{"id":332,"date":"2021-05-31T15:23:25","date_gmt":"2021-05-31T19:23:25","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathology\/?post_type=chapter&#038;p=332"},"modified":"2025-11-14T22:49:05","modified_gmt":"2025-11-15T03:49:05","slug":"classification-causes-of-heart-failure-2","status":"publish","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathology\/chapter\/classification-causes-of-heart-failure-2\/","title":{"raw":"Types and Causes of Left Heart Failure","rendered":"Types and Causes of Left Heart Failure"},"content":{"raw":"<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Objectives<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nBy the end of this section, you will be able to:\r\n<ul>\r\n \t<li>Define heart failure, ejection fraction, and hypertrophy.<\/li>\r\n \t<li>Differentiate between the heart failure types: right- vs left-sided, systolic vs diastolic, heart failure with preserved vs reduced ejection fraction.<\/li>\r\n \t<li>Explain the common causes of heart failure.<\/li>\r\n \t<li>Differentiate between concentric vs eccentric hypertrophy.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<h2>What is Heart Failure?<\/h2>\r\nHeart failure is when your heart muscle can not contract strongly enough to eject all of its blood to its destination. As a result, the heart can't deliver the blood needed for the body to function well AND a redistribution (i.e. backup) of blood due to the poor pumping. As a result, heart failure will have signs and symptoms in both the cardiovascular and non-cardiac systems.\r\n<h2>What is Ejection Fraction? Is Ejection Fraction Always Compromised during Heart Failure?<\/h2>\r\nEjection fraction (EF) 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 heart failure may (or may not) affect ejection fraction. How can you tell? It depends on whether the changes in the heart structure (type of hypertrophy) are predominantly affecting heart pumping (systole) or resting\/filling (diastole).\r\n<h2>Types of Left Heart Failure<\/h2>\r\nThe type of heart failure depends on the location of the poor pumping.\u00a0 If the right ventricle is too weak in pumping, this is called \"right sided heart failure.\"\u00a0 If the left ventricle has poor pumping abilities, this is called \"left-sided heart failure.\"\r\n\r\nLeft sided heart failure can be subdivided into two subtypes:\r\n<ul>\r\n \t<li>systolic failure (a.k.a. heart failure with reduced ejection fraction. Subdivided into mildly reduced and reduced EF)<\/li>\r\n \t<li>diastolic failure (a.k.a. heart failure with preserved ejection fraction)<\/li>\r\n<\/ul>\r\n<h2>Conditions that Lead to Heart Failure<\/h2>\r\n<div>\r\n\r\nHeart failure is a result of injury to the heart and\/or the heart can't keep up with what the body needs due to a variety of reasons.\u00a0 Regardless of which type of heart failure, heart failure is commonly caused by:\r\n<ul>\r\n \t<li>Asking the heart to work abnormally hard\u00a0 for too long due to some kind of increased resistance downstream of the ventricle (i.e. [pb_glossary id=\"471\"]afterload[\/pb_glossary]):\r\n<ul>\r\n \t<li>Valvular disease, chronic high blood pressure, severe lung disease<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>The heart muscle is directly hurt by:\r\n<ul>\r\n \t<li>Not enough oxygen or nutrients to feed the heart muscle during pumping (e.g. decrease blood flow to coronary arteries due to coronary artery disease)<\/li>\r\n \t<li>Increased workload for remaining undamaged heart tissue (e.g. previous myocardial infarction causing loss of viable heart tissue)<\/li>\r\n \t<li>Aging<\/li>\r\n \t<li>Damage due to infection or inflammation<\/li>\r\n \t<li>Certain medications and illicit drugs<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Heart is not 'made well' (i.e. abnormal structure) thus can't contract and fill efficiently. Examples of\u00a0 abnormal structure are:\r\n<ul>\r\n \t<li>Congenital (i.e. since birth) heart defect of muscles and\/or valves,<\/li>\r\n \t<li>Defects in heart's electrical system causing arrhythmias - resulting in heart beating too fast, slow, or irregular.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h2>Concentric versus Eccentric Hypertrophy<\/h2>\r\n<div>\r\n<h3>What is Hypertrophy?<\/h3>\r\nHearts, like any muscle, get bigger and thicker when it has a lot of resistance\/workload to frequently push against. It's like lifting hand weights to increase the size of the bicep.\u00a0 The cells in heart tissue get individually larger - not more numerous. This enlargement of muscle cells - whether it's cardiac or skeletal muscle - is known as [pb_glossary id=\"271\"]hypertrophy[\/pb_glossary].