where does the blood in the right atrium come from
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Anomalous pulmonary venous connection (or anomalous pulmonary venous drainage or anomalous pulmonary venous return) is a congenital defect of the pulmonary veins. Total anomalous pulmonary venous connection Total anomalous pulmonary venous connection, also known as total anomalous pulmonary venous return, is a rare cyanotic congenital heart defect in which all four pulmonary veins are malpositioned and make anomalous connections to the systemic venous circulation. (Normally, pulmonary veins return oxygenated blood from the lungs to the left atrium where it can then be pumped to the rest of the body). A right-to-left shunt such as a patent foramen ovale, patent ductus arteriosus or an atrial septal defect must be present, or else the condition is fatal due to a lack of systemic blood flow. In some cases, it can be detected prenatally. There are four variants: Supracardiac (50%): blood drains to one of the innominate veins (brachiocephalic veins) or the superior vena cava; Cardiac (20%), where blood drains into coronary sinus or directly into right atrium; Infradiaphragmatic (20%), where blood drains into portal or hepatic veins; and a mixed (10%) variant. TAPVC can occur with obstruction, which occurs when the anomalous vein enters a vessel at an acute angle and can cause pulmonary venous hypertension and cyanosis because blood cannot enter the new vein as easily. Signs and symptoms right ventricular heave Loud S1 fixed split S2 S3 gallop systolic ejection murmur at left upper sternal border cardiomegaly right axis deviation on ECG Snowman sign or 'figure of 8 configuration' on chest radiograph right ventricular hypertrophy cyanosis, tachypnea, dyspnea since the overloaded pulmonary circuit can cause pulmonary edema Cottage-loaf sign, that is, chest X-ray appearance similar to a cottage loaf, also known as the 'snow man' sign or 'figure of 8' sign. Treatment In TAPVC without obstruction, surgical redirection can be performed within the first month of life. The operation is performed under general anesthesia. The four pulmonary veins are reconnected to the left atrium, and any associated heart defects such as atrial septal defect, ventricular septal defect, patent foramen ovale, and/or patent ductus arteriosus are surgically closed. With obstruction, surgery should be undertaken emergently. PGE1 should be given because a patent ductus arteriosus allows oxygenated blood to go from the circulation of the right heart to the systemic circulation. Partial anomalous pulmonary venous connection A Partial anomalous pulmonary venous connection (or Partial anomalous pulmonary venous drainage or Partial anomalous pulmonary venous return) is a congenital defect where the left atrium is the point of return for the blood from some (but not all) of the pulmonary veins. It is less severe than total anomalous pulmonary venous connection which is a life-threatening anomaly requiring emergent surgical correction, usually diagnosed in the first few days of life. Partial anomalous venous connection may be diagnosed at any time from birth to old age. The severity of symptoms, and thus the likelihood of diagnosis, varies significantly depending on the amount of blood flow through the anomalous connections. In less severe cases, with smaller amounts
Anomalous pulmonary venous connection
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The tricuspid valve, or right atrioventricular valve, is on the right dorsal side of the mammalian heart, at the superior portion of the right ventricle. The function of the valve is to allow blood to flow from the right atrium to the right ventricle during diastole, and to close to prevent backflow (regurgitation) from the right ventricle into the right atrium during right ventricular contraction (systole). Structure The tricuspid valve usually has three cusps or leaflets, named the anterior, posterior, and septal cusps. Each leaflet is connected via chordae tendineae to the anterior, posterior, and septal papillary muscles of the right ventricle, respectively. Tricuspid valves may also occur with two or four leaflets; the number may change over a lifetime. Function The tricuspid valve functions as a one-way valve that closes during ventricular systole to prevent regurgitation of blood from the right ventricle back into the right atrium. It opens during ventricular diastole, allowing blood to flow from the right atrium into the right ventricle. The back flow of blood is also known as regression or tricuspid regurgitation. Tricuspid regurgitation can result in increased ventricular preload because the blood refluxed back into the atrium is added to the volume of blood that must be pumped back into the ventricle during the next cycle of ventricular diastole. Increased right ventricular preload over a prolonged period of time may lead to right ventricular enlargement (dilatation), which can progress to right heart failure if left uncorrected. Clinical significance Infected valves can result in endocarditis in intravenous drug users. Patients who inject narcotics or other drugs intravenously may introduce infection, which can travel to the right side of the heart, most often caused by the bacteria S. aureus. In patients without a history of intravenous exposure, endocarditis is more frequently left-sided. The tricuspid valve can be affected by rheumatic fever, which can cause tricuspid stenosis or tricuspid regurgitation. Some individuals are born with congenital abnormalities of the tricuspid valve. Congenital apical displacement of the tricuspid valve is called Ebstein's anomaly and typically causes significant tricuspid regurgitation. Certain carcinoid syndromes can affect the tricuspid valve by producing fibrosis due to serotonin production by those tumors. The first endovascular tricuspid valve implant was performed by surgeons at the Cleveland Clinic. Tricuspid regurgitation Tricuspid regurgitation is common and is estimated to occur in 65–85% of the population. In the Framingham Heart Study presence of any severity of tricuspid regurgitation, ranging from trace to above moderate was in 82% of men and in 85.7% of women. Mild tricuspid regurgitation tends to be common, benign, and in structurally normal tricuspid valve apparatus can be considered a normal variant. Moderate or severe tricuspid regurgitation is usually associated with tricuspid valve leaflet abnormalities and/or possibly annular dilation and is usually pathologic which can lead to irreversible damage of cardiac muscle and worse outcomes due to chronic prolonged right ventricular volume overload. Additional images See also Tricuspid atresia Cavo-tricuspid isthmus Lancisi's sign Right atrial enlargement References External links Photo of model: circulation/tricuspidvalve04
Tricuspid valve
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In anatomy, a persistent left superior vena cava is the most common variation of the thoracic venous system. It is present in between 0.3% and 0.5% of the population, and is an embryologic remnant that results from a failure to involute. Presentation In persistent left superior vena cava, the left brachiocephalic vein does not develop fully and the left upper limb and head and neck drain into the right atrium via the coronary sinus. In isolation, the variation is considered benign, but is very frequently associated with cardiac abnormalities (e.g. ventricular septal defect, atrioventricular septal defect) that have a significant mortality and morbidity. It is more frequent in patients with congenital heart defects. The (right) superior vena cava is almost always unaffected by the presence of persistent left superior vena cava. Diagnosis If an anomaly is detected during a routine ultrasound, a fetal echocardiogram is performed to determine whether a fetus has the condition. Otherwise, it is often unnoticed unless an extenuating circumstance warrants further examination of the heart, usually much later in life. CT and MRI scans in a parasagittal section may show a "pipe" sign where the left superior vena cava occurs. Treatment If no other cardiac abnormalities are present, persistent left superior vena cava will not be treated, as it is usually asymptomatic and unharmful. If it drains into the left atrium, then deoxygenated blood enters the circulation to the body, and cyanosis may occur. References External links Congenital vascular defects
Persistent left superior vena cava
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In anatomy, the venae cavae (; : vena cava ; ) are two large veins (great vessels) that return deoxygenated blood from the body into the heart. In humans they are the superior vena cava and the inferior vena cava, and both empty into the right atrium. They are located slightly off-center, toward the right side of the body. The right atrium receives deoxygenated blood through coronary sinus and two large veins called venae cavae. The inferior vena cava (or caudal vena cava in some animals) travels up alongside the abdominal aorta with blood from the lower part of the body. It is the largest vein in the human body. The superior vena cava (or cranial vena cava in animals) is above the heart, and forms from a convergence of the left and right brachiocephalic veins, which contain blood from the head and the arms. References Veins
Venae cavae
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Regurgitation is blood flow in the opposite direction from normal, as the backward flowing of blood into the heart or between heart chambers. It is the circulatory equivalent of backflow in engineered systems. It is sometimes called reflux. Types of heart valve regurgitation The various types of heart valve regurgitation via insufficiency are as follows: Aortic regurgitation: the backflow of blood from the aorta into the left ventricle, owing to insufficiency of the aortic semilunar valve; it may be chronic or acute. Mitral regurgitation: the backflow of blood from the left ventricle into the left atrium, owing to insufficiency of the mitral valve; it may be acute or chronic, and is usually due to mitral valve prolapse, rheumatic heart disease, or a complication of cardiac dilatation. See also Mitral regurgitation. Pulmonic regurgitation: the backflow of blood from the pulmonary artery into the right ventricle, owing to insufficiency of the pulmonic semilunar valve. Tricuspid regurgitation: the backflow of blood from the right ventricle into the right atrium, owing to imperfect functioning (insufficiency) of the tricuspid valve. Regurgitation in or near the heart is often caused by valvular insufficiency (insufficient function, with incomplete closure, of the heart valves); for example, aortic valve insufficiency causes regurgitation through that valve, called aortic regurgitation, and the terms aortic insufficiency and aortic regurgitation are so closely linked as usually to be treated as metonymically interchangeable. Regurgitant fraction Regurgitant fraction is the percentage of blood that regurgitates back through the aortic valve to the left ventricle due to aortic insufficiency, or through the mitral valve to the atrium due to mitral insufficiency. It is measured as the amount of blood regurgitated into a cardiac chamber divided by the stroke volume. This fraction affords a quantitative measure of the severity of the valvular lesion. Normally, no blood regurgitates, so the regurgitant fraction is zero. In patients with severe valvular lesions, regurgitant fraction can approach 80%. Epidemiology Tricuspid and mitral regurgitation Tricuspid regurgitation is common and is estimated to occur in 65–85% of the population. In The Framingham Heart Study presence of any severity of tricuspid regurgitation, ranging from trace to above moderate was in 82% of men and in 85.7% of women. Mild tricuspid regurgitation tend to be common and benign and in structurally normal tricuspid valve apparatus can be considered a normal variant. Moderate or severe tricuspid regurgitation is usually associated with tricuspid valve leaflet abnormalities and/or possibly annular dilation and is usually pathologic which can lead to irreversible damage of cardiac muscle and worse outcomes due to chronic prolonged right ventricular volume overload. In a study of 595 male elite football players aged 18–38, and 47 sedentary non-athletes, it was found that 58% of the athletes had tricuspid regurgitation vs. 36% in non-athletes and mitral regurgitation was found in 20% football players and 15% in controls. Football players with tricuspid regurgitation had larger tricuspid annulus diameter, compared to athletes without tricuspid regurgitation. Athletes with tricuspid regurgitation also had enlarged right atrium diameter when compared to control
Regurgitation (circulation)
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Venous blood is deoxygenated blood which travels from the peripheral blood vessels, through the venous system into the right atrium of the heart. Deoxygenated blood is then pumped by the right ventricle to the lungs via the pulmonary artery which is divided in two branches, left and right to the left and right lungs respectively. Blood is oxygenated in the lungs and returns to the left atrium through the pulmonary veins. Venous blood is typically colder than arterial blood, and has a lower oxygen content and pH. It also has lower concentrations of glucose and other nutrients and has higher concentrations of urea and other waste products. The difference in the oxygen content of arterial blood and venous blood is known as the arteriovenous oxygen difference. Most medical laboratory tests are conducted on venous blood, with the exception of arterial blood gas tests. Venous blood is obtained for lab work by venipuncture (also called phlebotomy), or by finger prick for small quantities. Color The color of human blood ranges from bright red when oxygenated to a darker red when deoxygenated. It owes its color to hemoglobin, to which oxygen binds. Deoxygenated blood is darker due to the difference in shape of the red blood cell when oxygen binds to haemoglobin in the blood cell (oxygenated) versus does not bind to it (deoxygenated). Though veins might make it appear as such, human blood is never naturally blue. The blue appearance of surface veins is caused mostly by the scattering of blue light away from the outside of venous tissue if the vein is at 0.5 mm deep or more. Veins and arteries appear similar when skin is removed and are seen directly. References Blood
Venous blood
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Atrial septal defect (ASD) is a congenital heart defect in which blood flows between the atria (upper chambers) of the heart. Some flow is a normal condition both pre-birth and immediately post-birth via the foramen ovale; however, when this does not naturally close after birth it is referred to as a patent (open) foramen ovale (PFO). It is common in patients with a congenital atrial septal aneurysm (ASA). After PFO closure the atria normally are separated by a dividing wall, the interatrial septum. If this septum is defective or absent, then oxygen-rich blood can flow directly from the left side of the heart to mix with the oxygen-poor blood in the right side of the heart; or the opposite, depending on whether the left or right atrium has the higher blood pressure. In the absence of other heart defects, the left atrium has the higher pressure. This can lead to lower-than-normal oxygen levels in the arterial blood that supplies the brain, organs, and tissues. However, an ASD may not produce noticeable signs or symptoms, especially if the defect is small. Also, in terms of health risks, people who have had a cryptogenic stroke are more likely to have a PFO than the general population. A cardiac shunt is the presence of a net flow of blood through a defect, either from left to right or right to left. The amount of shunting present, if any, determines the hemodynamic significance of the ASD. A right-to-left-shunt results in venous blood entering the left side of the heart and into the arterial circulation without passing through the pulmonary circulation to be oxygenated. This may result in the clinical finding of cyanosis, the presence of bluish-colored skin, especially of the lips and under the nails. During development of the baby, the interatrial septum develops to separate the left and right atria. However, a hole in the septum called the foramen ovale allows blood from the right atrium to enter the left atrium during fetal development. This opening allows blood to bypass the nonfunctional fetal lungs while the fetus obtains its oxygen from the placenta. A layer of tissue called the septum primum acts as a valve over the foramen ovale during fetal development. After birth, the pressure in the right side of the heart drops as the lungs open and begin working, causing the foramen ovale to close entirely. In about 25% of adults, the foramen ovale does not entirely seal. In these cases, any elevation of the pressure in the pulmonary circulatory system (due to pulmonary hypertension, temporarily while coughing, etc.) can cause the foramen ovale to remain open. Types The six types of atrial septal defects are differentiated from each other by whether they involve other structures of the heart and how they are formed during the developmental process during early fetal development. Ostium secundum The ostium secundum atrial septal defect is the most common type of atrial septal defect and comprises 6–10% of all congenital heart diseases. It involves a patent
