anatomy and phys II final part 1

• a) liquid portion of blood
• b) H2O mostly about 91%
• c) Plasma Proteins 9%

• a) Albumin
• b)Globulins
• c)Fibrinogen

• a) 58% of plasma proteins, most
• b) regulates movement of H2O between the tissue spaces in blood vessels by contributing to the Plasma Colloid Osmotic Pressure(PCOP)

• a) 38% of plasma proteins
• b) 2 functions= some are antibodies
• -protective proteins formed in response to antigens
• -some are transport molecules and bind to other substances

• a) 24% of plasma proteins
• b) contribute to the formation of blood cells

Red blood cells

• a) structure
• b) function
• c)Hemoglobin
• d)Life history of RBC
• e) breakdown of Hemoglobin from lysed RBC

• 1) Bioconcave discs with edges thicker than middle
• -increses surface area(can do more with gases without gettin bigger)
• - increases flexibility- allows to get through tight areas ( more efficient)
• 2)At maturity RBC's have no nucleus or cellular organelles
• 3) Main intracellular component is protein called Hemoglobin(Hb)
• = lipids, ATP, Carbonic anhydrase

• transport O2 and CO2
• - O2 from lungs to tissues
• -CO2 from tissues to lungs

• -protein made up of four polypeptide chains and four heme grps
• - 4 polypeptide chains: 2 alpha and 2 beta subchains
• -4 Heme grps: w/ in each grp is an Fe atom and the rest is pigment
• -O2 binds to Fe portion of Heme ( Hb O2 = oxyhemoglobin )
• -CO2 binds to globin portion (Hb CO2 = carboxyhemoglobin)

• 1) RBC production is called erythropoiesis (stimulated by low plasma O2 levels)
• 2)Erythropoiesis is regulated by the hormone erythropotein ( made in the kidneys)
• 3) immature RBC's are called reticulocytes
• 4) females = 4.3-5.2mil/mm cubed ; males = 5.1-5.8 mil/mm cubed
• 5) lifespan of RBC in females= 110 days; males= 120 days

• 1) remenants get trapped in two organs ( liver and spleen/rbc graveyard)
• a) macrophages enzymatically seperate Heme from globin
• - globin is broken down into amino acids ( then amino acids are used for protein synthesis)
• - heme ( Fe portion is transported to bone marro and used to make more Hb)
• ( pigment is converted to bilirubin and becomes part of bile secreted by the liver)

• 3 steps
• - vascular spasm
• - platelet plug formation (has its own three steps)
• - Coagulation
• Fibronolysis occurs after 3 steps

• 1) Immediate but temporary closure of damage blood vessel
• - due to reflexive retraction of smooth muscle within vessel wall
• 2) Triggered by two different things
• - endothelin from damages blood vessel endothelial cells
• - nervous system due to stimulation of local pain receptors(nociceptors)

• 1) an accumulation of platelets at injury cite
• 2) occurs in a series of steps
• a) Platelet adhesion
• b) Platelet release reaction
• c) Platelet aggragation

• 1) injured endothelial cells produce a protein called Von WillenBrand Factor
• - allows platelets to bind to collagen that has been exposed due to injury

• 1) Platelets bound to collagen and become activated , which causes platelets to release chemicals from their cytoplasmic granules
• a) ADP
• -Thromboxane A2 are released from granules ( recruits more platelets to injury cites)

Plasma protein fibrinogen facilitates binding of platelets together PGI1 released from damaged endothelial cells (limits the aggragation to only damaged area)

• - Prothrombin turns into Thrombin (by prothrombin activator from damaged endothelial cells) (prothrombin is made by liver and is not active)
• - Fibrinogen turns into Fibrin ( by Thrombin) (Fibrinogen is mage by the liver and Fibrin is what holds the clot together)

-cells around clot release a protein called Tissue Plasminogen Activator (TPA)

plasminogen -----> Plasmin (activated by TPA) (plasminogen is made by liver and Plasmin causes hydrolysis of fibrin holding clot together)

• - Edothelin
• - Von WillenBrand Factor
• - PGI2
• - Prothrombin activator
• - Tissue Plasminogen Activator

• double layered closed sack surrounding the heart
• a) fibrous pericardium
• - tough fibrous CT
• - prevents fro moverdistension of heart, anchors w/ in the mediastium
• b) Serous pericardium ( simple squamous epithelium)
• - 2 layers ( Parietal pericardium- thoracic cavity / Visceral pericardium- heart itself surrounds it)

