The ejection fraction (EF) is defined as the percentage of end diastolic volume that is ejected during ventricular systole. EF usually applies to the left ventricle (LV).
Normal EF ranges from 55% to 70%.
Physiology Principles
Ejection fraction: EF = (EDV ESV)/EDV
End diastolic volume (EDV): The volume of blood within the ventricle immediately prior to systole
End systolic volume (ESV): The volume of blood within the ventricle immediately after systole
Alternatively, the stroke volume is equal to the difference between the EDV and ESV (SV = EDV ESV)
EF = SV/EDV
As the LV pressure becomes higher than the aortic pressure during systolic contraction, the aortic valve opens. A portion/fraction of the EDV is ejected into the aorta until the aortic valve closes again and the LV begins its isovolemic relaxation phase. Even at a constant contractility, the measured EF can vary with varying preload and afterload.
Frank Starling Law: A larger LV end diastolic volume leads to increased cardiac muscle length with a higher force of contraction that consequently results in an increased EF. This mechanism is exhausted in failing hearts.
Echocardiography is the most frequently used technique to measure EF using M-mode, 2D and 3D modalities.
M-mode measures the fractional shortening (FS) of the mid-LV end diastolic internal diameter during systole. Doubling the FS value can be used to obtain a rough estimate of EF in the absence of optimal images or in the interest of time. Its accuracy is decreased in a ventricle with asymmetric contractility along different planes. The normal range for FS is 2545%.
2D echocardiography uses Simpson's method to calculate EDV and ESV of the LV. The method is based on the division of the LV into multiple discs and summation of individual disc volumes. The data is acquired from apical (transthoracic) or mid-esophageal (TEE) 2- and 4-chamber views and is less affected by abnormal size or asymmetry of the ventricle. Fractional area change (FAC), which is a rough estimation of EF, measures percent change in the area during systole and is calculated by tracing the end diastolic and systolic area of the mid-LV. It is not accurate in a ventricle with asymmetric contractility along its long axis.
3D echocardiography eliminates some of the inherent geometrical assumptions and mathematical modeling needed in the M-mode and 2D methods because the LV image is acquired in its true shape and provides more accurate assessment in the presence of regional dysfunction.
Left ventriculography:
A contrast agent is injected directly into the LV cavity and images are obtained during diastole and systole, most commonly in a 30° right anterior oblique view.
This method is commonly used during diagnostic or therapeutic cardiac catheterization/angiography.
Contraindicated in patients at risk for contrast-induced nephropathy
Magnetic resonance imaging:
Has a high accuracy due to excellent resolution with minimal inter-observer variability and is considered the gold standard
It also uses Simpson's method to calculate LV volume.
Associated with minimal adverse effects
Computed tomography:
Requires IV contrast administration
A slow sinus rhythm is necessary to obtain good quality images.
Can also evaluate any calcification in the coronary arteries
Nuclear medicine technique:
Involves injection of radiotracer material intravenously and analyzing recorded cardiac images
for example, a patient's red blood cells are labeled with Technetium-99 and re-injected intravenously followed by imaging of the LV at a high frame rate.
Anatomy
Depolarization leads to calcium influx into the myocardial cells. The amount of calcium influx coupled with preload (length of cardiac muscle) and afterload (systemic vascular resistance, blood viscosity, aortic valve stenosis) determine the force of contraction.
The heart works as a closed circuit; therefore left and right ventricles, although different in size, thickness, and chamber pressure, have identical EF.
Regional wall motion and aneurysmal abnormalities will impact EF calculations that use linear measurements.
Physiology/Pathophysiology
EF is a good clinical indicator of LV systolic function. A low EF indicates systolic dysfunction due to myocardial ischemia or non-ischemic cardiomyopathy and often leads to signs and symptoms of congestive heart failure (CHF). CHF in the presence of normal EF indicates significant diastolic dysfunction. The lifetime risk of developing CHF is 20% for both men and women.
In the presence of normal ventricular contractility, a higher EDV (e.g., increased venous return or aortic insufficiency) will result in increased EF. Therefore, it is important to report the preload status at the time of the EF measurement.
Low afterload (e.g., low systemic vascular resistance or severe mitral regurgitation) will also result in a higher EF. A normal measured EF in these conditions may actually indicate contractile dysfunction.
Perioperative Relevance
The primary goal in patients with low EF is to:
Focus on the etiology of systolic dysfunction
Optimize preoperative cardiovascular status
Maintain baseline hemodynamics
Minimize cardiovascular stress
In patients with ischemic heart disease, optimize preoperative medical management, decrease preoperative anxiety, and decrease myocardial oxygen demand by controlling heart rate, contractility, and wall tension. Improve myocardial oxygen supply by maintaining optimal hemoglobin levels, oxygenation, and coronary perfusion pressure (CPP).
Elective surgery should be delayed in the presence of active heart failure.
Avoid excessive myocardial suppression by anesthetic agents; expect slow circulation time for all drugs and slow emergence from anesthesia.
Invasive cardiovascular monitoring may be necessary to guide intravascular volume status and control hemodynamics closely.
Patients with significantly low EF (<35%) may have had cardiac resynchronization therapy and/or an implantable cardioverter-defibrillator device placed that will need to be managed appropriately.
Patients with chronic CHF have down-regulation of -1 receptors that might make them less responsive to -agonist therapy in improving contractility and EF. Chronic -blocker therapy up-regulates -1 receptors in these patients and has been shown to improve survival.
The prevalence of diastolic heart failure increases with age. LV hypertrophy from chronic hypertension or aortic stenosis also contributes to increased stiffness and decreased compliance. Maintain preload and adequate diastolic time. Lusitropic agents such as milrinone may be effective in improving cardiac output. Most anesthetic agents do not impair diastolic function.
Pediatric Considerations
The myocardium in children, especially neonates, is less compliant compared to an adult heart. Therefore, it is much more sensitive to small changes in in heart rate, preload, and afterload.
Equations
SV = EDV - ESV; where SV is stroke volume, EDV is end diastolic volume, and ESV is end systolic volume
EF = (100 × SV)/EDV; where EF is ejection fraction, SV is stroke volume, and EDV is end diastolic volume
Lloyd-JonesDM, LarsonMG, LeipEP, et al.Lifetime risk for developing congestive heart failure: The Framingham Heart Study. Circulation. 2002;106:30683072.
RamaniGV, UberPA, MehraMR.Chronic heart failure: Contemporary diagnosis and management. Mayo Clin Proc. 2010;85:180195.
San RománJA, Candell-RieraJ, ArnoldR, et al.Quantitative analysis of left ventricular function as a tool in clinical research: Theoretical basis and methodology. Rev Esp Cardiol. 2009;62:535551.
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