|Cardiomyopathy In Your Dog|
|Subaortic Stenosis In Your Puppy|
|Pulmonary Hypertension And Right-Side Heart Failure|
|Heart Disease In Your Dog|
This is one of several articles I have written over the years about the various heart problems that your dog might face. This particular one describes the most common heart problem that occurs in our small, medium and toy dog breeds, and in mixed breed dogs of similar size. It is called Congestive Heart Failure or CHF because the end result is unacceptably poor blood flow (poor circulation = congestion).
Your pet’s heart is a complex organ. Many things can go wrong with it - but eventually they all tend to lead to CHF.
The most common cause of CHF in dogs is a heart valve that does not work properly. Another article of mine describes Canine Dilated Cardiomyopathy (DCM), a problem more common in larger breeds of dogs (ref). DCM often leads to the same congestive heart failure described here. Still another article on subaortic stenosis, describes an inherited heart condition that sometimes occurs in puppies. (ref) Subaortic stenosis or SAS also leads to congestive heart failure. An older article of mine discusses heart problems in general in dogs and cats. (ref) If you read them, you will find that much of the information in them repeats. That is because all failing hearts are destined to go through similar stages of decline - regardless of the initial cause. The end result of heartworm infection is CHF as well. (ref)
The most common cause of heart failure in people and the most common cause of heart failure in dogs are quite different. In us humans, it is damage to the heart muscle itself due to blocked coronary arteries (ref) (a heart attack [ref] ) that usually begins the process of CHF. For reasons unknown, dogs and cats are extremely resistant to coronary artery disease. When we become overweight, our coronary arteries tend to clog. When our dogs become overweight they are subject to chronic generalized (systemic) inflammation and diabetes - but not heart attacks. (ref)
As I mentioned earlier, in our dogs heart failure is most commonly due to malfunctioning of the valves that direct blood flow through the heart (particularly the mitral valve). (ref) Even though people and dogs develop heart disease for different reasons, the mechanics and results of what is occurring in your pet’s heart is very similar to what occurs in a damaged human heart. Because of that, all of the medications your veterinarian or your physician relies on and all of the techniques he/she uses to diagnose the problem are the same.
Your dog's circulatory system is highly complex. Its proper function relies on complicated interactions between messenger chemicals, hormones, nerves and organs. I am going to try to keep my explanations as simple and readable as I can. If you want more depth, many pdfs on the web cover heart and circulation in considerably more detail.
The heart of all mammals and birds is made up of four chambers (reptiles have only 3 - two atria and one partially divided ventricle, fish and amphibians only two). The upper left and right chambers are called the atria (atrium) and the lower left and right chambers are called the ventricles. Each of the four chambers has an inlet and an exit valve to prevent back-flow of blood. In smaller and medium size breeds of dogs it is these valves – particularly the mitral valve which divides the left atrium from the left ventricle - that often fails first. That leads to an enlarged, inefficient heart. You can enlarge the first diagram at the top or go to it here to understand the anatomy of your dog's heart and see the mitral valve better.
Blood returning from your dog's body enters the right atrium (RA) chamber. I marked it RA on the diagram. At this point, the blood needs to be re-loaded with oxygen. When the RA contracts, the blood is squeezed through a valve, the tricuspid valve (TCV), into the lower right chamber, the right ventricle (RV). When that chamber contracts, the blood is squeezed through another valve, the pulmonic valve (PV or pulmonary semilunar valve), and on into an artery that lead to your dog's lungs (PA or pulmonary artery). In the lungs, the blood is re-oxygenated and CO2 is removed. The blood then flows back to its heart through the pulmonary veins (PulV) and arrives in the left upper chamber, the left atrium (LA). When the left atrium contracts, the blood is squeezed into the lower left and strongest heart chamber, the left ventricle (LV). To get there, the blood must pass through another valve, the mitral valve (MV). I mentioned that the mitral valve tends to be the one that fails first.
