Long cross-clamp time with warm heart surgery.
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Biomedical subjects
Publications and source records attributed to A Panos.
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Patients with acute-onset mitral insufficiency and cardiogenic shock after myocardial infarction have a high incidence of operative death and morbidity. Patients with ventricular dysfunction, myocardial ischemia, and limited cardiac reserve undergoing an urgent operation represent a challenge to modern methods of myocardial protection. To improve results of operation a new technique was devised with continuous infusion of cold oxygenated blood cardioplegia during the entire cross-clamp period. Between 1984 and 1988, 19 consecutive patients with severe mitral regurgitation and cardiogenic shock (systolic blood pressure less than 60 mm Hg) after myocardial infarction underwent urgent myocardial revascularization, mitral valve replacement, or both. Left ventricular ejection fraction was less than 40% in 16 of 19 patients. All patients had suffered myocardial infarction within 4 weeks of operation and underwent an urgent operation within 24 hours of the onset of hemodynamic compromise. Severe three-vessel coronary artery disease was present in 16 of the 19 patients. A continuous infusion of blood cardioplegia was instituted at aortic cross-clamping and continued throughout the cross-clamp period. Infusion of continuous blood cardioplegia was also instituted through each completed distal vein graft. Myocardial septal and left ventricular apical temperatures were maintained at 10 degrees +/- 2 degrees C throughout the cross-clamp period. There were two in-hospital deaths (mortality, 10.5%) and low output syndrome was present in 10 patients (53%). At a mean follow-up of 2.5 years, there was one late death and 14 of the 16 remaining patients were in New York Heart Association functional class I or II.(ABSTRACT TRUNCATED AT 250 WORDS)
A technique of modifying the Cabrol shunt using preserved bovine pericardium and a patch of autologous pericardium to deal with postoperative hemorrhage from an ascending aortic operation is described. A fistula to the right atrium was created for autotransfusion. This simple technique is very useful for dealing with the catastrophic complication of such postoperative hemorrhage.
Patients undergoing thoracoabdominal aortic aneurysm repair are at high risk of operative morbidity and death. Aortic clamping and unclamping stresses the myocardium, interrupts visceral and limb perfusion, and leads to metabolic acidosis. Use of a simple technique to preserve distal perfusion during the period of aortic clamping may reduce perioperative morbidity. We describe a technique of visceral and limb perfusion that may reduce surgical risk in high-risk patients.
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The efficacy of pulmonary artery balloon counterpulsation (PABC) has been previously demonstrated. Clinically this is usually achieved by suturing a Dacron graft to the side of the pulmonary artery with an intra-aortic balloon pulsating inside the graft. PABC via the percutaneous route has not been previously reported, although it has been demonstrated experimentally that an intrapulmonary artery balloon inserted via the outflow of the right ventricle provides effective counterpulsation. The morphologic effects of PABC on the heart and lungs have not been previously demonstrated. This study evaluates the feasibility of PABC via the percutaneous route and assesses the morphologic changes of PABC on the heart and lungs of pigs. Results indicate that PABC via the percutaneous route is technically feasible. However, after 24 h of PABC morphologic changes occurred in the heart and lungs, consisting of valvular and mural thrombi and hemorrhage. Histopathologic evaluation of the lungs revealed interstitial and intra-alveolar hemorrhage and pulmonary emboli. The etiology of these pathologic changes are likely multifactorial. Further studies are necessary to fully delineate the short and long term effects of PABC prior to initiation of clinical trials with this new percutaneous assist device.
