Physiology (Cardio 2) Flashcards
Overall takeawayes
- Circulatory system exhanges substances between the blood and the tissue
- Blood gives things to tissie and tossie puts waste into blood
- Arterioles control regulate blood flow
- Capilaries regulate exchange
What is the blood composed of
Overall - Plasma + Hemocrit
1. Proteins (Albumin, Globulin, Fibrogin)
- Albumin = most abdinent (comes from the liver)
- Globulin = comes from the immune system
2. Water (Water + ions + nutrients)
3. Hemocrit - cells (RBCs, WBCs, Platlets)
- RBCs = most abduent
- When spin down blood the cells go to the bottom)
Plasma = proteins + water
Garden hose analogy
The pressure the hose delivers to force wtaer out is based on:
1. How much flow
2. How narrow the tuve is
IF squeeze the hole = water goes faster = goes faster as you increase the resistance???
Hemodynamics (Pressure equation)
Pressue of blood vessel = Flow X Resistence
- Flow = pump = heart –> when heart squeezes you get cardiac output
- Resistence = Blood vessels dialating
dP = Flow (q) X resistence (R)
Cardiac output
Cardiac output = flow –> Cardiac output = stroke volume X herat rate
CO – heart squeezes and relaxes
- Squeezes once per second ; squeeze 100 mL –> squeeze 10 times = squeeze 1 mL
Normal cardiac output
Cardiac output is usuallly 4 Liters/minutae
Normal flow = 4 liters/minute
Pumps and circuts in the body
There are two pumps and two circuts in the body
- Heart
- Pulomary
BOTH = dP = flow (flow = Cardiac output) X resistence –> dBP = CO X systemic vascular resistice
- Pressure in lungs = flow X resistnce
AND dbP = Flow X Pulimary vascular resistence –> dBP = Cardiac output X Pulimary vascular resistnce
Cardiac output and systemic vascular resistnce –> lead to blood pressure
Stroke volume
How much volume per stroke
CO = How much volume per stroke X how many strokes
- Heart beats fast = higher Cardiac output
- Heart is good at squeezing = higher cardiac output ; Bad at squeezing = lower cardiac output
BP equation
BP = Cardiac output X resistnce –> dBP = Cardiac output X Systemic vacular resstnce
Cardiac output = deterined by heart squeezing per minute
ALL together stroke vlume, CO, Resistnce, Blood pressure
Stroke volume and Heart rate –> gives cardiac Output
Cardiac output and systemic vascular resistice –> gives Blood pressure
Anatmy of the cardiovascular system (overall)
- Heart
- Pulminary circulation
- Systemic circulation
Heart Pumps
Heart = has two pumps (one on the left and one on the right)
- right = pumps blood to the lungs
- Left = pumps blood to the body
Heart division
Heart = 2 Sides
- Blue = dosxyganted blood going to the lungs
- red = oxygenicated blood going to the body
Image: Right side = red blood –> going to the body –> blood turns to blue because th body uses teh oxygen –> deoxygnated blood goes to the heart –> blood go to the lung to get reoxugented
Pulminary circulation
Pulminary circulation:
- Has blood flow
- has gas exchnage (Exchanges CO2 and O2)
- Uses hemoglobin
See in image in the left side - blood with CO2 goes to the lungs - the CO2 is exchnaged for O2 in the lungs - O2 rich blood goes back to the heart –> blood goes to the body
Systemic Circulation
Oxygeated blood going from the heart to the tissues (red blood goes to the body) –> tissues use the oxygen –> deioxygenated (blue) blood goes back to the heart
What carries oxygen in the blood
Hemoglobin (carrier of has that will be exchnaged)
O2 dissolves in water at low levels –> BUT binds to hemoglobin at higher levels = hemoglobin carries O2
Pulminary Circulation (image 2)
Blue = goes to the lungs –> gets O2 –> now have red blood with O2
Oxygen exchange in the lungs
Overall - O2 exchnage happens in the capilary
O2 enters the aveoli (because have O2 in air???) –> O2 diffuses across averoli and goe sto cells –> Cells go to the body
Systemic Circulation
