Inconsistent effectiveness of myocardial preservation among cardiac chambers during hypothermic cardioplegia

The purpose of this study was to examine the selective and differential natures of ischemic injuries among three cardiac chambers (right atrium, right ventricle, and left ventricle) from the viewpoint of ultrastructural morphometric study. Twenty consecutive adult patients undergoing cardiac operations were studied. The duration of aortic crossclamp time varied from 36 to 142 minutes (mean 83.4 +/- 36.4 minutes). Two serial specimens (preischemic and ischemic) were obtained from the right atrium, the right ventricle, and the left ventricle, respectively. A total of 120 biopsy specimens was obtained from these 20 patients. The average mitochondrial surface area of the left ventricle was 0.308 +/- 0.062 micron 2 in the preischemic stage and 0.352 +/- 0.083 microns 2 in the ischemic stage. This represented a 14.3% increase in mitochondrial surface area after ischemic injury (p less than 0.01). The mitochondrial surface area of the right ventricle showed an average increase of 43.7%, from 0.252 +/- 0.036 micron 2 in the preischemic stage to 0.362 +/- 0.087 micron 2 in the ischemic stage (p less than 0.0005). With respect to the mitochondrial surface area of the right atrium, there was an increase of 88.0%, from 0.217 +/- 0.044 micron 2 in the preischemic stage to 0.408 +/- 0.084 micron 2 (p less than 0.0005). The difference of mitochondrial swelling among three chambers was statistically significant (right atrium versus right ventricle versus left ventricle, p less than 0.0005). Moreover, the differences of mitochondrial swelling between any two chambers were also highly significant (right atrium versus right ventricle, p less than 0.0005; right ventricle versus left ventricle, p less than 0.01; right atrium versus left ventricle, p less than 0.0005). In conclusion, our findings suggest that from the viewpoint of ultrastructural morphometric study myocardial injury after an average of 83 minutes of ischemic arrest is poorer in the right chambers of the heart than in the left ventricle, with the right atrium having the poorest preservation.     

Effects of elevated coronary sinus pressure on left ventricular function after the Fontan operation. An experimental and clinical correlation

An experimental model was devised to evaluate the effects of elevated coronary sinus pressure on left ventricular performance. Thirteen mongrel dogs were used. The coronary sinus was cannulated and its entire blood flow diverted into a reservoir. The pressure in the coronary sinus was increased from 5 to 25 torr by elevating the drainage reservoir in a stepwise fashion. Cardiac index, coronary arteriovenous difference, rate of rise of left ventricular pressure, left ventricular systolic time intervals, and coronary blood flow were measured. When the coronary sinus pressure reached 15 torr, there was a significant decrease in cardiac index (3.60 +/- 0.5 to 2.70 +/- 0.6 L/min/m2, p less than 0.001), coronary blood flow (13.7 +/- 3.1 to 7.0 +/- 2.1 ml/min, p less than 0.001), rate of rise of left ventricular pressure (1,567 +/- 275 to 1,331 +/- 314, p less than 0.05), and an increase in coronary arteriovenous difference (62.8% +/- 9.3% to 70.5% +/- 5.4% saturation, p less than 0.03). These experimental results were correlated with postoperative catheterization findings in 24 patients with the Fontan procedure. Patients with a mean right atrial pressure less than 15 torr had a left ventricular ejection fraction of 93% +/- 6% of predicted, whereas patients with a right atrial pressure of 15 torr or more had a left ventricular ejection fraction of 75% +/- 13% of predicted (p less than 0.001). These experimental and clinical data strongly suggest that elevated coronary sinus pressure has deleterious effects on ventricular function after the Fontan procedure. Modifications of the procedure, such as using the rudimentary right ventricle when feasible or diverting coronary sinus flow to the pulmonary venous atrium, might decrease coronary sinus hypertension and improve long-term results.     

