query: process that causes the last 30 of ventricular volume to fill

pos: Cardiac cycle valves, open during ventricular diastole to permit filling. Late in the filling period the atria begin to contract (atrial systole) forcing a final crop of blood into the ventricles under pressure—see cycle diagram. Then, prompted by electrical signals from the sinoatrial node, the ventricles start contracting (ventricular systole), and as back-pressure against them increases the AV valves are forced to close, which stops the blood volumes in the ventricles from flowing in or out; this is known as the "isovolumic contraction" stage. Due to the contractions of the systole, pressures in the ventricles rise quickly, exceeding the pressures in the

pos: Systole by the left ventricle in one minute. The ejection fraction (EF) is the volume of blood pumped divided by the total volume of blood in the left ventricle. 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

pos: Cardiac cycle two ventricles, one to the pulmonary artery and one to the aorta. Notably, near the end of the "Diastole", the atria begin contracting, then pumping blood into the ventricles; this pressurized delivery during ventricular relaxation (ventricular diastole) is called the "atrial systole", aka "atrial kick". The time-wise increases and decreases of the heart's blood volume (see Wiggers diagram), are also instructive to follow. The red-line tracing of "Ventricular volume" provides an excellent track of the two periods and four stages of one cardiac cycle. Starting with the Diastole period: the low-volume plateau of "Isovolumic relaxation" stage, followed by a rapid

pos: Systole diagram at the P/QRS phase (at right margin). Then the contractions of atrial systole cause the right ventricle to fill with oxygen-depleted blood through the tricuspid valve. When the right atrium is emptied—or prematurely closed—right atrial systole ends, and this stage signals the end of "ventricular diastole" and the beginning of "ventricular systole" (see Wiggers diagram). The time variable for the right systolic cycle is measured from (tricuspid) valve-open to valve-closed. The contractions of atrial systole fill the left ventricle with oxygen-enriched blood through the mitral valve; when the left atrium is emptied or closed, left atrial systole is ended

pos: Cardiac cycle the panel labeled "Diastole". Here it shows pressure levels in both atria and ventricles as near-zero during most of the diastole. (See gray and light-blue tracings labeled "Atrial pressure" and "Ventricular pressure"—Wiggers diagram.) Here also may be seen the red-line tracing of "Ventricular volume", showing increase in blood-volume from the low plateau of the "Isovolumic relaxation" stage to the maximum volume occurring in the "Atrial systole" sub-stage. Atrial systole is the contracting of cardiac muscle cells of both atria following electrical stimulation and conduction of electrical currents across the atrial chambers (see above, "Physiology"). While nominally a component of the

neg: Heart failure with preserved ejection fraction the left ventricle can lead to diastolic dysfunction. Other causes of left ventricular stiffening include: Causes of isolated right ventricular diastolic failure are uncommon. These causes include: Structural changes that occur with HFpEF are often radically different from those associated with heart failure with reduced ejection fraction (HFrEF). Many patients experience increased thickening of the ventricular wall in comparison to chamber size, termed concentric hypertrophy. This leads to increased left ventricular mass and is typically accompanied by a normal, or slightly reduced, end diastolic filling volume. Conversely, HFrEF is typically associated with eccentric hypertrophy, characterized by an increase in cardiac

neg: Volume overload considered according to which chamber is affected. Left ventricular volume overload Right ventricular volume overload Volume overload Volume overload refers to the state of one of the chambers of the heart in which too large a volume of blood exists within it for it to function efficiently. Ventricular volume overload is approximately equivalent to an excessively high preload. It is a cause of cardiac failure. In accordance with the Frank–Starling law of the heart, the myocardium contracts more powerfully as the end-diastolic volume increases. Stretching of the myofibrils in cardiac muscle causes them to contract more powerfully due to a

neg: Aortic insufficiency I, which is converted to angiotensin II. In the case of chronic aortic insufficiency with resultant cardiac remodeling, heart failure will develop, and it is possible to see systolic pressures diminish. Aortic insufficiency causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart. The volume overload, due to elevated pulse pressure and the systemic effects of neuroendocrine hormones causes left ventricular hypertrophy (LVH). There is both "concentric hypertrophy" and "eccentric hypertrophy" in AI. The concentric hypertrophy is due to the increased left ventricular pressure overload associated with AI, while the eccentric hypertrophy is due to volume

neg: Ventricular remodeling Ventricular remodeling In cardiology, ventricular remodeling (or cardiac remodeling) refers to changes in the size, shape, structure, and function of the heart. This can happen as a result of exercise (physiological remodeling) or after injury to the heart muscle (pathological remodeling). The injury is typically due to acute myocardial infarction (usually transmural or ST segment elevation infarction), but may be from a number of causes that result in increased pressure or volume, causing pressure overload or volume overload (forms of strain) on the heart. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to

neg: Aortic insufficiency decreases as it relaxes and begins to fill up with blood from the left atrium. This relaxation of the left ventricle (early ventricular diastole) causes a fall in its pressure. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood in the aorta from going back into the left ventricle. In terms of the diagnosis of aortic regurgitation a common test for the evaluation of the severity is transthoracic echocardiography, which can provide two-dimensional views of the regurgitant jet, allow measurement of velocity, and estimate jet volume. The findings

neg: Cardiac physiology that are now relaxed and in diastole. This increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves. Since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction. In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary

neg: Isovolumetric contraction backflow to the atria. At this stage, which corresponds to the R peak or the QRS complex seen on an ECG, the semilunar valves (aortic and pulmonary valves) are also closed. The net result is that, while contraction causes ventricular pressures to rise sharply, there is no overall change in volume because of the closed valves. The isovolumetric contraction phase lasts about 0.03 s, but this short period of time is enough to build up a sufficiently high pressure that eventually overcomes that of the aorta and the pulmonary trunk upon opening of the semilunar valves. This process, therefore, helps

neg: Frank–Starling law cardiac outputs were not equivalent, blood would accumulate in the pulmonary circulation (were the right ventricle producing more output than the left) or the systemic circulation (were the left ventricle producing more output than the right). Premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction occurs at its regular time, the filling time for the LV increases, causing an increased LV end-diastolic volume. Due to the Frank–Starling mechanism, the next ventricular contraction is more forceful, leading to the ejection of the larger than normal volume of blood, and bringing the