• a) 2 atria and 2 ventricles
• b) inter atria septum ( divides atria into left and right)
• c) interventricular septum (divides ventricles into left and right)

• Auricles- structures on superior surface
• Internal Posterior wall-smooth
• Internal Poster wall- ridged w/ pectinate muscles
• -smooth/ridged region is seperated by the crista terminalis

• 1)On the right side of the interatrial septum is an oval depression called the fossa ovalis
• -remnant of the foramen ovale, this was an opening between Right and Left atria in embryo/fetus
• 2) Atria are recieving chambers
• -right atria
• -left atria

• Recieves deoxygenated blood from three veins
• 1) Superior Vena Cava- from region above diaphragm
• 2) Inferior Vena Cava- from region below diaphram
• 3) Coronary sinus- from heart itself

• recieves oxygenated blood from lungs via four pulmonary veins
• -2 from left and 2 from right lungs

• Known as "distributing chambers"
• -Right ventricle
• - Left ventricle

receives blood from the right atrium and pumps it to the pulmonary trunk to take to lungs

receives from left atrium and pumps blood to the aorta to be taken to blody tissue

• a) allow blood to flow from atria to ventricles( OPEN), but prevent blood from flowing backwards into the artia
• -snapped closed when ventricles are contracted
• b) The AV valve between the Right atrium and Right ventricle = Tricuspid valve
• c) the AV valve between the Left atrium and the Left ventricle = Bicuspid valve

• a) allows blood to flow out of ventricle into aorta/pulmonary trunk (open)
• b) SL valve between right ventricel and pulmonary trunk = Pulmonary SL valve
• c) SL valve between left ventricle and the aorta = Arota SL vlave

Pulmonary Circuit

Systemic Circuit

• right side of the heart takes blood to lung picks up O2 and drops off CO2
• Route: Deoxy Blood---superior/inferior vena cava ---right atrium
• ---tricuspid valve---right ventricle---pulmonary SL valve---pulmonary trunk

• Left side of ther heart brings oxy blood from lungs to tissues
• Route: Oxy blood---pulmonary vein---left atrium---bicuspid valve
• ---left ventricle---aortic SL valve---aorta---tissues

• 1) Cellular Components 6)Regulation of Heart
• 2) Electrical Events
• 3) Heart Sounds
• 4)Abnormailities
• 5)Cardiac Output

• Contractile Cells
• Conductile Cells

muscle cells for actual heart pumping ( have actin and myosin )

make up 99% of cardiac cells

• -Make heart auto rythymic
• a) self excitable cells that generate theis own action potentials
• b) the action potentials then initiate action potentials in contractile cells

AP in contractile cell

AP in conductile cell

• 1) electrical stimulation cause Na channels to open; Na influx ; intracellular positivity
• 2)at threshold, more Na channels open; causing the steep uprise

• 3) Plateau Phase:
• a) "slow" Ca channels open; Ca influx; they stay open
• for several tenths of a second; keeping inside of cell positive and
• inhibits repolarization
• b) membrane pereability to K decreases by 5times, further inhibiting repolarization
• 4) Repolarization:
• a) Ca channels close
• b) membrane permeability increase for K allows for K eflux (intracellular negativity)

• 1) conducting system
• 2) AP trace

• a) Sino atrial(SA) node- heart "pacemaker" because it depolarizes the fastest and begins sequence of citation
• b) Internodal Pathway- electrical connection between SA and AV nodes
• c)Atrioventricular(AV) node- depolarization is delayed here ( AV nodal Delay) to give atria time to fully contract
• and empty blood into ventricles before ventricles are stimulated to contract
• d) Bundle of His- divided left and right bundle brnaches within intraventricular septum / AP progated to apex
• e) Purkinge Fibers- penetrate heart apex, then the wind superiorly toward base of the heart
• cause ventricles to contract upward

• have no resting potentials ( electrical signals runnging)
• a) membrane gradually depolarizes to threshold due to:
• i. Decreased permeability to K, decrease K eflux
• ii. Constant Na influx through "Leaky channels"
• iii. "transient" Ca channels open; Ca eflux

• b) Fast uprise/ spike at threshold due to Ca influx through "longer lasting" Ca channels
• c) Repolarization- increased K permeability: K eflux
• d) K channels or gates begin to close; decrease K eflux
• BACK TO BEGINING "a"

• Uses electrodes placed on body surface to detect a summation of all AP's being transmitted
• through heart at a given time