Right atrial isolation: a new surgical treatment for supraventricular tachycardia. II. Hemodynamic effects

Surgical isolation of the body of the right atrium presents a unique hemodynamic situation in which the synchronous right atrial contraction (kick) is lost but the synchronous left atrial contraction is preserved. The hemodynamic effects of this procedure were evaluated by pacing at selected atrial sites postoperatively to simulate (1) sinus rhythm with a synchronous right atrial kick, (2) sinus rhythm without a synchronous right atrial kick, (3) right atrial tachycardia propagated to the entire heart (propagated right atrial tachycardia), and (4) right atrial tachycardia confined to the isolated right atrium with sinus rhythm in the rest of the heart (confined right atrial tachycardia). Hemodynamic data recorded under these four conditions showed that (1) during sinus rhythm, synchrony of right atrial contraction had no significant effect on any of the hemodynamic parameters studied and (2) conversion from propagated right atrial tachycardia to confined right atrial tachycardia resulted in an increase in mean arterial pressure (65 +/- 5 to 78 +/- 3 mm Hg, p less than 0.005) and stroke volume index (9 +/- 1 to 19 +/- 3 ml/beat/m2, p less than 0.005) with a decrease in left atrial pressure (9 +/- 2 to 5 +/- 1 mm Hg, p less than 0.05) and right atrial pressure (6 +/- 1 to 5 +/- 1 mm Hg, p less than 0.05). Moreover, cardiac hemodynamic performance remained within normal limits for up to 14 weeks. Thus the right atrial isolation procedure does not adversely affect cardiac hemodynamics despite the loss of synchronous right atrial contraction during sinus rhythm, and the procedure prevents hemodynamic deterioration during right atrial tachycardia.     

Comparison of blood cardioplegia to electrolyte cardioplegia on the effectiveness of preservation of right atrial myocardium: mitochondrial morphometric study

The right atrium differs from the left ventricle in two respects during cardioplegic arrest: a higher proportion of noncoronary collateral flow is delivered to the right atrium, and the atrium is frequently excluded from topical ice cooling because of its higher position relative to the left ventricle. These factors result in early rewarming of atrial myocardium. To the best of our knowledge, the surgical literature contains no reports on whether blood cardioplegia can provide better atrial myocardial preservation than electrolyte cardioplegia. Twenty consecutive patients who underwent cardiac operations were randomly selected to receive blood cardioplegia (Group 1) or electrolyte cardioplegia (Group 2). Hypothermia was achieved by systemic cooling and continuous topical cooling with ice slush. Stereological morphometric study of mitochondria was performed on 40 biopsy specimens taken from the right atrium prior to aortic cross-clamping (preischemia) and at the end of ischemia. In Group 1, total aortic cross-clamp time was 72.8 +/- 32.5 minutes. The mean mitochondrial surface area before ischemia was 0.224 +/- 0.032 mu 2 and after ischemia, 0.336 +/- 0.032 mu 2, a 50.0% increase in mitochondrial size. In Group 2, total aortic cross-clamp time was 69.7 +/- 30.9 minutes. The mean mitochondrial surface area before ischemia was 0.205 +/- 0.025 mu 2 and after ischemia, 0.439 +/- 0.111 mu 2, an average increase in mitochondrial size of 114.2%. There was no significant difference between the two groups in mitochondrial size before ischemia. However, after ischemia the mean mitochondrial surface areas were significantly different (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of protamine sulfate are dependent on the presence and type of circulating heparin

Man's response to clinical doses of protamine is highly variable. We investigated the influence of circulating heparin in nine swine (mean age 6 weeks, weight 10 kg). Through a sternotomy we implanted an electromagnetic flow probe around the pulmonary artery for cardiac output determination and catheters into the ascending aorta, pulmonary artery, right atrium, and left atrium for pressure monitoring. Each animal was allowed to recover and was studied awake on 3 consecutive days. Protamine, 3 mg/kg, beef lung heparin, 300 U/kg, and pork mucosal heparin, 300 U/kg, followed by protamine, were given in rotation by intravenous bolus. Protamine alone had no effect. Beef lung heparin followed by protamine induced a marked increase in pulmonary artery pressure (mean 38 +/- 3 to 51 +/- 5 mm Hg in 3 minutes). Pulmonary vascular resistance doubled (mean 0.12 +/- 0.01 to 0.23 +/- 0.04 R within 4 minutes), returning to normal within 15 minutes. Cardiac index and aortic pressure changed minimally. Pork mucosal heparin followed by protamine induced a similar but greater increase in mean pulmonary arterial pressure; however, cardiac index fell significantly (p less than 0.05, 207 +/- 16 to 117 +/- 16 ml/kg/min-1 at 1 minute) despite a regular rhythm and adequate left atrial filling pressure. Thus cardiac contractility was depressed. Systemic hypotension occurred in three of nine pigs. Both mean pulmonary vascular resistance and systemic vascular resistance increased (0.12 +/- 0.01 to 0.67 +/- 0.25 R and 0.40 +/- 0.04 to 1.09 +/- 0.25 R, respectively), significantly (p less than 0.05) more with pork than beef heparin. These data demonstrate that cardiovascular response to protamine neutralization varies significantly in regard to the type of heparin used. Furthermore, circulating heparin is required to produce those effects previously attributed to protamine alone.     

