Heart failure

• Cardiac output is defined as:

  CO (mL/min) = heart rate (bpm) x stroke volume (mL/beat)
• Left sided heart failure is the most common type of heart failure. Causes include coronary artery disease, myocardial infarction and hypertension
• Left sided HF leads to back flow into the pulmonary veins, leading to pulmonary oedema
• Symptoms of left sided HF:

  • dysponea
  • reduced exercise tolerance
  • orthopnoea
  • paroxysmal nocturnal dyspnoea
  • nocturnal cough (with or without pink frothy sputum)
  • wheeze (cardiac asthma)
• Right heart failure is generally as a result of left sided heart failure due to raised intrathoracic pressure
• In right heart failure blood backs up into the vena cava, leading to peripheral/systemic oedema
• Cor pulmonale is right ventricle dysfunction/failure due to a primary disorder of the respiratory system. The respiratory disorder leads to pulmonary hypertension and therefore increased preload
• Signs of right HF:

  • peripheral oedema
  • ascites
  • facial engorgement
  • pulsation in neck + face (tricuspid regurgitation)
• systolic heart failure = reduced left ventricle ejection fraction. Less blood is being pumped out of the heart during systole leading to increased blood remaining in the heart. This leads to ventricular stretch, dilation and remodelling.
• Diastolic heart failure = preserved left ventricle ejection fraction. Ventricular relaxation and filling is impaired.
• Less than 50% function means reduced LVEF
• Ejection fraction = (stroke volume / end diastolic volume) x 100
• Signs of HF on CV exam:

  • Tachycardia at rest
  • Hypotension
  • Narrow pulse pressure
  • Raised JVP
  • Displaced apex beat (due to left ventricular dilatation)
  • Parasternal heave - RVH
  • Gallop rhythm on auscultation (pathognomic for CHF)
  • Murmurs associated with valvular heart disease (e.g. an ejection systolic murmur in aortic stenosis)
  • Pedal and ankle oedema
• New York heart association classification is a way of rating a patients dyspnoea from I - IV. IV means the patient is symptomatic at rest.
• The RAAS is activated in HF due to reduced cardiac output and renal hypoperfusion. Angiotensin II and aldosterone lead to the retention of sodium and water. This increases the preload.
• The sympathetic nervous system is activated by heart failure. It is activated by Baroreceptors and the RAAS. This increases heart rate and therefore afterload.
• Natriuretic peptides are released from the heart in response to abnormal stretch and volume overload. BNP (brain natriuretic peptide) is released from the ventricles which leads to vasodilation.
• Causes of heart failure include:

  • ischaemic heart disease
  • hypertension
  • valvular disease (commonly AS)
  • arrhythmias (commonly AF)
  • dilated cardiomyopathy
• For suspected heart failure, measure NT-proBNP

  • > 2000 ng/L needs an urgent referral for specialist assessment and TTE within 2 weeks
  • 400-2000 ng/L needs a specialist assessment and TTE within 6 weeks
  • <400 ng/L is unlikely to be heart failure
• TTE is a transthoracic echocardiogram. It can assess for valve disease plus the systolic and diastolic function of the ventricles.
• Gold standard imaging for heart failure is a cardiac MRI but TTE is first line
• An ECG should be performed for suspected heart failure:

  • Tachycardia
  • Left axis deviation - LVH
  • Left ventricle hypertrophy
  • ST and T wave abnormalities
  • LBBB - wide QRS
  • P wave abnormalities - atrial enlargement
  • Atrial fibrillation as a potential cause or due to enlarged atria
• CXR findings suggestive of heart failure:

  • Alveolar oedema (perihilar/bat-wing opacification)
  • Kerley B lines (interstitial oedema)
  • Cardiomegaly (cardiothoracic ratio >50%)
  • Dilated upper lobe vessels
  • Effusions (e.g. pleural effusions – blunted costophrenic angles)
• Management of reduced LVEF:

  1. ACEi + Beta blocker (can use ARB if not tolerating ACEi)
  2. Mineralocorticoid receptor agonist + ACEi / ARB + Beta blocker
  3. Specialist- digoxin, ivabradine, valsartan
• When commencing a patient on an ACEi / ARB make sure to check U&Es before and 1-2 weeks after. Also check after every dose increase.

