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Where is the majority of blood found in the circulatory system?
- in the systemic veins (aka body veins, contains venuoles, and small and large veins)
Which vessel is able to expand as they accumulate additional amounts of blood? which vessel cant do this?
- veins can expand to accommodate excess blood --> leads to pooling in the veins
- arteries cant do this, need to keep their shape more to keep pressure high
WHat is the average pressure in the veins? arteries?
- veins = 2 mmHg
- arteries = 100 mmHg
Why do veins have such a low pressure?
- because veins expand when theres a lot of blood in them, so instead of increased blood leading to increased pressure (which would happen if the volume stayed constant), blood pressure stays low
what do veins need help from to bring blood back to the heart from lower limbs?
- since the pressure is so low, veins need the help of skeletal muscles (present around the veins, not in the vein wall) to act as a pump, to bring blood to heart from lower limbs
- as the skeletal muscles contract, they squeeze the vein to propel blood
- youd assume that by squeezing the vein means that the blood goes in either direction, but to prevent this, there are venous valves that ensure only ONE way flow of blood back to the heart
what do veins need help from to bring blood back to the heart from abdominal and thoracic regions?
- the act of breathing + contraction of the diaphragm + pressure in the abdomen from breathing = squeezes the veins to propel blood
- youd assume that by squeezing the vein means that the blood goes in either direction, but to prevent this, there are venous valves that ensure only ONE way flow of blood back to the heart
Veins need the help of skeletal muscle to help them pump blood back to the heart. what do arteries use to help pump blood?
- they have fibres within their own cells that help pump blood
- in the aorta and other larger arteries, there are numerous layers of elastin fibres between the smooth muscle cells of the tunica media (the middle layer in arteries)
- These large elastic arteries expand when the pressure of the blood rises as a result of the ventricle's contraction
- They recoil like a stretched rubber band when the blood pressure falls during relaxation of the ventricles
- The elastic recoil drives blood during the diastolic phase when the heart is resting and not providing pressure
What is elastic recoil?
Describes how the arteries pump blood during the diastolic phase (when the heart is resting and not providing pressure)
Compare elasticity of small vs large arteries
- small arteries and arterioles are less elastic than large arteries and so their diameter only changes slightly during elastic recoil
How many capillaries in the body?
40 billion +
Any cell in the body is at max ______ um away from a capillary
60-80
Vasoconstriction ______ blood flow to the capillary bed, and vasodilation _______ blood flow to the capillary bed
- decreases, increases
How thick are capillaries?
1 cell thick
What 2 things do capillaries lack and how is this advantageous?
- capillaries lack smooth muscle and connective tissue
- makes it easier to exchange materials between blood and tissue
a) it takes _______ mins for blood to circulate all the way around the body
b) heart beats _________ beats in a day
a) 1 min
b) 100000 beats in a day
Do veins or arteries have a bigger lumen?
Veins have a bigger lumen because
1) theyre dealing with less pressure so their walls are less muscular
2) they dont even use their walls for muscular contraction they rely on neighbouring skeletal muscle cells for this
Jean Leonard Marie Poiseuille (19th century physician) said that resistance depends on three major factors. What are they?
- tube/blood vessel length
- viscosity of the blood
- tube/blood vessel radius
What is the formula for flow?
Flow = driving force / resistance
Explain the relationship between decreased vessel radius and flow rate of blood
- decreased radius = increased resistance between RBCs = decreased blood flow
What is blood vessel radius controlled by?
Smooth muscle contraction
a) Describe the relationship between increased blood viscosity and flow rate
b) Describe the relationship between increased hematocrit and flow rate
a) increased viscosity = increased friction between RBCs = increased resistance = decreased flow
b) increased hematocrit = increased interactions between RBCs = increased clots = decreased vessel radius = decreased flow
What is hematocrit?
the ratio between RBCs and the total blood volume
- if high, can cause clot formation
Describe the relationship between increased blood vessel length and flow rate
- increased length = increased friction (theres just more wall there so friction increases) = increased resistance = decreased blood flow
a) what is the only artery in the body that carries deoxygenated blood?
b) what is the only vein in the body that carries oxygenated blood?
a) pulmonary artery
b) pulmonary vein
What is the pharynx?
a muscular passage connecting the nasal cavity with the larynx
What is the larynx? what comes after the larynx?
