Anatomy - Notes

Cardio-Vascular

Middle region of the thorax 

This is where the heart is located 

Mediastinum ○

Diaphragm 

When you breathing and the diaphragm is moving up and down, the heart is going to have movement in your thorax area cause the PC is attached to the diaphgragm



Pericardium attaches the heart to the diaphragm  Bottom border ○ Base (top)  Right border  Left border  Apex (bottom) 

Down the diaphragm 

Inferior surface 

Borders ○

Sits to the right side and is rotated to the left … when we look at the heart from the front view, we see more of the right side 

General 

Costal cartilage (rib) □

Intercostal space □

Terms 

Superior left Inferior border of second costal Superior right Third costal cartilage

Inferior right Sixth cartilage

Inferior left Intercostal space between fifth and sixth □

Orientation 

Surface Projection ○

Sternal angle … followed down by the four sternabrae 

Middle region Heart, ascending aorta, pulmonary trunk

Anterior portion Lymph node, thymus gland (note in infants this is large, as large as a lung … as you age it shrinks) Posterior region Descending aorta, esophagus, lymph nodes, vagus nerve, thoracic duct

Superior region Aortic arch, esophagus, trachea □

Regions 

Side view of Mediastinum (left) ○

Right atrium 

Right ventricle 

Little flap like thing □

Left auricle 

Don’t see it full on … just see it peeking through □

Left ventricle 

Don’t see the right ventricle I believe □

Note 

Anterior Surface Features ○

Can see more of the left of the heart □

General 

Aorta 

Superior vena cava 

Left atrium 

Left ventricle 

Right ventricle (some of it) 

Right atrium 

Inferior vena cava 

Posterior Surface Features ○

Location and Orientation •

Have vessels sitting within the grooves. Don’t want vessels moving when the heart moves, so the coronary vessels lie in them … they are tracks 

General ○

Lies between atria and ventricles 

Coronary Sulcus ○

Lies between left and right ventricles 

Interventricular Sulcus ○

Groovy Heart (Sulci) •

It comes off the LV, arches up and then descends behind the heart □

Aorta 

Comes off RV and takes blood to the lungs □

Pulmonary trunk 

Off the Heart ○

Returning blood from upper body to the heart 

Superior Vena Cava  To the Heart ○ Big Vessels ○ Vessels •

CV Anatomy

Returning blood from upper body to the heart 

Returning blood from lower body to the heart 

Inferior Vena Cava 

Supplies blood to the heart muscle 

General □

Right coronary •Comes off arch of aorta

Wraps all the way to the back of the heart, but before that it branches to the marginal artery, and then in the back it will branch into the posterior ventricular artery

•

Left coronary •Comes off arch of aorta

Branches very quickly, into the circumflex and the LAD •

Marginal artery •Comes from right coronary Goes down the front of the heart •

Circumflex artery •Comes from left coronary Goes to the back of the heart •

Is in the coronary sulcus •

Left Anterior Descending (LAD)

Comes from left coronary •

Is in the interventricular sulcus •

□

Coronary Arteries ○

Small cardiac vein □

Anterior cardiac vein □

Middle cardiac vein (on the back side) □

Runs in the interventricular sulci up the heart, in the same groove as the LAD 

It will curve into the coronary sulcus (where the circumflex is) and will go to the back of the heart 

Great cardiac vein (wraps to the back) □

This is where the coronary veins comes together and this is where the blood gathers before it is returned to the right atrium 

Coronary sinus (on the back side) □

Coronary Veins ○

Anterior ○

Great cardiac vein □

Coronary sinus □

Right coronary arteries □

Comes off the right coronary at the back of the heart in the interventricular sulci 

Posterior interventricular artery □

Coronary Vessels ○

Posterior ○

Lumen is the inside of the artery, and in partially obstructed arteries there is atherosclerotic plaque, which narrows the artery 

This obstruction starts right after birth to everyone 

If the LAD is obstructed, will get an MI cause there is no anastomosis protecting it 

Obstructed Arteries ○

There to protect the heart □

General 

Dense irregular connective tissue □

Protects and anchors the heart □

Prevents overstretching □

Fibrous pericardium 

Secretes serous fluid 

Parietal layer □

Reduces friction 

Serous fluid in between □

Visceral later (epicardium) □ Serous Pericardium  Pericardium ○ Epicardium □

Where the specialized cardiac muscles are 

Myocardium □

Similar lining to what is in your blood vessels (endothelium) 

These are non-thrombogenic surfaces -- wont get clumping of components of the blood, like platelets and plaque formation 

Endocardium □

Layers 

The left side of the heart is much thicker than that of the right side … this is cause the left side of the heart has to work much harder in order to deliver its flow …

□

Thickness is depending on the function of the chamber □ Thickness  Fluid, pus  Pericarditis □

Can be caused by viral function and rheumatic fever 

Myocarditis □

Potentially fatal if not treated  Endocarditis □ Inflammation  Heart Wall ○

Pericardium and Heart Wall • Right Atrium  Right Ventricle  Left Atrium  Chambers ○ Chambers •

Left Atrium 

Left Ventricle 

Blood goes from the body into the right atrium and then flows into the right ventricle. It will go from there through the pulmonary trunk to the lungs. Then oxygenated blood comes from the lungs into the left atrium, down to the left ventricle, and then out through the aorta to the body tissues.



Body → Right Atrium → Right Ventricle → Pulmonary trunk → Lungs → Left Atrium → Left Ventricle → Aorta 

Flow ○

= fleshy logs 

When you look at the inside of the heart, you notice a buumpy surface inside … i.e. raised cardiac muscle 

Trabeculae Carnae ○

Help blood to travel in a specific path 

Right side of the heart 

Three leaflets (cusps) … from these come out chordae tendineae (like parachute strings) … to this is attached is the papillary muscle 

Tricupsid ○

Left side of the heart 

Two leaflets 

Bicupsid (mitral) ○

So when the blood enters the ventricles, they need to contract to let the blood through the aorta or pumonary trunk. That pressure is huge and you don’t want blood to back-flow to the atria.



The pressure makes the chordae tendieae muscles to go taut, the papillary muscle contracts and these things prevents the cusps everting or opening up back into the atria

 How ○ Congenital, Scarring  Mitral □ Aortic □ Stenosis 

When you have the eversion of the cusps going back into the atria 

Mitral valve prolapse (MVP) □

Prolapse 

Disorders ○

Helps maintain the diameter of the valves □

Attachment side for muscle fibers □

Electrically separates the atria from the ventricles □

General 

Wraps around the heart □

Like a wet towel and how you wring it, the fibrous skeleton is similar in how the muscle squeezes the heart □

Orientation 

Fibrous Skeleton ○

…. Didn’t copy this … 

Des scribed above I think 

Operation of the AV Valves ○

Between the ventricles and the aorta/pulmonary trunk □

Don’t have the chordae tendenae and papillary muscle □

General 

When the pressure in the ventricle is higher than that in the vessel, the valves open □

When the pressure is less, the valves close □

How 

Operation of the Semilunar Valves ○

Valves •

Closure of the cusps (this as well?) and the turbulence of the blood going up against the cusps is whats causing the heart sounds 

Heart sound is not listened to right at the spot of the valve, but a different spot is the echo is what is heard best 

General ○

Heard at the right sternal border at the second intercostal space □

Aortic valve 

Best heard on the left side in the second intercostal space … close to the sternal border □

Pulmonary Valve 

Point in the third intercostal space where you can hear both the aortic and pulmonary valve sounds □

Erb's Point (LLSB) 

Heard to the left hand side even though this is at the right □

Best heard around the 4th or 5th intercostal space □

Tricuspid valve 

Heard to the left hand side □

Best heard in 5th intercostal space … at the midclavicular line □

Mitral (bicuspid) valve 

All Pig Eat Too Much ○ Heart Sounds • Heart location ○ Heart orientation ○

Heart surface features ○

Coronary vessels ○

Main arteries and veins ○

Chamber and valves of the heart ○

Heart sounds ○

Summary •

Decreases. When the heart contracts, the surface coronary vessels stay open, but the ones that are feeding the myocardium act ually get compressed. So during ventricular contraction, there is little blood supply going directly to the heart tissue.

