Skeletal Muscle Structure Review PDF

STRUCTURE OF SKELETAL MUSCLE Functions of controlled muscle contractions Moving the body muscles help us move our whole body or specific body parts let us pick up and control tandling objects mus...

STRUCTURE OF SKELETAL MUSCLE Functions of controlled muscle contractions Moving the body muscles help us move our whole body or specific body parts let us pick up and control tandling objects muscles things around us movingthings internally muscles push things through hollow organs emptying organs muscles help certain organs release their contents 3 TYPES OF MUSCLES Skeletal straited voluntary stripped somatic 2 Cardiac striated involuntary Autonomic 3 Smooth unstraited involuntary skeletal Muscle makes 401 of body weight made up of muscle fibers that run parallel to each other Grouped together by connective tissue All the forces moving in one direction Inside each muscle fiber are myo fibrils Each myo fibril has a pattern of thick and thin filaments help muscles contract  KELETAL MUSCLE HIERARCHY Epimysium outer layer surrounds whole muscle 2 Whole Muscle an organ 3 Perimysium surrounds fascicles 1 Muscle Fiber a cell 5 surrounds a single muscle fiber Endomysium 6 Myo fibril specialized intracellular structure Thick myosin thin actin filament cytoskeletal elements e Myosin actin protein molecules arcomere small functional unit of muscle it 2 line to 2 line ones myosin actin A BAND DARK BANDS thick filaments and parts of thin filaments overlap Defines one end of myosin to the other in sarcomere ZONE lighter middle of A band area in the where the thin filaments don't reach From one end of actin to the other end 4 LINE holds the thick structure that filaments together vertically in the center of A band where myosin structurally connect BAND LIGHT BANDS where only thin filaments are present not with thick overlapping where A band ends and the next A band begins 2 LINE dense line in the 1 band that marks the boundary of a sarcomere Flat cytoskeletal disc when muscles grow they add more sarcomeres at ends of myo fibrils not by making each sarcomere bigger ITIN large elastic protein that runs from M line to the 2 lines within the sarcomere largest protein in the body made up of 30,000 amino acids 3 ROLES OF TITIN Scaffolding helps keep the thick thin filaments stable and aligned properly in the muscle maintains sacromere structure Elastic Spring makes muscles elastic helps them return to their normal length after stretching 3 Signal Transduction helps send signals for muscle growth stimulating titin muscle grows CROSS BRIDGES structures that stick out from each thick filament and reach toward the surrounding thin filaments where they overlap Extend in 6 directions from each thick filament toward the nearby thin filaments A single muscle fiber can have up to 16 billion thick filaments and 32 billion thin Represents myosin actin forming together Force generating capacity directly correlated to number of cross bridges 4405in thick filaments in muscle consists of two identical subunits the tails twist together the heads form cross bridges that connect to the thin filaments during muscle contraction ach cross bridge head has 2 key parts that are important for muscle contraction 1 Actin binding site connects to thin filaments 2 Myosin ATPase site uses energy from ATP to help the muscle contract Enzyme that lowers threshold of ATP If myosin head meets actin provides force inside sarcomere If it can't can it do anything ACTIN thin filaments Has two strands twisted together Each actin molecule has a spot where it can connect with a cross bridge myosin during muscle contraction Includes two other proteins 1 Tropomyosin threadlike protein that lies along the actin strand covers the actin binding sites blocking the connection with myosin prevents contraction 2 Troponin protein complex made of three parts 1 One binds to tropomyosin 2 One binds to Actin 3 One binds to calcium when calcium is not present troponin holds tropomyosin in the blocking position when calcium binds to troponin it changes shape causing tropomyosin to move away and allow the muscle to contract SLIDING FILAMENT MECHANISM During muscle contraction cross bridges on the thick filaments repeatedly attach bend and pull the thin filaments inward The thin filaments slide closer to the middle of the sarcomere from opposite sides The thick thin filaments don't actually get shorter they just slide past each other The 2 bands move closer together making the muscle contract TOWER STROKE happens when myosin binds to actin and pulls the thin filament inward helping the muscle contract once tropomyosin moves out of the way myosin can attach to actin Myosin is a motor protein that walks along the actin filament like kinesin when the binding site on actin is open myosin's head tilt at a hinge point and connects to actin The myosin head then tilts 45 degress pulling the thin filament toward the center of the sarcomere creating the power stroke that drives muscle contraction The length of muscle affects the muscle A single power stroke pulls the thin filament inward a little but its only a small part of the total distance the muscle needs to shorten The cycle continues with repeated cross bridge actions Each cycle ends when the link myosin between allowing myosin to actin breaks return to its starting position and get ready to bind again This happens asynchronously some myosin heads are still attached while others are resetting Helps keep thin filaments from sliding back to its resting position between power strokes allowing for smoother and more effective muscle contraction EXCITATION CONTRACTION COUPLING ACh at the NMJ neuromuscular junction between the motor neuron and muscle fibers skeletal muscles to contract triggers whenAch is released it fiber changes how permeable the muscle is leads to action potential that travels across the whole surface of the muscle cell membrane sarcolemma The action potential then spreads to two structures 1 Transverse Tubules T tubules 2 Sarcoplasmic Reticulum SR TRANSVERSE TUBULES Structures that form at the junctions of the Atl bands in muscle fibers the muscle cell membrane dips inward to create T tubules that run straight into the center of the muscle fiber connected Sarcolemma so when an action potential to occurs on the surface it also travels down into the T tubules depth of muscle Allows the electrical signal to spread quickly throughout the entire muscle fiber the in the reticulum SR important for signal causes changes sarcoplasmic muscle contraction SARCOPLASMIC RETICULUM modified type of endoplasmic reticulum in muscle cells Forms a network of interconnected compartments that surround each myo fibril mesh sleeve Different parts of the SR wrap around each Atl bands The ends of these segments create terminal cristernae lateral sacs which are slightly separated from the T tubules by a small gap The SR stores calcium and when an action potential travels down a T tubule it trigger the release of calcium from the SR into the muscle cell's cytosol Released calcium exposes the binding sites on actin allowing myosin to attach and initiate muscle contraction the on actin is once binding sites exposed 1 cross bridges bind Myosin 2 Power stroke 3 Release Reset TP POWERED CROSS BRIDGE CYCLYING involves myosin heads that have two sites 1 Actin where myosin connects to actin binding sites 2 ATPase site an enzyme that breaks down ATP Before myosin links to actin it breaks down ATP occurs on the myosin head storing energy After ATP is broken down ADP and inorganic phosphate Pi stay attached to myosin when myosin actin come into contact the myosin head releases Pi during the power stroke which pulls the thin filament inward After the power stroke ADP is released freeing up the ATPase site on myosin for a new ATP molecule to attach Myosin and actin stay linked until a new ATP molecule binds to myosin which reduce the strength of their connection allowing the cycle to start again teatergized briefing BIG 9 18 gizes Powerstrokehappens Binds to Actin wontbe Hagggens all over abletorelax thetension Muscle tension ZIGOR MORTIS occurs after death without new ATP to attach to the ATPase site on myosin myosin can't detach from actin After death the amount of calcium in the cytoplasm increases causingtropomyosin to move away from the actin binding sites Charged myosin then binds to actin and the power stroke happens but because no new ATP can be made the myosin heads can't release from actin causes the muscles to become stiff and locked in place The proteins in the muscles will break down leading to the stiffness gradually going away over a few days Relaxation muscle occurs