\u00a0 The muscle cell hypertrophies because it is adding more contractile proteins to enable greater contractile strength. Going back to the bicep example - the larger bicep is because each individual bicep muscle cell undergoes hypertrophy even though it has not changed in muscle cell number. This would be an example of physiologic hypertrophy.\r\n\r\nThus, the walls of muscle hypertrophy when there is chronically a lot of resistance\/workload. That means each cardiomyocyte is undergoing hypertrophy, rather than dividing into more cells ([pb_glossary id=\"272\"]hyperplasia[\/pb_glossary]), as cardiomyocytes can't undergo cell division.\r\n\r\nDuring hypertrophy, cells of the heart wall can:\r\n\r\na) Become bigger in circumference. These plumper cardiomyocytes make the heart wall grow thicker from the outside in, resulting in the heart becoming heavier. The larger in circumference the cells get, the harder it is for oxygen and nutrients to diffuse inside the cell, which will eventually cause metabolic problems. This is the basis of concentric hypertrophy and remodeling.\r\n\r\nor\r\n\r\nb) Become longer in length and more narrow in circumference. These narrower cardiomyocytes are 'stretched out' because the heart wall is undergoing more tension with over-filling with blood volume. To adapt to this stretching, the heart remodels by replacing contracting cardiomyocytes with non-contractile cardiac cells. As a result, the heart wall get thinner with weaker contractile strength. This is the basis of eccentric hypertrophy.\r\n\r\nc) Remodel (i.e. change their cellular make up in tissue). When the cardiomyocytes do not get enough oxygen and\/or nutrients (e.g.\u00a0 heart attack, extreme hypertrophy) or receive increased inflammatory signals (e.g. inflammation, infection), the cardiomyocytes will die. As a result, the cardiomyocytes are then replaced with connective tissue - principally collagen - which is NOT contractile. The heart tissue becomes less contractile, making it harder to empty the chamber. In addition, the collagen- filled heart wall becomes stiffer and not as stretchy to fill easily.\r\n<h4>Concentric Hypertrophy<\/h4>\r\nConcentric hypertrophy occurs when the left ventricular wall has increased demand and\/or afterload.\u00a0 If this is within physiological means, the heart gets bigger (ie concentric hypertrophy) to meet the demand. This is the case with larger body sizes and atheletes.\r\n\r\nHowever, if the heart is remodelling due to a chronically increased resistance to push against, this leads to a pathological concentric hypertrophy and remodeling (a.k.a. concentric remodeling).\u00a0 The LV wall gets thicker (due to plumper cardiomyocytes) resulting in\u00a0 the space within the ventricle (i.e. lumen) shrinking. This shrinkage of lumen means less volume of blood available to fill during diastole. At first, ejection fraction is preserved despite less diastolic filling, thus giving rise to the alternate terms of \"[pb_glossary id=\"80\"]diastolic heart failure [\/pb_glossary]\" or \"heart failure with preserved ejection fraction.\"\u00a0 Because ejection fraction is preserved, the body is getting sufficient supply of blood and thus there would be few signs\/symptoms.\r\n\r\nHowever, as the wall gets thicker, it becomes stiffer and not as \"stretchy\" to fill easily.\u00a0 Eventually, there will be a point where the diastolic filling volume will not be enough to maintain sufficient ejection fraction, regardless of how well the LV wall can pump. This is when signs and symptoms will begin to be noticed.\r\n<h4>Eccentric Hypertrophy<\/h4>\r\nWhen the heart chambers get overloaded with volume, the cells of the heart wall will compensate by becoming thinner &amp; longer.\u00a0 This overfilling will cause the heart to remodel into a larger lumen with thinner walls and less contractile strength. If this eccentric hypertrophy occurs in the ventricle, this would be [pb_glossary id=\"82\"]systolic failure[\/pb_glossary] or \"heart failure with reduced ejection fraction\" as the volume to pump is sufficient but the pumping ability is too weak. Unfortunately, as ejection fraction is reduced, there will be even more fluid left in the chamber - thus complicating the already chronic volume overload.\r\n<div>\r\n\r\n&nbsp;\r\n\r\n<\/div>\r\n<div class=\"textbox textbox--exercises\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Critical Thinking and Histopathology Exercises<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\nNow that you have viewed the gross specimen of concentric hypertrophy, consider the following questions.