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Biomedical subjects

M J Buckley

Publications and source records attributed to M J Buckley.

At least 127 records · Page 7Linked to original sources
PubMed1986

Effect of experimental cardiopulmonary bypass on systemic and transcardiac thromboxane B2 levels.

Systemic and cardiac metabolism of thromboxane was studied in a canine model (n = 13) of standard cardiopulmonary bypass and surgical cardioplegia. Sterile techniques were applied and no donor blood was used. Systemic samples (thoracic aorta) and transcardiac gradients (coronary sinus - aortic root) were obtained (1) 5 minutes after cannulation, (2) 20 minutes after the onset of partial bypass, (3) 5 seconds after the first administration of cardioplegic solution (CP-1), and (4) 5 seconds after the second administration of cardioplegic solution (CP-2). Cardioplegic doses were administered 30 minutes apart and consisted of 500 ml of hypothermic (8 degrees C), hyperkalemic (25 mEq potassium chloride) solution infused into the aortic root at 60 to 70 mm Hg. Thromboxane B2 was determined by a double-antibody radioimmunoassay (picograms per milliliter +/- standard error of the mean). Onset of partial bypass was followed by a significant rise in systemic arterial thromboxane B2 levels: after cannulation, 115 +/- 21 pg/ml; after the onset of partial bypass, 596 +/- 141 pg/ml; p less than 0.01). Significant transcardiac thromboxane B2 gradients were found during the first and second cardioplegic washouts (CP-1: aortic root 73 +/- 12 pg/ml, coronary sinus 306 +/- 86 pg/ml, p less than 0.01; CP-2: aortic root 65 +/- 11 pg/ml, coronary sinus 355 +/- 98 pg/ml, p less than 0.01). Transcardiac gradients of 6-keto-prostaglandin F1 alpha and thromboxane B2 were obtained at CP-1 and CP-2. Gradients of 6-keto-prostaglandin F1 alpha were not different from thromboxane B2 gradients during CP-1 but were significantly higher than thromboxane B2 gradients during CP-2. In a subgroup of five dogs, transcardiac thromboxane B2, lactate, and platelet gradients were measured simultaneously. Cardiac thromboxane B2 generation was found only in the presence of cardiac lactate production. Transcardiac platelet gradients were significantly higher at CP-1 (13,900 +/- 3,000/mm3) than at CP-2 (4,000 +/- 1,230/mm3) (p less than 0.05), whereas thromboxane B2 gradients were similar at CP-1 and CP-2. Our study demonstrates that thromboxane B2 is released into the coronary circulation during surgical cardioplegic arrest with anaerobiosis.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Prosthetic valve endocarditis. Analysis of factors affecting outcome of therapy.

We analyzed the outcome of 116 patients with prosthetic valve endocarditis treated between 1975 and 1983 and used multivariate analysis to identify risk factors for in-hospital mortality and bad outcome during follow-up. Complicated prosthetic valve endocarditis was defined as the presence of a new or changing heart murmur, new or worsening heart failure, new or progressive cardiac conduction abnormalities, or prolonged fever during therapy. Complicated prosthetic valve endocarditis was present in 64% of patients; factors associated with complicated prosthetic valve endocarditis included aortic valve infection (odds ratio 4.3, p = 0.002) and onset of endocarditis within 12 months of the cardiac operation (odds ratio 5.5, p = 0.0001). The in-hospital mortality rate for prosthetic valve endocarditis was 23%; patients with complicated prosthetic valve endocarditis had a higher mortality than patients with uncomplicated infection (odds ratio 6.4, p = 0.0009). Combined medical-surgical therapy was used in 39% of patients; surgical therapy was more common in patients with complicated prosthetic valve endocarditis (odds ratio 16, p less than 0.0001) and in patients infected with coagulase-negative staphylococci (odds ratio 3.9, p = 0.003). Survival after initially successful therapy for prosthetic valve endocarditis was adversely affected by the presence of moderate or severe congestive heart failure at hospital discharge (p = 0.03). Bad outcome during follow-up (death, relapse of prosthetic valve endocarditis, or subsequent cardiac operation related to sequelae of the original infection) was more common in the medical than the medical-surgical therapy group (p = 0.02). The difference in long-term outcome between patients treated initially with medical or with medical-surgical therapy was particularly evident in those with complicated prosthetic valve endocarditis (p = 0.008). The presence of complicated prosthetic valve endocarditis is a central variable in assessing prognosis and planning therapy; the majority of patients with complicated prosthetic valve endocarditis are best treated with medical-surgical therapy. Those who are not treated surgically during their initial hospitalization are at high risk for progressive prosthesis dysfunction and require careful follow-up.

