H. V. Schaff

Routine Use of Autotransfusion Following Cardiac Surgery: Experience in 700 Patients

An autotransfusion technique has been developed for collection and reinfusion of shed mediastinal blood. This system has been routinely applied in the postoperative management of 592 consecutive adult and 108 pediatric cardiac surgical patients. Two hundred seventy-one adult patients (46%) and thirty-six pediatric patients (33%) actually received autologous blood. Autotransfusion volume ranged from 50 to 21,350 ml per patient. In 1976 at our institution, homologous transfusion requirements averaged 8.4 +/- 0.7 units per adult patient. During 1978, with the routine use of postoperative autotransfusion, bank blood transfusions were lowered to 4.2 +/- 0.3 units per patient (p less than 0.001). In contrast to perioperative autotransfusion techniques, collection and reinfusion of shed mediastinal blood is particularly useful for intravascular volume replacement in patients with serious postoperative bleeding.

Diagnosis and Management of Postoperative Pericardial Effusions and Late Cardiac Tamponade Following Open-Heart Surgery

The clinical and laboratory findings of 28 patients identified as having late pericardial effusions were examined. Eleven of these patients were asymptomatic; 9 patients had moderate symptoms including fatigue, malaise, weight gain, and dyspnea on exertion, and 8 patients with similar symptoms had evidence of cardiac tamponade. Ten patients underwent right heart catheterization in the intensive care unit; normal hemodynamics were confirmed in 4 and cardiac tamponade in 6 patients. Pericardiocentesis was effective in decompressing cardiac tamponade in 7 of 8 patients. One patient required operative subxiphoid drainage after unsuccessful pericardiocentesis. In addition, 5 patients with moderate clinical symptoms and pericardial effusions, who did not have cardiac tamponade, underwent pericardiocentesis because of a need for chronic anticoagulant therapy. The remaining patients were managed successfully by observation, discontinuation of warfarin when possible, fluid restriction, and diuretic therapy. All but 1 patient was symptomatically improved. A diagnostic and therapeutic schema is presented as an aid to early recognition of this troublesome and potentially lethal complication.

The Harmful Effects of Ventricular Distention during Postischemic Reperfusion

To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27 degree C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dp/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n = 8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated impaired subendocardial blood flow after 5 minutes of reflow (0.75 +/- 0.06 vs 0.96 +/- 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and persistent elevation of intramyocardial carbon dioxide (CO2) tension (68 +/- 4 vs 51 +/- 4 mm Hg, Group 2 vs Group 1). In addition, postischemic ventricular function was significantly worse in Group 2 hearts (60 +/- 7 vs 79 +/- 3% of control dP/dt, Group 2 vs Group 1, and 53 +/- 6 vs 81 +/- 5% of control left ventricular developed pressure, Group 2 vs Group 1). These data demonstrate that even mild distention during early reperfusion can result in reduced subendocardial perfusion and delayed washout of tissue CO2. Although myocardial blood flow and CO2 tension subsequently returned to normal in the distended hearts, left ventricular performance remained significantly depressed. This injury can occur clinically in nonvented hearts prior to the resumption of effective ventricular contraction.

Effect of potassium cardioplegia on myocardial ischemia and post arrest ventricular function.

