Commonly asked Heart Failure Viva Questions

Basics and definitions

1. Define heart failure.
   A clinical syndrome caused by structural or functional cardiac abnormality, resulting in symptoms and/or signs due to elevated intracardiac pressures or inadequate cardiac output.
2. What are the major types of heart failure based on ejection fraction?
   • HFrEF: LVEF ≤40%
   • HFmrEF: LVEF 41%-49%
   • HFpEF: LVEF ≥50%, with evidence of raised filling pressures
   • HFimpEF: prior LVEF ≤40% that improves to >40%
     These definitions match the ACC/AHA/HFSA guideline summary.
3. Differentiate systolic from diastolic heart failure.
   • Systolic failure: impaired LV contractility, usually reduced EF.
   • Diastolic failure: impaired ventricular relaxation/filling with usually preserved EF.
4. What is the difference between acute and chronic heart failure?
   Acute HF is rapid onset or worsening of symptoms/signs requiring urgent treatment. Chronic HF is persistent HF, which may remain stable or become decompensated.
5. What are the ACC/AHA stages of heart failure?
   • Stage A: at risk for HF
   • Stage B: pre-HF, structural heart disease or raised biomarkers but no symptoms
   • Stage C: symptomatic HF
   • Stage D: advanced HF requiring specialized interventions
6. What is the NYHA functional classification?
   • I: no limitation
   • II: slight limitation
   • III: marked limitation
   • IV: symptoms at rest

Causes and pathophysiology

1. List common causes of heart failure.
   Ischaemic heart disease, hypertension, valvular heart disease, cardiomyopathy, arrhythmias, congenital heart disease, myocarditis, infiltrative disease, thyroid disease, severe anaemia, and high-output states.
2. What are common precipitants of acute decompensated heart failure?
   Acute coronary syndrome, uncontrolled hypertension, arrhythmia especially AF with rapid ventricular response, infection, non-adherence to drugs/diet, renal dysfunction, pulmonary embolism, anaemia, thyroid dysfunction, and drugs such as NSAIDs.
3. Explain the compensatory mechanisms in heart failure.
   Sympathetic activation, RAAS activation, ADH release, salt-water retention, ventricular hypertrophy and remodelling. Initially supportive, these ultimately increase afterload, congestion, fibrosis, and disease progression.
4. What is ventricular remodelling?
   Progressive change in ventricular size, shape, and function after myocardial injury or chronic pressure/volume overload. It contributes to worsening systolic function and functional mitral regurgitation.
5. What is forward failure and backward failure?
   • Forward failure: reduced cardiac output causing fatigue, cool peripheries, renal hypoperfusion.
   • Backward failure: raised filling pressures causing pulmonary and systemic venous congestion.
6. What is high-output heart failure? Give examples.
   HF despite elevated cardiac output, due to reduced systemic vascular resistance or increased demand. Examples: severe anaemia, thyrotoxicosis, AV fistula, beriberi, sepsis, and Paget disease.

Clinical features and examination

1. What symptoms suggest left-sided heart failure?
   Exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, fatigue, cough, wheeze, and reduced exercise tolerance.
2. What symptoms suggest right-sided heart failure?
   Peripheral oedema, abdominal distension, early satiety, right upper-quadrant discomfort, weight gain, and nocturia.
3. Why does orthopnoea occur?
   Lying flat increases venous return and central blood volume, raising pulmonary venous pressure and worsening pulmonary congestion.
4. Why does paroxysmal nocturnal dyspnoea occur?
   During sleep there is fluid redistribution from peripheral tissues into the central circulation, increasing pulmonary congestion. Reduced adrenergic drive may also contribute.
5. What are important signs of heart failure?
   Raised JVP, peripheral oedema, pulmonary crackles, displaced apex beat, S3 gallop, tachycardia, cool peripheries, hepatomegaly, ascites, and pleural effusion.
6. What does an S3 gallop indicate?
   Rapid ventricular filling into a dilated or poorly compliant ventricle. In an adult with symptoms, it supports volume overload and HFrEF.
7. What is the significance of raised JVP?
   It indicates elevated right atrial pressure and systemic venous congestion.
8. Why might a patient with severe chronic HF have no basal crepitations?
   Chronic elevation in pulmonary venous pressure may lead to lymphatic adaptation. Also, right-sided congestion can predominate.
9. How do you examine for hepatojugular reflux?
   Apply firm, sustained pressure over the right upper abdomen for about 10 seconds while observing the JVP. A sustained rise suggests impaired right ventricular accommodation and elevated filling pressures.

