Assessing Acute Decompensated Heart Failure – Strategies and Tools
Mortality is particularly high for patients with cardiogenic shock, with an in-hospital mortality of around 50 %. In general, readmission rates are high, with typical values of around 20–25 % at six months6
and 30 % at 12 months.8
to improve the post-discharge care of such patients, with many now entering chronic disease management programmes.
Characteristics of Patients
Surveys and registries in Europe and North America report a consistent picture of the characteristics of patients admitted with acute heart failure.6
The typical patient is elderly (median age in the
early 70s) and there is a slight predominance of men. Almost 70 % will present with acute decompensation of chronic heart failure and the remainder with acute de novo heart failure, most patients having a history of both coronary artery disease and hypertension. Co-morbidity is very common, atrial fibrillation, type 1 diabetes, renal dysfunction and chronic lung disease being often present. Preserved systolic function is found in perhaps one-third of patients, particularly in elderly women. Acute coronary syndrome is frequently present in de novo cases (up to 40 %), but is less common in decompensation of chronic heart failure. Arrhythmia and infection are also frequently seen, as is non-compliance with medication for those with a history of heart failure. Progressive valvular heart disease such as progressive mitral regurgitation (which may accompany adverse LV remodelling) may also be an important cause of acute decompensation. Critical aortic stenosis may present as de novo acute heart failure, especially in the elderly not under medical follow-up.
Initial Evaluation
There is a clear consensus on what constitutes good practice for evaluating patients with acute heart failure,1,9 base for this consensus is sparse.
although the evidence Possible evidence of low perfusion:
First, a thorough history taking and physical examination to identify cardiac and non-cardiac disorders and behaviours that might cause or accelerate the development or progression of heart failure should be undertaken. The physical examination should include assessment of the patient’s heart rate, blood pressure (taking note that hypotension is usually pathological, whereas normotension does not always ensure adequate organ perfusion), volume status, peripheral perfusion, skin temperature and venous filling pressure. Cardiac auscultation for S3 or S4 and valvular abnormality, and auscultation for lung crackles and pleural effusions should be performed.
Second, the following investigations should be considered: •
• •
Narrow pulse pressure Sleepy/obtunded Low serum sodium
Cool extremities Hypotension with ACE inhibitor Renal dysfunction (one cause)
ACE = angiotensin-converting enzyme; JV = jugular vein; PND = paroxysmal nocturnal dyspnoea; est. PAsys = estimated arterial systolic pressure. Source: modified from Nohria, et al., 2005,3
with permission. •
laboratory investigations: full blood count, urea and electrolytes, serum creatinine, plasma glucose, liver function tests, international normalised ratio and troponin if appropriate – noting that mild elevation is not uncommon in acute heart failure, even in the absence of a clinical history of acute coronary syndrome;
•
electrocardiogram (ECG) to provide information on heart rate, rhythm and conduction abnormalities, and perhaps on likely aetiology, such as ST elevation myocardial infarction;
chest radiograph to assess the degree of pulmonary congestion, cardiomegaly, pleural effusion and lung pathology – bearing in mind the limitations of a supine chest radiograph;
arterial blood gases to assess oxygenation, pCO2 and acid–base balance, particularly in patients with respiratory distress or signs of
low organ perfusion. A rising lactate is usually a very late feature of severe cardiogenic shock. Beware of the unreliability of data from non-invasive pulse oximetry in patients with poor peripheral perfusion;
EUROPEAN CARDIOLOGY •
natriurietc peptides: their measurement may be helpful in excluding heart failure in the emergency setting, although it may take time for the peptide concentrations to rise in very acute cases. The evidence base is much stronger for the value in prognostication, based on both baseline values and on how much the peptide concentration falls prior to discharge. There is little evidence of benefit of serial monitoring in patients during admission (see discussion below); and
2D and Doppler echocardiography, which can provide important information on the underlying cardiac dysfunction. Regional and global LV function as well as right ventricular (RV) systolic function can be assessed, along with LV diastolic function, ventricular dyssynchrony, valvular structure and function (allowing, for example, to exclude critical aortic stenosis in patients presenting with de novo acute heart failure), pericardial abnormality (allowing
129 ACS and HF
Cardiogenic shock
Right HF
Pulmonary oedema
The median length of stay was nine days in Europe, with an in-hospital mortality of 6–10 % rising to 15 % by three months6 months.7
and to 30 % by 12 Much effort has been expended Hypertensive AHF Acutely
decompensated chronic HF
Figure 1: Types of Acute Heart Failure
ACS = acute coronary syndrome; AHF = acute heart failure; HF = heart failure. Source: Dickstein, et al., 2008.1
Figure 2: Simple Clinical Classification of Acute Heart Failure Patients According to Haemodynamics
Congestion at rest NO YES NO AB Dry and warm Wet and warm Low
perfusion at rest
YES LC Dry and cold Wet and cold
Signs/symptoms of congestion
Orthopnea/PND JV distension Hepatomegaly Oedema Rales (rare in chronic heart failure) Elevated est. PAsys Valsalva square wave Abdominojugular reflux
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