Tissue velocities are given in Figure 2. Before surgery, reduced preload caused no significant change in E′max septal (P = 0.39), while there was significant reduction in E′max lateral (0.7 ± 0.03 cm s−1, P < 0.01). Elevated preload produced a significant increase in both E′max septal (0.7 ± 0.04 cm s−1, P < 0.001) and E′max lateral (1.5 ± 0.4 cm s−1, P < 0.001). After surgery, reduced preload did not produce significant changes in either E′max septal (P = 0.15) or in E′max lateral (P = 0.10). Elevated preload produced a significant increase in E′max septal (1.2 ± 0.04 cm s−1, P < 0.01), and marginally significant in E′max lateral (P = 0.06). Tissue velocities in both the septal and lateral portion of the mitral annulus were significantly higher when preload was increased, compared to when it was decreased.
There were no statistical differences when comparing the alterations in tissue velocities associated with preload interventions before and after surgery (P = 0.11 for E′max septal and P = 0.37 for E′max lateral, when comparing Trendelenburg with anti-Trendelenburg position before and after surgery).
There were no significant correlation between diastolic tissue velocities and PAOP. For E′max septal before and after surgery P values were 0.08 and 0.95 and r-values were 0.28 and 0.01, respectively. For E′max lateral before and after surgery P values were 0.22 and 0.54 and r-values were 0.2 and 0.1, respectively.
In the present study tissue velocities were altered during preload alterations in patients in general anaesthesia undergoing coronary surgery. When tissue velocities were compared between the Trendelenburg position and the anti-Trendelenburg position we found significant differences in tissue velocities in the septal and the lateral portion of the mitral annulus, both before and after surgery.
Conventional Doppler echocardiography has become the principal tool in assessing diastolic function in daily practice. Doppler measurements of the mitral inflow signal together with flow patterns of the pulmonary vein and 2D echocardiography have reasonable accuracy in assessment of diastolic function, but in many cases the information from these Doppler indices will be inconclusive. This method is affected by most haemodynamic factors, included preload  and is therefore difficult to interpret in the perioperative period due to rapid changes in preload, afterload and contractility.
The search for preload independent means to quantify diastolic function has lead to increased interest in tissue velocities, which selectively detect myocardial wall velocities. Movement of the mitral annulus reflects changes in LV long-axis dimension because the cardiac apex is relatively fixed during the cardiac cycle. In absence of great distortion of the ventricular shape or severe regional wall motion abnormalities, changes in long-axis dimensions could reflect LV volume. This method is of value in differentiating between constrictive pericarditis and restrictive cardiomyopathy  and between hypertrophic cardiomyopathy and athlete's hearts and LV hypertrophy due to hypertension . Additionally, the method can detect regional LV dysfunction during ischaemia  and has better accuracy than conventional echocardiography when global systolic function is not affected .
Several investigators have found TDE to be preload independent. Sohn and colleagues  studied the effects of preload alterations on E′ max in the medial portion of the mitral annulus in patients with normal and abnormal diastolic function. They found no significant changes in E′ max medial during volume infusion (500–700 mL saline) in awake patients with known relaxation abnormalities (defined by mitral inflow variables) or during nitroglycerin in awake patients with normal LV systolic and diastolic function. Accordingly, Nagueh and colleagues  found no relationship between E′ max and PAOP in patients with different types of heart diseases. In heart transplant recipients Aranda and colleagues  found TDE to be preload independent during interventions with nitroglycerin.
In recent years several studies in conscious human beings and animals indicate that TDE measurements are preload dependent. Dumesnil and colleagues  found a significant reduction of E′ max in the lateral portion of the mitral annulus during the Valsalva procedure in conscious human beings with and without impaired relaxation (defined by mitral inflow variables). By using the Valsalva procedure, Pei-Ying and colleagues  also concluded that TDE velocities are preload dependent in conscious healthy human beings. However, the effects of the Valsalva procedure were not verified by pressure measurements. Dincer and colleagues  evaluated the effects of haemodialysis on TDE measurements in the lateral, medial, posterior and anterior portion of the mitral annulus and found significant reductions in velocities in all measured sites after haemodialysis (500–4300 mL extracted).
All these studies are performed on conscious human beings. Different preload interventions are used and many are inaccurate regarding changes in end-diastolic volume. Firstenberg and colleagues  tested the hypothesis that tissue velocities are insensitive to acute alterations in preload in healthy dogs during anaesthesia and positive-pressure ventilation. Caval occlusion via balloon catheter was used for preload interventions. Volumetric calculation of end-diastolic and end-systolic volumes was obtained by electrical impedance calibrated by 2D echocardiography and TDE was measured in the medial portion of the mitral annulus. They found that E′ max is preload depended and that E′ max is modulated by the rate of LV relaxation. Preload dependency seems less strong when diastolic function is impaired. Accordingly, Nagueh and colleagues , in patients with heart diseases, and Jacques and colleagues , in anaesthetized dogs, also found that preload dependency for tissue velocities is reduced when LV relaxation is impaired.