Investigations

1. What baseline investigations would you order in suspected heart failure?
   ECG, chest radiograph, natriuretic peptide, echocardiography, CBC, renal function/electrolytes, liver function, glucose/HbA1c, thyroid function, iron studies, urinalysis, and assessment for ischaemia where appropriate.
2. What is the role of echocardiography?
   It assesses EF, chamber size, regional wall-motion abnormality, diastolic function, valve disease, pulmonary pressures, right ventricular function, and structural causes.
3. What are common ECG findings in heart failure?
   Prior MI/Q waves, LVH, AF, bundle branch block, tachyarrhythmias, bradyarrhythmias, or nonspecific ST-T changes. A completely normal ECG makes significant HF less likely but does not exclude it.
4. What chest X-ray findings support heart failure?
   Cardiomegaly, upper-lobe venous diversion, Kerley B lines, bilateral perihilar "bat-wing" opacities, pleural effusions, and alveolar oedema.
5. What are Kerley B lines?
   Short horizontal peripheral lines at the lung bases due to interlobular septal oedema.
6. What is BNP or NT-proBNP and why is it useful?
   Natriuretic peptides are released in response to myocardial wall stress. Low values help exclude HF; raised values support the diagnosis but may also occur in renal failure, AF, pulmonary embolism, and older age.
7. When can natriuretic peptide values be falsely low?
   Obesity, early or treated HF, and sometimes HFpEF.
8. Why are renal function and electrolytes monitored closely in HF?
   They are affected by congestion, low perfusion, and therapy such as diuretics, ACE inhibitors, ARBs, ARNIs, and mineralocorticoid receptor antagonists.
9. How do you confirm HFpEF?
   Symptoms/signs of HF, LVEF ≥50%, plus objective evidence of raised LV filling pressures or structural/functional abnormalities, such as raised natriuretic peptides, left atrial enlargement, LV hypertrophy, or echocardiographic diastolic dysfunction.

Chronic HFrEF treatment

1. What are the four foundational drug classes for HFrEF?
   1. ARNI, or ACE inhibitor/ARB if ARNI is unsuitable
   2. Evidence-based beta-blocker
   3. Mineralocorticoid receptor antagonist
   4. SGLT2 inhibitor
      This is a core guideline-directed medical therapy approach.
2. Name evidence-based beta-blockers in HFrEF.
   Bisoprolol, carvedilol, and metoprolol succinate. Nebivolol may be used in selected older patients depending on local guidance.
3. What is the role of loop diuretics?
   They relieve symptoms and signs of fluid retention, such as pulmonary oedema and peripheral oedema. They improve congestion but are not the main disease-modifying therapy.
4. Why should beta-blockers not be initiated or rapidly up-titrated in a congested, unstable patient?
   Their initial negative inotropic effect can worsen acute decompensation. Start or increase only after the patient is euvolaemic and clinically stable.
5. What are the important adverse effects of ACE inhibitors/ARBs/ARNIs?
   Hypotension, worsening renal function, hyperkalaemia, and rarely angioedema. ACE inhibitors can cause cough.
6. What is an ARNI?
   Sacubitril/valsartan combines neprilysin inhibition with angiotensin receptor blockade. Sacubitril increases natriuretic peptide activity; valsartan blocks the AT1 receptor.
7. What washout is needed when changing from an ACE inhibitor to sacubitril/valsartan?
   A 36-hour washout is required to reduce angioedema risk.
8. What are indications for an MRA in HFrEF?
   Symptomatic HFrEF, provided renal function and serum potassium permit. Monitor for hyperkalaemia and renal dysfunction. Spironolactone may cause gynaecomastia.
9. What is the role of SGLT2 inhibitors in HFrEF?
   Dapagliflozin and empagliflozin reduce HF hospitalization and cardiovascular events in HFrEF, including in people without diabetes.
10. When is ivabradine used?
    In symptomatic HFrEF with LVEF ≤35%, sinus rhythm, resting heart rate generally ≥70/min despite maximally tolerated beta-blocker, or when beta-blockers are unsuitable.
11. When is hydralazine with isosorbide dinitrate used?
    When ACE inhibitor/ARB/ARNI cannot be used, and in selected patients despite optimal therapy, according to local guideline recommendations.
12. When is digoxin useful?
    It may reduce HF hospitalization in selected HFrEF patients and can help rate control in AF. It does not improve survival in HFrEF. Toxicity is more likely with renal dysfunction, hypokalaemia, and interacting drugs.

