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ALS 2304, Week 13: Cardiovascular Physiology

by: Mara DePena

ALS 2304, Week 13: Cardiovascular Physiology ALS 2304

Mara DePena
Virginia Tech
GPA 3.62

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There notes cover the first week of lectures on cardiovascular physiology.
Animal Physiology and Anatomy
Dr. Cline
Class Notes
Heart, Blood, flow, layers, valves, cardiac, cycle, Conduction, EKG, fibrillation, contraction, innervation, norepinephrine, heartrate
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This 7 page Class Notes was uploaded by Mara DePena on Sunday April 24, 2016. The Class Notes belongs to ALS 2304 at Virginia Polytechnic Institute and State University taught by Dr. Cline in Spring 2016. Since its upload, it has received 19 views. For similar materials see Animal Physiology and Anatomy in Agricultural & Resource Econ at Virginia Polytechnic Institute and State University.

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Date Created: 04/24/16
ALS 2304 CARDIOVASCULAR PHYSIOLOGY LAYERS OF THE HEART  Three major layers: o Epicardium- Outermost, protective layer. o Myocardium- Thickest layer, individual cardiac fibers. Striated, involuntary contraction, intercalated discs, gap junction, near instantaneous transfer of action potentials.  Cardiac muscle fibers are shaped like a Y and connect to three other fibers. This allows the muscle to contract in three dimensions at once, while a skeletal muscle can only contract at two.  The intercalated discs hold the muscle fiber together.  Gap junctions are holes between the cells that allows the cytoplasm from one cell to be continuous with another, allowing for ion transfer. However, in the heart, it is not the transfer of ions that is important, but the transport of action potentials. They are propagated from one cell to the next. If you fire an action potential on one cell it will eventually be propagated to all cells of the heart. o Endocardium- CT and squamous cells. Line inside of heart and form valves. Innermost, protective, faces blood. Doesn’t allow gaseous exchange between cells of heart and blood inside.  Forms flimsy valves. BLOOD FLOW  Two different types of valves: o Atreoventricular (flimsy)  Mitral (bicuspid) and tricuspid valve.  Must withstand highest pressure.  Between atrium and ventricle.  Close due to changes in pressure.  Blood flows down. o Semilunar (rigid, do not prolapse)  Open as pressure increases, blood flows through pulmonary trunk and into aorta.  Blood flows up.  Pressure that makes atreoventicular valve close is less than the pressure that makes the semilunar valve open; this valve takes more pressure to open. For an instant, no valves are open.  Opens when ventricle contracts and pushes blood up. Holds pressure in aorta or pulmonary trunk.  The aorta is an elastic artery, which squeezes the blood and sends it into the periphery/head of the capillary bed.  Blood pressure in the aorta slowly decreases as the blood drains into the periphery. o These valves only respond to changes in pressure, and only work if the pressure is correct.  If you’ve too low of a blood pressure, valves won’t close. Heart will cease to function as a pump.  Least expensive way to euthanize an animal: Inject air into a vein. The air goes to the heart and expands/contracts in vesicle. When the ventricle expands, so does the air, and there is not enough pressure drop to open or shut the valves. The valves cease to function.  If a valve flips backward, it is a prolapse valve, which no longer functions as a valve. o Stops blood flow, animal dies. o Prolapse is prevented by cordae tendinae, as atrioventricular valves are very flimsy. They attach to the heart valve and to the capillary muscle of the ventricle wall. AUSCULTATION POINTS  Two heart sounds are closure of atrioventricular valves and then closure of semilunar valves.  With a heart murmur, the valve does not close all of the way. It is a leaking heart valve. Blood flows backward and vibrates, making a sound. CARDIAC CYCLE  Period when heart is contracting versus relax. Period of high versus low blood pressure.  Exists for both atria and ventricles. Ventricles are about 95% of the heart so we typically talk about the cardiac ventricular cycle.  Systole- Contraction, pressure when heart is actually pumping. First number when you get your blood pressure. Tells you about the vigor of heart contraction. o Cardiac muscle cells are stimulated by nerves. Vagus nerve specifically. Self excitable; can cut heart out of animal and it will beat on its own until deprived of oxygen. Autonomic nervous system accelerates or decelerates beating. Contracts as a unit. Long absolute refractory period, similar to skeletal muscle contraction. o Contracts and remains contracted for a sustained amount of time. Why? Sodium and calcium flow in, potassium flows out. Calcium prevents the potassium from flowing out, which delays the potassium exit and elongates the action potential. This is why the action potential takes much longer in the heart than in the skeletal muscles or neurons.  