Chapter 7 – Peripheral Nervous System

Chapter 7 – Peripheral Nervous System (p. 248-256)

Somatic Nervous System: 1 neuron, a motor neuron, exits CNS and leads to target cells, skeletal muscle

fibers Neurotransmitter = acetylcholine (Ach)o Nicotinic is the receptor type

Terminal button “synapse” = Neuromuscular Junctiono Where the skeletal muscle meets the somatic neurono Occurs in the motor end plate, this is only found on skeletal muscleso Where the neuron meets and communicates with the skeletal muscle fibers

One neuromuscular junction on a skeletal muscle fiber Somatic is only efferent enervation to skeletal muscle Only depolarization elicited, so only cation channels opened – EPP (end plate

potential) A FIBER in a muscle means cell Nicotine is the receptor in the skeletal muscle cell

Figure 7.5: Events at a neuromuscular junction.1. An action potential in a motor neuron is propagated to the axon terminal (terminal button).2. This local action potential triggers the opening of voltage-gated Ca2+ channels and the subsequent entry of Ca2+ into the terminal button.3. Ca2+ triggers the release of acetylcholine (ACh) by exocytosis from a portion of the vesicles.4. ACh diffuses across the space separating the nerve and muscle cells and binds with receptor-channels specific for it on the motor end plate of the muscle cell membrane.5. This binding brings about the opening of these nonspecific cation channels, leading to a relatively large movement of Na+ into the muscle cell compared to a smaller movement of K+ outward.6. The result is an end-plate potential. Local current flow occurs between the depolarized end plate and the adjacent membrane.7. This local current flow opens voltage-gated Na+ channels in the adjacent membrane.8. The resultant Na+ entry reduces the potential to threshold, initiating an action potential, which is propagated throughout themuscle fiber.9. ACh is subsequently destroyed by acetylcholinesterase, an enzyme located on the motor end-plate membrane, terminating the muscle cell’s response.

Any communication is excitatory so if you do not want to communicate with a muscle or let it relax you just don’t talk to it.

Skeletal muscle is Neurogenic the neuron tells the muscle to contract, generates contraction of fiber

Neuromuscular Junction: Somatic motor neuron terminal button Muscle fiber (cell) Motor end plate only found in skeletal muscles, this is where all the

neuromuscular junction happens Acetylcholine (ACh)-gated cation channels (increase Na+ and minor K+

permeability) Contains voltage gated sodium and potassium channels End Plate Potential (EPP)

Acetylcholinesterase (AChE) the a means there is an exnzyme, it breaks down aCh. Kills off neurotransmitter, we need to keep that area clean

In skeletal muscle the NMJ is in the middle of the fiber With this we are only going to excite our skeletal muscle fibers This is only going to be excitatory NO inhibition Skeletal muscle will always get to threshold if the somatic neuron fires no matter

what. If will not reach threshold if something dramatically goes wrong but most of the time, always, it will reach threshold and fire.

Each skeletal muscle fiber has a neuromuscular junction Each skeletal muscle fiber has to be told to contract. Each individual axon terminal is connected to a neuromuscular junction

Selected Neuromuscular Agents Black Widow Spider Venom

o Affects the NMJ by causing a burst of aCh in the buttono By this its flooding the synapse and the Acetylcholinesterase (AChE) can

not clean it up fast enough, this causes a massive contractiono Not big a deal to us but to small things like mice it will be a problemo Causes huge muscle contractions

Clostridium botulinum toxin (botulism, BoTox) o Smallest amount to cause death, most lethalo Bacteria that causes botulism

Ex. machine that labeled the salmon canso Its in botoxo It blocks the release of Ach so sarcoplasmic reticulum wont contracto In very small doses they can get the small muscles to stop twitching

Curare o Plant based drug from Africao Blocks the aCh cation channelso Use to be used in surgeries to calm the muscles down

Organophosphates o Not natural, military nerve gaseso Not organic so when it binds it binds permanently to Acetylcholinesterase

