Hospitalised Heart Failure

81
HOSPITALISED HEART FAILURE

Transcript of Hospitalised Heart Failure

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HOSPITALISED HEART FAILURE

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CONCLUSIONS

⦿ Complications similar in mild or severe symptoms ⦿ Complications similar in range of LVEF ⦿ Inertia/difficulty in providing evidenced-base care ⦿ Aim to refer every HF admission

● HF Team ● Cardiology

⦿ All new cases need imaging to guide therapy

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OUTLINE OF TALK

⦿ Some bits and bobs for your approach to acute heart failure

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Hospital admissions and the economic burden of heart failure

HF is estimated to cost around 2% of the NHS budget

(NHS budget for 2017–2018,

~£125 billion)1,3

Acute HF – leading cause of

hospital admission in patients

aged ≥65 years2

1 million inpatient bed-days

(2% of all NHS inpatient bed-days)1

70% of HF costs to the NHS are due to

hospitalisation1

HF, heart failure; NHS, National Health Service.

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The mortality rate for patients with treated heart failure remains high1

Inpatient mortality

rates increased

slightly and 1-year mortality

rates fell during

2016/2017 compared to

2015/2016Discharge

HOSPITAL

Hospitalisation

In-hospital mortality

rate

9.4%

30-day post-

dischargemortality

~6.0%

30 days

1-year mortality

23.3%

1 year

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⦿ NICE

● NT-proBNP

● >400ng/L

● >2000ng/L ⦿ NUH

● BNP

● >100ng/L

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ADAPTIVE/MALADAPTIVE CONSEQUENCES⦿ ‘Deleterious’ - Activation of RAAS - Sympathetic activation - Endothelin production - Endothelial dysfunction - Cytokine activation

⦿ ‘Beneficial’ - Natriuretic Peptide release

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Natriuretic peptides are important biomarkers in heart failure1-4

• Natriuretic peptides are released in response to stretching of the heart muscles

• As heart failure progresses, activation of the sympathetic nervous system and RAAS leads to increased blood volume and sustained myocardial stretch, resulting in elevated levels of circulating BNP and inactive fragment NT-proBNP

proBNP

BNPNT-proBNP

Vasodilation ▼ Blood pressure ▼ Sympathetic tone ▼ Aldosterone levels

▼ Fibrosis ▼ Hypertrophy ▲ Natriuresis / diuresis

Inactive fragments

NeprilysinPassive clearance

(muscle, liver, kidney)

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FACTORS THAT CAN TRIGGER ACUTE HEART FAILURE

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ASSESSMENT TIPS IN AHF

⦿ Up to 20% of CXR can be normal ⦿ ECG rarely normal ⦿ Immediate echocardiography

● If shocked

● Suspect mechanical complication ⦿ A normal BNP can be effective rule out ⦿ Utilise haemodynamic assessment if in doubt ⦿ Thoracic ultrasound may be useful

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OXYGEN VERSUS CPAP VERSUS NIPPV - C3P0

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THORACIC ULTRASOUND

A LINES B LINES

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Lung US: normal findings

Pleural sliding on 2D and M mode (Sea-shore sign)

Sea - waves

shore - sandy

Pleural sliding

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Lung US: normal findingsPleural Sliding on 2D and M mode (Sea-shore

sign) and lung pulse

Lung Pulse see with each heart beat green arrows (look at QRS on the ECG)

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INPATIENT MANAGEMENT TIPS

⦿ Daily weights

● Usually more useful/accurate than fluid balance

● Ensure same time, post-void, same scales, same clothes ⦿ Aim 0.5kg-1kg maximum loss per 24h ⦿ Diuretic therapy

● Double usual dose and convert to IV

● Increase daily when weight/UO static

● U&E every 48h

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INPATIENT MANAGEMENT TIPS - ACUTE ON CHRONIC

⦿ If established on HF therapy try to continue ⦿ If BP required, stop non-prognostic drugs first

● Calcium blockers, alpha blockers, nitrates, nicorandil etc ⦿ If HF therapy needs temporary cessation

● MRA first, then BB, then ACE/ARB

● Try to reduce rather then abruptly stop ⦿ Try to aim for a previously known ‘dry weight’ ⦿ No need to get to ‘bone dry’

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INPATIENT MANAGEMENT - NEW CASES

⦿ Do not start BB in HFrEF until nearing euvolaemia / low JVP

● Common cause of hypotension and hypoperfusion

● Common cause of prolonging positive response

⦿ No need for aggressive BB/ACE/MRA in >40% LVEF

● Fluid balance and co-morbidity control is key

⦿ All new presentations, especially with high BNP, requiring admission/IV therapy should have inpatient transthoracic echocardiography and Cardiology review

