Echocardiography can be a valuable tool in evaluation of the patient with unexplained hypotension (see Table 23–2). Both TTE and TEE can help quickly distinguish among a primary cardiac etiology resulting in decreased cardiac output versus a noncardiac etiology such as hemorrhage with hypovolemia. While TTE may provide sufficient imaging in the critically ill patient, visualization of cardiac structures is often impaired and TEE is therefore required. In one series of 2508 TEE studies in critically ill patients over 15 years, hemodynamic instability was the most frequent indication for TEE (39%), followed by suspected endocarditis (19%), assessment of ventricular function (9%), suspected aortic disease (8%), suspected pericardial tamponade (3%), and chest trauma (1%).71 Similarly, Burns et al72 demonstrated in acutely ill trauma patients that approximately two-thirds of patients improved because of changes in management resulting from the TEE findings. For example, several patients with what would be deemed as having acceptable filling pressures based on pulmonary arterial catheterization in fact had inadequate filling when visualized on TEE.72 In another study of 308 critically ill patients, 40% of patients were evaluated by TEE for hypotension; of these, the cause of the hypotension was identified in 67% of the cases, leading to a management change in 31% of patients.73
TEE Assessment of Cardiac Etiologies of Hypotension
Echocardiography can delineate the cardiac etiology resulting in hemodynamic instability, ie, cardiogenic shock, acute valvular insufficiency, or concurrent cardiac abnormalities. One of the mainstays of echocardiographic evaluation in patients with unexplained hypotension is left and right ventricular systolic function assessment, which can usually be accomplished by real-time visualization alone through a combination of short-axis and long-axis views of the left and right ventricles. In one study, 115 critically ill patients were evaluated by TEE, with the most common indication being hemodynamic instability (67% of patients).74 Of these, 26% were found to have left ventricular dysfunction with left ventricular ejection fraction of less than 30%, suggesting that this is not an uncommon cause of hypotension in ill patients. In several series, echocardiography has been found to be more reliable than Swan-Ganz catheter pressure in determining the cause of hypotension.75–77 Further, left ventricular dysfunction can occur in the setting of septic shock,78 and hence left ventricular function assessment in such patients can be important to guide subsequent therapy.
In addition to ventricular dysfunction, cardiac hypotension can be caused by pericardial tamponade and/or severe valvular disease. In a study of 61 critically ill patients with unexplained, sustained (>60 minutes) hypotension, a TEE-guided diagnosis of nonventricular limitation to cardiac output (ie, valvular or pericardial) was associated with improved survival to discharge (81%) versus a diagnosis of ventricular disease (41%) or hypovolemia/low systemic vascular resistance (44%).76 TTE was inadequate in 64% of these patients, and TEE contributed new, clinically significant diagnoses (ie, not seen by TTE) in 28% of patients, leading to surgical interventions in 20%. The authors suggest that TEE makes a clinically important contribution to the diagnosis and management of unexplained hypotension and is prognostic in critically ill patients.76 TEE can also diagnose myocardial infarction and related mechanical complications as detailed earlier in this chapter.
TEE Assessment of Hypovolemia as a Cause of Hypotension
Echocardiography can represent an important tool for the diagnosis of hypovolemia, documenting a small left ventricular volume and hyperdynamic motion. With TEE, left ventricular volume can be measured by subjective assessment of LV size or by quantitative determination of left ventricular cross-sectional area at end-diastole using the transgastric short-axis view at the level of the midpapillary muscles.79 In some patients, often those with a history of hypertension, an acquired dynamic left ventricular outflow tract obstruction can occur when volume depletion occurs, with the same hemodynamic consequences as obstructive hypertrophic cardiomyopathy. Elevated left ventricular outflow tract gradients and systolic anterior motion of the mitral valve with secondary mitral regurgitation may be seen, resulting in progressive hypotension and development of a systolic murmur. Gradients exceeding 100 mm Hg have been noted, and hemodynamic assessment with pulmonary artery catheterization may be misleading, showing an elevated pulmonary capillary wedge pressure suggesting an increased left ventricular filling volume.38 This abnormality resolves with volume repletion and removal of pharmacologic agents aimed at increasing contractility and/or reducing vascular resistance.
