1. Chest X-ray
Chest X-ray (CXR) is one of the most commonly available imaging tests used in the emergency department, especially in patients with dyspnoea, which frequently detect pulmonary disorders. Still, it may also demonstrate cardiac abnormalities
[1][2]. Sometimes it can be useful as the first-step imaging test to distinguish acute heart failure (AHF) from acute lung disease
[3]. Despite its absence in the main diagnostic pathway of chronic heart failure (CHF), CXR remains a recommended additional test
[4]. In addition to its diagnostic role, CXR may also have a prognostic value. Heart failure (HF) signs in CXR are associated with worse clinical outcomes for patients suffering from HF
[5]. Llorens et al. showed that alveolar oedema found in CXR resulted in an 89% (95%CI 30–177%) higher in-hospital death rate and a 38% higher 1-year mortality
[6].
Historically left and right heart failure was distinguished, with the first being more prevalent. The impact of left heart failure (HFpEF and HFrEF) on the lungs often leads to lung congestion, while right heart failure leads to systemic congestion expressed as distension of the jugular veins, peripheral oedema and organ dysfunction; thus, pulmonary symptoms are more obscure. However, right and left heart failure may coexist; in such cases, right HF is an important indicator of poor prognosis
[7][8]. Moreover, right heart failure may also be a consequence of lung disease (e.g., COPD, interstitial lung disease (ILD), pulmonary embolism or pericardial diseases), which may impact imaging of the lungs.
The values of CXR are accessibility, low cost and low radiation risk (an estimated effective dose for CXR in posteroanterior view is 0.05 mSv and 0.10 mSv for posteroanterior and lateral projection)
[9]. Therefore, CXR was applied as the first-step tool in the diagnosis of HF for many years, mostly in the acute setting. However, CXR is not deprived of limitations. Firstly, its diagnostic value in diagnosing HF is relatively low. A systematic review emphasised its moderate to high specificity (76–83%) but lower sensitivity (67–68%) in HF diagnosis
[10]. The relatively low sensitivity of CXR in diagnosing HF results from the fact that radiographic signs of pulmonary oedema and vascular redistribution may be missed in radiogram as they depend on the patient’s position (recumbent vs. erect) and limited visualisation of retrocardiac opacities in PA radiogram. Additionally, the increased lymphatic flow may transiently balance the increase of hydrostatic pressure, thus preventing progress to pulmonary oedema visible in CXR
[11][12][13]. Secondly, gravity has an impact on the results of CXR. Changing the position of the patient from orthostatic to supine may disturb the fluid flow resulting in a misleading impression of the patient’s condition
[14]. Thus, the position of the patient should be taken into account in the comparison of the lobar vasculature. To sum up, CXR currently seems to be an insufficient imaging technique, and when HF is suspected, the need for further studies, including echocardiography (ECHO) or lung ultrasonography (LUS), is indisputable.
2. Pulmonary Features of HF in CXR
There are some elements in the pulmonary picture that are strongly connected with HF. The most spectacular is pulmonary oedema, a hallmark feature of AHF. Studies show that it is present in 28.7% of patients admitted to the hospital for AHF
[15]. In addition, more than half of patients presenting with CHF will require hospitalisation for pulmonary oedema at least once in a lifetime
[16].
From the pathophysiological point of view, the pathway to developing pulmonary oedema consists of three stages depending on increasing pulmonary capillary wedge pressure (
Figure 1). It begins when the disruption of cardiac function increases hydrostatic pressure and redistribution in the lung vasculature (Phase 1). The overflow of lung vasculature results in fluid accumulation in the interstitium and the interlobular septa forming the first stage—interstitial oedema (Phase 2). When this space is overloaded, and lymphatics become congested, the excess fluid begins to accumulate in the alveoli, thus progressing to the subsequent stage—alveolar oedema (Phase 3)
[11].
Figure 1. Consecutive phases of HF according to the pulmonary capillary wedge pressure (PCWP). Various pulmonary findings in CXR have been mentioned. CTR—Cardiac thoracic ratio; CXR—Chest X-ray.
