Saline Contrast

Echocardiographic contrast agents are substances that enhance the reflected ultrasound signal. Simple agitated saline contrast can be used to detect intracardiac shunts, commonly at the atrial level. To detect an intracardiac shunt, a contrast study can be done with agitated saline. In this technique, a 10-mL syringe containing 8 mL of normal saline is connected to a second 10-mL syringe containing 1 cm³ of air via a three-way stopcock. Brisk exchange of the saline between the syringes creates microbubbles, which are then rapidly injected as an intravenous bolus, resulting in opacification of the right chambers of the heart. Saline contrast bubbles are too large to pass through the pulmonary capillaries but may appear in the left atrium and left ventricle as a result of passage across an intracardiac (ASD or patent foramen ovale [PFO]) or intrapulmonary communication; occasionally, a cough or Valsalva maneuver may transiently increase right-sided heart pressures and facilitate right-to-left crossover of bubbles.⁸ Pulmonary arteriovenous malformations (AVMs) will demonstrate appearance of very small saline contrast in the left atrium; however, these bubbles are typically smaller than those that transit across an intracardiac shunt, and usually appear late after injection (after >7-10 beats) and persist after the right side of heart empties of contrast saline, representing the typical transit time of the contrast saline through the pulmonary bed and the AVM into the pulmonary veins. An example of saline contrast echocardiography with a right-to-left interatrial shunt is shown in Figure 8.3.

Contrast for Left Ventricular Opacification

Commercially available contrast agents, specifically formulated to pass through the pulmonary capillary bed, can be used to opacify intracardiac chambers in order to enhance endocardial border definition. When activated, contrast agents yield perfluorocarbon microbubbles encapsulated in either a lipid or albumin shell, which exhibit lower acoustic impedance than blood and enhance the intrinsic backscatter of blood.⁹ The most important clinical use of contrast agents in critical care is for left ventricular opacification (LVO), to be used when standard TTE images are suboptimal, which occurs in 25% or more of cases in the critical care setting.¹⁰ These agents are useful in improving image quality in technically difficult echocardiograms and can provide significant additional diagnostic information, especially on LV function, the presence of LV apical thrombus, and detection of LV wall motion abnormalities.¹¹ Importantly, contrast for LVO has also been shown to reduce the need for other, more involved imaging modalities in the critical care population, such as TEE.^12–14 An example of contrast used for LVO in a patient with technically difficult echo windows is shown in Figure 8.4. In patients in whom contrast for LVO is used, the enhanced Doppler signals with the use of contrast can also be utilized for detection and measurement of faint tricuspid regurgitation (TR) signals for the estimation of pulmonary artery (PA) pressure, especially important in the critical care scenario.¹⁰

Systolic Function

Although there are a variety of methods to assess LV systolic function by echocardiography (Doppler calculation of stroke volume, dP/dt using mitral regurgitation [MR] signal, tissue Doppler systolic velocity, and systolic strain and strain rate), the most commonly used and clinically relevant is the calculation or estimation of LV ejection fraction (EF).24,25 As recommended in current guidelines,²⁴ calculation of left ventricular ejection fraction (LVEF) by method of discs (Fig. 8.5) is recommended, although visual estimation of LVEF is reliable when technically adequate images are evaluated by experienced echocardiographers.²⁶ EF (end-diastolic volume − end-systolic volume/end-diastolic volume) is dependent not only on intrinsic contractility but also on LV preload and afterload. Therefore, both factors should be considered when assessing LV systolic function. In general, LV systolic function is hyperdynamic when LVEF is greater than 70%, normal at 55% to 70%, mildly depressed at 45% to 54%, moderately depressed at 30% to 44%, and severely depressed at less than 30% (Table 8.1).²⁴ In the presence of regional dysfunction, EF from multiple views should be integrated to accurately assess LV systolic function. To improve the accuracy of EF calculation by echocardiography, it is essential to avoid foreshortened apical views and to use intravenous contrast material when needed to enhance endocardial border definition (see Fig. 8.4). Aside from measurements of systolic function, 2D echocardiography is of great use in reliably assessing LV dimensions, wall thickness, volumes, and mass.²⁴ Reliable assessments of LV dimensions and EF, particularly when combined with knowledge of filling pressures, can be used to guide and assess the response to therapeutic measures of volume infusion or intravenous administration of inotropic/vasodilator or vasopressor drugs.

