Chronic heart failure

See also pp. 143–51. There has been a marked change in the epidemiology of cardiac presentations to EDs over the last 20 years. The epidemic of premature deaths and morbidity associated with coronary artery disease and consequent acute myocardial infarction (AMI) in middle-aged men appears to have ended. In place of middle-aged men with AMIs, EDs are seeing older patients presenting with chronic heart failure (CHF). Fortunately, our ability to manage patients with heart failure has improved considerably and it is likely that this will be further enhanced with major pharmacologic advances in the next few years. The article by Prendergast and Bunney1 is timely in reminding emergency physicians of some of the conceptual advances in heart failure diagnosis and treatment over the last few years. The diagnosis of heart failure is still ultimately dependent on a consensus by clinical experts. There is no ‘gold standard’ test that will give a dichotomous ‘yes/no’ answer. The clinical presentation, exclusion of other causes for symptoms, together with X-rays, ECG and echocardiography, usually result in a high probability of the correct diagnosis. This is especially the case if patients are observed over a prolonged time frame and response to treatment is measured. Diagnosis can be more difficult when there are multiple comorbidities such as pneumonia, chronic obstructive airways disease (COAD) and pulmonary embolus as well as heart failure. To assist with this diagnostic problem, a brain natriuretic peptide (BNP) assay has been promoted and is used extensively in the USA and, to a lesser extent, Europe. The test can be performed either as a laboratory or bedside test. It has not been used widely in Australasia to date, partly because of cost and partly because of scepticism regarding its usefulness. There has been much discussion regarding the potential patient groups that may benefit from a more accurate diagnostic test. Packer et al.2 argued that BNP is most accurate when used in patients with severe cardiac failure, without comorbidities such as renal impairment and advanced age. This group is usually easy to diagnose clinically. Unfortunately, BNP levels are not necessarily of great diagnostic assistance in complex patients with multiple comorbidities. Despite this, two large studies have suggested that this test is reasonably accurate in diagnosing heart failure and may significantly alter our management approach to patients presenting with shortness of breath (SOB). The multicentre BNP study3 found an increase in diagnostic accuracy from 74% to 81%. A study by Meuller et al. in Basel4 found a significant decrease in length of stay (LOS) and admissions to hospital and ICU by using the BNP test in emergency presentations. In the Australasian context, it is hard to imagine how improved diagnostic accuracy would significantly change the decision to admit to hospital and ICU in the first few hours. Decisions regarding LOS and admission are rather determined primarily by severity of initial symptoms as well as associated comorbidities and social issues. Whether improved diagnosis with BNP will improve outcomes is not certain. Many emergency physicians treat both COAD and heart failure in the first instance until the diagnosis becomes clear. Treatment of COAD with nitrates or diuretics for incorrectly diagnosed heart failure could possibly increase LOS (by dehydrating the patient or causing hypotension), it is less likely that incorrect use of nebulized bronchodilators and steroids would cause significant harm to patients with heart failure. There is only one way to determine the impact of using this test – undertake a prospective randomized controlled study of BNP in the Australasian setting. In the ED setting, where patients present with acute decompensated heart failure and shortness of breath, there has been very little advancement in treatment apart from the introduction of continuous positive airways pressure (CPAP) ventilation. Patients are treated acutely in much the same way, whether the underlying diagnosis is diastolic or systolic heart failure. Improved understanding of the physiology of acute heart failure in recent years has led to a reduction in the reliance on diuretics.5 Acute decompensation is largely attributed to a redistribution of fluid causing raised pressure in the pulmonary vasculature, pulmonary oedema and sympathetic overdrive rather than an absolute increase in body water. Some patients may even have extracellular fluid depletion. The acute management should therefore focus on supporting ventilation, redistributing fluid and reducing sympathetic overdrive. A rapid diuresis may actually worsen sympathetic overdrive through renin-angiotensin system activation. In Australasian EDs this has translated into a practical approach of sitting the patient upright, applying oxygen, giving nitrates and CPAP. Small amounts of morphine may be used as an anxiolytic and judicious use of frusemide may be appropriate in patients with fluid overload. The use of angiotensin converting enzyme (ACE) inhibitors acutely is not widely practised, although there is some evidence for their use. Overall, the evidence base for our practice is poor, apart from CPAP. The classification of heart failure into diastolic and systolic dysfunction has helped in the understanding of aetiology and may potentially be useful in directing long-term treatment of the CHF patient. Systolic heart failure has well-established treatment regimens including the use of ACE inhibitors, beta blockers and diuretics.6 This may be augmented by aldosterone receptor antagonists and/or angiotensin receptor blockade as appropriate. In contrast, treatment of diastolic heart failure is largely empirical, focusing on treatment of underlying causes such as hypertension, ischaemia and diabetes. This may be supplemented by judicious use of diuretics to relieve volume overload and consideration of rate-limiting drugs such as non-dihydropyridine calcium antagonists and beta-blockers to prolong diastolic filling time.7 A recent study of angiotensin receptor blockade versus placebo revealed largely neutral findings (CHARM).8 The fact that non-dihydropyridine calcium channel blockers are absolutely contraindicated in systolic heart failure and potentially beneficial in diastolic heart failure is sufficient reason alone to differentiate diastolic from systolic heart failure. Currently, echocardiography is the only way to provide this information, and therefore may increasingly emerge as a useful tool in the ED. There are a number of new drugs that may be useful in the treatment of decompensated heart failure. Levosimendan (a calcium sensitizing drug) and nesiritide (BNP) have been trialled but the way in which these drugs fit into the established management strategies in the ED currently remains uncertain. Endothelin blockade for treating decompensated heart failure presenting to EDs did not prove successful (VERITAS) and this trial has ceased.9 Vasopressin receptor antagonists are another potential pharmacologic approach but still in the development phase.10 Given the increased incidence of CHF, ageing of the population and likely coexistence of multiple comorbidities, the challenge for emergency physicians in diagnosing acute SOB will only increase. The need for more precise diagnosis is also likely to increase because of more targeted therapies. Decompensated heart failure is clearly going to be a major diagnostic and management challenge in the ED in the years to come. None declared.