HARD QUIZ HF DRUGS

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Questions and Answers

Which of the following actions is NOT associated with the use of diuretics in CHF?

Decreased ventricular preload

Increased systemic vascular resistance (SVR) (correct)

Decreased blood volume

Decreased pulmonary edema

Which diuretic class is used to address potassium loss associated with other diuretics?

Potassium sparing diuretics

Thiazide diuretics

Aldosterone antagonists (correct)

Loop diuretics

Which specific drug is a combined α1 and β-blocker, as mentioned within this text?

Furosemide

Carvedilol (correct)

Metoprolol

Eplerenone

Which of the following drug classes is NOT considered a cardiostimulatory (inotropic) drug?

Calcium channel blockers (C) Signup and view all the answers

What is the primary reason for the use of β-blockers in patients with CHF?

To reduce sympathetic overstimulation and its consequences (B) Signup and view all the answers

Which of these drug categories is primarily used in acute heart failure?

Sympathomimetics (C) Signup and view all the answers

In chronic heart failure, what is the primary mechanism for the use of loop diuretics?

To decrease ventricular preload (D) Signup and view all the answers

What is the primary effect of Aldosterone antagonists in CHF?

To reduce mortality when used with ACE Inhibitors and loop diuretics (B) Signup and view all the answers

Which of the following statements regarding dopamine is TRUE?

Dopamine can be used to treat acute renal failure (C) Signup and view all the answers

Which of the following statements regarding Sympathomimetics is TRUE?

Sympathomimetics decrease the reuptake of calcium in the sarcoplasmic reticulum. (B) Signup and view all the answers

Which of the following drug classes is NOT typically used in the treatment of heart failure?

Anticoagulants (B) Signup and view all the answers

A patient with heart failure is prescribed an ACE inhibitor. Which of the following best describes the primary mechanism of action of this drug class?

Blocking the conversion of angiotensin I to angiotensin II (B) Signup and view all the answers

Which drug class is primarily used to reduce the sympathetic nervous system's effects on the heart in heart failure?

Beta-blockers (C) Signup and view all the answers

What is a primary therapeutic goal of using diuretics in managing patients with heart failure?

Reducing fluid overload and pulmonary congestion (A) Signup and view all the answers

Which class of drugs directly increases the force of myocardial contraction?

Inotropic drugs (D) Signup and view all the answers

What is a primary action of SGLT2 inhibitors related to heart failure treatment?

Reducing sodium glucose reabsorption in the kidney, leading to decreased blood volume. (C) Signup and view all the answers

Which of the following drug classes is considered a RAAS inhibitor?

Aldosterone antagonists (D) Signup and view all the answers

How do direct-acting vasodilator drugs primarily work in the context of heart failure?

By directly increasing blood vessel diameter. (B) Signup and view all the answers

What is a primary action of low doses of dopamine?

Positive inotropy and chronotropy (A) Signup and view all the answers

Which statement about dobutamine is correct?

It primarily acts on β1-adrenoceptors. (D) Signup and view all the answers

What adverse effect is associated with sympathomimetic inotropic drugs?

Proarrhythmia (C) Signup and view all the answers

What is the mechanism of action (MOA) for inodilators like milrinone?

Increase intracellular cAMP in the heart and vasculature (C) Signup and view all the answers

What is a significant risk associated with cardiac glycosides like digoxin?

Low therapeutic index (A) Signup and view all the answers

Which of the following is the primary mechanism by which neprilysin inhibitors exert their therapeutic effect in heart failure?

Inhibiting the breakdown of ANP, promoting vasodilation and attenuating RAAS. (B) Signup and view all the answers

What is the primary effect of arterial vasodilators on the left ventricle in a patient with heart failure?

Decrease in ESV, decrease in EDV, and increase in SV. (A) Signup and view all the answers

A patient with heart failure is prescribed an ARNI. What does 'ARNI' stand for and what is its combined mechanism of action?

Angiotensin Receptor Neprilysin Inhibitor; blocks angiotensin II receptors and inhibits neprilysin. (C) Signup and view all the answers

Which of the following best describes the effect of beta-blockers on cardiac remodeling and function in patients with heart failure?

Reverse remodeling, decreasing chamber size and increasing EF over several months. (D) Signup and view all the answers

What is a key physiological effect of ACE inhibitors that contributes to a reduction in cardiac remodeling?

