Paxil and Ventricular Septal Defects

Author: Robert H Hilley IV
Just like the atrial chambers (the left atrium and right atrium), the ventricular chambers also have a wall dividing them. The left ventricle and the right ventricle are divided by the ventricular septum and it is this septum that prevents arterial blood from mixing with venous blood.
When arterial blood mixes with venous blood, there are a multitude of potential side effects that could occur to a person as a result of this mixing. First and foremost, the main effect of the mixing the blood together is that the oxygenated and non-oxygenated blood groups will intermingle with each other, creating an imbalance between the blood coming in and leaving the heart. Some of the blood coming into the heart will already be oxygenated and some blood will leave the heart with poor oxygenation. This poorly oxygenated blood will circulate around the body and organs that are very sensitive to changes in blood oxygen levels (such as the Brain) may become damaged if a prolonged period of poor blood oxygenation takes place.
Additionally, there are also blood pressure concerns that can arise from the mixing of arterial and venous blood, not to mention the possibility of chronic pulmonary hypertension problems. These are the kinds of problems that can result from a hole in heart condition, especially if that condition is a ventricular septal defect (a hole in the ventricular septum). In general it is a very undesirable problem to have because of the large number of complications that can result from it.
The Connection to Paxil
In 2005 (especially late 2005 in the September to December month range), a lot of information was revealed about the side effects of Paxil. From the FDA warnings against pregnant women taking Paxil to multiple studies that showed the drug's propensity to cause multiple birth defects, Paxil and all selective serotonin reuptake inhibitors (SSRIs) were deemed dangerous to fetal matter and as such all pregnant women were urged to avoid taking those kinds of drugs.
Amongst the rather large list of birth defects that had been traced to the use of Paxil was ventricular septal defect. In many ways, this defect is worse for infants than it is for adults, because adults by and large, with medical assistance in some cases, have learned to deal with the problems of having a ventricular septal defect. In newborn children, obviously that acclimation is not there and conditions like pulmonary hypertension that result from a ventricular septal defect can be very painful for the child to experience and very stressful for the parent to see.
As with most things relating to the world of drug taking, knowledge and information are a person's best allies. If you are pregnant and suffering from depression, try to seek alternatives to taking SSRI drugs such as Paxil. If you must take these types of drugs, do so only under the supervision of a medical professional and do not under any circumstances take the drug without the permission of one. The list of mothers today that
regret taking Paxil during their pregnancy is vast and many of them feel nothing but sorrow for the painful lives their children now lead.
Robert H Hilley IV http://www.roberthilley.com

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Double Outlet Right Ventricle

Morphology

Double outlet right ventricle (DORV) is a partial abnormality of ventriculoarterial connection and intracardiac ventricular septation. It is a congenital anomaly in which both great arteries arise wholly or in large part from the right ventricle. Both the arrangement of the atrioventricular valves and the ventriculoarterial connections are quite variable, and lie somewhere in between those noted in the tetralogy of Fallot and those in D-transposition. The aorta and main pulmonary artery are dextrorotated from the normal arrangement, and are classically side-by-side or nearly so. There is often both a subaortic and a subpulmonary infundibulum, in contrast to classic tetralogy of Fallot in which there is only a subpulmonary conus, or to D-transposition in which there is only a subaortic conus. The great vessel relationships also lie somewhere in between that of the tetralogy of Fallot and of D-transposition, resulting in both aorto-mitral and aorto-tricuspid discontinuity.

The actual diagnosis of DORV takes into account the morphology of only a very small part of the heart, namely that of the ventriculoarterial junction. There are numerous additional abnormalities of atrial arrangement and atrioventricular connections, any of which can be associated with the abnormal ventriculoarterial connection. When present, these anomalies, such as atrial isomerism or discordant or double-inlet atrioventricular connections, dominate the clinical picture and are referred to in other sections. Only the largest subset of double outlet ventricle are considered in this section, those with the usual atrial arrangement and concordant atrioventricular connections. Within this subsets, there are many anatomical variants, the most important variable feature being the location of the ventricular septal defect. The location of the ventricular septal defect forms the basis for both a morphological and operative classification, although within this spectrum of variability, any position of the aorta can combine with any position of the main pulmonary artery and any location of the ventricular septal defect thereby creating an infinite number of morphological possibilities. Only rarely is DORV found in the presence of an intact ventricular septum, and in almost all such circumstances the features would suggest that intrauterine or postnatal closure of a preexisting ventricular septal defect took place.


