Introduction
Diagnostic imaging of patients in the cardiothoracic intensive care unit (ICU) can pose unique challenges. Where possible, the patient should be imaged in situ using mobile chest X-ray (CXR) and ultrasound, including transthoracic (TTE) and transoesophageal echocardiography (TOE), unless computed tomography (CT) is specifically required. An outline of the advantages and limitations of each imaging modality is followed by presentation of the optimal use and escalation of imaging to diagnose specific cardiorespiratory conditions in the context of this highly specialised setting.
Cardiothoracic Imaging Modalities
Chest X-ray
Chest X-ray (CXR) has a high diagnostic accuracy for the assessment of the position of lines, tubes and drains. When compared with this area and imaging of the lungs and pleural spaces, the accuracy of CXR is less impressive for cardiovascular disease, and hence CXR should never delay other definitive cardiovascular imaging in the ICU patient. In established cardiorespiratory disease, serial CXR has an additional role in the investigation of evolving respiratory compromise or non-response to treatment. Despite ease of use, daily routine bedside CXR is no longer encouraged because this does not appear to improve outcomes in ICU patients compared with a directed approach.
In the majority of ICU patients, the CXR is acquired bedside with the patient in the semi-erect or supine position. This has several effects: (a) This gives an anteroposterior (AP) projection, with apparent enlargement of cardiac and mediastinal structures compared to the posteroanterior (PA) projection obtained in the ambulatory setting; (b) An optimal full-inspiratory view is rarely attainable; (c) Distribution of fluid and air in the pleural space is altered, where a pneumothorax will locate to the anterior pleural space and pleural effusions settle posteriorly on supine CXR, albeit loculations may limit the free movement of pleural collections particularly. This may happen when there is longstanding pleural disease, prior malignancy or previous surgical intervention, and ultrasound or CT will often be preferable; (d) Forward slumping may obscure apical pulmonary disease or pneumothorax; (e) Rotation – as judged by medial clavicles not being equidistant from the midline relative to the spinous processes – may mimic mediastinal disease; and (f) Artefacts such as skin folds, hair braids, asymmetrical soft tissues, monitoring leads and other radio-opaque equipment overlying the field of interest, may degrade the diagnostic quality and should be minimised prior to imaging.
Ultrasound
Bedside thoracic ultrasound is predominantly used for assessment of pleural effusions, and to confirm CXR findings. Ultrasound may give clues to the nature of a pleural effusion, and has an important role in image-guided thoracic interventions. In experienced hands, ultrasound can also assess for pneumothorax, but emphysematous lung has the potential to cause misdiagnosis and ultrasound is of limited practical use. Extensive subcutaneous emphysema and severe obesity may limit adequate visualisation of the pleural spaces. Echocardiography is invaluable in the assessment of cardiac valves and chamber function as well as any pericardial disease, and has been dealt with in a dedicated chapter (see Chapter 3).
Computed Tomography
Thoracic CT is of immense value in the assessment of the ICU patient, particularly when CXR findings are equivocal or if complex disease processes are suspected. CT adds valuable information to CXR findings in up to 70%, changing management in 22%. The cross-sectional nature of CT allows more detailed interrogation of disease processes and can also provide image guidance for interventions. CT has a particular role when cardiac and great vessel disease such as pulmonary embolus (PE) and acute aortic syndrome are suspected, but is also a key diagnostic tool for the diagnosis of postoperative thoracic collections, pleural or pulmonary sepsis, malignancy, complications of mechanical ventilation, concurrent pulmonary pathologies, and in the assessment of life support device related complications. The diagnostic yield of CT must be weighed against the risks of transporting the ICU patient to the imaging department. Potentially nephrotoxic intravenous iodinated contrast medium should be used with caution, and where potential benefit outweighs risk, attention to pre-emptive renal protection and coordination of the timing of contrast administration with haemodialysis are helpful. Radiation constraints are less of an issue in this setting, however repeated CT imaging should be monitored.