○

When the heart is contracting, coronary blood supply …

•

If this happens, remembering that the papillary is the anchor for the chordae tendianae, the cusps don’t have tension and the refore you have back-flow

What might be the consequence of a heart attack that injured a segment of the papillary muscle. How would the flow of blood b e altered?

If this happens, remembering that the papillary is the anchor for the chordae tendianae, the cusps don’t have tension and the refore you have back-flow into the atria. One condition associated with this is mitral valve regurgitation

All about oxygen delivery ○

Start with two tubes that eventually start forming into a heart like shape 

Embryo ○

Heart looks similar to post-natal heart, except there are differences in features 

Fetal ○

Birth is a transition point 

Right is deoxygenated blood and left is oxygenated 

Postnatal/Adult ○

Function drives Development • Four chambers ○ RA → RV → Lungs → LA → LV → Body ○ Adult Heart •

This is concerned with removal of CO2 and waste products from blood … goal is to remove waste and get blood oxygenated 

This is the right side of the heart  Pulmonary side ○ Left side  Delivery system 

Transport waste to the right side of the heart 

Systemic side ○

Circulatory System •

Arteries Blood away from the heart Veins Blood towards the heart ○

Closed left side and closed right side □

Don’t have mixing unless there is a defect □

Two Closed Circuits 

Pumping through the pulmonary circulation and then the systemic circulation □

Arranged in Series 

Pressure on the left side of the heart is higher because of the vascular (?) resistance than on the right side of the heart □

Left side is supplying whole body … right side to the pulmonary vasculature □

Pressure  Characteristics ○

Post Natal Circulation •

Open circuits (left and right sides are not seperated … oxygen-medium blood is an indicator of this) □

Circulation operates in parallel … right and left occurs at the same time □

Right side has higher pressure due to the pressure associated with the vasculature of the pulmonary system … 

Left side has a lower pressure because it has a low systemic resistance due to the placenta being there 

Pressure □ Characteristics 

Oxygen exchange occurs at the placenta, not at the lungs □

Through diffusion … no mixing between the two blood systems (of the mother and fetus I think) □

Oxygen exchange 

Flows from the placenta through the umbilical cord and umbilicus … then at the liver point ish there is mixing of the blood cause there is blood coming from the fetus from the inferior vena cava that is deoxygenated … I think this is through the ductus venosus (?)

□

In the right atrium, there is an opening to the left side through the foramen ovalae … this lets the blood go to the aorta quickly □

Some blood makes it to the pulmonary trunk through … and therefore there is the ductus arteriosus to let the blood go from the pulmonary trunk to the aorta

□

During the later stages of fetal development, this is important cause you're trying to get the lungs to work at birth … so want to start to get that system primed and ready



5-7% of the blood still goes to the pulmonary trunk to the lungs □

Blood returns from the fetus through the umbilical arteries □

□ Blood flow 

Allows the mothers blood to bypass for the most part the liver … the maternal circulation is already filtering the blood so t he fetal liver doesn’t need to do this …

 Ductus venosus □ Foramen ovalae □ Ductus arteriosus □ Shunts  Fetal Circulation ○ Fetus • Birth •

CV Development

This causes an increase in the pressure in the left hand side 

Placenta is lost … □

Lungs open and the pressure associated with the right side will drop 

First breath … □

All of them? 

Shunts are closed … □

Events 

Umbilical vein → Ligamentum teres □

Umbilical artery → Medial Umbilical ligaments □

Ductus venosus → Ligamentum venosus □

Ductus arteriosus → Ligamentum arteriosum □

The FO is a depression in the atrial septum … this can be seen in specimens 

Foramen ovalae → Fossa ovalis □

Closures in postnatal circulation … Shunts and Ligaments 

What happens … ○

Birth •

Two thin tubes of cardio tissue … two start to expand and fuse … 

2 Weeks ○

Fused to one tube 

Starts to get sacculations … is like a wavy tube 

TA - Truncus Arteriosus Becomes the pulmonary trunk and the aorta BC - Bulbus Cordis RV

V - Ventricle LV

A - Atrium RA, LA, R+L Auricles SV - Sinus venosus RA, Coronary sinus, SA node □

Features 

Note that valves are in alignment □

Heart starts to elongate and then fold into an S-shaped configuration 

4 Weeks ○

Looking at it from top-down, there are from the sides ridges forming which grow towards each other and form a septum and that splits the tube into the two great vessels



See pic ◊

So I'm thinking that its not the tube that is twisting, but the septum or divider inside of it that is twisting ◊

This develops in a spiral formation … there is a 1800_{rotation occurring with the spiraling}



PT sits in front of the aorta and the aorta curves behind the PT □

Arch of the aorta goes over the pulmonary arteries □

Locations 

Separation of tubes □

This septum does this … these are the semilunar valves 

Truncus Arteriosus 1 vessel and 4 cusps

Aorta + PT Now there are 2wo vessels with 3 cusps each 

Formation of Valves □

Aorticopulmonary (spinal) Septum 

No Separation of Aorta and PT 

In the fetus its no problem but after birth the baby can become cyanotic ◊

Blood mixes from the left and right sides of the heart … oxygenated and deoxygenated 

Persistent Truncus □

Septum fails to spiral 

There you have one circuit cycling oxygenated and one deoxygenated … the deoxy is never getting reoxyed ◊

Not an issue in the fetus cause there are bypasses and shunts … but in post-natal life this is fatal unless there are other defects such that the circuit becomes open

◊

Patent ductus arteriosus 

Opening between the atria –

Atrial septal defect 

Opening between the ventricles –

Ventricular septal defect 

Fatal in life without PDA, ASD and VSD ◊

In this case, Aorta comes of right side and PT from the left side 

Transposition of Great Vessels □

Septum has divided the right and half part unequally … one side is expanded and the other is stenosed 

Factor Effect Obstruction or shunt

Obstruction

Blood flow Reduced blood flow to pulmonary artery Right ventricle

pressure and size

Pressure and size increases … natural response of body is to maintain what it sees in normal and therefore if there is an increase in pressure, the tissue response is to increase in size … this is so the pressure is distributed over more tissue, decreasing pressure on each individual piece of tissue

Acyanotic or cyanotic

Acyanotic … it’s a moderate obstruction in the case study so its acyanotic … if it was a full obstruction then it would be cyanotic possibly

◊ Factor-Effect 

Stenosis □

Normally in birth there is an immediate closure of DA … and over time there is tissue accumulation to fully close it Patent Ductus Arteriosus

□ Problems 

Truncus Arteriosus (Division) ○

Tubular Heart •

Normally in birth there is an immediate closure of DA … and over time there is tissue accumulation to fully close it 

Here there will be an opening between the aorta and PT … blood will go from aorta to PT cause pressure is higher in the left hand side 

