in Chapter 17 we're gonna talk about normal cardiac function so we're gonna start talking about the heart which is located in the mediastinal cavity just in the central portion of the thorax the heart has both a base and an apex the base is the superior part of the heart and the apex is the inferior point where the ventricles converge at that inferior point it turns out that in the heart we have four different chambers we have the two superior atria and two inferior ventricles and these valves separate the heart chambers from their associated great vessels as well so the tricuspid valve separates the right atrium from the right ventricle the mitral or bicuspid valve separates the left atrium from the left ventricle and the pulmonic valve separates the right ventricle from the pulmonary trunk and the aortic valve separates the left ventricle from the aorta now the heart moves a lot which means that it could potentially experience a lot of friction on its surrounding tissues in order to reduce that friction the heart surrounded by a pericardial sac that helps protect the hearts and there's two layers of pericardium where the serious and fibrous pericardium the serous pericardium is more of a lubrication type of membrane that directly surrounds the outside surface of the heart it helps lubricate and prevents friction on the outside of the heart the fibrous pericardium is actually more of a tougher sort of tissue that surrounds even the serous pericardium and it actually prevents overfilling of the heart so looking at just general heart anatomy what we see in this picture is a cutaway view of the heart and some of the deeper structures so we find we have a right atrium and right ventricle these the two superior heart chambers deep too that are sort of inferior we have the ventricles so we have the right ventricle and the left ventricle and the atria and ventricles are separated by what we call the atrioventricular valves or AV valves this is the right atrial ventricular valve also called the tricuspid valve this is the left atrial ventricular valve also called the mitral valve now the right ventricle would pump blood up through the pulmonary trunk which branches into the pulmonary veins I'm sorry arteries which bring blood towards the lungs now what separates the pulmonary trunk from the right ventricle is the pulmonary semilunar valve or pulmonic valve and this effectively prevents backflow of blood from the pulmonary arteries back into the heart the left ventricle and you can see that the walls of the left ventricle are thicker because there's more muscle here the left ventricle pumps blood through the aortic semilunar valve up through the aorta and out to the rest of the body and so we talk about the left ventricle as being part of what we call the systemic circuit or systemic circulation which are all of the arteries that bass that go out to all of your major organs so it makes sense that the left ventricle we need to have thicker walls because has to pump blood farther and have has more resistance to overcome in terms of just general blood flow through the heart we'll start with the superior and inferior vena cava the superior vena cava drains blood from the head neck upper limbs and posterior thorax the inferior vena cava drains blood from everything that's inferior to the heart itself so what we find that is that blood from the head neck upper limbs and posterior thorax and everything below the heart will drain directly into the right atrium so this venous blood drains back in the right atrium when the right atrium contracts residual amount of blood will fill the right ventricle what happens next is that the ventricles will contract and the right ventricle will pump blood up through the pulmonary semilunar valve through the pulmonary trunk which branches into the left and right pulmonary arteries these pulmonary arteries carry this deoxygenated blood to the lungs whereby it becomes oxygenated then that oxygenated blood comes back to the heart through the pulmonary veins which we have left and the right pulmonary veins which drain into the left atrium then the left atrium when this contracts will blood into the left ventricle through the mitral valve or left AV valve and when the left ventricle contracts it'll pump blood up through the aortic semilunar valve did a Horta and beyond now the wall of the heart as we mentioned earlier is surrounded by a pericardium so and we have two types of pericardium serous and fibrous pericardium member serous membrane is more of a lubrication membrane and there's two layers to the serous membrane we have the visceral and parietal layers the visceral pericardium of serous pericardium is what's directly attached to the outside of the heart we also call this epicardium now this epicardium or visceral pericardium is separated from the parietal pericardium by a pericardial space in this pericardial space is actually a fluid filled space filled with serous fluid serous fluid is essentially a highly filtered blood plasma that has lubrication qualities to it and by separating these two layers with a fluid layer here we find that is that the heart will beat or pump within its own sort of fluid cavity that way it doesn't rub up against nearby tissues as much now this outer layer here then we have our parietal pericardium which is actually going to be