Heart Failure

Left-Sided Heart Failure: From Cellular to Clinical

Jennifer Kong and Helen Dyck

Learning Objectives

By the end of this section, you will be able to:

  • Define ejection fraction.
  • Describe the pathophysiology and histopathology of left-sided heart failure.
  • List common signs and symptoms of left-sided heart failure.
  • Explain the development and histological appearance of pulmonary edema due to left sided heart failure.
  • Correlate the signs and symptoms listed on a patient chart/card with your understanding of the pathophysiology of left-sided heart failure.

Pathogenesis of Left-Sided Heart Failure

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

Transverse Plane of normal vs. hypertrophic heart by Jennifer Kong, licensed under All rights reserved

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

 

Gross Anatomy of Concentric Hypertrophy by Helen Dyck, licensed under All rights reserved

 

Critical Thinking and Histopathology Exercises

Now that you have viewed the gross specimen of concentric hypertrophy, consider the following questions.  Record your answers for yourself before viewing the next video on the “Histopathology of Heart Failure”.

  • Recall the histology of the H&E stained normal heart.  How much sarcoplasm (pink) was there in comparison to nuclei (purple)?
  • Thinking about the pathophysiology of concentric hypertrophy, what would you expect to see in the cardiomyocyte?  Will there be a change in sarcoplasm and/or nuclear size?
  • Cardiac remodelling is common in hypertrophy and heart failure – particularly the increased presence of collagen. What would these non-contractile cells and proteins look like histologically?

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

Pulmonary Consequences of Left-sided Heart Failure by Jennifer Kong, licensed under CC-BY-NC

Histopathology of Pulmonary Edema Due to Left-Sided Heart Failure

With excess blood filling the pulmonary vasculature, there is increase pressure in the pulmonary vessels.  This will cause two immediate effects:

  1. Increased pulmonary blood pressure (pulmonary hypertension) can ‘push’ fluid out of the pulmonary capillaries.
  2. Alveoli fill with fluid from the blood in the pulmonary capillaries causing more complications:
    •  a barrier to gas exchange between the airways and pulmonary capillaries. –> decreased oxygenation of blood and retention of CO2.

These effects result in pulmonary edema – or “excess fluid in the lungs”.  The fluid in the lungs are very similar to plasma in the blood  – thus it is fluid filled with protein and nutrients.

One can see this fluid  at the gross anatomy level and histologically:

Histopathology of Pulmonary Edema Due to Left-sided Heart Failure by Jonathan Bush, licensed under All rights reserved

Pathology of Pulmonary Edema Due to Left-Sided Heart Failure

Gross Anatomy of Pulmonary Edema Due to Left-sided Heart Failure by Helen Dyck, licensed under All rights reserved

Signs and Symptoms 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.

Summary Exercises

Consolidate your knowledge of left sided heart failure by creating a mind map or diagram of the pathophysiology of Left-sided heart failure.  Consider including these concepts to help you deepen your understanding

  • Chronically high afterload (e.g. stiff aortic valve that is hard to open)
  • Increased sarcoplasm (pink) and larger nuclei
  • Reduced ejection fraction
  • Increase LV wall thickness

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

definition

License

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Pathology Copyright © 2022 by Jennifer Kong and Helen Dyck is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.

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