In dealing with patients with hypotension and shock, one must distinguish among a cardiac etiology resulting in primary reduction in cardiac output, a purely noncardiac entity such as hemorrhage with hypovolemia, and cardiac entities resulting in hemodynamic instability such as acute valvular insufficiency. It is also important to identify concurrent cardiac abnormalities that may complicate either diagnosis or therapy. Figures 22.1, 22.2, 22.3, 22.4, 22.5 and 22.6 were recorded in patients in a medical or surgical intensive care unit with a variety of acute illnesses. Patients with severe infection and sepsis may have acute, severe left ventricular dysfunction in the absence of coronary disease or preexisting cardiomyopathy. Figure 22.1 was recorded in a patient hospitalized with sepsis, hypotension, and malperfusion. The echocardiogram documented severe left ventricular systolic dysfunction that improved after treatment of gram-negative sepsis.

Patients with preexisting pulmonary disease may be hospitalized with acute respiratory compromise related to decompensated pulmonary disease and/or decompensation of concurrent congestive heart failure. When a patient presents in this manner, it can be difficult to ascertain the contribution of underlying primary cardiac disease from that secondary to pulmonary disease. Figure 22.4 was recorded in a patient presenting with multilobar pneumonia requiring ventilatory support who had clinical right heart failure. Notice the marked enlargement of the right ventricle and right atrium with secondary tricuspid regurgitation and evidence of right ventricular pressure overload. Pulmonary hypertension confers a worsened prognosis for patients with acute severe medical illness. Severe pulmonary hypertension may result in a syndrome in which overall cardiac output is limited by right heart flow. In advanced cases, this may compromise left ventricular filling and make patients susceptible to significant hypotension in the presence of vasodilation related to either medical therapy or sepsis.

Because of the critically ill nature of these patients, and the fact that many are often on ventilatory support, transthoracic imaging may be suboptimal. It is often feasible, however, to evaluate the status of left ventricular function and exclude systolic dysfunction as a cause of hypotension even in poor-quality images. The routine use of second harmonic imaging and selective use of intravenous contrast for left ventricular opacification is beneficial to enhance visualization of left ventricular function in ventilated patients in an intensive care unit (Fig. 22.7). Although it may be possible to determine the status of left and right ventricular function from transthoracic echocardiography using contrast echocardiography, detailed evaluation of valvular anatomy and hemodynamics may require transesophageal echocardiography. Several studies have demonstrated the incremental value of transesophageal echocardiography for elucidating the underlying mechanism of hypotension or hypoxia in patients hospitalized in an intensive care unit with a broad range of disorders.

One cause of hypotension in critically ill patients, especially in a surgical or trauma intensive care unit, is hemorrhage and hypovolemia. This can be documented on an echocardiogram when a small left ventricular volume and hyperdynamic motion are noted (Fig. 22.2). This is reliable evidence of intravascular volume depletion and has obvious therapeutic implications. On occasion, one encounters a patient with progressive
hypotension in whom the use of intravenous pressors results in no improvement or further deterioration. There is a subset of patients, many of whom have a history of hypertension, who with volume depletion develop acquired dynamic left ventricular outflow tract obstruction which mimics obstructive hypertrophic cardiomyopathy. Systolic anterior motion of the mitral valve with secondary mitral regurgitation also may be seen. The overall hemodynamic result of this syndrome is progressive hypotension with the development of a prominent systolic murmur (due to outflow tract obstruction and/or mitral regurgitation). The etiology of the hypotension in this situation is the relatively low left ventricular stroke volume due to hypovolemia, complicated by outflow tract obstruction. Left ventricular outflow tract gradients exceeding 100 mm Hg have been noted because of this phenomenon. In this instance, right heart catheterization reveals an elevated pulmonary capillary wedge pressure that is then assumed to reflect left ventricular filling volume. When the syndrome of significant mitral regurgitation with outflow tract obstruction is identified, one should recognize that the elevated pulmonary capillary wedge pressure is the result of a hyperdynamic but noncompliant left ventricle and mitral regurgitation. Failure to appreciate this phenomenon results in the inappropriate course of increasing pressor support and diuretics, which obviously has the effect of worsening rather than improving the clinical situation. Figure 22.8 was recorded in a patient with this syndrome. Recognition of hypovolemia with dynamic outflow tract obstruction should lead to the appropriate management decision to resuscitate the patient with fluids and withdraw agents, which increase contractility and/or reduce vascular resistance.