neg: Ventricular remodeling process. Ventricular remodeling may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an aspect of cardiomyopathy, of which there are many types. Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload. The cardiac myocyte is the major cell involved in remodeling. Fibroblasts, collagen, the interstitium, and the coronary vessels to a lesser extent, also play a role. A common scenario for remodeling is after myocardial infarction. There is myocardial necrosis (cell death) and disproportionate thinning of the heart. This thin, weakened area is unable to withstand the pressure and volume load

neg: Cardiac cycle through the atria and fill the ventricular chambers—just before the return of the systole (contractions), ejecting the new blood volume and completing the cardiac cycle. (See Wiggers diagram: "Ventricular volume" tracing (red), at "Systole" panel.) Cardiac diastole is the period of the cardiac cycle when, after contraction, the heart relaxes and expands while refilling with blood returning from the circulatory system. Both atrioventricular (AV) valves open to facilitate the 'unpressurized' flow of blood directly through the atria into both ventricles, where it is collected for the next contraction. This period is best viewed at the middle of the Wiggers diagram—see

neg: Ventricular hypertrophy Ventricular hypertrophy Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur. Ventricular hypertrophy can result from a variety of conditions, both adaptive and maladaptive. For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume; but can also occur as a consequence of ventricular remodeling following a heart attack. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the

neg: Atrial septal defect flow of blood through the pulmonic valve rather than any structural abnormality of the valve leaflets. In unaffected individuals, respiratory variations occur in the splitting of the second heart sound (S). During respiratory inspiration, the negative intrathoracic pressure causes increased blood return into the right side of the heart. The increased blood volume in the right ventricle causes the pulmonic valve to stay open longer during ventricular systole. This causes a normal delay in the P component of S. During expiration, the positive intrathoracic pressure causes decreased blood return to the right side of the heart. The reduced volume in

neg: Tricuspid insufficiency result being incompetence of the tricuspid valve. Other common causes of right ventricular dilation include right ventricular infarction, inferior myocardial infarction, and cor pulmonale. In regards to "primary" and "secondary" causes they are: In terms of the mechanism of tricuspid insufficiency it involves the expansion of the tricuspid annulus (fibrous rings of heart). Tricuspid insufficiency is linked to geometric changes of the tricuspid annulus (decreased tricuspid annular release). The leaflets shape are normal but prevented from normal working mechanism due to a distortion of spatial relationships of leaflets and chords. It is also contemplated that the process via which tricuspid

neg: Pulsus paradoxus 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. Pulses paradoxus is therefore an exaggeration or an increase in the fall of systolic BP beyond 10

neg: Pathophysiology of heart failure terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and thus decrease the ability to relax during diastole. Enlargement of the ventricles can also occur and contributes to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and inefficient contraction of the heart. The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to abnormal ventricular heart rhythms) and

neg: Pathophysiology of heart failure caused by diastolic dysfunction is generally described as the backward failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. The "stiffness" and contractility of the ventricular walls in diastole was first described by Pierre-Simon Laplace. This causes inadequate filling of the ventricle and therefore results in an inadequate stroke volume (SV). SV is a mathematical term amenable to manipulation of many variables. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right

neg: Ventricular hypertrophy by hypertrophy and to prognosticate outcomes. In most situations, described above, the increase in ventricular wall thickness is a slow process. However, in some instances hypertrophy may be "dramatic and rapid." In the Burmese python, consumption of a large meal is associated with an increase in metabolic work by a factor of seven and a 40% increase in ventricular mass within 48 hours, both of which return to normal within 28 days. As described in the previous section, it is believed that the eccentric hypertrophy is induced by volume-overload and that the concentric hypertrophy is induced by pressure-overload. Biomechanical approaches

neg: Tricuspid atresia connection, an atrial septal defect (ASD) must be present to fill the left ventricle with blood. Also, since there is a lack of a right ventricle there must be a way to pump blood into the pulmonary arteries, and this is accomplished by a ventricular septal defect (VSD). The causes of Tricupsid atresia are unknown. An atrial septal defect (ASD) and a ventricular septal defect (VSD) must both be present to maintain blood flow-from the right atrium, the blood must flow through the ASD to the left atrium to the left ventricle and through the VSD to the right ventricle

neg: Die casting casting processes. Therefore, to make die casting an economic process, a large production volume is needed. Other disadvantages are that the process is limited to high-fluidity metals, and casting weights must be between 30 grams (1 oz) and 10 kg (20 lb). In the standard die casting process the final casting will have a small amount of porosity. This prevents any heat treating or welding, because the heat causes the gas in the pores to expand, which causes micro-cracks inside the part and exfoliation of the surface. Thus a related disadvantage of die casting is that it is only for

neg: Volume overload Volume overload Volume overload refers to the state of one of the chambers of the heart in which too large a volume of blood exists within it for it to function efficiently. Ventricular volume overload is approximately equivalent to an excessively high preload. It is a cause of cardiac failure. In accordance with the Frank–Starling law of the heart, the myocardium contracts more powerfully as the end-diastolic volume increases. Stretching of the myofibrils in cardiac muscle causes them to contract more powerfully due to a greater number of cross-bridges being formed between the myofibrils within cardiac myocytes. This is true

neg: Volume overload up to a point, however beyond this there is a loss of contractile ability due to loss of connection between myofibrils; see figure. Various pathologies, listed below, can lead to volume overload. Different mechanisms are involved depending on the cause, however the common theme is that of a high cardiac output with a low or normal afterload. The output may be high due to the inefficiency in valve disease, or it may be high due to shunting of blood in left-to-right shunts and arteriovenous malformations. Left ventricular volume overload may produce inverted u waves on the electrocardiogram. Causes may be

neg: Hypertrophic cardiomyopathy each is different. Beta blockers are used in both cases, but treatment with diuretics, a mainstay of CHF treatment, will exacerbate symptoms in hypertrophic obstructive cardiomyopathy by decreasing ventricular preload volume and thereby increasing outflow resistance (less blood to push aside the thickened obstructing tissue). Major risk factors for sudden death in individuals with HCM include prior history of cardiac arrest or ventricular fibrillation, spontaneous sustained ventricular tachycardia, family history of premature sudden death, unexplained syncope, LV thickness greater than or equal to 30 mm, abnormal exercise blood pressure and nonsustained ventricular tachycardia. "Spike and dome" pulse and "triple ripple

