Heart Ventricles
Myocardium
Cerebral Ventricles
Third Ventricle
Fourth Ventricle
Heart Failure
Lateral Ventricles
Heart Defects, Congenital
Cerebral Ventricle Neoplasms
Heart Diseases
Fetal Heart
Heart Valves
Ventricular Function, Left
Heart Block
Echocardiography
Hemodynamics
Dogs
Myocytes, Cardiac
Heart Septum
Cardiomegaly
Ventricular Function, Right
Stroke Volume
Myocardial Ischemia
Phasic right coronary artery blood flow in conscious dogs with normal and elevated right ventricular pressures. (1/10358)
We studied phasic right coronary blood flow in well trained normal dogs and dogs with pulmonic stenosis. We installed electromagnetic flow transducers and pressure tubes under anesthesia to monitor right coronary blood flow, cardiac output, central aortic blood pressure, and right ventribular pressure. In normotensive dogs, systolic flow amplitude equaled early diastolic flow levels. The ratio of systolic to diastolic flow at rest was substantially greater in the right coronary bed (36+/-1.3%) than in the left circumflex bed (13+/-3.6%). Right diastolid flow runoff, including the cove late in diastole, resembled left circumflex runoff. Blood flow to the normotensive right (37+/-1.1 ml/min 100(-1) g) and the left (35+/-1.0 ml/min(-1) g) ventricular myocardium indicated equal perfusion of both cardiac walls. Throttling of systolic flow was related directly to the right ventricular systolic pressure level in the dogs with pulmonic stenosis. Retrograde systolic flow occurred in severe right ventricular hypertension. The late diastolic runoff pattern in dogs with pulmonic stenosis appeared the same as for the normotensive dogs. We obtained systolic to diastolic flow ratios of 1/3 the value of normotensive hearts in high and severe pulmonic hypertension. Electrocardiograms and studies of pathology suggested restricted blood flow to the inner layers of the right myocardium in the dogs with severe and high right ventricular hypertension. Normotensive and hypertensive peak hyperemic flow responses were similar, except for an increased magnitude of diastolic flow, with proportionately less systolic flow in hypertensive states. (+info)Regulation of chamber-specific gene expression in the developing heart by Irx4. (2/10358)
The vertebrate heart consists of two types of chambers, the atria and the ventricles, which differ in their contractile and electrophysiological properties. Little is known of the molecular mechanisms by which these chambers are specified during embryogenesis. Here a chicken iroquois-related homeobox gene, Irx4, was identified that has a ventricle-restricted expression pattern at all stages of heart development. Irx4 protein was shown to regulate the chamber-specific expression of myosin isoforms by activating the expression of the ventricle myosin heavy chain-1 (VMHC1) and suppressing the expression of the atrial myosin heavy chain-1 (AMHC1) in the ventricles. Thus, Irx4 may play a critical role in establishing chamber-specific gene expression in the developing heart. (+info)Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis. (3/10358)
Insulin-like growth factor (IGF)-1 inhibits apoptosis, but its mechanism is unknown. Myocyte stretching activates p53 and p53-dependent genes, leading to the formation of angiotensin II (Ang II) and apoptosis. Therefore, this in vitro system was used to determine whether IGF-1 interfered with p53 function and the local renin-angiotensin system (RAS), decreasing stretch-induced cell death. A single dose of 200 ng/ml IGF-1 at the time of stretching decreased myocyte apoptosis 43% and 61% at 6 and 20 hours. Ang II concentration was reduced 52% at 20 hours. Additionally, p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF-1 via the induction of Mdm2 and the formation of Mdm2-p53 complexes. Concurrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes exposed to IGF-1. Conversely, Bcl-2 and the Bcl-2-to-Bax protein ratio increased. The effects of IGF-1 on cell death, Ang II synthesis, and Bax protein were the consequence of Mdm2-induced down-regulation of p53 function. In conclusion, the anti-apoptotic impact of IGF-1 on stretched myocytes was mediated by its capacity to depress p53 transcriptional activity, which limited Ang II formation and attenuated the susceptibility of myocytes to trigger their endogenous cell death pathway. (+info)Adenoviral gene transfer of the human V2 vasopressin receptor improves contractile force of rat cardiomyocytes. (4/10358)