(AChE). Cant clean out the synapse which causes to massive skeletal contraction

o Band in the US o Permanent binding

Myasthenia gravis (Neostigmine) o A autoimmune disorder own immune system tags then attacks one of

your productso The receptor-gated channel thinks its being bound or triggered by Ach so

it opens the cation channel.o Down regulated Ach receptors, skeletal muscles become least sensitive to

Ach

o Starts in the face, start loosing facial expression. Problems with swallowing can go down diaphragm.

o Neostigmine is the best drug for this. It binds to the Acetylcholinesterase (AChE) , this doesn’t allow the synapse to be cleaned and builds up Ach so it can bind to the small amount of Ach receptors that are left.

Basic Structure of overall skeletal muscle: Strong and flexible Muscle FasicleMuscle Fiber cell (a single muscle cell)Myofibril (with

sarcomeres, functional unit) Connective tissue around each fascicle, they are an insulator to get muscle fiber

fired, but it wont affect the fiber next to it. Dark and light bands are the striations of the muscle Sarcomere means flesh, functional unit

Muscle Fiber = Muscle Cell• Sarcolemma (covers the whole muscle cell), sarcoplasm (covers each individual

myofirbril)• Huge multinucleated cells• Transverse Tubules

• Allow depolarization of the membrane to quickly penetrate to the interior of the cell

• Inside the sarcolemma• Sarcoplasmic Reticulum (lateral sacs)

• Are surrounding the transvers tubules and then covers like a net all over the muscle fibers

• Surrounding the sarcomeres of the myofibrils

DRAW SARCOMERE FOR EXAM

Sliding Filament Theory• Thin filaments (of actin with troponin & tropomyosin) make-up the walls of

the sarcomere “compartments”– H zone is the lighter portion in the center of the A band where there are no

thin filaments– Calcium binds to troponin making tropomyosin move away and thick

filament will bind to the thin filament• Thick filaments (of myosin) make-up the central core, that pulls in the walls

– A band is darker because of the presence of the thick filaments– The thick filament grabs the thin filament and pulls it towards the M-line

and shortens (CONTRACTION)• I-Band shrinks and H-zone shrink when sarcomere shorten, sarcomere shortens

and A-band remains the same length• FILAMENTS DO NOT CHANGE LENGTH they just overlap each other to

shorten the sarcomere• There are two binding sites

o Actin & ATPo But you cannot bind to both at the same time

Cross bridge Cycle (connection between the thin and thick filaments) Starting point = relaxed no contraction Tropomysoin are blocking the binding sites Myosin are cocked and ready which means ATP has been there and broken down Acting kicks off only ADP = triggers power stroke Then gets stuck and ATP binds to myosin head and releases

Cross bridge Cycling• Contraction

o When nervous system tells the muscle fiber to contract all the myofibrils, sarcomeres contract

• Troponin-tropomyosin complexo At rest blocks myosin from grabbing actin - when contracting are moved -

with Ca 2+ • Cross bridges

o Myosin bound to actin (forms a bridge/connect)• Attach - power stroke - release - recock

1. Think Filament and myosina. Muscle relaxed - myosin-head cocked & ready, just needs a binding site,

still bound to ADP2. ATACHES: Myosin head binds when actin binding site becomes available (Ca2+

binds to troponin, moving tropomyosin out of the way) - knocking off ADP

3. POWERSTROKE: Myosin-head “power strokes”, pulling actin walls toward the M-line

4. Releases: Myosin-head releases when ATP binds to it , If no ATP available – you’re stuck: rigor mortis

5. Re-cocks: Myosin-head hydrolyzes (breaks) ATP to ADP and uses the energy to recock the myosin-head. If Ca2+ still available then crossbridge cycle starts again.

a. Attach - Power stroke - Release - Recock6. If Ca2+ no longer available - then the muscle has been returned to its “cocked and

ready” positiona. Muscle twitch = the smallest muscle contraction, in skeletal muscle

If Calcium is cleared out that doesn’t mean they all stop at the same time, its like pouring water out of a bucket. Some water touches the floor first then the rest follows

Energy released is used to cock the myosin head To get each myosin to release you need an ATP for each head How are we using ATP?

o We use ATP to stop contraction by releasing ito Heat can be given off as ATP

Cross Bridge Activity1. Binding: Myosin cross bridge binds to actin molecule.2. Power stroke: Cross bridge bends, pulling thin myofilament inward.3. Detachment: Cross bridge detaches at end of power stroke and returns to original conformation.4. Binding: Cross bridge binds to more distal actin molecule; cycle repeats.

