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BIOL 273
Heidi Engelhardt

BIOL 273 Midterm #2 Notes Cardiovascular Physiology Introduction • In the simplest terms, a cardiovascular system is a series of tubes (the blood vessels) filled with fluid (blood) and connected to a pump (the heart) o Pressure generated in the heart propels blood through the system continuously o The blood picks up oxygen at the lungs and nutrients in the intestine, delivering them to cells, while simultaneously removing cellular wastes for excretion The Cardiovascular System Consists of the Heart and Blood Vessels • The cardiovascular system is composed of the heart, the blood vessels, and the cells and plasma of the blood o Blood vessels that carry blood away from the heart are called arteries o Those which return blood to the heart are called veins • The heart is divided into left and right halves by a central wall called a septum o Each half has an atrium (receives blood to the heart from blood vessels) and a ventricle (pumps blood out to the blood vessels) o SEE FIGURE 14.1, PAGE 451 • The right side of the heart gets blood from the tissues then sends it to the lungs to be oxygenated (recycled almost?) • The left side of the heart receives blood from the lungs which was just oxygenated and then gives it out to the tissues • In the figure you can see blue and red blood – this is because de-oxygenated blood is bluish, and so for example blood going to the lungs for oxygenation or blood coming back to the heart from the tissues (as we can see in our veins) would be blue • So blood flows from the right atrium into the right ventricle, then out through the pulmonary arteries (since any blood outgoing from the heart is in arteries) to the lungs • Then the lungs finish their duty and the blood goes through pulmonary veins to the left atria, then the left ventricles o So this pulmonary artery/vein combination is known as the pulmonary circulation • And then blood finally leaves the heart for the rest of the body, and the first step is for it to enter a large artery called the aorta o From here we branch into smaller arteries, and then finally capillaries, which are very small thin-walled vessels where the exchange of material between blood and tissues actually takes place • After going through the capillaries, we are now on our way back to the heart, and so we enter veins – going from small ones to larger ones o The veins from the upper part of the body are called superior vena cava, while the lower ones are called inferior vena cava o And both of these, as mentioned previously, end up in the right atrium The Heart Has 4 Chambers • The heart lies in the center of the thoracic cavity o SEE ALL OF FIGURE 14.7, PAGE 456 • It is encased in a tough membranous sac, the pericardium o And there is pericardial fluid, which lubricates the external surface of the heart as it beats within the sac • The heart itself is mostly composed of cardiac muscle, also known as myocardium o It is covered by thin inner and outer layers of epithelium and connective tissue • The left and right sides of the heart are separated by the interventricular septum • The heart contracts as one – first the atria contract together, then the ventricles contract • If you look at the diagrams, you will see that the blood enters the ventricles at the top of the chamber, but also leaves from there o This means that the ventricles have to contract from the bottom up so that blood can be squeezed out at the top • The heart contains 4 fibrous connective tissue rings which surround the openings to the major arteries and the openings between the chambers o The tissue acts as an insulator (blocks electrical signals) Heart Valves Ensure One-Way Flow in the Heart • SEE FIGURE 14.7, PAGE 457 • There is one set of valves between the atria and the ventricles (because we always want to be going from the atria to the ventricles) • And the other set of valves is between the ventricles and the arteries • The passageways between the atria and the ventricles are guarded by the atrioventricular, or AV, valves o These things are thin flaps of tissue attached at their base to a ring of connective tissue o The flaps are slightly thickened at the edge and are attached on the ventricular side to collagenous cords, the chordae tendineae  SEE FIGURE 14.9BD, PAGE 460 o And then the cords are tethered (on the other end) papillary muscles, which are moundlike extensions of ventricular muscle • So when the ventricle contracts, we have all this blood pushing up against the valve, but because of these heartstrings (chordae tendinae), the valve does not get pushed all the way through into the atrium o The valve on the right side is called the tricuspid valve because it has three flaps, but the left side is the bicuspid or mitral valve (it has 2 flaps) • And then the second set of valves is from the ventricles into the arteries – these ensure that blood which is pumped out of the heart doesn’t return to it • They are called the semilunar valves because they look like a