When the left ventricle is full, it contracts. Its enormous muscular power forces the blood through another valve, the aortic valve (AV), on down the aorta (A) and throughout the dog's body. This contraction is the pulse you feel in your pet’s groin or chest and which your veterinarian hears through his or her stethoscope.
These four chambers to not fire one after another like a car motor. They all work together in rhythmic waves to keep the blood flow continuous. When the powerful left ventricle contracts, blood pressure is at its highest (systolic blood pressure ). Between contractions it is at its lowest (diastolic blood pressure).
Animate The Heart's Electrical System:
There has to be a bandmaster to coordinate the heart’s contractions. The signals for heart muscles to contract are electrical signals and the heart contains a system of wire-like nerves (perkinje fibers) to distribute those signals.
It all begins in a small area at the top of the right atrium. (the yellow bean-shaped structure in my fanciful animation) There, a structure called the sino-atrial node (SA Node) rhythmically fires off an electrical pulse. It is somewhat like a metronome. The signal first reaches the muscles of the upper chambers (atria); so they contract. Then it reaches another node, the AV node, that is located near the bottom of the right atrium. The AV node passes the electrical pulse to the ventricles causing them to contract and force blood on its way to the lungs or body. So the initial pacemaker for the whole system is the SA node. The heart won’t stop beating if the nodes fail – but it will not pump blood efficiently.
When the electrical system fails, heart blocks, abnormal pulse rhythms, and uncontrolled quivering (fibrillation) of the heart (or portions of it) occur. These electrical signals are what are measured by an electrocardiograph (ECG aka EKG).
I mentioned that we do not know why dogs do not develop plaque in the arteries of their hearts leading to heart attacks in the way it occurs in people. And that Instead, it is the valves directing the flow of blood through the heart that tend to wear out. About three-quarters of heart problems in dogs are due to heart valve problems.
Any valve, or multiple valves, can wear out; but the most common one to wear out first is the mitral valve – the one that must close before the pet's left ventricle can force blood throughout its body. Its job is the hardest of the four valves because the pressure difference across this valve is the greatest of all the valves every time your pet's heart beats.
When the mitral valve no longer opens and closes fully, the dog's heart begins to changes in shape and increase in size. Pressure in the wrong locations causes its walls to become thinner. And as the heart’s shape changes and it stretches, other valves no longer close properly. In dogs that have been diagnosed with a mitral valve problem (mitral insufficiency), cardiologists often find that the tricuspid valve between the right atrium and right ventricle is also dysfunctional - not opening or closing completely.
Mitral valve, or mixed valve, problems are given many different names. Some are: "acquired mitral regurgitation", "mitral insufficiency", "mitral valve prolapse", "mitral/tricuspid valve regurgitation", "leaky valve disease", "chronic valvular fibrosis", "endocardiosis" and "mucoid valvular degeneration". They all describe different aspects of the same underlying problem. In these dogs, the two flexible portions (cusps) of the mitral valve become stubby, thickened or lumpy (nodular) and no longer open and close satisfactorily. When this happens, something akin to backfire occurs (the valve "regurgitates") and blood flows in the wrong direction.
Heart valves and their thready nest of attachments (ref) are an excellent place for bacteria that have entered a dog's blood stream to become trapped – particularly if the valve is already somewhat misshapen. Many suspect that pets with severe dental disease - a source of infection - have mitral murmurs more frequently than those that don’t. Dentists have noticed the same thing. (ref) Dog studies confirm it. (ref) I have seen heart murmurs disappear in pets after a course of antibiotics.
In many cases, valve problems result in heart murmurs that your veterinarian can detect on a routine examination. However, not all heart murmurs lead to CHF. When heart murmurs are detected, other tests need to be run to determine if the murmur is something you should be concerned about or not. Anemia, valve infections (endocarditis), hyperthyroidism, fever and pregnancy have all be known to cause heart murmurs. Quirks in heart anatomy and anatomical heart defects can also cause them. When nothing major is found to be wrong, these are called innocent heart murmurs.
The majority of dogs 8-10+ years of age have these defects to varying degrees. At first, the leak is minor and produces no more than a high-pitched murmur with no health problems. When it is the mitral valve producing the murmur, it is most audible on the left side of the chest just behind the dog’s elbow.