The IAS begins with the formation of a septum that comes down from the roof of the aorta and downwards towards the endocardial cushion (midpoint between the atria and the ventricles) … this first septum = septum primum … it will continue to grow to the cushions but there will still be an opening called the foramen primum, which allows the open circuit in the fetal heart

□

Get holes within the septum primum to keep the open circulation, and these are perfurations called the foramen secundem (?)… □

Then get a second septum that is much thicker called the septum secundem come down beside the septum primum, and the hole that remain here is the foramen ovalae

□

The remaining tissue that is left from the septum primum is called the valve of the foramen ovalae □

Pressure is higher on the right hand side, so blood will move from right to left ◊

Blood will cause the septum primum to open (or in other word the valve of the foramen ovalae) … when the pressure build up on the left hand side, the valve will close

◊ Before birth 

Pressure is higher on the right side, the valve of the foramen ovalae closes and unless there is problems it will be closed ◊

After birth 

This is an opening in the heart ◊

The foramen ovalae fails to close ◊

ASD (Atrial septal defect) 

Foramen ovalae □

Formation of Interatrial Septum 

Partitioning of Chambers ○

From next lecture … •

It would be the same as the patent atrial septum (on the slides), which is that blood flow will be pushed from the left ventricle to the right ventricle. ○

Baby Noah is going to be acyanotic … so oxygenated blood is being pushed to the right side … the blood that is still on the left side is not getting mixed with deoxygenated blood and therefore Noah will be acyanotic (will still get enough oxygen)

○

If Baby Noah had a patent ventricular septum, what would be the effect

•

If there is problem with the formation of the membranous portion, there may also be a problems with the formations of the great vessels 

Starts growing from the bottom of the ventricle and grows to the endocardial cushion … the last bit of it that attaches to the cushion is the membranous

portion, which is important cause formation of this membranous component is associated with the separation of the truncus arteriorsis into the aorta and

the pulmonary trunk ○

The ridges are similar to the ones seen which played a role in the formation of the spinal septum □

Formed from the endocardial cushions and the bulbar ridges 

Associated with the partitioning of truncus arteriosus 

Membranous portion ○

Interventricular Septum •

There is some debate as to what causes the malformation 

Defect involving the membranous portion of the interventricular septum ○

Combination of four different defects that are occurring (numbering below is not necessarily #'s of occurrence or importance) ○

1) Larger than normal aorta (overriding aorta cause it overrides both ventricles) … picks up blood from both the left and right ventricles so it is picking up deoxygenated and oxygenated blood



2) Stenosed pulmonary trunk 

In the membranous portion □

3) Interventricular septal defect 

Thickness of a tissue responds to changes in pressure … so in response to the higher pressure in the RV (cause there is blood flowing from the LV to RV) + increased pressure due to the resistance caused by the stenosed pulmonary valve/trunk … therefore it grows in size

□

4) Enlarged (hypertrophied) right ventricle 

Tetrology ○

Can be cyanotic cause we have mixing deoxygenated and oxygenated blood  Baby ○ Tetralogy of Fallot • Tricuspid ○ Bicuspid ○

From subendocardial mesenchymal tissue that proliferates and develops outgrows 

Formation ○

The way this valve is formed is that you have outgrowth of tissue … but the shape of the valves is specific so it is sculpted by programmed cell death (apoptosis) … this is similar to what we see in our fingers

 Note ○

Formation of the Atrioventricular Valves •

95% of the heart 

Responsible for pumping action 

Striated, involuntary muscle 

This is kind of like the fibrous skeleton that we talked about earlier □

Fibers swirl diagonally around heart in bundles 

General ○

Sacolemma = cell membrane 

AP is started, then travels through the atria and then the ventricles (entire myocardium) □

Functional syncytium 

Desmosomes (cell junctions) □

Gap junctions (allow AP's to move from one cardiac muscle cell to another) □

Intercalated discs 

Cardiac Muscle Tissue ○

Myocardium •

Heart's pacemaker □

Sets the rhythm … spontaneously depolarizes and keeps doing so until it reaches the threshold 

AP's that come from the SAN travel to the AV Node … 

SAN ○

This is a spot between the atrium and the ventricles 

This is one exception to this □

When we looked at the fibrous covering (skeleton?), that was preventing electrical connections between the atria and the ventricles, we said that this was so that there wasn’t signals going between atria and the ventricles



During this time, the ventricles will be able to fill before they start their contraction □

When the AP hits the AV Node, there will be a pause which is important cause you want the atria and the ventricles to contract at different times 

From the the AV node, the signal goes to the AV bundles … 

AV Node ○

This is going down the interventricular septum 

Also referred to as the bundle of Hiss 

At the Purkinje fibers, the signal is starting at the apex of the heart and will travel through these fibers up the walls of the ventricles and eventually depolarizing the entire ventricle

□

Signal continues to the right and left bundle branches … and continues down to the purknije fibers … which are modified cardiomyocytes 

AV Bundles ○

SA node → anterior, middle, and posterior internodal tracts → transitional fibers → AV node → penetrating fibers → distal fibers → Bundle of His (AV bundle) → right and left bundle branches → Purkinje fibers → myocardium

 Summary ○

Conduction System •

Due to Na+_{inflow when voltage-gated fast Na}+_{channels open} □

This will stop with inactivation of the fast channels and Na+_{influx will drop} □

Note that contraction will not occur right at the depolarization, it will occur a little bit after □

1) Rapid depolarization 

Due to Ca2+_{inflow when voltage-gated slow Ca}2+_{channels open and K}+_{outflow when some K}+_{channels open} □

Note: Strength of heart contractions influenced by substances that alter movement of Ca2+_{through the channels} □

E.g. epinephrine … when you have an increase, it increases the contraction force by increasing the amount of Ca2+_{that can increase the} cytosol …

□ 2) Plateau 

Due to closure of Ca2+_{channels and K}+_{outflow when additional voltage-gated K}+_{channels open} □

3) Repolarization 

Steps ○

Note that the depolarization comes first, then the contraction 

Similar to both cardiac and skeletal muscle □

Electrical activity (AP) → Mechanical response (contraction) 

Contraction ○

Time interval during which a second AP/contraction cannot be triggered 

Refractory period lasts longer than the period of contraction 

Refractory period ○

Can occur in skeletal muscle, but not in cardiac muscle 

This is b/c the refractory period is longer than the period of contraction … cant have a contraction after another after another 

Because the pumping action of the heart depends on the ventricles being able to alternate between relaxation and contraction … □

Important 

Tetanus ○

AP in a Ventricular Contractile Fiber •

ECG or EKG ○

Note that this is composite of all fiber's AP … in previous slides, we saw the AP of a single cardiac myocyte 

Composite record of AP produced by all the heart muscle fibers ○

Detected at surface of the body ○

Electrocardiogram •

CV Physiology

○

Associated with a period of atrial contraction (when atria are in systole) □

Note that you can't detect when the atria are relaxing … don’t see this wave b/c the electrical activity level is so low that it is swamped out by depolarization activity

□ P 

Associated with a period of ventricular contraction (ventricular systole) □

QRS 

Represents when the ventricles are starting to repolarize and relax □ T  3 recognizable waves ○ Systole = contraction  Diasatole = relaxation  Note ○

Depolarization of atrial contractile fibers and this produces the P wave □

AP starts first and then contraction of the atria afterwards □

1) AP potential in the SAN 

After the P wave spike type of thing, this is the part of atrial contraction □

Also at this time we get that pause in the AV node, giving the ventricles time to fill up □

