Cardiac output, coronary flow, ventricular fibrillation and survival following varying degrees of myocardial contusion (original) (raw)
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Journal of the American College of Cardiology, 1983
©1983 by the Amencan College of Cardiology in anatomic sections were analyzed and compared with those of remote normal-appearing regions. The contused region showed increased end-diastolic wall thickness and impaired regional systolic function. Further, there was a visible increase in the echo brightness in the contused region. Regional perfusion was normal and thus the functional impairment of the contused myocardium was not due to ischemia. Other abnormalities observed on the two-dimensional echocardiograms included pericardial effusion and discreteintramyocardial sonolucentzones due to hematomas. Contused myocardium can be identified on a twodimensional echocardiogram by 1) increased end-diastolic wall thickness, 2) increased echo brightness , and 3) impaired regional systolic function. Two-dimensional echocardiography can also demonstrate other complications of cardiac trauma such as intramyocardial hematoma and hemopericardium. can examine the entire heart in multiple tomographic plane s and ultrasonic equipment can easily be moved to and used in an emergency setting, two-dimensional echocardiography is potentially valuable in the evaluati on of cardiac trauma. The purpose of our study was to assess the usefulne ss of two-dimensional echocardiography in the diagnosis of myocardial contusion resulting from blunt chest trauma. Methods We used two-dimensional echocardiography in a canine model of myocardial contusion. Twenty-five mongrel dog s. weighing 14 to 28 kg. were studied. Animal preparation. The dogs were anesthetized with intravenous sodium pentothal (500 mg) and chloralose (100 mg/kg body weight), intubated and ventilated using a Har
Effects of Cardiac Contusion in Isolated Perfused Rat Hearts
Shock, 2003
Myocardial contusion is frequently suspected after blunt chest trauma, but the exact mechanisms of resulting cardiac dysfunction and the time course for enzymatic alterations have not yet been fully understood. Therefore, we investigated pathophysiological aspects of myocardial contusion in a controlled animal model. Male Wistar rat hearts were studied in an isolated perfusion model and were divided into two groups: control (n = 4) and heart contusion (n = 6) groups. The cardiac contusion was produced by a single blow with a weighted pendulum (m = 44 g, height = 20 cm). Functional implications of the contusion were examined in an "isolated perfused heart" model. Troponin 1 concentrations were determined in the perfusate. Cardiac contusion resulted in an increase of coronary perfusion pressure (CPP) of 9 mmHg (P < 0.05, 20 min postcontusion versus baseline and control), followed by a significant increase of left ventricular end-diastolic pressure (LVEDP) of 6 mmHg (P < 0.05, 20 min postcontusion versus baseline and control). Heart contusion was followed by an early increase of troponin 1 (+0.82 ng/mL). The troponin 1 concentration decreased again and, after 20 min, baseline levels were reached. The control group showed no such changes. In this model, high troponin1 levels after cardiac contusion suggest direct damage to the myocardium. First functional response was shown by the alteration of the coronary perfusion, followed by impaired diastolic function, which persisted even after lowering of the troponin 1 levels.
The Journal of Thoracic and Cardiovascular Surgery, 1989
Physical and mechanical effects of cardioplegic injection on flow distribution and myocardial damage in hearts with normal coronary arteries The physical and mechanical effects of injecting crystaDoid cardioplegic solution under various pressures and flows was studied (in canine hearts) to establish a safe method for administering it in the presence of normal coronary arteries. A constant pressure system (300 mm Hg = 15 psi) was maintained in the solution reservoir, and flows and pressures were varied with the use of cannulas of different inner diameters: 0.8, 1.35, 1.6, 2.3, 2.58, and 2.80 mm. Cardioplegia distribution was measured by 15~m radioactive microspheres. Peak flow rate, total flow, and mean flow rate per infusion were measured by an inIineelectromagnetic flowmeter probe. Direct aortic root pressure, time to standstiU, and myocardial temperatures were recorded by continuous monitoring. Cardiac isoenzymes were measured in the coronary sinus, peripheral blood, and directly in the myocardial tissue. Histologic changes 'in the left ventricle were examined by light microscopy. The results showed that the higher the flow and pressure, the shorter the prearrest period, the better the flow distribution, and the faster the myocardial temperature drop. Mean aortic root pressures higher than 110 mm Hg and peak flow rates greater than 1500 mljmin caused a higher incidence of mechanical-physical trauma to the vascular endothelium and the endocardium, but ceDuiar protection was good. Low pressure (less than 30 mm Hg) and peak flows (less than 125 mljmin) showed a higher incidence of cellular (myocardial) ischemia, focal necrosis, and uneven flow distribution. An aortic root pressure of 61 ± 5 mm Hg, a mean peakflow rate of 622 ± 52 mljmin, and a total flow of 600 mI for the first injection seem to offer the best cellular protection with minimal physical injury to the endothelium and endocardium for a mean canine heart weight of 236 gm.
Annals of the New York Academy of Sciences, 1969
The sudden onset of ischemia in myocardium is followed within a few seconds by a series of striking functional changes: The area becomes cyanotic; cooler; hydrogen accumulates; electrocardiographic changes appear; and, within 30 to 60 seconds, contraction ceases in the affected myocardium. These changes within the ischemic focus are directly related to the development of local anoxia, which causes the affected cells to shift from an aerobic to an anaerobic form of metabolism, resulting in a substantial decrease in energy production. Although injured and nonfunctional, these severely ischemic, markedly anoxic cells are viable and survive for a period of time. Early restoration of the coronary blood flow to an ischemic focus is followed by almost instantaneous restoration of aerobic metabolism and contractile function. However, if the period of ischemia is more prolonged, restoration of the blood supply is not followed by restoration of function, since the affected cells are either dying or dead. The severely ischemic viable cells are reversibly injured, whereas the severely ischemic dead cells are irreversibly injured. Our chief interest has been in determining what event or series of events within the cells dictates the onset of irreversible injury.'
