AP II Unit 1 Flashcards
What is the equation for MAP?
DBP + 1/3(SBP - DBP)
Why is the pressure lower in the pulmonary circuit?
There is less vascular resistance relative to the systemic circuit
What is the ratio of pressure in the pulmonary system relative to the systemic?
1/7, another way to say it is the pressure in the pulmonary circuit is about 1/7th the pressure in the systemic
What is the average pressure outside the L/R atrium?
R = 0
L = 2
Which vessels are least compliant?
Large arteries
What make up the various pressure in an average capillary (include values for the pressures)?
Colloid osmotic pressure (28 keeping fluid in), interstitial fluid colloid pressure (8 pulling fluid out) interstitial fluid pressure (-3 pulling fluid out) and the capillary hydrostatic pressure that changes as you go down the capillary (meaning you start out favoring filtration then eventually switch to reabsorption)
Why is there such a stark difference in velocity for the aorta and vena cava?
The total cross sectional area of the aorta is 4.5 cm sq, and the vena cava is 18 cm sq, due to the higher cross sectional area there are more routes for the blood to take, therefore decreasing velocity
How many capillaries do we have?
10^10, or 10,000,000,000
What are the only venous vessel that do not have valves?
Cranial sinus’s
What maintains our vascular tone?
Norepi released by the SNS
What is the only vessel that does not receive direct SNS innervation?
Capillaries
Which vessels have more SNS innervation, artery or veins?
Veins
How is blood distributed in the body (give numbers)?
Systemic circulation = 84% (64% in the venular system, 13% in the arteries and 7% in the capillaries/arterioles)
Heart = 7%
Pulmonary circulation = 9%
How many CC are in the pulmonary circuit, heart and systemic circulation?
Pulm = 450 cc
Heart = 350 cc
Systemic = 4200
Per lecture, where can the body release an extra store of blood from?
The spleen
What makes up the colloid pressure (give numbers for the pressure added in terms of mmHg)?
Albumin (21.8), globulins 6.0) and fibrinogen (0.2)
Describe the relationship of metabolism to blood flow?
If metabolism goes up, BF goes up, if metabolism goes down, BF goes down. For example: you have increased CO2, a waste product, and this signal the vessels to dilate to increase blood flow
What are the measurement terms for the tricuspid valve?
Point of phlebo-static axis or the iso-gravimetric point
What is the ratio of gravitation mmHg added per unit of distance from the iso-gravimetric point?
1 mmHg per 1.36 cm
What formula are most of our CV biophysics derived from?
Ohm’s law
What governs blood flow?
Resistance (R) and the pressure difference (delta P)
What is the formula to find resistance?
R = delta P / Flow (F)
What is your resistance if conductance is high/low?
High conductance = low resistance
Low conductance = high resistance
Describe Distensibility
This is compliance with the original size of the container taken into account. A small container that grows very large = high distensibility, a small container that grows little = low distensibility.
In a tube, where is flow fastest?
In the middle of the tube
What is the relationship of Reynolds number to turbulence?
The higher Reynolds number, the greater the likelihood of turbulence
What is the relationship of pressure and volume?
As volume increases, pressure increases
What does arteries having low compliance mean if you add volume?
If you add even a small amount of volume there should be a drastic increase in pressure (the walls don’t stretch well to accommodate the extra volume)
Describe the slope of a line describing the pressure/volume relationship
Flat/low slope = high compliance (vein)
Steep/high slope = low compliance (artery)
What is the primary determinant of what our CO is?
Venous return, the heart can only pump out what is returned to it
What is the relationship of compliance to pulse pressure?
High compliance = narrow pulse pressure
Low compliance = wide pulse pressure
What BP changes would you expect with arteriosclerosis?
Higher SBP, lower DBP and wider pulse pressure
In arteriosclerosis, what other change would likely increase DBP?
HTN
Why does DBP tend to decrease if SBP increases?
To keep the MAP as close to 100 as possible, if the SBP increases the kidney’s will respond by decreasing DBP to try and keep the MAP as close to 100 as it can
What is the pulmonary pressure range? Mean pressure?