To our knowledge the present study is the first to investigate preload dependency for tissue velocities in patients in general anaesthesia undergoing coronary surgery. It should be noted that two of the patients had aortic valve replacement in addition to coronary surgery. This may alter the characteristics of the ventricle. However, these two patients did not qualitatively affect the data. During general anaesthesia almost all aspects of the cardiovascular system are affected. The patients in the present study were given isoflurane, diazepam, fentanyl, thiopental and pancuronium. Isoflurane leads to decreased systemic vascular resistance , depressed baroreceptor reflexes  and reduced myocardial contractility . Barbiturates predominant cardiovascular effect is venodilatation followed by pooling of blood in the periphery , while myocardial contractility is depressed to a lesser extent than after volatile agents . Diazepam reduces systemic vascular resistance and slightly depresses the baroreceptor reflex . Opioids blunt significant haemodynamic responses to noxious stimuli and produces minimal myocardial depression, with minimal decreases in preload and afterload, little depression of great vessels and atrial baroreceptors and no effect on coronary vasomotion . Pancuronium usually produces a moderate increase in HR, and to a lesser extent cardiac output, with small or no changes in systemic vascular resistance [22,23].
Our data confirm and extend findings previously obtained in awake human beings [8–10] and anaesthetized animals [6,7], indicating that tissue velocities are not preload independent and that there are no relationship between filling pressure and tissue velocities . E′ max shows preload dependency in both the septal and lateral mitral annulus in anaesthetized human beings undergoing cardiac surgery. We also found that tissue velocities are preload dependent in the early postsurgery period. Yalcin and colleagues  reported that TDE was not significantly altered during preload alterations (Trendelenburg, anti-Trendelenburg and inhalation of amyl nitrate) in awake patients with chronic ischaemic syndrome. General anaesthesia, as discussed above, and positive-pressure ventilation, which will affect venous return and cardiac function directly, are the two most apparent causes for this discrepancy.
In the present study the absolute changes in tissue velocities are relatively small (≈20%) seen in relation to the huge variations in RAP and PAOP (>10 mmHg). It should be noted that all our patients were on β-blockade. In anaesthetized dogs, Firstenberg and colleagues  has demonstrated that β-blockade blunts the preload dependency for tissue velocities. The fact that the effects of preload on tissue velocities are less pronounced in models of diastolic dysfunction [4,6,7] might also contribute to the small alterations in E′ max seen in our patients, as all of our patients either were on medication or had coexisting diseases that affect the diastole (Table 1).
We found that velocities in the septal portion of the mitral annulus are lower than in the lateral portion of the mitral annulus. This finding is consistent with findings in healthy conscious patients . In our study population, all patients have stenosis in the left anterior descending artery (LAD). This fact may also contribute to the lower velocities in the septal compared to the lateral portion of the mitral annulus.
This study was performed in a clinical setting on patients scheduled for elective coronary surgery. All patients in the study were monitored with a PAC. We used tilting of the operation table as preload interventions and RAP and PAOP as indicators of the preload changes. The patients were first examined in flat supine position, then in a state of decreased preload and finely in a state of increased preload. RAP and PAOP do not reflect changes in fibre length or changes in end-diastolic volume in all situations . One can alter end-diastolic volume without detecting it in the end-diastolic ‘pressure’ parameters used. This may partly explain why we found preload dependency in tissue velocities (compared within the individual patient), but detected no significant correlation between PAOP and tissue velocities (comparison at three PAOP levels for the 15 patients). All patients had a period of physiologic stabilization between the interventions. Examinations were obtained by TOE and measurements were made both in the septal and lateral portion of the mitral annulus. The most frequent alteration of preload in surgical patients is hypovolaemia. To ensure a normovolaemic state prior to the first part of the experiment, we gave a Ringer acetate infusion of 0.5 mL kg−1 h−1 of fasting.
We conclude that tissue velocities of the mitral annulus are preload dependent in patients in general anaesthesia both before coronary arterial bypass surgery and in the early postsurgery phase.
The authors thank the staff at the surgical and anaesthesiological departments, Feiring Heart Clinic and especially R. Salamanka for valuable technical assistance during the study. During the practical part of the study A. A. Jonassen had a fellowship financed by Feiring Heart Clinic.
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Keywords:© 2007 European Society of Anaesthesiology
ANAESTHESIA GENERAL, SURGERY CARDIAC; CORONARY ARTERY BYPASS; ECHOCARDIOGRAPHY DOPPLER; MYOCARDIAL CONTRACTION