G. W. Maier

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.

Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs.

The influence of chest compression rate on initial resuscitation success and 24 hr survival after prolonged manual cardiopulmonary resuscitation (CPR) was investigated in 26 morphine-anesthetized dogs (17 to 30 kg). After placement of aortic and right atrial micromanometers and induction of ventricular fibrillation, manual CPR was commenced immediately and continued for 30 min. One group of 13 dogs underwent manual CPR at a compression rate of 60/min, and the other group at a rate of 120/min. The compression durations in the two groups were not significantly different (51.7 +/- 1.8% at 60/min vs 51.6 +/- 1.9% at 120/min). No drugs other than sodium bicarbonate were administered during CPR. A maximum of three attempts was permitted to defibrillate the heart. Successfully defibrillated animals were followed for 24 hr, during which time no treatment, other than naloxone, was given to reverse the effects of morphine. Arterial blood pH, PCO2, and PO2 were not significantly different in the two groups throughout the CPR period. When compared with the compression rate of 60/min, the compression rate of 120/min produced more successfully defibrillated animals (12/13 at 120/min vs 2/13 at 60/min, p less than .002) and more 24 hr survivors (8/13 at 120/min vs 2/13 at 60/min, p less than .03). All 24 hr survivors were conscious and able to sit, stand, and drink normally. One 24 hr survivor in each group had difficulty walking. Improved survival with the high-rate compression technique was consistent with the significantly higher mean aortic (systolic and diastolic) and coronary perfusion pressures attained with high-rate compressions (all p less than .002). Although the clinical applicability of these findings has yet to be demonstrated, they provide empirical support for the recent decision to increase the chest compression rate for manual CPR recommended by the American Heart Association, and indicate that the hemodynamic and survival benefits of faster compression rates in this experimental preparation were not dependent on covariant alterations in compression duration.

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 ⩾ 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 < 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.

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.

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.

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.

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. Tran pericardial 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.

Mechanical determinants of myocardial oxygen consumption in conscious dogs

A new practical descriptor of metabolic to mechanical myocardial energy transfer (MET), termed the virtual work model, was evaluated in 32 conscious dogs and in 8 isolated canine hearts. An index of total mechanical energy expenditure (TME) was calculated as the sum of external energy (stroke work) and an internal energy index of heat (left ventricular end-diastolic volume times left ventricular mean ejection pressure). Physiological comparison of TME (x-axis) and myocardial oxygen consumption (MVO2; y-axis) yielded highly linear MET relationships (mean r = 0.93 +/- 0.07), with an average slope of 0.86 +/- 0.39 (SD) and a y-intercept of 9.1 +/- 6.4 mW/ml myocardium. The linear MVO2-TME relationship did not vary under steady-state vs. dynamic vena caval occlusion, increased heart rate, increased afterload, or increased inotropic state with calcium infusion. Compared with five other indexes of myocardial energetics, the virtual work model of MET was the most linear, the most practical in not requiring determination of the end-systolic pressure-volume relationship, and the most accurate predictor of MVO2 under normal and altered hemodynamic conditions.

Diastolic Myocardial Mechanics and the Regulation of Cardiac Performance

Over the past 15 years, the primary goal of our physiology laboratory has been to improve the understanding of basic myocardial function in both normal and diseased hearts. Very early in our studies, it became evident that existing descriptors of myocardial performance were deficient, and initial efforts were expended to develop basic models of ventricular geometry, diastolic properties, and systolic function. Later work has been directed toward applying these models to the study of pathophysiology in ischemic heart disease and chronic volume overload. Although this investigation is still in progress, enough information is currently available to provide insight into basic aspects of diastolic myocardial function, to propose several hypotheses on how the heart adapts to clinical heart disease, and to provide direction for future clinical investigation of myocardial mechanics in humans. This chapter will review these topics primarily through publications from our laboratory, each of which contains full references.

An Energetic Analysis of Myocardial Performance

Cardiovascular dynamics is one of the oldest lines of medical research, having its origins in the work of William Harvey in the seventeenth century. Yet despite its long history, conceptual understanding of cardiac performance is advancing more rapidly than ever, and many different scientifc approaches are currently yielding exciting new insights. This chapter reviews 15 years of work from our laboratories at Duke University on the quantitative assessment of diastolic and systolic ventricular function. Our approach to the analysis of chamber geometry, ventricular interaction, and diastolic mechanical properties is described, leading to the observation of a fundamentally linear relationship between myocardial energy production (net external work) and end diastolic fiber length. This relationship is further validated and expanded to provide a useful estimate of myocardial inotropism that is applicable to pathophysiologic analysis of myocardial ischemia and hypertrophy. Finally, recent extensions of this technique to human studies have proven useful to the understanding of cardiopulmonary interactions and valvular heart disease. As knowledge of myocardial adaptive mechanisms improves, enhanced diagnostic and therapeutic capabilities could translate into significant advances in patient care.