Downregulating sympathetic nerves and reducing vasopressin release. (D) Signup and view all the answers

Which of the following drug combinations would be MOST effective at reducing both preload and afterload in the treatment of heart failure?

A combination of an ARNI and a beta-blocker. (C) Signup and view all the answers

How does hydralazine lead to vasodilation, and what is its primary effect on the cardiovascular system?

It opens K+ channels and inhibits vascular SR Ca++ release, reducing mostly arterial afterload. (A) Signup and view all the answers

Which of the following describes the effect of increased blood volume in the context of heart failure?

Increased renal sodium retention and RAAS activation. (D) Signup and view all the answers

If a patient's heart failure symptoms include pulmonary edema and impaired gas exchange, which of the following would be the LEAST appropriate course of action?

Administering an arterial vasodilator to increase preload. (B) Signup and view all the answers

A patient with heart failure has a reduced cardiac output. Which of the following is a primary physiological consequence observed due to this reduced cardiac output?

Reduced exercise tolerance and dyspnea. (A) Signup and view all the answers

Study Notes

Heart Failure Drugs - Lecture 09

Heart failure drugs aim to improve cardiac function and reduce symptoms, thereby decreasing morbidity and mortality.
If possible, address underlying conditions like valve disease, coronary artery disease, and arrhythmias.
Reduce clinical symptoms and morbidity, including pulmonary congestion, systemic edema, and dyspnea.
Improve cardiovascular function, including organ perfusion and increase cardiovascular functional reserve.
Reduce mortality.

Learning Objectives

Describe major cardiovascular, pulmonary, and renal complications of heart failure.
Describe the therapeutic targets and goals for treating heart failure.
Detail how different drug classes (vasodilators, RAAS inhibitors, beta-blockers, inotropic drugs, diuretics, SGLT2 inhibitors) treat heart failure, providing specific examples.
Explain drug treatment differences in acute versus chronic heart failure (HFrEF vs HFpEF).

Cardiovascular, Pulmonary, and Renal Signs and Symptoms of Heart Failure

Reduced cardiac output and organ perfusion, leading to reduced exercise tolerance.
Dyspnea, even at rest.
Pulmonary edema.
Impaired lung gas exchange.
Fluid retention due to increased blood volume.
Renal sodium retention.
RAAS activation and increased vasopressin.
Elevated systemic vascular resistance.
Sympathetic activation.
Cardiac remodeling.
Arrhythmias.

Therapeutic Goals

Correct any underlying problems like valve disease, coronary artery disease, and arrhythmias.
Reduce clinical symptoms and morbidity.
Improve cardiovascular function, including organ perfusion and functional reserve.
Reduce mortality.

Drug Treatment - Physiological Targets

Renin-angiotensin-aldosterone system (RAAS): ACE inhibitors, ARBs, and ARNIs reduce afterload, preload, blood volume, and cardiac remodeling.
Cardiac sympathetic activation: Beta-blockers reduce cardiac remodeling and arrhythmias.
Volume overload and edema: Diuretics decrease blood volume, venous pressures, and preload.
Improving cardiac metabolic function: SGLT2 inhibitors.

Vasodilators

RAAS inhibitors, neprilysin inhibitors, and direct-acting arterial and venous dilators improve heart function.

Vasodilator Effects on Frank-Starling Curves

Mixed vasodilators (reduce afterload and preload) include ACE inhibitors, ARBs, and sodium nitroprusside.
Arterial vasodilators (reduce afterload) include hydralazine.
Venous vasodilators (reduce preload) include isosorbide dinitrate.

Reducing Afterload in Patients with Systolic Dysfunction (HFrEF)

Reducing afterload with an arterial vasodilator drug leads to decreased ESV, EDV, and increased SV and EF.
Failing hearts are more responsive to afterload changes than normal hearts.

Specific Drugs

ACE Inhibitors: Block angiotensin II formation, dilate arteries and veins, reduce vasopressin release, and attenuate cardiac remodeling. Examples: lisinopril, enalapril.
ARBs: Block angiotensin II receptors, similar actions to ACEIs. Examples: valsartan, losartan.
Neprilysin Inhibitors: Inhibit neprilysin, increase circulating ANP, reduce RAAS system activity, and dilate vessels. Combined with ARBs (valsartan) in ARNI drugs to treat heart failure.
Hydralazine: Direct-acting arterial vasodilator, reduces afterload primarily.
Isosorbide Dinitrate: Nitrodilator, primarily dilates veins, reduces preload.

