The comparative electrophysiologic and hemodynamic effects of a large dose of ropivacaine and bupivacaine in anesthetized and ventilated piglets.

Ropivacaine is less potent and less toxic than bupivacaine. We administered these two local anesthetics in a cardiac electrophysiologic model of sodium thiopental-anesthetized and ventilated piglets. After assessing the stability of the model, bupivacaine (4 mg/kg) and ropivacaine (6 mg/kg) were given IV in two groups (n = 7) of piglets. No alteration in biological variables was reported throughout the study. Bupivacaine and ropivacaine similarly decreased mean aortic pressure from 99 +/- 22 to 49 +/- 31 mm Hg and from 87 +/- 17 to 58 +/- 28 mm Hg, respectively, and decreased the peak of the first derivative of left ventricular pressure from 1979 +/- 95 to 689 +/- 482 mm Hg/s and from 1963 +/- 92 to 744 +/- 403 mm Hg/s, respectively. Left ventricular end-diastolic pressure was similarly increased from 6 +/- 5 to 9 +/- 5 mm Hg and from 6 +/- 4 to 12 +/- 4 mm Hg, respectively. Bupivacaine and ropivacaine similarly lengthened the cardiac cycle length (R-R; from 479 +/- 139 to 706 +/- 228 ms and from 451 +/- 87 to 666 +/- 194 ms, respectively), atria His (from 71 +/- 15 to 113 +/- 53 ms and from 64 +/- 6 to 86 +/- 10 ms, respectively), and QTc (QTc = QT x R-R(-0.5), Bazett formula; from 380 +/- 71 to 502 +/- 86 ms and from 361 +/- 33 to 440 +/- 56 ms, respectively) intervals. Bupivacaine altered to a greater extent the PQ (the onset of the P wave to the Q wave of the QRS complex) (from 97 +/- 20 to 211 +/- 60 ms versus from 91 +/- 8 to 145 +/- 38 ms, P < 0.05), QRS (from 58 +/- 3 to 149 +/- 34 ms versus from 60 +/- 5 to 101 +/- 17 ms, P < 0.05), and His ventricle interval (from 25 +/- 4 to 105 +/- 30 ms vs from 25 +/- 4 to 60 +/- 30 ms, P < 0.05) than ropivacaine. A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent. IMPLICATIONS: A 6 mg/kg ropivacaine dose induced similar hemodynamic alterations as 4 mg/kg bupivacaine. However, bupivacaine altered the variables of ventricular conduction (QRS and His ventricle) to a greater extent.     

Hemodynamic effects of endothelin in anesthetized dogs

The purpose of the present study was to investigate and compare the hemodynamic responses that can be elicited in anesthetized dogs by intravenous administration of endothelin at rates of 300 (group E-I, n = 9) and 600 pmol.kg-1 (group E-II, n = 9) for 15 minutes. In group E-I, no significant pressure response was observed after administration of endothelin and cardiac index remained unchanged throughout the experiment. However, right and left ventricular work indices increased significantly but left ventricular maximum dp/dt and pulmonary vascular resistance decreased significantly. In group E-II, mean arterial pressure increased significantly by elevating systemic vascular resistance with marked decrease in cardiac index. However, right and left ventricular work indices remained unchanged throughout the experiment. On the other hand, each dose of endothelin significantly increased pulmonary capillary wedge pressure and left ventricular end-diastolic pressure but decreased heart rate. The present data revealed that the hemodynamic effects were different according to the doses of endothelin infused. In conclusion, our results show that endothelin (600 pmol.kg-1 BW) produces a long lasting increase in arterial pressure and endothelin-induced pressure responses are caused by an elevation in systemic vascular resistance.     

