Physiology of Heart Failure
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Questions and Answers

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

  • Increase in heart rate and vasoconstriction (correct)
  • Increase in peripheral resistance and retention of sodium and water
  • Release of natriuretic peptides and vasodilation
  • Decrease in preload and afterload

    • Which of the following is NOT a direct effect of activation of the renin-angiotensin-aldosterone system in heart failure?

  • Retention of sodium and water
  • Increased peripheral resistance
  • Vasodilation (correct)
  • Increased formation of angiotensin II

    • What is the effect of increased preload on stroke volume and cardiac output?

  • Increases stroke volume and cardiac output (correct)
  • Increases stroke volume but decreases cardiac output
  • Decreases stroke volume and cardiac output
  • Has no effect on stroke volume and cardiac output

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

    <p>Reduction in myocardial fibrosis</p> Signup and view all the answers

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

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

    Which of the following is a consequence of the long-term increase in the work of the heart in heart failure?

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

    What is the effect of activation of natriuretic peptides on peripheral resistance?

    <p>Decrease in peripheral resistance</p> Signup and view all the answers

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

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

    What is the effect of increased release of angiotensin II on cardiac preload?

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

    What is the initial effect of stretching of the heart muscle on the heart's contraction?

    <p>Stronger contractions</p> Signup and view all the answers

    What is the term for heart failure characterized by the ventricle's inability to pump effectively?

    <p>Systolic failure</p> Signup and view all the answers

    What is the primary consequence of excessive thickening of the ventricular wall?

    <p>Decreased ventricular volume</p> Signup and view all the answers

    What is the primary difference between compensated and decompensated heart failure?

    <p>Ability of adaptive mechanisms to restore cardiac output</p> Signup and view all the answers

    What is a typical sign of heart failure?

    <p>Dyspnea on exertion</p> Signup and view all the answers

    What is the primary goal of therapeutic strategies in heart failure?

    <p>All of the above</p> Signup and view all the answers

    What type of heart failure is characterized by a normal functioning left ventricle?

    <p>Diastolic heart failure</p> Signup and view all the answers

    What type of agents are reserved for acute heart failure signs and symptoms?

    <p>Inotropic agents</p> Signup and view all the answers

    What is the recommended daily fluid intake for heart failure patients?

    <p>Less than 1.5 to 2 liters</p> Signup and view all the answers

    Which of the following drugs may precipitate or exacerbate heart failure?

    <p>Nonsteroidal anti-inflammatory drugs</p> Signup and view all the answers

    What is the primary mechanism by which heart failure leads to the activation of the renin-angiotensin-aldosterone system?

    <p>Diminished renal perfusion pressure</p> Signup and view all the answers

    What is the effect of angiotensin-converting enzyme inhibitors on bradykinin levels?

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

    What is the primary effect of ACE inhibitors on the heart?

    <p>Decrease vascular resistance and venous tone</p> Signup and view all the answers

    Which of the following is NOT an indication for ACE inhibitors in heart failure?

    <p>Diastolic heart failure</p> Signup and view all the answers

    Which of the following ACE inhibitors is NOT listed as an option for heart failure treatment?

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

    What is the effect of angiotensin II on the heart?

    <p>Vasoconstriction and increased blood pressure</p> Signup and view all the answers

    What is the mechanism by which ACE inhibitors decrease aldosterone secretion?

    <p>By blocking the enzyme that cleaves angiotensin I to form angiotensin II</p> Signup and view all the answers

    What is the effect of ACE inhibitors on epinephrine levels in heart failure?

    <p>Decrease epinephrine levels</p> Signup and view all the answers

    What is the significance of food intake when administering captopril?

    <p>It decreases the absorption of captopril.</p> Signup and view all the answers

    What is the primary mechanism of action of ACE inhibitors?

    <p>Inhibition of the enzyme responsible for the production of angiotensin II.</p> Signup and view all the answers

    Which of the following is a rare but potential adverse effect of ACE inhibitors?

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

    What is the advantage of Angiotensin Receptor Blockers (ARBs) over ACE inhibitors?

    <p>ARBs provide more complete blockade of angiotensin II action.</p> Signup and view all the answers

    What is the primary reason for using ARBs in heart failure patients?

    <p>As a substitute for ACE inhibitors in patients with severe cough or Angioedema.</p> Signup and view all the answers

    What is the dosing frequency of valsartan?

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

    Which of the following ARBs undergoes extensive first-pass hepatic metabolism?

    <p>Losartan.</p> Signup and view all the answers

    What is the primary route of elimination of ARBs and their metabolites?

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

    What is the similarity between ACE inhibitors and ARBs in terms of adverse effects?

    <p>They have similar adverse effect profiles.</p> Signup and view all the answers

    What is the primary mechanism by which sacubitril is transformed to its active form?

    <p>Esterases in the plasma</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 half-life of sacubitril and valsartan?

    <p>10 hours</p> Signup and view all the answers

    What is the effect of ivabradine on heart rate?

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

    What is the indication for ivabradine in patients with HFrEF?

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

    What should patients taking ivabradine do to increase absorption?

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

    What is the consequence of inhibiting neprilysin with sacubitril?

    <p>Increased bradykinin levels</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

    What is the effect of ivabradine on cardiac output?