Comparison of the effectiveness of myocardial preservation in right atrium and left ventricle

Ten patients underwent cardiac operations during which myocardial preservation was provided by systemic hypothermia, topical cardiac cooling, and cold blood cardioplegia. The duration of ischemia ranged from 45 to 142 minutes (mean, 84.2 +/- 36.2 minutes). Two serial specimens (preischemic and ischemic) were obtained from the right atrium and the left ventricle, respectively; thus, a total of 40 biopsy specimens was obtained from these 10 patients. A combination of grading of ischemic injury and stereological morphometric measurement of mitochondria was performed to assess the effectiveness of myocardial preservation. Our findings from the mitochondrial score studies (grading of ischemic injury) were as follows. In the right atrium, the average mitochondrial score rose from 0.337 +/- 0.235 in the preischemic stage to 1.969 +/- 0.492 in the ischemic stage. In contrast, the average mitochondrial score for the left ventricle was only elevated from 0.380 +/- 0.161 to 1.353 +/- 0.396. The difference between preischemia of the right atrium and left ventricle is not statistically significant, but the difference between ischemia of these chambers is significant (p less than 0.01). Our stereological morphometric studies revealed that in the left ventricle, the average mitochondrial surface area was 0.316 +/- 0.046 micron 2 in the preischemic stage and 0.347 +/- 0.073 micron 2 in the ischemic stage, a 9.8% increase in mitochondrial size (not significant). In contrast, the mitochondrial surface area of the right atrium showed a mean increase of 65.8%, from 0.231 +/- 0.038 micron 2 in the preischemic stage to 0.383 +/- 0.057 micron 2 in the ischemic stage (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

The hemodynamic effects and mechanism of action of pulmonary artery balloon counterpulsation in the treatment of right ventricular failure during left heart bypass

The efficacy of pulmonary artery balloon counterpulsation (PABC) was evaluated in improving right ventricular (RV) output during left heart bypass for global cardiac failure. In 13 pigs, a 40-ml balloon was positioned within a graft anastomosed to the pulmonary artery distal to the pulmonary valve, and left heart bypass was instituted from the left atrium to the carotid artery. Global myocardial failure was produced by an infusion of propranolol (range, 25 to 78 mg). In this model, RV output decreased despite volume loading to a right atrial pressure of 15 mm Hg and atrioventricular sequential pacing at 100 beats per minute. Pulmonary artery balloon counterpulsation increased both RV output (from 519 +/- 76 to 1,117 +/- 110 ml/min; p less than 0.01) and RV systolic stroke work (from 1.3 +/- 0.4 to 2.3 +/- 0.6 gm-m; p less than 0.01). Right atrial pressure decreased (from 15.5 +/- 0.9 to 10.7 +/- 1.0 mm Hg; p less than 0.01) in 8 of the pigs studied during RV failure. In 5 pigs, ventricular fibrillation occurred without a stable model of RV failure, and there was no cardiac output before or after counterpulsation. The mechanism of action of PABC was studied by placing a flow probe around a large branch of the right pulmonary artery. During RV failure, balloon inflation caused flow through the pulmonary circulation, and ventricular systole resulted in filling of the graft. During ventricular fibrillation, balloon inflation and deflation produced only a to-and-fro movement of blood in the pulmonary artery branch without net forward flow.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ninety consecutive corrective operations for tetralogy of Fallot with or without minimal right ventriculotomy

