Vena Cava Pressure Research Articles

Elevation of superior vena caval pressure increases extravascular lung water after endotoxemia.

In many sheep Escherichia coli endotoxin results in pulmonary hypertension, increased microvascular permeability, pulmonary edema, and increased central venous pressure. Since lung lymph drains into the systemic veins, increases in venous pressure may impair lymph flow sufficiently to enhance the accumulation of extravascular fluid. We tested the hypothesis that, following endotoxin, elevating the venous pressure would increase extravascular fluid. Thirteen sheep were chronically instrumented with catheters to monitor left atrial pressure (LAP), pulmonary arterial pressure (PAP), and superior vena caval pressure (SVCP) as well as balloons to elevate LAP and SVCP. These sheep received 4 micrograms/kg endotoxin, and following the pulmonary hypertensive spike the left atrial balloon was inflated so that (PAP + LAP)/2 = colloid osmotic pressure. It was necessary to control PAP + LAP in this way to minimize the sheep-to-sheep differences in the pulmonary hypertension. We elevated the SVCP to 10 or 17 mmHg or allowed it to stay low (3.2 mmHg). After a 3-h period, we killed the sheep and removed the right lungs for determination of the extravascular fluid-to-blood-free dry weight ratio (EVF). Sheep with SVCP elevated to 10 or 17 mmHg had significant increases in EVF (5.2 +/- 0.1 and 5.6 +/- 1.2) compared with the sheep in which we did not elevate SVCP (EVF = 4.5 +/- 0.4). These results indicate that sustained elevation in central venous pressure in patients contributes to the amount of pulmonary edema associated with endotoxemia.

Vena caval pressure and PPV : Chen F. N. (1985) Hemodynamic effects of positive pressure ventilation: vena caval pressure in patients without injuries to the inferior vena cava. J. Trauma25, 347

Vena caval pressure and PPV : Chen F. N. (1985) Hemodynamic effects of positive pressure ventilation: vena caval pressure in patients without injuries to the inferior vena cava. J. Trauma25, 347

Early variceal rebleeding after successful distal splenorenal shunt.

Of 77 patients with repeated variceal hemorrhage who underwent distal splenorenal shunt, five (6.5%) developed rebleeding despite a patent splenorenal anastomosis. Three of the five patients died. Early variceal rebleeding usually indicates shunt thrombosis but may occur with a patent anastomosis. Anatomic or functional left renal vein and/or splenic vein hypertension producing incomplete variceal decompression is generally the cause. Ineffective separation of the main portal vein from the gastrosplenic venous plexus may coexist and further intensify variceal congestion. Urgent angiographic studies and direct shunt catheterization with measurement of splenic vein, left renal vein, and inferior vena cava pressures should be performed to plan appropriate therapy. A significant gradient between the splenic and renal veins is evidence of an unsatisfactory anastomosis and should be managed by balloon angioplasty or reoperation. High splenic and left renal vein pressures with a gradient of more than 10 mm Hg between the renal vein and the inferior vena cava indicate renal vein hypertension. Initial therapy should include serial injection sclerotherapy, as renal vein hypertension will usually resolve over time as additional collaterals develop. However, persistent or recurrent variceal hemorrhage may require total portal decompression to bypass the restrictive left renal vein segment.

Norepinephrine on venous compliance and unstressed volume in cat liver.

Hemodynamic relationships between flows, pressures, and blood volume have been examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows, and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml X min-1 X 100 g liver-1 and when hepatic outflow pressure was varied from 0 to 9.5 mmHg, before, during, and after intravenous infusion of norepinephrine (2 micrograms X min-1 X kg body wt-1). Portal pressure was 1-2 mmHg higher than lobar venous pressure and 8-9 mmHg higher than inferior vena caval pressure, showing that the major site of resistance in the portal circuit was in the large hepatic veins. Intrahepatic pressure was linearly related to total hepatic flow, and norepinephrine increased the intercept but not the slope of this relationship. Hepatic blood volume was linearly related to intrahepatic pressure with a calculated compliance of 2.5-3.0 ml X mmHg-1 X 100 g liver-1 and a calculated unstressed volume at zero pressure of 10-15 ml/100 g liver. Norepinephrine did not significantly change vascular compliance but caused a marked reduction of 15-20 ml/100 g liver in calculated unstressed volume. Thus norepinephrine reduced hepatic blood volume by 15-20 ml/100 g liver at any given intrahepatic pressure. It is concluded that venoconstriction in the hepatic bed occurs by a decrease in unstressed volume with little change in compliance. Unstressed volume represents a true blood volume reserve, independent of passive influences, which can be mobilized by the central nervous system.

