Exam I Flashcards
What is clearance, and what is it a function of?
Volume of plasma cleared of a certain component per unit time.
Function of how the kidney handles a compound (filterability)
What does clearance of free water (or free water clearance) refer to?
Volume of water removed from the body per unit time.
Is our free water clearance high or low if we have an abundance of ADH?
Low - body holds on to free water.
Is our free water clearance high or low if we have an absence of ADH?
High - lack the ability to hang on to free water in the absence of ADH.
Does free water clearance tell us the quantity of electrolytes removed from the body?
No - free water clearance tells us how much water is removed from the body WITHOUT taking into account electrolytes.
What is a ballpark normal MAP at the beginning of systemic circulation (aorta)?
100mmHg
What is a normal systolic/diastolic BP pressure?
120/80
What is the formula for MAP?
Diastolic BP + 1/3(systolic - diastolic)
i.e.
BP 120/80
80 + 1/3(120-80)
80+1/3(40)
80+13ish = 93mmHg
^Note that this is not a MAP of 100mmHg. 100mmHg is a ballpark, but the formula will give us an accurate MAP.
What is the area of highest resistance in all circulation?
Arterioles
Pressure downstream of arterioles will be ___ due to high resistance at the arterioles.
Low
Pressure upstream from arterioles will be ___ due to high resistance at the arterioles.
High
Within the systemic capillary, what is the pressure at the arteriolar end?
What about the venous end?
What is ΔP?
30mmHg
10mmHg
ΔP = 20mmHg (difference between pressures)
As we move further from the aorta, what happens to the BP? Why?
Lower and lower BP due to moving from areas with high resistance to low resistance.
What is the BP at the start of a venule?
10mmHg
Where is the start of systemic circulation, and what is the BP?
Aorta; 100mmHg
Where is the end of systemic circulation, and what is the BP?
Right atrium; 0mmHg (in a healthy adult).
The normal pressure inside of the right atrium is 0mmHg. How does this change in someone in the ICU with heart failure?
The pressure of the right atrium will likely be elevated.
What is ΔP of systemic circulation in a healthy adult?
100mmHg
Where is the start of pulmonary circulation?
Pulmonary arteries
What is the normal pulmonary arterial pressure (PAP)?
What is another name for this?
16mmHg
Sometimes referred to as mPAP (mean pulmonary arterial pressure).
What is the normal systolic/diastolic pressure of the pulmonary circuit?
25/8 in a healthy adult.
^Note: If we use the formula given for MAP, we won’t get 16mmHg for the mPAP. Daddy said just use 16mmHg for a healthy adult.
Where is the end of the pulmonary circuit?
Left atrium
What is the pressure within the left atrium in a perfectly healthy person?
2mmHg
What is ΔP of the pulmonary circuit?
16mmHg - 2mmHg = 14mmHg
What is pulse pressure?
Difference between systolic and diastolic. (i.e. 120/80 has a pulse pressure of 40mmHg)
Ideal pulse pressure is 40mmHg.
Is pulse pressure greater in the arteries or the veins? Why?
Arteries. Arteries are more stiff, so they have more change in pressure when volume is introduced vs. veins stretch out and accommodate extra fluid.
Is pulse pressure greater in the aorta or the large arteries? Why?
The large arteries have a slightly greater pulse pressure than the aorta. This is because the large arteries are much less stretchy than the aorta. (fluid fed into a stiff container will have a greater pressure variance).
When it comes to stretchiness, how does the aorta work through the cardiac cycle?
The aorta is pretty stretchy if it’s healthy.
Systole - walls of the aorta are stretched.
Diastole - walls come closer together and act like a second heart pump, which helps pump blood downstream during diastole.
If someone had severe arterial stenosis, what would their pulse pressure be like and why?
They would have a very wide pulse pressure. Systolic would be very high, and diastolic pressures would be very low.
When fluid is put into a container with no give, it takes a lot of pressure which elevates systolic pressure.
When fluid is not being put into a stiff container, the pressures are very low.
If someone is given 1L of fluid, does it impact pressure within the veins?
Not really.. veins are very stretchy and accommodate lots of extra blood/fluid. Veins don’t really have a pulse pressure.
How does stroke volume (SV) impact pulse pressure?
Tight walls + High SV = wide pulse pressure.
In general, increasing SV increases pulse pressure, vice versa.
Why does the pulmonary circuit have a low pulse pressure?
Number 1 reason for low pulmonary pressure is that the vascular resistance is low.
What term are we using this semester for stretchiness, and where does it apply?
Compliance.
Can use the term in blood vessels within the heart and lungs, as well as the airway.
What is compliance? What is the formula?
Some change in volume over change in pressure.
(ΔV/ΔP) = Compliance
If a container doesn’t have much give, lots of pressure is needed to fill said container. Does this container have high or low compliance?
Low
If the volume is small and pressure is high, the container will have ___ compliance.
Low
If the volume is high, and the pressure is low, the container will have ____ compliance.
High
In the equation ΔV/ΔP, what does a high number mean? How about a low number?
High number = more compliant
Low number = less compliant
Within the CV system, what is the unit of pressure we use?
mmHg
Within the pulmonary system (airway), what is the unit of pressure that we use?
cmH20
How do you solve for vascular resistance?
ΔP/F
ΔP is the change in pressure
F is blood flow
example:
(100-0mmHg)/(5L/min) = vascular resistance, or SVR if we use a conversion factor
What is a normal SVR?
Between 800-1600 (he didn’t say units, may or may not need this, it was in passing)
What must venous return equal?
Cardiac output
Does a block in perfusion have to do more with cardiac output, or venous return?
Venous return
Can’t pump what isn’t there
What has a wider pulse pressure - left ventricle, or aorta?
Left ventricle.
Diastolic pressure of the left ventricle is low. What does this permit?
Filling
Systolic pressures of the left ventricle are high. What does the permit?
Pressure slightly exceeds aortic pressure. This allows blood to flow into the aorta during systole.
Which has a wider pulse pressure - the right ventricle, or the pulmonary artery?
Right ventricle - allows for the same mechanics as the left ventricle/aorta.
What is the peak systolic pressure within the right ventricle?
25mmHg
Arterioles have ____ walls and ____ openings. Why?
Thick walls with small openings.
This is due to high resistance from vascular smooth muscle within the arterioles.
Veins are more compliant than arteries. Why?
Wider internal diameter, stretchy, accommodates lots of volume.
There is a small smooth muscle layer, but much thinner than what is seen in arterioles.
Capillaries have ___ walls.
Thin
What is continuous with the chambers of the heart, and all blood vessels within circulation?
Thin endothelial cells that make up capillaries.
The aorta has a ___ opening, and ____ wall.
Wide opening; thick wall
Is the aorta stretchy? When might it not be?
In a healthy adult, yes.
As we age, the aorta becomes less stretchy and more rigid.
A person with a rigid aorta will have a ____ pulse pressure.
Wider
What is a normal cardiac output for a healthy adult, and where does it flow?
5L/min
Flows through the entire system.. aorta, capillaries, vena cava, etc. All areas get 5L/min output.
What is the formula for cardiac output?
CO = SV x HR
What is a normal heart rate (HR)?
72BPM
What is a normal Stroke Volume (SV)?
70mL
What is blood flow (velocity) determined by?
Cross sectional area
i.e., we have one aorta, but have two vena cava.. thus a larger cross sectional area in the vena cava, resulting in a slower blood flow/velocity within the vena cava.
What is the formula for velocity of blood? What do the symbols stand for?
V = F/A
V = velocity
F = flow
A = cross sectional area
An increase in cardiac output will do what to velocity of flow?
Increase velocity
A reduction of cross sectional area will do what to velocity of flow?
Increase velocity
Where in the capillary is filtration preferred?
Arterial end
Where in the capillary is reabsorption preferred?
Venous end
How do nutrients move through capillaries?
Capillaries generally are permeable to electrolytes, glucose, nutrients, gasses etc.
Fluid that is not reabsorbed by the venous side of a capillary is reabsorbed by what?
The lymphatic system.
How far below a pressure source will the pressure be 1mmHg higher?
13.6mm
Why does pressure increase as you go below a pressure source?
Blood and water are heavy in a column.
If a column of water is 13.6mm tall, what will be the pressure at the bottom?
1mmHg
What is the Isogravimetric point? Where is it?
It is the point in the body that there is no effect on pressure from gravity.
It is located in the middle of the tricuspid valve.
What name did we give the Isogravimetric point while we worked bedside?
Phlebostatic axis
In a standing adult, how much higher will the pressure be at the umbilicus compared to the Isogravimetric point?
+22mmHg
If an adult is standing, but not moving around.. what would the venous pressure be in the large foot veins compared to the isogravimetric point?
+90mmHg
Will pressure be higher or lower if measured above the isogravimetric point while standing?
Lower
Why is the pressure in the sagittal sinus subatmospheric (negative) when standing?
Is this a concern if exposed to open air? Why?
These vessels are rigid, have meninges/connective tissue supporting them. They are not very compliant.
Yes; if exposed to open air, air would be sucked into the CV system and cause an air embolism.
The neck veins are 0mmHg in pressure, even when measured above the isogravimetric point. Why aren’t they below 0mmHg?
If they were below 0mmHg, they would collapse. They are very wide, and also very thin walled. They are very compliant.
There is a column of blood within the veins that run from the upper arm to the vena cava. This results in a pressure difference of what? Why is this important?
+6-8mmHg in the upper arms both in the veins and arteries while standing.
Important because sitting BP in the arm will be slightly higher than true BP.
What is the pressure in the large foot veins as compared to the isogravimetric point while supine (recumbent)?
