens when the ventricles start to contract and blood attempts to head back to the atria. The dub sound is from the aortic and pulmonary valves closing as the ventricles begin to relax and blood attempts to head back into the ventricles. When listening with a stethoscope, different sounds may arise when valves are not functioning properly. If valves do not open properly, a condition known as stenosis, the sound may have a higher pitch. if valves don’t close properly, known as valve regurgitation, a swishing sound or whooshing sound may be detectable. We call these heart murmurs Heart arrhythmias are irregular heart contractions, may also be noticed while listening with a stethoscope  Cardiac Muscle & It’s Properties Cardiac Muscle The heart is an organ a bit larger than your clenched fist, which contracts and relaxes. Contraction and relaxation is possible because the majority of the heart is made up of cardiac muscle cells, known as cardiomyocytes. We have two types of cardiomyocytes: contractile cells, which are responsible for pumping blood through the heart and nodal/conducting calls, with are responsible for spreading electrical activity through the heart Contractile Cells The three requirements needed for a myofiber to contract and relax: ATP, and AP Similarities between skeletal myofibril and cardiomyocytes mmmm skeletal myofiber cardiomyocytes striated (thick and thin filaments) striated (thick and thin filaments) Ca2+ to contract (SR) Ca2+ to contract- difference is where calcium comes from- in cardiomyocytes some calcium can Mitochondria (for ATP) come from extracellular fluid and sarcoplasmic reticulum (the extracellular fluid calcium helps release Need AP (not neuron) the intracellular calcium → we call this calcium-induced calcium release) LOTS of mitochondria (for ATP) need AP- cardiomyocytes actually don’t require outside neurons, the heart can create its own action potential from nodal cells found within the heart itself Differences between skeletal myofibril and cardiomyocytes mmmun skeletal myofibril cardiomyocytes cylindrical cells branched cells Multinucleated single nucleus not electrically connected Electrical connected through gap junctions (special protein channel) Gap Junction- special channels that allow ions to pass and other small molecules between one cell and the next Nodal and Conducting Cells cell (can communicate directly) Intercalated Discs- helps lock the two cells together by Self-excitable → generates action potentials to spread way of special proteins known as desmosomes. Where through heart for contraction (makes sure that the heart gap junctions are found contracts in the appropriate order that it needs to contract eg. Atria then ventricles) Calcium-Induced Calcium Release S2. Electrical Activity In The Heart  Sinoatrial Node: Generating an Action Potential Electrical Activity and the Heart SA Nodal & conducting cells are self-excitable. We find these nodal & conducting cells in various places throughout the heart including the Sinoatrial Node, Atrioventricular (AV) Node, Atrioventricular bundle, and Subendocardial branches The Sinoatrial node is found in the upper right atrium, it is often considered the pacemaker of your heart. It sets your heart rate, determines how many beats per minute. RECAD OF NEURON Depolarization: Cell becomes more positive than RMP High conc of potassium inside cell (intracellular) and Neuron has RMP of approx -70mV. Repolarization: positive cell returns to RMP high conc. of sodium outside the cell (extracellular) Threshold is -55 What is different between a neuron that creates an AP and a nodal cell that creates an AP? Concentrations are the same from SA node also *kinda has a RMP, no stable RMP prevents + leaking Threshold in the nodal cell also has to be reached- Ca2+ and Na+ both move in to reach threshold, try to prevent & throug n their K+ from moving out when graded potential occurs ownvoltageare SA node is a pacemaker bc if your heart rate is 70bpm then the SA node fired 70 AP per minute, 100bpm means 100 AP were fired per minute Doesn’t stay at RMP for long Timeframe of AP in heart is much slower than neuron Depolarization Repolarizatinot Yellow line is graded potential- different than neuron graded potential because we have both Na+ and ca2+ entering while also preventing K+ from leaking out of the cell, this “graded potential” is now known as the pacemaker potential - Still have depolarization and repolarization, but no hyperpolarization Depolarization→ opening calcium voltage gated channels e n i Pacemaker Potential ↑ Na +, + Cat Nk+ , Repolarization→ opening of K+ channels, K+ leaking out i s The Conducting Pathway Through the Heart Focusing on how action potential reaches ALL contractile cells of your heart. Contractile cells in both atria and contractile cells in both ventricles of the heart need to receive these action potentials to help move calcium in from the extracellular fluid, which is