Pneumothorax during positive-pressure mechanical ventilation

The hemodynamic and respiratory effects of unilateral pneumothorax were studied during positive-pressure mechanical ventilation in five sheep. The sheep were anesthetized, intubated, and placed on mechanical ventilation with positive end-expiratory pressure (5 cm H2O). After baseline studies, including chest roentgenograms, were taken, increments of air were injected into the right pleural cavity. Measurements were repeated at pneumothoraces of 500, 1,000, and 1,500 ml. There was a steady fall in cardiac output (p less than 0.02) at pneumothoraces of 1,000 and 1,500 ml. The decrease in cardiac stroke volume paralleled that of cardiac output. Heart rate rose (p less than 0.05) at a pneumothorax of 1,500 ml. There appeared to be a linear relationship between the percent increase in pneumothorax as estimated by roentgenogram and the percent fall in cardiac output (r = 0.991). There was a steady rise in mean pulmonary arterial, pulmonary arterial capillary wedge, superior vena caval, and inferior vena caval pressures, although the changes in inferior vena caval pressure were not statistically different from baseline. Peak airway pressure increased from baseline at pneumothoraces of 1,000 and 1,500 ml. Both right and left end-expiratory intrapleural pressures increased and were statistically different (p less than 0.01) from baseline. However, there was a substantially greater rise in right intrapleural pressure than left. Arterial oxygen tension remained physiological throughout the study. This study indicates that cardiac output decreases as the amount of pneumothorax increases in sheep during mechanical ventilation. This study also demonstrates that, during positive-pressure mechanical ventilation, a relatively benign-appearing pneumothorax by chest roentgenogram may be associated with a significantly depressed cardiac output. In addition, arterial oxygen tension may not be useful in predicting the onset of pneumothorax during mechanical ventilation.

Hemodynamic Effects of Positive Pressure Ventilation

In order to investigate the effect of positive pressure ventilation on vena cava blood flow, intraoperative manometric measurements were made in three patients with blunt abdominal trauma. These patients had intra-abdominal hemorrhage but no injury to the vena cava. The vena cava pressure increased with stepwise increases in the inspiratory pressure of the ventilator. The implications of this for the management of injuries to the inferior vena cava are: control of blood loss from caval wounds requires blockage of retrograde and antegrade caval blood flow; temporary cessation can stop retrograde caval flow from the right atrium and allow identification and repair of the caval defect; and retrograde caval blood flow can be used to flush out air bubbles and blood clots.

Colloid osmotic pressure in decompensated cirrhosis. A 'mirror image' of portal venous hypertension.

Colloid osmotic pressure in plasma (IIP) and ascitic fluid (IIA) and hydrostatic pressures in the hepatoportal system were measured simultaneously in 20 patients with decompensated cirrhosis. IIP was significantly decreased (mean, 21 mm Hg, versus normal, 30 mm Hg; P less than 0.01), and IIA was significantly below that of plasma (average, 25% of IIP; P less than 0.01). Portal pressure (transmural), determined as wedged hepatic venous minus inferior vena caval pressure (WHV--IVCP), was significantly increased (mean, 18 mm Hg, versus normal, 3 mm Hg; P less than 0.01) and inversely correlated to IIA/IIP (r = -0.77, P less than 0.001). WHV--IVCP was in most patients in the same order as and closely correlated to effective colloid osmotic pressure (IIP--IIA) (r = 0.88, P less than 0.001). No relationship was found between WHV--IVCP and IIP. The results indicate that a fall in colloid osmotic pressure in the interstitial space and ascitic fluid is related to and most likely secondary to the elevated portal pressure in decompensated cirrhosis. Effective colloid osmotic pressure may therefore be regarded as a 'mirror image' of transmural portal pressure. The role of colloid osmotic pressure in the genesis and perpetuation of ascites should be reconsidered in the light of these findings.

