Since its introduction into the intensive care environment in the early 1980s, echocardiography has been recognised as an invaluable tool. Transthoracic echocardiography (TTE) provides a non-invasive, portable imaging modality, which allows for rapid diagnosis and cardiovascular monitoring in the critically ill. Transoesophageal echocardiography (TOE) produces better resolution images and is often utilised as an adjunct, or when TTE image quality is inadequate.
Focused echocardiography provides a goal directed ultrasound examination to address specific diagnostic and monitoring questions.
In the critically ill patient echocardiography has been shown to provide supplemental information to physical examination and other monitoring modalities. It may be performed for diagnostic reasons, as a haemodynamic monitor, to assess volaemic status, or for procedural guidance.
A focused TTE evaluation comprises four views of the heart: parasternal long-axis and short-axis, apical four-chamber and subcostal views (Figure 3.1). Each view provides basic information on biventricular function, volaemic status, valvular function, and the presence of pleural or pericardial collections. When integrated with clinical examination and other haemodynamic parameters, point-of-care echocardiography provides a bedside tool for diagnosis and monitoring of cardiovascular pathophysiology. Multiple focused cardiac scanning protocols are now in use across the globe (e.g. FICE, FEEL, FATE) and extended algorithms have been developed to allow basic assessment of valvular pathology and quantification of ventricular function. Focused scanning requires not only the development of skills to obtain adequate ultrasound images, but also the knowledge to interpret the findings and the experience to request a comprehensive study when indicated. Consequently, training and accreditation programmes are now established to ensure competency and focused echo is a skill to be possessed by all critical care physicians.
Figure 3.1 Basic focused transthoracic echocardiography views. PLAX, parasternal long-axis; PSAX, parasternal short-axis; A4C, apical four-chamber; SC, subcostal.
Left ventricular (LV) systolic function (LVSF) is frequently altered in the critically ill, either as a cause of decompensation, or as a consequence of critical illness: the incidence of LVSF in septic shock, for example, may be as high as 60%.
Advances in perioperative management and myocardial protection have seen a reduction in the incidence of postcardiotomy cardiogenic shock, but it may still occur in up to 6% of cardiac surgical procedures, and is associated with high mortality. Early postoperative detection or exclusion of LV dysfunction is paramount to initiate prompt and appropriate therapy.
Although some studies have reported good correlation between qualitative and quantitative assessment, objective quantification of LVSF is recommended and allows for interobserver comparisons.
Fractional shortening (FS), derived from M-mode linear measurements, is a quick and reproducible measure of LVSF. However, it is only representative of a single dimension, and in the presence of regional wall motion abnormalities (RWMA) may give an inaccurate measure of global LVSF.
Ejection fraction (EF) is calculated from estimates of LV end-diastolic volume (LVEDV) and end-systolic volume (LVESV). EF derived from the FS, using the Teichholz method, is limited by its assumptions of the geometric LV shape, and is no longer recommended. The modified Simpson rule involves tracing the LV cavity in the four-chamber and two-chamber views at end-diastole and end-systole to estimate LVEDV and LVESV (Figure 3.2). Three-dimensional echocardiography has also been shown to produce accurate and reproducible measures of LV volumes. EF is calculated as:
EF = (LVEDV – LVESV) / LVEDV.
Figure 3.2 TOE midoesophageal four-chamber (a) and two-chamber (b) views, showing biplane method (modified Simpson’s rule) to derive left ventricular ejection fraction.
The presence of RWMA before and after cardiac surgery is not uncommon, but the detection of new defects warrants further investigation. After coronary artery bypass grafting (CABG) surgery, a new RWMA suggests myocardial ischaemia or possibly infarction from multiple causes including a compromised coronary artery bypass graft occlusion, coronary vasospasm, inadvertent left circumflex artery ligation during mitral valve (MV) surgery (presenting with LV lateral wall akinesia), coronary ostial compromise after aortic root surgery and others. The 17-segment LV model is typically used and each segment is scored as follows:
1 normokinesia, normal regional wall motion
2 hypokinesia, reduced regional wall motion
3 akinesia, no movement of one or more segments
4 dyskinesia, paradoxical movement of one or more segments in relation to other LV areas.
However, RWMA may occur in the absence of significant coronary artery disease: postoperative epicardial pacing induces abnormal motion of the interventricular septum (IVS) and posterior LV; stress induced (Takotsubo) cardiomyopathy classically presents with apical akinesia and ballooning; the inferior and inferolateral LV walls are most often affected in myocarditis.