Excitation contraction coupling Excitation is how do you generate the excitation in your skeletal muscle

o In the NMJo Excite sarcoplasmic reticulum drops its calcium and begins to suck it

back up againo Always guaranteed to reach threshold unless something bad happenso Somatic Nervous System

The contraction is the cross bridge cycleo Pulling the thin filament to the m-line

BASICALLY going from NMJ to Cross Bridge Cycle The trigger point is the voltage gated channels from the sarcoplasmic

reticulum is the intermediate point that brings the NMJ and the Cross bridge cycle together

STEPS:1. An action potential arriving at a terminal button of the neuromuscular junction stimulates release of acetylcholine, which diffuses across the cleft and triggers anaction potential in the muscle fiber.

2. The action potential moves across the surface membrane and into the muscle fiber’s interior through the T tubules. An action potential in the T tubule triggers release of Ca2+ from the sarcoplasmic reticulum into the cytosol.

3) Ca2+ binds to troponin on thin filaments.

4) Ca2+ binding to troponin causes tropomyosin to change shape, physically moving it away from its blocking position; this uncovers the binding sites on actin for the myosin cross bridges.

5) Myosin cross bridges attach to actin at the exposed binding sites.

6) The binding triggers the cross bridge to bend, pulling the thin filament over the thick filament toward the center of the sarcomere. This powerstroke is powered by energy provided by ATP.

7) After the power stroke, the cross bridge detaches from actin. If Ca2+ is still present, the cycle returns to step 5.

8) When action potentials stop, Ca2+ is taken up by the sarcoplasmic reticulum. With no Ca2+ on troponin, tropomyosin moves back to its original position, blocking myosin cross bridge binding sites on actin. Contraction stops and the thin filaments passively slide back to their original relaxed positions.

3 ways we controlling strength on Contraction:1. Twitch summation Calcium is going to control the strength, by controlling

calcium you control contraction, controlling each individual fibera. Larger and larger contractions as we sum the twitches

2. Length-tension relationship how much the muscle can stretch to how much the muscle can contract

3. Motor unit / recruitment we only triggers a few fibers, not the whole muscle. This is good to pick up a little object. When you pick up something heavy you recruit more muscle fibers

Muscle fatigue: The inability to perform the action you are trying to doo The Two things that cause muscle fatiguea. Lack of ATPb. Change in pH – especially acidity lower pH, more alkaline will also make

an impact but less likely it will occur

Fig 8-13 Graph (TWITCH SUMMATION)

Skeletal Muscle Resting Membrane potential is about -90MVo Means that it is potassium’s equilibriumo Very leaky to potassium

o When opening a cation channel Na going in because potassium is gone from the membrane being very leaky to K

Skeletal muscle is about 1-2ms long just like nerve cell The strongest part of the curve is in the middle where you have more calcium, that

means the most myosin heads are moving The length of twitch varies 50-100ms length of twitch Tetnus (tetanic) FULL FORCE TWITCH SUMMATION

o Biggest muscle contraction that a muscle can give youo Can cause locked jawo Starts from the heado High frequency/action potentials

Length-Tension Relationship There is an optimal stretch in your muscle to give you max strength As you over stretch you loose strength, you pull all myosin away from actin , they

actually cant reach they are just standing there staring You want optimal overlap between the thick and the thin filaments For ice skaters, they use their gluteus Maximus and lean forward/over to get their

optimal maximal strength stretch because it works best like this Put muscle in the right place to get the max strength stretch Found in skeletal muscle, smooth muscle doesn’t have any its good because we

want to move fecal material down intestines. You do in cardiac muscle! Difference is that in cardiac muscle:

