Treatment of Acute Heart Failure - What We Have Learned to Date and How to Put it Into Practice

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DOI
https://doi.org/10.15420/ecr.2006.1.100

Acute heart failure (HF) is a clinical entity characterised by rapid onset of symptoms and signs secondary to abnormal cardiac function, with reduced cardiac output and pulmonary and/or systemic congestion.1

De Novo Acute HF and Acute Decompensation of Chronic HF

There are two subtypes of acute heart failure - de novo and acute decompensation of chronic HF.1 In the first, HF is of sudden onset, with no previous history of the condition - a typical example is massive myocardial infarction (MI), resulting in left ventricular systolic dysfunction and HF. The second type is characterised by decompensation of chronic HF, as a result, for example, of a respiratory infection.

Aetiology

The most commonly identified aetiology of acute HF is coronary heart disease, found in 60-70% of patients in many series.2 Less common causes include hypertensive crises, myocarditis and endocarditis.1

Relevance of Acute HF

Due to the ageing of the population and to improved survival after acute MI the prevalence of chronic HF and the incidence of acute HF are increasing.1 The economic cost of HF in developed countries represents 1-2% of total annual health budgets.3 The syndrome is progressive and is characterised by multiple episodes of decompensation, which are one of the most common causes of hospitalisation.4,5 This is the main burden on resources, accounting for 70-75% of total expenditure on HF.6,7 Mean hospital stay due to AHF is above 10 days.8 The rate of rehospitalisation within 12 months of admission for AHF is extremely high, at around 45%.9 Besides this, hospitalisation for AHF should be seen as an extremely serious clinical event, since in-hospital mortality is around 8%8 and six-month mortality is estimated at 25-30%.10,11 The recently published Acute Decompensated Heart Failure (ADHERE) Registry showed that it is possible to stratify the risk for in-hospital mortality in these patients using three simple parameters, recorded on admission - serum urea, systolic blood pressure and serum creatinine.12

Forms of Presentation

The European Society of Cardiology (ESC) guidelines list six forms of clinical presentation for acute HF:1

  • Acute pulmonary oedema. This is defined as a setting of severe dyspnoea and orthopnea, accompanied by crackles throughout the pulmonary fields - radiological confirmation is desirable. Arterial oxygen saturation on ambient air prior to treatment is usually <90%.
  • Cardiogenic shock. This is characterised by tissue hypoperfusion, despite adequate preload and heart rate of >60bpm. This is usually accompanied by hypotension - systolic blood pressure (BP) <90mmHg or a drop in mean BP of >30mmHg - and/or low urine output (<0.5ml/kg/h, which corresponds to <35ml/hour for an individual weighing 70kg).
  • Acute decompensated HF. This setting has less severe characteristics and does not fulfil criteria for acute pulmonary oedema, cardiogenic shock or hypertensive acute HF. It may be de novo or due to chronic decompensated HF.
  • Right heart failure. According to the guidelines, this syndrome is characterised by low cardiac output with hypotension, jugular distension and hepatomegaly.
  • Hypertensive acute HF. This is defined by signs and symptoms of HF with chest radiograph compatible with acute pulmonary oedema, accompanied by high BP and relatively preserved left ventricular systolic function.
  • High output HF. The clinical setting is one of pulmonary congestion, high heart rate caused by tachyarrhythmia, anaemia, thyrotoxicosis, etc., high cardiac output and warm extremities. It can sometimes be accompanied by low blood pressure as in septic shock.
Therapeutic Strategy

In acute HF, short-term therapeutic aims may outweigh long-term aims.13 While in chronic HF neurohormonal blockade is the mainstay of treatment, in acute HF ‘the immediate goals are to improve symptoms and to stabilise the haemodynamic condition’.1 The instability and poor prognosis of these patients requires an emergent approach.1 This involves three steps to be taken as rapidly as possible:

  • clinical and haemodynamic stabilisation;
  • prompt diagnostic assessment; and
  • definitive treatment of the cause - when possible - or correction of the triggering factor, when identified.1,14

Clinical and haemodynamic stabilisation involves two essential and complementary aims - rapid restoration of oxygenation and of cardiac output. To obtain adequate oxygen saturation, simple oxygen therapy, continuous positive airway pressure (CPAP) or, when necessary, invasive ventilation can be used.