whencalcium returns to the terminal cisternae after electrical activity stops The SR actively pumps calcium out of the cytosol and back into its storage When calcium levels drop the binding sites on actin are covered again by tropomyosin preventing myosin from attaching to actin leads to muscle relaxation he process of excitation concentration coupling has to happen before myosin actin can interact Delay between the action potential and when the muscle starts to contract so more action potentials can stack up more cat for more action potentials LATENT PERIOD when the action potential is finished but the muscle hasn't started contracting E After the contraction begins there's another delay until the muscle reaches There's also a while delay SR calcium is being pumped back into the terminal cisternae which is the area in the storage ZELAXTION TIME The time from when the muscle is at its peak tension until it fully relaxes The muscle's response to a action potential lasts longer than the action potential itself single Allows muscles to produce contractions with varying strengths WHOLE MUSCLES made up of groups of muscle fibers that are bundled together and attached to bones muscles different sizes can be covered by connective tissue which goes from the outside of the muscle into each individual fiber the connective tissue continues ends of the muscle beyond the forming strong tendons Tendons attach the muscles to the bones allowing movement MUSCLE TENSION transferred to the bone as the muscle contracts and tightens Tension is produced inside the sarcomere contractile component of the muscle The tension doesn't go straight to the bone but transmitted through the tendons Tendons have some passive elasticity and act like a spring connected in series with the contractile component The tendons stretch and store some energy when the muscle contracts helping to transfer the force to the bone 3 TYPES OF CONTRACTION ISOTONIC load remains constant while the muscle changes length constant tension ISO KINETIC velocity speed remains constant while the muscle changes length constant motion ISOMETRIC muscle remains the same length as tension increases constant length No motion CONCENTRIC TENSION muscle shortens as it contracts ECCENTRIC TENSION muscle lengthens while it is still contracting hevelocity speed of muscle shortening is connected to the amount of load the muscle is working Move faster aganist to capacity produce force decreases The heavier the load the slower the muscle shortens Muscles use energy to do but most of that energy turns into heat work is only done when something W Force distance moves FORCE the muscle tension required to overcome the load weight of object Amount of work depends on how heavy the object is and how far you move it The way muscles bones joints work together like a lever system LEVER rigid structure that moves around a pivotpoint ULCRUM pivot point Bones act as the levers Joints act as the fulcrum Skeletal muscles provide the power to move the bones Result in torques Angular movement EFFORT ARM POWER part of the lever between the fulcrum joint and where the muscle applies force RESISTANCE ARM LOAD part of the lever between fulcrum and where the weight load is acting MECHANICAL ADVANTAGE using less force to lift somethingheavy force Ankles YECHANICAL DISADVANTAGE needing more force but to move the load faster or being able over a larger range of motion speed Elbow Knee MOMENT ARM Distance between the fulcrum Access of ROT and the point where a force is applied plays a role in how much torque is produce EF EA RFX RA 35kg 5cm 175kg.cm amountoftorqueappliedbybicep distancefromaccess rot 5cm 35kg 175kg.cm lessforcebutthedistanceisgreater 2torquesare i useatoreuesare make it concentric More effort force if fi Muscle shortens Refinance make it eccentric Moretorque on resistance force Muscle lengthens g Eff Accy Effit Effy arm resistance Resistance Muscle contractions can vary in strength TWITCH a single action potential in a muscle fiber causes a weak contraction Muscle fibers work together in groups to create stronger or weaker contractions 2 ways to adjust the strength of a contraction 1 Number of muscle fibers contracting increases with more motor unit recruitment 2 Tension developed by each contracting fiber that is activated The strength of a muscle contraction depends on how many muscle fibers are working The more fibers that contract the more tension force the muscle can produce Larger muscles have more fibers create more tension Each muscle is controlled by several motor neurons These neurons spread out and connect to individual muscle fibers one neuron can control many muscle fibers but each fiber is controlled byonly one neuron when a neuron sends a signal all the fibers it connects to contract at the same time OTOR UNIT is made up of a motor neuron and all the muscle fibers it controls MOTOR UNIT RECRUITMENT The muscle fibers in a motor unit are spread out across the whole muscle so when they contract together it creates an even concentraction throughout the muscle Each muscle has many motor units when only a few motor units are activated the muscle contracts weakly Activating more motor units leads to a stronger concentration Motor Neuron goes off All its fibers go off too Ex Generate 6N Force everyfiber generates 1N Motor unit 1 Motor unit 3 generates 7N will still allow movement The bodyneedsto recruite the rightamount of force to produce movement Moreforce is fine fib fifteen makes a ratio How to change forcegenerated increasemotor unit recruitement More neuronsgo off theirfibersactivated the number of muscle fibers involved in a muscle's contraction depends on 2things 1 Number of motor units recruited 2 Number of muscle fibers permotor unit innervation ratio ASYNCHRONOUS RECRUITMENT what the body uses it to avoid fatigueduring lighter contraction where motor units take turns being active givessomefibers a rest while others work  he strength of a whole muscle contractiondepends on 2 things 1 Number of muscle fibers contracting 2 Tension developed by each contracting fiber Factors effect how much tension each fiber can produce Frequency of stimulation Starting length of the fiber at the onset of contraction Extent of fatigue Thickness of the fiber A single action potential causes just a witch but if a muscle fiber is stimulated repeatedly it can contract longer and stronger TWITCH SUMMATION when the tension increases with repeated stimulation of a muscle fiber Happens because the actional potential is much shorter than the twitch Allows for more concentrations before the fiber relaxes Mainly happensbecausethere's longer increase in calcium levels inside the muscle cells when the frequency of action potentials increases more calcium is released allowing it to interact with all the troponin There is more time for the series elastic component to help transmit the tension from the muscle fibers to the bones f the muscle is stimulated very quickly and doesn't get a chance to relax it reaches tetanus TETANUS smooth sustained contraction of maximal strength by the motor units activated  Rate coding There's a connection between how long a muscle is before it starts to contract and how strong it can contract afterward Each muscle has an optimal length where it can produce the most tension in alotofactionpotential The relationship between length and tension can be understood using the sliding filament theory how muscles contract Contractile Activity at lo optimal length The muscle can produce the maximum tension The thin filaments overlap well with the thick filaments where the cross bridges are made Contractile Activity at lengths greater than to The muscle is stretched The thin filaments the thick filaments get pulled away from leading to no tension contractile Activity at lengths less than to The thin filaments from the opposite sides of the sarcomere overlap which limits the ability to form cross bridges The ends of the thick filaments get pushed aganist the z lines making it hard for the muscle to shorten any further when the muscle is more than 801 shortened less calcium is released during contraction for reasons that aren't understood fully  Active insufficiency 41 iii 491 increased lengthcauses E.fi iii ni f iiiiii stretched muscle contested genienne Passive insufficiency lengthenedat 1joint 4 Steps in the muscle process of excitation contraction and relaxion need ATP 1 Myosin ATPasesplits ATP provides energy for the power stroke when myosin pullson actin to contract the muscle 2 Binding of ATP to myosin Breaksthe cross bridge betweenmyosin and actin after a contraction 3 Active Transport of Ca ᵗ ATP is used to pump calcium back into the