Adult↗
PubMed1985

Risk factors for the development of prosthetic valve endocarditis.

Risk factors for the development of prosthetic valve endocarditis (PVE) were analyzed in 2642 patients undergoing initial valve replacement at the Massachusetts General Hospital from 1975 to 1982. Follow-up was available for 2608 patients (98.7%); the mean length of follow-up was 39.8 months. PVE developed in 116 patients (4.4%). The actuarial risk of PVE was 3.1% at 12 months and 5.7% at 60 months. A Cox model was used to identify risk factors for PVE. Recipients of multiple valves had a higher risk of PVE than single valves (p = .01). There was no difference in the risk of PVE for patients receiving aortic valves vs those receiving mitral valves. Recipients of mechanical valves had a higher risk of PVE than recipients of porcine valves in the first 3 months after surgery (p = .02), but the risk of PVE was higher for porcine valve recipients 12 months or more after surgery (p = .004). Despite this difference in the time course of development of PVE, there was no significant difference in the cumulative risk of PVE by 5 years of follow-up between mechanical and porcine valve recipients. Male sex was a risk factor for PVE within 12 months of aortic valve replacement (p = .008) but not thereafter; sex did not influence the risk of PVE after mitral valve replacement. Older patients had a higher risk of late PVE after multiple (p = .04) or mitral valve replacement (p = .08), but not after aortic valve replacement.

Endocarditis↗
PubMed1985

Myocardial revascularization with combined aortic and mitral valve replacements.

Although the results of coronary artery bypass grafting plus single aortic or mitral valve replacement have been documented, the risk of myocardial revascularization with combined aortic and mitral valve replacement is not well defined. We present a series of 33 consecutive patients undergoing myocardial revascularization with combined aortic and mitral valve replacement during a period of almost seven years. There were 21 men and 12 women with a mean age of 67 years. All patients had congestive heart failure, and 21 (64%) had angina pectoris. Mean New York Heart Association functional classification was 3.4; eight patients (24%) had ejection fractions less than 0.40, and 13 patients (41%) had cardiac indices less than 2.0 L/min/m2. All operations were performed with hypothermic crystalloid potassium cardioplegia. The number of coronary arteries grafted varied from one to four (mean, 1.7 grafts per patient). Four patients died while in the hospital (12.1%). There were no perioperative myocardial infarctions. At a follow-up of 2 to 80 months (mean 40.7 months), death had occurred in eight (27.6%) of the 29 hospital survivors. Actuarial survival rate at 72 months was 60.7%. Although no preoperative factors predicted late death, early deaths were related significantly to severe mitral regurgitation, low ejection fraction, high New York Heart Association classification and extensive coronary artery disease (p less than 0.05). Myocardial revascularization with combined aortic and mitral valve replacement can be performed with an acceptable early mortality rate but with an appreciable late mortality rate.

Actuarial Analysis↗
PubMed1985

Early detection of cardiac allograft rejection with proton nuclear magnetic resonance.

