# Calculating heart stroke volume

## stroke

CO is a product of blood volume per heart stroke and heart rate. The higher/better the stroke volume (weak, strong, stronger contractions) the fewer heart beats (more for weak, less for strong, least for stronger) are required to meet demand (held constant for illustration) for blood oxygen. A well-condition individual requires fewer heartbeats due to strong contractions. It is the stroke that determines EF...not the CO, as CO can vary by an increase or decrease of HR.
This happens by a system of vasodilation and vasoconstriction coupled with the pumping rate and stroke volume of the heart. Rather than make frequent changes in volume, the body changes the configuration of the total container (all the vessels) and increases the speed at which the resource is renewed.
Stroke volume is a calculation to determine ejection fraction (EF)...the amount of blood pumped into circulation with each heartbeat. The calulation for EF is volume of blood in the left ventricle at systole (pumping) phase. Subtract the volume left in the ventricle after diastolic (filling) phase. Then divide the volume of blood during systole for a fraction...that would be EF. Your EF idicates you have a normal pumping heart. Normal is 50 to 70%.
EF is a compensating factor and helps maintain a balancing flow of blood between the right and left side of the heart. Stroke volume is inverse to the heart rate. Slow heart rate the greater the stroke volume which indicates the heart rate is also a compensating factor...the slower the heart rate the more time to fill. Wide pulse pressure (no medication, etc) can be the outcome of increased CO due to fitness, anxiety, hyperthyroidism, etc.
Over many, many years, with high blood pressure and being very overweight, the inside of your ventrical gets thicker, and the volume inside therefore decreases, decreasing stroke volume and causing your heart rate to become higher and your heart then has to work harder to pump the same amount of blood, which over many years causes the ventricular walls to stiffen. I hope that clarifies some of it.
The volume of blood left in a ventricle at the end of contraction is end-systolic volume. The difference between end-diastolic and end-systolic volumes is the stroke volume, the volume of blood ejected with each beat. Ejection fraction (Ef) is the fraction of the end-diastolic volume that is ejected with each beat; it is stroke volume divided by end-diastolic volume. Normal in a man is 50-68%.
The left venticle will dilate to increase blood flow with each stroke and the heart rate will increase the cardiac output (amount of blood pumped per minute). If the system is dysfunctional, medication, etc. can change the dynamics. For instance heart failure increases blood volume and the kidneys react as if the individual is losing blood...the increase of volume further distresses the heart and kidneys continue to believe the system is losing blood.
For a perspective, diastole dysfunction compromises left ventricle filling volume, inadequate stroke volume and operating at a high pressure regimen. LV filling volume is reduced due to increased wall size crowding out available space. Inadequate stroke volume is usually due to wall thickening and stiffening and loss of elasticity. High pressures can dilate upper chamber to compensate for gradient pressure across the mitral valve. That is the pathology.
A faster heartbeat does not provide enough time to fill as at rest, and the timing of contractions are less. The percent of blood pumped with each heartbeat is less reducing stroke volume (lower EF). The heart rate has increased to provide the necessary blood/oxygen to meet the system's demand for the diminished stroke volume. The CT scan indicates there is substanital soft plaque buildup within the linings of the vessels.
To maintain adequate blood flow with a decrease in stroke volume is to increase the heart rate. The math for cardiac output is stroke volume times heart rate for one minute. Frankly, I don't believe you have significant MVR because you should also have the symptoms of shortness of breath with exertion and muscle fatigue.
An echo calculates heart chamber diminsions and volume of blood pumped with each stroke. The math equation is diastole volume (peak filling) minus systole (volume after pumping) divided by diastole for the percentage. You can calculate your fraction shortening (FS) which is similar to EF but relies on dimensions rather than volume. To calculate subtract systole dimension from diastole dimension and divide by diastole for percentage. FS is an estimate of myocardial contractility.
When there is a significant drop in CO the vessel enthelium cells sends a message to increase the blood volume (recognized and not able to distinquish if there is a serious blood loss). The system controls stroke volume by venus return. Stroke volume AND heart rate determine CO (cardiac output). I believe you may be confused by not recognizing the determinants of the venus return phenomonon. Heart rate is result of sympthetic and parasympthetic input.
So I am thinking that I am just very deconditioned and my stroke volume is low and I need to wait for changes in muscle growth and circulation in my legs too. Am I too old to really increase my heart efficiency and stroke volume now?
For instance, how are systemic vascular resistance, blood volume, stroke volume, cardiac output, etc affected. I am wondering if an HOCM heart relies on a hyperdynamic state from hyperthyroidism, and if going euthyroid will harm the cat.
d expect the stroke volume to be inverse to the Heart Rate - e.g. a well-conditioned person would have a low HR with a low BP but a high stroke volume with every beat. As far as poisoning, it'd seem natural for the system to go into high gear to remove the poison - but 4 months would sure be a long time for that, unless it created some semi-permanent change in you somehow.
In this phase due to F/S phenomonon the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation (volume overload can be do to other causes), and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume dilates left ventricle.
Diastolic volume (filling phase) per stroke is blood volume measured at end of diastolic (maximum filling capacity...relaxed state) minus the volume at the end of systole (minimum amount of blood left in the chamber). Divide end diastolic volume into the difference between end systole and end diastole is the fraction (%) pumped with each stroke. CHF by definition is an EF below 29% (left side non-compliance) indicating there may be an insufficient blood/oxygen supply meeting system demand.
If you were nervous or stressed out than that can cause your heart to beat faster and more powerfully (stroke volume increases) and it makes much more obvious. Again, perfectly normal and nothing to be concerned over.
This is why athletes hearts can pump blood so much more efficiently around the body. The heart muscle increases and the internal volume increases, allowing more blood to be pushed out with each stroke.
Return of systemic blood to the heart is impeded by the pressure inside the chest. The output of the heart is reduced and stroke volume falls. This occurs from 5 to about 14 seconds in the illustration. The fall in stroke volume reflexively causes blood vessels to constrict with some rise in pressure (15 to 20 seconds). This compensation can be quite marked with pressure returning to near or even above normal, but the cardiac output and blood flow to the body remains low.
When the EF is 30% or less it is medically considered heart failure range and often the heart is unable (weak heart muscles) to pump into circulaion the blood/oxygen received from the lungs and the blood backs up into the lungs and fluids leak into the tissues (pulmonary edema) and causes congested heart failure. Lasix is prescribed to reduce the fluid build up in the lungs.