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Questions and Answers
What is the recommendation for patients in Stage A heart failure?
What is the recommendation for patients in Stage A heart failure?
What characterizes Stage C heart failure?
What characterizes Stage C heart failure?
Which of the following interventions is specifically associated with Stage D heart failure?
Which of the following interventions is specifically associated with Stage D heart failure?
In the context of heart failure prevention, which stage recommends drugs for patients with structural heart disease but without any heart failure signs or symptoms?
In the context of heart failure prevention, which stage recommends drugs for patients with structural heart disease but without any heart failure signs or symptoms?
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What is primarily recommended for patients with heart failure with reduced ejection fraction (HFrEF) in Stage C?
What is primarily recommended for patients with heart failure with reduced ejection fraction (HFrEF) in Stage C?
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Which symptom is commonly associated with chronic heart failure aside from fatigue?
Which symptom is commonly associated with chronic heart failure aside from fatigue?
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What is the primary purpose of the New York Heart Association (NYHA) Functional Classification System?
What is the primary purpose of the New York Heart Association (NYHA) Functional Classification System?
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Which diagnostic test can be used to demonstrate ventricular hypertrophy?
Which diagnostic test can be used to demonstrate ventricular hypertrophy?
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What is the first step in the treatment of chronic heart failure?
What is the first step in the treatment of chronic heart failure?
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What is one of the main goals of treating chronic heart failure?
What is one of the main goals of treating chronic heart failure?
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Which type of heart failure is characterized by reduced left ventricular ejection fraction?
Which type of heart failure is characterized by reduced left ventricular ejection fraction?
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What is one of the primary symptoms of heart failure?
What is one of the primary symptoms of heart failure?
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What causes diastolic dysfunction in heart failure?
What causes diastolic dysfunction in heart failure?
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Which of the following compensatory mechanisms occurs in response to decreased cardiac output?
Which of the following compensatory mechanisms occurs in response to decreased cardiac output?
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What is the leading cause of heart failure?
What is the leading cause of heart failure?
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What term refers to heart failure with normal left ventricular ejection fraction?
What term refers to heart failure with normal left ventricular ejection fraction?
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What complication often results from fluid overload in heart failure?
What complication often results from fluid overload in heart failure?
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What process refers to the structural changes in the heart due to chronic activation of neurohormonal systems in heart failure?
What process refers to the structural changes in the heart due to chronic activation of neurohormonal systems in heart failure?
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Study Notes
Heart Failure
- Heart failure (HF) is a syndrome associated with signs and symptoms due to abnormalities in cardiac structure or function.
- HF may be caused by abnormalities in systolic function, diastolic function, or both.
- HF with reduced systolic function (reduced left ventricular ejection fraction, LVEF) is called HF with reduced ejection fraction (HFrEF).
- Diastolic dysfunction with normal LVEF is called HF with preserved ejection fraction (HFpEF).
Pathophysiology
- Causes of systolic dysfunction (decreased contractility) include reduced muscle mass (e.g., myocardial infarction [MI]).
- Causes of diastolic dysfunction (restriction in ventricular filling) include increased ventricular stiffness and ventricular hypertrophy.
- Coronary artery disease and hypertension are the leading causes of HF.
- Decreased cardiac output (CO) activates compensatory responses to maintain circulation, including:
- Tachycardia and increased contractility through sympathetic nervous system activation.
- Increased preload (through sodium and water retention), increasing stroke volume.
- Vasoconstriction.
- Ventricular hypertrophy and remodeling.
- Compensatory mechanisms initially maintain cardiac function but contribute to disease progression.
- Chronic activation of neurohormonal systems results in a cascade of events, affecting the myocardium and leading to changes in ventricular size, shape, structure, and function (ventricular remodeling).
Clinical Presentation
- Patient presentation may range from asymptomatic to cardiogenic shock.
- Primary symptoms include dyspnea (especially on exertion) and exercise intolerance, fatigue.
- Other pulmonary symptoms include orthopnea, paroxysmal nocturnal dyspnea (PND), tachypnea, and cough. Fluid overload can lead to pulmonary congestion and peripheral edema.
- Nonspecific symptoms may include fatigue, nocturia, hemoptysis, abdominal pain, anorexia, nausea, bloating, ascites, poor appetite or early satiety, and weight gain or loss.
Diagnosis
- Ventricular hypertrophy can be demonstrated on chest radiographs or electrocardiograms (ECGs).
- Chest radiographs may show pleural effusions or pulmonary edema.
- Echocardiogram can quantify LVEF to determine if systolic or diastolic dysfunction is present.
