Lecture 10.2 - Investigation and Management of Heart Failure PDF

Diagnosis: ◦In patients with suspected heart failure, the first step is taking a detailed history and performing a clinical examination ◦The next step is measuring a BNP, which is used to risk stratify patients and determine the urgency of referral ◦At this point, an ECG...

Diagnosis: ◦In patients with suspected heart failure, the first step is taking a detailed history and performing a clinical examination ◦The next step is measuring a BNP, which is used to risk stratify patients and determine the urgency of referral ◦At this point, an ECG should be performed in all patients ◦Consideration should be made regarding further blood tests, chest radiograph, urinalysis and lung function testing (if alternative diagnosis is suspected) History taking: ◦Exercise tolerance - how far can they walk before becoming breathless? Has this changed? ◦Orthopnoea - how many pillows do they need to sleep? Do they sleep upright in armchair? ◦PND - do they wake in the middle of the night feeling breathless? ◦Bendopnea - SOB when bending forward ◦Cough - often dry (pink, frothy, sputum-rarely) ◦Weight change - gain or loss? ◦Comorbidities? ‣ Influence the presentation, clinical course, prognosis and response to therapy ◦Social and family history Physical examination: ◦General: ‣ Lower limb swelling ‣ Breathlessness (especially after stairs) ‣ Tachycardia ◦Cardiovascular/respiratory: ‣ Displaced apex beat ‣ Bibasal crackles ‣ Sacral oedema Bedside investigations: ◦Temperature - normal ◦Oxygen saturation - hypoxia may be present ◦Blood pressure - likely elevated: hypertension can result in heart failure ◦Respiratory rate - can be elevated: especially R heart failure/after exertion ◦Heart rate - likely elevated: effect of noradrenaline to maintain CO Investigations - NICE: ◦Severe symptoms - need admission to hospital ◦12 lead ECGs - all patients with suspected chronic heart failure should have an ECG ◦Blood tests: ‣ N-terminal pro-B type natriuretic peptide level ‣ Urea and electrolytes, eGFR, FBC, iron studies, TFT, LFT, HbA1c, fasting lipids ‣ Urine dipstick  ‣ Chest X-ray N-terminal pro-B-type natriuretic peptide level: ◦Cardiac neurohormone ◦Synthesised in ventricular cardiomyocytes in response to increase stress on ventricular wall ◦Inactive peptide released alongside BNP (active hormone) when there is increased pressure on the ventricular wall ◦Released in equal amounts to BNP but degrades less quickly ◦Low levels of NT-pro-BNP (< 4000 ng/L) have strong negative predictive value for heart failure (97%) Blood tests: ◦U&E and eGFR - markers of kidney function ◦FBC and iron studies - anaemia (presence of anaemia has poorer prognosis) ◦LFT - marker of hepatic congestion ◦TFT - marker of increased metabolic demand Chest X-ray: ◦Sensitive marker of cardiomegaly ◦The heart width should not make up more than 50% of the thoracic window Echocardiography: ◦A transthoracic echocardiography (TTE) is the main investigation for the confirmation of heart failure ◦The main determinant of a TTE is to look at the ejection fraction of the heart ◦This helps to differentiate the type of heart failure ◦Will also identify valvular abnormalities, filling abnormalities and changes in contraction (regional wall motion abnormalities) Other possible investigations - non-routine: ◦Cardiac MRI (cMRI) - useful if TTE is non-diagnostic ◦Coronary angiogram - identification (and treatment) of coronary artery disease ◦Lung function tests - if right sided heart failure is suspected (e.g. cor pulmonale from COPD) ◦Holter monitoring - arrythmia identification Management: ◦Patient education and lifestyle changes (modifiable risk factors) are vital parts of overall management ‣ Stop smoking ‣ Adaptations in the home ‣ Annual flu vaccine, one-off pneumococcal vaccine ‣ Supervised exercise-based rehabilitation ‣ Depression and anxiety screening ‣ Ensure co-morbidities are optimally managed ◦Several effective drug therapies have been developed which reduces the progression of heart failure - but it cannot be 'cured' Classification: ◦New York Heart association (NYHA) functional classification ◦Heart failure can also be classified based on the symptoms that patients experience  ‣ Class I (mild) - no symptomatic limitation of physical activity ‣ Class II (mild) - slight limitation of physical activity. No symptoms at rest ‣ Class III (moderate) - marked limitation of physical activity. No symptoms at rest ‣ Class IV (severe) - inability to carry out physical activity without symptoms. May have symptoms at rest Drug therapies: ◦Think about compensatory mechanisms - these are the targets of drug therapies ‣ ACE inhibitors: Prevent conversion of angiotensin I to angiotensin II ◦Reduce preload ◦Reduce afterload Examples: Ramipril, lisinopril, enalapril, captopril Produces bradykinin -> dry cough in ~20% of patients If problematic, consider ARB (angiotensin receptor blockers: Losartan, Candesartan) Stop in acute kidney injury ‣ Angiotensin receptor blockers ‣ Beta blockers: Prevent stimulation of beta adrenergic receptors Reduce heart rate - longer time for ventricular filling Consider cardiac selective beta blockers Propanolol, atenolol ‣ Mineralocorticoid receptor antagonists: Also called aldosterone antagonists Can be considered as add-on therapy if ACE-1 and beta blockers are insufficient Reduce sodium reabsorption (increase water excretion by the kidney) Reduces blood pressure and circulating volume Careful with electrolyte levels Spironolactone, eplerenone ‣ Loop diuretics: No effect on heart failure prognosis but offers symptomatic benefit Promote excretion of water from the kidney to reduce circulating volume and reduce pulmonary and peripheral oedema Highly effective Furosemide, bumetanide IV preparation of furosemide can be used in acute heart failure ‣ Drug management of co-morbidities ◦These are specifically for heart failure with reduced ejection fraction ◦There is insufficient evidence for common drug classes in HFpEF Second-line treatment: ◦Can only be initiated under specialist advice ‣ Sacubitril (prevents breakdown of natriuretic peptide)/valsartan (ARB) ‣ Ivabradine (inhibit cardiac pacemaker currents) ‣ Hydralazine (potent vasodilator) ‣ Digoxin (increased contractility)  Device therapy: ◦Implantable cardiac defibrillator (ICD): ‣ A device that monitors your heart rate and delivers a strong electrical shock to restore the heartbeat to normal in the event of tachycardia ◦Cardiac resynchronisation therapy: ‣ Send electrical signals to ventricles to make them pump together (biventricular pacing) ◦Intra aortic balloon pump therapy ◦Heart transplant