Lecture 4 + 5 Heart faliure Flashcards

1
Q

Describe the difference between acute and chronic heart failure, including the key symptoms associated with each.

A

Acute heart failure presents with sudden onset of severe shortness of breath and acute pulmonary edema, requiring immediate medical attention.
Chronic heart failure involves ongoing symptoms like fatigue, reduced exercise tolerance, ankle edema, sudden weight gain, persistent cough, and confusion, punctuated by acute heart failure episodes.

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2
Q

How does the pathophysiology of heart failure lead to compensatory mechanisms in the body? Explain the main compensatory effects resulting from the stimulation of the sympathetic nervous system, RAAS, and AVS.

A

In heart failure, compensatory mechanisms aim to maintain blood circulation by increasing cardiac output through ventricular remodeling, maintaining tissue perfusion via increased arterial blood pressure from systems like RAAS and sympathetic nervous system. This leads to effects like cardiac remodeling, fluid retention, vasoconstriction, increased heart rate, and increased blood pressure.

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3
Q

Define N-Terminal-proBNP and explain its role in heart failure diagnosis. How does it differ in levels between heart failure and normal conditions?

A

N-Terminal-proBNP is a peptide released when the heart walls are stretched or under pressure overload, like in heart failure. It stimulates fluid and sodium loss and mild vasodilation. High levels are seen in heart failure, aiding in diagnosis. In normal conditions, levels of N-Terminal-proBNP are lower.

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4
Q

What are the key diagnostic methods used for chronic heart failure? Explain the importance of each method in evaluating the condition.

A

Diagnostic methods for chronic heart failure include detailed history and examination, electrocardiography, NT-proBNP levels, echocardiogram, chest x-ray, blood tests, 6-minute walk test, and coronary angiogram. These tests help in assessing symptoms, heart rhythm, heart function, fluid overload, exercise tolerance, and potential blockages in the heart.

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5
Q

Describe the signs and symptoms associated with heart failure. How do these manifestations impact the daily life and well-being of individuals with this condition?

A

Signs and symptoms of heart failure include breathlessness, reduced exercise tolerance, fatigue, ankle edema, sudden weight gain, dizziness, cough, loss of appetite, palpitations, confusion, and more. These symptoms can significantly impact daily life, causing limitations in physical activities, emotional distress, and overall reduced quality of life.

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6
Q

Explain the main differences in the compensatory responses seen in acute and chronic heart failure. How do these responses contribute to the progression of the condition over time?

A

In acute heart failure, compensatory responses are immediate and intense, aiming to stabilize the condition rapidly. In chronic heart failure, these responses are ongoing but may become maladaptive, leading to further deterioration of heart function. Over time, these responses can contribute to the worsening of heart failure and its symptoms.

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7
Q

Describe the mechanism of action of ACE inhibitors in heart failure management. How do ACE inhibitors reduce sodium and water retention? What is their impact on left ventricular remodelling?

A

ACE inhibitors prevent the production of angiotensin II, leading to reduced sodium and water retention and vasoconstriction. They also help reduce left ventricular remodelling in heart failure patients.

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8
Q

How should ACE inhibitors be initiated in heart failure patients? What is the recommended dosing strategy for ACE inhibitors?

A

ACE inhibitors should be started at a low dose and increased every 2 weeks to the maximum tolerated or target dose. Examples include ramipril and perindopril.

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9
Q

Explain the mechanism of action of Angiotensin Receptor Blockers (ARBs) in heart failure management. When are ARBs typically used in patients intolerant to ACE inhibitors?

A

ARBs block the binding of angiotensin II to its receptor. They are often used in heart failure patients who are intolerant to ACE inhibitors.

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10
Q

Describe the role of Angiotensin Receptor-Neprilysin Inhibitors (ARNIs) in heart failure management. When can ARNIs be considered as a replacement for ACE inhibitors?

A

ARNIs are more effective than ACE inhibitors in trials and can replace ACE inhibitors in patients who remain symptomatic on the maximum tolerated dose. They act on the RAAS and natriuretic peptide system.

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11
Q

What is the mechanism of action of beta blockers in heart failure? How do beta-adrenoceptor blockers affect the sympathetic nervous system in heart failure patients?

A

Beta blockers in heart failure suppress the sympathetic nervous system, which the heart relies on for maintaining cardiac output. They help reduce the overdrive of the sympathetic nervous system.

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12
Q

Describe the dosing regimen for Entresto®, a combination drug containing sacubitril and valsartan. How is the dosing of Entresto® titrated in heart failure patients?

A

Entresto® is initially dosed at 24/26 mg twice daily for 3-4 weeks, then increased to 49/51 mg twice daily for 3-4 weeks if tolerated, and further increased to 97/103 mg twice daily if tolerated.