TDI-derived myocardial velocities (Fig. 8.6) have been utilized to assess global LV systolic properties.²⁷ This approach is dependent on TD technology to record mitral annulus and myocardial signals, which can be acquired from any area of the heart. However, because of their dependence on Doppler principles, they are of limited value when proper alignment cannot be achieved between the ultrasound beam and the plane of cardiac motion. TDI measurements of systolic annular velocity have been shown to reflect systolic dysfunction, even in the presence of normal LVEF (such as in hypertrophic cardiomyopathy [HCM] or infiltrative cardiomyopathy [ICM]).^27–29 Using speckle tracking imaging, a 2D echocardiographic technique that measures myocardial motion over time, myocardial deformation (strain) and rate of deformation (strain rate) can also be used to assess LV systolic function.^30,31 As in TDI, strain and strain rate can detect significant myocardial systolic abnormalities, even in the presence of preserved LVEF.^32,33 As with TDI, this is of particular importance in patients with diastolic heart failure, hypertensive heart disease, HCM, and infiltrative disease, when normal EF can coexist with significant and clinically important abnormalities of systolic function.

Diastolic Dysfunction

LV diastolic dysfunction in the intensive care unit (ICU) may be present as a result of cardiac as well as systemic disorders that can affect cardiac function: coronary and hypertensive heart disease, diabetes mellitus, amyloidosis, and HCM. A careful assessment of LV diastolic function by echocardiography can contribute essential information for the management of these patients.34–36 In general, LV diastolic function refers to LV relaxation (measured as the rate of decay of LV systolic pressure during the isovolumic relaxation period) and LV chamber stiffness. In turn, chamber stiffness is calculated using measurements of LV volume and pressure during the diastolic filling period. However, prediction of LV filling pressures integrates the effects of the preceding hemodynamic variables as well as other factors such as RV filling, pericardial constraint, and LA function on LV diastolic function.

The recommended clinical approach for the assessment of LV diastolic function (European Association of Echocardiography [ASE] guideline algorithms) begins with the 2D examination to determine LV dimensions and volumes and the presence and extent of LV hypertrophy, using standard ASE criteria (Figs. 8.7 and 8.8).³⁷ Patients with a depressed EF or LV hypertrophy have impaired LV relaxation. Therefore, even in the absence of any corroborating Doppler information, one can still conclude that LV relaxation is impaired in these patients. Furthermore, this information can be combined with the mitral inflow pattern to predict filling pressures. It is also important to measure left atrial (LA) volume using apical four- and two-chamber views because LA volume is related to the extent of diastolic dysfunction when increase in LA volume parallels deterioration of LV diastolic function.³⁸ Mitral inflow is obtained using pulse Doppler, with a 1- to 2-mm sample volume placed at the level of mitral valve tips.³⁹ Early diastolic flow and velocity (E) occur in response to a positive pressure gradient between the LA and the LV, resulting from a rapidly decreasing LV pressure due to LV relaxation and early diastolic suction. In late diastole, LA contraction leads to another positive pressure gradient and late diastolic flow or the A velocity. With normal LV relaxation, early diastolic flow predominates and the E/A ratio is greater than 1. However, when LV relaxation is impaired, LV diastolic pressure is elevated and a reduced E velocity is observed. This leads to a higher LA preload and contraction velocity. Therefore, the E/A ratio decreases in the presence of impaired LV relaxation. Because LA pressure usually increases to maintain forward stroke volume, early diastolic transmitral pressure gradient increases, leading to a higher E velocity and E/A ratio. Because of the simulation to normal mitral inflow, this pattern is referred to as a pseudonormal mitral inflow pattern. In more advanced disease with markedly elevated LA pressure, the E velocity increases even further, resulting in a “restrictive” inflow pattern, in which E/A ratio is 2 or greater. It is possible to unmask the presence of impaired LV relaxation in these cases by performing a Valsalva maneuver. The decrease in venous return during the strain phase of Valsalva results in a decrease in LA pressure and E/A ratio.^40–42 TD-derived early diastolic mitral annular velocity (e′) can be recorded by pulsed Doppler at mitral annulus. When combined with E, E/e′ ratio is obtained, which has been shown to be a reasonable correlate of LV filling pressure,⁴¹ although multiple diastolic echo-Doppler variables need to be synthesized to result in an accurate assessment of LV diastolic function.^43–45