crucial to facilitate the release of calcium-induced calcium released. Once calcium is in high contractions in the cytoplasm, then these contractile cells can do what they are meant to do—contract The pathway and coordination of contraction is so important. The atria and ventricles CANNOT both contract at the same time bc blood wouldn’t leave the heart. Instead, the atria contract first to move blood to the ventricles, and then the ventricles must contract to move blood out into the pulmonary arteries (right ventricle) and aorta (left ventricle) NOT E: the atria and ventricle contractile cells are not directly connected by gap junctions. Instead, to pass an AP from the atria to the ventricles, it MUST pass through the AV node. SA node has an intrinsic rate of 100 AP per minute. Why is your heart rate not 100 bpm? *pacemaker potential That AP can’t just stay in the SA node, we need the whole heart to contraction, we need to conduct that AP throughout the rest of the heart so that every muscle cell intrinsic rate : 100 Ap/min = in the atria and every contractile muscle cell in the ventricle contract. They need an AP to do that. How do we leave the SA node, which creates the AP, and then move it through the rest of the heart? One the SA node creates an AP, its neighbouring cells happen to be the atrial cardiomyocytes, so it travels to the atrial cardiomyocytes by gap junctions and cause those cells to be positively charged (by Ca2+) and create their own AP. AP is going to leave SA node, spread through the atria, atria get excited and depolarize( depolarization has to happen before they’re going to contract) atrial cardiomyocytes are going to to contract and move the blood into the ventricles. But we also have to send that AP then to the ventricles so they can contract and push the blood out of the heart. So, the next site that that AP is going to travel to is the atrioventricular node. The AV node provides the connection to send that AP between the atria and the ventricle. We have a pause, the AP slows down before it gets passed into the ventricles. We want to make sure that the atria finishes contracting before the ventricle contracts (we don’t want the top and the bottom of the heart contracting at the same time). Ap down From the AV node, AP heads to the arioventricular bundle, the atrioventricular slows I so atria can finish contracting bundle then spilts into bundle branches and AP travels down left and right befor ventricle contracts branches because we have a right and left ventricle that are going to need to contract simultaneously. 7 · - > Ventricular Cardiomyocytes Ap travels very fast ; Now we reach a system that is found in both the right and left walls of the · contracts very fast ventricles called the subendocardial branches. This is going to spread the AP (through gap junctions) from the base of the ventricles (the apex) towards the top of the ventricles. AP travels very fast here. Causing ventricular cardiomyocytes to contract from bottom up very fast Can the Sinoatrial Node Ever Fail? All nodal & conducting cells are self-excitable and create AP. However, it is the SA node that acts as the pacemaker of the heart because the intrinsic rate of generating action potentials in the SA node is fastest of all the nodal & conducting cells of the heart. Therefore, it depolarizes and spreads its AP before the rest have a chance to spontaneously fire action potentials. If the SA node were to fail, the AV node could take over as the pacemaker, since it is the next fastest to create action potentials. This would then spread the AP to the ventricles via the conducting system. Pacemaker Our hearts need to beat often enough to deliver blood and, most importantly, oxygen to our organs and tissues. If our heart rate it too low, it is called bradycardia, which can be dangerous and in some cases, surgery to insert a pacemaker may be required. A pacemaker may also be implanted if the heart has an irregular rhythm, called arrhythmia. A pacemaker → tiny device that is usually implanted under the collarbone, tiny wires attach the device to the heart which electrically stimulate the heart to contract, just like the sinoatrial node You often can't feel the pacemaker & only kicks when your heart needs it  Changing Your Heart Rate Resting heart rate is likely around 70-80 beats per minute. The average heart rate for a biological male is closer to 70 beats per minute, while the average heart rate for a biological female is around 80 beats per minute, simply because females tend to have smaller hearts. A trained athlete will possibly have a slower heart rate, maybe as low as 40-60 beats per minute. This is because your heart is more efficient at pumping blood as the cardiac muscles con contraction more forcefully, and, therefore, has to pump less often. We also discovered that the rate of the SA node is about 100 beats per minute. Your heart may also reach 140,150, or even 160 beats per minute