8 - 25, and 16
What other pressure can the MAP formula (DBP + 1/3 (SBP - DBP) be used on?
Pulmonary artery pressures to find the PA mean pressure
Where do signals from the aortic baroreceptors go?
To the vagus nerve, making it an afferent pathway
Where can you find baroreceptors?
The aortic arch and the bifurcation of the internal/external carotids
Where do signal from the baroreceptors in the bifurcations go?
To Hering’s nerve and then the glossopharyngeal nerve that then go to the vaso-motor center
Describe how baroreceptors work
The work like stretch sensors, if BP increases, the vessel stretches, as it stretches the permeability to Na increases which leads to a greater frequency of AP firing which the brain interprets as an increased BP
What is the equation to predict the electrical change due to BP?
Delta I (change in frequency of APs) / Delta P (change in pressure)
What would happen to MAP if we lost our baroreceptors?
MAP would still be maintained ~100, but there would be greater frequency of deviations from that 100
What are the 4 phases of the pressure volume loop?
I = filling, II = isovolumetric contraction, III = ejection, IV = Isovolumetric relaxation
What starts and ends phase I of the pressure volume loop?
Mitral valve opening then closing
How many CC’s of blood does atrial kick provide?
~ 10cc
What happens in the LV as pressure increases?
The mitral valve closes, then as pressure clears 80 mmHg, the aortic valve opens
What occurs during phase II of the pressure volume loop?
Isovolumetric contraction, meaning the volume of blood is not changing, but the ventricle is squeezing to increase pressure
When does the aortic valve close?
When the pressure in the aorta exceeds the pressure in the LV
What is a normal stroke volume?
70 cc
What is the normal ESV and EDV?
ESV = 50, EDV = 120
If the mitral valve leaks, how does the body compensate to the decrease in CO (some blood leaks back into the atria)?
Increase venous return. More blood coming back to the heart = higher stroke volume to compensate for blood leaking back to the atria. So the higher total volume in the heart should get us back to a SV of ~70cc
Normal range for preload? Normal afterload?
2 - 6 mmHg and 80 mmHg
How do you measure contractility in a pressure volume loop?
By drawing a line from the X-axis to the top left of the loop. The steeper the line the stronger your contractility, the flatter the line, the weaker your contractility
What mediates a change in contractility?
A beta agonist
What is the relationship of RAP to venous return?
The lower the RAP the more venous return (bigger delta P), the higher RAP is, the less venous return
Why is venous return (independent of other compensations) capped at 6 L/min?
Because if the RAP gets too negative it will collapse the large veins feeding into the right atrium
What is the mean systemic filling pressure?
7 mmHg
How does the body increase Psf (systemic filling pressure)?
Squeeze the reservoir of blood, or rather constrict the venous system to increase blood return
How does the body reduce Psf (systemic filling pressure)? What external event could also reduce it?
Vascular relaxation. Another cause would be due to volume loss
At rest what is the max the heart can pump under normal sympathetic stimulation? Maximal sympathetic stimulation?
13 L/min and ~25 L/min
What is the relationship of RAP to CO/SV?
As RAP increases, CO/SV would increase
Why does a small increase in RAP lead to a drastic increase in CO/SV?
The frank starling mechanism, as volume in the heart expands the myocytes better align and stronger cross bridge cycling can occur
What 2 mechanisms increase HR as right atrial stretch increase?
Primary one is the direct atrial stretch reflex (the intrinsic mechanism) and the Bainbridge reflex (extrinsic factor to the heart) occurs due to an increase in CVP (remember, CVP is different from RAP, though the 2 are very similar)
What is the relationship of contractility to RAP if contractility is the only factor being changed?
As contractility increases, RAP decreases (increasing venous return), as contractility decreases, RAP increases (decreasing venous return, helpful if the heart isn’t pumping well)
What innervation is more present/active at the heart?
PNS innervation
What change to CO would you expect with a small change to RAP in a healthy heart?