connected to our fibrous pericardium the fibrous pericardium is a is a thicker layer of tissue that isn't really involved with lubrication it's thick and tough as sort of a fibrous tissue it actually prevents overfilling of the heart because the heart can pump blood so quickly that it can return blood to itself so quick tremendously that these heart chambers could potentially overfill so that's this fibrous pericardium prevents over filling of the hearts which is interesting now we talked about the right side of the heart as being part of the pulmonary circulation circulation because the right side of the heart will effectively pump blood towards the lungs through the pulmonary arteries now the left side of the heart then will receive that oxygenated blood from the lungs through the pulmonary veins and we talked about the left side of the heart is being part of the systemic circulation because it will pump blood through the aorta out towards the rest of your body whereby your body's tissues can use that oxygenated blood to support their metabolism and also help dump off their waste into the bloodstream and then veins will help carry those deoxygenated blood from organs back towards the right side your heart and the whole cycle completes so we have a right side on the left side of the heart we talked about the right atrium and right ventricle as being part of the pulmonary circulation and the left atrium left ventricle is being part of the systemic circulation now we know the heart is a muscular organ and as a muscular organ it needs to get its own blood supply now it's sort of almost counterintuitive to think about the heart is needing to receive its own blood if it's pumping blood but remember the heart chamber walls are thick enough to where you're gonna need blood vessels that go through the muscle and deliver nutrients through the way of capillaries to deeper areas of the tissue so this is actually achieved by the coronary arteries so the coronary arteries actually emerge from the aorta almost immediately as that a Horta begins so what this means is that the left ventricle pumping oxygenated blood out of the aorta well a small fraction of that blood that's being pushed up through the aorta will leave the aorta and enter the left and right coronary arteries now the left coronary artery will branch into a left anterior descending or left anterior interventricular artery as well as a circumflex artery and these mostly deliver oxygenated blood to the left ventricle and left side of the heart whereas the right coronary artery will branch out into a right marginal artery I'm sorry right marginal artery as well as a posterior interventricular artery which proceeds around the posterior part of the heart and so the right corner are a mostly delivers blood to the right structures of the heart like the right atrium and right ventricle now these vessels will become smaller and smaller and smaller until they get to the capillary level of blood vessels these capillaries will help deliver nutrients to the muscle tissue the heart as well as pick up wastes from that tissue and then those capillaries will reconverge into the coronary veins which carry deoxygenated and metabolic wastes rich blood back towards the heart so though in the for the coronary veins but we find that are things like your middle cardiac vein and on the anterior side we would have we would have the great cardiac vein on this side and all of these veins will reconverge at a place called the coronary sinus now the coronary sinus is basically a sinus of blood so it's a large chamber that can fill up with venous blood and this coronary sinus will actually drain blood back into the right atrium where it's delivered back into the pulmonary circulation and the whole cycle can repeat again now we talked about the cardiac cycle as all of the events that occur within each heartbeat and there are two main phases to the cardiac cycle we have systole and diastole if you have those systolic phases and diastolic phases and so what will happen is that systole is actually a state of contraction so while the hearts contracting we talk about this as being systole or systolic and diastolic is a state of heart muscle relaxation we refer to this as being diastole or diastolic and the events that occur in one cardiac cycle or basically is that interval in one heartbeat so what we find then is that once our atria enter systole this will force blood into the ventricles and the ventricles will fill with blood the amount of blood that fills those ventricles we call end systolic volume I'm sorry end diastolic volume and right before the ventricles contracts that volume of blood that's in the ventricles is the end diastolic volume now once the ventricles start to contract this occurs briefly after the atria start to relax or enter diastole and so the one the vector will start to contract this stimulates the closure of the AV valves because Bloods gonna be forced up against those valves causing the valves to snap shut in fact these AV valve snaps shut with so much force this causes the first heart sound or lub noise and the love dub sound or love dub lub dub lub dub so love is s 1 which is the closure of the AV valves during the beginning of ventricular systole now later on and ventricular systole the semilunar valves will open allowing blood to leave