Eighty-eight patients with tetralogy of Fallot and two patients with ventricular septal defect and pulmonary atresia underwent repair without right ventriculotomy (n = 43) or with a minimal right ventriculotomy (n = 47) of 10 to 15 mm. The ventricular septal defect was closed through the tricuspid valve in 75 patients. The pulmonary valve was either preserved or reconstructed to maintain its competence. The age at operation was 1 or 2 years in 51 patients. There was one operative death and there were no late deaths. The results of postoperative cardiac catheterization in the present series of patients (n = 34) were compared with those of control patients (n = 21) who had repairs with a conventional right ventriculotomy in the preceding period. There was no significant difference in right ventricular/left ventricular systolic pressure ratio or in cardiac index either at rest or during isoproterenol infusion between the two groups. The incidence of significant pulmonary regurgitation (Grade greater than or equal to 2/4) was less (p less than 0.05) in the present patients (47%, n = 34) than in the control patients (81%, n = 21). The right ventricular end-diastolic volume index (ml/m2) was smaller in the present patients than in the control patients both at rest (91 +/- 37 versus 142 +/- 28, p less than 0.01) and during isoproterenol infusion (81 +/- 21 versus 109 +/- 30, p less than 0.01). The right ventricular ejection fraction was higher in the present patients than in the control patients during isoproterenol infusion (57% +/- 4% versus 49% +/- 6%, p less than 0.01). The incidence of ventricular arrhythmias (Lown's grade greater than or equal to 2) was less in the present patients (6/35) than in the control patients (36/65) (p less than 0.005). This method of repair for tetralogy of Fallot carries no more risk than the conventional method, and the results are better with respect to postoperative right ventricular function and ventricular arrhythmia.     

Hemodynamic changes and right heart support during vertical displacement of the beating heart

BACKGROUND: Hemodynamic instability during heart displacement in off-pump multivessel coronary artery bypass grafting might be related to right heart dysfunction. The Enabler (HemoDynamics Systems Ltd, Upper Yoqneam, Israel) is a cannula pump that expels blood from the right atrium into the pulmonary artery. We studied the hemodynamic changes and the role of the enabler during heart displacement. METHODS: Nine anesthetized sheep were assessed for hemodynamic changes during 90-degree heart displacement with or without Enabler support. Hemodynamic parameters included cardiac output, systemic arterial blood pressures, and left and right heart filling pressures. RESULTS: Heart displacement caused a significant decrease in cardiac output and systemic blood pressure (46%+/-5%, p = 0.001; and 20%+/-5%, p = 0.009, respectively), with a concomitant 137%+/-24% (p = 0.003) increase in central venous pressure. No significant change in left atrial pressure was observed. Activation of the Enabler caused a significant increase in cardiac output and systemic blood pressure (67%+/-15%, p = 0.01; and 17%+/-7%, p = 0.04, respectively), as well as a decrease in central venous pressure by 49%+/-8% (p = 0.0001). CONCLUSIONS: Heart displacement causes hemodynamic instability mainly by right heart dysfunction. The Enabler significantly stabilized circulation during vertical displacement of the beating heart.     

Effects of left heart bypass on right ventricular performance. Evaluation of the right ventricular end-systolic and end-diastolic pressure-volume relation in the in situ normal canine heart

Although left heart bypass has gained popularity as a powerful technique to assist the severely failed left heart, apparent right heart failure has often developed during the bypass procedure. We investigated whether the coexisting right heart failure is attributable to the left heart bypass in 16 open-chest dogs. We evaluated the effects of left heart bypass on the right ventricular systolic properties by the slope of the end-systolic pressure-volume relation and its effects on the diastolic properties by chamber compliance. Overall right ventricular performance was assessed by the end-diastolic pressure versus cardiac output relationship. The left heart bypass decreased the slope slightly when the assisted flow ratio exceeded 75% (-14% +/- 8% at the assisted flow ratio of 100%, p less than 0.02) and thus had a deleterious influence on right ventricular performance. The left heart bypass, on the other hand, had a counteracting beneficial influence on right ventricular performance through the increase in chamber compliance (38% +/- 5%, p less than 0.01) and the decrease in pulmonary arterial input resistance (-15% +/- 12%, p less than 0.01). The net effect of the left heart bypass was the increase in cardiac output (20% +/- 2%, p less than 0.05) for any given right ventricular end-diastolic pressure. We conclude that in normal hearts the left heart bypass augments right ventricular performance. We ascribe these beneficial effects to diastolic ventricular interdependence and afterload unloading.     