crescent moon o Either the aortic valve or pulmonary valve o They have 3 cup-like leaflets which fill up with blood then snap closed when backward pressure is exerted on them o SEE FIGURE 14.9C, PAGE 460 Cardiac Muscle Cells Contract without Nervous Stimulation • Most cardiac muscle is contractile, but 1% of the myocardial cells are specialized to generate action potentials spontaneously – this means that the heart can contract without any outside signal • The signal for contraction, then, comes from specialized myocardial cells known as auto-rhythmic cells called pacemakers o But these things are smaller and contain less contractile fibers than a contractile cell, so they don’t contribute to the contractile force of the heart • Here are ways cardiac muscle is different from skeletal muscle but the same as smooth muscle: o They are smaller than skeletal muscle fibers and have a single nucleus per fiber o Individual cardiac muscle cells branch and join neighboring cells end-to- end to create a complex network  SEE FIGURE 14.10B, PAGE 461  The part (cell junction) where the cells join together is called an intercalated disk  Here we have interdigitated membranes linked by desmosomes which tie adjacent cells together – this allows force to be transferred between cells  The t-tubules are much larger for myocardial cells, and they actually branch inside the cell  The sarcoplasmic reticulum is smaller than of skeletal muscle (cardiac muscle depends more on extracellular Ca2+ to initiate contraction)  Mitochondria make up about 1/3 of a muscle cell because they need so much energy, as they extract a lot of oxygen  Cardiac muscle cells are electrically connected to each other via gap junctions in the intercalated disks – thus the signals can travel fast, and the heart can beat all as one Cardiac EC Coupling Combines Features of Skeletal and Smooth Muscle • So before, we needed acetylcholine to cause an action potential, and then excitation-contraction (EC) coupling would start • In cardiac cells, we don’t need acetylcholine, although EC coupling is still initiated through an action potential o This AP is spontaneous in the pacemaker cells, and it quickly spreads into the contractile cells through gap junctions • When an action potential enters a contractile cell, it spreads along the sarcolemma and into the t-tubules, where it opens voltage-gated Ca2+ channels in the membrane o Ca2+ enters and in turn opens ryanodine receptor-channels (RyR) in the sarcoplasmic reticulum o Now these RyR in turn are Ca2+ channels, so here we have the phenomenon where we have Ca2+ induced Ca2+ release o Because we get stored Ca2+ flowing out of the SR and into the cytosol, and enough RyR channels doing this summates to form a Ca2+ signal o Then as usual, the Ca2+ diffuses across the cytosol to the contractile elements, where we bond to troponin and crossbridge formation starts, and so on  We still have the same sliding filament movement going on as before • When relaxation comes, it’s because Ca2+ unbinds from the troponin – we have something called Ca2+ ATPase which takes the calcium ions back into the sarcoplasmic reticulum o Ca2+ can also be removed through Na-Ca antiport proteins, which trade Ca2+ for Na which is outside the cell • SEE FIGURE 14.11, PAGE 462 Cardiac Muscle Contraction can be Graded • One good thing cardiac muscle cells have is the ability to execute graded contractions o So the strength is proportional to the number of crossbridges which are active, and this in turn is determined by how much Ca2+ is bound to troponin • Therefore, the catecholamines epinephrine and norepinephrine are regulatory molecules which affect the amount of Ca2+ available for cardiac muscle contraction o These things activate beta adrenergic receptors, which open more voltage gated Ca2+ channels • We can also increase this through the phosphorylation of a regulatory protein known as phospholamban, because this enhances Ca2+ATPase activity, which makes more Ca2+ available for the calcium-induced calcium release • But the thing is, it also removes calcium from the cytosol more quickly, so while the contractions are stronger, they are also shorter When Cardiac Muscle is Stretched, it Contracts More Forcefully • We also have sarcomere length affecting the force of contraction in cardiac muscle Action Potentials in Myocardial Cells vary According to Cell Type • OK, so in myocardial contractile cells, the action potentials are slightly different than those in neurons and skeletal muscle, and here is how: o SEE FIGURE 14.14, PAGE 464 o Phase 4: We have resting membrane potential here at -90 mV, no problem o Phase 0: depolarization – voltage gated Na+ channels open and so Na comes in and rapidly depolarizes the cell to +20 mV before these channels start closing o Phase 1: initial repolarization: the Na+ channels close and K+ channels open, and K= leaves through open K+ channels o Phase 2: the plateau: BUT…we suddenly have a decrease in K+ permeability and Ca2+ permeability INCREASES…You see, voltage gated Ca2+ channels have slowly been opening during Phases 0 and 1, and so we have some Ca coming in and K going out, and this levels us out for a while o Phase 3: rapid repolarization: but then the Ca2+ channels close and K permeability goes up, and then we go back down to -90 • So the influx of Ca2+ during Phase 2 lengthens the total duration of a myocardial action potential • Now this is important: This longer action potential helps prevent tetanus, which is when action potentials are short and so close together the muscle is in like a “sustained contraction mode”, when action potentials keep coming and coming and even somewhat overlap each other o Essentially, the refractory period and the contraction end almost simultaneously due to the longer action potential Myocardial Autorhythmic Cells • These things can generate action potentials spontaneously because they have an unstable membrane potential – it starts at -60 mV and slowly drifts upward toward threshold • And so we call this a pacemaker potential • Whenever it depolarizes to threshold, the autorhythmic cell fires an action potential • For now, we believe that the reason for this weirdness is that there are channels in these cells which are different from the channels of other excitable tissues o When the cell membrane potential is at -60 mV (the lowest it can go), channels which are permeable to Na and K open up o We call these channels I channels because they allow current (I) to flow f • And the subscript f is because it is ‘funny’ current because it behaves strangely o And then, K is going out but Na is coming in, and Na does its thing faster, and so the autorhythmic cell slowly depolarizes • KNOW TABLE 14.4, PAGE 467 Electrical Conduction in the Heart Co-ordinates Contraction • It is important that individual myocardial cells depolarize and contract in a co- ordinated fashion if the heart is to create enough force to circulate the blood • The depolarization starts in the sinoatrial node (SA node), which is autorhythmic cells in the right atrium which serve as the main pacemaker of the heart o Then we go through an internodal pathway of autorhythmic fibers which connects us to the atrioventricular node, which is the doorway into the right ventricle o Now we move into Purkinje fibers in the atrioventricular bundle (A-V bundle)  Purkinje fibers are specialized conducting cells which transmit electrical signals very rapidly o And these fibers take us to the apex of the heart, dividing into left and right bundle branches • SEE FIGURE 14.9, PAGE 469 • Note that the action potentials spread across the atria and encounter the fibrous skeleton of the heart at the junction of the atria and the ventricles, and it can move no more o So the AV node is the only pathway through which action potentials can reach the contractile fibers of the ventricles o Why is this important?  Because all the blood pumped out of the ventricles leaves through openings at the *top*, and so we want contractions to start from the bottom of the ventricles (an apex-to-base contraction)  As well, the muscles in the walls in the ventricles are like a spiral (see Figure 14.10), and so the apex and base of the heart come closer together and the blood squeezes out the opening at the top o The AV node also serves to delay the action potentials just a bit, so that the atria can contract before the ventricles – this is called the AV node delay Pacemakers Set the Heart Rate • The cells of the SA node set the pace of the heartbeat • Interestingly enough, other autorhythmic cells such as the AV node and the Purkinje fibers, have unstable resting potentials and therefore can act as pacemakers o But since they are slower than the SA node, they usually don’t set the beat The Electrocardiogram Reflects the Electrical Activity of the Heart • An electrocardiogram (or ECG) is a recording of the electrical activity of the heart made from electrodes placed on the surface of the skin • There are two major components of an ECG: waves and segments o Waves (as usual) are deflections above or below the baseline o Segments are sections of baseline between two waves o Intervals are combinations of waves and segments • There are three major waves on a normal ECG: o P wave – this is depolarization of the atria o Combined waves of the QRS complex – the progressive wave of ventricular depolarization (atrial repolarization is also part of this) o T wave – repolarization of the ventricles • SEE FIGURE 14.21 AND 14.22, PAGES 472-3 The Heart Contracts and Relaxes Once During a Cardiac Cycle • A cardiac cycle is the period of time from the beginning of one heartbeat to the beginning of the next o Each cycle has two phases – diastole (when the cardiac muscle relaxes) and systole (when it is contracting) • SEE FIGURE 14.25, PAGE 475 • Discussion of stages in aforementioned picture: o First stage: the heart is at rest (atrial and ventricular diastole)  The atria are filling with blood from the veins, and the ventricles have just completed a contraction  The ventricles relax and the AV valves