Uses:
1. Blood flow
2. Oxygenation
3. Hemoglobin
Oxygenated (red) blood goes to the body –> blood goes to the tissues –> tissue puts waste into the blood + O2 is unloaded from the hemaglobin in blood –> blood goes back to the heart
O2 movment overall
O2 is in the air –> O2 goe sinto the lungs –> O2 goes inot the blood –> Blood gives O2 to the peripheral tissue
Blood vessel histology
Blood vessels all have 3 layers:
1. Intima - Single layer of endothelial cells
- Has internal elastic lamina
2. Media - Smooth muscle cells
- Middle layer of vessel wall
- External elastic lamina
- Arteries = have a big media layer ; veins are weeker = have a smaller media layer
3. Adentitia - Smooth muscle cells + connective tissue + ECM
Atery cross histology cross-section
Intima - single layer of endothelial cells on inside
Media - large layer of smoooth muscle
Adventia - on the outside
Circulatory Vasculator
Arteries + capilares + veins –> bring blood to the heart and blood from the heart to the lungs
Arteries function
Arteries send blood to the periphery
Pressure change in different vessels
Biggest drop in systemic pressure is across arterioles
- Blood pressure drops for smaller vessels
- As you go form Aorta –> Arteries –> arterioles = getting smaller vesells BUT capilaries to venuals to veins the vessels get bigger
Capilaries
Capilaries - Thin walled vessels with pores
- Pores = allow for diffusion
Arteries regulate blood flow into the capilaries
Have diffision across capilary (Capilary = where exchange occurs)
- Difusion of water + ions + nutrients (Ex. glucose) + gasses (CO2 and O2) + Small proteins
Capilary structure
Capilaries = connect arteries and veins –> can have an exchnage of substances across capilaries
- Example - put O2 from artery (oxygenated) blood to deoxygenated vein blood
Forces in the Capilaries
- Hydrostatic pressire - pushes fluid out of the capilary (Put water out of the capilary)
- Oncatic pressure - Water going into the capilary
- Water goes up the concetration gradient (Going towards area of high solutes)
As the water leaves the capilary due to hydrostatic pressire - you have an increase in concetration of the protein in the capailary (because les diliuted form the water) –> water goes in towards the region of high portein concetratio (goes into the capilary)
Different forces in different areas of the capilary
Start of the capilary = have hydrostatic pressure = water goes out of the capilary –> end of the capilary have oncatic pressure (water goes in)
Starlings law - fluid movement = k[Pc+Pii] - (Pi + PiC)
Hydristatic vs. Oncotic pressure
Hydrostatic = Tissue Pi and capilary Pc
- Start of the capilary = lost of pressure to get the fluid out
Oncotic = Tissie Pii and Capipary PiC
- End of the capilary = high oncotic pressire –> fluid goes into the capilary
Capilary Functions (Overall)
- Gas Exchnage (Oxygen, CO2, NO)
- Nutrient Exchange (Glucose + Amino Acids)
- Fluid Exchange (Water)
Capilary Functions mechanism Gas exchnage
Gas Exchange:
1. O2 goes into the tossie because it flows down the concetration gradient (High O2 coming from the heart to low O2 going to a vein)
2. Have a lot of CO2 in the tisue (where the dexegnated blood is) = CO2 flows down gradient into the blood
- Get CO2 from blood vessels
Peripheral Arterial disease
Disease where the blood vessels get narrow
Narrow blood vessels = less blood is delivered to the tossie = less )2 and nutrinets go to the tissue + have a build up of waste in the tissue
Venous system
Function - Transports blood from the periphery back to the heart
Starts as venules (Smallest) –> goes to be bigger veins –> veins converge to create the vena cava (biggest)
Most blood = in the venous system - 64% (2/3) of blood is slowly being moved in the veins to the heart
Overall - Oxygenated blood is used in the system –> goes back deoxygenated in the veins