neg: Ventricular action potential Ventricular action potential In electrocardiography, the ventricular cardiomyocyte membrane potential is about −90 mV at rest, which is close to the potassium reversal potential. When an action potential is generated, the membrane potential rises above this level in four distinct phases. The beginning of the action potential, phase 0, specialized membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell. This causes the membrane potential to rise at a rate of about 300 V/s. As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation. The

neg: Kussmaul's sign Kussmaul's sign Kussmaul sign is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart dysfunction. Ordinarily the JVP falls with inspiration due to reduced pressure in the expanding thoracic cavity and the increased volume afforded to right ventricular expansion during diastole. Kussmaul sign suggests impaired filling of the right ventricle due to a poorly compliant myocardium or pericardium. This impaired filling causes the increased

neg: Arterial stiffness to blood vessels in target organs such as the brain or kidneys. This effect may be exaggerated if the increase in arterial stiffness results in reduced wave reflection and more propagation of the pulsatile pressure into the microcirculation. An increase in arterial stiffness also increases the load on the heart, since it has to perform more work to maintain the stroke volume. Over time, this increased workload causes left ventricular hypertrophy and left ventricular remodelling, which can lead to heart failure. The increased workload may also be associated with a higher heart rate, a proportionately longer duration of systole and

neg: Digoxin node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves, owing to improved filling. Overall, the heart rate is decreased while blood pressure is increased, resulting in a net increase in stroke volume, leading to increased tissue perfusion. This causes the myocardium to work more efficiently, with optimized hemodynamics and an improved ventricular function curve. Other electrical effects include a brief initial increase in action potential, followed by a decrease as the K conductance increases due to increased intracellular amounts of Ca ions. The

neg: Acute kidney injury valve and bypass procedures, emergency surgery, and preoperative intraaortic balloon pump are risk factors most strongly correlated with post-cardiopulmonary bypass acute kidney injury. Other well-known minor risk factors include: female gender, congestive heart failure, chronic obstructive pulmonary disease, insulin-requiring diabetes, and depressed left ventricular ejection fraction. "Prerenal" causes of AKI ("pre-renal azotemia") are those that decrease effective blood flow to the kidney and cause a decrease in the glomerular filtration rate (GFR). Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function. Notable causes of prerenal AKI include low blood volume (e.g.,

neg: Mitral insufficiency Frank–Starling mechanism, in which increased ventricular pre-load stretches the myocardium such that contractions are more forceful. The regurgitant volume causes a volume overload and a pressure overload of the left atrium and the left ventricle. The increased pressures in the left side of the heart may inhibit drainage of blood from the lungs via the pulmonary veins and lead to pulmonary congestion. If the MR develops slowly over months to years or if the acute phase cannot be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops

neg: Ventricular septal defect defect) include the incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene are usually associated with isolated (non syndromic) ASD in humans when one copy is missing. During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mmHg) than the

neg: Pressure–volume loop analysis in cardiology increases. The ESPVR becomes flatter and shifts to the right as inotropy decreases. End-diastolic pressure volume relationship (EDPVR) describes the passive filling curve for the ventricle and thus the passive properties of the myocardium. The slope of the EDPVR at any point along this curve is the reciprocal of ventricular compliance (or ventricular stiffness). For example, if ventricular compliance is decreased (such as in ventricular hypertrophy), the ventricle is stiffer. This results in higher ventricular end-diastolic pressures (EDP) at any given end-diastolic volume (EDV). Alternatively, for a given EDP, a less compliant ventricle would have a smaller EDV due to

neg: Pressure–volume loop analysis in cardiology to be load-dependent and inferior to hemodynamic parameters defined by the PV plane. An increase in contractility is manifested as an increase in dP/dt during isovolumic contraction. However, dP/dt is also influenced by preload, afterload, heart rate, and myocardial hypertrophy. Hence, the relationship between ventricular end-diastolic volume and dP/dt is a more accurate index of contractility than dP/dt alone. Likewise, an increase in diastolic function or an increase in relaxation (lusitropy) causes increased dP/dt during isovolumic relaxation. Hence, dP/dt has been used as a valuable tool in the analysis of isovolumic relaxation. However, studies have shown that this parameter may

neg: Pressure–volume loop analysis in cardiology reduced outflow resistance (due to mitral regurgitation) that tends to decrease afterload during ejection. The net effect of these changes is that the width of the PV loop is increased (i.e., ventricular stroke volume is increased). However, ejection into the aorta (forward flow) is reduced. The increased ventricular stroke volume in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium. Pressure–volume loop analysis in cardiology A plot of a system's pressure versus volume has long been used to measure the work done by the system and its

neg: End-diastolic volume right ventricular end-diastolic volume (RVEDV) ranges between 100 and 160 mL. The right ventricular end-diastolic volume index (RVEDVI) is calculated by RVEDV/BSA and ranges between 60 and 100 mL/m. Factors effecting end diastolic volume: Right atrial pressure = 2–6 mmHg Left atrial pressure = 7mmHg Ventricular pressure = 0mmHg By Hilal Amin Mir End-diastolic volume In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right and/or left ventricle at end load or filling in (diastole) or the amount of blood in the ventricles just before systole. Because greater EDVs cause greater distention of the ventricle, "EDV"

neg: Volume (thermodynamics) volume of the working fluid, such as, for example, the fluid within a piston. Changes to this volume may be made through an application of work, or may be used to produce work. An isochoric process however operates at a constant-volume, thus no work can be produced. Many other thermodynamic processes will result in a change in volume. A polytropic process, in particular, causes changes to the system so that the quantity formula_1 is constant (where formula_2 is pressure, formula_3 is volume, and formula_4 is the polytropic index, a constant). Note that for specific polytropic indexes a polytropic process will

neg: Aqueductal stenosis the ventricular system. This blockage causes ventricle volume to increase because the CSF cannot flow out of the ventricles and cannot be effectively absorbed by the surrounding tissue of the ventricles. Increased volume of the ventricles will result in higher pressure within the ventricles, and cause higher pressure in the cortex from it being pushed into the skull. A person may have aqueductal stenosis for years without any symptoms, and a head trauma, hemorrhage, or infection could suddenly invoke those symptoms and worsen the blockage. Many of the signs and symptoms of aqueductal stenosis are similar to those of hydrocephalus.