open, allowing blood to flow into the ventricles – this causes them to expand o Completion of ventricular filling: atrial systole  Alright, so now most of the blood is in the ventricles, and the atria contracts to get the rest of the blood in there  The wave of depolarization sweeps across the atria and contraction (atrial systole) begins  Interestingly, the pressure in the atria forces some blood back into the veins which have delivered it there o Early ventricular contraction and the first heart sound  The depolarization wave is moving slowly through the conducting cells of the AV node, and then down the Purkinje fibers to the apex of the heart (as we discussed earlier)  Ventricular systole beings, as the spiral bands of muscle start squeezing  Here we have the AV valves closing because of the increased pressure, and so we hear the first heart sound, the “lub” of “lub- dup”  Now the AV and semilunar valves are both closed so the blood has nowhere to go, but the ventricles keep contracting and increasing the pressure – this is called isovolumic ventricular contraction because the volume of blood is not changing  (Almost a side note): The atrial muscle fibers are relaxing, and blood flows into them again (but this happens independent to whatever is going on in the ventricles) o The heart pumps: ventricular ejection  The ventricles contract and they generate enough pressure to open the semilunar valves and push blood into the arteries  High-pressure blood is forced into the arteries and pushes the low- pressure blood farther into the vasculature o Ventricular relaxation and the second heart sound  At the end of ventricular ejection, the ventricles begin to repolarize and relax, and so ventricular pressure decreases  We get to a point where the arteries have a higher pressure than the ventricles, and so blood actually flows back into the heart (pressure gradient)  This closes the semilunar valves, and the sound created by this is the second heart sound (the dup of lub-dup)  And now the ventricles once again are a sealed chamber  This part is called isovolumic ventricular relaxation – the volume of blood in the ventricles is not changing Pressure-Volume Curves Represent One Cardiac Cycle • We can also describe the cardiac cycle using a pressure-volume graph o SEE FIGURE 14.26, PAGE 477 o The cycle begins at point A, where we have completed a contraction and we hold the minimum amount of blood we will ever hold…We are also at minimum pressure  At this point we also have blood flowing into the atrium  Once the pressure in the atrium exceeds the pressure in the ventricle, the mitral valve (between the atrium and ventricle) opens and blood flows in and the volume of the ventricle increases along with the pressure o The rest of the filling is done by atrial contraction, and now the ventricles hold the maximum amount of blood and the pressure is highest (Point B)  The volume of blood at this point is called the end-diastolic volume (EDV) o Next we have the ventricle contracting, and pressure increases even more, enough that the aortic valve opens (point C) o Then the blood gets pushed out into the aorta (point D)  Now, the heart does not empty itself of blood every time  There is some left in the ventricles at the end of each contraction, and this is called the end-systolic volume (ESV) • SEE FIGURE 14.27, PAGE 479 A few terms • Stroke volume is the amount of blood pumped by one ventricle during a contraction o Volume of blood before contraction – volume of blood after contraction = stroke volume o Or, EDV – ESV = stroke volume • Cardiac output is the volume of blood pumped per ventricle per unit of time o Heart rate x stroke volume Heart Rate is Varied by Autonomic Neurons and Catecholamines • The sympathetic and parasympathetic branches of the autonomic division influence heart rate through antagonistic control o Parasympathetic activity slows heart rate o Sympathetic activity speeds it up • Both autonomic branches alter the rate of conduction through the AV node – either enhancing or slowing its ability to conduct action potentials Multiple Factors Influence Stroke Volume • Force of contraction (and therefore stroke volume) is affected by: Length of the muscle fiber at the beginning of contraction and the contractility of the heart o Contractility is the intrinsic ability of a cardiac muscle fiber to contract at any given length Length-Tension Relationships and Starling’s Law of the Heart • So definitely, the greater the sarcomere length (but not over some optimum number), the more tension is created • And then the more tension we have, the more stroke volume we get • And then if we get more blood in the ventricles, we are going to have more forceful contractions • This relationship between stretch and force was discovered by Frank-Starling o SEE FIGURE 14.29, PAGE 481 • The graph shows that stroke volume is proportional to force • As additional blood enters the heart, the heart contracts more forcefully – this relationship is know
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