The oxygen consumption paradox of “stunned myocardium” in dogs
Basic Research in Cardiology, 1990
The contractile state of the heart is a major determinant of myocardial oxygen consumption. Since regional myocardial contractility can be severely impaired following a transient coronary occlusion, post-ischemic myocardium is frequently assumed to consume less oxygen. To test this assumption, regional myocardial function and oxygen consumption were studicd in anesthetized dogs during 2 h of myocardial rcperfnsion following either a 15-min (Group I) or 4-h (Group I1) left anterior descending coronary artery occlusion. Both groups developed similar post-ischemic regional dysfunction characterized by paradoxical motion (negative shortening). Measured as a percent of baseline segment shortening, anterior wall function in Group I (n = 8) and Group II (n = 5) at 30 min of reperfusion was-33 _-4-11% and-34 _+ 16 % (p = NS) and at 120 min was-23-9 % and-40 + 16 % (p=NS). However, the two groups showed a marked difference in regional myocardial oxygen consumption during rcperfusion. Despite the abnormal wall motion, regional oxygen consumption in Group I at 30 and 120 min of reperfusion was unchanged from prc-ischcmic levels as measured as a percent of baseline: 104+20% (p=NS) and 111_+21% (p=NS). In contrast, regional oxygen consumption in Group II was markedly depressed from baseline at 30 and 120 min of reperfusion: 42 _+ 7 % (p < .01) and 40 _+ 8 % (p < .01). To determine whether the dissociation between regional myocardial oxygen consumption and function in Group I was related to mitoehondrial uncoupling, six additional dogs were studied. Tissue samples were obtained from post-ischemic myocardium after 120 min of reperfusion following a 15-rain coronary artery occlusion, and compared to non-ischemic myocardium. There were no differences in the in vitro mitochondrial respiratory rates or oxidative phosphorylation capacity between the post-ischemic and non-ischemic myocardinrn. Thcrefore, in the post-ischemlc myocardium, significant depressions in regional contractility may not be associated with falls in oxygen consumption. Following a 15-min coronary artery occlusion, the injured myocardium maintains a paradoxically high oxygen consumption with normal mitochondrial function despite decreased contractility and abnormal wall motion.
Effects of Acute Regional Myocardial Ischemia on Left Ventricular Function in Dogs
Circulation Research, 1970
The immediate functional deficit resulting from acute regional myocardial ischemia was evaluated in 40 anesthetized dogs. Ventricular function curves, maximum dp/dt, isovohimetric force-velocity curves, and peak systolic and resting diastolic length-tension curves were assessed at fixed heart rate and constant aortic pressure before and during occlusion of the anterior descending coronary artery 2 to 3 cm distal to its origin. Mild, moderate, or marked depression of the ventricular function resulted from occlusion of the anterior descending artery, depending upon the anatomy of the intercoronary collateral vessels. Maximum loss of function was apparent 2 minutes after occlusion, and was quantitatively reproducible by reocclusion after an intervening period of unobstructed flow. Resting diastolic length-tension relations were not significantly altered by occlusion of the anterior descending artery. In 12 dogs, force-velocity relations were determined during the inscription of ventricular function curves and in every instance when depressed function was evident from the ventricular function curve, the simultaneously determined forcevelocity curve also demonstrated impaired performance. At low preload levels, however, the force-velocity curves inscribed before and during occlusion of the anterior descending artery were not very dissimilar; with increasing ventricular volumes, the force-velocity curve inscribed during coronary artery occlusion progressively shifted downward and to the left of the control curve. Maximum velocity, however, appeared to be unchanged suggesting that this index of contractility is not a satisfactory method for assessing cardiac performance during acute regional myocardial ischemia.
Performance of the right ventricle under stress: relation to right coronary flow
Journal of Clinical Investigation, 1971
ventricular performance was studied relative to right coronary artery flow in the chloralose-anesthetized, open chest dog. The right coronary artery was cannulated for measurement and control of flow and pressure. Under control conditions, right coronary artery occlusion caused no change in cardiac output, or right and left ventricular pressures, although right ventricular contractile force fell markedly. With right coronary artery flow intact, incremental pulmonary artery obstruction caused a corresponding decline in cardiac output and elevation of right ventricular end-diastolic pressure with eventual total right ventricular failure and systemic shock. With right coronary artery occlusion, identical degrees of pulmonary artery obstruction resulted in more pronounced changes in cardiac output and right ventricular end-diastolic pressure with right ventricular failure occurring at a much lower level of right ventricular stress. However, with right coronary artery flow intact, the right ventricular decompensation induced by pulmonary artery obstruction, could be reversed by raising right coronary artery perfusion to levels above normal, thus increasing right ventricular performance and restoring cardiac output. We conclude that right ventricular failure and resultant systemic hypotension due to severe pulmonary artery obstruction can be reversed simply by right coronary artery hyperperfusion, and that, although a normally contractile right ventricular free wall is not essential to maintain cardiac performance at rest, during right ventricular systolic stress, overall cardiac performance becomes increasingly dependent on the right ventricle. The data further imply that increased myocardial impingement on right coronary artery flow dur