2) Atrial systole contraction 

This produces the QRS thing □

3) Depolarization of ventricular contractile fibers produces QRS complex 

After the depolarization of the contractile fibers and the whole QRS spikes thing is done, we get the actual ventricular systole (contraction) □

Referred to the ST segment -- the space between the drop in the S and the start of the T wave □

4) 

Produces T wave □

This is just before the ventricle will relax □

5) Repolarization of ventricular contractile fibers 

After the T wave bump, we see the actual ventricular contraction □

6) Ventricular diastole 

Left to Right ○

ECG Waves, Systole and Diastole •

Can connect the ECG with pressure 

Pressure is being generated cause you have blood in your heart … contraction of muscles and blood pushing against the chambers 

Pressure is measured in mmHg 

Note: Diagrams are showing the left side of the heart cause the pressures are much higher 

General ○

When the atria is finishing its contraction, the bicuspid is closed and we have a moment in time when all four valves are closed … this is an isovolumetric contraction … everything is staying the same (nothing is lengthening or shortening

□

As pressure is rising in the left ventricles cause they are filling with blood, the blood closes the valves and you get rising pressure in the left ventricle

□ Atrial Systole 

Pressure in LV keeps rising as the fibers continue to contract … then the pressure will rise above the pressure in the aorta, which normally is 80 mmHg … once its passes this it opens the aortic valves … blood will go into the aorta

□

Note that the pressure in the aorta will be increasing but the pressure in the LV will also be increasing □

Then the pressure of both will start to fall and the aortic valve will close when the LV pressure drops below that in the aorta … at this point there is the dicrotic wave which is a slight bump/increase in pressure in the aorta due to the blood … this is caused by the turbulence of the blood falling against the semilunar valves … pressure in aorta will stabilize at 80 mmHg

□

Ventricular Systole 

Pressure in LV will continue to drop as it goes to the relaxation phase … the bicuspid valves will open and the cycle will start again □

Relaxation Period 

Steps ○

S1 Closure of AV valves (distinct) [right before isovolumetric contraction?] S2 Closure of SL valves (distinct)

S3 Blood turbulence during filling of ventricles phase (quieter) S4 Contraction of the atria (quieter)



If blood is flowing smoothly (laminar flow), this will not generate sound. It is when its moving against something causing turbulence is what causes sound □ Note:  Heart Sounds ○

Cardiac Cycle: ECG and Pressure Waves •



After the ventricles relax such that they can be filled with blood, initially we get this kind of passive filling, but then there is a boost where the atria actually contract to push blood to the ventricles

 ○

During the beginning of ventricular contraction, we have in the ventricles EDV … before they are gonna contract at the end of relaxation phase, the volume of blood is referred to EDV

□

EDV (End-Diastolic Volume) 

At the end of contraction phase (after the ventricles have expelled the blood), whatever blood that is left over after contraction is referred to as ESV

□

ESV (End-Systolic Volume) 

= EDV - ESV □

Remember that the LV is pushing against a greater pressure than RV … its able to expel the same amount of blood cause of that thicker heart wall



Each ventricle expels the same amount of blood per beat (left will do the same as right) □

Stroke Volume 

Stroke Volume ○

From next class

# of heart beats per minute ○

Autorhythmic rate of 100 beats per minute (bpm) 

Pacemaker cells in SA node ○

Slowed down by parasympathetic stimulation 

In athletes this might be lower like 40 bpm 

Native HR = 70 bpm ○

Heart Rate •

Volume of blood ejected from the left ventricle (or right ventricle) into the aorta (or PT) each minute ○

CO = HR x SV ○

E.g. when you are running 

When is increase needed? ○ = 5250 ml/min □ CO (ml/min) = HR (75 bpm) x SV (70 ml/beat)  Example ○

Cardiac Output (CO) •

CR = CO (max) - CO (rest) Cardiac Reserve

Have a reserve -- ability to put out more cardiac output 

CR = CO (max) - CO (rest) ○

How does CR change with training or heart failure?

○

Degree of stretch on the heart before it contracts □

The more you stretch the heart, the more blood you will be able to push out ◊

↑ heart muscle is stretched (during diastolic filling) → ↑ force of contraction → ↑ volume of blood ejected into the aorta 

Frank-Starling Law of the heart □

↑ Ejection volume = ↑ Stroke Volume = ↑ CO □

□

Factor Increase Decrease

Duration of ventricular diastole (time when ventricles fill with blood)

Slow HR … more chance to fill ventricle with blood … so slow HR = increase in duration

Extremely rapid HR

Venous return Increase in venous return (e.g. exercise) Low venous return (e.g. severe blood loss) □

Preload 

Forcefulness of contraction of individual ventricular muscle fibers □

Strength of contraction at any given preload □

From ECF and sarcoplasmic reticulum 

Due to changed in influx of Ca2+ □

Type of Agent Positive inotropic Negative inotropic

Changes in contractility Increase Decrease

Examples of inotropic substances •Symp stimulation (e.g. adrenaline) Hormones (e.g. glucagon) • Drugs (digitalis) • Increase K+ • Acidosis (excess H+₎ •

Calcium channel blockers •

□

Many drugs are considered inotropic … either positive or negative … so either increasing or decreasing contractility of fiber s 

Inotropic = affects force of muscle contraction □

Contractility 

Formal definition: Pressure ventricles must overcome before the semilunar valves open 

Is that point where ventricular pressure has to get to the point of the pressure of the aorta … this was normally 80mmHg □

Pressure in the aorta approx 80 mmHg 

Normal afterload □

More blood will remain in the ventricles … therefore ESV will be higher 

Increase in afterload leads to a decrease in SV □

Factor Increase Decrease

Blood Pressure Elevated arterial BP (hypertension) Blood loss (hemorrhage)

Vessel Structure Narrowing of arteries by atherosclerosis Widespread vasodilatation (sepsis, anaphalaxsis) 

Changes in Afterload □

Afterload 

Factors that regulate stroke volume ○

Stroke Volume •

Factor Increase Decrease

Autonomic Regulation Symp (e.g. NE) Parasymp (e.g. ACh)

Chemical Regulation •Hormones (e.g. E, NE, thyroid) Cations (e.g. Ca2+₎ • Hypoxia (↓ O2) • Acidosis (↑ H + ) • Alkalosis (↑ pH) • Cations (e.g. Na+_{, K}+₎ •

Other factors •Age (have ↑ resting HR)

↑ body temp (e.g. fever, excersise) •

↓ with age •

Decreased body temp •

○

Regulation of Heart Rate • Cerebral cortex □ Limbic centers □ Hypothalamus □

From higher brain centers 

Proprioceptors □

Chemoreceptors (monitors blood chemistry) □

Baroreceptors (monitors BP) □

From sensory receptors 

Input to CV Center ○

In the medulla oblongata 

Cardiovascular Center ○

Affects the ability of the heart to contract … and how much SV comes out … what rate of repolarization will be □

Output to Heart ○

Nervous System Control of the Heart •

Affects the ability of the heart to contract … and how much SV comes out … what rate of repolarization will be □

Increased rate of spontaneous depolarization in SA/AV nodes □

Increased contractility of atria and ventricles to increase SV □

Cardiac Accelerator nerves (symp) 

Decreased rate of depolarization in SA/AV nodes which decreases HR □

Vagus nerves (CN10, parasymp) 

Note the our slide is WRONG ○

○

Neural Regulation: Example •

R & L Coronary Arteries 

Ascending Aorta ○

Right Common carotid □ Right Subclavian □ Brachiocephalic trunk  Left Subclavian  Left Carotid 

Arch of the aorta ○

Pericardium, esophagus, bronchi, diaphragm, intercostal and chest muscles, mammary gland, skin, vertebrae and spinal cord 

Thoracic aorta ○

I think the diaphragm signals the change between thoracic and abdominal aorta 

Note: ○

Abdominal and pelvic viscera and lower extremities 

Same as celiac artery? 

