Failure of methylprednisolone to protect myocardial function or prevent myocardial edema following ischemic cardiac arrest.
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Biomedical subjects
Publications and source records attributed to V L Gott.
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Myocardial performance in the immediate postoperative period was studied 49 cardiac surgical patients treated with nitroprusside alone. With a thermodilution catheter positioned in the pulmonary artery, cardiac output was calculated and cardiac index, systemic vascular resistance index, and stroke work index were derived before after treatment with nitroprusside. The drug was a administered to all patients because of elevated systemic vascular resistance index. Based on their mean arterial pressure and cardiac index before treatment, the patients fell into two groups. Group I patients (N = 25) had elevated mean arterial pressure and normal cardiac index. Group II patients (N = 24) had normal mean arterial pressure and subnormal cardiac index. Nitroprusside administration resulted in a significant reduction of systemic vascular resistance index in all patients. In Group I the mean arterial pressure was lowered significantly while cardiac index increased only slightly. In Group II there was no change in arterial pressure, but cardiac index improved significantly. The results not only confirm that nitroprusside is effective in managing postoperative hypertension, but also demonstrate that in patients with postoperative left ventricular failure, the drug can improve cardiac output by reducing systemic vascular resistance without significantly lowering arterial blood pressure.
To assess the effects of moderate potassium cardioplegia (37 mEq/l KCl) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and 1 hour after ischemic arrest. Normothermia (37 degrees C) was maintained in the remaining 16 hearts, eight without KCl and eight with KCl. Hypothermia (27 degrees C) was maintained in the remaining 16 hearts, eight with KCl and eight without KCl. Myocardial oxygen (PmO2) and carbon dioxide tensions (PmCO2) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO2 compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 +/- 6% of control and max dP/dt = 99 +/- 5% of control). These data suggest that the beneficial effects of postassium cardioplegia and 27 degrees hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO2 correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.
Previous investigators have suggested that calcium may play a role in the pathogenesis of myocardial cell damage following ischemia and reperfusion. Twenty-six in-situ blood perfused isovolumic canine preparations were divided into four groups. Group I dogs were maintained normocalcemic during 45 min of reperfusion following 45 min of hypothermic (27 degrees C) ischemic arrest; Group II dogs received CaCl2 (7 mg/kg) after 15 min of reperfusion; Group III dogs received citrate solution (0.8 ml/kg citrate-phosphate-dextrose [CPD]) after 15 min of reperfusion; Group IV dogs received 7 mg/kg of CaCl2 at 5 min after receiving the same citrate dose as Group III after 15 min of reperfusion. In Group II hearts, calcium improved the left ventricular contractility (P < 0.05 vs Group I) without causing additional cellular or subcellular injury. Calcium also appeared to increase myocardial stiffness (alpha(n)) compared to Group I hearts (P < 0.01). In Group III hearts, citrate reduced contractility (P < 0.01 vs Group I) and increased myocardial edema (P < 0.005 vs Group I) without any apparent improvement in cellular or subcellular preservation. In Group IV hearts, calcium reversed the depression of contractility caused by citrate, resulted in no additional morphologic injury, increased myocardial stiffness compared to Group I or Group III (P < 0.005), and minimized myocardial edema (P < 0.005 vs Group I or III). These results suggest that calcium administered after 15 min of reperfusion improves the depression of contractility that follows hypothermic ischemic arrest without causing additional myocardial damage.