neg: Ventricle (heart) heart pumping volume is ~5 liters/min, resting. Maximum capacity pumping volume extends from ~25 liters/min for non-athletes to as high as ~45 liters/min for Olympic level athletes. In cardiology, the performance of the ventricles are measured with several volumetric parameters, including end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV) and ejection fraction (E). Ventricular pressure is a measure of blood pressure within the ventricles of the heart. During most of the cardiac cycle, ventricular pressure is less than the pressure in the aorta, but during systole, the ventricular pressure rapidly increases, and the two pressures become equal to each

neg: Right ventricular hypertrophy Right ventricular hypertrophy Right ventricular hypertrophy (RVH) is a form of ventricular hypertrophy affecting the right ventricle. Blood travels through the right ventricle to the lungs via the pulmonary arteries. If conditions occur which decrease pulmonary circulation, meaning blood does not flow well from the heart to the lungs, extra stress can be placed on the right ventricle. This can lead to right ventricular hypertrophy. It can affect electrocardiography (ECG) findings. An ECG with right ventricular hypertrophy may or may not show a right axis deviation on the graph. There are various symptoms that can be seen: Common causes include:

neg: Ejection fraction 54 per cent remaining in the ventricle at the end of systole'. Folse and Braunwald in 1962 used the ratio of forward stroke volume/EDV and observed that 'estimations of the fraction of the left ventricular end-diastolic volume that is ejected into the aorta during each cardiac cycle, as well as of the ventricular end-diastolic and residual volumes, provide information that is fundamental to a hemodynamic analysis of left ventricular function'. In 1965 Bartle et al. used the term ejected fraction for the ratio SV/EDV, and the term ejection fraction was used in two review articles in 1968 suggesting a wide

neg: QT interval roughly be expected to be equal to or below 0.38 s. Prolonged QTc causes premature action potentials during the late phases of depolarization. This increases the risk of developing ventricular arrhythmias, including fatal ventricular fibrillation. Higher rates of prolonged QTc are seen in females, older patients, high systolic blood pressure or heart rate, and short stature. Prolonged QTc is also associated with EKG findings called Torsades de Pointes, which are known to degenerate into ventricular fibrillation, associated with higher mortality rates. There are many causes of prolonged QT intervals, acquired causes being more common than genetic. An abnormally prolonged QT

neg: Tachycardia-induced cardiomyopathy be incomplete. In addition, despite improvement in the left ventricular ejection fraction, studies have demonstrated that patients with prior TIC continue to demonstrate signs of negative cardiac remodeling including increased left ventricular end-systolic dimension, end-systolic volume, and end-diastolic volume. Additionally, recurrence of the tachyarrhythmia in patients with a history of TIC has been associated with a rapid decline in left ventricular ejection fraction and more severe cardiomyopathy that their prior presentation, which may be a result of the negative cardiac remodeling. There have also been cases of sudden death in patients with a history of TIC, which may be associated

neg: Ventricular tachycardia right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is scarring of the heart muscle from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit "around" the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT. Polymorphic ventricular tachycardia, on the other hand, is

neg: Tricuspid valve 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 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

neg: Autotransfusion of fluid. When a volume adequate to fill the wash bowl has been collected, processing may begin. The volume required to fill the bowl is dependent on the hematocrit (HCT) and size of the centrifuge wash bowl. If the patients HCT is normal, the amount needed to process a unit is roughly two times the bowl volume. When aspirating the blood it is important to utilize the following technique whenever possible: Following these techniques will help reduce hemolysis of the red cells and will help increase the amount of red cells that will be salvaged. Antibiotics which are plasma bound

neg: Full-mold casting cutter. If the volume is large, then the pattern can be mass-produced by a process similar to injection molding. Pre-expanded beads of polystyrene are injected into a preheated aluminum mold at low pressure. Steam is then applied to the polystyrene which causes it to expand more to fill the die. The final pattern is approximately 97.5% air and 2.5% polystyrene. The finished patterns can be hot glued to pre-made pouring basins, runners, and risers to form the final pattern. The pattern is then coated with a refractory material. The coated pattern (2) is placed in a flask and packed carefully

neg: Lost-foam casting be cut using a hot-wire foam cutter. If the volume is large, then the pattern can be mass-produced by a process similar to injection molding. Pre-expanded beads of polystyrene are injected into a preheated aluminum mold at low pressure. Steam is then applied to the polystyrene which causes it to expand more to fill the die. The final pattern is approximately 97.5% air and 2.5% polystyrene. Pre-made pouring basins, runners, and risers can be hot glued to the pattern to finish it. Next, the foam cluster is coated with ceramic investment, also known as the refractory coating, via dipping, brushing,

neg: Bendopnea Bendopnea Bendopnea is a newly described symptom of heart failure, meaning shortness of breath when leaning forward. It was introduced by Thibodeau et al. in 2014. Patients with heart failure often experience this when bending over to tie a shoe or putting socks on. It has been defined as occurring within 30 seconds of bending over, but could occur in as few as 8 seconds. When a patient is in heart failure, it often means the ventricular filling pressures are high at baseline. When said person bends forward, it causes a further increase in ventricular filling pressures, especially in patients

neg: Pulsus paradoxus equalizes between all of the chambers of the heart. Following a zero-sum game principle, as the right ventricle receives more volume it can push the septum into the left ventricle further reducing its volume in turn. This additional loss of volume of the left ventricle that "only" occurs with equalization of the pressures (as in tamponade) allows for the further reduction in volume, so cardiac output is reduced, leading to a further decline in BP. However, in situations where the left ventricular pressure remains higher than the pericardial sac (most frequently from coexisting disease with an elevated left ventricular diastolic