Venous Disease
Veins don’t work –> blodd builds up in leg –> don’t get gas or nutrient xchnage –> tissue breaks down
Lymphatic system
Overall - vascular system in the body that is seperate from blood
- Takes away waste
- vessles that drain interstaial space
- Empty out into venous circulation at the thoracic duct
- Thin-walled vessels
- Sewer system that collects water
Fluid flows out of the blood (flows out of the capilaries) –> fluid goes to the lymphatic system –> vessels come out of thoracic duct go to drain the fluid
What does the lymphatic system collects
Lymphatc = collectx water and waste from the tissue + collects virsues/bacteria/antigens (monitors issues)
Extra fluid in tisue = taken up by the lympathic tissue
Split of lymphatic system
Comes off the venous system –> goe sto large lympathtic vessles –> goes to lymph node
Filariasis
Worm (Wucheria bancrofti) infects people through masquitoes –> worm enters the lympahtic system – blocks the lympatic system
Infects the leg lymphatic system = lymph return is blocked = leg sweels
What determines systemic vascular resistence
Vasculature is constantly regulated by opposing forces of vasoconstriction and vasodilation
- Blood vessles always relac and dilate at the same time (two forces oppse each other)
- If you stop contracting the vessel = the vessl will dilate (because if no contraction then it would be able to dilate)
Regulation of blood flow
3 Systems regulation dilation and contraction:
1. Nueronal - brain contrls blood flow through nuerons
2. Hormonal - Kidney controls blood flow through hromones
3. Local - Arterial control blood flow
ALL three systems are active at the same time
Regulation of blood flow (Sensors)
There are receptors all throughout the body –> repctors sense the blood pressure and prodvide feedback to all of the systems to reponde (Dilate or constrict the area)
Sensors in the body detect BP –> Sensors tel the brain, kidney, and local factors –> nerves, hormons, local factors respond and regulate the heart and blood vessles
Things that regulate blood flow
- Receptors
- Afferent nerves
- Brainstem
- Efferent nerves
- Vascular response
Regulation of blood flow (brain)
Regulation is completed through nuerons –> done through the autonomic nervous system
- Autonomic = involtary (hard to control conciously)
- Driven by nerves going to the body
Uses Sympthetic + Parasympathetic
Regulation of Blood flow Sympathtic vs. parasympathetic
Sympathetc (fight or flight) –> constricts Blood vessels
- Uses Pond/medula + spinal cord + arteries + norepinephrine
- Have Vasomotor center in the brain stem –> sends nuerons to blood vessels and heart
Parasympathetic –> relaxes
- Uses brain + Spinal cord + heart/other ogans + Acetylcholine
- PNS does not innervate vessels
Regulation of blood flow (Barororeceptor)
Brain gets reponse about blood pressure form the sensors in the body –> brain response to sense and controls blood flow
Barrarorecptors = sense BP in body –> Sends signal to the brain
- If Barorector sense high BP –> Brain sends signal to nerve to stop constricting = decrease the BP
Goes form sensors in aortic arch _ coratic + atria + ventricles –> Autonimic nervous system –> signals go to vessels and heart
IMAGE - shows the path of system
Hypertension of Fast Heart rate in ER
If someone has hypertention of Fast heart rate i the ER –> doctors can massage the coroted –> receptors think that the BP is high –> Bararorecpotors will tell the brain to send signals to the nervous system to respond
Chemorecptor regulation of blood flow
Chemorecptors - sense the Oxgen level in blood –> sends message to the brain –> brain sends message to the autonmic system
- Example - if the blood needs more O2 then the brain will signal to breath faster
- Affect = decreases O2 or increases CO2
- Aorta + cortid + medulla (where receptors are?)
