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Biomedical subjects

C O Olsen

Publications and source records attributed to C O Olsen.

33 records · Page 2Linked to original sources
PubMed1982

Cardiovascular effects of ventilation with positive expiratory airway pressure.

The broad clinical application of positive and expiratory pressure (PEEP) in the treatment of a variety of respiratory disorders has led to the observation that positive airway pressure can result in cardiac dysfunction. Recent attempts to integrate and extend the results of past research have led to diverse explanations of the overall cardiopulmonary effects of PEEP. This review summarizes previous work in the field and attempts to explain the basis of the divergent conclusions of previous investigators. Data are presented from several experimental models, as well as studies in postoperative patients to formulate an overall analysis of the influence of airway pressure on the central circulation. It appears that the effects of PEEP are primarily mechanical and are mediated through a combination of right ventricular preload limitation and outflow obstruction. Both effects are additive in limiting left ventricular preload and can be ameliorated by volume loading in the absence of significant right ventricular or pulmonary vascular disease. Neural, humoral and ventricular interactive forces appear to be insignificant under most circumstances. The clinical implications of these advances in the current understanding of PEEP are reviewed.

Animals↗
PubMed1982

The effects of airway pressure on cardiac function in intact dogs and man.

Ventilation with positive end-expiratory pressure (PEEP) is associated with reduced cardiac output, but the mechanisms involved are controversial. Possible explanations include increased intrathoracic pressure, reflex changes in myocardial inotropism, pulmonary vascular obstruction and abnormal ventricular interaction. Three types of conscious canine preparations were developed to examine simultaneously each of these factors during ventilation with PEEP. In addition, similar measurements were obtained in patients after cardiac surgical procedures and compared with the results of animal experiments. The primary cause of reduced cardiac output during PEEP appeared to be a diminished end-diastolic volume of the left ventricle, and this appeared to be the result of elevated intrathoracic pressure and increased impedance to blood flow through the lungs. Abnormal interventricular septal shifting and reflex autonomic alterations did not appear to be significant in the normal cardiovascular system. These data provide insight into the cardiac effects of PEEP and emphasize the importance of simultaneous quantification of biventricular performance when assessing cardiopulmonary function.

Animals↗
PubMed1982

Dimensional characteristics of left ventricular function after coronary artery bypass grafting.

During coronary artery bypass grafting, 20 patients underwent epicardial placement of miniature ultrasonic dimension transducers across the minor-axis diameter of the left ventricle to monitor cardiac function postoperatively. Left atrial or left ventricular pressure was measured in all patients, and thermodilution cardiac outputs were obtained routinely. Data from 1, 6, 12 and 20 hours postoperatively were analyzed. Directional changes in systolic shortening of the left ventricular diameter correlated well with stroke volume measured by thermodilution techniques and could be used as an on-line index of cardiac output. In five patients who had preoperative abnormalities in wall motion, systolic bulging of the minor-axis diameter was seen initially after revascularization and then gradually resolved over the next 12 hours. Systolic bulging that did not resolve was the earliest indication of a perioperative myocardial infarction in another patient. The end-diastolic diameter increased progressively in all patients in the first 12 hours postoperatively and was associated with stabilization of cardiac function. This improvement in diastolic left ventricular filling was not reflected (p greater than 0.2) by changes in mean left atrial pressure. Therefore, ultrasonic assessment of left ventricular diameter is a simple, precise and safe method of monitoring systolic and diastolic ventricular function postoperatively.

Adult↗
PubMed1981

Dynamic geometry of the intact left ventricle.

Knowledge of left ventricular chamber dynamics is central to our understanding of cardiac physiology. The complicated changes in left ventricular geometry observed in the dog during various phases of the cardiac cycle can be represented as distinct linear relationships between chamber eccentricity and intracavitary volume during diastole and ejection, and probably represent structural properties of the ventricular wall. Chamber geometry of the left ventricle is a major determinant of overall myocardial function. The slope of the radius of curvature (r) to wall thickness (h) relationship is a geometric constant that determines the mural force at any given transmural pressure. Chronic pressure and volume overload produce changes in this geometric relationship as a result of increased mural force resisting ejection. The adaptive mechanism of ventricular hypertrophy in this setting alters the r/h ratio and returns systolic mural force toward normal. Coronary occlusion induces acute changes in regional geometry characterized by holosystolic wall bulging and systolic wall thinning, which shift the r/h relationship upward and to the left. The geometric alteration during ischemia probably increases systolic mural force and could adversely affect myocardial function. Recent studies with patients have shown the r/h ratio to be of value in distinguishing between reversible and irreversible impairment of myocardial performance. Because most myocardial diseases produce major alterations in the structure of the ventricular wall, analysis of dynamic chamber geometry may prove of prognostic value in assessing patients with cardiac disorders.