Direct Transhepatic Assessment of Hepatic Vein Pressure and Direction of Flow Using a Thin Needle in Patients With Cirrhosis and Budd—Chiari Syndrome

Portal pressure can be accurately measured transhepatically with a Chiba needle. Since 1980, we have used transhepatic hepatic vein pressures as our zero reference for transhepatic portal pressure measurements. To validate the latter technique, we performed hepatic vein catheterization and transhepatic hepatic vein puncture in 11 patients undergoing portal pressure measurement. Transhepatic hepatic vein puncture was simple, providing pressures as reproducible as those obtained by hepatic vein and inferior vena cava catheterization. These pressures were minimally higher than simultaneous free hepatic vein and inferior vena caval pressures, possibly reflecting the more proximal location of the small hepatic vein radicles often entered by this technique. Transhepatic hepatic vein puncture is an accurate way to determine hepatic vein pressure and, combined with transhepatic portal vein pressure measurement, completely obviates the need for venous catheterization for portal pressure determination. Transhepatic hepatic vein pressure was also measured in 3 patients with Budd-Chiari syndrome. In these patients, transhepatic hepatic vein pressure was elevated and equaled or exceeded portal vein pressure. Abnormal venous collaterals were identified in all patients. Transhepatic portal pressure studies are also an appropriate way to evaluate patients suspected of having hepatic outflow obstruction.

The morphogenesis of the vacuolation of liver cells.

The morphogenesis of the vacuolation of liver cells caused by congestion was studied in the rat. Congestion of the liver was produced by constriction of the inferior vena cava just below the diaphragm. Vacuoles appeared within 5 min after the constriction (inferior vena cava pressure: 50 mm H2O or more). Vacuolation began as a small and saccular invagination of the sinusoidal surface of the liver cell membrane, and at the initial stage the vacuolar lumen connected with the space of Disse through a narrow slit. The small vacuoles increased in size and became larger by fusing with each other. The limiting membrane of vacuoles showed identical enzymological activities to those in the liver cell membrane. Vacuoles contained some components of blood and horseradish peroxidase injected into the femoral vein. These findings suggest that vacuolation of liver cells is formed by invaginations of liver cell membrane.

Plasma-to-ascitic fluid transport rate of albumin in patients with decompensated cirrhosis. Relation to intraperitoneal albumin.

Albumin-kinetics and haemodynamic studies were performed in 20 patients with decompensated liver cirrhosis in order to improve the knowledge on genesis and perpetuation of hepatic ascites, especially with respect to determinants of intraperitoneal protein. A positive relationship was found between the plasma-to-peritoneal transport rate of albumin (index of 'lymph-imbalance') and the mass of intraperitoneal albumin (rlog = 0.82, P less than 0.001), indicating a significant role of 'lymph-imbalance' to sequestration of protein in the peritoneal cavity. Ascitic fluid albumin concentration was on the average 0.22 of that of plasma and directly correlated to the plasma concentration (rlin = 0.68, P less than 0.01). The hydrostatic pressure difference across the splanchnic microvasculature (assessed as wedged hepatic vein minus inferior vena caval pressure) was directly correlated to the effective (plasma minus ascitic fluid) oncotic pressure (rlin = 0.74, P less than 0.001) but significantly higher than that (P less than 0.005), indicating a 'non-equilibrium' in the splanchnic Starling forces. The results point to a multivariate genesis and perpetuation of cirrhotic ascites as laid down in the 'lymph-imbalance' theory of ascites formation, whereas a 'fluid equilibrium' theory seems to be too simple, especially with respect to explain protein sequestration in the peritoneal cavity.