(keep in mind something else is modifying RAP, usually a result of PSF), a small increase in RAP leads to a drastic increase in CO, and vice versa, a small decrease in RAP leads to a drastic decrease in CO
What change would you expect to RAP with an increase in PSF and no change to contractiltiy?
Massive increase in RAP
What typically drives venous return?
Metabolic needs/waste products
What variable is generally the same/closely related to RVR (resistance to venous return)?
SVR - systemic vascular resistance
What is the primary controller of venous return?
PSF
Relationship of RVR to venous return?
Inverse, the higher RVR the less return due to more of an “impediment” to flow. If RVR is lower there is more return due to a lessening of impediment to flow.
What likely happened to decrease RVR in someone who is vigorously exercising?
Relaxation of the blood vessels; the person is doing a lot of work consuming oxygen and doing work leading to a lot of waste products that need to be wasted and oxygen stores that need to be replenished
What would happen if you gave an arterial specific vasodilator in regards to CO?
SVR decreases -> decrease RVR -> easier to get blood back to the heart, CO increases (assuming contractility is unchanged)
What would happen to CO if you gave a venous specific vasodilator?
CVP and PSF would reduce leading to a reduction in CO
What would likely be the overall change with a mixed vasodilator?
The arterial/venous would fight each other a bit, but overall the venous one would “win” and CO would slightly decrease
What vasodilator would you give to increase CO, venous or arterial?
Arterial
What vasodilator would you give to decrease the workload of the heart?
Venous
What would happen to PSF if you increased compliance? Decrease?
Increase = less tone = decrease in PSF
Decrease = more tone = increase in PSF
What would happen if you gave a mixed arterial/venous constrictor?
The overall effect would be a slight decrease in CO
What is the primary compensation if CO drops?
Constriction of veins = increase in CVP/PSF = greater venous return = (hopefully) increase in CO
If the CO is chronically low, what mechanism will the body enact to try and correct the problem?
Begin retaining volume to compensate for the lack of CO to increase PSF at a cost of increase RAP and therefore more stretch on the heart
Describe the basic trend of what occurs during an MI to try and restore CO
1) drop in CO, 2) first compensation is to increase venous tone via increased SNS outflow to increase CO, 3) begin to retain fluid to decrease SNS outflow 4) retain enough fluid to return CO and SNS outflow to baseline
How can an epidural or spinal decrease CO?
If the anesthetic drifts high enough it can knock out SNS reflexes. More of a risk with intra-thecal administration rather than epidural
What is the drug of choice if BP drops from a spinal? Why?
Neo, because if you have wiped out the SNS reflexes, we have lost venous tone. Meaning this is a filling (PSF) problem not a contractility problem
What would happen to RVR after administration of 3 units of PRBCs?
PSF would increase (more volume) and the walls of the venous system would stretch reducing RVR, both factors would greatly increase CO and venous return (primary change though is still increase in PSF)
What changes would you expect with an AV fistula (assuming other variables remain constant)?
You now have a low resistance path from a high pressure circuit to the low, this would reduce RVR and therefore make it easier for blood to go from arterial to venous circulation. PSF wouldn’t change much (you aren’t changing tone or constriction) but CO should substantially increase because it is easier for blood to return to the heart
What changes to ESV/EDV would you expect if preload increased?
ESV is static, EDV increases and SV increases
What changes to ESV/EDV would you expect if preload decreased?
ESV is static, EDV decreases and SV decreases
What changes to ESV/EDV would you expect if afterload increased?
Increase in ESV, EDV is static and decreased SV
Describe the changes in increased afterload that modify ESV
You need more pressure to overcome the increase in afterload, more time spent in contraction = less time spent in ejection and the aortic valve slams shut earlier due to the reduction in delta P. Combined: less blood leaves the heart in systole = increase in ESV
What changes to ESV/EDV would you expect if afterload decreased?
It is easier for the heart to pump, and it will pump back whatever is returned to it.
