Assisted venous drainage presents the risk of undetected air microembolism.

OBJECTIVES: The proliferation of minimally invasive cardiac surgery has increased dependence on augmented venous return techniques for cardiopulmonary bypass. Such augmented techniques have the potential to introduce venous air emboli, which can pass to the patient. We examined the potential for the transmission of air emboli with different augmented venous return techniques. METHODS: In vitro bypass systems with augmented venous drainage were created with either kinetically augmented or vacuum-augmented venous return. Roller or centrifugal pumps were used for arterial perfusion in combination with a hollow fiber oxygenator and a 40-micrometer arterial filter. Air was introduced into the venous line via an open 25-gauge needle. Test conditions involved varying the amount of negative venous pressure, the augmented venous return technique, and the arterial pump type. Measurements were recorded at the following sites: pre-arterial pump, post-arterial pump, post-oxygenator, and patient side. RESULTS: Kinetically augmented venous return quickly filled the centrifugal venous pump with macrobubbles requiring continuous manual clearing; a steady state to test for air embolism could not be achieved. Vacuum-augmented venous return handled the air leakage satisfactorily and microbubbles per minute were measured. Higher vacuum pressures resulted in delivery of significantly more microbubbles to the "patient" (P <.001). The use of an arterial centrifugal pump was associated with fewer microbubbles (P =.02). CONCLUSIONS: Some augmented venous return configurations permit a significant quantity of microbubbles to reach the patient despite filtration. A centrifugal pump has air-handling disadvantages when used for kinetic venous drainage, but when used as an arterial pump in combination with vacuum-assisted venous drainage it aids in clearing air emboli.

Trauma to the lung.

Injuries to the lung parenchyma occur following both blunt and penetrating trauma and usually are associated with injury to adjacent structures. In most cases, patients with lung injury require little more than chest-tube insertion and supportive care. A thoracotomy is required, however, in approximately 10% of these patients, half of whom will need pulmonary repair or resection. Because serious morbidity and mortality can follow lung injuries, surgeons must have a broad understanding of the causes, types, and pathophysiologies of lung injuries and be able to promptly diagnose and appropriately treat them.

Extracorporeal membrane oxygenation as an adjunct treatment for primary graft failure in adult lung transplant recipients.

Primary graft failure is a catastrophic event in lung transplantation. Failure is characterized by profound abnormalities of gas exchange that are frequently unresponsive to alterations in mechanical ventilation. This condition can be fatal and, if less severe, is usually associated with significant permanent damage to the allograft. We report the use of extracorporeal membrane oxygenation as a means to support lung transplant recipients with severe graft failure. Since 1991, extracorporeal membrane oxygenation has been used on 17 occasions for the temporary support of 16 adult lung transplant recipients. All patients met or exceeded standard National Institutes of Health guidelines for institution of extracorporeal membrane oxygenation. Nine double lung, six single lung, and one heart-lung recipients were supported for 1 to 12 days (mean 4.6 +/- 2.2 days). Extracorporeal membrane oxygenation was instituted early, within 7 days of transplantation, in ten patients. Eight early patients (80%) were successfully weaned from extracorporeal membrane oxygenation. Seven of ten (70%) patients were long-term survivors, and five of the seven had normal lung function. In comparison, there were no survivors among six recipients placed on extracorporeal membrane oxygenation for late (> or = 7 days) graft dysfunction. Extracorporeal membrane oxygenation is a lifesaving adjunct in recipients with acute graft failure after lung transplantation. Ischemia-reperfusion injury and acute graft dysfunction after lung transplantation can be successfully reversed with early aggressive intervention.

Successful plication for postoperative diaphragmatic paralysis in an adult.

Diaphragmatic paralysis developed in an adult after a cardiac operation. The patient suffered from recurrent fevers and could not be weaned from mechanical ventilatory support. Diaphragmatic plication was performed and enabled rapid and sustained weaning from respiratory support.

Direct-current injury from external pacemaker results in tissue electrolysis.

In two patients undergoing open heart operations, electrochemical burns developed at the sites of connection to an external pacing system. Investigation revealed that failure of the pacing generator caused a small, continuous, direct current to pass through the patients, resulting in electrolysis at the sites of contact with the pacing and grounding wires. This electrolytic reaction was recreated in a mock pacing system and resulted in tissue injury and disintegration of the pacing wire. Guidelines to help recognize and prevent this complication are presented.

Acute rejection after cardiac transplantation: detection by interstitial myocardial pH.