Supplies panrcreas, duodenum and spleen 

Celiac trunk □

Superior Mesenteric □

From this comes the common iliac artery  Inferior Mesentaric □ Suprarenal  Renal  Gonadal  3 Paired Glands □ There are 4  Lumbar Arteries □ Branches  Abdominal aorta ○

There are reference slides that show all these parts and what comes off of them … look at the slides 

Note: ○

Aorta: 4 Principle Divisions •

Head, neck, chest and upper limbs 

Superior Vena Cava ○

Great cardiac vein, middle cardiac vein, small cardiac vein 

Coronary Sinus ○

Abdomen, pelvis and lower limbs 

Inferior Vena Cava ○

Venous blood from GI organs and spleen go to the liver before going to the inferior vena cava (and then back to the heart) … you need to filter that blood



Superior and inferior mesenteric drain into hepatic portal vein which is going to go to the liver 

Hepatic Portal System ○

Veins •

Carry blood from the heart 

Artery → Arterioles → Capillaries 

Arteries ○

Site of gas and nutrient exchange 

Waste removal 

Capillaries ○

Return blood to the heart 

Capillaries → Venules → Veins  Veins ○ Blood Vessels • Pressure vessels ○

Smooth layer that blood is going be flowing up against 

Endocardium in the heart is a continuum of the endothelium in the aorta and PT 

Endothelium □

Basement membrane □

Is a giant sheet of elastic ____ with holes punched in … with this elastic lamina and the holes it allows the artery to be stretched easily



Internal elastic lamina □

Tunica Intima 

Cells responsible for contraction 

Smooth muscle cells □

Elastic fibers □

Also fenestrated (has holes) 

External elastic lamina □

Tunica Media 

Elastic and collagen fibers □

Arteries that supply other arteries Vasa vasorum

□

Tunica Externa (Adventita)  Structure ○ Arteries •

Vascular System

Arteries that supply other arteries 

Great vessels want to supply tissue with nutrients … problem is the great vessels are large enough that the O2and nutrients cant

reach the outer wall … and therefore have these vaso vasorum 

Tiny vessels that supply O2and nutrients to the outer walls of the great vessels



D = 15mm □

T = 1mm □

Largest of the arteries (e.g. aorta)  Pressure reservoir □ Conducting arteries □ ◊ ◊ Tissue makeup □ Characteristics 

More of a propelling vessel 

Help to conduct blood to the muscular arteries □

What we want is whether the heart is relaxing or contracting, we want blood flow either way. Don’t want blood flow to stop … the aorta expands and it contracts, and when it does that it is still pushing blood to the systemic circulation regardless of whether we are in relaxation or contraction

◊

Must resist pressure from the contractions of the heart (systole) and provide pressure between heart beats (diastole) □

Tunica media is full of elastic fibers of connective tissue □

Elastic arteries expand when the blood pressure increases and contract when the blood pressure decreases evening out the pulse pressure □ In depth  Elastic ○ D = 6mm □ T = 1mm □ Dimensions  □

Have a lot more smooth muscle tissue … core difference is really in the amount of elastic tissue (EL) and smooth muscle (SL) they have

□

Tissue Makeup 

More of a contraction vessel 

Medium-sized arteries with more muscle than elastic fibers in tunica media □

Walls are relatively thick ◊

“Distributing arteries” – direct blood flow ◊

Capable of greater vasoconstriction and vasodilation to adjust rate of flow □

Brachial artery in the arm ◊

radial artery in the forearm ◊ Examples: □ In depth  Muscular ○

Elastic and Muscular Arteries ○

D: 37 um □

T: 6um □

Referred to as resistance arteries  □ Tissue make-up  Arterioles  D: 9um □ T: 0.5um □ Exchange vessels  □ Tissue make-up 

Have endothelial cells forming a ring □

In the middle have a red blood cell □

Nucleus of endothelial cell □

Structure 

Capillaries 

Arterioles and Capillaries ○

Nucleus of endothelial cell □

Spaces between the endothelial cells ◊

Intercellular clefts □

Cell that forms around the endothelial cells of the capillaries ◊

Pericyte □

Tight junctions □

Brain, lungs, muscle ◊

Basement membrane 

Nucleus of endothelial cell  Lumen  Intercellular cleft  Have: ◊ Continuous □

Need lots of perfusion  Kidney ◊ Fenestrations (pores) ◊ Fenestrated □

Need bigger things moving out of the capillaries 

Red bone marrow, liver ◊

Large intercellular cleft 

Incomplete basement membrane  Have: ◊ Sinusoid □ Types 

At the capillary level … 

At the terminal end of the arteriole have something called a metarteriole 

Allow blood flow into the capillary bed and blood to perfuse the tissues □

If we follow the blood we have the postcapillary venule, which is then going to go into the venous circulation □

When open 

The blood will bypass the capillary bed and go right from the arteriole end to the venous end through something called the thoroughfare channel

□

This is to control the rate of blood flow and where blood is going to □

When closed 

At the metarteriole end have precapillary spincters 

Ability of the sphincters to open and close … 

Vasomotion 

Microvascular (Capillary) Bed ○

Volume reservoirs (2/3 of blood volume) ○

Helps assist blood returning to the heart and fight gravity … can't have the blood fall back down  Valves ○ Endothelium □ Basement membrane □ Tunica Intima 

Smooth muscle cells □

Tunica Media 

Elastic and collagen fibers □

Particularly in the larger veins 

Vasa vasorum □

Tunica Externa (Adventita)  Structure ○ D: 20um  T: 1um  Size □

Almost no elastic tissue  Tissue-make up □ Venule  D: 5mm  T: 0.5mm  Size □

Has some elastic tissue (little) 

Tissue-make up □

Vein 

Veins and Venules (from next lecture) ○

Contraction of muscle □

Compressed veins □

Milks blood to heart □

Skeletal muscle pump 

Inhale … diaphragm moves down □

↑ pressure in abdomen □

Compresses abdominal vessels □

Also milks the blood □

Respiratory pump 

Venous Return (from next slide) ○

Veins •

Veins have a much thinner muscular layer and tunica externa 

Veins have no elastic layers but they do have valves 

Anatomically ○

Arteries vs. Veins •

Veins have no elastic layers but they do have valves 

Veins have almost no blood pressure to resist which means the vessel wall can be much thinner and weaker 

The valves are necessary to prevent back flow and assist in venous blood return 

Physiologically ○

From next lecture …

Interstitial fluid that is surrounding the capillary and the cells 

Background (of the pic) ○

On this side, there is net filtration □

Arterial end 

On this side, there is net reabsorption □

Venous end 

Two ends ○

Note: Fluids and proteins that escape get pulled into the lymphatic system □

85-90% reabsorption 

Starling's Law of the Capillaries ○

The pressures associated with that are minimal so we will forget about them □

Interstitial fluid 

Blood hydrostatic pressure □

Result of water in the blood pressing against the blood vessel wall □

Higher at the arterial end than at the venous end □

HP 

Blood colloid osmotic pressure □

Associated with proteins present in the blood … not all can enter interstitial space and these therefore cause this pressure □