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The effect of pulsatile cardiopulmonary bypass on intramyocardial gas tensions and regional myocardial blood flow was studied in 10 mongrel dogs. Following application of a critical stenosis to the circumflex coronary artery (CIRC), animals were placed on total bypass with vented, fibrillating hearts. During three 45 minute periods of perfusion, animals alternately received pulsatile or linear flow with perfusion pressure carefully maintained at 80 mm. Hg. In myocardium supplied by the stenosed CIRC, intramyocardial oxygen tension (PO2) rose from 13 +/- 3 to 19 +/- 5 mm. Hg when a period of linear flow was followed by a period of pulsatile flow (p less than 0.025). Similarly in the CIRC-supplied area, intramyocardial carbon dioxide (PCO2) decreased from 128 +/- 12 to 99 +/- 12 mm. Hg (p less than 0.005) with conversion from linear to pulsatile flow. Myocardial blood flow (microsphere technique) to endocardial and epicardial layers of the CIRC-supplied area was significantly greater (p less than 0.05) during pulsatile than during linear perfusion. In contrast, when periods of pulsatile bypass were followed by periods of linear perfusion, myocardial PO2 fell from 25 +/- 6 to 9 +/- 3 (less than 0.02) and myocardial PCO2 rose from 82 +/- 12 to 154 +/- 12 mm. Hg (p less than 0.001). These data suggest that (1) fibrillation-induced regional ischemia distal to a critical coronary stenosis can be reduced by pulsatile perfusion during bypass and (2) the mechanism for the reduction in regional ischemia is improved myocardial blood flow.
In a randomized prospective study of patients having cardiac surgery, autologous blood collected from mediastinal tubes was autotransfused preferentially in 63 patients (ATS), whereas 51 patients received bank blood for transfusion (control). Comparison of the two groups showed no significant difference in regard to age, sex, operations performed, or total postoperative bleeding (ATS 813 +/- 121 ml. per square meter versus control 711 +/- 93 ml. per square meter; N.S.) Although mean postoperative blood replacement was similar in the two groups (ATS 4.3 +/- 0.6 units per patient versus control 4.8 +/- 0.6 units per patient), requirements for transfusion of stored bank blood were reduced by 50 percent in the ATS group (ATS 2.4 +/- 0.3 units per patient versus control 4.8 +/- 0.6 units per patient; p less than 0.005). Coagulation studies demonstrated that this blood was defibrinogenated; yet it contains significantly more platelets and clotting factors than does bank blood. In this study, autotransfusion of shed mediastinal blood was safe and simple. It significantly reduced bank blood requirements and resulted in substantial financial savings for the patients and the hospital.
The extent of myocardial protection afforded by a procaine cardioplegic solution during cardiac ischemia has been evaluated and compared with the protection seen using a potassium cardioplegic solution. An isolated cat heart model was employed, and ventricular function parameters, intramyocardial gas tensions, and postischemic myocardial edema were measured and compared following 60 minutes of induced ischemia at 37 degrees C. and 27 degrees C. There was no significant improvement in recovery of postarrest ventricular function when procaine cardioplegia was used during normothermic ischemia. When used at 27 degrees C., however, both cardioplegic solutions were associated with significantly better recovery of postarrest ventricular function, although there was less myocardial edema formation in the potassium-treated hearts. Results of this study indicate that procaine-induced cardioplegia provides myocardial protection during anoxic cardiac arrest which is additive to that afforded by hypothermia alone. In addition, procaine cardioplegia results in postarrest functional recovery which is similar to that seen with potassium cardioplegia.
Myocardial carbon dioxide tension and intramyocardial S-T segment voltage have previously been shown to provide useful quantitative indexes of the severity of regional myocardial ischemia. This study was designed to determine if (1) changes in intramyocardial S-T segment voltage and myocardial gas tensions, with the addition of atrial pacing, could be used to assess the functional significance of a coronary stenosis, and (2) if changes in S-T voltage recorded in intramyocardial electrodes proved a more sensitive indicator of ischemia than changes recorded in epicardial electrodes. In 12 open chest dogs, a variable constrictor and an electromagnetic flow probe were placed on the proximal left circumflex coronary artery. Myocardial carbon dioxide and oxygen tensions were recorded with mass spectrometry and unipolar intramyocardial S-T segment voltage with multicontact plunge electrodes. Intramyocardial S-T voltage and myocardial carbon dioxide tension showed parallel increases with atrial pacing in the presence of subcritical, critical and supercritical coronary stenoses. In the presence of a critical stenosis, S-T segment changes recorded in deepr myocardial layers were of greater magnitude than those recorded near the epicardial surface. These findings suggest that the severity of myocardial ischemia can be assessed by measuring intramyocardial S-T voltage or myocardial gas tensions at resting and paced heart rates. They also suggest that intramyocardial S-T voltage is a more sensitive indicator of the severity of pacing-induced myocardial ischemia than epicardial S-T changes. Application of this technique to patients undergoing coronary revascularization could allow intraoperative determination of the functional significance of questionable angiographic lesions and a more rational approach to the assignment of priorities to individual arteries when multiple bypasses are being considered.
