CARDIOVASCULAR ANESTHESIA Section Editor Joseph G . Reves
Effect of Preoperative Normovolemic Hemodilution on Left Ventricular Segmental Wall Motion During Abdominal Aortic Surgery Patrick Catoire, MD, Michel Saada, and Francis Bonnet, MD
MD,
Ngai Liu,
MD,
Laurent Delaunay,
MD,
A. Rauss,
Dkpartement d’anesthesie Reanimation, HBpital Henri Mondor, Crkteil, France
Preoperative normovolemic hemodilution (PNH) has been proposed for patients scheduled to undergo aortic surgery. Coronary artery disease is frequent in these patients. The aim of the study was to assess the effect of PNH on hemodynamics and segmental wall ‘motion (SWM) evaluated by transesophageal echocardiography in such patients. Twenty patients with coronary artery disease were allocated randomly to either PNH or no PNH; PNH was performed after anesthetic induction using dextran 60,000. Patients were operated on under general anesthesia and monitored intraoperatively with electrocardiographic lead CM,, radial and pulmonary artery catheters, and transesophageal echocardiography positioned to obtain a short-axis view. Hemodynamic and transesophageal echocardiographic data were collected after anesthetic induction and after PNH, before and 5 min after aortic clamping, after unclamping, and at
P
reoperative normovolemic hemodilution (PNH) has been proposed to avoid homologous blood transfusion in patients scheduled to undergo aortic surgery (1,2). Hemodilution decreases blood viscosity and may also improve oxygen delivery to tissues in these patients (3). However, patients who undergo abdominal aortic surgery frequently have coronary artery disease (CAD) (4),and CAD classically contraindicates PNH on the basis of results of experimental studies (5,6).Nevertheless, animal studies fail to document any sigruficant negative effect of hemodilution on myocardial ischemia (7,8), and human studies do not in fact confirm the deleterious effect of PNH in
Supported by a grant from the Delegation a la Recherche Clinique de YAssistance Publique-Hopitauxde Paris, Paris, France. Accepted for publication July 2, 1992. Address correspondence to Dr. Bonnet, Departement d’Anesthesie Rkanimation, HBpital Henri Mondor, 51, avenue du Markchal de Lattre de Tassigny, 94010 CrCteil, France.
654
Anesth Analg 1992;75:654-9
the end of surgery. Aortic clamping induced a significant increase in systemic vascular resistance and arteriovenous difference in oxygen and a decrease in cardiac index ( P < 0.05), but the effect of aortic clamping was inversely related to hemodilution. The SWM score (graded from 1 = normal to 5 = dyskinesia) was significantly increased after aortic clamping, mainly in the anterior segment (P < 0.05). Four patients in the control (no PNH) group and one in the PNH group developed new S W M abnormalities indicative of myocardial ischemia during surgery ( P = NS). This study suggests that PNH may improve hemodynamic tolerance to aortic clamping in patients with coronary artery disease. The observed changes in S W M indicate that PNH may not worsen myocardial ischemia in patients scheduled to undergo aortic surgery. (Anesth Analg 1992;75:65&9)
patients with CAD. Laxenaire et al. (9) showed that in patients with CAD undergoing PNH for peripheral arterial disease, myocardial perfusion evaluated with thallium scintigraphy was not impaired. Recent studies performed during coronary artery bypass surgery showed that as much as 15%normovolemic hemodilution is well tolerated by the myocardium (10,ll). Van der Linden et al. (12) showed that global myocardial function is preserved after PNH for abdominal aortic surgery (AAS).Patients undergoing AAS are likely to develop intraoperative myocardial ischemia and hemodynamic disturbances owing to clamping and unclamping of the aorta (13). Segmental wall motion (SWM) and wall-thickening abnormalities have been shown to be sensitive, early indices of myocardial ischemia, and transesophagealechocardiography (TEE) easily detects these changes (14). The current study was therefore conducted in such patients to assess the effect of PNH on hemodynamics and SWM during AAS, hypothesizing that PNH may not worsen myocardial ischemia. 01992 by the International Anesthesia Research Society 0003-2!399/92/$5.00
ANESTH ANALG 1992:75654-9
Methods After approval by our hospital ethical committee and informed consent were obtained, all patients with CAD scheduled for infrarenal AAS were eligible for the studv. The diagnosis of CAD was made if the patient met at least one of the following criteria: 1. Presence of typical angina pectoris; 2. A documented previous myocardial infarction (Q waves on the ECG and increase in creatinine phosphokinase isoenzymes at the time of occurrence); 3. Ischemic ST segments (STsegment depression of 1.0 mm or ST segment elevation of 2.0 mm at 60 ms of the J point) or Q waves on the ECG; 4. A positive exercise treadmill test; 5. Fixed or reversible defect on dipyridamole thallium-201 angioscintigraphy; 6. Significant stenosis (>75%) of at least one main coronary artery on coronary arteriography.