the ventricles through their respective great vessels like if it's the right ventricle blood will leave the pulmonary trunk if it's left ventricle blood belief in the aorta and as those ventricles start to relax or once they enter diastole when we find then is that pressure in the pulmonary trunk in aorta could be higher than pressure in the now relaxing ventricles which means that there will be a tendency for blood to want to flow back to where pressure is lower however we have the semilunar valves that prevent that backflow of blood from the pulmonary trunk or the aorta it's the closing of these semilunar valves during ventricular diastole that causes s 2 and s 2 is the second heart sound which is the dub noise and love dub in fact these simulator' valves closed with so much force it creates an audible sound we call s 2 so s 1 is actually going to be occurring during ventricular systole and it's due to closure of the AV valves s 2 occurs during ventricular diastole and it's due to closure of the signal intervals so if we if we can hear problems with either s 1 or s 2 this can indicate issues with these particular valves whether it's AV valves which would which occur during s 1 and/or the same liter valves which closed during s 2 now ventricular ejection is the amount of blood that's basically ejected by the ventricle in one contraction and another word we took we call this a stroke volume so stroke volume is the amount of blood that's ejected during each contraction now there's a way we can calculate stroke volume and we can basically look at this as end diastolic volume - and systolic volume remember n - volume is the amount of blood that fills the ventricles at the end of diastole right before ventricular systole so this means that this is should be a large volume of blood if we subtract the amount of blood that filled the ventricles - our insiste Dalek volume which is the amount of blood that remains in the ventricles at the end of systole hence the name and systolic volume so it's the amount of blood that filled the ventricle - the amount of blood that's left behind the ventricle well that tells us about how much blood left the ventricles which their stroke volume it's it could be important or stroke flowing because we can calculate cardiac output as a function of stroke volume and a normal ejection fraction should be about sixty to eighty percent so what we should find then is that approximately you know 60 or 80 percent of the of the blood that filled the ventricles should be ejected during a normal amount of stroke volume if this ejection fraction is below normal it could indicate cardiomyopathy or basically muscle disease where the maybe the muscle can't functionally contract strong enough to pump enough blood out of the ventricle during each beat now there are two types of cardiac muscle cells we have the the muscle cells called the cardiac myocytes that produce mechanical pumping functions as well as other cardiomyocytes whose sole purpose is to conduct electrical impulses remember we talked about the heart as being autorhythmic which means it can generate its own electrical impulses at a certain rhythm or frequency and these electrical impulses will spread throughout the heart in a directed and coordinated manner that way blood is effectively pumped through the heart chambers and out of the heart now these electrical cells their sole purpose is to basically conduct those electrical impulses around the heart once these electrical impulses reach the cardiomyocytes these electrical impulses are action potentials can stimulate the contraction phase of these muscle cells to begin mechanical pumping functions of the heart so what these cells look like then are striated so they have striations which relate to the sarcomeres or contraction proteins you find deep within the cardiac muscle cells now these cardiac muscle cells are also branched many of them are branched into Y shaped patterns these cells are short and they're interconnected by what we call these intercalated discs so microscopically these intercalated discs look like these basically little borders or lines like these thicker dark lines now these intercalated discs are basically full of gap junctions and desmosomes remember gap junctions are protein tubes that allow for molecules to spread from one cell to the next and desmosomes are a supporting type of protein that can hold these cells together very tightly so knowing that these cells are interconnected by gap junctions then we can guess then that electrical currents could spread from one cardiac muscle cell to the next through these gap junctions and this is one of the ways that electrical currents can basically spread rapidly across the heart now inside of a cardiac muscle cell we find that our a lot of myofibrils and these myofibrils are basically big ol bundles of protein there's two main types of protein you find in each myofibril we have the thick filaments and thin filaments the thick filaments are comprised of myosin heads that are basically enzymes that use ATP to produce contraction force and then the thin filaments are mostly comprised of actin which serve as the binding sites for the myosin heads so what this means these myofibrils are composed of comprised of proteins that effectively pull on one another to produce contraction which is basically a