0mmHg - no gravity effects in a supine patient, no pressure difference
How do the veins combat retrograde blood flow?
One way valves; act as shelves to limit effect of gravity on pressure.
Skeletal muscle contraction also helps move blood to the heart.
As we age, what happens to our venous valves? What does this result in, and what is the risk?
They wear down and don’t function properly over time. This results in varicose veins, which is mostly aesthetic. However, it can increase the risk of blood clots.
What is another name for supine? (other than flat)
Recumbent
If someone is in a recumbent position, what is the effect of gravity on their veins?
Not very much effect - will see normal pressures. (i.e. foot would not be +90mmHg from isogravimetric point)
What do we rely on to keep veins narrow enough to allow valves to work?
Compression, AKA skeletal muscle contraction
What effect does gravity have on arterial pressure in a standing position?
There are no valves in arteries, so the pressure of a given artery is the following:
Pressure of what is coming from the heart + effects from gravity = significantly elevated BP
i.e., in the foot there would be 100mmHg + 90mmHg = 190mmHg pressure.
If you stand still and do nothing, what happens to cardiac output? Why?
There is a decrease in cardiac output due to less venous return. Blood pools in the legs.
If you strap some poor bloke to a piece of plywood, paralyze them, and move the plywood around and different angles, what would happen to the person?
They would quickly pass out because there is no muscle activity to move the blood around. This is what happens in surgery.
What is the formula for vascular compliance? Aside from the circulatory system, where can this formula be used?
ΔV/ΔP
Lungs
What is the difference between compliance and distensibility?
Distensibility takes into account the original volume of a container.
A large container that does not accept volume easily (i.e., uses a lot of pressure to get fluid in it) is said to have ___ distensibility.
Low
If something is distensible, it is said to be _____.
Expandable
If something has a small start volume with a high compliance, it is said to have ____ distensibility.
High
What is resistance?
Descriptor of how difficult it is to move something from one point to another.
What is inverse to conductance?
Resistance
All blood vessels control blood flow due to changes of what?
Tissue metabolism to replenish what is being used by the cells.
Resistance is changed, this impacts flow. Resistance is the single most important variable.
Changes in resistance occur as vessels constrict and relax. This changes diameter, which helps determine flow. What is the formula for this?
F = (πΔPr4)/(8n1)
Note: the 4 is supposed to be an exponent but I can’t type it.
Therefore, resistance and flow are related to diameter to the 4th power.
A small change in diameter of a vessel has what change on resistance?
A huge change
What is the formula for ohms law, and what does it stand for?
V=IR
Voltage = current x resistance
What is the formula for ohms law, but for the CV system? What does it stand for?
ΔP = F x R
Change in pressure = Blood flow x Vascular resistance
If there is a larger ΔP, there is ____ opportunity for blood flow.
More
The ____ system has much higher pressure, but much less volume.
Arterial
The _____ system has much lower pressure, but much more volume.
Venous
In an artery, if you add a little volume what happens to pressure?
It goes way up (less compliant).
In a vein, if you add a lot of volume, what happens to pressure?
It hardly goes up at all (more compliant).
In a graph with volume on the X axis, and pressure on the Y axis, what would a horizontal line (or low slope) represent?
Venous system; highly compliant
In a graph with volume on the X axis, and pressure on the Y axis, what would a vertical line (or high slope) represent?
Arterial system; lower compliance
In the arterial system, ____ is more likely to change. In the venous system, ____ is more likely to change.
Pressure; Volume
Someone with sympathetic inhibition with the normal amount of arterial volume will have a ____ pressure. Why?
Significantly lower; Arterial pressure is highly dependent on SNS tone.
Venous pressure also drops with sympathetic inhibition.
Someone with sympathetic stimulation with a normal amount of blood in the arterial system will have a ____ blood pressure.
Sky high
With sympathetic stimulation, venous pressure rises slightly. What can the body do with this?
Use expanded venous pressure to help return blood to the heart, which then gets pumped by the heart and can help raise pressure.
What is Reynolds number? & what does it indicate?
Hypothetical number (No units)
when above 2000 it indicates there is going to be turbulent flow
What is the formula for Reynolds number?
(V x D x P) / n
What does V stand for in Reynolds formula & what happens when it is increased?
V = velocity
increased velocity increases the risk for turbulent flow
What does D stand for in Reynolds formula & what happens when it is increased?
D = diameter
increased diameter increases the risk for turbulent flow
What does P stand for in Reynolds formula? & what happens when it is increased?
P = density
increased density increases the risk for turbulent flow
Which vessels are at greatest risk for turbulent flow?
Aorta & large arteries
Why do we rarely see turbulent flow in the venous system?
Velocity is so slow
What occurs during the first phase of the cardiac cycle?
Filling phase – most filling is passive
The volume remaining after the previous cardiac cycle is referred to as?
End Systolic Volume (ESV)
What is the normal ESV?
50 mL
The last portion of filling during phase 1 is aided by what?
Atrial contraction
In a healthy heart, about how much ventricular filling is aided in by atria contraction?
10 mL
In a sick heart, about how much ventricular filling is aided by the atrial contraction?
25% or greater
Why is the atrial kick important in a sick heart vs a healthy heart?
The ventricle has difficulty filling and relies on atrial contraction forcing the blood into the ventricle while a healthy heart has no issue filling passively
What occurs during the second phase of the cardiac cycle?
The heart begins to contract, pressure in the ventricle begins to increase enough to close mitral valve but not enough to over come aortic valve –> both mitral & aortic valve are closed at this point
The volume at the end of filling is known as?
End diastolic volume (EDV)
What is a normal EDV?
120mL
During phase 2, since both Aortic & Mitral valve are closed, the ventricle volume does not change, this is referred to as?
Isovolumetric Contraction
What occurs during the 3rd phase of the cardiac cycle?
Ventricular contraction – pressure in the ventricle exceeds the pressure in the aorta & ejection occurs
How is stroke volume (SV) calculated?
The difference between the ventricular volume at the end of diastole & the end of systole
EDV - ESV = SV
What is a normal SV?
120 - 50 = 70mL
Normal SV = 70 mL
What marks the end of phase 3 & the beginning of phase 4?
The aortic valve closing due to pressure in the ventricle being lower than the pressure in the aorta
During phase 4 both the Mitral & Aortic valve remain closed & volume in the ventricle does not change, this is referred to as?
Isovolumetric Relaxation
Why does the Mitral valve remain closed during phase 4?
The pressure in the ventricle is still too high post systole
What must occur for the mitral valve to open & mark the end of phase 4?
The pressure in the ventricle must be lower than the pressure in the atria – normal left atrial pressure is 2mmHg – left ventricle must have a pressure lower than 2mmHg
The pressure generated during peak systole is how much normally?
120mmHg
The pressure at which marks the diastolic pressure where the aortic valve opens is how much normally?
80mmHg
What valve is in the center of the heart (roughly)? What is another name for this point?
Tricuspid valve.
Isogravimetric point.
What does the Carl J Wiggers diagram depict?
Relationship between valves, ventricular pressure, atrial pressure, chamber volumes, electrical activity, and sounds of the heart.
Be able to draw this for the test.
When right atrial pressure is 0 mmHg, what is cardiac output?
5L/min
What is cardiac output tied to?
Venous return
What is the normal right atrial pressure?
0 mmHg
If RA pressure is higher than 0 mmHg, what happens to venous return?
Venous return is reduced (which would then reduce CO without other changes).
What pressure is the Mean Systemic Filling Pressure (PSF)?
7 mmHg
What happens to venous return when RA pressure is sub atmospheric? (below 0 mmHg). Is this always the case?
Larger ΔP, resulting in increased venous return.
No - RA pressure -4 mmHg through 0mm Hg is considered the transitional zone. The lower pressure becomes in this range, the higher venous return. Anything below -4 mmHg results in a plateau of venous return at 6L/min. Large veins can collapse from being in a vacuum as well.
What is flow dependent on?
ΔP
ΔP = Average pressure in CV system - right atrial pressure (which is the end of the CV system)
What is another name for the average pressure within the CV system?
Mean Systemic filling pressure (PSF)
How is the average pressure in the CV system calculated?
Sum/average of all blood vessel pressures within the CV system.
What contributes more to mean systemic filling pressure (PSF) - veins or arteries? Why?
Veins - while they have low pressure, they have significantly more volume than arteries.
What is ΔP of the CV system?
Beginning of the CV system - end of CV system
OR
mean systemic filling pressure (PSF) - RA pressure (CVP)
OR
7 mmHg - 0 mmHg = 7mmhg
Normal ΔP of a healthy CV system is 7 mmHg
If the heart was paused and all blood was left to settle wherever it wanted to within the CV system, what would the pressure be?
7 mmHg - this is also the mean systemic filling pressure (PSF).
What happens if ΔP of the CV system is increased (i.e., RA pressure increased)?
Harder for filling
What exactly changes mean systemic filling pressure (PSF)? What is most effective?
Tightening up veins/arteries.
Contracting systemic veins - hold most of our volume.
If the SNS contracts the veins just a little bit, what happens to pressure? Why?
Significant increase in pressure due to large volume of veins + arteries are relatively stiff but receive venous volume. This results in a large pressure increase.
What is resistance to venous return?
Describes how easy it is for the blood to get back to the heart.
Why do we need synthetic catecholamines while under general anesthesia?
SNS is knocked out - this results in lack of venous squeeze, which returns a large portion of blood to the veins. In doing so, pressure drops within the arteries significantly.
In a static patient (nothing changing), CO is maxed at about 6L/min assuming -4 mmHg RA pressure.