- The New York Heart Association (NYHA) Functional Classification System classifies symptoms according to subjective evaluation.
- NYHA Class I: No limitation of physical activity.
- NYHA Class II: Slight limitation; asymptomatic at rest, but symptoms with normal level of activity.
- NYHA Class III: Marked limitation; asymptomatic at rest, but symptoms with less than normal level of activity.
- NYHA Class IV: Unable to carry out any physical activity without discomfort; symptoms of HF at rest.
Treatment of Chronic Heart Failure
- Goals of treatment include improving quality of life, relieving or reducing symptoms, preventing or minimizing hospitalizations, and prolonging survival.
- General Approach: Determine etiology/precipitating factors; treat underlying disorders; manage HF using a staging system.
- Stages:
- Stage A: At-risk for HF (no signs or symptoms; no structural heart disease).
- Stage B: PreHF (no signs or symptoms; structural heart disease).
- Stage C: HF (HF signs or symptoms; structural heart disease).
- Stage D: Advanced HF (persistent HF symptoms despite maximal tolerated GDMT).
- Recommendations vary depending on stage and type of HF (HFrEF or HFpEF), and may include drugs, guideline-directed medical therapy (GDMT), and specialized interventions.
Treatment of Chronic Heart Failure - Nonpharmacological
- Interventions include restriction of fluid intake and dietary sodium (<2-3 g sodium/day) with daily weight measurements.
- Limit fluid intake in patients with hyponatremia or persistent volume retention despite diuretic use to 2 L/day.
- Revascularization or anti-ischemic therapy in patients with coronary disease may reduce HF symptoms.
- Avoid drugs that can worsen HF when possible.
Treatment of Chronic Heart Failure - Pharmacologic
- Stage C HFrEF: ACE inhibitor, ARB, or ARNI plus β-blocker, SGLT2 inhibitor, and aldosterone antagonist.
- Fluid retention: Administer diuretic.
- Specific situations: Hydralazine-nitrate combination (African American patients), ivabradine, vericiguat, or digoxin may be considered in select patients.
A-Diuretics
- Diuretic therapy (in addition to sodium restriction) is recommended for all patients with clinical evidence of fluid retention.
- Thiazide diuretics are relatively weak and not frequently used alone, but can be combined with loop diuretics for better diuresis.
- Loop diuretics (furosemide, bumetanide, torsemide) are usually necessary for fluid retention and euvolemia.
- Adverse effects of diuretics include hypovolemia, hypotension, hyponatremia, hypokalemia, hypomagnesemia, hyperuricemia, and renal dysfunction.
B-ACE Inhibitors
- Improve symptoms, slow disease progression, and decrease mortality in HFrEF patients.
- Sacubitril/valsartan is preferred over ACE inhibitors for HFrEF.
- Discontinue ACE inhibitors 36 hours prior to starting sacubitril/valsartan.
- Common adverse effects include hypotension, renal dysfunction, hyperkalemia, and a cough.
- Angioedema is a serious potential side effect and requires close monitoring.
C-ARB Blockers
- Alternative to ACE inhibitors and preferred over ACE inhibitors for patients intolerant to ACE inhibitors.
- ARBs do not affect bradykinin, which is linked to ACE inhibitor cough and angioedema.
- Only candesartan, valsartan, and losartan are recommended due to demonstrated efficacy in clinical trials.
- Adverse effects include hypotension, hyperkalemia, and renal insufficiency.
D-ARNI
- Use of valsartan/sacubitril is recommended to reduce morbidity and mortality in HFrEF (NYHA II-IV).
- Neprilysin is an enzyme that breaks down bradykinin and natriuretic peptides; reducing neprilysin activity enhances vasodilation, diuresis, and natriuresis.
- ARNI is preferred over ACE inhibitors or ARBs for HFrEF.
- Discontinue ACE inhibitors 36 hours before initiation; no waiting period is required for ARBs.
E-Beta-Blockers
- Antagonize sympathetic nervous system effects, slowing disease progression, and reducing HF mortality and hospitalizations.
- Carvedilol, metoprolol succinate (CR/XL), and bisoprolol are the only beta-blockers shown to reduce mortality in large HF trials.
- Initiate in stable patients without evidence of fluid overload, titrating dose slowly.
- Monitor for bradycardia, heart block, hypotension, fatigue, impaired glycemic control, and bronchospasm.
F-Aldosterone Antagonists
- Block aldosterone receptors, improving outcomes.
- Spironolactone and eplerenone are examples.
- Use with caution in patients with impaired renal function, elevated potassium.
- Patients may experience gynecomastia, impotence, and menstrual irregularities.
