Term
| What percent of total body mass is blood mass? How would you calculate blood volume? |
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Definition
| Blood mass = 7-8% of body mass. To calculate volume, take the blood mass in kg and make it liters (since blood density is very close to water). |
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Term
| What percent of systemic blood volume is in veins? Capillaries? |
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Definition
| 75-80% in veins, only about 5% in capillaries. |
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Term
| What percent of blood volume is ejected from ventricles during systole (i.e. what is a normal Ejection Fraction)? How do you calculate EF, and why do you care? |
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Definition
60% is normal.
EF = SV/EDV
EF is a useful index of systolic function. |
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Term
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Definition
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Term
| What is stress? What are the units? |
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Definition
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Term
| Is systolic pressure higher in the aorta or resistance arterioles (such as the dorsal pedal artery)? |
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Definition
| Resistance vessels! Dorsal pedal, e.g., is 135/70 vs. the aorta at 110/75. However, MEAN pressure at the resistance arterioles is lower than mean pressure in the aorta. |
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Term
| What is the difference between the systolic and diastolic pressures in an artery? What does this mean in a clinical evaluation? |
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Definition
| Pulse pressure. This is the variation in pressure you feel on your fingertips when feeling patient's pulse. |
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Term
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Definition
Diastolic pressure + 1/3 pulse pressure
"1/3 up, 2/3 down"
This is b/c pulsating pressure spends more time on the diastolic end. |
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Term
| What is the driving pressure in the circulation? Distending pressure? |
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Definition
Driving pressure: pressure is greater upstream than down.
Distending pressure: pressure is greater inside circulation than outside. |
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Term
| What are normal pressures within the left ventricle during systole and diastole? |
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Definition
Systole: 120-160 mmHg
Diastole: 4-10 mmHg |
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Term
| What are normal mean pressure within the left atrium? How does this relate to left ventricular pressure? |
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Definition
4-10 mmHg
This is slightly higher than left ventricular diastolic pressure, because 80% of left ventricular filling is passive. |
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Term
| What are normal pressures within the right ventricle during systole and diastole? |
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Definition
Systole: 20-28 mmHg
Diastole: 0-5 mmHg |
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Term
| What are normal pressures within the aorta during systole and diastole? |
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Definition
Systole: 120-160 mmHg
Diastole: 80-120 mmHg |
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Term
| What are normal mean pressure within the right atrium? How does this relate to right ventricular pressure? |
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Definition
| 0-5 mmHg. Mean atrial pressure must be slightly greater than ventricular diastolic pressure. |
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Term
| What are normal pressures within the pulmonary artery during systole and diastole? |
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Definition
Systole: 20-28 mmHg
Diastole: 8-12 mmHg |
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Term
| What is mean capillary pressure? |
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Definition
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Term
| What mmHg change in ventricular diastolic pressures can result in shock or hypertension? |
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Definition
Just a few mmHg decrease (from 4-10 in the left heart or 0-5 in the right heart) can result in shock.
Just a few mmHg increase can result in systemic or pulmonary hypertension. |
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Term
| What is LaPlace's relationship mathematically and in words? |
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Definition
pi (stress) = P (internal chamber pressure) x r (chamber radius)/2h (wall thickness)
An increase in chamber dimension without a proportional increase in wall thickness results in increased wall stress. |
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Term
| Are cardiovascular pressures proportional to body size amongst mammals? Why/why not? |
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Definition
| No - they are very consistent across species. This is related to the fact that myocardial sarcomeres generate similar forces across species, and r/h ratio (chamber radius to wall thickness) is conserved. |
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Term
| How can you estimate CO in an animal? |
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Definition
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Term
| What is the formula for CO? |
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Definition
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Term
| What is the velocity of blood flow in capillary beds? |
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Definition
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Term
| What is the formula for TPR? What is the implication for controlling arterial pressure? |
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Definition
TPR = (MAP-RAP)/CO
where MAP is the mean aortic pressure and RAP is right atrial pressure.
