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Canadian Journal of Anesthesia 53:168-173 (2006)
© Canadian Anesthesiologists' Society, 2006
Cardiothoracic Anesthesia, Respiration and Airway

Acute diastolic dysfunction in thoracoabdominal aortic aneurysm surgery

[Dysfonction diastolique aiguë pendant l’opération d’un anévrysme aortique thoraco-abdominal]

Ashraf Fayad, MD*, Homer Yang, MD*, Howard Nathan, MD*, Gregory L. Bryson, MD* and Claudio S. Cina, MD{dagger}

* From the Department of Anesthesia, University of Ottawa; and the
{dagger} Department of Surgery, McMaster University, Hamilton, Ontario, Canada.

Address correspondence to: Dr. Ashraf Fayad, Department of Anesthesia, University of Ottawa, B309, 1053 Carling Avenue, Ottawa, Ontario K1Y 4E9, Canada. Phone: 613-761-4940; Fax: 613-761-5209; E-mail: afayad{at}ottawahospital.on.ca


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: To report transesophageal echocardiographic (TEE) findings consistent with intraoperative acute diastolic dysfunction in a series of patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair.

Methods: A series of nine consecutive patients underwent TAAA repair with intraoperative TEE monitoring. Surgical repair was performed with the adjunct of a left atrio-femoral bypass. Invasive arterial and venous pressures were monitored. Intraoperative TEE was utilized to assess the diastolic function before, and during aortic cross clamping. Diastolic dysfunction was defined as a mitral inflow pulsed wave Doppler (E: A ratio) < 1.

Results: All patients demonstrated an E: A ratio > 1 (1.3 ± 0.08) before aortic cross clamping. During cross clamp, the E: A ratio decreased to < 1 (0.75 ± 0.05) in six of nine patients consistent with diastolic dysfunction. The three patients who did not develop E: A changes were receiving ß-blockers pre-operatively. Patients with diastolic dysfunction were treated with nitroglycerin infusions, which resulted in restoration of their E: A ratios > 1 (1.2 ± 0.09). Three of the patients with intraoperative diastolic dysfunction developed postoperative myocardial infarction.

Conclusions: Chronic diastolic dysfunction is a well-known entity. This report describes acute diastolic dysfunction, which was observed frequently in patients undergoing TAAA during aortic cross clamp. Further research is required to confirm this phenomenon and determine its possible association with increased postoperative cardiac morbidity.


   Introduction
TOP
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
DIASTOLIC dysfunction is the inability of the left ventricle (LV) to relax, an energy-requiring step which is related to intracellular calcium metabolism.1 It is a well-recognized problem in patients with high after-load, e.g., hypertension or aortic stenosis. "Diastolic dysfunction is present in virtually all patients with systolic dysfunction; however, diastolic dysfunction can be present without systolic dysfunction."2 Nearly half of patients with congestive heart failure have diastolic dysfunction despite a normal ejection fraction,3 suggesting that the left ventricular systolic and diastolic function may be uncoupled.4,5 As a result, many traditional monitors of cardiac systolic function may not reflect the extent of diastolic dysfunction. In thoracoabdominal aortic aneurysm (TAAA) repair, there is a significant increase in the afterload upon application of the aortic cross clamp. The acute impact of the aortic cross clamp on the left ventricular diastolic function has not been described previously.

Echocardiography plays a unique role in allowing the non-invasive measurement of intracardiac flows and velocities to assess diastolic function. An analysis of echocardiographic Doppler mitral inflow (E: A ratio), pulmonary venous flow, deceleration time (DT) and isovolumic relaxation time allows assessment of the severity of diastolic dysfunction.6 Intraoperative measurement of diastolic function during TAAA repair using transesophageal echocardiography (TEE) is a challenging task. This is due to the patient’s position, the busy and limited environment at the head of the patient, and the rapid resuscitation maneuvers required at the time of aortic clamping. In this study, a simplified approach was used to assess diastolic function by measuring the mitral inflow waves (E: A ratio) before, and immediately after application of the aortic cross clamp.

The purpose of this study was to document the possible occurrence of acute diastolic dysfunction secondary to aortic cross clamping, identified by TEE in patients undergoing TAAA repair.


   Methods
TOP
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
This was a prospective cohort study of consecutive patients undergoing TAAA repair in a tertiary vascular centre with TEE monitoring between March 2003 and June 2004. After obtaining Research Ethics Board approval and patient consent for publication of personal health information, demographics, characteristics, medications, type of aneurysm (Crawford Classification),7 comorbid diseases and the preoperative cardiac investigations were recorded. Intraoperative changes in systolic and diastolic function, as assessed by TEE, were documented during aortic cross clamping.

