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Inotropes – Angina and Heart Failure Management

by Pravin Shukle, MD
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    00:01 Let's go on to heart failure. Heart failure is kind of a sister disease to angina treatment because we use many of the similar kinds of treatments.

    00:12 Now, how we treat heart failure is a little bit different. We can use inotropes and those inotropes include cardiac glycosides, beta agonists, and PDE inhibitors. We can use vasodilators like the PDE inhibitors, nitrates, and the loop diuretics. And we can use classic cardiac remodelling agents like loop diuretics, ACE inhibitors, ARBs, spironolactone, and the new nesiritide.

    00:42 Let's move on to the cardiac glycosides. The prototypical agent in this drug class is digoxin.

    00:48 There are other cardiac glycosides out there. Digoxin is derived from the digitalis plant, it's also called the foxglove plant.

    00:57 It inhibits the sodium-potassium-ATPase pump. This results in an increased in sodium levels in the cell.

    01:07 This results in less excretion of calcium through the cotransporter and higher levels of calcium within the cell.

    01:14 With higher levels of calcium within the cell, you have increased calcium release from the sarcoplasmic reticulum.

    01:21 Now, the strength of contraction is going to be increased because you have more calcium.

    01:27 So, strength of contraction is proportional to intercellular calcium.

    01:31 Interestingly enough, you'll also have a reduction in heart rate.

    01:36 Digoxin reduces symptoms of heart failure, and it reduces hospitalization due to heart failure, but it does not prolong life.

    01:45 This is based on major studies looking at this particular agent in heart failure.

    01:50 Dosing. It has a very narrow therapeutic window. So, we actually have to monitor digoxin levels in patients.

    01:58 The drug can accumulate in the body, so that's why we monitor the serum levels. You can get digoxin toxicity.

    02:05 This beautiful picture here is just a picture of the foxglove plant, which actually grows as a weed where I grew up.

    02:14 Interactions of digoxin. It interacts with quinidine, which is also derived from a similar plant.

    02:20 The toxicity is increased with low potassium levels, and low magnesium levels, and low serum calcium levels.

    02:27 So, when you're going to administer digoxin to a patient, make sure you check the electrolytes.

    02:34 Toxicity can also result in arrhythmia, nausea, vomiting, and diarrhoea.

    02:40 The arrhythmia is occuring due to intercellular calcium overload.

    02:46 How do you treat it? Number 1, correct your electrolyte abnormality. Number 2, we can give antiarrhytmic drugs.

    02:53 Lidocaine, phenytoin and propranolol are some of the agents that we use.

    02:59 There is actually a product called digibind, which is fragments of binding material that bind the product or bind the digoxin in the serum and bring it out of activity. We do not use antiarrhythmics in patients who have heart block, because the antiarrhytmics are not gonna help them.

    03:22 Consider pacemaker therapy. Now, at one time, we used to use a ton of digoxin, and at that time, we used to see a lot of patients coming in with significant heart block from digoxin toxicity.

    03:34 We used to get maybe one or two a night in our hospital, and so we used to use temporary pace in quite a bit.

    03:40 With the reduction of use of digoxin over the years, we are doing less and less of this.

    03:48 Let's move on to beta 1 agonists. These drugs are mostly used in the intensive care unit or in the coronary care unit.

    03:56 These are IV drugs. Dobutamine and dopamine. They are not appropriate for chronic long term failure, because these drugs are subject to tolerance. They can also cause arrhythmia so we don't like to use them if we don't have to.

    04:12 There is no oral version of this medication. So, taking a pill of this particular drug is just not an option.

    04:21 Milrinone is a phosphodiesterase inhibitor that is now being used in heart failure.

    04:26 Once again, this is an ICU or CCU drug. It has positive inotropic effects because it releases cyclic AMP by inhibiting the PDE3 molecule.

    04:38 This increases intracellular levels of calcium. And by increasing intracellular levels of calcium, you have an increased strength of contraction or inotropy.

    04:49 Now, remember the word inotropy comes from the Greek God Inos who is the god of strength.

    04:54 So, whenever you hear inotropy, your ino, that's strength of contraction.

    05:00 That is a vasodilatory action that milrinone has as well, and we think that it's having a direct action right at the level of vascular smooth muscle. It can be arrhythmogenic, and so we tend to avoid it in long term chronic heart failure patients.

    05:16 It can actually increase mortality in chronic heart failure. So, it's really not a great choice in those patients.


    About the Lecture

    The lecture Inotropes – Angina and Heart Failure Management by Pravin Shukle, MD is from the course Cardiovascular Pharmacology. It contains the following chapters:

    • Overview Heart Failure
    • Cardiac Glycosides
    • β1 Agonists
    • Phosphodiesterase Inhibitors

    Included Quiz Questions

    1. Quinidine
    2. increased calcium levels.
    3. increased magnesium levels.
    4. increased potassium levels.
    1. The naturopathic product foxglove has combined with digoxin to cause toxicity.
    2. The metoprolol and the nifedipine combined to cause excessive bradycardia and dizziness.
    3. The furosemide and perindopril have combined to cause excessive hypotension and dizziness.
    4. The homeopathic mixture has caused the blood pressure to drop.
    1. ...have a narrow therapeutic window.
    2. ...have a moderate therapeutic window.
    3. ...have a wide theraputic window.
    4. ...have a high therapeutic window.
    1. ...inhibits the Na/K ATP ase, which results in increased calcium within the cell, and an increased cardiac contractile force.
    2. ...induces the Na/K ATP ase, which results in increased calcium within the cell, and an increased cardiac contractile force.
    3. ...inhibits the Na/K ATPase, which results in decreased calcium within the cell, and an increased cardiac contractile force
    4. ...induces the Na/K ATPase, which result in decreased calcium within the cell, and an increased cardiac contractile force.
    1. ...decreases heart failure symptoms, reduces heart rate, but does not prolong life or save lives.
    2. ...decreases heart failure symptoms, reduces heart rate, and saves lives.
    1. ...is a phosphodiesterase inhibitor, which will increase cAMP levels in the cell, and increase contractile force.
    2. ...is a phosphodiesterase inhibitor, which will decrease AMP levels in the cell, and increase contractile force.
    3. ...is a phosphodiesterase inhibitor, which will decrease cAMP levels in the cell, and increase contractile force.
    4. ...is a phosphodiesterase inhibitor, which will increase AMP levels in the cell, and increase contractile force.

    Author of lecture Inotropes – Angina and Heart Failure Management

     Pravin Shukle, MD

    Pravin Shukle, MD


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