Download Heart Failure - Acute Medicine @ BHH

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prevalence ~900,000 people
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average age of diagnosis 76
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most common cause is CAD
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30-40% mortality at 1y after diagnosis (worse than most cancers)
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5% of all acute admissions (projected to rise by 50% over next 25 years)
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1 million inpatient bed days per annum
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2% of annual NHS budget (70% of cost due to hospitalizations)
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1 in 4 patients are readmitted within 3m of discharge
Class
Symptoms
I
No limitation of physical activity: ordinary physical activity does not
cause fatigue, palpitations, dyspnoea or angina
II
Slight limitation of physical activity: comfortable at rest but
ordinary activity causes fatigue, palpitations, dyspnoea or angina
III
Marked limitation of physical activity: comfortable at rest but less
than ordinary activity causes fatigue, palpitations, dyspnoea or
angina
IV
Unable to carry out any physical activity without discomfort:
symptoms of cardiac insufficiency at rest and discomfort increases
with any physical activity
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67-year-old male, diabetes, COPD, MI 2005, CKD2
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ECHO 2008 mild AS and LVEF 33%
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NYHA II at last heart failure clinic appointment
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aspirin 75mg OD, simvastatin 40mg ON, metformin 500mg BD,
furosemide 40mg OD, ramipril 2.5mg OD, bisoprolol 1.25mg OD
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admitted to AMU with 1/52 Hx of increasing SOBOE (ET reduced
from 200 to 50yds), orthopnoea and oedema
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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?
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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
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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
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FBC, U&E, LFT, CRP, Ca2+, Mg2+, PO43-, lipids, glucose, TFTs
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Infection screen
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CXR
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ECG
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ECHO
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cMRI
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CT or conventional coronary angiography
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Spirometry
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NT-proBNP or BNP and hsTnI in selected cases
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CXR – venous congestion, upper lobe diversion, enlarged heart
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ECG – AF rate 98/min
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urea 14, creatinine 155 (138), other bloods unremarkable
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suddenly deteriorates at 02:00 with MEWS = 6
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RR 34, SpO2 88% on 2l O2, HR 144, BP 169/102, no urine since
admission
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cyanosed, clammy, agitated, JVP +5cm, bibasal crackles ++
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ABG: pH 7.29, pO2 7.6, pCO2 7.2, BE -8.3, lactate 3.2
1.
WHAT IS THE DIAGNOSIS?
2.
WHAT IS THE TREATMENT NOW?
ACUTE HEART FAILURE
IV diuretic bolus e.g. furosemide 50mg +/- IV morphine 2.5-5mg
sBP >110mmHg: IV vasodilator e.g. GTN 50mg in 50ml @ 0.6-6ml/h (10-100μg/min)
Inadequate
ventilation
or
oxygenation
Oxygen
NIV
ETT and IV
Lifethreatening
tachy- or
bradyarrhythmia
Systolic BP
<85mmHg
or shock
DCCV
Pacing
Stop
vasodilators
and βblockers
Inotrope /
Vasopressor
Consider
IABP
Inadequate
diuresis
Acute
mechanical
cause or
valvular
dysfunction
ACS
Catheterize
Increase
diuretics
Consider
low-dose
dopamine
or UF
Urgent
ECHO
Surgical or
percutaneous
intervention
Antithrombotic
therapy
Coronary
reperfusion
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limited evidence for beneficial ‘venodilatory’ effects of IV diuretics
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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)
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increased risk of other SE e.g. ototoxicity with high-dose furosemide
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continuous IV infusion of diuretics increases diuresis with lower cummulative doses
but no effect on symptoms or safety at 72h
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IV GTN causes venodilatation and reduced LV filling pressures (i.e. preload); arterial
dilatation (reduced afterload) at higher doses may decrease myocardial O2 demand
and improve CO
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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
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risk of sudden hypotension and increased myocardial ischaemia with nitrates
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Consider as adjunct to pharmacological Rx if severe respiratory
distress, refractory hypoxaemia or T2RF
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Contraindicated if significant hypotension
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CPAP and BiPAP are probably equivalent
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Improves symptoms, respiratory parameters and ABGs
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Earlier meta-analyses showed improved outcomes with NIV
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More recent meta-analyses (including results of large 3CPO
trial) failed to show any effect on intubation rates, LOS or
mortality
Congestion at rest?
orthopnoea, elevated JVP,
oedema, rales, ascites
Yes
Poor perfusion at rest?
cold extremities, narrow
pulse pressure, drowsiness
No
Yes
No
A: Warm & Wet C: Warm & Dry
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
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76-year-old Afro-Caribbean female
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HTN, CKD3 (renovascular disease) and OA
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diagnosis of HF with LVEF 26% on ECHO
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GFR fell from 44 to 31mL/min on initiation of ACE-i - stopped
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admitted with worsening oedema and SOBOE (NYHA III)
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bisoprolol 5mg, doxazosin 4mg, furosemide 80mg, simvastatin
40mg, naproxen 500mg
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BP 143/88mmHg, HR 84/min
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ECG: sinus rhythm, non-specific BBB (QRS 0.16s)
1.