Stays approx the same at both ends □

Causes stuff to go into the capillary □

OP 

When HP > OP, there is net out flow of fluid out of capillary (filtration?) □

When OP > HP, there is net flow of fluid into the capillary (reabsorption) □

HP and OP 

Pressure ○

All small molecules can pass into the interstitial space but large molecules (> albumin size) cannot and stay in the blood 

Molecule movement ○

Dynamics of Capillary Exchange •

Fluid and proteins escape from vascular capillaries ○

Fluid = lymph (not interstitial fluid anymore) 

Excess interstitial fluid collected by lymphatic capillaries ○

This is for maintaining fluid levels and homeostasis 

Returned to the blood ○

Role of Lymphatic System •

○

Function as blood reservoir 

E.g. you need to start running, this is possible □

Blood is diverted from it in times of need 

60% of blood volume at rest is in systemic veins and venules ○

15% of blood volume in arteries and arterioles ○

Blood Distribution •

mL/min 

CO = Volume of blood flowing through a tissue/organ/vessel in a given time ○

Sometimes the stomach gets more blood and sometimes gets less 

Flow to individual organs varies continually ○

CO = HR x SV 

Total blood flow is cardiac output ○

Blood Flow and Cardiac Output •

Pressure (force) exerted by the blood on the walls of a vessel 

Water in the blood exerts the pressure on the walls of the vessels and this is known as blood pressure □

Generated by contraction of the ventricles 

General ○

Pressure falls steadily in systemic circulation with distance from left ventricle 

Slide 13 ○

Blood Pressure •

Farther we get away from the heart and the LV and aorta, our pressure drops. By the time we get to the capillaries its 35 and by the RA its 0.

◊

Mean Arterial BP 

This is the tracing of the blood pressure 

Difference in the peaks and troughs decreases as we get farther away from the LV, and by the time we get to the capillaries there are no peaks/troughs anymore … the wave is non-existent anymore

◊

Systolic/Diastolic BP 

□

If decrease in blood volume is over 10%, BP drops 

Water retention increases blood pressure 



Pulse pressure = Systolic (ventricular contraction) - Diastolic (ventricular relaxation) 

Mean pressure = Average pressure in the system 

Is this the same as mean pressure and mean arterial blood pressure 

= MAP = diastolic BP + 1/3 (systolic BP – diastolic BP) □

E.g. MAP = 80 + 1/3(120 – 80) = 93 mmHg □

MAP 

Blood Pressures - Terminology ○

Average pressure during entire cardiac cycle 

Significance - system is designed to maintain mean ABP 

Any changes in SV and HR therefore can change MABP □

Mean ABP = CO x Total peripheral resistance (TPR) 

MABP ○

Difference in systolic and diastolic 

120-80 = 40 mmHg 

If a person has hypertension, they have increase in systolic pressure which can change pulse pressure 

See what happens is that a small change in systolic/diastolic pressure creates a large change in the pulse pressure 

This is what we are measuring at different pulse points 

Pulse Pressure ○

Give indication on heart rate, strength and perfusion □

Roughly equivalent to heart rate □

Common carotid artery 

Used for patients with peripheral arterial disease □

Radial artery 

Dorsalis pedis artery 

Pulse and Pulse Points ○ Heart rate  Peripheral resistance  Blood volume 

Remember CO is equal to total blood flow 

Pressure = flow x resistance □

Flow = pressure / resistance □

Equations 

Factors Affecting BP ○

Blood is fluid going through vessels in body … resistance in the inside wall of the vessel … it will be a type of drag force … friction is greatest in inner SA?



Smaller radius = more friction = more resistance □

Blood vessel radius 

Thicker blood = more resistance (dependent on the # of blood cells and water content ratio … when youre dehydrated you have m ore viscous blood)

□

Blood viscosity (thickness) 

Longer the blood vessel = more resistance □

Blood vessel length 

Friction between blood and the vessel's walls ○

These vessels after changing their diameter … if they become smaller, they make the resistance greater 

Arterioles control BP by changing diameter ○

Systemic vascular resistance Vascular Resistance

Same as TPR 

Systemic vascular resistance ○

Constriction of veins leads to increase in venous return ○

•

Monitor pressure changes 

Baroreceptor reflexes □

Monitor changes in chem composition in the blood  Chemoreceptor relfexes □ Types  Neural ○ Epinephrine and NE  Types □ ↑ symp stimuation  Explanation □ Short-term   RAA system □

Released from the posterior pituitary 

In response to dehydration / ↓ in blood volume (e.g. hemorrhage)  Causes vasoconstriction  ↑ BP  ADH □

Released by cells in atria 

Cases vasodilation 

Promotes loss of salt/water  ↓ BP  ANP □ Long-term  Hormonal ○

In carotid sinus area and aorta, there are these baro and chemo receptors. 

Signal sent to medulla oblongata 

Message goes down spinal cord and then out where they act on SAN and AVN to alter contraction of the heart, heart rate and so on to regulate change in BP



Parasymp and symp mechanisms in place 

Example 

Receptor Reflexes ○

Regulation of Blood Pressure •

□ Example

Rapid resting heart rate 

Weak, rapid pulse 

Clammy, cool skin 

Sweating 

Diagnosis: hypovolemic shock 

Car accident - Michael ○

Inadequate perfusion □

Cells forced to switch to anaerobic respiration □

Lactic acid builds up □

Cells and tissues become damaged & die □

Shock is failure of cardiovascular system to deliver enough O2 and nutrients 

Definition ○

Remember the goal: Maintain MABP 

Activate RAA system □

Secrete antidiuretic hormone □

Activate sympathetic nervous system □

Release of local vasodilators □

Compensation Mechanisms 

Shock and Homeostasis ○

Effects of Shock •

O2, CO2, nutrients, hormones, heat & waste products 

Transportation ○

pH through the use of buffers 

Heart-absorbing/coolant properties of water in blood plasma □

Variable rate of flow through the skin □

Body temp 

Water content of cells influenced by blood osmotic pressure 

Regulation ○

Blood loss … clotting 

Disease … phagocytic white blood cells, antibodies etc. 

Protection ○

Functions of Blood •

Water, proteins, glucose, hormones, ions, metabolites, etc. □ Albumin  Fibrinogen  Globulins 

Other (e.g. coagulation factors) 

Proteins: □

Plasma … Liquid ECM … 55% of whole blood  Plasma ○ <1% □ Buffy coat □

Leukocytes (WBC) and platelets  45% of whole blood □ Erythrocytes (RBC)  Formed Elements ○

Blood is connective tissue 

Plasma is similar to interstitial fluid but has more protein  Key points ○ Components of Blood • Hemoglobin 

Red cell count 

Hematocrit (packed cell volume without plasma) 

Morphology (shape of cells) 

Increase is indicative of infection □

White cell count  % of dif WBC's □ Differential  Platelets 

Complete Blood Count (CBC) ○

Haematology Blood Tests • Diameter : 7.5um  Thickness: 2 um  Dimensions ○

Greatest surface area to volume ratio of a simple shape □

Biconcave disc 

It has to travel through vessels without being damaged … has to manipulate itself to travel through capillaries which sometimes allow only one cell at a time