No reliable, noninvasive technique is currently available for the early detection of cardiac transplant rejection. In this study, pulse nuclear magnetic resonance (NMR) spectroscopy was used (20 MHz) to detect cardiac allograft rejection in rats. Proton spin-lattice relaxation time (T1), proton spin-spin relaxation time (T2), and water content were measured in both recipient and donor hearts at 2, 4, 6, and 8 days after transplantation. Pathologic specimens were scored on a 0 to 4+ scale of increasing evidence of rejection by light microscopy. Three kinds of heterotopic transplants were performed for a total of 90: (1) Lewis rats received Lewis rat isografts, (2) Lewis rats received Brown Norway rat allografts, and (3) Lewis rats received cyclosporin A-treated allografts (15 mg/kg/day). T1 in group 2 was significantly higher than that in group 1 as early as day 2 (670 + 25 vs 616 + 11 msec, p less than .001), when histologic scores were not different. T2 in group 2 was also higher than that in group 1 (48.0 +/- 5.0 vs 41.1 +/- 2.6, p less than .005). T1 and T2 in group 2 increased from day 4 and correlated well with the water content of the hearts (r = .70 and r = .75, respectively). Cyclosporin A completely suppressed the increase of T1 and T2 in group 2. Treatment with cyclosporin also suppressed the histologic rejection scores. Our data suggest that proton relaxation time measurement may be a sensitive technique for detecting the onset of rejection and examining the therapeutic effects of cyclosporin. NMR imaging, which highlights T1 and T2 separately, should provide a sensitive noninvasive means of assessing myocardial graft rejection.

Animals↗
PubMed1985

Prostaglandin E1. A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement.

Patients undergoing mitral valve replacement, particularly those with severe pulmonary hypertension and/or congestive heart failure, may develop life-threatening right heart failure in the immediate postbypass period. We have observed that such patients have intense pulmonary vasoconstriction. The markedly increased pulmonary impedance may aggravate the right heart failure and prevent recovery of right ventricular function in this setting. Therefore, we studied the effects of high-dose prostaglandin E1 (30 to 150 ng/kg/min), a potent pulmonary vasodilator, in combination with massive infusion of norepinephrine (up to 1 microgram/kg/min) into the left atrium in five consecutive patients with refractory right heart failure and pulmonary hypertension after mitral valve replacement. This pharmacologic approach takes advantage of the pulmonary vasodilating effects of prostaglandin E1, while offsetting associated systemic vasodilation and resulting hypotension. All five patients had rapid pulmonary vasodilator responses followed by marked improvement in right ventricular function. All survived the operation and none had right ventricular infarction or chronic right heart failure postoperatively.

Adult↗
PubMed1984

Predictors of survival after tricuspid valve surgery.

The long-term survival rate of 74 consecutive patients who underwent multiple cardiac valve surgery including tricuspid valve surgery was analyzed to identify predictive preoperative clinical variables. Univariate analysis revealed that male sex (P less than 0.04), symptoms of New York Heart Association functional class IV heart failure (p less than 0.004), ascites or pulmonary edema (p less than 0.01), high preoperative bilirubin level (p less than 0.012), mean pulmonary artery pressure greater than 40 mm Hg (p less than 0.038) and pulmonary vascular resistance greater than 6 Wood units (p less than 0.02) were each associated with an increased risk of death after surgery. Stepwise multivariate analysis indicated that severity of preoperative edema and mean pulmonary artery pressure were the most predictive combination of independent variables. These 2 variables were used to calculate an estimated probability of 1-year survival after surgery for patients with multivalvular cardiac decompensation. Recognition of these preoperative variables should assist the clinician in determining the risk of surgical intervention.

Adult↗
PubMed1984

Long-term survival of patients with treated aortic dissection.

Retrospective data on the treatment of aortic dissection at the Massachusetts General Hospital from 1963 to 1978 are reported. During this period, 160 patients with spontaneous aortic dissection were treated by definitive medical or definitive surgical therapy. Patients were classified according to type (proximal versus distal) and duration (acute versus chronic) of dissection. Long-term follow-up (mean 48 months, range 1 to 147) was available in 156 cases. Hospital and late survival in each of the categories of dissection were evaluated in relation to those features of the dissection itself and of the subsequent therapy that correlated with ultimate survival. Results show that: 1) chronic presentation was the most significant determinant of both hospital and late survival; 2) in acute dissection, prognosis was determined largely by the presence or absence of major complications, regardless of ultimate therapy; the only complication without adverse effect on survival was aortic insufficiency; 3) late survival after discharge from the hospital was similar for patients with all types of dissection and modes of therapy; and 4) the incidence of late complications from aortic dissection was lower than previously reported. Thus, the success of early definitive medical and surgical treatment was sustained on long-term follow-up.