Atrial septal defect
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Diastole ( ) is the relaxed phase of the cardiac cycle when the chambers of the heart are refilling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles. The term originates from the Greek word (diastolē), meaning "dilation", from (diá, "apart") + (stéllein, "to send"). Role in cardiac cycle A typical heart rate is 75 beats per minute (bpm), which means that the cardiac cycle that produces one heartbeat, lasts for less than one second. The cycle requires 0.3 sec in ventricular systole (contraction)—pumping blood to all body systems from the two ventricles; and 0.5 sec in diastole (dilation), re-filling the four chambers of the heart, for a total of 0.8 sec to complete the cycle. Early ventricular diastole During early ventricular diastole, pressure in the two ventricles begins to drop from the peak reached during systole. When the pressure in the left ventricle falls below that in the left atrium, the mitral valve opens due to a negative pressure differential (suction) between the two chambers. The open mitral valve allows blood in the atrium (accumulated during atrial diastole) to flow into the ventricle (see graphic at top). Likewise, the same phenomenon runs simultaneously in the right ventricle and right atrium through the tricuspid valve. The ventricular filling flow (or flow from the atria into the ventricles) has an early (E) diastolic component caused by ventricular suction, and then a late one created by atrial systole (A). The E/A ratio is used as a diagnostic measure as its diminishment indicates probable diastolic dysfunction, though this should be used in conjunction with other clinical characteristics and not by itself. Late ventricular diastole Early diastole is a suction mechanism between the atrial and ventricular chambers. Then, in late ventricular diastole, the two atrial chambers contract (atrial systole), causing blood pressure in both atria to increase and forcing additional blood flow into the ventricles. This beginning of the atrial systole is known as the atrial kick—see Wiggers diagram. The atrial kick does not supply the larger amount of flow (during the cardiac cycle) as about 80 percent of the collected blood volume flows into the ventricles during the active suction period. Atrial diastole At the beginning of the cardiac cycle the atria, and the ventricles are synchronously approaching and retreating from relaxation and dilation, or diastole. The atria are filling with separate blood volumes returning to the right atrium (from the vena cavae), and to the left atrium (from the lungs). After chamber and back pressures equalize, the mitral and tricuspid valves open, and the returning blood flows through the atria into the ventricles. When the ventricles have completed most of their filling, the atria begin to contract (atrial systole), forcing blood under pressure into the ventricles. Now the ventricles start to contract, and as pressures within the ventricles rise, the mitral and tricuspid valves close producing the first heart sound (S1) as
Diastole
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In the fetal heart, the foramen ovale (), also foramen Botalli or the ostium secundum of Born, allows blood to enter the left atrium from the right atrium. It is one of two fetal cardiac shunts, the other being the ductus arteriosus (which allows blood that still escapes to the right ventricle to bypass the pulmonary circulation). Another similar adaptation in the fetus is the ductus venosus. In most individuals, the foramen ovale closes at birth. It later forms the fossa ovalis. Development The foramen ovale () forms in the late fourth week of gestation, as a small passageway between the septum secundum and the ostium secundum. Initially the atria are separated from one another by the septum primum except for a small opening below the septum, the ostium primum. As the septum primum grows, the ostium primum narrows and eventually closes. Before it does so, bloodflow from the inferior vena cava wears down a portion of the septum primum, forming the ostium secundum. Some embryologists postulate that the ostium secundum may be formed through programmed cell death. The ostium secundum provides communication between the atria after the ostium primum closes completely. Subsequently, a second wall of tissue, the septum secundum, grows over the ostium secundum in the right atrium. Blood then passes from the right to left atrium only by way of a small passageway in the septum secundum and then through the ostium secundum. This passageway is called the foramen ovale''. Closure The foramen ovale often closes at birth. At birth, when the lungs become functional, the pulmonary vascular pressure decreases and the left atrial pressure exceeds that of the right. This forces the septum primum against the septum secundum, functionally closing the foramen ovale. In time the septa eventually fuse, leaving a remnant of the foramen ovale, the fossa ovalis. Function A fetus receives oxygen not from its lungs, but from the mother's oxygen-rich blood via the placenta. Oxygenated blood from the placenta travels through the umbilical cord to the right atrium of the fetal heart. As the fetal lungs are non-functional at this time, the blood bypasses them through two cardiac shunts. The first is the foramen ovale (the valve present between them called eustachian valve) which shunts blood from the right atrium to the left atrium. The second is the ductus arteriosus which shunts blood from the pulmonary artery (which, after birth, carries blood from the right side of the heart to the lungs) to the descending aorta. Clinical significance In about 25% of adults the foramen ovale does not close completely, but remains as a small patent foramen ovale ("PFO"). In most of these individuals, the PFO causes no problems and remains undetected throughout life. PFO has long been studied because of its role in paradoxical embolism (an embolism that travels from the venous side to the arterial side). This may lead to a stroke or transient ischemic attack. Transesophageal echocardiography is considered the most accurate investigation to demonstrate a patent foramen ovale. A
Foramen ovale (heart)
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In the anatomy of the heart, the valve of the coronary sinus (also called the Thebesian valve, after Adam Christian Thebesius) is a valve located at the orifice of the coronary sinus where the coronary sinus drains into the right atrium. It prevents blood from flowing backwards into the coronary sinus during contraction of the heart. Anatomy The valve of the coronary sinus is a thin, semilunar (half-moon-shaped) valve located on the anteroinferior part of the opening into the right atrium. It is formed by as semicircular fold of the lining membrane of the right atrium. It is situated at the base of the inferior vena cava. Variation The valve may be completely absent; it is present in 73-86% of individuals. The valve may vary in size. It may be double, or it may be cribriform (containing numerous small holes). Function The valve prevents regurgitation of blood into the sinus during diastole (i.e. the contraction of the atrium). References Cardiac anatomy
Valve of coronary sinus
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The Fontan procedure or Fontan–Kreutzer procedure is a palliative surgical procedure used in children with univentricular hearts. It involves diverting the venous blood from the inferior vena cava (IVC) and superior vena cava (SVC) to the pulmonary arteries. The procedure varies for differing congenital heart pathologies. For example in tricuspid atresia, the procedure can be done where the blood does not pass through the morphologic right ventricle; i.e., the systemic and pulmonary circulations are placed in series with the functional single ventricle. Whereas in hypoplastic left heart syndrome, the heart is more reliant on the more functional right ventricle to provide blood flow to the systemic circulation. The procedure was initially performed in 1968 by Francis Fontan and Eugene Baudet from Bordeaux, France, published in 1971, simultaneously described in July 1971 by Guillermo Kreutzer from Buenos Aires, Argentina, presented at the Argentinean National Cardilogy meeting of that year and finally published in 1973. Indications The Fontan Kreutzer procedure is used in pediatric patients who possess only a single functional ventricle, either due to lack of a heart valve (e.g. tricuspid or mitral atresia), an abnormality of the pumping ability of the heart (e.g. hypoplastic left heart syndrome or hypoplastic right heart syndrome), or a complex congenital heart disease where a bi-ventricular repair is impossible or inadvisable. The surgery allows blood to be delivered to the lungs via central venous pressure rather than via the right ventricle. Patients typically present as neonates with cyanosis or congestive heart failure. Fontan completion is usually carried out when the patient is 2–5 years of age, but is also performed before 2 years of age. Types There are four variations of the Fontan procedure: Ventricularization of the Right Atrium (The original Fontan's Technique) Atriopulmonary connection (the original Kreutzer's Technique) Intracardiac total cavopulmonary connection (lateral tunnel) (described by Marc De Leval and Aldo Castañeda, separately) Extracardiac total cavopulmonary connection (described by Carlo Marceletti and Francisco Puga for Heterotaxy Syndrome) Approach The Fontan-Kreutzer procedure is the third procedure in the staged surgical palliation. It is performed in children born with congenital heart disease without two functional ventricles and an effective parallel blood flow circuit. The first stage is known as the Norwood procedure. This stage generally involves combining the pulmonary artery and aorta to form a larger vessel for blood to get to the body. An artificial tube or shunt can be placed from this larger vessel to the pulmonary arteries so that blood can get from the heart to the lungs. The wall between the left and right atrium can be removed to allow the mixing of oxygenated and de-oxygenated blood. The second stage is called the hemi-Fontan or the Bidirectional Glenn procedure. This intermediary stage incorporates the shifting of oxygen-poor blood from the top of the body to the lungs. The superior vena cava (SVC), which carries blood returning from the upper parts of the body, is disconnected from the heart and instead redirects the blood into the pulmonary arteries. The inferior vena cava (IVC),
Fontan procedure
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A venous heart is the type of heart in which only blood with CO₂ circulates. Venous hearts receive blood from veins and pumps it for oxygenation. This type of heart is generally found in fishes. Structure Venous hearts only have the right side of heart, which contains an atrium (also known as auricle) and an ventricle. The heart is made of two chambers, unlike human hearts which have four chambers. Blood circulation The blood circulation system via venous heart is close-looped. A venous heart is single circuit and the heart pumps blood all over the body with only a single loop. Deoxygenated blood circulates to the atrium from the body, and afterwards the deoxygenated blood moves to the ventricles from the atrium. Next, the blood reaches the gills for purification. Like all hearts, venous hearts are also engaged in the distribution of nutrients, oxygen, hormones and other necessities to all parts of the body, and remove metabolic waste. References Fish anatomy
Venous heart
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A double inlet left ventricle (DILV) or "single ventricle", is a congenital heart defect appearing in 5 in newborns, where both the left atrium and the right atrium feed into the left ventricle. The right ventricle is hypoplastic or does not exist. Both atria communicate with the ventricle by a single atrio-ventricular valve. There is a big shunt left-right with a quickly evolutive pulmonary hypertension. Without life-prolonging interventions, the condition is fatal, but with intervention, the newborn may survive. Even if there is no foetal sickness, the diagnosis can be made in utero by foetal echocardiography. Presentation Infants born with DILV cannot feed normally (breathlessness) and have difficulty gaining weight. The mixed blood in systemic circulation leads to hypoxia (lack of oxygen to the body and organs), so infants develop cyanosis and breathlessness early. Diagnosis Treatment In the first few days, if there is no pulmonary valve stenosis, a pulmonary valve banding is necessary to prevent pulmonary hypertension and the ductus must be kept open to allow blood-flow using medication containing prostaglandin. At same time, if necessary, the atrial and ventricular septum communications must be enlarged. When possible Glenn procedure is done. Later, surgical options include the Damus–Kaye–Stansel procedure, the Fontan procedure, and the Norwood procedure. The goal of all of these is separating the pulmonary and the systemic circulation. Usually, DILV is associated with other cardiac malformations. Prognosis Mortality is very high in the first 2 years, 85%, but after it decreases and between 2 and 15 years old the mortality is only around 9%. Diagnosis must be made within few days or even hours to prevent death. References External links Congenital heart defects
Double inlet left ventricle
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Cor triatriatum (or triatrial heart) is a congenital heart defect where the left atrium (cor triatriatum sinistrum) or right atrium (cor triatriatum dextrum) is subdivided by a thin membrane, resulting in three atrial chambers (hence the name). Cor triatriatum represents 0.1% of all congenital cardiac malformations and may be associated with other cardiac defects in as many as 50% of cases. The membrane may be complete or may contain one or more fenestrations of varying size. Cor triatriatum sinistrum is more common. In this defect, there is typically a proximal chamber that receives the pulmonic veins and a distal (true) chamber located more anteriorly where it empties into the mitral valve. The membrane that separates the atrium into two parts varies significantly in size and shape. It may appear similar to a diaphragm or be funnel-shaped, band-like, entirely intact (imperforate) or contain one or more openings (fenestrations) ranging from small, restrictive-type to large and widely open. In the pediatric population, this anomaly may be associated with major congenital cardiac lesions such as tetralogy of Fallot, double outlet right ventricle, coarctation of the aorta, partial anomalous pulmonary venous connection, persistent left superior vena cava with unroofed coronary sinus, ventricular septal defect, atrioventricular septal (endocardial cushion) defect, and common atrioventricular canal. Rarely, asplenia or polysplenia has been reported in these patients. In the adult, cor triatriatum is frequently an isolated finding. Cause Cor triatriatum dextrum is extremely rare and results from the complete persistence of the right sinus valve of the embryonic heart. The membrane divides the right atrium into a proximal (upper) and a distal (lower) chamber. The upper chamber receives the venous blood from both vena cavae and the lower chamber is in contact with the tricuspid valve and the right atrial appendage. Mechanism and Symptoms The natural history of this defect depends on the size of the communicating orifice between the upper and lower atrial chambers. If the communicating orifice is small, the patient is critically ill and may succumb at a young age (usually during infancy) to congestive heart failure and pulmonary edema. If the connection is larger, patients may present in childhood or young adulthood with a clinical picture similar to that of mitral stenosis. As the malformed membrane calcifies with age, thus further narrowing such opening, decreased cardiac output produces features of pulmonary venous hypertension and right heart failure—including symptoms of dyspnea and orthopnea, easy fatigability, palpitations and shortness of breath, among others. Cor triatriatum may also be an incidental finding when it is nonobstructive. Diagnosis Primarily diagnosed with imaging, such as echocardiogram (ultrasound of the heart), CT, and/or MRI. Treatment Treatment of Cor triatriatum varies among cases and is dependent upon presentation of symptoms—incidental finding of the condition in asymptomatic patients does not typically require immediate medical management, but for those exhibiting dyspnea and pulmonary congestion, surgical intervention is required. The disorder can be treated surgically by removing the membrane dividing the atrium. The surgery, which usually occurs by first excising the diaphragm and then