\u00a0 Record your answers for yourself before viewing the next video on the \"Histopathology of Heart Failure.\"\r\n<ul>\r\n \t<li>Recall the histology of the H&amp;E stained normal heart.\u00a0 How much sarcoplasm (pink) was there in comparison to nuclei (purple)?<\/li>\r\n \t<li>Thinking about the pathophysiology of concentric hypertrophy, what would you expect to see in the cardiomyocyte?\u00a0 Will there be a change in sarcoplasm and\/or nuclear size?<\/li>\r\n \t<li>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?<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<h2>Histopathology of Left-Sided Heart Failure<\/h2>\r\n<div><\/div>\r\n[h5p id=\"34\"]\r\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Histopathology of Left-sided Heart Failure by Jonathan Bush, licensed under <a href=\"https:\/\/choosealicense.com\/no-license\/\">All rights reserved<\/a><\/sup><\/p>\r\n\r\n<h2>Clinical Manifestations of Left Sided heart failure<\/h2>\r\n[h5p id=\"443\"]\r\n\r\n&nbsp;\r\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Clinical Manifestations of Left sided Heart Failure by Jennifer Kong, licensed under under\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\" rel=\"noopener\">Creative Commons Attribution-NonCommercial 4.0 International License<\/a><\/sup><\/p>\r\n&nbsp;\r\n\r\n...\r\n<div>\r\n<h2>Pulmonary Consequences of Left-Sided Heart Failure<\/h2>\r\nBecause 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.\r\n\r\n<\/div>\r\n<h2 style=\"text-align: left\">Histopathology of Pulmonary Edema Due to Left-Sided Heart Failure<\/h2>\r\nWith excess blood filling the pulmonary vasculature, there is increase pressure in the pulmonary vessels. This will cause two immediate effects:\r\n<ol>\r\n \t<li>Increased pulmonary blood pressure (pulmonary hypertension) can 'push' fluid out of the pulmonary capillaries.<\/li>\r\n \t<li>Alveoli fill with fluid from the blood in the pulmonary capillaries causing more complications:\r\n<ul>\r\n \t<li>\u00a0a barrier to gas exchange between the airways and pulmonary capillaries. --&gt; decreased oxygenation of blood and retention of CO2.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\nThese effects result in pulmonary edema - or \"excess fluid in the lungs.\" The fluid in the lungs are very similar to plasma in the blood\u00a0 - thus it is fluid filled with protein and nutrients.\r\n\r\nOne can see this fluid\u00a0 at the gross anatomy level and histologically:\r\n\r\n[h5p id=\"35\"]\r\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Histopathology of Pulmonary Edema Due to Left-sided Heart Failure by Jonathan Bush, licensed under <a href=\"https:\/\/choosealicense.com\/no-license\/\">All rights reserved<\/a><\/sup><\/p>\r\nFurther 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.\u00a0 For greater detail, refer to our chapter on\u00a0 <a href=\"https:\/\/pressbooks.bccampus.ca\/pathology\/part\/pneumonia-and-pulmonary-edema\/\">Pneumonia and Pulmonary Edema<\/a>.\r\n<div class=\"textbox textbox--exercises\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Summary Exercises<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n<div data-wp-editing=\"1\">\r\n<div class=\"textbox textbox--exercises\">\r\n<div class=\"textbox__content\">\r\n\r\nConsolidate 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\r\n<ul>\r\n \t<li>Chronically high afterload (e.g. stiff aortic valve that is hard to open)<\/li>\r\n \t<li>Increased sarcoplasm (pink) and larger nuclei<\/li>\r\n \t<li>Reduced ejection fraction<\/li>\r\n \t<li>Increase LV wall thickness<\/li>\r\n<\/ul>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<h2>Section Review<\/h2>\r\n<ul>\r\n \t<li class=\"textbox__content\">You can have both concentric and eccentric cardiomyopathy if the heart has to deal with both increased pressure and increased volume.<\/li>\r\n \t<li class=\"textbox__content\">Both systolic and diastolic failure have the same end result: the heart can't pump enough blood out to feed the body.<\/li>\r\n \t<li>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 &amp; fatigue since muscles can't get sufficient oxygen nor nutrients.<\/li>\r\n \t<li>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 remodeled 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.<\/li>\r\n \t<li>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).<\/li>\r\n \t<li>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 [pb_glossary id=\"1431\"]auscultation[\/pb_glossary].<\/li>\r\n \t<li>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).