BACKGROUND: In congestive heart failure, high systemic levels of the hormone arginine vasopressin (AVP) result in vasoconstriction and reduced cardiac contractility. These effects are mediated by the V1 vasopressin receptor (V1R) coupled to phospholipase C beta-isoforms. The V2 vasopressin receptor (V2R), which promotes activation of the Gs/adenylyl cyclase system, is physiologically expressed in the kidney but not in the myocardium. Expression of a recombinant V2R (rV2R) in the myocardium could result in a positive inotropic effect via the endogenous high concentrations of AVP in heart failure. METHODS AND RESULTS: A recombinant adenovirus encoding the human V2R (Ad-V2R) was tested for its ability to modulate the cardiac Gs/adenylyl cyclase system and to potentiate contractile force in rat ventricular cardiomyocytes and in H9c2 cardiomyoblasts. Ad-V2R infection resulted in a virus concentration-dependent expression of the transgene and led to a marked increase in cAMP formation in rV2R-expressing cardiomyocytes after exposure to AVP. Single-cell shortening measurements showed a significant agonist-induced contraction amplitude enhancement, which was blocked by the V2R antagonist, SR 121463A. Pretreatment of Ad-V2R-infected cardiomyocytes with AVP led to desensitization of the rV2R after short-term agonist exposure but did not lead to further loss of receptor function or density after long-term agonist incubation, thus demonstrating resistance of the rV2R to downregulation. CONCLUSIONS: Adenoviral gene transfer of the V2R in cardiomyocytes can modulate the endogenous adenylyl cyclase-signal transduction cascade and can potentiate contraction amplitude in cardiomyocytes. Heterologous expression of cAMP-forming receptors in the myocardium could lead to novel strategies in congestive heart failure by bypassing the desensitized beta-adrenergic receptor signaling. (+info)An inhibitor of p38 mitogen-activated protein kinase protects neonatal cardiac myocytes from ischemia. (5/10358)
Cellular ischemia results in activation of a number of kinases, including p38 mitogen-activated protein kinase (MAPK); however, it is not yet clear whether p38 MAPK activation plays a role in cellular damage or is part of a protective response against ischemia. We have developed a model to study ischemia in cultured neonatal rat cardiac myocytes. In this model, two distinct phases of p38 MAPK activation were observed during ischemia. The first phase began within 10 min and lasted less than 1 h, and the second began after 2 h and lasted throughout the ischemic period. Similar to previous studies using in vivo models, the nonspecific activator of p38 MAPK and c-Jun NH2-terminal kinase, anisomycin, protected cardiac myocytes from ischemic injury, decreasing the release of cytosolic lactate dehydrogenase by approximately 25%. We demonstrated, however, that a selective inhibitor of p38 MAPK, SB 203580, also protected cardiac myocytes against extended ischemia in a dose-dependent manner. The protective effect was seen even when the inhibitor was present during only the second, sustained phase of p38 MAPK activation. We found that ischemia induced apoptosis in neonatal rat cardiac myocytes and that SB 203580 reduced activation of caspase-3, a key event in apoptosis. These results suggest that p38 MAPK induces apoptosis during ischemia in cardiac myocytes and that selective inhibition of p38 MAPK could be developed as a potential therapy for ischemic heart disease. (+info)Taurine modulates I(Kr) but I(Ks) in guinea-pig ventricular cardiomyocytes. (6/10358)
1. Effects of taurine on the delayed rectifier K+ current (I(K)) in isolated guinea-pig ventricular cardiomyocytes were examined at different intracellular Ca2+ concentration ([Ca2+]i), using whole-cell voltage and current clamp techniques. Experiments were performed at 36 degrees C. 2. Addition of taurine (10-20 mM) decreased the action potential duration (APD) at pCa 8, but increased the APD at pCa 6. Taurine (20 mM) enhanced I(K) at 70 mV by 22.4 +/- 3.1% (n = 6, P < 0.01) at pCa 8, whereas taurine inhibited the I(K) by 27.1 +/- 2.7% (n = 6, P < 0.01) at pCa 6. These responses behaved in a concentration-dependent manner. 3. The I(K) is composed of the rapid and slow components (I(Kr) and I(Ks)). When [Ca2+]i was pCa 6, taurine at 20 mM reduced the tail current of I(Kr) at 70 mV by 16.5 +/- 2.7% (n = 5, P < 0.05) and that of I(Ks) at 70 mV by 27.1 +/- 2.8% (n = 6, P < 0.01). In contrast, at pCa 8, the tail currents of I(Kr) and I(Ks) at 70 mV were enhanced by 13.4 +/- 3.2% (n = 7, P < 0.05) and by 22.4 +/- 3.1% (n = 7, P < 0.01), respectively. The voltages of half-maximum activation (V1/2) for I(Kr) and I(Ks) were not modified by taurine. 4. Addition of E-4031 (5 microM) to taurine had a complete blockade of the tail current of I(Kr), but not I(Ks). The remained tail current (I(Ks)) in the presence of E-4031 (5 microM) was not affected by taurine (20 mM), but was blocked by 293B (30 microM). 5. These results indicate that taurine modulates I(Kr) but not I(Ks), depending on [Ca2+]i, resulting in regulation of the APD. (+info)A comparison of an A1 adenosine receptor agonist (CVT-510) with diltiazem for slowing of AV nodal conduction in guinea-pig. (7/10358)