Exclusion criteria were the absence of CAD as previously defined, a hematocrit 30% segment shortening; 2 = mild hypokinesia (slightly reduced thickening and 10%-30% segment shortening); 3 = severe hypokinesia ( 4 0 % segment shortening and minimal thickening); 4 = akinesia (no thickening and no segment shortening); 5 = dyskinesia (wall thinning and no shortening of the segment). An increase of more than one grade, or a change from grade 4 to 5, was considered indicative of ischemia (14). Interobserver discrepancies defined as an SWM evaluation of more than one grade difference were resolved by a third experienced echocardiographer. During the postoperative period, ischemic events were defined by new Q waves or ischemic ST segment changes on ECG, by a creatinine kinase level >350 IU/mL, with a percentage of creatine kinase-MB >6%. The PNH was performed after anesthetic induction before surgery. Blood withdrawal and compensation were done at the same time using two antebrachial venous 16-gauge catheters each inserted in a different arm. Final expected hematocrit was 30%. To achieve this, the volume of harvested blood was determined from initial hematocrit and body weight. All the hematocrits were measured by a cooximeter (Radiometer-Copenhagen, Denmark). The final hematocrit was verified and the hemodilution continued until the hematocrit reached 30%. Compensation was achieved using dextran 60,000 (Hemodex).AIIergic reaction was prevented by the administration of 3 g of dextran 1000 (Promit). Dextran 60,000 infusion was restricted to 75% of the circumflex artery
Effect of Preoperative Normovolemic Hemodilution on Left Ventricular Segmental Wall Motion During Abdominal Aortic Surgery Patrick Catoire, MD, Michel Saada, and Francis Bonnet, MD
MD,
Ngai Liu,
MD,
Laurent Delaunay,
MD,
A. Rauss,
Dkpartement d’anesthesie Reanimation, HBpital Henri Mondor, Crkteil, France
Preoperative normovolemic hemodilution (PNH) has been proposed for patients scheduled to undergo aortic surgery. Coronary artery disease is frequent in these patients. The aim of the study was to assess the effect of PNH on hemodynamics and segmental wall ‘motion (SWM) evaluated by transesophageal echocardiography in such patients. Twenty patients with coronary artery disease were allocated randomly to either PNH or no PNH; PNH was performed after anesthetic induction using dextran 60,000. Patients were operated on under general anesthesia and monitored intraoperatively with electrocardiographic lead CM,, radial and pulmonary artery catheters, and transesophageal echocardiography positioned to obtain a short-axis view. Hemodynamic and transesophageal echocardiographic data were collected after anesthetic induction and after PNH, before and 5 min after aortic clamping, after unclamping, and at
P
reoperative normovolemic hemodilution (PNH) has been proposed to avoid homologous blood transfusion in patients scheduled to undergo aortic surgery (1,2). Hemodilution decreases blood viscosity and may also improve oxygen delivery to tissues in these patients (3). However, patients who undergo abdominal aortic surgery frequently have coronary artery disease (CAD) (4),and CAD classically contraindicates PNH on the basis of results of experimental studies (5,6).Nevertheless, animal studies fail to document any sigruficant negative effect of hemodilution on myocardial ischemia (7,8), and human studies do not in fact confirm the deleterious effect of PNH in
Supported by a grant from the Delegation a la Recherche Clinique de YAssistance Publique-Hopitauxde Paris, Paris, France. Accepted for publication July 2, 1992. Address correspondence to Dr. Bonnet, Departement d’Anesthesie Rkanimation, HBpital Henri Mondor, 51, avenue du Markchal de Lattre de Tassigny, 94010 CrCteil, France.