<\/li>\r\n<\/ul>\r\n<h2><\/h2>\r\n<ul>\r\n \t<li class=\"textbox__content\"><\/li>\r\n<\/ul>\r\n<h1>Review Questions<\/h1>\r\n<div class=\"h5p\">[h5p id=\"232\"]<\/div>\r\n<div>[h5p id=\"233\"]<\/div>\r\n<div class=\"pdf\">\r\n\r\n<strong>1. Concentric hypertrophy will have a larger lumen size for filling and is thus associated with systolic failure.<\/strong>\r\n<ul>\r\n \t<li>True<\/li>\r\n \t<li>False<\/li>\r\n<\/ul>\r\n<strong>2. Put the types of left-sided heart failure in the correct column.<\/strong>\r\n<table style=\"border-collapse: collapse;width: 100%\" border=\"0\">\r\n<tbody>\r\n<tr>\r\n<td style=\"width: 50%\">caused by increased resistance (afterload)\r\n\r\ncaused by overfilling of the heart\r\n\r\neccentric hypertrophy<\/td>\r\n<td style=\"width: 50%\">diastolic filling is reduced\r\n\r\ncontraction during systole is weaker\r\n\r\nconcentric hypertrophy<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\" border=\"0\">\r\n<tbody>\r\n<tr>\r\n<td style=\"width: 675.562px\"><strong>Abnormally Thick Ventricular Walls\u00a0<\/strong><\/td>\r\n<td style=\"width: 675.562px\"><strong>Abnormally Thin Ventricular Walls<\/strong><\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 675.562px\">&nbsp;\r\n\r\n&nbsp;\r\n\r\n&nbsp;<\/td>\r\n<td style=\"width: 675.562px\"><\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<strong>3. Choose the correct statement.<\/strong>\r\n<ul>\r\n \t<li>Heart failure occurs when the heart cannot pump out sufficient blood with each ejection.<\/li>\r\n \t<li>Heart failure involves enlargement of the heart walls, due to hyperplasia.<\/li>\r\n \t<li>Heart failure is caused by chronically circulating reduced blood volume.<\/li>\r\n \t<li>Heart failure is mainly divided into those with preserved vs reduced ejection fraction.<\/li>\r\n<\/ul>\r\n<div><\/div>\r\n<div class=\"textbox\">\r\n<h2>Answer Key<\/h2>\r\n<ol>\r\n \t<li>False<\/li>\r\n \t<li>\r\n<table class=\"lines\" style=\"border-collapse: collapse;width: 100%\" border=\"0\">\r\n<tbody>\r\n<tr>\r\n<td style=\"width: 675.562px\"><strong>Abnormally Thick Ventricular Walls\u00a0<\/strong><\/td>\r\n<td style=\"width: 675.562px\"><strong>Abnormally Thin Ventricular Walls<\/strong><\/td>\r\n<\/tr>\r\n<tr>\r\n<td style=\"width: 675.562px\">concentric hypertrophy\r\ndiastolic filling is reduced\r\ncaused by increased resistance (afterload)<\/td>\r\n<td style=\"width: 675.562px\">caused by overfilling of the heart\r\nContraction during systole is weaker\r\neccentric hypertrophy<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<\/li>\r\n \t<li>Heart failure occurs when the heart cannot pump out sufficient blood with each ejection.<\/li>\r\n<\/ol>\r\n<\/div>\r\n<div><\/div>\r\n<div><\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>","rendered":"<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Objectives<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>By the end of this section, you will be able to:<\/p>\n<ul>\n<li>Define heart failure, ejection fraction, and hypertrophy.<\/li>\n<li>Differentiate between the heart failure types: right- vs left-sided, systolic vs diastolic, heart failure with preserved vs reduced ejection fraction.<\/li>\n<li>Explain the common causes of heart failure.<\/li>\n<li>Differentiate between concentric vs eccentric hypertrophy.<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<h2>What is Heart Failure?<\/h2>\n<p>Heart failure is when your heart muscle can not contract strongly enough to eject all of its blood to its destination. As a result, the heart can&#8217;t deliver the blood needed for the body to function well AND a redistribution (i.e. backup) of blood due to the poor pumping. As a result, heart failure will have signs and symptoms in both the cardiovascular and non-cardiac systems.<\/p>\n<h2>What is Ejection Fraction? Is Ejection Fraction Always Compromised during Heart Failure?<\/h2>\n<p>Ejection fraction (EF) 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 heart failure may (or may not) affect ejection fraction. How can you tell? It depends on whether the changes in the heart structure (type of hypertrophy) are predominantly affecting heart pumping (systole) or resting\/filling (diastole).<\/p>\n<h2>Types of Left Heart Failure<\/h2>\n<p>The type of heart failure depends on the location of the poor pumping.\u00a0 If the right ventricle is too weak in pumping, this is called &#8220;right sided heart failure.&#8221;\u00a0 If the left ventricle has poor pumping abilities, this is called &#8220;left-sided heart failure.&#8221;<\/p>\n<p>Left sided heart failure can be subdivided into two subtypes:<\/p>\n<ul>\n<li>systolic failure (a.k.a. heart failure with reduced ejection fraction. Subdivided into mildly reduced and reduced EF)<\/li>\n<li>diastolic failure (a.k.a. heart failure with preserved ejection fraction)<\/li>\n<\/ul>\n<h2>Conditions that Lead to Heart Failure<\/h2>\n<div>\n<p>Heart failure is a result of injury to the heart and\/or the heart can&#8217;t keep up with what the body needs due to a variety of reasons.