neg: Left ventricular hypertrophy causes a patient to have an irregular ECG. Patients with LVH may have to participate in more complicated and precise diagnostic procedures, such as imaging, in situations in which a physician could otherwise give advice based on an ECG. Left ventricular hypertrophy Left ventricular hypertrophy (LVH) is thickening of the heart muscle of the left ventricle of the heart, that is, left-sided ventricular hypertrophy. While ventricular hypertrophy occurs naturally as a reaction to aerobic exercise and strength training, it is most frequently referred to as a pathological reaction to cardiovascular disease, or high blood pressure. It is one aspect of

neg: Heart failure with preserved ejection fraction heart to be over-filled (High output cardiac failure). Although the term diastolic heart failure is often used when there are signs and symptoms of heart failure with normal left ventricular systolic function, this is not always appropriate. Diastolic function is determined by the relative end diastolic volume in relation to end diastolic pressure, and is therefore independent of left ventricular systolic function. A leftward shift of the end-diastolic pressure-volume relationship (i.e. decreased left ventricular distensibility) can occur both in those with normal and those with decreased left ventricular systolic function. Likewise, heart failure may occur in those with dilated left

neg: Ventricular remodeling remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that lead to progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume. Physiological remodeling is reversible while pathological remodeling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand make mismatches inevitable. Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological

neg: Heart failure with preserved ejection fraction atrio-ventricular valves open (mitral valve at left side and tricuspid valve at right side) and the blood passes from the atria into the ventricles. First, ventricles are filled by a pressure gradient but near the end, atria contract (atrial kick) and force more blood to pass into ventricles. Atrial contraction is responsible for around 20% of the total filling blood volume. (In atrial fibrillation, this additional 20% filling volume is lost and the patient may experience systolic heart failure symptoms). Complete left ventricular filling is essential to maintain maximum cardiac output. Left ventricular filling is dependent upon ventricular relaxation and

neg: Pressure–volume loop analysis in cardiology atrium during ventricular systole. The constant backflow of blood through the leaky mitral valve implies that there is no true phase of isovolumic contraction. Since the afterload imposed on the ventricle is reduced, end-systolic volume can be smaller than normal. There is also no true period of isovolumic relaxation because some LV blood flows back into the left atrium through the leaky mitral valve. During ventricular diastolic filling, the elevated atrial pressure is transmitted to the LV during filling so that LV end-diastolic volume (and pressure) increases. This would cause the afterload to increase if it were not for the

neg: Spontaneous cerebrospinal fluid leak of spinal fluid" and "ventricular collapse". In 1940, Henry Woltman of the Mayo Clinic wrote about "headaches associated with decreased intracranial pressure". The full clinical manifestations of intracranial hypotension and CSF leaks were described in several publications reported between the 1960s and early 1990s. Modern reports of spontaneous CSF leak have been reported to medical journals since the late 1980s. Tetracosactide is a corticosteroid that causes the brain to produce additional spinal fluid to replace the volume of the lost CSF and alleviate symptoms, and has been given intravenously to treat CSF leaks. In three small studies of 1-2 patients

neg: Diving reflex respiratory and cardiac workload causes increased blood flow to the cardiac and respiratory muscles. Stroke volume is not greatly affected by immersion or variation in ambient pressure, but bradycardia reduces the overall cardiac output, particularly due to the diving reflex in breath-hold diving. Bradycardia is the response to facial contact with cold water: the human heart rate slows down ten to twenty-five percent. Seals experience changes that are even more dramatic, going from about 125 beats per minute to as low as 10 on an extended dive. During breath-holding, humans also display reduced left ventricular contractility and diminished cardiac output,

neg: Pulmonary edema heart sound. Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure pulmonary edema may form when mean pulmonary pressure rises from the normal of 15 mmHg to above 25 mmHg. Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic. By convention cardiogenic refers to left ventricular causes. Injury to the lung may also cause pulmonary edema through injury to the vasculature and

neg: Cardiac rhythm problems during space flight use of the anti-arrhythmic drug amiodarone all prolong QTc without increasing the incidence of ventricular arrhythmias. It is possible that space flight presents a similar situation. However, at this time, that determination cannot be made due to lack of data. Therefore, the data must be collected. In general, subjects in bed rest studies do not exhibit increases in ventricular ectopy, although numerous studies have shown decreases in left ventricular mass and/or volume. During bed rest, left ventricular mass has been shown to decrease by eight percent after 6 weeks, which was thought to be related to decreased physiological loading. Ground-based

neg: Ventricular tachycardia a summation pattern (fusion complexes). Less common is ventricular tachycardia that occurs in individuals with structurally normal hearts. This is known as idiopathic ventricular tachycardia and in the monomorphic form coincides with little or no increased risk of sudden cardiac death. In general, idiopathic ventricular tachycardia occurs in younger individuals diagnosed with VT. While the causes of idiopathic VT are not known, in general it is presumed to be congenital, and can be brought on by any number of diverse factors. Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk

neg: Moniliformin Moniliformin Moniliformin is an unusual mycotoxin, a feed contaminant that is lethal to fowl, especially ducklings. Moniliformin is formed in many cereals by a number of "Fusarium" species that include Fusarium moniliforme, Fusarium avenaceum, Fusarium subglutinans, Fusarium proliferatum, Fusarium fujikuroi and others. It is mainly cardiotoxic and causes ventricular hypertrophy. Moniliformin actually causes competitive inhibition of the activity of pyruvate dehydrogenase complex of respiratory reaction, which prevents pyruvic acid, product of glycolysis, to convert to acetyl CoA. Ultrastructural examination of right ventricular wall of 9 month old female mink ("Mustela vison") fed acute doses of moniliformin (2.2 and 2.8 mg/kg

neg: Pressure-volume loop experiments balloon to occlude the inferior vena cava, a procedure that reduces cardiac preload. EDPVR and ESPVR are valuable because they are load-independent indices of left ventricular function. They also measure left ventricle Compliance/Stiffness (EDPVR) and Contractility (ESPVR) respectively. Other parameters derived from series of loops are: Pressure-volume loop experiments Pressure Volume loops are widely used in basic and preclinical research. Left ventricular PV loops are considered to be the gold standard for hemodynamic assessment and are widely used in research to evaluate cardiac performance. While it has long been possible to measure pressure in real time from the left ventricle,

