Physiology of Heart Failure
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Questions and Answers

What is the primary mechanism by which the renin-angiotensin-aldosterone system increases peripheral resistance?

  • Increasing the formation of angiotensin II (correct)
  • Enhancing the release of aldosterone
  • Directly stimulating the release of natriuretic peptides
  • Inhibiting the activity of β-adrenergic receptors

    • Which of the following is NOT a compensatory response to heart failure?

  • Activation of the renin-angiotensin-aldosterone system
  • Increased parasympathetic activity (correct)
  • Increased sympathetic activity
  • Release of natriuretic peptides

    • What is the primary effect of increased sympathetic activity on the heart in heart failure?

  • Increased heart rate and contractility (correct)
  • Decreased heart rate and contractility
  • Decreased venous return and cardiac preload
  • Increased peripheral resistance and cardiac output

    • Which of the following is a beneficial effect of natriuretic peptides in heart failure?

    <p>Vasodilation and reduction of myocardial fibrosis</p> Signup and view all the answers

    What is the primary mechanism by which increased preload increases cardiac output?

    <p>Increased stroke volume through the Frank-Starling mechanism</p> Signup and view all the answers

    What is the ultimate effect of the renin-angiotensin-aldosterone system on cardiac function?

    <p>Increased peripheral resistance and cardiac workload</p> Signup and view all the answers

    What is the role of neprilysin enzyme in the body?

    <p>To degrade natriuretic peptides and other vasoactive peptides</p> Signup and view all the answers

    What is the primary stimulus for the release of renin in heart failure?

    <p>Decreased blood flow to the kidney</p> Signup and view all the answers

    Which of the following is a long-term consequence of the compensatory responses to heart failure?

    <p>Further decline in cardiac function and increased symptoms</p> Signup and view all the answers

    What is the effect of inhibiting neprilysin on bradykinin levels?

    <p>It increases the levels of bradykinin</p> Signup and view all the answers

    What is the effect of natriuretic peptides on sodium levels in the blood?

    <p>They remove sodium from the blood and excrete it in the urine</p> Signup and view all the answers

    What is the therapeutic use of an ARNI in patients with HFrEF?

    <p>To replace an ACE inhibitor or ARB in patients with HFrEF who remain symptomatic on optimal doses of a β-blocker and an ACE inhibitor or ARB</p> Signup and view all the answers

    What is the effect of sacubitril/valsartan on afterload, preload, and myocardial fibrosis?

    <p>It decreases afterload, preload, and myocardial fibrosis</p> Signup and view all the answers

    What is the benefit of using an ARNI over an ACE inhibitor in patients with HFrEF?

    <p>ARNI improves survival and symptoms of HF</p> Signup and view all the answers

    What is the reason for combining an ARB with a neprilysin inhibitor?

    <p>To avoid the risk of angioedema</p> Signup and view all the answers

    What happens to sacubitril in the body?

    <p>It is transformed to an active drug by plasma esterases</p> Signup and view all the answers

    What is the primary mechanism of digoxin elimination in the body?

    <p>Renal excretion</p> Signup and view all the answers

    What is the initial indicator of digoxin toxicity in patients?

    <p>Anorexia, nausea, and vomiting</p> Signup and view all the answers

    What is the effect of decreased serum potassium levels on digoxin toxicity?

    <p>Increased risk of toxicity</p> Signup and view all the answers

    What is the primary mechanism of action of ivabradine?

    <p>Inhibition of HCN channel and reduction of heart rate</p> Signup and view all the answers

    What is the mechanism of action of β-adrenergic agonists in increasing cardiac contractility?

    <p>Increase in intracellular cAMP</p> Signup and view all the answers

    What is the benefit of ivabradine in patients with HFrEF?

    <p>Increase in stroke volume and improvement in HF symptoms</p> Signup and view all the answers

    What is the effect of phosphodiesterase inhibitors on cardiac contractility?

    <p>Increase in cardiac contractility</p> Signup and view all the answers

    What is the contraindication for the use of ARNI in patients with a history of?

    <p>Hereditary angioedema or angioedema associated with ACE inhibitor or ARB</p> Signup and view all the answers

    What is the primary function of neprilysin in the body?

    <p>Breaking down vasoactive peptides</p> Signup and view all the answers

    What is the main adverse effect of ARNI similar to that of an ACE inhibitor or ARB?

    <p>Angioedema</p> Signup and view all the answers

    What is the possible consequence of severe digoxin toxicity?

    <p>Ventricular tachycardia</p> Signup and view all the answers

    What is the recommended dosing frequency for sacubitril/valsartan?

    <p>Twice daily</p> Signup and view all the answers

    What is the common complication of thiazide or loop diuretics in patients receiving digoxin?

    <p>Hypokalemia</p> Signup and view all the answers

    What is the pharmacokinetic characteristic of ivabradine?