lateral sacs in the sarcoplasmic reticulum during relaxation 4 Nat kt Pump Activity ATPhelpsmove sodium out of the cell and potassium back into the cell after a contraction which helps restore the cell's resting state Muscle fibers can create new ATP using different methods 1 Creatine Phosphate Phosphagen Alactic Pcr Fast and burns out quickly fatigues faster need ATP 2 Oxidative Phosphorylation Aerobic requires 02 Slow ATP production slow fatigue long lasting ATP more efficient for longer activities endurance 3 Glycolysis Breakdown of glucose ATP Medium speed mediumfatigue ATP Fatigues a little slower than Pcr gets ATP from breakdown of carbs 4 Lactate production possible result of glycolysis Not a bad or good thing Fatigue can comefrom either the muscle or CNS muscle fatigue happens when a muscle can't respond to signals with the same strength anymore This fatigue acts as a defense mechanism to stop the muscle from getting so tired that it can't produce ATP which could lead to a state like rigor mortis Tossible factors of muscle fatigue Increased inorganic phosphate builds up from breakingdown ATP Calcium leakage calcium may leak out of the cell preventing it from beingpumped back into SR Depleted Glycogen the muscle runs low on its stored energy glycogen Seripheral Fatigue fatigue in muscle the inability of a muscle to continue contractingeffectively duringprolonged exercise Ex Running a marathon Central Fatigue fatigue in the brain happens when the CNS can't activate motor neurons effectively anymore muscles can still work eventhough the muscles are capable of performingthey may not be activated fully Psychologicalfactors central fatigue is often linked to mental states feeling uncomfortable bored etc makes a person less motivated to continue exercising Ex getting up in the morning muscles are not fatigued but you are Protective Mechanism XERCISE POST EXERCISE OXYGEN CONSUMPTION Increased O2 consumption is necessary to recover from exercise Helps prevent recover fromfatigue Repay the oxygen debt that was created during the workout Restore creatine phosphate energy source used by muscles Remove Lactate builds up during intense exercise and can cause fatigue Partially refill glycogen stores the energy reserves in muscles that getdepletedduring exercise muscle fibers are classified into 3 main types based on how they produce and use ATP 1 SLOW OXIDATIVE FIBERS TYPE I slow twitch innervated by small slow twitch nerve 2 FAST OXIDATIVE FIBERS TYPE 119 fast twitch innervated by large fast twitch nerve 3 FAST GLYCOLYTIC FIBERS TYPE I contracts quickly uses stored energy without oxygen the main difference between the fibers are how they contract and the methodsthey use to generate ATP FAST FIBERS have more active myosin ATPase can split ATP faster allowing for quicker contractions Fatigue faster because they burn through ATPfaster OXIDATIVE VS GLYCOLYTIC FIBERS different fiber types vary in their ability to produce ATP Fibers with a greater ability to synthesize ATP are better at resistingfatigue Glycolytic faster ATP production mediumfatigue Oxidative Glycolytic depend on each other Ability to produce use ATP GENETIC AND MUSCLE FIBERS the type of muscle fibers a person has is mostly determined by the activities they often perform Muscle fibers can adapt in response to the demandsplaced on them 1 Improvement in oxidative capacity muscles can increase their ability to use oxygen more effectively by building more enzymes that help with energy production Increasing the number of capillaries to deliver more 02 Enhancing how efficiently they use 02 during exercise 2 Muscle Hypertrophy the muscle fibers getbigger increased diameter because they produce more myosin actin more filaments allow for more cross bridging between actin myosin leading to stronger contractions influence of Testosterone helps build more myosin actin in muscle fibers muscle growth iber type changes can change fast muscle types from one form to another All fibers in a single motor unit are the same type but the speed is determined by the neuron The oxidative capacity can change between fiber types Muscle Atrophy when muscles shrink and weaken due to Lack of use disuse Nerve damage denervation Aging sarcopenia Limited Repair of Muscle Satellite cells can turn into myoblasts and help form new muscle fibers similar to existing ones muscle fiber types are mostly determined by genetics Training Effects with specifictypes of training muscle fibers can shift between types Type 119 fast can shift to type I slow or type I Aging Effects we lose type IIa fast motor units End up with a higher percentage of type I slow fibers leading to a decline in explosive strength and speed Motor Activities can be divided into 3 types Reflex Movements Automatic movements caused by skeletal muscle contraction and happen without thinking simplest type of movement 2 Voluntary Movements Most complexmovements Goal directed and can be started or stopped whenever you want Cerebral cortex in the brain is responsible for controlling these movements Rhythmic Activities repetitive movements walking chewing you consciously start and stop them but once they start they continue in a reflex manner 3 Main Neural Inputs that control how motor neurons activate muscle fibers 1 Input from Afferent Neurons happens at the spinal cord level and usually responds to sensations like body position or pain Triggers spinal reflexes automatic muscle responses 2 Primary Motor cortex Corticospinal system go straight to motor neurons in the spinal cord Responsible for controlling fine precise movements using hands fingers 3 Brain Stem Multineuronal motor system connects with many brain areas Helps regulate body posture and controls involuntary movements of large muscle groups keeping balance or standing upright he corticospinal motor system and the multi neuronal system work together and overlap in their functions When you perform voluntary movements like sending a text your body also makes subconscious posture adjustments without thinking about it Only the primary motor cortex for voluntary movements and the brain stem for posture large muscle control have direct control over motor neurons other brain areas don't directly control motor neurons theyinfluencemovement directly by adjusting the motor signals coming from the motor cortex or brain stem MUSCLE TONE ongoing involuntary low level state of tension in a muscle even at rest Maintains postural stability Tightness comes from 2 thing 1 Muscle Elasticity resist passivestretching 2 Minimal stimulation by motor neurons produce constant state ofpartial muscle contraction Controlled by reflexes that help with posture and signals from the brain Nervous system move activated muscle based on contraction history Maintain resting tone on purpose muscle receptors help the brain and nervous system manage how muscles work To control movement properly the brain needs constant updates about how stretched or tense the muscles are Proprioceptors special sensors located in muscles and joints provide the information 1 Muscle spindles track how long a muscle is 2 Golgi tendon organs sense changes in muscle tension Muscle spindles are found throughout the main part of a skeletal muscle INTRAFUSAL FIBERS special muscle fibers that make up muscle spindles Have a central part that doesn't contract but have contractile parts at both ends EXTRAFUSAL FIBERS regular muscle fibers that contract along their entire length Each muscle spindle has its own nerve supply Efferent gamma motor neuron sending signals to the intrafusal fibers Afferent sending sensory information back to the brain Stretch Reflex Helps the body sense and resist changes in muscle length when extra weight is added When a muscle is stretched the special fibers inside the muscle spindles intrafusal also stretch This stretching increases the firing rate of the sensory nerve fibers which then connect to the alpha motor neurons that control regular muscle fibers extra fusal As a result the muscle contracts to counteract the stretch Example patellar tendon reflex knee jerk reaction GAMMA MOTOR NEURONS help contract the ends of the special muscle fibers intrafusal inside the muscle spindles Not strong enough to affect the overall tension of the muscle but they prevent the spindle fibers from going slack when the main muscle fibers extra fusal shorten Keeps the muscle spindles effective in sensing changes in muscle length ALPHA GAMMA COACTIVATION both gamma and alpha motor neurons are stimulated at the same time Takes the slack out of the spindle fibers while the whole muscle is shortening If the muscle doesn't shorten as much as expected when the weight is heavier than