2.1. Phase 1—Redistribution in the Lung Vasculature
At first, cardiac failure leads to fluid redistribution and increased hydrostatic pressure in the large veins and the lung vessels. The process has its consequences in CXR images. To begin with, the first noticeable sign is the enlarged vascular pedicle width. It is assessed by measuring the distance between the two virtual vertical parallel lines on the CXR. The first line runs through the point at which the superior vena cava crosses the right main bronchus, while the second line passes through the beginning of the left subclavian artery
[17] (
Figure 2). The normal range of the perpendicular width should be less than about 48 ± 5 mm in the erect position with about a 20% increase in the supine
[18]. The meta-analysis of 8 studies on 363 participants suggested that vascular pedicle width correlates with volume overload, which may help in the management of patients with HF
[19].
Figure 2. Vascular pedicle width. (Created with BioRender.com).
The next feature of fluid redistribution as a consequence of HF visible in CXR are prominent pulmonary hila and enlarged veins of the upper lobes, known as cephalisation
[20]. Under normal conditions, veins of the upper lobes have a smaller diameter than veins in the lower lobes due to gravity, but in HF, upper lobe vessels increase in size. According to the study by Mueller-Lenke et al., cephalisation had a sensitivity of 19.6% and specificity of 92.6% in recognising HF, respectively
[21]. It is a subtle sign, present when the image is taken in an upright position and lost when the patient is in the supine position
[22].
2.2. Phase 2—Interstitial Oedema
The subsequent consequence of HF is interstitial oedema, which in CXR is reflected by: (1) distortion in the hilar image, (2) peribronchovascular cuffing (colloquially—“donut sign”), (3) thickening of interlobar or interlobular fissures
[14]. The last feature is also known as the Kerley lines. The three types of Kerley lines are distinguished: A, B and C
[23]. Kerley A lines represent the thickening of connections between the central and peripheral lymphatic systems. They are the longest Kerley lines spanning about 2 to 6 cm from the hilum to the upper lobes
[24]. The second type—the B lines, are the most common finding in HF. They are short, 1 to 2 cm long, perpendicular to the pleura, emerging from the surface of the inferolateral areas of the lung
[22]. Should the interstitial oedema incidents repeat, the interlobular fissures may undergo fibrosis, thus creating the so-called chronic Kerley B lines
[25]. From the above-mentioned signs representing interstitial oedema, Kerley B lines are the most prominent in both values—sensitivity (23.4%) and specificity (95.8%)
[21]. The third type—Kerley C lines, are the least frequent. These lines differ from the other Kerley lines in that they neither spread from the hilum nor reach the pleura and are the smallest in length.
2.3. Phase 3—Alveolar Oedema
If excess fluid accumulates within the alveolar space, pulmonary oedema may manifest as alveolar oedema. Typically, its appearance on CXR is in the form of mostly bilateral higher density opacities in central and basal lung areas
[20], what is referred to as the angel wing, bat wing or butterfly pattern
[25]. The bat wing sign develops only in about 10% of pulmonary oedema cases. Furthermore, the sign may be asymmetrical, e.g., when the radiograph was taken while the patient was in a lateral position. It occurs mainly in the course of AHF, progressing so rapidly that it overloads the compensation mechanisms and covers the presence of interstitial oedema
[26]. The rate of filtering of the excess fluid through the capillary wall in AHF may cause significant functional changes before morphological abnormalities appear on CXR. This explains why clinical symptoms tend to develop before radiological findings can be seen. The same applies to the resolution of the radiological findings—they resolve at a slower rate than clinical symptoms
[26]. This may also explain the limited sensitivity of chest X-rays in patients with acute decompensated HF admitted to the ED
[27].