\u00a0 Regardless of which type of heart failure, heart failure is commonly caused by:<\/p>\n<ul>\n<li>Asking the heart to work abnormally hard\u00a0 for too long due to some kind of increased resistance downstream of the ventricle (i.e. <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_471\">afterload<\/a>):\n<ul>\n<li>Valvular disease, chronic high blood pressure, severe lung disease<\/li>\n<\/ul>\n<\/li>\n<li>The heart muscle is directly hurt by:\n<ul>\n<li>Not enough oxygen or nutrients to feed the heart muscle during pumping (e.g. decrease blood flow to coronary arteries due to coronary artery disease)<\/li>\n<li>Increased workload for remaining undamaged heart tissue (e.g. previous myocardial infarction causing loss of viable heart tissue)<\/li>\n<li>Aging<\/li>\n<li>Damage due to infection or inflammation<\/li>\n<li>Certain medications and illicit drugs<\/li>\n<\/ul>\n<\/li>\n<li>Heart is not &#8216;made well&#8217; (i.e. abnormal structure) thus can&#8217;t contract and fill efficiently. Examples of\u00a0 abnormal structure are:\n<ul>\n<li>Congenital (i.e. since birth) heart defect of muscles and\/or valves,<\/li>\n<li>Defects in heart&#8217;s electrical system causing arrhythmias &#8211; resulting in heart beating too fast, slow, or irregular.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h2>Concentric versus Eccentric Hypertrophy<\/h2>\n<div>\n<h3>What is Hypertrophy?<\/h3>\n<p>Hearts, like any muscle, get bigger and thicker when it has a lot of resistance\/workload to frequently push against. It&#8217;s like lifting hand weights to increase the size of the bicep.\u00a0 The cells in heart tissue get individually larger &#8211; not more numerous. This enlargement of muscle cells &#8211; whether it&#8217;s cardiac or skeletal muscle &#8211; is known as <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_271\">hypertrophy<\/a>.\u00a0 The muscle cell hypertrophies because it is adding more contractile proteins to enable greater contractile strength. Going back to the bicep example &#8211; the larger bicep is because each individual bicep muscle cell undergoes hypertrophy even though it has not changed in muscle cell number. This would be an example of physiologic hypertrophy.<\/p>\n<p>Thus, the walls of muscle hypertrophy when there is chronically a lot of resistance\/workload. That means each cardiomyocyte is undergoing hypertrophy, rather than dividing into more cells (<a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_272\">hyperplasia<\/a>), as cardiomyocytes can&#8217;t undergo cell division.<\/p>\n<p>During hypertrophy, cells of the heart wall can:<\/p>\n<p>a) Become bigger in circumference. These plumper cardiomyocytes make the heart wall grow thicker from the outside in, resulting in the heart becoming heavier. The larger in circumference the cells get, the harder it is for oxygen and nutrients to diffuse inside the cell, which will eventually cause metabolic problems. This is the basis of concentric hypertrophy and remodeling.<\/p>\n<p>or<\/p>\n<p>b) Become longer in length and more narrow in circumference. These narrower cardiomyocytes are &#8216;stretched out&#8217; because the heart wall is undergoing more tension with over-filling with blood volume. To adapt to this stretching, the heart remodels by replacing contracting cardiomyocytes with non-contractile cardiac cells. As a result, the heart wall get thinner with weaker contractile strength. This is the basis of eccentric hypertrophy.<\/p>\n<p>c) Remodel (i.e. change their cellular make up in tissue). When the cardiomyocytes do not get enough oxygen and\/or nutrients (e.g.\u00a0 heart attack, extreme hypertrophy) or receive increased inflammatory signals (e.g. inflammation, infection), the cardiomyocytes will die. As a result, the cardiomyocytes are then replaced with connective tissue &#8211; principally collagen &#8211; which is NOT contractile. The heart tissue becomes less contractile, making it harder to empty the chamber. In addition, the collagen- filled heart wall becomes stiffer and not as stretchy to fill easily.<\/p>\n<h4>Concentric Hypertrophy<\/h4>\n<p>Concentric hypertrophy occurs when the left ventricular wall has increased demand and\/or afterload.\u00a0 If this is within physiological means, the heart gets bigger (ie concentric hypertrophy) to meet the demand. This is the case with larger body sizes and atheletes.