anticipated the muscle spindle receptors send signals to the alpha motor neurons to fire more and help adjust for the extra load GOLGI TENDON ORGANS Location in the tendons of muscles Function respond to changes in the tension of the muscle not its length Structure made up of nerve endings that are wrapped around bundles of connective tissue How they work when the main muscle fibers extrafusal contract they pull on the tendon which tightens the connective tissue bundles and pulls on the bone Activates the nerve receptors sending signals to the brain about the tension in the muscle Helps us be aware of how tense a muscle is Old Belief GTOstriggered a spinal reflex that stopped muscle contraction caused sudden relaxation when muscletension gets too high help prevent injury Current Belief GTOs act mainly as sensors They don't initiate a reflex on their own Other mechanisms in the body help stop muscle contraction to prevent damage from excessive tension Skeletal Muscles have automatic reactions when the skin feels pain Withdrawal reflex used to withdraw from a painful stimulus Crossed Extensor reflex ensures the other limb is ready to support your body when you pull the injured limb away  Deoxygenatedor CIRCULATORY SYSTEM transport system of the body 25 Heart pump establishes pressure gradient Biti Eary Blood vessels passageways Adaptive re Blood transport medium besidespulmonary systemic Blood flows nonstop through circulatory system moving in 2 loops 1 Pulmonary circulation travels between heart lungs 2 Systemic circulation travels between heart all body systems The heart is located in the middle of the chest Apex lower tip thumps on the left side The heart is divided into 2 halves each with 4 chambers Atria upper chambers ventricle lower chambers left ventricle is thicker Blood flows in a complete circuit through the heart Both left right sides of the heart pump blood at the same time Both pump equal amounts of blood to the Right pumps blood lungs pulmonary Left pumps blood to the rest of the body systemic The heart has pressure operated values that make sure blood flows the right way ATRIOVENTRICULAR AV VALVES located between the atria and ventricles Let blood flow from the atria to the ventricles when the ventricles are filling up Stop blood from flowing backward into the atria when the ventricles are pumping blood on LEFT Eight a Left A Tricuspid valve Mitral Bicuspid Value Right Atrioventricular value Left Atrioventricular valve SEMILUNAR VALVES between the ventricles and major arteries Aortic semilunar value Pulmonary semilunar valve There are no valves between the atria and the veins because blood backflow into the veins isn't a issue big A small pressure difference between the atria and veins The veins compressed when the heart contracts vena cavae get partially The heart's fibrous skeleton is made of 4 rings of tough connective tissue the rings support the 4 heart values and help keep their structure  Right Left Pressure in ventricle closes cusp Papillary muscles contract and pulls Chordae Tendineae and prevents cusp semilunar from opening semilunar iii Iii HEY IEEE assumes allcoffattile During embryonicdevelopment the heart starts as a single tube that bend and twists causing the cardiac muscle fibers to form in a spiral pattern The heart wall has 3 layers 1 Endocardium inner layer 2 Myocardium thick middle layer made of muscle 3 Epicardium outer layer when the ventricles contract the heart twists reducing the size of testingstateis closed the chambers and pulling the apex upward creates a wringing motion that pushes blood upwardthrough the Havetobepressuredopen Exiles Entree semilunar values efficiently he heart muscle has alot of mitochondra and a rich blood supply with nearly one capillary for each myocardial fiber muscle gets enoughoxygen nutrients Heart lives aerobically  SYNCYTIUM mechanically electrically connected cells Gapjunctions ardiac muscle fibers are connected by intercalated discs which help the heart cells work together as a single unit mechanically electrically functional system intercalated discs have 2 types of junctions 1 Desmosomes hold the cells together tightly keeping them connected contractions during mechanical 2 Gap Junctions allow action potentials to pass quickly from one cell to another electrically The atria and ventricles each act as their own functional syncytium meaning the cell in each chamber work together as a unit here are no gap junctions between the atria and ventricles and the fibrous skeleton between them prevents electrical signals from passing directly helping control the timing of contractions separates top bottom of heart Atrium ventricle don't connect The heart has an endocrine function releases hormones The atria and ventricles each produce hormones that help regulate blood pressure These hormones tell the kidneys to get rid of excess salt in the urine which helps reduce water retention and lower blood pressure ERICARDIAL SAC double walled protective covering surrounds the heart Has a fibrous outer layer for protection Has a secretory lining that produces pericardial fluid reduces friction as the heart beats The heart's contraction is triggered by action potentials AUTO RHYTHMICITY AUTOMATICITY the heart can generate the potentials on its own self exciting here are 2 types of specialized cardiac muscle cells 1 CONTRACTILE CELLS do the actual work but don't normally start their own action pumping potentials 99.1 of heart cells they can reach action potentials but they're slow Don't reach threshold on their own 2 AUTORHYTHMIC CELLS these cells don't contract and spread the action potentials that trigger the contractile cells to pump The genferate syncytium if one cell reaches action potential they all do Pacemaker cells happens first Unlike nerve and skeletal muscle cells resting potential until stimulated have a constant Cardiac autorhythmic cells don't have a resting potential have electric potential their membrane potential gradually depolarizes slowly increases between action potential until it reaches a threshold Pacemaker potential acemaker Potential is caused by a complex interaction of different ions moving in and out of the cell these cycles of drifting membrane potential and firing of action potentials allow the auto rhythmic cells to regularly generate electrical signals which spread throughout heart causing it to beat rhymically n auto rhymic cells the action potential works differently Rising phase influx of calcium Cart through long lasting voltage gated Ca't channels that causes the depolarization Falling phase when potassium K exits the cell and the long lasting cast channels close The slow closure of K channels helps trigger the next depolarization During the rising phase the influx of cast is paired with active reuptake of cast by the SR ER calcium ATPase pump Refills the cell's cart stores and resets the cast clock and the membrane clock preparing the cell for the next cycle of slow depolarization and action potential Becausethey are naturally leaky to sodium they reach threshold on its own INO ATRIAL SA NODE the heart's natural pacemaker located in the right atrial wall near the superior vena cava sets the rhythm for the heart's contractions sinus rhythm TRIO VENTRICULAR AV NODE small bundle of specialized cells at the base of the right atrium near the septum delays the signal from the SA node to allow the atria to finish contracting before the ventricles contract Help signal get down to ventricle BUNDLE OF HIS AV BUNDLE specialized cells that start at the AV node and travel down the septum between the ventricles splits into the left and right bundles that curve around the tips of the ventricles Allow signal to transfer through ventricle URKINJE FIBERS small fibers that branch out from the bundle of His and spread throughout the ventricular myocardium ensuring the ventricles contract in a coordinated manner increase speed of transmission by 6x Inter atrial Pathway spreadssignalsthroughout atrium Internodal Pathway connects SA to AV Different autorhythmic cells in the heart have different rates of slow depolarization which affects how often they generate action potentials Results in varying heart rates for different parts of the heart SA node fastest generating action potentials at 70 80 or 80 100 BPM AV node slower at 40 60 or 60 80 BPM Bundle of His and PurkinjeFibers even slower at 20 40 or 40 60 BPM Since the SA node has the fastest rate of action potential initiation it naturally becomes the heart's pacemaker Once an action potential is generated in any cardiac muscle cell it quickly spreads through the entire myocardium ensuring coordinated contractions All cells are avhythmicdepending