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.

Midesophageal four-chamber view in a patient with active ischemia and restricted posterior mitral valve leaflet (red arrow) . Note the posteriorly directed wall hugging (Coanda effect) mitral regurgitant jet. LA, Left atrium; LV, left ventricle.

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).

Midesophageal long-axis view in a patient with significant aortic stenosis. Note the poor leaflet separation of the aortic valve indicating high positive predictive value of severe aortic stenosis. LA, Left atrium; LV, left ventricle.

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.

Descending thoracic aorta short-axis view in a patient with an aortic dissection. The true lumen (red arrow) is round in shape with laminar flow in color-flow Doppler, and the false lumen (green arrow) is crescentic in shape with spontaneous echo contrast indicative of slow flow.

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.

Midesophageal four-chamber view in a patient with a large pericardial effusion (red arrow) . LA, Left atrium; RA, right atrium; RV, right ventricle.

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.

Pulsed-wave echocardiographic interrogation of the left ventricular outflow tract by using the deep transgastric view in a patient with tamponade physiology showing respiratory variability. HR, Heart rate.

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

Decreased RV Contraction

• •
  

  TAPSE <16 mm

  
  
• •
  

  RV FAC <35%

Evidence of Elevated PA Pressures

• •
  

  Pulmonary artery diameter >21 mm

  
  
• •
  

  “D-shaped” ventricular septum

Worsening TV Regurgitation

• •
  

  Severe TV regurgitation noted by vena contracta >0.7 cm

EDD, End-diastolic diameter; FAC, fractional area change; PA, pulmonary artery; RA, right atrial; RV, right ventricular; RVEDD, right ventricular end-diastolic diameter; RVOT, right ventricular outflow tract; TAPSE, tricuspid annular-plane systolic excursion; TV, tricuspid valve.

Transgastric midpapillary short-axis view in a patient with massive right ventricular dilation and pressure overload. Note the deviated interventricular septum leading to a D-shaped left ventricle (LV) instead of the normal O-shaped orientation. RV, Right ventricle.

The TAPSE method is best measured by placing the M-mode cursor on the tricuspid annulus in the modified bicaval or transgastric RV inflow-outflow views and measuring the distance the annulus moves from systole to diastole ( Fig. 10.7 ). A distance of less than 17 cm is considered abnormal. For purposes of rescue echocardiography, a qualitative assessment of the TAPSE and the RV free wall in the ME RV inflow-outflow and four-chamber views is preferred.

An example of tricuspid annular plane excursion using M-mode echocardiography on the tricuspid annulus. The red arrow points to the tricuspid annulus. A visual estimation of the annular movement suggests good right ventricular function.

Pulmonary Embolism

The immobility and hypercoagulability associated with surgical procedures increase the risk of PE fivefold. This risk is only partially mitigated by prophylactic measures. Early diagnosis and treatment can reduce the overall mortality rate 10-fold. The examiner should have a high suspicion for PE in hemodynamically unstable patients with malignant disease, prolonged immobilization, obesity, or tobacco use, as well as in patients who use oral contraceptives, hormone replacement therapy, or antipsychotic drugs. The surgical procedures with the highest risks of PE are those associated with hip fractures, acute spinal cord injuries, and general trauma. The pathophysiology of PE begins with an abrupt increase in pulmonary artery pressures. Hypoxia and vasoconstriction worsen pulmonary vascular resistance. RV wall tension and oxygen demand increase, leading to subendocardial ischemia, RV dilation, and regional wall motion abnormalities (RWMAs). The intraventricular septum shifts left, and this shift reduces LV diastolic filling and SV. Overall, the cardiac pathophysiology of PE is complex, involving an interplay of wall tension, ischemia, structural damage, and inflammation.

