PALi Cardiology Revision: Heart Failure

1. PALi Cardiology Revision:Heart Failure Lucille Ramani 0707070r@student.gla.ac.uk

2. Heart Failure Definition “a complex of signs and symptoms that occurs when the heart fails to pump adequate CO” Epidemiology • Prevalence: 3-20 per 1000 • 5% emergency admissions •  by 50% in the next 25 years • 50% dead by 5 years • Mainly a disease of the older population (>65 years)

3. Aetiology

4. Right Heart Failure (RHF) • Aetiology: • Chronic pulmonary disease corpulmonale • Left-sided heart failure • Patent ductusarteriosus • Isolated right-sided cardiomyopathy • Tricuspid valve disease •  RV pressure  backward failure  systemic venous congestion

5. RHF: Clinical Features • Symptoms • Fatigue • Dyspnoea • Anorexia, nausea • Nocturia • Signs •  JVP • Smooth, tender hepatomegaly • Ascites • Pitting oedema (sacral, ankle) • Hypotension • Cyanosis, cool peripheries

6. LHF: Aetiology • Ischaemic heart disease • Chronic systemic HTN • Cardiomyopathy (usually dilated) • Mitral / Aortic valve disease • Mitral regurgitation: volume overload ( preload ) • Aortic stenosis: pressure overload ( afterload) • Consequence = pulmonary congestion

7. LHF: Clinical Features • Symptoms • Fatigue • Dyspnoea: exertional; orthopnoea; paroxysmal nocturnal • Cough ± frothy pink sputum; haemoptysis • Signs • Few, but prominent at late stage • Weight loss; muscle wasting • Cardiomegaly • Pulmonary oedema (creps) • Hypotension; cool peripheries • S3 and tachycardia: triple gallop rhythm

8. Pathophysiology • Compensatory mechanisms become overwhelmed and thus pathological (cardiac decompensation) • Key concepts: • CO is a function of preload and afterload • Preload: end-diastolic wall stress (initial stretching of myocytes) • Afterload: the resistance against which the heart has to pump • Frank-Starling mechanism: change in SV in response to change in preload •  in preload via Rx is beneficial •  in workload and symptoms arising from venous congestion

9. Compensatory Changes •  filling pressures to maintain SV • Dilation: increased wall tension  ischaemia • Hypertrophy to balance pressure overload • Sinus tachycardia • Neurohormonal mechanisms • Activation of RAAS -  systemic vascular resistance - Aldosterone release (Na+ and water retention) - ADH release (water retention) •  Sympathetic activity ( catecholamines) -  HR, force of contraction and peripheral vasoconstriction

10. Diagnosis • Bloods; cardiac enzymes/markers • BNP (>100pg/mL = 95% specificity and 98% sensitivity • ECG • Transthoracic doppler ECHO: EF<0.45

11. ) Chest X-ray Findings • Alveolar oedema (“Bat’s wings”) • KerleyB lines (interstitial oedema) • Cardiomegaly • Dilated prominent upper lobe vessels • Pleural Effusions • LV dysfunction  dilation of pulmonary vessels  leakage of fluid into interstitium  pleural effusion  alveolar oedema (pulmonary oedema)

12. Management • Aims: • Treat cause, e.g. valve disease • Treat exacerbating factors, e.g. anaemia, HTN • Relieve S+S • Augment survival • General Measures: • Smoking cessation • Salt reduction and fluid restriction if severe • Maintenance of optimal weight and nutrition • Vaccinations: pneumoccocal (once only) and annual influenza • Assess for depression • Monitor: functional capacity, fluid status, cardiac rhythm

13. Pharmacological Rx • Diuretics • Routinely loop diuretics, e.g. Furosemide 40mg/24h po (increase prn) • Can add spironolactone or metolazone • ACEi • Long-acting, e.g. lisinopril 10mg/24h po • Start with small dose and increase every 2 weeks until at target (30-40mg) • Warn patients of side effects: hypotension (esp after first dose- advise to lie down); dry cough; hyperkalaemia; taste disturbance • Check U+E and creatinine before starting and with each titration

14. Pharmacological Rx • Beta-blockers • Initiate after ACEi and diuretic • Start low, go slow e.g. carvedilol 3.125mg/bd 25-50mg/bd (at least 2 week increments) • Angiotensin-II receptor antagonists • Alternative if intolerant of ACEi • Digoxin • Use if diuretics, ACEi or BB do not control symptoms or if in AF • 0.125mg-0.24mg/24h po • Monitor U+E and maintain potassium at 4-5mmol/L

15. Acute HF • Most commonly occurs in context of acute MI  extensive loss of ventricular muscle • Also: PE, cardiac tamponade, rupture of IV septum (producing VSD), AF • Clinical presentation: • Acute worsening (decompensation) of chronic HF • Acute pulmonary oedema: respiratory distress, crackles, pink frothy sputum • Cardiogenic shock: hypotension, tachycardia, oliguria • Investigations: • CXR • ECG; consider ECHO and BNP • U+E; cardiac markers; ABGs

16. Acute HF Management • Different to chronic; Rx before Ix • Sit pt up + high-flow O2 (100% if no lung disease) • IV access and ECG (Rx any arrhythmia, e.g. AF) • Diamorphine 2.5-5mg IV slowly • Furosemide 40-80mg IV slowly • GTN spray 2 puffs sublingual then infusion of isosorbidedinitrate 2-10mg/h • If pt worsening- first get help, then: • Further dose of furosemide • Consider ventilation or increasing nitrate infusion

17. MEQ Past Paper

18. Further Questions • What are the possible causes for deterioration in HF? (3) • Immediate treatment of acute HF and how you would administer this? (3)

19. Thank-you! Any Questions?