Biomedical subjects

G W Maier

Publications and source records attributed to G W Maier.

26 records · Page 2Linked to original sources

PubMed1987

Sequence of mitral valve motion and transmitral blood flow during manual cardiopulmonary resuscitation in dogs.

According to the thoracic pump model of cardiopulmonary resuscitation (CPR), the heart serves as a passive conduit for blood flow from the pulmonary to the systemic vasculature, necessitating an open mitral valve and anterograde transmitral blood flow during chest compression. To assess the applicability of this model to manual CPR techniques, two-dimensional echocardiograms were recorded from the right chest wall and/or the esophagus in nine dogs (18 to 26 kg) during manual CPR. The aortic valve opened with chest compression and closed with release, while the pulmonary and tricuspid valve leaflets closed with compression and opened during release. The mitral valve remained open during ventilation alone and during abdominal compressions. With the onset of brief, high-velocity (high-impulse) chest compressions, the mitral valve closed rapidly and the left ventricle was deformed, whether compressions were applied to the sternum or the left mid-chest wall. The mitral valve reopened with release of each compression. Left atrial echocardiographic contrast injections confirmed the absence of anterograde transmitral blood flow during high-impulse compression and its presence during release. Failure of mitral leaflet approximation during chest compression was observed only when a very low-velocity, prolonged (low-impulse) compression technique was used, or when regions that did not directly overlie the heart were compressed. Consistent with these observations, simultaneous recordings of the left ventricular and left atrial pressures during high-impulse sternal compressions in five dogs (19 to 25 kg) demonstrated peak and mean left ventriculoatrial pressure gradients of 38.5 +/- 4.0 and 13.5 +/- 2.9 mm Hg, respectively, and these pressure gradients declined with less impulsive compressions. The observations made during all but low-impulse chest compressions are inconsistent with the thoracic pump model, and support direct cardiac compression as the primary mechanism of forward blood flow with more impulsive manual chest compression techniques.

Animals↗

PubMed1986

The influence of manual chest compression rate on hemodynamic support during cardiac arrest: high-impulse cardiopulmonary resuscitation.

Considerable effort has been expended in recent years by a number of laboratories to improve methods of cardiopulmonary resuscitation. This article briefly summarizes 5 years of investigation by our group on hemodynamic support during external cardiac massage. In most studies, long-term canine preparations were used, and implanted transducers allowed precise hemodynamic measurements. Although cardiac output was depressed with all CPR methods, manual chest compressions of high velocity, moderate force, and brief duration at a rate of 120/min seemed to optimize systemic and coronary blood flow. This method was termed high-impulse CPR. High-impulse techniques now have been applied extensively in the clinical setting, and preliminary observations also support their efficacy in man. Based on this experience, it is suggested that the American Heart Association guidelines be changed to recommend a manual chest compression rate of 120/min during closed-chest cardiac massage.

Animals↗

PubMed1985

Diminished stroke volume during inspiration: a reverse thoracic pump.

In 12 conscious dogs, a three-dimensional array of pulse-transit ultrasonic transducers was used to measure left ventricular anterior-posterior minor, septal-free wall minor, and basal-apical major diameters. Matched micromanometers measured left ventricular, right ventricular, and intrapleural pressures. Electromagnetic ascending aortic blood flow and right ventricular transverse diameter were measured in five of the dogs. A major cause of the inspiratory decline in stroke volume in this preparation appeared to be reflex tachycardia and autonomic changes associated with inspiration. However, when heart rate was controlled by atrial pacing or pharmacologic autonomic attenuation (propranolol and atropine), stroke volume still decreased around 10%, with an inspiratory decrease in pleural pressure of 10 mm Hg. Based on the measurements of ventricular dimension, venous return to the right ventricle appeared to be augmented significantly during inspiration and the transient increase in right ventricular volume was associated with leftward interventricular septal shifting and altered diastolic left ventricular geometry. However, left ventricular end-diastolic volume was changed minimally, implying that alterations in preload were not important. Moreover, transmural left ventricular ejection pressure, calculated as intracavitary minus pleural pressure, was not significantly changed, and it seemed that neither pressure nor geometric components of afterload were altered significantly by inspiration. The inspiratory fall in left ventricular stroke volume correlated best with the decline in intracavitary left ventricular ejection pressure referenced to atmospheric pressure. It is hypothesized that during ejection, left ventricular pressure referenced to atmospheric pressure is the hydraulic force effecting stroke volume and that the decline in this effective left ventricular ejection pressure is responsible for the inspiratory fall in stroke volume through a reverse thoracic pump mechanism.

Animals↗

PubMed1984

The physiology of external cardiac massage: high-impulse cardiopulmonary resuscitation.