- Uses autonimic
- Can cause vasoconstriction = increases the Heart rate + increases reporation = gets more O2
Homonal regulation of blood flow (overall)
Have vasoconstrictors and vasodilators - hormones can increase or decrease BP
Uses teh Kidneys –> Kidneys sense BP
Vasoconctrictors:
1. Adrenal gland (make Epinepheran + cortisol)
2. Kidneys (make renin)
3. Pituitaruy (makde Vassopresing - ADH)
Vasodilators:
1. Tisues (local regulators) - Produce Hypoxia + CO2 + Adenosine + Bradykinin + Histamine + Seratonin
Kidneys sensing Low BP
Major hormones that control BP from kidney = angiotensinoin and aldosterone
Example - if the kidneys sense decrease in BP –> kidney sends hormon Renin –> renin acts on teh angiotensionin(from the liver) –> get angiotensinoin 1 –> ACE acts on angiotensinoin 1 –> get angiotensinoin 2 –> angiotensinoin 1 is a vasoconstrictor = vascoconstrocts
- End = get angiotensinoin 2 = acts on Blood vessles
- rapid responce
Kidney = also induces aldostereone –> aldosterone will induce to kep salt and wtaer + pee less
- Long term effect (slower repsonde)
Affect of brain + kidney
Burrorecptors = doted lines –> go to brain stem –> integrates signals –> sends signals to the heart + blood vessels
Kidney = sense BP = makes renin + andiogenstsin
Local Mediators (Overview)
Every tissue regulates blood flow locally –> produces things to constrict or dilate arteries
- example - if have too much nuertnets –> have atretial vasoconstriction
- if need O2 or Amino acids = have vasodilation (done locally + through brain + through kidney)
Have vasodialtors and vasoconstrictors
Vasodilators - Nitric Oxide
Vasoconstroctors:
1. Peptides - Endothelins + Angiotensin
2. Arachadonic Acid - EDHP + Thromboxane
What leads to vasodlation
Have metabolic demands (Decreased O2 or Increased Co2 or Adenosine) –> leads to vasodilation
NO mechanism
Endotheliam cell = contrls dilation at local level through NO product
- Endothelial cell has eNOS
NO diffuses to the smoothe muscle (diffsuses across the cell layer) –> activated mediater to cause dilation (mediator = cGMP ; smooth muscle has cGMP) –> Get H+ or CO2 or K+ to tissue cell –> get
NO structure
NO is a free radical = very reactive + has a short half life
NO diffuses across cell memebranes
NO reacts with superxides + metals + thiols
NO = gas –> has no protein rceptor
NO synthesis
Synthesized by NO synthetase
Agrinine (Amino acid) + O2 –> Cirtiline (Amino Acod) + NO
Enzyme = Nitric Oxide sythetase - Uses NADPH + FAD + FMN + H4 biopterin
Overall - Rip electron off of NAPHD to create NO
Affect of NO on Vasculator
NO = vasodialtaor (causes the arterial to dialte)
- Endthelial cell disfunction (I THINK if have issue with enodthelial cells = have isue with NO = issue with dialation)
If have a disease in NO = have issue with dialation
NO:
1. Vasodilator
2. Has Antithormotoc activity (affects platlets)
3. Has anti inflamatory activity (affects lymphocytes)
How does NO cause vasodilation
Endothelial cells have NOS = make NO –> NO diffuses to smooth muscle cells –> NO turns on signaling cascade (NO activates gunylate cyclase –> Gunaylate cyclase make cGMP –> get kinase –> have a relaxation of the smooth muscle cell
NO Overall
NO is produces by blood vessels + some drugs
NO Dilates the blood vessels + protects blood vessels from disease
- Loss of NO predisposes to artheroscelrosis
What causes local vasoconstriction
Have metabolic demands –> get Enodthelin + Angiotensi 2 + superoxide + EdHF + Thromboxan –> Get vassoconstriction
Many things that constrict affect vessel dilation –> moleculaes diffuse from the tissue –> hits the vessel –> consticts the vessel
Vascular disease
- Hemerage
- Shock
- Hypertension
- Artherosclrosis
Hemorrage
Overall: Loss of blood
- Heart rate goes up
- Blood pressure goes down
- Have vasoconstriction (causes people to become pale)
IF you lose 10-20% of blood –> body can compensate
- Body senses that you have a decrease in BP and tries to incerase BP
Compensatory mchanism =
1. Barororecotors - sense BP is lowered –> tells the brain –> tells the vessles to constrict (fast resposne)
