Echocardiography in Noncardiac Surgery

Acute Valvular Dysfunction

Although it must be considered in the differential diagnosis, acute new valvular insufficiency is an unlikely cause of hemodynamic instability. If it occurs, it is more likely to occur on left-sided valvular structures. Potential causes of acute aortic valve (AV) and mitral valve (MV) insufficiencies are listed in Table 10.1 . The echocardiographic evaluation of valvular dysfunction is similar regardless of the acuity of the dysfunction. Assessment of valvular regurgitation with rescue echocardiography should be limited to a rapid, qualitative assessment. Quantitative measures such as effective regurgitant orifice area and regurgitant volume may be inaccurate in acute regurgitation. Visual assessment of the regurgitant jet with color-flow Doppler (CFD) focusing primarily on the vena contracta is the preferred approach. It is unlikely that any regurgitation that is less than moderate to severe would cause significant hemodynamic instability. The detection of new-onset severe mitral regurgitation intraoperatively should prompt an evaluation for myocardial ischemia (i.e., wall motion abnormalities). Because the papillary muscles originate from the underlying myocardial walls, wall motion abnormalities may lead to papillary muscle dysfunction with resultant leaflet tethering and mitral regurgitation ( Fig. 10.1 ). One or both of the leaflets may be affected, so the determination of central versus eccentric jets does not include or exclude myocardial ischemia.

Because chronic regurgitation leads to myocardial remodeling, moderate to severe regurgitation in the setting of a normal ventricular size should alert the clinician to the high probability of new-onset dysfunction. Noting new-onset regurgitation or a large change in chronic regurgitation is more important than grading the severity of the regurgitation. Acute or subacute regurgitation in the setting of hemodynamic instability may be either the cause or a manifestation of changes in ventricular function and loading induced by another cardiac abnormality. Treatment of the underlying abnormality may improve the regurgitation.

Although new acute valvular pathology is a less likely intraoperative event, hemodynamic instability that results from an unrecognized presence of existing valvular disease is much more likely. For example, the induction of anesthesia in a patient with previously undiagnosed aortic stenosis may lead to hypotension with resultant myocardial ischemia. Prompt diagnosis and therapy are key to maintaining adequate coronary perfusion pressure and preventing a downward spiral of worsening hemodynamics. Again, the detection of aortic stenosis in the noncardiac operating room is more qualitative than quantitative. Calculating gradients is time consuming and may underestimate the severity in the setting of coexisting LV systolic dysfunction. Semiquantitatively, leaflet separation may be calculated or estimated in the midesophageal (ME) AV long-axis view (LAX). Leaflet separation greater than 15 mm denotes the lack of aortic stenosis, but leaflet separation of less than 8 mm carries a 97% positive predictive value of severe aortic stenosis ( Fig. 10.2 ). Additionally, the ME AV short-axis (SAX) view may demonstrate significant calcium deposition and leaflet restriction and allow the estimation of AV area via planimetry (i.e., the tracing of the AV opening).

Acute Aortic Disease

The mortality rate is high in acute dissection of the thoracic aortic and increases with a delay in diagnosis. Helical computed tomography, magnetic resonance imaging (MRI), and TEE are equally reliable for diagnosing or ruling out a dissection, but TEE has the advantage of portability. The thoracic aorta may be visualized throughout the ME ascending aortic, upper esophageal aortic arch, and descending thoracic aortic views. Recognition of a blind spot preventing visualization with TEE of the distal ascending aorta and proximal aortic arch caused by the interposition of the trachea between the esophagus and aorta is essential to preventing a missed diagnosis.

The diagnosis of dissection is based on the detection of an intimal flap that divides the aorta into true and false lumina. The characteristics of the true and false lumens are summarized in Table 10.2 . In general, the true lumen tends to be smaller and round in shape during systole, with systolic expansion and early laminar flow on color-flow Doppler. The false lumen is typically larger and irregular or crescentic in shape with systolic compression and late turbulent flow ( Fig. 10.3 ). On occasion, the false lumen contains spontaneous echo contrast or frank thrombus from the sluggish flow. TEE is also valuable in assessing for intimal tears, intramural hematomas, and penetrating ulcers. Equally important as identifying dissection is identification of associated complications such as acute aortic regurgitation and pericardial effusions with or without tamponade.

Cardiac Tamponade

Proper identification of pericardial tamponade is vital because the hemodynamic consequences can be devastating, and the treatment is specific: maintain contractility and preload and drain the pericardial fluid. The pericardium consists of two layers: visceral and parietal. The visceral layer adheres to the epicardium, and the parietal layer is the fibrous sac surrounding it. Five to 10 mL of pericardial fluid is normal. Potential causes of pathologic fluid accumulation are listed in Box 10.2 . The pericardium is of limited size and distensibility, thereby restraining the four chambers and dampening the effects of changes in intrathoracic pressure. Acute effusions are most likely secondary to trauma (including iatrogenic or surgical) or myocardial infarction. Pericardial tissue affected by chronic effusion tends to be more distensible and thus causes less hemodynamic instability. The effusion can envelop the space in a free-flowing fashion or may be loculated, affecting only a portion of the heart. Free-flowing effusions tend to accumulate in the dependent portion of the space. Pericardial fat is a relatively common finding in the anterior space and should not be confused with fluid accumulation. It tends to have a more granular appearance, rather than purely echolucent, and does not lead to chamber collapse.