The more you stretch the harder it contracts, the more blood you have in the heart the heart will push it out faster and stronger, the more you stretch the heart the stronger it contracts (natural length and tension relationship). If you receive 70ml in heart you better pump out 70ml

Motor Unit Is the somatic neuron plus all the fibers it connects to, For example: motor units

of 12 is 1 for somatic neurons and 11 fibers its communicating with. Smallest are about 4 Fine control you want about 3 fibers, knitting 30,40,50 motor units are in your thighs Come in different sizes Allow us to activate a subset in the whole muscle Somatic neurons only talk to the fibers Benefits: ability to recruit, allows for a range of strengths from a given muscle,

very efficient with ATP use, avoiding fatigue, don’t have to use the whole muscle at once, it allows you to rotate through the motor units in the muscle to allow you to use the muscle for a longer period of time

It’s a learned process, for example sometimes you may recruit too many and the object you are picking up is actually light, and sometimes you recruit less and the object is very heavy

2year olds are still trying to learn the motor unit recruitment process

Rotate through the motor units, rotate through fibers by recruiting different subsets of the muscles to allow the muscle to continue to work longer

Tension vs. Load If picking up 20lbs you need to put 20lbs of tension Load and strength and tension of muscle are directly related

GENERAL CONTRACTION TYPES Essentric conrtraction controlling drop, elongating of muscle Consentric contraction shortening of muscle Isometric muscle length does not change

Fueling muscles (creatine phosphate) Store it Longer life then atp, but cant use it directly. it acts like a immediate

recharger for ADP Recharge your old atp Replenish atp with creatine phosphate if atp is available Its in short supply, so go to cellular respiration for atp replenish with respiration charged with hi energy phosphate group can store it

o Glycolytic (anaerobic) specialistso Oxidative (aerobic) specialists

Glycolytic Specialized for anaerobic respiration 2 ATP/glucose, but very rapid “bursts” of ATP production lactic acid biproduct fast but inefficient White meat. Not that much myoglobin Chickens Bicep muscle Usain Bolt

Oxidative Specialized for aerobic respiration ~36ATP/glucose via high density of mitochondria Myoglobin the protein ( has a higher O2 affinity than hemoglobin), this is

what makes dark meat dark Highly vascular efficient but slow great for endurance, not huge burts no lactic acid, byproducts are CO2 and H2O great blood supply Dark meat

o Example: Erector spinae muscle Mev

Different people have different proportion of glycolytic and oxidativeGenetics and environment have a lot to do with itSkeletal Muscle Fiber Type (3)

Slow Oxidative (red, myoglobin) – Type Io Best at avoiding fatigueo Not using atp as quicklyo Lots of atp and no lactic acid build upo Cant change the slow to fast oxidative or fast glycolytic

Fast Oxidative (red, myoglobin) – Type IIa Fast Glycolytic (white) – Type IIx

o Fatigue fasto Biceps and shoulder muscleso Few mitochondriao High levels of glycogen

All muscles have all three fiber types - they vary with regard to specific muscle, genetics, & training

You can change the proportions/ shifts from fast oxidative/glycolytic Fiber size = fiber strength ALL skeletal muscles in the body have all e of these muscles, different muscle

will have different proprtions of each typeMuscle Size:• Hypertrophy tissue or organ gets larger because cells inside get larger/bigger

not because cell number gets larger (that’s hyperplasia)o Adult liver is larger then child liver due to hyperplasiao Skeletal muscle grows through hypertrophy

• Atrophy: loss of muscle size, due to cells getting smallero 2 types:o Disuse Atrophy

Not using it Astronauts, arm out of cast PT can decrease this

o Denervation Atrophy Somatic neurons not firing to the fibers Muscle not receiving somatic nerve

o Muscular dystrophy Loss of muscle tissue as a result of a lack of a protein called

dystrophin protein (in the sarcolemma it helps to maintain the stability of that structure of that cell)