□

Strong, flexible membrane 

If the RBC gets damaged, it can't repair itself □

No nucleus 

If the RBC gets damaged, it can't repair itself □

Lack mitochondria; generate ATP anaerobically 

Allows it to bind O2and CO2and NO □

2 beta chans and 2 alpha chains 

-globin is the protein compartment 

One oxygen molecule binds to one iron group … we have 4 iron groups … each hemoglobin molecule can bind to 4 O2molecules ◊

Hemo- is ring like structure that contains iron 

Structure □

Excess carrying capacity → reserve ◊

Never give off all the O2from the blood cells ◊

Hemoglobin-O2 saturation: 97% - lungs, 75% - tissue 

↑ temperature, ↑CO2, ↓ pH (i.e., ↑ acidity) ◊

Causes O2release more readily 

Helps to maintain P02in tissues ◊

Tissue oxygen buffer system  Characteristics □ Hemoglobin  Characteristics ○

Process by which formed elements of blood develop □ Hemopoiesis  Erythropoesis  Production ○ Erythrocytes (RBC's) •

Blood

Pluripotent stem cell → Myeloid stem cell → Proerythroblast → (nucleus ejected): Reticulocyte → (leaves red bone marrow and enters blood stream): RBC (erythrocyte)

 Steps □ Erythropoesis  120 days □

E.g. axial skeleton, ribs, pelvis … in infants is mainly in long bones ◊

Production (in red bone marrow) 

RBC death ◊

Phagocytosis ◊

Recycling of breakdown products ◊ Destruction  Steps □ Life-Span 

Giving blood or high altitudes causes hypoxia □

Change in O2 levels … if there is hypoxic situation where there isnt enough O2 , kidney's kick in … 

Its release also depends on the health of the kidney … diseased kidneys make not be able to produce enough of it □

If it's in vessels that is going to the kidneys, there will be less sensing of the low O2levels 

Atherosclerosis □

Kidney's release erythropoietin 

This causes red bone marrow to release more RBC's 

Results in increase O2 carrying capacity 

○

RBC Production •

Lisa is tired and cold. CBC (complete blood cell count) was ordered ○

Cause: Anemia … decrease in O2 supply 

Decreased red blood cells ○

O2 is needed for ATP and heat production … this naturally makes her tired and cold ○ Case Question • Nucleus  No hemoglobin 

Most live a few hours to days to even years 

Characteristics ○



1) Pluripotent stem cell → Myeloid stem cell → [Eosinophilic meyoblast → Eosinophil] + [Basophilic meyoblast → Basophil] + [Neutrophilic meyoblast → Neutrophil] + [Monoblast→ Monocyte]

□

2) Pluripotent stem cell → Lymphoid stem cell → Lymphoblast→ Lypmphocyte] □

Streams 

Contain granules in their cytoplasm … □

Eosinophil React with acidic dyes Basophil React with basic dyes Neutrophil Mixture

□ Granular 

Doesn’t have granules in its cytoplasm 

Monocyte □

Doesn’t have granules in its cytoplasm  Lymphocyte □ Agranular  Steps ○

Type Percentage Function

Neutrophil 60-70% •Phagocytize bacteria Functions

○

WBC Production •

Neutrophil 60-70% •Phagocytize bacteria Eosinophil 2-4% •Kill parasitic worms

Destroy antigen-antibody complexes •

Inactivate some inflammatory chemicals of allergy •

Basophil 0.5-1% •Releases heparin (anti-coagulant)

Releases histamine and other mediators of inflammation •

Lymphocyte 20-25% •Mount immune response by direct cell attack or via antibodies

Monocyte 3-8% •Phagocytosis (pacman)

Develop into macrophages (large eaters) in tissue •  Disc-shaped  2-4 microns in size  No nucleus 

Short life span (5-9) days 

Characteristics ○

Pluripotent stem cell → Myeloid stem cell → Megakaryoblast → Megakaryocyte → Platelets □

○

Form a platelet plug □

Blood clotting 

Vascular spasm 

Release chemicals that promote … □

Stop blood loss from damaged blood vessels 

Function ○

Platelet (thrombocyte) Production •

Sequence of responses that stops bleeding 

Quick, localized and controlled 

Medial intervention usually required for hemorrhage from larger blood vessels □

Prevents hemorrhage (loss of large amount of blood) from smaller blood vessels 

General ○

Vasoconstriction of the vessels □

Smooth muscle cells can contract, decreasing lumen diameter and we decrease the amount of blood flowing though … idea is to slow the flow of blood as its moving part the area of injury … want a chance for the hemostasis mechanism to kick in

□

1) Vascular spasm 

Endothelial layer is generally non-thrombogenic, but if its damaged the underlying layer is exposed to the blood 

Platelets are attracted to the collagen 

Adhesion □

Help formation of the platelet plug ◊

Initial platelets release ADP, serotonin, and thromboxane A2 (ex.s) 

Serotonin and TA2 help the smooth muscle cells constrict 

Platelets at the site start to elongate and have extensions and grab onto other platelets that come into contact with them ◊

ADP and TA2 help activate other platelets 

Release reaction □

Platelet plug 

A # platelets at the site of injury. 

ADP also helps platelets to become stick … makes the platelets adherent so that the plug is solid 

Aggregation □

2) Platelet plug formation 

Positive feedback cycle □

Coagulation = formation of fibrin threads □

Platelets 

Fibrin 

Usually red blood cells 

Blood Clot Contains … □

Cascade of reactions in which each clotting factor activates the next one in a fixed sequence 

Formation of Fibrin □

Clot in an unbroken vessel 

If a thrombus breaks off … it is known as an embolus 

Note: Thrombus □

3) Blood clotting 

Rapid … occurs within seconds ◊ Characteristics  Extrinsic □ Clotting Pathways 

Mechanisms to Reduce Blood Loss (Steps) ○

Hemostasis •

Happens in the small vessels 

Rapid … occurs within seconds ◊

In intrinsic, the activators are in direct contact with the blood, in extrinsic they are not initially in direct contact with the blood



Named cause have substances that are outside the blood vessel and the cell ◊

◊

Tissue trauma → (Tissue factor) → ______ → (Ca2+₎ →

Activates F10 (in presence of F5 and Ca2+_{) → Prothrombinase} ◊

Steps 

In intrinsic, the activators are in direct contact with the blood, in extrinsic they are not initially in direct contact with the blood ◊

Occurs within minutes ◊

Characteristics 

◊

→ Activates platelets → Platelet phospholipids released 

→ Activates F12 → (in presence of platelet phospholipids + Ca2+_{) → Activates F10 → (in presence of F5 and Ca}2+ _{and platelet} phospholipids) → Prothrombinase



Blood trauma (to the blood vessel e.g. endothelial layer → ◊

Steps  Intrinsic □

→ Fibrinogen (soluble) → Loose fibrin threads (insoluble) ◊



→ Activates F13 → works with the loose fibrin threads and strengthens them, making them stronger ◊

Prothrombinase (Ca2+_{) → Makes prothrombin get cleaved into Thrombin →} 

Common Pathway □

Clot plugs ruptured area of blood vessels □

By retraction you are able to pull the places closer together … this is pretty much the healing process 

Platelets pull on fibrin thread causing clot retraction □

Edges of the damaged blood vessel are pulled together □

Fibroblasts and endothelial cells repair the blood vessel wall □

Clot Retraction and Blood Vessel Repair 

Activated F12 + Tissue plasminogen activator (tPA) → Make inactive Plasminogen which is incorporated into the clot → plasmin (active) → which break down the fibrin and break the clot

□

□

Clot Lysis (Fibrinolysis) 

Preventing/Breaking up Clots 

Asprin  …  Antiplatelet agents □ Heparin  …  Vitamin K antagonists 

Anticoagulants suppresses or prevent blood clotting □

In certain patients that have a certain type of stroke, if this is given within the first few hours it can reverse some of th e damage ◊

Tissue plasminogen activator (tPA) 

… 

Thrombolytics break up clots □

Preventing/Breaking up Clots 

Antigens can promote the production of antibodies … seen as foreign substances □

Red blood cells have antigens on them 

In our plasma we have antibodies  General ○ □ Descriptions 

Donor 'A' to Recipient 'B' □

A antigen is being introduced into blood with an Anti-A antibody. Result could be death 

RBC's could end up clumping  RBC's can rupture  Toxic reaction  Problem □ Compatibility Ex. 