In some breeds, such as Cavalier KC Spaniels, increased susceptibility to valve heart disease is thought to be an inherited genetic defect.
When the powerful left ventricle contracts to force blood throughout the dog's body but the mitral valve can not stand up to the pressure, it leaks blood back into the left atrium (regurgitation). When that happens, the freshly oxygenated blood coming from the lungs has nowhere to go. The left atrium, where the blood was headed, is already too full with blood that should have moved from the left ventricle to the general circulation through the aorta. Pressure increases in that part of the circulation (increased pulmonary pressure, pulmonary hypertension). The lungs expand with this blood and some of it leaks out (pulmonary edema) through the lung's small capillaries and into the small spaces normally filled with air (the alveoli). This doesn’t happen independently. As the valves deteriorate, the heart also enlarges to try to keep up with its increasing workload. The enlarged (hypertrophied) heart begins to press on your dog’s windpipe. This, plus the excess fluid in its lungs, is the cause of its cough.
The right side of the heart deals with blood returning from the body. With time, the tricuspid valve which separates the right upper chamber (atrium) from the lower one (right ventricle) will also fail. When this happens, blood backs up into the venous side of the system, pooling fluid and leading to large, pear-shaped, bellies (ascites). The belly enlargement is not all due to free fluid – the dog's liver and spleen also become congested with blood and enlarge.
These events cause all sorts of things to happen. The pet’s heart rate speeds up (tachycardia). Enzymes are released that constrict blood vessels (increased vascular resistance and tone) of all blood vessels. Chemical changes occur as well - (angiotensin-converting enzyme or ACE, angiotensin II) and rising aldosterone hormone levels result in fluid and sodium retention. These events make the pet's pulmonary edema problem worse.
These events occur slowly and at different rates in different dogs. Dogs with mild to moderately enlarged hearts often show no signs at all. The first sign might be just a little reluctance on the part of your pet to play as actively as it once did. When an actual problem finally occurs, it is usually a dry cough accompanied by gagging. These coughs tend to be worst when the dog is lying down and at rest.
As the condition progresses, and as pressure builds up in the heart, first the left side and then the right side of the heart begin to enlarge. This enlargement is not accompanied by any increase in blood pumping efficiency. The more the heart enlarges, the less the four valves of the heart are able to seal themselves during each contraction.
Most pet owners find out that their dog has a heart murmur during one of its yearly routine health checkup. A listen with a stethoscope should always be part of your dog’s yearly health examination. When a heart murmur is detected, vets make other observations and will probably suggest some additional tests even though your pet appears to you to be completely healthy.
What you tell your veterinarian about your pet (its medical and life history) is just as important as your veterinarian's examination. As I mentioned before, most dogs that are developing CHF have subtle clues that something is amiss. Veterinarians rely on what you tell them about your dog to gather much of their decision making information. When a pet is relaxed at home it often shows symptoms that it doesn't exhibit during an office call. There are certain buzzwords that set a veterinarian off to thinking about your pet’s heart. Some of those are: “more tired than usual” “less active” “chronic cough” “panting” and “gagging”. Some of these pets have trouble finding a comfortable sleeping position at night. Some are graying prematurely around the muzzle. Many get tired climbing steps. Some chill easier due to poor circulation. Since older dogs are most affected, owners might assume that their pet is "just getting old". Others might write it off to age-related mental decline. (ref)
With the dog's history in mind, your veterinarian will begin to examine your pet. He/she will check its gums for evidence of poor circulation (blush gums = cyanosis). Your vet will judge the dog's respiratory rate and the quality and regularity of its pulse; then spend some time listening to your pet’s heart through a stethoscope. Stethoscopes have been around since 1816. But they still provide an amazing amount of useful information. Stethoscopes easily detect heart murmurs and give a clue as to which heart valve, if any, might be involved. Stethoscopes detect excess fluid in the lungs (pulmonary edema) and they judge the adequacy of the heart’s electrical system (detecting arrhythmias). With those results in mind, your vet will check how quickly your pets blood moves through the body using the capillary refill time (CRT) test on its gums.