shortening type of force that our muscle cells can use to produce a pumping action now our cardiac muscle cells are also full of a specialized type of endoplasmic reticulum called sarcoplasmic reticulum now sarcoplasmic reticulum is basically like a big old bag of calcium within these cardiac muscle cells and we know that calcium is important in the muscle contraction cycle because calcium serves is one of the initiating stimuli to get contraction to begin so it would make sense that you'd have a lot of sarcoplasmic reticulum within these cardiac muscle cells because it's one of the signals that can be released to get contraction to begin so effectively what happens is what's action potentials spread across these cardiac muscle cells they can those electrical impulses or action potentials can travel down these tubes going deep into the cell called a t2 Buhl and along the way these these t tubules have voltage-gated channels that allow for an influx of positively charged ions like calcium and sodium now these cations or positive charged ions can stimulate the release of additional calcium from the sarcoplasmic reticulum once you get a sufficient amount of calcium release from the SR that can actually go over to the myofibrils and help initiate those myofibrils to begin contraction so under a microscope you can see what these myofibrils can look like so here's one mile fibril under an electron microscope in fact this is a type of electron microscope picture called a transmission electron microscopes you're actually looking into the cell and what you're seeing here is basically a sarcomere so from z-disc to z-disk this is one sarcomere and within this you'd have the thick and thin filaments that pull on each other nearby you can find a lot of mitochondria as well so here you're seeing mitochondria and it makes sense you have a lot of mitochondria within these muscle cells because all of this requires a tremendous amount of ATP now remember the thick filaments are comprised of your mouse and heads and these myosin heads are basically enzymes that use the chemical energy and ATP to produce a contraction type of force the thin filaments have actin and actin serves as a binding site for the mouse and heads you find on the thick filament we also find associated with actin are proteins like tropomyosin and troponin tropomyosin is a type of ribbon shaped protein that wraps around actin thin filaments and it blocks the binding sites on actin while the muscles at rest troponin is a must as a protein that's associated with tropomyosin however troponin is a calcium sensitive protein so when calcium binds to troponin this initiates a conformational change in the protein that causes tropomyosin to move the way exposing the actin binding sites which then allow the myosin heads to bind and complete their power stroke or contraction cycle which produces a tension type of force that your muscle cells can use to pump blood so we're seeing here that is the contraction cycle so here's a thick filament here's our thin filament on the thick filament we find our myosin heads which effectively can use ATP to help contract and use that force of contraction to pull on the thin filament now while the muscles at rest what we find then is that this ribbon shape protein that wraps around the thin filament called triple myosin blocks the binding sites on tropomyosin troponin is a calcium sensitive protein and when calcium binds to troponin troponin effectively changes shape enough that it can pull on tropomyosin and it's then exposed the binding sites for actin once these actin binding sites are available and exposed the myosin binding site of myosin heads can bind to their active site on the thin filament on actin and for what we call a cross bridge once they bind these effectively flex and that process of flexion here contraction will sort of pull on the thin filament in a way that produces tension or force once they've flexed the myosin heads can actually have ATP a new ATP molecule bind which helps initiate the unbinding on the myosin head and the whole process will repeat so long as ATP and calcium are available and present now the role of calcium here like we talked about is that it helps initiate the contraction cycle so the concentration of calcium is going to be dependent on the amount of calcium that's released from sarcoplasmic reticulum and this is actually going to be what helps also determine how many actin sites are exposed as well as for how long which also determines how many cross bridges can be formed which also determines the extent of contraction so we talked about hormones like epinephrine that cause your heart to contract or beat more strongly epinephrine as a hormone has an effect on your cardiac muscle cells to increase the concentration of calcium in those muscle cells to a greater level also at a quicker rate so that when you increase the calcium concentrations that muscle cell rapidly enough this allows for more of the myosin heads to bind which that allows for more cross bridges to form which then produces a greater force of contraction now it turns out that it takes a significant amount of energy for muscle cells to relax as well because once that calcium ends up in the cytoplasm of the muscle cell it has to be pumped back in the sarcoplasmic reticulum otherwise you'd have a sustained