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The glossary is available to help your clients understand terms they may encounter as you explain their pet's heart disease to them.  Below is a list of definitions for commonly used medical terms related to the heart and its function in both health and disease.

Acquired heart disease
Acquired heart diseases are those that are not present at birth. The most common type of acquired heart disease in dogs is chronic valvular disease, a degenerative disease (sometimes called endocardiosis) of one or both of the atrioventricular (AV) valves [also called the mitral and tricuspid valves]). In chronic valvular disease, the affected heart valves gradually lose the ability to close effectively, causing the affected valves to leak (valve leakage is called regurgitation or insufficiency). Other common causes of acquired heart disease in dogs include heartworm disease and dilated cardiomyopathy (DCM). DCM causes the heart muscle to lose strength and the heart chambers to dilate.
The sum of forces resisting ejection of blood from the heart is the afterload. Afterload can also be thought of as the tension that the heart muscle must develop in order to force the ejection of blood from the ventricles. The amount of energy available for each contraction is relatively fixed and constant, determined by the level of nutrients and oxygen available to the heart muscle and the muscle's metabolic health -- if the heart needs more energy to develop wall tension, less is available to eject blood from the ventricle.
Aldosterone is a steroid-based hormone that is produced by the adrenal gland (cortex) in response to activation of the renin-angiotensin-aldosterone system. Aldosterone helps the body conserve salt and water in situations where this is necessary (for example, following water deprivation, vomiting or diarrhea). In chronic heart disease, however, aldosterone levels rise because of chronically low cardiac output, and chronically elevated aldosterone levels are toxic to the heart muscle and blood vessels. Strategies to lower aldosterone levels (e.g., angiotensin converting enzyme inhibitors) and aldosterone receptor blockers (such as spironolactone) are common strategies in the long-term management of heart failure to try to prevent the damage that excess aldosterone may cause.
Angiotensin Converting Enzyme Inhibitors (ACEI)
A group of medications that share the common action of inhibiting the activation of the renin-angiotensin-aldosterone system. These drugs are used in the treatment of heart failure, systemic hypertension and some forms of kidney disease. Commonly prescribed ACEIs include enalapril, benazepril, lisinopril and ramipril.
Aorta (Ao)
The aorta is the large, elastic vessel that normally receives the entire output of the left ventricle. The aorta is divided into three segments: the ascending aorta, the aortic arch and the descending aorta. The sinus of Valsalva is a prominent outpouching behind the aortic valve that is the origin of coronary arteries (the arteries that supply blood to the heart muscle itself).
Aortic & Pulmonic Valves
These are semilunar (half moon shaped) valves, similar in collagen structure and lining to the AV valves, but composed of three cusps each, and positioned so that they guard the exits from the left and right ventricles. As with the AV (mitral and tricuspid) valves, they open silently, and close (coapt) with a sharp sound (the second heart sound, S2).
Aortic stenosis (AS) or subaortic stenosis (SAS)
Aortic stenosis is (usually) a congenital heart defect that is caused by a developmental problem with the aortic valve. It is a relatively common defect in dogs, a less common defect in cats. The most common form involves the inherited formation of a fibrous ring just beneath the aortic valve (subaortic stenosis), an inherited condition common in Newfoundlands, Golden Retrievers, German Shepherds and some other large breed dogs. Aortic stenosis increases the resistance to the ejection of blood into the aorta from the left ventricle, and increases the workload on the left ventricle. These defects also increase the risk for infection of the abnormal valve (endocarditis).
Arrhythmia is any disturbance of the heart rhythm. Arrhythmias may be caused by disorders of electrical impulse formation, or disorders of impulse conduction. They may also be categorized by their anatomical site of origin (i.e., supraventricular, AV-nodal or ventricular). In general, the clinical importance of an arrhythmia is determined by the effect it has on the heart's pumping function and clinical well-being, and whether or not the arrhythmia puts the animal at significantly increased risk for sudden death.
