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Biomedical subjects

K J Elsperger

Publications and source records attributed to K J Elsperger.

16 recordsLinked to original sources
PubMed1990

The cardiac electrophysiology of postresuscitation hypokalemia in dogs.

Hypokalemia has been observed in man after out-of-hospital ventricular fibrillation and after cardioversion from ventricular tachycardia in the electrophysiology laboratory, and also in dogs following ventricular fibrillation (maximal effect 45-60 minutes after resuscitation). Since the electrophysiological effects of postresuscitation hypokalemia are unknown, we evaluated the effects of this hypokalemia on ventricular fibrillation thresholds (group 1) and on right ventricular effective refractory periods (group 2). In both groups, anesthetized dogs with normal hearts were divided into experimental animals that had 2 minutes of ventricular fibrillation followed by cardioversion without medications and control animals without ventricular fibrillation. In group 1, we measured serum potassium before ventricular fibrillation (or time 0 in control dogs) and then measured potassium and ventricular fibrillation threshold at 45, 60, 75, and 90 minutes after baseline. In group 2 animals we measured right ventricular effective refractory periods and serum potassium at baseline and sequentially from 7 to 180 minutes after resuscitation. In group 1, the maximum change in potassium from baseline was -0.8 +/- 0.3 mEq/L at 60 minutes after resuscitation as compared to -0.1 +/- 0.3 mEq/L in control animals at 60 minutes (P less than 0.01). At 60 minutes, ventricular fibrillation threshold was 8 +/- 3 mA in ventricular fibrillation animals and 7 +/- 3 mA in control animals (P = NS). In group 2 animals, the maximum change in serum potassium also occurred 60 minutes after resuscitation and was -0.8 +/- 0.3 mEq/L as compared to -0.2 +/- 0.2 mEq/L in control animals (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗
PubMed1989

Canine myocardial creatine kinase isoenzyme response to coronary artery occlusion.

The response of the myocardial creatine kinase system to acute coronary artery occlusion is not well defined. In the present study, we measured serial changes in myocardial creatine kinase and creatine kinase-MB activities after acute occlusion of the left anterior descending (LAD) coronary artery in 20 open-chest pentobarbital-anesthetized dogs. Tissue samples were obtained from both ischemic and nonischemic left ventricular myocardium at base line and 1-, 3-, and 5-h intervals after LAD occlusion and assayed for total creatine kinase and the isoenzymes creatine kinase-MM, and creatine kinase-MB. Total creatine kinase activity declined significantly in both the ischemic and the nonischemic tissue because of a decline in creatine kinase-MM activity. Concomitantly, creatine kinase-MB activity increased significantly in both the ischemic and the nonischemic tissue. These changes were observed when the duration of the LAD occlusion was 3 h or longer, but not when the duration of the occlusion was 1 h. Thus acute myocardial ischemia causes pronounced changes in the canine myocardial creatine kinase system. These rapid biochemical alterations occur both locally in ischemic tissue and remotely in nonischemic tissue.

Animals↗
PubMed1989

Postresuscitation electrolyte changes: role of arrhythmia and resuscitation efforts in their genesis.

Hypokalemia frequently occurs after resuscitation from ventricular fibrillation (VF) in man. To test the casual roles of VF and resuscitation variables in this electrolyte change, we studied six groups of dogs: VF with CPR and electrical cardioversion (n = 9), control dogs with no intervention (n = 9), CPR without arrhythmia (n = 5), electrical cardioversion without arrhythmia (n = 5), CPR and cardioversion without arrhythmia (n = 5), and rapid right ventricular pacing (n = 5) (pacing rate 374 +/- 68 beat/min; BP 79/52 mm Hg during pacing). Blood for K, Ca, Mg, and glucose analysis was collected before each intervention (or at baseline in control animals) and sequentially for 3 hr. Mg had a maximum change of 0.3 mEq/L in the VF group 7 min after resuscitation, but did not change in the other groups (p less than .005). Glucose had a maximum change of 79 mg/dl in the VF group 7 min after resuscitation but did not change in the other groups (p less than .005). Ca had a maximum decrease of 0.4 mg/dl in the VF group 15 min after resuscitation but did not decrease in the other groups (p less than .005). K had a maximum decrease of 0.8 mEq/L in the VF group 60 min after resuscitation, whereas decreases were less in the other groups (p less than .005). Thus, VF caused a rapid rise in Mg and glucose followed by a fall in Ca and K. These changes were independent of resuscitation efforts as well as the moderate hypotension induced by rapid right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of pretreatment with propranolol on potassium, calcium, and magnesium shifts after ventricular fibrillation in dogs.