Acute Disease↗
PubMed1984

Dynamic patch artificial myocardium; effects on the residual myocardial function.

Dynamic patch artificial myocardium (D-PATCH) has been developed to replace the damaged left ventricular (LV) wall in severe cardiogenic shock patients with a massive myocardial infarction. This study was undertaken to demonstrate the effects of (1) single D-PATCH support on the global cardiac function (group 1, 12 dogs, whole heart model), (2) single D-PATCH support on the LV function and myocardial metabolism (group 2, 6 dogs, right heart bypass model), and (3) the concomitant support of D-PATCH and aortic counterpulsation (CP) on the regional myocardial function of the residual LV wall (group 3, 6 dogs, right heart bypass model with ultrasonic piezoelectric crystals). In group 1, mean aortic pressure and cardiac output were increased 20-36% (p less than 0.01) and 17-50% (p less than 0.01) respectively, and mean left atrial pressure was decreased 16% (p less than 0.01) by D-PATCH assist. In group 2, under constant preload volume, afterload pressure and heart rate, tension time index (TTI) was decreased 21-26% (p less than 0.01) and myocardial oxygen consumption was also decreased 24-29% (p less than 0.001) by D-PATCH assist. In group 3, although peak LVP was increased by single D-PATCH assist, when heart was assisted concomitantly by D-PATCH and CP peak LVP was significantly decreased (18%, p less than 0.01). Percent LV segmental shortening was not increased by CP assist, but increased 143% (p less than 0.02) by D-PATCH assist. In conclusion, D-PATCH can improve the global LV function and myocardial metabolism of the ischemic failing heart, also improve the regional myocardial function of the residual LV wall. Thus, D-PATCH is effective for the salvage of ischemic myocardium while maintaining the global cardiac function.

Animals↗
PubMed1984

Cardiac prostacyclin kinetics during cardiopulmonary bypass.

We have investigated the response of systemic and myocardial prostacyclin metabolism to cardiopulmonary bypass and 30 minutes of hypothermic (22 degrees C), hyperkalemic (25 mEq K+) surgical cardioplegia. Thirteen adult mongrel dogs of either sex (range 21 to 36 kg) underwent sterile cardiopulmonary bypass without donor blood. Prostacyclin levels were obtained after cannulation, 20 minutes after onset of partial bypass, and 5 seconds after the onset of cardioplegia 1 (CP-1) and cardioplegia 2 (CP-2, 30 minutes later). Samples were drawn from the thoracic aorta, the aortic root below cross-clamping, and the coronary sinus. The stable metabolite of prostacyclin, 6-keto-PGF1 alpha was measured by double-antibody radioimmunoassay (pg/ml; values +/- standard error of the mean). We found that the onset of partial bypass is associated with significant increase in the systemic production of 6-keto-PGF1 alpha (122 +/- 33 versus 518 +/- 187; p less than 0.05), which persists throughout the experiment. A small but significant positive cardiac gradient of 6-keto-PGF1 alpha is found after cannulation (aortic root 122 +/- 33, coronary sinus 202 +/- 57, p less than 0.05). This gradient is more pronounced during partial bypass (aortic root 518 +/- 187, coronary sinus 686 +/- 186 p less than 0.05), when significant cardiac lactate extraction (p less than 0.005) is observed. After cross-clamping, a significantly increased gradient of 6-keto-PGF1 alpha is found during CP-1 (aortic root 74 +/- 10, coronary sinus 264 +/- 46, p less than 0.05 versus cannulation) in the presence of significant cardiac lactate production (p less than 0.005). A further significant increase in 6-keto-PGF1 alpha production is noted during the CP-2 infusion (aortic root 73 +/- 10, coronary sinus 483 +/- 83; p less than 0.01 versus CP-1), which is inversely related to cardiac oxygen uptake and endocardial/epicardial flow ratio. Our data demonstrate significant production of prostacyclin in the systemic and cardiac circulations during cardiopulmonary bypass and surgical cardioplegia. They further indicate that both ischemic and nonischemic stimuli regulate prostacyclin metabolism during cardiopulmonary bypass.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Vascular complications of intra-aortic balloon counterpulsation.