In regard to resistance to venous return, what happens to cardiac output if the resistance is considered easy?
Lower resistance to venous return, which increases venous return higher than the max of 6L/min, therefore allowing for an increase in CO.
In a static patient (nothing changing), CO is maxed at about 6L/min assuming -4 mmHg RA pressure.
In regard to resistance to venous return, what happens to cardiac output if the resistance is considered hard?
Higher resistance to venous return, resulting in less venous return. This further results in a decrease of cardiac output.
Maybe there is an obstruction.
As mean systemic filling pressure (PSF) increases, what happens to ΔP? What happens as a result?
ΔP increases, resulting in higher venous return. This increases cardiac output.
If normal ΔP is 7 mmHg, but was doubled to 14 mmHg, what happens to venous return/cardiac output?
It is also doubled.
If ΔP was halved from 7 mmHg to 3.5 mmHg, what happens to venous return/cardiac output?
It is also halved.
RA pressure is closely correlated to what?
CVP (central venous pressure)
Note: If measured close to the right atrium, they will be more or less the same. If measured far from the right atrium (like in a central line port), the CVP would be significantly higher than the RA pressure.
What two main things affect filling pressures?
- Blood volume
- Venous tone (remember, veins are a large container.. a change of resistance here can result in a large increase of volume in the arteries, which are a rigid container. This results in a large arterial pressure increase for a small resistance change in the veins).
What happens to intrathoracic pressure as PEEP is increased? What is the result of this? How can it be overcome?
Intrathoracic pressure is increased.
If nothing is changed, this results in decreased venous return due to collapsed veins, which then decreases cardiac output.
^ squeeze veins in increase internal pressure or add volume to the patient to overcome this
PEEP increases intrathoracic pressure, which decreases venous return. Which side of the heart does it decrease return to?
Both, left and right
What two things does cardiac output depend on?
Condition of circulatory system (venous return)
The heart (pumping function)
On the venous return curve graph, what does the point where cardiac function and venous return meet represent?
Cardiac output/venous return
What happens to cardiac output if:
Filling pressure (venous return) is increased without increasing cardiac function?
Moderate increase in cardiac output.
i.e. if RA pressure was 2 mmHg, CO would be 13L/min.
What happens to cardiac output if:
Strong stimulation of heart with unchanged venous return?
CO would go up a very small amount
What happens to cardiac output if:
Cardiac function and venous return were both increased?
Much higher cardiac output
If you had a RA pressure of 4 mmHg with normal sympathetic stimulation, what would your cardiac output be?
13L/min
If you take away the SNS and apply a strong PNS stimulus to the heart, what happens?
Pumping effectiveness is reduced. While there would be an increase in CO with increased RA pressure, it wouldn’t be nearly as high of a cardiac output as with normal sympathetic stimulation due to the lack of cardiac function.
What is the frank starling mechanism?
Ventricular walls in a normal heart are a little under stretched.
Increasing filling pressure stretches (within reason) and better aligns cross bridges, allowing for better pumping.
What are the three things that govern how we get augmented cardiac output when filling pressures increase?
1 - Frank starling mechanism
2 - Direct atrial stretch
3 - Bainbridge reflex
What is direct atrial stretch, and what does it do?
Property of the conduction system of the heart that does not require any other input from anywhere else in the body.
When atria are stretched, HR increases by 10-15% of normal.
Contractility is also increased, but daddy says focus on HR.
This allows for accommodation of extra venous return, resulting in increased cardiac output.
What is the Bainbridge reflex?
When atrial stretch is sensed by the heart, it sends afferent signals to the brainstem, which then increases the sympathetic output of the cardiac SNS nerves and decreases PNS output. This results in an increase in HR by 40-50%.
Requires signal to be sent to brainstem unlike direct atrial stretch which works purely from the heart.
What nerve is the afferent/efferent parts of the Bainbridge reflex carried by?
Vagus nerve
What level does the phrenic nerve come off of? What does it control?
c3-c5; Diaphragm
What is the sensory component of the Bainbridge reflex?
Vagus nerve
What level does the pudendal nerve come off of? What does it control?
S2-S4; Urination and defecation, can cause incontinence with prostate surgeries due to accidental snipping
In regard to the magnitude of HR change, which is greater: Direct atrial stretching, or Bainbridge reflex?
Bainbridge reflex (40-50% increase in HR)
What is the max cardiac output with maximum sympathetic stimulation in someone who does not train?
23L-25L/min
The Bainbridge reflex has a twofold component from the brainstem. What are the components?
Increased SNS outflow
Decreased vagal tone (decreased PNS output)
Why does someone with maximal sympathetic stimulation have a lower RA pressure (CVP) than someone with normal sympathetic stimulation?
The heart is pumping hard at an increased rate, this decreases RA pressure which increases ΔP (mean systemic filling pressure [PSF]) and helps increase venous return/cardiac output.
Reminder: PSF = average CV pressure - RA pressure
OR
7 mmHg - 0 mmHg
Why does someone with a strong PNS response have a higher CVP than someone with normal SNS stimulation?
HR is slower, less pumping action, pressures are higher. This decreases ΔP (mean systemic filling pressure [PSF]) which decreases venous return/cardiac output.
Reminder: PSF = average CV pressure - RA pressure
OR
7 mmHg - 0 mmHg
In someone with heart failure, what might their cardiac output curve look like? What are the implications of this?
Normal is sigmoid shaped.
15 degree line roughly as drawn in class.
A significantly high CVP would be needed to meet 5L/min. This may need to be done artificially (i.e. meds) to maintain life.
Depolarization on an EKG will be seen before there is actual pressure changes in the heart, why is there a delay?
It takes time for calcium to bind & the entire process to occur, so we see a delay between electrical changes & physical changes
During diastole pressure in the ventricle is?
Low
During systole pressure in the ventricle is?
High
When does diastole start?
When the aortic valve closes at the beginning of phase 4 or at the end of phase 3
When does systole start?
At the end of phase 1 at the EDV
The spike in ventricular pressure near the end of diastole is caused by what?
The contraction of the atria
There is essentially 3 parts of phase 1, which part does filling occur most in during phase 1?
The first 1/3 of phase is when most of the filling takes place
Why does the first 1/3 of phase 1 have the most filling?
The blood is built up behind the atria & once the AV valve opens blood floods into the ventricle
What happens during the 2/3 of phase 1?
Not much filling occurs as most of the blood was filled into the ventricle during the initial part of phase 1
What occurs during the 3/3 of phase 1?
The ventricle gets a little bit of extra filling from atrial contraction
If the mitral valve is stenotic, how might this affect CO? What happens if the patient were to become tachycardic?
A stenotic mitral valve would lead to slower filling from the atria to the ventricle, if the patient were to become tachycardic cardiac output may drop as there isnt enough time for the ventricle to fill
When is aortic pressure the lowest?
when the aortic valve first opens
When is aortic pressure the highest?
at the peak of phase 3
Cardiac output is a function of what?
Metabolic rate
If metabolic rate is high, cardiac output will be what?
High
If metabolic rate is low, cardiac output will be what?
Low
Which butterfly shaped organ governs most of the metabolic rate of tissues in the body?
Thyroid
Metabolic rate in a pt with hypothyroidism will be?
Low
What is the difference between cardiac output and cardiac index?
Cardiac index takes into account body surface area
An increase vascular resistance will have what effect on CO?
Decrease CO
- tissue do no need as much blood flow so arteries will constrict decreasing CO
What is the formula for Cardiac Index (CI)?
CI = (SV x HR)/BSA
What unit is Cardiac Index (CI) measured in?
L/Min/m2
2 = exponent
What is the normal Body Surface Area (BSA)?
1.7 meters squared is the normal BSA
Who has a higher Cardiac Index (CI), male or female? Is this always true?
Male
No - women in late pregnancy have an increased metabolism d/t fetus, which increases Cardiac Index (CI) as a result.
What is the normal Cardiac Index (CI) for a healthy 20 year old, 70kg patient?
3L/min/m2
What age does Cardiac Index (CI) max out at? How many L/min/m2 is this?
Age 10
4L/min/m2
Daddy says he expected birth to be higher since our metabolism is really high, but turns out from birth to 10y/o our cardiac index increases quickly
As we age, we lose muscle mass. Some people lose organs as they go along.. the result is needing less energy. What happens to cardiac index?
Naturally reduces as we get older.
What is the cardiac index (CI) of a reasonably healthy 80 year old?
2.4L/min/m2
In a patient with normal metabolic rate, will vascular resistance be normal?
Yes
In a patient with a reduction in metabolic rate, what will happen to cardiac output?
It will decrease d/t lower metabolic needs
How is our cardiac output affected with hypothyroidism?
Reduction of metabolic rate –> Reduces CO
How is our cardiac output affected with hyperthyroidism?
Increase of metabolic rate –> Increases CO (by reducing SVR)
What happens to CO as SVR is increased, assuming a low metabolic rate?
CO is reduced
An increase of metabolic activity does what to CO? how?
Increases CO by reducing SVR
If someone loses tissue/organs etc, the body has lower cardiac output. Why?
Less available blood vessels –> Higher SVR since there are less paths of flow for the blood
What is Beriberi?
Vitamin B1 deficiency that impacts the way cells use energy.. makes the cell less efficient, thus increases metabolism.
Only really seen in 3rd world countries, not really here.
What happens to SVR in a patient with an AV shunt?
There are extra paths for blood vessels to take within circulation. This results in a lower SVR.
Lower SVR –> Increased CO
Is CO dependent on RA pressure or LA pressure
Both pressures must be met to have a great CO.