contraction which we call tetanus which as far as the heart is concerned you wouldn't want tetanus to occur in the heart because then your heart muscle couldn't relax and therefore it couldn't fill up with blood again so it wouldn't function as an effective pump very well so it does take a lot of energy to have a muscle cell contract but also takes energy for muscles to relax as well so it takes ATP to actually pump or sorry ATP to help power these membrane pumps that can actually pump calcium back out of the cytoplasm back in the sarcoplasmic reticulum or out of the muscle cell so what we're seeing here is basically how ATP can be used to pump calcium back out in fact if calcium is removed more quickly than your heart muscle cells can relax more rapidly and you should expect then as well that you'd want this to occur once you seeing more rapid heartbeats because in order for the next beat to occur you need your heart muscle to relax so that epinephrine also has the effect of allowing calcium to be pumped out of cells more rapidly or pumped back into the sarcoplasmic reticulum more rapidly which means the heart muscle cells can relax more quickly which means you have a shorter amount of time before you can actually get another heart muscle cell contraction so it's an interesting effect there now we talked about calcium channel blockers you should expect then that if you block these calcium channels that heart muscles would probably our muscle cells would probably contractions that take a little bit longer to relax so it's going to help slow your heart rate down and decrease the frequency of heartbeats now we know that your heart requires a tremendous amount of ATP it turns out that we get most of our ATP from aerobic respiration or aerobic processes in ourselves so most of the ATP that we can make in our heart muscle cells comes from oxidative phosphorylation in the mitochondria which does require a significant amount of oxygen however the heart can still function under low oxygen conditions because it stores different forms of chemical energy like creatine phosphate or CP which is basically an enzyme that can are sorry it's a molecule that can store chemical energy in a more stable form and you can use this creatine phosphate to generate more ATP under conditions of low oxygen concentrations so this enzyme creatine kinase can take what's available ATP use some of the phosphate on that ATP to phosphorylate creatinine and that we can take creatine phosphate and basically store ATP for later use in the form of creatine phosphate now the reason why you want to store a ATP or basically these phosphate bonds on creatine phosphate is that CP is a more stable chemical versus ATP ATP is more unstable and therefore more likely to spontaneously to generate which means that you can just lose that chemical energy as heat instead of using that for work so it makes more sense to store chemical energy in the form of creatine phosphate in the long term now creatine kinase can be a useful way to determine myocardial cell damage let's say if you suspect someone having a heart attack what you can do then is actually take a sample of blood measure the concentrations that creatine kinase in their bloodstream as an indicator of how much muscle cell damage there may be because you normally shouldn't find an enzyme that's in a cardiac muscle cell and high concentrations in their bloodstream if you find this cardiac muscle cell enzyme in the bloodstream what that suggests then at least if it's in high concentration is that a you know a significant amount of cardiac muscle cells have died lysed open and therefore spilled out their proteins into the bloodstream now your heart will primarily use fatty acids and glucose to create ATP however under some more extreme conditions the heart can use lactate which is the conjugate base of lactic acid as well as ketones to also make some ATP so it's interesting that you know let's say during during extreme or intense exercise and you're generating a lot of lactic acid your heart can actually use lactate to make ATP or if you have extremely low blood glucose levels and you're you're making a lot of ketones to supply different metabolic processes or in your body while these ketones can also be used by your heart for ATP production now we know that the heart is rhythmically activated by action potentials and we also know that the heart is autorhythmic or can basically generate an action potentials on its own so it's important to talk about cardiac electrophysiology or basically the electrical processes of the heart because many different cardiac disorders are derived from abnormal electrical phenomena in the heart so we'll first talk about this cardiac resting potential and so resting potential is basically resting voltage which you find in these cardiac muscle cells now resting voltage is a negative value and all this means is basically the inside of the cell is is slightly more negative with reference to the outside of the cell and this difference in charge relates to the differences in protein and other ion concentrations inside nets of the cell it turns out we have a significant more potassium inside the cell and more sodium outside of the cell and this difference in ionic concentration is what's helped helps determine resting membrane potential now the cardiac