We will now look at the medications used to treat heart failure. The goal is to restore the maximum amount of function to the cardiovascular system with the least expense to other organs and tissues. Consistently, clients experiencing heart failure report that the major drawbacks to a good quality of life are shortness of breath and fatigue. We can control these by increasing cardiac output and thus reducing fluid retention.
Heart failure is not a simple disease, and therefore calls for a complex and integrated response using multiple medications to support the positive effects of symptom management. In general, the order of therapy may first call for initiation of loop diuretics to contain and control fluid overload in those individuals exhibiting overt heart failure symptoms such as dyspnea or peripheral edema.
Whether or not a diuretic is called for as the first line in pharmacologic intervention, the use of angiotensin converting enzyme (ACE) inhibitors are sure to be considered early on as a first-line treatment for heart failure.10 ACE inhibitors work by preventing the body from creating angiotensin, a substance in the blood that causes vessels to vasoconstrict and raise the blood pressure. ACE inhibitor patients have, in trials, consistently shown improved cardiac function, improved symptoms, and better test results. In a series of large-scale trials, use of ACE inhibitors in various phases of heart failure demonstrated a lower death rate from all causes and a decreased risk of hospitalization.9 Please note that while ACE inhibitors decrease some of the more visible symptoms and contribute a slowing effect, they do not seem to stop the disease progression. More studies are being conducted with some practitioners so enthused by early study returns that they are advocating that all patients with left ventricle problems be placed on an ACE inhibitor.
|ACE Inhibitors9||Initial Dose||Max Dose|
|Captopril||6.25mg three times daily||50mg three times daily|
|Enalapril||2.5mg twice daily||10-20mg twice daily|
|Fosinopril||5-10mg once daily||40mg once daily|
|Lisinopril||2.5-5.0mg once daily||20-40mg once daily|
|Quinapril||5mg twice daily||20mg twice daily|
|Ramipril||1.25-2.5mg once daily||10mg once daily|
|Trandolapril||1mg once daily||4mg once daily|
The antihypertensive group known as beta blockers is often prescribed in combination with ACE inhibitors. Beta-blockers block the chemical receptors known as beta-receptors. These receptors are located on the outside of heart cells and along the course of some of the major blood vessels. They aid in the process of controlling the rate at which the heart beats. There are different sub-types of beta-receptors found on heart cells. If a drug blocks all the beta-receptors it can find, it is called non-selective. If a drug blocks mainly one certain kind of beta-receptor, it is called selective. For example, of the newer medications, Coreg is non-selective and Toprol-XL is selective. There is now a huge amount of evidence supporting beta-blocker use in CHF. Beta-blocker patients have shown improved cardiac function and generally see their symptoms improve. Beta-blocker studies show that death from heart failure from all causes is lowered with less hospitalization time. The positive effects from beta blockers given in conjunction with ACE inhibitors appear to be additive, which makes them a desirable addition to heart failure treatment regimens.9
|Beta Blockers9||Initial Dose||Max Dose|
|Bisoprolol||1.25mg once daily||10mg once daily|
|Carvedilol||3.125mg twice daily|
25mg twice daily;
50mg twice daily if > 85 kg
|12.5-25mg once daily||200mg once daily|
Diuretics are almost inevitably prescribed with heart failure at some point, often very early following diagnosis because they are THE major treatment for fluid congestion (edema). The goal of diuretics is to reduce filling pressures in the heart by causing the patient to eliminate (urinate) excess fluid. Some prescribers operate on a rigid premise that their clients with CHF need a little extra fluid to maintain an optimal preload. Preload is how far heart fibers stretch when the heart is its fullest, just before it pumps blood out into the body. This is wrong according to heart failure specialists. A wedge pressure of 20mmHg is not necessary. A wedge pressure of 12mmHg, which is normally considered low for these patients, may be perfectly fine as fluid volumes must be regulated by each individual’s needs and condition. Wedge pressure is a direct measurement of blood flow pressure obtained from a balloon-tipped flexible tube inserted through either the inferior or superior vena cava, through the heart and into the pulmonary artery.
|Loop Diuretics9||Initial Dose||Max Dose|
|Bumetanide||0.5-1.0mg once or twice daily||10mg daily|
|Furosemide (Lasix)||20-40mg once or twice daily||600mg daily|
|Torsemide||10-20mg once daily||200mg daily|
Digoxin (Lanoxin, digitalis, and foxglove) has been a staple of heart failure treatment for over two thousand years. Would it surprise you that a few years ago it fell into disfavor as a treatment for CHF? A large drug trial known as The Digoxin Investigators Group (DIG) put 3,000 patients on a placebo and 3,000 on digoxin, then watched to see how digoxin affected end result mortality in the groups. Their findings showed that there was no difference whatsoever between digoxin users and those taking placebos. This resulted in a sudden reaction by clinicians prescribing digoxin for their heart failure clients. After all, why give something that doesn’t extend the longevity of the clients? Fortunately, this impulse reaction was recognized quickly as just that, a reaction over the wrong test criteria. Digoxin alone in heart failure patients does not noticeably lengthen a CHF sufferer’s lifespan. What it does do is help them to feel better during the course of the disease, and stay out of the hospital much more than those clients not on digoxin. It is a quality of life issue, not quantity of life.8,12
|Digitalis glycosides9||Initial Dose||Max Dose|
|Digoxin||0.125-0.25mg once daily||Routine blood levels determine effective dose|
That brings us to the shadier side of the medication spectrum. Many of the drugs used to treat heart failure actually increase the nearness of death. The patients feel and function better, but their use puts a burden on body systems, leading to a decreased lifespan. These include medications known as inotropes that make a person’s heart beat stronger.
