Antianginal and Heart Failure Medications Overview

<p>Increased nitric oxide production (B)</p> Signup and view all the answers

<p>Reduction of preload and afterload (A)</p> Signup and view all the answers

<p>They block different types of receptors (D)</p> Signup and view all the answers

<p>They decrease the frequency of angina attacks (C)</p> Signup and view all the answers

<p>They can dilate coronary arteries, improving oxygen supply (A)</p> Signup and view all the answers

<p>Reducing fluid retention and edema (D)</p> Signup and view all the answers

<p>Causing direct arterial vasodilation (D)</p> Signup and view all the answers

<p>Hydralazine and nitrates (C)</p> Signup and view all the answers

<p>By reducing inflammation and oxidative stress (B)</p> Signup and view all the answers

<p>Patients with HFrEF who have elevated heart rates (B)</p> Signup and view all the answers

<p>It increases myocardial contractility (D)</p> Signup and view all the answers

<p>If current (A)</p> Signup and view all the answers

<p>Diuretics (A), Digoxin (C)</p> Signup and view all the answers

<p>Inhibits the late phase of sodium current in cardiac myocytes (C)</p> Signup and view all the answers

<p>It selectively inhibits the If current channels in the SA node (C)</p> Signup and view all the answers

<p>Prevent thrombus formation in the coronary arteries (C)</p> Signup and view all the answers

<p>They block the conversion of angiotensin I to angiotensin II (C)</p> Signup and view all the answers

<p>ARBs do not enhance bradykinin levels (B)</p> Signup and view all the answers

<p>Decrease heart rate and reduce myocardial contractility (C)</p> Signup and view all the answers

<p>Block the action of aldosterone leading to reduced fluid retention (A)</p> Signup and view all the answers

<p>Loop diuretics (D)</p> Signup and view all the answers

<p>Ranolazine does not affect heart rate but Ivabradine decreases it (A)</p> Signup and view all the answers

<p>Beta-blockers (D)</p> Signup and view all the answers

<p>Cough due to bradykinin accumulation (B)</p> Signup and view all the answers

<p>Prevent thrombus formation to reduce ischemia (A)</p> Signup and view all the answers

<p>Promoting sodium and water absorption (D)</p> Signup and view all the answers

Chest pain caused by reduced blood flow to the heart muscle, making it work harder.

Medications used to manage angina by improving the balance between how much oxygen the heart needs and how much it gets.

Vasodilators that relax blood vessels, mainly in the veins, reducing the amount of blood returning to the heart and lowering oxygen demand.

A molecule produced by nitrates that activates an enzyme called guanylate cyclase, causing smooth muscle relaxation.

Drugs that block beta-adrenergic receptors, slowing heart rate, reducing contractility, and lowering blood pressure.

Drugs that block calcium channels in smooth and heart muscle, relaxing blood vessels and reducing workload.

Type of calcium channel blocker that mainly dilates blood vessels, lowering the resistance the heart has to pump against.

Type of calcium channel blocker that dilates blood vessels, slows heart rate, and reduces heart muscle force.

Diuretics help manage heart failure symptoms by getting rid of excess fluid, reducing swelling, shortness of breath, and fatigue. They don't prolong life, but they make patients feel better.

These drugs relax blood vessels, reducing the pressure the heart has to pump against (afterload) and the amount of blood returning to the heart (preload). This helps the heart work more efficiently.

SGLT2 inhibitors block the reabsorption of sugar in the kidneys, leading to more sugar excreted in the urine, which draws water out and lowers blood pressure. They also have additional heart-protective effects.

These treatments improve symptoms, reduce hospital stays, and can even help patients live longer, especially those with heart failure and diabetes.

Ivabradine slows the heart rate without making the heart muscle weaker. This allows the heart to fill with blood better, improving oxygen delivery.

Ivabradine is used for patients with heart failure who are still having symptoms despite taking beta-blockers, especially those with a fast heart rate.

Digoxin strengthens the heart muscle and slows the heart rate, improving its ability to pump blood effectively.

Digoxin is used to improve heart failure symptoms and exercise tolerance, especially in patients with atrial fibrillation.

Ranolazine reduces heart oxygen needs by blocking a specific sodium channel (I_Na) in heart muscle cells. This prevents excessive calcium buildup and reduces heart work.

Ivabradine slows your heart rate by selectively blocking the 'funny' current (If) in the SA node, the heart's pacemaker.

Antiplatelets like aspirin and clopidogrel prevent blood clots in coronary arteries by blocking platelet aggregation, which is the sticking together of blood cells that form clots.

Heparin prevents blood clots by inhibiting thrombin and factor Xa, which are crucial proteins involved in the blood clotting process.

Heart failure occurs when your heart cannot pump blood effectively to meet the body's needs, leading to symptoms like shortness of breath, fatigue, and fluid retention.

ACE inhibitors like enalapril block the production of angiotensin II, a powerful vasoconstrictor (blood vessel narrow), leading to lower blood pressure, vasodilation, and reduced heart workload.

ARBs like losartan work directly on the angiotensin II receptor, blocking its effects and achieving similar results as ACE inhibitors, but without the cough side effect.

Beta-blockers like metoprolol reduce heart rate, myocardial contractility (heart muscle strength), and blood pressure by blocking beta-receptors, which are stimulated by the 'fight-or-flight' response.

Aldosterone antagonists like spironolactone block the action of aldosterone, a hormone that retains sodium and water, leading to fluid buildup and high blood pressure. Blocking aldosterone helps reduce fluid retention and improves heart function.

Diuretics like furosemide increase urine production by promoting excretion of water and sodium, reducing fluid overload, also known as edema, and decreasing blood pressure.

ACE inhibitors improve heart function by decreasing the heart's workload through dilation of blood vessels, reducing afterload (resistance to blood flow) and preload (blood volume returning to the heart).

ARBs and ACE inhibitors both block the effects of angiotensin II, a potent vasoconstrictor. However, ARBs are preferred in patients who experience a cough side effect from ACE inhibitors.

Chronic use of beta-blockers not only improves heart function but also prevents further heart damage by reducing the remodeling of the heart muscle, a process where the heart becomes stiff and weak.

Aldosterone antagonists reduce scarring of the heart muscle (myocardial fibrosis) by blocking the effects of aldosterone, which is linked to heart muscle damage.