Individuals can be born without the protein or have a loss of this protein as they grow older

We are loosing cells not size It means any disease in which you get loss of muscle tissue

(degenerations), a much broader term than defined Include the diaphragm/muscles of swallowing

Individuals who are not making enough or not making enough of the protein and leads to destabilized sarcolemma’s/cells begin to die

Afferent Information back to brain Nociceptors all skeletal muscles have this and proprioceptors Proprioceptors

o Two types:o Muscle Spindles (Knee-Jerk reflex)

Buried in muscle cell collection of specialized intrafusal fibers that lie within a

connective tissue capsule parallel to the ordinary extrafusal skeletal muscle fibers. Interverted by its own gamma motor neuron and is supplied by two types of afferent sensory terminals, the primary (annulospiral) endings and the secondary (flower-spray) endings, both of which are activated by stretch.

o Golgi Tendons Organs Buried in tendons Entwined with the collagen fibers in a tendon and monitors

changes in muscle tension transmitted to the tendon.Smooth & Cardiac&Skeletal Muscle

Skeletal Smooth Cardiac Striated ( are from thick and thin

filaments, striations mean sarcomeres)

Voluntary ( only contracts because somatic NS tells it to, all control is in the NS)

Fiber size is huge Multinucleated (50-100) Transverse tubules Huge SR Cocking of myosin head is

automatic Somatic Nociceptors/proproceptors

Un-Striated (no sarcomeres), has thin and thick filaments but spread out like net, this means no troponin tropomysosin components so Ca cant bind.

Involuntary (affect by hormones, irritation, stretch, heat, controlled by whole environment)

Fiber size is small 1 nucleus (fattest part of

cell) Non existent (transverse

tubules) Diffusion Binding sites always

open Cant cock own myosin

heads but calcium is the trigger

Autonomic If stretch, contracts back myogenic

Striated (sarcomeres functions like SM) striations mean sarcomeres

Involuntary (affect by hormones, irritation, stretch, heat, controlled by whole environment)

Fiber size is intermediate 1-2 nuclei Not so much transverse tubules Diffusion/SR uses both Autonomic If stretches it doesn’t contract back myogenic

Smooth Muscle• Spindle shaped• Dense bodies instead of sarcomeres they have this• Very slow myosin activity for energy conservation• Ca2+-Calmodulin 2nd Messenger System Þ phosphorylated Myosin-head

activation LEADS TO THE COCKING OF THE MYOSIN HEADS• Very few signals that lead to a cascade of millions of reactions• Binding sits always available• ALL WE NEED TO KNOW IS THAT IT LEADS TO THE

COCKING OF THE MYOSIN HEADS• Tone, latch phenomenon

• Always a little calcium in there which means that we always got cell myosin heads going through their cycle, never really relaxed

• Can control the tube size/tone of tube

Multiunit vs Single Unit Smooth Muscle Mainly talk about single unit Multi units (NEUROGENIC)smooth muscle means that the individual smooth

muscle cells act like individual units you have to talk to each cell independently. Found in eye (to help focus), in the iris to help control dilation , attached to hair follicles

Single units (MYOGENIC)smooth muscle, all the cells are inner connected by huge numbers of gap junctions, like a tunnel that connects from one cell and the next, a wave of activity, you just communicate with a small bundle of cells and that will spread out. With that wave you have thousands of cells acting like one unit. Functional syncytium. Found in all the tubing in body

Two Types of Smooth Muscle (these refer to what is going to cause the muscle cell to contract, How do we excitation to skeletal muscle?)

o Neurogenic the nervous system telling muscle to contract Multiunit smooth muscle Affected by local environment (stretch, hormones, irritation)

o Myogenic muscle itself creates own excitement/contraction Single units smooth muscle

Functional Syncytiumo In all organs to help move stuff across our bodies.o Two Types of Smooth Muscle (functional syncytium)o Ventricular fibrillation

When your cells come out of sync and the heart is not working as one unit so they have to shock your heart with the electrodes to get it to all function at the same time. You lost your functional Syncytium.