action potential which is basically an electrical impulse that travels in a cardiac muscle cell occurs in three main phases we have a rising phase a plateau phase and a falling phase and what this what we're seeing this this particular graph is voltage over time so when an action potential travels across the cardiac muscle cell we find that is that we see rapid rises in voltage followed by a plateau in that voltage and a falling phase or when the voltage becomes more negative and it's due to the movement of various ions so we find that as the rising phase of the cardiac action potential is primarily due to a rapid influx of sodium through voltage-gated sodium channels and this influx of positively charged sodium makes the inside of the cell more positive which causes this rising phase here and then the plateau here is actually caused by an e flux of pitar influx of calcium and an e flux of potassium it's sort of the balance of this movement of the cations here that causes a slight plateau and then finally we get these voltage-gated calcium channels that closed and we primarily get a potassium efflux that helps bring our voltage back down to a resting value now this particular action potential looks different than other action potentials in your body like the ones you'd find in neurons and skeletal muscle are much more brief you know a neuron and skeletal muscle action potential is about one millisecond in duration whereas this one here is close to a hundred milliseconds which is one tenth of a second so the cardiac action potentials are longer and by having a longer action potential this helps sure a nice sort of lung contraction rather than a brief sort of quick twitch in muscle and you'd want to have a nice long contraction of muscle because the heart functions as a pump not as a trishing organ because if the heart only twitch that it wouldn't really pump blood very well now the rhythmicity of the heart comes from these autorhythmic cells which are part of your electrical conducting pathway of the heart so the auto all along this electrical conducting pathway especially in areas like the a trio of an sinoatrial node the atrioventricular node the bundle of branches and the Purkinje fibers and we call these autorhythmic because they can generate their own action potentials without the nervous system so without the nervous system we call this automaticity meaning that actually can occur on on its own without nervous system stimulation although the heart does get nervous system stimulation it could potentially beat and regulate its own heartbeat on its own now we talk about the SA node or sinoatrial node as being the pacemaker of the heart and the reason being is it generates action potentials at them at the fastest rate so because it's generating the fastest rate of action potentials it sort of sets the pace of all other pacemaker cells and what this electrical conducting pathway of the heart looks like is we have basically deep within the heart muscle tissue itself we find this electrical conducting system so here's the SA node and here's the AV node which are basically just collections of autorhythmic cells now the SA node and AV node are connected by internodal pathways which spread across the atria now the AV node is gonna be connected to an AV bundle or bundle 'his which then branches out into the bundle branches the bundle branches continue down the interventricular septum of the heart towards the apex where that then branches into the Purkinje fibers that can stimulate heart muscle from the apex and superior lis now it turns out the action potentials in the heart typically you will only travel in one direction from superior to inferior in the back up along the lateral aspects of the heart itself so what this means that action potentials begin in the SA node they spread across the atria through these internodal pathways to the atrioventricular node whereby at the atrioventricular node action potentials are held up for a brief period of time because the AV bundle of hisses as an anatomical bottleneck now which basically slows down action potentials once those action potentials travel down the AV bundle they'll travel through the bundle branches going to the left and the right and then along the bundle branches through the Purkinje fibers and then up back along the heart and the vegetables so we find that is that because action potentials travel in this particular direction we also see that that heart muscle will contract in a particular order as well so knowing that action potentials begin near the atria we find that as the atria are the first to contract because they're the closest to the initiation of those action potentials second to that then would be the ventricles contracting because it takes longer for action potentials to spread towards the ventricles and then the then they'll track contracts second now we can measure the electrical activities of the heart using an electrocardiogram or EKG which is shown over here EKG has many different waveforms but there are several key waveforms are out sort of a large ones we have the P wave here the QRS wave and a T wave here and sometimes a u wave which we'll come to in later chapters now the P wave is a change in the electromagnetic fields in your body due to electrical activity in the atria so P wave here in the EKG indicates atrial