Ventricular pump performance during hypocalcemia: clinical and experimental studies.

We have compared indices of ventricular function during rapid transfusion of citrated (1.5 ml/kg/min) or heparinized (1.5 ml/kg/min) autologous blood in six patients following discontinuation of cardiopulmonary bypass. Infusion of citrated blood was associated with a lowering of plasma ionized calcium concentration ([Ca++], from 0.90 +/- 0.04 to 0.71 +/- 0.4 mM, p less than 0.001) and an increase in pulmonary artery balloon-occluded pressure (PA0, from 9.4 +/- 2.6 to 15.5 +/- 1.7 mm Hg, p less than 0.u1), without a change in left ventricular stroke work index, stroke index, or cardiac index. Transfusion of heparinized blood caused no change in plasma [Ca++]. A rise in PA0, which was similar in magnitude to that observed during citrated blood transfusion, was associated with increased left ventricular stroke work index, stroke index, cardiac index, and mean arterial pressure. Although data obtained during citrated blood transfusion suggest the presence of transient left ventricular dysfunction, its magnitude is not readily expressed in terms of ventricular function curves when accompanied by a simultaneous change in [Cized closed-chest dog by volume loading during hypocalcemia, when mean arterial pressure, heart rate, and [Ca++] were in a steady state, both prior to and following beta blockade with propranolol. Function curves obtained during severe hypocalcemia ([Ca++] = 0.43 +/- 0.02 mM) were shifted significantly to the right and downward, when compared to those obtained during normocalcemia ([Ca++] = 1.06 +/- 0.03 mM). Hypocalcemia combined with beta blockade resulted in severe left ventricular failure, as demonstrated by a flat ventricular function curve.     

Hemodynamic evaluation of heterotopic heart transplantation.

To assess the relative contribution of native and donor hearts to total circulatory performance after heterotopic transplantation, we used cardiac catheterization to examine 10 patients. Left and right ventricular filling pressures significantly decreased by 41% and 36%, respectively, cardiac index increased by 25%, and pulmonary arteriolar resistance was reduced by 61%. Patients were subdivided into two groups according to the presence of one (group I) or two (group II) peaks on the aortic pressure curve. In group I, the donor left ventricle assumed total left ventricular work and 80% of right ventricular work. Because the native left ventricle could not generate enough pressure to open the aortic valve, its entire stroke volume was ejected into the common left atrium. In addition, in all four patients a native aortic regurgitation occurred in diastole and systole. In contrast, in group II, native left ventricular systolic pressure always exceeded aortic diastolic pressure. The donor left ventricle contributed 68% to systemic blood flow and the donor right ventricle 51% to pulmonary blood flow. Mild native aortic regurgitation was demonstrated in two patients only. Native left ventricular function deteriorated postoperatively in all patients (ejection fraction decreased from 0.22 +/- 0.09 to 0.14 +/- 0.08), but this deterioration was more marked in group I. Postoperative depression of native left ventricular function could not be ascribed to progression of coronary artery disease but was mainly due to reduced preload (competitive filling) and increased afterload. Thus in group I patients with more severe preoperative left ventricular dysfunction, the donor heart behaved like a total biventricular assist device. In contrast, in group II patients the donor heart acted like a partial biventricular assist device.     

Efficacy of nitroprusside therapy in postcardiotomy low-output syndrome necessitating intra-aortic balloon counterpulsation.