Cor triatriatum
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The inferior vena cava is a large vein that carries the deoxygenated blood from the lower and middle body into the right atrium of the heart. It is formed by the joining of the right and the left common iliac veins, usually at the level of the fifth lumbar vertebra. The inferior vena cava is the lower ("inferior") of the two venae cavae, the two large veins that carry deoxygenated blood from the body to the right atrium of the heart: the inferior vena cava carries blood from the lower half of the body whilst the superior vena cava carries blood from the upper half of the body. Together, the venae cavae (in addition to the coronary sinus, which carries blood from the muscle of the heart itself) form the venous counterparts of the aorta. It is a large retroperitoneal vein that lies posterior to the abdominal cavity and runs along the right side of the vertebral column. It enters the right auricle at the lower right, back side of the heart. The name derives from . Structure The IVC is formed by the joining of the left and right common iliac veins and brings collected blood into the right atrium of the heart. It also joins with the azygos vein (which runs on the right side of the vertebral column) and venous plexuses next to the spinal cord. The inferior vena cava begins as the left and right common iliac veins behind the abdomen unite, at about the level of L5. It passes through the thoracic diaphragm at the caval opening at the level of T8 - T9. It passes to the right of the descending aorta. Tributaries The specific levels of the tributaries are as follows: Because the inferior vena cava is located to the right of the midline, drainage of the tributaries is not always symmetrical. On the right, the gonadal veins and suprarenal veins drain into the inferior vena cava directly. On the left, they drain into the renal vein which in turn drains into the inferior vena cava. By contrast, all the lumbar veins and hepatic veins usually drain directly into the inferior vena cava. Development In the embryo, the inferior vena cava and right auricle are separated by the valve of the inferior vena cava, also known as the Eustachian valve. In the adult, this valve typically has totally regressed or remains as a small fold of endocardium. Variation Rarely, the inferior vena cava may vary in its size and position. In transposition of the great arteries the inferior vena cava may lie on the left. In between 0.2% to 0.3% of people, the inferior vena cava may be duplicated beneath the level of the renal veins. Function The inferior vena cava is a vein. It carries deoxygenated blood from the lower half of the body to the right atrium of the heart. The corresponding vein that carries deoxygenated blood from the upper half of the body is the superior vena cava. Clinical significance
Inferior vena cava
3310704
Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure (where central venous pressure increases, but right atrial pressure stays the same; VR = CVP − RAP). CVP has been, and often still is, used as a surrogate for preload, and changes in CVP in response to infusions of intravenous fluid have been used to predict volume-responsiveness (i.e. whether more fluid will improve cardiac output). However, there is increasing evidence that CVP, whether as an absolute value or in terms of changes in response to fluid, does not correlate with ventricular volume (i.e. preload) or volume-responsiveness, and so should not be used to guide intravenous fluid therapy. Nevertheless, CVP monitoring is a useful tool to guide hemodynamic therapy. The cardiopulmonary baroreflex responds to an increase in CVP by decreasing systemic vascular resistance while increasing heart rate and ventricular contractility in dogs. Measurement Normal CVP in patients can be measured from two points of reference: Sternum: 0–14 cm H2O Midaxillary line: 8–15 cm H2O CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP. In most intensive care units, facilities are available to measure CVP continuously. Normal values vary between 4 and 12 cm H2O. Factors affecting CVP Factors that increase CVP include: Cardiac tamponade Decreased cardiac output Forced exhalation Heart failure Hypervolemia Mechanical ventilation and the application of positive end-expiratory pressure (PEEP) Pleural effusion Pulmonary embolism Pulmonary hypertension Tension pneumothorax Factors that decrease CVP include: Deep inhalation Distributive shock Hypovolemia See also Jugular venous pressure Pulmonary capillary wedge pressure References External links Venous function and central venous pressure: a physiologic story - a technical discussion of the more modern understanding of central venous pressure; this may well conflict with the sources below. Central Venous Pressure and Pulmonary Capillary Wedge Monitoring Cardiovascular Physiology Medical terminology Medical monitoring Cardiovascular physiology
Central venous pressure
607130
Constrictive pericarditis is a condition characterized by a thickened, fibrotic pericardium, limiting the heart's ability to function normally. In many cases, the condition continues to be difficult to diagnose and therefore benefits from a good understanding of the underlying cause. Signs and symptoms Signs and symptoms of constrictive pericarditis are consistent with the following: fatigue, swollen abdomen, difficulty breathing (dyspnea), swelling of legs and general weakness. Related conditions are bacterial pericarditis, pericarditis and pericarditis after a heart attack. Causes The cause of constrictive pericarditis in the developing world are idiopathic in origin, though likely infectious in nature. In regions where tuberculosis is common, it is the cause in a large portion of cases. Causes of constrictive pericarditis include: Tuberculosis Incomplete drainage of purulent pericarditis Fungal and parasitic infections Chronic pericarditis Postviral pericarditis Postsurgical Following MI, post-myocardial infarction In association with pulmonary asbestos Pathophysiology The pathophysiological characteristics of constrictive pericarditis are due to a thickened, fibrotic pericardium that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. As pressure on the heart increases, the stroke volume decreases as a result of a reduction in the diastolic expansion in the chambers. This results in significant respiratory variation in blood flow in the chambers of the heart. During inspiration, pressure in the thoracic cavity decreases but is not relayed to the left atrium, subsequently a reduction in flow to the left atrium and ventricle happens. During diastole, less blood flow in left ventricle allows for more room for filling in right ventricle and therefore a septal shift occurs. During expiration, the amount of blood entering the left ventricle will increase, allowing the interventricular septum to bulge towards the right ventricle, decreasing the right heart ventricular filing. Diagnosis The diagnosis of constrictive pericarditis is often difficult to make. In particular, restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating them in a particular individual is often a diagnostic dilemma. Chest X-Ray - pericardial calcification (common but not specific), pleural effusions are common findings. Echocardiography - the principal echographic finding is changes in cardiac chamber volume. CT and MRI - CT scan is useful in assessing the thickness of pericardium, calcification, and ventricular contour. Cardiac MRI may find pericardial thickening and pericardial-myocardial adherence. Ventricular septum shift during breathing can also be found using cardiac MRI. Late gadolinium enhancement can show enhancement of the pericardium due to fibroblast proliferation and neovascularization. BNP blood test - tests for the existence of the cardiac hormone brain natriuretic peptide, which is only present in restrictive cardiomyopathy but not in constrictive pericarditis Conventional cardiac catheterization Physical examination - can reveal clinical features including Kussmaul's sign and a pericardial knock. Treatment The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. This procedure has significant risk involved, with mortality rates of 6% or higher in major referral centers. A poor outcome is almost always the
Constrictive pericarditis
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Raghib syndrome is rare a congenital heart defect where the left superior vena cava (LSVC) is draining into the left atrium in addition to an absent coronary sinus and an atrial septal defect. This can be considered a dangerous heart condition because it puts the individual at a high risk of stroke. Other defects that are often associated with Raghib syndrome can include ventricular septal defects, enlargement of the tricuspid annulus, and pulmonary stenosis. While this is considered an extremely rare developmental complex, cases regarding a persistent left superior vena cava (PLSVC) are relatively common among congenital heart defects. It is also important to note that the PLSVC often drains into the right atrium, and only drains into the left atrium in approximately 10 to 20% of individuals with the defect. In an individual with no underlying heart condition, the superior vena cava delivers blood returning from the body to the right atrium. Due to oxygen being used by various biological processes throughout the body, this blood has extremely low blood oxygenation levels. Therefore, the right side of the heart pumps this blood to the lungs where gas exchange takes place in the capillaries. The oxygenated blood is then transported back to the left side of the heart through pulmonary veins. The left atrium and left ventricle work to push the now oxygen saturated blood up through the aorta and out to the body. As stated earlier, individuals with Raghib syndrome experience drainage from the left superior vena cava into the left atrium. This means that the deoxygenated blood returning from the body is directly bypassing the lungs and entering the left atrium where it will be pumped back into the body causing cyanosis. The result of this can have major implications on several biological processes, often requiring surgical intervention. The coronary sinus is a vein continuing off of the great cardiac vein. It collects blood from the ventricular veins of the heart muscle during ventricle contraction and moves this blood into the right atrium. Essentially, this coronary sinus takes de-oxygenated blood from veins in the heart muscle (epicardial ventricular veins) and delivers it to the right side of the heart so it can be transported to the lungs and oxygenated again. It is extremely rare for an individual to be lacking this component of the heart. Lastly, a common aspect of Raghib syndrome is an atrial septal defect. This is when there is a hole in the septum dividing the right and left atriums of the heart. The size of this hole may vary significantly from individual to individual Some may not even notice the symptoms of this defect until they are well into adulthood, if at all. The main concern with an atrial septal defect, is it can cause the right side of the heart to become overworked. This is because the amount of blood being pumped to the lungs increases significantly as blood from the left atrium leaks back into the right atrium. Thus leading to damaged
Raghib syndrome
4506997
The sinus venosus is a large quadrangular cavity which precedes the atrium on the venous side of the chordate heart. In mammals, the sinus venosus exists distinctly only in the embryonic heart where it is found between the two venae cavae; in the adult, the sinus venosus becomes incorporated into the wall of the right atrium to form a smooth part called the sinus venarum which is separated from the rest of the atrium by a ridge called the crista terminalis. In most mammals, the sinus venosus also forms the sinoatrial node and the coronary sinus. Development In the embryo, the thin walls of the sinus venosus are connected below with the right ventricle, and medially with the left atrium, but are free in the rest of their extent. It receives blood from the vitelline vein, umbilical vein and common cardinal vein. The sinus venosus originally starts as a paired structure but shifts towards associating only with the right atrium as the embryonic heart develops. The left portion shrinks in size and eventually forms the coronary sinus (right atrium) and oblique vein of the left atrium, whereas the right part becomes incorporated into the right atrium to form the sinus venarum. Additional images See also Atrial septal defect Bulbus cordis Ducts of Cuvier Primitive ventricle Primitive atrium Ductus venosus Truncus arteriosus Sinus venosus atrial septal defect References External links - Gross anatomy of the adult heart - "Right atrium, internal structure, anterior view" Embryology of cardiovascular system de:Sinus venosus zh:静脉窦
Sinus venosus
26862016
Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another. Blood flow The heart functions as a pump and acts as a double pump in the cardiovascular system to provide a continuous circulation of blood throughout the body. This circulation includes the systemic circulation and the pulmonary circulation. Both circuits transport blood but they can also be seen in terms of the gases they carry. The pulmonary circulation collects oxygen from the lungs and delivers carbon dioxide for exhalation. The systemic circuit transports oxygen to the body and returns relatively de-oxygenated blood and carbon dioxide to the pulmonary circuit. Blood flows through the heart in one direction, from the atria to the ventricles, and out through the pulmonary artery into the pulmonary circulation, and the aorta into the systemic circulation. The pulmonary artery (also trunk) branches into the left and right pulmonary arteries to supply each lung. Blood is prevented from flowing backwards (regurgitation) by the tricuspid, bicuspid, aortic, and pulmonary valves. The function of the right heart, is to collect de-oxygenated blood, in the right atrium, from the body via the superior vena cava, inferior vena cava and from the coronary sinus and pump it, through the tricuspid valve, via the right ventricle, through the semilunar pulmonary valve and into the pulmonary artery in the pulmonary circulation where carbon dioxide can be exchanged for oxygen in the lungs. This happens through the passive process of diffusion. In the left heart oxygenated blood is returned to the left atrium via the pulmonary vein. It is then pumped into the left ventricle through the bicuspid valve and into the aorta for systemic circulation. Eventually in the systemic capillaries exchange with the tissue fluid and cells of the body occurs; oxygen and nutrients are supplied to the cells for their metabolism and exchanged for carbon dioxide and waste products In this case, oxygen and nutrients exit the systemic capillaries to be used by the cells in their metabolic processes, and carbon dioxide and waste products will enter the blood. The ventricles are stronger and thicker than the atria, and the muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation. Atria facilitate circulation primarily by allowing uninterrupted venous flow to the heart, preventing the inertia of interrupted venous flow that would otherwise occur at each ventricular systole. Cardiac muscle Cardiac muscle tissue has autorhythmicity, the unique ability to initiate a cardiac action potential at a fixed rate – spreading the impulse rapidly from cell to cell to trigger the contraction of the entire heart. This autorhythmicity is still modulated by the endocrine and nervous systems. There are two types of cardiac muscle cell: cardiomyocytes which have the ability to contract easily,
Cardiac physiology
7193171