The assessment of LV diastolic function should form an integral part of a routine examination, especially in patients presenting with heart failure. In fact, up to 50% of patients with CHF have isolated LV diastolic dysfunction (DD) in the presence of a normal LVEF. In addition, LVDD may play an important role in a subset of patients difficult to wean from mechanical ventilation.
Patients with dynamic LV outflow tract (LVOT) obstruction exhibit hypotension, a low cardiac index and high LV filling pressures, but deteriorate with inotropic administration. Typically seen in hypertrophic obstructive cardiomyopathy (HOCM) and post-MV repair surgery, it may also occur in severe hypovolaemia. Echocardiography is indispensable in making the correct diagnosis, allowing expeditious treatment revision to vasopressor therapy, volume loading and cessation of inotropic support. Echocardiography findings include the presence of a significant gradient in the LVOT, systolic anterior motion (SAM) of the MV and mitral regurgitation (MR).
Acute right ventricular (RV) failure after cardiac surgery carries a poor prognosis. It occurs frequently after heart transplantation and LV assist device (LVAD) implantation. RV dysfunction is a well-recognised complication of acute respiratory distress syndrome (ARDS) and RV-protective ventilation strategies have emerged to impact on RV function.
Due to its geometry, echocardiographic quantification of RV systolic function is challenging. Longitudinal measures of function, such as tricuspid annular plane systolic excursion (TAPSE) and tissue Doppler derived tricuspid lateral annular systolic velocity (Sʹ), provide excellent measures of RV function. They are easily obtainable by TTE, but with TOE, values can be underestimated due to linear malalignment. Their use in the perioperative setting is less robust: opening of the pericardium is accompanied by a significant decline in TAPSE and Sʹ without an associated decrease in global RV function. This makes preoperative and early postoperative comparisons unreliable. RV fractional area change (FAC) provides an accurate measure of global RV function (Figure 3.3), correlates with RVEF derived from magnetic resonance imaging and is an independent predictor of mortality. Global longitudinal strain and three-dimensional imaging offer alternative measures of RV performance.
Figure 3.3 TOE midoesophageal four-chamber right ventricular views in end-diastole (a) and end-systole (b), used to calculate right ventricular fractional area change.
In the early postoperative period, echocardiography is used to assess adequacy of valve repair, competence of valve replacement, detection of significant paravalvular leaks, recognition of patient-prosthesis mismatch, and iatrogenic valve injury.
Valvulopathies responsible for acute deterioration can be postischaemic, infective and traumatic in origin. Acute myocardial infarction (MI) may be complicated by papillary muscle rupture and severe MR. Infective endocarditis (IE) is a life threatening condition. TOE is recommended in patients with high clinical suspicion of IE. It is essential to determine the size and precise location of vegetations, extent of leaflet destruction and valvular dysfunction, the presence of abscess cavities or fistulae, and dehiscence of prosthetic valves (Figure 3.4). Echocardiography findings are crucial in predicting embolic risk and establishing the timing of surgical intervention.
Figure 3.4 TOE midoesophageal long axis view, showing vegetations (arrows) on the aortic valve (AV). LA, left atrium; LV, left ventricle.
Cardiac tamponade is a clinical diagnosis comprising haemodynamic instability associated with equalisation of diastolic filling pressures and large respiratory fluctuation in arterial pressure (pulsus paradoxus). After cardiac surgery, however, classic signs of cardiac tamponade are often mild and atypical presentations are not uncommon. Localised pericardial collections and thrombus formation may cause isolated left-sided compression, with normal right-sided pressures. A high index of suspicion is required postcardiac surgery and TTE or TOE often provides rapid confirmation of diagnosis (Figure 3.5). Loculated and posterior collections may necessitate TOE. In patients with significant pulmonary hypertension, RV diastolic collapse may be absent. In haemodynamically stable patients, echocardiography may be utilised to monitor the progression of a pericardial effusion.
Figure 3.5 TTE subcostal view, showing a large pericardial effusion (arrows). LV, left ventricle; RV, right ventricle.
Constrictive pericarditis (CP) results in impaired diastolic filling due to a rigid, non-compliant pericardium. Patients present with chest pain, dyspnoea and peripheral oedema. Although usually idiopathic in origin, it can occur post-MI and postcardiac surgery. It is important to differentiate it from restrictive cardiomyopathy (RCM).
Echocardiographic features to distinguish CP from RCM include a hyperechogenic pericardium, dynamic changes in LV diastolic filling velocity with respiration and preservation of myocardial relaxation velocities.