From 1966 to 1976 a flexible, heparin-coated shunt was used for operative procedures on the thoracic aorta and great vessels in 25 patients aged 15 to 78 years. Twenty patients had resection of aneurysms of the descending thoracic aorta. There was 1 death in 15 patients undergoing elective resection and 2 deaths (both from rupturing aneurysms) in 5 patients having emergency resection. The shunt was used in 5 patients who had procedures involving involving the great vessels. There have been no complications attributable to the shunt in either group. The advantages of this shunt include elimination of the need for systemic heparin, avoidance of hypertension during cross-clamping, and adequate perfusion of the distal cirulation without an interposed pump. Because of the ease of handling, low risk, and versatility, we consider the use of this shunt the preferred method for support in elective procedures of the thoracic aorta and great vessels.
Changes in myocardial carbon dioxide (PmCO2) and oxygen tension (PmO2) measured by mass spectrometry have been shown to reflect quantitatively progressive degrees of regional myocardial ischemia associated with stepwise reduction in coronary blood flow. The present study utilized mass spectrometry to assess the severity of regional myocardial ischemia developing during atrial pacing in the presence of a flow-limiting proximal critical coronary artend subendocardial layers was measured by the radioactive microsphere technique. Application of a "critical stenosis" resulted in a 6-mmHg decrease in PmO2 and a 17-mmHg increase in PmCO2 in the region of the myocardium supplied by the stenosed vessel. The addition of atrial pacing resulted in a 3-mmHg further decrease in Pmo2 and a 40-mmHg further increase in PmCO2. In the region of myocardium supplied by the critically stenosed vessel MBF increased in the subepicardial layer, but decreased or remained unchanged in the subendocardial layer. The failure of myocardial blood flow to increase in deeper myocardial layers in response to the increased myocardial oxygen demand of atrial pacing would provide a mechanism for the development of subendocardial ischemia in the presence of a critical coronary stenosis.
A patient with an aneurysm of the ascending aorta and calcific stenosis of a congenital bicuspid aortic valve, whose brother also had a stenotic congenital bicuspid aortic valve, is described. Predominant aortic stenosis at cardiac catheterization and the presence of an aneurysm distal to and not including the aortic valvular ring made the initial diagnosis of Marfan's syndrome unlikely. Cystic medial necrosis present in the aneurysmal wall probably arose as a consequence of poststenotic dilation. Adequate noninvasive evaluation of the ascending aorta requires echocardiographic studies, as well as a chest x-ray film.
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Left ventricular (LV) aneurysms were resected in 27 patients for treatment of congestive heart failure and in five patients for treatment of ventricular arrhythmia. There were eight early (25 per cent) and five late (15 per cent) deaths. Preoperative hemodynamics including analysis of left ventriculograms in the right anterior oblique position did not consistently predict survival. In contrast, coronary artery anatomy appeared to influence the mortality rate strikingly in patients with congestive heart failure. The hospital mortality rate was 6 per cent and the late mortality rate was 13 per cent for 16 patients with one-or two-vessel coronary artery disease, but with unobstructed LV lateral wall blood supply. All but one of the survivors obtained a good late result. In nine patients with two-and three-vessel coronary artery disease and obstructed LV lateral wall blood supply there were six hospital deaths and two late deaths. It is concluded that the presence or absence of occlusive disease in the arteries supplying the LV lateral wall is an important determinant of the mortality rate associated with resection of anterior apical LV aneurysms in patients with severe congestive heart failure.