TEE Assessment of Pulmonary Embolism as a Cause of Hypotension
Pulmonary embolus (PE) has been shown to be the cause of almost 5% of cardiac arrests, with PEA being the initial rhythm in 63%.32 In fact, one small study of 25 patients presenting with PEA in whom TEE was routinely performed showed that 14 had evidence of right ventricular enlargement; of these nine were subsequently found to have pulmonary embolism, with the remainder having cardiac contusion, right ventricular infarction, right ventricular hypertrophy, or cor pulmonale.80 Diagnosis of PE in the setting of cardiac arrest is an important one as prompt treatment with thrombolytics has been shown to result in a significantly higher return of spontaneous circulation than in those patients not receiving thrombolytics (81% vs 43%, respectively).32
PE is diagnosed on TEE by findings suggestive of acute right ventricular pressure overload such as right ventricular enlargement and/or hypokinesis in the context of an appropriate clinical scenario. In the absence of myocardial infarction, significant left-side valve or ventricular disease, or known pulmonary disease, this finding indicates a high probability of pulmonary embolus.4 This can often be accompanied by right atrial enlargement, tricuspid regurgitation, dilation of the inferior vena cava and flattening of the interventricular septum with a “D-shaped” left ventricular geometry in the short-axis views due to pressure overload on the right ventricle, and paradoxical septal motion. Of note, right ventricular dysfunction can also be due to an inferior myocardial infarction, myocardial contusion (ie, in the setting of trauma), sepsis, and acute sickle-cell crisis.10 Often termed “McConnell sign,” a relatively specific sign of right ventricular dysfunction due to pulmonary embolism (as opposed to other causes of right ventricular dysfunction) is characterized by a distinct regional pattern of right ventricular (RV) dysfunction with normal RV apical motion but akinesia of the mid-free RV wall.81 This regional RV dysfunction was found to have a sensitivity of 77%, specificity of 94%, positive predictive value of 71%, and a negative predictive value of 96% for the diagnosis of PE.
It should be noted that the echocardiographic findings of pulmonary embolus are typically seen after acute obstruction of more than 30% of the pulmonary arterial bed.82 However, a recent small study has suggested that a decreased acceleration time of pulmonary artery outflow is associated with even small pulmonary emboli obstructing less than 25% of the pulmonary vasculature (acceleration time in pulmonary embolism 85 ± 22 milliseconds vs 117 ± 35 milliseconds in controls without pulmonary embolism).83 This needs to be further validated before being used clinically, but suggests additional echocardiographic criteria to discriminate smaller pulmonary emboli. In addition, some studies have suggested that the right ventricular to left ventricular end-diastolic diameter ratio (RVEDD/LVEDD) may be an important prognostic factor in patients with pulmonary embolism. In one study of 950 patients hospitalized for acute pulmonary embolism, it was found that the sensitivity and specificity of an RVEDD/LVEDD greater than 0.9 for predicting hospital mortality were 72% and 58%, respectively, with the ratio also being an independent predictor of hospitality mortality (odds ratio 2.66).84
Although rarely seen on TTE, TEE may be able to directly visualize pulmonary emboli,85 usually in the main or right pulmonary arteries (Figure 23–11), with limited sensitivity for more distal or left pulmonary arterial clots. In one study of intraoperative TEE in 46 patients with known PE immediately prior to pulmonary embolectomy, using definitive location of thromboemboli determined from the surgical record as the “gold standard,” they found that echocardiographic evidence of right ventricular dysfunction was present in 96% and leftward interatrial septal bowing was present in 98% of examinations. However, the sensitivity of TEE for direct visualization at any specific location was only 26%, with the least sensitivity for the left pulmonary artery.22 Another study of TEE in patients with known severe PE showed that central pulmonary thromboemboli were directly visualized in 58.3% of patients evaluated, leading the authors to conclude that TEE seems to be a useful method for the diagnosis of severe PE, with the potential ability to clarify the diagnosis within a few minutes without further invasive diagnostic procedures.85 Regardless, the combination of indirect echocardiographic criteria in combination with potential direct visualization of pulmonary thromboemboli make TEE a valuable tool in the diagnostic workup.
Upper esophageal ascending aorta (ASC AO) short-axis view demonstrating a pulmonary embolus (arrow) in the right pulmonary artery (RPA) (left panel). The embolus is more readily visualized after contrast enhanced ultrasonography (right panel). (SVC, superior vena cava.)