electrical activity the QRS wave here indicates ventricular electrical activity and the T wave also indicates ventricular electrical activity now we can build on this and be a little more specific where the P wave actually represents atrial depolarization and depolarization is the same as the rising phase of the action potential where the voltage inside your muscle cells is becoming more positive because action potentials are beginning so P wave is atrial depolarization QRS wave is ventricular depolarization and we see there's a delay then between P and Q waves so we call this the PQ interval and this is an important interval because it tells us then that electrical activity is occurring in different periods of time and there may be a sufficient amount of delay then between the atria and ventricles that allows the ventricles to adequately fill with blood so the QRS wave is actually going to be ventricular depolarization and then the T wave here is vent is ventricular repolarization where the ventricles are starting to become more negative again and that decrease in voltage also creates a measurable change in electromagnetic fields of your body which we call the T wave here and you might wonder well if we have a P wave which is atrial depolarization where is atrial repolarization well atrial repolarization occurs during the QRS wave and it contributes to the shape of this wave although it contributes to a sort of a minor way atrial repolarization is sort of hidden or masked by the tremendous amount of electrical activity you find during the ventricles during ventricular depolarization which is what we call the QRS wave now it turns out that we know that our heart actually is also innervated by the autonomic nervous system so it receives both sympathetic and parasympathetic inputs parasympathetic nervous system innervates the heart but by the way of the vagus nerves which is cranial nerve number 10 and the vagus nerves can actually supply information to your SA and AV nodes and ultimately the function of the parasympathetic nervous system on the heart is to slow down the rate of heart muscle contraction in the absence of any court kind of parasympathetic or sympathetic information the heart would beat at approximately 100 beats per minute so that's its intrinsic rate of contraction but we know that while at rest your heart rate typically isn't around 100 beats per minute we find that is that there's a sort of basal or resting amount of parasympathetic activity that can inhibit your heart and slow it down to a more restful state you know around 70 beats per minute or so would be average or I suppose normal now the heart also receives sympathetic input in several different ways there are sympathetic nerves that originate from the the thoracic spine that can innervate the heart directly and stimulate heart muscle to contract more strongly and beat more rapidly and the heart also has beta 1 receptors that are sensitive to epinephrine and norepinephrine which can be released by the adrenal medulla so that the heart also receives hormonal stimulation in fact sympathetic hormones can increase heart rate and heart muscle contraction so the sympathetic effect on the heart is that it can increase its rate of contraction we call us a chronic tropic effect as well as the speed of conduction and conduction or drama tropic effect and the force of contraction which is an ionotropic effect so we talked about epinephrine and norepinephrine as being positive inotropic agents meaning that could actually stimulate the heart muscle to contract more strongly by binding to beta 1 receptors in the heart which influence calcium regulation in the heart which we talked about earlier sympathetic nervous system actually will slow heart rate but it turns out that the sympathetic nervous system doesn't really have much of an effect on must the the strength of muscle contraction mostly just the heart rate itself and the parasympathetic nervous system has different effects than the sympathetic nervous system because the parasympathetic nerves can activate a different variety of receptor we called muscarinic receptors which help to slow down your heart rate by also affecting or influencing calcium regulation within those cells now earlier we talked about the EKG or ECG which is electrocardiogram and there's different wave forms like pqrst a new wave the P wave corresponds with atrial depolarization QRS wave corresponds with ventricular depolarization T wave was ventricular repolarization and a u wave can occur during slow rates or during certain electrolyte imbalances like low potassium levels or hypokalemia so just looking at a normal EKG what we find that as our P wave QRS and T wave this one looks a little bit more detail than our previous one because we can find then it are some of the more minut inflections you can see here you know there are some other dips that can occur here and this is showing a more normal type of EKG or ECG here's that little u wave off the side which you're gonna you can see during bradycardia or slower heart rate or hypokalemia or low potassium now these waveforms should occur in certain intervals and we can actually measure their intervals to tell us a little bit about how the heart's conducting these action potentials so we talked about PR intervals and QRS intervals and ST segments