The pathophysiology of advanced heart failure is similar to that of heart failure in general, with the predominant symptoms caused by pulmonary congestion. Increased left ventricular filling pressure leads to pulmonary congestion.
For a detailed discussion of systolic versus diastolic failure, see the pathophysiology of acute heart failure section. In systolic heart failure, the contractility of the myocardium is reduced, decreasing effective stroke volume. Cardiac output is reduced, as it is directly dependent on both stroke volume and heart rate. Subsequently, this results in two mechanisms of direct failure:
The relative increase in pulmonary venous pressure drives fluid from the vasculature into the interstitium. This pushes tissue fluid into the alveoli themselves, reducing gas exchange and causing the classical symptoms of dyspnoea, paroxysmal nocturnal dyspnoea and orthopnoea, and in some cases chronic pleural effusion (Komamura, 2013). Mitral regurgitation is often present and due to its dynamic nature, may increase when volume overload is elevated. The pulmonary congestion often causes an increase in pulmonary vascular resistance and secondary right ventricular pressure, and may increase tricuspid regurgitation, which together with neurohumoral activation increases fluid retention, peripheral swelling and elevated jugular venous pressure. Chronic heart failure with a different mechanism usually induces myocardial fibrosis and diastolic dysfunction, often being a complication in systolic heart failure.
In diastolic heart failure, the myocardium is able to contract effectively, but relaxation is impaired – this may happen for several reasons, including increased ventricle stiffness or fibrosis. As with systolic failure, the compromised filling of the ventricles creates a back-pressure into the venous circulation, especially when the heart rate increases, with the same result of pulmonary congestion (Figure 1). In right-sided disease or chronic left heart failure with elevated pulmonary resistance and right ventricular dilation, the venous back-pressure will extend into the peripheral vasculature, and cause peripheral oedema and ascites (Drazner et al., 2012; Rosenberg & Manning, 2012; Komamura, 2013).
These conditions result in an activation of the sympathetic nervous system; neurohormonal compensatory mechanisms cause an increase in heart rate and systemic vascular resistance in an attempt to improve cardiac output (this is also covered in more detail in the pathophysiology of acute heart failure section). In the long-term these compensatory mechanisms begin to create a positive feedback loop – they exist to prioritise end-organ perfusion; however, they inevitably end up placing an increasing workload on a failing heart (Mentz & O’Connor, 2016).
In the short-term, boosting heart rate can increase cardiac output, and grant an increase in exercise tolerance. As mentioned previously, cardiac output is dependent on both stroke volume and heart rate, and in heart failure there is often an exclusive focus on the former, with a very clear body of evidence to support the value of changing stroke volumes. There is some evidence to suggest that, particularly in more advanced disease and the elderly population, chronotropic incompetence – the lack of increase in heart rate in response to stimulation – can contribute significantly to the symptoms of heart failure. Patients with heart failure often rely on an increase in heart rate to boost their cardiac output sufficiently to support increased demand, even during light exercise. It is as these mechanisms become dysfunctional that the burden of disease becomes more pronounced (Brubaker & Kitzman, 2013).
Renal dysfunction is a frequent comorbidity in heart failure and is linked to worse prognosis and quality of life, but there is limited understanding of the pathophysiology of renal dysfunction in advanced heart failure. Theoretical causes include the increased venous pressures and congestion seen in heart failure reducing renal perfusion, as well as the neurohormonal activation and increased oxidative stress that are part of the disease process of heart failure (Marti et al., 2013; Mentz & O’Connor, 2016).
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