This means the body can control arterial pressure either by changing CO or TPR. (Think of body's response to low BP) |
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Term
| How is blood flow diverted to specific organs? |
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Definition
| By changing the relative resistance of capillary beds: vasoconstriction increases resistance and vasodilation decreases resistance so blood "chooses" to go down the path of least resistance. |
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Term
| What is the definition of a compliance vessel? What are the most compliant vessels of the CV system? |
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Definition
| Changes its volume a lot for a small change in pressure...i.e. veins and then heart (during diastole). |
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Term
| What affect does increased preload have on SV and CO, according to Starling's law of the heart? |
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Definition
| Increasing preload increases SV and CO. |
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Term
| Is the normal heart preload dependent or independent? Afterload dependent or independent? What does this mean? |
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Definition
| The normal heart is preload dependent, meaning that great increases in CO result from small increases in preload. The normal heart is also afterload-independent, meaning that increases in afterload do not result in major decreases in SV or CO. On the other hand, diseased hearts do not respond normally to increased preload and afterload (can you picture how, on a graph of preload/afterload vs. CO?). |
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Term
| Is systolic or diastolic function more related to preload dependence? |
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Definition
| Diastolic. With diastolic dysfunction, a heart does not respond to increased preload with sufficient increase in CO. |
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Term
| Is systolic or diastolic function more related to afterload dependence? |
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Definition
| Systolic. Systolic dysfunction results in a heart that cannot generate sufficient pressures to overcome increased afterload, so it becomes afterload-dependent. |
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Term
| What are some cell-level events that affect contractility? |
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Definition
| How fast ATP is hydrolyzed (by myosin ATP-ase), the number of active actin-myosin binding sites, availability of calcium at the sarcomeres, sensitivity to calcium. |
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Term
| What are the effects of decreased contractility? |
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Definition
| Decreased CO at a given preload, or increased preload necessary to maintain a given CO. |
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Term
| What are the parts of the CV system to consider when thinking about etiology of cardiac disease? |
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Definition
Myocardial tissue
4 valves
2 atria and 2 ventricles
coronary vasculature
pericardium
electrical conduction system
arteries, veins, capillaries, lymphatics |
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Term
Describe what this equation means:
Body energy use rate = CO x (arterial nutrient energy - venous nutrient energy) |
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Definition
| The body can't perform work any faster than the heart can deliver it. Same holds for O2. Thus, heart disease, by decreasing the amount of oxygen and nutrients available to the body, necessarily limits activity levels. |
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Term
| What is the EDPVR? Is it normally a straight line? |
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Definition
| End Diastolic Pressure Volume Relationship describes the change in ventricular volume with change in pressure (and vice versa). This relationship is not generally constant/linear, rather the relaxed heart gets stiffer at higher volumes so increasing the volume further results in greater pressure increase. The curve represents distensibility and compliance of the heart's chamber. |
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Term
| What is Dr. Rush's favorite definition of preload? |
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Definition
| Diastolic wall stress (which relates to both pressure and volume in the ventricle at end diastole). |
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Term
| What is Dr. Rush's favorite definition of afterload? |
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Definition
| The pressure the heart ejects against, or end systolic pressure. |
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Term
| What are the determinants of cardiac performance? |
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Definition
| Preload, afterload, contractility, distensibility, heart rate, synergy of contraction (AV synchrony, inter-ventricular synchrony). They are not all totally independent (for example, HR usually changes in response to decreased contractility). |
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Term
| Does increasing HR affect the diastolic or systolic interval more? |
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Definition
| Diastolic. Thus, increasing HR usually has the effect of reducing preload, since less time in diastole means a less-filled ventricle. |
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Term
| How does the relationship between HR and SV (or CO) change in a trained athlete? |
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Definition
| The tipping point where increasing HR results in LOWER CO due to reduced preload occurs at a higher HR in trained athletes. |
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Term
| What is oxygen delivery to tissues a function of? |
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Definition
| CO and O2 extraction (i.e. the difference between arterial and venous oxygen fraction). |
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Term
| Match the following: pressure overload, volume overload, concentric hypertrophy, eccentric hypertrophy, increased preload, increased afterload. What are some disease conditions that could cause these? |
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Definition
Pressure overload, or systolic wall stress, results in concentric hypertrophy (increase in wall thickness, decrease in chamber radius). This could be caused by anything that increases afterload: valvular stenosis (pulmonary for the right ventricle, aortic for the left) or hypertension (pulmonary or systemic).