Serial hemodynamic measurements were obtained before, during, and after nitroprusside therapy over a 24 hour period in 19 patients requiring intra-aortic balloon pumping (IABP) for successful weaning from cardiopulmonary bypass. Nitroprusside, administered in doses ranging from 0.5 to 5 micrograms/kg/min, effected significant reductions in mean aortic pressure and systemic vascular resistance within 20 to 30 minutes. Mean aortic pressure decreased from 108 +/- 22 mm Hg to 85 +/- 27 mm Hg (p less than 0.005). Systemic vascular resistance decreased from 2,705 +/- 1,072 to 1,942 +/- 823 dynes sec cm-5 (p less than 0.005). 2n response to nitroprusside-induced decreases in left venticular afterload, cardiac indes increased from 1.83 +/- 0.58 to 2.04 +/- 0.54 L/min/m2 (p less than 0.025). Pulmonary capillary wedge pressure (PCW), right atrial pressure, right and left ventricular minute work indices, and the rate-pressure products did not change, indicating that nitroprusside administration during IABP further increased cardiac output without increasing ventricular filling pressure, ventricular work, or indices of myocardial oxygen consumption. The data suggest that nitroprusside, in conjunction with volume loading to optimal preload levels (PCW = 15 to 18 mm Hg), augments ventricular performance in postcardiotomy low-output syndrome by lowering impedance to left ventricular ejection through a direct dilator effect on vascular smooth muscle, without a direct effect on cardiac muscle. Thus it is a valuable pharmacologic adjunct during mechanical (IABP) support of the failing circulation.     

Preparation of the left ventricle for anatomical correction in patients with simple transposition of the great arteries. Surgical guidelines

Pulmonary artery banding in combination with an aortopulmonary shunt was performed on 16 patients with simple transposition of the great arteries to prepare the left ventricle for anatomical correction. Three groups were identified after operation: Group I (four patients) had increased pulmonary blood flow and tight pulmonary artery banding; Group II (four patients) had increased pulmonary blood flow and moderate pulmonary artery banding; Group III (eight patients) had normal pulmonary blood flow and moderate pulmonary artery banding. Postoperative low cardiac output was present in all patients in Group I, whereas mild heart failure was present in two patients in Group II and in two in Group III. There was one hospital death (6%). The follow-up period was 125 patient-months. Left ventricular systolic pressure rose from 63 +/- 11 torr before the operation to 101 +/- 35 torr after the procedure in Group I (p less than 0.05), from 59 +/- 10 to 93 +/- 33 torr in Group II (p less than 0.05), and from 55 +/- 10 to 84 +/- 16 torr in Group III (p less than 0.005). The increase in left ventricular muscle mass was from 44 +/- 2 gm/m2 preoperatively to 108 +/- 12 gm/m2 after operation in Group I (p less than 0.01), from 43 +/- 3 to 93 +/- 8 gm/m2 in Group II (p less than 0.02), and from 46 +/- 3 to 55 +/- 14 gm/m2 in Group III (p = no statistically significant difference). The postoperative change in left ventricular end-diastolic volume was from 100% +/- 17% to 133% +/- 23% of normal in Groups I and II (p less than 0.05) and from 123% +/- 29% to 107% +/- 36% of normal in Group III (p = no statistically significant difference). In preparing the left ventricle for anatomical correction, avoidance of severe pulmonary artery banding decreases the incidence of postoperative myocardial dysfunction, a moderate degree of volume overload and pulmonary artery banding provides the most effective stimulus for ventricular growth, and a small to moderate atrial septal defect is advantageous because it ensures the volume preload necessary for the development of the left ventricle.     

Hemodynamic effects of prolonged hyperoxia.

Experimental studies have consistently demonstrated the development of perivascular edema in the dog lung following prolonged exposure to 95% oxygen. This pathological change has been thought to result from capillary injury, but a direct effect secondary to left ventricular dysfunction has not yet been excluded. To evaluate the latter possibility, ten trained, awake dogs were prepared with monitoring of right and left atrial, systemic and pulmonary artery pressures, cardiac output, and mixed venous and arterial blood gases. Animals were exposed to an F1O2 greater than 0.95 for 48-70 hours. Radioactive 8-10 mu microspheres (141Ce, 51Cr, 85Sr, 46Sc) were injected into the left atrium at zero, six, 24, and 48 hours. PaO2 was 480 +/- 10 mm Hg during exposure, and the pulmonary shunt fraction increased from 11.3% to 16.9% (p less than 0.0001) during 70 hours. Left atrial pressure fell from 9 +/- 2 mm Hg to 3 +/- 3 mm Hg (p less than 0.0001), but cardiac output was constant at 2.7 +/- 0.1 l/min. Pulmonary arteriolar resistance increased from 183 +/- 20 dynes-sec-CM-5 to 791 +/- 30 at 70 hours (p less than 0.0001). Histologic sections of the lungs demonstrated the characteristic perivascular edema. Of particular interest was the fact that myocardial perfusion was significantly increased to all three layers of the ventricular wall at 24 and 48 hours. These data indicate that perivascular edema developing after exposure to high concentrations of oxygen is secondary to pulmonary capillary endothelial damage with no evidence that myocardial dysfunction occurs during this period.     

