Acute heart failure

• The definition is woolly and ranges from cardiogenic shock to acute pulmonary oedema to worsening peripheral oedema and gradually worsening SOB. Best considered as heart failure that brings you in to hospital
• Most do not present in acute pulmonary oedema. If they do, likely due to overzealous fluid prescribing, MI or arrythmia
• 60% of acute heart failure occurs de novo, with no known history of the condition
• Acute HF carries a mortality risk of around 9% during admission and a post-discharge mortality of a further 33% over the next year… worse than many cancers.
• Tips on history and exam
  • • Ask about orthopnoea and PND. Check JVP, ankles and chest
    • Can gain 5kg of weight prior to clinically obvious oedema evident
    • Pitting oedema to thighs = around 12L of extra fluid on board
    • Drowsiness and cool peripheries are poor prognostic signs
    • If cold and wet, refer to ICU early if a candidate
    • Patients may have enough fluid but in the wrong place (distribution issue) or might be volume overloaded (more subacute presentation, more likely caused by poor compliance with medications, deterioration of LV function or arrhythmia)

---

Phenotype the patient / assess severity

• Are they wet? Oedema, congestion on CxR/USS
• Are they poorly perfused? Cool peripheries, reduced GCS, hypotensive, lactic acidosis, AKI, deranged LFTs
• What’s the phenotype?
  • • Decompensated heart failure
      • • 65%
        • Can be 10-20kg over baseline weight
        • More gradual onset
        • Often low or normal BP and cardiac output (CO)
        • Can be ‘wet and warm’ or ‘wet and cold’
    • Cardiogenic shock
      • • Signs of poor perfusion
        • Needs urgent echo
        • Low BP (but rarely can be normotensive)
        • ‘Wet and cold’
    • Acute pulmonary oedema
      • • 20%
        • Most often secondary to ACS (in 50%) or arrythmia. May occur in the context of diastolic dysfunction or valve disease
        • Rapid onset
        • Sweaty, using accessory muscles, afraid, pink/frothy sputum, cold/clammy
        • Often hypertension, but BP can be normal
        • ‘Wet and warm’
    • Isolated RV failure
      • • Can be due to RV infarction or PE
        • Raised JVP and systemic hypoperfusion
        • Often low BP and CO
        • ‘Wet and cold’

• Consider eight possible precipitants of acute HF – then reverse/treat what you can
  • • Ischaemia
      • • Usually a relatively large infarct if acute HF occurs. Consider immediate angio
    • Hypertensive crisis
      • • Quite common, often overlooked
        • Adrenergic spiral, in extremis
        • Occurs in HF with preserved EF
        • Significant HTN
        • GTN works very well
    • Arrhythmia
      • • Quite common. Fast AF might be the trigger in 30% of cases (digoxin used a lot but slow to work)
        • Consider if drugs required (care with amiodarone which is negatively inotropic, and betablockers), DCCV or emergency pacing
    • Mechanical – Tamponade, valve problem (eg acute MR from chordal rupture), VSD, aorta problem etc – esp in context of ischaemia
    • Pulmonary embolism
    • Non-compliance with meds – perhaps the most common precipitant
    • Physiological stress – Infection, toxins, post-op, anaemia, pregnancy
    • Endocrine – Hyperthyroid, DKA, adrenal dysfunction

• Think about root causes of chronic HF (whether diagnosed or not – steers investigations and long-term management)
  • • Cardiovascular – HTN, IHD, valvular disease, sustained arrhythmias, congenital, cardiomyopathies, myo/pericarditis, infiltrative
    • Increased metabolic demand – peripartum cardiomyopathy, pagets, hyperthyroidism, anaemia, obesity
    • Drugs – incl ETOH, cocaine, cancer drugs
    • Pulmonary disease
    • Rare – storage disorders, endomyocardial disease (EO, carcinoid), neuromuscular disease