Volume overload, or diastolic wall stress, results in eccentric hypertrophy (normal or reduced wall thickness; increased chamber diameter). This can be caused by DCM or any condition resulting in volume overload or increased preload: tricuspid or pulmonic insufficiency or atrial septal defect (right ventricle) or mitral or aortic insufficiency, PDA, or ventricular septal defect (left heart). |
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Term
| Is DCM an example of volume overload? |
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Definition
| NO. Volume overload implies increase SV; DCM has reduced SV. However, both DCM and volume overload show eccentric hypertrophy. |
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Term
| Concentric hypertrophy: sarcomeres being laid down in series or parallel? Eccentric hypertrophy? |
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Definition
| Concentric: sarcomeres laid down in parallel. Eccentric: laid down in series. |
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Term
| What is referred to by the term diastolic dysfunction? |
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Definition
| Reduced rate and extent of diastolic ventricular relaxation. |
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Term
| Can systolic or diastolic dysfunction result in increased preload? |
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Definition
| Both. e.g. Decreased contractility (systolic dysfunction) can result in increased preload to bring SV back to normal. Or, decreased ventricular relaxation can result in decreased SV, which increased preload improves. |
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Term
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Definition
| Pathological elevation of venous pressure (i.e. preload). Most typically due to cardiac dysfunction (CHF), which could be either systolic or diastolic dysfunction. |
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Term
| What determines myocardial oxygen requirements? |
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Definition
Wall stress (i.e. preload)
HR
(i.e. CO)
"Sick" hearts require more O2 to do the same amount of work. |
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Term
What is the equation for compliance?
What's the opposite of compliance? |
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Definition
dV/dP (change in volume/change in pressure)
Elastance = dP/dV |
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Term
| What does the ESPVR look like? |
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Definition
| A straight line with large slope compared to EDPVR. |
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Term
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Definition
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Term
Match each term in CAPS with a term in lower case:
EDSVR preload
ESPVR distensibility
ESP contractility
EDP afterload
EDV |
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Definition
EDP or EDV: preload
ESP: afterload
ESPVR: contractility
EDPVR: distensibility |
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Term
| With increased preload, what happens to the shape of the PV loop? What does this mean in words? |
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Definition
It gets wider and (slightly) flatter.
This means EDV is greater (for a small increase in EDP), and SV increases. Normal heart is preload dependent. |
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Term
| With increased afterload, what happens to the shape of the PV loop? What does this mean in words? |
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Definition
It gets taller and (slightly) narrower.
This means pressure increases more during systole compared to normal. ESV increases, but only very slightly compared to pressure (thus decreasing SV)....because normal heart is afterload-independent. |
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Term
| What are arterial and venous PO2? |
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Definition
Arterial: 100 mmHg
venous: 40 mmHg |
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Term
| When is myocardial oxygen delivery maximized? Think about how this is affected by increased HR, and how this changes with exercise. |
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Definition
| During diastole. When HR increases, there is less time in diastole, so myocardial O2 delivery decreases. In a trained athlete, myocardial efficiency of O2 extraction increases. |
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Term
| What does increased afterload, with increased preload compensation, look like on a PV loop? |
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Definition
| Loops gets wider (increased preload) in addition to taller (increased afterload), to maintain CO. |
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Term
| How does decreased contractility affect your PV loop? |
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Definition
| The slope of the ESPVR decreases, so the PV loop is narrower (sits to the right of normal PV loop. ESV is greater (so there's a smaller SV). |
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Term
| What does decreased contractility, with increased preload compensation, look like on a PV loop? |
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Definition
| The loop is shifted to the right. EDV is higher due to the preload compensation, and ESV is smaller due to the decreased contractility, but overall SV is normal. |
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Term
| How does decreased distensibility affect your PV loop? |
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Definition
| EDV decreases, making your loop narrower (it sits on the left side of the normal PV loop). |
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Term
| What does decreased distensibility, with increased preload compensation, look like on a PV loop? |
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Definition
| Pressure increases more than normal for the increase in volume during end diastole, so the loop has the lower right corner "cut off." However, SV doesn't change significantly since the increase in preload essentially overcomes the reduced distensibility. |
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