What happens if RA pressure and LA pressure don’t line up where they are supposed to? (i.e. RA pressure not 0mmHg, LA pressure not +2mmHg)
Blood will buildup somewhere; blood will also be absent from filling pressures.. results in lower CO
What makes it easy for the RV to work/pump to lungs?
Low resistance of the pulmonary circuit.
Which side of the heart does more work? Why?
LV does more work because it pumps against a high pressure gradient in the aorta, compared to the RV pumping to a low resistance pulmonary circuit.
What is the plateau for CO for either side of the heart (normal SNS activity)
13L/min
If a patient is supine and CVP is measured just prior to the RA, which will be higher? RA pressure or CVP? Why?
CVP will be slightly higher. This is due to the inferior vena cava being slightly inferior in position to the RA in a supine position. Gravity changes CVP in this scenario.
If CVP is measured far from the RA, it is much higher than RA pressure. Why?
There needs to be a pressure gradient for blood to return to the heart.
A patient with heart failure has a poor CO curve. What are examples of what can be done here to sustain life?
LVAD/RVAD/BIVAD, drugs (the good kind) - bridge to keep someone alive until it can heal itself or be repaired.
How would organ/limb removal affect vascular resistance & CO?
It will increase vascular resistance & decrease CO
- the body will have less tissue to care for –> body doesnt need as much CO –> increase in vascular resistance –> decrease in CO
What affect would hyperthyroidism have on vascular resistance & CO?
Decrease vascular resistance & increase CO
- increased demand of blood flow by tissues –> decrease in arterial vascular resistance –> increase in CO
What is Beriberi?
Vitamin B1 deficiency – impacts the way cells use energy by making them less efficient
What affect does Beriberi have on vascular resistance & CO?
Decreases vascular resistance & increases CO
- cells become less efficient & require more blood flow –> decrease in arterial vascular resistance –> increase in CO
What is an AV shunt?
an extra connection between the arterial & venous system
What affect would an AV shunt have on the vascular resistance & CO?
Decreases vascular resistance & increases CO
- extra connection or pathway for blood to flow in a parallel system decreases vascular resistance –> increasing CO
CO is tightly linked to consumption of what?
oxygen
Weight loss drugs have what affect on the body?
They increase metabolic rate
If something causes metabolic rate to be increased with the addition of the SNS, what is the end result?
Arterial vascular resistance will decrease as blood flow demand is increased & the veins will constrict which will increase CO
In a patient with heart failure, what does the heart rely on to maintain adequate CO?
Increased filling pressure - will have increased CVP/RA pressure.
The main circulatory filling pressure is roughly the same as the mean systemic filling pressure. What is this number?
+7mmHg
If volume is added to the CV system, what happens to pressure?
Increases
If volume is removed from the CV system, what happens to the pressure?
It goes down.
If there is a strong SNS stimulus to the CV system, what happens to filling pressures? Why?
Increase of filling pressure
Squeezing veins helps move volume back to the heart –> increases CO/helps forward flow
In a patient with AV fistula, how will the BP be? What about the CO? Why?
Normal BP with high CO (d/t low resistance to venous return since there is an additional path for blood to flow)
What is the biggest obstacle that we will face as anesthesia providers in regard to venous return?
PEEP (increased intrathoracic pressure)
Assume someone is bleeding, and it isn’t controlled.
As we lose blood, what happens to the CV system? Can we stop this process?
Heart eventually doesn’t receive the nutrients it needs to survive.
Heart relies on the aorta (diastolic squeeze) to perfuse the coronary arteries. If this doesn’t happen d/t low pressures, the heart doesn’t get nutrients and begins to die (MI), then you die without intervention.
If we step in in the early stages of bleeding, this can be avoidable.
Is there a negative or a positive pressure in the pleural space normally?
Negative
If something causes metabolic rate to be increased withOUT the addition of the SNS, what is the possible end result?
The arteries will dilate however the veins will not constrict so filling pressure will drop & arterial pressure will crash due to lack of blood return to the heart from the veins –> CO will decrease
Where is the intrapleural space?
Between lungs and chest wall
How does air enter our lungs?
As the diaphragm moves down, it creates a negative pressure within the lungs. This draws outside air into the lungs.
What is the normal intrapleural pressure?
-4mmHg (-5cmH2O)
When we breathe in, is our CO higher or lower? Why?
CO is increased due to negative pressure within the pleural space
How is air forced out of the chest?
Abdominal contraction
If there is a sustained increase of thoracic pressure, what happens to CO?
Decreased CO (Need higher RA pressure to achieve the same CO
Aside from PEEP, what example was used in class that caused increased thoracic pressure?
Trauma/surgery (opening chest to the outside environment)
Reduces CO
If intrathoracic pressure is increased over a long period of time, what does the body do to compensate?
Increases mean systemic filling pressure (PSF), which increases the slope of the venous return curve –> normal cardiac output.
aka, tightens up system or adds volume via kidneys to maintain normal CO
What medical condition does the following describe: Fluid around the heart that isn’t normal.
Cardiac tamponade
Cardiac tamponade results in extra pressure around the heart. What happens as a consequence?
Reduction in filling –> CO decreases until death
How do you fix cardiac tamponade?
Get rid of the fluid around the heart –> fixed
What happens in a hypo effective heart with negative pleural pressure?
Lower max CO than normal, but RA pressure of 0mmHg would net you the max (6L/min).
CO curve shifted to the left
What happens in a hyper effective heart with increased intrapleural pressure?
CO curve shifted to the right -
Max CO is higher than normal
Need more RA pressure to maintain CO
If someone has enhanced pumping, how will their RA pressure change?
Decreased - d/t more blood being pumped away.
If someone has decreased pumping function, what happens to their RA pressure?
Increased - d/t blood being left behind and backing up
An arterial-specific vasodilator would do what to cardiac output? Why?
Cardiac output would increase due to improvement of the circulatory system
When a patient is given an arterial-specific vasodilator, cardiac output increases due to improvement of the circulatory system. What improvements are there?
- SVR is governed by the arteriole.
- Relaxed arterioles –> choke point less choked, resulting in reduction of arterial pressure, and increase of venous pressure –> results in a lower resistance to venous return, and a higher RA pressure which helps drive CO increase
What is an example of an arterial-specific vasodilator?
ACE inhibition
Does ACE inhibition reduce preload or afterload?
Afterload reducer
What is an example of a venular-specific vasodilator?
Nitroglycerin
What impact does vein dilation have on filling pressure and cardiac output? Why?
Large reduction in filling pressure (container is stretchy, fills with blood and removes it from the tight container [arteries]), which reduces ΔP, and thus reduces cardiac output.
There is no change to resistance to venous return (slope).
In a patient on nitroglycerin, a venular-specific vasodilator, would stimulating the SNS help improve cardiac output? Why or why not?
Not really.. Cardiac output must venous return. If the venous return is reduced, the CO will not be improved much with increased SNS stimulation.
Is nitroglycerin a preload or afterload reducer?
Preload - it reduces the amount of blood going back to the heart
Why do we typically put a patient who has chest pain on nitroglycerin, assuming they can tolerate it?
Reduces cardiac output –> reduction in metabolism –> preserves heart tissue that may be ischemic/infarcting
Caveat: Need enough BP/CO to maintain life, can’t dose too high, patient dependent.
Does nitroglycerin relax coronary vessels?
No. It is a preload reducer (venular-specific vasodilator) that reduces cardiac demand until the pathology can be corrected.
If someone is on a mixed vasodilator, what happens to their filling pressure? Resistance to venous return? What about cardiac output?
- Reduced filling pressure d/t venodilation
- Reduced resistance to venous return d/t arteriodilation (dilation of arteries reduces resistance to venous return and helps blood get to the other side of the heart)
When giving mixed vasodilators, what is a consideration in terms of the intended effect?
Reduction in filling pressure + reduction of resistance to venous return gives us a mixed result in effect.
The body normally manipulates what to maintain cardiac output?
Filling pressure
Being that mixed vasodilators both reduce filling pressure + reduce resistance to venous return, the body, which is more important/has a larger impact?
Reduction of filling pressure - that is why giving a mixed vasodilator reduces cardiac output even though resistance to venous return is lower.
Between filling pressure and resistance to venous return, which is most important (always)?
Filling pressure
What two things can change filling pressure?
Changing volume or changing tightness of the venous container
If volume was increased/decreased, or the veins were dilated/constricted, would resistance to filling pressure change?
No - the path that blood takes to get back to the right side of the heart is unchanged.
What does the abbreviation “Cv” stand for?
Compliance (venous); measure of stretchiness.
Reduction of venous compliance does what to filling pressure? Why?
Increases filling pressure; volume is squeezed out of veins to return to the heart.
What happens to mean systemic filling pressure (PSF) if there is a reduction of volume, or an increase of venous compliance? Does resistance to venous return change?
PSF would be lower; resistance to venous return remains the same.
If there was a reduction of volume, or an increase of venous compliance, PSF would be lower. If pumping effectiveness/muscle activity remained unchanged, what happens to cardiac output?
Change in filling pressure would result in a large cardiac output change
If arterioles are relaxed, SVR is reduced. What does this do to filling pressure?
Unchanged
If you use a vasopressor that constricts arterioles, it makes it harder to get blood from the left to right side of the heart. What does this do with resistance to venous return? SVR? PSF? CO? BP?
SVR is increased, and mean systemic filling pressure (PSF) remains the same.
Resistance to venous return is increased.
Ultimately, cardiac output max will drop here due to the drop in venous return.
BP remains about the same.. the pressure upstream will be higher, downstream will be lower. Overall, it’s a wash.