<\/p>\n<p>However, if the heart is remodelling due to a chronically increased resistance to push against, this leads to a pathological concentric hypertrophy and remodeling (a.k.a. concentric remodeling).\u00a0 The LV wall gets thicker (due to plumper cardiomyocytes) resulting in\u00a0 the space within the ventricle (i.e. lumen) shrinking. This shrinkage of lumen means less volume of blood available to fill during diastole. At first, ejection fraction is preserved despite less diastolic filling, thus giving rise to the alternate terms of &#8220;<a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_80\">diastolic heart failure <\/a>&#8221; or &#8220;heart failure with preserved ejection fraction.&#8221;\u00a0 Because ejection fraction is preserved, the body is getting sufficient supply of blood and thus there would be few signs\/symptoms.<\/p>\n<p>However, as the wall gets thicker, it becomes stiffer and not as &#8220;stretchy&#8221; to fill easily.\u00a0 Eventually, there will be a point where the diastolic filling volume will not be enough to maintain sufficient ejection fraction, regardless of how well the LV wall can pump. This is when signs and symptoms will begin to be noticed.<\/p>\n<h4>Eccentric Hypertrophy<\/h4>\n<p>When the heart chambers get overloaded with volume, the cells of the heart wall will compensate by becoming thinner &amp; longer.\u00a0 This overfilling will cause the heart to remodel into a larger lumen with thinner walls and less contractile strength. If this eccentric hypertrophy occurs in the ventricle, this would be <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_82\">systolic failure<\/a> or &#8220;heart failure with reduced ejection fraction&#8221; as the volume to pump is sufficient but the pumping ability is too weak. Unfortunately, as ejection fraction is reduced, there will be even more fluid left in the chamber &#8211; thus complicating the already chronic volume overload.<\/p>\n<div>\n<p>&nbsp;<\/p>\n<\/div>\n<div class=\"textbox textbox--exercises\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Critical Thinking and Histopathology Exercises<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p>Now that you have viewed the gross specimen of concentric hypertrophy, consider the following questions.\u00a0 Record your answers for yourself before viewing the next video on the &#8220;Histopathology of Heart Failure.&#8221;<\/p>\n<ul>\n<li>Recall the histology of the H&amp;E stained normal heart.\u00a0 How much sarcoplasm (pink) was there in comparison to nuclei (purple)?<\/li>\n<li>Thinking about the pathophysiology of concentric hypertrophy, what would you expect to see in the cardiomyocyte?\u00a0 Will there be a change in sarcoplasm and\/or nuclear size?<\/li>\n<li>Cardiac remodelling is common in hypertrophy and heart failure &#8211; particularly the increased presence of collagen. What would these non-contractile cells and proteins look like histologically?<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<h2>Histopathology of Left-Sided Heart Failure<\/h2>\n<div><\/div>\n<div id=\"h5p-34\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-34\" class=\"h5p-iframe\" data-content-id=\"34\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"histopath of LVH\"><\/iframe><\/div>\n<\/div>\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Histopathology of Left-sided Heart Failure by Jonathan Bush, licensed under <a href=\"https:\/\/choosealicense.com\/no-license\/\">All rights reserved<\/a><\/sup><\/p>\n<h2>Clinical Manifestations of Left Sided heart failure<\/h2>\n<div id=\"h5p-443\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-443\" class=\"h5p-iframe\" data-content-id=\"443\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"clinical manifestations of left sided heart failure\"><\/iframe><\/div>\n<\/div>\n<p>&nbsp;<\/p>\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Clinical Manifestations of Left sided Heart Failure by Jennifer Kong, licensed under under\u00a0<a href=\"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/\" target=\"_blank\" rel=\"noopener\">Creative Commons Attribution-NonCommercial 4.0 International License<\/a><\/sup><\/p>\n<p>&nbsp;<\/p>\n<p>&#8230;<\/p>\n<div>\n<h2>Pulmonary Consequences of Left-Sided Heart Failure<\/h2>\n<p>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.<\/p>\n<\/div>\n<h2 style=\"text-align: left\">Histopathology of Pulmonary Edema Due to Left-Sided Heart Failure<\/h2>\n<p>With excess blood filling the pulmonary vasculature, there is increase pressure in the pulmonary vessels. This will cause two immediate effects:<\/p>\n<ol>\n<li>Increased pulmonary blood pressure (pulmonary hypertension) can &#8216;push&#8217; fluid out of the pulmonary capillaries.