neg: Circular breathing lungs are nearly empty, the last volume of air is blown into the mouth, and the cheeks are inflated with part of this air. Then, while still blowing this last bit of air out by squeezing the cheeks, the musician must very quickly fill the lungs by inhaling through the nose prior to running out of the air in the mouth. If done correctly, by the time the air in the mouth is nearly exhausted the musician can begin to exhale from the lungs once more, ready to repeat the process again. Essentially, circular breathing bridges the gap between exhalations

neg: Natriuresis Natriuresis Natriuresis is the process of sodium excretion in the urine through the action of the kidneys. It is promoted by ventricular and atrial natriuretic peptides as well as calcitonin, and inhibited by chemicals such as aldosterone. Natriuresis lowers the concentration of sodium in the blood and also tends to lower blood volume because osmotic forces drag water out of the body's blood circulation and into the urine along with the sodium. Many diuretic drugs take advantage of this mechanism to treat medical conditions like hypernatremia and hypertension, which involve excess blood volume. Excess natriuresis can be caused by: Endogenous

neg: Pacemaker crosstalk thresholds. Crosstalk is more common in unipolar systems since they require a larger pacing spike. Crosstalk is sometimes referred to as crosstalk inhibition, far-field sensing, or self-inhibition. In some cases, crosstalk can occur in the pulse generator circuit itself, though more common causes include atrial lead dislodgement into the ventricle, ventricular lead dislodgement into the atrium, high atrial output current, high ventricular sensitivity, and short ventricular blanking period. In general, the treatment of crosstalk includes decreasing atrial pacing output, decreasing atrial pulse width, decreasing ventricular sensitivity, increasing the ventricular blanking period, activating ventricular safety pacing, and new atrial lead implant

neg: Cardiac physiology in blood pressure tracings. The semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase. In the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the atria into the

neg: Pressure–volume loop analysis in cardiology not be a valid measure of LV relaxation rate, especially during acute alterations in contractility or afterload. Tau represents the exponential decay of the ventricular pressure during isovolumic relaxation. Several studies have shown that Tau is a preload-independent measure of isovolumic relaxation. The accurate estimation of Tau is highly dependent on the accuracy of ventricular pressure measurements. Thus, high fidelity pressure transducers are required to obtain real time instantaneous ventricular pressures. Calculation of Tau (Glantz method) formula_5 where Due to the load dependency of the previous parameters, more accurate measures of ventricular function are available in the PV plane. End-systolic

neg: Francisco Torrent-Guasp with current theory) during ventricular diastole. Thus, it is the contraction of the ascending segment of the myocardial band that paradoxically increases the ventricular volume. The insights provided by the ventricular myocardial band model allows glimpses of possible advances in cardiac surgical procedures, notably those associated with the remodeling seen in hearts with systolic heart failure. This procedure aims to improve the shape of the ventricles in dilated hearts by removing part of the excess muscle tissue within the ventricular cavity (ventriculotomy). However, using Torrent-Guasp model, Drs. Suma and Burkberg replaced the ventriculotomy by placing a Dacron patch longitudinal to

neg: Cardiac physiology in the ventricle following contraction. This volume of blood is known as the end systolic volume (ESV). Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately 430 ms. During the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. When pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen

neg: Pulsus bigeminus Other causes include digitalis toxicity, induction of anesthesia, placement of surgical instrumentation into the thorax or as a benign, temporary phenomenon. In Pulsus Bigeminus not all of the conducted electrical activity will elicit sufficient ventricular contraction to produce a palpable pulse. This is important for two reasons. One, an ECG may give a ventricular contraction rate that does not correspond to the palpated pulse rate. Secondly, because not all beats are being conducted, patients may present with symptoms of low output heart failure, e.g. Dizziness, shortness of breath or hypotension, even with a normal ECG. Causes Include: A doctor can

neg: Mitral insufficiency are also common causes in acute cases, dysfunction, which can include mitral valve prolapse. The pathophysiology of MR can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase. Acute MR (as may occur due to the sudden rupture of a chorda tendinae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward

neg: Heart arrhythmia result of ventricular arrhythmias. Arrhythmias may occur at any age but are more common among older people. Arrhythmia may be classified by rate (tachycardia, bradycardia), mechanism (automaticity, re-entry, triggered) or duration (isolated premature beats; couplets; runs, that is 3 or more beats; non-sustained= less than 30 seconds or sustained= over 30 seconds). It is also appropriate to classify by site of origin: These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They are the most common causes of bradycardia: First, second and third degree block also can occur at

neg: Re-entry ventricular arrhythmia the alternative anatomically defined circuit accessory pathways and it may not reside in just one location. Ventricular fibrillation (VF) following ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. The original re-entrant circuit breaks down into multiple mini reentrant circuits. (VF becoming the grand finale of a single prolonged VT larger circus movement, propagating change in the "functional core" of the ventricular myocardium, dissipating mini reentrant circuits, exhibited as ventricular fibrillation.) Ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry due

neg: Ejection fraction the left heart, known as the left ventricular ejection fraction (LVEF), is calculated by dividing the volume of blood pumped from the left ventricle per beat (stroke volume) by the volume of blood collected in the left ventricle at the end of diastolic filling (end-diastolic volume). LVEF is an indicator of the effectiveness of pumping into the systemic circulation. The EF of the right heart, or right ventricular ejection fraction (RVEF), is a measure of the efficiency of pumping into the pulmonary circulation. A heart which cannot pump sufficient blood to meet the body's requirements (i.e., heart failure) will often,

neg: Hyperaldosteronism The causes of secondary hyperaldosteronism are massive ascites, left ventricular failure, and cor pulmonale. These act either by decreasing circulating fluid volume or by decreasing cardiac output, with resulting increase in renin release leading to secondary hyperaldosteronism. When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism, and decreased or normal but with high renin in secondary hyperaldosteronism. In endocrinology, the terms 'primary' and 'secondary' are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, "i.e.", the tumor's location. Hyperaldosteronism can also be caused by plant poisoning, where the patient has been

neg: Natriuresis natriuretic hormones include: This is a natural process in infants at the time of birth. Natriuresis Natriuresis is the process of sodium excretion in the urine through the action of the kidneys. It is promoted by ventricular and atrial natriuretic peptides as well as calcitonin, and inhibited by chemicals such as aldosterone. Natriuresis lowers the concentration of sodium in the blood and also tends to lower blood volume because osmotic forces drag water out of the body's blood circulation and into the urine along with the sodium. Many diuretic drugs take advantage of this mechanism to treat medical conditions like