1. The purpose of this study was to compare the pharmacological properties (i.e. the AV nodal depressant, vasodilator, and inotropic effects) of two AV nodal blocking agents belonging to different drug classes; a novel A1 adenosine receptor (A1 receptor) agonist, N-(3(R)-tetrahydrofuranyl)-6-aminopurine riboside (CVT-510), and the prototypical calcium channel blocker diltiazem. 2. In the atrial-paced isolated heart, CVT-510 was approximately 5 fold more potent to prolong the stimulus-to-His bundle (S-H interval), a measure of slowing AV nodal conduction (EC50 = 41 nM) than to increase coronary conductance (EC50 = 200 nM). At concentrations of CVT-510 (40 nM) and diltiazem (1 microM) that caused equal prolongation of S-H interval (approximately 10 ms), diltiazem, but not CVT-510, significantly reduced left ventricular developed pressure (LVP) and markedly increased coronary conductance. CVT-510 shortened atrial (EC50 = 73 nM) but not the ventricular monophasic action potentials (MAP). 3. In atrial-paced anaesthetized guinea-pigs, intravenous infusions of CVT-510 and diltiazem caused nearly equal prolongations of P-R interval. However, diltiazem, but not CVT-510, significantly reduced mean arterial blood pressure. 4. Both CVT-510 and diltiazem prolonged S-H interval, i.e., slowed AV nodal conduction. However, the A1 receptor-selective agonist CVT-510 did so without causing the negative inotropic, vasodilator, and hypotensive effects associated with diltiazem. Because CVT-510 did not affect the ventricular action potential, it is unlikely that this agonist will have a proarrythmic action in ventricular myocardium. (+info)Effects of tumour necrosis factor-alpha on left ventricular function in the rat isolated perfused heart: possible mechanisms for a decline in cardiac function. (8/10358)
1. The cardiac depressant actions of TNF were investigated in the isolated perfused rat heart under constant flow (10 ml min(-1)) and constant pressure (70 mmHg) conditions, using a recirculating (50 ml) mode of perfusion. 2. Under constant flow conditions TNF (20 ng ml(-1)) caused an early (< 25 min) decrease in left ventricular developed pressure (LVDP), which was maintained for 90 min (LVDP after 90 min: control vs TNF; 110 +/- 4 vs 82 +/- 10 mmHg, P < 0.01). 3. The depression in cardiac function seen with TNF under constant flow conditions, was blocked by the ceramidase inhibitor N-oleoylethanolamine (NOE), 1 microM, (LVDP after 90 min: TNF vs TNF with NOE; 82 +/- 10 vs 11 +/- 5 mmHg, P < 0.05). 4. In hearts perfused at constant pressure, TNF caused a decrease in coronary flow rate (change in flow 20 min after TNF: control vs TNF; -3.0 +/- 0.9 vs -8.7 +/- 1.2 ml min(-1), P < 0.01). This was paralleled by a negative inotropic effect (change in LVDP 20 min after TNF: control vs TNF; -17 +/- 7 vs -46 +/- 6 mmHg, P < 0.01). The decline in function was more rapid and more severe than that seen under conditions of constant flow. 5. These data indicate that cardiac function can be disrupted by TNF on two levels, firstly via a direct, ceramidase dependant negative inotropic effect, and secondly via an indirect coronary vasoconstriction. (+info)The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.
The myocardium is the middle layer of the heart wall, composed of specialized cardiac muscle cells that are responsible for pumping blood throughout the body. It forms the thickest part of the heart wall and is divided into two sections: the left ventricle, which pumps oxygenated blood to the rest of the body, and the right ventricle, which pumps deoxygenated blood to the lungs.
The myocardium contains several types of cells, including cardiac muscle fibers, connective tissue, nerves, and blood vessels. The muscle fibers are arranged in a highly organized pattern that allows them to contract in a coordinated manner, generating the force necessary to pump blood through the heart and circulatory system.
Damage to the myocardium can occur due to various factors such as ischemia (reduced blood flow), infection, inflammation, or genetic disorders. This damage can lead to several cardiac conditions, including heart failure, arrhythmias, and cardiomyopathy.
In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.
Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.
The cerebral ventricles are a system of interconnected fluid-filled cavities within the brain. They are located in the center of the brain and are filled with cerebrospinal fluid (CSF), which provides protection to the brain by cushioning it from impacts and helping to maintain its stability within the skull.
