ANP 1105 Muscles There are many factors that contribute to increased contractile force, these include a) Large

number of muscle fibers activated b) Large muscle fibers c) Asynchronous tetanic contractions d) Muscle and sarcomere length slightly over 100 of resting length The velocity and !uration of "ontraction de#end on$ 1) Load$ the greater the load, the longer latent #eriod %hich in turn results in slo%er contraction and shorter contraction duration The & sources %here muscle contraction gets its energy from is stored ATP, !irect #hos#horylation, Aerobic res#iration and anaerobic glycolysis a) Stored ATP ' as soon as you stimulate the muscle to contract, it is going to ma(e use of %hatever ATP there is available to be used) ' ATP for cross bridge movement and detachment* "a++ #um# ' These contains only &', seconds of stored ATP b) Direct Phosphorylation of ADP by creatine phosphate ' As soon as you try to do %or(, and ATP is used, this method %ill be initiated) The "P %ill transform and transfer its #hos#hate to A!P to ma(e ATP) The en-yme that cataly-es this reaction is called creatine (inase) ' This %ill last for 15'.0 seconds because the "P reserves %ill be diminished) /our muscles %ill be at ma0imum #o%er during this time) ' Creatine Phosphate is a uni1ue high energy molecule that is stored in muscles) The reaction is defined as "P + A!P creatine + ATP c) Aerobic respiration ' you %ill ne0t be loo(ing to%ards glucose for energy) /ou can metaboli-e it anaerobic2aerobically) The difference bet%een the t%o is utili-ing o0ygen) ' Aerobic gives you a high ATP yield* ho%ever, it is much slo%er because it re1uires many ste#s and re1uires continuous su##ly of 3. and other nutrients in order to create said ATP) ' Aerobic res#iration is much more efficient #er glucose molecule but it re1uires more time) 4t generates 56, ATP #er glucose d) ' ' ' Anaerobic glycolysis anaerobic gives you more ATP faster, but less #er glucose molecule) 4t only generates . ATP2glucose but it is fast 7sually it is #yruvic acid that enters the aerobic #ath%ay) 4t is converted to lactic acid)

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After, it is converted bac( to #yruvic acid once e0cercising is over and aerobic res#iration %ill ta(e over and re#lenish ATP stores) This is im#ortant because %hen your muscles are %or(ing at 80 or more, your muscles are contracting vigorously and it effects blood flo% to the muscles) Therefore %ith less blood flo%, insufficient 3. su##ly is getting to the muscles in order to use aerobic res#iration) Anaerobic #ath%ay #roduces 55 ATP of aerobic #ath%ay, but it is .)50 faster than aerobic #ath%ay)

Example: Short duration exercise 1', seconds$ ATP stored in the muscles are used first ,'10 seconds$ ATP is formed from creatine #hos#hate and A!P 10'&0 seconds until finish$ 9lycogen stored in muscles are bro(en do%n to glucose, %hich is o0idi-ed to generate ATP Example of prolonged duration exercise :ours$ ATP is generated by brea(do%n of several nutrient energy fuels by aerobic #ath%ay) This #ath%ay uses o0ygen released from myoglobin or delivered in the blood by haemoglobin) ;hen it ends, the o0ygen deficit is #aid bac() ' ' ' ' 4f an e0ercise is around 15'.0 seconds, %e %ill be using ATP stored and "P) This is because it is not an endurance activity, it is <ust a short burst of fairly intense activity) Tennis, soccer and 100m s%im are almost entirely anaerobic because it consists of short bursts of energy) A marathon is mainly aerobic$ %hen you first start training, and do re#eated e0ercise, you %ill slo%ly increase your aerobic endurance* meaning that your cells are slo%ly being more and more efficient %ith aerobic res#iration) "ells build u# myoglobin and more en-ymes for the aerobic metabolism of glucose* they build more mitochondria to be able to #rolong much longer)

Aerobic endurance: the length of time a muscle can use aerobic res#iration Anaerobic threshold: #oint at %hich muscle converts to anaerobic res#iration) uscle !atigue$ is the state of #hysiological inability to contract* it results from a relative deficit of ATP =total absence %ould cause contractures) ' there is a difference bet%een feeling tired and to the level %here your muscles are <ust unable to do it) ' 4f there is absolutely no ATP there %ill be rigor ' A build u# of lactic acid %ill disru#t #: levels in your body* and also, ion imbalances ) there are ions in unnecessary #laces =the Na+2>+ #um# re1uires ATP) "xygen Debt: the e0tra amount of o0ygen needed to be ta(en in to accom#lish the belo% ' #ost e0ercise, you need to re#lenish o0ygen reserves, convert lactic acid to #yruvic acid =lactic acid indirectly stimulates the res#iratory centre of the brain), re#lace glycogen stores, restoc( ATP and "P)

The liver also hel#s by converting additional lactic acid to glucose2glycogen This is %hy after a heavy e0ercise, you are still breathing heavily to re#lace this o0ygen debt) #eat production during muscle acti$ity ' ATP driven muscle contraction is only .0'.5 efficient) The rest of the energy is %asted and turned into heat energy %hich is dissi#ated by the body?s cooling mechanisms) uscle !iber Types The muscle combination in every #erson is different) This means that by genetics, some #eo#le are better runners than others, etc) @lo% and fast refer to their contractile ability and their metabolism rate for generating ATP) 30idative im#lies that they carry out aerobic res#iration) a) Slo% oxidati$e fibers: thin cells %ith slo% acting myosin ATPases* they contract slo%ly =redA lots of myoglobin)) The #rimary energy fuel is fat) ' contains lots of mitochondria, ca#illaries, aerobic en-ymes* 3B4!AT4CD ' fatigue resistant but they are not #o%erful =thin) ' these muscles are im#ortant for endurance ty#e activities) b) !ast glycolytic fibers: large, #ale =%hite), little myoglobin and almost t%ice the diameter of slo% o0idative fibers* there are fast acting myosion ATPases and contract 1uic(ly) ' fe% mitochondria, they are going to carry out anaerobic metabolism) They %ill need a good glycogen reserve) ' They %ill fatigue because there %ill be lactic acid #roduced and glycogen reserve %ill run out, but they are very #o%erful ' These muscles are used in short term, ra#id intense movements) c) !ast oxidati$e fibers: red or #in(, cell si-e is intermediate* fast acting myosin ATPases and contract 1uic(ly* high myoglobin content and o0ygen de#endent* fairly fatigue resistant) ' the are best for intermediate activities) /our muscles re1uire a different mi0 of these fibers in order to ada#t to certain circumstances) !ue to genetics, some #eo#le %ill have an advantage and abilities based on their muscle com#ositions) Smooth muscle ' ' are very %idely distributed in the body and it is going to be in #laces %here you have lumen) Tend to be smaller cells %here lots of nuclei are #ushed off to the side* it is filled %ith myofilaments)

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They %ill not be arranged in an orderly %ay so you %ill not see the striation that you see in s(eletal muscle) They %ill still have actin and myosin* they are able to carry out contraction in one smooth movement) The cells are se#arated by fine "T* sheets of closely o##osed fibers* usually at least . sheets %ith o##osite orientations) Alternating contractions of o##osing layers #rovide mi0ing, #eristalsis, e0#elling There are varcosities instead of neuromuscular <unctions) Eulbous s%elling of autonomic nerve fibers$ the release neurotransmitters into a %ide syna#tic cleft near smooth muscle cells This allo%s the %hole layer of smooth muscle cells to move as a singular unit The cells are s#indled meaning that they are fatter in the middle and get smaller as you move a%ay from the centrally located nucleus The @F are less develo#ed than s(eletal muscle* there are no T tubules because the cells are small and the events at the PM %ill have no #roblem travelling through the ga# <unctions) There is no striation but they do have interdigitating thic( and thin filaments$