• Displays electrical events that are responsible for mechanical events of contraction (systole)
• and relaxtion(diastole)

• P-wave -atrial depolarization about .1 sec after artia contract(systole)
• QRS complex- ventricle depolarization after ventricles contract ( hides atrial diastole)
• T-wave- ventricles repolarize .225 sec later ventricles relax

• use a Stethoscope to listen
• 1st is "Lubb"- AV valves closing (beginning of ventricular systole)
• 2nd is "Dubb"- SL valves closinf and begining of ventricular diastole

• 1)Tachycardia
• 2) Bradycardia
• 3) Arythmias

abnormal high rate- 100bpm

abnormal low rate- less than 60bpm

• are abnormal series of excitement
• 1) SA nodal Block (missing P-wave and HR decreases)
• 2) AV nodal Block - ventricles dont recieve all implulses from atria
• 3types: 1st(interval between P and QRS > .2 sec)
• 2nd (some P waves trigger QRS and some dont)
• 3rd ( complete heart block / atrial bpm 100 and ventricle bpm lower than 40)
• V-fib- ventricles never fully fill or empty( drecrease blood supply to tissues)

• 1) amount of blood pumped through heart per minute
• - HR times SV
• - SV is amount of blood the heart beats per beat

• 1)Intrinsic- the more the ventricle muscle is stretched the more
• forceful the next contraction would be
• - occurs when venous return increase (amount of blood entering the right atrium from superior vena cava)
• -if you increase venous return you increase SV and therfore CO

• Tunica Intima
• Tunica Media
• Tunica Adventitia

• contacts blood
• endothelial cells and basement membrane cells

smooth muslce and is innervated from sypmathetic nervous system which causes vasoconstriction and lack mean vasodialation

• outermost layer
• has collagen fibers tha anchor BV to the surrounding structure

• Continuous Capillaries
• Fenestrated Capillareis
• Sinusoidal Capillaries

• skin, muscle, and blood brain barrier
• most common
• least permeable
• intercellular clefts- unjoined membrane

• large pores (fenestrations)
• SI, Kidneys, Endocrine organs

• leaky capillaries
• most permeable
• liver, bone marrow. adrenal medulla, spleen
• Hepatic macrophages ( kuppfer cells)

• have much thinner tunica media and have larger lumens
• cna hold up to 65% of blood volume at one time
• are blood reservoirs
• venus valves- prevents blood from pooling to ensure one way flow to heart

Neural regulation

Chemical regulation

• Baroreceptors- sense pressure in Arch of Aorta and bifurcation of carotids
• monitors minute to minute fluctuations
• affaerent signals are sent from aorta to the vagus (X) adn from the carotids to the glosspharyngeal (IX)
• efferent signals are then sent to cardioregulatory systems and medulla oblongata

• 1) vasomotor center
• 2) Vagal Center
• 3) Processes invovled

• is sympathetic and recieve afferent signals from baroreceptors
• if BP decreases it will efferently stimulate nerves in the thoracic region( T1-T2)
• the release of norepinepherine or epinephrine one the Beta recpetors on the heart( increase CO and BP) and the alpha receptors on the blood vessels ( vasoconstriction to increase TPR)

• in under parasympathetic control and it recieves afferent signals from the baroreceptors
• -stimulated by an increase in BP
• -sends effernent signals via the vagus which causes the release of Ach on the M2 receptors on the heart
• -Decreases HR and CO
• - lack of stimulation from barorecptors causes vasodialation and decrease in TPR
• -this yeilds a decrese in BP

• -an increase in BP will excite the Vagal center and inhibit the vasomotor center( cause decrese in BP)
• - a decrese in BP will excite the Vasomotor center and inhibit the Vagal center ( cause increase in BP)

• 1) ADH( anti-diuretic hormone)
• 2) Renin

• vasopressin
• 1) made by hypothalamus
• 2) stored in Posterior pituitary
• 3) release of ADH is triggered by a decrese in BP
• 4) ADH targets the kidney tubule system ( cause more water reabsorbtion)
• 5) increse BC, venous return, SV, CO, and therefor BP

• 1) made by kidneys
• 2) triggered by decrese in BP
• 3) once in the blood it cuases and enzyme to catalyze production of Angiotensin 2
• - A2 targets adrenal gland and cause the adrenal cortex to release Aldosterone
• - aldosterone cause incres in NaCl reabsorbtion in circulatory system ( water follow osmatically)
• 4) increase H2O, BV, and therefor BP