1. distribute nutrients from digestive tract, liver and adipose tissue
2. transport O2 from lungs to entire body and CO2 from tissue to lungs
3. transport metabloic waste products from tissues to excretory systems (kidneys)
4. transport hormones from endocrine glands to targets and provide feedback
5. homeostasis of body temp
6. hemostasis (blood clotting) 

ischemia - caused by inadequate blood flow

- tissues become damaged from lack of O2, nutrients and build up of metabolic waste

- worse than hypoxia

hypoxia - adequate circulation present, but O2 supply reduced 

artereis - blood away from heart at high pressure

veins - blood towards heart at low pressure

• arteries
• arterioles
• capillaries
• venules
• veins 

right side of heart pumps blood to lungs

left side of heart pumps blood to body

pulmonary circulation - flow of blood from herat to lungs to heart

systemic circulation - flow of blood from herat to body to heart 

• deoxygenated blood enters from systemic circulation in from the inferior and superior vena cava, entering the right atria.
• blood is pumped into the right ventricle through the tricuspid valve. 
• blood is pumped from the right ventricle through pulmonary artery through the pulmonary semilunar valve.
• blood enters the  lungs from the pulmonary artery
• blood is oxygenated, and is sent through the pulmonary vein, where it passes through the to the left atrium
• pumped into the left ventricle through the bicuspid (mitral) valve
• blood passes through the aortic semilunar valves and is pumped out through the aorta into systemic circulation

[image]

• the coronary arteries branch off from the aorta and supply oxygenated blood to the wall of the heart
• deoxygenated blood collects in coronary veins.
• coronary veins merge into coronary sinus which drains directly into the right atrium
• blood in the coronary sinus is the only deoxygenated blood that doens't end up in the inferior or superior vena cava 

Diastole - the ventricles are relaxed and blood flows in from the atria which contract

Systole - ventricles contract

- build up of pressure in the ventricles cause AV valves to slam shut

- pressure rapidly increases in ventricles and the semilunar valves are forced open as blood rushes into the aorta/pulmonary artery

- very little blood seeps backwards into ventricle at end of contraction

- semilunar valves shut

[image]

"lub" - produced by closing of AV valves at begining of systole

"dub" - produced by semilunar valves closing at end of systole 

stroke volume - amount of blood pumped with each systole

cardiac output - total amount of blood pumped per min

Heart rate- number of times "lub-dub" cardiac cycle is repeated per min. 

CO = SV x HR

increases stroke volume by:

• filling heart with more blood, thus increasing amount that muscle fibers have to stretch, leading to more forceful contractions 

1. increase total volume of blood in circulation. Done by retaining water through decreasing urination
2. contraction of large veins propel blood towards heart. *valves important here- prevent backwards flow.

what is meant by the statement:

cardiac muscle is a fuctional syncytium.

the cardiac conduction system transmits action potential from artial syncytium to ventricle syncytiums.

depolarization is sent directly thourhg one cells cytoplasm to another through gap junctios. This is an electrical synapse only! There are no chemical synapses between cardiac muscles. 

• both fast sodium channels (aka voltage-gated sodium channels) and slow calcium channels are involved in cardiac muscle action.
• both open in response to threshold voltage

• slow calcium channels allow passage of Ca+ down gradient once threshold voltage met. It stays open longer than fast sodium channels causing membrane deoplarization to last longer. This creates a plateu phase. 

it is the automatic pacemaker of the heart. It transmits action potential through intercalated discs to the rest of the conduction cells in the heart 

phase 4 - self-depolarization

- automatic, slow depolarization caused by sodium leak channels, responsible for rhythmic, automatic excitation

- inward sodium leak brings cell potential to threshold for voltage-gated calcium channels to open

phase 0 - depolarization

-when voltage gated calcium channels open, membrane optential rapildy becomes postivie as calcium flows inwards

phase 3 - repolarization

- caused by closing of calcium channels and opening of K⁺ channels.