The left anterior descending artery (also LAD, anterior interventricular branch of left coronary artery, or anterior descending branch) is a branch of the left coronary artery. It supplies the anterior portion of the left ventricle. It provides about half of the arterial supply to the left ventricle and is thus considered the most important vessel supplying the left ventricle. Blockage of this artery is often called the widow-maker infarction due to a high risk of death. Structure Course It first passes at posterior to the pulmonary artery, then passes anteriorward between that pulmonary artery and the left atrium to reach the anterior interventricular sulcus, along which it descends to the notch of cardiac apex. In 78% of cases, it reaches the apex of the heart. Although rare, multiple anomalous courses of the LAD have been described. These include the origin of the artery from the right aortic sinus. Branches The LAD gives off two types of branches: septals and diagonals. Septals originate from the LAD at 90 degrees to the surface of the heart, perforating and supplying the anterior 2/3 of the interventricular septum. Diagonals run along the surface of the heart and supply the lateral wall of the left ventricle and the anterolateral papillary muscle. Segments Proximal: from LAD origin to, and including, the origin of the first septal branch (some definitions say to first diagonal, or to whichever comes first) Middle: from proximal segment to halfway of remaining distance to apex. A more technical definition is from the proximal segment to the point where the LAD forms an angle, as seen from a right anterior oblique view on angiography, which is often close to the origin of the second diagonal branch. Distal: from middle segment to apex, or in some cases beyond. Function The artery supplies the anterior region of the left ventricle, including: the anterolateral myocardium, apex, anterior interventricular septum, and anterolateral papillary muscle. The LAD typically supplies 45–55% of the left ventricle and is therefore considered the most critical vessel in terms of myocardial blood supply. Widow maker Widow maker is an alternative name for the anterior interventricular branch of the left coronary artery. The name widow maker may also apply to the left coronary artery or severe occlusions to that artery. This term is used because the left main coronary and/or the left anterior descending supply blood to large areas of the heart. This means that if these arteries are abruptly and completely occluded it will cause a massive heart attack that will likely lead to sudden death. The blockage that kills is made up of platelets streaming to the site of a ruptured cholesterol plaque. Even a small amount of plaque in this area can (for a variety of poorly understood reasons) rupture and cause death; bypassing chronic blockages or trying to open them up with angioplasty does not prevent heart attack but it can restore blood flow in case of a sudden blockage or heart attack and if performed within a rapid time
Left anterior descending artery
3046797
In humans, the circulatory system is different before and after birth. The fetal circulation is composed of the placenta, umbilical blood vessels encapsulated by the umbilical cord, heart and systemic blood vessels. A major difference between the fetal circulation and postnatal circulation is that the lungs are not used during the fetal stage resulting in the presence of shunts to move oxygenated blood and nutrients from the placenta to the fetal tissue. At birth, the start of breathing and the severance of the umbilical cord prompt various changes that quickly transform fetal circulation into postnatal circulation. Oxygenation, nutrient, and waste exchange Placenta The placenta functions as the exchange site of nutrients and wastes between the maternal and fetal circulation. Water, glucose, amino acids, vitamins, and inorganic salts freely diffuse across the placenta along with oxygen. Two umbilical arteries carry deoxygenated blood and waste from the fetus to the placenta where waste is exchanged for oxygen and nutrients. The oxygenated blood will then return to the fetus from the placenta via the umbilical vein. Oxygenation transport in fetus Hemoglobin is a structure found within the red blood cells that binds to and carries oxygen. Fetal hemoglobin enhances the fetus' ability to draw oxygen from the placenta. This is facilitated by the hemoglobin molecule that made up of two alpha and two gamma chains (2α2γ). Its oxygen-hemoglobin dissociation curve is shifted to the left, meaning that it is able to absorb oxygen at lower concentrations than adult hemoglobin. This enables fetal hemoglobin to absorb oxygen from adult hemoglobin in the placenta, where the oxygen pressure is lower than at the lungs. Around 6 months of age after birth, the gamma chains will gradually be replaced by beta chains. This new hemoglobin structure is known as hemoglobin A, composed of two alpha and two beta chains (2α2β). Hemoglobin A is the predominant form found in adults. Before birth Oxygenated blood from the placenta is carried to the fetus by the umbilical vein, which will drain into the inferior vena cava (IVC) through the ductus venosus or the liver. When oxygenated blood enters the IVC, it moves in parallel with deoxygenated blood from the fetal systemic veins, establishing a bilaminar blood flow as it enters the right atrium. The fetal heart contains two upper atria and two lower ventricles. It also contains two additional structures, the foramen ovale and the ductus arteriosus, that function as shunts for oxygenated blood. The function of these shunts is to bypass the lungs and maintain proper circulation to important fetal tissue. In the fetal stage, the lungs fill with fluid and collapse because the fetus is within the amniotic sac and the placenta is providing the oxygen it needs to grow. With the lung collapsed, pulmonary vascular resistance remains high during the fetal stage to prevent blood flow into the lungs. As oxygenated blood arrives at the right atrium, the eustachian valve helps direct the oxygenated blood into the foramen ovale, an opening between the right and left
Fetal circulation
25518103
Crista dividens is a structure in the developing heart of the human embryo that divides the right atrium in a way such that it creates a pan systolic murmur in the same way as the foramen ovale. Recognition of the absence of this murmur can indicate a potentially terminal cardiac defect in the newborn. Function The crista dividens plays a role in separating oxygenated blood from the ductus venosus and deoxygenated blood from the inferior vena cava (IVC) draining the caudal portion of the fetus into the left and right atria, respectively. The crista dividens is located on the inferior edge of the interatrial septum and faces the opening of the IVC. As blood enters the heart from the IVC, it hits the crista dividens and is divided into two streams, with one stream entering the right atrium and the other entering the left atrium. The ductus venosus joins the terminal portion of the IVC, just before the right atrium. Before the ductus venosus joins the IVC, it is positioned in such a way that the oxygenated blood flowing into the IVC from the ductus venosus preferentially passes on the side of the crista dividens that directs the blood stream toward the left atrium. The rest of the IVC (prior to the joining of the ductus venosus) carries deoxygenated blood from the caudal (inferior) part of the fetus, and is directed toward the side of the crista dividens that directs blood into the right atrium. References Embryology Cardiac anatomy
Crista dividens
5478650
The valve of the inferior vena cava (Eustachian valve) is a venous valve that lies at the junction of the inferior vena cava and right atrium. Development In prenatal development, the eustachian valve helps direct the flow of oxygen-rich blood through the right atrium into the left atrium and away from the right ventricle. Before birth, the fetal circulation directs oxygen-rich blood returning from the placenta to mix with blood from the hepatic veins in the inferior vena cava. Streaming this blood across the atrial septum via the foramen ovale increases the oxygen content of blood in the left atrium. This in turn increases the oxygen concentration of blood in the left ventricle, the aorta, the coronary circulation and the circulation of the developing brain. Following birth and separation from the placenta, the oxygen content in the inferior vena cava falls. With the onset of breathing, the left atrium receives oxygen-rich blood from the lungs via the pulmonary veins. As blood flow to the lungs increases, the amount of blood flow entering the left atrium increases. When the pressure in the left atrium exceeds the pressure in the right atrium, the foramen ovale begins to close and limits the blood flow between the left and right atrium. While the eustachian valve persists in adult life, it essentially does not have a specific function after the gestational period. Variation There is a large variability in size, shape, thickness, and texture of the persistent eustachian valve, and in the extent to which it encroaches on neighboring structures such as the atrial septum. At one end of the spectrum, the embryonic eustachian valve disappears completely or is represented only by a thin ridge. Most commonly, it is a crescentic fold of endocardium arising from the anterior rim of the IVC orifice. The lateral horn of the crescent tends to meet the lower end of the crista terminalis, while the medial horn joins the thebesian valve, a semicircular valvular fold at the orifice of the coronary sinus. At the other extreme, it persists as a mobile, elongated structure projecting several centimeters into the right atrial cavity. In this case, it may demonstrate an undulating motion in real time echocardiography; and when it is quite large, it may be confused with right atrial tumors, thrombi, or vegetations. Occasionally, the eustachian valve crosses the floor of the right atrium from the orifice of the IVC and inserts into the lower portion of the interatrial septum adjacent to the atrioventricular valves. However, higher insertion of a giant eustachian valve, which mimics the echocardiographic appearance of divided right atrium, is very rare. This type of abnormality may be confused with cor triatriatum dexter. Very rarely, such a configuration of a large eustachian valve may mimic a right atrial cystic tumor. The superior vena cava (SVC) does not have any homologous valve or valvule. Clinical significance The eustachian valve is frequently seen with transthoracic echocardiography from the parasternal long axis, the apical four-chamber and the sub-costal four-chamber views. The
Valve of inferior vena cava
146642
Coronary circulation is the circulation of blood in the arteries and veins that supply the heart muscle (myocardium). Coronary arteries supply oxygenated blood to the heart muscle. Cardiac veins then drain away the blood after it has been deoxygenated. Because the rest of the body, and most especially the brain, needs a steady supply of oxygenated blood that is free of all but the slightest interruptions, the heart is required to function continuously. Therefore its circulation is of major importance not only to its own tissues but to the entire body and even the level of consciousness of the brain from moment to moment. Interruptions of coronary circulation quickly cause heart attacks (myocardial infarctions), in which the heart muscle is damaged by oxygen starvation. Such interruptions are usually caused by coronary ischemia linked to coronary artery disease, and sometimes to embolism from other causes like obstruction in blood flow through vessels. Structure Coronary arteries Coronary arteries supply blood to the myocardium and other components of the heart. Two coronary arteries originate from the left side of the heart at the beginning (root) left ventricle. There are three aortic sinuses (dilations) in the wall of the aorta just superior to the aortic semilunar valve. Two of these, the left posterior aortic sinus and anterior aortic sinus, give rise to the left and right coronary arteries, respectively. The third sinus, the right posterior aortic sinus, typically does not give rise to a vessel. Coronary vessel branches that remain on the surface of the heart and follow the sulci of the heart are called epicardial coronary arteries. The left coronary artery distributes blood to the left side of the heart, the left atrium and ventricle, and the interventricular septum. The circumflex artery arises from the left coronary artery and follows the coronary sulcus to the left. Eventually, it will fuse with the small branches of the right coronary artery. The larger left anterior descending artery (LAD), is the second major branch arising from the left coronary artery. It follows the anterior interventricular sulcus around the pulmonary trunk. Along the way it gives rise to numerous smaller branches that interconnect with the branches of the posterior interventricular artery, forming anastomoses. An anastomosis is an area where vessels unite to form interconnections that normally allow blood to circulate to a region even if there may be partial blockage in another branch. The anastomoses in the heart are very small. Therefore, this ability is somewhat restricted in the heart so a coronary artery blockage often results in myocardial infarction causing death of the cells supplied by the particular vessel. The right coronary artery proceeds along the coronary sulcus and distributes blood to the right atrium, portions of both ventricles, and the heart conduction system. Normally, one or more marginal arteries arise from the right coronary artery inferior to the right atrium. The marginal arteries supply blood to the superficial portions of the right ventricle. On the posterior surface of the heart, the right coronary artery gives
Coronary circulation
2404687
An artificial heart valve is a one-way valve implanted into a person's heart to replace a heart valve that is not functioning properly (valvular heart disease). Artificial heart valves can be separated into three broad classes: mechanical heart valves, bioprosthetic tissue valves and engineered tissue valves. The human heart contains four valves: tricuspid valve, pulmonary valve, mitral valve and aortic valve. Their main purpose is to keep blood flowing in the proper direction through the heart, and from the heart into the major blood vessels connected to it (the pulmonary artery and the aorta). Heart valves can malfunction for a variety of reasons, which can impede the flow of blood through the valve (stenosis) and/or let blood flow backwards through the valve (regurgitation). Both processes put strain on the heart and may lead to serious problems, including heart failure. While some dysfunctional valves can be treated with drugs or repaired, others need to be replaced with an artificial valve. Background A heart contains four valves (tricuspid, pulmonary, mitral and aortic valves) which open and close as blood passes through the heart. Blood enters the heart in the right atrium and passes through the tricuspid valve to the right ventricle. From there, blood is pumped through the pulmonary valve to enter the lungs. After being oxygenated, blood passes to the left atrium, where is it pumped through the mitral valve to the left ventricle. The left ventricle pumps blood to the aorta through the aortic valve. There are many potential causes of heart valve damage, such as birth defects, age related changes, and effects from other disorders, such as rheumatic fever and infections causing endocarditis. High blood pressure and heart failure which can enlarge the heart and arteries, and scar tissue can form after a heart attack or injury. The three main types of artificial heart valves are mechanical, biological (bioprosthetic/tissue), and tissue-engineered valves. In the US, UK and the European Union, the most common type of artificial heart valve is the bioprosthetic valve. Mechanical valves are more commonly used in Asia and Latin America. Companies that manufacture heart valves include Edwards Lifesciences, Medtronic, Abbott (St. Jude Medical), CryoLife, and LifeNet Health. Mechanical valves Mechanical valves come in three main types – caged ball, tilting-disc and bileaflet – with various modifications on these designs. Caged ball valves are no longer implanted. Bileaflet valves are the most common type of mechanical valve implanted in patients today. Caged ball valves The first artificial heart valve was the caged ball valve, a type of ball check valve, in which a ball is housed inside a cage. When the heart contracts and the blood pressure in the chamber of the heart exceeds the pressure on the outside of the chamber, the ball is pushed against the cage and allows blood to flow. When the heart finishes contracting, the pressure inside the chamber drops and the ball moves back against the base of the valve forming a seal. In 1952, Charles A. Hufnagel implanted caged ball
Artificial heart valve
2859527
Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure (a drop more than 10 mmHg) and pulse wave amplitude during inspiration. Pulsus paradoxus is not related to pulse rate or heart rate, and it is not a paradoxical rise in systolic pressure. Normally, blood pressure drops less precipitously than 10 mmHg during inhalation. Pulsus paradoxus is a sign that is indicative of several conditions, most commonly pericardial effusion. The paradox in pulsus paradoxus is that, on physical examination, one can detect beats on cardiac auscultation during inspiration that cannot be palpated at the radial pulse. It results from an accentuated decrease of the blood pressure, which leads to the (radial) pulse not being palpable and may be accompanied by an increase in the jugular venous pressure height (Kussmaul's sign). As is usual with inspiration, the heart rate is slightly increased, due to decreased left ventricular output. Mechanism During inspiration, the negative intra-thoracic pressure results in an increased right venous return, filling the right atrium more than during an exhalation. The increased blood volume dilates the right atrium, reducing the compliance of the left atrium due to their shared septum. Lower left atrial compliance reduces the left atrium venous return and as a consequence causes a reduction in left ventricular preload. This results in a reduction in left ventricular stroke volume and will be noted as a reduction in systolic blood pressure in inspiration. Pulsus paradoxus is therefore an exaggeration or an increase in the fall of systolic BP beyond 10 mmHg during inspiration. Normally during inspiration, a person's systolic blood pressure decreases by ≤10 mmHg and heart rate slightly increases. This is because inspiration decreases intra-thoracic pressure relative to atmospheric pressure, which increases blood flow (systemic venous return) to the right atrium of the heart by reducing pressure on the veins, particularly the venae cavae. However, the decrease in intra-thoracic pressure and stretching of the lungs during inhalation also expands the compliant pulmonary vasculature so that blood pools in the lungs and decreases pulmonary venous return to the left atrium. Also, the increased systemic venous return to the right side of the heart expands the right heart and directly compromises filling of the left side of the heart by slightly bulging the septum to the left, reducing maximum volume. Reduced left-heart filling leads to a reduced stroke volume which manifests as a decrease in systolic blood pressure, leading to a faster heart rate due to the inhibition of the baroreceptor reflex, which stimulates sympathetic outflow to the heart. Under normal physiologic conditions the large pressure gradient between the right and left ventricles prevents the septum from bulging dramatically into the left ventricle during inspiration. However such bulging does occur during cardiac tamponade where pressure equalizes between all of the chambers of the heart. As the right ventricle receives more volume, it pushes the septum into the left ventricle further reducing its volume in turn. This additional loss of volume of
Pulsus paradoxus
44283452
Pulmonary vein stenosis is a rare cardiovascular disorder. It is recognized as being the stenosis of one or more of the four pulmonary veins that return blood from the lungs to the left atrium of the heart. In congenital cases, it is associated with poor prognosis and high mortality rate. In some people, pulmonary vein stenosis occurs after pulmonary vein ablation for the treatment of atrial fibrillation. Some recent research has indicated that it may be genetically linked in congenital cases. Signs and symptoms Pulmonary vein stenosis usually manifests during the initial years of life. Pneumonia recurrentis and tachypnea are common presentation symptoms rather than the typical early pulmonary hypertension symptoms. Patients may experience a new murmur, right ventricular heart failure, pulmonary edema, failure to thrive, or hemoptysis as the disease worsens and pulmonary hypertension becomes more noticeable. Causes Pulmonary vein stenosis can be congenital or acquired. A rare abnormality that accounts for 0.4% of congenital heart diseases, congenital pulmonary vein stenosis results from the common right or left pulmonary vein failing to integrate into the left atrium (LA) during the vessel's embryonic development, obliterating the pulmonary veins partially or completely on one or both sides. The main cause of pulmonary vein stenosis is radiofrequency ablation for atrial fibrillation. Pneumonia resulting from sarcoidosis may be caused by granulomatous involvement or extrinsic compression due to lymphadenopathies. Uncontrolled fibrosis surrounding the afflicted mediastinal lymph nodes is the hallmark of fibrosing mediastinitis, a rare consequence of tuberculosis and Histoplasma capsulatum infection that can cause invasion as well as obstruction of the surrounding pulmonary veins. Neoplasms next to the pulmonary veins have the potential to compress or infiltrate, resulting in stenosis. In the pediatric population, the most common cause of clinically significant pulmonary vein stenosis is complete anomalous pulmonary venous return repair. Localized obliteration can occur further into the center of the vessel or at the point where the pulmonary vein anastomoses into the left atrium. The literature contains isolated reports of lung transplantation, suture repair of a pulmonary vein cannulation site, and pulmonary vein injury resulting in obstruction following myxoma resection. Diagnosis Pulmonary vein stenosis may be identified by noninvasive procedures such as magnetic resonance imaging, multidetector CT angiography, radionuclide quantitative pulmonary flow imaging, and echocardiography with Doppler ultrasonography. Treatment Although clinical and imaging surveillance is recommended because the disease can change over time, mild and asymptomatic pulmonary vein stenosis may not require intervention. When it comes to the majority of pulmonary vein stenosis cases, whether congenital or acquired, surgery is the recommended course of action. References Further reading External links Boston Children's Hospital The Children’s Hospital of Philadelphia Vascular diseases
Pulmonary vein stenosis
2664415
The fossa ovalis is a depression in the right atrium of the heart, at the level of the interatrial septum, the wall between right and left atrium. The fossa ovalis is the remnant of a thin fibrous sheet that covered the foramen ovale during fetal development. Function During fetal development, the foramen ovale allows blood to pass from the right atrium to the left atrium, bypassing the nonfunctional fetal lungs while the fetus obtains its oxygen from the placenta. A flap of tissue called the septum primum acts as a valve over the foramen ovale during that time. After birth, the introduction of air into the lungs causes the pressure in the pulmonary circulatory system to drop. This change in pressure pushes the septum primum against the atrial septum, closing the foramen. The septum primum and atrial septum eventually fuse together to form a complete seal, leaving a depression called the fossa ovalis. By age two, about 75% of people have a completely sealed fossa ovalis. An unfused fossa ovalis is called a patent foramen ovale. Depending on the circumstances, a patent foramen ovale may be completely asymptomatic, or may require surgery. The limbus of fossa ovalis (annulus ovalis) is the prominent oval margin of the fossa ovalis in the right atrium. It is most distinct above and at the sides of the fossa ovalis; below, it is deficient. A small slit-like valvular opening is occasionally found, at the upper margin of the fossa, leading upward beneath the limbus, into the left atrium; it is the remains of the fetal aperture the foramen ovale between the two atria. Closure Almost immediately after the infant is born, the foramen ovale and ductus arteriosus close. The major changes that are made by the body occur at the first breath (in the case of heart and lung functions) and up to weeks after birth (such as the liver's enzyme synthesis). The foramen ovale becomes the fossa ovalis as the foramen closes while edge of the septum secundum in right atrium becomes anulus ovalis, so the depression beneath it becomes the fossa ovalis. This enables respiration and circulation independent from the mother's placenta. With the child's first breath, the lung sends oxygenated blood to the left atrium. As a result, pressure in the left atrium is higher than that of the right, and the increased pressure holds the interatrial flap (which covers the foramen ovale) shut, therefore closing the foramen ovale as well. In normal development, the closed foramen ovale fuses with the interatrial wall. During the first breath, vasoconstriction causes the ductus arteriosus to close, and during adult years, tissue occludes what once was the ductus arterious, creating the ligamentum arteriosum. Clinical significance Aneurysm Aneurysms can occur in adulthood if the foramen ovale is not closed correctly. An aneurysm happens when an artery becomes enlarged in a localized area due to weakening of the arterial wall. When this type of aneurysm occurs in the area of the fossa ovalis, an enlarged pouch is
Fossa ovalis (heart)
598465
The pulmonary circulation is a division of the circulatory system in all vertebrates. The circuit begins with deoxygenated blood returned from the body to the right atrium of the heart where it is pumped out from the right ventricle to the lungs. In the lungs the blood is oxygenated and returned to the left atrium to complete the circuit. The other division of the circulatory system is the systemic circulation that begins with receiving the oxygenated blood from the pulmonary circulation into the left atrium. From the atrium the oxygenated blood enters the left ventricle where it is pumped out to the rest of the body, returning as deoxygenated blood back to the pulmonary circulation. The blood vessels of the pulmonary circulation are the pulmonary arteries and the pulmonary veins. A separate circulatory circuit known as the bronchial circulation supplies oxygenated blood to the tissue of the larger airways of the lung. Structure De-oxygenated blood leaves the heart, goes to the lungs, and then enters back into the heart. De-oxygenated blood leaves through the right ventricle through the pulmonary artery. From the right atrium, the blood is pumped through the tricuspid valve (or right atrioventricular valve) into the right ventricle. Blood is then pumped from the right ventricle through the pulmonary valve and into the pulmonary artery. Lungs The pulmonary arteries carry deoxygenated blood to the lungs, where carbon dioxide is released and oxygen is picked up during respiration. Arteries are further divided into very fine capillaries which are extremely thin-walled. The pulmonary veins return oxygenated blood to the left atrium of the heart. Veins Oxygenated blood leaves the lungs through pulmonary veins, which return it to the left part of the heart, completing the pulmonary cycle. This blood then enters the left atrium, which pumps it through the mitral valve into the left ventricle. From the left ventricle, the blood passes through the aortic valve to the aorta. The blood is then distributed to the body through the systemic circulation before returning again to the pulmonary circulation. Arteries From the right ventricle, blood is pumped through the semilunar pulmonary valve into the left and right main pulmonary artery (one for each lung), which branch into smaller pulmonary arteries that spread throughout the lungs. Development The pulmonary circulation loop is virtually bypassed in fetal circulation. The fetal lungs are collapsed, and blood passes from the right atrium directly into the left atrium through the foramen ovale (an open conduit between the paired atria) or through the ductus arteriosus (a shunt between the pulmonary artery and the aorta). When the lungs expand at birth, the pulmonary pressure drops and blood is drawn from the right atrium into the right ventricle and through the pulmonary circuit. Over the course of several months, the foramen ovale closes, leaving a shallow depression known as the fossa ovalis. Clinical significance A number of medical conditions may affect the pulmonary circulation: Pulmonary hypertension describes an increase in resistance in the pulmonary arteries. Pulmonary embolism is occlusion
Pulmonary circulation
4479531
The small cardiac vein, also known as the right coronary vein, is a coronary vein that drains parts of the right atrium and right ventricle of the heart. Despite its size, it is one of the major drainage vessels for the heart. Anatomy Course The small cardiac vein runs in the coronary sulcus between the right atrium and right ventricle, and opens into the right extremity of the coronary sinus. Territory The small cardiac vein receives blood from the posterior portion of the right atrium and ventricle. Variation The small cardiac vein may empty into the coronary sinus, right atrium, or middle cardiac vein. It may be absent. References External links - "Anterior view of the heart." Veins of the torso
Small cardiac vein
646092
Mitral stenosis is a valvular heart disease characterized by the narrowing of the opening of the mitral valve of the heart. It is almost always caused by rheumatic valvular heart disease. Normally, the mitral valve is about 5 cm2 during diastole. Any decrease in area below 2 cm2 causes mitral stenosis. Early diagnosis of mitral stenosis in pregnancy is very important as the heart cannot tolerate increased cardiac output demand as in the case of exercise and pregnancy. Atrial fibrillation is a common complication of resulting left atrial enlargement, which can lead to systemic thromboembolic complications such as stroke. Signs and symptoms Signs and symptoms of mitral stenosis include the following: Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND) Palpitations Chest pain Hemoptysis Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation. Ascites and edema and hepatomegaly (if right-side heart failure develops) Fatigue and weakness increase with exercise and pregnancy. Natural history The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years. In individuals having been offered mitral valve surgery but refused, survival with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction. Cause Almost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Uncommon causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. It is the most common valvular heart disease in pregnancy. Other causes include infective endocarditis where the vegetations may favor increase risk of stenosis. Other rare causes include mitral annular calcification, endomyocardial fibroelastosis, malignant carcinoid syndrome, systemic lupus erythematosus, whipple disease, fabry disease, and rheumatoid arthritis. hurler' disease, hunter's disease, amyloidosis. Pathophysiology The normal area of the mitral valve orifice is about 4 to 6 cm2. In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. A normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during ventricular diastole will be equal. The result is that the left ventricle gets filled with blood during early ventricular diastole, with only a small portion of extra blood contributed by contraction of the left atrium (the "atrial kick") during late ventricular diastole. When the mitral valve area goes below 2 cm2, the valve causes an impediment to the
Mitral stenosis
1283378
The jugular veins are veins that take blood from the head back to the heart via the superior vena cava. The internal jugular vein descends next to the internal carotid artery and continues posteriorly to the sternocleidomastoid muscle. Structure and function There are two sets of jugular veins: external and internal. The left and right external jugular veins drain into the subclavian veins. The internal jugular veins join with the subclavian veins more medially to form the brachiocephalic veins. Finally, the left and right brachiocephalic veins join to form the superior vena cava, which delivers deoxygenated blood to the right atrium of the heart. The jugular vein has tributaries consisting of petrosal sinus, facial, lingual, pharylingual, the thyroid, and sometimes the occipital vein. Internal The internal jugular vein is formed by the anastomosis of blood from the sigmoid sinus of the dura mater and the inferior petrosal sinus. The internal jugular runs with the common carotid artery and vagus nerve inside the carotid sheath. It provides venous drainage for the contents of the skull. External The external jugular vein runs superficially to sternocleidomastoid. There is also another minor jugular vein, the anterior jugular vein, draining the submaxillary region. Clinical significance Pressure The jugular venous pressure is an indirectly observed pressure over the venous system. It can be useful in the differentiation of different forms of heart and lung disease. In the jugular veins pressure waveform, upward deflections correspond with (A) atrial contraction, (C) ventricular contraction (and resulting bulging of perspicuous into the right atrium during isovolumic systole), and (V) atrial venous filling. The downward deflections correspond with (X) the atrium relaxing (and the perspicuous valve moving downward) and (y) the filling of ventricle after the tricuspid opens. Components include: The a peak is caused by the contraction of the right atrium. The av minimum is due to relaxation of the right atrium and closure of the tricuspid valve. The c peak reflects the pressure rise in the right ventricle early during systole and the resultant bulging of the tricuspid valve—which has just closed—into the right atrium. The x minimum occurs as the ventricle contracts and shortens during the ejection phase, later in systole. The shortening heart—with tricuspid valve still closed—pulls on valve opens, the v peak begins to wane. The y minimum reflects a fall in right atrial pressure during rapid ventricular filling, as blood leaves the right atrium through an open tricuspid valve and enters the right ventricle. The increase in venous pressure after the y minimum occurs as venous return continues in the face of reduced ventricular filling. Diseases and conditions The jugular vein is prominent in heart failure. When the patient is sitting or in a semirecumbent position, the height of the jugular veins and their pulsations provides an estimate of the central venous pressure and gives important information about whether the heart is keeping up with the demands on it or is failing. Distension of the jugular is a potential sign of heart failure, cardiac tamponade,