2.4. Phase 3—Pleural and/or Pericardial Effusion
Lastly, HF may manifest as pleural or pericardial effusion. In the retrospective analysis by Korczyński et al., CHF was the most common aetiology in patients with pleural effusion, accounting for 37.4% of all cases
[28]. Interestingly, compared to patients with malignant and parapneumonic pleural effusion, HF-related pleural effusion was characterised by a lower fluid volume. In another retrospective review, 46% of 3245 patients diagnosed with acute decompensated HF presented signs of pleural effusion. In the analysed group, pleural effusion was bilateral in 58%, right-sided in 27%, and left-sided in 14% of cases, respectively
[29]. In most patients with pleural effusion due to HF, pleural fluid is classified as transudate according to the Light criteria. However, 25% of cases may fall into the exudative category, especially if a patient is treated intensively with diuretics. In such cases, to differentiate whether the fluid is of cardiac origin, it is beneficial to assess the level of pleural NT-proBNP. Porcel et al. suggest that a pleural fluid BNP concentration exceeding 1500 pg/mL supports cardiac aetiology
[30]. In addition, Morales-Rull et al. confirmed the viability of measuring NT-proBNP in serum while adding the parameters such as systolic pulmonary artery pressure and serum prealbumin in predicting PE development
[29].
On the other hand, pericardial effusion, a rare symptom of HF, is associated with an elevated filling pressure of the right heart. It usually coexists with other signs of advanced congestive HF. As the frequency of left-sided overload dominates over the right-sided, pericardial effusion occurs less frequently than pleural fluid accumulation
[31]. In the study conducted by Kataoka et al., from the 60 enrolled patients, 52 (87%) presented with pleural effusion, while only 12 (20%) had pericardial effusion, which was small to moderate in volume. No significant correlation between the pleural and pericardial effusion was found in that study
[31]. Although pericardial effusion is rarely observed in HF it is associated with an unfavourable outcome, even if it is haemodynamically irrelevant
[32][33][34]. In addition, in critically ill patients with relevant pericardial effusion treated in the Intensive Care Unit (ICU), a positive impact of pleural effusion drainage was documented
[35].
3. Cardiac Abnormalities Related to HF in CXR
The most prominent abnormality detectable in CXR in patients with HF is cardiomegaly. It is simply defined as the subjectively enlarged heart. However, in radiological images, it is most often presented in the form of the ratio between the width of the heart and the thoracic cage, called the cardiac thoracic ratio (CTR). If the CTR is higher than 0.5—cardiomegaly might be suspected. However, it is worth mentioning that the dimensions of the heart and vessels are influenced by how the CXR is performed. Routinely CXR is taken in the PA (posterior-anterior) projection, which means that the course of the X-ray comes from the back of the patient. However, when CXR is taken in the AP (anterior-posterior) projection, the silhouette of the heart and vessels is enlarged. Thus, it is essential to report the projection applied.
In the study by Knudsen et al., cardiomegaly was the most frequent feature of HF in the radiographic, being present in 50% of affected patients
[36]. Similar results were found in research by Fonesca et al., who observed that subjectively enlarged heart silhouette and CTR > 0.5 were present in CXR in 54% and 43% of subjects with HF, respectively
[37]. The results of another study also confirmed that cardiomegaly was the most sensitive radiographic finding in congestive HF diagnosis
[21]. However, the sensitivity of CXR in diagnosing cardiomegaly is rather limited. In the study by McKee et al., in a series of 244 patients with NSTEMI, which compared the accuracy of diagnosing cardiomegaly by CXR and echocardiography as the gold standard, the sensitivity of CXR to identify cardiomegaly was only 40%, specificity was 91%, positive and negative predictive values reached 56% and 84%, respectively. These findings show that CXR itself is insufficient for the diagnosis of HF and emphasise the need for implementing other diagnostic modalities, such as echocardiography
[38]. In HFpEF, cardiomegaly is rarely present in the CXR. However, the left atrial enlargement was described in the form of splaying of the carina
[39].
In conclusion, there is a considerable number of radiographic features of HF, which can be identified in CXR, and their correct radiological interpretation is of the essence. These features are specific but only moderately sensitive; thus, a chest radiogram as the only test is insufficient to confirm HF diagnosis
[4]. However, it is helpful in the diagnosis of many other diseases (e.g., pneumonia, interstitial lung diseases, pneumothorax). Thus, it is an important first-step imaging test in diagnosing dyspnoeic patients, but other tests are usually necessary
[4]. Recently, LUS has become an increasingly valuable tool for diagnosing patients with dyspnoea, particularly in the ED and ICU setting.