Devices and advanced therapy

1. When is an ICD considered in HFrEF?
   For primary prevention in selected patients with persistently reduced LVEF, usually ≤35% despite adequate optimized therapy, appropriate functional status, and a reasonable expected survival.
2. When is CRT indicated?
   In selected symptomatic HFrEF patients with LVEF ≤35%, despite optimal therapy, especially with sinus rhythm and broad LBBB QRS complexes. It improves ventricular synchrony.
3. What is advanced heart failure?
   Persistent severe symptoms, recurrent admissions, intolerance of guideline-directed therapy, refractory congestion or low output, and need for inotropes, mechanical support, transplant assessment, or palliative planning.
4. What advanced treatment options exist?
   Heart transplantation, durable LV assist device, temporary mechanical circulatory support in selected acute settings, intermittent or continuous inotropes in selected cases, and palliative symptom-focused care.

Acute heart failure and pulmonary oedema

1. How do you manage acute pulmonary oedema initially?
   ABCDE assessment, sit the patient upright, monitor ECG/BP/SpO₂, establish IV access, identify precipitant, give oxygen only if hypoxaemic, consider NIV if significant respiratory distress, administer IV loop diuretic if congested, and consider vasodilators if hypertensive and not hypotensive.
2. When are nitrates useful in acute heart failure?
   Particularly in hypertensive acute pulmonary oedema with adequate blood pressure. They reduce preload and afterload.
3. When are inotropes used?
   In cardiogenic shock or severe low-output HF with hypotension and evidence of hypoperfusion, usually in a monitored critical-care setting. Examples include dobutamine and milrinone.
4. What is cardiogenic shock?
   Cardiac pump failure causing persistent hypotension and tissue hypoperfusion, typically with cold peripheries, oliguria, altered mental state, raised lactate, and pulmonary congestion.
5. What are the "warm-cold" and "wet-dry" profiles?
   • Wet: congested
   • Dry: no congestion
   • Warm: adequately perfused
   • Cold: hypoperfused
     The commonest acute profile is warm and wet.
6. Why is routine oxygen not indicated in every patient with acute HF?
   Give oxygen for hypoxaemia, not routinely. Unnecessary oxygen can be harmful in normoxaemic patients.
7. What is the role of non-invasive ventilation?
   CPAP or BiPAP can improve oxygenation, reduce work of breathing, and help in acute cardiogenic pulmonary oedema, provided there are no contraindications.

HFpEF and practical questions

1. How is HFpEF managed?
   Treat congestion with diuretics; control blood pressure; manage AF, ischaemia, obesity, diabetes, sleep apnoea, and renal disease; use an SGLT2 inhibitor where appropriate. Unlike HFrEF, many traditional HFrEF drugs have less consistent outcome benefit in HFpEF.
2. Why is atrial fibrillation poorly tolerated in HFpEF?
   A stiff ventricle depends heavily on atrial contraction for filling. Loss of atrial kick and rapid ventricular rate can sharply raise filling pressure.
3. What lifestyle advice would you give a patient with chronic HF?
   Daily weight monitoring, salt moderation, individualized fluid advice, adherence to medicines, vaccination, exercise/cardiac rehabilitation where appropriate, smoking cessation, alcohol moderation, and early contact for worsening dyspnoea, oedema, or rapid weight gain.
4. What weight gain should raise concern for fluid retention?
   A rapid gain, often around 2 kg over several days, should prompt review according to the patient’s action plan and local protocol.
5. Which drugs can worsen heart failure?
   NSAIDs, verapamil and diltiazem in HFrEF, most thiazolidinediones, some antiarrhythmics, excess corticosteroids due to fluid retention, and medications that impair renal function or promote sodium retention.
6. What is cardiorenal syndrome?
   Bidirectional dysfunction in which acute or chronic cardiac dysfunction causes renal dysfunction, and renal dysfunction worsens cardiac disease. Venous congestion is often a major driver.
7. How would you counsel a patient discharged after HF admission?
   Explain medications and monitoring, provide a clear diuretic/self-care plan, arrange early follow-up, reinforce daily weights and symptom recognition, assess adherence and social barriers, and ensure they know when to seek urgent care.

High-yield viva closing question

1. What are the key goals of heart failure management?
   Relieve congestion and symptoms, improve quality of life and functional capacity, reduce hospital admissions, slow progression/remodelling, reduce mortality, treat the cause and precipitating factors, and plan timely device or advanced therapy referral where needed.