Comorbidities - Professor Richard Kirk 2023

Factors that contribute to anaemia include iron and vitamin deficiency, chronic inflammation, blood loss (phlebotomy) and medications (e.g. ACEi and ARBs).

Heart failure predisposes to infectious complications - frequent respiratory and gastrointestinal infections. Many of these are viral and vaccinations against them (influenza, rotavirus), passive RSV with palivizumab injections are appropriate. Similarly vaccination against haemophilus influenza and streptococcus pneumonia should be up to date. It may be hard to differentiate infection from an exacerbation of heart failure, especially if heart failure has been exacerbated by an infection. If both the procalcitonin (PCT) and NT-proBNP are elevated, it is likely that there is an infection with exacerbation of HF and in addition to appropriate antibiotic therapy, HF treatment may need to be escalated. If the NT proBNP has not increased then no change in HF therapy is required.

Heart failure occurs in some metabolic diseases e.g. Propionic acidaemia. In addition to treatment of the primary disorder HF treatment is often necessary, but if definitive treatment is possible e.g. liver transplantation, cardiac transplantation may be avoided.

Pulmonary hypertension may occur due to elevation of left atrial pressure. In the first instance the effect is post capillary pulmonary hypertension but the effect of chronic elevation may lead to permanent damage to the pulmonary vasculature and the development of fixed pulmonary vascular resistance. When suspected early recourse to cardiac catheterization to assess the pulmonary vascular resistance and its ability to reverse should be undertaken. In patients with dilated cardiomyopathy increasing HF therapy may reduce the left atrial pressure, if this is ineffective VAD may be required. In the case of restrictive physiology when the increase in pulmonary artery pressure may be silent listing for cardiac transplant may be considered as once the pulmonary vasculature becomes non- reactive, cardiac transplant is not possible and heart lung transplant becomes the only option with a significantly worse prognosis than cardiac transplant alone.  

Cardiac failure frequently leads to respiratory issues, which further compound the heart failure. A high left atrial pressure leads to pulmonary venous congestion and pulmonary oedema which in turn decreases lung compliance leading to restrictive lung function, impaired pulmonary lymphatic drainage and fluid retention, often with pleural effusions. Cardiomegaly is also a frequent cause of bronchial compression.