Inotropes come under names such as milrinone, dobutamine, xamoterol and ibopamine. They are recommended for use on a short-term basis in heart failure to aid during the stabilization of patients. Basically every inotropic drug that has been studied, including in some circumstances digoxin, increases the potential for death.
Another medication class that possesses both promise and danger is vasodilators. Vasodilators cause the blood vessel walls to widen or relax, allowing blood to flow more easily. We have already looked at one type of vasodilator, called ACE inhibitors. People who cannot tolerate an ACE inhibitor are often prescribed other types of vasodilators such as isosorbide dinitrate (Isordil), hydralazine (Apresoline), or nitroglycerin to relieve symptoms and improve tolerance for exercise. Other vasodilators that take less of a toll on the body when used are currently in the drug trial study stage. Flosequinan is one that actually received FDA approval before it had to be withdrawn from the market. The use of a kinder, gentler form of vasodilator would be a great aid in the control of heart failure, so it is with mixed eagerness and trepidation that the medical community is waiting to see if any oral forms of these newest agents get off the drawing board.
One of the newest medications has the potential of jumping straight into the ranks of the first-line prescribed medications, especially in those patients who are unable to tolerate an ACE inhibitor. Angiotensin II receptor blockers (ARBs) block the AT-1 receptor, decreasing the function of the angiotensin II receptors themselves.13 The benefit in this is that no matter how much angiotensin II there is, it can only cause limited amounts of harm since there would be no receptors for it to connect with. Currently, candesartan and valsartan have the best evidence base for use in the treatment of heart failure, though caution in use is warranted after a surge in adverse effect reports following generic status use in the Canadian health system.15
Still another new drug to hit the market is a potent vasodilator which has shown promise in use for acute decompensated heart failure. This potent adjunct to treatment is an injectable drug known as Natrecor (nesiritide). Approved for use by the FDA in August 2001, it is the synthetic version of one of the neurohormones called BNP that the body makes naturally in the heart's ventricle. Natrecor works by dilating blood vessels, decreasing the production of other pesky neurohormones and acting as a mild diuretic. These functions reduce the load on the heart, both preload and afterload (coming and going), making the heart’s job easier. Nesiritide is typically given to patients who remain dyspneic despite the use of IV loop diuretics and who are neither hypotensive or in cardiac shock.16 Nesiritide is generally given as an intravenous bolus of 2mcg/kg followed by a continuous infusion of 0.01 mcg/kg with close monitoring of hemodynamic effects.
There are some other types of medications that are commonly used with a diagnosis of heart failure even though they have minimal or no effect on the heart. While these adjuncts to treatment are not especially heart failure medications, they are so commonly prescribed for individuals with this diagnosis that it is important to mention them here.
Blood thinners (aspirin, coumadin) are prescribed to prevent the formation of blood clots and microemboli which occur with atrial fibrillation. As the pumping pressures of the heart decrease, the risk of forming blood clots and micro-emboli increases. Be aware that there is some debate as to the advisability of prescribing every heart failure patient with coumadin. Some very well-respected practitioners feel that coumadin is not warranted unless the patient has symptomatic atrial fibrillation. Others who are just as well respected disagree. We know that good reasons exist to individualize treatment for each person with heart failure, taking into consideration their unique individual needs.
Potassium helps control heart rhythm and is essential for the normal work of the nervous system and muscles. It is important to have just the right amount of potassium in the body, especially for the heart. The kidneys control the amount of potassium in the bloodstream and eliminate any excess through the urine. Since most diuretics remove potassium from the body, there is a risk of losing too much potassium. Patients taking diuretics are encouraged to eat foods high in potassium or are prescribed potassium supplements to compensate for the potassium loss. However, ACE inhibitors can cause the body to retain potassium, so this intricate juggling act needs to be taken into account as well.
Aldactone (spironolactone) competes with aldosterone for a certain receptor site, known as the mineralocorticoid receptor, and in doing so seems to prolong the survival rate in certain individuals with heart failure. The properties of Aldactone include a diuretic effect and interference in collagen build-up. In some heart failure studies, those clients taking Aldactone had a slight slowing of disease progression that could not be attributed to other causes, especially in the area of remodeling of the heart chambers. The exact reason for this is not fully known, and it is still unclear how to use the information should further studies show that it was not just a statistical set of flukes. In light of the positive indications for use, the 2017 ACC/AHA guidelines for chronic heart failure recommend Aldactone in patients with moderate to severe heart failure while carefully monitoring renal function and maintaining normal plasma potassium levels. The goal behind spironolactone use is a reduction in the number and length of hospitalizations of those tolerating it.17