Cardiac Failure

Range of syndromes characterised by impediment to ventricular filling or ejection due to structural or functional myocardial disease, classified by:

Stage C and D disease are also staged by function, using either the NYHA or INTERMACS grade.

Functional Staging of Heart Failure
NYHA INTERMACS Capacity
I Asymptomatic, with no physical limitations.
II Comfortable at rest.
Slight symptoms with ordinary activity.
III 7 Comfortable at rest.
Symptomatic with less than ordinary activity.
IV 6 Symptomatic at rest.
Exertion limited by symptoms.
5 Exertion intolerant.
4 Symptomatic at rest on oral therapy.
3 Stable on inotropes.
2 Progressive decline (‘sliding’) on inotropes.
1 Critical cardiogenic shock.
Notes:
  • Functional staging is used for stage C or D heart failure
  • INTERMACS staging may receive modifiers for requiring:
    • Temporary circulatory support
      For INTERMACS 1-3.
    • Arrhythmia For all grades.
    • Frequent flyer For INTERMACS 3-6.

Epidemiology and Risk Factors

  • Prevalence of chronic heart failure is ~2%
    • <2% in <60 year-olds
    • >10% in >75 year-olds
  • Lifetime risk of disease is ~20%
  • Annual mortality is 6-7% in patients with stable heart failure
    • ↑ to 25%/year in hospitalised patients

Pathophysiology

Heart failure with reduced ejection fraction:

Aetiology

Precipitating causes:

  • Cardiac
    • Arrhythmias
      • AF
    • Ischaemia
      • AMI
      • Angina
    • Hypertensive emergency
    • Mechanical
      • Valvular
      • Tamponade
      • PE
  • Neurological
    • Neuromuscular disease
  • Infective
    • Sepsis
    • Pneumonia
    • Myocarditis
  • Toxins
    • Alcohol
    • Beta-blockade
    • Calcium antagonists
    • Cocaine
    • Chemotherapy
  • Genetic
    • Muscular dystrophies
    • Desmoplakin cardiomyopathy
  • Other
    • Peripartum
    • Autoimmune
    • Giant Cell Myocarditis
      May recur after heart transplant.
    • Sarcoidosis
    • Iron overload

Assessment

Features of Cardiac Failure by Stage
Stage Features Caveats
A

Risk factors:

  • HTN
  • DM
  • Obesity
  • Diabetes
  • Cardiotoxic agent exposure
  • Family history
  • Genetic cardiomyopathy
  • Asymptomatic
B

Evidence of:

  • Structural heart disease
    • ↓ LVEF or RVEF
    • LVH
    • LV dilation
    • RWMA
    • Valvular heart disease
  • ↑ Filling pressures
    • Echocardiography
    • Invasive measurement
  • Persistent troponin elevation
  • ↑ BNP
  • Asymptomatic
  • No competing diagnosis
C Features of heart failure
D Marked features that interfere with daily life and result in recurrent hospitalisation

History

Symptoms of heart failure:

  • Dyspnoea
    May be secondary to:
    • Pulmonary oedema
      Pulmonary congestion due to raised LAP. Moderately sensitive but poorly specific.
    • Pleural effusion
      Fluid retention and elevated RAP/ Classically bilateral, due to pulmonary congestion.
  • Orthopnoea
    ↑ VR and pulmonary congestion in supine position.
    • More specific than dyspnoea, but insensitive
  • PND
    As orthopnoea, but with additional respiratory depression.
  • Palpitations
    Tachyarrhythmias and reduced exercise tolerance.
  • Early satiety
    Fluid retention.
  • Anorexia
    Fluid retention.
  • Fatigue
    Reduced skeletal muscle perfusion.

Examination

  • Cachexia
    Intestinal congestion, chronic inflammatory pathway activation.
  • Crepitations
    Secondary to pulmonary oedema.
  • Elevated JVP
    ↑ RAP.
  • Displaced apex beat
    LV dilatation.
  • Hepatomegaly
    ↑ RAP.
  • Hepatojugular reflex
    ↑ RAP.
  • Ascites
    Fluid retention.
  • Oedema
    Fluid retention and elevated filling pressures.
    • Insensitive
      Many elderly patients have oedema due to immobility.

Diagnostic Approach and DDx

Investigations

Bedside:

  • Blood gas
    • Lactate
    • SvO2
  • Bedside echocardiogram
    • Systolic function
    • Filling state
    • Structural disease
  • PAC
    May be useful in:
    • Cardiogenic shock
    • Uncertain haemodynamic state
      i.e. Mixed shock.