Intramyocardial pH was assessed as a potential marker for clinical evaluation and treatment of acute rejection following cardiac transplantation. Fifteen cats underwent forty operative procedures. Following intra-abdominal heterotopic heart transplantation, serial laparotomies were performed in the early (days 0 to 2), intermediate (days 5 to 7), and late (days 7 to 16) postoperative periods. Rejection was assessed by serial clinical examinations, ECG analyses, B-mode echocardiography, histological and ultrastructural analyses, and measurements of interstitial myocardial pH. Intramyocardial pH was measured by a new miniature (0.6 X 3.0 mm) fiberoptic pH transducer. At confirmed rejection, concomitant laparotomy and thoracotomy were performed and pH sensors were implanted in both native (anatomical) and graft hearts. Nine animals at rejection were given methylprednisolone and changes in graft and native heart pH were measured. The pH during absence of rejection, mild acute rejection, and severe acute rejection averaged 7.430 +/- 0.019, 7.233 +/- 0.040 (p less than .02), and 6.860 +/- 0.066 (p less than .02), respectively (mean +/- standard error of the mean). A progressive decline in pH was noted in each heart. In animals receiving steroids, graft heart pH increased over 90 minutes from 6.852 +/- 0.065 to 7.043 +/- 0.077 (p less than .05). Although pH decline may be secondary to either inflammatory or ischemic etiology, histological and ultrastructural analyses demonstrate a predominant inflammatory response with progressive mononuclear cell infiltration, interstitial edema, vascular wall edema, infiltration by polymorphonuclear neutrophil leukocytes, vacuolation of sarcoplasmic reticulum, and disarray of myocytes associated with falling pH. Degree of pH change correlated closely with degree of histological rejection, presence of ECG voltage decline, and change in wall thickness by ultrasound.

Continuous measurement of intramyocardial pH: relative importance of hypothermia and cardioplegic perfusion pressure and temperature.

The continuous measurement of intramyocardial pH was used to follow the progression of ischemia and permit correlation to functional recovery. Adequacy of myocardial preservation following 38 degrees C or 25 degrees C global ischemia alone or with the administration of one or two doses of 38 degrees C, 25 degrees C, or 1 degree C crystalloid cardioplegia at aortic root perfusion pressures of 90 mm Hg or 130 mm Hg was assessed. A new miniature myocardial transducer incorporating fiberoptic technology and dual pH and temperature-sensing capability was placed into the left ventricular free wall and septum of 44 sheep undergoing ischemic arrest during cardiopulmonary bypass. All groups underwent global ischemia until myocardial pH was 6.8. An intramyocardial pH level of 6.8 reliably correlated to similar levels of functional recovery in each group. Aortic root perfusion pressure of 130 mm Hg provided enhanced myocardial protection by increasing the total ischemic time (5 to 10 minutes) with one (p less than 0.01) or two (p less than 0.001) doses of cardioplegic solution until a given functional level of recovery was attained. Aortic root perfusion pressure of 90 mm Hg provided no added benefit in total ischemic time, rate of change of pH, or degree of recovery of function. Hypothermic (25 degrees C) global ischemia alone enhanced myocardial protection by providing increased time (p less than 0.01) until a given functional level of recovery was attained with a slower rate of change of pH (p less than 0.01) compared with normothermic (38 degrees C) global ischemia alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous measurement of intramyocardial pH: correlation to functional recovery following normothermic and hypothermic global ischemia.

The continuous measurement of intramyocardial pH was used to follow the progression of ischemia and was correlated to the recovery of left ventricular function following normothermic (38 degrees C) and hypothermic (25 degrees C) global ischemia. New miniature myocardial transducers, which incorporate fiberoptic technology and dual pH- and temperature-sensing capability, were placed into the left ventricular free wall and septum of 52 sheep undergoing cardiopulmonary bypass. Left ventricular stroke work as a function of mean left atrial pressure curves were generated before and after cardiopulmonary bypass by volume loading with whole blood. Functional recovery was determined by the ratio of the integrals of the preischemic and postischemic function curves. Control sheep (N = 11) did not undergo ischemia. Three groups (N = 41) underwent aortic cross-clamping until pH reached 7.0, 6.8, or 6.6. The preischemic myocardial pH averaged 7.42 +/- 0.01. Following both normothermic and hypothermic global ischemia, no significant difference was demonstrated in recovery of function between control (pH 7.4) and pH 7.0 groups at either temperature. However, recovery of function of the pH 6.8 and pH 6.6 groups was significantly decreased (p less than 0.01) versus control and pH 7.0 groups at both temperatures. No significant difference in recovery of function was demonstrated at any pH level when normothermic versus hypothermic groups were compared. However, hypothermia provided increased time (p less than 0.001) before each level of function was reached with a slower rate of change of pH (p less than 0.01) compared with the corresponding same pH group in sheep undergoing normothermic (38 degrees C) cardiopulmonary bypass.(ABSTRACT TRUNCATED AT 250 WORDS)