Dog owners inexperienced in listening to the hearts of dogs, sometimes confuse the normal fluctuations in heart rate (sinus arrhythmia) with abnormal arrhythmias. The heart rates of healthy dogs are more likely to increase with every inspiration than the heart rates of people. Veterinarians assign a loudness number to your pet’s heart murmur when one is present. The faintest murmur is given a 1 and the loudest a 6. By the time a mitral valve murmur is a 6 you can often even feel it over the dogs left chest.
Other dog owners put off seeing their veterinarian until their dog's problem is more advanced and serious. Those dogs have all the symptoms of the prior groups. But they also have a distended pot belly. The gums of their mouth are redder and the blood vesicles in the gums more prominent and spidery (injected). Their gums and tongue may turn purplish (cyanotic) when the dog exerts itself. They may faint. Heart murmurs in these dogs tend to be louder, lungs tend to give sounds that indicate excess fluid (moist rales), a jugular pulse tends to be present, their pulse is weak and thready and their heart rate is elevated (tachycardia). In this advanced stage, the heart beat is often irregular and some beats may not be felt in its femoral area (groin) (a pulse deficit). Although the dog may have an enlarged tummy, its prominent ribs and spine show that its body has lost muscle mass (sarcopenia). Pooled fluids and distended organs can deceptively keep the dog's scale weight deceptively high.
As heart function declines, the pet’s body is able to adjust and compensate for weeks or months. However, at some point, its ability to compensate is no longer effective. At that point, dogs can go into sudden heart failure in what appears to be a matter of hours. Rapid, heavy breathing, blue tongue, excessive drooling, or collapse may be the first time some owners realize how seriously wrong things have become. In the impoverished area of South Texas where I live, many of those cases never see a vet. They are written of to "poisoning" or perhaps "snake bite".
If your veterinarian's physical exam and the dog's history make him or her
suspicious of a heart problem, the next thing to suggest are chest (thoracic) X-rays or an ultrasound examination. The vet needs to see how much space your pet’s
heart occupies in the dog's chest, the shape of the heart and the condition
of the dog's lungs. Failing hearts loose their normal silhouette detail. They also become rounder
(globular) in their outline.
In early CHF, your veterinarian will be looking for evidence that the left atrium is enlarge, If the heart's shadow (its image) occupies more than the 3rd to 6ths rib spaces it is larger than it should be. If an increase in heart mass (size) has pushed the windpipe (trachea) upward, that and lung fluid might account for its cough.
You have probably had one of these multi-wired machines applied to you. They measure the minute natural electrical impulses traveling through the heart. Many veterinarians rely on electrocardiograms (EKG) to detect early heart abnormalities. When the portion of the EKG paper tracing called the QRS complex lengthens and increases in height (amplitude) it signifies left ventricular enlargement. In CHF, heart rates are often faster than normal in the tracing and premature contractions of the ventricles give the tracing an abnormal or irregular rhythm. Interpretation of EKG results can require in-depth training beyond that of practicing veterinarians. Online services are available to assist in that. (ref)
Sometimes, it can be difficult for your veterinarian to distinguish between problems that originate in the heart and problems that originate in the lungs or elsewhere. In those cases, one of two test can be very helpful. These tests detect a marker chemical (a hormone) that is released by damaged hearts. The tests are ones that your regular veterinarian can run before deciding if it would be wise for your pet to be referred to a veterinary cardiologist. Like most test, it has it’s limitations. (ref) It is fine as a rule-out test for heart failure. But results can be in the gray or intermediate area where interpretation is difficult and significance unknown.
Both Antech Diagnostics and Idexx Laboratories, the two largest independent American veterinary diagnostic laboratories, offer tests that detect heart damage. Antech's is called Cardio-BNP and Idexx's is called the proBNP test.