Diastolic dysfunction may result in pulmonary congestion and heart failure in patients hospitalized with medical illnesses or in the postoperative period. These patients typically are

elderly and have a history of hypertension. In the operative or postoperative period, overly aggressive fluid resuscitation may result in congestive heart failure. The echocardiogram will typically reveal normal systolic function and left ventricular hypertrophy (Fig. 22.9). Mitral inflow patterns may be highly variable and show either delayed relaxation or a restrictive filling pattern. If intravascular volume overload is present, a pseudonormal inflow pattern is not uncommon.

Echocardiography can be effectively used in an intensive care unit for evaluation of unexplained hypoxia or inability to wean from ventilatory support. Etiologies of hypoxia that can be documented by echocardiography are listed in Table 22.1. A comprehensive echocardiographic examination is useful in patients with hypotension and shock to exclude a primary cardiac abnormality. If no primary cardiac abnormality is identified, including right-to-left shunting, then the etiology of hypoxia can reliably be assumed to be noncardiac and appropriate diagnostic and therapeutic efforts directed to pulmonary or other causes. A cause of hypoxia in the intensive care unit that is uniquely evaluated by echocardiography is the opening of a patent foramen ovale (PFO) with subsequent right-to-left shunting (Fig. 22.10). This generally requires not only the presence of a PFO but also a concurrent process that elevates right heart pressure such as pulmonary hypertension, acute pulmonary embolus, or right ventricular dysfunction. Additionally, reactive pulmonary hypertension of any etiology, including that provoked by bronchospasm, can result in sufficient elevation of right heart pressure that a patent foramen becomes a source for significant right-to-left shunting.

An additional source of right-to-left shunting is a pulmonary arteriovenous malformation (AVM). Arteriovenous malformations are seen in chronic liver disease as well as in Osler-Weber-Rendu syndrome. Most AVMs result in clinically inconsequential degrees of shunting and rarely result in clinically relevant, or even detectable, hypoxia. On occasion, large or multiple AVMs may result in substantial right-to-left shunting with clinically relevant hypoxia. Separation of an AVM from atrial level communication is discussed in Chapter 4 and relies on the timing and other characteristics of contrast appearance in the left side of the heart. Typically, contrast appearance in the left side of the heart related to an AVM is delayed by several cardiac cycles, but then builds persistently rather than appearing phasically, as is typically seen in atrial level shunts. (Fig. 22.11). The basis for this echocardiographic finding is that before it appears in the left side of the heart, contrast must pass through the entire pulmonary vascular circuit. This typically takes three to six cardiac cycles depending on cardiac output. The pulmonary circuit then acts as a reservoir of contrast that continues to flow into the left side of the heart even after the initial intravenous bolus has begun clearing from the right side of the heart.

For patients presenting to the emergency department with hypotension, shock, or major trauma (especially thoracic), many of the same considerations noted above regarding use of echocardiography in the intensive care unit apply. Obviously for patients
with major trauma, hemorrhagic shock is a consideration, in which case echocardiography can quickly document a small, underfilled ventricle. Additionally, in patients with major blunt chest trauma, such as after a high-speed motor vehicle accident, echocardiography can be instrumental in documenting cardiac involvement including myocardial contusion, pericardial effusion, or aortic trauma. By confirming the absence of significant cardiac involvement, echocardiography allows the clinician to redirect efforts to alternate explanations for hypotension.