Oxygen saturation of central or mixed venous blood indicates the degree of oxygen extraction and is one marker (with many caveats) of the adequacy of tissue perfusion and oxygen delivery.

Interpretation of Venous Oxygen Saturation
SmvO2 Interpretation
>75% Normal
50-75% ↑ VO2/↓ DO2
30-50% Exhaustion of extraction reserve
<30% Significant anaerobic metabolism
Notes ScvO2 is usually 2-3% lower than SmvO2 due to ↓ O2 extraction from the lower body, but will trend in parallel

Laboratory:

The level of an ↑ BNP and NT-proBNP both have prognostic significance.

  • Blood
    • Troponin
    • BNP
      Released in response to ↑ ventricular wall tension.
      • <100pg/mL is 90% sensitive/70% specific for excluding failure
      • Echocardiography indicated if >35pg/mL
      • May be normal in HFmrEF or HFpEF
    • NT-proBNP
      Prohormone of BNP.
      • Similar sensitivity to BNP with cut-off of >300pg/mL300
      • Echocardiography indicated if >125pg/mL
    • Monoclonal light chains
      If concern for cardiac amyloidosis.
  • Urine
    • Monoclonal light chains
      As blood.
  • Endomyocardial biopsy
    Indicated if suspecting a particular diagnosis, e.g.
    • Amyloidosis
    • Infiltrative disease
    • Acute rejection following transplant
    • Rapid deterioration despite optimal medical therapy

Imaging:

  • CXR
    • Pulmonary oedema
    • Venous congestion
    • Cardiomegaly
  • Serial echocardiogram
    Recommended for patients following a significant change in clinical status.
  • Cardiac MRI
    Excellent anatomical characterisation. Useful in:
    • Congenital heart disease
    • Unsuccessful echocardiography

Other:

  • 6MWT
    Distance correlates with VO2 and prognosis. Thresholds include:
    • >490m results in ↓ utility of the score
      Due to poorer correlation.
    • <300m correlates with NYHA III/IV symptoms
  • CPET
    VO2 <14mL/kg/min may indicate better survival with transplantation.

Diagnostic Approach and DDx

Management

Effective heart failure management relies on achieving balance between the competing goals of ensuring adequate organ perfusion whilst minimising myocardial work. The choice of therapy depends on the degree of cardiopulmonary reserve of the patient, and so patients can be divided into:

  • Haemodynamically stable
    Myocardial function adequate to meet demands. Anti-failure therapy aims to:
    • ↓ Rate of functional decline
    • Counteract maladaptive physiological processes
  • Haemodynamically marginal
    Myocardial function barely adequate to meet demands, such that many elements of anti-failure therapy may need to be ceased or reduced due to intolerance.
  • Haemodynamically unstable
    Myocardial function inadequate to meet demands; essentially on a cardiogenic shock spectrum. Therapy aims to:
    • ↑ Organ perfusion with inotropes and diuresis, whilst preventing excess myocardial work
      If this balance cannot be achieved with medical therapy, then mechanical support may be required.

Haemodynamically Stable Disease

  • Prevent further deterioration by controlling risk factors
  • Determine the ejection fraction
  • Early medical management with anti-failure therapies
    The **“four pillars”* of heart failure.
  • Consider ICD or CRT-D if EF <35%

This section is tailored towards management of stable heart failure in the critical care setting; lifestyle and risk factor modification is underrepresented.

Specific therapy:

Avoid β-blockade in patients with severely ↓ LVEF to avoid precipitating cardiogenic shock.