on what reaches action potential first will make the other cells reach action potential bnormal Pacemaker Activity can occur if the normal conduction system of the heart is disrupted SA NODE FAILURE if the SA node stops working due to heart attack the Av node takes over as the pacemaker but at a slower rate 40 60 BPM BLOCKBETWEEN ATRIA AND VENTICULAR if the impulse between the atria and ventricles gets blocked the atria will continue beating at 70 BPM the ventricles will beat more slowly 30 Bpm driven by purkinje fibers this slow heart rate is insufficient for normal function patient becomes comatose ECTOPICFOCUS if an area of the heart like purkinje fibers becomes inappropriately excited causes the heart to generate a premature action potential leading to premature ventricular contraction PVC This abnormal contraction disrupts the normal rhythm of the heart n anormal healthy heart the spread of cardiac excitation is carefully coordinated to ensure efficien sumping of blood 1 Atrial contraction before ventricular contraction the atria should fully contract and push blood into the ventricles before the ventricles start contracting Ensures that the ventricles are filled with blood before they pump it out 2 Coordinated contraction within each chamber All the muscle fibers in a chamber either atria or ventricles need to contract together as a unit Helps pump blood efficientlyfrom each chamber 3 Coordination between atria and ventricles The two atria and two ventricles need to contract simultaneously within their pairs Ensures that both atria and both ventricles are workingtogether to move blood through the heart and to the lungs or body TRIAL EXCITATION When the SA node generates an action potential it spreadsthroughout both atria INTERATRIAL PATHWAY ensures that both atria become depolarized contract simultaneously INTER NODAL PATHWAY directs the action potential from the SA node to the AV node which is the only electrical connection between the atria and ventricles conduction between the atria and ventricles AVNODE DELAY delay of about 100 msec at the AV node Allows the atria to finish contracting and fully fill the ventricles with blood before the ventricles begin contracting VENTRICULAR CONDUCTION SYSTEM crucial for quickly spreading the excitation throughout the ventricles ensures the ventricules contract efficiently Includes Bundles of His the right and left bundle branches Purkinje fibers Cardiac contractile cells are not autorhymthic Rely on action potentials from autorhymthic cells like the SA node to contract The action potential in cardiac contractile cells has Plateau Phase the membrane potential stays near its peak positive level for several 100 msec Helps extend the contraction of the heart muscle This prolongeddepolarization is caused by calcium cast entering the cell from the ECF The calcium entrytriggers a process called calcium induced calcium release from the SR Releases even more calcium into the cell leading to a strong muscle concentration The result is a stronger contraction 3 stronger than skeletal muscle and the contraction lasts about 300 msec The short refractory period in cardiac muscle prevents tetanus Tetanus in skeletal muscle can occur if the muscle is stimulated rapidly before it has finished relaxing leading to continous contractio In cardiac muscle the short refractoryperiod ensures that the heart muscle can't be stimulated again until it has fully relaxed the heart needs time to fill with blood before each contraction ELECTROCARDIOGRAM ECG EKG recording of the overall spread of electrical activity through the heart Doesn't directly record the electrical activity of individual cells Measures the electrical signals that travel through the body from the heart and reach the body surface Represents voltage differences detected by electrodes placed on the body's surface Depolarization and repolarization of the heart occur as a coordinated event across the entire heart so when the heart is fully depolarized or repolarized no voltage difference can be detected between electrodes During these phases no recording appears on the ECG ifferent parts of the ECG correspond to specific cardiac events P WAVE atrial depolarization electrical activity that causes the atria to contract and push blood into the ventricle QRS COMPLEX ventricular depolarization triggers the ventricle to contract and pump blood to the lungs and body T WAVE ventricular repolarization when the ventricles relax and prepare for the next beat ATRIAL KICK during resting diastole the atria ventricle open Blood passes ventricle gets full creates pressure to expand wall of ventricle  I 1 SA NODE FIRES the heart's electrical signalbegins in the SA node causes the atria to contract shown as the P wave on the ECG Atrial depolarization 6 2 2 PR SEGMENT AV NODALDELAY the electrical signal travels to the AV node pauses briefly allowing the ventricles to fill with blood 3 QRS COMPLEX After the signal leaves the AV node it quickly moves through the ventricles 5 3 causes them to contract and pump blood out to the body 4 Represented by the sharp spike on the ECG The atria is relaxing at the same time 4 ST SEGMENT Shows the time during which the ventricles are fully contracting and emptying the blood Flat line after QRS 5 T WAVE the ventricles begin to relax and prepare for the next heartbeat 6 TP SEGMENT the time when both atria and ventricles are relaxing and the heart is filling with blood again Ready for next heartbeat The ECG can find problems like Abnormal heart rate Tachycardia more than 100 Bradycardia less than 60 Abnormal heart rhythms heart doesn't beat in a regularpattern ATRIAL FLUTTER the atria beats very fast but in a regularpattern The ventricles can't keep up with this speed ATRIAL FIBRILLATION the atria beat quickly and in a veryirregular way the ECG won't show clear P waves Makes ventricles beat irregular and the heart might not pump blood effictively leads to a difference between the actual heartbeat and the pulseyou feel at the wrist VENTRICULAR FIBRILLATION the ventricles beat in a completely chaotic way NO pattern at all on the ECG Pumps very poorly if not treated within 4 minutes causes brain damage HEART BLOCK defects in cardiac conductingsystem Atria beats normally but the ventricles fail to be stimulated beat slower CARDIAC MYOPATHIES damage to the heart muscle Myocardial Ischemia heart doesn't getenough oxygen rich blood heart attack Necrosis some of the heart muscle cells die Abnormal QRS waveforms appear Heart Muscle Damage STRESS TESTS GXT aid in diagnosing heart or lung problems and check how fit a person is usually done on a bike or treadmill difficulty level slowly increasing Monitor ECG BP Positive Test the ECG shows problems or the person has symptoms like chest pain False Positive Test suggests a problem even if the person's heart is fine 10 201 of men and 30 of women UNCTIONAL CAPACITY TEST done by exercise experts to find out how much exercise a person can safely do create training programs research effects of exercise The heart works in a cycle where it contracts to pump out blood and relaxes to fill with blood systole when the heart contracts to push blood out Diastole when the heart relaxes to fill up with blood VENTRICULAR DIASTOLE FILLING PHASE the ventricles are relaxed and fill with blood happens in three parts early mid and late distole VENTRICULAR SYSTOLE PUMPING PHASE the ventricles contract to push blood out there's an initial stagewhere the ventricles are contracting but not pumping iso volumetric contrac then they pump the blood out ventricular ejection VENTRICULARDIASTOLE RELAXING PHASE ventricles relax but not yet iso volumetric relaxation Then start filling again filling During initial QRS as pressure begins to 1 ELECTROCARDIOGRAM ECG wild up what happens to the values shows the electricalsigns that cause the heart to contract and relax Av value closes P wave atrial contraction Atrial systole semilunarvalvescloseduringcontraction QRS ventricular contraction depolarization T wave ventricular relaxation 2 AORTICPRESSURE Shows the pressure in the aorta pressure goesup during ventricular systole and goes down 1 during ventricular diastole 3 LEFT VENTRICULAR PRESSURE 2 shows the pressure inside the left ventricle pressure rises sharplyduring ventricular contraction and falls during relaxation 3 4 LEFT ATRIAL PRESSURE Showspressure in the left atrium 4 Rises slightly when the atrium contracts to push blood into the ventricle 5 5 LEFT VENTRICULAR VOLUME Shows how much blood is in the left ventricle 6 volume increases during filling and decreasesduring ejection 70 Passive 30 from Atria 6 HEART SOUNDS the tub dub heart sounds are caused