Patients likely to have sustained cardiac trauma often have concurrent, thoracic, abdominal, or major limb trauma. As a consequence of this, the independent specific cardiac abnormalities may be masked by hypovolemia from hemorrhage. The majority of patients with significant cardiac and/or aortic trauma have multiple rib fractures, hemo- or pneumothorax, and other complications which render transthoracic imaging problematic. Because of chest trauma, atypical imaging windows may be necessary. Occasionally, after an intrathoracic procedure or major chest trauma, transthoracic echocardiography results in total failure to visualize any cardiac structures. This may be associated with strong and occasionally dynamic reverberation signals (Fig. 22.12). When this scenario is encountered, one should suspect either subcutaneous air, pneumothorax or pneumomediastinum. In these instances, transesophageal echocardiography is essential and can identify the majority of cardiac injuries. In skilled hands, it has been demonstrated to be equivalent to computed tomography for identification of aortic trauma (Figs. 22.13 and 22.14).

Forms of trauma other than blunt chest trauma include penetrating injuries from knife or bullet wounds. The echocardiographer should be cognizant of the unpredictable path of a high-velocity penetrating injury and the need for atypical imaging planes. In general, patients with any significant penetrating cardiac trauma will have a pericardial effusion, and its absence is circumstantial evidence that a penetrating cardiac injury has not occurred. Cardiac contusion and injury, however, can occur from the “shock” effect of bullet wounds to the chest, in which case penetration of cardiac structures will not be noted. Figures 22.15 and 22.16 were recorded in patients with penetrating cardiac trauma.

Sudden cardiac arrest can occur because of a variety of mechanisms and is typically classified as being arrhythmic, pulseless electrical activity, or asystolic. The underlying mechanisms can be distinct for each and outcomes are dependent on the nature of the arrest. Specific therapy may be indicated on the basis of the precipitating cause. Several studies have suggested the utility of a limited, rapid, bedside echocardiogram, often performed with handheld devices, to facilitate rapid diagnosis and decision making in patients suffering witnessed cardiac arrest. Figures 22.17 and 22.18 were recorded in patients shortly after resuscitation from cardiac arrest. Note in Figure 22.17 the global hypokinesis of the left ventricle with apical dyskinesis suggesting an underlying ischemic disease as the substrate. In Figure 22.18, note the normal hyperdynamic left ventricle with right ventricular dilation raising the possibility of an acute pulmonary embolus as the etiology. Obviously, management would be altered on the basis of these findings.

Determination of the feasibility of mitral valve repair relies on the preoperative transesophageal echocardiogram. In general, posterior leaflet pathology is more easily repaired than anterior, and in general any disease process that scars or foreshortens the mitral valve apparatus results in anatomy less likely to be successfully repaired than diseases associated with excess or redundant tissue.

When performing echocardiography for the purpose of assessing the mitral valve before repair, it is important that a thorough and detailed evaluation of the mitral valve be undertaken in a systematic fashion. The primary purpose of the examination is to determine the underlying anatomic abnormality responsible for the regurgitation or stenosis. It is important to recognize that there are three different viewing perspectives on mitral valve anatomy (Fig. 22.23). The surgeon will be viewing the mitral valve from within the left atrium so that the anterolateral commissures will be to the left of the field of view and

the medial commissures to the right. When viewed with either transesophageal or transthoracic echocardiography, this orientation will be reversed (assuming traditional recommended viewing formats on a video screen). Also, depending on whether the reference is a transthoracic or transesophageal echocardiogram, the anterior and posterior leaflets of the mitral valve will vary in position compared with the surgical perspective.

There are multiple imaging planes available from transesophageal echocardiography, each of which will interrogate a different aspect of mitral valve anatomy. Figure 22.24 depicts the location of each of the scallops of the anterior and posterior mitral valve leaflets as they relate to different two-dimensional transesophageal imaging planes. Even with substantial experience, it is occasionally difficult to identify the precise site of pathology and much experience is necessary before being able to render consistently accurate interpretations of mitral valve pathology with respect to the precise anatomy responsible for a regurgitant lesion.