Circulatory and ventilatory effects of hypervolaemia in artificially ventilated piglets

The influence of hypervolaemia upon circulation and pulmonary ventilation was studied in six piglets (body weights 8.5–10.5 kg). A new functional principle for artificial ventilation was used. The alveolar ventilation was unchanged at normovolaemia and hypervolaemia. Arterial blood gases were sampled and end-tidal carbon dioxide concentrations were measured continuously. Central circulation was followed by pressure recordings and an electromagnetic flow meter for cardiac output measurements. Mean values ± SEM of end-inspiratory tracheal pressures increased from 0.98 ± 0.06 kPa at normovolaemia to 1.57 ± 0.06 kPa at hypervolaemia (p < 0.02). In all animals total compliance decreased (p < 0.02). Simultaneously the insufflation time for the tidal volume decreased by 13 percent (p < 0.05). Arterial oxygen tensions decreased from 8.5 ± 0.48 kPa to 7.0± 0.77kPa (p< 0.05). During hypervolaemia aortic pressures increased from 13.1± 1.3kPato 14.9 ± 0.8 kPa(p< 0.05), pulmonary artery pressures from 2.8 ± 0.33 kPa to 5.0 ± 0.53 kPa (p < 0.02) and cardiac output from 1.07 ±0.17 l · min^-1 to 1.5 ± 0.19 l min ·^-1 (p< 0.02). The stroke work for the right heart increased by 74 per cent (p < 0.02) and for the left heart by 62 per cent (p < 0.02). Pulmonary vascular resistance was unchanged, while systemic vascular resistance was significantly decreased (p < 0.05). The positive effect upon systemic circulation gained by the use of excessive fluid therapy resulted in an overcirculation within the lungs which reduced pulmonary ventilation. This reduction could most probably be related to a closure of terminal airways secondary to lung hyperperfusion, increasing the pulmonary shunt.     

Hemodynamic and coronary vascular effects of dexmedetomidine in the anesthetized goat

Background: In phase III trials, the hemodynamic stabilising effect of the α₂-adrenergic agonist dexmedetomidine (DEX) is being investigated in patients with coronary artery disease. Coronary vascular effects of α₂-agonists have been studied in dogs and pigs, but both species have a different hemodynamic response to DEX than man. The aim of this study was to investigate the hemodynamic and coronary vascular effects in goats.
Methods: In 6 open-chest goats anesthetized with halothane, central and coronary hemodynamics and oxygen supply and demand were measured before and following IV bolus infusion of DEX in doses ranging from 0.1 to 10 μg/kg.
Results: With DEX doses of 1 μg/kg or higher, mean arterial pressure (MAP), systemic vascular resistance, coronary vascular resistance and arterio-mixed venous oxygen content increased within 2 min, but returned to baseline within 15 min. In contrast, there was a progressive and cumulative decrease in cardiac output (CO), heart rate, and dP/dt_max. Regional coronary venous oxygen extraction (C(a-cv)O₂) transiently increased after 3 μg/kg DEX and decreased 15 min after 10 μg/kg DEX. LVEDP transiently increased after 3 and 10 μg/kg DEX. The changes after DEX 10 μg/kg differed from those after lower doses: MAP (35%), CO (50%), stroke volume (33%), C(a-cv)O₂ (15%) and myocardial oxygen extraction (33%) were all decreased. Myocardial oxygen supply and demand decreased in parallel.
Conclusions: 1) The cardiovascular response to IV DEX in goats is similar to man. 2) In goats after DEX, systemic and coronary vasoconstriction are short-lived, and 3) the balance between myocardial oxygen supply and demand is maintained.     

Hemodynamic effects of induced hypotension by ketanserin in anesthetized dogs]

Hemodynamic effects of hypotension induced by ketanserin were investigated in 18 mongrel dogs under 0.87% halothane in oxygen (1 MAC). They were randomly allocated to one of two groups. Group C (n = 9) received no vasodilator therapy and served as a control and group K (n = 9) received 0.1% ketanserin solution. Mean arterial pressure decreased and was maintained at 60 mmHg for 60 minutes in group K. No change was noted in hemodynamic variables measured in group C throughout the experiment. During and after induced hypotension in group K, stroke volume index increased significantly compared with the control value. On the other hand, systemic vascular resistance was significantly reduced, reaching 50% of the control value at the end of the hypotensive period. Left ventricular maximum dp/dt showed a significant reduction during hypotension but then increased gradually to the control value. In addition, heart rate decreased significantly during and after induced hypotension, therefore these vasodilator effects were not accompanied by reflex tachycardia. Cardiac index remained unchanged throughout the experiment. Further, no changes in central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance were observed. In conclusion, the data indicate that ketanserin is a potent systemic vasodilator producing stable hemodynamics. It also reduces systemic vascular resistance without reflex tachycardia and this is a favorable effect of ketanserin.     