by values closing The first heart sound S1 occurs when the AV valves close tub The second heart sound S2 happens when the semilunar values aortic pulmonary close dub A PASSIVE FILLING Blood flows passively from the atria into the ventricles because both the atria and ventricules are relaxed The AV values are open and the semilunar valves are closed 3 ATRIAL CONTRACTION the atria contract to push more blood into the ventricles ventricles are still relaxed C ISOVOLUMETRIC CONTRACTION ventricles start contracting but no blood leaves yet because all values are closed Increases pressure in the ventricles No change in volume D VENTRICULAR EJECTION ventricles fully contract and blood is pushed out through the semilunar values into the aorta pulmonary artery E ISOVOLUMETRIC RELAXATION ventricles stop contracting and begin to relax All values are closed so no blood is flowing in or out of the ventricles Turbulent blood flow when blood doesn't flow smoothly can cause heart murmurs abnormal heart sounds value problems can turbulence cause STENOTIC VALVE valve that is stiff and narrowed Doesn't open fully causes a whistling sounds INSUFFICIENT VALVE valve that doesn't close properly causes blood to flow backward making a swishing sound the timing of murmurs refers to when they happen during the heartbeat SYSTOLIC MURMUR if the murmur is between the tub dub sounds when the heart is contracting AV valve issue DIASTOLIC MURMUR if the murmur is between the dub tub sounds when the heart is relaxing semilunar valve issue A LAMINAR FLOW smooth and organized blood flow blood moves in straight parallel lines without any disturbance Does not create sound because the flow is smooth and quiet How bloodtypically flows throughhealthy blood vessels B TURBULENT FLOW Disorganized chaotic blood flow blood moves in random directions Can be heard because the turbulence causes vibrations murmurs happens when there's a problem narrow or leaky heart value which disrupts the smooth flow of blood Resistance to flow CARDIAC OUTPUT Q amount of blood each ventricle pumps out in one minute Depends on heart rate and stroke volume CO HR SV Heart pumps about 5L of blood per minute At rest the heart pumps around 2.5 million L of blood During exercise the heart can pump 20 25 times more blood than when resting CARDIAC RESERVE ability to increase blood output during exercise the heart's capacity to pump more when needed EART RATE HR mainly controlled by the autonomic nervous system both sympathetic parasympathetic influence the heart and change HR and change HR and how strongly the heart contract RESERVE Maximum resting Ex Maximum HR Resting HR Parasympathetic system rest digest the vagus nerve releases Ach Ach binds to muscarinic receptors on the heart This slows down the HR byreducing the activity of the cAMP pathway involved in heart stimulation sympathetic system flight or fight release norepinephrine Norepinephrine binds to Beta 1 receptors of the heart speeds up the heart rate and makes the heart contract more forcefully by increasing the activity of the cAMP pathway EFFECT OF PARASYMPATHETIC STIMULATION Slows down the HRby affecting the SA node increases the amount of potassium leaving the SA node cells which makes the cell membrane more negative hypolarized makes it harder for the SA node to fire off electrical signals Slows down the natural reduction of potassium which makes the heart take longer to reach th threshold needed to generate next heart beat Reduces the activity of the AV node which slows the conduction of electrical signals between the atria and ventricles slows HR more weakens the contraction of the atrial muscles by shortening the time they spend in the plateauphase making the contraction less strong reducescontractile strength Little effect on ventricles becausethey hardly innervate ventricular cells EFFECT OF SYMPATHETIC STIMULATION Speeds up the HR by making the SA node fire more quickly speeds up the depolarization of the SA node reaches the threshold to fire electrical signals faster Happens because there's more Nat and cast moving into the cells Shortens the delay at the AV node speeding up the transmission of electrical signals to the ventricles Increases the speed at which the electrical signals travel through the heart's conduction system faster contractions Makes heart muscles in atria ventricles contract more forcefully by allowing more cast into the cells increases contractile strength Helps heart relax faster between beats by improving the function of the SERCA pump a protein that removes cast from the cell Allows the heart to be ready for the next beat more quickly arasympathetic and sympathetic effects on HR are antagonistic HR depends on the balance between these two parasympathetic more active the HR Slows DUAL INNERVATION sympathetic more active the HR speeds up organ innervated by both parasympathetic sympathetic ARDIO VASCULAR CONTROL CENTER controls the balance In the brainstem Detailed control because the Adjusts how much influence each system has on the heart work together EPINEPHRINE hormone that affects HR increases HR Black Line Inherent Activity of the SA node without any influence from the parasympathetic or sympathetic systems shows natural pace at which the heart would beat without external control SA node generates action potentials Red Line shows how the parasympatheticsystem slows down the SA node Takes longer for the SA node to reach threshold to fire which means the heart beats more slowly Slower HR Blue Line shows how the sympatheticsystem speeds up the SA node SA node reaches the threshold faster heart beats more quickly Faster HR Red Line slows by affecting the SA node down the HR Blue Line Epinephrine speed up the HR by making the SA node fire faster STROKE VOLUME the amount of blood pumped out by each ventricle with every heartbea INTRINSIC CONTROL VENOUS RETURN how much blood returns to the heart from the veins FRANK STARLING MECHANISM the more blood that returns to the heart the more the heart stretches the stronger it contracts pumping more blood out EXTRINSIC CONTROL SYMPATHETIC ACTIVITY when the sympathetic system is active it increases the strength of the heart's contraction allowing it to pump more blood with each beat even if the venous return doesn't change 1 Sympathetic Activity Extrinsic control sympathetic Activity epinephrine cause the heart to contract more strongly increases the of cardiac contraction strength allowing the heart to pump out more blood with each beat increases stroke volume 2 Venous Return Intrinsic control when it increases more blood fills the heart increases the end diastolic volume the heart stretches more increases the strength of the heart's contraction boosting stroke volume makes the heart pump harder based on how much blood returns to it END DIASTOLIC VOLUME EDU increased when more blood fills the heart before it contracts when increased increases SV Greater EDV stretches myocardium of the ventricle Align more myosin actin more crossbriding force more contractile TROKE VOLUME SV increased when the heart pumps out more blood intrinsic control the heart's natural ability to change how much blood it pumps SV based on how much blood it recieves EDU The more blood that returns the more blood the heart pumps out Doesn't pump out all the blood some remains in the heart Related to how stretched the heart muscle fibers are before they contract when the heart fills with more blood the muscle fibers stretch more LENGTH TENSION RELATIONSHIP when the heart muscle stretches more it contracts harder Normal Resting Length the heart's natural state when it isn't stretched much the heart pumps a moderate amount of blood low SV Increase in EDV point A B when more blood returns to the heart stretches more Allows the heart to pump more blood with each beat higher Sv Optimal Length where the heart is stretched just enough to pump the maximum amount of blood the ideal length for the heart's muscle fibers to contract most effectively Descending Limb if the heart stretches too much too much EDV can't contract as effectively and stroke volume decreases the heart normally doesn't reach this stage under normal conditions Advantages of the cardiac length tension relationship BALANCES BLOOD FLOW MEDV if one side of the heart gets more blood returning to it preload stretches more causes that side to pump out more blood larger SV keeping the blood flow balanced between the two sides INCREASES CARDIAC OUTPUT WHEN NEEDED sympathetic nervous system steps in when the body needs more blood constricts the veins and your muscles help push blood back to the heart increase the rate Increases the amount of blood returning to the heart EDU stretches