Arterial Blood Pressure (Systolic, Diastolic and Mean)
The pressure in the arteries is determined by the cardiac output and the resistance to blood flow into the arteries, according to the relationship that the Pressure = Cardiac Output X Systemic Vascular Resistance. The systolic blood pressure is the highest pressure measured during the heart's contraction phase (ventricular systole), and is higher than the diastolic blood pressure (the lowest pressure measured during the heart's relaxation phase). Low arterial pressure is called systemic hypotension, while high pressure is termed systemic hypertension. Normal systemic arterial pressures in the dog are approximately 120/80 with a mean arterial pressure of about 85-90 mm Hg. Pressures of 170/120 or above in a calm animal are too high (hypertensive). Mean arterial pressure must be maintained above 55-60 mmHg to maintain adequate organ perfusion.
Atrial or Brain Natriuretic Factor (Peptide) (ANF, ANP, BNP)
There are small peptide hormones produced in atrial and ventricular muscle cells, released in response to stretch, that enhance sodium excretion and dilate the veins, decreasing preload. Measurement of these substances in blood can give an indication of whether the heart is damaged or failing.
Atrioventricular (AV) Valve Apparatus
The valves are thin, tough structures made up of an inner collagen layer that is produced by cells called fibroblasts, along with a small amount of glycosaminoglycan (filler in between the cells and collagen bundles). Papillary muscles (part of the ventricular heart muscle) function as part of the AV valve apparatus in both the right and left ventricles. The papillary muscles are connected to the mitral (left) and tricuspid (right) AV valves via chordae tendineae, collagen cords that insert directly into the collagen structure of the valves. The valves open silently if they are normal. The contraction of the ventricles closes and tenses the valves. Valve closure is also called coaptation. The papillary muscles, chordae tendineae and valve leaflets act in concert to prevent AV valve leakage (called regurgitation or insufficiency) during contraction. Disease of any of the elements of the valve apparatus can result in AV valve leakage or regurgitation.
Atrioventricular Node (AV node)
Atrioventricular Node (AV node) is the only normal electrical connection between the heart's upper chambers (atria) and lower chambers (ventricles), located in the upper portion of the muscular wall that divides the left from the right ventricle (interventricular septum). Like the SA node, the AV node is not visible on echocardiography.
Beta Receptors
Beta adrenergic receptors are located in the heart, and they are responsible for the action of adrenaline and other sympathetic nerve transmitters on the heart (generally to increase heart rate and contractility). Chronic sympathetic stimulation results in a decrease in the number of beta receptors expressed on the surface of heart muscle cells that are available for stimulation, thus "numbing" the tissue to further stimulation and requiring ever larger amounts of stimulant to reach a response (called receptor down-regulation).
Capillaries are the smallest (microscopic - the size of blood cells) blood vessels in the body. They are made up of endothelial cells, and they form the barrier across which gas, fluid and electrolyte exchange occurs in all of the organs of the body. The capillaries are relatively fragile, and they normally leak a small amount of fluid into the tissues (which is in turn removed by the lymphatic system).
Cardiac Conduction System
The cardiac conduction system is the "electrical system" of the heart, made up of the Sinoatrial Node (SA Node), lnteratrial conduction pathways, Atrioventricular Node (AV node), Bundle of HIS (a bundle of specialized, rapidly conducting cells below the AV node), Left Main Bundle Branch (LBB), Left Anterior Fascicle or Branch (LAF), Left Posterior Fascicle or Branch (LPF), Right Bundle Branch (RBB) and Purkinje fibers (specialized, rapidly conducting cells that form the interface between the heart muscle cells and the conduction system).
Cardiac Output
Cardiac output refers to the volume of blood that the heart pumps in any defined unit of time. Cardiac Output = Heart Rate X Stroke Volume. Stroke volume, defined below, is the amount of blood ejected from the ventricle on a single contraction. Several methods are available for the clinical measurement of cardiac output, but all of the accurate ones involve some degree of invasive instrumentation, making the measurement uncommon in most veterinary practices.