---

General management and investigations

• Sit up, give oxygen
  • • Aim sats >90% as hypoxia causes vasoconstriction and can increase afterload.
    • High flow nasal cannula if required
    • Consider intubation for progressive respiratory failure despite O2 (although intubation in cardiogenic shock can cause arrest)
    • CPAP can be considered if hypoxic but this can impair systolic function. Safe though. Most useful in pulmonary oedema when BP often elevated.
• ECG
  • • If in fast AF, consider rhythm control, rate control, anticoagulation, and whether they need an early cardioversion (+/- TOE guided)
    • Look carefully for signs of ischaemia if any pain
• CxR – check for:
  • • Peripheral septal lines
    • Upper lobe diversion (prominence of upper lobe pulmonary veins which resembles a stag’s antlers)
    • Cardiomegaly
    • Perihilar haze or bats wings
    • Airspace opacification
    • Can be effusions but usually not
• Consider bedside echo / POCUS
  • • Subcostal view best with 4 Chambers, LV function, effusion, then tilt to liver to check IVC to check filling.
    • Over 3 B lines in 2 bilateral lung zones has a high sensitivity, specificity and positive likelihood ratio, with very low negative likelihood ratio for pulmonary oedema
    • Acute severe MR – consider MVR. Edge to edge repair sometimes done in secondary MR, or surgery
    • Critical AS – consider TAVI or AVR
    • Reduced EF – ensure GDMT prescribed once stabilised
• Departmental echo within 48 hours (sooner if new murmur/shock)
  • • Check previous echo and compare
    • Look at LV function, valves, RWMAs
    • Any evidence of HTN? Eg dilated aorta, LV wall thickness
    • Look for diastolic dysfunction
    • Always do an inpatient echo if admitted in acute HF and no previous scans. The one-year survival for those with HFrEF discharged on 3 classes of drugs is much better. Patients less likely to be readmitted too.
• Bloods
  • • NT-proBNP, TSH, trop, CRP, Hba1C, CK, LFTs, urinary PCR, Na and renal function (compare to baseline), lactate/pH
    • An NT-proBNP <300 pg/mL reliably excludes acute HF
    • Age-stratified rule-in cut-offs indicate acute HF is likely: >1800 pg/mL if aged >75 years, >900 pg/mL if aged between 55 and 75 years and >450 pg/mL if aged >55 years
    • BNP will also be elevated in anything that puts a load on the heart esp AF, sepsis, anaemia, uncontrolled HTN, lung disease (incl pulmonary HTN), myocarditis, PE
    • Other causes of raised BNP – stroke, renal or liver dysfunction, burns, infection, COPD
    • Obesity causes lower levels of BNP
• Consider PCI if any suggestion of ischaemia
• Diuretics (see below)
• LMWH if not anticoagulated
• Vasodilator eg GTN infusion
  • • Works well
    • 2-10 ml/h of a 1mg/ml preparation and check BP frequently
    • Especially good treatment if HTN predominates (caution if pregnant)
    • Tend to avoid if BP < 100 or 110
    • Avoid in significant aortic or mitral stenosis (check previous echo)
    • IV nitroprusside alternative
    • Better evidence than frusemide acutely
• Only give 2.5-5mg IV morphine if distressed / agitated (can make them worse)
• Avoid, stop or hold:
  • • Avoid cyclizine (increases LV/RV afterload)
    • Sometimes hold betablockers (but ensure restarted after discharge as part of GDMT)
    • Avoid CCB (verapamil, diltiazem)
    • Stop NSAIDs, glitazones
    • Consider stopping non-prognostic antihypertensives (so you have more room for prognostic meds which lower BP)
• Goal directed medical therapy (if HFrEF)
  • • Uptitrate / commence prognostic therapies – ie ACE-I, betablocker, digoxin, spironolactone, Entresto, SGLT2i
    • If new diagnosis of HF – can start once improving
    • Routine withdrawal of existing HF GDMT is not recommended in acute HF, as this is associated with worsened outcomes
    • SGLT2i – can start early in most cases (avoid in T1DM). Also used in HFpEF
    • See Chronic Heart Failure
• IV iron should be considered for iron deficient hospitalised HF patients with an LVEF <50%
• Refer to heart failure specialist nurse/team (and ensure follow up arranged if heading home soon)
• Phenotype-specific management
  • • Acute decompensated heart failure – diuretics, check prior diuretic compliance, consider combined diuretic therapy, inotropes if hypoperfusion
    • Pulmonary oedema – consider CPAP. diuretics.
    • RV failure – diuretics, optimise fluid status, look for PE
    • Shock – consider inotropes, pressors, PCI, mechanical assist devices, surgery, palliation
    • If wet and well perfused (most) – diuretics
    • If wet and poorly perfused (cold) – inotropes first line, consider vasopressor and give diuretic when perfusion corrected.
    • If dry and poorly perfused – give fluid challenge, consider inotropes and vasopressor

