Effects of left atrial pressure on pulmonary shunt and the dead space/tidal volume ratio.
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Biomedical subjects
Publications and source records attributed to W S Liu.
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Cardiovascular dynamics and left ventricular work were evaluated in 15 resting, standing, and treadmill-exercised calves before and at periodic intervals after their natural hearts (NH) were replaced with an artificial heart (AH). Standing produced increases in heart rate, cardiac output, oxygen uptake, and left ventricular work and decreases in mean aortic pressure and systemic vascular resistance in NH calves which were more marked with exercise. AH calves had higher aortic pressures, cardiac output, systemic vascular resistance, oxygen uptake, and left ventricular work during resting conditions in the first 2 postoperative weeks than did NH calves, which gradually returned to values similar to the latter by the fifth week after operation. Exercise was not tolerated early after AH implantation, but was after 5 to 6 weeks. Our results indicate that AH calves increase cardiac output with exercise by reducing systemic vascular resistance, whereas NH animals respond similarly, but also increase heart rate. The data suggest that a marked elevation in systemic vascular resistance early after AH implantation increases left ventricular work and prevents adequate rises in cardiac output to all but minor increases in metabolic requirements.
The effects of fentanyl (0.5 mg/kg iv), fentanyl with diazepam (1 mg/kg iv) and fentanyl, diazepam and pancuronium (0.1 mg/kg iv) on heart rate (HR), mean arterial blood pressure (BP), cardiac output (QT), urine flow rate and urine epinephrine and norepinephrine excretion were determined in nine dogs. Fentanyl did not significantly change QT or BP but did reduce HR and urine flow rate (P less than 0.05). Urine epinephrine and norepinephrine excretion rates were signicantly increased by fentanyl (P less than 0.05). Diazepam caused no significant further changes in QT, BP or HR 30 minutes after administration, but urine epinephrine and norepinephrine excretion rates were reduced to control (pre-fentanyl) levels. Addition of pancuronium after fentanyl and diazepam increased urine flow rate to pre-fentanyl levels and elevated QT, BP and HR above controls but produced no significant change in urine epinephrine or norepinephrine excretion. These data suggest that fentanyl increases catecholamine blood levels and imply that the latter may be one mechanism by which cardiovascular dynamics are maintained stable during fentanyl anaesthesia. Our findings also demonstrate that cardiovascular stimulation after pancuronium is not associated with increased urinary catecholamine excretion.
Peripheral vascular and myocardial effects of increasing concentrations of nitrous oxide (0 to 70 per cent) in oxygen were determined in 15 unanaesthetized calves before and after replacement in their natural heart (NH) with a pneumatically driven artificial heart (AH). Nitrous oxide produced concentration-related decreases in arterial and mixed venous pH and increases in minute ventilation and arterial and mixed venous carbon dioxide tensions in both NH and AH calves. Nitrous oxide resulted in significant increases in cardiac output, stroke volume and mean aortic, pulmonary artery and right atrial pressures in NH and AH calves, but did not significantly change systemic vascular resistance in either group of animals. Heart rate was increased in NH calves but was fixed in AH calves. Elevations in heart rate and cardiac output at nitrous oxide concentrations greater than 30 per cent and aortic pressure at 70 per cent nitrous oxide were significantly greater in NH than AH animals (P less than 0.05). These data demonstrate that nitrous oxide stimulates the cardiovascular system in spontaneously breathing mammals and that the changes result from improved venous return and an increase in myocardial chronotropy. Our findings also suggest that cardiovascular stimulation during nitrous oxide breathing may be related to increased concentrations of arterial and/or venous carbon dioxide.