- larynx contains the 'vocal cords': folds in the tissue lining of the larynx
- After the larynx is where there are 2 separate paths →
• air diverted toward the lungs goes into the trachea
• food toward the stomach goes to the esophagus
What are the 2 zones of the respiratory system?
conducting zone: just the tubes involved (like bronchi, bronchioles etc)
respiratory zone: where the gas exchange occurs
What do alveoli have that allow air to pass between them?
Pores
Name 3 key properties of the lungs
- inspiration and compliance
- expiration and elasticity
- surface tension
What is lung compliance?
the ease with which the lungs can expand under pressure
What is the lung compliance formula?
change in lung volume per change in transpulmonary pressure =
deltaV/deltaP
What does lung disease do to compliance?
Reduces it
Describe what happens when you breathe in
- When you breathe in, your lungs expand, your ribs expand, and your diaphragm contract downwards to create more space this expansion (requires high compliance)
Explain what happens when you breathe out
- when you breath out, your lungs contract, your ribs contract, and your diaphragm relaxes and expands upwards
- tension is released
What helps the lungs be elastic? (which is necessary for breathing to occur)
- elastin proteins increase during inspiration, and help with lung recoiling when you breath out
- tension reduced by elastic recoil during expiration
Why are the lungs said to be always in a state of elastic tension?
- bc theyre attached to the chest wall so they can never recoil/relax completely
what happens if the lungs arent attached to the inner wall of the chest?
they wont be able to inflate
Describe the 2 pleural membranes of the lungs. what do the 2 membranes secrete? where do they secrete this into?
- Parietal pleural membrane attaches outer part to the surface of the lungs to the chest cavity
- Visceral pleural membrane (inner) attaches parietal pleural membrane (outer)
- Produce mucous rich lubricating fluid (pleural fluid) into space between membranes (pleural space, PS, but not really a space, its filled with fluid to allow the 2 membranes to slide past each other without tearing anything, and also holds the two pleural membranes together)
What is surfactant, where is it secreted from, and what purpose does it have
- phospholipids and hydrophobic surfactant proteins, secreted into alveoli by type II alveolar cells
- purpose is to decrease the surface tension of the alveoli to keep them open during expiration (like the stuff in bubble mix)
When is surfactant produced in fetal development? What can happen to premature babies?
- surfactant is produced late in fetal life (bc in the womb babies don't breathe air)
- premature babies are sometimes born with lungs that lack sufficient surfactant and their alveoli are collapsed as a result
What is tidal volume?
volume of gas inspired or expired in an unforced respiratory cycle (~500 mls)
What is inspiratory reserve?
max vol of gas that can be inspired during forced breathing (after and not including a normal breath in)
What is expiratory reserve?
max vol of gas that can be expired during forced breathing (after accounting for tidal volume)
What is residual volume?
vol of gas remaining in lungs after max expiration
What is total lung capacity?
total amount of gas in the lungs after a max inspiration
What is vital capacity?
max amount of gas expired after a max inspiration
What is inspiratory capacity?
max amount of gas that can be expired after a normal tidal expiration (normal breath in + max breath in)
What is functional residual capacity?
amount of gas remaining in the lungs after a normal tidal expiration
What is anatomical dead space/dead volume?
air inside nose, mouth, larynx, trachea, bronchi and bronchioles→ where no gas exchange occurs
- about 150 mls
Describe the structure of Hb and how that relates to its function
- Has 2 beta and 2 alpha chains, and on each of the chains you have a heme group which is where oxygen can bind to
- Heme has Fe 2+ which is uses to hold onto oxygen
Describe O2 and CO2 movement in the lungs
1. Bicarbonate in RBCs is converted into CO2
2. Co2 is brought out of the RBCs, into the alveoli and out of the lungs
3. This changes the blood pH → acidity decreases
4. This increases Hb's affinity for oxygen (oxyHb formation happens in basic conditions) and oxyHb formation occurs
5. oxyHb goes off to the tissues
Describe O2 and CO2 movement in the tissues
1. CO2 gets unloaded from tissue cells to RBCs
2. CO2 gets converted to bicarbonate ion in the RBC
3. This changes the pH of the blood → acidity increases
4. This decreases Hb's affinity for oxygen, so disassociation happens
5. Oxygen is released into the tissues
a) When is Hbs affinity for oxygen increased? Where does this occur
b) when is Hbs affinity for oxygen decreased? where does this occur
a) when the blood pH is basic (bc CO2 is gone). occurs in the lungs
b) when the blood pH is acidic (bc CO2 is in the blood) . occurs in the tissues
Does the presence of CO2 in the blood make the blood more acidic or basic?