Imaging for Cardiac Emergencies
Chest Pain
Chest pain in the ICU requires urgent appraisal. The differential diagnosis is varied, ranging from life threatening emergencies to more benign conditions. A clue to the aetiology can be gained by focused history, physical examination and electrocardiogram, with imaging playing a smaller role.
Acute Coronary Syndrome
A minority of patients, particularly elderly and females with risk factors for atherosclerosis such as hypertension, chronic renal disease or previous cerebrovascular events, may sustain an acute myocardial infarction while being hospitalised for another reason. The first step in its management is expeditious recognition to optimise myocardial salvage and reduce mortality by a prompt attempt of reperfusion therapy. Non-invasive imaging such as ECG-gated cardiac CT is not recommended as it will not only delay consideration for primary percutaneous coronary intervention (PCI) or fibrinolysis but also often will be non-diagnostic, particularly in patients with cardiogenic shock, heart failure or ventricular tachyarrhythmia.
Acute Aortic Syndrome
Aortic dissection, intramural haematoma and penetrating ulcer together comprise acute aortic syndrome (Figure 7.1), which is classically encountered in patients with systemic hypertension or those with predisposing factors such as connective tissue disease. However, it can also occur in healthy vessels as a consequence of iatrogenic injury following intra-arterial catheterisation and intra-aortic balloon pump insertion. Potentially devastating consequences of aortic dissection include extension into the aortic annulus leading to severe aortic regurgitation, rupture into the pericardium causing cardiac tamponade or multiorgan ischaemia (coronary, cerebral, spinal, and visceral).
Figure 7.1 Acute aortic syndrome. Top panel, far left and middle images: ECG-gated CT in a 65 year old male with acute type A aortic dissection. The aortic root is dilated (black star) with a dissection flap (block black arrow) that extends into neck vessels (thin white arrow) and the ostium of the left main stem coronary artery (middle image, block white arrow). Top panel, far right image: rupture of descending thoracic aneurysm with high attenuation blood (white star) around the aorta. Bottom panel: different CT findings of acute aortic syndrome in different patients. Intramural haematoma with a rim of high attenuation material on the unenhanced CT (far left image); aneurysmal descending aorta with a dissection flap (middle image, thin black arrow); small penetrating ulcer in the descending thoracic aorta (far right image, notched arrow).
CXR has limited value in diagnosing acute aortic syndrome, with a sensitivity of 64% and a specificity of 86%. Typical features are useful when present, such as upper mediastinal widening, double aortic contrast and discrepancy between the diameters of the ascending and descending aorta, displacement of the trachea and of the left main bronchus, ill definition of the aortopulmonary window, left apical cap, pleural effusion, haemothorax and widening of the left paravertebral sulcus, but their absence cannot exclude the diagnosis. The CXR may be completely normal in 11–15%. Echocardiography has immense value in unstable patients as it is portable, quick and can even be used in theatres to facilitate diagnosis. The aortic root, valve and proximal ascending aorta can all be assessed with relative ease using echocardiography, which also has the ability to document ancillary findings such as impairment of ventricular function and haemopericardium. A major limitation of the transthoracic approach, TTE, is the inability to clearly visualise beyond the proximal ascending aorta. The transoesophageal approach, TOE, has a much higher sensitivity of up to 98% for detecting entry tear sites, coronary and great vessel involvement and differential flow characteristics in the false lumen. TOE, however, requires sedation and also cannot image the entire thoracic aorta.