  These medications are also used in hypertension so monitor patients blood pressure.
• Spironolactone is a MRA that can cause hyperkalaemia so make sure to monitor potassium levels
• For all types of heart failure, diuretics are used for relief from fluid congestion. Patients with reserved LVEF tend to be on low dose furosemide.
• Calcium channel blockers should be avoided in heart failure patients with reduced LVEF
• All heart failure patients should receive pneumococcal and influenza vaccinations. They should also have an echocardiogram every 6-12 months.
• The most common cause of right heart failure is left heart failure
• Stroke volume requires:

  • adequate preload
  • optimal myocardial contractility (Frank-Starling mechanism)
  • decreased afterload
• The most common causes of heart failure in the UK are coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension.

  Other causes of heart failure include:

  • Endocrine disease: hypothyroidism, hyperthyroidism, diabetes, adrenal insufficiency, Cushing’s syndrome
  • Medications: calcium antagonists, anti-arrhythmics, cytotoxic medication, beta-blockers.
• The acronym HIGH-VIS is useful to remember some of the causes of CHF:

  • Hypertension (common cause)
  • Infection/immune: viral (e.g. HIV), bacterial (e.g. sepsis), autoimmune (e.g. lupus, rheumatoid arthritis)
  • Genetic: hypertrophic obstructive cardiomyopathy (HOCM), dilated cardiomyopathy (DCM)
  • Heart attack: ischaemic heart disease (common cause)
  • Volume overload: renal failure, nephrotic syndrome, hepatic failure
  • Infiltration: sarcoidosis, amyloidosis, haemochromatosis
  • Structural: valvular heart disease, septal defects
• High-output cardiac failure occurs in states where demand exceeds normal cardiac output such as pregnancy, anaemia and sepsis.
• Gallop rhythm:

  • A gallop rhythm is a rapid triple rhythm resulting from the combination of a loud S3, with or without an S4, and tachycardia.
  • louder at the apex and the left sternal edge
  • if right ventricular then louder on inspiration
  • if left ventricular then louder on expiration
• Clinical findings on respiratory examination may include:

  • Tachypnoea
  • Bibasal end-inspiratory crackles and wheeze on auscultation of the lung fields
  • Reduced air entry on auscultation with stony dullness on percussion (pleural effusion)
• Clinical findings on abdominal examination may include:

  • Hepatomegaly
  • Ascites
• Lab investigations:

  • FBC: anaemia
  • U&Es: renal failure, electrolyte abnormalities due to fluid overload (e.g. hyponatraemia)
  • LFTs: hepatic congestion
  • Troponin: if considering recent myocardial infarction
  • Lipids/HbA1c: ischaemic risk profile
  • TFTs: hyperthyroidism/hypothyroidism
  • Cardiomyopathy screen
  • N-terminal pro-B-type natriuretic peptide
• Screening for cardiomyopathy includes the following blood tests:

  • Serum iron and copper studies (to rule out haemochromatosis and Wilson’s disease)
  • Rheumatoid factor, ANCA/ANA, ENA, dsDNA (to rule out autoimmune disease)
  • Serum ACE (to rule out sarcoidosis)
  • Serum-free light chains (to rule out amyloidosis)
• Cardiac MRI is the gold standard investigation for assessing ventricular mass, volume and wall motion. It can also be used with contrast to identify infiltration (e.g. amyloidosis), inflammation (e.g. myocarditis) or scarring (e.g. myocardial infarction). It is typically used when echocardiography has provided inadequate views.