Comparison of Flow Differences among Venous Cannulas

The efficiency of four methods of venous drainage during cardiopulmonary bypass was evaluated. Superior vena caval (SVC), inferior vena caval (IVC), right atrial (RA), and right ventricular (RV) pressures as well as RV blood flow were measured for cannulation with a single USCI 40F atrial cannula, a single Sarns 51F cavoatrial cannula, and double USCI 32F caval cannulas with and without caval tourniquets. Measurements for all cannulas were recorded in conditioned dogs during nor-mothermic cardiopulmonary bypass with the heart beating, with the heart fibrillated, and with the apex of the heart elevated in the circumflex position. Venous drainage using double caval cannulas with caval snares provided maximum decompression of the venous system (SVC pressure, − 3 ± 1.52 mm Hg [standard deviation]; IVC pressure, −1.67 ± 2.67 mm Hg to 0.4 ± 2.09 mm Hg). However, decompression of the right side of the heart with this method was the poorest (RA pressure, 5 ± 1.46 mm Hg to 9.60 ± 2.78 mm Hg; RV pressure, 5.67 ± 0.82 mm Hg to 12.5 ± 1.51 mm Hg; RV vent flow, 96 ± 4 ml/min to 370 ± 50 ml/min). The caval cannulas without tapes provided similar venous decompression but with better right-heart decompression (RA pressure, −0.71 ± 1.95 mm Hg to 0.60 ± 2.51 mm Hg; RV pressure, 2.13 ± 2.23 mm Hg to 11.6 ± 0.89 mm Hg; RV vent flow, 29 ± 5 ml/min to 75 ± 4.5 ml/min). The USCI 40F atrial cannula provided less efficient decompression of the inferior vena cava (IVC pressure, 4.33 ± 1.96 mm Hg to 7.17 ± 3.46 mm Hg). The Sarns 51F cavoatrial cannula had the most efficient right-heart decompression (RA pressure, −11.6 ± 2.19 mm Hg to −4.1 ± 1.7 mm Hg; RV pressure, −2.5 ± 1.57 mm Hg to 4.6 ± 1.2 mm Hg; RV vent flow, 0 ± 7 ml/min to 26 ± 9 ml/min). Placing the heart in the circumflex position adversely affected right heart decompression in all techniques except single cannulation with the 51F cavoatrial cannula. Likewise, venous decompression was affected adversely in all techniques except double cannulation with caval snares. With the single 40F atrial cannula, SVC and IVC pressures were both elevated. Only the SVC pressure was affected when the cavoatrial cannula was used.

Renal blood flow autoregulation in developing swine.

Pressure-flow relationships (P/F) in the renal circulation were determined in 62 swine, aged 1 day-2 mo, anesthetized with pentobarbital sodium. Aortic and inferior vena caval pressures and renal and femoral arterial flows were recorded. Blood gas composition and pH and body temperature were monitored. The P/F was first determined while perfusion pressure was decreased for 2 min at each pressure by suprarenal aortic occlusion. The left renal artery in 38 of these animals was then cannulated for in situ perfusion of the kidney with blood withdrawn from a carotid artery by a Masterflex pump. The P/F was subsequently determined by changing pump flow for 2 min at each flow while recording perfusion pressure. Records were analyzed for transient and steady-state effects. Readjustments in renal vascular resistance (RVR) were apparent within 5 s after changing pressure or flow. The RVR stabilized at a new level within 2 min. Graphs of steady-state data delineated an autoregulatory range in the P/F for animals as young as 2 wk of age. We conclude that renal blood flow autoregulation in this mammal is negligible at birth and develops progressively during the first postnatal month.

A Starling resistor regulates cerebral venous outflow in dogs.

This investigation was undertaken to determine whether a Starling resistor or venous waterfall effect exists between the sagittal sinus and the cerebral veins such that increases in sagittal sinus pressure (Pss) do not abolish cerebral venous outflow and to examine two possible contributions of extracranial venous valves in regulating outflow. Anesthetized dogs were subjected to positive end-expiratory pressure (PEEP) before and after intracranial pressure (Pic) was elevated by inflation of an epidural balloon. PEEP raised Pss equally in all animals, but Pic and cerebral venous pressure (Pcv) increased less in the presence of intracranial hypertension. When Pss was low, passage of a catheter in the cerebral vein in and out of the sagittal sinus demonstrated an abrupt drop in pressure as the sinus was entered. When Pss was raised and lowered independently of superior vena caval pressure (Psvc) the changes in Pic and Pcv were less when Pss was decreased than when it was increased. Sustained increases and decreases in Psvc caused increases and decreases in Pcv, Pic, Pss, and external jugular venous pressure (Pejv) regardless of whether external jugular venous valves were present or absent. We conclude that a Starling resistor between the sagittal sinus and the cerebral veins regulates cerebral venous outflow when Pss is increased by PEEP and other maneuvers that raise Psvc. The waterfall maintains Pcv and Pic at normal levels when Psvc and Pss are reduced. Extracranial venous valves are not essential to this mechanism.