  • Pharmacological
    • Anti-failure therapy
      The four pillars of antifailure therapy are indicated for HFrEF or HFimpEF, and consist of:
      • RAAS inhibition
        ↓ BP and maladaptive remodelling, ↓ mortality, hospitalisations, and progression. One of:
        • ARNI
          Recommended in NYHA II/III disease. Contraindicated if:
          • History of angioedema
          • ACEi use in previous 36 hours
        • A2RB
          Preferred if recent MI, intolerance to ACEi, or requirement for ARNI.
        • ACE inhibitor
          De-emphasised due to inferiority to ARNI.
      • β-blockade
        Improve symptoms and ↓ arrhythmia-related mortality. Use either:
        • Bisoprolol
        • Carvedilol
        • Slow-release metoprolol
      • Aldosterone antagonists
        ↓ Mortality and morbidity, indicated for NYHA II-IV disease.
        • Spironolactone 12.5-50mg PO OD
          • Commence at 25mg if eGFR >50mL/min/1.73m2
          • Double dose after 1 month
        • Contraindications:
          • eGFR >30mL/min/1.73m2
          • K+ <5.0mmol/L
            Incidence of hyperkalaemia is rare.
        • Requires regular review of potassium
      • SGLT2i
        ↓ Mortality, hospitalisations, dialysis, and rate of renal decline.
        • Empaglifozin 10mg daily
    • Diuresis
      Goal is to relieve clinical evidence of congestion at the lowest possible dose.
      • Diuretic therapy should be escalated in a stepwise fashion:
        • Loop diuretic
        • Thiazide
          May be added if:
          • Hypertension
          • Fluid retention refractory to loop diuretics
      • Exacerbations requiring hospital admission generally require:
        • Doubling the usual daily dose, and administering IV
          Results in a 4× effective furosemide dose.
        • Addition of a thiazide
      • Diuretic resistance can be managed in a stepwise fashion:
        • ↑ Furosemide dose
        • Add thiazide
        • Commence furosemide infusion
        • Sequential nephron blockade
    • Statin
      Indicated with any history of ACS. ↓ Failure and further cardiovascular events.
    • Additional therapies
      May be considered once the above therapies are instituted and doses have been optimised. Include:
      • Digoxin
        NYHA II-III HFrEF; ↓ hospital admissions but not mortality.
      • Ivabradine
        NYHA II-III HFrEF with LVEF <35% and in NSR >70bpm despite maximally tolerated dose of β-blocker.
    • GTN
      Indicated for relief of dyspnoea (in addition to diuretics) in patients without hypotension.
  • Procedural
    • ICD
      Indicated if LVEF <35% and estimated >1 year survival.
    • CRT-D
      Combination resynchronisation therapy and ICD is indicated if an ICD is indicated and there is preserved sinus rhythm with a LBBB. Benefit is proportional to the QRS width.
    • CABG
      Surgical revascularisation ↓ mortality hospital admission for patients with 3VD, left main (or equivalent) disease, and LVEF <35%. This benefit ↓ with ↑ age.
  • Physical
    • NIV
      CPAP is beneficial in APO, by improving oxygenation and ↓ LV afterload.

The principles of HFpEF management are similar, although the evidence base supporting therapies are much weaker. In general, treatment should include:

  • RAAS inhibition
  • Aldosterone antagonist
  • Diuretic PRN

Diuretic resistance can be defined as inadequate solute and water clearance despite 160mg/day of furosemide.

Diuretic Dosing
Class Drug Initial Daily Dose Maximum Total Daily Dose Duration of Action
Loop diuretics Bumetanide 0.5–1.0mg OD/BD 10mg 4–6h
Furosemide 20–40mg OD/BD 600mg 6–8h
Thiazide diuretics Chlorthiazide 250–500mg OD/BD 1000mg 6–12h
Chlorthalidone 12.5–25mg OD 100mg 24–72h
Hydrochlorothiazide 25mg OD/BD 200mg 6–12h
Indapamide 2.5mg OD 5mg 36h
Metolazone 2.5mg OD 20mg 12–24h

Benefit from β-blockade does not appear to be a class effect - only a limited number of agents are shown to have benefit.

β-Blocker Dosing for Heart Failure
Drug Initial Daily Dose Target Daily Dose Mean Achieved Dose
Bisoprolol 1.25mg OD 10mg OD 8.6mg
Carvedilol 3.125mg BD 25–50mg BD 37mg
Carvedilol CR 10mg OD 80mg OD
Metoprolol CR 12.5–25mg OD 200mg OD 159mg

GTN is particularly important with acute LV failure in the setting of hypertension - rapid afterload reduction can quickly unload the LV, reverse APO, and stave off the requirement for intubation. Rapid IV administration is best performed with invasive pressure monitoring.

Supportive care:

  • H
    • VTE prophylaxis
    • Correct iron deficiency

Disposition:

Preventative:

  • Risk factor modification
    • OSA treatment
    • Regular physical activity
    • Healthy dietary patterns
    • Smoking cessation
  • SGLT2 inhibitor
    Generally contraindicated in the critical care setting.
  • Anti-failure therapy
    ↓ Readmission in chronic failure.