Although TEE can help guide both diagnosis and management, it is not the gold standard. Echocardiography has high specificity and low sensitivity (90% and 56%, respectively). In fact, end-tidal carbon dioxide is a significantly better diagnostic tool. Although visualization of a clot, which can be found anywhere on the right side from the vena cava to the pulmonary artery, is pathognomonic of PE and can be seen in more than 80% of cases, the presence of a thrombus does not predict death. The ideal views to assess for thrombus include the ME bicaval, RV inflow–outflow, and ascending aorta SAX views. The main and right pulmonary arteries can be seen by withdrawal of the probe to the high esophagus until a cross-section of the ascending aorta is obtained. The left pulmonary artery is often obscured by the tracheobronchial tree. The most clinically useful echocardiographic findings in the setting of PE are those associated with acute RA and RV failure. Bowing of the interatrial septum to the left indicates high RA pressures, which can be particularly problematic in the setting of a patent foramen ovale. A patent foramen ovale in a patient with PE doubles the mortality rate and quintuples the rate of ischemic stroke, and aggressive thrombolytic treatment is therefore warranted. RV wall motion abnormalities are the most common echocardiographic findings in patients with PE. The extent of RV dysfunction correlates with the overall clot burden, with perfusion defects larger than 20% to 25% more likely to cause dysfunction and dilation. A reduced TAPSE correlates with mortality rates, and it can predict the extent of the clot burden as well as residual perfusion defects when the RV dilation has resolved.

Right ventricular dysfunction in the setting of PE predicts mortality rates, even in normotensive patients. The McConnell sign is suggested as a highly specific (94% specificity with 77% sensitivity) finding of a distinct pattern of RV RWMA in predicting PE. The sign consists of a hypokinetic free wall and a normal to hyperdynamic apex. This subsequently has been found to have reduced sensitivity and specificity, with some suggesting a “reverse” McConnell sign as an indication of PE. Therefore a particular array of RV RWMA does not accurately predict PE. RV pressure overload, however, does “flatten” the interventricular septum, thus reducing left-sided filling and CO. The subsequent reduction of coronary perfusion as well as the structural and inflammatory changes in the myocardium can additionally lead to LV dysfunction. A low ejection fraction (EF) is an independent predictor of death. In addition to the diagnosis of PE, echocardiography can aid in assessing the effectiveness of treatment. If a thrombus is visualized at presentation, continuous assessment of the thrombus during thrombolytic administration can show resolution of the clot and return of normal RV function. Echocardiography can also be useful in following the return of RV function over longer periods of time.

Left Ventricular Hypocontractility

Although LV dysfunction has many potential causes, the echocardiographic manifestations are similar. The SCA recommended a qualitative estimation of the LVEF when assessing candidates who may benefit from inotropic therapy. Visual estimation, or “eyeballing,” has been validated with Simpson’s biplane method, three-dimensional echocardiography, and radionuclide angiography. In addition, visual estimation of LV function can be accurately performed by noncardiologists and clinicians with only limited training. The primary method of visual estimation of LV contractility is through the FAC as seen in the TG LV midpapillary SAX view. The LV FAC is calculated by measuring the LV end-systolic and end-diastolic areas (LVESA and LVEDA, respectively) in the LV SAX view and using the following equation: [LVEDA − LVESA]/LVEDA. The normal values are similar to the normal values for EF. Initially, the calculation should be performed to assess contractile function. However, with more experience (≈≥20 studies), a visual estimate is reliable. However, in patients with regional dysfunction, the TG LV midpapillary SAX view may miss some pathologic features. A brief, qualitative assessment of the left ventricle in the four-chamber, two-chamber, and LAX views to look for hypokinetic walls aids in the diagnosis. Particular attention should be paid to the apex because it contributes a significant portion of the overall EF.