There are four ventricles in total: two lateral ventricles, one third ventricle, and one fourth ventricle. The lateral ventricles are located in each cerebral hemisphere, while the third ventricle is located between the thalami of the two hemispheres. The fourth ventricle is located at the base of the brain, above the spinal cord.
CSF flows from the lateral ventricles into the third ventricle through narrow passageways called the interventricular foramen. From there, it flows into the fourth ventricle through another narrow passageway called the cerebral aqueduct. CSF then leaves the fourth ventricle and enters the subarachnoid space surrounding the brain and spinal cord, where it can be absorbed into the bloodstream.
Abnormalities in the size or shape of the cerebral ventricles can indicate underlying neurological conditions, such as hydrocephalus (excessive accumulation of CSF) or atrophy (shrinkage) of brain tissue. Imaging techniques, such as computed tomography (CT) or magnetic resonance imaging (MRI), are often used to assess the size and shape of the cerebral ventricles in clinical settings.
The third ventricle is a narrow, fluid-filled cavity in the brain that is located between the thalamus and hypothalamus. It is one of the four ventricles in the ventricular system of the brain, which produces and circulates cerebrospinal fluid (CSF) around the brain and spinal cord.
The third ventricle is shaped like a slit and communicates with the lateral ventricles through the interventricular foramen (also known as the foramen of Monro), and with the fourth ventricle through the cerebral aqueduct (also known as the aqueduct of Sylvius).
The third ventricle contains choroid plexus tissue, which produces CSF. The fluid flows from the lateral ventricles into the third ventricle, then through the cerebral aqueduct and into the fourth ventricle, where it can circulate around the brainstem and spinal cord before being absorbed back into the bloodstream.
Abnormalities in the third ventricle, such as enlargement or obstruction of the cerebral aqueduct, can lead to hydrocephalus, a condition characterized by an accumulation of CSF in the brain.
The fourth ventricle is a part of the cerebrospinal fluid-filled system in the brain, located in the posterior cranial fossa and continuous with the central canal of the medulla oblongata and the cerebral aqueduct. It is shaped like a cavity with a roof, floor, and lateral walls, and it communicates rostrally with the third ventricle through the cerebral aqueduct and caudally with the subarachnoid space through the median and lateral apertures (foramina of Luschka and Magendie). The fourth ventricle contains choroid plexus tissue, which produces cerebrospinal fluid. Its roof is formed by the cerebellar vermis and the superior medullary velum, while its floor is composed of the rhomboid fossa, which includes several important structures such as the vagal trigone, hypoglossal trigone, and striae medullares.
Heart failure is a pathophysiological state in which the heart is unable to pump sufficient blood to meet the metabolic demands of the body or do so only at the expense of elevated filling pressures. It can be caused by various cardiac disorders, including coronary artery disease, hypertension, valvular heart disease, cardiomyopathy, and arrhythmias. Symptoms may include shortness of breath, fatigue, and fluid retention. Heart failure is often classified based on the ejection fraction (EF), which is the percentage of blood that is pumped out of the left ventricle during each contraction. A reduced EF (less than 40%) is indicative of heart failure with reduced ejection fraction (HFrEF), while a preserved EF (greater than or equal to 50%) is indicative of heart failure with preserved ejection fraction (HFpEF). There is also a category of heart failure with mid-range ejection fraction (HFmrEF) for those with an EF between 40-49%.
The lateral ventricles are a pair of fluid-filled cavities located within the brain. They are part of the ventricular system, which is a series of interconnected spaces filled with cerebrospinal fluid (CSF). The lateral ventricles are situated in the left and right hemispheres of the brain and are among the largest of the ventricles.
Each lateral ventricle has a complex structure and can be divided into several parts:
1. Anterior horn: This is the front part of the lateral ventricle, located in the frontal lobe of the brain.
2. Body: The central part of the lateral ventricle, which is continuous with the anterior horn and posterior horn.
3. Posterior horn: The back part of the lateral ventricle, located in the occipital lobe of the brain.
4. Temporal horn: An extension that projects into the temporal lobe of the brain.
The lateral ventricles are lined with ependymal cells, which produce cerebrospinal fluid. CSF circulates through the ventricular system, providing buoyancy and protection to the brain, and is eventually absorbed into the bloodstream. Abnormalities in the size or shape of the lateral ventricles can be associated with various neurological conditions, such as hydrocephalus, brain tumors, or neurodegenerative diseases.
Congenital heart defects (CHDs) are structural abnormalities in the heart that are present at birth. They can affect any part of the heart's structure, including the walls of the heart, the valves inside the heart, and the major blood vessels that lead to and from the heart.