When determining the severity of mitral regurgitation, it is critical to recognize that intracardiac hemodynamics in an anesthetized and ventilated open chest patient are substantially different than hemodynamics in the awake or mildly sedated patient. For this reason, there can be marked differences in the apparent severity of mitral regurgitation when comparing an intraoperative transesophageal echocardiogram with one performed on an ambulatory patient. In general, diseases resulting in functional mitral regurgitation will tend to have a reduction in the severity of mitral regurgitation when comparing the intraoperative with the preoperative studies. There is less reduction in the apparent severity of mitral regurgitation for patients with anatomic disruption of a valve leaflet than for those with functional mitral regurgitation. Figure 22.25 was recorded in two patients preoperatively and reveals severe mitral regurgitation. The lower panels were recorded in the same patients during an intraoperative study and reveal substantially less mitral regurgitation. Of note, blood pressure and heart rate were equivalent at the time of the examinations.

Evaluation of the mitral valve has been one of the more successful applications of three-dimensional echocardiography. This technique can be performed using a number of techniques which were discussed in Chapter 3. Its greatest impact has been with the utilization of new real-time three-dimensional scanners, capable of providing real-time, subpyramidal imaging
of the mitral valve from a perspective within the left atrium (Fig. 22.26). Experience suggests that real-time three-dimensional imaging confers an advantage with respect to complete evaluation of mitral valve pathology, including isolated mitral flail chordae and precise localization of flail scallops compared with routine, two-dimensional imaging, although the true clinical impact of this has yet to be demonstrated. Figures 22.27, 22.28 and 22.29 were recorded in patients with mitral pathology and demonstrate the unique capabilities of this type of imaging. Similar images can be obtained from reconstructed images but are
limited by artifacts inherent in stitching subvolumes and the fact that they do not provide true real-time images. Sophisticated on- and off-line analysis systems have been developed for quantitation of the three-dimensional mitral valve data set allowing determined quantitation of the actual amount of mitral valve tissue involved with a flail leaflet as well as the overall area of the mitral valve (Fig. 22.29). Experience to date suggests that this imaging technique confers substantial clinical value with respect to accuracy and speed of anatomical diagnosis, both before and following surgery for mitral valve disease. As current ultrasound platforms are still limited with respect to color Doppler imaging when operating in a threedimensional scanning mode, standard two-dimensional imaging with color flow Doppler is still essential for a complete evaluation.

Figures 22.30, 22.31 and 22.32 were recorded in a patient with dilated cardiomyopathy and severe functional mitral regurgitation. The mitral valve is anatomically normal; however, there is failure of coaptation, resulting in severe mitral regurgitation. In this instance, the mechanism of regurgitation can be demonstrated to be apical displacement of the papillary muscles in the dilated and spherical left ventricle. Note the central location of the mitral regurgitation jet that arises at the area of noncoaptation of the mitral leaflets. This type of mitral regurgitation can be addressed by placement of an annular ring, which corrects the abnormal coaptation of the mitral valve. For patients with functional ischemic mitral regurgitation, due to restricted motion, of one or both mitral valve leaflets, a similar surgical approach is taken.

The patient illustrated in Figures 22.33 and 22.34 has mitral regurgitation due to a flail scallop of the posterior mitral valve leaflet. In this instance, regurgitation is due to anatomic disruption of the mitral valve and the repair will necessitate resection of the flail scallop with reapposition of the intact margins. For a posterior flail, the most common repair is resection of the redundant portion of the flail leaflet with reapproximation of the intact edges. A mitral annular ring is then placed (Fig. 22.35). Depending on the initial pathology and the amount of resected
valve tissue, this may result in the valve being converted to a nearly unicuspid valve with the anterior leaflet providing the majority of functional valve tissue. More complex repairs may include transposition of a portion of a leaflet and its attached chordae to the opposite leaflet to provide intact chordae to the previously flail leaflet. Finally, prosthetic chords can be attached to a flail mitral leaflet and subsequently to a papillary muscle to replace chordal structures that are damaged beyond repair. The goal of mitral valve repair is to reduce the severity of mitral regurgitation to no more than mild without creating iatrogenic mitral stenosis. In the examples presented, note the smaller annular dimensions due to an annular ring as well as the areas of thickening on the mitral valve that represent areas of resection (Figs. 22.36 and 22.37).