Table of Contents
Layers of the Heart Wall
The layers of the heart wall and the blood vessels carry the same basic structure. The layers of the heart starting from the inside include endocardium, myocardium, and epicardium. They correspond to tunica intima, tunica media and tunica externa in the blood vessels.
The endocardium is the inner layer of the heart, consisting of the following components:
- Lamina epithelialis is composed of a flat single-layer squamous epithelium that provides a low-friction, non-thrombogenic surface.
- Basal lamina anchors the endothelium to the connective tissue.
- Lamina propria is the connective tissue layer of the heart containing a network of elastic fibers and smooth muscle cells. The lamina propria can be further divided into:
- Stratum subendotheliale
- Stratum myoelasticum (primary component of the heart valves)
- Tela subendothelialis is the layer connected to the myocardium. It contains the muscle fibres that initiate and conduct electrical impulses.
Structure of the heart valves
The heart valves exhibit the same general structure as the endocardium, with the addition of a specialized lamina propria, composed of dense collagenous connective tissue designed to withstand an especially high mechanical load. This specialized endocardium is also known as valvular endocardium, which has the following layers:
- Lamina epithelialis (one-layer squamous endothelium)
- Basal lamina
- Lamina propria (composed of a stratum subendotheliale and a stratum myoelasticum)
The stratum myoelasticum, the specialized tissue layer of the heart valves, is composed of fibrosa and spongiosa. The fibrosa is a layer of non-vascular, dense collagenous connective tissue. In the atrioventricular valves, it is located on the side facing the ventricles. In the semilunar valves, the fibrosa is located on the side facing the arteries. The spongiosa is a layer of loose connective tissue.
Cardiac skeleton located on the valvular plane
The cardiac skeleton is composed of dense collagenous connective tissue carrying the heart valves in a plane. The valves are anchored by four collagenous fibrous rings, the anuli fibrosi:
- Anulus fibrosus dexter et sinister (tricuspid and mitral valve)
- Anulus trunci pulmonalis et anulus aortae (pulmonary and aortic valve)
As the valves allow blood flow in only a single direction, or ‘valvular plane’ of the heart. The muscle tissue of the atria is almost completely insulated from that of the ventricles by electrically non-conductive cardiac skeleton. The only structure that conducts impulses through the cardiac skeleton is the bundle of His—part of the specialized muscle cells of the impulse-forming system and the conducting system. The bundle of His ensures that the ventricles contract after the atria. The collagenous muscle tissue structure of the cardiac skeleton also acts as a firm base and source of the heart musculature.
Endocarditis is an inflammation of the inner layer of the heart. It is caused by bacterial infection or an immune reaction to a streptococcus infection of the tonsillar ring—a secondary infection resulting from rheumatic fever. Endocarditis most frequently occurs in the valve region, especially on the left side of the heart, which bears a greater mechanical load. Endocarditis triggered by substance abuse using infected peripheral venous catheters and injection materials occurs primarily on the tricuspid valve because the pathogen travels directly via the venous system and enters the right side of the heart.
This muscular layer is the thickest of the three heart wall layers. Its thickness is determined by mechanical load and is thinner in the atria than in the ventricles and thicker in the left side of the heart. It is composed of a specialized form of striated muscle—the striated cardiac muscle tissue. Both cardiac and skeletal striated muscle tissues exhibit similar structures; however, a few key differences still remain.
What are the key differences between cardiac and skeletal muscle?
The cardiac muscle cells are connected by specialized cell contacts, the disci intercalares (intercalated discs). There are three types: maculae adhaerentes, fasciae adhaerentes, and gap junctions.
Skeletal muscle fibers are unbranched, whereas cardiac muscle cells form a three-dimensional network.
Skeletal muscle cells carry a peripheral nucleus, whereas cardiac muscle cells bear a nucleus located at the center. The oval or rectangular nucleus is extended in the direction of the myofibrils. At both ends of the nucleus is the sarcoplasm that contains glycogen granules, mitochondria, and lipofuscin. Lipofuscin is a brown pigment that accumulates in the cells with age.