There were two anesthesiologists for each case, one performing the intraoperative TEE, the other attending to the anesthetic. All patients received a standard volatile anesthetic technique supplemented by sufentanil 3 to 5 µg·kg–1 iv. Hemodynamic measurements included pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), right radial artery (proximal) pressure, right femoral artery (distal) pressure, and intracranial pressure measured through a lumbar cerebrospinal fluid drainage catheter.

Patients were positioned in the right lateral decubitus position. A left bronchial blocker was inserted to facilitate one-lung ventilation. Surgical exposure was achieved through a posterolateral thoracoabdominal incision and excision of the fifth rib. The left atrium was cannulated through the left upper pulmonary vein while the left femoral artery was cannulated with a femoral cannula to complete the left atrio-femoral bypass (LAFB) circuit. The normothermic LAFB flow was adjusted to maintain a proximal mean pressure of 60 mmHg. Details of the sequential repair with the LAFB, anesthesia, transfusion technique and cooling procedure for renal preservation have been reported elsewhere.8–11

A Vivid 3® echocardiography device (GE Medical Systems, Mississauga, ON, Canada) was used in this study. The TEE probe was inserted in the supine position after induction of anesthesia. Midesophageal and transgastric views were obtained in the right decubitus position. A transgastric short axis view was used to monitor the LV volume status and to detect any wall motion abnormalities. Mitral inflow waves were measured in the midesophageal four-chamber view using the conventional pulsed wave Doppler, by sampling at the level of the open mitral leaflets in diastole. The E: A ratio was measured manually before aortic cross clamping, at the time of application of the cross clamp, and every three minutes for 15 min, thereafter. The colour flow Doppler was used to help align the sample. The sweep speed was 50 mm·sec–1 A valsalva maneuver up to 30 cm H2O was applied whenever E:A ratio was > 1 to rule out a "pseudonormal" pattern. In keeping with the Canadian consensus guidelines,12 diastolic dysfunction in this study was defined as the inversion of the E: A ratio (E: A ratio < 1). Patients with impaired LV relaxation were treated with nitroglycerin infusion started at 2 µg·kg–1·min–1 and titrated to maintain the proximal mean arterial pressure > 60 mmHg. All patients were followed during the course of their stay in the intensive care unit (ICU). A 12-lead electrocardiogram was preformed on arrival at the ICU and repeated as required if ischemia was suspected. Troponin-T levels were measured immediately after ICU admission and every six hours for 48 hr, thereafter. A myocardial infraction was diagnosed when troponin-T levels exceeded 0.5 µg·L–1

Continuous variables were described with mean and standard deviation. Dichotomous variables were described as proportions.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Data from the nine consecutive patients who under-went TAAA repair with TEE monitoring are reported. There were five males and four females, aged 58 to 79 yr (mean 67 ± 5). Three had a type I aneurysm (involving the descending thoracic aorta) and six had a type II aneurysm (involving the entire descending aorta). Three patients were on ß-blockers, three were taking angiotensin converting enzyme inhibitors, and three were receiving diuretics. Preoperatively, all patients had LV function grade I (ejection fraction > 60%) or II (40–59%) with no significant coronary artery disease as determined by echocardiography and coronary angiography (Table IGo). With intraoperative TEE, it was possible to confirm the correct position of the left atrial cannula and measure mitral inflow E: A ratios in all patients. No technical difficulty was encountered in obtaining midesophageal or transgastric echocardiography views. However, some manipulations were required to obtain the relative views due to the lateral decubitus position.


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  		TABLE I Demographics and comorbidities of patients with acute diastolic dysfunction
 
Before aortic cross clamping, all patients demonstrated a normal pattern of mitral inflow with an E: A ratio > 1 in the four-chamber and the two-chamber midesophageal views (mean 1.3 ± 0.08). The E: A ratio remained unchanged with the application of the valsalva maneuver. Three to ten minutes after application of the aortic cross clamp, six patients (three females and three males; three with type I and three with type II TAAA) experienced a decrease in their E: A ratio (0.75 ± 0.05) consistent with acute impairment of LV relaxation. There were no changes on PAP, CVP, or PCWP during the episodes of diastolic dysfunction (Table IIGo). In addition, no wall motion abnormalities were detected during the acute diastolic dysfunction. Figure 1Go provides an example of acute diastolic dysfunction occurring during aortic clamping.


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  		TABLE II Measurement of intraoperative hemodynamics and outcomes
 

Figure 1
Figure 1
Figure 1
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  		FIGURE 1 Mitral inflow pulsed wave Doppler midesophageal four-chamber view in a patient who underwent thoracoabdominal aortic aneurysm repair and developed diastolic dysfunction during cross clamping.