Cardiogenic Shock
Severe heart failure that results in systemic hypotension and low cardiac output in combination with high venous pressures (fluid accumulation either in the lungs or a body cavity).
Chamber Stiffness
The geometry of the ventricle or atrium (the chamber includes the cavity) also affects its stiffness, and may influence diastolic function as well. Large, dilated, spherical chambers generally are stiffer than smaller, more ellipsoid ones, for example.
Chronotropy is a synonym for heart rate. Drugs or physiologic maneuvers that enhance chronotropy (positive chronotropes or things that elicit a positive chronotropic response) increase the heart rate.
Circulatory System
The system of organs and tissues, including the heart, blood, blood vessels, lymph, lymphatic vessels and lymph nodes, involved in circulating blood and lymph through the body.
Clinical Signs
Indications (signs) that you may observe or your veterinarian may find on physical examination that an animal is sick.
Compensated Valvular Insufficiency
Refers to the clinical situation where a valve is damaged and leaking, but the hemodynamic overload is not yet severe enough to result in overt clinical signs of heart failure.
Congenital Heart Disease
A heart disease or anatomical defect that is present at birth. Congenital diseases may be inherited, or they may be the result of events that occur during pregnancy (e.g., spontaneous mutation, viral infection, trauma, drug effects). Examples of common congenital heart diseases in dogs include patent ductus arteriosus, pulmonic valve stenosis, aortic valve stenosis, mitral or tricuspid valve dysplasias, ventricular or atrial septal defects, and tetralogy of Fallot. Many of these defects can be cured or successfully treated by catheter-based intervention, surgery, medications or some combination of those treatment modalities.
An inherent property of the heart that reflects the health of the muscle. Contractility is actually defined as the speed with which the cardiac myocytes would contract if there was no load placed on the heart (i.e., independently of preload and afterload).
General term for the time period during which the heart relaxes and aspirates blood from the great veins. Distinct mechanical events occur during ventricular diastole, which is an active and energy requiring process.
Diastolic Ventricular Function
How well the ventricle relaxes. Depends on active (e.g., reuptake of Ca by the sarcoplasmic reticulum and subsequent reorientation of the calcium sensitive regulatory proteins and breakage of the actin myosin crossbridges) and passive (e.g., the compliance of the connective tissue components of the ventricle) factors.
Dilated Cardiomyopathy (DCM)
A condition (which may be congenital or acquired) in which the heart becomes weakened and enlarged, and cannot pump blood efficiently.
Medications that cause increased urine production, usually by inhibiting the uptake of salt by the kidney. These drugs (e.g., furosemide) are used primarily to remove excess salt and water from the circulatory system, which may reduce fluid accumulations in heart failure.
Echocardiogram (Echo)
An echocardiogram (Echo) is a record of the examination of the heart using ultrasound. An echocardiogram potentially provides a detailed noninvasive picture of the heart's internal anatomy and function during contraction and relaxation, and also allows measurement of many aspects of blood flow into and out of the heart.
Electrocardiogram (ECG or EKG)
Electrocardiogram (ECG or EKG) is a record of the electrical activity (depolarization and repolarization) of the heart that is made by placing electrodes on the body surface. The ECG provides information on the heart rate and rhythm, and sometimes other heart-related issues (e.g., the metabolic state of the heart muscle).
Elevated Cardiac Filling Pressures
Increased right and/or left atrial and right and/or left ventricular end diastolic pressures.
Endocardiosis (chronic valvular disease, myxomatous degeneration of the heart valves)
Endocardiosis is the term that refers to a degenerative disease of the heart valves. Endocardiosis is not related to endocarditis, despite their similar sounding names. Endocardiosis is a common disease in dogs (the most common acquired heart disease in small breed dogs), and a much less common disease in cats. Endocardiosis is also called chronic valvular heart disease and myxomatous degeneration of the heart valves.
Endocarditis is the word for infection or inflammation of the endocardial lining of the heart valves or of the heart or great vessels themselves. Endocarditis is an infrequent disease in dogs and a rare disease in cats.