1) ratio of thic( $ thin A 1$1, =smooth) versus the 1$. =s(eletal)* but smooth muscle myosin has actin gri##ing heads along the entire length) They can achieve very strong contractions li(e this) .) they have tro#omyosin but no tro#onin) 4n order to move the tro#omyosin, a calcium binding #rotein called "almodulin is moving the tro#omyosin instead of tro#onin) 6) no sarcomeres$ thic( and thin filaments s#iral do%n smooth muscle cell) &) noncontractile intermediate filaments and dense bodies =attach to thin filaments) Contraction of Smooth uscle

echanism: ' electrical cou#ling via ga# <unctions slo% synchroni-ed contractions ' some smooth muscle cells are #acema(er cells 1) actin and myosin interact by sliding filament mechanism .) final trigger is rise in intracellular "a+ 6) sliding #rocess is energi-ed by ATP ' ' "ontraction of smooth muscle is slo%, sustained and fatigue resistant) There are fe% mitochondrion* most ATP is generated aerobically) This %or(s because smooth muscle cells %or( as an entire unit, so little %or( is done from each singular muscle cell)

Special features of smooth muscle contraction

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a) &esponse to stretch$ more stretch =1.0 resting length) therefore #roducing much more vigorous contraction) The stretching can induce brief contraction =gut) or can have stretch rela0ation res#onse =filling) as you eat and #ut #ressure on your stomach, the smooth muscle in your stomach %ill res#ond by rela0ing and e0#and as you eat b) Length and tension changes: stretches more than s(eletal* can generate more tension than s(eletal muscles =contracts in a cor(scre%'li(e manner)) @mooth can contract 150 versus s(eletal muscle that contracts only ,0 ) @mooth muscle can also be stretched by hormonal messages c) #yperplasia: e0am#le$ estrogen and uterine smooth muscle cells d) Secretory functions: collagen, elastin' ma(e their o%n connective tissue

Single'unit smooth muscle () *) +) ,) contracts as a unit and rhythmically electrically cou#led by ga# <unctions often s#ontaneous action #otentials all other smooth muscle characteristics

ultiunit smooth muscle Large air%ays to lungs, arteries, arrector #ili muscles of s(in hair follicles, internal eye muscles for focus) 1) muscle fibers structurally inde#endent of each other .) richly su##lied %ith nerve endings, each forms a motor unit %ith a number of muscle fibers 6) res#onds to neural stimulation %ith graded contractions =still regulated by autonomic ns, hormones)

#" E"STAS-S Control mechanisms As ;alter "annon describes it$ :omeostasis is the ability of the body Gto maintain relatively stable internal conditions even though there is continuous change in the outside %orld)H ' i) ii) iii) iv) not changing$ rather a dynamic state of e1uilibrium involving many systems$ ade1uate blood levels of vital nutrients heart activity2blood #ressure monitored and ad<usted as needed %astes must not accumulate body tem#erature

+ essential characteristics of homeostatic control mechanisms &eceptor: senses change =stimulus) and sends information =afferent #ath%ay) to the Control centre: determines a set #oint for variable maintenance* analy-es information and determines correct res#onse Effector: #rovides means for res#onse =out#ut along efferent #ath%ay) !eedbac. =negative2#ositive) allo%s for regulation %ithin a range2enhanced res#ose) /egati$e !eedbac. echanisms ' out#ut reduces or shuts off the stimulus) 1) 1 hormone regulating a #rocess$ negative feed bac( secretion .) #rocess regulated in o##osite directions by . different hormones =e0am#le$ blood glucose) the goal of negati$e feedbac.: #revent sudden, severe changes Positi$e feedbac. mechanism ' ' ' ' res#onse of mechanism enhances original stimulus out#ut is further stimulated change occurs in the same direction as original res#onse goal to be attained e0am#le$ blood clotting, %ill stimulate blood to clot in<ury, therefore reduce amount of blood lost) This is homeostatic because you are trying to (ee# a balance of amount of blood in the body)

#omeostatic imbalance Most diseases seen as a disturbance of homeostasis A homeostatic imbalance

Aging is associated %ith #rogressive decrease in our ability to maintain homeostasis greater ris(s for illness as you age) Example: temperature regulation ' ;hen you have a fever, your body drives to increase the tem#erature* %hich in turn %ill increase your body?s metabolism rate) ' 4t involves #ositive feedbac( because it %ill allo% the body to (ee# doing this in order to increase body tem#erature until a desired tem#erature is achieved) ' There is also negative feedbac( involved because once you hit an o#timal tem#erature* it %ill sto# the #ositive to (ee# increasing to maintain stability of tem#erature) Autonomic /er$ous System 0A/S) autoA self* nom A govern AN@ regulates bodily functions that you do not need to %orry about or do not re1uire to consciously thin( about doing these things =breathing, heart beating etc) thus given the descri#tion GautomaticH ' Performs a##ro#riate res#onse %ithout you mentally controlling these actions) ' The motor division is divided into . divisions 1) the somatic system is directed to the s(eletal muscles Parasym#athetc$ digestion, rest @ym#athetic$ 9et through stress AN@ A the system of motor neurons to smooth and cardiac muscle and glands to allo% res#onses usually %ithout our a%areness a) b) c) d) shunt blood to more needy areas s#eed2slo% heart and res#iratory rates ad<ust blood #ressure, body tem#erature increase2decrease gastric secretions ' '

The somatic nervous system contains long a0ons that are %ell myelinated because their neurosignals %ill need to travel long distances) Therefore, it must re1uire methods to increase the s#eed of transmission) Ac: is the neurotransmitter %hich is used to signal s(eletal muscle) ' ' ' The effector organs for the AN@ include smooth muscle =%all of blood vessel, bladder, etc) and it %ill target these muscles in order to control %hat is going on there) 4t %ill target glands such as the s%eat glands, secretory glands, and glandular tissue "ardiac muscle$ The sym#athetic nervous division %ill s#eed u# or slo% do%n heart rate %henever necessary)

4n the sympathetic ner$ous di$ision of the A/S1 it consists of neurons that are not as long as the somatic N@* it %ill target ganglia first) Then the ganglia %ill release nore#ine#hrine for the #ost ganglionic neuron %hich %ill target the designated area) Also, it can stimulate the adrenal medulla$ the inside of the medulla is made u# of neural tissue) /ou %ill have neuron stimulating neural tissue %hich is the adrenal medulla* the adrenal medulla %ill then release e#ine#hrine and nore#ine#hrine =nore#ine#hrine no% acting as a hormone)) 4t is sent into the blood stream to travel to the heart and other #arts of the body %hich is re1uired to be stimulated) Ior the #arasym#athetic division of the AN@, instead of directly arriving at a target, it lands on ganglion and it %ill release Ac: @7MMAF/ Somatic ner$ous system: effects s(eletal muscle A/S: smooth muscle, cardiac muscle and glands Path%ays and ganglia Somatic: thic(, heavily myelinated a0on from s#inal cord to s(eletal muscle* ra#id conduction of im#ulses =no ganglia) A/S: t%o'neuron chain$ #reganglionic neuron$ originates in the brain or s#inal cord* #reganglionic a0on syna#ses %ith .nd motor neuron =#ostganglionic) in ganglion outside "N@ #ostganglionic a0on to the effector organ "onduction is slo%* #reganglionic a0ons are thin and lightly myelinated* #ostganglionic a0ons are thinner and unmyleninated) Parasympathetic Di$ision ' ' ' ' active in non'stressful situations =resting and digestive system) (ee#s body?s energy use lo% %hile regulation house(ee#ing activities =digestion, elimination of feces and urine) G!H system$ digestion, defecation, diuresis D0am#le$ after you eat dinner, you read the ne%s#a#er) /our #arasym#athetic nervous division does the follo%ing$ digestion by stimulating events in your stomach* slo% do%n heart rate, #u#ils constrict in order to read, slo% res#iration rate)