FIGURE 1A Normal mitral inflow pulsed wave Doppler (E: A ratio > 1) before aortic cross clamping.

FIGURE 1B Decreased mitral inflow pulsed wave Doppler (E: A ratio < 1) during cross clamping.

FIGURE 1C Restoration of mitral inflow pulsed wave Doppler (E: A ratio) with a nitroglycerin infusion during cross clamping.

 
Patients with impaired LV relaxation were treated with nitroglycerin infusions, which resulted in normalization of the E: A ratio (1.2 ± 0.09) within two to seven minutes after initiation of the infusion. A graphical summary of E: A ratio changes is displayed in Figure 2Go.


Figure 2
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  		FIGURE 2 Changes in the mitral inflow pulsed wave Doppler ( E: A ratio) in the nine patients who underwent thoracoabdominal aortic aneurysm (TAAA) repair. Pre: before aortic cross clamping, post: during aortic cross clamping and NTG = with the nitroglycerin infusion. The dark dots represent the mean of the E: A ratios in patients with diastolic dysfunction during cross clamping.

 
Three of the patients with intraoperative diastolic dysfunction developed postoperative myocardial infarction based on increased serum troponin-T levels > 0.5 µg·L–1 None of the three patients who were receiving ß-blockers preoperatively developed intraoperative diastolic dysfunction or postoperative myocardial infarction.


   Discussion
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
In this cohort study, six of nine consecutive patients undergoing TAAA repair had a decrease of mitral inflow E: A ratio to < 1 during aortic cross clamp, consistent with acute diastolic dysfunction. This phenomenon was sudden in onset and reversible with nitroglycerin infusion. There were no changes in systolic function according to the echocardiographic LV transgastric images. In an animal study, diastolic LV dysfunction was induced by the application of the aortic cross clamp resulting in an elevated afterload in healthy hearts. This was determined by an elevation of the LV end-diastolic pressure and alteration in the LV pressure – internal diameter relationship.13

Diastolic function is assessed with Doppler echo-cardiography by measuring several parameters including mitral inflow waves, pulmonary venous flow, isovolumetric relaxation time (IVRT) and the DT. A typical Doppler transmitral blood flow velocity profile has a biphasic pattern. An initial peak velocity (E-wave) occurs during early diastolic filling, and a later peak flow velocity (A-wave) occurs during atrial systole. Normally, the flow velocity during early diastole is greater than that during atrial systole (E: A ratio is greater than 1). In patients undergoing TAAA repair with LAFB, the mitral inflow pattern was maintained while the pulmonary venous flow Doppler pattern was disturbed. Turbulent flow resulting from cannulation of the left atrium or one of the pulmonary veins renders measurements of pulmonary venous flow invalid. Because of the busy environment at the patient’s head and the amount of time required to manipulate the TEE probe to obtain the respective diastolic parameters in such a short period, IVRT and DT were not measured in this study. We chose to simplify our approach and measure the transmitral flow (E: A) ratio as an indicator of diastolic function.

Recently, colour M-mode and Doppler tissue imaging have emerged as new modalities to provide a complementary role in the assessment of diastolic function. However, Doppler mitral inflow velocity derived variables remain the cornerstone of the evaluation of diastolic function.14

In patients with diastolic dysfunction, a previous study demonstrated four abnormal filling patterns based on E: A ratio and other diastolic parameters:15 mild or impaired relaxation pattern (E: A ratio < 1), moderate or pseudo normal pattern (E: A ratio > 1 < 1.5), reversible severe or reversible restrictive pattern (E: A ratio > 1.5) and fixed severe or fixed restrictive pattern (E: A ratio > 1.5). Diastolic dysfunction seen in this study was either a mild or impaired relaxation pattern in response to aortic cross clamping.

Previous echocardiography studies have suggested that diastolic dysfunction may contribute to perioperative hemodynamic instability and adverse outcome following cardiac surgery.16 In this series, three of six patients with intraoperative diastolic dysfunction developed postoperative myocardial infarction, suggesting that the new onset of diastolic dysfunction may predict adverse outcome. It is unclear if the resolution of diastolic dysfunction associated with nitroglycerin infusion represents improved coronary blood flow or changes in ventricular loading conditions.

Preoperative diastolic dysfunction is prevalent among cardiovascular surgical patients17 and identifying high-risk vascular patients preoperatively may allow for the institution of prophylactic therapeutic strategies. It is of interest that acute diastolic dysfunction was absent in all three patients taking ß-blockers in the present study. Further research is required to determine a possible association between ß-blockade and the absence of diastolic dysfunction.