Hypokalemia and other electrolyte changes have been observed after resuscitation from ventricular fibrillation. We studied the effect of propranolol on postresuscitation electrolytes in a canine model of ventricular fibrillation and cardiac resuscitation by randomizing 40 anesthetized dogs to four groups: ventricular fibrillation--no drug (VF), ventricular fibrillation--propranolol pretreatment (VF-prop), control-no drug (NoVF), control--propranolol (NoVF-prop). We measured serum electrolytes at baseline and periodically for 3 hours. In VF dogs, serum potassium decreased from 3.9 +/- 0.4 to 3.2 +/- 0.2 mEq/L 60 minutes after resuscitation (p less than 0.001). The decrease in potassium was prevented (p less than 0.001) by propranolol. Serum calcium decreased from 10.6 +/- 0.8 to 10.2 +/- 0.8 mg/dl in VF dogs 15 minutes after resuscitation (p less than 0.05); this decrease was not blocked by propranolol (p = NS). Serum magnesium increased from 1.5 +/- 0.2 to 1.8 +/- 0.1 mEq/L in VF dogs 7 minutes after resuscitation (p less than 0.001); this rise was partially blocked by propranolol (p less than 0.01). Serum glucose increased from 105 +/- 6 to 183 +/- 27 mg/dl in VF dogs 7 minutes after resuscitation (p less than 0.001); this increase was diminished by propranolol (p less than 0.001). Thus propranolol prevents the decrease in serum potassium after ventricular fibrillation in this canine model, providing evidence that postresuscitation hypokalemia is caused by the beta-adrenergic effects of catecholamines secreted in response to cardiac arrest. Propranolol blocks the rise in magnesium and glucose but does not block the decrease in calcium after resuscitation.

Animals↗
PubMed1988

Serial changes in left ventricular wall motion by two-dimensional echocardiography following anterior myocardial infarction.

To evaluate the time course of spontaneous changes in wall motion following anterior infarction, we prospectively performed serial apical four-chamber two-dimensional echocardiography on 45 consecutive long-term survivors of initial transmural anterior infarction. Studies were performed on admission (1 +/- 1 days), 1 week after admission (6 +/- 2 days), at discharge (15 +/- 8 days), and at long-term follow-up (235 +/- 186 days). Ventricular size was expressed as end-diastolic area in square centimeters. Wall motion for this tomographic section was evaluated as the percent change in left ventricular area from end diastole to end systole (% LVA). Patients were grouped on the basis of significant differences for %LVA between the first and fourth studies. Group I (n = 14) had improved wall motion (23 +/- 5% to 38 +/- 9%); group II (n = 23) did not change (22 +/- 9% to 23 +/- 11%); and group III (n = 8) had worsened wall motion (28 +/- 6% to 18 +/- 7%). End-diastolic area did not change over the study period for groups I and II but increased significantly for group III (30 +/- 6 to 35 +/- 4 cm2, p less than 0.05). Most of the increase in end-diastolic area for group III was between the third and fourth study. The percent improvement (%IMP) in wall motion for patients in group I who did not have ventricular fibrillation outside the hospital expressed in days (t) following infarction fit an exponential curve (%IMP = 100-100e-(.108t) that predicts that 70% of eventual recovery will occur in the first 15 days post-infarction. We conclude that changes in left ventricular size and wall motion occur following anterior infarction with improvement or worsening occurring spontaneously in some patients. If improvement occurs, it should be evident within 2 weeks of infarction; infarct expansion in this select group of long-term survivors occurred primarily after discharge.

Clinical Enzyme Tests↗
PubMed1988

Early peak of creatine kinase-MB in acute myocardial infarction with a nondiagnostic electrocardiogram.