Haemodynamically Unstable Disease

  • Revascularisation
    For acute MI.
  • Inotropic support
    Use the lowest dose tolerated for the shortest amount of time possible.
  • Consider mechanical support
    If adequate organ function is not maintained by inotropes.
  • Transplantation workup

Resuscitation:

  • C
    • Inotropic support
      • Rotation may be required in long-term infusions to minimise tachyphylaxis
      • ↑ Arrhythmia burden
      • Appropriate for palliation and symptomatic relief
      • Choice is guided by:
        • Availability
        • Blood pressure
        • Arrhythmia burden

Specific therapy:

Inotropic support is covered in detail under Inotropes.

  • Pharmacological
  • Procedural
    • Revascularisation
      For acute MI.
    • Durable LVAD
      Selected patients with INTERMACS 3 disease. May be used as:
      • Destination therapy
      • Bridge-to-transplant
    • Heart transplantation
    • Temporary mechanical circulatory support
      Temporary mechanical support may for patients in cardiogenic shock as:
      • Bridge-to-decision
        Determine eligibility of transplant.
      • Bridge-to-bridge
        Stabilise prior to durable VAD insertion.
  • Physical

Temporary mechanical support may consist of ECMO, temporary LVAD, or temporary RVAD.

Supportive care:

Disposition:

Preventative:

Marginal and Ineffective Therapies

  • Non-dihydropyridine calcium channel blockers
    Negative inotropic effects may be poorly tolerated compared to β-blockers.
  • Glitazones
    ↑ Rate of hospitalisations.
  • Fluid restriction
    Unclear benefit: No change in hospitalisation or mortality.

Anaesthetic Considerations

Improving Organ Perfusion

  • Afterload
    Reduce with systemic vasodilators.
    • IV
      • GTN
      • SNP
      • Milrinone
  • Preload
  • Contractility
    • Cease negative inotropes
    • Inotropes
  • Rate
    ↑ to high normal (~90); CO may fall with ↑ tachycardia depending on the diastolic function.
  • Rhythm
    Restore sinus rhythm.

Reduce Myocardial Work

  • Afterload
    Reduce with systemic vasodilators.
    • PO
      • ACE-I
  • Contractility
    • Negative inotropes
      Improvement in ventricular filling, coronary perfusion, and myocardial oxygen demand.
  • Preload
  • Rate
  • Rhythm
    Restore sinus rhythm.

Mechanical Support

  • Respiratory
    • NIV
      Positive airway pressures CPAP, PEEP) reduces LV wall tension and afterload.
    • Mechanical ventilation
      In addition to the effects of ↑ airway pressure, mechanical ventilation substantially reduces work of breathing and therefore VO2. These gains may be significant (up to 30%), but is not a long-term solution.
  • Cardiac
    • IABP
    • VAD
      • Temporary
      • Permanent
    • ECMO

Additional Physiological Goals

Correct:

  • Hypoxia
  • Acidaemia
  • Electrolyte derangements
  • Anaemia
  • Thiamine deficiency

Marginal and Ineffective Therapies

Complications

  • C
    • AF
      • Present in ~30% of patients
      • May be either a cause or consequence
    • Malignant arrhythmias
      • ↑ Risk with:
        • Ischaemia
        • Electrolyte abnormalities
          Hypo/hyperkalaemia, hypomagnesaemia.
      • Psychotropic drugs
      • Digoxin
      • Antiarrhythmics
  • H
    • Thromboembolism

Prognosis

  • Death
    • High in symptomatic heart failure
      • 20-30% one-year mortality in mild cases
      • ⩾50% one-year mortality in severe heart failure
    • Predictors of poor outcome include:
      • High NYHA class
      • Reduced LVEF
      • Raised PCWP
      • Third heart sound
      • Reduced CI
      • DM
      • Hypernatraemia
      • Elevated catecholamines
      • Low predicted peak oxygen consumption with maximal exercise

Key Studies

References

  1. Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022 May 3;145(18):e895–1032.
  2. Stevenson LW, Pagani FD, Young JB, Jessup M, Miller L, Kormos RL, et al. INTERMACS Profiles of Advanced Heart Failure: The Current Picture. The Journal of Heart and Lung Transplantation. 2009 Jun 1;28(6):535–41.
  3. Metra M, Teerlink JR. Heart failure. Lancet. 2017;6736(17). doi:10.1016/S0140-6736(17)31071-1.
  4. ABC of heart failure: Clinical features and complications [Internet]. [cited 2019 Dec 9].
  5. Bloos F, Reinhart K. Venous oximetry. Intensive Care Med. 2005 Jul 1;31(7):911–3.