Sympathetic Di$ision ' ' ' Gfight or flightH system* also im#ortant during e0ercise$ increased heart rate, ra#id, dee# breathing, cold s%eaty s(in, dilated eye #u#ils GDH system$ e0ercise, e0citement, emergency, embarrassment 4t could be immediate short term stress or long term stress

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4t %ill gear you u# for things to come* all the things that %ill come into #lay %hen you are in a stressful situation)

Somatic ner$ous system and $ascular tone al#ha bloc(ing drugs to treat hy#ertension* blood shunting #ossible via vasoconstriction2vasodilation ' This is the only #lace in your body that is res#onsible for regulating blood vessel diameter) ' ;ith the heart, a tonic effect of slo%ing do%n heart rate) /ou %ill then override it %ith the @N@ %hen you are e0ercising or re1uire an increase of heart rate) Peripheral ner$ous system and tone: heart, smooth muscle of 94 and urinary tracts can be overridden by the @N@ -nteractions of the Autonomic di$isions: the most visceral organs receive dual innervation Antagonistic -nteractions: e0am#le$ activity of the heart, 94 system, res#iratory system S/S: 4f the @N@ is dominant, you %ould see$ increased heart rate, decreased 94, increase res#iratory system function P/S: if PN@ is dominant, you %ill see decreased heart rate, increased 94, decreased res#iratory system) Cooperati$e effects: regulation of e0ternal genitalia during intercourse a) PN@$ dilation of blood vessels in the #enis in males and clit in females) b) @N@$ e<aculation, refle0 #eristalsis of female?s vagina 2ni3ue &oles of the Sympathetic /S S/S regulation only: ' adrenal medulla: sym#athetic neurons going out to neural tissue to adrenal medulla in %hich in turn release e#ine#hrine and NP to stimulated target organs by releasing hormones into the blood stream) ' S%eat glands: ties in %ith tem#erature regulation ' Arrector pili muscles of the s.in: tem#erature regulation, fight or flight res#onse and tem#erature regulation ' 4idneys: filtering of the blood and %ill regulated the rate of filtering the blood by the dilation of blood vessels) ' Thermoregulatory res#onses to heat ' Fennin release from (idneys' result %ill be increased blood #ressure etabolic effects: () increases metabolic rate of body cells *) raises blood glucose levels +) stimulates mobili-ation of fats

,) increases mental alertness 5) increases s#eed2strength of muscle contraction They all lin( together and they are all res#onsible by the @N@ + Le$els of &egulation of Autonomic function () 6rain Stem and Spinal Cord Controls These are motor refle0es* there %ill be incoming information %ith regards to %hat is going on in those systems and %ill res#ond accordingly Motor centres in ventro'lateral medulla =e0am#le$ cardiovascular centre heart rate, blood vessels* also 94, res#iratory centres) Cagus nerve afferents convey sensory information *) #ypothalamic Controls: ' ' ' ' ' ' also is the site of hormone #roduction it is the integration centre of the #arasym#athetic and sym#athetic nervous system) 4t %ill it to collaborate and determine %hat is the best action to do during the s#ecific body state) :y#othalamus$ integration centre of AN@ Medial and anterior regions #arasym#athetic Lateral and #osterior areas sym#athetic :y#othalamus contains centres to coordinate heart activity, blood #ressure, body tem#erature, %ater balance, endocrine activity* also, centres that hel# mediate emotions and biological drives

+) Cortical Controls: ' ' ' e0am#le$ meditation and biofeedbac( allo% some conscious control over visceral activities e0am#le$ during meditation, you can consciously lo%er heart and breathing rates, o0ygen use, metabolic rate bio feedbac( to im#rove management of migraine headaches, stress and cardiac function

#omeostatic -mbalance of A/S ' e0am#le$ hy#ertension

T#E E/D"C&-/E S7STE A chemical substance released into the D0tra "ellular Iluid that regulates the metabolic function of other cells in the body)

' :ormones must bind to s#ecific rece#tors to influence target cell function ' hormones are specific* level of target cell activation de#ends on$ i) hormone concentration ii) target cell rece#tor content iii) affinity of hormone for rece#tor echanisms of #ormone Action ' a) b) c) d) e) hormones alter levels of cell activity$ membrane #ermeability2#otential =channels) synthesis of en-ymes %ithin cells en-yme activation2deactivation induction of secretory activity stimulation of mitosis

+ structural groups of hormones: i) ii) iii) amino acids, #e#tides, #roteins steroid hormones =derivatives of cholesterol)* they are li#ids, ma(ing them to be #ermeable to cell membranes eicosanoids =from arachadonic acid)

* main mechanisms of action: a) Peptide8protein hormones: bind to cell surface rece#tor activation of membrane'bound 9 #rotein #roduction of .nd messenger =eg$ cAMP, calcium) activation of #rotein (inases to regulate activity of (ey en-ymes b) Steroid hormones1 etc: entry into nucleus and activation of gene transcri#tion

#alf'life1 "nset and Duration of #ormone Acti$ity ' ' ' ' ' ' hormones are potent* they do not re1uire high concentrations) They are very strong =#otent) blood level of hormone de#ends on$ rate of synthesis, and rate of degradation2clearance from blood) #alf life: #ersistence of a hormone in the blood* usually J 1 min to 60 min time to onset of hormone action variable$ en9yme acti$ation ra#id =minutes)* en9yme synthesis hours to days some hormone ssecreted as prohormones* activated once reach target cell duration of hormone action also variable =hours to days)

Control of #ormone &elease ' ' usually negati$e feedbac( =set#oint)* sometimes #ositive feedbac( =goal) 6 ty#es of stimuli$ humoral, neural and hormonal

a) #umoral stimuli: hormone secretion in direct res#onst to change in blood level of a nutrient, ion Keg$ #arathyroid hormone =PT:) and blood calcium* insulin and blood glucoseL b) /eural stimuli: not as common, eg$ sym#athetic ns and e#ine#hrine release by adrenal medulla, hy#othalamic neurons and o0ytocin release) c) #ormonal stimuli: 6'tiered system involving hy#othalamus, #ituitary and target endocrine gland conce#t of hy#othalamic'#ituitary a0is)

Thyroid'releasing hormone =TF:), hy#othalamus Thyroid'stimulating hormone =T@:), anterior #ituitary Thyroid hormones =T6 and T&), thyroid gland :y#othalamus is neural* #roduces a number of releasing factors =hormones) %hich travel to anterior #ituitary via hy#o#hyseal #ortal system Pituitary :land: ' si-e and sha#e of #ea ' infundibulum connects #ituitary to hy#othalamus Posterior lobe: ' a0on terminals ' hormone storage area ' antidiuretic hormone o0ytocin They are structurally similar =nona#e#tides) but very different functions) &eleasing #ormone Thyroid releasing hormone =TF:) "orticotro#in releasing hormone ="F:) 9:4: =@omatostatin) 9F: or 9:F: 9onadotro#in releasing hormone =9nF:) P4:A do#amine PF:A TF:, o0ytocin Anterior Pituitary #ormone Thyroid stimulating hormone =T@:) Adrenocorticotro#ic hormone =A"T:) 9ro%th hormone Iollicle stimulating hormone =I@:) Luteini-ing hormone =L:) Prolactin Target :land Thyroid gland Adrenal glands Liver 3varies Testes Ereast

"$er$ie% of 6lood Circulation ' ' ' ' ' ' blood leaves the heart via arteries that branch re#eatedly until they become ca#illaries 30ygen =3.) and nutrients diffuse across ca#illary %alls and enter tissues "arbon dio0ide ="3.) and %astes move from tissues into the blood 30ygen'deficient blood leaves the ca#illaries and flo%s in veins to the heart This blood flo%s to the lungs %here it releases "3. and #ic(s u# 3. The o0ygen rich blood returns to the heart