Cardiac Muscle Intercalated disc one cardiac muscle cell attaches to the next cardiac muscle

cello Desmosomes (strong but stretchy) and gap junctions in intercalated discso 1-2 nucelio myogenic (and in smooth muscle), cell has to create excitement

Single units muscles use these two , Auto rhythmicity: Slow-Wave vs. Pacemaker• Slow-Wave Potentials some single unit cells use this to alternate their ion

permeability channelso Some Single-unit Smooth muscleso Alternating ion permeability’s - may or may not reach thresholdo Cells have alternating channels creating wave of polarity

• Pacemaker Potentials o Cardiac & some Single-unit Smooth muscleso Leaky to Na+ to threshold, at 60mv then you leak your way to thresholdo Involuntary, under control of the ANSo Nervous system adjusts ion permeability’s

o Under sympathetic innervation you release EPI and NOREPI, they make the cells leakier, leaks it faster and this causes it the increase rhythm of heart

o Under Para releases Ach and makes you less leaky, closes up channels, takes longer to leak your way to threshold and makes heart rhythm slower

Cardiovascular systemo Artery, Arteriole, Capillary (only sight for exchange between blood and tissue,

pick up waste products like CO2), Venuole, Vein

Systemic circulation the right side of the heart sends deoxygenated blood to the lungs to get “refreshed”, to get oxygenated. The left side of the heart receives oxygenated blood from pulmonary circulation and pumps it to the systemic circulation (rest of body)

In lungs fragile, low blood pressure, the volumes in the lungs are the same, pumping at the same time. Time and volume are the same for right and left lung, it’s the pressures that are completely different. Giraffe has the greatest blood pressure difference because of how separated his head is from the rest of the body.

Tracing a blood cell through the heart!Inferior/Superior Vena CavaRight Atrium Right Atrioventricular ValueRight Ventricle Pulmonary Semilunar Valve Pulmonary Artery Lungs Pulmonary Veins Left Atrium Left Atrioventricular Valve Left Ventricle Aortic Semilunar Valve Aorta Systemic Circulation

Beats of the heart

Single unit cells use both, cardiac only uses pacemaker potentials .

These two can affect how fast or how slow they will get to threshold but they don’t run the show

o 1st beat slamming shut of the Atroventricular Valveso 2nd beat Semilunar Valves Shut downo Its also good to know that the ventricles work harder if the pressure on the other

side of the valve is greater.o You also get the same blood pressure from the leg and arm

- Use pacemaker potentials to get beats- Ventricles contract bottom to top- If there are no blood in ventricles they will collapse, no air or open space- Right and Left sides eject same amount of heart, if not you will get a back up in the system-Arteries are elastic-Heart beats 70bpm

Valves: One way valves Laminar Flow do not hear it, its when you get turbulence, its always smooth,

this is how blood should always flow

What holds down the ventricles so blood wont go backwards? Pupillary muscle, the cords are called chordae tendineae You also never eject all the blood, only about 50%

4 major pacemaker cluster cells: (this is under parasympathetic stimulation, at rest)1. Sinoatrial Node

a. This is our fastest node, it leaks to threshold the fastest2. Atrioventricular Node

a. Sending signals to the ventricles3. Bundles of his with bundle branches

a. Sending signals to the ventricles4. Purkinjie fibers

a. Communicating with actual muscles

*All these cells are capable of leaking themselves to threshold

Plateau phase Open voltage gated calcium channels, calcium goes in K goes out. They’re

charges are canceling each other out.