Animals↗
PubMed1981

An improved transducer for measurement of cardiac dimensions with sonomicrometry.

Although pulse-transit sonomicrometry is an accurate and sensitive technique for measuring cardiac dimensions, transducer directionality has been a significant problem in certain applications. Construction of an improved ultrasonic dimension transducer is described for the measurement of global cardiac diameters. The transducer consists of a hemispheric piezoelectric crystal with a quarter-wavelength impedance matched faceplate. The in vitro acoustic characteristics of this transducer reveal a substantially improved beam pattern compared to the flat piezoceramic transducer commonly used. This improvement in transducer design greatly facilitates sonic alignment, enhances tracking throughout the cardiac cycle, and allows the measurement of more complex cardiac dimensions.

Acoustics↗
PubMed1981

The deformational characteristics of the left ventricle in the conscious dog.

We studied left ventricular minor and major axis diameters and equatorial wall thickness in eleven conscious dogs with chronically implanted pulse-transit ultrasonic dimension transducers. Left ventricular transmural pressure was measured with micromanometers. Left ventricular volume was varied by inflation of implanted vena caval or aortic occluders. The geometry of the left ventricle was represented as a three-dimensioal ellipsoidal shell. Left ventricular eccentricity was found to be a linear function of ventricular volume during both diastole and ejection. However, the relationship was not the same for diastole and ejection, and during diastole the left ventricle was mre spherical at large volumes and more elliptical at small volumes than during ejection. The rearrangements in geometry observed during isovolumic contraction appeared to be transitional stages from the diastolic to the ejection-phase relationship. Thus, during isovolumic contraction, the left ventricle became more elliptical at large volumes and more spherical at small volumes. These relationships were not altered significantly by increased afterload or inotropic interventions. We also observed that the diastolic deformation of the ventricular chamber occurred in a set and predictable manner that seemed to be determined by the three-dimensional mechanical properties of the myocardium. The geometric inter-relationships of the ventricular wall determined the relationship between diastolic transmural pressure and mural stress. These findings probably reflect basic structural characteristics of the myocardium and provide a convenient method for quantitatively representing the dynamic geometry of the left ventricle.

Animals↗
PubMed1981

The coronary pressure-flow determinants left ventricular compliance in dogs.

Displacement of the left ventricular diastolic pressure-dimension relationship (change in compliance) has been observed with alterations in coronary perfusion pressure. The relative contribution of coronary (myocardial) blood flow, as compared with the perfusion pressure at which flow occurs, was studied in 10 dogs during diastolic relaxation potassium arrest during cardiopulmonary bypass. The normalized left ventricular pressure-dimension relationships, obtained during passive, gradual filling of the left ventricle (0-20 mm Hg) were shifted progressively to the left as coronary perfusion pressure was increased. Myocardial blood flow was 0.06 ml/mg per min +/- 0.02 ml/mg per min (mean +/- SEM) at a coronary perfusion pressure of 40 mm Hg and increased to 0.38 ml/mg per min +/- 0.11 ml/mg per min as the coronary perfusion pressure was raised to 120 mm Hg. Addition of adenosine significantly increased myocardial blood flow by 109% at a coronary perfusion pressure of 80 and by 147% at a coronary perfusion pressure of 120 mm Hg, but caused no additional significant shifts in the pressure-dimension relationships, compared to the same coronary perfusion pressures without adenosine. Coronary perfusion pressure, and not coronary blood flow, is a more direct determinant of cardiac diastolic properties.

Adenosine↗
PubMed1981

Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. I. Myocardial blood flow and metabolism.

Using a canine model of subcoronary valvular aortic stenosis, we determined myocardial blood flow, high-energy phosphate content, and mitochondrial function in eight hearts with chronic left ventricular hypertrophy. Fourteen normal hearts were used for control data. Myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, left ventricular transmural biopsy specimens were taken for metabolic analyses. Subepicardial and subendocardial content of adenosine triphosphate (ATP) and creatine phosphate (CP) were assayed. Respiratory control indices for isolated mitochondria were measured by use of NAD-linked and FAD-linked substrates. Endocardial blood flow, subendocardial high-energy phosphate content, and respiratory control indices for NAD-linked substrate in the hearts with chronic left ventricular hypertrophy were significantly lower than the normal values. These data provide insight into the metabolic and myocardial blood flow abnormalities occurring in cardiac hypertrophy and provide a framework for understanding the altered response of hypertrophied hearts to ischemia.

Adenosine Triphosphate↗
PubMed1981

Characteristics of chronic left ventricular hypertrophy induced by subcoronary valvular aortic stenosis. II. Response to ischemia.

