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Flashcards in Cardiac Output Deck (54):

How do we normalize cardiac output to the size of an individual?

using cardiac index= CO/Body surface area
ex. (5.6 L/min/ 1.9 m^2= 3.0 L/min/m^2)


Does cardiac index change with age?

YES. At birth= 2.5
10 years old= 4.5 and then it drops steadily back to 2.5 around age 80.


What is cardiac output (CO)?

Thus, if HR remains constant, SV will increase proportionately with CO


What is stroke volume (SV)?

the difference in the ventricular blood volume at the end of diastole (end diastolic volume; EDV) and the ventricular blood volume at the end of systole (end systolic volume; ESV)


Does stroke volume vary?



What are the 3 determinants of SV?

1. preload
2. afterload
3. contractility (inotropicity)


What is preload?

the load on the heart prior to contraction (the EDV).


What is afterload?

the load on the heart after it begins to contract (aka the pressure (MAP) against which the heart has to work)


What is contractility (inotropicity)?

the strength at which the heart contracts


What is ejection fraction (EF)?

ratio of SV to EDV expressed as a percentage
EF= (SV/EDV) * 100
normally >55%
used to measure cardiac performance


On what does ejection fraction depend?

HR, preload, afterload, and contractility


Is ejection fraction a valuable index of the severity of heart disease?



What are the 2 main determinants of CO?

1. Load-dependent regulation: intrinsic properties (does not depend on extrinsic nerves or hormones).
2. Load-independent regulation:
-contractility (strength of contraction)
-heart rate


What is the frank-starling curve?
(see diagram)

demonstrates the relationship of SV or CO and degree of ventricular filling (EDV, end-diastolic fiber length, end-diastolic pressure, cardiac pressure)
*aka the heart pumps what it receives (if it receives more blood, it will pump more blood)


What is the pressure volume loop?
(see diagram)

equates left ventricular pressure to left ventricular volume. When you increase preload, you increase SV and ventricular pressure.


What are the 3 underlying mechanisms for the molecular basis of stroke volume?

1. sarcomere length-tension relationship
2. intracellular calcium release
3. length dependence of calcium sensitivity of contractile filaments


What happens to the length of the sarcomeres at the end of systole (beginning of diastole) and the end of diastole (beginning of systole)?

They are shorter. As the heart fills they then get longer and approach a more optimal overlap. So as the ventricles fill more, they are able to produce more force due to increased tension :)


What happens to the size of the calcium transients (aka calcium sensitivity) as sarcomeres stretch during ventricular filling (diastole)?

more calcium is released from the sarcoplasmic reticulum for a short period of time, but less is required to elicit contraction.


What is the importance of Starling's Law?

it explains the remarkable balance of the output between the right and left ventricles. If the right side were to pump 1% more blood than the left each minute without a compensatory mechanism, the entire blood volume of the body will be displaced into the pulmonary circulation in less than two hours!


What happens if the right ventricle pumps out more blood than the left?

pulmonary venous return to the left atrium increases, increasing left atrial pressure, increasing left ventricular filling, increasing left ventricular end-diastolic fiber length and thus increasing left ventricular SV. Thus, the left side accommodates this problem :)


What is the single most important determinant of ventricular preload?

* central venous pressure (CVP): aka the pressures within the SVC, IVC and pulmonary veins. Thus if CVP goes up, filling of the atria goes up.


What are the 6 major physiologic determinants of CVP?

1. venous smooth muscle tone: because 2/3 of blood is found in the venous system, changing this VENOUS smooth muscle tone (decreasing size) allows you to shunt blood to the arterial side if you need it at any one time.
2. blood volume
3. body position: because venous pressures are low and more sensitive to gravity.
4. intrathoracic pressure
5. skeletal muscle pump: increases extraluminal pressure drastically to pump blood back to the heart.
6. resistance to blood flow


Aside from CVP, what are the 3 minor determinants of ventricular preload?

1. atrial contribution to ventricular filling: more important at high heart rates.
2. pericardial sac pressure: normally not an issue, but an increase in this will limit diastolic filling.
3. ventricular compliance (distensibility): will decrease in hypertrophic cardiomyopathies limiting diastolic filling.


What happens to stroke volume as you increase afterload?
(see diagram)

it decreases. Think Aortic pressure for Afterload. Therefore with higher aortic pressures, the heart doesn't eject as much blood.


What is the main difference in changes of afterload?

the pressure at which the aortic valve opens. It will open at lower pressures when afterload is low, and open at higher pressures when afterload is high.


What happens to shortening velocity of cardiac muscle as you increase load (aortic arterial pressure)?

it shortens more slowly (decreases) and therefore ejects less blood per unit time. This is because the heart is spending more time in the ISOVOLUMETRIC contraction.


