The Frank-Starling relationship generally has been examined with filling pressure as the index of preload, resulting in a curvilinear function that plateaus at higher filling pressures. To investigate this relationship further in the intact heart, 32 dogs were chronically instrumented with left ventricular and pleural micromanometers and with regional (10 dogs) or global (22 dogs) ultrasonic dimension transducers. Seven days after implantation, left ventricular pressure and regional or global dimensions were recorded in the conscious state. After autonomic blockade, preload was varied by vena caval occlusion. Myocardial function was assessed by calculating regional or global stroke work, and preload was measured as end-diastolic segment length or chamber volume. The relationship between stroke work and either end-diastolic segment length or chamber volume (termed the preload recruitable stroke work relationship) was highly linear in every study (mean r = .97) and could be quantified by a slope (Mw) and x-intercept (L,). Previous nonlinear relationships between stroke work and filling pressure seemed to reflect the exponential diastolic pressure-volume curve. Over the physiologic range of systolic arterial pressures produced by infusion of nitroprusside or phenylephrine, no significant change was observed in Mw or Lw in the normal dog. Calcium infusion increased both regional and global M, by 71 + 19% and 65 + 9%, respectively (p < .02), with no significant change in LW. To normalize for ventricular geometry and heart rate, stroke work was computed from circumferential stress-strain data and converted to myocardial power output, which was then plotted against enddiastolic circumferential strain. This relationship also was highly linear, and the slope, Mmp (mW/cm3 of myocardium), is proposed as a potential measure of intrinsic myocardial performance independent of loading, geometry, and heart rate. Circulation 71, No. 5, 994-1009, 1985 QUANTIFICATION of cardiac function has been the goal of physiologists for nearly a century, but it has been difficult if not impossible to establish practical or reliable measures of intrinsic myocardial performance in the intact heart. Some indexes, such as ventricular function curves relating stroke work to filling pressures, were nonlinear and difficult to quantify.' Other parameters suffered from lack of preload or afterload From the

No abstract

Congenital fistulas are the most common of the coronary arterial malformations and with the widespread use of selective coronary arteriography are being recognized with increasing frequency. Twenty-eight patients with congenital coronary fistulas have been evaluated at the Duke University Medical Center between 1960 and 1981. An additional 258 patients have previously been reported in the literature, making a total of 286 available for review. The right coronary artery is most commonly involved, and the fistulous communication is most often to the right ventricle, right atrium or pulmonary artery. Slightly more than half of the patients with coronary fistulas are symptomatic at the time the diagnosis is made. Surgical correction is strongly recommended to prevent the development of congestive heart failure, angina, subacute bacterial endocarditis, myocardial infarction, and pulmonary hypertension, as well as coronary aneurysm formation, with subsequent rupture or embolization. There were no operative or late deaths in the patients who underwent operations. Moreover, there have been no recurrent fistulas during a mean follow-up period of ten years. The risks of operative correction appear to be considerably less than the potential for development of serious and potentially fatal complications, even in asymptomatic patients.

No abstract

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 < .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.

Origin of the right pulmonary artery from the aorta is a congenital malformation usually associated with serious symptoms in the first year of life and characterized by a poor prognosis. Sixty-five patients with this disorder have been reviewed in the literature, and 95% presented during the first year with signs of congestive heart failure. All had cardiomegaly by radiographic and electrocardiographic examination. An accurate diagnosis was established by cineangiography, and associated cardiovascular anomalies were present in 85%. Origin of the right pulmonary artery from the ascending aorta is much more common than origin of the left pulmonary artery from this vessel (8 to 1). Twenty-three patients were managed without operation with a 30% 1-year survival rate. Among those patients managed surgically, the survival rate was 84% at 1 year. It is now clear that operation should be done as early as possible to prevent irreversible changes occurring in the pulmonary arterial vasculature since microscopic features of pulmonary hypertension have been seen during the first month of life. One patient was operated on at 5 months with correction of the deformity. The pulmonary arterial pressure decreased to normal after operation. This child is now asymptomatic and his 10-year postoperative follow-up is the longest found in the literature.

In the experimental animal the basic and controversial problem was studied of the influence of cardiac contraction on coronary blood flow. Normally beating hearts were perfused at a constant pressure, and coronary inflow and outflow were determined. In order to assess the role of systole, prolonged periods of ventricular asystole and fibrillation were induced and observations were made of the changes in coronary flow. With the cessation of cardiac contraction blood flow in the coronary arteries and coronary sinus rose appreciably. The results of these studies support the concept that contraction of the heart muscle, by compression of the myocardial vascular bed, behaves as a throttling mechanism and impedes coronary flow. The method employed permits a separation and quantitation of the effects on coronary flow resulting from cardiac contraction and the vasomotor state of the coronary vessels.T HE effect of organized cardiac contraction on flow through the capillary bed of the myocardium remains unsettled despite much work that has been done to elucidate this basic problem. Evidence has accumulated in support of 2 opposing viewpoints. One concept is that the shortening of the muscle fibers during systole compresses the vascular bed in the myocardium and acts as a "throttling" mechanism. The opposing view is that cardiac contraction "massages" or "kneads" the blood through the vascular bed and increases coronary flow. The primary objective in this study has been an evaluation of the effect of organized myocardial contraction on coronary flow in the intact animal. This problem has been attacked by the elimination of this factor by the induction of ventricular asystole or ventricular fibrillation. Comparisons have been made of coronary flow in the beating heart perfused at a constant pressure with those in the nonbeating heart under the same conditions. METHODS Twenty-seven adult mongrel dogs were anesthetized with intravenous pentobarbital (25 mg./ Kg.). Respiration was maintained through an endotracheal tube connected to a demand-valve apparatus supplied with oxygen. The left chest was entered through the fourth intercostal space and the pericardium was opened. The appropriate From the

No abstract