neg: Arrhythmogenic right ventricular dysplasia False positives include other conditions with fatty infiltration of the ventricle, such as chronic alcohol abuse and Duchenne/Becker muscular dystrophy. False negatives are common, however, because the disease progresses typically from the epicardium to the endocardium (with the biopsy sample coming from the endocardium), and the segmental nature of the disease. Also, due to the paper-thin right ventricular free wall that is common in this disease process, most biopsy samples are taken from the ventricular septum, which is commonly "not" involved in the disease process. A biopsy sample that is consistent with ARVD would have > 3% fat, >40% fibrous

neg: Heart arrhythmia die suddenly of this cause every year in the US. SADS may occur from other causes. There are many inherited conditions and heart diseases that can affect young people which can subsequently cause sudden death without advance symptoms. Causes of SADS in young people include viral myocarditis, long QT syndrome, Brugada syndrome, Catecholaminergic polymorphic ventricular tachycardia, hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia. The term cardiac arrhythmia covers a very large number of very different conditions. The most common symptom of an arrhythmia is an awareness of an abnormal heartbeat, called palpitations. These may be infrequent, frequent, or continuous. Some

neg: Pulmonary hypertension flow. In common with other types of pulmonary hypertension, these changes result in an increased workload for the right side of the heart. The right ventricle is normally part of a low pressure system, with systolic ventricular pressures that are lower than those that the left ventricle normally encounters. As such, the right ventricle cannot cope as well with higher pressures, and although right ventricular adaptations (hypertrophy and increased contractility of the heart muscle) initially help to preserve stroke volume, ultimately these compensatory mechanisms are insufficient; the right ventricular muscle cannot get enough oxygen to meet its needs and right

neg: Ventricular fibrillation fibrillation to a more benign rhythm is rare in all but small animals. Defibrillation is the process that converts ventricular fibrillation to a more benign rhythm. This is usually by application of an electric shock to the myocardium and is discussed in detail in the relevant article. Ventricular fibrillation Ventricular fibrillation (V-fib or VF) is when the heart quivers instead of pumping due to disorganized electrical activity in the ventricles. It is a type of cardiac arrhythmia. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by death in the absence of treatment.

neg: TNNT2 myofilaments and leads to reduced contractile velocity of the ventricular muscle, which extends the rapid ejection phase and results in an increase in stroke volume, especially under increased afterload. In vitro studies showed that N-terminal truncated cTnT preserved the overall cardiac myofilament calcium sensitivity and cooperativity, but altered TnT’s binding affinities for tropomyosin, TnI and TnC proteins, and lead to slightly decreased maximum myosin ATPase activity and myofilament force production, which forms the basis of the selective decrease in contractile velocity of ventricular muscle to increase stroke volume without significant increase in energy expenditure. With the relatively short half life

neg: Phrixotoxin cardiac reactions, such as premature ventricular beats, ventricular tachycardia, and atrio-ventricular blocks. Neurological effects observed are motor impairment and convulsions. These effects are seen following both intravenous and intracisternal injection, making it likely that phrixotoxin-1 crosses the blood brain barrier . Injection of this venom into mice causes immediate general ataxia, lack to response stimuli and semi-paralysis. Inability to stand and breathing reduction occurs within minutes. Flaccid paralysis and slowing of breathing eventually cause death . Phrixotoxin Phrixotoxins are peptide toxins derived from the venom of the Chilean copper tarantula "Phrixotrichus auratus", also named "Paraphysa scrofa". Phrixotoxin-1 and -2 block

neg: Noble Causes on a global scale, they still harbor dark secrets and hidden agendas. Volume 9 collects issues #32-36. Long-kept secrets are revealed in the final volume of the Noble Causes saga as Image Comics’ most dysfunctional superhero family returns for their last collection of adventures. Volume 10 collects issues #37-40. Two-issue series. Collects volumes 1 to 5 (black & white) Collects volumes 6 to 9 and Noble Causes: Extended Family (black & white) Noble Causes Noble Causes is an American comic book series created and written by Jay Faerber, illustrated by a variety of artists and published by Image Comics. The

neg: Pulsus alternans his novel "Sons and Lovers": Then he felt her pulse. There was a strong stroke and a weak one, like a sound and its echo. That was supposed to betoken the end... Pulsus alternans Pulsus alternans is a physical finding with arterial pulse waveform showing alternating strong and weak beats. It is almost always indicative of left ventricular systolic impairment, and carries a poor prognosis. In left ventricular dysfunction, the ejection fraction will decrease significantly, causing reduction in stroke volume, hence causing an increase in end-diastolic volume. As a result, during the next cycle of systolic phase, the myocardial muscle

neg: Atrial septal defect remarkable left-to-right shunt, blood shunts from the left atrium to the right atrium. This extra blood from the left atrium may cause a volume overload of both the right atrium and the right ventricle. If untreated, this condition can result in enlargement of the right side of the heart and ultimately heart failure. Any process that increases the pressure in the left ventricle can cause worsening of the left-to-right shunt. This includes hypertension, which increases the pressure that the left ventricle has to generate to open the aortic valve during ventricular systole, and coronary artery disease which increases the stiffness

neg: Cavernous liver haemangioma diagnostic. Biopsy is avoided due to the risk of haemorrhage. Hepatic haemangiomas can occur as part of a clinical syndrome, for example Klippel-Trenaunay-Weber syndrome, Osler–Weber–Rendu syndrome and Von Hippel-Lindau syndrome. This large, atypical haemangioma of the liver may present with abdominal pain or fullness due to haemorrhage, thrombosis or mass effect. It may also lead to left ventricular volume overload and heart failure due to the increase in cardiac output which it causes. Further complications are Kasabach-Merritt syndrome, a form of consumptive coagulopathy due to thrombocytopaenia, and rupture. Cavernous liver haemangioma A cavernous liver haemangioma or hepatic haemangioma is a

neg: Mitral valve stenosis 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 cm, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the