Decrease in ESV, static EDV and increased SV
What changes would you expect to ESV/EDV with an increase in contractility?
Reduced ESV, static EDV (overall the heart is pumping out more blood) and increased SV
What changes would you expect to ESV/EDV with a decrease in contractility?
Increased ESV, static EDV, overall decrease to SV
What changes would you expect to the heart with mitral regurgitation?
Massive increase in EDV, moderate increase to ESV, and a massively dilated heart.
When do problems occur in the pressure volume loop of mitral regurgitation, and when does greatest retrograde flow occur?
Through phases II - IV, and greatest flow is during phase III because this is when pressure is greatest in the LV (and also the longest phase), and therefore the greatest delta P between the atria and ventricle
Describe how mitral regurgitation creates a vicious cycle
Blood black flows into the LA, decreasing SV. Heart’s response is to fill the heart with more blood. Heart stretches out, decreasing SV and body responds by filling heart with more blood. Continue until the heart is massively dilated out.
What changes would you expect to the heart with mitral stenosis?
Elevated resistance creates a problem filling. Due to the increase delta P, less blood gets to the LV. This leads to a reduction in EDV, small decrease to ESV and decrease in SV (the entire loop shifts to the left)
How would the body compensate to mitral stenosis?
Increase in PSF, blood volume until SV returns to normal
When would the most retrograde flow occur in aortic valve insufficiency?
During phase I (this is when the aorta is high pressure, but the LV is low pressure giving us a big delta P)
What is a common cause of mitral stenosis?
An auto-immune issue, such as strep or staph infections
What is the only valve with 2 cusps?
Mitral valve
When would the greatest majority of retrograde flow occur in aortic valve insufficiency?
Phase IV (this is when the aorta would have high pressure, and the LV would have low pressure). This leak continues through phase I until pressure begins to build in phase II
What would be a good treatment for aortic valve insufficency?
An afterload reducer, decrease pressure in the aorta = less retrograde flow during phase IV d/t a smaller delta P
What change would you expect to pulse pressure in aortic stenosis?
Pulse pressure would decrease (less blood is getting past, meaning less energy and therefore lower pressure despite the fact that LV pressure is sky high)
What basic vital signs changes are indicative of aortic stenosis?
Increased HR with a narrowed pulse pressure
What happens to coronary perfusion in aortic stenosis?
Less time for coronary perfusion; they can only perfuse when LV pressure drops, and in aortic stenosis the LV pressure is much higher and stays higher for a longer period of time. Add in a fast HR, and there is even less time spent in diastole for the coronaries to perfuse
What variables tend to make aortic stenosis rough on coronary perfusion?
High wall pressure + decreased SV + elevated HR = poor coronary perfusion
What changes to ESV/EDV would you expect in severe CHF?
Massively increased EDV and ESV
What is the afterload reducer of choice in CHF?
ACE/ARB
What is the unit of coronary blood blow per unit of cardiac muscle mass?
70 ml/min per 100 grams of muscle
What is the normal coronary perfusion rate?
225 ml/min
What 2 factors make diastole favorable in terms of pressure to perfuse the coronaries?
LV pressure is low, and the heart has just used up a lot of oxygen and created a lot of waste products producing a beat. In order to get ride of waste products and replenish oxygen the vessels dilate.
So the 2 factors are low LV pressure and dilated coronaries after systole
Why is there a short period of retrograde coronary blood flow?
The pressure from the LV makes the pressure in the coronaries high, briefly making it high enough for blood to flow into the aorta
What are the 2 primary variables in determining coronary perfusion?
Delta P and time for the Delta P to do something
What is the oxygen extraction ratio of the heart? And systemic ratio?
Heart = 75%
Systemic = 25%
What is a downside of the coronary oxygen extraction ratio? Benefit?
Con = there are minimal oxygen reserves because the heart pulls out so much oxygen
Pro = because the ratio is so high, the heart only needs 1/3 of the blood flow relative to the systemic circuit to achieve the same level of oxygenation
What is the normal oxygen content of arterial blood?