Acidic
What 2 things can Hb bind?
O2 and CO2
What is carbonic anhydrase?
- an enzyme present in RBCs that converts CO2 into bicarbonate ion (HCO3-)
- CO2 needs to get converted bc it has low solubility in the blood
What are carbamino compounds?
- CO2 attached to Hb (not converted)
- pretty small amount though, most of CO2 is converted to bicarbonate ion for it to be transferred in the blood
Give the bicarbonate equation
CO2 + H20 --> H2CO3 ----(spontaneous) ----> H+ + HCO3-
Total atmospheric pressure increases by one atm every ______ below sea level. what does this mean for the amount of dissolved gases in the blood at 20 and 30 m (due to the law of partial pressures)
- 10 m
-If a diver goes down 10 m, then the partial pressures and amount of dissolved gasses in their blood plasma will be twice the values at sea level
- At 20 m, they are 3 times the value
- At 30 m, they are 4 times the value
What happens to the human lungs >30 m below sea level?
the human lung would be permanently damage, and shrink from the chest wall
How do free divers go farther than 30m under sea level without dying?
- Mammalian diving reflex
- Drop in heart rate (bradycardia)
- Vasoconstriction in the peripheral areas of the body (blood shuttled away from limbs to benefit heart, lungs, brain)
- Spleen releases RBCs reserve carrying O2
- Blood shift → plasma fills up lung blood vessels
What does SCUBA stand for?
SCUBA stands for self contained underwater breathing apparatus
How do scuba divers avoid O2 toxicity at low depths underwater?
- they take air tanks with a gas mix that is the same as atmospheric air (21% O2, 78% nitrogen, 1% trace gases)
- other gas mixes could be used (eg less nitrogen to prevent nitrogen narcosis or decompression sickness)
What is nitrogen narcosis?
increased nitrogen dissolved in the plasma membranes
What is decompression sickness? How can you treat it?
- N2 gas bubbles in tissues enter the blood and block small blood channels producing pain (the bends) and possibly more serious damage
- happens when scuba divers ascend to the surface too quickly (the high conc. of nitrogen that got into the cells dont have time to diffuse through the alveoli, and cause bubbles instead)
- Primary treatment for N2 gas bubbles is hyperbaric oxygen therapy=
- Normal blood O2 conc. = 0.2 - 0.3 ml O2/100ml
- Treat = Give 100% O2 at 3 ATM pressure, raises plasma concentration to ~6ml O2/100ml (high dose oxygen can get nitrogen out of your tissues)
What is acute mountain sickness?
At 5000 ft...
- Headache - low arterial pressure stimulates vasodilation increasing blood flow and pressure in the skull
- Balanced with Hypocapnia (low CO2 in the blood due to hyperventilation) causes cerebral vasoconstriction
At 9000 ft...
- pulmonary edema (excess fluid in the lungs), shortness of breath
At 10000 ft...
- Cerebral edema (excess fluid in the brain)
Where is the one place that people actually do live at incredibly high altitudes? how are they able to do this?
- the one exception where people live at incredibly high altitudes is El Alto, Bolivia
- they live at 13,615 ft (highest settlement in the world)
- bodies have undergone adaptation to carry more oxygen (eg they have more Hb in their blood to compensate for the fact that theres so little oxygen is in the air, so what every oxygen they can breathe in is going to bind to a Hb)
How thick is the LV? the RV? How much greater is the work performed by the LV than the RV? WHY?