654
Anesth Analg 1992;75:654-9
the end of surgery. Aortic clamping induced a significant increase in systemic vascular resistance and arteriovenous difference in oxygen and a decrease in cardiac index ( P < 0.05), but the effect of aortic clamping was inversely related to hemodilution. The SWM score (graded from 1 = normal to 5 = dyskinesia) was significantly increased after aortic clamping, mainly in the anterior segment (P < 0.05). Four patients in the control (no PNH) group and one in the PNH group developed new S W M abnormalities indicative of myocardial ischemia during surgery ( P = NS). This study suggests that PNH may improve hemodynamic tolerance to aortic clamping in patients with coronary artery disease. The observed changes in S W M indicate that PNH may not worsen myocardial ischemia in patients scheduled to undergo aortic surgery. (Anesth Analg 1992;75:65&9)
patients with CAD. Laxenaire et al. (9) showed that in patients with CAD undergoing PNH for peripheral arterial disease, myocardial perfusion evaluated with thallium scintigraphy was not impaired. Recent studies performed during coronary artery bypass surgery showed that as much as 15%normovolemic hemodilution is well tolerated by the myocardium (10,ll). Van der Linden et al. (12) showed that global myocardial function is preserved after PNH for abdominal aortic surgery (AAS).Patients undergoing AAS are likely to develop intraoperative myocardial ischemia and hemodynamic disturbances owing to clamping and unclamping of the aorta (13). Segmental wall motion (SWM) and wall-thickening abnormalities have been shown to be sensitive, early indices of myocardial ischemia, and transesophagealechocardiography (TEE) easily detects these changes (14). The current study was therefore conducted in such patients to assess the effect of PNH on hemodynamics and SWM during AAS, hypothesizing that PNH may not worsen myocardial ischemia. 01992 by the International Anesthesia Research Society 0003-2!399/92/$5.00
ANESTH ANALG 1992:75654-9
Methods After approval by our hospital ethical committee and informed consent were obtained, all patients with CAD scheduled for infrarenal AAS were eligible for the studv. The diagnosis of CAD was made if the patient met at least one of the following criteria: 1. Presence of typical angina pectoris; 2. A documented previous myocardial infarction (Q waves on the ECG and increase in creatinine phosphokinase isoenzymes at the time of occurrence); 3. Ischemic ST segments (STsegment depression of 1.0 mm or ST segment elevation of 2.0 mm at 60 ms of the J point) or Q waves on the ECG; 4. A positive exercise treadmill test; 5. Fixed or reversible defect on dipyridamole thallium-201 angioscintigraphy; 6. Significant stenosis (>75%) of at least one main coronary artery on coronary arteriography.
Exclusion criteria were the absence of CAD as previously defined, a hematocrit 30% segment shortening; 2 = mild hypokinesia (slightly reduced thickening and 10%-30% segment shortening); 3 = severe hypokinesia ( 4 0 % segment shortening and minimal thickening); 4 = akinesia (no thickening and no segment shortening); 5 = dyskinesia (wall thinning and no shortening of the segment). An increase of more than one grade, or a change from grade 4 to 5, was considered indicative of ischemia (14). Interobserver discrepancies defined as an SWM evaluation of more than one grade difference were resolved by a third experienced echocardiographer. During the postoperative period, ischemic events were defined by new Q waves or ischemic ST segment changes on ECG, by a creatinine kinase level >350 IU/mL, with a percentage of creatine kinase-MB >6%. The PNH was performed after anesthetic induction before surgery. Blood withdrawal and compensation were done at the same time using two antebrachial venous 16-gauge catheters each inserted in a different arm. Final expected hematocrit was 30%. To achieve this, the volume of harvested blood was determined from initial hematocrit and body weight. All the hematocrits were measured by a cooximeter (Radiometer-Copenhagen, Denmark). The final hematocrit was verified and the hemodilution continued until the hematocrit reached 30%. Compensation was achieved using dextran 60,000 (Hemodex).AIIergic reaction was prevented by the administration of 3 g of dextran 1000 (Promit). Dextran 60,000 infusion was restricted to 75% of the circumflex artery