Use of the Pneumatic Antishock Garment

To the Editor.— The report entitled Caution in Pneumatic Antishock Garment Use concerns me greatly. The time course for the events from birth is described sketchily. One is left with the impression that the patient underwent cardiopulmonary resuscitation for a considerable interval (how soon after parturition?) before help was summoned. Proper application of the pneumatic antishock garment after an interval of seven minutes without vital signs would increase intraabdominal and inferior vena caval pressure 1 and act as a barrier to cephalad migration of blood 2 and, presumably, air. Creation of a negative intrathoracic pressure would also be obviated by mechanical ventilation. One should look more closely at the negative intrathoracic pressures created on the release of chest compression during cardiopulmonary resuscitation before sounding an alarm against therapy with the pneumatic antishock garment. To deny therapy of potential lifesaving magnitude like that of a properly applied pneumatic antishock garment

Left Renal Vein to Inferior Vena Cava Pressure Relationship in Humans

Pullback pressures from the left renal vein to the inferior vena cava were done on 50 normal patients. A gradient more than 1 mm. Hg was found in only 1 patient. The significance of these results as they relate to the etiology of varicocele formation and essential hematuria is discussed.

Hemodynamic effects of hydralazine in infants with a large ventricular septal defect.

To evaluate the effects of acute afterload reduction, hydralazine, 0.2 mg/kg, was administered at cardiac catheterization to seven infants who had a large ventricular septal defect (VSD). The infants were 2.5 - 11 months old (mean 5.1 months). Before and 5, 15, 25 and 35 minutes after hydralazine, aortic, pulmonary capillary wedge, pulmonary artery, right atrial and superior vena caval pressures and saturations, heart rate and oxygen consumption were measured. Hemodynamic effects were noted after 5 minutes but were most pronounced 35 minutes after hydralazine. Prehydralazine baseline data were therefore compared with values 35 minutes after hydralazine. Pulmonary flow did not changes, but systemic flow increased significantly (4.5 +/- 0.2 to 6.7 +/- 0.5 liters/min/m2 [mean +/- SEM], p less than 0.001). The pulmonary-to-systemic flow ratio decreased by 32% (3.4 +/- 0.4 to 2.3 +/- 0.2, p less than 0.001) and the absolute left-to-right shunt decreased by 24% (10.8 +/- 1.3 to 8.2 +/- 1.2 liters/min/m2, p less than 0.01). Hydralazine caused a significant decrease in systemic resistance (13.9 +/- 0.7 to 9.5 +/- 0.7 U, p less than 0.001). Pulmonary resistance, aortic, pulmonary artery and pulmonary capillary wedge pressures, heart rate and oxygen consumption did not change after hydralazine. Right atrial pressure decreased slightly (4.0 +/- 0.6 to 2.4 +/- 0.6 mm Hg, p less than 0.05). In conclusion, hydralazine caused a significant increase in systemic blood flow and a significant decrease in both pulmonary-to-systemic flow ratio and absolute left-to-right shunt in seven infants with a large VSD. These effects appear to be related to the decrease in systemic resistance that occurred with hydralazine. Although limited to the acute setting, these findings suggest that hydralazine may be beneficial in the management of infants with a large VSD.

The role of cava-pulmonary (Glenn) anastomosis in the palliative treatment of congenital heart disease

The value of the cava-pulmonary anastomosis (Glenn procedure) was assessed by reviewing the entire experience with this procedure in 83 children at The Hospital for Sick Children, Toronto, from 1961 to 1980. The over-all operative mortality rate was 9.6%, but only 2% in the second half of the series. The average follow-up is 9.4 years per patient. The late mortality rate has been 20%. By actuarial analysis, 84% of survivors were alive 9 years after operation; 54% had adequate palliation and 46% had required further operation. Long-term palliation was significantly better when the anastomosis was performed after 5 years of age. A previous arterial pulmonary artery shunt had no effect on either patient or shunt survival. Patients with tricuspid atresia had a better long-term survival rate than, but similar shunt survival to, those children with transposition, single ventricle, or miscellaneous cardiac anomalies. Angiography in 36 survivors showed patent shunts in 35 and no arteriovenous fistulas. Clinical status was not related to superior vena caval pressure or angiographic findings, indicating that Glenn shunt failure is a functional problem. The procedure is most useful for patients over 5 years of age who have complex heart disease not amenable to total repair. It is also on appropriate initial procedure in young patients over 18 months of age for whom direct atrium--pulmonary artery anastomosis is proposed as the future definitive treatment.

Mechanism by which positive end-expiratory pressure increases cerebrospinal fluid pressure in dogs.