- LV wall is thicker (8-10 mm) vs the RV wall (2-3 mm)
- work performed by LV is much greater (factor of 5-7) than RV
- since the right side (right atria and right ventricles) only pump to the lungs, its thinner than the left side (left atria/ventricles) bc that side pumps blood out to the body
What are the 2 types of AV (atrioventricular) valves?
- tricuspid valve = separates right atrium with right ventricle (has 3 flaps)
- bicuspid valve/mitral valve = separates left atrium with left ventricle (has 2 flaps)
What are the 2 types of semilunar valves?
- aortic valve = between the left ventricle and aorta
- pulmonary valve = between the right ventricle and pulmonary artery
What are septal defects?
Any defect in the heart that causes blood in various heart chambers to mix
Describe steps of the heart mechanism
1. deoxygenated blood from the lower extremity comes in from the inferior vena cava, and deoxygenated blood from the upper extremity comes in from the superior vena cava
2. from the superior and inferior vena cavas, blood goes into the right atrium
3. Right atrium contracts, which increases pressure of the chamber and forces blood through the tricuspid valve and into the right ventricle. As the pressure in the atrium starts to decrease, the tricuspid valve closes again to prevent backflow
4. The right ventricle contracts, increasing pressure within the ventricle chamber, forcing blood through the pulmonary semilunar valve and into the pulmonary arteries. As the pressure in the ventricles starts to decrease, the pulmonary semilunar valve closes again to prevent backflow
5. From pulmonary arteries, the deoxygenated blood goes to the lungs where it gets oxygenated
• note that the pulmonary arteries are the only artery that carries deoxygenated blood
6. From the lungs, oxygenated comes back to the heart through the pulmonary veins
• note that the pulmonary veins are the only vein that carries oxygenated blood
7. From the pulmonary veins → left atrium
8. Left atrium contracts, increasing pressure in that chamber and forcing blood through the bicuspid/mitral valve and into left ventricle. As pressure decreases in the left atria, the mitral valve shuts again to prevent backflow
9. The left ventricle contracts, which increases pressure in the ventricle and forces blood through the aortic semilunar valve, and into aorta. Once the pressure decreases in the ventricle, the aortic semilunar valve shuts to prevent backflow
10. Oxygenated blood leaves the aorta and goes to the tissues
How long after the atria contract do the ventricles contract? (not considering the overlap)
0.1-0.2 s
What is stroke volume?
the amount of ejected blood during systole coming from the ventricles in 1 heart beat (2/3 of total blood in the ventricles)
What is end diastolic volume?
how big the heart can fill at the end of diastole (blood rushes into the ventricles)
What is end systolic volume?
how much blood is left after the ventricles pump blood out during systole
- usually end systolic volume is 1/3 of the end diastolic volume
end diastolic volume - end systolic volume = ?
stroke volume
What is the ratio between end diastolic and end systolic volumes an indicator for?
How well your heart is pumping
What is the formula for cardiac output?
heart rate x stroke volume
a) assuming stroke volume stays the same, what happens to cardiac output when your heart starts beating faster (eg during exercise)?
b) What happens to cardiac output during heart disease (assuming heart rate stays the same)?
a) cardiac output increases
b) cardiac output decreases (bc stroke volume goes down)
Explain the parts of the cardiac cycle
- each cardiac cycle lasts 0.8 seconds
- 0-0.3 seconds = the ventricles contract in systole, and the atria are relaxed
- 0.3 seconds - 0.7 seconds = the ventricles relax in diastole, and the atria are still relaxed
- 0.7-0.8 seconds = the ventricles are relaxed in diastole, but the atria contract in diastole
- so it takes longer for the ventricles to contract in systole than it takes the atria to contract in diastole, and systole lasts the entire contraction of the ventricles (0.3 seconds), while the atria only contract at the end of diastole (diastole lasts 0.5 seconds)
What is the SA node?
- aka sinoatrial node
- functions as pacemaker
- located in the RA, near the opening of the superior vena cava
What is the vagus nerve?
- innervates the SA node
- can adjust HR (so SA node is basically self sufficient to keep heart pumping except when things are out of order (HR is too fast), then vagus nerve can slow down HR)
- note that vagus can only slow down HR not speed it up
Where is the AV node? where is the bundle of His/ AV bundle?