- leads to outward flow of K⁺from cell

- results in neg membrane potential

[image]

Phase 0 - depolarization

- action potentials that propagate through intercalated discs stimulate the myocytes to reach the threshold for voltage gated Na+ channels to open

- influx of Na+ causes membrane potential to become positive

Phase 1- initial repolarization

- Na+ channels inactivate and K+ channels open

- efflux of K+ causes slight drop in cell potential 

- increased potential from initial Na+ influx cuases opening of voltage gated Ca2+ channels

Phase 2- plateau phase

- iflux of Ca2+ ions balance K+ efflux ions resulting in equilbrium of the cell membrane potential

Phase 3 - repolarization

- Ca2+ channels close and K+ channels stay open

- K+ continues to leave cell, making cell potential negative

Phase 4- resting membrane potential

- Na+/K+ATPase and slow K+ leak channels reach equilbrium of innward and outward current

- -90mV

 [image]

• Action Potential generated at sinoatrial (SA) node
• spread to atria and causes contraction OR travels down internodal tract to atrioventricular (AV) node
• action potential impulse delayed breifly at AV node
• travels down AV bundle (bundle of His) to either right or left bundle branches
• travels to Purkinje fibers where impulse spreads evenly over ventricles

[image]

Parasympathetic - continually inhibits automic depolarization of SA node

• the vagus nerve (a cranial nerce) causes SA node to release acetylcholine (ACh) which inhibits SA's deoplarization
• vagal tone - contant level of inhibition by vagus nerve

Sympathetic - stimulatory action during "fight or flight"

• causes heart to release norepinephrine
• causes epinephrine release which acts on cardiac muscle cells 

• monitors pressure in heart
• if pressure too high, notifies central nervous system which corrects prob by increasing vagal tone and decreaseing sympathetic input
• if pressure too low, opposite effect 

ΔP = Q x R

ΔP - pressure gradient from arterial to venous system

Q - blood flow

R - peripheral resistance 

Systemic arterial pressure def.

pulse pressure def and how it is measured. 

systemic arterial pressure - "blood pressure"

- force of blood on walls of arteries

pulse pressure - difference between systolic and diastolic pressure

• 120/80 
• 120 - systolic pressure
• 80 - diastolic pressure 

describe local autoregulation.

it is the principal determinant of what?

tissue in need of extra blood flow is able to "request" it itself because when wast builds up, vasodilation occurs. 

principle determinant of coronary blood flow 

• electrolytes
• buffers
• sugars
• blood proteins
• lipoproteins
• CO2
• O2
• metabloic waste products

• Na+
• K+
• Cl-
• Ca+
• Mg+

• albumin - maintenance of oncotic pressure, the osmotic pressure in capillaries due only to plasma proteins
• immunoglobulins - immune system
• fibrinogen - blood clotting (hemostasis)
• lipoproteins - transport lipids in bloodstream

urea - excess nitrogen

bilirubin - excess heme

aka white blood cells

fight infection and dispose of debris

erythropoeitin which is made in the kindey, stimulates RBC production in bone marrow.

Old RBCs are eaten by phagocytes in the spleen and liver

how do RBCs differ from normal cells?

What do they rely on for their ATP synth?

RBCs don't have nucleus or organelles like mitochondria

rely on glycolsis for ATP synth

• ABO blood group - I^A, I^B, i
• Rh (rhesus) blood group
• RR or Rr = expresion of protein on RBC (+)
• rr = absence of protein (-)

• Antibodies to A and B antigens prouced at infancy and cause clumping and destruction of RBCs with incorect antigen
• eg A+ blood creates anti B-antibodies
• antibodies to Rh antigen created after person with Rh- blood exposed to Rh+ blood
• eg hemolytic disease of newborns/erythroblastosis fetalis
• when mother's anti-Rh antibodies cross placental barrier to clump/destory Rh+ baby's blood

• universal recipients - AB+ blood since it does not make antibodies to any blood group antigens
• universal donor - O^- since it has no surface antigens

• amoebid motility - crawling
• chemotaxis - movement by direct chemical stimuli

• plateltes - aggregate at the site of damage to blood vessel walls and form a platelet plug
• when bleeding occurs, the plamsa protein fibrinogen is converted to fibrin by thrombin.
• fibrin, a thread like protein, forms mesh to hold platelets together and forms a scab.

platelets have no nuceli.

they are derived from fragmentation of megakaryocytes (large bone marrow cells) which are derived from the same stem cells that give rise to RBCs and WBCs.

• RBCs have millions of hemoglobin molecules
• each hemoglobin molecule has four polypeptide units
• each subunit has one molecule of heme
• heme contains an iron atom which binds to O2