Intravenous pharmacological therapy is crucial to haemodynamic improvement and vasodilators, diuretics and/or inotropics can be used, depending on the clinical situation.1,14,15 Vasodilators are a first-line therapy if hypoperfusion is associated with an adequate blood pressure and signs of congestion with low diureses (European Society of Cardiology (ESC) class I recommendation).1 Diuretics are indicated in patients with acute HF and fluid retention (ESC class I recommendation).1 Inotropes are indicated in the presence of peripheral hypoperfusion with or without congestion or pulmonary oedema refractory to diuretics and vasodilators - ESC class IIa recommendation.1Figure 1 depicts the general strategy for the treatment of acute HF according to the ESC guidelines.1

Monitoring of the clinical status and effects of treatment should be initiated as early as possible after hospital admission. In most cases non-invasive monitoring is sufficient1,16 and includes the assessment of symptoms and vital signs, pulse oximetry, continuous electrocardiograph (ECG) monitoring, urinary flux measurement and assessment of renal function and serum electrolytes.1 Invasive monitoring has a class IIb recommendation and is generally reserved for haemodynamically unstable patients who are not responding in a predictable fashion to therapy and in those with hypoperfusion combined with pulmonary congestion. It should be removed as soon as possible.1

The initial evaluation of acute HF includes the appraisal of symptoms and the clinical assessment of tissue perfusion and of pulmonary and systemic congestion.1 Laboratory evaluation strongly suggested by the ESC guidelines includes blood and platelet counts, C-reactive protein (CRP), urea, creatinine and serum electrolytes, blood glucose, creatine kinase MB, troponin I/T and D-dimer.1 In severe HF, international normalised ratio and arterial blood gases should be considered.1 Transaminases, plasma b-type natriuretic peptide (BNP) or N-terminal prohormone BNP and urinalysis should be considered.1 Chest X-ray carries a class I recommendation.1 The ECG is essential in assessment of acute coronary syndromes. Echocardiography-2D is key and plays a pivotal role in prompt diagnostic assessment, identifying treatable causes or correctable triggering factors. It bears a class I recommendation according to the ESC guidelines.1,14

Definitive treatment, when possible, may involve invasive or surgical methods.1,14 Decompensating factors should be investigated and treated; they include, among others, infection, lack of adherence to therapy, uncontrolled hypertension and supraventricular arrhythmias with rapid ventricular rate.1

Goals of the Treatment of Acute HF

Apart from the immediate goals of improving symptoms, reducing signs of HF and stabilising the haemodynamic condition, others, like the normalisation of renal and hepatic function, as well as the decrease of neurohormonal markers such as BNP, are important.1 Of relevance are also longer-term outcomes, probably dependent on the limitation of myocardial damage. These include the reduction of the duration of hospital stay and re-admissions and of mortality.1 Tolerability of the therapeutic intervention is also relevant.

Organisation of Care

The specific local conditions of each hospital will dictate the organisation of care.

In view of the poor prognosis associated with this syndrome, careful planning of differential treatment of these patients is warranted. To quote the guidelines of the ESC, ‘Best results are achieved if patients with acute heart failure are treated promptly by expert staff in areas reserved for heart failure patients. ... An experienced cardiologist and/or other suitably trained staff should treat AHF patients’ (class I recommendation of the ESC guidelines).1 The Society’s guidelines on intensive cardiac care units - commonly known as coronary care units - state that ‘the intensive cardiac care unit (ICCU) is becoming the treatment centre for patients suffering from severe cardiac arrhythmias and decompensated heart failure ... For these reasons the requirements of the ICCU will increase, not decrease’.17 Among the patients to be admitted to such units are ‘(ii) patients [with] heart failure that requires intravenous therapy or haemodynamic monitoring or support of an intraaortic balloon, (iii) patients in cardiogenic shock, (vii) patients with acute pulmonary oedema unresolved by initial therapy and depending on the underlying conditions and (ix) patients after a heart transplant with acute problem’.17 With regard to selection of patients to be admitted to intermediate cardiac care units, the following is included: ‘patients with uncontrollable cardiac insufficiency not responsive to regular oral therapy, especially those with co-morbidities’.17

The role of cardiologists in the treatment of acute HF in Europe will become increasingly important. The traditional concept of coronary care units and intermediate cardiac care units as places to treat acute coronary syndromes is being replaced by that of ICCUs, which are being asked to take on new responsibilities that include the management and treatment of patients with acute HF.