• AV node = located at the junction of all 4 chambers
- bundle of His = a portion of the AV node thats further down the heart than the top of the AV node
What is the intraventricular septum?
- tissue that divides the right and left ventricles
What are purkinje fibres?
- fibres in the intraventricular septum that spread the signal down the ventricles
What are the 3 regions of the heart that can spontaneously generate action potentials?
- SA node
- AV node
- Purkinje fibres
Describe the steps of electrical activity in the heart
1. Impulse starts at SA node and spreads across both atria through gap junctions
2. Goes to AV node
3. Continues through AV bundle (or "bundle of His", a portion of the AV node)
4. Descends down the intraventricular septum (divides right & left ventricles) via the Purkinje fibers in the ventricle wall
5. Spreads from endocardium (inside of the heart) to epicardium (outside the heart) causing both ventricles to contract simultaneously (aka the signal starts in the middle of the heart but spreads to the peripheries)
Describe the timing of electrical activity (speed) in the heart
1. SA node = signal spreads quickly (0.8-1.0 m/s)
2. AV node= signal slows (0.03 - 0.05 m/s)
3. Bundle of His = signal increases again
4. purkinje fibres = signal conduction rate peaks (5 m/s)
What is an ECG?
- measured potential differences of the heart (electrodes are placed on skin)
- note that an ECG is NOT the recording of just 1 action potential, but an amalgamation of all action potentials that occur in the heart
Explain the pattern you see on an ECG
- P wave = spreading of signal across both atria
- PR segment = period of time after both atria depolarize but before the ventricles depolarize (contract)
- QRS wave = spreading through the purkinje fibres, and contraction of ventricles (atria also relax here but you don't see atrial repolarization on an ECG cause its hidden by the QRS wave)
o Aka systole
- ST segment = ventricle walls start to relax, but are still depolarized
- T wave = repolarization of ventricles (diastole starts here)
How do you diagnose a heart attack based on an ECG?
- To diagnose a heart attack, docs look for stemi: ST segment elevation
- occurs when the left ventricle is damaged (like due to a clot during a heart attack), so the segment leading up to repolarization doesn't occur properly
What happens when you hyperstimulate the vagus nerve?
- bradychardia
- the vagus nerve slows down the HR
Bradychardia = _____ bmp (approx)
Tachychardia = ______ bmp (approx)
- 42 bmp and 125 bmp
What is inotropy?
Increased strength in heart contractions
What does increased epi do to the heart? When is it secreted?
- it increases HR and inotropy
- Activation→ times of stress (exercise, HF, hemorrhage, emotional stress, pain)
- Vasoconstriction in systemic arteries and veins
- Low concentration of epi causes vasodilation of muscle and liver vessels
- High concentration of epi causes vasoconstriction of muscle and liver vessels
What does increased norepi do to the heart? when is it secreted?
adrenal medulla is ~20% of catecholamine release, the rest is spillover from sympathetic nerves innervating blood vessels (mostly retaken up by nerves but some goes into general circulation)
- Incr. HR and inotropy
- More transient (impermanent) than epic
• baroreceptors (senses BP) & vagal mediated slowing of HR in response to elevation in arterial pressure
• aka the body can correct a rise in HR due to norepi faster than it can with epi
- Vasoconstriction in systemic arteries and veins
- Overall, increases cardiac output and systemic vascular resistance
• leads to increased arterial BP
What are alpha or beta blockers?
- drugs given to combat high BP
- drugs bind to epi or norepi so that it doesnt bind its alpha/beta receptor
- thus HR slows and BP decreases
- note you can only bind one receptor at a time (blocking both gives too many problems)
How do alpha/beta blockers work?
- e.g. moderate of Epi + alpha-adrenergic blockade = vascular beta-adrenoreceptor unopposed and will lead to large hypotensive (lowering of BP) response due to systemic vasodilation
- aka if you give someone with high Epi levels alpha blockers, the alpha adrenergic receptors will be blocked but not the beta adrenergic receptors
- and if these receptors are blocked, you get vasodilation
When epi binds its beta adrenergic receptor in the adenylate cyclase pathway, what happens after cAMP is activated in the heart?
- cAMP activates PKA
- PKA works to increase contractility of the heart