when exercising. How high can our heart really get? This is age-dependent and can be approximated by the following equation: max heart rate= 220-your age in years The Mechanisms That Allow Our Heart to Speed Up or Slow Down ANS plays a significant role in pacing the heart, that's b/c the SA node cell Meeting receives input from both branches of the autonomic nervous system. It receives in put from the sympathetic nervous system (fight or flight) and parasympathetic nervous system (rest and digest) 1 K + leaking out The parasympathetic system (PSNS) is the system responsible for keeping your S SNS due decreasait to Ach " binding V & E ↓ Ach heart below 100bpm when your just sitting around resting PSNS -N choline muscarine Ach also pacemaker & ↓ decreases potential - SLOWING DOWN- The PSNS will communicate with a tissue, like the SA node, using neurotransmitters. The neurotransmitter is acetylcholine (Ach). Ach is going to bind to receptors on the cells of the SA node. Those receptors are called muscarinic - & receptors. How is that going to slow the heart rate down? wewant old tohappea slope By taking a longer time to reach threshold, so the pacemaker potential is going to take (decrease the a longer time to hit threshold. By What decreasing the slope, we wont hit an AP as quickly, therefore slowing the heart rate down How do you prevent the pacemaker potential from hitting threshold quite as quickly? We don't want it to get as positive as quickly/ make it longer for the inside of the cell to become more positive. When Ach binds to muscarinic receptors, it will decrease sodium permeability (less sodium will come in). Same thing with calcium. Also, when Ach binds to muscarinic receptors, it allows K+ to leak out (increasing permeability to potassium). So, whenever we activate our PSNS system, our rest& digest system, it decreases the scope of the pacemaker potential which is naturally going to slow your heart rate down. - SPEEDING UP- Activating our sympathetic nervous system (SNS), our fight or flight system, is responsible for increasing our heart rate above 100 bpm. Adrenergic receptors will bind SNS. norepinephrine to neurotransmitters released by the SNS. The neurotransmitter released by the SNS Tr is a is norepinephrine (NE). When these bind, the heart rate speeds up. ↑ PSNS - anpacemaker * anal & ↑NEincreases When we want to speed up the heart rate, we need it to hit threshold faster (than 0. 6 sec). Therefore we need to make the inside of the cell more positive faster. When NE and receptor bind, it activates cell to increase how much sodium f comes in. Same thing with calcium. wewantto happea ed faster (increasing the scope of pacemaker potential Important to note that the sympathetic system also triggers the release of epinephrine. This hormone can also act on cells of the SA node by binding to adrenergic receptors, and therefore, both norepinephrine and epinephrine can speed up heart rate  The Electrocardiogram (ECG) The electrocardiogram (ECG) gives healthcare providers important information about electrical activity in the heart. During this test, 10 sticky disks, known as electrodes are placed in various locations on the skin of the chest, arms, and legs. Depending on how the information is recorded, it can give 12 “views” of the hearts electrical activity from different directions. For example, from the front of the heart or sides of the heart. Therefore, it is referred to as a 12-lead ECG. It’s can be used to help diagnose heart arrhythmias, heart attacks, and conduction issues of the heart. How is the hearts electrical activity recorded from our skin? Your body fluids conduct electricity well. So as this AP is moving through your heart, we can pick it up from the surface of the skin by using electrodes. The ECG doesn’t give you an idea of what a single cell is doing, It gives you a sum of all electrical events in the heart. So it’s telling you how is those AP spreading across the whole heart, not necessarily through one AP or one place, but a global view of whats happening in the heart. From an ECG, you will see three obvious waves, each providing some information: The P Wave The QRS Wave The T Wave this electrical event is the result of this electrical event is the result of the this electrical event is the result of the DEPOLARIZAT ION of the atria of the heart. DEPOLARIZAT ION of the ventricles. Notice how REPOLARIZAT ION of the ventricles. Repolarization This is not measuring a single action potential much larger it is than the P wave. This is is also “up” in the ECG. During the AP, you have nut the sum of all action potentials occurring in because the ventricles have a much larger mass always seen repolarization as making the voltage of the atria. If you were to measure the time from and therefore more cells than the atria. With more a cell more negative. In fact, all three of these the start of one P wave to the next P wave, cells comes a larger electrical