If you use a drug that relaxes arterioles, it becomes easier to get blood from the left to the right side of the heart. What does this do with resistance to venous return? SVR? PSF? CO?
SVR is decreased, and mean systemic filling pressure (PSF) remains the same.
Resistance to venous return is decreased.
Ultimately, cardiac output max will increase here due to the increase in venous return.
Venous constriction does what to mean systemic filling pressure (PSF)?
Increases PSF
Arterial constriction does what to resistance to venous return?
Reduces slope of venous return curve.
Changing the slope of the venous return curve indicates what when giving a drug that causes arterial and venous constriction?
Arterial constriction.
When giving a drug that causes arterial and venous constriction, increases in filling pressure are due to
venous vasoconstriction
If venous compliance is reduced, what happens to filling pressure? CO?
Increased filling pressure –> Increased CO
What is the purpose of constricting arteries?
Shunting blood away from where it’s not needed.
When venous compliance is reduced, what happens to SVR? How does this change the venous return curve?
SVR increases, which decreases the slope of the venous return curve.
What is the purpose of constricting being?
Return more blood to the heart.
How do the kidneys help heart failure patients survive (long term/short term)?
Instead of constricting veins to get improved venous return, the kidneys do the following -
Long term: The kidneys expand blood volume.
Short term: High levels of catecholamines.
By expanding volume, patients with heart failure don’t have to live with high levels of catecholamines.
Which drug mentioned in class is almost ENTIRELY an arterial specific dilator?
Hydralazine
If a pt has an MI and the body hasnt had an opportunity to compensate, what would happen to the CO & RAP?
The CO would decrease as the heart is not able to pump adequately & the RAP would increase do to the hearts ineffective pumping
In a pt who experienced an MI, what is the initial response from the body & what effect does it have on the CO & RAP?
The SNS is stimulated & releases catecholamines that increase venous tone which in turn increase filling pressure –> increases CO
RAP remains high as the heart is still inadequately pumping
If possible, how does the body dial back sympathetic stimulation while maintaining CO in a patient with a failing heart?
By telling the kidneys to retain volume –> expands blood volume
If blood volume is expanded in a failing heart & SNS is dialed back, how does this affect RAP & filling pressure?
Both RAP & filling pressure will be elevated and act as the new normal to maintain adequate CO
What does high sympathetic activity of the heart predispose it to ?
Arrhythmias
- calcium channels can open prematurely due to high SNS
Why do we have to be careful in pts with a failing heart when removing volume?
Pts become volume dependent to maintain adequate CO – excess volume results in higher RAP & filling pressures
The pressures available to fill the heart with blood is defined as?
Preload
The pressure at the end of phase 1 is?
Preload
The pressure the heart has to pump against is defined as?
Afterload
The difference that might exist in SV if preload & afterload are maintained is defined as?
Contractility
The pressure at the end of phase 2 or the beginning of phase 3 is defined as?
Afterload
What is a normal afterload pressure in a healthy heart?
80mmHg
If preload is increased in a healthy heart what should we expect as the result?
expect to see increased filling pressure –> increase in EDV –> increased SV –> increased BP
If preload is reduced, what would the result be?
Less filling & less volume in the ventricle at the end of diastole –> leads to reduction in stroke volume d/t reduction in EDV
How does an increase in afterload affect the heart?
an increased afterload means the diastolic pressure will be higher & the heart will have to generate a higher pressure to open the aortic valve
How will a higher afterload affect the phases of the heart?
- The heart will spend more time in phase 2 trying to generate enough pressure to open the aortic valve that phase 3 will be shortened
- a higher afterload will also close the aortic valve sooner which further decreases time spent in phase 3
- this will ultimately decrease SV
What is the inner most layer of the pericardium?
The visceral layer
- apart of the serous
- thin transparent membrane
- allows the heart to move without friction
What is the middle layer of the pericardium? & what is it attached to?
Parietal layer
- glued to fibrous layer
- helps heart slide
What is the outermost layer of the pericardium?
Fibrous pericardium
- rigid, tough, thick layer
How does an AP move from cell to cell?
Gap junctions
Valves are referred to as?
Cusps or leaflets
What are the valves attached to? & what prevents them from being blown back into the atria?
valves are attached to chordae tendinae which is attached to papillary muscle which are a continuation of the ventricular muscle
- The papillary muscle prevents the valves from being blown back into the atria & they contract with the ventricle
What is the normal ejection fraction for daddy’s class?
58%
70/120 = 0.58 x 100 = 58
Which valve only has 2 cusps?
Mitral
What functional split separates electrical activity in the atria from the ventricle?
The cardiac cartilaginous ring
What is the only pathway in a normal heart where conduction from the atria can reach the ventricle?
Bundle of his
Which valve has a third cusp that isnt large enough to be considered its own? what is it referred to as?
Mitral
- called the commissural cusp – part of the posterior cusp
where is the opening for the right coronary artery found?
The right cusp of the aortic valve
Where is the opening for the left coronary artery found?
The left cusp of the aortic valve
What does the left coronary artery split into?
The left anterior descending & the circumflex arteries
What path does the LAD follow?
runs down the front & middle of the heart
What path does the Circumflex follow?
runs down the side & back of the heart
In most people, the RCA supplies which large artery at the base of the heart?
Posterior descending artery
- in some people the PDA is a branch of the LCA
Which is largest vein found on the posterior inferior part of the heart?
The great cardiac vein
What comes off of the great cardiac vein & where does it empty into?
The coronary sinus comes off the great cardiac vein & empties into the RA
- it carries deoxygenated blood to be returned to the lungs
When is right coronary flow the highest?
during systole –> but pretty much continuous throughout the cardiac cycle
When is left coronary flow the highest?
during diastole
when is there retrograde flow in the coronary arteries?
Early systole as the coronary arteries & nice & plump from receiving blood during diastole then the pressure in the ventricles increases during systole which causes blood to move back & read as a negative pressure
How does tachycardia affect coronary perfusion?
It reduces time spent during in diastole –> reduces coronary perfusion time & less filling time
When aortic pressure is high, coronary perfusion is?
High
When aortic pressure is low, coronary perfusion is?
Low
What happens to the heart if there is high after load?
High energy expenditure + cardiac remodeling
Drop BP to make demand lower
What drug example was given in class to reduce after load?
ACE inhibitors, Hydralazine
In a patient with reduced after load, does the aortic valve open/close at a higher or lower than normal pressure? What does this allow for?
Diastolic pressure = after load
Decreased after load = lower diastolic pressure
Aortic valve will open/close at lower pressures
Allows for longer phase 3 time, which increases SV
In a patient with decreased after load, what are the changes in the pressure/volume curve? What about time in different phases?
Increased time in phase 1 & 3
Decreased time in phase 2 & 4
Increase of SV in phase 3
Lower ESV d/t higher SV
HR will decrease
Lowering after load, all other things equal, will do what to HR?
Decrease HR - reducing after load will increase SV. To maintain the same CO, HR must drop
What is contractility? How is it shown on the pressure/volume curve?
Measure of heart squeeze, depicted by diagonal line on pressure/volume curve on the top left. The steeper the line, the more contractility.
If afterload/preload is constant with a normal EDV, what will happen to SV if contractility is increased?
SV will also increase. More squeeze = more ejected
ESV will be lower (Higher SV = Lower ESV)
EDV will be normal
If someone has decreased contractility, what happens to SV?
Also decreases SV assuming preload/afterload remains the same.
Decrease in SV = Increase in ESV
What happens if contractility is reduced with an unchanged HR?
Given that the SV will be lower, if HR is not increased, there will be a reduction of CO
What happens if you decrease contractility with a normal CO?
HR will rise to maintain CO
Contractility has a direct relationship with what?
Bloop pressure
What happens to blood flow with mitral regurgitation/insufficiency? Why?
Blood moves backwards from the LV to LA.
LA will be filled by both LV and the pulmonary system.
Occurs when pressure is higher in ventricle than the atria (assuming valve is insufficient). Normally, there is no back flow.
A patient has mitral regurgitation. During systole, what happens to blood flow?
It flows backwards and forwards. The pressure in the atria is less than the ventricles, so back flow occurs.
With mitral regurgitation, when is there the most back flow into the atria during P4 of the pressure/volume cycle?
The beginning of P4. This is due to high ventricular pressures with low atrial pressures. blood follows the gradient until the ventricle is more relaxed in late P4
Which has a bigger leak with mitral regurgitation: End of P3, or start of P4?
End of P3
With mitral regurgitation, which phases have back flow into the LA? What does this lead to?
P2, 3, and 4
Lower ESV, higher EDV
If someone has a normal functioning heart/valves, what should P2 and P4 look like? Why?
Straight vertical. These are isovolumetric phases (no volume change normally).
You look at a pressure/volume curve and note that P2 and P4 are curved. What can this tell you right away?
There is a valve problem, specifically regurgitation/insufficiency.
What is the problem with mitral valve stenosis?
The valve doesn’t open fully, so there is a problem with ventricular filling.
Note: This is a filling problem without compensation that reduces SV d/t reduced filling during diastole. The body compensates, but eventually will be come an issue (later flash cards)
If we don’t do anything to fix mitral stenosis, what happens to our EDV and SV? What will have to change to maintain life?
EDV - lower d/t problem filling
SV - reduced since there is not enough “gas in the tank”
HR - will have to increase to make up the difference to maintain CO
What compensations are there for mitral stenosis?
Increase filling pressure
Increase atrial pressure
Increase blood volume
Increase preload
^Helps with filling, but note that this extra pressure will be sitting in the LA/lungs. Note that on a pressure/volume curve that this won’t be seen unless it is a atrial graph unlike the ventricular one in our pptt.