    <p>Has no effect on cardiac output</p> Signup and view all the answers

    Study Notes

    Heart Failure

    • Heart failure is a condition in which the heart is unable to pump enough blood to meet the body's needs.
    • Compensatory mechanisms are activated in heart failure to enhance cardiac output, including:
      • Increased sympathetic activity, which increases heart rate and force of contraction, and vasoconstriction to enhance venous return and cardiac preload.
      • Activation of the renin-angiotensin-aldosterone system, which increases peripheral resistance and retention of sodium and water, leading to increased blood volume and pressure.
      • Activation of natriuretic peptides, which leads to vasodilation, natriuresis, inhibition of renin and aldosterone release, and reduction of myocardial fibrosis.
    • Myocardial hypertrophy is a compensatory response in heart failure, where the heart increases in size, and the chambers dilate and become more globular.
    • There are two types of heart failure:
      • Systolic failure (HFrEF), where the ventricle is unable to pump effectively due to excessive elongation of fibers, resulting in weaker contractions.
      • Diastolic failure (HFpEF), where the ventricle does not fill adequately due to thickening of the ventricular wall and subsequent decrease in ventricular volume.

    Acute (Decompensated) Heart Failure

    • Acute heart failure occurs when the adaptive mechanisms fail to maintain cardiac output, leading to worsening signs and symptoms of heart failure.
    • Typical signs and symptoms of heart failure include:
      • Dyspnea on exertion
      • Orthopnea
      • Paroxysmal nocturnal dyspnea
      • Fatigue
      • Peripheral edema

    Therapeutic Strategies in Heart Failure

    • Heart failure is typically managed by:
      • Fluid limitations (less than 1.5 to 2 L daily)
      • Low intake of sodium (less than 2000 mg/d)
      • Treatment of comorbid conditions
      • Diuretics, inhibitors of the renin-angiotensin-aldosterone system, and inhibitors of the sympathetic nervous system
      • Inotropic agents (reserved for acute heart failure signs and symptoms in mostly the inpatient setting)
    • Drugs that may precipitate or exacerbate heart failure, such as:
      • Nonsteroidal anti-inflammatory drugs (NSAIDs)
      • Alcohol
      • Non-dihydropyridine calcium channel blockers
      • Some antiarrhythmic drugs

    Angiotensin-Converting Enzyme (ACE) Inhibitors

    • ACE inhibitors are a part of standard pharmacotherapy in HFrEF.
    • ACE inhibitors block the enzyme that cleaves angiotensin I to form the potent vasoconstrictor angiotensin II.
    • ACE inhibitors also:
      • Diminish the inactivation of bradykinin
      • Reduce the secretion of aldosterone
      • Decrease vascular resistance (afterload) and venous tone (preload), resulting in increased cardiac output
    • Actions on the heart:
      • Decrease vascular resistance (afterload) and venous tone (preload)
      • Blunt the usual angiotensin II–mediated increase in epinephrine and aldosterone seen in HF
    • Indications:
      • Patients with asymptomatic and symptomatic HFrEF
      • Patients with all stages of left ventricular failure
    • Pharmacokinetics:
      • Orally active
      • Food may decrease the absorption of captopril, so it should be taken on an empty stomach
      • Except for captopril, ACE inhibitors are prodrugs that require activation by hydrolysis via hepatic enzymes
      • Renal elimination of the active moiety is important for most ACE inhibitors except fosinopril
    • Adverse effects:
      • Postural hypotension
      • Renal insufficiency
      • Hyperkalemia
      • A persistent dry cough
      • Angioedema (rare)

    Angiotensin Receptor Blockers (ARBs)

    • ARBs are orally active compounds that are competitive antagonists of the angiotensin II type 1 receptor.
    • Actions on the cardiovascular system:
      • Similar to ACE inhibitors, ARBs decrease vascular resistance (afterload) and venous tone (preload)
      • Mainly used as a substitute for ACE inhibitors in patients with severe cough or angioedema
    • Pharmacokinetics:
      • Orally active
      • Dosed once-daily, with the exception of valsartan which is twice a day
      • Highly plasma protein bound and, except for candesartan, have large volumes of distribution
      • Elimination of metabolites and parent compounds occurs in urine and feces
    • Adverse effects:
      • Similar to ACE inhibitors

    Angiotensin Receptor-Neprilysin Inhibitors (ARNIs)

    • ARNIs are a combination of an angiotensin receptor blocker and a neprilysin inhibitor.
    • Actions on the cardiovascular system:
      • Similar to ACE inhibitors, ARNIs decrease vascular resistance (afterload) and venous tone (preload)
      • Reduce the heart rate, leading to increased stroke volume and improved symptoms of HF
    • Pharmacokinetics:
      • Sacubitril is transformed to active drug by plasma esterases
      • Both drugs have a high volume of distribution and are highly bound to plasma proteins
      • Elimination of metabolites and parent compounds occurs in urine and feces
    • Adverse effects:
      • Similar to ACE inhibitors, with the added potential for hypotension and bradykinin-mediated angioedema

    Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Channel Blockers

    • HCN channel blockers, such as ivabradine, selectively slow the (If) current in the SA node, reducing the heart rate.
    • Actions on the cardiovascular system:
      • Reduction of heart rate without a reduction in contractility, AV conduction, ventricular repolarization, or blood pressure
      • Increases stroke volume and improves symptoms of HF
    • Indications:
      • Patients with HFrEF who are in sinus rhythm with a heart rate above 70 beats per minute and are on optimized HF pharmacotherapy
      • Patients who are on an optimal dose of β-blocker or have a contraindication to β-blockers
    • Pharmacokinetics:
      • Administered with meals to increase absorption
      • Has a high volume of distribution and is highly bound to plasma proteins
      • Elimination of metabolites and parent compounds occurs in urine and feces

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    Description

    This quiz covers the compensatory physiological responses in heart failure, including increased sympathetic activity, renin-angiotensin-aldosterone system, and ventricular remodeling.

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