The ventricular septal defect was classified by Lev as being subaortic, subpulmonary, doubly-committed, and noncommitted.

a) Subaortic ventricular septal defect. Double outlet right ventricle with subaortic ventricular septal defect is the most common sub-type, and is morphologically a close cousin to tetralogy of Fallot. The ventricular septal defect, which is the primary outlet from the left ventricle, is located beneath the outflow tract supporting the aortic valve, and as in the tetralogy of Fallot, is positioned between the limbs of the septomarginal trabeculation. In this setting, the leaflets of the aortic valve often override the crest of the ventricular septum, and there can be doubt about which ventricle the aorta is most connected to, particularly when the morphology of tetralogy of Fallot is also present. Then, although there is discontinuity between the aortic valve and both atrioventricular valves, there still remains fibrous continuity between the mitral and tricuspid valves - that is, for the ventricular septal defect to be perimembranous. This feature is of surgical importance, since it indicates that the conduction tissue is closely related to the margin of the interventricular communication at its postero-inferior rim. Only rarely with a subaortic interventricular communication is there discontinuity between the mitral and tricuspid valves. Irrespective of the infundibular morphology, the interventricular communication is the only direct outlet of the left ventricle. Therefore, stenosis of the interventricular communication effectively produces subaortic obstruction although there is, of course, free access to the aortic outflow tract from the right ventricle. In the majority of cases however, the subaortic outflow tract is widely patent from both ventricles, and the outlet septum, which in this setting is an exclusively right ventricular structure, is deviated in antero-cephalad direction to produce subpulmonary obstruction. Almost always the arterial trunks are normally related when the interventricular communication is subaortic, or side-by-side with the aorta to the right. In one rare variant, however, the aorta can be anterior and to the left of the pulmonary trunk (with usual atrial arrangement and concordant atrioventricular connections). Although the ventricular septal defect is almost always in subaortic position with this rare pattern, making it possible in most cases for the surgeon to connect the aorta directly to the left ventricle, the septal defect can rarely occupy the locations to be described below when the aorta is left-sided.

b) Subpulmonary ventricular septal defect. With this arrangement, the ventricular septal defect is between the limbs of the septomarginal trabeculation, but in a subpulmonary (rather than a subaortic) location. This pattern, the second most frequent, is associated with parallel alignment of the arterial trunks, the aorta being to the right and slightly or markedly anterior to the pulmonary trunk. It is the orientation of the outlet septum, an exclusively right ventricular structure, that is the central feature, and the resulting lesion is usually described as the Taussig-Bing heart. Such hearts exhibit a spectrum of malformation determined by the precise connection of the overriding pulmonary valve. In most cases, there is mitral to tricuspid discontinuity, so that the defect has a muscular postero-inferior rim. Rightward deviation of the outlet septum producing subaortic obstruction is also frequent, as is aortic coarctation. Straddling and overriding of the mitral valve is the other malformation frequently associated with this pattern of DORV.


c) Doubly-committed, juxta-arterial ventricular septal defect. This subgroup of double outlet right ventricle is also closely related to tetralogy of Fallot. The central feature of this subgroup is complete absence of the muscular outlet septum, so that there is fibrous continuity between the facing leaflets of the aortic and pulmonary valves. The large interventricular communication is located immediately beneath both the aortic and valves, which have a marked tendency to override. The defect can be associated with mitral - tricuspid continuity and therefore be perimembranous, or with mitral - tricuspid discontinuity, and have a muscular postero-inferior rim. Reminiscent of the tetralogy of Fallot, the raphe between the arterial valves is deviated in an antero-cephalad direction to produce pulmonary stenosis with overriding of the aortic valve. Hence, this variant can be diagnosed as tetralogy of Fallot, although it is best considered as DORV with a doubly-committed and juxta-arterial ventricular septal defect, and describe the mode of ventriculoarterial connection.

