The symptoms of acute heart failure are difficult to unpick from those of more chronic disease. Unless there is a specific provoking cause – such as pneumonia or a myocardial infarction, (which will occur with symptoms relative to that insult) – acute heart failure is either a presentation with symptoms that can be attributed to heart failure, or a worsening from baseline of symptoms of chronic heart failure. For this reason, in this section we will be talking more generally about heart failure.
Heart failure as a clinical syndrome has a variable course in individuals, and symptoms may become apparent at different times in different people. There is also a distinction to be made between right- and left-sided symptoms, although in practice the picture is usually mixed. Right-sided symptoms typically relate to venous back-pressure in the systemic circulation, while left-heart failure more commonly causes pulmonary congestion and related symptoms (Mentz & O’Connor, 2016).
The most common presenting symptom is dyspnoea (shortness of breath). This is secondary to pulmonary oedema and venous congestion – it may also be contributed to by a pleural effusion (Figure 5). Key distinctions to establish are the presence of postural changes in symptoms: lying flat will tend to exacerbate symptoms of dyspnoea, so distinguishing how someone sleeps is a useful guide. Do they sleep sitting, propped up by cushions, or are they able to lie flat?
An acute exacerbation of heart failure may well be apparent in chronic heart failure patients. By establishing their current status and how it relates to their baseline, it is possible to gauge the severity of their symptoms. Paroxysmal nocturnal dyspnoea may also be a component of their respiratory symptoms. So-called ‘bendopnoea’ – shortness of breath on bending over double – has also been found to be linked to increased ventricular filling pressures (Mentz & O’Connor, 2016; Marti et al., 2013; Platz et al., 2015).
Anginal chest discomfort is another key symptom, typically described as heavy or dull central chest heaviness brought on by exercise, and relieved by rest. This ischaemic-type symptom may reflect a cardiac hypoperfusion and pulmonary congestion secondary to pump failure rather than classical coronary atherosclerosis. Given that in the majority of patients' heart failure is a result of ischaemic heart disease, this may be an unnecessary distinction clinically as often the coronary anatomy has been investigated (Mentz & O’Connor, 2016).
Fatigue results from lack of supply of oxygenated blood on a chronic level and is another common long-term sign of left heart failure (Marti et al., 2013).
As mentioned earlier, heart failure that can be attributed to the right-side of the heart is more likely to present with findings related to venous back-pressure of the systemic circulation. Weight-gain secondary to fluid retention, swollen peripheries (Figure 6), and abdominal distension due to ascites are all possible symptoms of right-heart failure (Mentz & O’Connor, 2016; Marti et al., 2013; Platz et al., 2015).
Peripheral oedema is often present in chronic advanced heart failure or in exacerbation of chronic heart failure with varying causes, such as infection, noncompliance, therapy resistance and renal complications.
The examination findings in acute heart failure again reflect the systems that are disrupted, much like the symptoms.
Respiratory findings in pulmonary oedema will be heard as crepitations on auscultation. Cardiac asthma may also be audible as a wheeze. Dullness to percussion and reduced breath sounds at the lung bases should raise the possibility of pleural effusion. From a symptomatic perspective, it may make sense to drain this fluid to improve lung expansion and gas exchange in acute disease.
The most discriminating examination findings are an S3 gallop – an additional heart sound in mid diastole – and the presence of a raised jugular venous pressure (Figure 7) (Drazner et al., 2001; Mentz & O’Connor, 2016).
Other clinical signs include the presence of ascites (clinically presenting as abdominal distension with a positive fluid wave test or shifting dullness to percussion), hepatomegaly due to venous congestion, cool extremities as a result of hypoperfusion, a narrow pulse pressure, and pitting oedema in dependent body areas (figure 6) (Mentz & O’Connor, 2016; Marti et al., 2013).
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