In intact chronically instrumented dogs, left ventricular dynamics were studied during cardiopulmonary resuscitation (CPR). Electromagnetic flow probes measured cardiac output and coronary blood flow, ultrasonic transducers measured cardiac dimensions, and micromanometers measured left ventricular, right ventricular, aortic, and intrathoracic pressures. The dogs were anesthetized with morphine, intubated, and fibrillated by rapid ventricular pacing. Data were obtained during manual external massage with dogs in the lateral and supine positions. Force of compression was varied from a peak intrathoracic pressure of 10 to 30 mm Hg, and compression rate was varied from 60 to 150/min. Increasing force of compression increased stroke volume up to a peak intrathoracic pressure of approximately 20 mm Hg, beyond which stroke volume remained constant or declined. Stroke volume appeared to result primarily from direct transmission of manual compression force to the heart rather than from positive intrathoracic pressure because peak cardiac or vascular pressures or the change in these pressures were consistently two to four times greater than the corresponding intrathoracic pressures during manual compression. With increasing compression rate, stroke volume remained relatively constant, and total cardiac output increased significantly: 425 +/- 92 ml/min at 60/min, 643 +/- 130 ml/min at 100/min, and 975 +/- 219 ml/min at 150/min (p less than .05). Left ventricular dimensions decreased minimally at higher manual compression rates. In four patients undergoing CPR, systolic and diastolic arterial blood pressure increased with faster compression rates, correlating well with data obtained in the dog. Dynamic coronary blood flow in canine experiments decreased to zero or negative values during compression. Antegrade coronary flow occurred primarily during noncompression periods and seemed to be related to diastolic aortic perfusion pressure; coronary flow at a compression rate of 150/min averaged 75% of control. Therefore stroke volume and coronary blood flow in this canine preparation were maximized with manual chest compression performed with moderate force and brief duration. Increasing rate of compression increased total cardiac output while coronary blood flow was well maintained. Direct cardiac compression appeared to be the major determinant of stroke volume during manual external cardiac massage.

Animals↗

PubMed1984

Pericardial influences on ventricular filling in the conscious dog. An analysis based on pericardial pressure.

Twenty-five dogs were chronically instrumented to investigate the effects of the normal pericardium on cardiac function. Pulse-transit ultrasonic transducers were implanted to measure multiple ventricular dimensions. The pericardium was incised transversely at the base of the heart and precisely reapproximated, so as to disturb its characteristics minimally. One week later, the dogs were studied in the conscious state, and left ventricular, right ventricular, pericardial, and pleural pressures were measured with matched micromanometers. Data were recorded before and after blood volume expansion. Absolute end-diastolic pericardial pressure varied directly with pleural pressure during the respiratory cycle. Transpericardial pressure (pericardial-pleural pressure) varied little with respiration and was related directly to ventricular diameter during the cardiac cycle with peak transpericardial pressure uniformly occurring at end-diastole. With volume infusion, normalized end-diastolic minor axis diameter and left ventricular transmural pressure (left ventricular-pleural pressure) increased significantly from 0.14 +/- 0.01 and 9.5 mm Hg +/- 1.0 mm Hg, respectively, in the control state to 0.20 +/- 0.01 and 19.3 mm Hg +/- 1.2 mm Hg after volume loading. End-diastolic transpericardial pressure also increased significantly from 2.3 +/- 0.5 mm Hg to 4.1 +/- 0.3 mm Hg, and represented approximately 21% of transmural left ventricular pressure. When measurements were obtained sequentially after implantation, transpericardial pressure was initially high but decreased with time, presumably due to pericardial creep. After volume loading, right ventricular end-diastolic transmural pressure averaged 9.6 mm Hg, and pericardial pressure constituted 42% of right ventricular pressure. Thus, pericardial restraining effects may predominantly influence right ventricular filling and affect the left ventricle through series interaction. In the normal conscious dog, transpericardial pressure remains low over the entire physiological range, and the direct influence of the normal pericardium on diastolic filling of the left ventricle appears to be minimal.

Animals↗

PubMed1983

Dynamic ventricular interaction in the conscious dog.

In nine conscious, chronically instrumented dogs, ultrasonic dimension transducers measured left ventricular anterior-posterior and septal-free wall minor axis and major axis diameters. Matched micromanometers measured right and left ventricular transmural and transeptal pressures. Ventricular pressures and volumes were varied by inflation of implanted vena caval and pulmonary artery occluders, and the functional significance of the two types of ventricular interaction, i.e., direct and series, was determined. The left ventricle was represented by a modified ellipsoidal geometry. Left ventricular stroke volume calculated from the dimension data correlated well with that measured directly from ascending aortic electromagnetic flow probes during all interventions (r greater than or equal to 0.96). Partial pulmonary artery occlusion significantly increased right ventricular diastolic and systolic pressures as compared to values obtained during control and venal caval occlusion. During pulmonary artery occlusion, latitudinal septal eccentricity was increased throughout the cardiac cycle compared to control and vena caval occlusion (P less than 0.05), indicating leftward interventricular septal shifting and significant alteration of left ventricular shape. The normalized diastolic pressure-volume curve was shifted to the left with pulmonary artery occlusion compared to control and indicated a decrease in left ventricular chamber compliance. However, when selected cardiac cycles with similar end-diastolic volumes from vena caval and pulmonary artery occlusions were compared, parameters of left ventricular systolic function (stroke volume, percent systolic shortening, peak aortic blood flow, peak left ventricular pressure, and its first derivative) remained relatively constant. These data suggest that mean myocardial fiber length is the major preload determinant of left ventricular systolic function independent of chamber pressure and shape, and that direct ventricular interaction mediated by interventricular septal shifting has minimal effects on systolic myocardial performance in this model. Thus, series ventricular interaction during acute imbalances in biventricular loading, where the output of the right ventricle determines the input of the left, seems to be far more important than direct interaction to the regulation of overall cardiac function.

Animals↗

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

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↗