Composition of 6lood ' ' ' 1) .) 6) ' blood is the body?s only fluid tissue it is com#osed of li1uid #lasma and formed elements formed elements include$ erythrocytes, or red blood cells =FE"s) leu(ocytes, or %hite blood cells =;E"s) #latelets hematocrit the #ercentage of FE"s out of the total blood volume

Physical Characteristics and ;olume ' ' ' ' ' ' blood is a stic(y, o#a1ue fluid %ith a metallic taste color varies from scarlet to dar( red the #: of blood is 8)65'8)&5 tem#erature is 6M degress " Average volume$ 5',L for males, and &'5L for females Elood accounts for a##ro0imately M of body %eight

!unctions of 6lood ' 1) .) 6) blood #erforms a number of functions dealing %ith$ substance distribution regulation of blood levels of #articular substances body #rotection

Distribution: blood trans#orts$ ' o0ygen from the lungs and nutrients from the digestive tract ' metabolic %astes from cells to the lungs and (idneys for elimination ' hormones from endocrine glands to target organs &egulation: blood maintains$ ' a##ro#riate body tem#erature by absorbing and distributing heat ' normal #: in body tissues using buffer systems =bicarbonate ions) ' ade1uate fluid volume in the circulatory system =osmotic #ressure) Protection Elood #revents blood loss by$ ' activating #lasma #roteins and #latelets ' initiation clot formation %hen a vessel is bro(en Elood #revents infection by$ ' synthesi-ing and utili-ing antibodies ' activating com#lement #roteins ' activating ;E"s to defend the body against foreign invaders 6lood plasma Elood #lasma contains over 100 solutes, including$ ' ' ' ' ' proteins: albumin =ma<or osmotic #rotein, made by the liver), globuliuns, clotting #roteins, and others Lactic acid1 urea1 creatinine "rganic nutrients: glucose, carbohydrates, amino acids Electrolytes: sodium =ma<or osmotic ion), #otassium, calcium, chloride, bicarbonate &espiratory gases: o0ygen and carbon dio0ide

!ormed Elements ' ' ' ' ' ' erythrocytes, leu(ocytes, and #latelets ma(e u# the formed elements only ;E"s are com#lete cells FE"s have no nuclei or organelles, and #latelets are <ust cell fragments They are made from stem cells, don?t regenerate* made in bone marro% =stem cells) constantly creating red and %hite blood cells Most formed elements survive in the bloodstream for only a fe% days Most blood cells do not divide but are rene%ed by cells in the bone marro%)

"3MP3NDNT@ 3I ;:3LD EL33!

Erythrocytes 0&6C) ' biconcave discs, anucleate, essentially no organelles ' ma<or factor contributing to blood viscosity ' filled %ith haemoglobin =:b), a #rotein that functions in gas trans#ort ' contain the #lasma membrane #rotein s#ectrin and other #roteins that 1) give erythrocytes their fle0ibility and .) allo% them to change sha#e as necessary) ' ;or( force of the circulatory system) ' They have no nucleus and they are <ust bags of #rotein =:b) %hich carry out the ma<or function of blood %hich is gas trans#ort) ' @ome ca#illaries are smaller than the si-e of red blood cells) ' The FE" structure is o#timi-ed to carry out the bloods function) ' erythrocytes are an e0am#le of the com#lementarity of structure and function structural characteristics contribute to its gas trans#ort function ' biconcave sha#e has a huge surface area relative to volume ' erythrocytes are more than N8 haemoglobin ' ATP is generated anaerobically, so the erythrocytes do not consume the o0ygen they trans#ort ' it is damaging to the (idneys considered as a buffer, therefore you do not %ant it to disru#t #: levels in the body %ill also ma(e blood more thic( and less flo%' li(e)

Erythrocyte !unction ' ' ' FE" are dedicated to res#iratory gas trans#ort) :b reversibly binds %ith o0ygen and most o0ygen in the blood is bound to :b :b is com#osed of the #rotein globin, made u# of t%o al#ha and t%o beta chains, each bound to a heme grou#

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Dach heme grou# bears an atom of iron, %hich can bind to one o0ygen molecule Dach :b molecule can trans#ort four molecules of o0ygen)

#emoglobin 0#b) ' 30yhemoglobin :b bound to o0ygen* o0ygen loading ta(es #lace in the lungs ' !eo0yhemoglobin :b after o0ygen diffuses into tissues =reduced :b) ' "arbaminohemoglobin :b bound to carbon dio0ide* .0 on heme, rest on #e#tide ' "arbon dio0ide binds to the #e#tide bac(bone, Not heme) ' The ma<ority of carbon dio0ide ends u# converted to bicarbonate in FE"s by carbonic anhydrase) Production of Erythrocytes ' hemato#oiesis$ blood cell formation ' hemato#oiesis occurs in the red bone marro% of$ 1) a0ial s(eleton and girdles .) e#i#hyses of the humerus and femur 6) #roduces about 60mL2day ' 10 to .0 billion FE" are #roduced by blood everyday, O 100000 FE"2second ' :emocytoblasts give rise to all formed elements ' :emocytoblasts are stem cells and they give rise to stem cell research) Production of Erythrocytes: Erythropoiesis ' a hemocytoblast is transformed into a #roerythroblast ' #roerythroblasts develo# into early erythroblasts The develo#mental #ath%ay consists of three #hases$ 1) ribosome synthesis in early erythroblasts .) :b accumulation in late erythroblasts and normoblasts 6) e<ection of the nucleus from normoblasts and formation of reticulocytes ' reticulocytes then become mature erythrocytes

&egulation and &e3uirements for Erythropoiesis circulating erythrocytes$ number remains constant and reflects a balance bet%een FE" #roduction and destruction

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too fe% FE" lead to tissue hy#o0ia* cannot deliver enough o0ygen to tissues too many FE" causes undesirable blood viscosity* blood gets too viscous and it #um#s uncontrollably

Drythro#oiesis is hormonally controlled and de#ends on ade1uate su##lies of iron, amino acids, and E vitamins) #ormonal Control of Erythropoiesis Drythro#oietin =DP3) is released by the (idneys %hich is triggered by =sensing o0ygen levels in the blood)$ ' hy#o0ia due to decreased FE"s ' decreased o0ygen availability ' increased tissue demand for o0ygen ' o0ygen availability is the signalPP Dnhanced erythro#oeisis increases the ' FE" count in circulating blood ' 30ygen carrying ability of the blood) !ialysis #atients become anemic because they are unable to trigger DP3 to synthesi-e ne% FE" 1) Stimulus: :y#o0ia due to decreased FE" count, decreased amount of haemoglobin, decreased availability of 3. .) (idney =and liver to smaller e0tent) releases erythro#oietin) 6) erythro#oietin stimulates red bone marro% &) enhanced erythro#oiesis increases FE" count 5) 30ygen carrying ability of blood increases) Dietary &e3uirements of Eryhtropoiesis Drythro#oiesis re1uires$ ' #roteins, li#ids and carbohydrates ' iron, vitamin E1., and folic acid ' ' ' The body stores iron in :b =,5 ), the liver, s#leen, and bone marro%) 4ntracellular iron is stored in #rotein'iron com#le0es such as ferritin and hemosiderin "irculating iron is loosely bound to the trans#ort #rotein transferring

!ate and Destruction of Erythrocytes ' ' ' the life s#an of an erythrocyte is 100'1.0 days 3ld FE"s become rigid and fragile, and their :b begin to degenerate because you start to get o0ygen damage done to the #roteins) !ying FE"s are engulfed by macro#hages

' ' ' ' ' ' '

:eme and globin are se#arated and the iron is salvaged for reuse :eme is degraded to a yello% #igment called bilirubin The liver secretes bilirubin into the intestines as bile The intestines metaboli-e it into urobilinogen This degraded #igment leaves the body in feces, in a bro%n #igment called stercobilin 9lobin is metaboli-ed into amino acids and is released into circulation :b released into the blood is ca#tured by ha#toglobin and #hagocytised)