Although the intra-aortic balloon pump (IABP) saves many lives, complication rates as high as 36% have been reported. Many of the complications require surgical attention. In 794 patients of the Massachusetts General Hospital in Boston, an IABP was inserted into either the femoral or iliac artery between Nov 1, 1968, and June 30, 1981. Eighty-seven major vascular complications occurred in 70 (8.8%) of them. Of those 70 patients, 95% denied previous symptoms of vascular disease, and 78% had had normal pulses before insertion. The two most common complications were limb ischemia (n = 36) and arterial trauma (n = 20). Other complications included sepsis (n = 14), wound problems (n = 10), and hemorrhage (n = 7). No limbs were lost. Analysis of each group of complications allowed specific conclusions to be drawn concerning prevention, early diagnosis, and the most appropriate treatment.

Adult↗
PubMed1983

Myocardial protection by lidocaine during cardioplegia.

This study was undertaken to examine the effects of lidocaine (L) (400 mg/liter) in a normokalemic crystalloid (S) (K +: 5 meq/liter, Na+: 120 meq/liter) and in a hyperkalemic crystalloid cardioplegic solution (K) (K+: 25 meq/liter, Na+: 120 meq/liter) during 90 min of hypothermic (28 degrees C) aortic occlusion followed by 45 min of reperfusion (R). Four groups of dogs were studied: group 1 (S), n = 6; group 2 (S + L), n = 6; group 3 (K), n = 6; group 4 (K + L), n = 6. Left ventricular (LV) function was defined as percentage changes in center of mass between pre- and postarrest function curves. Regional myocardial flow was measured with 9 mu radioactive microspheres and myocardial metabolism monitored by lactate and oxygen utilization. Ventricular biopsies were obtained for measurement of myocardial ATP, creatine phosphate, and water content. Percent recovery of LV function curves at the end of (R) was 59.2 +/- 3.9% in group 1, 85.0 +/- 4.3% in group 2, 71.5 +/- 4.9% in group 3, and 87.0 +/- 4.5 in group 4 (group 1 vs group 2, P less than 0.01; group 3 vs group 4, P less than 0.05). Metabolic recovery was evaluated at 5, 20, and 45 min of (R). Only group 3 (K) demonstrated persistent lactate production at 5 min of (R) (P less than 0.01). The hyperkalemic groups failed to return to control levels of oxygen utilization after 5 min of (R) (group 3, P less than 0.05; group 4, P less than 0.05). LV endocardial/epicardial myocardial blood flow ratio demonstrated greater increase in hyperkalemic groups (group 3, P less than 0.01; group 4, P less than 0.01) at 5 min of (R). ATP was significantly decreased in groups 1, 3 and 4, but not in group 2 at the end of ischemia (group 1, P less than 0.01; group 3, P less than 0.01; group 4, P less than 0.05) and after 45 min of (R) (group 1, P less than 0.05; group 3, P less than 0.01; group 4, P less than 0.01). These results demonstrate that lidocaine has a myocardial protective effect which is superior to standard hyperkalemic cardioplegia. Moreover, lidocaine has an additive salutary effect during potassium cardioplegia. Persistent metabolic derangements post reflow in the hyperkalemic groups suggest deleterious effects of hyperkalemia on subendocardial protection.

Animals↗
PubMed1983

Electrophysiologic studies before and after myocardial revascularization in patients with life-threatening ventricular arrhythmias.