What complication can severe mitral valve stenosis cause d/t compensation?
Pulmonary HTN/edema with impaired gas exchange d/t high LA/lung pressure from increased filling pressure/volumes.
What is happening in aortic valve insufficiency?
Blood is moving backwards from the aorta to the LV
Expect blood to move backwards when the valve is closed & when aortic BP is higher than LV pressure
In aortic valve insufficiency, what part of P4 will there be the most back flow? Why?
The end of P4/beginning of P1 will have the most back flow into the ventricle. The pressure in the ventricle is the lowest at this point, so there is a wider pressure gradient, allowing for greater back flow.
Note: There is back flow any point where ventricular pressure is less than aortic pressure.
Normally, P1 has filling only from the atria into the ventricle. How does this change with aortic valve insufficiency? How does this change EDV and SV? What will this lead to?
There is filling from both the aorta AND the atria, leading to a much higher EDV, and a larger SV as well. Eventually, this will lead to dilated ventricular walls, which will cause the valves to function even worse.
The higher the EDV, the more risk there is for what? Is this helpful at all?
Ventricular dilation/stretching.
Higher EDV is helpful early on as it helps increase SV to make up for backward flowing blood, but overtime it leads to poor function from dilation.
With aortic valve insufficiency, the higher the EDV, the (better or worse?) the valve problem is?
Worse
If a pressure/volume curve is wider than normal, is it a stenotic or regurgitant valve?
regurgitant
If a pressure/volume curve is more narrow than normal, is it a stenotic or a regurgitant valve?
Stenotic
In aortic insufficiency, does the aortic valve open at a higher or lower diastolic pressure than normal?
Lower
In aortic valve insufficiency, is peak systole higher or lower than normal? Why?
Higher, to accommodate elevated SV.
Aortic stenosis has a ____ pulse pressure.
Narrow
What are some common causes of aortic valve stenosis?
High cholesterol; infection on valves
Aortic insufficiency has a ____ pulse pressure due to blood leaking the wrong way, leading to ___ aortic pressure.
Wide; low
After the age of 50, what valve condition will everyone have to some extent?
Aortic valve stenosis
What effects does aortic valve stenosis have?
Harder to get blood through aortic valve.
Reduction in ejection time
Reduces SV
Increases ESV
Very slight increase in EDV
Longer P2 d/t increased pressure requirement to get through the aortic valve, resulting in a shorter P3/P1
How should we treat aortic valve stenosis?
Like a high after load issue
Pressures in the ventricle are very high in patients with aortic valve stenosis. Is aortic pressure high?
No - the valve is a place of high resistance. An area after a place of high resistance will have a lower pressure. The MAP may even be normal in the aorta.
If someone has chronic aortic valve stenosis, what compensation must be made by the heart to maintain life?
Increased HR to maintain CO.
What happens to preload with aortic valve stenosis? Why?
It is increased significantly. If the heart struggles to maintain CO, volume is expanded. This is helpful early on (high filling pressure), but overtime it will lead to wall thickening. This will increase filling pressure requirement.
What is the hallmark characteristic of aortic stenosis?
Narrowed pulse pressure.
Where is the end of P2 with aortic valve stenosis?
It depends on the severity of the stenosis. The pressure in the aorta may be so low that the aortic valve may open prematurely.
If there is permanent damage, or damage that is not repaired on the heart, what happens to the contractility slope? What about ESV? SV? What about accommodation?
Contractility slope is decreased (less contractility)
Greater ESV
Lower SV
Higher HR to allow for normal CO/relatively normal BP
In a patient with heart damage (temporary or permanent), how do you treat it?
Reduce the oxygen demand/energy requirements by:
Treating with an after load reducer results in greater SV, and reduced ESV.
In a patient with depressed contractility (untreated), what happens with filling pressure/preload? What should we be careful of?
Increases lots to maintain cardiac output. Volume is expanded after healing from an MI.
Careful when removing volume from these patients. They are volume dependent.
What problem comes from high filling pressures of a patient with heart failure?
Dilation of the heart - harmful
What valve is in the left side of the heart between the atria and ventricle?
Bicuspid AKA mitral (two leaflets; anterior and posterior)
What valve is in the right side of the heart between the atria and ventricle?
Tricuspid (three leaflets)
Anterior, posterior, and septal cusps
In the tricuspid valve, which cusp is fastened to the wall of the septum?
The septal cusp
How many leaflets/cusps do the pulmonary and aortic valve have?
Three
Calcified valves would cause what valve disease?
Stenosis
Is coronary blood flow better during systole, or diastole? Why?
Diastole
Coronary blood flow is dependent on resistance, resistance being a function of ventricular pressures. Pressures are lowest in diastole, meaning more blood can flow through the coronary arteries
Which valvular issue inhibits coronary blood flow more? aortic regurgitation or stenosis?
Stenosis - ventricular pressures are much higher here, leading to increased resistance within the walls of the ventricle. This leads to less blood flow from the coronary arteries.
Is there ever retrograde coronary perfusion? Why or why not?
For ejection to occur, ventricular pressure has to be higher than aortic pressure. This high ventricular pressure “squeezes” the blood out of the coronary arteries and dumps it back into the aorta.
^So yes. Delta P is negative during systole in the coronary arteries
What does deep spinal anesthesia do to our SNS? Heart? Circulation?
SNS - Knocks out a lot of SNS chains
Heart - activity reduced d/t SNS chains being knocked out, but not very much given the SNS doesn’t do all too much for us HR wise.
Circulation - filling pressure will be lower d/t lower HR/SNS.
Overall: If we have normal circulation with a small reduction in pumping effectiveness from spinal anesthesia, CO will only decrease to around 4.8L/min.. not really a big deal. Not a heart problem. It is a circulatory problem (lack of filling pressure).
On a CVP waveform, what is the A wave?
Contraction of the atria (peak systolic of the waveform usually)
On a CVP waveform, what is the C wave?
Backward bulging of the AV valves (small notch after the A wave)
On a CVP waveform, what is the X descent?
Once valves stop bulging backwards, the atria is empty. This reduces atrial pressure, producing a downstroke on the waveform that is X
On a CVP waveform, what is the V wave?
Blood buildup in the atria early in diastole
On a CVP waveform, what is the Y descent?
Just after the V wave, it is a result of blood going through the open AV valve.
AV valve being open = Y descent.
What is the order of waves on the CVP waveform?
A, C, X, V, Y
Daddy said ignore the H wave
When we breathe in, what happens to thoracic pressure?
Decreases thoracic pressure, which helps CO due to drawing blood into the chest
When breathing out, what happens to thoracic pressure? Why?
Increases d/t abdominal muscle contraction. Reduces CO d/t decreased venous return.
When inhaling and exhaling, will PAP/CVP correlate, or no?
Yes
What happens to CVP and PAP on inspiration?
Decreases
What happens to chest veins during inspiration?
The pressure within the veins decreases, as well as the pressure around them which makes the pressure even lower.
Because of this, more blood is pulled into the thorax.
Why is there a momentary drop in CO followed by an increase of CO upon inspiration?
The drop in thoracic pressure allows for veins to be filled with blood first, THEN the heart.
Note: the initial pressure drop can pull blood from the right atrium as well until the blood can return from the veins.
Which is thicker - veins, or the right atrium?
RA
Upon inspiration, how long does the decrease of CO last?
A beat or two, then CO will increase once blood makes it from the veins to the heart.
Other than CVP decreasing upon inspiration, does anything else decrease?
Right sided Afterload decreases (lower pulmonary resistance)
Is the left side of the heart impacted by inspiration in the same ways that the right side is?
Yes, HOWEVER
The initial CO drop will be much greater in the left side than the right side.
This is due to the LV pumping to the aorta, which is not impacted by inspiration. There is no left side after load change. The only change is a decreased LA preload.
Upon inspiration, one side of the heart definitely has a lower CO, while the other is currently debatable depending on who you ask. Which is which?
Left side definitely drops
Right side probably drops, but maybe increases depending on who you ask
What is a normal SVR?
800-1600 dynes x sec/cm5
What is a normal PVR?
40-180 dynes x sec/cm5
What does CGS stand for? What is it?
Centimeters grams seconds; unit of measurement with hemodynamic values
What is the equivalent of a CGS (centimeters grams seconds) unit?
Dynes x sec/cm5
If someone has a nutrient delivery problem, what would their SVR be?
Lower end of normal - lower SVR that way nutrients can make it to the site that it is needed.
Lower SVR allows for more blood flow.
Higher metabolism reduces SVR to allow for more blood flow.
How do you find PRU (peripheral resistance unit)?
(Beginning of CV system - end of CV system)/ 5L/min
(100mmHg - 0mmHg)/ 5L/min = 83.3mL/sec
He then said we’d round this to 100mL/sec to make it easy
AKA
(100mmHg - 0mmHg)/ 100mL/sec = 1PRU
What is 1 PRU (peripheral resistance unit) equal to?
1 mmHg
How is PRU (Peripheral resistance unit) converted to CGS (centimeters grams seconds)?
PRU x 1333 = CGS
When our heart rate increases, a third of diastole is removed. Which third is this, and why?
The 2nd third of diastole.
The majority of filling happens in the first third of diastole, and the last third is atrial kick (~10mL). Not much filling occurs in the second third of diastole. This allows for increased HR.
What consideration should be made with elevated HR/skipping the second third of diastole?
The coronary arteries are perfused during diastole.
Higher HR –> Less time in diastole –> Less coronary artery perfusion time. This can be a concern with a sick heart.