Pulmonary compliance and shunt were evaluated preoperatively, 30 minutes after cardiopulmonary bypass, and two hours postoperatively in 132 calves undergoing open-heart surgery with halothane and oxygen anesthesia. The calves were divided into 11 groups with respect to maintenance of the lungs during bypass. In Group 1 the lungs were collapsed during bypass. In all other groups the lungs were mechanically ventilated, statically inflated, or both, with either pure oxygen or nitrous oxide, 50 per cent, in oxygen. All groups had similar compliance and shunt values before operation and sustained significant decreases in compliance and increases in shunt 30 minutes after bypass. Calves exposed to positive-pressure breathing during bypass had higher shunt and lower compliance values after bypass and postoperatively than those not exposed to mechanical ventilation, irrespective of the inflating gas or presence or absence of any amount of static airway pressure. Animals not ventilated during bypass had compliance and shunt values that were not significantly different from preoperative values, while calves that were ventilated had compliance and shunt values that were still significantly altered two hours postoperatively. These data demonstrate that positive-pressure breathing during bypass decreases pulmonary compliance after bypass and postoperatively and increases intrapulmonary shunt, but that the gas inflating the lungs during bypass does not influence either of these variables. The findings also suggest that static pulmonary inflation during bypass offers no advantage over allowing the lungs to remain collapsed.
Urine excretion rates of norepinephrine were measured in 15 children with Tetralogy of Fallot and 25 with atrial septal secundum defects anaesthetized with halothane or morphine before, during and for two hours after surgical correction of their cardiac defects. All patients were paralyzed with d-tubocurarine, the tracheae were intubated and respiration was controlled. Urine was obtained for 90 minutes before induction, during induction, before, during and after bypass and postoperative. Patients with TF had significantly higher pre-operative urine norepinephrine excretion rates than patients with ASD. In TF children anaesthetized with halothane norepinephrine excretion was significantly decreased during induction and during operation but increased post-operatively. Children with ASD and anaesthetized with halothane did not have urine norepinephrine excretion rates that were significantly different from post-operative values until the postoperative period. ASD children anaesthetized with morphine had marked elevations in norepinephrine excretion during induction and all subsequent study periods. On the other hand, morphine anaesthetized TF children did not have a significant increase in urine norepinephrine excretion until bypass had been established. Increased norepinephrine excretion was maintained in these patients during all subsequent study periods. These data, when combined with our results in patients with acquired heart disease, demonstrate that disease can alter norepinephrine responses to morphine anaesthesia. In addition our results suggest that dosage of morphine and morphine blood levels might also modify norepinephrine excretion.
Renal effects of large doses of fentanyl (1 mg/kg) were determined in 14 mongrel dogs before and after addition of 50 per cent nitrous oxide. Fentanyl significantly increased urine osmolarity and decreased urine output and free water clearance but did not change inulin or PAH clearances. The arterial blood pressure and cardiac output were significantly decreased after 0.1 mg/kg fentanyl and these changes were then maintained during the remainder of the study period. Addition of nitrous oxide produced no further changes in cardiac output and arterial blood pressure but did increase urine output, PAH, inulin and free water clearances and decreased urine osmolarity. These data demonstrate that high doses of fentanyl have significant antidiuretic properties in the dog and these probably are related to the release of antidiuretic hormone. Our results also indicate that addition of nitrous oxide reverses fentanyl induced antidiuresis.
The cardiovascular effects of diazepam 0.5 and 1.0 mg/kg and diazepam with pancuronium 0.1 mg/kg after fentanyl 0.5 mg/kg were determined in thirteen dogs premedicated with atropine. Fentanyl produced significant reductions in heart rate, cardiac ouptut and arterial blood pressure. Administration of 0.5 mg/kg of diazepam after fentanyl did not significantly alter stroke volume, arterial blood pressure or peripheral vascular resistance but did increase heart rate and cardiac output. Additional diazepam did not further change the heart rate, but did reduce stroke volume, cardiac output, arterial blood pressure and peripheral vascular resistance. Administration of pancuronium after fentanyl and diazepam produced marked elevations in heart rate, cardiac output and arterial blood pressure. There was no difference in mean heart rate and cardiac output when values prior to fentanyl and those obtained three minutes following pancuronium were compared. These data demonstrate that large doses of fentanyl decrease heart rate, cardiac these changes can be partially reversed with diazepam 0.5 mg/kg and completely antagonized with pancuronium 0.1 mg/kg.