Additional differences between cardiac and skeletal muscle:
Cardiac muscle cells have a basal lamina and a surrounding network of capillaries to support their high metabolic rate. The sarcoplasmic reticulum is less developed than in skeletal muscle. In cardiac muscle cells, the transverse tubules of the sarcolemma (i.e. the T-system) are located next to the Z-lines and form the primary calcium reservoir; the longitudinal system (the L-system) is less pronounced. The T-tubules and L-tubules form a dyad. The higher metabolic demands of the cardiac muscle cells result in a smaller diameter and larger quantities of sarcoplasm and mitochondria.
The heart is a specialized organ in the cardiovascular system, whose function is to pump blood throughout the body via contraction of cardiomyocytes. There are two types of cardiomyocytes: the cells of the working musculature, as well as the pacemaker cells that initiate and conduct electrical impulses and function as myoendocrine cells to regulate the circulatory function.
The cardiac working musculature
Function: contraction of the cardiac muscle
The three layers of the cardiac working musculature are oriented in a corkscrew fashion in relation to each other. The external longitudinal layer runs from the cardiac skeleton to the Vortex cordis. The middle layer is composed of circular fiber bundles and is especially thick in the left ventricle, in order to support a greater pumping force. The inner layer is composed of fibers that radiate from this circular layer, and includes the trabeculae carneae and the musculi papillares.
If the pumping action of the heart is weakened due to a pre-existing condition (e.g., valve defects, heart attack), blood may be retained within a portion of the circulatory system. According to the location, cardiac insufficiency is defined as right, left or global cardiac insufficiency. Each of these has specific consequences for the human body.
Right cardiac insufficiency
Blood retention in the systemic circulation causes a volume burden on the right heart. Symptoms are engorgement of the neck veins and peripheral edema that is compensated by nocturnal reabsorption, resulting in nocturia.
Left cardiac insufficiency
Blood retention in the pulmonary circulation leads to pressure in the lungs, resulting in pulmonary edema and dyspnea.
Specialized cells of the cardiac musculature
The pacemaker cells initiate and conduct the electrical impulses.
Function: the spontaneous, rhythmic initiation and conduction of electrical impulses.
The conduction system has several components: the sinoatrial node, the atrioventricular node, the bundle of His, the bundle branch block and the Purkinje fibers. The pacemaker runs from the right atrium, down through the ventricular septum, to the cardiac apex. It crosses the cardiac skeleton—the collagenous connective tissue layer that separates the atrial and ventricular musculature. The pacemaker components are arranged hierarchically. The sinoatrial node is the primary pacemaker with the highest characteristic frequency. If it malfunctions, the atrioventricular node situated downstream can use its lower characteristic frequency to act as the primary pacemaker. Pacemaker cells contain a high quantity of glycogen and few myofibrils and are larger than the cells of the working musculature.
Pacemaker cells have a high quantity of glycogen and few myofibrils and are larger than the cells of the working musculature.
Function: endocrine regulation of the circulatory system.
Atrial natriuretic peptide (ANP), otherwise known as cardiodilatin, is secreted in the cardiac cells of the atrial auricles. This peptide hormone prevents cardiac overload via two mechanisms:
- ANP causes a reduction in blood volume by signaling the kidneys to reabsorb less NaCl. NaCl is excreted along with water, causing increased diuresis.
- ANP stimulates vasodilation of the blood vessel walls, reducing peripheral vascular resistance.
Secretion of ANP is stimulated by increased stretching of the right atrium (e.g., due to cardiac insufficiency) or when activated by the sympathetic nervous system.
BNP (brain natriuretic peptide) is produced by cardiomyocytes in the ventricles. Secretion is stimulated mainly by increased ventricular stretching (e.g., due to cardiac insufficiency). BNP and ANP exhibit antifibrotic and antihypertrophic effects on the heart.
Cardiac muscle hypertrophy
Cardiac muscle hypertrophy refers to an increase in cardiac muscle mass. It is caused by enlarged cardiomyocytes as a reaction to chronic overload either physiologically (additional loading is the desired outcome of high-performance sport), or pathologically, by increased ventricular pressure or volume load.