Congenital heart defects can range from mild to severe and can cause various symptoms depending on the type and severity of the defect. Some common symptoms of CHDs include cyanosis (a bluish tint to the skin, lips, and fingernails), shortness of breath, fatigue, poor feeding, and slow growth in infants and children.
There are many different types of congenital heart defects, including:
1. Septal defects: These are holes in the walls that separate the four chambers of the heart. The two most common septal defects are atrial septal defect (ASD) and ventricular septal defect (VSD).
2. Valve abnormalities: These include narrowed or leaky valves, which can affect blood flow through the heart.
3. Obstruction defects: These occur when blood flow is blocked or restricted due to narrowing or absence of a part of the heart's structure. Examples include pulmonary stenosis and coarctation of the aorta.
4. Cyanotic heart defects: These cause a lack of oxygen in the blood, leading to cyanosis. Examples include tetralogy of Fallot and transposition of the great arteries.
The causes of congenital heart defects are not fully understood, but genetic factors and environmental influences during pregnancy may play a role. Some CHDs can be detected before birth through prenatal testing, while others may not be diagnosed until after birth or later in childhood. Treatment for CHDs may include medication, surgery, or other interventions to improve blood flow and oxygenation of the body's tissues.
Cerebral ventricle neoplasms refer to tumors that develop within the cerebral ventricles, which are fluid-filled spaces in the brain. These tumors can arise from various types of cells within the ventricular system, including the ependymal cells that line the ventricles, choroid plexus cells that produce cerebrospinal fluid, or other surrounding tissues.
Cerebral ventricle neoplasms can cause a variety of symptoms depending on their size and location, such as headaches, nausea, vomiting, vision changes, imbalance, weakness, or difficulty with mental tasks. The treatment options for these tumors may include surgical resection, radiation therapy, and chemotherapy, depending on the type and extent of the tumor. Regular follow-up care is essential to monitor for recurrence and manage any long-term effects of treatment.
Heart disease is a broad term for a class of diseases that involve the heart or blood vessels. It's often used to refer to conditions that include:
1. Coronary artery disease (CAD): This is the most common type of heart disease. It occurs when the arteries that supply blood to the heart become hardened and narrowed due to the buildup of cholesterol and other substances, which can lead to chest pain (angina), shortness of breath, or a heart attack.
2. Heart failure: This condition occurs when the heart is unable to pump blood efficiently to meet the body's needs. It can be caused by various conditions, including coronary artery disease, high blood pressure, and cardiomyopathy.
3. Arrhythmias: These are abnormal heart rhythms, which can be too fast, too slow, or irregular. They can lead to symptoms such as palpitations, dizziness, and fainting.
4. Valvular heart disease: This involves damage to one or more of the heart's four valves, which control blood flow through the heart. Damage can be caused by various conditions, including infection, rheumatic fever, and aging.
5. Cardiomyopathy: This is a disease of the heart muscle that makes it harder for the heart to pump blood efficiently. It can be caused by various factors, including genetics, viral infections, and drug abuse.
6. Pericardial disease: This involves inflammation or other problems with the sac surrounding the heart (pericardium). It can cause chest pain and other symptoms.
7. Congenital heart defects: These are heart conditions that are present at birth, such as a hole in the heart or abnormal blood vessels. They can range from mild to severe and may require medical intervention.
8. Heart infections: The heart can become infected by bacteria, viruses, or parasites, leading to various symptoms and complications.
It's important to note that many factors can contribute to the development of heart disease, including genetics, lifestyle choices, and certain medical conditions. Regular check-ups and a healthy lifestyle can help reduce the risk of developing heart disease.
Heart transplantation is a surgical procedure where a diseased, damaged, or failing heart is removed and replaced with a healthy donor heart. This procedure is usually considered as a last resort for patients with end-stage heart failure or severe coronary artery disease who have not responded to other treatments. The donor heart typically comes from a brain-dead individual whose family has agreed to donate their loved one's organs for transplantation. Heart transplantation is a complex and highly specialized procedure that requires a multidisciplinary team of healthcare professionals, including cardiologists, cardiac surgeons, anesthesiologists, perfusionists, nurses, and other support staff. The success rates for heart transplantation have improved significantly over the past few decades, with many patients experiencing improved quality of life and increased survival rates. However, recipients of heart transplants require lifelong immunosuppressive therapy to prevent rejection of the donor heart, which can increase the risk of infections and other complications.
The fetal heart is the cardiovascular organ that develops in the growing fetus during pregnancy. It starts to form around 22 days after conception and continues to develop throughout the first trimester. By the end of the eighth week of gestation, the fetal heart has developed enough to pump blood throughout the body.