What is the advantage of this elongated action potential?  Facilitates the movement of the blood. Blood needs time to flow.  Diastole- Relaxation, no contraction of the heart. Tells you about the fitness of the vasculature, or how tightly it is squeezing upon the heart. INTRINSIC CONDUCTION SYSTEM  Not individual cardiac muscle fibers; these are the auto rhythmic/pacemaker cells, which are neurons. o Sits there and fires action potential. Hands it off to the cardiac muscle fibers that surround it. Set inherent rhythm of heartbeat. o Has leaky sodium channels. Never close. When sodium moves across a neuron it initiates action potentials. Since these channels are always leaking, membrane potential becomes more positive and then drives the neuron to fire. There is no way to close these channels. When the sodium channel leaks enough, the voltage gated calcium channel opens and calcium comes into the cell. This drives the spike, unlike in a normal neuron. The sodium behaves like a slow EPSP. Potassium channels then open up and return the cell to its starting state. o Unstable resting potentials called pacemaker potentials. o The pacemaker slope controls heart rate by being affected by the autonomic nervous system.  All ventricle cells are interconnected by gap junctions. Action potential takes a lot of time to pass through. Without something to accelerate the action potentials, only parts of the heart would pump. Our body has a conduction system to speed things up.  SA Node- Sets heart rate, major pacemaker region of heart. At head of right atria. o Fires in response to leaky sodium channel and opening of calcium channel. Where action potential starts, spreads to two atria. o Two atria contract. Right contracts slightly ahead of left because that is where the SA node is. o Layer of insulation at top of heart. One hole in insulation, at AV node.  AV Node- Can generate action potentials as well. o Action potential falls into the ventricle. o Delay mechanism, holds onto action potential as It bounces off walls. o Atria and ventricles cannot contract simultaneously because we need differences in pressure for the blood to flow. o AV delay- Action potential ricochets back and forth in the node. Then releases it into the ventricle.  Goes through the Bundle of His. This branches into the right and left bundle branches which go down into the septum of the heart and come back on the walls of the vesicle. Terminal vesicles on these are the Purkinje fibers, which deliver the action potentials to the individual cardiac muscle cells. ELECTROCARDIOGRAM (EKG)  An amp meter measures the flow of current, if the needle goes in the negative direction you are discharging your battery. If it goes in the positive, you are recharging. It tells you where electrons are flowing.  EKG is nothing more than an amp meter.  When the heart is not beating, the EKG is flat lined because there is no net flow of charge. You start out with the flat line EKG.  Action potential flows in all directions.  P-wave- Corresponds to atrial depolarization, thanks to SA node.  At flatline, there is an action potential in the AV node.  The action potential is sent to the ventricles. Top of right side depolarizes slightly ahead of the left, charge is flowing more in the negative direction. There is then a huge positive deflection because the left atrium is much larger. This is the QRS complex, with the Q being the beginning of depolarization of the right atrium, the R being the depolarization of the left, and the S being the completion of depolarization.  The ventricles then contract, closing the atrioventricular valves and opening the semilunar valves. While the ventricle is depolarization, the atria relax. You can’t see this since the ventricles make up so much of the mass of the heart.  T-wave- Ventricle repolarization, which is not as dramatic as as depolarization.  If you have a flat line, check that the leads are on correctly! VENTRICULAR FIBRILLATION  Poorly understood.  Electrical impulses through the heart.  Two atria/ventricals start to ricochet action potentials back and forth and will not clear.  Heart will enter state of flutter or stay contracted. o If ventricle contracts very rapidly, there’s not enough time for blood to flow. o Heart stops.  You send a very violent electrical shock through the heart. This stops the heart momentarily and then it will restart itself with a normal rhythm. o Why does this happen/work?  Nobody really understands. CARDIAC MUSCLE CONTRACTION  Action potential falls into the T tubule and opens up a calcium channel.  The calcium channel is an L-type calcium channel.  Calcium flows down its concentration gradient into the cytoplasm of the cardiac muscle fiber. Some of the calcium associates with the thick and thin filament and causes contraction.  