    <p>Extensive first-pass metabolism by cytochrome P450 3A4</p> Signup and view all the answers

    What is the benefit of using ivabradine in patients with HFrEF?

    <p>Improvement in symptoms in patients with a heart rate above 70 beats per minute</p> Signup and view all the answers

    What is the effect of ARNI on bradykinin levels?

    <p>Increase in bradykinin levels</p> Signup and view all the answers

    What is the primary route of excretion for sacubitril?

    <p>Urine</p> Signup and view all the answers

    What is the effect of inhibiting the HCN channel on the heart rate?

    <p>Decreases the heart rate</p> Signup and view all the answers

    What is the benefit of using ivabradine in patients with HFrEF?

    <p>Improves symptoms of HF</p> Signup and view all the answers

    What is the effect of sacubitril on bradykinin levels?

    <p>Increases bradykinin levels</p> Signup and view all the answers

    What is the primary mechanism of action of ivabradine?

    <p>Inhibition of the HCN channel</p> Signup and view all the answers

    What is the recommended administration of ivabradine?

    <p>Administered with meals</p> Signup and view all the answers

    What is the effect of sacubitril on afterload?

    <p>Decreases afterload</p> Signup and view all the answers

    What is the contraindication for the combination of sacubitril and valsartan?

    <p>History of hereditary angioedema or angioedema associated with an ACE inhibitor or ARB</p> Signup and view all the answers

    Study Notes

    Heart Failure

    • Heart failure evokes three major compensatory mechanisms to enhance cardiac output:
      • Increased sympathetic activity
      • Activation of the renin-angiotensin-aldosterone system
      • Activation of natriuretic peptides

    Compensatory Mechanisms

    • Increased sympathetic activity:
      • Baroreceptors sense a decrease in blood pressure and activate the sympathetic nervous system
      • Stimulation of β-adrenergic receptors results in an increased heart rate and a greater force of contraction
      • Vasoconstriction enhances venous return and increases cardiac preload
      • An increase in preload increases stroke volume, which in turn increases cardiac output

    Activation of the Renin-Angiotensin-Aldosterone System

    • A fall in cardiac output (COP) decreases blood flow to the kidney, prompting the release of renin
    • Release of renin results in increased formation of angiotensin II and aldosterone
    • Increased peripheral resistance (afterload) and retention of sodium and water
    • Increased volume returns to the heart, increasing cardiac preload

    Activation of Natriuretic Peptides

    • Increase in preload also increases the release of natriuretic peptides
    • Natriuretic peptides (atrial, B-type, and C-type) have differing roles in heart failure
    • Atrial and B-type natriuretic peptides are the most important
    • Activation of natriuretic peptides results in:
      • Vasodilation
      • Natriuresis
      • Inhibition of renin and aldosterone release
      • Reduction in myocardial fibrosis

    Pharmacological Treatment

    • Digoxin:
      • Increases the force of contraction (inotropic effect)
      • Long half-life of 30-40 hours
      • Eliminated by the kidney, requiring dose adjustment in renal dysfunction
      • Common adverse reactions: anorexia, nausea, vomiting, blurred vision, and cardiac arrhythmias
      • Toxicity can be managed by discontinuing digoxin, determining serum potassium levels, and replenishing potassium if necessary

    β-Adrenergic Agonists

    • β-Adrenergic agonists (dobutamine and dopamine):
      • Cause positive inotropic effects and vasodilation
      • Increase intracellular cAMP, leading to the activation of protein kinase
      • Protein kinase phosphorylates slow calcium channels, increasing entry of calcium ions into the myocardial cells and enhancing contraction

    Phosphodiesterase Inhibitors

    • Milrinone:
      • Increases the intracellular concentration of cAMP
      • Results in an increase in intracellular calcium and cardiac contractility

    Angiotensin Receptor-Neprilysin Inhibitor

    • Sacubitril/valsartan:
      • Combines the actions of an angiotensin receptor blocker (ARB) with neprilysin inhibition
      • Inhibition of neprilysin results in increased concentration of vasoactive peptides, leading to:
        • Natriuresis
        • Diuresis
        • Vasodilation
        • Inhibition of fibrosis
      • Decreases afterload, preload, and myocardial fibrosis
      • Improves survival and symptoms of heart failure compared to therapy with an ACE inhibitor

    Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Blocker

    • Ivabradine:
      • Selectively slows the If current in the SA node, reducing heart rate
      • Does not reduce contractility, AV conduction, ventricular repolarization, or blood pressure
      • Used in heart failure with reduced ejection fraction (HFrEF) to improve symptoms in patients who are in sinus rhythm with a heart rate above 70 beats per minute and are on optimized HF pharmacotherapy

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    Description

    Learn about the effects of increased intracellular calcium levels on heart contraction and the compensatory mechanisms in heart failure, including sympathetic activity and beta-adrenergic receptor stimulation.

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