When should the hypoplastic right ventricle be used in a Fontan operation? An experimental and clinical correlation

Eight anesthetized dogs underwent closure of the tricuspid valve and a Fontan procedure, and the right ventricular cavity was reduced in stepwise fashion. There was an increase in right atrial pressure from 9.3 +/- 2.2 to 14.1 +/- 2.4 mm Hg (p less than 0.001), a decrease in pulmonary artery pulse pressure from 10.8 +/- 2.2 to 6.8 +/- 2.2 mm Hg (p less than 0.01), and a decrease in cardiac index from 2.7 +/- 0.3 to 2.2 +/- 0.2 L/min/m2 (p less than 0.001) when the ventricular size was dropped from 50% to 25% of normal. The difference between mean pulmonary artery pressure and mean right atrial pressure, which reflects the positive stroke work index of the ventricle, disappeared once the right ventricular cavity was reduced to 25% of normal (15.0 +/- 6.1 versus 14.1 +/- 2.4 mm Hg; p = not significant). Experimental results were correlated with postoperative catheterization data from 19 patients with tricuspid atresia who had the Fontan operation. Mean right atrial pressure was 18 +/- 4.6 mm Hg and cardiac index was 2.35 +/- 0.65 L/min/m2 in patients with a direct atrium-pulmonary artery anastomosis or an atrioventricular anastomosis with a right ventricular cavity less than 30% of normal versus 13 +/- 3.2 mm Hg and 3.42 +/- 0.46 L/min/m2 for those with an atrioventricular connection and a right ventricular cavity greater than 30% of normal (p less than 0.05 and p less than 0.02, respectively). The right ventricle enlarged from 27% +/- 6% of normal preoperatively to 35% +/- 10% of normal on follow-up (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of amrinone in low cardiac output after mitral valve replacement

The efficacy of amrinone was assessed in the treatment of low cardiac output states occurring within 24 h after mitral valve replacement in an open prospective trial. It included 7 women and 5 men, aged 58 +/- 10 years. Four patients had also had simultaneous aortic valve replacement. Patients entered in the study if their cardiac index (CI) remained less than 2.2 l.min-1.m-2 after pulmonary wedged pressure (Ppw) had been increased to at least 15 mmHg, the patient having a temperature greater than 36 degrees C. Amrinone was given so as to increase Cl by at least 30% and to decrease Ppw by at least 30%. Patients were given a mean of 1.5 mg.kg-1 amrinone during the first hour, followed by a constant rate infusion of 9 +/- 3 micrograms.kg-1.min-1 over at least 24 h. The usual haemodynamic parameters were measured and calculated before giving amrinone, and after 1, 3, 6, 24, and 48 h. After 1 h of treatment, systolic arterial pressure, cardiac index, systolic index and left ventricular stroke work increased by 22, 42, 23, and 47% respectively, whilst Ppw decreased by 27% (p less than 0.01). Heart rate rose and systemic vascular resistance decreased but not significantly. Right atrial pressure, right ventricular stroke work, pulmonary artery pressure and pulmonary vascular resistance did not change. These effects were all maintained throughout the 48 h infusion. Amrinone had to be replaced by another agent (a beta-agonist) in 3 cases because of arrhythmia, lack of efficacy or thrombocytopaenia. In this setting, amrinone increased left ventricular performance with little effect on the right ventricle.     