the heart more pumps out more blood automatically higher SV COMBINED EFFECT Along with higher SV the sympathetic nervous system also increases HR the combined effect of more BPM and more blood per beat results in a much higher cardiac output The body can meet the body's increased demand for oxygen and nutrients during times of activity or stress Example Going up the stairs 13570 65 Increasing skeletal muscle pump i EDV  Green Line normal relationship between EDV and SV AS EDV increases the SV increases A certain EDV results in B SV Purple Line the sympathetic NS increases the heart's pumping ability even at the same EDV the heart pumps more blood when it's stimulated by the SNS A same EDV C higher SV EXTRINSIC CONTROL OF SV factors originating outside the heart SYMPATHETIC STIMULATION INCREASES CONTRACTILITY CONTRACTILITY how strongly the heart contracts for a given amount of blood filling it EDU Norepinephrine NE and epinephrine E release during sympathetic stimulation cause more calcium to enter the heart muscle cells extra calcium contract harder Pumps more blood increases SV Shifts the Frank Starling curve to the left the heart can pump more blood at any given level of filling EDU EJECTION FRACTION percentage of blood the heart pumps out compared to how much it fills up SV EDU higher ejection fraction means the heart is pumping more of the blood it holds in ventricles SYMPATHETIC STIMULATION INCREASES SV Affects the veins causes the veins to constrict pushes more blood back to the heart increases venous return When more blood returns to the heart EDU increases larger SV Difference from skeletal Muscles Skeletal muscles increase their force of contraction by witch summation recruitment of motor units 1 Cardiac Output co Depends on HR SV 2 Heart Rate HR 2 3 parasympathetic slows it sympathetic speed it 3 Stroke volume SV Intrinsic control Extrinsic control 4 Venous Return 4 increases EDV SV higher BP makes the heart work harder AFTERLOAD the amount of work the heart has to do after it starts contracting when the heart's ventricles contract they need to generate enough pressure to push open the semilunar valves force blood into the major arteries If BP in the arteries is high the ventricles need to work even harder to create enough pressure to overcome that resistance This extra workload from high BP can damage the heart and lead to heart failure IEART FAILURE HF the heart can't pump enough blood to meet the body's needs for 02 and nutrients or remove waste efficiently SYSTOLIC HEART FAILURE heart has trouble pumping blood out of the ventricles Decreased contractility heart muscles aren't strong enough to pump ejection fraction is reduced because the heart isn't squeezing as well causes damage to the heart muscle works aganist high blood pressure which weakens it Diastefas he fifth neg with blood becomes stiff and can't relax properly between beats her the heart starts to fall in systolic heart failure the body tries to compensate or adjust to help the heart keep up INCREASED SYMPATHETIC ACTIVITY SNS kicks in to make the heart beat faster and pump harder by releasing NE Helps the heart pump more blood for a short time but the heart becomes less responsive to NE RETENTION OF SALT WATER BY THE KIDNEYS Kidneys hold more salt and H2O to increase the blood volume More blood volume means more blood returns increases EDU the extra blood stretches the heart muscle fibers allowing the heart to pump out a norma amount of blood even though the heart is weakened Help the heart temporarily but can lead to more stress on the heart make HF worse DECOMPENSATED SYSTOLIC HF the heart's ability to contract weakens even more the compensating measures stop working FORWARD FAILURE when the heart can't pump enough blood to the rest of the body because SV keeps getting smaller the body's tissue don't get enough blood to meet their needs BACKWARD FAILURE the heart can't pump out all the blood that's coming back to it leads to a back up of blood in the veins As blood backs up causes congestion in the veins build up of blood CONGESTIVE HF DIASTOLIC HF stiff heart muscle caused by the build up of collagen in the heart's muscle tissue Titin Tension increased tension in the heart's muscle fibers can prevent proper filling calcium removal tissues when the heart can't remove calcium from its cells fast enough doesn't relax properly prevents the ventricles from filling completely  Green Line shows normal relationship between how much blood fills the heart and how much blood is pumped out Red Line shows a failing heart weakened contractility SV is lower than it should be Red Line shows sv of a failing heart without help Purple Line shows the failing heart with sympathetic stimulat boosts contractility helps heart pump harder increases SV Cardiac Muscle cells have alot of Mitochondria 401 Heavily dependent on 02 delivery and aerobic metabolism The heart gets most of its oxygen and nutrients from the blood through the coronary arteries during diastole phase only when semilunar valve is closed can't use the 02 in the blood inside its chambers because the walls of the heart are too thick for 02 to diffuse through During systole the heart muscle compresses the major branches of the coronary arteries Not much blood can flow through them the aortic semilunar valve partially blocks the entrance to the coronary arteries limiting blood flow to heart The heart adjusts its coronary blood flow based on how much 02 it needs even when the diastol phase is shorter due to increased heart activity OXYGEN DEMAND heart needs more 02 when working harder less time for blood to flow into the coronary arteries during diastole because heart is beating faster VASODILATION coronary vessels expand which increases the blood flow to the heart delivers more 02 LIMITED OXYGEN RESERVE heart doesn't have a large oz reserve in its blood supply like other tissues Most tissues can extract only about 25 of 02 from their blood leaving a 75 reserve they can use when needed the heart already uses 65 of 02 from its blood leaving 35 reserve the heart must increase blood flow to get more 02 ADENOSINE heart produces more adenosine when working hard Acts as a signal to dilate the coronary blood vessels allowing more blood to flow to the heart muscle supply the extra oxygen it needs Paracrine The heart can tolerate wide variations of types of nutrients it can use for energy Fatty Acids Glucose Lactate Because the heart can use different energy sources the main problem when there is reduced coronary blood flow is the lack of 02 Primary danger is 02 deficiency CORONARY ARTERY DISEASE CAD when coronary arteries become narrowed or blocked Deprives heart of 02 reduce blood flow to the heart responsible for 50 of deaths Causes Myocardial Ischemia VASCULAR SPASM temporary spasm or constriction of the coronary arteries reduce bloo flow reduced 02 ATHEROSCLEROSIS progressive disease where fatty deposits plaque build up inside the arteries causes arteries to narrow and harden reduce blood flow OCCLUSION OF VESSELS atherosclerosis leads to blockage of arteries Results in myocardial ischemia or heart attack THROMBOEMBOLISM when a blood cot travels through the bloodstream as an embolus Blocks a blood vessel either gradually or suddenly cutting off blood flow SERIPHERAL ARTERY DISEASE PAD atherosclerosis happens in blood vessels outside the brain and heart most commonly in the legs Reduces blood flow to the legs pain cramping ANGINA PECTORIS chest pain that occurs when the heart isn't getting enough 02 come from the build up of lactate when the heart has to use anaerobic metabolism Stimulates nerve endings causes discomfort EART ATTACK when part of the heart tissue dies due to lack of 02 caused by a blocked coronary artery aorta The Respiratory system isn't involved in every part of how the body uses oxygen and gets rid of CO2 CELLULAR RESPIRATION intracellular metabolic processes carried out in the mitochondria use O2 and CO2 as waste EXTERNAL RESPIRATION how 02 and Co2 are exchanged between the lungs blood and body cells 4 main steps 1 Air goes in and out the lungs 2 O2 and CO2 are swapped between air and alveoli 3 Blood transports the gasesthrough the body 4 02 and CO2 are exchanged between tissue cells 1 Air enters leaves lungs Oz goes into the alveoli CO2 is pushed out into the air 2 Gas exchange in the lungs 02 moves from alveoli to the blood Co2 moves from the blood into alveoli 3 Blood carries gases Blood moves O2from lungs to tissues brings CO2 from tissues to lungs 4 Gas exchange in tissues 02 moves from blood into cells CO2 moves from cells into the blood to be carried back to the lungs FUNCTIONS OF NONRESPIRATORY Route for water loss and