d) Noncommitted ventricular septal defect. This is the most complex variant of double outlet right ventricle. Most commonly, the defect is noncommitted because it is perimembranous and opens into the right ventricle beneath the septal leaflet of the tricuspid valve, or because the tension apparatus of the atrioventricular valves is interposed between the margins of the defect and the subarterial outflow tracts. The surgical correction of these variants is quite difficult, and complete repair may not be possible. Rarely is the defect noncommitted because it is within the inlet or apical trabecular components of the muscular septum. To this extent, there is a conflict between the anatomical and functional definitions of a noncommitted defect. What is anatomically a committed defect may be rendered noncommitted functionally because of the interposition of vital structures, usually a valvar tension apparatus, between the defect and the arterial valves. These features are of profound surgical important, and must be taken into account in order to decide when a defect is noncommitted or subarterial.

Hemodynamics

The hemodynamics are dependent on the position of the ventricular septal defect, the relationships of the great arteries, and the presence of associated cardiac malformations, such as outflow obstruction and atrioventricular valve abnormalities. Variable degrees of cyanosis are present in all patients, depending on the location of the ventricular septal defect and the volume of pulmonary blood flow. Patients with DORV and unrestricted pulmonary blood flow have hemodynamics indistinguishable from those with an nonrestrictive ventricular septal defect; those with pulmonary stenosis have hemodynamics analogous to tetralogy of Fallot; and those with subaortic stenosis (Taussig-Bing heart) have hemodynamics similar to transposition of the great arteries with a large ventricular septal defect.

Clinical Findings

The clinical findings are also quite variable, although most patients present in early infancy. Patients with double outlet right ventricle and pulmonary stenosis present analogously to those with tetralogy of Fallot, cyanosis may be initially mild but may progress, and young infants may exhibit cyanotic spells. Patients with a large nonrestrictive ventricular septal defect and no outflow tract obstruction usually present at around 3 months of age with congestive heart failure and minimal signs of cyanosis, and finally those with double outlet right ventricle, unrestricted pulmonary blood flow and left ventricular outflow tract obstruction may present with severe congestive signs and poor peripheral perfusion.
Echocardiography localizes the position of the ventricular septal defect, demonstrates the relationships of the outflow tracts and the presence of obstruction(s) if present, and defines any atrioventricular valve abnormalities. Importantly, echocardiography is able to assess the tricuspid-pulmonic valve distance, and define the presence of straddling atrioventricular valves. Cardiac catheterization is performed to further define the anatomy, to obtain data on pulmonary vascular resistance and to identify coexistent conditions.

Medical & Surgical Management

Palliative operative procedures include pulmonary artery banding in cases of excessive pulmonary blood flow, and placement of systemic-pulmonary shunts in cases of pulmonary outflow tract stenosis. Palliative procedures are currently utilized only in cases in which definitive correction is anatomically not feasible. The goal of corrective operative management is to achieve a biventricular repair, in which the left ventricle is connected to the aorta, and the right ventricle to the main pulmonary artery. There are three main variables to be considered when deciding upon the most suitable operation, these being the location of the ventricular septal defect, the degree of tricuspid - pulmonary discontinuity, and the presence of right or left ventricular outflow tract obstruction. Often time, the decision on which operation to perform depends on the intraoperative findings.

Repair with subaortic or doubly-committed ventricular septal defect.