Forward Cardiac Output
Forward cardiac output is the volume of blood that the heart (LV) pumps in a defined unit of time into the effective systemic circulation. There may be occasions when a large regurgitant output (the Regurgitant Fraction is the volume of blood regurgitated divided by the total cardiac output) renders even an elevated cardiac output inadequate, because the forward output is low.
A muscular pump that circulates blood around the body. In mammals (e.g., dogs, cats and humans), the normal heart has an electrical system, along with 4 distinct chambers and 4 valves. Under normal circumstances, the action of the heart is coordinated to ensure that blood is returned from the body to the right side of the heart via the veins, pumped to the lungs for oxygenation, returned to the left side of the heart from the lungs, and pumped out to the body to supply oxygen and nutrients to all of the organs.
Heart Disease
Heart disease is an abnormality of the heart (or of the arteries supplying the heart) that impairs its normal function.
Heart Failure
The inability of the heart to pump enough blood to meet the body's needs. This can be due to inadequate blood flow out of the heart (low output signs) or due to high venous pressure in either the right or left ventricle leading to signs of congestion. Congestive heart failure is associated with increased fluid buildup in areas such as the lungs, or the abdominal or chest cavity.
Heart Murmur
Heart murmur is the sound made by turbulent blood flow in the heart. The importance of a heart murmur is determined by the underlying cause of the turbulent blood flow, and may range from an incidental finding in an otherwise normal animal, to an indication of the presence of serious heart disease.
Heart Rate
Heart rate refers to how many times per minute the heart is electrically activated. This may be divided into the atrial rate and the ventricular rate. Practically, the heart rate is often used interchangeably with the pulse rate, although occasions arise where the heart rate as measured on the electrocardiogram exceeds the pulse rate because some electrical activations of the ventricle fail to generate a pulse.
Hepatic Venous Congestion
Hepatic venous congestion is elevated hepatic venous pressure.
Impedance is resistance to pulsatile flow, and is unfortunately difficult to calculate in a clinical setting.
Indices (measurements) of Afterload
Afterload can be estimated from measurements of ventricular muscle wall tension, aortic impedance or systemic vascular resistance. If cardiac output is known in addition to arterial blood pressure, the systemic vascular resistance can be calculated. Ventricular wall tension can be estimated from simultaneous echocardiographic measurements of wall thickness combined with intraventricular pressure measurements. Wall tension is directly proportional to the pressure in the chamber, directly proportional to the diameter of the chamber and inversely proportional to the wall thickness.
Indices (measurements) of Contractility
Many exist, none are perfect. Most measure the efficiency or extent of ventricular ejection (LV Ejection Fraction (LVEF), LV change in diameter, %ΔD). Clinically, the echocardiographic indices of contractility are the most frequently used.
Indices (measurements) of Diastolic Ventricular Function
Several exist, and in general they are more problematic than indices of systolic ventricular function. Indices of diastolic ventricular function rely on some index of how ventricular filling is proceeding, or on the velocity of blood flow into the ventricle during various phases of diastole.
Indices (measurements) of Preload
Preload is estimated clinically by a variety of methods, most accurately by measuring the pressure in the ventricle just before contraction occurs. The right ventricular diastolic pressure (RVEDP) accurately estimates only right ventricular preload, because the pulmonary vascular circuit is interposed between the right and left ventricles (in addition to the pulmonic valve, left atrium and mitral valve), and it is possible (and common) for the left ventricular diastolic pressure to be severely elevated despite a normal or near normal right ventricular end diastolic pressure. Likewise, the left ventricular diastolic pressure is an inaccurate estimator of right ventricular preload. Because it is difficult to place and maintain a catheter in the left ventricle, the pulmonary artery diastolic pressure (or using a special balloon catheter with an end hole to "shut off" the vessel behind the hole and expose the hole only to the pressure distal to it, the pulmonary artery wedge (PAW) or pulmonary capillary wedge pressure (PCWP) is often used to estimate the left ventricular diastolic pressure. Right ventricular preload is usually estimated via a catheter in the cranial vena cava (Central Venous Pressure, CVP) or in the Right Atrium (Right Atrial Pressure, RAP).