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13
Q

What are the common side effects of ACE inhibitors in heart failure patients? When should ACE inhibitors be contraindicated?

A

Common side effects of ACE inhibitors include hyperkalemia, cough, and hypotension. They are contraindicated in patients with a history of angioedema, bilateral renal artery stenosis, or pregnancy.

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14
Q

Explain the monitoring recommendations for patients on ARNIs in heart failure management. What parameters should be monitored regularly for patients on ARNIs?

A

Patients on ARNIs should be monitored for electrolytes (including renal function) and blood pressure regularly. There is a risk of hypotension associated with ARNIs.

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15
Q

How should beta blockers be monitored in heart failure patients? What parameters should be regularly checked for patients on beta blockers?

A

Blood pressure and heart rate should be monitored regularly in heart failure patients on beta blockers to ensure they are within the target range.

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16
Q

Describe the mechanism of action of Mineralocorticoid Receptor Antagonists (MRAs) and their recommended use in patients with HFrEF. What are the common side effects and monitoring parameters associated with MRAs?

A

Mineralocorticoid Receptor Antagonists (MRAs) work by preventing aldosterone binding to the mineralocorticoid receptor, counteracting sodium and water retention. They are recommended in addition to ACE-I/ARNI and BB in HFrEF. Common side effects include gynaecomastia, hyperkalaemia, and renal dysfunction. Monitoring parameters include U&E, BP, and potassium levels.

17
Q

How do Sodium-Glucose-Co-Transporter-2 inhibitors (SGLT-2i) work and why are they recommended in HFrEF patients? What are the risks associated with SGLT-2i and what should be monitored regularly?

A

Sodium-Glucose-Co-Transporter-2 inhibitors (SGLT-2i) inhibit glucose re-absorption in the proximal renal tubules, recommended in HFrEF regardless of diabetes status. Risks include dehydration, small initial reduction in eGFR, and contraindication in critical limb ischaemia. Monitoring should include volume depletion, blood glucose, BP, and renal function.

18
Q

Define the role of Loop diuretics in managing heart failure. How are they dosed and monitored? What are the common side effects and when is a loop and thiazide combination used?

A

Loop diuretics relieve congestive symptoms and fluid retention in heart failure. They are dosed low and adjusted based on response, tolerance, and renal function to achieve ‘dry weight’. Monitoring includes U&E, renal function, and BP. Side effects may include electrolyte disturbances, gout, dizziness, and AKI. A loop and thiazide combination is used for resistant oedema.

19
Q

Describe the benefits of IV iron in patients with HFrEF and iron deficiency. What evidence supports its use and what outcomes are improved?

A

IV iron benefits patients with HFrEF and iron deficiency by reducing the risk of hospital admissions for heart failure and cardiovascular death. Evidence shows improved outcomes, but there is a lack of strong evidence for oral iron. IV iron has shown to be beneficial in reducing adverse events in this patient population.

20
Q

How is heart failure with mid-range ejection fraction (HFmrEF) managed differently from other forms of heart failure? What are the key recommendations for treatment in HFmrEF patients based on recent guidelines?

A

HFmrEF (EF 41-49%) is managed similarly to other forms of heart failure with the addition of SGLT2 inhibitors based on recent guidelines. Recommendations include diuretics for symptom control, SGLT2 inhibitors for improved outcomes, and consideration of ACE/ARNI/ARB, MRA, and BB based on clinical judgement and co-morbidities.

21
Q

Explain the importance of ACE inhibitors, ARNIs, and beta-blockers in the management of heart failure with reduced ejection fraction (HFrEF). How do these medications reduce the risk of hospitalization and death in HFrEF patients?

A

ACE inhibitors, ARNIs, and beta-blockers are essential in managing HFrEF as they reduce the risk of hospitalization and death. These medications improve cardiac function, decrease symptoms, and prevent adverse remodeling of the heart. By targeting different pathways, they collectively improve outcomes and quality of life in HFrEF patients.

22
Q

Describe the treatment approach for HFpEF with ejection fraction greater than 50%. What are the recommended medications and strategies for managing this condition?

A

In HFpEF with EF>50%, treatment involves diuretics for symptom control, SGLT2 inhibitors for reducing morbidity/mortality, and managing co-morbidities like HTN and angina with ACE inhibitors, beta-blockers, and mineralocorticoid receptor antagonists.

23
Q

What are the recommended interventions for acute heart failure (AHF)? List the drugs and treatments commonly used in AHF management.

A

In AHF, interventions include IV diuretics (e.g., furosemide), IV vasodilators (e.g., nitrates), inotropic agents (e.g., dobutamine), thromboembolism prophylaxis (e.g., enoxaparin), oxygen therapy, and optimizing long-term medications before discharge.