What is the most important part of the second third of diastole?
Coronary perfusion. Not so much on filling
Chordae tendineae & papillary muscles prevent valves from being blown out. Do they prevent bulging?
No. The bulge is what the C wave it on a CVP waveform.
How is PRU (peripheral resistance unit) of the pulmonary circulation found?
(16mmHg - 2mmHg)/ 100mL/sec = 0.14 PRU
The pulmonary circulation has 0.14 PRU. How many times greater is the PRU value for systemic circulation?
Pulmonary PRU is about 1/7th of the systemic circulation.
Multiplying 0.14 by 7 should give us the vascular resistance of the systemic circulation
What is meant when someone is right coronary dominant?
When the RCA splits into the PDA
- this occurs in about 75% of folks
What is meant when someone is left coronary dominant?
When the Circumflex artery splits into the PDA
- occurs in about 15% of people
If the walls of the ventricle become hypertrophic, how will this affect filling pressure?
The filling pressure will be increased as the ventricular compliance is reduced
If the walls of the ventricle become very compliant, how will this affect filling pressure?
The filling pressure is decreased as ventricular compliance is increased
What can lead to LV hypertrophy?
AS & uncontrolled HTN
What can lead to LV dilation?
AR
Why do we have to be cautious when giving volume to a kid?
They do not have the starling component so their ventricles can not accommodate to an increase in venous return & rely on increasing HR
The 1st heart sound that is heard is a function of?
AV valves closing
- valves vibrate & bulge back into atria producing sound
Which is the longest of the 4 normal heart sounds?
what is the duration?
what is its pitch?
1st heart sound
0.14 sec
low pitch
When is the 1st heart sound heard?
Beginning of systole
The 2nd heart sound is a function of what?
Closure of the pulmonic & aortic valves
What is the duration & pitch of the 2nd heart sound?
0.11 sec & high pitched
What causes the physiological splitting of the 2nd heart sound?
The pulmonic valve staying open longer than the aortic valve on deep inspiration due to the afterload being reduced for the ride side of the heart but not the left side
The 4th heart sound is a function of?
Atrial contraction
- not normally heard in a healthy pt – exaggerated when the atria has to work harder
The 3rd heart sound is a function of?
a low compliance ventricle –> the ventricle fills after as the walls are thickened & require more pressure to fill to a normal volume
When is the 3rd heart sound heard?
HF or kids
When will AS be heard?
systole
When will AR be heard?
Early diastole
When will MS be heard?
loudest at the end of diastole
When will MR be heard?
Early systole
Where can you hear the Aortic valve?
Medial right sternum - 2nd intercostal space
Where can you hear the Pulmonic valve?
Medial left sternum - 2nd intercostal space
Where can you hear the Tricuspid valve?
Medial left sternum - 5thintercostal space
Where can you hear the Mitral valve?
Lateral left sternum - 5th intercostal space
What is the term used to describe when the RCA & Circumflex combine together to form the PDA?
Anastomosis
Which type of coronary arteries are more prone to ischemia?
The sub endocardial coronary arteries in LV
Concentric hypertrophy is defined as?
sacromeres stacked in parallel
Eccentric hypertrophy is defined as?
sacromeres added in series
What medication is utilized to stop growth factors which slows fibroblasts?
ACE inhibitors
What makes difficult to diagnosis thyroid issues?
it is difficult to quantify thyroid hormone it is a fat soluble hormone that hides in plasma proteins
What is a hallmark sign of too much thyroid hormone?
Unexplained high HR at rest with no other comorbidities
What are the two compounds related to thyroid hormone?
T-3 – has 3 iodides attached to a tyrosine
T-4 – has 4 iodides attached to a tyrosine
Which thyroid compound does they thyroid release most?
T-4 – 93%
T-3 – 7%
What is another name for T-4?
Thyroxine
What is the amount of iodide we need annually to keep our body happy?
50mg
An enlarged thyroid is referred to as?
A goiter
how does the hypothalamus communicate with the thyroid hormone?
Thyrotropin releasing hormone (TRH)
Goes to anterior pituitary which releases Thyroid stimulating hormone (TSH)
Which goes to thyroid and thyroid releases T3/4
What is another term used to describe TSH?
Thyrotropin
Where is TSH produced?
Anterior pituitary gland – adrenohypophysis
What controls the pituitary gland?
Hypothalamus
How does the Hypothalamus communicate with the pituitary?
Thyrotropin releasing hormone (TRH)
What are the nodules found on the sides of the thyroid gland?
Parathyroid
What does the Parathyroid control?
Calcium levels in blood
What is the name for T3?
Triidothyronine
Where are the motor neurons of voice box housed?
Vagus nerve
Which nerve that branches off the vagus gives us the ability to speak?
Recurrent laryngeal nerve
Being that thyroid hormone is very lipid soluble, how does it get to the cell when in the CV system?
Catches a ride on plasma proteins – TBG (thyroxine binding globulin), thyroxine binding pre-albumin & albumin
- all three plasma proteins are produced by the liver
Excess thyroid hormone affects almost everything except for BP, why is that?
SVR decreases to increase flow to vessels but HR increases as well so BP essentially does not change
What is the majority of thyroid hormone that reaches the cell?
T-4
What is the active form of Thyroid hormone?
T-3
How long does it take for thyroid hormone to take affect if given synthetically?
6-8hrs
If the pituitary gland developed a tumor, how would this affect thyroid hormone?
Pituitary would increase its release of TSGH –> which would act on Thyroid to release more thyroid hormone
How would the hypothalamus react to a pituitary tumor causing hyperthyroidism?
The hypothalamus would stop releasing TRH
If the thyroid gland developed a tumor causing excess release of thyroid hormone, how would the Pituitary & hypothalamus respond?
Hypothalamus would stop releasing TRH & pituitary would slow the release of TSH
If the hypothalamus were to develop a tumor, how would this affect thyroid hormone production?
The hypothalamus would release an excess of TRH –> which would act on pituitary to release excess TSH –> TSH TSH would act on thyroid to release more thyroid hormone
- there is nothing to combat the hypothalamus
What are the two mediastinum divisions?
Superior & Inferior
How many subdivisions are there of the inferior mediastinum division?
3
Anterior
Middle
Posterior
What is included in the anterior section of the inferior mediastinum division?
Whatever is in front of the heart
What is included in the Middle section of the inferior mediastinum division?
This section is the meat and potatoes - it has most of the “stuff” in it.
- Heart
- Pericardium
- Ascending aorta
- Superior vena cava
- Pulmonary trunk
- Pulmonary arteries/veins
- Pericardiophrenic nerve
What is included in the Posterior section of the inferior mediastinum division?
- Abdomen (biggest part of this section)
- Esophagus
- Thoracic aorta
- Vagus nerve (can be here, or in the middle section)
- Azygos vein
- Hemizygos vein
- Thoracic ducts
NOTE: Lymph dumps content to venous system - these vessels combine with veins in the posterior mediastinum. Don’t need to locate this, just know it.
How does the ascending aorta attach to the heart?
Directly
What does the pericardiophrenic nerve do?
- Responsible for sensory perception in the pericardium
- Supplies enervation to diaphragm
Pericarditis hurts. What nerve sends the pain signal?
Pericardiophrenic nerve (has blood vessels within middle section of the inferior mediastinum that supply it)
What is located in the superior mediastinum?
- Thoracic part of the trachea
- Thoracic part of the esophagus
Within the posterior section of the inferior mediastinum, where is the thoracic aorta located?
Back of chest cavity next to vertebra
What causes the second heart sound?
Closure of the pulmonary and aortic valves
How do the pulmonary/aortic valves close?
Based on pressure differential; both have a slightly different pressure differential.
The aortic and pulmonic valve have different pressure differentials required to close. What would deep inspiration cause?
Makes the pressure differential more obvious - left sided afterload will not be impacted as it is aortic, but right side afterload is reduced.
Regardless of output of the right side of the heart, this will cause the pulmonic valve to stay open a little longer than the aortic valve on deep inspiration.
What causes splitting of the 2nd heart sound?
The pulmonic valve staying open a little longer than the aortic valve due to change in pressure differentials.
Can you hear a second heart sound split easily?
Not really
We use a phonocardiogram, which allows us to identify the sounds a bit better. They can be out of our ability to hear naturally.
How low of a frequency can we normally hear? Is this always the case?
20Hz - note, some heart murmurs are lower pitched than this, which is why we need a phonocardiogram to hear heart sounds sometimes.
We lose this ability (hearing high/low) as we age
What happens to your pressure waveform if there is an air bubble in the art line?
It acts as a spring and overdamps the waveform.
The bubble compresses when pressure goes up.
No dicrotic notch will be seen.
Note: Blood clots in art line will do this as well.
What might be the problem other than air bubbles or blood clots in the art line if it is overdamped?
Gain on amplifier may not be turned up enough.
The bubble will look the same as if the gain was too low - troubleshoot your lines.
If you have a underdamped art line waveform, will there be a dichrotic notch?
Many - they are artifacts due to the gain on the amplifier being turned too high
What are the two types of anastomosis between the left and right coronary arteries by way of the circumflex branch?
Physiologic (good, think circle of Wilis, want extra options for blood flow in critical areas)
Nonphysiologic - doesn’t really matter
Doesn’t exist in everyone, but maybe more common than we think. Unknown d/t difficulty and expense of testing required to diagnose.
What is a right side dominant coronary artery system?
Posterior PDA comes from the right coronary artery
What is an epicardial blood vessel?
Larger blood vessels outside/on the surface of the heart.