In the spectrum of double outlet right ventricle that is tetralogy of Fallot-like, namely in the presence of a subaortic or doubly-committed, juxta-arterial ventricular septal defect, and adequate tricuspid - pulmonary discontinuity to allow for an unobstructed intraventricular baffle, (usually at least equal to the diameter of the aortic annulus), a Kawashima intraventricular repair can generally be performed, in which the ventricular septal defect is baffled directly to the aorta by use of a tunnel.[306, 310] When the morphology is not favorable for an intraventricular repair, due either to insufficient tricuspid - pulmonary discontinuity or to pulmonary stenosis, then the pulmonary valve may be sacrificed in order to gain sufficient space to place an intraventricular baffle. Right ventricular to pulmonary artery continuity is then established by a conduit, the so-called Rastelli operation. Three other operations, not in common use include réparation à l’étage ventriculaire (REV operation)[61], Nikaidoh’s aortic translocation operation[54], and the pulmonary translocation operation. These operations are described in greater detail below. Resection of the outlet septum or enlargement of the ventricular septal defect may also be necessary to avoid outflow obstruction.

Repair with subpulmonary ventricular septal defect.

In the spectrum of double outlet right ventricle that is D-transposition-like, namely that there is a subpulmonary ventricular septal defect and insufficient tricuspid - pulmonary discontinuity, two options are available for complete repair without the use of a conduit. These include the arterial switch operation, in which an intraventricular patch diverts blood from the ventricular septal defect to the pulmonary valve and a standard arterial switch operation is performed[53], and the pulmonary translocation operation, (see below). A third option is the Damus-Kaye-Stansel operation, in which an intraventricular patch diverts blood from the ventricular septal defect to the pulmonary valve, the main pulmonary artery is divided at its bifurcation, the proximal end is anastomosed to the ascending aorta, and the right ventricular outflow tract reconstructed with a valved conduit from the right ventricle to the distal divided end of the main pulmonary artery. Resection of the outlet septum or enlargement of the ventricular septal defect may also be necessary to avoid outflow obstruction.

Repair with noncommitted ventricular septal defect.

The most common form of noncommitted ventricular septal defect is the atrioventricular septal defect, which extends under the septal leaflet of the tricuspid valve. Several authors have suggested that when this defect occurs with pulmonary stenosis, (which thereby precludes an arterial switch operation), the procedure of choice is patch closure of the ventricular septal defect with creation of a generous anterior and superior extension. The ventricular septal defect extension is then baffled to the aorta as for the standard intraventricular repair described previously. However, in view of the known tendency for surgically created ventricular septal defects to close spontaneously, as well as the inherent risk of creating subaortic stenosis with the tunnel repair, this approach is generally best avoided.
Certain anatomic forms of double outlet right ventricle require surgical approaches that are more closely related to those used for management of a functional single ventricle[538]. In these forms of double outlet right ventricle, the right ventricle is quite hypoplastic, and the defect results in essentially a single functional ventricle. In this subgroup, there is frequently a straddling tricuspid valve and sometimes a superior-inferior ventricular relationship. In other forms of double outlet right ventricle the left ventricle is hypoplastic, and frequently there is hypoplasia or atresia of the mitral valve. However, in still other patients there are two relatively well-formed ventricles, but the ventricular septal defect is of the atrioventricular septal defect type, and construction of a baffle to divert the left ventricular output to the aorta may be extremely difficult without disruption of the tricuspid chordal attachments and anterior enlargement of the ventricular septal defect. Under all of these circumstances, a univentricular palliation may be elected. When a univentricular palliation is considered, the critical surgical features are the function of the atrioventricular valves and obstruction to outflow from both ventricles into the aorta. There is a high incidence of obstruction to either the aorta or the pulmonary artery in patients with double outlet right ventricle, in addition, straddling tricuspid valves and common atrioventricular valves are not infrequently regurgitant in patients with double outlet right ventricle.

