Perioperative echocardiography-guided hemodynamic therapy in high-risk patients: a practical expert approach of hemodynamically focused echocardiography

If cardiac filling is impaired by pericardial effusion/tamponade as shown in Fig. 1 ("obstructive shock"), evacuation (interventional or surgical) has the highest priority. Not only in the cardiac surgery setting, but also due to trauma or due to chronic disease, a relevant accumulation of fluid in the pericardium can occur. Within the "Focused Assessment with Sonography in Trauma" algorithm (FAST) the orienting visualization of all four heart chambers with the possibility of visualizing pericardial effusion is therefore an integral part of initial trauma assessment [36‐39]. Echocardiographic signs of hemodynamically relevant pericardial effusions with a given clinical history and/or symptomatology may include: identification of pericardial effusion with consecutive hypovolemia of all heart chambers, collapse of the right cardiac chambers and/or dilatation of the inferior vena cava (SIVC). When using a TTE, the S4C view should be used, while for TEE, the ME4C should be used initially.

Once any immediate impairment of cardiac filling has been ruled out, the second step is to estimate the volume status/responsiveness of the patient, as both hypo- and hypervolemia can reduce SV and thus DO₂. To assess the volume status, the 4-chamber views (4C) as well as the short axis views (SAX) at the level of the papillary muscles are suitable for obtaining a quick overview.

Although resting diameters for cardiac chambers are gender and body surface area specific [40], the size of the left ventricle (LV) and the right ventricle (RV) should be measured with regards to overall volume status. An end-diastolic left ventricular diameter (LVEDD) of 35–55 mm may reflect normal LV and a basal RV diameter ≤ 41 mm may reflect normal RV size. Qualitatively, substantial hypovolemia may be identified by the “kissing papillary muscle” sign of the corresponding ventricle. This sign is best witnessed during the systolic period, whereby the opposite myocardial walls of the associated ventricle come in contact with one another. Occasionally, hypovolemia will aggravate a dynamic flow obstruction in the left ventricular outflow tract (LVOT) in case of LV hypertrophy. It should be noted, that a pronounced concentric hypertrophy as evidenced by a myocardial wall thickness of > 14 mm (i.e., due to severe aortic stenosis or as primary disease as displayed in Fig. 2) must be excluded prior to the diagnose of hypovolemia [41]. In addition, a preoperative dilated LV (e.g. LVEDD 65 mm) with a reduced global systolic function may be interpreted as “hypovolemic” if the LVEDD is within normal range (e.g. LVEDD 50 mm) and DO₂ is reduced.

With regards to atrial volume status, a visual assessment of the interatrial septum (IAS) in the 4-chamber views (4C, ME4C) can be used for qualitative estimation of atrial filling pressures. During states of low bi-atrial filling such as during global hypovolemia, a hypermobile IAS is commonly observed. With increasing left atrial filling pressure, the IAS appears permanently convex to the right (as displayed in Fig. 3), whereas with increased right atrial filling pressure, the IAS appears permanently convex to the left atrium in combination with left cardiac hypovolemia [42]. In the context of global hypervolemia, all heart chambers appear "overfilled” or “stretched" and the IAS is usually fixated in the middle [43, 44].

Volume status/responsiveness can be estimated by measuring the superior vena cava (SVC) via TEE or the inferior vena cava (IVC) via TTE as shown in Fig. 4. The SIVC diameter and its respiratory variation may be used to estimate right atrial filling pressure [45]. The normal diameter for the SIVC is < 21 mm in awake and spontaneously breathing patients [46]. Due to the increased intrathoracic pressure exerted during mechanical inspiration, venous return is reduced and the IVC distends ("SIVC-Distensibility index, DI") [47]. The more pronounced the intravascular hypovolemia, the greater the volume responsiveness, thus the greater the IVC distensibility [48]. An SIVC-DI of > 18% in controlled ventilated septic patients indicated a positive volume response with an increase in cardiac output (CO) after fluid resuscitation [49‐53]. In patients with preserved spontaneous respiration, sufficient sensitivity and specificity of the SIVC-DI can also be achieved [54]: the patient is asked to inhale deeply once and exhale passively afterward, while an ultrasound measurement is continuously recorded. An SIVC diameter variability of ≥ 48% represents a positive volume responsiveness. The same is also possible with TEE using the SVC collapse index (SVC-CI) [55]. Due to the intrathoracic position, the SVC will be compressed during mechanical inspiration. Here, a SVC-CI > 36% indicates a positive volume responsiveness. However, like many other methods, these easy-to-determine quantitative variables are subject to individual cut-off variations (e.g. SIVC-DI "grey zone" 8—30%) [53, 56‐59]. Therefore, in addition to the quantitative determination of these two indices, the approach shown in Table 1 may be helpful in deciphering the measurements taken from the SIVC/SVC [60‐62]. Again, physicians have to interpret echocardiographic findings in the clinical context: fluid substituon will be indicated in a trauma patient with low blood pressure, overall small heart chambers and a small vena cava inferior.