WHAT ARE THE TREATMENT OPTIONS?
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
CRT-P or CRT-D
LVAD +/- heart
transplant
Digoxin if in AF or HR
still >70
CRT-P reduces hospital admissions and mortality and improves symptoms and
exercise capacity if symptomatic despite maximal medical therapy if:
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life expectancy >1y, good functional status, sinus rhythm
AND
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NYHA III-IV with EF ≤35% AND QRS ≥120ms (LBBB) OR QRS ≥150ms (non-LBBB)
OR
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NYHA II with EF ≤30% AND QRS ≥130ms (LBBB) OR QRS≥150ms (non-LBBB)
Possible benefit from CRT-P if:
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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
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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
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started on hydralazine 37.5mg TDS and ISDN 20mg TDS
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α-blocker stopped
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ivabradine 2.5mg BD added for rate control
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dose of furosemide increased to 120mg OD
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fluid restricted to ≤2l/d
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referred to HFNS for consideration of CRT-P
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no significant decline in renal function but no significant diuresis
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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?
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Poor compliance, excess salt intake, concomitant NSAID use
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Renal impairment (reduced active secretion of diuretics and
decreased peak urinary concentrations)
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Compensatory hyperplasia/hypertrophy of epithelial cells in
DCT and increased Na+ reabsorption with chronic loop diuretic
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Reduced biovailability or delayed absorption of diuretics due
to intestinal mucosal oedema
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Compensatory post-diuretic salt retention (when urinary drug
concentrations < diuretic threshold)
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Reduce dietary salt intake (<2g/d) and stop NSAIDs
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Increase diuretic dose in renal failure (e.g. furosemide 240mg daily)
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Add in thiazide diuretic e.g. metolazone, bendroflumethiazide or
indapamide (monitor U&E closely)
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Switch to bumetanide or torasemide (bioavailability 80% compared
with 40% for furosemide) or IV diuretics
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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
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consider ultrafiltration with CVVH: increased weight loss and
reduced readmissions c/w diuretics (UNLOAD)
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82-year-old female
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T2DM, HTN, AF
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2x admissions this year with pulmonary oedema
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review in AEC with results of outpatient ECHO
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breathless after walking 50 yds, mild ankle oedema, raised JVP
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ramipril 2.5mg, gliclazide 40mg BD, furosemide 40mg OD
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BP 159/91, HR 88/min irregularly irregular, CBG 15.1mmol/L
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BNP 252pg/mL (<35pg/mL), HbA1c 9.5%, other bloods normal
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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
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symptoms and signs of CHF with EF >40%
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normal LVEF on ECHO in up to 50% with ACPOE (rule out reversible cause of LVSD)
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older, female, hypertensive, diabetic, AF (CAD less common)
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similar prognosis to HF-REF
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impaired LV relaxation during diastole and E/A reversal on ECHO
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no treatment proven to reduce mortality
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perindopril (PEP-CHF), irbesartan (i-PRESERVE) and candesartan (CHARMPRESERVED) may improve symptoms and reduce admissions
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β-blockers (e.g. nebivolol), rate-limiting CCBs (e.g. verapamil) and digoxin may
increase diastolic filling times by reducing ventricular rate
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diuretics for congestive symptoms
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optimize Rx of comorbidities e.g. HTN, diabetes, AF (and CAD)
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78-year-old male, previous CABG
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EF 15%
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NYHA IV (breathless at rest)
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LBBB on ECG
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admitted with worsening oedema
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unable to tolerate ACE-i/ARB and spironolactone due to CKD4
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sBP 90mmHg, SpO2 90% on air
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asked to see urgently by nurse ?dying (DNACPR in place)
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asleep, Cheyne-Stokes respiration, apnoeic periods with SpO2 84%
1.
WHAT IS THE DIAGNOSIS?
2.
WHAT ARE THE TREATMENT OPTIONS?
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Periodic breathing or central sleep apnoea (CSA)
Occurs in up to 50% with severe HF (NYHA III-IV) during sleep
Heightened chemoreceptor sensitivity to CO2, increased circulating
catecholamine levels and hypoxaemia
Hyperventilation
Hypocapnia – CO2 levels fall below apnoeic threshold
Apnoea
Sympathetic activity ++
PaCO2 levels rise above apnoea threshold
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Daytime somnolence, fatigue, PND, hypoxaemia/diastolic dysfunction,
increase in fatal arrhythmias and mortality
Nocturnal O2 < CPAP < BiPAP < adaptive servoventilation (ASV)