Blood chemistry and urine tests are usually normal until heart disease is well advanced. When any of those routine tests are abnormal, it is usually because organs have become starved for oxygen or congested with pooling blood. Although routine blood tests cannot diagnose heart disease, they do let your veterinarian know how well your pet will tolerate the heart medicines it will be needing.
Visualization of the heart as it is actually beating (realtime) is the most informative way to evaluate heart health.
There are three kinds of machines, M-mode (a single beam) , two dimensional (a cross-sectional "slice" of the beating heart) and 3-D echocardiographs that combines a doppler to assess blood flow. The last is the most sophisticated and, in the hands of a skilled operator, yields the most information.
When one has that training, a great deal of knowledge can be gathered about the current condition of your pet’s heart. Using these machines, each of your pet’s heart valves can be measured as to its thickness and shape. One can also view how far the valve is pushed into abnormal positions as the heart beats (eg valvular prolapse) and how much it fails to open and close. The amount of blood flowing in the wrong direction (regurgitation) and the increased blood volume of a weakened heart are also evident.
No known medications will repair damaged hearts; and stem cell approaches are still in their infancy - their benefits unproven. (ref) What medications will do is allow your pet to live more comfortably for a time.
Veterinarians concentrate on giving your dog medications that help eliminate excess fluids leaking from its sluggish circulation (=diuretics), drugs that decrease the pressure (work load) your dog's heart must pump against (=ACE inhibitors), and drugs that increase the force of its heart contraction (=positive ionotropes like pimobendan). I'll go over them in that order. Late in heart disease or whenever required, we give your dog medications to keep its heart’s electrical system running smoothly. Generally, more than one type of medication needs to be given so that all these problems are addressed.
Diuretics accomplish the first goal. They rid your dog's chest and abdomen of excess fluid ("water"). They do that by encouraging the pet to urinate. They are very effective in lessening coughs and respiratory distress, when lung fluid buildup (pulmonary edema) is the underlying cause. The most commonly used diuretic in dogs is furosemide (Lasix®). Diuretic doses and frequency vary between canine patients depending on the severity of their condition. Giving too much or too frequently during the day can dehydrate your pet or lead to kidney damage.
Furosemide diuretic has been the mainstay treatment for CHF for many years. It is very effective in flushing excess fluid out of your dog's body and, in most cases, causes relatively few side effects. It, like bumetanide (ref), are called loop diuretics because they do their work at small tube loops (loop of Henle) that are present in the filtering apparatuses of your dog’s kidneys. (ref)
Dogs on Lasix, particularly at higher doses, need to have their blood potassium level and kidney function monitored every few months and they need to be observed for dehydration. Pets that start furosemide for heart issues generally stay on it for the remainder of their lives.
The improvement you see in your pet, once it begins taking furosemide, can be dramatic. As fluid drains from its lungs, its cough should rapidly go away and it should breath freer. The amount of fluid pooled in its abdomen should also decrease. Remember however that the drug has done nothing to improve your dog’s heart function. It does its helpful work in the pet's kidneys.
When your dog begins taking furosemide, you will notice that it will drink and urinate more. Do not restrict its access to water – give it all it desires. You will have to make arrangements for it to relieve itself during the night. I have not seen problems when I limit a pet’s access to water in the evening and replace their water bowls in the morning in an attempt to help them sleep through the night – but that is something you need to discuss with your veterinarian. On higher doses of furosemide or other loop diuretics, your dog might require a potassium supplement.
When a high end (near maximum) dose of furosemide diuretic is no longer sufficient to control fluid buildup in your pet’s lungs (pulmonary edema) or its tummy (ascites), another diuretic, spironolactone, can be added to the medications your pet receives. Spironolactone has the advantage of not depleting your dog’s potassium reserves.
You need to be patient. Unlike furosemide, it takes 2-4 days for the full effects of spironolactone to be achieved. Spironolactone can increase the toxicity and effects of digoxin, so if your pet is taking digoxin, its digoxin dose might need to be lowered. Spironolactone can also increase serum potassium which can also be dangerous. To monitor your dog's potassium level, a blood sample needs to be taken and measured for serum electrolytes (and kidney function). That is often done on the 3rd-4th day after beginning the medication, the 7th day and periodically thereafter.