Erythrocyte Disorders Anemia: blood has abnormally lo% o0ygen carrying ca#acity ' it is a sym#tom rather than a disease itself ' blood o0ygen levels cannot su##ort normal metabolism ' signs2sym#toms include fatigue, #aleness, shortness of breath, and chills Anemia -nsufficient erythrocytes ' #emorrhagic anemia: result of acute or chronic loss of blood ' #emolytic anemia: #rematurely ru#tured FE"s ' Aplastic anemia: destruction or inhibition of red bone marro% Anemia decreased haemoglobin content 4ron deficiency anemia results from ' a secondary result of hemorrhagic anemia ' inade1uate inta(e of iron'containing foods ' im#aired iron absor#tion Pernicious anemia results from ' deficiency of vitamin E1. ' lac( of intrinsic factor needed for absor#tion of E1. Treatment is intramuscular in<ection of E1.* a##lication of Nascobal Anemia abnormal haemoglobin Thealassemias$ absent or faulty globin chain in :b ' FE"s are thin, delicate, and deficient in :b @ic(le cell anemia$ results from a defective gene coding for an abnormal :b called haemoglobin @ =:b@) ' :b@ has a single amino acid substitution in the beta chain ' This defect causes FE"s to become sic(le'sha#ed in lo% o0ygen situations Polycythemia Polycythemia$ e0cess FE"s that increase blood viscosity Three main #olycythemias are$ ' #olycythemia vera

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secondary #olycythemia =smo(ers, burn victims)* lose fluid, therefore increase in hematocrit blood do#ing DP3 abuse

Platelets ' #latelets are fragments of mega(aryocytes %ith a blue'staining outer region and a #ur#le granular center ' #latelet formation regulated by thrombo#oietin ' granules contain clotting factors and en-ymes ' #latelets function in the clotting mechanism by forming a tem#orary #lug that hel#s seal brea(s in blood vessels ' #latelets not involved in clotting are (e#t inactive by N3 and #rostocyclin released from endothelium ' Lifes#an is 510 days* .50'500000 #latelets2mL :enesis of Platelets ' the stem cell for #latelets is the hemocytoblast @tem cell !evelo#mental #ath%ay

:emocytoblastMega(aryoblastPromega(aryocyteMega(aryocyte Platelets #emostasis @eries of reactions for sto##age of bleeding) !uring hemostasis, three #hases occur in ra#id se1uence ' vascular s#asms$ immediate vasoconstriction in res#onse to in<ury ' #latelet #lug formation ' coagulation =blood clotting)

#emostasis: ;ascular Spasms ' vasoconstriction in res#onse to in<ury ' triggered by damage, chemicals from D"s and #latelets, #ain refle0es ' their #ur#ose is to reduce blood flo% #emostasis: Platelet Plug !ormation

Platelets do not stic( to each other or to blood vessels 7#on damage to blood vessel endothelium #latelets$ ' ;ith the hel# of von ;illebrand factor =C;I) adhere to collagen ' Are stimulated by thrombo0ane A. ' @tic( to e0#osed collagen fibers and form a #latelet #lug ' Felease serotonin and A!P, %hich attract still more #latelets The #latelet #lug is limited to the immediate area of in<ury by #rostacyclin =P94.) released by endothelial cells #emostasis: Coagulation ' ' ' i) ii) iii) ' A set of reactions in %hich blood is transformed from a li1uid to a gel "oagulation follo%s intrinsic and e0trinsic #ath%ays The final three ste#s of this series of reactions are$ Prothrombin activator is formed Prothrombin is converted into thrombin* s%itch that turns on clotting #rocess Thrombin cataly-es the <oining of fibrinogen into a fibrin mesh see events of coagulation diagram on #revious #age

Detailed E$ents of Coagulation -ntrinsic: regulates clotting outside of the body =e0am#le$ tube) or in slightly damaged vessel) @lo%er Path%ay to factor B and PA Extrinsic: clotting is associated %ith body and vessel damage and release of Tissue Iactor Ie%er ste#s to factor B and PA Iactors numbered in order of discovery, N3T role in #ath%ay

Coagulation Phase (: T%o path%ays to Prothrombin Acti$ator ' May be initiated by either the intrinsic or e0trinsic #ath%ay i) Triggered by tissue'damaging events ii) 4nvolves a series of #rocoagulants iii) Dach #ath%ay cascades to%ard factor B ' 3nce factor B has been activated, it com#le0es %ith calcium ions, PI6, and factor Ca to form #rothombin activator These are the #rocesses leading u# to the formation of #rothrombin activator) ;hen you activated the e0trinsic #ath%ay, it activates the intrinsic #ath%ay) The more severe the %ound, the more #ath%ays %ill be o#en to do this #rocess more ra#idly) ' ' The formation of #rothrombin activator =PA) is the rate'limiting ste# After PA accumulates, clotting #roceeds in 10'15 seconds esh

Coagulation Phase +: Common Path%ays to the !ibrin ' '

thrombin cataly-es the #olymeri-ation of fibrinogen into fibrin insoluble fibrin strands form the structural basis of a clot

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fibrin causes #lasma to become a gel'li(e tra# fibrin in the #resence of calcium ions activates factor B444 that$ cross'lin(s fibrin, strengthens and stabili-es the clot

Clot &etraction and &epair clot retraction stabili-ation of the clot by s1uee-ing serum from the fibrin strands ' Fe#air i) Platelet'derived gro%th factor =P!9I) stimulates rebuilding of blood vessel %all ii) Iibroblasts form a connective tissue #atch iii) @timulated by vascular endothelial gro%th factor =CD9I), endothelial cells multi#ly and restore the endothelial lining "$er$ie% of Coagulation '

Clot remo$al: !ibrinolysis ' removal of clot %hen no longer needed ' Iibrin clots is digested by Plasmin =#recursorA #lasminogen) ' Plasminogen is activated by tissue Plasminogen Activator =tPA) released by endothelial cells ' Eegins %ithin . days and continues until clot is dissolved !actors Limiting Clot :ro%th or !ormation ' t%o homeostatic mechanisms #revent clots from becoming large i) @%ift removal of clotting factors by normal blood flo% ii) 4nhibition of activated clotting factors -nhibition of Clotting !actors ' fibrin acts as an anticoagulant by binding thrombin and #reventing its #ositive feedbac( effects of coagulation ' Thrombin not absorbed to fibrin is inactivated by antithrombin 444 in #lasma ' :e#arin on the endothelium enhances antithrombin 444 activity !actors Pre$enting 2ndesirable Clotting ' unnecessary clotting is #revented by endothelial cells lining the blood vessels ' Platelet adhesion is #revented by$ i) The smooth endothelial lining of blood vessels ii) N3 :e#arin and P94. secreted by endothelial cells iii) Citamin D 1uinine, a #otent anticoagulant #emostasis Disorders : Thromboembolytic Conditions ' Thrombus a clot that develo#s and #ersists in an unbro(en blood vessel i) Thrombi can bloc( circulation, resulting in tissue death ii) "oronary thrombosis thrombus in blood vessel of the heart ' ' ' Embolus a thrombus freely floating in the blood stream Pulmonary emboli can im#air the ability of the body to obtain o0ygen "erebral emboli can cause stro(es

Pre$ention of 2ndesirable Clots ' @ubstances used to #revent undesirable clots i) As#irin$ an anti#rostaglandin that inhibits thrombo0ane A. ii) :e#arin$ an anticoagulant used clinically for #re and #ost o#erative cardiac care iii) ;arfarin$ used for those #rone to atrial fibrillation #emostasis Disorders: 6leeding Disorders ' Thrombocytopenia: condition %here the number of circulating #latelets is deficient i) Patients sho% #etechiae due to s#ontaneous, %ides#read hemorrhage

ii) iii) iv) ' ' ' '