Inodilators are medications that both increase myocardial contractility and open up constricted blood vessels (arteries and veins), potentially improving cardiac output without increasing the workload on the heart. The most frequently used inodilator in veterinary medicine is pimobendan.
Laminar Flow
Laminar flow refers to nondisturbed, smooth flow. The flow in the cardiovascular system under most normal circumstances is laminar, and therefore silent to the human ear.
Inotropy is another word for contractility (i.e., a positive inotrope is a drug that increases contractility, and a positive inotropic response is one in which contractility was enhanced).
Another word for relaxation or diastolic function. Something that is a positive lusitrope improves diastolic function.
Muscle Stiffness
Refers to the resistance of the muscle to physical deformation, which makes it hard for the heart to fill with blood when it is relaxed. The heart muscle may become stiff for a variety of reasons, some of which are poorly understood. Conditions that often increase heart muscle stiffness include inadequate blood flow to the muscle (called ischemia), hypertrophy (increasing muscle thickness), muscle failure, calcium loading, inadequate oxygen supply (called hypoxia), scarring, inflammation and metabolic defects. Stiff heart muscle requires a higher filling pressure to achieve a given diastolic ventricular chamber volume.
Myocardial Failure
Myocardial failure specifically denotes that the heart muscle (myocardium) is not working properly. Myocardial failure may result from a number of pathologic processes affecting the myocardium, including inflammation, metabolic derangement or most commonly a condition of unknown cause, cardiomyopathy. Systolic myocardial failure (the usual association with myocardial failure when used without a timing modifier) implies that the heart fails to contract normally because of muscle weakness; diastolic myocardial failure implies that the heart fails to relax properly. The most common association with myocardial failure in clinical veterinary medicine is canine dilated cardiomyopathy, where systolic myocardial failure of unknown etiology is the underlying defect that leads to the syndrome of heart failure.
Myocardial Hypertrophy
Myocardial hypertrophy refers to the addition of muscle proteins to existing heart muscle cells (myocytes). The actual number of heart muscle cells (cardiac myocytes) rarely changes in the adult animal. The stimuli to hypertrophy (the signals that trigger increased production of muscle proteins by the cell) are imperfectly understood, but different stimuli result in different patterns of hypertrophy. Hypertrophy as a response to pumping increased blood volume (e.g., valvular insufficiency requires the heart to pump greater volumes of blood in order to maintain normal forward cardiac output, since a portion of each stroke volume is leaked backward through the insufficient valve into an inappropriate chamber) is generally called eccentric hypertrophy, since the chamber involved becomes larger (dilated) as the muscle mass increases. Hypertrophy that occurs as a response to pressure loading of the heart (e.g., hypertension) is called concentric hypertrophy, since the chamber involved becomes smaller as the muscle mass increases.
Myocardial Oxygen Consumption (MVO2)
The amount of oxygen needed by the heart muscle to produce energy for structural maintenance and contraction. The prime determinants of myocardial oxygen consumption include the heart rate, the amount of tension that must be generated in the heart muscle in order to eject blood, and the intrinsic contractility of the muscle. The higher the heart rate, the greater the wall tension, and the greater the intrinsic contractility of the muscle, the more oxygen is required to supply the metabolic demands of the myocardium.
Patent Ductus Arteriosus (PDA)
The ductus arteriosus is a normal structure in the fetus, shunting blood away from the pulmonary artery into the descending aorta. At birth, the ductus normally constricts and closes in response to biochemical changes that occur with oxygenation of the lungs. In some situations (an inherited condition in some dogs), the ducus fails to constrict, and remains patent - hence the name PDA. This defect generally should be corrected as early as possible, and it has an excellent prognosis once repaired.
Pericardial Effusion
Pericardial effusion is fluid accumulation around the heart in the pericardial space. Cardiac Tamponade refers to the situation where a sufficient volume of fluid accumulates rapidly enough to raise the intrapericardial pressure above the normal central venous pressure, inhibiting normal venous inflow to the heart.
