^{Pathogenesis of Left-Sided Heart Failure by Jennifer Kong, licensed under CC-BY-NC}

What is Ejection Fraction?  Is Ejection Fraction Always Compromised during Heart Failure?

Ejection fraction is the percentage of blood ejected into the aorta after the left ventricle contracts.  Normally, only 50-75% of the LV volume is ejected into the aorta with each beat: this volume being sufficient to feed both the heart itself and the rest of the body.  However, the impaired pumping ability of Left-sided heart failure may (or may not) affect ejection fraction.  How can you tell?  It depends on whether the changes in the heart structure are predominantly affecting heart pumping (systole) or resting/filling (diastole).

Transverse Plane of Heart Specimens

Anatomy of Left-Sided Heart Failure (Concentric Hypertrophy) – DHPLC Specimen: B0611

Histopathology of Left-Sided Heart Failure

^{Histopathology of Left-sided Heart Failure by Jonathan Bush, licensed under All rights reserved}

Pulmonary Consequences of Left-Sided Heart Failure

Because the left ventricle can not eject sufficient blood into the aorta, there will be leftover blood in the left ventricle. This results in blood backing up from the left ventricle into the left atrium and then the lungs.  Because the lungs have many, many pulmonary vessels which are in close contact with alveoli, there are many pulmonary consequences. This will manifest in problems with breathing and oxygenation.

Pathophysiology of Pulmonary Consequences of Left-Sided Heart Failure

^{Clinical Manifestations of Left-sided Heart Failure by Jennifer Kong, licensed under CC-BY-NC}

Further complications of pulmonary edema will lead to issues with oxygenation of blood and infection since the nutrient-rich fluid in alveoli becomes a very good environment for the growth of pathogens – thus causing pneumonia.

Section Review

• Left sided heart failure occurs when the left ventricle can’t pump as much blood out to the rest of the body.  It can be due to poor pumping abilities (i.e. reduced ejection fraction) or reduced ventricular filling due to heart remodelling to non-compliant tissue (i.e. ejection fraction is normal).  The former can be termed as systolic heart failure and the latter as diastolic heart failure. Regardless of the type, the patient will have signs of symptoms of insufficient blood flow – manifested as weakness & fatigue since muscles can’t get sufficient oxygen nor nutrients.
• To adapt to changes in resistance and/or pumping, the left ventricle will remodel.  The left ventricle can remodel to include more collagen protein that is more stiff, thus making the remodelled ventricle to be less elastic.  To increase pumping force, the cardiomyocytes of the left ventricle can increase its size, filling it with more contractile protein units.  This requires more nuclear activity to the demand for more synthesis of new contractile proteins.
• Because a reduced volume of blood is ejected out of the left ventricle, there is a back-up of blood into the left atrium which has a small fixed volume.  Hence, the blood will continue to back up into the lungs causing pulmonary vessels to be overfilled with blood causing increased blood pressure (pulmonary hypertension).
• Pulmonary hypertension of the pulmonary capillaries will cause leakage of protein-rich plasma-like fluid out of the blood into the alveolar air space causing pulmonary edema. The presence of alveolar fluid can be heard as “crackles” during auscultation.
• The fluid in the alveoli will cause a barrier in gas exchange at the alveolar level, causing poor blood oxygenation (visibly evident with cyanosis) and dyspnea.  Pulmonary edema is also an environment which pathogens are likely to grow, leading to lung infections (pneumonia).

Review Questions