30-40% mortality at 1y after diagnosis (worse than most cancers) 2% of annual NHS budget (70% of cost due to hospitalizations)

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2 prevalence ~900,000 people average age of diagnosis 76 most common cause is CAD 30-40% mortality at 1y after diagnosis (worse than most cancers) 5% of all acute admissions (projected to rise by 50% over next 25 years) 1 million inpatient bed days per annum 2% of annual NHS budget (70% of cost due to hospitalizations) 1 in 4 patients are readmitted within 3m of discharge

3 Class Symptoms I II III IV No limitation of physical activity: ordinary physical activity does not cause fatigue, palpitations, dyspnoea or angina Slight limitation of physical activity: comfortable at rest but ordinary activity causes fatigue, palpitations, dyspnoea or angina Marked limitation of physical activity: comfortable at rest but less than ordinary activity causes fatigue, palpitations, dyspnoea or angina Unable to carry out any physical activity without discomfort: symptoms of cardiac insufficiency at rest and discomfort increases with any physical activity

4 67-year-old male, diabetes, COPD, MI 2005, CKD 2 ECHO 2008 mild AS and LVEF 33% NYHA II at last heart failure clinic appointment aspirin 75mg OD, simvastatin 40mg ON, metformin 500mg BD, furosemide 40mg OD, ramipril 2.5mg OD, bisoprolol 1.25mg OD admitted to AMU with 1/52 Hx of increasing SOBOE (ET reduced from 200 to 50yds), orthopnoea and oedema RR 20, SpO2 94% on air, BP 156/82mmHg, HR 94/min 1. WHAT IS THE DIAGNOSIS? 2. WHAT ARE THE POTENTIAL TRIGGERS? 3. WHAT INVESTIGATIONS ARE REQUIRED?

5 Syndrome of rapid onset of symptoms and signs secondary to cardiac dysfunction due to: 1. Acute myocardial injury ischaemia, acute valvular dysfunction, pericardial effusion/tamponade, myocarditis, aortic dissection, acute VSD/ventricular wall rupture, cardiac contusion 2. Afterload/chronotropy/inotropy/lusitropy mismatch hypertensive crisis, arrhythmia, thyrotoxicosis 3. Decompensation of chronic heart failure

6 Poor compliance with HF treatment Excessive salt intake Addition of new drug e.g. NSAID, steroid, thiazolidinedione, diltiazem Alcohol or drug abuse Uncontrolled hypertension Infection/sepsis esp. pneumonia AKI AECOPD Arrhythmia e.g. AF Ischaemia/ACS or valvular dysfunction Hyper- or hypothyroidism Anaemia Electrolyte disturbances e.g. hypocalcaemia, hypophosphataemia Iatrogenic fluid overload

7 FBC, U&E, LFT, CRP, Ca 2+, Mg 2+, PO 3-4, lipids, glucose, TFTs Infection screen CXR ECG ECHO cmri CT or conventional coronary angiography Spirometry NT-proBNP or BNP and hstni in selected cases

8 CXR venous congestion, upper lobe diversion, enlarged heart ECG AF rate 98/min urea 14, creatinine 155 (138), other bloods unremarkable suddenly deteriorates at 02:00 with MEWS = 6 RR 34, SpO 2 88% on 2l O 2, HR 144, BP 169/102, no urine since admission cyanosed, clammy, agitated, JVP +5cm, bibasal crackles ++ ABG: ph 7.29, po 2 7.6, pco 2 7.2, BE -8.3, lactate WHAT IS THE DIAGNOSIS? 2. WHAT IS THE TREATMENT NOW?