We investigated possible mechanisms by which positive end-expiratory pressure (PEEP) increased cerebrospinal fluid pressure (PCSF) in anesthetized mechanically ventilated dogs. In part I of the study, PEEP was applied in 5 cmH2O increments each lasting 1-2 min, before and after a snare separated the spinal from the cerebral subarachnoid space in each animal. Next, with the spinal cord still ligated, the dogs were ventilated without PEEP while superior vena cava pressure (PSVC) was raised in 5 cmH2O increments by means of a fluid reservoir connected with the superior vena cava. Cerebrospinal fluid pressure in the cisterna magna increased immediately and in parallel with PEEP before and after the spinal subarachnoid space was occluded and also increased when PSVC was raised independently; in all circumstances the increase in PCSF correlated closely with PSVC (r = 0.926). In part II of the study, arterial blood gases were drawn before and after PEEP was applied in the same increments and for the same duration as in part I. Cerebrospinal fluid pressure measured with a hollow skull screw again rose in parallel with PEEP, whereas arterial carbon dioxide tension rose only slightly at 60 s. In part III of the study, mean arterial pressure (Pa) was allowed to decrease with PEEP or was held constant by distal aortic obstruction and volume infusion. Cerebrospinal fluid pressure increased regardless of Pa, but the increase was greater when Pa was held constant than when it fell with PEEP. We conclude that PEEP increases PCSF primarily by increasing PSVC and decreasing cerebral venous outflow. This effect is augmented if cerebral arterial inflow is increased as well.

Intragastric pressure measurement: A guide for reduction and closure of the silastic chimney in omphalocele and gastroschisis

In newborn infants with omphalocele or gastroschisis, traditional criteria for reduction of the herniated viscera either primarily or after application of a Silastic chimney have been the baby's color, respiratory rate, and lower extremity turgor. These are not always accurate or immediately apparent. In order to define more objective guidelines for reduction, measurements of intragastric pressure through a gastrostomy tube using a water manometer were carried out. The validity of this pressure measurement was demonstrated in five puppies where intra-abdominal pressure correlated well with inferior vena cava pressure and intragastric pressure measured through a gastrostomy tube (R = .98 and .99, respectively). Over a 3.5-yr period, 25 newborn infants with omphalocele (9) or gastroschisis (16) were treated. Ten underwent primary closure, and 15 were treated by placement of a Silastic chimney with serial reduction and closure. Manual reductions were performed once or twice daily to a maximum intragastric pressure of 20 cm water. Greater pressures demonstrated cardiovascular and respiratory comprise both experimentally and clinically. The mean time required for removal of the Silastic chimney was 4.7 days. There were no infections related to the chimney. There were 2 early and 5 late deaths, a 28% mortality rate. The remaining patients are alive and well. Intragastric pressure measurement in patients with omphalocele or gastroschisis provides objective criteria for safe primary closure and Silastic chimney reduction, shortens the time of reduction, and reduces the number of associated circulatory, respiratory, and septic complications.

211 CARBOHYDRATE METABOLISM IN THE IMMATURE HEART

Metabolic activity of the heart is best observed using a system in which the heart is isolated from other organs but is allowed to support a work load comparable to that in the living animal. A model is described in which the isolated heart of a newborn piglet is perfused in a manner reproducing fetal flow patterns and work loads. Perfusion is carried out using Krebs-Henseleit buffer equilibrated with O2 95%, CO2 5% supplemented with glucose (glu) 10 mM(n=7), pyruvate(pyr) 20 mM(n=5) or lactate (lact) 20 mM(n=5) in a 250 cc recirculating system for 1 hr. Buffer is infused via the inferior vena cava and mean pressure in both great arteries is adjusted to 60±3 mmHg with left atrial pressure 6±2 mmHg paced at 180/min. Pressure development and total cardiac output were stable over 1 hr. In glu-perfused hearts, O2 uptake (VO2)=2572±323, glu uptake=439±44 and lact production=24±31 μmol/hr/g dry heart. In pyr-perfused hearts VO2=2725±297, pyr uptake=929±90 and lact production=112±50 μmol/hr/g dry heart. In lact-perfused hearts VO2=2082±180, lact uptake=690±111 μmol/hr/g dry heart. Tissue ATP and creatine phosphate following perfusion were 20.4±0.6 and 19.1±1.1 μmol/g dry heart, respectively, after pyr and lact perfusion for 1 hr. Glycogen content after 1 hr working perfusion with pyr was 166±20 μmol glu equivalent/g dry heart. These results quantify O2 requirements of the newborn heart and indicate normal function may be supported without significant contribution from anaerobic glycolysis.