Beta-blockers in Chronic Heart Failure (CHF)

Newer beta-blockers are efficacious (reduce hospitalizations and death).
Beta-blockers reverse heart remodeling, decrease chamber size, and increase ejection fraction.
Typically used with diuretics, ACE inhibitors, or ARBs.

Beta-blockers in CHF (cont.)

Excessive beta-adrenergic stimulation in CHF downregulates beta receptors, thereby reducing inotropic reserve.
Excessive sympathetic activation contributes to hypertrophy and dysfunctional changes in signal transduction mechanisms.
Positive antiarrhythmic benefits are observed.

Diuretics

Increase sodium and water excretion by the kidneys.
Reduce blood volume and CVP.
Reduce ventricular preload and pulmonary/systemic edema.
Reduce SVR (chronic therapy).
Minimal effect on ventricular stroke volume and cardiac output except in cases of overdose.
Types of diuretics include loop diuretics, thiazide diuretics, and K+-sparing diuretics.
Furosemide is the primary loop diuretic for CHF.
Less potent thiazide diuretics are used in mild CHF.
Potential problems include K+ loss and excessive volume reduction (monitor for arrhythmias).
Spironolactone and eplerenone are aldosterone antagonists for K+-sparing, improving mortality when used with ACE inhibitors or loop diuretics, especially post-MI CHF.

Cardiostimulatory/Inotropic Drugs

Beta-agonists, PDE inhibitors, and digoxin are used in these cases.

Sympathomimetics

Mimic sympathetic effects by stimulating beta-adrenoceptors.
Used only for acute, not chronic, heart failure. Types include Dopamine/Dobutamine.
Dopamine is used in low doses to cause systemic vasodilation and in high doses for α₁-mediated vasoconstriction.
Dobutamine primarily acts on β₁-adrenoceptors, increasing cardiac output and reducing preload, but can be arrhythmogenic and has a short half-life.

Inodilators – Phosphodiesterase (PDE3) Inhibitors

Increase cAMP in the heart and vasculature.
Cause systemic vasodilation, mild-to-moderate positive inotropy, and tachycardia.
Used only for acute heart failure and increase mortality and arrhythmogenic potential in chronic failure. Drugs including Milrinone and Inamrinone are examples.

Cardiac Glycosides (Digoxin)

Inhibit Na+/K+-ATPase, leading to intracellular Ca++ increase, enhancing inotropy, and increasing ejection fraction.
Decrease heart rate (parasympathomimetic effect).
Inhibit sympathetic activity.
Low therapeutic index; easily toxic.

Pharmacokinetics

Digoxin has a half-life of 40 hours and requires renal elimination.
Digitalization (reaching steady state without loading doses) takes 5-7 days.
Renal function and lean body mass are crucial considerations.
Digoxin toxicity is increased by low potassium, low magnesium, and high calcium.

SGLT2 Inhibitors

Lower blood glucose by inhibiting SGLT2.
Increase urinary glucose excretion.
Cause natriuresis, diuresis, and lower arterial pressure, without increasing heart rate.
Clinical trials show benefits for HFpEF (with or without diabetes) and in patients with mildly reduced ejection fractions (HFmrEF). These generally improve diastolic stiffness and diastolic function.

Acute vs. Chronic Therapy in HFrEF

Acute systolic failure: Loop diuretics, arterial and mixed vasodilators, PDE inhibitors, and sympathomimetics (beta agonists).
Chronic systolic failure: Diuretics, ACEIs, ARBs, ARNI, newer beta-blockers, and SGLT2 inhibitors.

HFpEF: Drug Treatment Guidelines

No clearly defined guidelines; treatment focuses on comorbidities. Common drugs include: beta-blockers, calcium-channel blockers (e.g., verapamil), SGLT2 inhibitors, aldosterone receptor antagonists, and diuretics if necessary for severe edema. Also, K+-sparing diuretics are key.

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Description

This quiz covers Lecture 09 on heart failure drugs, focusing on their therapeutic implications and mechanisms. You'll learn about various drug classes, their roles in treating heart failure, and the differences in treatment between acute and chronic conditions. Additionally, the quiz addresses the complications related to cardiovascular, pulmonary, and renal systems.