Jugular vein
20995276
Right atrial pressure (RAP) is the blood pressure in the right atrium of the heart. RAP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system. RAP is often nearly identical to central venous pressure (CVP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when venous tone (i.e the degree of venous constriction) is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure (where central venous pressure increases, but right atrial pressure stays the same; VR = CVP − RAP). Factors affecting RAP Factors that increase RAP include: Hypervolemia Forced exhalation Tension pneumothorax Heart failure Pleural effusion Decreased cardiac output Cardiac tamponade Mechanical ventilation and the application of positive end-expiratory pressure (PEEP) Pulmonary Hypertension Pulmonary Embolism Left to right shunted Atrial Septal Defect Factors that decrease RAP include: Hypovolemia Deep inhalation Distributive shock See also Pulmonary capillary wedge pressure Jugular venous pressure Central venous pressure References External links Cardiovascular Physiology Concepts Cardiovascular Physiology Medical terminology Medical monitoring Cardiovascular physiology
Right atrial pressure
242360
Systole ( ) is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood. Etymology The term originates, via Neo-Latin, from Ancient Greek (sustolē), from (sustéllein 'to contract'; from sun 'together' + stéllein 'to send'), and is similar to the use of the English term to squeeze. Terminology, general explanation The mammalian heart has four chambers: the left atrium above the left ventricle (lighter pink, see graphic), which two are connected through the mitral (or bicuspid) valve; and the right atrium above the right ventricle (lighter blue), connected through the tricuspid valve. The atria are the receiving blood chambers for the circulation of blood and the ventricles are the discharging chambers. In late ventricular diastole, the atrial chambers contract and send blood to the ventricles. This flow fills the ventricles with blood, and the resulting pressure closes the valves to the atria. The ventricles now perform isovolumetric contraction, which is contraction while all valves are closed. This contraction ends the first stage of systole. The second stage proceeds immediately, pumping oxygenated blood from the left ventricle through the aortic valve and aorta to all body systems, and simultaneously pumping oxygen-poor blood from the right ventricle through the pulmonic valve and pulmonary artery to the lungs. Thus, the pairs of chambers (upper atria and lower ventricles) contract in alternating sequence to each other. First, atrial contraction feeds blood into the ventricles, then ventricular contraction pumps blood out of the heart to the body systems, including the lungs for resupply of oxygen. Cardiac systole is the contraction of the cardiac muscle in response to an electrochemical stimulus to the heart's cells (cardiomyocytes). Cardiac output is the volume of blood pumped by the ventricles in one minute. The ejection fraction is the volume of blood pumped divided by the total volume of blood in the left ventricle. Types of systole Atrial systole Atrial systole occurs late in ventricular diastole and represents the contraction of myocardium of the left and right atria. The sharp decrease in ventricular pressure that occurs during ventricular diastole allows the atrioventricular valves (or mitral and tricuspid valves) to open and causes the contents of the atria to empty into the ventricles. The atrioventricular valves remain open while the aortic and pulmonary valves remain closed because the pressure gradient between the atrium and ventricle is preserved during late ventricular diastole. Atrial contraction confers a minor-fraction addition to ventricular filling, but becomes significant in left ventricular hypertrophy, or thickening of the heart wall, as the ventricle does not fully relax during its diastole. Loss of normal electrical conduction in the heart—as seen during atrial fibrillation, atrial flutter, and complete heart block—may eliminate atrial systole completely. Contraction of the atria follows depolarization, represented by the P wave of the ECG. As both atrial chambers contract—from the superior region of the atria toward the atrioventricular septum—pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular valves. At the start
Systole
64449141
Carbon dioxide angiography is a diagnostic radiographic technique in which a carbon dioxide (CO2) based contrast medium is used - unlike traditional angiography where the contrast medium normally used is iodine based – to see and study the body vessels. Since CO2 is a non-radio-opaque contrast medium, angiographic procedures need to be performed in digital subtraction angiography (DSA). History The use of carbon dioxide as a contrast agent goes back to 1920s when the gas was used to visualize retroperitoneal structures. In the 1950s and early 1960s, CO2 was injected intravenously to delineate the right atrium for the detection of pericardial effusion. This imaging technique developed from animal and clinical studies which demonstrated that CO2 was safe and well tolerated with venous injections. In the early 1970s, Dr. Hawkins and Dr. Cho started using and studying CO2 as a contrast agent also for peripheral vascular imaging and intervention. With the advent of digital subtraction angiography (DSA) technique in 1980s, CO2 has evolved into a safe and useful alternative contrast agent in both arteriography and venography. Because of its lack of renal toxicity and allergic potential, CO2 is a preferred contrast agent in patients with renal failure or iodinated contrast medium allergy, and particularly in patients who require large volumes of contrast medium for complex endovascular procedures. Technique CO2 angiography is intended only for peripheral procedures. In case of procedures in the arterious system it is allowed to inject CO2 only below the diaphragm; while in the venous system it can also be investigated supradiaphragmatic, provided that the cerebral vessels are excluded. Taking this aspect into consideration, the practical approach follows that of the iodinated contrast procedures. The contrast injection can be carried out, similarly, both with manual devices and with automatic injectors (Automated Carbon Dioxide Angiography, ACDA). Properties Being naturally present in the human body, CO2 is the only 100% biocompatible contrast agent, meaning no adverse reactions, such as allergy, nephrotoxicity, and hepatotoxicity. Carbon dioxide is a negative contrast medium and it has a low radiopacity (while iodinated contrast media are defined as positive contrast media due to their high radiopacity). Contrast is caused by the different X-ray absorption coefficients between the tissue and the contrast agent. In the vascular imaging results produced using CO2, vessels look brighter rather than the surrounding tissues, because the contrast medium absorbs less X-ray radiations rather an iodine-based contrast medium, where the vessel are displayed in black. The CO2 does not mix with blood. At atmospheric pressure CO2 is in gaseous form and, when it comes out from the catheter, it forms a train of bubbles which displaces blood, causing a transient ischemia, in relation to the bloodstream (systolic pressure). When added together by DSA “stacking” software, the result is a composite diagnostic image of the frames. Carbon dioxide is highly soluble, allowing multiple injections without a maximum dosage (per procedure, while it is 100 mL per injection by the literature), but, in case of multiple injections, should be considered and adequate time interval
Carbon dioxide angiography
44942975
The bronchial circulation is the part of the systemic circulation that supplies nutrients and oxygen to the cells that constitute the lungs, as well as carrying waste products away from them. It is complementary to the pulmonary circulation that brings deoxygenated blood to the lungs and carries oxygenated blood away from them in order to oxygenate the rest of the body. In the bronchial circulation, blood goes through the following steps: Bronchial arteries carry oxygenated blood to the lungs Pulmonary capillaries, where there is exchange of water, oxygen, carbon dioxide, and many other nutrients and waste chemical substances between blood and the tissues Bronchial veins drain venous blood from the large main bronchi into the azygous vein, and ultimately the right atrium. Venous blood from the bronchi inside the lungs drains into the pulmonary veins and empties into the left atrium; since this blood never went through a capillary bed it was never oxygenated and so provides a small amount of shunted deoxygenated blood into the systemic circulation. Blood reaches from the pulmonary circulation into the lungs for gas exchange to oxygenate the rest of the body tissues. But bronchial circulation supplies fully oxygenated arterial blood to the lung tissues themselves. This blood supplies the bronchi and the pleurae to meet their nutritional requirements. Because of the dual blood supply to the lungs from both the bronchial and the pulmonary circulation, this tissue is more resistant to infarction. An occlusion of the bronchial circulation does not cause infarction, but it can still occur in pulmonary embolism when the pulmonary circulation is blocked and the bronchial circulation cannot fully compensate for it. References Angiology
Bronchial circulation
2456407
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the systemic circulation to be filled with relatively deoxygenated blood. The causes of tricuspid atresia are unknown. In most cases of tricuspid atresia, additional defects exist to allow exchange of blood between the loops of systematic circulation and pulmonary circulation, filling in the role of the missing atrioventricular connection. An atrial septal defect (ASD) must be present to fill the left atrium and the left ventricle with blood. Since there is a lack of a right ventricle, there must also be a way to pump blood into the pulmonary artery. This can be accomplished by a ventricular septal defect (VSD) connecting the left ventricle to the pulmonary artery or by a patent ductus arteriosus (PDA) connecting the aorta to the pulmonary artery. In the latter case, prostaglandin E1 is used to maintain the PDA connection until emergency corrective surgery can be completed. As oxygenated blood is mixed with deoxygenated blood in both cases, there is a reduction in the oxygen-carrying capacity. It is also possible for tricuspid atresia to appear without the life-saving defects. In this case, the systemic and pulmonary circulations would be cut off from each other and no useful breathing can occur. An experimental procedure called fetal balloon atrial septostomy can be used to artificially create the required defect in utero. Presentation progressive cyanosis poor feeding tachypnea over the first 2 weeks of life holosystolic murmur due to the VSD left axis deviation on electrocardiography and left ventricular hypertrophy (since it must pump blood to both the pulmonary and systemic systems) Normal or mildly enlarged heart Cause Tricuspid atresia is caused by complete absence of the tricuspid valve. The underlying cause of this absence remains unknown. This prevents direct blood flow between the right atrium and the right ventricle. This usually causes the foramen ovale to remain open after birth, leading to atrial septal defect. Pathophysiology As there is no communication between the right atrium and the right ventricle, there must be an atrial septal defect to allow blood to flow into the left cardiac chambers. Due to the lack of blood flow into the right ventricle, it will be hypoplastic. In most cases, there will also be a ventricular septal defect allowing some blood into the pulmonary circulation. Due to the lack of blood flow into the pulmonary circulation, there is poor oxygenation of blood, leading to progressively worsening cyanosis. Diagnosis The majority of cases can be diagnosed prenatally during a routine anomaly scan. If evidence of a congenital heart disease is found, the diagnosis can be confirmed by a foetal echocardiogram. If it is not diagnosed prenatally, it may be diagnosed shortly after birth with physical examination, which would reveal cyanosis
Tricuspid atresia
12368695
Crisscross heart is a type of congenital heart defect where the right atrium is closely associated with the left ventricle in space, and the left atrium is closely associated with the right ventricle. Although it is classified as a defect, the criss-cross is more of a spatial anomaly than a functional one, and it is possible for the heart to have relatively normal functioning. The ventricles are rotated either clockwise or counterclockwise resulting in the twisting of their connection. The actual blood flow stream through the ventricles is not interrupted. Symptoms and signs Crisscross heart is a very rare congenital heart defect, and results in many different symptoms, even though the heart still has the ability to perform its major function of pumping blood throughout the body. Individuals who have this disease will experience cyanosis which is a blue tint to the skin because of inadequate blood flow to the body, this symptom will be seen especially around the mouth. Other symptoms include pallor, extreme dyspnea, pulmonary valve stenosis, cardiac murmurs and a deviated ventricular septum. Pallor can be described as a pale color of the skin, and dyspnea is difficulty breathing. Pulmonary valve stenosis is the narrowing of the pulmonary valve which leads to decreased blood flow to the pulmonary artery. Cardiac murmurs are sounds that can be heard when using a stethoscope that make a swooshing noise rather than a normal “lub-dup”. Lastly a deviated ventricular septum is when there is a hole between the ventricle walls resulting in blood between the ventricles flowing freely between each other. Anatomy In an anatomically correct heart the right atrium and right ventricle are working together to supply blood to the pulmonary artery, similarly to how the left atrium and the left ventricle work simultaneously to supply blood to the aorta. During the process of the heart contracting and releasing the right atrium and left atrium contract at the same time, while the left ventricle and right ventricle relax. In opposition, when the left atrium and right atrium are relaxed the left ventricle and right ventricle contract pushing blood to either the aorta or pulmonary artery. In an anatomically correct heart the atria are smaller than the ventricles. The ventricles include more muscle in order to push high quantities of blood throughout the body. Normal blood flow throughout the heart begins at the superior vena cava coming from the upper half of the body and the inferior vena cava coming from the lower half of the body. Next blood will be in the right atrium and will flow uninterrupted through the tricuspid valve through to the right ventricle. The blood from the right ventricle should go to the pulmonary artery via the pulmonary valve. The blood from the pulmonary vein enters the left atrium, then flows through the mitral valve to the left ventricle. After the left ventricle is filled with blood the aortic valve opens allowing blood to go through, which the blood then enters the aorta and goes to
Crisscross heart
3188445
