Drugs Used in Acute and Chronic Congestive Heart Failure (CHF)

The drugs used in the treatment of acute and chronic congestive heart failure (CHF) are an important topic for the NEET PG exam since CHF is a common and serious cardiac condition. It affects a large number of people globally, which makes it essential for medical students to understand the drugs used to treat the condition.

Read this blog to get a quick overview of this high-yield pharmacology topic and strengthen your NEET PG Exam preparation.

Overview                 

It is a chronic condition in which the heart doesn’t pump blood properly. Hence, fluid accumulates in the back of the heart. This leads to congestive symptoms like

• Breathlessness
• Hepatomegaly
• Increase in JVP 

When a person has acute CHF, the body starts compensatory mechanisms. It will increase sympathetic activities as the heart is not pumping properly. Hence, in acute CHF, when there is low cardiac output, it increases the sympathetic activities which ultimately increases the production of catecholamines like adrenaline, noradrenaline etc. This will stimulate the β1 receptors which will eventually maintain the cardiac output.

The β1 overactivity in the JG cells of the kidney, will lead to the release of renin. Renin converts angiotensinogen into angiotensin first. Angiotensin first is converted into angiotensin second with the help of the enzyme ACE. Angiotensin second then stimulates the AT1 receptors which are present at several places. This can lead to vasoconstriction, release of aldosterone and release of catecholamines like adrenaline, noradrenalin etc.

Aldosterone that has been released will lead to

• Retention of sodium and water.
• Removal of potassium and hydrogen.

Problems with sympathetic over-activity

• It leads to vasoconstriction.
• They can cause edema because of water retention.
• They can increase the level of aldosterone, which can lead to left ventricular hypertrophy. As a result of which, cardiac remodeling will lead to the death of the person.

Hence in chronic CHF, inotropic drugs do not play a major role in the treatment. In chronic CHF, the aim of the treatment will be the following:

• To decrease the work of heart
• To remove the accumulated fluid
• To prevent left ventricular hypertrophy (LVH).

Inotropic drugs are given only if the patient hasn’t gotten better even after compensatory mechanisms.

Drugs used in chronic CHF

Work of heart is decreased by administering vasodilators like - 

• Drugs which dilate arteries like hydralazine (decreases after load). 
• Drugs which dilate veins like nitrates (decrease preload).
• Drugs which dilate both arteries and veins like sodium nitroprusside, angiotensin converting enzymes and angiotensin receptor blockers. These drugs decrease both preload and afterload as they dilate both arteries and veins.

Drugs that remove fluid retention are loop diuretics.

Drugs that prevent the left ventricular hypertrophy decreases the mortality/ increase the longevity of the person. No other drug decreases mortality. This is done by 4 types of drugs:

• Β1 blockers (drugs whose names end with LOL)
• ACE inhibitors (whose names end with PRIL)
• AT1 receptor blockers (drugs whose names end with SARTAN)
• Aldosterone antagonists (whose names ends with SPIRONOLACTONE)

Inotropic drugs

• Are used in the case of acute CHF and chronic CHF.

Digoxin

• In chronic CHF, we use oral inotropic drugs. The main drug being digoxin group of drugs.
• MECHANISMS OF DIGOXIN
  • It inhibits Na-K pumps. By inhibiting this pump, it increases the intracellular calcium which can lead to increase in contractility. 
  • It has a vagomimetic effect as well. Hence, it decreases the conduction from atrium to ventricle. This causes atrial fibrillation.
• SIDE EFFECTS OF DIGOXIN
  • Nausea
  • Vomiting
  • It can cause almost any arrhythmia. The most common being ventricular bigeminy. Non-Paroxysmal Atrial Tachycardia with AV block is the most common arrhythmia caused by digoxin.
  • Gynecomastia (Other drugs that cause gynecomastia are spironolactone, cimetidine and estrogen – DISCO drugs)
  • Xanthopsia/yellow vision.
• MEAN FACTORS WHICH INCREASE THE RISK OF TOXICITY OF DIGOXIN
  • During electrolyte imbalance. That is, in the case of hypokalemia, hypomagnesemia or hypercalcemia.
  • Certain drugs like quinidine, verapamil/clarithromycin, amiodarone and thiazides, increase the risk of toxicity.
  • Renal failure.
• When toxicity occurs, the person will have arrhythmia. Hence the drug of choice for digoxin induced ventricular arrhythmias is lignocaine. If arrhythmia is not controlled even then, Digoxin Immune Fab is the drug to go for. This is a fraction of antibodies against digoxin which is known as DIGIBIND. This will bind digoxin and stop its action. This is used in case of severe digoxin toxicity.

New drugs in CHF treatment

• Brain Natriuretic peptide (BNP) is the main target. The function of BNP is the loss of Na or natriuresis. Also, it is a powerful vasodilator. BNP is neutralized in the body with the help of NEP (neutral endopeptidase). We can administer the BNP from outside. The drug used is Nesiritide. This is a recombinant BNP.
• Problems of BNP
  • It is not effective orally.
  • It is very short acting.
• NEP inhibitor/neprilysin inhibitor can be given for CHF. These are the ones whose name ends with “tril”(sacubitril).

A combination of ACE (“pril”) inhibitor and NEP inhibitor (“tril”) has been developed. This is known as Patrilats like omapatrilat and sanpatrrilat. They have the property of both ‘prils’ and ‘trils.’ 

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