ABO Blood Group System ○

Based on an antigen discovered in the Rhesus monkey □

Rh+ is more common than Rh-

85% of European population 

Rh antigen on RBC surface = Rh+ □

Normally plasma doesn’t contain anti-Rh antibodies □

Antibodies develop only in Rh- blood type and only with exposure to the antigen □ General  Rh- mother □ Fetus that is Rh+ 

At birth there can be leaking of fetal blood across placenta … as such the Rh+ antigens can be introduced to the mum 

First Pregnancy □

Produces anti-Rh antibodies 

Between Pregnancies □

Has Rh+ fetus 

Antibodies in the mum can go into the fetal blood and bind with the RBC's of the fetus 

Second Pregnancies □

Removes fetal blood from mother's system 

Treatment □

Hemolytic Disease of Newborn 

Rh Blood Groups ○

Antigens and Antibodies •

Lymph (fluid)



Lymphatic vessels



Structures/organs containing lymphatic tissue



Red bone marrow



Consists of

○

Drain excess interstitial fluid from tissue spaces and return it to the blood



Transportation of dietary lipids & lipid-soluble vitamins from GI tract



Recognize microbes or abnormal cells

□

Kill directly or secrete antibodies

□

Carry out immune responses



Functions

○

….



Dynamics of Capillary Exchange

○

Fluid and proteins escape from vascular capillaries



Fluid = lymph (not interstitial fluid anymore)



Excess interstitial fluid collected by lymphatic capillaries



This is for maintaining fluid levels and homeostasis



Returned to the blood



Formation of Lymph

○

Opening between the cells … have anchoring filaments that anchor the cells to the surrounding tissue



Get stretching of the openings and we get fluid go into the lymphatic capillaries



Closed at the end



Merge to become larger vessels…



Lymphatic capillaries



Lymphatic Vessels and Circulation

○

Skeletal muscle pump



Respiratory pump



More valves than veins

□

Valves prevent back-flow



Flow of Lymph

○

CCC is the beginning of thoracic duct

□

Picks up lymph fluid from all of the lower body + area behind the ribs + upper part of left body as well

□

Cisterna chyli → Thoracic (left lymphatic) duct



Fluid from the upper right part of the body

□

Right lymphatic duct



Enters the venous system at the junction between the subclavian and the left jugular vein … it will then go into the heart



Lymph Drainage Routes

○

Lymphatic fluid is filtered here



Cervical

□

Axillary

□

Inguinal

□

Location (major)



Tonsils

□

Thymus

□

Largest single lymphatic tissue



Lymphatic area

◊

White pulp



Reservoir for the RBC's

◊

Red pulp



Spleen

□

In the intestinal region



Peyer's patches

□

Location (other)



Lymph Nodes

○

Lymphatic System

•

Lymphatics

Don’t need to send so much blood to lungs as there is no gas exchange there at this point … only send blood there to develop lung •

What is doing the gas exchange is the placenta •

There are two of them to make sure that the blood bypasses the lungs ○

One is between the atria and ventricles … blood from the umbilical vein goes to right atria to right ventricle to normally the pulmonary trunk, but instead we have the foramen

ovalae … this is between the atria

○

Second is between the pulmonary trunk and the aorta … some of the blood from the placenta will be going to right ventricle and then P. trunk, but b/c the pressure there is higher in the P trunk than in the aorta, the blood will go right to the aorta to go right to systemic circuit … ductus arteriosus ?

○ Bypasses/Shuts •

There is large resistance, and therefore there is lots of pressure on the right hand side (of the body) cause the right ventricle is pumping against a closed door ○

In adults, there is higher pressure in the left hand side ○

Pulmonary Circuit •

Blood needs to travel through the ascending aorta, then the thoracic aorta, then the abdominal aorta, then the common iliac, and then the internal ilial, then the paired umbilical arteries

○

When you do ultrasound, want to see 3 things … one large umbilical vein and two smaller umbilical arteries ○

Oxygenation •

Note: The liver is also bypassed through the ductus venousus, such that the oxygenated blood from the placenta gets to the ri ght atrium quickly through the inferior venca cava … also this will now be mixed blood, partly oxygenated and partly deoxygenated

•

Need to have higher pressure on one end of a tube as compared to another to have blood flow in that tube … ○

Heart is there to make the pressure ○

Pressure •

As the tube becomes smaller, resistance increases and therefore need the more and more amounts of pressure to get the same flow of blood through the tube …

○

Resistance is inversely proportional to radius ○

Resistance •

Heart is most concerned with keeping flow ○

Note •

Case Study - Blue Baby

This has something to do with the pulmonary vasculature being stretched (later on in the lecture?) ○

During birth and the first breath, by opening and expanding the lungs you get a huge fall in the pulmonary vascular resistance, causing the pressure in the right side of the heart drops as compared to the left

•

Also, the placenta is lost at birth … it was a low resistance sponge, and therefore its loss results in higher pressures in the left side

•

Normal gestation should be 40 weeks •

Problems are ten days after birth •

Lots of breathing is happening … indicates that the kid is having problems oxygenating the blood

•

Legs being cool means legs are not getting enough blood … and mottled means that it looks like mottled cheese •

White marking in the black are the pulmonary arteries … where blood is going for gas exchange in the lungs … black = air in the lungs

• • Heart is bigger

Apex of heart is lifted •

There is a lot of blood in the pulmonary circuit … what happens is that the plasma goes into the airways … problem with water in the airways is that oxygen doesn’t diffuse well through a watery barrier

Which shunt didn’t close … •

Lack of blood in lower limbs suggests … that there is blood being diverted from the systemic circuit to the pulmonary circuit

•

Note that in the fetal state oxygenated blood comes from the umbilical veins, through the inferior vena cava, into the right atrium, bypass the lungs and the pulmonary trunk by going through the foramen ovalae to the left ventricle … •

The little bit of blood that does make it to the pulmonary trunk is shunted as well to the aorta through the ductus arteriosus …

Echo is to confirm doctors suspicions … that there is a patent (still open) ductus arteriosis

•

Systole - ventricles are contracting, generating pressure in aorta

•

Diastole - just back pressure in aorta •

Will cause heart murmur cause of blood turbulence ○

Open ductus arteriosis •

Like giving ibuprofen … gets rid of relaxant prostaglandins leaving contractatory PG's which will hopefully close the shunt … didn’t work in this case ○

Indomethesin •

To close the shunt ○

Surgical clip •

PDA = open ductus arteriosis •

Start to hear in diatole as well cause over time, resistance in right side keeps dropping (starting from right after birth), and therefore at some point even in diastole the pressure in the aorta will be high enough to push blood to the pulmonary trunk

○ Murmur •