9 ACUTE HEART FAILURE IV diuretic bolus e.g. furosemide 50mg +/- IV morphine 2.5-5mg sbp >110mmHg: IV vasodilator e.g. GTN 50mg in 0.6-6ml/h (10-100μg/min) Inadequate ventilation or oxygenation Lifethreatening tachy- or bradyarrhythmia Systolic BP <85mmHg or shock Inadequate diuresis Acute mechanical cause or valvular dysfunction ACS Oxygen NIV ETT and IV DCCV Pacing Stop vasodilators and β- blockers Inotrope / Vasopressor Consider IABP Catheterize Increase diuretics Consider low-dose dopamine or UF Urgent ECHO Surgical or percutaneous intervention Antithrombotic therapy Coronary reperfusion

10 limited evidence for beneficial venodilatory effects of IV diuretics high dose diuretics increase fluid loss but reduction in circulating volume may cause organ hypoperfusion (e.g. AKI) and increased myocardial stress (activation of RAAS and SNS) increased risk of other SE e.g. ototoxicity with high-dose furosemide continuous IV infusion of diuretics increases diuresis with lower cummulative doses but no effect on symptoms or safety at 72h IV GTN causes venodilatation and reduced LV filling pressures (i.e. preload); arterial dilatation (reduced afterload) at higher doses may decrease myocardial O 2 demand and improve CO better outcome (decreased rates of intubation and MI) with high-dose nitrates plus low-dose diuretics vs. low-dose nitrates plus high-dose diuretics in one study risk of sudden hypotension and increased myocardial ischaemia with nitrates

11 Consider as adjunct to pharmacological Rx if severe respiratory distress, refractory hypoxaemia or T2RF Contraindicated if significant hypotension CPAP and BiPAP are probably equivalent Improves symptoms, respiratory parameters and ABGs Earlier meta-analyses showed improved outcomes with NIV More recent meta-analyses (including results of large 3CPO trial) failed to show any effect on intubation rates, LOS or mortality

12 Congestion at rest? orthopnoea, elevated JVP, oedema, rales, ascites Yes No Poor perfusion at rest? cold extremities, narrow pulse pressure, drowsiness No A: Warm & Wet C: Warm & Dry Yes B: Cold & Wet D: Cold & Dry A. diuretics > nitrates B. nitrates > diuretics, withold β-blockers and ACE-i, consider inotropes C. target profile, optimize and titrate chronic therapy D. exclude hypovolaemia, consider invasive monitoring, cautious filling, inotropes, IABP

13 76-year-old Afro-Caribbean female HTN, CKD3 (renovascular disease) and OA diagnosis of HF with LVEF 26% on ECHO GFR fell from 44 to 31mL/min on initiation of ACE-i - stopped admitted with worsening oedema and SOBOE (NYHA III) bisoprolol 5mg, doxazosin 4mg, furosemide 80mg, simvastatin 40mg, naproxen 500mg BP 143/88mmHg, HR 84/min ECG: sinus rhythm, non-specific BBB (QRS 0.16s) 1. WHAT ARE THE TREATMENT OPTIONS?

14 Diuretics ACE-inhibitor ARB if ACE-i not tolerated β-blocker H-ISDN if ACE-i AND ARB not tolerated MR antagonist Ivabradine if in SR and HR >70/min Digoxin if in AF or HR still >70 CRT-P or CRT-D LVAD +/- heart transplant

15 CRT-P reduces hospital admissions and mortality and improves symptoms and exercise capacity if symptomatic despite maximal medical therapy if: life expectancy >1y, good functional status, sinus rhythm AND NYHA III-IV with EF 35% AND QRS 120ms (LBBB) OR QRS 150ms (non-lbbb) NYHA II with EF 30% AND QRS 130ms (LBBB) OR QRS 150ms (non-lbbb) Possible benefit from CRT-P if: permanent AF AND NYHA III-IV with EF 35% AND QRS 120ms AND AV nodal ablation OR pacing required for slow AF OR HR 60 resting and 90 on exertion OR indication for conventional pacing AND NYHA II-IV AND EF 35% irrespective of QRS duration CRT-D if: previous ventricular arrhythmia OR symptomatic (NYHA II-III) with EF 35% after 3m of maximal medical therapy

16 started on hydralazine 37.5mg TDS and ISDN 20mg TDS α-blocker stopped ivabradine 2.5mg BD added for rate control dose of furosemide increased to 120mg OD fluid restricted to 2l/d referred to HFNS for consideration of CRT-P no significant decline in renal function but no significant diuresis no improvement in oedema or reduction in body weight over next 4d 1. WHY IS SHE NOT RESPONDING TO INCREASED DIURETICS? 2. WHAT ARE THE OPTIONS TO TREAT HER FLUID OVERLOAD?

