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Questions and Answers
What is the primary purpose of using diuretics in heart failure patients?
What is the primary purpose of using diuretics in heart failure patients?
Which adverse effect is commonly associated with loop diuretics?
Which adverse effect is commonly associated with loop diuretics?
How does ivabradine function in heart failure treatment?
How does ivabradine function in heart failure treatment?
Why are SGLT2 inhibitors beneficial in heart failure management?
Why are SGLT2 inhibitors beneficial in heart failure management?
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What is a notable side effect of using ivabradine?
What is a notable side effect of using ivabradine?
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What cardiovascular effects are associated with inotropic drugs?
What cardiovascular effects are associated with inotropic drugs?
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Which class of medication should be monitored closely for the risk of urogenital infections?
Which class of medication should be monitored closely for the risk of urogenital infections?
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What is the mechanism of action of digoxin in treating heart failure?
What is the mechanism of action of digoxin in treating heart failure?
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What effect does digoxin have on heart rate and myocardial oxygen demand?
What effect does digoxin have on heart rate and myocardial oxygen demand?
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What is the recommended serum drug concentration range of digoxin for patients with HFrEF?
What is the recommended serum drug concentration range of digoxin for patients with HFrEF?
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Which electrolyte imbalance increases the risk of digoxin toxicity?
Which electrolyte imbalance increases the risk of digoxin toxicity?
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What is the primary route of elimination for digoxin?
What is the primary route of elimination for digoxin?
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Which medication is primarily used for the short-term treatment of acute decompensated heart failure?
Which medication is primarily used for the short-term treatment of acute decompensated heart failure?
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What mechanism do B-adrenergic agonists use to improve cardiac performance?
What mechanism do B-adrenergic agonists use to improve cardiac performance?
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What role does soluble guanylate cyclase (sGC) play in heart function?
What role does soluble guanylate cyclase (sGC) play in heart function?
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Which of the following signs can be an initial indicator of digoxin toxicity?
Which of the following signs can be an initial indicator of digoxin toxicity?
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What is a significant risk associated with the use of mineralocorticoid receptor antagonists (MRAs) like spironolactone?
What is a significant risk associated with the use of mineralocorticoid receptor antagonists (MRAs) like spironolactone?
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Which statement about angiotensin receptor blockers (ARBs) is correct?
Which statement about angiotensin receptor blockers (ARBs) is correct?
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Which class of drugs is recommended to mitigate harmful sympathetic nervous system activation in heart failure patients?
Which class of drugs is recommended to mitigate harmful sympathetic nervous system activation in heart failure patients?
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What is the ideal treatment setting for angiotensin receptor-neprilysin inhibitors (ARNIs)?
What is the ideal treatment setting for angiotensin receptor-neprilysin inhibitors (ARNIs)?
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What common adverse effect is associated with both ACE inhibitors and angiotensin receptor blockers (ARBs)?
What common adverse effect is associated with both ACE inhibitors and angiotensin receptor blockers (ARBs)?
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What is a key advantage of using ARBs over ACE inhibitors?
What is a key advantage of using ARBs over ACE inhibitors?
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What is the recommended approach when starting beta-blocker therapy in patients with heart failure?
What is the recommended approach when starting beta-blocker therapy in patients with heart failure?
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Which medication can produce adverse effects such as gynecomastia?
Which medication can produce adverse effects such as gynecomastia?
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Which of the following are major causes of heart failure?
Which of the following are major causes of heart failure?
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What role does the sympathetic nervous system play in heart failure?
What role does the sympathetic nervous system play in heart failure?
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What effect does the activation of the renin–angiotensin–aldosterone system (RAAS) have?
What effect does the activation of the renin–angiotensin–aldosterone system (RAAS) have?
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Which of the following best describes the role of natriuretic peptides in heart failure?
Which of the following best describes the role of natriuretic peptides in heart failure?
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What is the primary action of angiotensin-converting enzyme (ACE) inhibitors in treating heart failure?
What is the primary action of angiotensin-converting enzyme (ACE) inhibitors in treating heart failure?
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What consequence can result from excessive fluid retention in heart failure?
What consequence can result from excessive fluid retention in heart failure?
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How does myocardial dysfunction contribute to heart failure?
How does myocardial dysfunction contribute to heart failure?
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What is a common feature of the compensatory mechanisms activated in heart failure?
What is a common feature of the compensatory mechanisms activated in heart failure?
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Study Notes
Heart Failure Pharmacology
- Heart failure (HF) is the inability of the heart to pump sufficient blood due to impaired filling and/or ejection capabilities.
- Major causes include ischemic heart disease, hypertension, valvular disorders, arrhythmias, cardiomyopathies, and conditions like severe anemia or anticancer drugs like doxorubicin.
- Chronic activation of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) results in cardiac remodeling, myocyte loss, hypertrophy, and fibrosis, leading to a decline in heart function.