Electrophysiologic studies with programmed cardiac stimulation were performed in a selected group of 17 patients with severe proximal coronary artery disease involving at least 2 major vessels and left ventricular ejection fractions greater than 30% who were undergoing coronary artery bypass graft surgery after prehospital cardiac arrest or ventricular tachycardia (VT) unassociated with acute myocardial infarction. Before surgery and without antiarrhythmic drug therapy, programmed cardiac stimulation induced ventricular fibrillation (VF) in 4 patients, and VT (greater than or equal to 5 beats) in 11 patients. Inducible VT or VF was suppressed by antiarrhythmic drugs in 7 of 13 patients in whom they were tried. Patients underwent coronary artery bypass graft surgery unassociated with perioperative myocardial infarction. When studied again an average of 19 days after surgery, 10 patients had no inducible VT or VF without antiarrhythmic drug therapy; 6 had induced VT. One patient had spontaneous VT. An effective antiarrhythmic regimen that suppressed inducible or spontaneous VT, or both, was defined by serial electrophysiologic studies in 4 patients, whereas 3 patients continued to manifest electrically inducible VT with all antiarrhythmic regimens tested. All but 1 patient, in whom postoperative VT could not be suppressed, are free of arrhythmias after a mean follow-up period of 23 months (range 6 to 53). It is concluded that myocardial revascularization alone may improve the abnormal electrophysiologic findings in certain patients; however, this effect of coronary artery bypass graft surgery is unpredictable, and pre- and postoperative electrophysiologic studies are recommended as part of the evaluation of these patients.

Aged↗
PubMed1983

Pulsatile and nonpulsatile cardiopulmonary bypass: review of a counterproductive controversy.

In the controversy over pulsatile and nonpulsatile perfusion, most authors have failed to recognize the fundamental physical differences between the two methods. Pulsatile perfusion is polymorphic and its form varies with both the pulsatile source and the vascular system being perfused; nonpulsatile perfusion is by definition unvarying and uniform. While many studies of hemodynamics, metabolism, organ function, microcirculation, and histology show benefits derived from pulsatile perfusion, others do not. The simplest explanation for these conflicts is that different investigators employ different forms of pulsatile perfusion, only some of which are effective. Failure to quantitate adequately the pulsatile components of flow in these studies prevents differentiation between effective and ineffective forms of pulsatile flow and makes comparison of studies difficult. Future research in this area should be directed toward definition of effective pulsatile perfusion by adequate measurement of the pulsatile components of perfusion.

Cardiopulmonary Bypass↗
PubMed1983

Temperature gradients and rewarming time during hypothermic cardiopulmonary bypass with and without pulsatile flow.

Pulsatile perfusion during cardiopulmonary bypass (CPB) has been reported to have a number of beneficial effects, including attenuation of hormonal stress responses and improved organ blood flow and function. To determine the effect of pulsatile perfusion on temperature gradients and the time required for cooling and rewarming during CPB, we studied 21 patients scheduled for elective coronary artery operations. The patients were divided into two comparable groups: Group 1 (N = 11) had standard nonpulsatile perfusion, while in Group 2 (N = 10), a pulsatile pump was used. Rectal and esophageal temperatures were monitored, as were deltoid muscle temperatures and upper arm and finger skin temperatures in the same extremity. Ambient temperature, bypass flow and pressure, and bypass time were similar in both groups. Time required to cool to the lowest esophageal temperature was virtually identical for both groups (Group 1, 17 +/- 3 min; Group 2, 17.6 +/- 5 min), as was rewarming time (Group 1, 26.8 +/- 11 min; Group 2, 27.2 +/- 6 min). There were no significant differences in temperature measurements between groups except briefly during rewarming when finger skin temperature rose more rapidly in Group 1 (p less than 0.05). Temperature changes following CPB were the same for both groups, with rectal and esophageal temperatures showing an inverse relationships. These data demonstrate that pulsatile flow does not substantially alter rewarming time or temperature gradients during hypothermic CPB.

Aged↗
PubMed1983

Blood cardioplegia delivery. Deleterious effects of potassium versus lidocaine.