⦿ A repeat generic TTE in a known case rarely adds useful information

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HYPONATRAEMIA

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MANAGEMENT: DOSING

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Neprilysin Inhibition Potentiates Actions of Endogenous Vasoactive Peptides That Counter

Maladaptive Mechanisms in Heart Failure

Endogenous vasoactive peptides

(natriuretic peptides, adrenomedullin, bradykinin, substance P,

calcitonin gene-related peptide)

Inactive metabolites

Neurohormonal activation

Vascular tone Cardiac fibrosis,

hypertrophy Sodium retention

Neprilysin Neprilysin inhibitor

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0

16

32

40

24

8

Enalapril (n=4212)

360 720 10800 180 540 900 1260Days After Randomization

4187 4212

3922 3883

3663 3579

3018 2922

2257 2123

1544 1488

896 853

249 236

LCZ696 Enalapril

Patients at Risk

1117

Kap

lan-

Mei

er E

stim

ate

of

Cum

ulat

ive

Rat

es (%

) 914

ENTRESTO (n=4187)

HR = 0.80 (0.73-0.87) P = 0.0000002

Number needed to treat = 21

PARADIGM-HF: Cardiovascular Death or Heart Failure Hospitalization (Primary Endpoint)

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The AE profile of Entresto was similar to enalapril1

1. McMurray et al. N Engl J Med 2014;371:993–1004.

Fewer patients in the Entresto group than in the enalapril group stopped their study medication because of an AE (10.7 vs 12.3%, p=0.03)

Event, n (%)Entresto(N=4187)

Enalapril(N=4212) p value

HypotensionSymptomatic 588 (14.0) 388 (9.2) <0.001Symptomatic with SBP <90 mmHg 112 (2.7) 59 (1.4) <0.001

Elevated serum creatinine≥2.5 mg/dL (221umol/L) 139 (3.3) 188 (4.5) 0.007≥3.0 mg/dL (265umol/L) 63 (1.5) 83 (2.0) 0.10

Elevated serum potassium>5.5 mmol/L 674 (16.1) 727 (17.3) 0.15>6.0 mmol/L 181 (4.3) 236 (5.6) 0.007

Cough 474 (11.3) 601 (14.3) <0.001Angioedema (adjudicated in a blinded fashion by an expert committee)

No treatment or use of antihistamines only 10 (0.2) 5 (0.1) 0.19Catecholamines or glucocorticoids without hospitalisation 6 (0.1) 4 (0.1) 0.52Hospitalised without airway compromise 3 (0.1) 1 (<0.1) 0.31Airway compromise 0 0 ---

AE, adverse event; SBP, systolic blood pressure.

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NOT JUST ABOUT OPTIMAL DRUG THERAPY…

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CARDIAC RESYNCHRONISATION THERAPY

LBBB >130MS

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PARADIGM-HF: Risk of sudden death1

1. Desai et al. Eur Heart J 2015;36:1990–1997.

0.02

0.000 1080900180 360 540 720 1260

0.04

0.06

0.08

0.10

41874212

38913860

24782410

1005994

6% (Entresto) vs 7.4% (Enalapril)Hazard ratio=0.80 (95% CI: 0.68-0.94)p=0.0008.

EnalaprilEntresto

Days since randomisation

Cum

ulat

ive

prob

abili

ty

No. at riskEntresto:Enalapril:

*ARR, RRR are based on median F/U at 27 months. ARR, absolute risk reduction; CI, confidence interval; F/U, follow-up; RR, risk reduction; RRR, relative risk reduction.

20%RRR

1.4% ARR

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COMMON HEART

FAILURE SYNDROMES

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ISCHAEMIC HEART DISEASE - VIABILITY

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MITRAL REGURGITATION

TRIVIAL MODERATE

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AORTIC STENOSIS

NORMAL SEVERE

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IRON DEFICIENCY IS COMMON IN HEART FAILURE⦿ Lead to anaemia/skeletal muscle dysfunction

⦿ Worse prognosis in HF if present

⦿ Trials (FAIR-HF and CONFIRM-HF) have examined effects of intravenous iron replacement

● Improved NYHA class

● Reduced hospitalisations

● Improved Peak VO2 (EFFECT-HF)

● No effects seen with oral iron supplementation (IRONOUT HF)