Levo-Transposition of the great arteries is an acyanotic congenital heart defect in which the primary arteries (the aorta and the pulmonary artery) are transposed, with the aorta anterior and to the left of the pulmonary artery; the morphological left and right ventricles with their corresponding atrioventricular valves are also transposed. Use of the term "corrected" has been disputed by many due to the frequent occurrence of other abnormalities and or acquired disorders in l-TGA patients. In segmental analysis, this condition is described as atrioventricular discordance (ventricular inversion) with ventriculoarterial discordance. l-TGA is often referred to simply as transposition of the great arteries (TGA); however, TGA is a more general term which may also refer to dextro-transposition of the great arteries (d-TGA). Signs and symptoms Simple l-TGA does not produce any visually identifiable features at birth. However, systemic blood pressure then becomes much higher than pulmonary blood pressure. The morphological right ventricle, evolved to handle a low blood pressure, will over a period of years hypertrophy and may fail, because of the high pressure it is forced to work against. This may produce symptoms such as dyspnea or fatigue. Complex l-TGA may produce immediate or more quickly-developed symptoms, depending on the nature, degree and number of accompanying defect(s). If a right-to-left or bidirectional shunt is present, the list of symptoms may include mild cyanosis. Pathogenesis In a normal heart, oxygen-depleted ("deoxygenated") blood is pumped from the right atrium into the right ventricle, then through the pulmonary artery to the lungs where it is oxygenated. The oxygen-rich ("oxygenated") blood then returns, via the pulmonary veins, to the left atrium from which it is pumped into the left ventricle, then through the aorta to the rest of the body, including the heart muscle itself. With l-TGA, deoxygenated blood is pumped from the right atrium into the morphological left ventricle (which lies on the right side of the heart), then through the pulmonary artery to the lungs. The oxygenated blood then returns, via the pulmonary veins, to the left atrium from which it is pumped into the morphological right ventricle, then through the aorta. Variations and similar defects l-TGA is often accompanied by other heart defects, the most common type being intracardiac shunts such as atrial septal defect (ASD) including patent foramen ovale (PFO), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). Stenosis of valves or vessels may also be present. When no other heart defects are present it is called 'simple' l-TGA; when other defects are present it is called 'complex' l-TGA. Diagnosis l-TGA can sometimes be diagnosed in utero with an ultrasound after 18 weeks gestation. However, many cases of simple l-TGA are "accidentally" diagnosed in adulthood, during diagnosis or treatment of other conditions. Treatment Simple l-TGA has a very good prognosis, with many individuals being asymptomatic and not requiring surgical correction. In a number of cases, the (technically challenging) "double switch operation" has been successfully performed to restore the normal blood flow through the ventricles. References External links Congenital heart
Levo-Transposition of the great arteries
3170526
The coronary sinus () is the largest vein of the heart. It drains over half of the deoxygenated blood from the heart muscle into the right atrium. It begins on the backside of the heart, in between the left atrium, and left ventricle; it begins at the junction of the great cardiac vein, and oblique vein of the left atrium. It receives multiple tributaries. It passes across the backside of the heart along a groove between left atrium and left ventricle, then drains into the right atrium at the orifice of the coronary sinus (which is usually guarded by the valve of coronary sinus). Structure Origin The coronary sinus arises upon the posterior aspect of the heart between the left atrium, and left ventricle. The coronary sinus commences at the union of the great cardiac vein, and the oblique vein of the left atrium. The origin of the coronary sinus is marked by the Vieussens valve of the coronary sinus which is situated at the endpoint of the great cardiac vein. Course The coronary sinus runs transversely in the left atrioventricular groove (coronary sulcus) on the posterior aspect of the heart. The sinus, before entering the right atrium, is considerably dilated - nearly to the size of the end of the little finger. Fate The coronary sinus drains through the posterior wall of right atrium at the orifice of the coronary sinus. This orifice is located at the posteroinferior aspect of the right atrium, just medial and to the left of the orifice of inferior vena cava, and between the inferior vena cava and the right atrioventricular orifice/tricuspid valve. The orifice is usually guarded by the valve of coronary sinus (a thin, crescent-shaped valve located on the anteroinferior part of the opening into the right atrium). Tributaries The coronary sinus receives blood mainly from the small, middle, great, and oblique cardiac veins. It also receives blood from the left marginal vein and the left posterior ventricular vein. Great cardiac vein (run upwards in the anterior interventricular sulcus to the left atrioventricular groove to form the coronary sinus; Middle cardiac vein (ascends posterior interventricular sulcus to drain into coronary sinus); Small cardiac vein (accompanies right coronary artery in the right atrioventricular groove to drain into the right side of the coronary sinus; Posterior vein of left ventricle (accompanies the left marginal artery, ascends the posterior wall of left ventricle to drain into the coronary sinus); Oblique vein of left atrium. All veins that empty into the coronary sinus except for the oblique vein of the left atrium have valves at their junction with the coronary sinus. The anterior cardiac veins do not drain into the coronary sinus but drain directly into the right atrium. Some small veins known as Thebesian veins drain directly into any of the four chambers of the heart. Microanatomy The wall of the coronary sinus is partly muscular. Function The coronary sinus is responsible for venous return of about 55% of the cardiac blood supply. Clinical significance
Coronary sinus
3038536
The interatrial septum is the wall of tissue that separates the right and left atria of the heart. Structure The interatrial septum is a that lies between the left atrium and right atrium of the human heart. The interatrial septum lies at angle of 65 degrees from right posterior to left anterior because right atrium is located at the right side of the body while left atrium is located at the left side of the body. The interatrial septum represents the posterior wall of the right atrium. Development The interatrial septum forms during the first and second months of fetal development. Formation of the septum occurs in several stages. The first is the development of the septum primum, a crescent-shaped piece of tissue forming the initial divider between the right and left atria. Because of its crescent shape, the septum primum does not fully occlude the space between the left and right atria; the opening that remains is called the ostium primum. During fetal development, this opening allows blood to be shunted from the right atrium to the left. As the septum primum grows, the ostium primum progressively narrows. Before the ostium primum is completely occluded, a second opening called the ostium secundum begins to form in the septum primum. The ostium secundum allows continued shunting of blood from the right atrium to the left. To the right of the septum primum, the septum secundum begins to form. This thick, muscular structure initially takes on the same crescent shape as the septum primum, except that it originates anteriorly, whereas the septum primum originates posteriorly. As the septum secundum grows, it leaves a small opening called the foramen ovale. The foramen ovale is continuous with the ostium secundum, again providing for continued shunting of blood. The ostium secundum progressively enlarges and the size of the septum primum diminishes. Eventually, the septum primum is nothing more than a small flap that covers the foramen ovale on its left side. This flap of tissue is called the valve of the foramen ovale. It opens and closes in response to pressure gradients between the left and right atria. When the pressure is greater in the right atrium, the valve opens; when the pressure is greater in the left atrium, the valve closes. Because the lungs are nonfunctional in fetal life, pressure in the pulmonary circulation is greater than that of the systemic circulation. Consequently, the right atrium is generally under higher pressures than the left atrium, and the valve of the foramen ovale is normally open. At birth At birth, there is a reversal in the pressure gradient between the atria, resulting in functional closure of the valve of the foramen ovale. Permanent anatomical closure of the foramen ovale occurs with time in normal infants. Inappropriate closure of the foramen ovale results in patent foramen ovale. Clinical significance An Atrial septal defect is a relatively common heart malformation that occurs when the interatrial septum fails to develop properly. Persistence of the ostium secundum is
Interatrial septum
21148921
Hypoplastic right heart syndrome or HRHS is a congenital heart defect in which the structures on the right side of the heart, particularly the right ventricle, are underdeveloped. This defect causes inadequate blood flow to the lungs, and thus a cyanotic infant. Symptoms and signs Common symptoms include a grayish-blue (cyanosis) coloration to the skin, lips, fingernails and other parts of the body. Other pronounced symptoms can be rapid or difficult breathing, poor feeding due to lack of energy, cold hands or feet, or being inactive and drowsy. Notably, patent ductus arteriosus and patent foramen ovale, normally dangerous defects, are necessary for a newborn with HRHS to survive. If either formation does close, the child will go into shock, signs of which can include cool or clammy skin, a weak or rapid pulse, and dilated pupils. Causes It is mostly unknown what causes hypoplastic right heart syndrome in a given individual. It is thought that a family history of similar heart defects can increase the risk, and there are some genes hypothesized to be factors. However, it can also manifest in a child whose family is completely lacking in congenital heart abnormalities. Pathogenesis When the right side of the heart is more underdeveloped than the left side, this is known as hypoplastic right heart syndrome. HRHS is known for the pulmonary atresia valves, the tricuspid valve, right ventricle, and the pulmonary artery all failing to form properly. HRHS also causes the right ventricle to be a fair amount smaller than the left side. In people with hypoplastic right heart syndrome, the heart is not able to adequately pump blood to the lungs. The result of this is an inadequate supply of oxygenated blood to be circulated to the body. The severity of underdevelopment varies for each individual. A special team of pediatric cardiologists is required to develop a treatment plan. Anatomy A healthy heart has four chambers, each separated by valves that open and close to control blood flow between the chambers. When the heart beats, oxygen-poor blood enters the right atrium. The blood then flows into the right ventricle, where it pumps into the pulmonary artery to travel to the lungs for oxygen. Oxygen-rich blood returns to the left atrium, where it then travels into the left ventricle. The left ventricle pumps the oxygenated blood into the aorta to be circulated to the rest of the body. Crucial steps in heart formation are development of the ventricles and atrium formation, as well as septation and valve formation. Any disturbances of such processes may lead to various congenital heart diseases and defects that could be initiated by various genetic, epigenetic or environmental factors. The most common heart malformations from genetic or epigenetic problems are: stenosis of the aorta and pulmonary trunk, which is a narrowing of the vessels, atrial and/or ventricular septal defect, tricuspid atresia, and hypoplastic left and right heart syndrome. When an individual has hypoplastic right or left heart syndrome, it means that more than one of these
Hypoplastic right heart syndrome
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A cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system. It may be described as right-left, left-right or bidirectional, or as systemic-to-pulmonary or pulmonary-to-systemic. The direction may be controlled by left and/or right heart pressure, a biological or artificial heart valve or both. The presence of a shunt may also affect left and/or right heart pressure either beneficially or detrimentally. Terminology The left and right sides of the heart are named from a dorsal view, i.e., looking at the heart from the back or from the perspective of the person whose heart it is. There are four chambers in a heart: an atrium (upper) and a ventricle (lower) on both the left and right sides. In mammals and birds, blood from the body goes to the right side of the heart first. Blood enters the upper right atrium, is pumped down to the right ventricle and from there to the lungs via the pulmonary artery. Blood going to the lungs is called the pulmonary circulation. When the blood returns to the heart from the lungs via the pulmonary vein, it goes to the left side of the heart, entering the upper left atrium. Blood is then pumped to the lower left ventricle and from there out of the heart to the body via the aorta. This is called the systemic circulation. A cardiac shunt is when blood follows a pattern that deviates from the systemic circulation, i.e., from the body to the right atrium, down to the right ventricle, to the lungs, from the lungs to the left atrium, down to the left ventricle and then out of the heart back to the systemic circulation. A left-to-right shunt is when blood from the left side of the heart goes to the right side of the heart. This can occur either through a hole in the ventricular or atrial septum that divides the left and the right heart or through a hole in the walls of the arteries leaving the heart, called great vessels. Left-to-right shunts occur when the systolic blood pressure in the left heart is higher than the right heart, which is the normal condition in birds and mammals. Congenital shunts in humans The most common congenital heart defects (CHDs) which cause shunting are atrial septal defects (ASD), patent foramen ovale (PFO), ventricular septal defects (VSD), and patent ductus arteriosi (PDA). In isolation, these defects may be asymptomatic, or they may produce symptoms which can range from mild to severe, and which can either have an acute or a delayed onset. However, these shunts are often present in combination with other defects; in these cases, they may still be asymptomatic, mild or severe, acute or delayed, but they may also work to counteract the negative symptoms caused by another defect (as with d-Transposition of the great arteries). Acquired shunts in human Biological Some acquired shunts are modifications of congenital ones: a balloon septostomy can enlarge a foramen
Cardiac shunt
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The heart is a muscular organ situated in the mediastinum. It consists of four chambers, four valves, two main arteries (the coronary arteries), and the conduction system. The left and right sides of the heart have different functions: the right side receives de-oxygenated blood through the superior and inferior venae cavae and pumps blood to the lungs through the pulmonary artery, and the left side receives saturated blood from the lungs. Heart location, orientation, and projection to the chest The heart has the shape of a pyramid, with its apex pointing towards the left nipple while its base forms the posterior surface of the heart. Other surfaces are the anterior, inferior (or diaphragmatic), and two pulmonary surfaces facing the lungs. Its longest dimension (apical to base) is broadly 12–13 cm, while the average weight is 250 grams in females and 300 grams in males. Its primary role is to receive the blood from the body, pump it to the lungs to be oxygenated, and receive it once more to pump it again to the rest of the human body tissues. Heart rate, defined as the number of times the heart beats per minute, can fluctuate due to the body's varying needs for oxygen and nutrients. In addition, heart rates can increase when the sympathetic nervous system is activated but decrease when the parasympathetic nervous system is activated. Although the parasympathetic nervous system prevails, specific mental, physical, or environmental stressors trigger the sympathetic nervous system, and thus, increase heart rate. The right side of the heart (which consists of the right atrium and the right ventricle) receives the desaturated blood, while the left side (consisting of the left atrium and left ventricle) receives the oxygenated blood. The pericardium is a thick membrane that covers the heart. It consists of two layers: the fibrous pericardium and the serous pericardium. It forms two recesses: the transverse recess and oblique recess. The transverse recess lies behind the aorta and pulmonary trunk, while the oblique recess lies behind the left atrium. The serous pericardium is thin and covers the heart. It is also called the epicardium. The fibrous pericardium is much thicker. Together they form the pericardial cavity, a thin sac hosting a small amount of fluid. Fibrous skeleton The four cardiac valves are kept in their place partly because of the fibrous skeleton of the heart, which is a collection of connective tissue. It consists of the right fibrous trigone (which along with the membranous septum forms the central fibrous body), the left right fibrous trigone, and the conus tendon. The right fibrous trigone is the strongest part of the skeleton. It lies to the right of the aortic valve and connects it with the mitral and tricuspid valves. It is pierced by the bundle of His. Lastly, the aortomitral curtain is also a part of the fibrous skeleton; it is formed by fibrous tissue connecting two of three of the aortic valve leaflets (the right and non-coronary leaflet) with anterior leaflet of the