Hemodynamic effects of levosimendan following cardiac surgery

The hemodynamic effect of levosimendan was compared to that of dobutamine in a trial enrolling 30 adults undergoing scheduled cardiac surgery with cardiopulmonary bypass. Fifteen patients were randomly assigned to receive levosimendan in a single dose of 18 microg x kg(-1) followed in 15 to 20 minutes by start of infusion at a rate of 0.2 microg x kg(-1) min(-1) for 24 hours (levosimendan group). Another 15 randomized patients received dobutamine infused at a rate of 7.5 microg x kg(-1) min(-1). Hemodynamic parameters were measured before starting infusion of the drug and after 24 hours of treatment. Changes in the main hemodynamic parameters were as follows. In the levosimendan group heart rate (beats/min) was 87.15 (SD 10.22) at baseline and 87.91 (6.00) at 24 hours; mean arterial pressure (mm Hg) was 83.96 (10.57) at baseline and 86.41 (13.29) after 24 hours; cardiac index (L/min/m2) was 2.21 (0.23) at baseline and 2.53 (0.35) at 24 hours; systemic vascular resistance (dyn/sec(-1)/cm(-5)) was 1436.74 (311.48) at baseline and 1378.35 (320.68) at 24 hours. In the dobutamine group heart rate (beats/min) was 84.28 (2.18) at baseline and 96.02 (9.10) after 24 hours; mean arterial pressure (mm Hg) was 83.59 (9.05) at baseline and 74.29 (6.33) at 24 hours; cardiac index (L/min/m2) was 2.16 (0.28) at baseline and) 3.02 (0.34) at 24 hours; systemic vascular resistance (dyn/sec(-1)/cm(-5)) was 1578.93 (334.88) at baseline and 1136.68 (158.60) at 24 hours. We found that mean arterial pressure and both systemic and pulmonary vascular resistance decreased significantly in the levosimendan group (P < 0.05), but not in the dobutamine group. On the other hand, both heart rate and cardiac index increased in the levosimendan group only (P < 0.05). We conclude that levosimendan improves hemodynamic stability in patients who have undergone cardiac surgery and that it is a good alternative for treating postoperative low cardiac output syndrome.     

Hemodynamic effects of infusions of alpha-human atrial natriuretic peptide in anesthetized dogs]

The purpose of this study is to investigate and compare the hemodynamic effects of infusion of alpha-human atrial natriuretic peptide (alpha-hANP) at three different doses. Mongrel dogs were anesthetized with 0.87% halothane in oxygen. alpha-hANP was infused for one hour with a constant rate at either 0.3, 1.0, or 10.0 micrograms.kg-1.min-1, respectively. They were randomly divided into four groups. Group A-1 received 0.3 micrograms.kg-1.min-1 of alpha-hANP; Group A-2 received 1.0 micrograms.kg-1.min-1 of alpha-hANP; Group A-3 received 10.0 micrograms.kg-1.min-1 of alpha-hANP; and Group C received normal saline as the vehicle and served as the control. Control values were obtained before infusion of alpha-hANP or vehicle was started, and hemodynamic variables were measured at 30 minutes intervals for two hours. Mean arterial pressure (MAP) of the group C showed no significant changes from control value. During and after infusion of alpha-hANP, MAP in the group A-2 and A-3 was significantly lower than the control values. The decrease in MAP of the group A-2 was the greatest. Heart rate decreased significantly at 60 minutes after termination of the infusion in all four groups. The reduction of cardiac index (CI) in the group-3 was the greatest. In the group A-3, it decreased for 31% from the control value at 60 minutes during infusion. However, this change was not significant. In contrast, the reduction in CI of the group A-2 was minimal. Mean pulmonary artery pressure (MPAP) of the group C showed no significant change from the control value. The patterns of changes in MPAP were similar to those of the alpha-hANP infused groups. It decreased progressively during the infusion. Systemic vascular resistance (SVR) was essentially unchanged in the group C. In the group A-2, SVR decreased slightly during the infusion period and then tended to increase after the infusion of alpha-hANP. In contrast, in the group A-1 and A-3, SVR increased progressively. The changes in left ventricular maximum dp/dt (LV dp/dt max) of the group C were minimal. The reduction in LV dp/dt max was more pronounced in group A-2 than in group A-3. In conclusion, our data show that hypotensive effects of alpha-hANP are associated with the reduction in cardiac output due to the decrease of cardiac contractility. However, the changes of hemodynamic variable are not dose-dependent.     