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Murmurs, Arrythmias, Heart Disease, & Failure

Author: Linda Mar Veterinary Hospital
Basic heart function
The heart is divided into four chambers. The right atriumreceives unoxygenated blood which then goes past the tricuspid valve into the right ventricle. From here, blood is pumped into the lungs through the pulmonic arteries as it passes by the pulmonic valve. Blood flows to the lungs where it is oxygenated. The blood returns via pulmonary veins into the left atrium. From here, blood flows past the mitral valve into the left ventricle. From here, blood is pumped out to the rest of the body via the aorta as it passes by the aortic valve. This sequence of events is coordinated by an electric impulse triggered by the SA node to result in a regular rhythmic lup-dup of the heart as it consistently relaxes and contracts.
Heart disease results from any abnormality of the heart. While heart disease can result in heart failure, it can be present and never lead to heart failure. Murmurs can be associated with heart disease that may be minor or serious in nature. Arrythmias are usually associated with serious heart disease. The heart disease may or may not necessitate treatment.
Heart failure is the end-result of heart disease and occurs when the heart is decompensating from its heart disease and is working inefficiently to cope with the body's needs. It is associated with signs of congestion/edema, poor perfusion and low blood pressure. This condition always necessitates treatment.
Signs
Some pets may have significant heart disease without signs. However, their condition can change quickly with stress or exertion as the heart starts to fail.
Most dogs with significant heart failure will show some or all of the following signs- coughing, especially at night, fatigue, tiring with exercise, a change in gum color from pink to a bluish color, difficulty breathing or rapid, shallow breathing at rest. These signs occur due to accumulation of fluid in or around the lungs and in the abdomen.
Most cats, however, show no signs before complete failure occurs. They can go from being apparently normal cats to open mouth breathing or fast, shallow breathing or having inabilityto use their legs when they have a clot (emboli) originating from the heart that lodges in their aorta. Cats can also suddenly die at home and pass away before anything can be done to help them.
Problems with the heart
Arrythmias
These may be primary, that is, associated with the heart directly and resulting from a heart condition. Arrythmias can also be secondary to problems with other organs in the body or occur in reaction to toxins or anesthesia.
Arrythmias may be heard during a routine physical exam where the animals shows no outward signs of a problem; they may be heard when an animal presents for fatigue, collapse or "seizure" like signs.
Arrythmias are categorized according to the chamber with which they are associated. Arrythmias of the atrium are called supraventricular, while arrythmias of the ventricles are called ventricular. Bradyarrythmia is a decreased heart rate, while tachyarrythmia is an elevated heart rate.
Murmurs
Murmurs result when there are changes within the heart. These can be from thickening of the valves (endocardiosis), narrowing near the valves (stenosis), thickening or thinning of the chambers (cardiomyopathy) or infection of the heart (endocarditis).
Murmurs may be heard during a routine physical exam where the animal has no symptoms of a problem (asymptomatic). Murmurs may be heard when the animal is showing signs of heart failure (fatigue, difficulty breathing, fainting or coughing).
Sometimes, with soft murmurs in puppies and kittens, they can be "innocent", that is, they will eventually disappear and cause no problems for the animal. A murmur that develops later in life, after six months of age, is more likely to be from disease. Murmurs are graded in loudness on a scale from 1 to 6, one being a soft, barely heard murmur to six being able to be heard without a stethoscope. While murmur loudness is useful in its description, it often doesn't correlate directly with the severity of the heart problem.
Murmurs can indicate a primary heart problem or can be secondary to other conditions such as anemia in dogs and cats (when the blood is thin and more prone to turbulence) or hyperthyroidism in cats (when having elevated levels of thyroid hormone put an excessive strain on the heart).
Congenital Heart Conditions
Animals can be born with a heart condition resulting from a congenital malformation. These are seen in young animals and can be hereditary. For this reason, these animals should not be bred. Certain breeds of dogs and cats are more likely to have certain congenital heart conditions, but even mixed breeds can be affected. Some common congenital heart defects are:
Patent Ductus Arteriosis (PDA)
A shunt is present in the fetal state that fails to close in the young animal, resulting in a direct connection between the pulmonary artery and aorta. The flow of blood is usually left-to-right; occasionally, though, if pressure builds up in the lungs, the flow can be right-to-left. These conditions are treated differently.
Pulmonic Stenosis and Aortic Stenosis There are areas of constriction or narrowing near or at the pulmonic or aortic valves.
Atrial Septal Defect (ASD) and Ventricular Septal Defect (VSD)
There are openings due to an incomplete wall between the two atria or two ventricles.
Mitral or Tricuspid Valve Dysplasia
There are malformed mitral or tricuspid valves that result in abnormal blood flow.
In general, subaortic and pulmonic stenosis and patent ductus arteriosus are the most common congenital abnormalities in dogs, and ventricular septal defect and tricuspid valve dyplasia are the most common congenital abnormalities in cats.
Hernias
Peritoneopericardial diaphragmatic hernias refer to the condition in which an animal is born with an opening of the diaphragm and the pericardial sac, allowing herniation of abdominal contents into the chest cavity and into the sac that surrounds the heart.
Acquired Heart Conditions
Most heart disease in animals is acquired, that is, associated with a condition that develops over time. Certain breeds of dogs and cats are more likely to have certain acquired heart disease.
The most common conditions are:
Mitral valve disease (MVD)
This occurs when there is thickening of the mitral valve on the left side of the heart; this results in abnormal blood flow. It is also known as mitral regurgitation.
Cardiomyopathy
These are disease of the heart muscle. This condition is common in older small breed dogs.
  • Dilative, the most common form in dogs, is when the chamber walls are thin and the chamber size is enlarged. There is a higher incidence in Boxers, Doberman pinschers, Cocker spaniels and Great Danes.
  • Hypertrophic, the most common form in cats, is when the chamber walls are thickened, and there is less room for blood inside the chamber.
  • Restrictive and mixed forms of cardiomyopathy are two other forms that can occur in cats.
Pericardial disease
This refers to accumulation of fluid in the sac that surrounds the heart (pericardial sac); this can occur from cancer, trauma, infection or for no known reason (idiopathic).
Heartworm disease
This can occur in dogs and is acquired via mosquitoes; cats living in areas frequented with mosquitoes carrying the heartworm larvae can occasionally acquire this disease. Heartworms, left untreated, will lead to heart failure.
Cardiac tests
Tests are required to differentiate between the different forms of heart disease and indicate what type of treatment is needed.
Radiographs
These show the overall heart size and arteries and veins of the lungs. It can show if one side of the heart is larger than the other and suggest what chambers may be enlarged. It can also check for the presence of fluid associated with the lungs (pulmonary edema or effusion) and for the presence of abdominal fluid (ascites) and other organ enlargement, especially, the liver.
Echocardiogram
This is an ultrasound of the heart, the most useful test there is to determine the presence and type of heart disease. Itallows for the measurement of the chambers (the wall thickness) and for the evaluation of heart valves' efficiency. It indicates overall heart performance and helps to dictate what type of treatment is needed. Follow-up echocardiograms show if the treatment is working or not.
Electrocardiogram (ECG or EKG)
This shows the heart's rate and rhythm and helps to determine what type of arrythmias are present. It can also suggest if there is chamber enlargement.
Blood and urine tests
A blood panel and urine test showing organ function is valuable in evaluating the body as a whole. Sometimes, the heart can affect other organs; sometimes, the animal has concurrent disease. It is important to have a "baseline" of the body'sfunction, before heart medication is started. Some values, especially kidney function and electrolytes, may need to be rechecked over time once treatment is started.
Blood pressure
Hypertension can occur with both heart and kidney disease and can make the animal's condition worse. High blood pressure is treatable and it's control may help the pet's heart condition.
Monitoring
Home monitoring
Since a pet is more relaxed at home, heart and respiratory rates taken at home are more accurate than those in the hospital. It is important to learn to monitor a pet's breathing pattern since this can be a clue of fluid accumulation in the chest and even a pet's heart rate can indicate if the heart disease is under control or not.