1 dL (100 ml) has 20 ml of oxygen
Describe the difference in anatomical ANS innervation of the heart
SNS = widespread all over the heart
PNS = concentrated area via the vagus nerve. R vagus = R atrium, L vagus = goes over the L atrium and rests on the SA node
Where do the sympathetic ganglia that affect the heart originate? When do they stop appearing?
C-spine or cervical part of the cord, they stop showing up by T2
What nerve runs parallel to the heart before spreading out and providing innervation to the diaphragm?
The phrenic nerve
Describe the 3 pericardial layers
The outer fibrous pericardium, the parietal serous pericardium (attached to the fibrous pericardium) and the visceral serous pericardium (attached to the heart)
What valves are on the right side of the heart? Left?
Right = Pulmonic and tricuspid
Left = Aortic and mitral (bicuspid)
What heart valve condition affects 2% of the population?
Bicuspid aortic valve
Describe how the heart anatomy creates conditions to favor blood going into the coronaries not related to pressure/delta P
The cusps of the valves sit in a bowl that helps redirect blood into the coronaries
Describe the basic physiology of what creates a heart murmur
The vibration of the cartilaginous rings
What is the 1st heart sound?
The A/V (mitral and tricuspid) valves closing
What is the 2nd heart sound?
The aortic and pulmonic valves closing
How long are the AV heart sounds? Aortic/Pulmonic?
AV = 0.14 seconds
AP = 0.11 seconds
When does the majority of ejection occur?
The first 1/3 of the ejection phase
When does the bulk of filling occur?
The first 1/3 of diastole
When would you hear the third heart sound?
During the later 2/3 of filling (the heart is full at this point. Sound only occurs in an unhealthy heart, ie CHF)
When does the 4th heart sound occur?
When the atria contract, or the last 1/3 of filling/diastole
What is the range of human hearing?
20 hertz to 20 kilohertz
What is the loudest heart murmur?
Aortic stenosis
When would you hear mitral regurgitation?
When backwards flow would be a problem when the valve is closed, so systole
When would you hear aortic regurgitation?
When backwards flow would be a problem when the valve is closed, so diastole
What is the primary compensation to improve SV in aortic stenosis?
Increase HR
What is the relationship of distance from the RA to CVP?
The further away from the RA you are, the more CVP should increase
What would happen to RAP if the LV was struggling to beat?
Blood would back up into the pulmonary circuit -> backs up into the RV -> which then backs up into the RA increasing RAP
What occurs to CVP during positive pressure ventilation?
The extra pressure collapses the veins, and to compensate the body increases CVP to open them back up again
When would you hear aortic stenosis?
During systole
What pressure changes would you expect with mitral stenosis?
Large increase in LAP, increase in CVP and increase in pulmonary pressure
When would you hear mitral stenosis?
During diastole (filling) and would be loudest at the beginning of diastole
What general concerns would you have with mitral stenosis?
Electrical issues because as the LA dilates it can affect the SA/AV nodes. Elevated LAP increasing pulmonary pressures thereby increasing pressures on the right side of the heart which can’t handle elevated pressures well
What is the only valve problem that does not carry LV dysfunction concerns?
Mitral stenosis
How does MAP change with aortic regurgitation?
Decreases; the valve doesn’t close properly, so instead of MAP staying at 80, it drops down to 50 since the blood can now flow back into the LV
When would you hear aortic regurgitation?
During diastole, loudest at the beginning of diastole
Describe diastasis
The middle 1/3 of diastole, not much is happening here (ventricle is mostly full from the first 1/3 of diastole). If sick, then the filling from diastasis is much more important
When does systole electrically end?
As the t-wave is ending. Of note; the heart is contracting THROUGH the t-wave, only part of the heart has been repolarized as this stage
Why is BP not entirely accurate in estimating CO?
Because CO can drop and compensations can keep BP looking normal. You can lose 1/5 of your blood, CO will now suck, but BP will look ok.
What happens to CVP/venous blood flow during normal negative pressure ventilation?