Preload is the amount of tension on the heart muscle cell in diastole, just prior to contraction. This tension (stretch) determines the degree of overlap between the actin and myosin filaments within the muscle cell (which in turn determines the number of potential muscle-shortening cross bridges that can be formed to cause the muscle to contract). The ventricular geometry and arrangement of muscle cells within that geometry will affect the degree of actual stretch on the muscle for any given amount of LV diastolic pressure.
Pulmonary Artery (PA)
The pulmonary artery is the large vessel that receives the entire output of the right ventricle. The main pulmonary artery normally gives rise to right and left pulmonary arteries of approximately equal size; the pulmonary arteries divide further and deliver blood to the lungs for oxygenation. In the fetus, the ductus arteriosus connects the main pulmonary artery (or occasionally the left PA) to the descending aorta to shunt blood away from the unoxygenated pulmonary circulation. The ductus normally closes during the first hours to days of life in domestic species (hours in the dog and cat, up to 2 days in the horse). Failure of this vessel to close results in a common congenital heart defect called patent ductus arteriosus (PDA).
Pulmonary Venous Congestion
Pulmonary venous congestion is elevated pulmonary venous pressure.
Pulmonic Stenosis (PS)
Pulmonic stenosis is a common congenital heart defect in dogs, and a less common defect in cats. It is caused by a developmental defect in the pulmonic valve, such that the valve is too narrow (stenotic), which increases the resistance to the ejection of blood from the right ventricle into the main pulmonary artery. This defect is often correctable by a catheter-based intervention that can be highly successful if done at a young age.
A radiograph is a photographic image of internal structures produced by passing X-rays through the body. Allows a relatively detailed examination of the exterior surface of the heart, and an even more detailed examination of the anatomy of the lungs and chest cavity.
Renin - Angiotensin Aldosterone System (RAAS)
Renin is a peptide hormone released from the juxtaglomerular apparatus of the kidney in response to reductions in renal blood flow, increases in sympathetic stimulation (via the renal sympathetic nerves or circulating levels of catecholamines), and other humoral changes (including potassium, prostaglandins and other signals). Renin converts angiotensinogen to angiotensin I, and the angiotensin converting enzyme converts angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor (to maintain blood pressure when cardiac output falls) and also a primary stimulus for aldosterone release (enhances sodium retention) as well as a secondary stimulus for anti-diuretic hormone (ADH or argentine vasopressin) release (increases thirst and expands blood volume).
Resistance in the cardiovascular system refers to resistance to the steady (or constant) flow of blood.
Shock refers to inadequate cardiac output to meet tissue needs associated with low venous pressures, and most often with systemic hypotension. Various insults (e.g., hemorrhage, volume depletion, sepsis) can result in this condition by a variety of pathophysiologic mechanisms.
Sinoatrial Node (SA Node)
Sinoatrial Node (SA Node) is a cluster of electrically active cells located high in the right atrium. These cells are the normal pacemaker of the heart. The SA node is too small to see with the naked eye, and is not visible on echocardiography.
Stroke Volume
Stroke volume is the amount of blood ejected from the heart per contraction. The stroke volume multiplied by the heart rate equals the cardiac output. At any given heart rate, the stroke volume is directly (positively) related to the contractility and preload, and inversely (negatively) related to the afterload. In other words, stroke volume generally increases with increased contractility and/or preload, and decreases with increased afterload.
Sympathetic nervous system (fight or flight hormones)
The sympathetic nervous system is the branch of the autonomic (i.e., unconscious) nervous system that is responsible for "fight or flight" responses. This system is activated by chemicals generally called catecholamines (including epinephrine or adrenaline and norepinephrine or noradrenaline). When released in response to normal stimuli (e.g., fear or acute injury) these chemical signals generally increase the heart rate, the strength of contraction, the blood pressure and the heart's ability to relax and function well at high heart rates. When released chronically in response to pathologic stimuli (e.g., chronic valvular or muscle disease), these chemicals damage the heart muscle. For this reason, catecholamine blocking drugs (e.g., beta adrenergic blockers) are sometimes used in the chronic management of heart disease to try and prevent chronic damage to the heart muscle.
