Fluorocarbons: A Potential Treatment of Cerebral Air Embolism in Open-Heart Surgery

This study was designed to assess whether an oxygenated fluorocarbon solution could reduce ischemic brain damage related to arterial air embolism. Air embolism was produced by injecting air bubbles into the carotid artery of barbiturate-anesthetized rats breathing 100% oxygen. Results were assessed on electrocorticogram. In an additional set of experiments, mass spectrometry was used to provide continuous monitoring of intracerebral tissue oxygen (Po₂) and carbon dioxide (Pco₂) tensions and intermittent measurement of cerebral blood flow (CBF). Fluorocarbon or saline solution (containing the emulsifying agent of fluorocarbons) was given intravenously after the initial air embolism (0.2 ml), and injections of air (0.1 ml) were repeated thereafter every five minutes.The maximal amount of air required to achieve complete and irreversible flattening of the electrocorticogram was 1.60 ± 0.06 ml (mean ± standard error of the mean) in the saline-treated rats and 5.20 ± 0.44 ml in the fluorocarbon-treated group (p < 10^-7). In the second experiment, air embolism caused CBF to rise in both groups, the average percent of increase being higher in treated (41.6%) than in control animals (38.3%) (p < 0.02). However, in the control group, the increase in CBF did not prevent intracerebral tissue Po₂ from decreasing by 7.4 ± 7.0% over the same period; conversely, in the fluorocarbon group, Po₂ levels fell by only 2.5 ± 3.7% (p < 0.001 versus controls), but this time-averaged percentage was calculated over a longer period of cumulative ischemia because of the greater number of air emboli tolerated by treated animals.We conclude that fluorocarbons seem to be effective in extending the tolerance of the brain to ischemic damage secondary to air embolism. Their protective mechanism most likely involves increased availability of oxygen for ischemic tissues and possibly indirect reduction of the size of air bubbles through enhanced denitrogenation of blood.     

Limitations of Potassium Cardioplegia during Cardiac Ischemic Arrest: A Phosphorus 31 Nuclear Magnetic Resonance Study

Cold K⁺ cardioplegia is commonly used to preserve the myocardium during surgical ischemia. Since the K⁺-induced membrane depolarization could cause a Ca²⁺-mediated breakdown of adenosine triphosphate, this study compared the influence of different electrolytes on high-energy phosphate metabolism during cardioplegic arrest and subsequent recovery of mechanical function. An isolated working heart was subjected to hypothermic ischemia for one hour. Metabolic studies were assessed on phosphorus 31 nuclear magnetic resonance (NMR). Results show that (1) K⁺ cardioplegia is harmful when the Ca²⁺ content is equal to 2 mEq/L; (2) deleterious effects of K⁺ are markedly reduced by lowering the Ca²⁺ content; (3) the most adequate preservation is provided by a Mg²⁺-rich–Ca²⁺-poor perfusate; (4) this protection is not enhanced by addition of K⁺. Finally, ³¹P NMR appears particularly appropriate for evaluating myocardial protection techniques since it allows noninvasive serial monitoring of high-energy phosphate content and subsequent correlation with functional recovery after ischemia.     

Author Index

During aortic valve surgery, cardioplegic solution is delivered through direct cannulation of both coronary ostia. Since this approach may cause an intimal injury leading to acute dissection or late ostial stenosis, we have evaluated retrograde coronary sinus perfusion (RCSP) as a means of delivering cardioplegia in 12 patients undergoing aortic valve replacement. The retroperfusion of the cardioplegic solution was performed with a balloon-tipped catheter inserted into the coronary sinus through the right atrium. The perfusion pressure averaged 40 mm Hg. Twelve patients undergoing antegrade coronary perfusion served as controls. Both groups were matched for preoperative and intraoperative data. The postoperative evaluation focused on hemodynamic status, as evidenced by serial measurements of right-sided pressures and cardiac output at 1, 6, 12, 18, and 24 hours after operation. The stroke volume index and the left ventricular and right ventricular systolic stroke work indexes were then calculated. There was no statistically significant difference between the two groups. We conclude that RCSP is a simple, safe, and effective means of cardioplegic protection during aortic valve surgery.     

Furosemide during sustained left atrial hypertension in functionally anephric dogs: intravascular and extravascular pulmonary fluid volumes. V

The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 +/- 2.1 mm Hg to 30.2 +/- 4.0 mm Hg (P less than 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 +/- 0.8 cc/kg at control to 21.7 +/- 2.0 cc/kg at 120 min, P less than 0.001), as had PBV (6.2 +/- 2.1 cc/kg to 9.1 +/- 3.1 cc/kg P less than 0.01). After furosemide injection (N = 6), LA pressure declined (mean peak reduction of approximately 6 mm Hg at 60-75 min, P less than 0.01), aortic and pulmonary arterial pressure both declined (P less than 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 +/- 0.4 cc/kg, P less than 0.01). In the untreated dogs, EVLW continued to climb (P less than 0.05 vs treated dogs at 75 min postfurosemide).(ABSTRACT TRUNCATED AT 250 WORDS)     

Anatomical Correction of Transposition of the Great Arteries

This method of true anatomical repair of transposition of the great arteries (TGA) avoids the transection and suture of the coronary arteries and does not require any tubes of foreign material. Because the transection goes through the infundibulum under the aortic annulus, the complete aortic root together with the coronary arteries and a muscular subvalvular rim can be sutured to the pulmonary annulus.The technical simplicity of this procedure allows its application in TGA with intact ventricular septum in the newborn when the left ventricular pressure is still high or after the left ventricle has been “prepared” by previous banding of the main pulmonary artery.     

The aorta-to-coronary radial artery bypass graft. A technique avoiding pathological changes in grafts

A technique of aorta-to-coronary artery bypass grafting using the patient's radial artery is proposed with the aim of reducing the incidence of late pathological changes in the graft. Experience with 40 radial artery grafts in 30 human patients has shown excellent short-term results and has demonstrated the primary importance of mechanical dilation of the arterial graft before implantation to counteract its spasm. Even though several advantages favor use of the radial artery over the vein for grafting (arterial structure, elasticity, regularity of the lumen) and over the mammary artery (graft size and length, resistance of the arterial wall), the ultimate fate of the radial artery graft needs a longer follow-up to be determined with certainty.     

Massive mitral regrgitation from chordal rupture and coronary artery disease

The precise mechanism that causes spontaneous rupture of chordae tendineae remains unknown. That it may occur in patients with no disease other than underlying or associated coronary artery occlusion has not been previously reported. Six patients with chordal rupture were found among 600 patients who underwent operation for mitral regurgitation in a 6-year period. All 6 patients without exception underwent simultaneous mitral valve replacement and coronary revascularization. The salient clinical features of these patients are summarized, and 1 case is reported in detail.     

Posterior Rupture of the Interventricular Septum after Acute Myocardial Infarction: Successful Early Surgical Repair

A patient with a large posterior ventricular septal defect complicating an acute inferior myocardial infarction is reported. Because of medically intractable biventricular failure, temporary circulatory assistance was initiated using intraaortic balloon pumping. Emergency coronary angiography, ventriculography, and subsequent operation were carried out. Operative repair involved closure of the septal defect with the use of a Dacron patch, infarctectomy, and aortocoronary bypass grafting and resulted in long-term survival of the patient.