Cardiac electrophysiologic effects of fentanyl and sufentanil in canine cardiac Purkinje fibers

The electrophysiologic effects of high concentrations of the opioid agonists, fentanyl and sufentanil, on isolated canine cardiac Purkinje fibers were studied. Changes in action potential parameters were examined at the following concentrations: fentanyl 94.6 nM, 0.19 microM, and 0.95 microM; sufentanil 8.6 nM, 86.4 nM, 0.17 microM, and 0.26 microM. Naloxone 5.5 microM was administered after maximal changes were induced by fentanyl in order to explore the possibility of an opioid receptor interaction. Action potential parameters measured were Vmax of phase 0, amplitude, overshoot, maximum diastolic potential, action potential duration at 50%, and 90% repolarization and membrane responsiveness. Fentanyl 0.19 microM and sufentanil-0.17 microM caused a significant lengthening of action potential duration at 50 and 90% repolarization, 6.4% and 7.3%, and 10.2% and 12.4%, respectively, P less than 0.05. Other action potential parameters were not significantly affected by the opioids. Naloxone 5.5 microM alone did not alter action potential characteristics and failed to reverse action potential prolongation produced by fentanyl. The authors suggest that fentanyl and sufentanil prolong action potential duration in canine cardiac Purkinje fibers via direct membrane actions.     

Hemodynamic effects of external cardiac massage in trauma shock

The effectiveness of closed chest cardiopulmonary resuscitation (CCCPR) in maintaining cardiac output has been well studied in cardiac arrest. Trauma surgeons most often encounter shock secondary to hypovolemia or cardiac tamponade, and the effectiveness of CCCPR in that setting has not been established. To determine the hemodynamic effects of external massage in profound shock, hypotension was induced in baboons. Pressures obtained with external massage were compared to spontaneous intra-arterial pressures before compression. Although external massage increased systolic pressures in both tamponade and hypovolemia, diastolic pressures were consistently decreased. We conclude that CCCPR does not augment arterial pressure in the clinical situations associated with decreased LVEDV and is unlikely to provide organ perfusion for trauma victims.     

Differential effects of halothane and enflurane on end-systolic pressure-diameter relationship in anesthetized,mechanically ventilated dogs

To clarify the difference of negative inotropic effects, we evaluated the effects of 0, 0.5, and 1 MAC halothane and enflurane on systolic performance in anesthetized, mechanically ventilated, vagotomized dogs. Left ventricular myocardial contractility was assessed by the slope of the end-systolic pressure-diameter relationship (Ees), which have been reported to be independent of alterations in preload and afterload but sensitive to changes in myocardial contractility. Both anesthetics decreased heart rate and dose-dependently decreased left ventricular systolic pressure. Enflurane decreased heart rate and left ventricular systolic pressure more than an equivalent MAC of halothane. Both anesthetics increased left ventricular end-diastolic diameter without any change in % shortening of the left ventricular internal diameter. TheEes was decreased to a similar extent at both 0.5 and 1 MAC halothane. TheEes was decreased with increasing concentrations of enflurane. TheEes was significantly larger (P<0.05) with 1 MAC of halothane than with 1 MAC enflurane. These results suggest that halothane preserves myocardial contractility better than enflurane in the presence of fentanyl.     

