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Questions and Answers
Which of the following is a compensatory mechanism in Heart Failure?
Which of the following is a compensatory mechanism in Heart Failure?
What is a consequence of decreased cardiac output in Heart Failure?
What is a consequence of decreased cardiac output in Heart Failure?
What is a key component of pathology progression in Heart Failure?
What is a key component of pathology progression in Heart Failure?
What is a cause of diastolic dysfunction?
What is a cause of diastolic dysfunction?
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What is a consequence of increased afterload in Heart Failure?
What is a consequence of increased afterload in Heart Failure?
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What is a type of infiltrative myocardial disease that can cause diastolic dysfunction?
What is a type of infiltrative myocardial disease that can cause diastolic dysfunction?
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What is a consequence of persistent activation of compensatory responses in Heart Failure?
What is a consequence of persistent activation of compensatory responses in Heart Failure?
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What is a definition of ventricular hypertrophy?
What is a definition of ventricular hypertrophy?
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What is a cause of shunts and high-output states?
What is a cause of shunts and high-output states?
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What is a consequence of tachycardia in Heart Failure?
What is a consequence of tachycardia in Heart Failure?
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Study Notes
Heart Failure
- Heart failure (HF) is a progressive clinical syndrome resulting from the heart's inability to pump sufficient blood to meet the body's metabolic needs.
Neurohormonal Model of Heart Failure
- The neurohormonal model is the current paradigm for understanding heart failure.
- Initiating events lead to decreased cardiac output, becoming a progressive systemic disease mediated by neurohormones and autocrine/paracrine factors.
- Drug therapies that target neurohormonal imbalances slow disease progression but do not stop it.
Neurohormones and Autocrine/Paracrine Factors
- Neurohormones involved in heart failure include angiotensin II, norepinephrine, aldosterone, and natriuretic peptides (ANP, BNP, and CNP).
- Autocrine/paracrine factors include proinflammatory cytokines (e.g., TNF-α, IL-6, and IL-1β), which have negative inotropic effects, reduce β-receptor-mediated responses, increase myocardial cell apoptosis, and stimulate remodeling.
Heart Failure Exacerbation
- Heart failure exacerbation occurs when previously compensated patients develop worsening symptoms that require hospitalization.
- Factors that exacerbate heart failure include noncompliance with medications and dietary recommendations, cardiac events, non-cardiac events, and inadequate or inappropriate medications.
- Most causes of heart failure exacerbation are preventable.
Drugs that Exacerbate Heart Failure
- Certain drugs can exacerbate heart failure, including:
- Negative inotropic effect drugs: antiarrhythmics, β-blockers, calcium channel blockers, and cardiotoxic drugs (e.g., doxorubicin and trastuzumab).
- Sodium and water retention drugs: nonsteroidal anti-inflammatory drugs, cyclooxygenase-2 inhibitors, thiazolidinediones, glucocorticoids, androgens, estrogens, and sodium-containing drugs.
Clinical Presentation
- Patient presentation may range from asymptomatic to cardiogenic shock, with symptoms including dyspnea, orthopnea, paroxysmal nocturnal dyspnea, chest pain, pulmonary edema, fatigue, nocturia, and confusion.
Factors Affecting Prognosis
- Factors affecting prognosis in heart failure include age, gender, left ventricular ejection fraction, renal function, extent of underlying coronary artery disease, diabetes, anemia, blood pressure, and heart failure etiology.
Etiology
- Heart failure can result from any disorder that affects the heart's ability to contract and/or relax.
- Coronary artery disease is the most common cause of systolic heart failure, accounting for nearly 70% of cases.
- Diastolic dysfunction is a common cause of heart failure, especially in the elderly, females, obese individuals, and those with hypertension, atrial fibrillation, and diabetes.
Compensatory Mechanisms in Heart Failure
- The heart's decrease in pumping capacity results in compensatory responses to maintain cardiac output.
- Compensatory responses include tachycardia and increased contractility, fluid retention and increased preload, vasoconstriction and increased afterload, and ventricular hypertrophy and remodeling.
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Description
Learn about the neurohormonal model of heart failure, its progression, and the role of neurohormones and autocrine/paracrine factors. Understand how drug therapies target neurohormonal imbalances to slow disease progression.