Systole is a general term for the time period during which cardiac contraction occurs. Atrial systole refers to the contraction of the atria; ventricular systole to the contraction of the ventricles. The adjective, systolic, refers to events or phenomena that occur during systole. For example, systolic myocardial performance concerns the performance of the heart muscle during the period of contraction, and a systolic murmur is one that occurs sometime between the first heart sound (S1) and the second (S2), during the period of systole.
Transient Heart Sound
Transient heart sound consists of brief, short duration sounds (like lub dup, for S1 S2, the first and second heart sound). Transient heart sounds are generally made by valves closing and tensing (or prolapsing, as with some systolic "clicks"), or by rapid deceleration and subsequent vibration of the ventricles and columns of blood, such as occurs in the third or fourth heart sounds.
Turbulent Flow
Turbulent flow is disturbed flow, whereby the fluid flow contains swirls and eddies, with the particles in the flow going at a variety of different velocities and in many directions. The tendency for a flow to become turbulent depends on a number of factors, and is directly proportional to the velocity of the blood and the diameter of the vessel, and inversely proportional to the viscosity of the blood. Thus high velocity flow in a large vessel is very likely to be turbulent. Low velocity flow is not likely to become turbulent, and at any given velocity, the higher the viscosity, the less likely the flow will become disturbed. Because heart murmurs are generally caused by turbulent flow, situations that result in high velocity blood flow, dilated vessels and / or low blood viscosity (e.g., anemia) predispose to the formation of heart murmurs.
Valvular Insufficiency or Regurgitation
Valvular insufficiency or regurgitation describes the situation in which one or more of the heart valves leaks, setting up a situation where blood no longer flows in one direction only. Potential causes of valvular insufficiency include chronic valvular disease (a degenerative disease sometimes called endocardiosis), infection of the valves (called endocarditis), congenital malformations of the valves, dilatation of the heart chambers or great vessels severe enough to cause valve leakage, and traumatic injury of the valve. Valvular regurgitation or insufficiency refers to the leakage of blood in a retrograde direction through any valve. This generally happens during the period when the valve is supposed to be closed. Thus, AV valve regurgitation or insufficiency generally occurs during systole, when the AV valves (Mitral and Tricuspid) are supposed to be closed, and semilunar valve insufficiency (aortic and pulmonic valves) occurs during diastole, when those valves should be closed.
Valvular Stenosis
Stenosis refers to a pathological narrowing in the area of a heart valve or great vessel close to a valve. The pressure on the proximal side of a stenosis is always elevated, while that on the distal side remains normal. Thus in the example of pulmonary valve stenosis, the pressure in the right ventricle would be higher than normal (the degree of abnormal elevation of RV pressure would indicate the severity of the stenosis), and the pressure in the pulmonary artery would remain normal. Stenosis causes disturbances of flow (turbulence) and dysfunction of the valve or vessel during the time when the valve is normally open, so that mitral or tricuspid stenosis manifest as disturbed flow (and heart murmurs) during diastole (when blood normally flows undisturbed across the mitral and tricuspid orifices), and aortic and pulmonic stenosis cause disturbed flow during systole.
Venous Hypertension
Venous hypertension is defined as elevated pressures within veins. Venous hypertension elevates the pressure in the capillaries, which in turn tend to leak more fluid into the tissues or body cavity where they are found.

Call the Cardiology Care Network Hotline tollfree at 888-962-7763 for answers to any questions that you have about your pet's heart disease, or to schedule an appointment through the NCSU Heart Failure Program. The Cardiology Care Network Technician is available between the hours of 9AM - 5PM Monday - Friday; Outside of regular business hours, emergency assistance is available 24 hours / day, 7 days / week through the NCSU-VTH Emergency service (phone 919-513-6911).

Sponsored by an educational grant
from Boehringer Ingelheim Vetmedica, Inc.