SUMMARY To assess the effects of moderate potassium cardioplegia (37 mEq/l KCI) on the severity of myocardial ischemia during arrest and on post arrest ventricular function, 32 isolated, isovolumic feline hearts were studied before, during and I hour after ischemic arrest. Normothermia (37°C) was maintained in 16 hearts, eight without KCI and eight with KCI. Hypothermia (27°C) was maintained in the remaining 16 hearts, eight with KCI and eight without KCI. Myocardial oxygen (PmO,) and carbon dioxide tensions (PmCO,) were measured by mass spectrometry. Maximum developed intraventricular pressure (max DP) and max dP/dt were used as indices of performance. Compared with normothermic or hypothermic arrest alone, the addition of potassium cardioplegia resulted in a significant reduction in the peak PmCO2 measured during the arrest period. Hypothermia alone resulted in morphologic evidence of improved myocardial preservation and a significant reduction in peak PmCO, compared with normothermia. Post arrest ventricular function was best with the combination of hypothermic arrest and potassium cardioplegia (max DP = 96 ± 6% of control and max dP/dt = 99 ± 5% of control). These data suggest that the beneficial effects of potassium cardioplegia and 27° hypothermia are additive, and that reduction in myocardial ischemia as evidenced by a reduction in peak PmCO, correlated with improvement in ventricular performance in the post arrest period and with preservation of myocardial structure.

Mechanism of defective oxygen extraction following global ischemia

Abstract Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O 2 E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O 2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O 2 . Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O 2 E determinations, myocardial O 2 ( P m O 2 ) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O 2 E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O 2 E was not associated with increased A-V shunting. P m O 2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O 2 E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O 2 E, therefore, must be an impaired capacity for utilization of delivered O 2 at the cellular level.

Reduced oxygen extraction during reperfusion: A consequence of global ischemic arrest☆

Abstract Myocardial oxygen utilization has been shown to be impaired following prolonged global ischemia in experimental and clinical studies. The precise nature of this defect in O2 utilization has not been well defined and the present study was designed in an attempt to elucidate the defect. Forty-six isolated, isovolumic feline heart preparations were utilized and three groups of 10 hearts each were subjected to 60 min of normothermic ischemic arrest. Left ventricular function, assessed by developed pressure (DP) and dP dt , coronary blood flow (CBF), myocardial oxygen consumption ( M V O 2 ), and oxygen extraction (O2E) were measured before and after ischemia. One group (I) had unmodified reperfusion; the second group (II) received epinephrine during reperfusion to increase contractility, and the third group (III) received nitroprusside post-ischemia to increase CBF. The remaining hearts, none of which underwent ischemic arrest, were divided into two groups, one of which (IV) was subjected to a period of reduced perfusion pressure with the above parameters examined, and in the final group (V) a period of epinephrine infusion was performed. In Group I hearts after ischemia, dP dt , CBF, M V O 2 , and O2E were all significantly reduced when compared to preischemic levels. Epinephrine infusion postarrest (Group II), although increasing dP dt , CBF, and M V O 2 , did not change the postischemic depression of O2E. With nitroprusside infusion to postischemic depression of oxygen extraction was still apparent. By contrast, epinephrine infusion in the nonarrested hearts (V) increased oxygen extraction as well as dP dt , CBF, and M V O 2 . These data suggest that the primary defect in postischemic oxygen utilization after prolonged ischemia is an impairment in oxygen extraction. Furthermore, the data demonstrate that oxygen extraction remains depressed following arrest in spite of changes in CBF and ventricular function.

Partial anomalous pulmonary venous return with intact atrial septum: report of four cases.

Four patients are reported who underwent repair of partial anomalous pulmonary venous drainage with intact atrial septum. One patient also had azygos continuation of the inferior vena cava and two patients had associated mitral stenosis. Diagnostic considerations and guidelines for operative repair are presented.

Failure of methylprednisolone to protect myocardial function or prevent myocardial edema following ischemic cardiac arrest

Abstract The results of the present study suggest that, in hearts subjected to hypothermic global ischemia and reperfusion, pretreatment with methylprednisolone: (1) does not reduce indexes of myocardial ischemia during the period of cross clamp, (2) does not improve myocardial contractility during the reperfusion period despite significantly increasing coronary blood flow, (3) does not afford additional protection to myocardial structure by either light or electron microscopy, (4) does result in increased myocardial edema, and (5) does result in an increase in isovolumic end-diastolic pressure, which is most likely the result of decreasing left ventricular cavity size and not a result of an increase in left ventricular wall stiffness.