2. Chemorecotors - Makes angiostenin + holds onto salt and water over time
3. Vasoconstriction
4. Renal mechanisms
Mechanim of loss of Blood Pressure in Hemerage
Less blood in the system = Cardiac outpuc decreases = Blood pressure decreases
- Based on equation BP = Cardiac output X systemic vascular reisstence (CO decreased = BP decreases)
IF have a really low BP (lose >20% of blood) = body can’t compensate = get hypotension = tissues don’t get blood = brain can’t think + muscles can’t constrict
Shock
Hypotension (I THINK can cause shock - list below causes hypotnesion = causes shock)
- Heart attcked = decrease BP
- Issue in brain (autonmic not working) = Decrease BP
- Sepsis = barriocetprois in body don’t work = local system doesn’t work
Inability to profuse tissues
Organ dysfunction (urine + mental)
Differential diagnosis –> Hypovlemia + cardiogenic + nueroggenic + septic
Clincal role of NO
NO = acts as immune effector
- NO kills viruses + bacteria + aytpical bacteria + fungi + Parasites
If have lots of bacteria –> body makes a lot of NO to kill bacteria = get vasodilataion –> if have too much NO then get too much dialation
Sepsis and NO
Sepsis = caused by overproduction of NO –> can lead to hypotension ad death
- get hypotension because NO dilates the blood vessles to much
Have infecation/bateria –> get NO –> dilated vessles too much –> get hypotension
What happens if arteries dilate
Arteries dilate = resistnce decreased = BP decreased
Based on dP equation (dBP = CO X systemic vascular resistence)
Hypertension
When blood pressure is >130/85
- When healthy - brain and kidney keep BP at 120/80 (normal) but sometimes the kdiney increases teh BP to 130/85
- Clasifications = unknown + renal + endocrine
Often due to kidney not working + kidney does not extrecet slay and water at normal blood pressures
BP throughout the day
BP varies throughout the dau (highest 1-5 AM) + varies if excersizing
Normal kidney response vs. hypertension
Noormally when you eat salty food + water –> kidneys see BP and makes les angiostnin + aldronin BUT somtimes the kidneys decide to want a higher BP = release hormones and hold onto more sat and water = keeps high BP
Hypertension mechanism
Normal = hypervolemia –> increase BP –> kidneys sense BP –> Kidneys extretes salt + water == Volume decreases –> BP decrease
During Hypertension –> Kidneys want the avergae BP to be higher –> kidneys sense 120 as low –> kidneys work to incerase the BP by releasing antiostensin + holding onto water = BP rising over the course of years
- Kidney regulates body fluid and blood pressure
- Renin-angiotensi-aldosterone hormeon system is activated = kidney retains excess salt and water
- Have increase CO + release of angiotensin = increase resistence
IF BP is 130/80 = need lifestyle chnage (need t treat because overtime high BP can caus eissues)
Atheroscelorsis
Disease of the arteries - hardening of the arteries
Risk factors - smoking + diabetes + cholestrol + family history
- High cholestrol for a long period of time –> get atheroscelrosis –> get heart attack
When have damage to endothelial lning = cuases issues
- Pathogensis = endothelial damage + inflamation
Inducers - Nicotone + oxidized LDL
Atheroscelorsis + damage to endothelium
High choletral = endothelium will be enflamed –> white blood cells will become adherant to the endothelum –> inflamatories enter the vessel wall to scuh the cholestral out –> have fatty secretion –> have wall off and scarr invades the vessels –> vessels become filled with lipids + smoothers + smooth muscle –> blocks the vessle –> get heart attck or stroke
- have stroke if occurs in brain
Overall - have smooth muscle migration + form cell formation + T-cell activarion + adherance and agregasion of platelets + adgerane and entry of luekocyes = block the vessel
- Can also have macrophage accumilation + formation of necrotic core + fibrous cap formation
Ruptured cap in Atherosckerosis
Have plaque ruptire + thinnning of fiberous cap + hemoerrahe from plaque microvessels