The negative pressure stretches the veins out, dropping CVP and increasing venous return = increased CO
What happens to CVP/venous blood flow during positive pressure ventilaion?
The positive pressure collapses the veins, increasing CVP and decreasing venous return = decreased CO
What is an example of positive pressure on the heart that is not related to ventilation?
Cardiac tamponade -> increasing positive pressure and therefore reducing CO
What happens to CVP/PAP during inspiration? Expiration?
Inspiration = both decrease
Expiration = both increase and return to baseline
What happens to R/L CO during normal inspiration?
R = RAP decreases but so does the afterload (pulmonary circuit) and the two even out to mildly increase CO
L = LAP has dropped (because PAP or the left atrial filling pressure) but the afterload isn’t affected, so CO mildly decreases
How much should BP decrease during the respiratory cycle?
About 10 mmHg
What does the a-wave represent?
Atrial contraction at the end of diastole
What does the c-wave represent?
The tricuspid valve bulging backwards during ventricular isovolumetric contraction (increasing pressure) ands pushing on the valves during early systole
What does the v-wave represent?
Systolic filling of the atrium, pressure in the atria is building but the mitral valve is still closed
What does the h-wave represent?
Diastolic plateau during mid to late diastole
What does the x-descent represent?
Atrial relaxation, occurs during mid systole
What does the y-descent represent?
The rapid drop in atrial pressure as blood goes into the ventricles, occurs during early diastole
What happens to venous return of RVR increases/decreases?
Increase = decrease in venous return
Decrease = Increase in venous return
What units does the guyton formula for SVR/PVR leave you in? What is the formula?
PRU’s
SVR = MAP - RAP / CO , PVR = MPAP - PAWP / CO
What do you need to remember to do when using guyton resistance formulas?
That CO of L/min needs to be converted into ml/sec
What units does miller’s SVR/PVR formula leave you in?
dyne/sec/cm^5 or mmHg/L/min (they’re synonomous)
What is the miller formula for SVR/PVR?
SVR = (MAP - CVP / CO) x 80
PVR = (MPAP - PAWP / CO) x 80
What is the conversion factor for PRU to CGS?
1 to 1333
Normal CO and SVR?
5 L/min and 1600 dynes/sec/cm^5
Normal PVR?
80, range of 40 - 180
Normal SV/ESV/EDV?
EDV = 120, ESV = 50, SV = 70
Normal arterial/mixed venous oxygen content?
Arterial = 20 ml/dL
Venous = 15 ml/dL
Normal oxygen consumption rate?
250 ml/min
How do you calculate oxygen consumption?
CO x the arterial/venous oxygen content difference (normally 5 ml/dL)
5 L/min (get units to match via dL) x 10 = 50 dL/min
5 ml/dL x 50 dL/min = 250 ml / min
Common cause of over/under dampening on an arterial waveform?
Over = bubbles in the tubing or a clot
Under = too much gain
Where do the coronary arteries received their blood?
The R/L cusps of the aortic valve (R for RCA, L for LCA)
Describe the pathway of the coronary blood returning to venous circulation
Coronaries -> great cardiac vein -> coronary sinus -> IVC -> RA to be re-oxygenated
What branch of the LCA can connect with RCA circulation?
The circumflex artery (not present in all people)
What 2 vessels does the LCA split into?
Circumflex and LAD
What vessel normally branches off the RCA?
The PDA
How often does the PDA branch from the LCA? Why is this a concern?
LCA branch = 15%, RCA branch (normal setup) = 85%. This is a concern because if it branches off the LCA, we are now far more reliant on LCA blood flow, so there is a higher likelihood of something going drastically wrong
Pneumonic to listen for valves?
APe To Man -> Aortic, pulmonic, tricuspid, mitral or APTM (all physicians take money)
What is the difference between our sets of baroreceptors?
Carotids = setpoint of 100 mmHg
Aortic arch = setpoints of 130 -150 mmHg
Why is the difference of setpoints in our baroreceptors advantageous?