"aused by su##ression or destruction of bone marro% =e0am#le$ malignancy, radiation) Platelet counts less than ,00002mm6 is diagnostic for this condition Treated %ith %hole blood transfusions 4nability to synbthesi-e #rocoagulants by the liver results in severe bleeding disorders "auses can range from vitamin > deficiency to he#atitis and cirrhosis 4nability to absorb fat can lead to vitamin > deficiencies as it is a fat'soluble substance and is absorbed along %ith fat Liver disease can also #revent the liver from #roducing bile, %hich is re1uired for fat and vitamin > absor#tion

' #emophilias hereditary bleeding disorders caused by lac( of clotting factors i) :emo#hilia A$ most common ty#er =M6 of all cases) due to a deficiency of factor C444 ii) :emo#hilia E$ due to a deficiency of factor 4B iii) :emo#helia "$ mild ty#e, due to a deficiency of factor B4 ' ' ' ' :emo#hilia A and E are B'lin(ed :emo#hilia " is autosomal recessive @ym#toms include #rolonged bleeding and #ainful and disabled <oints Treatment is %ith blood transfusions and the in<ection of missing factors

6lood Transfusions ' ;hole blood transfusions are used$ i) ;hen blood loss is substantial =15'60 %ea(ness, #allor* greater than 60 shoc() ii) 4n treating thrombocyto#enia =bone marro% damage) ' Pac(ed red cells =cells %ith #lasma removed) are used to treat anemia #uman 6lood :roups ' FE" membranes have glyco#rotein antigens on their e0ternal surfaces ' These antigens are$ i) 7ni1ue to the individual ii) Fecogni-ed as foreign if transfused into another individual iii) Promoters of agglutination and are referred to as agglutinogens ' Presence or absence of these antigens is used to classify blood grou#s ' :umans have 60 varieties of naturally occurring FE" antigens ' The antigens of the AE3 and Fh blood grou#s cause vigorous transfusion reactions %hen they are im#ro#erly transfused ' 3ther blood grou#s =M, N, !ufy, >ell, and Le%is) are mainly used for legalities ' The AE3 blood grou#s consist of$ i) T%o antigens =A and E) on the surface of the FE"s ii) T%o antibodies in the #lasma =anti'A and anti'E)

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AE3 blood grou#s may have various ty#es of antigens and #reformed antibodies =agglutinins) Agglutinins absent in ne%borns, a##ear by . months, #ea( at M'10 years Agglutinogens and their corres#onding agglutinins cannot be mi0ed %ithout serious haemolytic reactions

&h 6lood :roups ' There are eight different Fh agglutinogens, three of %hich =", !, and D) are common ' Presence of the Fh agglutinogens on FE"s is indicated as F:+ ' Anti'Fh antibodies are not s#ontaneously formed in Fh' individuals ' :o%ever, if an Fh' individual receives Fh+ blood, anti'Fh antibodies form ' A second e0#osure to Fh+ blood %ill result in a ty#ical transfusion reaction #emolytic Disease of the /e%born ' :emolytic disease of the ne%born$ Fh+ antibodies of a sensiti-ed Fh' mother cross the #lacenta and attac( and destroy the FE"s of an Fh+ baby ' Fh' mother becomes sensiti-ed %hen e0#osure to Fh+ blood causes her body to synthesi-e Fh+ antibodies ' The druge Fho9AM can #revent the Fh' mother from becoming sensiti-ed ' Fho9AM is an anti'F: agglutinin antisera ' Treatment of haemolytic disease of the ne%born involves #re'birth transfusions and e0change transfusions after birth Transfusion &eactions ' transfusion reactions occur %hen mismatched blood is infused ' !onor?s cells are attac(ed by the reci#ients #lasma agglutinins causing$

i) !iminished o0ygen'carrying ca#acity ii) "lum#ed cells that im#ede blood flo% iii) Fu#tured FE"s that release free haemoglobin into the bloodstream ' "irculating haemoglobin #reci#itates in the (idneys and causes renal failure 6lood Typing ' %hen serum containing anti'A or anti'E agglutinins is added to blood, agglutination %ill occur bet%een the agglutinin and the corres#onding agglutinogens ' #ositive reactions indicate agglutination A6" 6lood Typing Elood Ty#e Eeing Tested FE" Agglutinogens @erum Feaction Anti'A AE A and E + E E ' A A + 3 None ' @erum Feaction Anti'E + + ' '

#eart Anatomy ' a##ro0imately the si-e of your fist ' T%o side'by'side #um#s ' Location i) @u#erior surface of dia#hragm ii) Left of the midline, from .nd rib to 5th intercostal s#ace iii) Anterior to the vertebral column, #osterior to the sternum iv) GmediastinumH + layers of the heart ' Pericardium$ outer sac ' Myocardium$ muscle, bul( of mass ' Dndocardium$ inner lining Co$ering of the #eart: Anatomy Pericardium a double %alled sac around the heart com#osed of$ ' A su#erficial fibrous #ericardium ' A dee# t%o'layer serous #ericardium i) The #arietal layer lines the internal surface of the fibrous #ericardium ii) The visceral layer or e#icardium lines the surface of the heart iii) They are se#arated by the fluid filled #ericardial cavity Co$ering of the #eart: Physiology The #ericardium$ ' #rotects and anchors the heart ' #revents overfilling of the heart %ith blood ' allo%s for the heart to %or( in relatively friction'free environment D#icardium visceral layer of the serous #ericardium

#eart <all yocardium cardiac muscle layer forming the bul( of the heart ' branching muscle cells arranged in bundles ' #rovides su##ort for great vessels and valves ' directs s#read of action #otentials across heart

fibrous s(eleton of the heart crisscrossing, interlacing layer of connective tissue, insulation, su##orts great vessels Endocardium endothelial layer of the inner myocardial surface* continuous %ith vessels leaving and entering the heart External #eart: a=or ;essels of the #eart 0Anterior $ie%) Cessels returning blood to the heart include$ ' su#eriour and inferior vena cava, one goes to organs above heart, the other goes belo% ' right and left #ulmonary veins Cessels conveying blood a%ay from the heart$ ' #ulmonary trun(, %hich s#lits into right and left #ulmonary arteries ' Ascending aorta =three branches) brachioce#halic, left common carotid, and subclavian arteries External #eart: ;essels that supply8drain the #eart ' Arteries right and left coronary =in atrioventricular groove), marginal, circumfle0, and anterior interventricular arteries ' Ceins small cardiac, anterior cardiac, and great cardiac veins External #eart: a=or ;essels of the #eart 0posterior $ie%) Cessels returning blood to the heart include$ ' right and left #ulmonary veins ' su#erior and inferior vena cava Cessels conveying blood a%ay from the heart include$ ' aorta ' right and left #ulmonary arteries ;essels that Supply8Drain the #eart 0posterior $ie%) ' arteries right coronary artery =in atrioventricular groove) and the #osterior interventricular artery =in interventricular groove) ' veins great cardiac vein, #osterior vein to left ventricale, coronary sinus, and middle cardiac vein Atria of the #eart ' atria are the receiving chambers of the heart ' each atrium has a #rotruding auricle ' #ectinate muscles mar( atrial %alls ' blood enters right atria from su#erior and inferior vena cava and coronary sinus ' blood enters left atria from #ulmonary veins ;entricles of the #eart ' ventricles are the discharging chambers of the heart ' Pa#illary muscles and trabeculae carneae muscles mar( ventricular %alls ' Fight ventricle #um#s blood into the #ulmonary trun(

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Left ventricle #um#s blood into the aorta

Path%ay of 6lood Through the #eart and Lungs ' right atrium tricus#id valve right ventricle ' right ventricle #ulmonary semililunar valve #ulmonary arteries lungs ' lungs #ulmonary veins left atrium ' left atrium bicus#id valve left ventricle ' left ventricle aortic semilunar valve aorta ' aorta systemic circulation