Trendelenburg versus PASG application--hemodynamic response in man

Diminished venous return is the primary determinant of reduced cardiac output in hemorrhagic hypoperfusion. In this study the hemodynamic response of two therapies commonly employed to increase venous return in hemorrhagic hypoperfusion--pneumatic antishock garment (PASG) application and Trendelenburg (TREND) positioning--were compared in normovolemic man. Five patients had PASG pressure of 20 mm Hg compared with 10 degrees Trendelenburg, eight patients had 20 and 40 mm Hg PASG application compared with 10 degrees Trendelenburg. PASG application at both 20 and 40 mm Hg resulted in a significant increase in CVP (11.1 +/- 1.9 baseline to 16.0 +/- 2.7 PASG 40; p less than 0.01) left atrial pressure (LAP) (10.1 +/- 1.3 baseline to 14.4 +/- 1.8 PASG 20; p less than 0.01) pulmonary capillary wedge pressure (PCWP) (11.6 +/- 2.0 baseline to 16.8 +/- 3.4 PASG 40; p less than 0.01) and esophageal pressure (Pes) (5.0 +/- 0.8 baseline to 8.6 +/- 0.9 PASG 40; p less than 0.01). However, transmural right and left atrial pressure (RATP, LATP) and cardiac index (CI) were unchanged. Ten degrees of Trendelenburg resulted in no increase in CVP, PCWP, RATP, or LATP, but CI (2.67 +/- 0.07 baseline to 2.82 +/- 0.1 TREND; p less than 0.01) was significantly increased. Systemic vascular resistance index (570 +/- 46 TREND vs. 668 +/- 53 PASG 40; p less than 0.01) was significantly less in Trendelenburg compared to PASG at 40 mm Hg. The data demonstrate that elevation in CVP, LAP, and PCWP following PASG application is secondary to an increase in intrathoracic pressure (as measured by Pes).(ABSTRACT TRUNCATED AT 250 WORDS)     

Isolated biventricular working rat heart preparation.

The isolated perfused heart from small animals has been used extensively for hemodynamic and metabolic studies. The left working heart preparation proved superior to the Langendorff model for functional evaluations but has not allowed study of right heart function. A simple and inexpensive biventricular working heart preparation has been developed by modifying the left working rat heart model. Under general anesthesia the heart was removed surgically leaving sufficient vessels attached to it. Cannulation of the aorta, left atrium, right atrium, and pulmonary artery was completed in 10 minutes. A pressurized compliance chamber allowed rapid and reliable regulation of aortic impedance. For the 7 hearts that were subjected to 3-hour biventricular perfusion (their end points expressed as percent of their initial values), the aortic output (95% +/- 3%), pulmonary flow (88% +/- 9%), mean aortic pressure (109% +/- 5%), mean pulmonary pressure (100% +/- 2%), heart rate (106% +/- 8%), myocardial adenosine triphosphate level (85% +/- 8%), and creatine phosphate level (89% +/- 4%) were all maintained at physiologic levels. For the 11 hearts that were converted from left working heart preparation to biventricular working mode, significant improvement in stroke volume, aortic and cardiac output, and pressure development were observed. Experimental results indicate that the biventricular working model for isolated perfused rat hearts is superior to the left working preparation for studying the function of the total heart. Further study of the biventricular perfused working rat heart appears warranted.     

Dynamic cardiomyoplasty for hemodynamic support during acute pulmonary hypertension. An experimental study.

The efficacy of dynamic cardiomyoplasty for hemodynamic support during acute pulmonary hypertension was studied. Five dogs underwent a right latissimus dorsi cardiomyoplasty. Each dog was later studied in a short-term experiment. A graded acute pulmonary hypertension was induced by infusion of glass microspheres into the pulmonary artery. This resulted in decrease in pulmonary artery flow, systemic pressure, and systemic flow. The cardiomyoplasty was then stimulated with a new R wave synchronous rate-responsive pulse-train stimulator (Prometheus system). This pacemaker delivers a pulse train with the duration of stimulation determined as a proportion of the RR interval. At an optimal level of hemodynamic impairment, the dynamic cardiomyoplasty was able to immediately improve pulmonary artery flow 26.4% +/- 5.84% (standard error of the mean) (p less than 0.005, paired t test), mean systemic arterial pressure 11.6% +/- 3.7% (p less than 0.05), and thoracic aortic flow 15.7% +/- 6.3% (p less than 0.05). The degree of improvement in hemodynamic variables could be correlated with the magnitude of hemodynamic impairment present (e.g., r = 0.78; p less than 0.005 for pulmonary blood flow). We conclude that a significant beneficial effect of dynamic cardiomyoplasty on hemodynamics in short-term canine pulmonary hypertension is demonstrated in this study. Thus cardiomyoplasty may be useful in patients with right heart failure associated with increased pulmonary vascular resistance.