This study compared the time from the onset of symptoms to the peak of the creatine kinase-myocardial band (CK-MB) in 34 consecutive patients with acute myocardial infarction. Patients were separated into two groups: group 1 (n = 21) had diagnostic (greater than or equal to 0.1 mV) ST segment elevation on the initial ECG, and group 2 (n = 13) did not have diagnostic ST segment elevation on the initial ECG. In group 1 the time to the peak CK-MB was 16.2 +/- 50 hours vs 10.0 +/- 2.0 hours for group 2 (p = 0.0001). Peak CK-MB was 331 +/- 276 IU/L in group 1 vs 81 +/- 54 IU/L in group 2 (p less than 0.005). In group 1 there were 16 patients who subsequently had a Q wave myocardial infarction as opposed to one patient in group 2 (p = 0.0001). Patients who do not have diagnostic ST segment elevation on the initial ECG have an early but low peak of CK-MB and typically have a non-Q wave infarction. These findings are consistent with early spontaneous restoration of blood flow during the infarction process in these patients. This early restoration of blood flow may provide the substrate for the high incidence of recurrent ischemic events noted in patients with non-Q wave myocardial infarction.

Aged↗
PubMed1987

Serum potassium, calcium and magnesium after resuscitation from ventricular fibrillation: a canine study.

Serum electrolytes were measured before and sequentially for 3 hours after resuscitation from ventricular fibrillation in a canine model that was designed to approximate the human cardiac arrest and resuscitation process. Twenty anesthetized dogs were resuscitated from ventricular fibrillation; 7 required epinephrine during resuscitation and 13 did not. To control for the effects of anesthesia, 10 dogs were anesthetized and instrumented, but ventricular fibrillation was not induced. Serum potassium decreased from 3.7 +/- 0.3 mmol/liter at baseline to 3.2 +/- 0.4 mmol/liter 45 minutes after resuscitation in the experimental dogs resuscitated without epinephrine, as compared with 3.6 +/- 0.3 to 3.4 +/- 0.2 mmol/liter in control dogs (p = 0.07 versus control dogs by two-way analysis of variance) and returned toward baseline at the end of 3 hours. Serum calcium decreased from 9.6 +/- 0.6 mg/dl at baseline to 8.9 +/- 0.9 mg/dl at 5 minutes after resuscitation as compared with 9.4 +/- 0.7 to 9.5 +/- 0.7 mg/dl in control dogs (p less than 0.05 versus control dogs) and returned to baseline by 3 hours. Serum magnesium decreased from 1.5 +/- 0.1 to 1.3 +/- 0.2 mEq/dl by 3 hours in resuscitated dogs as compared with 1.6 +/- 0.2 to 1.5 +/- 0.2 mEq/dl in control dogs (p = 0.06 versus control dogs). These changes in serum potassium, calcium and magnesium were independent of the administration of epinephrine during the resuscitation process. Changes in potassium were independent of arterial pH or bicarbonate therapy. Serum glucose increased after ventricular fibrillation but not in control dogs (p less than 0.0005 versus control). No changes in other electrolytes were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Two-dimensional echocardiographic identification of complicated aortic root endocarditis: implications for surgery.

Two-dimensional echocardiography successfully displayed the location and extent of aortic root complications, annular abscess or mycotic aneurysm in nine patients with aortic valve endocarditis. Five of the nine patients had prosthetic valve endocarditis and four had native valve endocarditis. The infective process extended into the paravalvular structures, including the interventricular septum (seven patients), right ventricular outflow tract (three patients), interatrial septum (one patient) and anterior mitral valve leaflet (four patients). The amount of aorto-left ventricular discontinuity caused by these complications was quantitated in degrees of annular circumference on the parasternal short axis image and in distance on the parasternal long axis image. The echocardiographic findings were confirmed at surgery and were helpful in the preoperative anticipation of the type of surgical procedure required: aortic valve replacement or composite aortic valve and root replacement. Five patients had prosthetic valve endocarditis with calculated aorto-left ventricular discontinuity of 173 +/- 55 degrees on parasternal short axis images and 1.36 +/- 0.72 cm on parasternal long axis images. Initial surgical repair included three composite aortic root-valve prosthesis implants, one reconstructive procedure with valve replacement and one simple aortic valve replacement. During a follow-up period of 18 months (range 1 to 35), a second reparative procedure was required for only one patient to repair an aortic conduit to coronary artery venous bypass graft. Four patients had native valve endocarditis with calculated aorto-left ventricular discontinuity of 100 +/- 17 degrees on parasternal short axis images and 0.88 +/- 63 cm on parasternal long axis images. Initial surgical repair included two reconstructive procedures with valve replacement and two simple aortic valve replacements. During a follow-up period of 30 months (range 16 to 42), three of these four patients required a second reparative procedure: one each for repair of a paraprosthetic leak, a ventricular septal defect and persistent aorto-left ventricular discontinuity. Two-dimensional echocardiography accurately detected aortic annular abscess and mycotic aneurysm complicating aortic valve endocarditis and the resultant degree of aorto-left ventricular discontinuity. Circumferential aorto-left ventricular discontinuity with these complications is greater for prosthetic than native valve endocarditis and predicts a more extensive surgical repair.(ABSTRACT TRUNCATED AT 400 WORDS)