Multidetector CT has sensitivity and specificity of almost 100%. The high negative predictive value in combination with rapid image acquisition and wide availability has made CT the investigation of choice in an acute setting. Triple rule out is a new concept that can be used in the same study to evaluate the aorta, coronary arteries and pulmonary vasculature. It requires ECG-gating and should ideally be performed using a scanner with 64 slice or higher detector number. The need for simultaneous opacification of pulmonary and systemic circulation can be particularly challenging in haemodynamically unstable patients and in some circumstances it is better to do one focused examination rather than an all-in-one approach. Initial unenhanced data are useful to demonstrate crescentic foci of high attenuation in the aortic wall due to intramural haematoma or a thrombosed false lumen. On a contrast-enhanced examination, the classical feature of dissection is an intimal flap that separates the true lumen that is contiguous with the undissected vessel from the false lumen. The false lumen generally has a larger cross-sectional area, thin linear strands of low attenuation material representing the incompletely sheared media (cobweb sign) and a wedge of haematoma (beak sign) that forms to create a space for the development of the false lumen. Occasionally, circumferential dissection can be complicated by intimo-intimal intussusception (windsock sign). Secondary features of aortic dissection include displacement of intimal calcification, delayed enhancement or thrombosis of the false lumen and complications such as mediastinal and pericardial haematoma and compromise from coronary, neck vessel, mesenteric, renal and peripheral vascular involvement. Penetrating ulcers are shown as focal crater-like pouching of the aortic wall with irregular edges in the presence of extensive aortic atheroma, which is most common in the middle and distal thirds of the thoracic aorta.
CT is the imaging modality of choice for suspected rupture. A peripheral hyperattenuation crescent within the thrombus of an aneurysm on an unenhanced CT is a sign of acute or impending rupture, as is the close apposition of the posterior aortic wall to the spine (draped aorta sign). Rupture into mediastinal, pericardial or pleural spaces gives rise to high attenuation haematoma in the respective anatomical space. Fistulous communication with the tracheobronchial tree or oesophagus is a recognised complication. CT may not show the communication, but development of haemoptysis/haematemesis and new onset of pulmonary haemorrhage/consolidation should raise the clinical suspicion.
Pulmonary Oedema
Pulmonary oedema may be hydrostatic as seen in cardiac disease, renal failure or overhydration. Alternatively, it may be non-cardiogenic due to increased permeability oedema as encountered in acute respiratory distress syndrome (ARDS) (Figure 7.2). Differentiating cardiogenic and non-cardiogenic pulmonary oedema is arduous, and most optimally would require measurement of pulmonary capillary wedge pressure. Image findings in hydrostatic pulmonary oedema depend on the degree of elevation of the pulmonary capillary wedge pressure: (a) no abnormality (<12 mmHg); (b) early oedema (12–15 mmHg) with vascular engorgement and peribronchovascular cuffing; (c) interstitial oedema (15–25 mmHg) with progressive blurring of the pulmonary vessels with engorgement of peribronchovascular spaces, Kerley lines and subpleural effusions; and (d) alveolar oedema (> 25 mmHg) with nodular or acinar areas of increased opacity that evolve into frank consolidation. CXR can detect the majority of these changes and is often adequate, particularly when the morphological findings are complemented by haemodynamic data. CT is reserved for cases where there is a need to distinguish hydrostatic oedema from other causes. The combination of upper lobe predominant ground-glass opacification with a central distribution and central airspace consolidation favours hydrostatic oedema. Conversely, ARDS classically gives rise to a gravitational anteroposterior density gradient within the lung due to dense consolidation in the dependent region and normal or hyperexpanded lung in the non-dependent regions, which merge into a background of diffuse ground-glass opacification. Additionally, ARDS persists for days to weeks, does not respond to diuretic therapy and may progress to a reticular pattern due to secondary fibrosis.
Figure 7.2 Pulmonary oedema and acute respiratory distress syndrome with pneumothorax.
Far left image: CXR with pulmonary oedema in a 60 year old male in the aftermath of acute myocardial infarction. Note the intra-aortic balloon pump (block white arrow) and Swan–Ganz catheter (thin arrow). Middle image: CXR of a 45 year old male with acute respiratory distress syndrome on extracorporeal membrane oxygenation (black block arrow). There is a supine, right-sided pneumothorax (white star) with deepened costophrenic sulcus and contralateral mediastinal shift suggestive of tension pneumothorax. Far right image: axial CT thorax in a different patient with acute respiratory distress syndrome. Note the gravitational, dependent consolidation in the posterior lung segments with diffuse ground-glass opacification and fibrosis. There is a left pneumothorax (white star) and surgical emphysema (black arrow head).