Delivery of cardioplegic (CP) solutions to all regions of the myocardium is critical for optimal myocardial protection during cardiac surgery. However, there are little data regarding the effects of CP agents upon coronary vascular resistance (CVR) and CP delivery. Accordingly, we evaluated blood CP (Hct 30) delivery and CVR during 75 minutes of multi-dose hypothermic blood CP arrest in an in vivo isolated dog heart preparation. Three groups of dogs were studied: K(K+ = 30 mEq/L; n = 6), L (Lidocaine = 400 mg/L; K+ = 4 mEq/L; n = 6), and KL (K+ = 30 mEq/L, Lidocaine 400 mg/L; n = 6) during total cardiopulmonary bypass and moderate systemic hypothermia (28 C). Basal CVR was calculated by measuring total coronary flow (HR 120/min; mean aortic pressure = 80 mmHg) in the empty beating heart. After aortic cross-clamping, the blood CP solution was infused into the aortic root at a constant pressure (80 mmHg) and constant temperature (16 +/- 2 C) for 60 seconds at 15 minute intervals for a total arrest time of 75 min. Total CP flow, CVR, O2 consumption, lactate extraction/production, and K+ balance during 75 minutes of arrest and 30 minutes of reperfusion were determined. The distribution of the CP solution in the left ventricle was measured with radioactive microspheres (9 +/- 1 mu). Biopsy specimens were taken to measure wet to dry ratios. Values are mean +/- SEM. Data were analyzed by BMDP-P2V. During the first CP infusion, after aortic cross-clamping, no differences in CVR or CP distribution were found among the three groups. However, CVR was increased significantly in the K group during the second CP infusion (O': 0.98 +/- 0.20 mmHg/ml/min/100 g; 15': 2.66 +/- 0.82; p less than 0.001). The CVR remained high for the remainder of the arrest period. Moreover, total, epi- and endocardial flow decreased significantly (54%, p less than 0.001). In groups L and KL, no significant changes in CVR were seen. Groups K and KL showed a significant K+ extraction during the first CP infusion. During the early reperfusion period, K+ washout occurred in these two groups, which was not seen in the L group. There was no significant difference between the three groups in myocardial O2 consumption, lactate metabolism, and water content during the arrest and the reperfusion period. In conclusion, high concentrations of K+ (30 mEq/L) can markedly increase CVR and impair blood CP delivery and distribution. These effects can be prevented by lidocaine. These findings warrant reassessment of the various additives to CP solutions and their effects on CVR and CP distribution during multi-dose hypothermic CP arrest.

Animals↗
PubMed1983

Serial changes in left ventricular ejection fraction in the early hours after aortocoronary bypass grafting.

To determine the course of left ventricular ejection fraction (LVEF) in the early hours after aortocoronary bypass grafting, 24 patients underwent serial gated bloodpool scanning. Twenty-two had received propranolol until the day of surgery. ECGs showed no evidence of perioperative infarction. Preoperatively, the mean (+/- SD) LVEF was 0.56 +/- 0.13; after bypass, it was 0.38 +/- 0.11 at 4 hours, 0.42 +/- 0.12 at 5 hours, 0.43 +/- 0.11 at 6 hours, 0.48 +/- 0.13 at 7 hours, 0.52 +/- 0.15 at 8 hours, and 0.54 +/- 0.15 at 10 to 14 days. The LVEFs at 4, 5, and 6 hours postoperatively were significantly lower than preoperatively (p less than 0.05). Postoperative mean heart rate was higher at all times; mean temperature was depressed at 4 and 5 hours and elevated at 7 and 8 hours; and mean arterial blood pressure was depressed at 7 hours, 8 hours, and 10 to 14 days (p less than 0.05). The degree of the early postoperative LVEF depression correlated with the daily preoperative propranolol dose (p less than 0.05) and was unrelated to bypass time, aortic cross-clamp time, or changes in temperature, heart rate, and blood pressure. The LVEF at 10 to 14 days postoperatively was not significantly different from the preoperative value. The LVEF is depressed in the early hours after aortocoronary bypass grafting and approaches the preoperative value with time. The magnitude of the early depression appears to be related to the preoperative propranolol dose, but does not significantly correlate with factors related to surgical technique.

Adult↗