What happens to SV if you decrease afterload?

it goes up, along with contractility (inotropicity)


What are the 3 determinants of ventricular afterload?

1. aortic diastolic pressure (MAP)
2. aortic compliance (distensibility): more pathological because it shouldn't change beat to beat
3. aortic valve resistance: typically very low


How does the Frank-Starling curve shift with a decrease in afterload?

up and to the left (because you're increasing SV when you decrease afterload)


How does the Frank-Starling curve shift with an increase in afterload?

down and to the right (because you're decreasing SV when you increase afterload)


At what afterload (MAP) does the CO start to become effected?

160 mm Hg and the higher this goes, the lower the CO


What happens to end systolic volume when we increase contractility?

we lower end systolic volume (because we pumped out more; aka higher stroke volume).


Does the aortic valve close at lower, or higher pressure when we increase contractility?

higher pressure


What happens to contractility if we increase afterload?

it decreases


What happens to contractility if we decrease afterload?

it increases


* Is stroke volume a function of preload?



Is stroke volume and preload depended or independent of contractility?

independent regulation (inotropic)


* What is stroke work?

the area of the pressure volume loop or (SV * MAP)


What is the mean arterial blood pressure (MAP)?

Pdiastole + (Psystolic-Pdiastolic)/3
Aka diasotolic pressure + 1/3 the pulse pressure


What is pulse pressure?

Psystolic - Pdiastolic


What is the molecular basis for cardiac contractility?

1. calcium kinetics= size of the transient rise in intracellular Ca++ that occurs during depolarization
2. Myosin ATPase activity= motor (converts one form of energy into another) that converts chemical energy (ATP) into mechanical energy. If you increase this, you increase contractility.
3. ATP levels (normal= 5 mM)
4. Number of cross-bridges (ex. hypertrophy increases myosin and actin).


What happens when we shiver?

we make use of the myosin motor and because no motor is 100% efficient, we lose some energy in the form of heat. Thus when we shiver, we are accessing the inefficiency of the myosin motor to generate heat.


What are some ways to measure contractility?

1. peak ventricular systolic pressure
2. shift in the position of aortic valve closure in the pressure-volume loop (it will close at higher pressures with increased contractility; up and to the left on the curve)
3. dP/dTmax= maximal rate of change of ventricular pressure rise (mm Hg/sec) during the isovolumetric period (easily measured clinically). So you're looking at wether the slope increases or decreases during that short isovolumetric contraction period (right after the mitral valve closes).
* Note that these indices are not completely independent of preload and afterload and thus NOT ideal measures of contractility.


What will happen ever so slightly to end diastolic pressure when contractility increases over time?

it will decrease


How much can heart rate vary?

from less than 50 bpm to greater than 200 bmp during maximal exercise.
*remember this is a load independent regulation


Do heart rate changes cause proportional changes in cardiac output?

not necessarily


What happens to the duration of the cardiac cycle as heart rate increases?

it decreases. Thus, the time for ventricular filling also decreases leading to reduced EDV and reduced SV


What happens to CO as heart rate increases?

it will go up, but only a little bit because SV is reduced as a consequence.
Remember CO= SV * HR


How does CO compare to increases in HR for untrained individuals when compared to trained athletes?

CO has a larger increase in trained athletes compared to untrained individuals, with increases in HR.


How does SV compare to increases in HR for untrained individuals when compared to trained athletes?

high HR in untrained individuals compromises SV (it actually decreases), but in trained athletes SV only increases as HR increases :)


What happens with decreases in heart rate?

cardiac output remains constant because as diastolic filling time goes up (preload increases) and SV increases! Thus these offset the decrease in HR :)


At what low HR does CO become compromised?

20 bpm


What is the Fick Method of measuring CO?

the quantity of O2 in pulmonary artery plus that added as it passes through the lungs must be equal to that in the pulmonary venous blood (conservation of mass).


How is the Fick Principle (indicator dilution method) carried out to measure CO?

-take 3 measurements: O2 content of lungs, venous blood in right heart, and arterial blood in left heat. Venous blood is 160 ml/L and arterial is 200 ml/L.
So to find CO (in liters), if you know 200 ml/L O2 are entering the lungs every minute, and 40 ml/L is absorbed as the blood passes through the lungs, then 5 L of blood must pass through the lungs each minute to absorb this amount of O2.
CO= (200ml/min / 40ml/L) = 5 L
-You can also inject a dye or warm saline on the venous side and measure the dye concentration in a peripheral artery.
CO= (mg of dye injected * 60) / (average dye conc. per dl of blood for duration of curve (mg/dl) * duration of curve (sec)