Pulmonary venous (PV) flow can also be analyzed to predict LV filling pressures. PV flow signals are readily recorded in the majority of patients seen in the outpatient laboratory but can be challenging in the critical care setting. Antegrade forward flow from the pulmonary vein into the left atrium occurs during systole (S) and early and mid-diastole (D). After atrial contraction, retrograde flow (Ar) from the left atrium into the pulmonary vein occurs. At the earlier stages of diastolic dysfunction where LV end-diastolic pressure is increased, the peak velocity and duration of Ar (velocity > 30 cm/second and Ar-A duration ≥ 35 ms) become more prominent.42,46 Subsequently, with the rise in mean LA pressure, antegrade systolic flow decreases, whereas the D velocity increases with a shortening of its deceleration time. Assessment of PA systolic and diastolic pressures (see later) can provide helpful corroborating evidence of the status of LV filling pressures. In the absence of pulmonary parenchymal and vascular disease, and in the presence of significant cardiac valvular disease or cardiomyopathy, one can reasonably infer that PA pressures are increased due to an elevated LA pressure. Figure 8.9 shows an example of a patient with preserved LVEF with elevated LV filling pressures as assessed by integrated diastolic assessment with multiple echo-Doppler variables.

Hypertrophic Cardiomypathy

HCM is an inherited disorder that is characterized by unexplained LV hypertrophy in the absence of longstanding hypertension or infiltrative disease.⁴⁹ At the pathologic level, there is myocyte disarray, with replacement of healthy myocytes with fibrosis. Therefore, on echocardiography, thick LV walls with elevated LV mass are seen. Early in the disease, LV function is usually hyperdynamic, although late in the disease, LVEF can become depressed (“burned-out HCM”). There are various morphologic types of HCM, including septal hypertrophy (Fig. 8.17), concentric (uniform) hypertrophy, apical hypertrophy, and hypertrophy concentrated in LV walls other than the septum. It is important to understand that LV obstruction with resultant dynamic gradients can occur in any of these morphologic types, thus the differentiation between obstructive and nonobstructive HCM. Echocardiography is uniquely positioned to differentiate these morphologic types, determine LV systolic function, assess for left ventricular outflow tract (LVOT) obstruction, identify associated MR, and determine LV filling pressures and PA pressure.⁵⁰ Obstruction in HCM is most often caused by systolic anterior motion (SAM) of the mitral valve (Fig. 8.18), which physically obstructs the LVOT, resulting in a significant gradient. From the clinical point of view, HCM patients can present to critical care with hypotension, congestive heart failure, arrhythmias, stroke, and cardiac arrest; echocardiography is crucial in differentiating the underlying disease state and functional/morphologic associations with these presentations.

Dilated Cardiomyopathy

DCM refers to nonischemic global LV systolic dysfunction often associated with RV dysfunction. Although viral myocarditis can cause this same picture, in general, DCM refers to familial inherited cardiomyopathy but can be caused by a variety of conditions including alcohol abuse, chemotherapeutic agents, and endocrine disorders. As genetic methods for diagnosing inherited DCM become more refined, an increasing proportion of idiopathic nonischemic cardiomypathy is found to be inherited.⁵¹ From the echocardiographic standpoint, DCM is readily diagnosed by dilated LV with depressed EF and often RV dysfunction; for final diagnosis, exclusion of a sufficient degree of coronary artery disease to explain degree of LV dysfunction is necessary.⁵² Secondary MR and TR can be seen by color and spectral Doppler interrogation, and LV filling pressure and PA pressure assessments are important in clinical management. An example of a patient with DCM is seen in Figure 8.19.

Infiltrative/Restrictive Cardiomyopathy

ICMs are characterized by the deposition of abnormal substances that cause the ventricular walls to become progressively rigid, thereby impeding ventricular filling.⁵³ This impedance to normal LV filling is termed “restrictive filling;” hence the other name, “restrictive cardiomyopathy.” However, because any cardiomyopathic process can have restrictive filling (ischemic, dilated, hypertrophic), the preferred term is ICM. Some ICMs can cause LV and RV thickening, such as the archetypal ICM cardiac amyloidosis (Fig. 8.20), although others can cause ventricular thinning, such as sarcoidosis. From the echocardiographic point of view, thickened ventricular walls with restrictive LV filling and at time depressed LVEF are seen in amyloidosis;⁵⁴ the differentiation from HCM and hypertensive heart disease is made by the presence of low ECG voltages in ICM, as normal myocytes are replaced by amyloid. For sarcoidosis, many LV patterns can be seen, but focal LV aneurysms are typical; heart block on ECG is also often seen.