References
  1. Nieminen M S, Bohm M, Cowie M R et al., on behalf of the Task Force on Acute Heart Failure of the European Society of Cardiology, Executive summary of the guidelines on the diagnosis and treatment of acute heart failure, Eur Heart J (2005);26: pp. 384-416.
    Crossref | PubMed
  2. Cleland J G, Swedberg K, Follath F et al., The EuroHeart Failure Survey programme - a survey on the quality of care among patients with heart failure in Europe. Part 1: patient characteristics and diagnosis, Eur Heart J (2003);24: pp. 442-463.
    Crossref | PubMed
  3. Berry C, Murdoch D R, McMurray J J V, Economics of chronic heart failure, Eur J Heart Fail (2001);3: pp. 283-291.
    Crossref | PubMed
  4. Silva Cardoso J, Fonseca C, Rebocho M J et al., Heart transplant in Portugal, current status and future perspectives, Rev Port Cardiol (2002);21: pp. 1,077-1,097.
    PubMed
  5. Teixeira J S, Fioeza A C, Silva Cardoso J, National Donation Network: what reality for heart transplantation?, Rev Port Cardiol (2003);22: pp. 923-933.
    Crossref | PubMed
  6. Adams K F Jr, Zannad F, Clinical definition and epidemiology of advanced heart failure, Am Heart J (1998);135: pp. S204-S215.
    Crossref | PubMed
  7. O'Connel J B, The economic burden of heart failure, Clin Cardiol (2000);23: pp. 6-10.
    Crossref | PubMed
  8. Morais-Sarmento P, Fonseca C, Marques F, Ceia F, Aleixo A, Acutely decompensated heart failure: characteristics of hospitalized patients and opportunities to improve their care, Rev Port Cardiol (2006);25: pp. 13-27.
    PubMed
  9. Krumholz H M, Em P, Tu N et al., The treatment target in acute decompensated heart failure, Rev Cardiovasc Med (2001);2 (Suppl); pp. S7-S12.
  10. Cleland J G K, Gemmel I, Khand A, Boddy A, Is the prognosis of heart failure improving?, Eur J Heart Fail (1999);1: pp. 229-241.
    Crossref | PubMed
  11. Mebazaa A, on behalf of the Steering Committee and SURVIVE study investigators. Survival of patients with acute heart failure in need of intravenous inotropic support, American Heart Association Scientific Sessions, Dallas, Texas, 13-16 Nov 2005.
  12. Fonarow G C, Adams K F, Abraham W T, Yancy C W, Bosacrdin W J, for the ADHERE Scientific Advisory Committee, Study Group, and Investigators. Risk stratification for in-hospital mortality in acutely decompensated heart failure. Classification and regression tree analysis, JAMA (2005);293: pp. 572-580.
    Crossref | PubMed
  13. Follath F, personal communication (2005).
  14. Bristow R B, Lowes B D, Management of heart failure, in Braunwald's Heart Disease. A Textbook of Cardiovascular Medicine, 7th edition, WB Saunders Company, (2005); pp. 603-624.
  15. Follath F, Franco F, Silva-Cardoso J, The European experience on the practical use of levosimendan in patients with acute heart failure syndromes, Am J Cardiol (2005);96: pp. 80-85.
    Crossref | PubMed
  16. The ESCAPE investigators and ESCAPE study coordinator, Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness, JAMA (2005);294: pp. 1,625-1,632.
    Crossref | PubMed
  17. Hasin Y, Danchin N, Filippatos G S et al., on behalf of the working group on acute cardiac care of the European Society of Cardiology, Recommendations on the structure, organization, and operation of intensive cardiac care units, Eur Heart J (2005);26: pp. 1,676-1,682.
    Crossref | PubMed