Abscess↗
PubMed1987

Analyses of creatine kinase isoenzymes and isoforms in serum to detect reperfusion after acute myocardial infarction.

Isoenzymes and isoforms of creatine kinase (CK, EC 2.7.3.2) were measured to assess reperfusion after acute myocardial infarction (AMI). In streptokinase-treated and in spontaneously reperfused AMI patients, total CK, CK-2 activity and concentration, and CK-3(3) isoform activity peaked significantly (p less than 0.05) earlier than conventionally treated, non-reperfused patients. The ratio for CK-3(3) to CK-3(1) activities peaked significantly (p less than 0.05) earlier in both the streptokinase-treated and spontaneously reperfused groups, and indicated a greater release of enzyme (higher ratio) than in the conventionally treated patients. The ratio of CK-3(3)/3(1) also peaked significantly (p less than 0.05) earlier in all three groups than did total CK, CK-2, and CK-3(3) activities or concentrations. The clearance rates of total CK, CK-2, and CK-3(3) were not significantly different in all three groups. Thus, the ratio CK-3(3)/3(1) was the earliest indicator of infarction in both reperfused and non-reperfused patients.

Creatine Kinase↗
PubMed1986

Two-dimensional echocardiographic detection of left ventricular posterior wall motion abnormalities using an inferior angulation view.

Two-dimensional echocardiography is frequently used to detect left ventricular (LV) wall motion abnormalities. Modification of the apical 4-chamber view by inferior angulation of the transducer provides a superior image for detection of regional wall motion abnormalities of the LV posterior wall. The inferior angulation image was prospectively compared with the standard parasternal short-axis image for detection of posterior LV wall motion abnormalities as defined by contrast left ventriculography in 63 consecutive patients. Posterior wall akinesia was present on the contrast left ventriculogram in 22 of the 63 patients. The parasternal short-axis image was judged technically inadequate for interpretation in 7 patients (11%). The inferior angulation image was technically adequate for interpretation in all patients. The sensitivity, specificity and accuracy of the inferior angulation image for detection of LV posterior wall motion abnormality was 91%, 80% and 84%, respectively, vs 67%, 71% and 70% for the parasternal short-axis image. The differences between the sensitivity, specificity and accuracy for the 2 views were not statistically significant. These observations indicate that the inferior angulation image provides a useful plane for routine echocardiographic analysis of regional LV wall motion either as a primary method to detect posterior wall motion abnormality or as a confirmatory view to document posterior wall motion abnormality.

Adolescent↗
PubMed1986

Mechanisms of remote myocardial dysfunction during coronary artery occlusion in the presence of multivessel disease.