The fetal heart is similar in structure to the adult heart but has some differences. It is smaller and more compact, with a four-chambered structure that includes two atria and two ventricles. The fetal heart also has unique features such as the foramen ovale, which is a hole between the right and left atria that allows blood to bypass the lungs, and the ductus arteriosus, a blood vessel that connects the pulmonary artery to the aorta and diverts blood away from the lungs.
The fetal heart is responsible for pumping oxygenated blood from the placenta to the rest of the body and returning deoxygenated blood back to the placenta for re-oxygenation. The rate of the fetal heartbeat is faster than that of an adult, typically ranging from 120 to 160 beats per minute. Fetal heart rate monitoring is a common method used during pregnancy and childbirth to assess the health and well-being of the developing fetus.
The heart atria are the upper chambers of the heart that receive blood from the veins and deliver it to the lower chambers, or ventricles. There are two atria in the heart: the right atrium receives oxygen-poor blood from the body and pumps it into the right ventricle, which then sends it to the lungs to be oxygenated; and the left atrium receives oxygen-rich blood from the lungs and pumps it into the left ventricle, which then sends it out to the rest of the body. The atria contract before the ventricles during each heartbeat, helping to fill the ventricles with blood and prepare them for contraction.
Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.
During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.
Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.
Heart valves are specialized structures in the heart that ensure unidirectional flow of blood through its chambers during the cardiac cycle. There are four heart valves: the tricuspid valve and the mitral (bicuspid) valve, located between the atria and ventricles, and the pulmonic (pulmonary) valve and aortic valve, located between the ventricles and the major blood vessels leaving the heart.
The heart valves are composed of thin flaps of tissue called leaflets or cusps, which are supported by a fibrous ring. The aortic and pulmonic valves have three cusps each, while the tricuspid and mitral valves have three and two cusps, respectively.
The heart valves open and close in response to pressure differences across them, allowing blood to flow forward into the ventricles during diastole (filling phase) and preventing backflow of blood into the atria during systole (contraction phase). A properly functioning heart valve ensures efficient pumping of blood by the heart and maintains normal blood circulation throughout the body.
Ventricular function, in the context of cardiac medicine, refers to the ability of the heart's ventricles (the lower chambers) to fill with blood during the diastole phase and eject blood during the systole phase. The ventricles are primarily responsible for pumping oxygenated blood out to the body (left ventricle) and deoxygenated blood to the lungs (right ventricle).
There are several ways to assess ventricular function, including:
1. Ejection Fraction (EF): This is the most commonly used measure of ventricular function. It represents the percentage of blood that is ejected from the ventricle during each heartbeat. A normal left ventricular ejection fraction is typically between 55% and 70%.
2. Fractional Shortening (FS): This is another measure of ventricular function, which calculates the change in size of the ventricle during contraction as a percentage of the original size. A normal FS for the left ventricle is typically between 25% and 45%.
3. Stroke Volume (SV): This refers to the amount of blood that is pumped out of the ventricle with each heartbeat. SV is calculated by multiplying the ejection fraction by the end-diastolic volume (the amount of blood in the ventricle at the end of diastole).
4. Cardiac Output (CO): This is the total amount of blood that the heart pumps in one minute. It is calculated by multiplying the stroke volume by the heart rate.
Impaired ventricular function can lead to various cardiovascular conditions, such as heart failure, cardiomyopathy, and valvular heart disease. Assessing ventricular function is crucial for diagnosing these conditions, monitoring treatment response, and guiding clinical decision-making.
Left ventricular function refers to the ability of the left ventricle (the heart's lower-left chamber) to contract and relax, thereby filling with and ejecting blood. The left ventricle is responsible for pumping oxygenated blood to the rest of the body. Its function is evaluated by measuring several parameters, including:
1. Ejection fraction (EF): This is the percentage of blood that is pumped out of the left ventricle with each heartbeat. A normal ejection fraction ranges from 55% to 70%.
2. Stroke volume (SV): The amount of blood pumped by the left ventricle in one contraction. A typical SV is about 70 mL/beat.
3. Cardiac output (CO): The total volume of blood that the left ventricle pumps per minute, calculated as the product of stroke volume and heart rate. Normal CO ranges from 4 to 8 L/minute.
Assessment of left ventricular function is crucial in diagnosing and monitoring various cardiovascular conditions such as heart failure, coronary artery disease, valvular heart diseases, and cardiomyopathies.