The major function of the calcium is that it binds to a ryodine receptor, intercellular receptors for calcium. Ryodine is a particular type of calcium found on the sarcoplasmic reticulum. The ryodine channel receptor complex opens and calcium spills into the cytoplasm to cause contraction.  The complex is open longer because the L-type calcium channel is going to open longer. Why? Because the action potential is elongated. The concentration of calcium remains higher longer, which makes the contraction longer.  Just as soon as the calcium starts leaving the RyR, channels that consume ATP will store it back in the SR. Calsequestrin and calreticulum are present there.  There is also a sodium-calcium exchanger, where sodium comes in and calcium comes out.  Driving calcium out stops contraction.  About 80% of the calcium for contraction comes from the SR, and about 80% goes back in. 15% that is cleared back out goes through the Ca-Na exchanger, and there is a separate calcium channel that simply pumps out calcium and nothing else by consuming ATP, which is about 5%. EXTRINSIC HEART INNERVATION  The nervous system overrides the normal rhythm of the heart.  Stimulated by the sympathetic cardioacceleratory center (collection of several nuclei in medulla oblongata). o Stimulates thoracic region of the spinal cord. This is also known as the cardioacceleratory center. o Goes through spinal nerves onto SA and AV nodes and increases the pacemaker slope. This also synapses onto the ventricles, and dumps norepinephrine onto the ventricular wall. This also targets the individual cardiac fibers themselves.  Inhibited by the parasympathetic cardioinhibitory center (collection of several nuclei medulla oblongata). o Synapses on dorsal motor nucleus of vagus nerve, which increases firing frequency. ACh comes out of this and then dumps it onto SA and AV node. o This decreases pacemaker slope. How does that decelerate heart rate?  It takes longer to fire the SA node, therefore heart rate slows. CONTRACTILITY AND NOREPINEPHRINE  When a beta receptor is blocked, the heart rate slows down by going back to its inherent rhythm.  Once NE binds to a beta receptor, the beta receptor has a g-protein coupled complex (gas) that activates AC. It creates cAMP and activates kinase which opens up a calcium channel on the plasma membrane. It also targets the SR and allows calcium to come out more freely (accelerates release).  This kinase also facilitates crossbridging of the thick and the thin filament.  With increased Ca and increases crossbridging ability, the vigor of contraction is also increased. o This does not accelerate heart rate (only increases velocity of blood pumping), but heart rate would be accelerated simultaneously.  Why? Because you are also dumping the NE onto the SA node. INCREASED HEART RATE: EPINEPHRINE  Does the same thing the NE does, but comes from the adrenal gland.  Gets into the heart through the blood itself. Has to travel.  NE causes vigor to increase first, then you wait for circulation for epinephrine to go in. DECREASED HEART RATE: ACh  Binds to its receptor and inhibits activation of AC.  Activates K channel and suppresses excitability of membrane of the SA node. Causes slope to fall.  Slope falls because it takes longer so the sodium to overpower the potassium leaving. CARDIAC OUTPUT AND RESERVE  Cardiac output- Amount of blood pumped by each ventricle in one minute. Product of heart rate and stroke volume.  Heart rate- Beats per minute.  Stroke volume- Amount of blood pumped out by a ventricle with each beat.  Cardiac reserve- Difference between resting and maximal cardiac output.  Factors Affecting CO o Posture  Greater when standing up than lying down  Have to pump blood against gravity  Increased vigor to overcome gravity o Extreme temperatures  Severe cold  Trying to warm the extremities  After a certain point, will decrease blood flow to extremities, trying to keep blood flow to internal organs  Focuses on heart, brain, lungs  Severe heat  Blood flow increases as you are trying to keep heat close to the skin o Eating  Increases blood flow to carry the nutrients away from the digestive system under the control of VIP FRANK-STARLING LAW  Applies to skeletal and cardiac muscles.  Degree of stretch of cardiac muscles before they contract is the critical factor controlling stroke volume.  If z discs are very close together, the muscle can’t exert much pressure because the thick filament is colliding with the z disc and doesn’t have room to travel.  If you pull the sarcomere really far apart, you won’t be able to apply much tension because there will be less crossbriding.  If you stretch the heart too far apart, it doesn’t have enough power to contract.  You have the most strength at a certain sarcomere distance.  Several mechanisms prevent overstretching of the heart. The paracardium is one.


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