Hydrochlorthiazide or chlorthiazide are alternative options to spironolactone when furosemide is no longer sufficient to keep your dog's fluid buildup under control.
The most common ACE inhibitor used to treat CHF in dogs is enalapril. But benazepril, captopril, lisinopril and other ACE medications are also used. Drugs in this class differ in their absorbability and the stress they put on the kidneys and liver. (ref) Their effects on your dog are not immediate and it can take a week or so before you see improvement.
These medications all decrease the effort your pet’s heart must exert to pump blood throughout its circulation by relaxing and expanding blood vessels throughout the body. They do this by reducing the formation of a hormone in the lungs, (angiotensin II), that increases your pet’s heart work load (peripheral or systemic vascular resistance). Angiotensin II is also bad for failing hearts because it increased the production of a hormone your pet’s adrenal glands produce (aldosterone) that causes sodium and water retention and high blood pressure (the RASS system). In doing so, ACE inhibitors lower blood pressure and decrease salt (sodium) and water retention. Their doses need to be periodically adjusted in response to the improvement you see or desire to see in your dog.
Dogs in heart failure often have fragile kidneys as well. Since ace inhibitors, as well as the diuretics, can occasionally have negative effects on the kidneys (azotemia), kidney function needs to be checked before these drugs are given and then monitored periodically. Doses need to be kept to the effective minimum and the diuretic dose may need to be adjusted downward as the ACE inhibitor dose increases.
ACE-inhibitor medications have the opposite effect of furosemide diuretic, they tend to raise blood potassium - sometimes to dangerously high levels. This is another reason periodic blood monitoring is desirable.
Vomiting and a poor appetite are occasional side effects of ACE inhibitors. Those problems can usually be dealt with without stopping the pet's medication.
Enalapril is approved for once-a-day use in dogs; but seems to work more effectively for me when the pet's total daily dose is divided and given half in the morning and half in the evening. It will occasionally cause nausea, diarrhea and loss of appetite. If the dose is higher than necessary, low blood pressure can occur, leading to listlessness and weakness.
Benazepril (Lotensin®, Fortekor®) is another ACE-inhibitor commonly used in dogs with Congestive Heart Failure. Like enalapril, it is usually given along with a diuretic and like enalapril, it can be given with or without food. The ability of a portion (50%) of the drug to leave the body through the liver perhaps makes it a better choice than enalapril in dogs with kidney disease. All enalapril must leave via your dog's kidneys. In humans, the danger of compounding pre-existing kidney problems appears slightly less for benazepril than for enalapril.
Hydralazine is not an ACE-inhibitor, but it has similar effects. This potent medication dilates blood vessels and in so doing lowers the resistance that the heart must pump against. Because the drug can cause dangerously low blood pressure and a racing heart (tachycardia), it must be used cautiously. It is best given and monitored in an animal hospital setting under close veterinary observation until its effects in your dog become known.
This is currently debated. One might assume that reducing your dog's heart workload before severe damage occurred might postpone that damage. The only study I know of to date in dogs did not find that to be the case. But it was a study of Cavalier King Charles Spaniels - a breed with multiple, genetic, health-related problems.
So some veterinary cardiologists go with their instincts and prescribe ACE-inhibitors before the pet’s heart has deteriorated to the point where the dog needs it - much the way the ACE medications have been used to ward off strokes in humans (ref) Other animal study situations have not found that strategies to be advantageous. (ref)
Pimobendan (Vetmedin®), combined with the other two groups I have already mentioned, has rapidly become a standard first line treatment for congestive heart failure in dogs. All positive ionotropes like pimobendan increase the strength of heart muscle contractions.
Calcium is important in the mechanism of muscle contraction. (ref) The force of heart muscles contraction is related to the amount of calcium ion present in your dogs circulation. Pimobendan increases your dog's heart muscle sensitivity to the calcium that is already there.