Heart block is a cardiac condition characterized by the interruption of electrical impulse transmission from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This disruption can lead to abnormal heart rhythms, including bradycardia (a slower-than-normal heart rate), and in severe cases, can cause the heart to stop beating altogether. Heart block is typically caused by damage to the heart's electrical conduction system due to various factors such as aging, heart disease, or certain medications.
There are three types of heart block: first-degree, second-degree, and third-degree (also known as complete heart block). Each type has distinct electrocardiogram (ECG) findings and symptoms. Treatment for heart block depends on the severity of the condition and may include monitoring, medication, or implantation of a pacemaker to regulate the heart's electrical activity.
Echocardiography is a medical procedure that uses sound waves to produce detailed images of the heart's structure, function, and motion. It is a non-invasive test that can help diagnose various heart conditions, such as valve problems, heart muscle damage, blood clots, and congenital heart defects.
During an echocardiogram, a transducer (a device that sends and receives sound waves) is placed on the chest or passed through the esophagus to obtain images of the heart. The sound waves produced by the transducer bounce off the heart structures and return to the transducer, which then converts them into electrical signals that are processed to create images of the heart.
There are several types of echocardiograms, including:
* Transthoracic echocardiography (TTE): This is the most common type of echocardiogram and involves placing the transducer on the chest.
* Transesophageal echocardiography (TEE): This type of echocardiogram involves passing a specialized transducer through the esophagus to obtain images of the heart from a closer proximity.
* Stress echocardiography: This type of echocardiogram is performed during exercise or medication-induced stress to assess how the heart functions under stress.
* Doppler echocardiography: This type of echocardiogram uses sound waves to measure blood flow and velocity in the heart and blood vessels.
Echocardiography is a valuable tool for diagnosing and managing various heart conditions, as it provides detailed information about the structure and function of the heart. It is generally safe, non-invasive, and painless, making it a popular choice for doctors and patients alike.
Hemodynamics is the study of how blood flows through the cardiovascular system, including the heart and the vascular network. It examines various factors that affect blood flow, such as blood volume, viscosity, vessel length and diameter, and pressure differences between different parts of the circulatory system. Hemodynamics also considers the impact of various physiological and pathological conditions on these variables, and how they in turn influence the function of vital organs and systems in the body. It is a critical area of study in fields such as cardiology, anesthesiology, and critical care medicine.
I believe there might be a misunderstanding in your question. "Dogs" is not a medical term or condition. It is the common name for a domesticated carnivore of the family Canidae, specifically the genus Canis, which includes wolves, foxes, and other extant and extinct species of mammals. Dogs are often kept as pets and companions, and they have been bred in a wide variety of forms and sizes for different purposes, such as hunting, herding, guarding, assisting police and military forces, and providing companionship and emotional support.
If you meant to ask about a specific medical condition or term related to dogs, please provide more context so I can give you an accurate answer.
Heart function tests are a group of diagnostic exams that are used to evaluate the structure and functioning of the heart. These tests help doctors assess the pumping efficiency of the heart, the flow of blood through the heart, the presence of any heart damage, and the overall effectiveness of the heart in delivering oxygenated blood to the rest of the body.
Some common heart function tests include:
1. Echocardiogram (Echo): This test uses sound waves to create detailed images of the heart's structure and functioning. It can help detect any damage to the heart muscle, valves, or sac surrounding the heart.
2. Nuclear Stress Test: This test involves injecting a small amount of radioactive substance into the patient's bloodstream and taking images of the heart while it is at rest and during exercise. The test helps evaluate blood flow to the heart and detect any areas of reduced blood flow, which could indicate coronary artery disease.
3. Cardiac Magnetic Resonance Imaging (MRI): This test uses magnetic fields and radio waves to create detailed images of the heart's structure and function. It can help detect any damage to the heart muscle, valves, or other structures of the heart.
4. Electrocardiogram (ECG): This test measures the electrical activity of the heart and helps detect any abnormalities in the heart's rhythm or conduction system.
5. Exercise Stress Test: This test involves walking on a treadmill or riding a stationary bike while being monitored for changes in heart rate, blood pressure, and ECG readings. It helps evaluate exercise capacity and detect any signs of coronary artery disease.
6. Cardiac Catheterization: This is an invasive procedure that involves inserting a catheter into the heart to measure pressures and take samples of blood from different parts of the heart. It can help diagnose various heart conditions, including heart valve problems, congenital heart defects, and coronary artery disease.
Overall, heart function tests play an essential role in diagnosing and managing various heart conditions, helping doctors provide appropriate treatment and improve patient outcomes.
