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Questions and Answers
What type of receptors does carvedilol antagonize?
What type of receptors does carvedilol antagonize?
Which of the following β-blockers is not β1-selective?
Which of the following β-blockers is not β1-selective?
What is the primary reason for starting β-blockers at low doses and gradually increasing them in patients with HF?
What is the primary reason for starting β-blockers at low doses and gradually increasing them in patients with HF?
Which of the following medications should be used with caution when combined with β-blockers?
Which of the following medications should be used with caution when combined with β-blockers?
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What is the primary benefit of using β-blockers in HF?
What is the primary benefit of using β-blockers in HF?
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What is the primary mechanism by which β-blockers reduce cardiac workload?
What is the primary mechanism by which β-blockers reduce cardiac workload?
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What is the primary effect of natriuretic peptides on the heart?
What is the primary effect of natriuretic peptides on the heart?
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What is the function of neprilysin in the body?
What is the function of neprilysin in the body?
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What is the primary effect of β-Adrenergic agonists on myocardial cells?
What is the primary effect of β-Adrenergic agonists on myocardial cells?
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Which of the following is NOT a characteristic of β-Adrenergic agonists?
Which of the following is NOT a characteristic of β-Adrenergic agonists?
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What is the primary route of administration for β-Adrenergic agonists?
What is the primary route of administration for β-Adrenergic agonists?
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Which of the following β-Adrenergic agonists is most commonly used other than digoxin?
Which of the following β-Adrenergic agonists is most commonly used other than digoxin?
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What is the setting where β-Adrenergic agonists are primarily used?
What is the setting where β-Adrenergic agonists are primarily used?
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Which of the following is a effect of β-Adrenergic agonists?
Which of the following is a effect of β-Adrenergic agonists?
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What is the primary mechanism of action of β-Adrenergic agonists?
What is the primary mechanism of action of β-Adrenergic agonists?
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What is the result of the action of β-Adrenergic agonists on myocardial cells?
What is the result of the action of β-Adrenergic agonists on myocardial cells?
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What is the result of β-adrenergic agonists leading to an increase in intracellular cyclic adenosine monophosphate (cAMP)?
What is the result of β-adrenergic agonists leading to an increase in intracellular cyclic adenosine monophosphate (cAMP)?
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What is the effect of phosphorylating slow calcium channels by protein kinase?
What is the effect of phosphorylating slow calcium channels by protein kinase?
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What is the result of β-adrenergic agonists activating protein kinase?
What is the result of β-adrenergic agonists activating protein kinase?
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What is the mechanism of action of β-adrenergic agonists in relation to cyclic adenosine monophosphate (cAMP)?
What is the mechanism of action of β-adrenergic agonists in relation to cyclic adenosine monophosphate (cAMP)?
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What is the effect of increased intracellular calcium on myocardial cells?
What is the effect of increased intracellular calcium on myocardial cells?
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What is the role of protein kinase in the mechanism of action of β-adrenergic agonists?
What is the role of protein kinase in the mechanism of action of β-adrenergic agonists?
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What is the result of β-adrenergic agonists increasing intracellular cAMP?
What is the result of β-adrenergic agonists increasing intracellular cAMP?
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What is the effect of protein kinase phosphorylating slow calcium channels?
What is the effect of protein kinase phosphorylating slow calcium channels?
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Study Notes
Adverse Effects of Digoxin
- Digoxin has a narrow therapeutic index, and toxicity is a common adverse drug reaction leading to hospitalization.
- Initial indicators of toxicity include anorexia, nausea, and vomiting.
- Patients may also experience blurred vision, yellowish vision (xanthopsia), and cardiac arrhythmias.
- Hypokalemia predisposes patients to digoxin toxicity, as digoxin competes with potassium for binding on the Na+/K+-ATPase pump.
Interactions with Digoxin
- Digoxin should be used with caution with other drugs that slow AV conduction, such as β-blockers, verapamil, and diltiazem.
- Inhibitors of P-gp, such as clarithromycin, verapamil, and amiodarone, can significantly increase digoxin levels.
β-Adrenergic Agonists
- β-Adrenergic agonists, such as dobutamine and dopamine, improve cardiac performance by causing positive inotropic effects and vasodilation.
- They increase entry of calcium ions into myocardial cells and enhance contraction.
- Dobutamine is the most commonly used inotropic agent other than digoxin.
Mechanism of Action of β-Adrenergic Agonists
- β-Adrenergic agonists lead to an increase in intracellular cAMP, which results in the activation of protein kinase.
- Protein kinase then phosphorylates slow calcium channels, increasing the entry of calcium ions into the myocardial cells and enhancing contraction.
Phosphodiesterase Inhibitors
- Milrinone increases the intracellular concentration of cAMP, resulting in an increase of intracellular calcium and, therefore, cardiac contractility.
Recombinant B-Type Natriuretic Peptide
- Nesiritide is a recombinant form of human B-type natriuretic peptide that has beneficial vasodilatory, natriuretic, diuretic, and neurohormonal effects.
- It is administered intravenously for the management of patients with decompensated congestive heart failure.
- Through binding to natriuretic peptide receptors, nesiritide stimulates natriuresis and diuresis, reducing preload and afterload.
β-Blockers in HF
- Three β-blockers have shown benefit in HF: Bisoprolol, carvedilol, and long-acting metoprolol succinate reduce morbidity and mortality associated with HFrEF.
- Carvedilol is a nonselective αβ-adrenergic receptor antagonist, while bisoprolol and metoprolol succinate are β1-selective antagonists.
Diuretics
- Diuretics relieve pulmonary and peripheral edema caused by congestive heart failure.
- They decrease the plasma volume and subsequently decrease venous return to the heart (preload), reducing cardiac workload and oxygen demand.
Angiotensin Receptor-Neprilysin Inhibitor (ARNI)
- Natriuretic peptides (atrial and brain natriuretic peptides) cause natriuresis, reducing the work on the heart and reducing blood pressure.
- Neprilysin is the enzyme responsible for breaking down these natriuretic peptides.
- Angiotensin receptor-neprilysin inhibitor (ARNI) therapy inhibits neprilysin, increasing the levels of natriuretic peptides and reducing blood pressure.
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Description
Learn about the adverse effects of digoxin in patients with heart failure, including toxicity symptoms, cardiac arrhythmias, and more. Identify the initial indicators of toxicity and the risks of hypokalemia.
