As we learned in Part 1 of this article, EF is one of the most, if not THE most important thing to know about any patient that you are preoping because of the profound implications of EF on a patient’s overall health as well as how the patient will respond to anesthesia.
Here’s how the American Heart Association classifies ejection fraction:
- 50 - 70% -- Normal
- 40 - 49% -- Borderline
- Less than 40% -- Reduced
The Cleveland Clinic refines this a bit more:
- 55 - 70%-- Normal
- 40 - 54% -- Slightly below normal
- 35 - 39% -- Moderately below normal
- Less than 35% -- Severely below normal
Ejection fraction is important because it determines how much blood gets pumped out of the heart with every heartbeat. The volume of blood that gets pumped out with each contraction of the heart is known as “stroke volume” (normal is about 70 - 100cc). Stroke volume times a patient’s heart rate equals cardiac output. So a patient with a stroke volume of 100cc and a heart rate of 60 would have a cardiac output of 6,000cc per minute (6.0 liters per minute).
Remember, the heart is just a pump for blood. A cardiac output of 5 - 6 liters per minute (correspondingly less for small adults and children) is the normal output of the pump. The other organs and tissues of the body need to receive this much oxygenated blood in order to perform normally. Imagine that rather than talking about a heart and tissues we are talking about an irrigation pump and crops. It is pretty easy to understand that in order for the crops to survive, the irrigation pump needs to continue to deliver an adequate amount of water every day.
So how does the body respond to a decrease in ejection fraction? Initially, it will try to compensate. The first thing that happens is that the heart rate will increase, i.e., the heart will pump a smaller stroke volume more times per minute. Over a longer period of time, the heart will dilate (get bigger) so that even if it has an ejection fraction of only 40%, the 40% ejected will be a larger stroke volume because the capacity of the left ventricle when it is full (left ventricular end diastolic volume) has increased.
Eventually however, these compensatory mechanisms are not enough and the patient’s cardiac output will decrease. This causes systemic effects as every organ and every tissue in a patient’s body receives less oxygen than normal.
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