Vetmedin also opens up (dilates) blood vessels throughout the body easing resistance and pressure in the circulatory system. That also improves the efficiency with which your dog's heart functions as a pump. In one clinically controlled trial, dogs with congestive heart failure survived on average of (median) 42 days without Vetmedin and 217 days when Vetmedin was part of their treatment.
Digoxin and digitoxin (ref) are two other drugs in the positive ionotrope class. They too increase the force of heart contractions by increasing the heart’s sensitivity to blood calcium, but they have many negative side effects. These include vomiting, depression, refusal to eat and cardiac rhythm abnormalities.
Dogs receiving this medication need to be very closely monitored and their dose finely adjusted to their needs and their ability to tolerate the drug. Digoxin and digitoxin are slightly different, the first is excreted through the kidneys and the second metabolized by the liver. So digitoxin is probably a better choice when a dog's kidney function is poor.
I have seen too many cases of toxicity in dogs to be a fan of either drug. When they are given, it should be under the supervision of a veterinary cardiologist. (ref)
Dogs with irregular heartbeats or fainting episodes (syncope) may benefit from this group of medications. Their use must be carefully monitored and they are usually begun after fainting episodes, or heart beat irregularities detected on an electrocardiogram or through the use of a Holter monitor that records your dog’s heart rate over time.
The best-known drugs in this class are propranolol and atenolol. These medications protect your dog's heart from excessive levels of stress hormones (catecholamines, adrenaline and noradrenaline) often present in the blood of dogs with advanced CHF. In doing so, they lower blood pressure, reduce the heart’s oxygen demand and also help protect against heart beat abnormalities (arrhythmias).
These drugs appear more effective in combating the sudden heart deterioration of Dilated cardiomyopathy and atrial fibrillation when combined with digoxin.
The most commonly used drug in this class is diltiazem. Diltiazem increases the diameter of blood vessels (a vasodilator), increasing blood flow and slowing heart rate. It is used primarily in the acute form of heart failure seen most often in larger breeds of dogs - the dilated cardiomyopathy (ref) I linked to just above.
Theophylline and aminophylline are the most commonly used drugs in this group used in dogs. They work by increasing the diameter of the passages (bronchioles) in your pet’s lungs. Their primary use is in conditions affecting the lungs – not the heart. But they seem to reduce the frequency of fainting in some dogs with CHF.
Cough suppressants are generally not necessary in dogs with CHF. Coughs due to lung congestion need to be treated with diuretics – not masked with cough suppressants. However, if x-rays show that your pet’s lungs are clear of fluid (dry) and the coughing is due to an enlarged heart pressing on its windpipe (trachea), these cough suppressants might be helpful.
We all want to do everything in our power to keep our pets with us as long as we can. Dog food companies know that. But the products they market are not a substitute for the science-based medicines that I have been discussing.
Many pet food companies make low-sodium diets designed for pets with heart failure. They know that you know that low sodium diets are suggested for human heart issues. They sell these only through veterinarians to maximize profits. There are no published studies I know of that confirm their benefits in dogs with CHF. Most contain added taurine and this and that mentioned in the popular press. Taurine has been found to be beneficial in a subset of dogs with cardiomyopathy - but not for dogs with valve-related CHF. The same goes for l-carnitine. Neither of them are toxic so those dog foods are OK to use.
In the few studies available, restricted sodium diets did not pan out (not successful) in lowering blood pressure in dogs. (ref1, ref2) Lowering blood pressure is the chief reason low sodium diets are suggested for humans with heart disease. Dogs and humans are different in that respect but the dog food companies prefer to ignore that.
Still, low sodium diets might be helpful in lessening fluid retention. But you must not restrict your dog's salt intake too severely or too soon into the disease. Sodium is in your dog's blood for a reason. (ref)
Coenzyme Q is a natural substance that is involved in the body’s energy generation. (ref) Its level in our bodies naturally declines as we age. It is found in high levels in the red flesh of mackerel but it is present in tuna and salmon as well. Much of it is destroyed by cooking. It is sold where human supplements are sold. The results of its use in humans with heart disease have been problematic. Some studies found it beneficial but others did not. Some human cardiologists recommend it for heart disease, others feel there is not enough evidence one way or the other.