17 Poor compliance, excess salt intake, concomitant NSAID use Renal impairment (reduced active secretion of diuretics and decreased peak urinary concentrations) Compensatory hyperplasia/hypertrophy of epithelial cells in DCT and increased Na + reabsorption with chronic loop diuretic Reduced biovailability or delayed absorption of diuretics due to intestinal mucosal oedema Compensatory post-diuretic salt retention (when urinary drug concentrations < diuretic threshold)

18 Reduce dietary salt intake (<2g/d) and stop NSAIDs Increase diuretic dose in renal failure (e.g. furosemide 240mg daily) Add in thiazide diuretic e.g. metolazone, bendroflumethiazide or indapamide (monitor U&E closely) Switch to bumetanide or torasemide (bioavailability 80% compared with 40% for furosemide) or IV diuretics Split dosing i.e. BD/TDS or switch to torasemide (duration of action 18-24h compared with 4-6h for furosemide) or give continuous IV infusion e.g. furosemide 10mg/h consider ultrafiltration with CVVH: increased weight loss and reduced readmissions c/w diuretics (UNLOAD)

19 82-year-old female T2DM, HTN, AF 2x admissions this year with pulmonary oedema review in AEC with results of outpatient ECHO breathless after walking 50 yds, mild ankle oedema, raised JVP ramipril 2.5mg, gliclazide 40mg BD, furosemide 40mg OD BP 159/91, HR 88/min irregularly irregular, CBG 15.1mmol/L BNP 252pg/mL (<35pg/mL), HbA1c 9.5%, other bloods normal ECHO: good LV systolic function (LVEF 63%), moderate LVH, E/A reversal of doppler waveform across mitral valve 1. WHAT IS THE DIAGNOSIS 2. HOW SHOULD SHE BE TREATED

20 symptoms and signs of CHF with EF >40% normal LVEF on ECHO in up to 50% with ACPOE (rule out reversible cause of LVSD) older, female, hypertensive, diabetic, AF (CAD less common) similar prognosis to HF-REF impaired LV relaxation during diastole and E/A reversal on ECHO no treatment proven to reduce mortality perindopril (PEP-CHF), irbesartan (i-preserve) and candesartan (CHARM- PRESERVED) may improve symptoms and reduce admissions β-blockers (e.g. nebivolol), rate-limiting CCBs (e.g. verapamil) and digoxin may increase diastolic filling times by reducing ventricular rate diuretics for congestive symptoms optimize Rx of comorbidities e.g. HTN, diabetes, AF (and CAD)

21 78-year-old male, previous CABG EF 15% NYHA IV (breathless at rest) LBBB on ECG admitted with worsening oedema unable to tolerate ACE-i/ARB and spironolactone due to CKD 4 sbp 90mmHg, SpO 2 90% on air asked to see urgently by nurse?dying (DNACPR in place) asleep, Cheyne-Stokes respiration, apnoeic periods with SpO 2 84% 1. WHAT IS THE DIAGNOSIS? 2. WHAT ARE THE TREATMENT OPTIONS?

22 Periodic breathing or central sleep apnoea (CSA) Occurs in up to 50% with severe HF (NYHA III-IV) during sleep Heightened chemoreceptor sensitivity to CO 2, increased circulating catecholamine levels and hypoxaemia Hyperventilation Hypocapnia CO 2 levels fall below apnoeic threshold Apnoea Sympathetic activity ++ PaCO 2 levels rise above apnoea threshold Daytime somnolence, fatigue, PND, hypoxaemia/diastolic dysfunction, increase in fatal arrhythmias and mortality Nocturnal O 2 < CPAP < BiPAP < adaptive servoventilation (ASV)