<\/li>\n<li>Alveoli fill with fluid from the blood in the pulmonary capillaries causing more complications:\n<ul>\n<li>\u00a0a barrier to gas exchange between the airways and pulmonary capillaries. &#8211;&gt; decreased oxygenation of blood and retention of CO2.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<p>These effects result in pulmonary edema &#8211; or &#8220;excess fluid in the lungs.&#8221; The fluid in the lungs are very similar to plasma in the blood\u00a0 &#8211; thus it is fluid filled with protein and nutrients.<\/p>\n<p>One can see this fluid\u00a0 at the gross anatomy level and histologically:<\/p>\n<div id=\"h5p-35\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-35\" class=\"h5p-iframe\" data-content-id=\"35\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"Histopath of pulmonary edema\"><\/iframe><\/div>\n<\/div>\n<p style=\"text-align: center;background-color: #f0f0f0;padding: 5px\"><sup>Histopathology of Pulmonary Edema Due to Left-sided Heart Failure by Jonathan Bush, licensed under <a href=\"https:\/\/choosealicense.com\/no-license\/\">All rights reserved<\/a><\/sup><\/p>\n<p>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 &#8211; thus causing pneumonia.\u00a0 For greater detail, refer to our chapter on\u00a0 <a href=\"https:\/\/pressbooks.bccampus.ca\/pathology\/part\/pneumonia-and-pulmonary-edema\/\">Pneumonia and Pulmonary Edema<\/a>.<\/p>\n<div class=\"textbox textbox--exercises\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Summary Exercises<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<div data-wp-editing=\"1\">\n<div class=\"textbox textbox--exercises\">\n<div class=\"textbox__content\">\n<p>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<\/p>\n<ul>\n<li>Chronically high afterload (e.g. stiff aortic valve that is hard to open)<\/li>\n<li>Increased sarcoplasm (pink) and larger nuclei<\/li>\n<li>Reduced ejection fraction<\/li>\n<li>Increase LV wall thickness<\/li>\n<\/ul>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<h2>Section Review<\/h2>\n<ul>\n<li class=\"textbox__content\">You can have both concentric and eccentric cardiomyopathy if the heart has to deal with both increased pressure and increased volume.<\/li>\n<li class=\"textbox__content\">Both systolic and diastolic failure have the same end result: the heart can&#8217;t pump enough blood out to feed the body.<\/li>\n<li>Left sided heart failure occurs when the left ventricle can&#8217;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 &#8211; manifested as weakness &amp; fatigue since muscles can&#8217;t get sufficient oxygen nor nutrients.<\/li>\n<li>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 remodeled 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.<\/li>\n<li>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).<\/li>\n<li>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 &#8220;crackles&#8221; during <a class=\"glossary-term\" aria-haspopup=\"dialog\" aria-describedby=\"definition\" href=\"#term_332_1431\">auscultation<\/a>.<\/li>\n<li>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).<\/li>\n<\/ul>\n<h2><\/h2>\n<ul>\n<li class=\"textbox__content\"><\/li>\n<\/ul>\n<h1>Review Questions<\/h1>\n<div class=\"h5p\">\n<div id=\"h5p-232\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-232\" class=\"h5p-iframe\" data-content-id=\"232\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"Types and causes of heart failure\"><\/iframe><\/div>\n<\/div>\n<\/div>\n<div>\n<div id=\"h5p-233\">\n<div class=\"h5p-iframe-wrapper\"><iframe id=\"h5p-iframe-233\" class=\"h5p-iframe\" data-content-id=\"233\" style=\"height:1px\" src=\"about:blank\" frameBorder=\"0\" scrolling=\"no\" title=\"Left sided heart failure\"><\/iframe><\/div>\n<\/div>\n<\/div>\n<div class=\"pdf\">\n<p><strong>1. Concentric hypertrophy will have a larger lumen size for filling and is thus associated with systolic failure.<\/strong><\/p>\n<ul>\n<li>True<\/li>\n<li>False<\/li>\n<\/ul>\n<p><strong>2. Put the types of left-sided heart failure in the correct column.<\/strong><\/p>\n<table style=\"border-collapse: collapse;width: 100%\">\n<tbody>\n<tr>\n<td style=\"width: 50%\">caused by increased resistance (afterload)<\/p>\n<p>caused by overfilling of the heart<\/p>\n<p>eccentric hypertrophy<\/td>\n<td style=\"width: 50%\">diastolic filling is reduced<\/p>\n<p>contraction during systole is weaker<\/p>\n<p>concentric hypertrophy<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<table class=\"grid\" style=\"border-collapse: collapse;width: 100%\">\n<tbody>\n<tr>\n<td style=\"width: 675.562px\"><strong>Abnormally Thick Ventricular Walls\u00a0<\/strong><\/td>\n<td style=\"width: 675.562px\"><strong>Abnormally Thin Ventricular Walls<\/strong><\/td>\n<\/tr>\n<tr>\n<td style=\"width: 675.562px\">&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/td>\n<td style=\"width: 675.562px\"><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p><strong>3. Choose the correct statement.