Myocardial dysfunction may occur in areas remote from an acutely occluded coronary artery if those areas are served by a critically stenosed vessel. Although subendocardial hypoperfusion of such remote myocardium has been demonstrated in experimental preparations of this situation, this study was undertaken to determine whether actual reductions in subendocardial perfusion below control levels were necessary for such dysfunction to occur. A 20 mg dose of pentobarbital was injected into the left anterior descending artery (LAD) in 14 anesthetized dogs to create a large anterior regional wall motion abnormality without drawing significant collateral flow from the circumflex vascular bed. Circumflex subendocardial flow was found to rise during injections of pentobarbital and occlusion of the LAD (1.12 +/- 0.38 and 1.17 +/- 0.34 ml/min/g, respectively, vs control 0.91 +/- 0.23 ml/min/g; p less than .05) in the absence of circumflex stenosis. In the presence of circumflex stenosis, circumflex subendocardial flow fell during left anterior descending occlusion (0.59 +/- 0.21 vs 0.89 +/- 0.19 ml/min/g control; p less than .01) but did not change during pentobarbital injections in the LAD (0.77 +/- 0.36 ml/min/g). In the absence of circumflex stenosis, circumflex segment shortening increased during injection of pentobarbital or occlusion of the LAD (14.3 +/- 4.9% and 14.4 +/- 3.5%, respectively, vs 12.3 +/- 3.3% control). In the presence of circumflex stenosis, it did not change (12.5 +/- 4.0% pentobarbital, 11.8 +/- 3.6 LAD occlusion vs 13.1 +/- 4.0% control). We concluded that the presence of large regional wall motion abnormalities may increase the oxygen consumption of remaining myocardium and that dysfunction of that myocardium may result from relative hypoperfusion if blood flow cannot increase appropriately.

Animals↗
PubMed1985

Reactive oxygen species may cause myocardial reperfusion injury.

The pathogenic mechanisms responsible for heart damage following temporary coronary artery occlusion are unknown. Some damage may be mediated by a normal cellular enzyme, xanthine dehydrogenase, which converts to xanthine oxidase during myocardial ischemia. Reperfusion, with restoration of oxygen supply, may then lead to formation of superoxide by xanthine oxidase, possibly initiating a cascade of oxidative events. In support of this, reperfusion of transiently ischemic canine myocardium leads to a rapid loss of cellular glutathione and a decrease in catalase activity, both indicative of enhanced generation of activated oxygen. Allopurinol--an inhibitor of xanthine oxidase--ameliorates both biochemical damage and functional deficits ordinarily triggered by ischemia and reperfusion, suggesting one possible mode of pharmacologic intervention following acute myocardial infarction.

Allopurinol↗
PubMed1985

Regional function and perfusion at the lateral border of ischemic myocardium.

To determine whether function is depressed in areas of myocardium adjacent to an area of myocardial ischemia, 16 open-chest dogs were studied with both two-dimensional echocardiography and ultrasonic microcrystals. Regional myocardial blood flow was measured with radioactive microspheres during control periods and after coronary arterial ligation. Segments of myocardium adjacent to the area of ischemia were found to have no significant change in transmural blood flow (1.02 +/- 0.38 ml/g/min control vs 0.95 +/- 0.3 ml/g/min after ligation) or subendocardial flow (1.18 +/- 0.41 ml/g/min control vs. 1.19 +/- 0.37 ml/g/min after ligation). Regional function assessed echocardiographically as percent change in segment area was significantly depressed in these normally perfused adjacent areas (69.5 +/- 18.8% control vs 52.5 +/- 19.8% after ligation; p less than .01). There was a significant relationship between proximity to border of infarction and degree of adjacent dysfunction (r = .50, p less than .01 for echocardiography; r = .70, p less than .01 for ultrasonic microcrystals). It is concluded that systolic performance is depressed in nonischemic myocardium directly adjacent to the lateral border of an area of acute myocardial ischemia.

Animals↗
PubMed1984

Two-dimensional echocardiographic detection of right-sided cardiac intracavitary thromboembolus with pulmonary embolism.

Five patients with pulmonary embolism, in whom right-sided intracardiac thromboembolus was detected by echocardiography and confirmed by either angiography, surgery or postmortem examination, are described. One of these patients died from massive pulmonary embolism after right heart catheterization. In two patients treated medically, either partial or total lysis of the thromboembolus was demonstrated echocardiographically; in another two patients, the right atrial thromboembolus was successfully removed surgically. Typical locations and echocardiographic characteristics of right-sided thromboemboli are described. The potential usefulness of two-dimensional echocardiography in both the diagnosis and the management of patients with right-sided intracardiac thromboembolism is discussed.

Adolescent↗