If we go beyond the carotid setpoint and are at maximal carotid stimulation, then the aortic baroreceptors can still function and sense the higher pressure
What else is found in the regions of our baroreceptors?
The chemoreceptors (blood gas sensors)
How much dose the direct atrial stretch reflex increase our HR? Bainbridge?
DAS = 10 - 15% increase in HR
Bain = 50 - 60% increase in HR and SV
How does the atrial stretch reflex impact the kidneys?
The increased stretch releases ANP which gets the kidneys to make PGs -> vasodilation of the kidneys -> increases RBF/GFR -> increase UOP to reduce volume and therefore strain on the atria
What happens to the kidneys in response to increased atrial stretch?
SNS tone to the kidneys decrease, which increases perfusion to the kidney which allows it to get rid of more fluid d/t increase in blood flow
What hormonal changes occur in the kidneys in response to increased atrial stretch?
Decreases ANG II, aldosterone and ADH = more UOP
What happens in our veins if they are over-filled?
They stretch out which reduces blood velocity. This reduction in velocity increases the risk of blood clots
What is BNP?
Brain natriuretic peptide. Similar to ANP, it is made by the ventricle when they are overloaded. Causes the same effects as ANP though not quite as useful for the ventricle as ANP is for the atria
General trend of CO/CI in regards to age?
Both decrease as you age and metabolic/activity decrease
2 examples of what can reduce metabolic rate?
Hypothyroidism, loss of limbs
What can increase metabolic rate?
Hyperthyroidism, Beri-Beri, anemia, pulmonary disease, AV shunts, Paget’s disease (bones grow larger and weaker)
How do the deeper endocardial coronaries get perfused?
Because they squeeze longer than epicardial they use up more nutrients/oxygen. Since they burn more, the dilate more than the epicardial, this easier pathway can help encourage blood to travel farther to get to the endocardial vessels
How much blood flow does the thyroid get?
5x its mass
How many arteries feed the thyroid?
4, superior thyroid arteries (branches of the external carotids) x2 and inferiors thyroid arteries (branches of the subclavian arteries) x2
How much thyroid hormone can the thyroid gland store?
2-3 months worth
What do the nodules of the para-thyroid do?
Release PTH to regulate calcium
Describe the anatomy of the laryngeal nerves
The right laryngeal nerve comes down, recurs at the brachiocephalic artery before ascending, the left comes down recurs at the aorta before ascending
What is the “floating bone”?
Hyoid bone
Name T1 - T4
T1 = mono-idod-tyrosine
T2 = di-iodo-tyrosine
T3 = Tri-iodo-thyronine
T4 = thyroxine
What is the predominate and the active versions of thyroid hormone?
Predominate = T4
Active = T3
How does a taste receptor work?
Salt leaks into the cell, making it more excitable and therefore sends an electrical impulse
Describe how iodide gets into the thyroid cell
Co-transporter of iodide and 2 Na go in, then the Na/K pump spits the Na back out
What is the primary oxidizing agent of iodide?
Peroxidase
What stores tyrosine and T3/4?
Thyroglobulin
What releases T3/4 from thyroglobulin? Where does this occur?
Protease’s and lysosomes and in the thyroid (thyroglobulin does NOT transport the hormones in circulation)
What triggers the release of thyroglobulin?
TSH
What is the ratio of T3 to T4?
T4 = 93%
T3 = 7%
What transports T3/T4 in the CV system? List in order of importance
TBG (thyroxine binding globulin), pre-albumin and albumin
What produces TSH?
The pituitary gland, specifically the anterior (hypophysis)
Describe the basic process of stimulating the thyroid
Hypothalamus releases TRH -> binds to the pituitary gland -> releases TSH -> binds to thyroid -> T3/T4 released
What is the basic intracellular effect of T3/4?
Increase transcription -> more proteins being made = increase in metabolism
How does a cell activate T4?