Box 10.2

Causes of Pericardial Effusions

• Trauma

• Inflammation

• Infection

• Malignant disease

• Renal or hepatic failure

• Post–myocardial infarction status

Pressures within the pericardium and cardiac chambers during fluid accumulation follow a recognized pattern. Initially, fluid accumulation in the pericardial space compresses the right ventricle and causes the filling pressures to rise with little effect on the stroke volume (SV) of either ventricle. As the pericardial pressures rise, the right ventricle begins to collapse, but the thicker-walled left ventricle is unaffected. In the final stage, both the RV and LV SVs are significantly affected as the pericardial pressure determines passive flow. The external pressure on the cardiac chambers also exaggerates the normal respiratory variation in RV and LV SVs. In mechanically ventilated patients, elevated intrathoracic pressure compresses the superior vena cava (SVC) and inferior vena cava and thus reduces RV preload and SV. At the same time, LV preload and SV are enhanced by increasing return from the inflated lungs. Intrathoracic and pericardial pressures decrease on expiration, augment flow into the right ventricle, and push the interventricular septum into the left ventricle. Diastolic filling and LV SV are thus reduced. In a physiologically normal patient, these hemodynamic swings are minimal. Box 10.3 lists the values for normal respiratory variation in the right and left ventricles, and Table 10.3 summarizes the changes in SV associated with cardiac tamponade.

Box 10.3

Normal Respiratory Variation

• RV inflow <25%

• LV inflow <15%

• RV outflow <10%

• LV outflow <10%

LV, Left ventricular; RV , right ventricular.

The limited TEE examination should be performed in its entirety because some hemodynamically significant effusions may be difficult to visualize. Pericardial effusions are viewed as darkened echolucent areas between the heart and the parietal pericardium. No universally accepted rule exists for quantification, but effusions measuring less than 1 cm are considered small, effusions of 1 to 2 cm are considered moderate, and those larger than 2 cm are considered large ( Fig. 10.4 ). Echogenic “stranding” in the pericardial space alerts the examiner to the possibility that the effusion is inflammatory or hemorrhagic. In the case of extreme hemodynamic instability, a large pericardial effusion should be considered to cause cardiac tamponade regardless of the results of the continuing study.

Pulsed-wave Doppler (PWD) interrogation of RV inflow or outflow may reveal exaggerated respiratory variations. These changes are the earliest signs of tamponade physiology and are followed by exaggerated variations in LV inflow and outflow. Because of the position and variable anatomy of the right ventricle, Doppler assessment of RV inflow and outflow can prove difficult, particularly within the time constraints of rescue echocardiography. LV inflow is best assessed in the ME four-chamber view with the PWD cursor placed at the MV leaflet tips ( Table 10.4 ). LV outflow is best assessed by placing the PWD cursor in the LV outflow tract (LVOT) seen in the deep transgastric (TG) view ( Fig. 10.5 ). The sweep speed should be 25 to 50 mm/s to view the variability most clearly.

With increasing fluid accumulation, the pericardial pressure starts to exceed the right atrial (RA) pressure, thereby causing exaggerated atrial systolic (i.e., ventricular diastolic) contraction that extends into atrial diastole (i.e., ventricular systole). Assessment of this collapse is best performed in the ME RV inflow-outflow view or the ME four-chamber view. As the pericardial pressure increases further, the right ventricle begins to collapse in diastole. The RV outflow tract is most likely to collapse, and thus the preferred view is the RV inflow-outflow view ( Box 10.4 ). A similar collapse of the thicker left-sided structures would indicate very high pericardial pressures. After the diagnosis is established, echocardiography can be a useful adjunct to guide needle placement during pericardiocentesis.

Box 10.4

Summary of Echocardiographic Findings in Pericardial Tamponade

• Pericardial effusion

• Late diastolic or early systolic right atrial collapse

• Diastolic right ventricular collapse

• Increased respiratory variation in mitral inflow and left ventricular outflow tract

Right Ventricular Dysfunction

RV failure, defined as the inability of the right ventricle to provide adequate blood flow to the left ventricle in the setting of normal or elevated central venous pressure, is associated with a high mortality rate in both cardiac and noncardiac surgical procedures. Potential causes of RV failure are numerous and include RV contractile dysfunction as seen in ischemia, volume overload, sepsis, and nonischemic cardiomyopathy and the acute elevations in pulmonary artery pressures seen in hypoxia, acute respiratory distress syndrome, LV dysfunction, and PE. Abrupt, catastrophic RV dysfunction can result when the contractile reserve is reduced secondary to a feedback loop involving RV dysfunction, reduced cardiac output (CO), and decreased coronary perfusion causing worsening RV dysfunction.

Because the anatomy and function of the right ventricle are complex, geometric modeling and quantitative analysis are very difficult. For this reason, the echocardiographic assessment of RV function in the emergency setting should be qualitative, and this approach is as good as MRI at detecting dysfunction. Box 10.5 summarizes the echocardiographic manifestations of RV dysfunction. Visual assessment begins with inspection of right-sided chamber sizes to look for dilation of the right ventricle and right atrium. Encroachment into the left side with right-to-left bowing of the interatrial septum (seen best in the ME four-chamber and bicaval views) and a D-shaped intraventricular septum (seen best in the LV SAX view) indicates elevated right-sided pressures ( Fig. 10.6 ). RV contractility can then be assessed by the fractional area change (FAC) or the tricuspid annular-plane systolic excursion (TAPSE) methods. The RV FAC is calculated by measuring the RV end-systolic and end-diastolic areas (RVESA and RVEDA, respectively) in the ME four-chamber view and using the following equation: [RVEDA – RVESA]/RVEDA. A reduced FAC has significant prognostic value in myocardial ischemia and PE.

Box 10.5

Echocardiographic Parameters of Right Ventricular Dysfunction

Dilated Right Ventricle

• Basal RVEDD >4.2 cm

• Mid-RVEDD >3.5 cm

• RVOT EDD >2.7 cm

Dilated Right Atrium

• RA area >18 cm ²

• RA length >5.3 cm

• RA diameter >4.4 cm

• Bowing into left atrium

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