Taken together from a clinical point of view, one has to differentiate between (a) “global” hypovolemia (i.e. all heart chambers are reduced in size due to a significant reduction in total circulating blood volume—additional fluid substitution will lead to an increase in SV), (b) “relative” hypovolemia (i.e. all heart chambers appeared to be “normally” filled, however, additional fluid substitution may cause an increase in SV—“volume responsiveness”) or (c) “partial” hypovolemia (i.e. LV hypovolemia in case of RV failure). In the latter, fluid substitution will mostly not be effective in increasing left ventricular SV because of the incapability of the RV to transport the blood forward into the pulmonary circulation and left heart, thus worsening RV cogestion. The determination of the exact hypovolemic cause will be detrimental in defining the amount and type of fluid resuscitation necessary.

A restricted RV function is associated with increased perioperative mortality [63‐65]. In addition, as already mentioned, a sufficient LV function depends on a sufficient preload provided by the RV [66]. Therefore, the morphology and function of the RV should be assessed prior to LV assessment [67].

In addition to the points mentioned in step 2, this is achieved visually with the help of the volume/diameter relation between the right and left ventricle, the "RV/LV-Index". A normal ratio is ~ 0.6, an RV/LV index ≥ 1.0 indicates a severe RV dilatation as shown in Fig. 5 [68].

In case of RV dysfunction, hypertrophy of the free right ventricular wall (> 5 mm) may indicate a chronic disease process [69]. The thickness of the right ventricular wall is best measured from subcostal at the level of the anterior tricuspid valve tip under recess of trabeculae and papillary muscles. Alternatively, measurement of the thickness of the right ventricle may be performed in the PLAX [45].

Contractility of the RV is visually assessed in the 4-chamber views. With a normal RV function, the free RV wall should move inwards [45]. For simple quantitative evaluation of the RV function, the amount of systolic movement of the lateral tricuspid valve annulus towards the apex (Tricuspid Annular Plane Systolic Excursion, TAPSE) can be used (Fig. 6). A TAPSE of ≥ 17 mm indicates normal systolic RV function [45]. If RV dilatation and systolic impairment are observed, this mostly reflects severe, and hemodynamic relevant RV dysfunction.

In addition to advanced diagnostics and consecutive therapy of the primary cause of RV dysfunction (e.g. lysis in pulmonary embolism or revascularization in RV infarction), hemodynamic optimization should aim at optimizing RV preload, ensuring coronary perfusion pressure, as well as inotropic support and pulmonary afterload reduction if indicated [67, 70‐73]. Importantly, optimizing RV preload must be performed with great caution to avoid volume overload. RV volume overload is detrimental not only for the contractile function of the RV, but also for coronary perfusion, venous, and intramural perfusion pressure of other organs such as the kidney. Furthermore, LV output is dependent upon the physiological geometry of the RV and the septum. Hence, RV overloading can displace the interventricular septum towards the LV (“paradoxical septum shift”), thereby restricting LV contractility. If the required therapeutic interventions are not successful, extracorporeal support—if available—may be considered [72, 74]. If the RV is assessed as "non-dilated, normal systolic function", hemodynamically relevant RV dysfunction is excluded and one can proceed to step 4.

In the fourth step, the LV should now be assessed in an analogous manner to the RV with regard to size and global systolic function (see also steps 2 and 3). The left ventricular ejection fraction (LVEF) is determined to quantify global systolic function. For normal clinical concerns, however, a qualitative assessment of the LVEF ("eye balling") may be equivalent to a quantitative [75]. The transthoracic parasternal short axis view (PSAX) or the transgastric central papillary short axis view (TGSAX) as well as 4-chamber views (4C or ME4C) allow for a quick orientation (Fig. 7) [76].