Cardiogenic Shock
Cardiogenic shock is characterised by systemic hypotension and tissue hypoxia secondary to decreased cardiac output. Diagnostic evaluation should be carried out in conjunction with resuscitative efforts. Ultrasonography and TTE are essential bedside imaging modalities, which allow rapid assessment of multiple organ systems including cardiac chambers for biventricular function, proximal aorta for aortic dissection, pleural and pericardial spaces for effusions, and the abdominal cavity for peritoneal fluid and organ appearances. A portable CXR is useful for the exclusion of pneumothorax, whilst targeted imaging such as thoracic CT should be considered in patients in whom the aetiology of the circulatory failure remains unclear despite initial bedside imaging. Coronary angiography should not be delayed in patients with suspected myocardial infarction who might be candidates for revascularisation.
Pericardial Tamponade
Tamponade can occur due to collection of fluid, blood, pus, air or soft tissue within the pericardial space (Figure 7.3). Although challenging, it is foremost a clinical diagnosis and must be considered in all patients with unexplained cardiogenic shock or pulseless electric activity. TTE is the most appropriate initial imaging modality as it facilitates assessment of the haemodynamic impact and may guide diagnostic and therapeutic pericardiocentesis. Progressively enlarging cardiac silhouette resulting in a globular featureless water-bottle appearance is a characteristic feature on serial CXRs. However, tamponade due to pneumopericardium can cause reduction in the size of the cardiac silhouette with sharp outlining of the pericardium by radiolucent air. CT is not routinely indicated for the diagnosis and should be reserved for cases where there is diagnostic uncertainty. The attenuation value of the collection on a precontrast scan can give a clue to its nature, with haemopericardium typically being of higher attenuation than simple fluid. Imaging features such as compression of the cardiac chambers and coronary sinus, straightening of the right heart border, interventricular septal bowing, distension of the systemic veins and reflux of contrast medium into the azygos vein may be seen even on non-ECG gated CT. Although the addition of gating will improve the anatomical and functional delineation, the need for prompt treatment should override any potential delays in image acquisition. Percutaneous drainage should be performed using image guidance, and echocardiography, fluoroscopy or CT have all been shown to be successful, with the relative use of each technique much depending on the institutional and individual preferences.
Figure 7.3 Pericardial tamponade.
Top panel: pneumopericardium (left image, black arrows) and globular cardiac silhouette secondary to pericardial effusion (right image) on CXR. Lower panel: pericardial collections on CT. Haematoma (left image, black star) with compression of the underlying cardiac chambers, and ventricular assist device catheters in situ. Circumferential pericardial thickening and enhancement (right image, block white arrow) secondary to a purulent collection (white star) with an enhancing left pleural collection (thin white arrow).
Right Ventricular Failure
The aetiology varies from worsening of compensated right ventricular failure, frequently seen in chronic left-sided heart or pre-existing lung disease such as emphysema, to acute right ventricular failure in massive pulmonary embolus, right-sided myocardial infarction, ARDS or sepsis (Figure 7.4). Pulmonary artery catheterisation provides reliable and continuous monitoring of haemodynamic parameters whilst echocardiography allows for bedside evaluation of cardiac function although estimates of RV systolic and pulmonary artery pressure can be inaccurate in patients with chronic lung disease and those undergoing IPPV. CXR is of limited value and can demonstrate generic features such as cardiomegaly and proximal pulmonary artery dilatation. It can be useful for tracking of lung parenchymal changes like atelectasis or consolidation and pleural effusions, and for the assessment of lines, tubes and drains. CT can be more useful in detailing this pathology.