This is another one of the product out there that there is no harm in giving in reasonable amounts. Your dog might appreciate some lightly cooked, deboned mackerel - I know mine would. Prescription diets designed for heart failure in dogs generally keep coenzyme Q levels high . Perhaps it will do some good.
Omega-3 fatty acid supplements are in the same category. (ref1, ref2) The mackerel is a great source of them as well. If you purchase capsules, buy them at a human health food store so you known they are mercury-free.
Over time, pets with CHF loose weight due to loss of muscle mass (cardiac cachexia). Their abdomens may seem large to you, that is due to a congested liver and pooled fluids, but their ribs and spine become very prominent due to muscle wasting. This is a result of their low cardiac output. It is important that you do everything you can to encourage your dog with CHF to eat. Protein and vitamins needs to be high in its diet. Geriatric pets often have poor teeth – so feeding them their food in a softened, fresh or canned form is often best. You might look into Entyce® as an appetite stimulant. If you want to add your observations on Entyce to my blog, let me know.
When your pet can no longer catch its breath after exertion, or during heart emergencies, supplemental oxygen will help. All pet emergency centers should have sealed cages to administer oxygen. But trips to an emergency center are stressful to your pet and you in themselves. Human home oxygen concentrators work just as well. You can improvise an oxygen “tent” at home for small pets or use an improvised face mask for larger dogs. PURE OXYGEN CAUSES ORDINARY THINGS IN YOUR HOME TO BECOME VERY FLAMABLE. If you contemplate using oxygen at home for your dog, have a human respiratory therapist instruct you in its use. Small canisters of oxygen do not last long and are expensive to refill. But they are another option.
Dogs become very uncomfortable when leaked fluid in their chest restricts their normal respiration. Draining this fluid (thoracocentesis) can give them temporary relief. It it generally done in emergency situations to gain more time for the effects of diuretics, like furosemide to occur.
Diuretic medications will usually remove the excess fluid (ascites) that pools the tummies of dogs with congestive heart failure as well. When diuretics don’t, it is usually because the dog's kidneys are damaged as well as its heart. (ref) When it brings discomfort to your dog, this fluid can also be tapped and drained periodically (abdomenocentesis). However, when that is done too frequently, removing abdominal fluid can deplete the dog's blood albumin reserves.
Our pets can be so happy to see us when we get home that they overexert themselves. As much as your pet may enjoy it, encouraging your dog to work its heart at maximum capacity is not a good idea when CHF is an issue. Modify the style of your play-time and your pets life style to minimize its daily exertion. Its your closeness that means the most to your dog's happiness.
Dogs with mild to moderate heart disease can have a good quality life for many years. Every dog differs in the rate at which CHF advances and no statistics are available for me to provide you with. In humans, half of patients are alive 5 years after a CHF diagnosis. The shorter natural lives of our pets shorten that time. How suddenly the heart problem appeared in your pet tends to predict survival time. The more sudden the onset, the shorter the dog is likely to live. In dogs with dilated cardiomyopathy (DCM) leading to CHF, the average patient survives only 4.2 months. (ref) However, when valve failure is the cause of CHF, pets tend to survive much longer.
Your nursing care, and your veterinarian’s assistance are key factors in maximizing your pet’s lifespan once CHF has been recognized. All dogs on therapy for CHF should be monitored every 3-6 months and their therapy adjusted according to the results. It is wise to include a thyroid hormone check, a blood chemistry panel, ECG, and chest radiographs - but your assessment at home of your pets energy level and general comfort are just as valid indicators of when medications might need to be added, changed or their doses adjusted.
In some parts of the World, it is an option in cases where the anchoring fibers (chordae tendineae) that hold your pet's left upper heart valve (mitral valve prolapse) in place have torn. Veterinarians at Nihon University in Tokyo are perfecting that procedure. (ref) In the USA, I would discuss the issue with cardiologists at the Vet School in Davis CA. (ref)