The LAD and PDA are what kind of blood vessels? (aside from coronary arteries)
Epicardial vessels
Note: Networked with deeper endocardial and subendocardial coronary arteries
Which coronary vessels have the lowest pressure during systole?
Epicardial
Which coronary vessels have the highest pressure during systole? Which area especially?
Endocardial/subendocardial vessels
Deep left ventricular wall
Subendocardial coronary vessel pressure is close to what?
Ventricular pressure
Ischemia is most likely to occur in which coronary vessels?
Subendocardial left ventricular vessels
Which area of the heart is most likely to have retrograde coronary perfusion during the start of systole?
Left ventricle (especially subendocardial)
When is the murmur for aortic stenosis?
Systole
When is the murmur for mitral stenosis?
Diastole
When is the murmur for aortic regurgitation?
Diastole (louder in early diastole)
When is the murmur for mitral regurgitation?
Systole
What change on a CVP waveform would be seen with mitral regurgitation?
Much higher V wave
All valve problems cause some sort of what?
Backup - some helpful, some not so much
In what patient population is the loss of atrial kick devastating?
Bad valves/heart failure
Why does afib lower output from the atria?
Chambers of the heart are uncoordinated
A patient with heart failure has a physiologic response by the kidneys and increases volume. What is a consideration in long term treatment?
Diuretics
Reliant on forward flow, but also don’t want to dilate the heart. Need to find a fine balance.
What is eccentric left ventricular hypertrophy? How are extra contractile filaments laid out?
Dilation; in sequence
Tylerism - if you add things together in a line (sequence), they get long or dilated
What is Concentric left ventricular hypertrophy? How are extra contractile filaments laid out?
Thicker walls/hypertrophy; stacked on top of each other.
Tylerism - Stacked things are thicker. Concentric = concentrated. Concentrated things are all on top of each other.
What can cause concentric left ventricular hypertrophy?
Aortic stenosis
Long term untreated HTN
What is the problem with concentric LVH?
Thick walls are less compliant, which causes a filling problem and diastolic dysfunction.
What are some causes of eccentric LVH?
- Congenital cardiomyopathy
- Aortic valve insufficiency
- MI
What can be given to slow down congenital cardiomyopathy from dilating the heart? (Eccentric LVH)
ACE inhibitor - either way patients will die in their mid 20s
When someone has an MI, why do they get eccentric LVH? (dilated)
Heart patches itself up, but areas with patches don’t have as much muscle. That means they will be more likely to stretch out over time.
What is the problem with eccentric LVH?
Heart wall is thinner, leading to harder time pumping with as much pressure or against pressure.
Systolic dysfunction.
What is systolic dysfunction, as seen in eccentric LVH?
Heart has trouble producing normal SV/BP.
If we have a small area in the heart with a perfusion issue, is this a problem?
What does this depend on?
Sure, but not a horrible one as we have collateral circulation that can help provide nutrients.
Depends on the ability of nearby vessels to dilate. If unable to dilate (drop SVR to allow more flow), will be much more likely to have a larger area of infarct.
What would cause someones vessels to be unable to dilate?
Pathology such as:
- HLD
- EToH abuse
- DM
- HTN
- “lots of things”
What lays down scar tissue in the heart if it is damaged?
Fibroblasts
What is the problem with fibroblasts patching up the heart when it is damaged?
It doesn’t know when to stop - will lead to too much scar tissue which adds risk of eccentric LVH (dilated cardiomyopathy)
Also can lay down scar tissue onto of functioning muscle tissue, further weakening the heart.
What do we give patients to help slow down scar tissue deposition by fibroblasts on the heart?
Ace inhibitors - inhibits the growth factor needed by fibroblasts.
What is systolic stretch, and why is it a problem?
Area of ventricular wall not working right (i.e. too much scar tissue, damaged tissue, etc)
–> leads to systolic stretch.
When the rest of the heart contracts, this area does not. This causes an outward stretch of the nonfunctional area.
The area bows out during systole, leading to a lower EF***
What is graves disease?
An autoimmune disease.
The body creates antibodies that activates TSH receptors. This increases thyroid gland activity.
Key observations: Goiter, exophthalmos (protruding eyes)
What is the cause of goiter?
Antibodies in graves disease activate TSH receptors in the thyroid, leading to goiter. (Thyroid produces a ton of thyroid hormone)
What is the problem with exophthalmos?
Protecting the cornea - if protruding enough, they can be injured.
How can graves disease be treated?
Some sort of treatment that gets rid of the bad antibodies (i.e. plasmapheresis)
If you don’t meet your iodine needs, what happens in the body?
- Unable to produce building blocks for thyroid hormone
- Thyroid gland doesn’t produce enough hormone
- Hypothalamus releases lots of TRH to try to get pituitary to release TSH
- Anterior pituitary releases lots of TSH
- Thyroid gland cannot make T3/4 because it doesn’t have the iodine precursor components
Results in goiter.
Fix? Have some table salt.. has iodine in it
What is Hoshimotos Thyroiditis?
Body produces antibodies that bind/attack the thyroid gland until total destruction.
Starts from irritation of thyroid gland, and is more common in asian populations.
What is a great treatment for thyroid cancer?
Radioactive iodine.
No other part of the body takes up iodine.
Small doses over a long period of time get the thyroid activity normalized.
For thyroid cancer, what is the radioactive isotope used for treatment?
I-131
What happens if you have a large amount of iodine intake in a short period of time?
- Interferes with thyroid hormone production (too much traffic of iodine)
- Cell system in place to attach iodine to tyrosine gets confused
- Similar to redox reactions (i.e. too much oxygen leads to bad results)
What is an example of receiving too much iodine in a short period of time?
Amiodarone can cause this.
Amiodarone is packaged in solution with high levels of iodine. Giving too much will drop T3/T4 levels.
Can giving someone high iodine intake over a short period of time ever be beneficial?
Yes - with acute hyperthyroid issues (thyroid storm, brain issues). High iodine in a short period slows production of T3/T4.
What can happen if you have low thyroid hormone levels?
- Note that the thyroid uses cholesterol and fatty acids to create T3/T4
- Cholesterol and fatty acid levels will increase (increased risk of atherosclerosis)
- Will get tougher, thicker blood vessels
- Need to treat promptly to prevent the above
Are people generally compliant with their thyroid medication? (synthetic thyroid hormone). Why?
People hate the drug.
Messes with sleep/relaxation
Causes palpations, anxiety, restlessness in higher doses.
Healthy patients generally will take it. Old unhealthy patients are typically not compliant.
What is shock?
Problem getting nutrients required to tissues
What are the five types of shock?
- Cardiogenic
- Hypovolemic
- Neurogenic
- Anaphylactic
- Septic
What is cardiogenic shock?
A pump problem.
If you have an MI, or can’t meet CO needs, this will result.
What type of shock can bleeding or embolism cause?
Hypovolemic/obstructive
What is neurogenic shock?
Caused by most anesthetics, especially volatile
Takes SNS offline, which nulls the help from the CV system to keep BP up. Need synthetic catecholamines to help overcome this.
What is the concern with giving a high level full spinal anesthetic block?
Potential loss of CNS below the level of anesthetic, leading to SNS being offline and drop of BP without synthetic catecholamines.
What is anaphylactic shock?
Reaction from immune system (latex allergy? Peanut? Etc)
Body panics and releases histamine from mast cells
If there is enough histamine, there is no vascular tone. Big issue with the veins (no venous return, drops filling pressure with a huge CO drop)
What is septic shock?
Shock caused by bacteria, generally gram +.
Blood vessels dilate, making it harder to deliver nutrients to the cells.
Which of the five shock states are the most common?
Hypovolemic shock - can happen with blood loss or too little volume conservation (i.e. drinking only 8oz of fluid a day)
What happens within the body if there is a short hemorrhage?
- Catecholamines released
- Kidneys conserve volume
- Fluid shifts to maintain CO
What is our normal blood volume?
5L (hct/plasma)
Lots of water in the cells and between them
What is non progressive shock?
Progressive shock?
Non-progressive:Body compensations occur, but body can recover.
Progressive: Body compensations occur, but body cannot recover without intervention. (MODS, coronary/kidney/brain/brainstem loss of perfusion)
How much blood volume can be lost without impacting CO/BP?
10%
How much blood volume loss will drop CO, but keep BP reasonable?
20% (1L blood loss if healthy)
If you lose >20% blood, what is your outcome?
If you are not near a healthcare facility, you may not be able to live.
What areas of the body hold extra fluid that can be shifted into circulation if needed?
- Spleen (Hg/RBC)
- Pulmonary system (couple 100mLs)
- GI system can shunt where needed
More systems online? Easier to recover
More systems offline? Harder to fix/survive
Is arterial BP a substitute for measuring CO? Why or why not?
No. Arterial BP is a good snapshot of the system, but does not tell you CO.
i.e. you can have a normal BP with a blood loss of 20%, but have a reduced CO.
In heart failure, what does the kidney do? What is the issue with this? How might we fix this?
The kidney looks at the BP. When it sees that it is low, it retains fluid and electrolytes to increase preload/RAP.
The problem? The kidney doesn’t know when to stop, and will keep retaining fluid until it reaches its BP goal (which it might never do, the heart may not be capable of it anymore). Filling pressures can be elevated to a point where it is no longer helpful.
Treatment: Give diuretics to maximize the patients CO. If the patient can live at a BP of 80 instead of 100, this may be the better choice rather than killing the patient.
What is PPV?
Pulse pressure variation
Does FloTrac add enough information to us to assure adequate cardiac output?
Daddy says no. We can take what we have available and use the information, but look at the full picture.
Good to see BP