<\/strong><\/p>\n<ul>\n<li>Heart failure occurs when the heart cannot pump out sufficient blood with each ejection.<\/li>\n<li>Heart failure involves enlargement of the heart walls, due to hyperplasia.<\/li>\n<li>Heart failure is caused by chronically circulating reduced blood volume.<\/li>\n<li>Heart failure is mainly divided into those with preserved vs reduced ejection fraction.<\/li>\n<\/ul>\n<div><\/div>\n<div class=\"textbox\">\n<h2>Answer Key<\/h2>\n<ol>\n<li>False<\/li>\n<li>\n<table class=\"lines\" style=\"border-collapse: collapse;width: 100%\">\n<tbody>\n<tr>\n<td style=\"width: 675.562px\"><strong>Abnormally Thick Ventricular Walls\u00a0<\/strong><\/td>\n<td style=\"width: 675.562px\"><strong>Abnormally Thin Ventricular Walls<\/strong><\/td>\n<\/tr>\n<tr>\n<td style=\"width: 675.562px\">concentric hypertrophy<br \/>\ndiastolic filling is reduced<br \/>\ncaused by increased resistance (afterload)<\/td>\n<td style=\"width: 675.562px\">caused by overfilling of the heart<br \/>\nContraction during systole is weaker<br \/>\neccentric hypertrophy<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/li>\n<li>Heart failure occurs when the heart cannot pump out sufficient blood with each ejection.<\/li>\n<\/ol>\n<\/div>\n<div><\/div>\n<div><\/div>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"glossary\"><span class=\"screen-reader-text\" id=\"definition\">definition<\/span><template id=\"term_332_471\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_471\"><div tabindex=\"-1\"><p>the pressure\/resistance against which the heart must work in order to eject blood for each contraction<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_332_271\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_271\"><div tabindex=\"-1\"><p>tissue is enlarged due to each individual cell becoming larger, often with an increase of cytoplasmic contents such as contractile proteins as in the case with muscle tissue<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_332_272\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_272\"><div tabindex=\"-1\"><p>tissue that is enlarged due to an increased number of new cells<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_332_80\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_80\"><div tabindex=\"-1\"><p>The left ventricle can't fill well during diastole because the ventricular walls can't relax well and\/or the ventricular lumen size is reduced<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_332_82\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_82\"><div tabindex=\"-1\"><p>The left ventricle is unable to contract strongly enough during systole. As a result, not enough blood leaves the heart to nourish the rest of the body<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><template id=\"term_332_1431\"><div class=\"glossary__definition\" role=\"dialog\" data-id=\"term_332_1431\"><div tabindex=\"-1\"><p>listening with a stethoscope for changes in sounds produced by movement of air, blood, food digestion, etc.<\/p>\n<\/div><button><span aria-hidden=\"true\">&times;<\/span><span class=\"screen-reader-text\">Close definition<\/span><\/button><\/div><\/template><\/div>","protected":false},"author":1076,"menu_order":7,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["jen-2"],"pb_section_license":""},"chapter-type":[],"contributor":[59],"license":[],"class_list":["post-332","chapter","type-chapter","status-publish","hentry","contributor-jen-2"],"part":324,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/332","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/users\/1076"}],"version-history":[{"count":25,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/332\/revisions"}],"predecessor-version":[{"id":9822,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/332\/revisions\/9822"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/parts\/324"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapters\/332\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/media?parent=332"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/pressbooks\/v2\/chapter-type?post=332"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/contributor?post=332"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathology\/wp-json\/wp\/v2\/license?post=332"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}