Although the peripheral vascular effects of epinephrine have been characterized in animal models, similar studies have not been carried out in man. To determine the vascular effects of epinephrine the systemic circuit must be conceptually and surgically opened to allow for independent control of flow and pressure. This unique situation exists in man only while on total cardiopulmonary bypass with an external reservoir and pump interposed between the right atrium and the aorta. Under these conditions, peripheral vascular compliance, arteriolar and venous resistance, and the systemic time constant (a measure of the drainage characteristics of the vascular bed, in units of time) can be determined directly. Nine anesthetized patients undergoing normothermic cardiopulmonary bypass were studied before and during epinephrine infusion (5 micrograms/kg/min) after the aorta was cross-clamped and the heart had been isolated from the rest of the peripheral circulation. At constant blood flow epinephrine infusion increased blood pressure and reservoir volume (effectively decreasing blood volume) by an average of 360 ml. Although systemic vascular compliance decreased (due to venoconstriction), resistance to venous return decreased. Analysis of transient blood volume changes after a step change in right atrial pressure at constant blood flow revealed that blood was effectively draining from two vascular compartments with different time constants, as previously demonstrated in animal experiments. Epinephrine caused redistribution of blood flow away from the compartment with the longest time constant by constricting the arterioles leading to it. This accounts for the major increase in venous return and is almost entirely the mechanism of increased cardiac output in the normal individual after its administration, independent of its effects on the heart. In an attempt to localize the long and short time constant vascular compartments, three normal volunteers were studied. Thallium-201 whole body imaging at rest and after maximal treadmill exercise showed redistribution of blood flow away from the mesenteric bed and towards the muscle compartments. Although two similar compartment models of the circulation have been suggested by others, to our knowledge this type of analysis has not been carried out in man.
Pulsus paradoxus is the pathological exaggeration of the normal transient decrease in arterial blood pressure that occurs during spontaneous inspiration. The transient increase in arterial pressure associated with positive pressure inspiration is termed reversed pulsus paradoxus (RPP). Cardiorespiratory interactions and the mechanism of these effects have been studied extensively in animals, and to a lesser extent, in humans. In this clinical investigation pulsus paradoxus and RPP were studied in 10 postoperative cardiac patients with invasive monitoring and mediastinal pressure catheters placed intraoperatively. From end-expiration to end-inspiration, RPP was accompanied by decreased transmural pressures in the right atrium, left atrium, and aorta. Left ventricular end-systolic volume measured by radionuclide studies diminished during a positive pressure inspiration, without a significant change in end-diastolic volume. These results are consistent with decreased left ventricular afterload as the major mechanism of RPP. During spontaneous breathing, inspiration was associated with converse effects, a fall in arterial pressure and an increase in transmural right atrial, left atrial, and aortic pressures from end-expiration to end-inspiration. End-systolic volume was significantly larger at end-expiration than end-inspiration, with no change in end-diastolic volume. These findings suggest that an increase in left ventricular afterload during inspiration is responsible for the observed pulsus paradoxus.
We present a case of left ventricular (LV) rupture that occurred on the second day after inferolateral myocardial infarction (MI). An aggressive diagnostic approach with rapid coronary angiography prior to surgical repair provides a benefit characterized postoperatively by complete recovery of myocardial contractility in the akinetic infarcted area. We believe that coronary artery disease associated with subacute ventricular rupture may, in fact, be better investigated and simultaneously treated under a protocol of early surgical repair.
A technique was developed to permit multiple large biopsies of the in vivo myocardium to measure certain metabolites (ATP, CP, myocardial glycogen, lactate) with minimal chance of ventricular fibrillation or severe alterations in the heart's ability to maintain BP. Adult pigs with normal hearts (n = 9) as well as with hypertrophy (n = 5) created by aortic banding 3-4 months prior were anesthetized, intubated, and ventilated. After a sternotomy, the pericardium was opened and the epicardial surface was cleared of any adhesions. Biopsies were taken from the distal to proximal end of the heart. A suture (3-O Prolene) was placed in a figure-eight pattern in the area to be biopsied. A piece of the myocardium (50-100 mg) was grasped using a pair of narrow dressing forceps and frozen in liquid nitrogen. When the sample was completely frozen, a No. 11 scalpel blade, held at a 90 degrees angle to the epicardium throughout the cut, was used to carve out the full thickness biopsy. The sample was placed immediately in liquid nitrogen. The myocardial defect was repaired by using the previously placed suture buttressed with pieces of subcutaneous fat to prevent tearing the epicardial surface. This in vivo biopsy method has negligible complications and can be repeated or taught with constant reliability.