Cardiac myocytes are the muscle cells that make up the heart muscle, also known as the myocardium. These specialized cells are responsible for contracting and relaxing in a coordinated manner to pump blood throughout the body. They differ from skeletal muscle cells in several ways, including their ability to generate their own electrical impulses, which allows the heart to function as an independent rhythmical pump. Cardiac myocytes contain sarcomeres, the contractile units of the muscle, and are connected to each other by intercalated discs that help coordinate contraction and ensure the synchronous beating of the heart.
The heart septum is the thick, muscular wall that divides the right and left sides of the heart. It consists of two main parts: the atrial septum, which separates the right and left atria (the upper chambers of the heart), and the ventricular septum, which separates the right and left ventricles (the lower chambers of the heart). A normal heart septum ensures that oxygen-rich blood from the lungs does not mix with oxygen-poor blood from the body. Any defect or abnormality in the heart septum is called a septal defect, which can lead to various congenital heart diseases.
Cardiomegaly is a medical term that refers to an enlarged heart. It can be caused by various conditions such as high blood pressure, heart valve problems, cardiomyopathy, or fluid accumulation around the heart (pericardial effusion). Cardiomegaly can be detected through imaging tests like chest X-rays or echocardiograms. Depending on the underlying cause, treatment options may include medications, lifestyle changes, or in some cases, surgery. It is important to consult with a healthcare professional for proper diagnosis and treatment.
The endocardium is the innermost layer of tissue that lines the chambers of the heart and the valves between them. It is a thin, smooth membrane that is in contact with the blood within the heart. This layer helps to maintain the heart's internal environment, facilitates the smooth movement of blood through the heart, and provides a protective barrier against infection and other harmful substances. The endocardium is composed of simple squamous epithelial cells called endothelial cells, which are supported by a thin layer of connective tissue.
Right Ventricular Function refers to the ability of the right ventricle (RV) of the heart to receive and eject blood during the cardiac cycle. The right ventricle is one of the four chambers of the heart and is responsible for pumping deoxygenated blood from the body to the lungs for re-oxygenation.
Right ventricular function can be assessed by measuring various parameters such as:
1. Right Ventricular Ejection Fraction (RVEF): It is the percentage of blood that is ejected from the right ventricle during each heartbeat. A normal RVEF ranges from 45-75%.
2. Right Ventricular Systolic Function: It refers to the ability of the right ventricle to contract and eject blood during systole (contraction phase). This can be assessed by measuring the tricuspid annular plane systolic excursion (TAPSE) or tissue Doppler imaging.
3. Right Ventricular Diastolic Function: It refers to the ability of the right ventricle to relax and fill with blood during diastole (relaxation phase). This can be assessed by measuring the right ventricular inflow pattern, tricuspid valve E/A ratio, or deceleration time.
4. Right Ventricular Afterload: It refers to the pressure that the right ventricle must overcome to eject blood into the pulmonary artery. Increased afterload can impair right ventricular function.
Abnormalities in right ventricular function can lead to various cardiovascular conditions such as pulmonary hypertension, heart failure, and arrhythmias.
Stroke volume is a term used in cardiovascular physiology and medicine. It refers to the amount of blood that is pumped out of the left ventricle of the heart during each contraction (systole). Specifically, it is the difference between the volume of blood in the left ventricle at the end of diastole (when the ventricle is filled with blood) and the volume at the end of systole (when the ventricle has contracted and ejected its contents into the aorta).
Stroke volume is an important measure of heart function, as it reflects the ability of the heart to pump blood effectively to the rest of the body. A low stroke volume may indicate that the heart is not pumping efficiently, while a high stroke volume may suggest that the heart is working too hard. Stroke volume can be affected by various factors, including heart disease, high blood pressure, and physical fitness level.
The formula for calculating stroke volume is:
Stroke Volume = End-Diastolic Volume - End-Systolic Volume
Where end-diastolic volume (EDV) is the volume of blood in the left ventricle at the end of diastole, and end-systolic volume (ESV) is the volume of blood in the left ventricle at the end of systole.
Myocardial ischemia is a condition in which the blood supply to the heart muscle (myocardium) is reduced or blocked, leading to insufficient oxygen delivery and potential damage to the heart tissue. This reduction in blood flow typically results from the buildup of fatty deposits, called plaques, in the coronary arteries that supply the heart with oxygen-rich blood. The plaques can rupture or become unstable, causing the formation of blood clots that obstruct the artery and limit blood flow.
Myocardial ischemia may manifest as chest pain (angina pectoris), shortness of breath, fatigue, or irregular heartbeats (arrhythmias). In severe cases, it can lead to myocardial infarction (heart attack) if the oxygen supply is significantly reduced or cut off completely, causing permanent damage or death of the heart muscle. Early diagnosis and treatment of myocardial ischemia are crucial for preventing further complications and improving patient outcomes.