While chronic diastolic dysfunction is a well-known entity, limited information is available regarding acute diastolic dysfunction. In this study, conventional Doppler mitral inflow velocities were used to measure diastolic function. This is the first report of a new onset, reversible E: A ratio < 1, identified by TEE during aortic clamping in TAAA repair. Further studies using all diastolic parameters in addition to the newer Doppler techniques, which are less sensitive to intraoperative preload changes, will be needed to confirm this phenomenon. The prognostic significance of intraoperative acute diastolic dysfunction and the potential influence of perioperative ß-blockade are intriguing, and warrant further observational and interventional research.


   Footnotes
 
Accepted for publication June 20, 2005. Revision accepted September 13, 2005.


   References
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Bonow RO, Udelson JE. Left ventricular diastolic dysfunction as a cause of congestive heart failure. Mechanisms and management. Ann Intern Med 1992; 117: 502–10.[Medline]

2 Sigurdsson G, Rovner A, Thomas JD, Savage RM. Diastolic dysfunction in the perioperative setting. In: Savage RM, Aronson S (Eds). Comprehensive Textbook of Intraoperative Transesophageal Echocardiography. TK, Lippincott Williams and Wilkins; 2005: 171–85.

3 Vasan RS, Larson MG, Benjamin EJ, Evans JC, Reiss CK, Levy D. Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction. Prevalence and mortality in a population-based cohort. J Am Coll Cardiol 1999; 33: 1948–55.[Abstract/Free Full Text]

4 Bella JN, Palmieri V, Liu JE, et al. Relationship between left ventricular diastolic relaxation and systolic function in hypertension. The Hypertension Genetic Epidemiology Network (HyperGEN) Study. Hypertension 2001; 38: 424–8.[Abstract/Free Full Text]

5 Inouye I, Massie B, Loge D, et al. Abnormal left ventricular filling: an early finding in mild to moderate systemic hypertension. Am J Cardiol 1984; 53: 120–6.[Medline]

6 Yamada H, Goh PP, Sun JP, et al. Prevalence of left ventricular diastolic dysfunction by Doppler echocardiography: clinical application of the Canadian consensus guidelines. J Am Soc Echocardiogr 2002; 15: 1238–44.[Medline]

7 Crawford SE, Crawford JL, Safi HJ, et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 1986; 3: 389–404.[Medline]

8 Rakowski H, Appleton CP, Chan KL, et al. Canadian consensus recommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. J Am Soc Echocardiogr 1996; 9: 736–60.[Medline]

9 Cina CS, Irvine KP, Jones DK. A modified technique of atriofemoral bypass for visceral and distal aortic perfusion in thoracoabdominal aortic surgery. Ann Vasc Surg 1999; 13: 560–5.[Medline]

10 Cina CS, Bruin G. Acute normovolemic hemodilution (ANH) in surgery of the thoracoabdominal aorta. A cohort study to evaluate coagulation parameters and blood products utilization. J Cardiovasc Surg (Torino) 1999; 40: 37–43.[Medline]

11 Cina CS, Clase CM, Bruin G. Effects of acute normovolaemic haemodilution and partial exchange transfusion on blood product utilization, haemostasis and haemodynamics in surgery of the thoracoabdominal aorta. A cohort study in consecutive patients. Panminerva Med 2000; 42: 211–5.[Medline]

12 Cina CS, It SC, Clase CM, Bruin G. A cohort study of coagulation parameters and the use of blood products in surgery of the thoracic and thoracoabdominal aorta. J Vasc Surg 2001; 33: 462–8.[Medline]

13 Leite-Moreira AF, Correia-Pinto J, Gillebert TC. Afterload induced changes in myocardial relaxation: a mechanism for diastolic dysfunction. Cardiovasc Res 1999; 43: 344–53.[Abstract/Free Full Text]

14 Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician’s Rosetta stone. J Am Coll Cardiol 1997; 30: 8–18.[Abstract]

15 Khouri SJ, Maly GT, Suh DD, Walsh TE. A practical approach to the echocardiographic evaluation of diastolic function. J Am Soc Echocadiogr 2004; 17: 290–7.

16 Bernard F, Denault A, Babin D, et al. Diastolic dysfunction is predictive of difficult weaning from cardiopulmonary bypass. Anesth Analg 2001; 92: 291–8.[Abstract/Free Full Text]

17 Doolan LA, Jones EF, Kalman J, Buxton BF, Tonkin AM. A placebo-controlled trial verifying the efficacy of milrinone in weaning high-risk patients from cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1997; 11: 37–41.[Medline]





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