Pulmonary circuit$ short, lo% #ressure @ystemic circuit$ Long #ath%ay, 50 #ressure =more resistance) Coronary Circulation ' ' ' coronary circulation is the functional blood su##ly to the heart muscle itself collateral routes ensure blood delivery to heart even if ma<or vessels are occluded bloc(age results in$ Angina #ectoris myocardial infarction

Coronary Circulation ' many anastomoses, %hich #rovide alternate routes for nourishment if a given artery begins to be occluded* total occlusion results in com#lete bloc(age) 1) actively deliver blood %hen heart is rela0ed .) largerly ineffective %hen ventricles are contracting ' heart 512.00 of body but re1uires 512.0 of blood su##ly =es#ecially left ventricle) Coronary $enous supply Irom ca#illaries cardiac veins =great, middle and small) coronary sinus right atrium Also some anterior cardiac veins directly into right atrium anteriorly

#eart ;al$es ' heart valves ensure unidirectional blood flo% through the heart ' atrioventricular =AC) valves lie bet%een the atria and the ventricles ' AC valves #revent bac(flo% into the atria %hen ventricles contract ' "hordae tendineae anchor AC valves to #a#illary muscles ' Aortic semilunar valve lies bet%een the left ventricle and the aorta ' Pulmonary semilunar valve lies bet%een the right ventricle and #ulmonary trun( ' @emilunar valves #revent bac(flo% of blood into the ventricles ' No valves for vena cava and #ulmonary veins

Atrio$entricular ;al$e !unction

@emilunar Calve Iunction

icroscopic Anatomy of #eart uscle ' cardiac muscle is striated, short, fat, branched, and interconnected ' the connective tissue endomysium acts as both tendon and insertion ' intercalated discs anchor cardiac cells together and allo% free #assage of ions ' heart muscle behaves as a functional syncytium ' 1 or . nuclei2cell ' Iull of mitochondria =.5 vs . s(eletal) ' Fesist fatigue Physiological properties of cardiac muscle fibers %ith those of s.eletal muscle cells "ardiac Muscle @(eletal Muscle ' shorter, fatter ' longer, cylindrical ' single or double nuclei ' multinucleate ' intercalated dis(s =desmosomes, ga# ' structural inde#endence* motor <unctions) A interde#endence* this unit grou#ing allo%s cardiac muscle to contract as a ' functional inde#endence single unit ' .'5 of volume is mitochondria ' .0'&0 of volume is mitochondria* ' 7niform myofibrils give distinct very de#endent on an o0ygen su##ly striations in order to function #ro#erly and %ill ' Many T'tubules* com#le0 "a++ use strictly aerobic metabolism delivery ' Myofibril diameters vary and much ' "om#le0 sarco#lasmic reticulum branching gives indistinct striations ' Feadily uses anaerobic ' Ie%er T'tubules* less elaborate "a++ metabolism delivery ' 4ntensity determines fuel ty#e ' Less develo#ed sarco#lasmic used reticulum ' Almost e0clusively aerobic metabolism ' Abundance of fuel ty#e determines fuel used

-ntercalated discs and * aspects of their structure to the support of Cardiac !unction ' an area %here there is a high concentration of ga# <unctions and desmosomes) i) Desmosomes for strong cell'cell adhesion during contraction ii) :ap =unctions for electric cou#(ing functional syncytium The individual muscle cells have to be strongly attached to each other in order to ad<ust to daily activities) Cardiac uscle Contraction ' cardiac muscle contraction is similar to s(eletal muscle contraction ' :eart muscle differs in that i) 4s self e0citable =autorythmic cells) and neural #ath%ays only influence rate and force ii) "ontracts as a unit* sometimes you re1uire faster heart beating, sym#athetic N@ %ill stimulate heart to #um# faster) 4t %ill be in dominant influence of the @N@) ;hen at rest, the PN@ %ill be in dominance iii) :as a long =.50ms) absolute refractory #eriod* this #revents your heart from getting tetanic contractions) Electrical properties of contractile cardiac muscle cells %ith those of autoryhtmic cardiac muscle cells ' heart contraction stimulated by action #otentials$ action #otential A signal* muscle t%itchA res#onse ' fig sho%s action #otential of ventricular Pur(in<e fibers =remember AP of neuron is 1'.msec)* total se1uence A about 600 msec Special characteristics of cardiac muscle cells 1) All or none la%$ a##lies to organ rather than individual cells) Eecause cardiac muscle cells are connected electrically, %hen one is stimulated, all of them %ill go) 3nly one #ercent of cardiac cells are autorythmic) The other are <ust regular .) Stimulation$ autorythmicity of =1 ) cardiac cells 6) absolute refractory period$ .50 msec vs 1'. msec for action #otential stimulating s(eletal muscle) This allo%s the heart to be a #um#) The need individual contractile events to be se#arated from each other)

Phase 1A de#olari-ation due to Na+ influ0 =#ositive feedbac() Phase .A #lateau maintained by "a.+ influ0 =Gslo%H "a.+ channels) Phase 6A re#olari-ation %ith >+ efflu0

Cardiac Action Potential and Contraction of Cardiac uscle ' absolute refractory #eriod A muscle t%itch allo%s heart to fill again ' heart needs to be stimulated in <ust one location* %hole organ res#onds ' activation of contraction basically as in s(eletal muscle Autorythmic cell1 properties that allo% them to spontaneously depolari9e1 %hy is SA node the #eart Pacema.er ' pacema.er A @A node because$ has the fastest autorythmicity ' SA node is located in the right atrium ' Sinus rhythm determines heart rate ' Autorythmic cells have unstable resting #otential* this means that their resting membrane #otential is slo%ly moving to the #ositive direction) There is a decreasing #ermeability to #otassium) The >+ is going out of the cell) ' Pacema(er #otentials action #otentials ' 4n autorythmic cells, action #otential due to$ calcium channels Pacema.er and Action

-ntrinsic conduction system of the heart allo%s it to function as a pump AP generated by @A node #asses to$ .) AC node =short delay)$ Eottlenec(* it is easy for signal to #ass do%n to the ventricles) 3nly one #ath%ay) Therefore, it %ill be direct and it gives time for atria to contract and fill u# ventricles before the ventricles contract 6) AC bundle &) rt and lt bundle branches 5) Pur(in<e fibers

Eottle nec( is from atria to ventricles* only #lace %here there is no insulation %here the im#ulses can get through ' Iast #ath%ay for Q6'5* then short distances left for AP to diffuse through rest of myocardium ' 0).. sec =..0msec) from initiation at @A node to de#olari-ation of last of ventricular cells &ate of @A node de#olari-ation regulated by autonomic ns$ 1) Parasympathetic /S: decreases diastolic de#olari-ation rate by ma(ing cells more #ermeable to >+* ma(es diastolic #otentials more negative .) Sympathetic /S: increases de#olari-ation and re#olari-ation rates ' tonic #arasym#athetic dam#ening effect on heart rate* constantly slo%ing do%n the @A node) Sinus rhythm: normal regular heartbeat set by the sinoatrial node 6radycardia: heart is slo%er than normal heart rate Tachycardia: heart is faster than normal heart rate Delineate the extrinsic inner$ation of the heart and contrast the influences of P/S and S/S on heart rate ' cardiac centres located in medulla oblongata

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fibers to #rimarily @A node, AC node, coronary arteries Cardioaccelatory centre 0sympathetic) motor neurons in T1'T5 =referring to thoracic region) level of s#inal cord #ostganglionic neurons eventually to heart increase both rate and force of heartbeat Cardioinhibitory centre 0parasympathetic) to dorsal vagal nucleus in medulla inhibitory im#ulses to heart via branches of vagus nerve