Electrocardiogram measures change in electricity in your body Heart is creating the electrical system We don’t see the atria repolarization because that’s when the ventricles depolarize Ventricles are the most full right before they eject

Cardiac function • Systole (between P and QRS)

o Contraction• Diastole

o Relaxation• Stroke volume (SV) = end diastolic volume – end systolic volume

o Ejection volume, how much volume of blood do the ventricles contract• EDV Ventricles are most full

o Volume at the End of ventricle relaxtion phase• ESV Ventricles are least full

o Volume After ventricles contract• Isovolumetric contraction (all valves are shut)

• All four valves shut• Between QRS and T• Pop open semilunar valve

• Isovolumetric relaxation (all valves are shut)• Pop up open AV • After the C

• T or F during atrial contractions the semilunar valves are open• Dicrotic Notch blood bouncing valves when they close shut. Blood causing

little waves• Repolarization is the return of the ions to their previous resting state,

which corresponds with relaxation of the myocardial muscle• electrical impulse causes the ions to cross the cell membrane and causes

the action potential, also called depolarization

Cardiac Disorders• Arrhythmias Iregular Heart Beat

Bradycardia slow resting HR, HR<50, only exception are athletes Tachycardia Fast resting HR, HR>100 Premature ventricular contraction Ventricles cause an extra beat Complete heart block Scar Tissue, The atria is beating faster than

ventricles Ectopic focus irritation or inflammation

Atrial or Ventricular Fibrillation For atria fibrillation you are not ejecting blood anywhere, get defibrillator. Not getting a functional syncytium meaning that the gap junctions are not running the show

o Loose all pumping contractiono No Ventricular fibrillation medicine

Heart Sounds • Lub & dup• Heart murmurs abnormal heart sound, caused by valve problems

– Stenotic valves The valves are stiff and do not open up all the way, causes turbulence. Makes whisper noise

– Insufficient valves, regurgitation• Not closing right, you are getting regurgitation of blood

backwards. Bubbling noise• Laminar vs. turbulent flow

– When you get turbulent you can hear it

Cardiac output How hard the heart is beating At rest pumping about 5L of blood Cardiac Output (CO) = stroke volume x heart rate Cardiac reserve = COmax – COrest

Frank-Starling LawDEF> The cardiac muscle fiber’s length, which is determined by the extent of venous filling, is normally less than the optimal length for developing maximal tension. Therefore, an increase in end-diastolic volume (that is, an increase in venous return), by moving the cardiac muscle fiber length closer to optimal length, increases the contractile tension of the fibers on the next systole. A stronger contraction squeezes out more blood. Thus, as more blood is returned to the heart and the end-diastolic volume increases, the heart automatically pumps out a correspondingly larger stroke volume.

Cardiac muscle length-tension relationship• End-diastolic volume – stretches heart• Heart failure SV decreases at the same EDV as normal heart

• During compensation for heart failure, reflex sympathetic stimulation shifts the Frank–Starling curve of a failing heart to the left, increasing the contractility of the heart toward normal. A compensatory increase in end-diastolic volume as a result of blood volume expansion further increases the strength of contraction of the failing heart. Operating at a longer cardiac muscle fiber length, a compensated failing heart is able to eject a normal stroke volume

• Congestive heart failure

Cardiac Blood Flow

• Myocardial ischemia o Blood flow to your heart muscle is decreased by a partial or complete

blockage of your heart's arteries (coronary arteries). The decrease in blood flow reduces your heart's oxygen supply.

• Myocardial infarction (heart attack) • Coronary artery disease (CAD) • Atherosclerosis • Thrombus • Embolus • Occlusion

o Loss of blood flow in a region of the hearto When vessels contract it squeezes hearto Metabolic activity really active tissue= increase blood flow

The higher the activity the higher vasodilation of coronary vesselsChapter 10 Blood Vessels

Arteries Arterioles Capillaries Venioles Veins

• Arteries– Away from the heart– Thick, elastic walls– High pressure

• Arterioles– Control to the tissues– Walls mostly smooth muscle– Constricting walls – decreases blood flow

• Capillaries– Only site of exchange (between tissues & bloood)– Only one squamous cell thick (endothelial cell)

• Venules– Very tiny veins

• Veins– Very loose, baggy walls– Contricting walls – increases blood flow (venous return)– Very low pressure, returns blood to the heart

*If you have all the blood vessels open your blood pressure drops significantly

*Most coronary blood flow occurs during diastole because the coronary vessels are compressed almost completely closed during systole.