If the LV appears non-dilated with normal systolic function (LVEF > 50%), relevant systolic LV dysfunction is excluded. However, isolated diastolic LV dysfunction (Heart failure with preserved ejection fraction, HFpEF) may be present, thereby affecting overall hemodynamic functioning [77]. Evaluation of diastolic function is outside of the scope of a hemodynamic focused echocardiography. If diastolic dysfunction is suspected, an expert consultation should be made in order to guide further diagnostics and therapy [78]. Qualitatively, a pronounced dilation of the left atrium (LA) in conjunction with a “stiff” and/or hypertrophied LV with normal systolic function in a breathless patient may be related to HFpEF [79]. In symptomatic patients LV afterload should be reduced and fluid substitution should be restricted [24, 80].

In the case of a non-dilated LV with slightly to moderately reduced global systolic function (heart failure with mid-range ejection fraction (HFmrEF), LVEF 40–49%), cardiac preload should be optimized and inotropic support may be administered to improve DO₂ [74, 81]. In a dilated LV with severely reduced global systolic function (heart failure with reduced ejection fraction (HFrEF) with LVEF < 40%) an intensified inotropic therapy in conjunction with preload optimization is indicated in situations of hemodynamic instability. A vasopressor may be considered in case of cardiogenic shock with persistent hypoperfusion, despite treatment with an inotropic agent, to increase blood pressure and vital organ perfusion pressure [24]. If conservative therapy does not improve DO₂, mechanical support and/or implantation of a left ventricular microaxial pump may be discussed. Lastly, if (new) regional wall motion abnormalities are detected, specifically LV wall hypokinesia, akinesia or dyskinesia [82], this may hint at specific cause such as myocardial infarction or Takotsubo syndrome, which require specific diagnostic testing (e.g. electrocardiogram, cardiac enzymes, coronary angiography) and treatment.

Echocardiography allows for a comprehensive morphological and functional assessment of the heart valves. The visual and thus qualitative evaluation of valves in the hemodynamic focused examination is used to assess valve opening and closure as well as to recognize morphological abnormalities. Hemodynamic relevant valve dysfunction may be excluded if thin leaflets with a normal opening/closing and without turbulent flow in color Doppler have been determined in ≥ 2 cross-sectional views. If a thickened or calcified valve with a restricted opening is apparent, hemodynamic relevant stenosis may be suspected, especially in the case of antegrade flow accelerations/turbulences in color Doppler. In addition, hemodynamic relevant regurgitation might be suspected if an exaggerated leaflet motion or visuable coaptation defect during valve closing is observed in conjunction with a wide, turbulent colour jet (“vena contracta”) depicting significant backward flow (Fig. 8) [34]. However, in case of hemodynamically relevant valve abnormalities in the focused examination, a detailed evaluation should be carried out immediately by a certified examiner [83‐85].

Transthoracic and transesophageal echocardiography are capable of rating cardiac output, although discontinuously, using continuous-wave (cw) Doppler across the left ventricular outflow tract (LVOT) / aortic valve (AV) measuring the velocity time integral (VTI) (Fig. 9) [86]. Prior to this, aortic stenosis must be excluded (see Step 5). A VTI of 18–22 cm indicates normal stroke volume, whereas a VTI < 18 cm is suspective of decreased stroke volume and > 22 cm of an increased one [86]. In a prospective observational study Mercado et al. found out that in critically ill mechanically ventilated patients the transthoracic echocardiography was an accurate and precise method for estimating cardiac output [87]. In contrast, amongst patients undergoing cardiac surgery, echocardiography is not interchangeable with cardiac output monitoring by pulmonary catheter thermodilution [88]. Thus, after and/or simultaneously to initial echocardiographic evaluation, a continuous hemodynamic monitoring should be implemented in hemodynamic unstable patients to assess therapeutic success. In patients with refractory shock associated with a right ventricular dysfunction, a pulmonary artery catheter in addition to echocardiography is recommended [89]. Most other conditions may be monitored by transpulmonary thermodilution [90].