Pathophysiology of Heart Failure
- Heart failure (HF) involves the inability of the heart to pump sufficient blood.
- Major causes include ischemic heart disease, hypertension, valvular disorders, arrhythmias, cardiomyopathies, and less commonly severe anemia or anticancer drugs.
- Chronic activation of the SNS and RAAS leads to cardiac remodeling with myocyte loss, hypertrophy, and fibrosis.
Compensatory Mechanisms in HF
- Increased sympathetic activity: Low blood pressure activates baroreceptors triggering the SNS. This increases heart rate and contraction strength.
- RAAS activation: Reduced renal blood flow stimulates renin release, activating angiotensin II and aldosterone.
- Natriuretic peptides: These peptides counteract excess fluid by inducing vasodilation and sodium excretion.
- Myocardial dysfunction: Heart muscle stretching initially increases contractile strength, but eventually, excessive stretching weakens contractions leading to systolic (HFrEF) or diastolic (HFpEF) failure.
Heart Failure Symptoms
- Common symptoms include coughing, shortness of breath, swelling in the abdomen (ascites), swelling in ankles and legs, and tiredness.
Pharmacologic Treatment of HF
- Positive inotropic effect drugs (increase the force of heart contractions).
- ACE inhibitors (reduce afterload).
- Angiotensin II receptor blockers (ARBs): similar to ACE inhibitors.
- Mineralocorticoid receptor antagonists (MRAs): reduce sodium retention and cardiac remodelling.
- Angiotensin Receptor-Neprilysin Inhibitors (ARNI): reduce afterload, preload, and myocardial fibrosis.
Diuretics
- Diuretics, like furosemide, reduce plasma volume and preload, relieving fluid overload symptoms.
- Electrolyte monitoring is essential to prevent complications like dehydration, hyponatremia, and hypokalemia.
Beta-Blockers
- These drugs mitigate SNS activation preventing norepinephrine buildup and cardiac remodeling.
- Gradual dose increase is critical to avoid adverse effects.
- Carvedilol also possesses anti-oxidant properties.
Hyperpolarization-activated cyclic nucleotide-gated channel blocker (HCN) blocker
- Ivabradine selectively slows the If current in the SA node, reducing heart rate without affecting contractility, AV conduction, and ventricular repolarization.
- Useful in patients with HFrEF, especially where beta-blockers are not tolerated.
Vaso- and Venodilators
- Venous dilators (eg., nitrites) reduce preload while arterial dilators (eg., hydralazine) reduce afterload.
- Used in patients unable to tolerate ACE inhibitors and ARBs or needing additional vasodilation.
Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors
- SGLT2 inhibitors (dapagliflozin and empagliflozin) reduce plasma volume through glucosuria and natriuresis, thus lowering preload and afterload.
- May reduce HF hospitalizations and mortality in patients with HFrEF.
Inotropic Drugs
- Inotropic drugs enhance cardiac contractility through intracellular calcium.
- Typically reserved for acute severe HF due to associated mortality in the long term.
- Digitalis glycosides, phosphodiesterase inhibitors, and B-adrenergic agonists are examples of inotropic drugs.
Cardiac Glycosides
- Cardiac glycosides, most notably digoxin, inhibit Na+/K+ ATPase, increasing calcium and contractility.
- Useful in symptoms of HFrEF.
- Requires careful monitoring due to a narrow therapeutic range.
Phosphodiesterase Inhibitors
- Phosphodiesterase inhibitors, for example milrinone, increase intracellular cAMP, resulting in increased calcium.
- Improve cardiac contractility, and reduce pulmonary vasculature resistance in acute HF and pulmonary hypertension.
B-Adrenergic Agonists
- B-adrenergic agonists (eg., dobutamine and dopamine) increase myocardial calcium entry and contraction; thus improving cardiac performance, via positive inotropic effects and vasodilation.
- Typically used in acute decompensated HF cases.
Soluble guanylate cyclase stimulators
- Vericiguat directly stimulates sGC which leads to increase in cGMP resulting in improved left ventricular compliance, reduced inflammation, and prevention of hypertrophy and fibrosis.
- Contraindicated in pregnancy and co-administration with nitrates/phosphodiesterase inhibitors due to risk of excessive hypotension.
Acute vs. Chronic HF Management
- Chronic HF is managed with lifestyle changes (fluid/sodium restriction) and optimized drug combinations.
- Acute decompensated HF may use inotropes and intravenous vasodilators for rapid stabilization. Avoiding NSAIDs are crucial.
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Description
This quiz covers the pharmacology and pathophysiology of heart failure, focusing on its causes, mechanisms, and compensatory responses. Learn about the role of the sympathetic nervous system and renin-angiotensin-aldosterone system in cardiac remodeling and heart function decline.