Anatomy of the human heart
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The foramen secundum or ostium secundum is a in the septum primum, a precursor to the interatrial septum of the human heart. It is not the same as the foramen ovale, which is an opening in the septum secundum. Development The foramen secundum () is formed from small perforations that develop in the septum primum. The septum primum is a that grows down between the single primitive atrium of the developing heart to separate it into left and right atria. Closure Once a baby is born, blood should flow through the lungs, which now function to provide oxygen to the blood. The foramen secundum and foramen ovale act as a shunt where blood bypasses the lungs and does not become oxygenated. To provide proper blood flow as a newborn, the foramen secundum and foramen ovale must close at birth. Since the lungs now require a significant amount of blood flow, the vessels going to and from the lungs undergo dilation. While the pulmonary artery and pulmonary veins are dilating, the umbilical artery and umbilical vein are severed at the cutting of the umbilical cord, or the funiculus umbilicalis. This combination results in a reversal of pressure differences between the atria, and the septum primum is permanently forced against the septum secundum. This holds true even during atrial diastole, when the pressure is significantly less than atrial systole. Function The septum primum is on the left side of the heart in the left atrium while the septum secundum is much thicker and is located on the right side, in the right atrium. During development, blood shunts from the floor of the right atrium through the foramen ovale in the septum secundum then up through the foramen secundum in the septum primum. The foramen secundum is positioned so that blood exits in the ceiling of the left atrium and then out through the left ventricle and the aorta. The position of the foramen secundum and the size of the septum primum are crucial to ensuring that blood not flow backwards from the left atrium to the right atrium. The septum primum, being much thinner, is easily pressed against the septum secundum if blood attempts to flow in the reverse direction, effectively sealing off both the foramen secundum and the foramen ovale. Clinical significance An ostium secundum that persists at large size can be a source of atrial septal defects. Foramen secundum atrial septal defects are the most common atrial septal defects. This defect can arise as a result of defects of the septum primum and the septum secundum. For the septum primum, the problem can arise as a result of excess resorption of the septum during the process of apoptosis in order to form the foramen secundum. For the septum secundum, its inadequate growth can cause atrial septal defect since it is supposed to grow and eventually overlap the foramen secundum so as to form the oval foramen. As the right atrial pressure is normally lower than the mean left atrial pressure,
Foramen secundum
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A lumped parameter cardiovascular model is a zero-dimensional mathematical model used to describe the hemodynamics of the cardiovascular system. Given a set of parameters that have a physical meaning (e.g. resistances to blood flow), it allows to study the changes in blood pressures or flow rates throughout the cardiovascular system. Modifying the parameters, it is possible to study the effects of a specific disease. For example, arterial hypertension is modeled increasing the arterial resistances of the model. The lumped parameter model is used to study the hemodynamics of a three-dimensional space (the cardiovascular system) by means of a zero-dimensional space that exploits the analogy between pipes and electrical circuits. The reduction from three to zero dimensions is performed by splitting the cardiovascular system into different compartments, each of them representing a specific component of the system, e.g. right atrium or systemic arteries. Each compartment is made up of simple circuital components, like resistances or capacitors, while the blood flux behaves like the current flowing through the circuit according to Kirchoff's laws, under the action of the blood pressure (voltage drop). The lumped parameter model consists in a system of ordinary differential equations that describes the evolution in time of the volumes of the heart chambers, and the blood pressures and fluxes through the blood vessels. Model description The lumped parameter model consists in a system of ordinary differential equations that adhere to the principles of conservation of mass and momentum. The model is obtained exploiting the electrical analogy where the current represents the blood flow, the voltage represents the pressure difference, the electric resistance plays the role of the vascular resistance (determined by the section and the length of the blood vessel), the capacitance plays the role of the vascular compliance (the ability of the vessel to distend and increase volume with increasing transmural pressure, that is the difference in pressure between two sides of a vessel wall) and the inductance represents the blood inertia. Each heart chamber is modeled by means of the elastances that describe the contractility of the cardiac muscle and the unloaded volume, that is the blood volume contained in the chamber at zero-pressure. The valves are modeled as diodes. The parameter of the model are the resistances, the capacitances, the inductances and the elastances. The unknowns of the system are the blood volumes inside each heart chamber, the blood pressures and fluxes inside each compartment of the circulation. The system of ordinary differential equations is solved by means of a numerical method for temporal discretization, e.g., a Runge-Kutta method. The cardiovascular system is split into different compartments: the four heart chambers: left and right atrium and left and right ventricles; the systemic circulation that can be split into arteries, veins and, if needed, in other compartments accounting for different blood vessels; the pulmonary circulation that can be split into arteries, veins and, if needed, in other compartments accounting for different blood vessels. Downstream of the left atrium and ventricle and right atrium and ventricle there
Lumped parameter model for the cardiovascular system
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The Bainbridge reflex or Bainbridge effect, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors (Cardiac Receptors) located in both sides of atria at the venoatrial junctions. History Francis Arthur Bainbridge described this as a reflex in 1918 when he was experimenting on dogs. Bainbridge found that infusing blood or saline into the animal increased heart rate. This phenomenon occurred even if arterial blood pressure did not increase. He further observed that heart rate increased when venous pressure rose high enough to distend the right atrium, but denervation of the vagi to the heart eliminated these effects. Subsequent work demonstrated a stretch-induced increase in heart rate in isolated hearts or even the fully separated sinoatrial node (SAN). Thus, the positive chronotropic (from Χρόνος, Greek for 'time', and τρέπειν, Greek for 'to bend/turn') response of the heart to stretch must, in part, at least, be caused and accomplished by mechanisms located within the SAN. This led to the suggestion to refer to the response discovered by Bainbrindge as an 'effect' rather than a 'reflex'. Mechanism of Action Increased blood volume results in increased venous return to the heart, which leads to increased firing of B-fibers. B-fibers send signals to the brain (the afferent pathway of the neural portion of the Bainbridge reflex), which then modulates both sympathetic and parasympathetic pathways to the SA node of the heart (the efferent pathway of the neural portion of the Bainbridge reflex), causing an increase in heart rate. "Effects on cardiac contractility and stroke volume are insignificant." Bainbridge reflex can be blocked by atropine and can be abolished by cutting the vagus nerve. The local response of sino-atrial node pacemaker cells to stretch involves stretch-activated ion channels, as was demonstrated by stretching single isolated pacemaker cells while recording their cellular electrical activity. Control of heart rate The Bainbridge reflex and the baroreceptor reflex control heart rate. The baroreceptor reflex can correct for a change in arterial pressure by increasing or decreasing heart rate. In contrast, the Bainbridge reflex responds to changes in blood volume. The Bainbridge reflex is seen in dogs, but experiment has shown that it is not as significant in primates. There is evidence, however, that the Bainbridge reflex does occur in humans, as after delivery of an infant when a large volume (up to 800 mL) of uteroplacental blood is returned to the mother's circulation, resulting in tachycardia Venous return As venous return increases, the pressure in the superior and inferior vena cava increase. This results in an increase in the pressure of the right atrium, which stimulates the atrial stretch receptors (low pressure receptor zones). These receptors in turn signal the medullary control centers to increase the heart rate (Tachycardia). Unusually, this tachycardia is mediated by increased sympathetic activity to the SAN with no fall in parasympathetic activity. Increasing the heart rate serves to decrease the pressure in the superior and inferior venae
Bainbridge reflex
7904695
Tricuspid regurgitation (TR), also called tricuspid insufficiency, is a type of valvular heart disease in which the tricuspid valve of the heart, located between the right atrium and right ventricle, does not close completely when the right ventricle contracts (systole). TR allows the blood to flow backwards from the right ventricle to the right atrium, which increases the volume and pressure of the blood both in the right atrium and the right ventricle, which may increase central venous volume and pressure if the backward flow is sufficiently severe. The causes of TR are divided into hereditary and acquired; and also primary and secondary. Primary TR refers to a defect solely in the tricuspid valve, such as infective endocarditis; secondary TR refers to a defect in the valve as a consequence of some other pathology, such as left ventricular failure or pulmonary hypertension. The mechanism of TR is either a dilatation of the base (annulus) of the valve due to right ventricular dilatation, which results in the three leaflets being too far apart to reach one another; or an abnormality of one or more of the three leaflets. Signs and symptoms The symptoms of TR depend on its severity. Severe TR causes right-sided heart failure, with the development of ascites and peripheral edema. In severe cases of right heart failure due to TR, venous congestion of the kidneys and liver may lead to cardiorenal syndrome (kidney failure secondary to heart failure) and cardiohepatic syndromes (liver failure secondary to heart failure) respectively. Venous congestion from TR and right heart failure may also lead to anasarca (diffuse swelling) and decreased intestinal absorption due to the swelling surrounding the intestines, in severe cases this may lead to cachexia and malnutrition. A pansystolic heart murmur may be heard on auscultation of the chest. The murmur is usually of low frequency and best heard on the lower left sternal border. It increases with inspiration, and decreases with expiration: this is known as Carvallo's sign. However, the murmur may be inaudible due to the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard at the lower sternal border, and increasing in intensity with inspiration. On examination of the neck, there may be giant C-V waves in the jugular pulse. With severe TR, there may be an enlarged liver detected on palpation of the right upper quadrant of the abdomen; the liver may be pulsatile on palpation and even on inspection. Causes The causes of TR may be classified as congenital or acquired; another classification divides the causes into primary or secondary. Congenital abnormalities are much less common than acquired. The most common acquired TR is due to right ventricular dilatation. Such dilatation is most often due left heart failure or pulmonary hypertension. Other causes of right ventricular dilatation include right ventricular infarction, inferior myocardial infarction, and cor pulmonale. In regards to primary and secondary causes they are: Mechanism In terms of the mechanism of tricuspid insufficiency,
Tricuspid regurgitation
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The proper development of the atrioventricular canal into its prospective components (The heart septum and associated valves) to create a clear division between the four compartments of the heart and ensure proper blood movement through the heart, are essential for proper heart function. When this process does not happen correctly, a child will develop atrioventricular canal defect which occurs in 2 out of every 10,000 births. It also has a correlation with Down syndrome because 20% of children with Down syndrome have atrioventricular canal disease as well. This is a very serious condition and surgery is necessary within the first six months of life for a child. Half of the children who are untreated with this condition die during their first year due to heart failure or pneumonia. Atrioventricular canal defect is a combination of abnormalities of the heart and is present at birth. There is a problem when there are holes present in the walls that separate chambers (septa), as well as when valves are incorrectly constructed. There are other names for these heart abnormalities such as endocardial cushion defects or atrioventricular septal defect'Development In a normal heart there are four chambers. These are the right and left atria, and right and left ventricles. The right atrium and right ventricle function to pump blood to the lungs while the left atrium and left ventricle pump blood to the rest of the body. There are heart valves in place that inhibit back-flow between these chambers. Clinical relevance Atrioventricular canal defect An atrioventricular canal defect is developed because of the improper formation of the endocardial cushions, and their job is to separate the different parts of the heart during development when they fuse. It is strongly associated with Down's syndrome. The structures that develop from the fusion of the endocardial cushions are: The interatrial septum divides the left and right atrium The interventricular septum divides the left and right ventricles. The mitral valve and tricuspid valve are formed by the proper division of an early common valve being separated into two. Atrioventricular canal defect may be divided into partial or complete'' forms. In the partial form, openings between the left and right atria and improper formation of the mitral valve exist. In the complete form, there is free movement in all chambers because there is a large hole where the atria and ventricles meet, and instead of there being two valves there is one common valve. Surgery is usually conducted in-between the 3rd and 6th month of life, and with this condition the earlier the better. Usually, intracardiac repair involves closing the holes in the septum and the creation of two new atrioventricular valves from the underdeveloped common valve leaflet. See also Atrioventricular septal defect Atrioventricular septum References Embryology of cardiovascular system
Atrioventricular canal