Via iodinase which strips an iodine off, making T3 out of T4
Describe how the thyroid gets bigger
Excessive TSH stimulation = buildup of thyroglobulin
Describe Hashimoto’s disease
The immune system makes antibodies that binds to the thyroid that then signal the body to attack the gland -> hypo-thyroidism
Describe the patho behind Graves
Another auto-immune issue, but this time the anti-bodies mimic TSH causing hyper-thyroidism
Why is radioactive iodine generally a safe treatment?
Because the only place in the body iodine goes to is the thyroid, so the radioactive iodine shouldn’t be uptaken in any other part of the body
What does propylthiouracil (PTU) do?
It inhibits thyroid peroxidase, meaning you knock out the conversion of Iodide into Iodine, makin it a potential treatment for hyperthyroidism
Why is breaking down ATP to adenosine dangerous?
ATP, ADP and AMP are generally “trapped” in the cell, but adenosine can leave the cell. So if the heart breaks AMP down into adenosine, it can leave the heart, and now the heart can no longer produce energy
What is the rate of adenosine production in the heart?
2% of what it needs every 30 minutes
Describe the difference of eccentric and concentric LV failure
Concentric = concentric rings of a tree, severe hypertrophy. It’s a filling problem because the LV is so thick/big
Eccentric = dilated LV failure, so stretched out it can’t pump
Concentric LVH causes?
Aortic valve stenosis, chronic HTN
Eccentric LVH causes?
Aortic/mitral regurg, VSD, systolic dysfunction
Both eccentric and concentric are both technically LV hypertrophy, describe the difference in how the extra sarcomeres are added
Concentric = you stack them on top of each other (making the muscle thicker)
Eccenntric = add them end to end, creating a bigger “space” for blood to come in (dilate out)
What change to preload would you expect with concentric LVH?
A higher preload; the LV is thick and less compliant, meaning you need higher pressure to fill it
In unexplained tachycardia, what are 2 probable causes per lecture?
Elevated thyroid hormone or a heart related pathology
Describe coronary steal
Collateral circulation is in place, you have an MI and the collateral circulation is keeping everything perfused. Heart demand increases, and now the tissue that the progenitor circulation normally perfused pulls blood towards it and there is now less going through the collateral circulation to perfuse the damaged area
What are 2 ways the heart can repair itself?
Angiogenesis and laying down scar tissue via fibroblasts
Why does the heart need to tighten up scar tissue?
If it doesn’t, when the heart tries to contract the scar tissue will bulge out, this causes the heart to waste energy and CO will decrease
What puts you at greater risk for electrical abnormalities, eccentric or concentric LVH?
Eccentric
How much blood volume can you lose but still adequately perfuse?
20%
Describe the 3 phases of shock
Non-progressive = the body can fix itself
Progressive = need intervention or outside help
Decompensated/irreversible = you’re screwed
What is the pressure of no return in shock (once you hit this, you can’t recover)?
45 mmHg
How can shock end up causing septic shock?
Intestines die/slough, bacteria proliferate and spread. They then release endotoxins (myocardial depressant factor) causing septic shock
Per lecture, what 3 factors can quickly cause you to dilate out in shock?
Acidosis, endotoxin and elevated K
How does anesthesia cause a mild form of shock?
You wipe out the SNS drive = reduction in PSF = decrease in blood returning to the heart = drop in CO
What are 2 synthetic treatments to try and pull volume back into circulation?
Dextran - sugar molecule
Hetastarch - a big carb
Both act to mimic oncotic pressure to draw fluid back into the capillaries
If your CO goes from 5 to 20, how much of a percent increase is it?
300% (each increment of 5 is a “double” or 100% increase, so 5+5+5+5 is 3 “doubles” occurring, so 300%)
How can a severe MI turn into a vicious cycle?
Normal SNS response to get CO up is tighten the central veins and retain water. This will keep going if CO is low. If the CO never returns to baseline, then this cycle will keep going until your heart stretches to an extreme point.
What drug class “overrides” the kidneys desire to maintain a map of 100?
Diuretics
What is the relationship of preload to pulse pressure?
Low preload = lots of pulse pressure variation
High preload = less pulse pressure variation