and QT intervals and we'll come back to these intervals later when we talk about the diseases of the heart that affects its electrical properties now the determinants of cardiac output relate to things that can affect stroke volume and heart rate so cardiac output is the amount of blood that's pumped out of your heart during one minute and normal resting cardiac output it's about five to six liters of blood and going back to our blood chapter we learned about this is about the normal blood volume so even at rest your heart can pump the entirety of your Bloods volume in one minute now we can calculate cardiac output as stroke volume times heart rate remember stroke volume is the amount of blood that's ejected from your heart in each contraction heart rate is the amount of contractions per minute so what cardiac output tells us then is the amount of blood that's pumped at your heart per minute and we know that cardiac output is also proportional to blood pressure so if you can increase cardiac output you can increase blood pressure if you decrease cardiac output this could potentially decrease blood pressure now we know that heart rates influenced by the sympathetic nervous system and the parasympathetic nervous system so remember of the parasympathetic nervous system will slow heart rate down to its resting level of 70 beats per minute or less whereas the sympathetic nervous system can speed up heart rate to more maximal levels like in the hundreds of beats per minute now there are other determinants of heart rate as well like atrial or ventricular distension can actually suppress I'm sorry can actually speed up heart rate we call this the bane reflux so the Bainbridge reflux is when the atria stretch this sexually stimulates the heart to increase its rate of contraction and you expect that this makes sense because of the atria are stretching you want the heart to keep up with venous return and so this would also speed up the heart rate in order to keep blood flowing along in a more normal amount now there are baroreceptors throughout your body like baroreceptors in the in the carotid bodies which is where your common carotid will branch off into internal next you'll accredits these bear receptors can detect blood pressure so blood pressure Falls then we have will have a sympathetic reflex which relates to the vasomotor center of your medulla which acts to increase heart rate and if blood pressure's too high we can have a parasympathetic reflex that can act to inhibit heart rate to decrease cardiac output and therefore decrease our blood pressure so there are other determinants of heart rate things like anxiety fear stress excitement trauma fever drugs or vagus nerve stimulation and these are all things to consider while you're doing sort of clinical assessments because if someone's heart rate and blood pressure appear to be really high these are all confounding sort of situational variables that could give you sort of false data or data that does is an indicative of you know sort of this the state of that person outside of that particular circumstance now there's also something called the frank-starling law in the heart as well and the frank-starling law tells us that when we have increased preload preload is relates to the amount of blood that fills the ventricles so preload is synonymous with end diastolic volume but when we have an increase in preload or end diastolic volume this causes our sarcomeres in the myofibrils to stretch which results in more forceful contraction which increases stroke volume so we find then is a really neat phenomenon the heart is that with increased ventricular filling you get more forceful contraction which increases stroke volume so if you can increase your venous return to the heart you can increase the amount of blood that those those ventricles which then causes the ventricles to stretch more which then also stimulates stronger contractions which increase stroke volume so just by increasing venous return you can actually get increases in cardiac output by influencing how strongly your heart muscle contracts now there are other hormones that are made by the heart like the natural peptides we have atrial natriuretic peptide and B type natural peptide these are produced by the cardiomyocytes in response to stretch and what these hormones do and we've talked about these in previous chapters is they actually act on the kidneys to inhibit the reabsorption of sodium which then also promotes the loss of water and if you lose water then you're gonna decrease blood pressure and it makes sense then that the heart would release these hormones when the heart muscle is stretched chronically because you should expect then that heart muscle could be overfilled and stretched if the blood pressure is too high so these hormones are released by the heart to help diminish blood pressure in the long term in fact you can look at the concentrations of a and P and B and P as markers of chronic hypertension now there are different tests of cardiac function like ECG which can tell us about conduction of electrical activity in our heart echocardiography which can tell us give us sort of an image of the heart in real time or cardiac catherization which can give us a more direct assessment of cardiac function like direct blood pressure changes in any of the heart chambers