A heart rate can be measured by placing a hand on the pet's chest and inside the thigh to feel the femoral artery. An inexpensive stethoscope can serve this purpose also. Count the
heart rate for 15 seconds and multiply the number by four to get the number of beats per minute. Similarly, the respiration rate can be counted. A normal resting heart and respiratory rate for a dog, respectively, is 100-120 beats per minute and 12-20 respirations per minute. A normal resting heart and respiratory rate for a cat, respectively, is 120-160 beats per minute and 24-32 respirations per minute.
Hospital monitoring
Rechecks for radiographs to evaluate lung changes, ultrasound to evaluate heart function, rechecks of blood pressure levels, and blood and urine tests to evaluate organ function while on medications are all important to assuring the pet a good quality of life while coping with heart disease or heart failure. The goal is to make the heart last longer and prevent complications of heart disease and failure by giving daily medications.
Treatment
Treatment is usually medical and is directed at helping the heart cope with the results of its inefficient state. There are many human drugs that are used to manage pets with heart disease and in heart failure. However, is surgery is rarely of help; only in patients with left to right patent ductus arteriosis (PDA) may benefit from surgery.
Diet
Since sodium/ salt can retain water and further increase work on the heart, feeding a prescription low sodium diet is recommended for pets in heart failure. However, it does not appear to be beneficial in preventing heart failure. Diet changes for a pet with heart problems include not feeding salty snacks and commercial dog and cat foods since they tend to have a lot of sodium. However, low sodium diets are less palatable, and some pets refuse to eat them. Examples of low-sodium prescription diets are: Hill's H/D for dogs and Purina's CV for cats. For dogs, there is also a home-made diet formulation.
Diuretics
This is a class of drugs that result in increased urine output as they "draw" fluid out of the lungs. Examples of commonly used drugs are lasix (Furosemide or Disal), spironolactone
(Aldactone) and hydrochlorothiazide (Chlorothiazide). These drugs are overall safe, but animals must be monitored for dehydration, electrolyte imbalances and for the worsening of kidney failure, if present.
Angiotension converting enzyme (ACE) inhibitors
This is a class of drugs that reduce the work load on the heart and lower blood pressure. Examples of commonly used drugs are enalapril (also known as Vasotec or Enacard) or benazapril (Lotensin). These drugs are overall safe, but animals must be monitored for negative effects on the kidneys and excessive lowering of blood pressure.
Digitalis
This is a class of drugs that increase the strength of contractions of the heart. They also have anti-arrythmic effects and are used to control supraventricular arrhythmias. Examples of commonly used drugs are digoxin (Lanoxin) and digitoxin (Crystodigin). These drugs can be toxic and must be used carefully. Blood levels can be monitored as a guide to dosing the drug. Excessively high levels can cause a decreased appetite, kidney dysfunction or ventricular arrhythmias.
Calcium channel blockers
This is a class of drugs that relax the heart tissue and decrease the rate of an excessively fast heart rate, such as in cases of hypertrophy, so the heart can fill more efficiently. They can also be used to treat hypertension. Examples include dilitazem (Cardizem) and amlodipine (Norvasc). These drugs are overall safe but blood pressure must be monitored.
Beta adrenergic blockers
This is a class of drugs that decrease the heart rate and relax the heart muscle in cases of hypertrophy. Examples include atenolol (Tenormin) and sotalol (Betapace).
Oxygen therapy
While it is helpful in an emergency situation for a pet in fulminant heart failure in a hospital, it is not practical for home application.
Nutritional supplements
Taurine- in the past, taurine deficiency was a common cause of dilated cardiomyopathy in cats. Due to supplementation in cat foods, it is a rare condition now. Some forms of dilated cardiomyopathy in dogs, especially that occurring in Cocker spaniels, can be responsive to taurine supplementation.
Carnitine- Some dogs, especially Boxers with dilated cardiomyopathy, may benefit with supplementation of carnitine.
If you have questions regarding this disease, please don't hesitate to call your veterinarian.
The above is general veterinary information. Do not begin any course of treatment without consulting your regular veterinarian. All animals should be examined at least once every 12 months.


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