Hemodynamic effects of pressure support ventilation in cardiac surgery patients

Hemodynamic consequences of pressure support ventilation (PSV) were compared with intermittent mandatory ventilation (IMV) in 20 patients following aortocoronary bypass. On the morning following surgery, all patients were weaned by IMV to a rate of eight breaths per minute, tidal volume of 12 ml/kg and inspired oxygen concentration of 40 per cent. With patients awake and able to breath spontaneously, PSV was begun at 20 cm of water. In patients with static lung compliance, less than 0.06 l/cm H2O, 30 cm H2O of PSV was used. Subsequently, all patients were weaned to PSV 10 cm of water, continuous positive airway pressure (CPAP) at 5 cm water and extubated. Hemodynamic data including oxygen transport were obtained at each level of PSV and at IMV prior to weaning. Analysis using ANOVA showed comparable hemodynamic and oxygen transport parameters for PSV of 30 cm H2O in comparison with IMV. PSV at levels of 20 and 10 cm H2O produced statistically significant increases in heart rate, mean arterial pressure, central venous pressure, and pulmonary capillary wedge pressure. Cardiac output was stable, and these increases were not clinically significant. In awake patients following cardiac surgery, PSV up to 30 cm H2O can be safely applied without hemodynamic embarrassment in patients with good left ventricular ejection fractions.     

Hemodynamic effects of flunitrazepam in cardiac patients during anesthetic induction

The hemodynamic effects of flunitrazepam were studied in eight coronary patients (group I) and in six patients with compensated cardiac failure (group II) during the induction of anesthesia with droperidol 5 mg and fentanyl 4 micrograms . kg-1. A right sided cardiac catheterization was performed to measure cardiac output by thermodilution. In coronary patients, the hemodynamic parameters were only slightly modified (NS). Cardiac output (-12.7%) and oxygen consumption (-20.4%) decreased; Pvo2 increased from 6.4 +/- 0.1 to 7.3 +/- 0.3 kPa. In patients with cardiac failure, significant cardiovascular changes were not observed. Arterial pressure (-13%), cardiac output (-2.6%), oxygen consumption (-6%) and systemic vascular resistance (-13.4%) decreased; Pvo2 increased from 6.4 +/- 0.5 to 6.8 +/- 0.7 kPa. In both groups, heart rate and pulmonary capillary wedge pressure were unchanged. There was only a significant difference (p less than 0.05) between the decrease in systemic resistance in group II and in the absence of change in systemic resistance in group I. Decrease in oxygen consumption be decrease in oxygen demand could explain the slight decrease in cardiac output. Flunitrazepam was a good hypnotic for the induction of anesthesia in normovolaemic coronary patients and in patients with compensated cardiac failure.     

七氟醚诱导及维持麻醉对心脏瓣膜手术病人血液动力学的影响

目的:研究七氟醚及七氟醚-N_2O吸入诱导及维持麻醉对心脏瓣病人血液动力学的影响。方法:44例患者分两组,组1以七氟醚、组2以七氟醚-N_2O诱导,均以七氟醚-N_2O维持麻醉。采用SwanGanz导管技术监测血液动力学变化。结果:诱导过程病人舒适,入睡平稳,几无呛咳屏气及躁动等不良反应发生。诱导后两组HR、PTRI、PVRI和SVRI无变化,但MAP、CI、LVWI、LVSWI及RVWI明显降低(P<0.05),组1尚伴SI和RVSWI减低(P<0.05)。劈胸骨后,两组RAP、PTRI、PORI、SVRI增高,CI、SI、LVWI、LVSWI、RVWI及RVSWI进一步减低(P<0.05)。CPB开始前,两组LVWI、LVSWI、RVWI及RVSW仍继续下降(P<0.01)。结论:心脏瓣膜病人以1.0 MAC七氟醚或1.2 MAC七氟醚-N_2O诱导是可取的,但以此浓度维持麻醉,对强烈刺激反应的抑制仍嫌不足。