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Cardiac Output

Cardiac output is the volume of blood the left ventricle pumps out to the body per minute. The main purpose of the heart is to maintain cardiac output at an appropriate level to perfuse all of our organs. The units for cardiac output are volume/time (mL/min). Cardiac output can be expressed as the product of stroke volume (SV) and heart rate (HR).

Cardiac output increases if SV increases (if the heart pumps out more volume per heartbeat, more blood is pushed out to the body per minute). Cardiac output increases in HR increases (if the heart beats more times per minute, it pushes more blood out to the body per minute).

If cardiac output decreases to a significant degree (where our organ systems are not being perfused properly), this is considered heart failure (HF). In fact, the hallmark of HF is low cardiac output.


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Stroke Volume

Stroke volume (SV) is the amount of blood that is pumped out of the left ventricle (LV) in one heartbeat. SV depends on both a.) the ability of the LV to fill with blood properly, and b.) the ability of the LV to pump that blood properly.

Stroke volume depends on three main factors:

  1. Contractility: As contractility increases, SV increases. If LV myocytes are more contractile (able to generate more force during each contraction), then they will be able to pump out a greater volume of blood per heartbeat.
  2. Preload: As preload increases, SV increases. If more blood is returning to the heart from the venous system, then the LV will fill with more blood during each round of diastole. As long as the LV maintains its contractile force, then more blood in the LV at the start of each contraction means that more blood will be pumped out with each heartbeat.
  3. Afterload: As afterload increases, SV decreases. If the pressure in the body that the LV needs to push against during each heartbeat increases, then it will be harder for the LV to push out the same amount of blood as it would it were pushing out to a lower pressure system. Therefore, if the force the LV can generate with each contraction is held constant, then the LV will pump out a lower volume of blood as the pressure it pumps against rises.

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Heart Rate

Heart rate (HR) is the number of times the heart beats per minute. Typically, as HR increases, cardiac output also increases (if the heart beats more times per minute, it pushes more blood out to the body per minute).

Heart Rate and Stroke Volume

As HR increases, stroke volume (SV) decreases. This is because as HR increases, the time for ventricular filling between heartbeats gets shorter. In this case, less blood fills the LV during diastole and, therefore, less blood is available to pump out with each heart beat (and SV goes down, which has the potential to decrease cardiac output). These opposing effects on cardiac output get tricky to think about when we consider the fact that cardiac output is the product of HR and SV. However, the general rule of thumb is still that as HR increases, cardiac output increases, because an increase in HR increases the cardiac output to a greater degree than a decrease in SV decreases the cardiac output.

Heart Rate and Contractility

Increases in HR produce increases in contractility. ***.

Regulation of Heart Rate

The heart rate is normally set at the depolarization rate of the SA node, which is considered the "pacemaker" of the heart. The SA nodal cells--and therefore heart rate--are regulated by the autonomic nervous system. The autonomic nervous system effects on heart rate are "chronotropic effects".


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Contractility

Contractility is a property of atrial and ventricular myocytes and refers to the ability of these myocytes to generate force during muscle contraction to push out blood.

Contractility is one of the main determinants of stroke volume (SV): As contractility increases, SV increases. If myocytes become more contractile, they are able to generate more force--and therefore pump harder and eject more blood--with each heartbeat.

Contractility can be estimated by the left ventricle's (LV) ejection fraction (EF), or the percentage of blood in the LV that is pumped out with each heartbeat. If contractility of the LV increases, the EF will increase, because the LV will be able to generate more force to pump out more blood during systole, given a constant starting volume.

Regulation of Myocyte Contractility

The main way myocytes can increase contracility is by increasing their amount of intracellular Ca2+ during cardiac muscle contraction. There are two main ways atrial and ventricular myocytes can increase the amount of Ca2+ available for muscle contraction: 1.) increase the Ca2+ influx during the plateau phase of an action potential, and 2.) increase the amount of Ca2+ stored/released from the sarcoplasmic reticulum. Ca2+ movements in myocytes--and therefore contractility--are regulated by the autonomic nervous system. The autonomic nervous system effects on contractility are "inotropic effects".

Contractility is also increased with increased preload. ***.


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Ejection Fraction

Ejection fraction (EF) is the percentage of blood in a filled left ventricle (LV) that is pumped out to the body in one heartbeat. The LV does not typically pump out 100% of the blood that it contains at the end of diastole (ventricular filling). A normal EF is around 55-70%, meaning that the left ventricle only pumps out about 55-70% of the blood it contains with each heartbeat. Ejection fraction can be expressed as:

EF can be used as an estimation of the contractility of the cardiac muscle, or the force the cardiac myocytes generate during each contraction. If contractility of the LV increases, the EF will increase, because the LV will be able to generate more force to pump out more blood during systole, given a constant starting volume.

Ejection Fraction and Heart Failure

In important clinical correlate of EF is when it is used to describe heart failure. In general, heart failure is characterized by a decrease in cardiac output. However, there are two kinds of heart failure, which depend on whether EF is reduced or not reduced (preserved):

  • Heart failure with reduced EF (HFrEF): This refers to "systolic heart failure (HF)". When a person has HF with systolic dysfunction, it means that they have a problem pumping blood out of the LV. Let's say that in a normal heartbeat, the LV gets filled with 100mL of blood by the end of diastole and pumps out 60mL of blood during systole (so the EDV is 100mL, and the SV is 60mL). This gives us a normal EF of 60%. In systolic HF, the problem is with pumping--so we will fill normally (EDV of 100mL), but we won't pump normally (we have SV of, let's say, 40mL). This will certainly decrease our cardiac output (because we went from pumping out 60mL of blood every heartbeat to just 40mL), so we will be diagnosed with HF. Our new EF will be 40% (40mL/100mL), which is below the normal limit of 55-70%, so we will have "HF with reduced EF".
  • Heart failure with preserved EF (HFpEF): This refers to "diastolic heart failure (HF)". When a person has heart failure with diastolic dysfunction, it means that their LV can pump fine, but they have a problem with filling the ventricle. Let's again say that in a normal heartbeat, the LV gets filled with 100mL of blood by the end of diastole and pumps out 60mL of blood during systole (so the EDV is 100mL, and the SV is 60mL, giving us a normal EF of 60%). In diastolic HF, we won't fill normally during diastole (we have an EDV of, let's say 70mL, instead of our normal 100mL). We don't have any problem with pumping during systole, so for every heartbeat, we still pump out about 60% of our LV's blood volume. But 60% of 70mL is only around 40mL (so our SV for each heartbeat is only 40mL). This will certainly decrease our cardiac output (because we went from pumping out 60mL of blood for every heartbeat to just 40mL), so we will be diagnosed with HF. However, 40mL/70mL gives us an EF of 60%, which is normal, so we will have "HF with preserved EF".