Away from heart (elastic

wall)

Only place of exchange

between blood & tissues

Returning blood to heart

Blood Vessel Diameter• Vascular tone• Vasoconstriction• Vasodilation

– active hyperemia (fig. 10-10, p 353)• Local vasoactive mediators (NO, endothelin; histamine)• Other factors: temperature, sympathetic nervous system

Capillary Exchange• Capillary beds• Precapillary sphincter• Pores

List and Define the ways exchange across a capillary occur Diffusion small molecules that can move high concentration to low

concentration (Na and Cl leaving) through channels or through the cell Transcytosis move larger things through capillary walls by exocytosis and

endocytosis. The way you move larger molecules like insulin Bulk Flow Bulk flow is the result of filtration and reabsorption between the

capillaries and the interstitial fluid due to fluxes in blood pressure and osmotic pressures

Bulk flow Filtration pushing fluids put through capillary wall Reabsorption forcing fluids out and sucking them in. The way you clean/rinse

tissues The more you increase BP the increase the filtration and the less absorption

happens Anything that increases filtration or reabsorption gets the extra fluid in the tissues.

This causes EDEMAo Edema can be localized or systemico Edema as a result of increases in capillary blood pressure, capillary

permeability, interstitial fluid colloid osmotic pressure (inflammation)o Filtration is a constant process, its high in the beginning and decreases in

the end

Blood Flow in the Veins• Venous capacity, venous return

– Venoconstriction (vasoconstriction of veins) improves flow• Skeletal muscle pump, respiratory pump, heart as “suction pump” and force of

blood pressure• Many veins have valves, constricted skeletal muscles act as transient valves• Blood volume at rest is usually in the systemic veins

Vasopressin Constrict blood vessel, increases BP

Another word for this is ADH, anti diuretic hormone Blood volume increase with ADH and helps BP Found in posterior pituitary

Medullary CV control center & hormones• Afferent:

– Carotid sinus & aortic arch baroreceptors• Cardiovascular Control Center in medulla oblongata of brain stem• Efferent: (bodys emergenry to increase BP)

– Autonomic N.S.– Vasopressin– Renin-angiotensin-aldosterone system, increase MAP

Disorders• Coronary artery disease (CAD) this is atherosclerosis of the heart• Atherosclerosis plaque usually forms an eclusion = inflamation• Thrombus problem for blood flow but trouble Is when it breaks free then

becomes an embolus which turn into thromb, blood clot or plaque • Embolus anything blocking a vessel• Occlusion cant get into any artery• Hypotension systolic under 100mmhg, low blood pressure• Hypertension high blood pressure• Circulatory shock sudden drop in BP• Hemorrhage Bleeding

Circulatory Shock (decreases MAP)

Hypvolumetric shock (decreases CO)o Severe blood and fluid loss

o Less BVo BP decreaseso Pass out to save the brain because the blood gets to the brain faster when

you are horizontalo Uses anaerobic respirationo Lactic acid build up, keep them warmer

Cardiogenic shock(decreases CO)o Heart is problem, weakened heart, result of long term age and diseaseo Heart not able to get proper SV, BP decreases

Vasogenic shock(Decrease TPR)o Problem with blood vesselo Infection or allergic reaction can be the cause

Ex. sting ray exampleo Massive Vasodilation so there will be a TPR decreaseso Septic shock and anaphalactic shock

Neurogenic shock (Decrease TPR)o Problem with ANSo Lost of vascular toneo Decreases Sympathetic system: increases

contractility Increases venous return And increase HR

3 ways the Cardiac Output is affected?1. Increase HR by increase SA node2. Increase contracting of muscle3. Increase tone or vasoconstriction of veins, which increases venous return

These are also 3 ways to increase Stroke Volume