Epicardium = pericardium serosum, visceral lobe
The epicardium is the visceral lobe of the pericardium serosum that firmly adheres to the heart, forming part of the pericardial sac. Similar to all other serous membranes, it is composed of:
- Tunica serosa—serosa epithelium, composed of a single-layered squamous mesothelium
- Lamina propria—serosa connective tissue with numerous elastic fibers, along with blood and lymph vessels
- Tela subserosa—a sliding layer whose adipose tissue cushions the surface of the heart and envelopes the coronary vessels in the sulci.
Both the outer and inner surfaces of the heart are low-friction and elastic, perfectly suited to withstand the high mechanical load on an active heart.
The pericardium is the connective tissue surrounding the heart. It has two components:
- Pericardium serosum (serous epicardial membrane = visceral lobe and parietal lobe)
- Pericardium fibrosum
The richly vascularised tela subpericardialis is situated between these layers.
The pericardium serosum is the serous membrane surrounding the heart. Similar to all serous membranes, it carries two serous lobes:
- Lamina visceralis = epicardium (the outer layer of the cardiac wall)
- Lamina parietalis, which firmly adheres to the Pericardium fibrosum.
Both lobes merge at a reflecting fold to form the cavitas pericardica or pericardial cavity. This capillary-rich space is filled with a few milliliters of serous fluid, an ultrafiltrate derived from the blood, which facilitates low-friction sliding movements of the organs.
The collagenous pericardium fibrosum reinforces the lamina parietalis. This layer has very little elasticity.
The reflecting folds of the serous lobes (mesocardiacum) form the following sinuses:
- Sinus transversus pericardii
- Sinus obliquus pericardii
In addition, the heart is attached to its surroundings via the following structures:
- Ligamenta phrenicopericardiaca
- Membrana bronchopericardiaca
- Ligamenta sternopericardiaca
Components of the CVS
- Lymph nodes scattered throughout the body (thymus, spleen)
- Returns excess body fluid to the blood
- Transports fats from intestines to blood
Main classes of blood vessels
- Convey blood away from the heart to the body tissues
- Bifurcate into smaller vessels (arterioles) as they travel further from the heart until they feed into the capillaries
- Exchange oxygen, carbon dioxide, nutrients, and waste products
- Return blood to the heart
- Become progressively smaller as they split and travel further away from the heart (venules)
Components of the CVS
Main classes of blood vessels
- Happens where two or more vessels merge to supply the same body region.
- Veins tend to form many more anastomoses than arteries do.
Diseases of the Heart
Pericardial effusion is defined as the accumulation of fluid in the pericardium. This condition can have a variety of causes:
- A myocardial ischemia can cause extensive necrosis of the cardiac wall leading to formation of weak points that rupture and cause hemorrhage into the pericardium.
- Ruptured aneurysm of the aorta ascendens
- Hemorrhagic diathesis
- Physical trauma
- Transudate due to right cardiac insufficiency or hypoalbuminemia
Effusion caused by a viral infection
- E.g., Coxsackievirus
Purulent effusion = empyema
- During the course of sepsis;
- When the infection spreads from the surrounding structures to the heart
Pericardial effusion leads to increased pressure on the pericardial cavity and afferent veins, causing incomplete filling of the heart during diastole. Decreased blood ejection during systole lowers the blood pressure and results in shock.
Causes of infection of the pericardial sac include:
- Viral, bacterial or fungal infection; can also occur via spread from surrounding structures (e.g., pneumonia)
- Uremic pericarditis caused by chronic kidney infection
- Irradiation of the thorax
- Autoimmune disorders such as SLE (systemic lupus erythematosus);
- Post-traumatic consequence of a heart attack or Dressler syndrome following surgery.
Pericarditis calcarea is caused by recurring inflammation of the pericardium, which leads to tissue scarring and calcification, preventing flexible and low-friction gliding of the pericardial lobes. The heart can no longer completely dilate during the filling phase, causing venous blood retention and resulting in visible internal and external symptoms. Pericarditis calcarea may also lead to secondary diseases warranting surgical intervention.