When LV dysfunction is encountered, it is important to identify myocardial ischemia as the mechanism quickly because early revascularization improves outcomes. The echocardiographic manifestations of myocardial ischemia occur earlier and are more sensitive than the electrocardiogram (ECG), even in anesthetized patients. Segmental wall thickening of less than 30% suggests ischemia and can manifest within seconds. Distinguishing between new-onset RWMAs and hypokinesis from chronic ischemia can be difficult. Intraoperative pharmacologic stress testing is ideal, but it is often not practical in the urgent setting. Acute ischemia therefore must be diagnosed by a change in RWMA from baseline by two grades (e.g., from normal to severe hypokinesis) in two or more segments. Infarcted myocardium often appears thinner and brighter than surrounding tissue and is therefore easily distinguished from myocardium with acute ischemia. Complications of ischemia such as acute diastolic dysfunction, mitral regurgitation, and papillary muscle rupture can also aid in the diagnosis.

In addition to LV ischemia, the stress, inflammation, and catecholamine excess associated with acute illness can reduce LV contractility. Potentially reversible secondary cardiomyopathies can develop in patients with numerous noncardiac critical illnesses. Sepsis-induced cardiomyopathy, for example, may occur in more than half of patients, with sepsis as a result of inflammatory mediators, bacterial endotoxins, catecholamines, and microcirculatory dysfunction. LV and RV dysfunction ensues, with global and RWMAs, as well as worsening measures of diastolic function. The myocardial toxicity from excess catecholamines, whether through septic shock, drug administration, or stress, can also induce LV dysfunction. Stress-induced cardiomyopathy, also known as takotsubo cardiomyopathy, is a form of catecholamine-mediated ventricular dysfunction induced by physical or emotional stress. Takotsubo cardiomyopathy most often manifests with normal to hyperkinetic basal function and hypokinesis of the apex, likely secondary to an increased density of β-adrenergic receptors in the apex. The LV apex often appears to “balloon” out, and this is the most prominent feature found on echocardiography.

Left Ventricular Hypercontractility and Left Ventricular Outflow Tract Obstruction

An often overlooked consequence of a hyperdynamic left ventricle, whether secondary to low afterload, hypovolemia, or inotropic support, is dynamic LVOT obstruction (LVOTO). Although often associated with hypertrophic cardiomyopathy, LVOTO has been reported in the setting of hypertension, type 1 diabetes, myocardial ischemia, pheochromocytomas, takotsubo cardiomyopathy, valvular replacements and repairs, and catecholamine administration. The mechanism of LVOTO remains unclear and varies by cause. The primary mechanism likely results from localized increases in flow velocity during ejection that results from a narrow LVOT from LV thickening or hypovolemia. This change causes the anterior mitral leaflet and chordae to be drawn toward the septum through both a Venturi effect and a hydrodynamic “drag.” This process distorts the mitral leaflet coaptation and results in middle to late systolic mitral regurgitation. Precipitating factors that further narrow the LVOT include hypovolemia, sepsis, inotropic agents, and diuretic agents. LVOTO should be considered in any hemodynamically unstable patient with risk factors for LVOT narrowing whose hemodynamic status worsens with inotropic support.

On echocardiographic examination, the left ventricle likely appears underfilled and hypercontractile. LV hypertrophy of varying degrees and morphologic features may be present. It is often possible to see movement of the anterior leaflet of the MV toward the upper septum in the ME LAX view ( Fig. 10.8 ). CFD may show mitral regurgitation with an anteriorly directed jet that begins in middle to late systole. CFD may also show turbulent flow in the LVOT ( Fig. 10.9 ). This finding is often the initial indicator of altered ejection dynamics in LVOTO. The hallmarks of LVOTO are a dagger-shaped spectral Doppler pattern in the LVOT and midsystolic closure of the AV. Early systolic ejection is usually normal because it takes time for the flow velocity to build. Obstruction occurs late in ventricular contraction, thus causing flow to diminish transiently and resulting in partial closure of the AV. M-mode interrogation of the AV in the ME LAX view shows a “notch” indicating midsystolic partial closure of the AV with a secondary opening. In addition, this dynamic property of the obstruction yields a late-peaking continuous-wave Doppler pattern as the gradient tends to develop in middle to end systole, producing a dagger shape ( Fig. 10.10 ). The peak velocity of the wave is high, consistent with an elevated pressure gradient. The gradient can be measured by tracing the waveform.

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