---

Diuresis

• If already on it, double dose (or up to 2.5x usual dose) and switch to IV (as gut oedema might limit absorption)
• Dose depending on fluid status, BP and how unwell they are. Can give Furosemide 40 mg daily or Bumetanide 1 mg daily. Trial 40mg furosemide BD if more unwell, 80mg BD if very unwell
• Might need higher doses if pre-existing renal impairment
• Relatively contraindicated if systolic < 90
• Doses of >120mg frusemide should be split into BD
• Watch renal function daily
• Bed rest helps diuresis
• Usually treated with IV diuretics until euvolaemic and ready to discharge
• Diuresis and renal function
  • • Often fluid overload is the cause of renal impairment, so requires diuresis. Frusemide might cause decline in renal function but relieving oedema can help kidney perfusion.
    • Worsening renal function in this setting is not analogous to AKI (there is often no tubular injury). Renal function may actually improve with diuresis so don’t be too stingy with diuretics just because renal function is a little off. Worsening renal function is fine, as long as it is accompanied by a good diuretic response – this is key
    • Decline in renal function actually corresponds with a better prognosis than no change
    • Knowing how much to tolerate a drop in eEFR is difficult. Some say accept rise in creatinine up to 50%. If creatinine rises by > 30% or hyperkalaemic you might withhold Ramipril and spironolactone, but you can keep going with frusemide.
    • Consider the context and the cause (eg drugs, renal hypoperfusion, cardiogenic shock, congestion, sepsis, gout)
    • If anuric – make decisions about RRT
    • If creatinine up to 300, and patient looks unwell, consider frank discussions about end of life
• Hypokalaemia on diuresis – continue furosemide, replace K+ (orally is fine, unless <3)
• How to know much diuresis is enough? Can look at:
  • • Urine output – aim for >100-150ml/hr. Not every patient needs to be catheterised.
    • Urinary spot Na – aim for >50-70mEq/L (same as mmol/L) at 2-6 hours after furosemide given IV. This might be best, as you don’t have to wait to work out the urine output
    • Daily weights
      • • Aim for weight decrease of > 1-1.5kg every 24 hours, some would say 2-3kg/day but may be too much for most.
        • Once euvolaemic or at dry weight, switch back to oral diuretics
        • Often very inaccurate so not the preferred test of diuresis
        • If in range, continue diuretics BD. If lower – double dose, and continue to increase until max dose met
        • Once weight stable for 48 hours – can be discharged (the At Home team can sometimes continue diuresis)
    • Some advise discharging only once euvolaemic, as residual oedema at discharge is associated with increased HF mortality and readmissions. However, hospital at home teams can sometimes facilitate ongoing diuresis
• Input/output chart
  • • Can fluid restrict 1-1.5L/day (2-2.5L/day if patient at dry weight) – but actually no evidence for this!
    • Useful if low Na, maybe not for all comers.
    • Tends to piss off patients rather than making them better. Same with Na restriction.
• If not winning
  • • If loop diuretic not working well, give more, or add on / switch to bumetanide (more predictable, esp if lots of gut oedema / ascites, bumetanide better absorbed)
    • Can add metolazone 5mg (could start at alternate days), or spironolactone if hypokalaemia
    • Or start furosemide infusion (eg 120mg / 24 hours). Can go up to 360mg / 24 hours if being aggressive
    • If still struggling with lots of diuretics, ultrafiltration is an option for a few patients

---

Issues

• Hypotension
  • • Critical care/cardiology review early
    • Stop CCB and nitrates
    • Don’t necessarily stop betablocker and ACEI – it depends. Sometimes better to reduce dose and remember that BP of 100 or 90 systolic might be normal for them.
    • Digoxin can increase BP in AF and is safe (even in renal dysfunction). Can load 500mcg, then 500mcg 12 hours later. Then stop.
    • Can usually still give loop diuretics in hypotensive pulmonary oedema (alone if no signs of hypoperfusion, and with inotropes if there is)
• Hyponatraemia
  • • If chronic, don’t worry too much, though this suggests prognosis is poor and is common in advanced disease
    • Don’t do osmolalities if on diuretics (might stop diuretics and check osmolalities if it persists)
    • Have honest conversation with patient about the balancing act
    • Fluid restrict first
    • If really not winning, you can use twice normal saline (hypertonic) alongside a frusemide infusion
• Bradycardia – consider stopping/reducing betablockers, CCBs, amiodarone
• Severe AS
  • • Avoid vasodilators, eg nitrates. Consider emergency TAVI or surgical valve replacement (provided life expectancy > 1 year)
    • Correct other causes of high flow status eg anaemia, thyrotoxicosis, AV shunts

---

Advanced strategies and other measures

• Often used as a bridge – to either a decision, to candidacy, to transplant, to recovery, or as a destination therapy if the patient is ineligible for transplant
• Refer early to specialist unit if severe myocarditis, rapidly progressive DCM or young and severe ischaemic LV impairment
• Inotropes
  • • No good evidence of benefit
    • Useful if poorly perfused
    • If mixed venous sats <65% and metabolic acidosis – consider dobutamine
    • Consider pressors like norad alongside, especially if infected
• Mechanical assist devices
  • • Can be used short term or longer term
    • Lots on the market – Impala, LVAD
    • Lots of contraindications – incl PVD, high bleeding risk
• CPAP
  • • Can reduce venous return and BP – be careful if BP already low
    • Can be useful if tiring, or acidaemia
• ECMO
• Heart transplant
• Advance Care Planning and palliative care input
  • • Being admitted for gross fluid retention is often a sign patient is nearing end-stage disease, esp if admissions becoming increasingly frequent
    • Consider switching off ICDs
• Revascularise when fit if required
  • • Consider inpatient CTCA or angiogram if ischaemic cardiomyopathy suspected