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Peripheral vascular and direct cardiac effects of calcium chloride were determined in a new animal model, the unanesthetized calf, before and after replacement of its natural heart (NH) with a pneumatically driven artificial heart (AH). Calcium (5 and 10 mg/kg) significantly increased cardiac output (Qt) and reduced systemic vascular resistance (SVR) before and after AH implantation. Increases in Qt in AH calves and reductions in SVR in both NH and AH calves were, however, transient, being present 5 minutes but not 15 minutes after both doses of calcium. Increases in Qt and reductions in SVR were significantly (P less than .05) greater after 10 mg/kg than after 5 mg/kg calcium in NH and AH calves. Both doses of calcium produced greater (P less than .05) increases of Qt in NH than in AH animals but similar reductions in SVR. Pulmonary vascular resitance, heart rate and pulmonary arterial and right atrial pressures were not significantly altered by either dose of calcium in NH or AH calves. Mean aortic pressure was influenced by 10 mg/kg calcium only, being transiently reduced in AH calves and increased in NH animals. Pulmonary shunt (QS/Qt) was increased by both doses of calcium in NH calves but only by 10 mg/kg in AH animals. Correlations of mean change in QS/Qt with mean change in Qt were high both before (r=.99) and after (r=.97) AH implantation. These data demonstrate that calcium significantly reduces SVR in a dose-related manner as well as exerting a positive inotropic effect on the myocardium.
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The effects of oxygen and 60% nitrous oxide and oxygen on the pressure and volume of Portex low-pressure (LP) and high-pressure (HP) endotracheal tube cuffs were determined in 120 intubated patients undergoing thoracic surgical procedures. Cuffs were filled with either room air or a sample of the inspired gases. All cuffs had sustained significant increases in cuff volume and pressure by the end of the procedure except those filled with inspired gases. LP cuffs had lower initial and final cuff pressures than HP cuffs, but pressure and volume changes were similar with both types. Cuff gas analysis revealed that cuff volume changes were due to diffusion of oxygen and nitrous oxide into the cuff and failure of nitrogen to diffuse out. These findings suggest that cuff overexpansion during anesthesia or prolonged ventilation may be an important cause of tracheal trauma.
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Quantitation of peripheral vascular versus direct cardiac effects of isoproterenol (0.002 mg/kg) was attempted in a new pharmacologic animal model, the unanesthetized calf, before and after replacement of its natural heart with a pneumatically driven artificial heart (AH). Isoproterenol significantly increased (rho less then 0.01) cardiac output and pulmonary shunt and decreased aortic blood pressure before and after AH replacment. Elevation of cardiac output and pulmonary shunt was greater (rho less than 0.05) and depression of aortic pressure less (rho less than 0.05) before AH replacement than after. Isoproterenol did not change pulmonary artery (PA) or right atrial (RA) blood pressures before AH implantation but did reduce (rho less than 0.05) PA diastolic and mean pressures and increase mean RA pressures after. Systemic vascular resistance was significantly (rho less than 0.01) reduced by isoproterenol before and after AH implantation. Heart rate, 02 uptake, respiratory rate, tidal volume, and minute volume were all markedly increased before AH implantation but unchanged after. These findings demonstrate that approximately half the increase in output and pulmonary shunt and all changes in 02 uptake and respiratory dynamics after administration of isoproterenol are related to cardiac effects of the drug. Our data also suggest that the unanesthetized bovine before and after AH replacement is a unique model for study of the differential pharmacology of drugs with respiratory, cardiac, and peripheral vascular effects.
The cardiovascular effects of 2 and 3 mg/kg of meperidine plus 60 to 67% N2O in O2 on cardiovascular dynamics in man were measured before and after the administration of 0.08 mg/kg of IV pancuronium. N2O and 2 mg/kg of meperidine did not change heart rate (HR) but produced a marked reduction (-49%) in cardiac output (QT) plus significant decreases in stroke volume (SV) and blood pressure (BP) and an increase in peripheral arterial resistance (PVR). Additional meperidine did not further alter any of the variables; however, surgical stimulation caused significant increases in HR, BP, and PVR. SV and QT were not significantly changed by surgical stimulation and were still markedly depressed when compared to control values. Pancuronium produced marked increases in HR, SV, QT, and BP and a reduction in PVR. These changes were maximal 4 to 8 minutes after pancuronium and returned toward pre-pancuronium values thereafter. These data demonstrate that N2O-meperidine anesthesia results in a moderate reduction in BP but a marked depression in QT. The findings also indicate that pancuronium reverses the cardiovascular depression produced by N2O-meperidine and is therefore, a desirable muscle relaxant when the above technic is employed.
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