The increased susceptibility of hearts with chronic left ventricular hypertrophy (CLVH) to damage during ischemia has been suggested but not documented. The purpose of this study was to isolate ischemic events in hearts with CLVH from reperfusion events. Using physiological and biochemical parameters, we compared the rate and extent of myocardial injury during ischemic contracture between eight canine hearts with CLVH induced by subcoronary valvular aortic stenosis and 14 normal canine hearts. Preischemic myocardial blood flow was determined by injection of tracer microspheres. During cardiopulmonary bypass, each heart was instrumented with a left ventricular balloon and made globally ischemic. At control, contracture initiation, and contracture completion left ventricular transmural biopsy specimens were assayed for subepicardial and subendocardial adenosine triphosphate (ATP) and creatine phosphate (CP). Mitochondrial respiratory control indices for NAD-linked and FAD-linked substrates were measured. Preischemic endocardial blood flow in hearts with CLVH was significantly lower than in normal hearts. At control, subendocardial ATP and CP and the respiratory control index for NAD-linked substrate were significantly lower in hearts with CLVH than in normal hearts. Hearts with CLVH reached contracture initiation significantly sooner than normal hearts. All hearts demonstrated significant decreases in high-energy phosphate content and mitochondrial function during ischemia. Reperfusion injury notwithstanding, we concluded that hearts wih CLVH are more susceptible to ischemic injury than are normal hearts, perhaps related to lower endocardial blood flow, lower subendocardial high-energy phosphate stores, and depressed mitochondrial function prior to ischemia.

Adenosine Triphosphate↗
PubMed1981

Response of hypertrophied myocardium to ischemia: correlation with biochemical and physiological parameters.

The increased susceptibility of hypertrophied hearts to ischemic injury during cardiac operations has long been recognized. Although the imbalances in oxygen supply and demand which may occur with hypertrophy during hypotension, ventricular fibrillation, or reperfusion have been extensively studied, the biochemical response of hypertrophied myocardium to ischemia has not been fully elucidated. In the present investigation, rat hearts in which hypertrophy was induced by chronic pressure overload were used to examine the relationship of the physiological parameter, ischemic contracture, to high-energy phosphate content and mitochondrial function during global ischemia. Hypertrophied hearts developed ischemic contracture after significantly shorter duration of ischemia than did normal hearts (5.8 +/- 0.3 minutes versus 10.1 +/- 0.7 minutes). High-energy phosphate content was lower in hypertrophied hearts at control and at ischemic contracture initiation and completion than in normal hearts, whereas mitochondrial function was consistently greater in the hypertrophy group. This investigation demonstrates that the hypertrophied myocardium, independent of flow-related events, is more vulnerable to ischemic injury than normal myocardium and suggests that the increased susceptibility may result from lower high-energy phosphate stores present at the onset of ischemia. The results emphasize the need for rapid cardiac arrest with the induction of ischemia in hypertrophied myocardium and suggest the potential for increasing myocardial high-energy phosphate content in the hypertrophied ventricle by interventions such as arrested perfusion with substrate containing oxygenated cardioplegic solutions prior to the onset of planned ischemia.

Animals↗
PubMed1981

Metabolic deterioration during global ischemia as a function of time in the intact normal dog heart.

High-energy phosphate content and mitochondrial function were analyzed at the initiation and completion of ischemic contracture in dog hearts exposed to normothermic ischemia while on cardiopulmonary bypass. Contracture initiation and completion were detected by a balloon catheter placed within the left ventricle. In seven dogs, inner and outer layers of the myocardium were assayed for adenosine triphosphate (ATP) and creatine phosphate (CP). ATP and CP content in these two layers were compared prior to ischemia and at contracture initiation and completion. Inner layer ATP levels were 23.88 +/- 0.73 (mean +/- SM) mu moles/gm dry weight prior to ischemia, 5.14 +/- 0.49 at initiation, and 0.73 +/- 0.2 at completion. Inner layer CP content was 41.29 +/- 0.87 prior to ischemia, 3.49 +/- 0.34 at initiation, and 4.06 +/- 0.48 at completion. Mitochondrial respiratory control indices (RCI) were assayed in a second group of seven dogs prior to ischemia, at contracture initiation, and at contracture completion and were, respectively, 11.5 +/- 1.18, 3.1 +/- 0.43 and 1.76 +/- 0.29 (alpha ketoglutarate as substrate). Despite the specific degrees of metabolic deterioration associated with the events of contracture, ischemic time required to develop contracture initiation and completion was variable, ranging from 29.5 to 72 minutes for initiation and 60.25 to 101 minutes for completion. A third group of five dogs had biopsy specimens taken for ATP at fixed ischemic time intervals, and at 45 minutes of ischemia they were found to have greater ranges in ATP values than the ranges associated with contracture initiation. In contrast to ischemic time, the physiological events of ischemic contracture are reliable predictors of the degree of metabolic injury in the intact dog heart exposed to normothermic ischemic arrest during cardiopulmonary bypass.

Adenosine Triphosphate↗