heat elimination Inspired air gets warmed and humidified before being expired lose H2O heat to inspired air Important because gases cannot diffuse through dry membranes Enhances venous return respiratory pump keeps the body's acid levels balanced important for normal function in warming Enables speech singing and other vocalizations Protects aganist inhaled foreignmatter helps trap remove like dust or germs from the air things Lets you smell Removes modifies activates or inactivates materials that pass respiratory system includes the airways that bring air into the lungs the lungs muscles in the chest abdomen involved in breathing The airways nose throat windpipe move air in and out between the outside world alveoli Alveoli are the only place where oxygenfrom the air can get into your blood Co2 from your blood canleave thebody The lungs are designed to exchange gases 02 Co2 efficiently Fick's Law says that gases move faster when the distance is short and the surface area is 99Th the lungs this helps gas exchangehappen quickly Gas exchange actuallyhappens in the alveoli Air barrier encircledby pulmonary capillaries Blood barrier Type 1 Alveolar cells flat cells that make up most of the alveoli's walls Type 11 Alveolar cells make up about 5 of the alveoli and produce surfactant keeps alveoli from collapsing Alveolar Macrophages immune cells that help protect the lungs by removing harmful particles or bacteria he surface of the alveoli is huge giving more space for gas exchange The network of capillaries around alveoli is so dense that each alveolus is surrounded by a sheet of blood making the exchange of gases very efficient Each lung is divided into sections called lobes and each lobe gets air through a branch of the bronchi Lungs are made up of Highly branced airways bronchi bronchioles Alveoli tiny sacs where gasexchangehappens Blood vessels that carry blood through the lungs Elastic tissue smooth muscle around the small airways and arterioles In the bronchioles There is no muscle in the walls of the alveoli DIAPHRAGM dome shaped muscle that separates the chest from the abdomin Helps with breathing has openings for the esophagus blood vessels that pass between the chest abdomin Skeletalmuscle Contracts pullsaway from the lungs Inspiration PLEURAL SAC separates each lung from thoracic wall Double layered closed sac around each lung PLEURAL CAVITY space inside the sac sac produces a small amount of intra pleural fluid INTRAPLEURAL FLUID acts like a lubricant allowing the lungs and chest wall to move smoothly as you breathe Lollipoprepresents the lung water filled balloon represents pleural sac The Pleural sac has 2 layers 1 Visceral Pleura inner layer that directly touches the lung 2 Parietal Pleura outer layer that touches the chest wall The relationship between different pressures inside outside the lungs is key for breathing These pressures are controlled by muscle movement Atmospheric Pressure the pressure of the air around us which is 760 mmHg at sea level Intra Alveolar Pressure the pressure inside the tiny air sacs in the lungs 760mmHg Intrapleural Pressure pressure inside the pleural sac which surrounds the lungs around 756 mmHg Slightly lower than atmospheric pressure The pressure inside the pleural sac does not equalize with the pressure in the air or lungs keeps lungs elevated The balance of pressure helps air move in out of the lungs during breathing The pressure inside the alveoli is higher than the pressure inside the pleural sac More pressure pushing outward from the lungs than inward TRANSMURAL PRESSURE GRADIENT difference in pressure helps the lungs stretch to fill the space inside the chest Because of the pressure difference the lungs always try to expand to fill the chest as it moves when the chest moves the lungs follow along and expand or contract with it The lungs won't collapse and can fill with air when breathing The Intra pleural pressure is subatmospheric The lungs are elastic they pull inward away from thoracic wall The transmural pressure gradient stops the lungs from collapsing completely but the lungs still pull inward a little The movement expands the intra pleural space and drops the pressure by 4 mmHg PNEUMOTHORAX air in the chest causes intrapleural inter alveolar pressure to equalize with atmospheric pressure No transmural pressure gradient will exist to stretch the lung it collapses Air moves in out of the lungs because of intra alveolar pressure Air flows from high to low Air moves into the lungs when the pressure is lower than outside Air moves out when the pressure is higher than outside BOYLES LAW when the volume of the lungs change the pressure changes too Larger volume lower pressure Smaller volume higherpressure Respiratory Muscles don'tdirectly act on the lungs Change size of thoracic cavity causes the lungs to expand or contract A volume is small higher pressure Gas molecules are squeezed into a small place causing them to bump into each other more often increasing pressure B volume pressure are equal molecules are evenly spread out so pressure is stable C volume is larger lower pressure molecules have more space to move around so they don't bump into each other lower pressure VSPIRATION contraction of inspiratory muscles expansion ofthoraciccavity Diaphragm External intercostal muscles outside of ribs whentheycontract it pullsthe ribs ACCESSORY MUSCLES help chest expand even more for forceful inspiration EXPIRATION relaxation of inspiratory muscles passive process doesn't require energy ORCED EXPIRATION contraction of expiratory muscles make thoraciccavitymuscles Abdominal muscles push diaphragm upward Active process requires energy A External intercostal Muscles Diaphragm are relaxed B External intercostal Muscles contract the ribs expanding the chest lifting The Diaphragm also contracts moving downward increasin the size of the chest cavity Makes the space inside the so air flows in lungs bigger c The inspiratory muscles relax allowing the ribs diaphragm to return to their normal positions D To force more air out the abdominal muscles internal intercostal muscles contract pushing the diaphragm up the ribs flattening Make the chest cavity smaller pushing more air out quickly  A The pressure inside the lungs 760 mmHg is the same as the outside air so no air is moving in or out B As the chest expands the pressure inside the lungs drops slightly to 759 mmHg which pulls air in because air flows from higher pressure outside to lower pressure inside C As the lungs shrink back the pressure inside increases 761 mmHg slightlyoutside pushing air out because the air moves from higherpressure inside to lower pressure Airflow into out of the lungs depends on two main things 1 The pressure difference between the air outside inside the lungs 2 The resistance of the which is airways mostly determined by how wide In a the resistance is very low so air flows easily healthy respiratory system Parasympathetic simulation part of the nervous system causes BRONCHOCONSTRICTION the bronchioles get smaller making it harder for air to flow through Sympathetic simulation epinephrine cause BRONCHO DILATION the widen allowing air to flow more airways easily F F airflow JP P pressure difference between atmosphere inside of the lungs R resistance in airways radius of bronchioles F is directly proportional to DP if DP increases so does F F is inversely proportional to R if R increases Fdecreases CHRONIC OBSTRUCTIVE PULMONARY DISEASE COPD group of lung diseases that cause the airways to become narrower Makes it hard to breathe because of increased resistance in the airways CHRONIC BRONCHITIS long term inflammation of the airways in the becomes swollen to irritation lungs Airway produce too much mucus due Excess mucus blocks airways leads to narrowing ASTHMA Airways get blocked The walls of the airways become thick swollen Excess mucus clogs the airways The airways become hyperresponsiveof the smooth muscle tighten or constrict suddenly EMPHYSEMA collapse of smaller airways Breaks down the walls of the alveoli which reduces the surface area available for gas exchange auder to breathe out than breathing in During inspiration the chest expands which helps open the it easier airways making when someone breathes out forcefully the pressure inside the alveoli the pressure inside the pleural sac increases As air moves through the smaller airways the pressure drops slightly due to friction can cause the pressure in the airways to fall below the pressure in the pleural space leading to airway collapse before all the air is out The high intrapleural pressure can squeeze collapse these smaller airways especially those without supportive cartilage  n COPD wi