G-SGLT2 Inhibitors
- SGLT2 inhibitors block glucose and sodium reabsorption in the kidneys, leading to osmotic diuresis and natriuresis.
- Recommended in symptomatic HFrEF, irrespective of diabetes type.
- Patients should avoid abrupt position changes due to potential orthostasis with over-diuresis.
H-Nitrates and Hydralazine
- Isosorbide dinitrate (ISDN) is a venodilator.
- Hydralazine is a direct arterial vasodilator that reduces the systemic vascular resistance (SVR).
- These are added to black patients with HFrEF.
I-Ivabradine
- Ivabradine slows heart rate, which also improves outcomes.
- Start in patients already taking maximally tolerated beta-blocker dosages.
- It is contraindicated in patients unable to tolerate a beta-blocker, caution should be taken in patients who have a contraindication to β-blocker use.
J-Digoxin
- Digoxin has neutral effects in HF; it's not a first-line medication but may improve symptoms and reduce hospitalizations for select patients with symptomatic HFrEF despite GDMT or those intolerant to other GDMT.
- Digoxin can help control ventricular rate in HFrEF with supraventricular arrhythmias.
K-Vericiguat
- Vericiguat modulates endothelial dysfunction by activating soluble guanylate cyclase.
- It regulates contractility and diastolic function.
- May be considered in additional optimized HF therapy to potentially mitigate morbidity and mortality in patients at high risk for HFrEF.
- Not indicated in HFpEF due to lack of benefit and safety data.
Evaluation of Therapeutic Outcomes - Chronic HF
- Assess daily patient activities, assess efficacy of diuretic therapy by disappearance of excess fluid retention.
- Monitor daily weights- Changes of 1.4-2.3 kg are important to report.
- Monitor for potential worsening of symptoms due to beta-blocker therapy.
- Monitor electrolytes (potassium and magnesium) and renal function (BUN, serum creatinine, eGFR).
Evaluation of Therapeutic Outcomes - Acute HF
- Assess efficacy of drug therapy with daily monitoring of weight, fluid intake, and output, and HF signs and symptoms.
- Monitor for electrolyte depletion, symptomatic hypotension, and renal dysfunction regularly.
- Assess vital signs frequently.
General Approach - Acute Decompensated Heart Failure (ADHF)
- ADHF involves patients with new or worsening signs/symptoms resulting from volume overload or low cardiac output; requiring medical intervention.
- Admission to an ICU may be needed; administer IV loop diuretics as first-line treatment for ADHF patients with volume overload.
- Consider non-invasive ventilation for patients in respiratory distress due to acute pulmonary edema.
- Provide pharmacologic thromboprophylaxis to patients with limited mobility; consider mechanical thromboprophylaxis. -Temporary mechanical circulatory support may be considered until underlying issues are corrected, cardiac transplantation is the best option for patients with the irreversible form of advanced HF.
- Hold or reduce beta-blocker dosages of patients if recent changes are responsible for acute decompensation.
- ACE inhibitors, ARBs, ARNI, and aldosterone antagonists may need to be temporarily withheld when renal dysfunction is present.
- Place all patients with congestive symptoms on a strict sodium restriction diet (< 2 g daily).
Pharmacologic Therapy for HFpEF
- Initiate SGLT2 inhibitors in HFpEF patients without contraindications.
- Use diuretics for relief of volume overload.
- The addition of aldosterone antagonists, ARNI, or ARBs may be considered.
B-Vasopressin Antagonists - (e.g. Tolvaptan)
- Used for hypervolemic and euvolemic hyponatremia in HF.
- Monitor patients closely to avoid excessively rapid increases in serum sodium; discontinue if necessary.
- Use with caution.
C-Vasodilators
- Reduce preload by increasing venous capacitance and improving symptoms of pulmonary congestion.
- Arterial vasodilators reduce afterload and increase cardiac output (CO).
- IV nitroglycerin is often the vasodilator of choice in ADHF.
- Sodium nitroprusside is a mixed arteriovenous vasodilator; use prudently due to hypotension risk.
D-Inotropic Therapy
- Correct low cardiac output (CO) in hypoperfused patients with inotropes (e.g., dobutamine, milrinone, norepinephrine, or dopamine).
- These are temporizing measures used for cardiogenic shock or severely depressed CO and low systolic BP
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Description
This quiz covers the fundamentals of heart failure (HF), including its definitions, classifications, and underlying causes of systolic and diastolic dysfunction. Additionally, it explores the pathophysiological mechanisms associated with heart failure, such as decreased cardiac output and compensatory responses. Test your knowledge on this critical cardiac condition.