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Abstract
There are different approaches that prevent or lessen myocardial ischemia and insult during CABG. Those approaches include efficacy of surgical coronary revascularization and pharmacologically by modulating the myocardial oxygen supply-demand ratio for example with beta-adrenergic blockers, alpha 2 agonists, or calcium channel blockers.
One of the recent approaches for reducing perioperative ischemia is focusing on myocardial oxygen demand at the cellular or mitochondrial level to prepare the myocyte to tolerate longer time of ischemia and so less ischemic insults. This technique is called preconditioning.
Preconditioning of the myocardium was firstly described with ischemia. Laboratory and clinical investigations have demonstrated that single or multiple brief periods of ischemia are not necessarily deleterious and instead can be beneficial and protect the myocardium against subsequent prolonged ischemic insults. The brief period of ischemia appear to precondition the myocardium against the reversible and irreversible tissue injury, including stunning, infarction and development of malignant arrhythmias. On the other hand, exposures of myocardium to volatile anesthetics induce similar cardioprotective effect against ischemia activating the same mediators and receptors of ischemic preconditioning (IPC), enhance and augment IPC. Anesthetic preconditioning (APC) is a well documented phenomenon with effective cardioprotection against ischemia in many experimental studies applied on different animal species, also on isolated human myocardium independent of improvement in oxygen demand -supply ratio. Recently, APC was reported with few clinical studies using different parameters to evaluate the preconditioning or the cardioprotective effect.
Some of intravenous anesthetics as propofol have negative effect against APC and others as midazolam have neutral effect. Mechanisms of APC involve three stages: 1- the primary stimuli as stimulation of adenosine A 1, opioid and adrenergic receptors and release of bradikinin, NO and ROS .2-Amplification of primary stimuli and linking to the KATP channels as G protein, Phospholipases and protein kinase C. 3- Activation of sarcoplasmic KATP and mitochondrial KATP channels which are the end effector of the APC and IPC.
Aim of the work: evaluation of cardioprotective effect (APC) of sevoflurane against ischemia induced by aortic crossclamping in comparison to propofol in coronary artery bypass graft surgeries
Methodology: this study was conducted on 38 patients admitted to National Heart Institute undergoing elective coronary artery bypass graft surgeries (CABG). Patients were randomly equally allocated to one of two groups (19 /group): Sevoflurane G (G1) and Propofol G (G2) Inclusion criteria involved patient age between40-60 years, both sexes, ejection fraction more than 40%, procedures with cardiopulmonary bypass (CPB) and aortic cross clamping applied on patients with two or three coronary vessels diseases. Exclusion criteria involved, patients with repeated coronary surgery, concurrent valve repair or aneurysm resection, ABG initiated on beating heart even followed with CPB, patients treated with theophylin or oral antidiabetics , preoperative cTnT level ≥ 0.01 ng /ml and patients with history of esophageal varices . In G1 Sevoflurane was used for induction and maintenance of general anesthesia and in G2 propofol was used for induction and maintenance. In both group, induction was achieved with bolus of fentanyl 8-12 ug /kg slowly, lidocaine 1, 5 mg /kg, propofol (titration with maximum dose 2mg/kg) or sevoflurane (2-3 %) titration and endotracheal intubation was obtained with 0.1 mg/kg pancronium i.v. Maintenance in both groupG1 and with fentanyl boluses 100-200 ug i.v. In G1, with sevoflurane 0.5-2% and in G2 with propofol infusion at (100-200) ug /kg/min titrated according to ABP as needed. Nitroglycerine infusion 1-2 ug /kg /min were administered in both. Procedure was achieved with full heparinzation, CPB, systemic hypothermia 30 0C, aortic crossclamping, cold crystalloid cardioplegia. During bypass anesthesia was maintained with propofol. After separation from the bypass, using the transoesophageal doppler cardiac output and systemic vascular resistance was assessed. If CI was lower than 2.2 L/kg/min adrenaline support was applied (adrenaline infusion starting with 50 ng /kg/min and increased according to response) with correction of hpyovolemia. If there SVR was lower than 1000 dyn.s.cm-5 vasopressors (noradrenaline) was used. Measurements: 1) Hemodynamic data, MAP, HR, CVP, and by the transoesophageal Doppler, CI), SVR. Data were recorded at different times: before induction (basal), before the start of CPB (pre), 15 min after the end of the CPB (post), before discharge from theater (End). 2) The pattern of recovery of the myocardium after the bypass was assessed by the need for cardiac support by; (a) number of patients needed cardiac support and (b) adrenaline infusion rate. 3) ECG finding suggesting ischemia (S-T segment elevation or depression. 4) Incidence of Ventricular fibrillation (after crossclamping off). 5) Cardiac troponin T level, before induction (basal), 6 hrs after cross-clamping (T6), 12 hrs after cross-clamping (T12) .Cardiac troponin T >0.01 ng /ml was considered positive. 6) Time of cross clamping and CPB was recorded.
Results : There was no statistical significant difference between both group regarding demographic data (age ,sex height ,BSA, ) ,preoperative medications , diseases or echo findings ,time of CPB time and aortic crossclamping or number of coronary grafts. There was no statistical significant difference between both groups regarding HR, MAP, SVRI or CVP. There was no statistical significant difference between both group regarding ventricular fibrillation or ECG ischemic changes. Post bypass-CI in G1 (2.6±0.3 L/min/m2) was statistically significantly higher than in G2 (2.1±0.1 L/min/m2) There was high statistical significant difference between both group. P value = (0.0009) < 0.001. Average of adrenaline support in G1 was (75 ±25 ng /kg/min) and in G2 was (150 ± 50 ng/kg/min) with high statistical significant difference between both group, p value = (0.0001) < 0.001 . Number of patients who received adrenaline support in G1 was 8(42% ) and in G 2was 13 ( 68% ) with statistical significant difference between both group , p value =( 0.0128 ) < 0.5 . At T6, cTnT in G1was 1.1± .1 ng /ml and in G2 was 1.8 ±.2 ng/ml with high statistical significant difference between both group, p value = (0.0004) < 0.05. At T12, cTnT in G1was 4.2± .4 ng / ml and in G2 was 6.3± .7 ng / ml with high statistical significant difference between both group, p value = (0.0002) <0 .0001.