neg: Split S2 due to an increase in ventricular emptying time, whereas the aortic valve (A component of S) closes slightly earlier due to a reduction in left ventricular volume and ventricular emptying time. Thus the P component of S is delayed relative to that of the A component. This delay in P versus A is heard as a slight broadening or even "splitting" of the second heart sound; though it is usually only heard in the pulmonic area of the chest because the P is soft and not heard in other areas. During expiration, the chest wall collapses and decreases the negative

neg: Fourth heart sound itself does not require treatment; rather plans should be laid to stop the progression of whatever causes the underlying ventricular dysfunction. The S4 heart sound is a secondary manifestation of a primary disease process and treatment should be focused on treating the underlying, primary disease. Fourth heart sound The fourth heart sound or S is an extra heart sound that occurs during late diastole, immediately before the normal two "lub-dub" heart sounds (S and S). It occurs just after atrial contraction and immediately before the systolic S and is caused by the atria contracting forcefully in an effort to overcome

neg: Incipient wetness impregnation Incipient wetness impregnation Incipient wetness impregnation (IW or IWI), also called capillary impregnation or dry impregnation, is a commonly used technique for the synthesis of heterogeneous catalysts. Typically, the active metal precursor is dissolved in an aqueous or organic solution. Then the metal-containing solution is added to a catalyst support containing the same pore volume as the volume of the solution that was added. Capillary action draws the solution into the pores. Solution added in excess of the support pore volume causes the solution transport to change from a capillary action process to a diffusion process, which is much slower.

neg: Ventricular escape beat an ectopic beat. It can be considered a form of ectopic pacemaker activity that is unveiled by lack of other pacemakers to stimulate the ventricles. Ventricular pacemaker cells discharge at a slower rate than the SA or AV node. While the SA node typically initiates a rate of 70 beats per minute (BPM), the atrioventricular node (AV node) is usually only capable of generating a rhythm at 40-60 BPM or less. Ventricular contraction rate is thus reduced by 15-40 beats per minute. If there are only one or two ectopic beats, they are considered escape beats. If this causes a

neg: Pressure–volume loop analysis in cardiology defined by the afterload and inotropic state of the heart. Increased afterload or decreased inotropy shifts the curve down and to the right. Decreased afterload and increased inotropy shifts the curve up and to the left. Arterial elastance (Ea) is a measure of arterial load and is calculated as the simple ratio of ventricular end-systolic pressure to stroke volume. In mathematical terms, formula_8 By characterizing both the ventricular and arterial systems in terms of pressure and stroke volume, it is possible to study the ventriculo-arterial coupling (the interaction between the heart and the arterial system). In dilated cardiomyopathy, the ventricle

neg: Implantable cardioverter-defibrillator (Abbott). Implantation of ICD is meant to prevent sudden cardiac death and is indicated under various conditions. Two broad but distinct categories are primary and secondary prevention. Primary prevention refers to patients who have not suffered a life-threatening arrhythmia episode. Secondary prevention has the strongest evidence for benefit and it refers to survivors of cardiac arrest secondary to ventricular fibrillation or hemodynamically unstable sustained ventricular tachycardia after reversible causes are excluded. Similarly, ICD use in primary prevention is to prevent cardiac death in patients who are at risk for sustained ventricular tachycardia or ventricular fibrillation. This population accounts for the

neg: Cardiac resynchronization therapy from the axillary or cephalic veins. Right ventricular access is direct, while left ventricular access is conferred via the coronary sinus (CS). CRT defibrillators (CRT-D) also incorporate the additional function of an implantable cardioverter-defibrillator (ICD), to quickly terminate an abnormally fast, life-threatening heart rhythm. CRT and CRT-D have become increasingly important therapeutic options for patients with moderate and severe heart failure. The key indication for CRT is left bundle branch block (LBBB) of the heart, a cardiac abnormality leading to delayed left ventricular contraction. LBBB causes a QRS prolongation of >120 ms on the electrocardiogram, contributing to poor left ventricular

neg: Pressure–volume loop analysis in cardiology hearts, the SV is highly sensitive to afterload changes. Ventricular stroke work (SW) is defined as the work performed by the left or right ventricle to eject the stroke volume into the aorta or pulmonary artery, respectively. The area enclosed by the PV loop is a measure of the ventricular stroke work, which is a product of the stroke volume and the mean aortic or pulmonary artery pressure (afterload), depending on whether one is considering the left or the right ventricle. Cardiac output (CO) is defined as the amount of blood pumped by the ventricle in unit time. In mathematical

neg: Frank–Starling law fibers, caused by ventricular filling, determines the sarcomere length of the fibres. Therefore the force (pressure) generated by the cardiac muscle fibres is related to the end-diastolic volume of the left and right ventricles as determined by complexities of the force-sarcomere length relationship. Due to the intrinsic property of myocardium that is responsible for the Frank-Starling mechanism, the heart can automatically accommodate an increase in venous return, at any heart rate. The mechanism is of functional importance because it serves to adapt left ventricular output to right ventricular output. If this mechanism did not exist and the right and left

neg: Syncope (medicine) irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which is rapidly fatal without cardiopulmonary resuscitation

neg: Heart failure with preserved ejection fraction chamber size without an accompanying increase in wall thickness. This leads to a corresponding increase in left ventricular end diastolic volume. Cellular changes generally underlie alterations in cardiac structure. In HFpEF cardiomyocytes have been demonstrated to show increased diameter without an increase in length; this is consistent with observed concentric ventricular hypertrophy and increased left ventricular mass. HFrEF cardiomyocytes exhibit the opposite morphology; increased length without increased cellular diameter. This too is consistent with eccentric hypertrophy seen in this condition. Changes in the extracellular environment are of significant importance in heart disease. Particularly, regulation of genes that alter fibrosis contribute

neg: Systole in isovolumetric, or fixed-volume, contraction phase until maximal pressure (dP/dt = 0) occurs, causing the pulmonary and aortic valves to open in ejection phase. In ejection phase, blood flows from the two ventricles down its pressure gradient—that is, 'down' from higher pressure to lower pressure—into (and through) the aorta and the pulmonary trunk respectively. Notably, cardiac muscle perfusion through the heart's coronary vessels doesn't happen during ventricular systole; rather, it occurs during ventricular diastole. Ventricular systole is the origin of the pulse. The pulmonary (or pulmonic) valve in the right ventricle opens into the pulmonary trunk, also known as the