LONG TERM HEART FAILURE THERAPY
LONG TERM THERAPY FOR HEART FAILURE
When the heart is not able to pump out the volume of blood it receives (“backward failure”) or cannot pump out enough blood to supply oxygen to the body (“forward failure”), the goal is to avoid or resolve a life-threatening crisis. Once the short term disaster is resolved, we look to a more long term therapy plan.
THE BASICS OF SHORT TERM HEART FAILURE
In the short term, the body has an assortment of mechanisms to preserve circulation to the heart and brain and keep blood pressure up. The problem is that these mechanisms evolved for protection against blood pressure drop due to bleeding (as in predator attack). Protection against heart failure is an added benefit in the short term but in the long term problems arise.
So let’s say blood pressure drops. It could be because a predator has taken a bite out of an large blood vessel and there is bleeding or it could be because the heart just is not moving an adequate quantity of blood forward. Either way the tissues of the body need more blood supply and they need it quickly. What does the body do?
So, in short, our heart works harder, our vessels close off, and we retain salt. This is all wonderful but if the heart is weak, it cannot hand the extra blood volume brought on by retaining salt, nor can it push blood through constricted vessels or continue pumping faster and harder all the time.
LONG TERM HEART FAILURE MANAGEMENT
Managing the failing heart is all about creating a balance for what a sick heart can handle and lifting the heart's burden that has been created by the protective mechanisms of the crisis. Our patient should be comfortable and able to perform modest exercise. We want to minimize discomfort due to coughing, fluid build-up, or collapse.
Heart failure can be staged according to the severity of the signs and therapy can be selected from the options reviewed below based on the patient's stage.
In most heart failure scenarios, the heart is unable to handle the blood volume with which it is presented. Fluid backs up and leaks out, creating either fluid in the lung (“pulmonary edema”) or fluid build up in the belly. In the long term, the last thing we want is to retain sodium and give the heart more blood volume to pump.
A sodium restricted diet is helpful in relieving some of the heart’s burden if the pet will eat it. Classically the Hills diet called h/d is the most restricted in sodium but as it is so very bland, many pets will not accept it so k/d or other diets made for kidney disease are used and generally found more palatable. Using purified water for drinking may also help as many areas contain water with high sodium levels.
Poor appetite bodes poorly in heart failure as is loss of muscle tone. One must balance the blandness of the low sodium diet with keeping the pet’s appetite up.
OMEGA 3 FATTY ACIDS
Supplementation with omega 3 fatty acids is currently being researched as a possible treatment for the drastic weight loss (“cardiac cachexia”) that occurs with some cases of heart failure. If a pet enjoys these fishy flavored supplements, this may be a particularly helpful way to encourage appetite.
People often ask how much restriction in exercise they should impose. Some exercise is good for the pet’s well-being and life quality. Avoid exercise that leads to excessive panting or weakness.
A diuretic is a drug that increases urine production. In a heart failure crisis where the lungs are filling with fluid because the heart cannot pump blood in quantities large enough to prevent fluid build-up, diuretics are life-saving. The dose needed for long term comfort is highly individual and may change depending on the stage of disease. Furosemide is almost always the first diuretic used as it is one of the most powerful. It is often used in combination with an ACE Inhibitor or with the newer drug, pimobendan (which strengthens heart contractions), for long term therapy. Spironolactone is another diuretic commonly used especially in patients that do not respond adequately to furosemide alone.
“ACE” stands for Angiotensin Converting Enzyme. We briefly mentioned the Renin-Angiotensin system above. Angiotensinogen is an inactive product made by the liver. It circulates all the time and converts to a substance called Angiotensin I at a rate so slow as to be completely innocuous. When blood pressure drops, special receptors in the kidney detect the drop and release a hormone called “renin.” Renin is a catalyst. It makes the conversion of Angiotensinogen to Angiotensin I happen much faster to create a large amount of circulating Angiotensin I. The final activation occurs in the lung where Angiotensin Converting Enzyme converts Angiotensin I to Angiotensin II, completing the transformation from Clark Kent to Superman.
During an emergency we need Superman but on a day to day basis we want less Superman and more Clark Kent.
By using medication to inhibit Angiotensin Converting Enzyme, we get less sodium retention and we keep blood vessels open. When the heart is overwhelmed by the amount of blood it is asked to pump forward (i.e. it receives more blood than it can pump out), it is very helpful to dilate peripheral blood vessels. Another analogy might involve a freeway system or turnpike with an inefficient tollbooth. Opening up more side streets, reduces traffic on the main freeway. Opening up peripheral blood vessels means less blood volume for the overloaded heart to pump.
One of the effects of the ACE Inhibitor is reduced blood flow through the kidney. The kidney’s normal function depends on receiving good blood flow. Borderline kidney function may suffer from ACE Inhibitor use particularly when it is combined with diuretics (as it usually is for heart failure) thus necessitating monitoring tests for kidney function. ACE inhibitors can also drop blood pressure excessively and may lead to retention of potassium.
This drug is a relative newcomer to the cardiac drug armamentarium. It works by helping the heart pump more efficiently and more strongly. It also dilates blood vessels both going to and from the heart thus giving the "extra" blood a place to go so as not to overload the heart. Relatively stable heart failure patients are commonly started on this medication in addition to a diuretic and sometimes also with an ACE inhibitor.
Dogs are often prescribed digoxin in combination with the above medications. It yields several benefits:
The biggest down side is what is called a “narrow therapeutic range.” This means that there isn’t much leeway between a dose that helps and a toxic dose. Blood levels must be regularly monitored. Upset stomach can be a side effect. Concurrent use of certain other drugs can influence the strength of any given dose of digoxin so it is important for your veterinarian to know of all medications your pet is taking. The advent of pimobendan has made the use of digoxin far less common.
It is important to realize that heart failure is a symptom of a structural heart disease.
LEARN HOW TO CHECK YOUR PET’S RESPIRATORY RATE
A patient with heart failure distress will generally have an increased respiratory rate. A pet with controlled heart failure may have a respiratory rate that is greater than normal. It is very helpful to know what is normal for your pet and check several times daily. Simply watch the number of chest excursions during a 15 second period. A change in respiratory rate is a good sign the pet needs a check up with the vet. If the pet is a cat, be sure the pet is not purring when respiratory rate is checked and do not count panting for dogs.
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Page last updated: 8/28/2014