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IRON REPLACEMENT⦿ Incorporated into international guidelines ⦿ Current IRONMAN trial recruiting and powered for hard

clinical endpoints

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RENAL IMPAIRMENT

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MECHANISMS OF GFR CHANGES DURING CCF TREATMENT

⦿ Venous congestion

● MAP is important but the MAP/CVP gradient more

● Congestion key driver in WRF

● Causes an inflammatory response in parenchyma

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CONGESTION

Low eGFR seems to be only associated with poorer outcome with persistent congestion

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MANAGEMENT OF RAAS-I WITH WRF

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Statement from the British Society for Heart Failure Board on sick-day guidance and acute kidney injury1

“It is important to remember that patients presenting with decompensated heart failure often suffer deterioration in renal function as a consequence of the fluid overload. Diuresis is the

mainstay of treatment in these situations and withholding drugs may well

do more harm – tailoring care to the individual is key”

“Some deterioration in renal function when commencing ACEi, ARB or mineralocorticoid

receptor antagonist is common in patients with heart failure but in the vast majority of cases

does not require cessation of the drug(see ESC Guidelines)”

1. British Society for Heart Failure. Acute kidney injury and sick day rules/guidance: implications for patients with chronic heart failure – a statement from the BSH Board. 2016. Available at: http://www.shfnf.co.uk/wp-content/uploads/2016/05/BSH-Acute-kidney-injury-and-sick-day-rules.pdf. Accessed August 2018.

ACEi, angiotensin-converting enzyme inhibitor; AKI, acute kidney injury; ARB, angiotensin receptor blocker; ESC, European Society of Cardiology.

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ARE WE GOOD AT DIAGNOSIS AND TREATMENT?

⦿ White, middle-class, middle-aged man = sorted

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Died during trialAlive at the end

NYHA Class II NYHA Class III

24%N=476

76%N=1542

37% of deaths were sudden

17%N= 1003

83%N= 4916

35% of deaths were sudden

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Died during trialAlive at the end

NYHA Class II NYHA Class III

24%N=476

76%N=1542

37% of deaths were sudden

17%N= 1003

83%N= 4916

35% of deaths were sudden

Patients with mild symptoms are not stable, and progress, even on optimal treatment

Mild symptoms DO NOT equal mild disease

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Best-practice tariffs offer financial incentives to improve the care of patients with heart failure by making specialist care more available1

Best-practice tariffs are financial incentives for hospitals to meet criteria based on nationalguidance and expert opinion that define ‘best practice’ for managing that condition

1. Br J Cardiol. Heart failure learning module 1: background, epidemiology and pathophysiology. Costs to the NHS. 2017. Available at: https://bjcardio.co.uk/2017/11/heart-failure-module-1-background-epidemiology-and-pathophysiology-2/4/. Accessed August 2018.

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NATIONAL HEART FAILURE AUDIT

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NUH HF SERVICE

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NUH HEART FAILURE

⦿ 3 heart failure consultants (John, Jenny, Bara)

● 5 clinics

● Imaging, devices, cardiomyopathy, inherited ⦿ 3 heart failure nurses

● 1x inpatient referrals at QMC

● 1x clinic - new referrals & post-discharge reviews

● 1x NCH-based & for ambulatory IV diuretic service ⦿ Fortnightly MDT ⦿ Can directly refer to HF team rather than CATS/Cardiology ⦿ HF guidelines on intranet: BNP, Echo, Therapy, Referral

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Detailed discharge summaries are particularly important for patients with heart failure, who are subject to high rates of re-admission yet often lack key information

Key items recommended for heart failure discharge summaries

✓✓✓✓✓

✓✓✓✓✓

Echocardiographic evidence to support the diagnosis

Details of the cardiologist and other MDT members who saw the patient during the admission

Record of dry weight on discharge

Record of blood pressure and heart rate on discharge

All ECG findings (rhythm, QRS duration, whether paced, whether LBBB)

All drugs and doses on discharge

Contraindications (when drugs of prognostic benefit for LVSD are not prescribed, reason should be given)

Haemoglobin, creatinine, urea and electrolytes, and eGFR on discharge

Follow-up arrangements within 2 weeks of discharge

If there is a care plan in place with a specified contact person

Improving communication between primary and secondary care1

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AMBULATORY DIURETIC SERVICE

⦿ For patients where IV diuretic is only reason for stay ⦿ Any aetiology ⦿ Will run from Oxton Ward ⦿ Heart failure specialist nurse led ⦿ Initial recruitment from Cardiology beds / community

● Aim to accept referrals from anywhere after learning curve

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FUTURE THERAPIES

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PULMONARY ARTERY PRESSURE MONITORING

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Any questions?