EC: tracing and the nature of the information it is encoding Electrocardiogram: records electrical changes during heart activity relies on conductile activity of body fluids i) P'%a$e > atrial de#olari-ation ii) ?&S complex > ventricular de#olari-ation iii) T'%a$e > ventricular re#olari-ation Note$ D"9 records only voltage =current flo%) and time* sho%s only electrical events, but from these can deduce contractile events) 4t is not sho%ing you atrial contraction, it is sho%ing you de#olar and re#olari-ation of atria and ventricles)

@tandard limb leads for recording D"9 tracings There are 1. leads altogether Measure com#osite of all APs from nodal and contractile cells Three bi#olar leads measure voltage difference bet%een arms or bet%een arms and legs)

Diagnostic EC: inter$als ' RF@ com#le0A ventricular de#olarisation and contraction =GbigH FA :y#ertro#hy)) Dither bigger heart from %or(ing out and e0cercising or muscle failure of a #art of the heart so that the other functional #arts are com#ensating for the damaged #art* hence more #ressure)

P'F =or P'R) interval A time from atrial e0citation to ventricular e0citation2contraction ' @'T segment A entire ventricle de#olari-ed =cardiac ischemia) ' R'T interval A time from ventricle de#olari-ation to re#olari-ation =ventricular arrhythmias @A node$ sinus rhythm =85b#m) @A im#airedA Sunctional Fhythm by AC node =&0',0 b#m)* heart rate is slo%er* not getting de#olari-ation throughout the atria* blood is not to##ing u# in the ventricles) :eart bloc(A defective AC node =uncou#ling of P'%ave) Sinus &hythm 0a) and non'functional SA node

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*nd degree heart bloc. and $entricular fibrillation

Explain the e$ents of each phase of the cardiac cycle Systole: contraction of heart* #um#ing 37T Diastole: rela0ation of heart* filling Cardiac cycle: atrial systole + diastole ventricular systole + diastole @tart A mid'to'late diastole$ 1) Period of $entricular filling: mid to late diastole #ressure lo% =but Patria O Pventricles) AC valves 3PDN* @L valves "L3@D!) After 80 ventricular filling, AC valves begin to close P %ave and atrial systole* atrial #ressure increases and final 60 of blood enters ventricles =end diastolic volume or D!C) atrial diastole for rest of cycle .) ;entricular systole 0comprises ?&S complex and T %a$es): ventricles begin to contract increased #ressure closes AC valves T #eriod of isovolumetric contraction =volume constant* a closed system) increased #ressure o#ens @L valves ventricular e<ection #hase =aortic #ressure u# to 1.0 mm:g)* #ressure is building u# in ventricles but it is not high enough yet to be #ushed out 6) -so$olumetric relaxation: early diastole ventricles rela0* #ressure decreases ra#idly* bac(flo% of aortic2#ulmonary blood closes @L valves =dicrotic notch)* ventricles a closed system A isovolumetric rela0ation &) 6ac. to 0(): atria continued in diastole and have been filling* %hen #ressure O ventricular #ressure, AC valves o#en and %e are bac( at =1)

85 beat2min$ each cardiac cycle A 0)M seconds Atrial systoleA 0)1 sec Centricular systoleA 0)6 sec Ruiescent #eriodA 0)& sec . features driving "ardiac "ycle a) blood flo% through heart controlled entirely by #ressure changes

b) blood flo%s from higher to lo%er #ressure through any available o#ening* this is %hy it is so im#ortant for the AC valves to shut %hile e<ection occurs) UU electrical activity of left and right hearts is almost simultaneous) Physiological significance of the first and second heart sounds There are . distinguishable sounds that can be heard through a stethosco#e a) first heart sound: closure of AC valves A beginning of systole b) second heart sound: closure of semilunar valves A end of systole :eart sounds due to vibrations of heart2chest due to valve closure #eart urmurs: 1) due to $al$ular obstruction high velocity <et of blood through narro% o#ening higher #itch of sounds .) due to $al$ular insufficiency lea(age of blood bac( causes sounds %hen there should be silence Abnormal 6lood !lo% 4n the e0am#le, there is #ulmonary valve stenosis) The narro%ed #ulmonary valve o#ening causes the blood to be turbulent and noisy %hich is heard as a heart murmur on auscultation)

Aortic $al$e sounds are heard in the .nd intercostal s#ace at right sternal margin Pulmonary $al$e sounds are heard in .nd intercostal s#ace at the left sternal margin itral $al$e sounds are heard over heart a#e0 =in 5th intercostal s#ace) in line %ith middle of clavicle Tricuspid $al$e sounds ty#ically heard in right sternal margin of 5th intercostal s#ace

Cardiac "utput 0C") in terms of heart rate and stro.e $olume "3 A amount of blood #um#ed from left ventricle into aorta2min ' average "3 for resting, healthy male A 5L2min ' @CA D!C T D@C =D!CA end diastolic volume, D@CA end systolic volume) "3A :F 0 @C = :F is heart rate, and @C is stro(e volume) -nfluence of exercise on #& and S; ' "3 increases &'5 times in a fit #erson ' "3 increases 8 times in a %ell trained marathon runner ' "ombined effects on :F and @C =cardiac reserve) Detailed mechanisms for the regulation of #& and S; ' :eart rate is determined by rate of s#ontaneous de#olari-ation of @A node i) autonomic fibers innervating @A node ii) circulating hormones =e)g$ e#ine#hrine) iii) #lasma electrolyte concentration ="a++, Na+, >+, :+) iv) body tem#erature =useful ins surgery) ' ' ' ' ' Nore#ine#hrine =sym#athetic N@)$ increases the rate of s#ontaneous de#olari-ation heart rate is increased Ach =#arasym#athetic N@)$ decreases rate of s#ontaneous de#olari-ation =>+ influ0 hy#er#olari-es #acema(er cells) heart rate is decreased &esting conditions: PN@ is dominant =vagal tone) Tachycardia 0O150'180 b#m) leads to reduced cardiac out#ut This is because that the heart is #um#ing too fast* %hich in turn, ventricles %ill not have enough time to fill u# to o#timal volume) Therefore the "3 %ill decrease)

!ran. Starling La% of the #eart and intrinsic regulation of S;

Preload: Iran( @tarling La% of the :eart$ %ithin defined limits, the heart %ill #um# %hatever volume of blood it receives* over a fairly %ide range, there is a #ro#ortional relationshi# bet%een D!C and stro(e volume

"ardiac muscle has o#timal length for contraction =A length'tension relationshi#)* resting A shorter than o#timal lengthP ' each ventricle is regulated inde#endently and beat'to'beat$ I@ mechanism hel#s ensure that each ventricle #um#s same volume of blood over a #eriod of time) ' D0am#le$ if right heart O left heart O 5 1ml2beat in N0 minutes, the %hole blood volume in lungs if the right heart gets ahead of the left heart* increased return to left heart let it catch u#) 4f you have high EP, you do not allo% the heart to rest ade1uetly) The ventricles have to %or( harder to overcome semilunar bac( #ressure) 4n e0ercise, you are only doing this for a short #eriod of time, allo%ing the heart to recover) Afterload and its influence in stro.e $olume Afterload > #ressure that ventricles must overcome to force o#en valves and e<ect blood from the heart ' healthy$ 5M0mm:g in aorta* 10mm:g in #ulmonary trun( not a mahor determinant of @C ' hy#ertension reduces ability of ventricles to e<ect blood increased D@C and decreased @C * types of extrinsic influences on stro.e $olume ' Iactors outside the heart %hich change vigour of contraction %ithout changing D!C change in contractility not due to greater initial fiber length but involves change in the rate and strength of contraction due to increased "a++ influ0 i) sympathetic stimulation: =Nore#ine#hrine) increases rate of contraction and rela0tion ii) drugs such as digoxin: increase heart contractility iii) parasympathetic /S: =Ach) antagoni-es sym#athetic stimulation -nteraction bet%een contractility and !ran. Starling La% to influence stro.e $olume '