Coronary-subclavian steal: correction of recurrent angina and cerebrovascular symptoms.

Six months following aortic valve replacement and myocardial revascularization using the left internal mammary artery as a pedicle graft, recurrent angina and cerebrovascular symptoms occurred in our patient. Cardiac catheterization demonstrated a subtotal stenosis of the proximal left subclavian artery and a patent internal mammary artery graft with angiographic steal from the myocardium. The angina and cerebrovascular symptoms were relieved with correction of the proximal subclavian stenosis by balloon angioplasty. This demonstrates the importance of aortic arch and subclavian evaluation and selected angiography prior to myocardial revascularization using the internal mammary artery as a pedicle graft.

Effects of left ventricular loading by negative intrathoracic pressure in dogs.

There are many factors, both intrinsic and extrinsic to the left ventricle, that can affect its function when negative intrathoracic pressure is imposed. In this study, we examined whether the left ventricular response to the afterload imposed by negative intrathoracic pressure was similar to that imposed by partial aortic constriction. We used steady-state right heart bypass to control pulmonary venous return to the left ventricle and reflex blockade to maintain constant heart rate and contractility. To impose negative intrathoracic pressure we used a pressure chamber fitted over a midsternal thoracotomy, which allowed steady negative pressure to be applied to all intrathoracic surfaces. Left ventricular volumes were measured from biplane cineradiograms of multiple 1-mm markers implanted in the left ventricular midwall. With cardiac output and heart rate constant, we compared the left ventricular response to two different levels of negative intrathoracic pressure and to increasing aortic pressure by partial aortic constriction. In each case, negative intrathoracic pressure produced a rise in the left ventricular end-systolic and end-diastolic volumes as well as transmural pressures similar to the effects of partial aortic occlusion. Thus, when cardiac output, heart rate, and contractility are maintained constant and all external restraints on the left ventricle are removed, the left ventricle responds in a similar manner to an increase in hydraulic load whether produced by a decrease in intrathoracic pressure or by partial aortic occlusion.

Interaction between cardiac chambers and thoracic pressure in intact circulation.

A comprehensive model that describes the interaction between the cardiovascular system (CVS) and the intrathoracic pressure (ITP) based on a lumped parameter vascular representation and a time-varying elastance concept for the four cardiac chambers is presented. Special attention is given to two possible mechanisms of interventricular interaction; the constraining effects of the pericardium and direct interventricular interaction that results from the fact that the two ventricles share a common interventricular septum. The response of the CVS to positive and negative perturbations in the ITP and to injection of fluid into the pericardium was simulated and compared with experimental literature data. The results show that 1) the total heart volume is relatively constant throughout the cycle both for ITP of 0 and +15 mmHg, which is consistent with experimental data in dogs, thus suggesting that intrinsic properties of the cardiac chambers rather than a restricting pericardium is the mechanism for that observation. 2) The pericardium has a major role in modifying the transient and steady-state response to a step decrease in the ITP with a transient decrease in left ventricle (LV) end-diastolic volume followed by gradual increase afterwards. 3) The response to sudden injection of fluid into the pericardial space is a larger transient decrease in right ventricle than LV volume, which is consistent with experimental data. 4) Transmission across the septum has a relatively minor role in modifying the response of the CVS to negative pressure. Thus the model reasonably predicts the effects of intrathoracic and pericardial pressures on the circulation in a reflex-blocked animal and provides a means for placing multiple potential mechanisms in proper hierarchial order with regard to contributions to LV and overall CVS function.

Use of negative intrathoracic pressure to obtain end-systolic pressure volume relations in dogs.

Left ventricular contractility can be assessed from the end-systolic pressure-volume relationship (ESPVR). In this study we test the hypothesis that the same ESPVR can be obtained by varying LV loading with different levels of negative intrathoracic pressure as by varying LV filling. In six dogs mean aortic transmural pressure was used to approximate LV end-systolic pressure and LV volume was determined from data gathered from biplane cineradiograms of multiple markers placed in the LV midwall. In each preparation right heart bypass allowed control of cardiac output while the thoracic pressure was varied with a box surrounding a midsternal thoracotomy. Reflex effects were minimized by ganglionic blockade and bilateral vagotomy. ESPVRs were obtained by varying the cardiac output at constant thoracic pressure or by changing intrathoracic pressure at constant cardiac output. The slopes of the ESPVRs were not significantly different. This result implies that LV loading by negative intrathoracic pressure, in this highly controlled preparation, can be used to generate a systolic LV elastance similar to that obtained by varying LV filling.

Effects of lung inflation on blood flow during cardiopulmonary resuscitation in the canine isolated heart-lung preparation.

Using an isolated, fibrillated canine heart-lung preparation, we studied the effects of simultaneous lung inflation and chest compression on blood flow in a model of cardiopulmonary resuscitation. The heart and lungs were placed in an artificial thorax with the great vessels and trachea exteriorized and attached to an artificial perfusion circuit and respirator, respectively. The blood volume of the system was adjusted to obtain various levels of static equilibrium pressure. Blood flow was obtained by cyclically raising and lowering the pressure in the artificial thorax, simulating the changes in pleural pressure that occur during cardiopulmonary resuscitation. Lung inflation during the compression phase caused an increase in cardiopulmonary resuscitation blood flow when the change in pleural pressure was small and when static equilibrium pressure was high. In contrast, lung inflation caused a decrease in blood flow when changes in pleural pressure were high and when blood volume was low. These results suggest that the driving pressure for blood flow during chest compression may be increased by lung inflation when the pulmonary blood vessels are filled with blood. However, blood may become trapped in the right heart and unavailable for transfer to the periphery during chest compression if lung inflation causes the alveolar blood vessels to collapse.