event. Measurements waves (P, QRS, and T) have an upward (more you could determine the heart rate of the time it takes from the P wave to the start positive) and then downward (more negative) of the QRS wave can indicate whether electrical component. That is because the direction of the conduction is normal between the atria and the wave (up or down) is determined by the direction ventricles. Other measurements, like the Q-T of the electrical activity toward a particular interval, can give indications about cardiac conditions electrode. If the electrical activity is heading towards the electrode, it is shown as an increase in voltage. As the electrical activity is heading away from that same electrode, it measures a decrease in voltage. If the atria depolarizers, why don’t they also repolarize? Well, they do. The atria Repolarization at about the same time as the QRS wave. And because the atria are smaller, their repolarization is masked by the large QRS activity as the ventricles are depolarization. So we don’t see a unique wave created by the atrial repolarization like we do for ventricular repolarization. S3. The Cardiac Cycle  Overview of the Cardiac Cycle Terminology Systole: this describes the period in time when cardiomyocytes are contracting (top number) Diastole: this describes the period in time when cardiomyocytes are relaxing (bottom number) The Cardiac Cycle Every single heartbeat you experience involves a series of different events known as the cardiac cycle. 1. Isovolumetric ventricular systole: this is when the ventricles start contracting but they aren’t yet able to pump blood out of the heart. Hence the term isovolumetric is used, as the volume of the ventricles don’t change 2. Ventricular systole: this is when the ventricles are contracting AND moving blood out of the heart and into the aorta (L ventricle) or pulmonary arteries (R ventricle) 3. Isovolumetric ventricular diastole: this is when the ventricles start relaxing but they aren’t yet able to fill with blood. Notice the word Isovolumetric here since ventricular volume isn’t changing 4. Late ventricular diastole: this is when the ventricles are relaxing AND starting to fill with blood from the atria 5. A trial systole: this is when the atria are contracting, moving blood into the ventricles NOT E: the atria do relax (atrial diastole), but similar to what we saw with the ECG, this takes place when the ventricles are contracting, so we don’t refer to it as one of the cardiac cycle phases sovolumetric ventricular systole very : narrow area; notice the 2345 ventricular volume is not here changing 2 Ventricular systole : ventricles start pumping blood into the aorta the ; ventricular volume starts decreasing in this phase 3 sovolumetric ventricular diastole : narrow area ; ventricles are relaxing but blood is not ventricles yet; volume entering isn't changing ↑ Late ventricular diastole : ventricles are now relaxing and to fill my blood They don't starting. actually fill up during this phase though they continue to fill during - atrial systole - 5 Atrial Systole : phase where atria pump blood into the ventricles this ; you can also see Phase before # at the left of the graph u Pressure (mmHg) → This diagram is showing pressure on the left side of the heart and into the aorta. We will only focus on the left side. Pressure are measured in millimeters of mercury (mmHg) In this top panel, we are seeing the pressure of the aorta, where blood is ejected into from the left ventricle. We also see pressure in the left atrium, which will receive blood from the pulmonary veins. Lastly, we see pressure in the left ventricle that will receive blood from the atrium and pump it into the aorta Mu Ventricular Volume (mL) → this shows the changes in volume within the left ventricle during different stages in the cardiac cycle. The volume is decreasing during ventricular systole and increasing starting in late ventricular diastole Mu Electrocardiogram → P wave, QRS complex, and T wave  * left side I only focusing on b /C different pressure on right side* left side pressure right !A side pressure ↳ Fressure 5 Phases (Blood always moves down a pressure gradient : High pressure - > low pressure 2) value (open or closed? 3) ECG before contraction - Av value - before relaxation Not an atomically correct ↑blood will only try and move back up close so that can't happen if ↑Pres in Atria then. ventricle, but , values Because the cardiac cycle is exactly that- a cycle- phases 1-5 repeat every single time you have a heartbeat Ventricular Systole: 2 Phases ventricles contract still contracting - # & - -see "equal volume" T even though ventricular contraction the volume in the is occurring , ventricle wont change [ - in order to getenticulation , you need entricularorization p [ no new ECG events QRS (ventricular depolarization) * started in atrial contraction/phases decrease ventricular volume & it's lowest leaving) change level here