Haemodynamic changes associated with thermodilution cardiac output determination during myocardial ischaemia or pulmonary oedema in dogs

Since the technique of thermodilution (TD) cardiac output measurements per se causes haemodynamic alterations, the authors examined whether the alterations elicited by iced injectate are augmented in the presence of myocardial ischaemia (MI) or pulmonary oedema (PE), compromised conditions frequently associated with critically ill patients. MI (N = 7) or PE (N = 7) was induced by clamping the anterior descending coronary artery or by a slow infusion of oleic acid into the right atrium, respectively, in anaesthetized dogs. Injection of iced injectate, 3 ml, caused similar changes in heart rate, mean systemic and pulmonary arterial pressures, pulmonary blood flow, right ventricular dP/dt, and right atrial pressure in dogs with and without MI or PE. Cardiac output estimated by TD correlated closely with pulmonary blood flow measured by electromagnetic flowmeter in both MI and PE (r > 0.9). No profound alterations in haemodynamics were observed at any injection during TD cardiac output measurements under MI or PE. These results indicate that TD cardiac output determination does not cause serious haemodynamic alterations, and can estimate right ventricular output accurately under MI and PE.     

Haemodynamic changes associated with thermodilution cardiac output determination during metabolic acidosis or hypoxic hypoxia in dogs

Haemodynamic alterations elicited by iced injectate during thermodilution cardiac output measurements were evaluated in the presence of metabolic acidosis or hypoxic hypoxia in 14 instrumented anaesthetized dogs. The alterations in some haemodynamic variables during slowing of the heart rate following injection of 3 ml iced injectate were slightly greater in metabolic acidosis and hypoxic hypoxia as compared to animals without metabolic acidosis or hypoxic hypoxia (P < 0.05), but the changes were clinically insignificant. No serious haemodynamic changes were found during any cardiac output measurement by thermodilution in the presence of metabolic acidosis or hypoxic hypoxia. The values of cardiac output measured by thermodilution correlated closely with those of pulmonary blood flow measured by an electromagnetic flowmeter in the metabolic acidosis and hypoxic hypoxia groups (r > 0.9). It is concluded that thermodilution using iced injectate will estimate right ventricular output accurately in conditions of metabolic acidosis and hypoxic hypoxia.     

Mechanism for slowing of heart rate and associated changes in pulmonary circulation elicited by cold injectate during thermodilution cardiac output determination in dogs

The authors investigated the mechanism for slowing of heart rate (HR) and associated changes in the pulmonary hemodynamics caused by cold injectate during thermodilution method. To clarify whether the slowing of HR after cold injectate is due to the cooling of the sinoatrial (SA) node or a reflex mediated by the autonomic nerves, we directly measured the myocardial temperature of the SA node region by a thermistor probe, and evaluated the HR responses to iced injectate after autonomic blockade in anesthetized dogs. Additionally, pulmonary blood flow (PBF) was continuously measured by an electromagnetic flowmeter during the delivery of injectate. The direction and magnitude of changes in HR after injectate were significantly dependent upon the injectate temperature (P less than 0.01). Thereby, the changes in HR correlated well with those in myocardial temperature of the SA node region (r = 0.987, P less than 0.01). However, the HR responses to injectate were unaffected by cervical vagotomy or stellate ganglionectomy. A significant decrease in PBF was noted in most cases during the slowing of HR. It was concluded that the slowing of HR after cold injectate during thermodilution in dogs is primarily due to the direct cooling of the SA node.     

The hemodynamic effects of newborn caudal anesthesia assessed by transthoracic echocardiography: a randomized, double-blind, controlled study

Background: Caudal anesthesia has been increasingly used in abdominal, urinary tract, and lower extremity surgery of infants. However, little was known about the hemodynamic effects of caudal anesthesia in them, especially in neonates. The purpose of this prospective study was designed to investigate the hemodynamic alterations by transthoracic echocardiography in newborn baby after caudal anesthesia with plain Bupivacaine or with epinephrine added Bupivacaine. Methods: Thirty full‐term newborn infants scheduled for lower abdominal or urinary tract surgery were randomly allocated into three groups (n = 10 each) as follows: (i) GA group: general anesthesia with sevoflurane; (ii) GA+CP group: GA with sevoflurane, combined with caudal anesthesia of plain Bupivacaine (1.25 ml·kg^?1 of 0.2%); (iii) GA+CA group: sevoflurane GA combined with caudal anesthesia of epinephrine‐added Bupivacaine (1.25 ml·kg^?1 of 0.2% Bupivacaine plus 1/200 000 epinephrine). Cardiac output (CO), arterial blood pressure, and heart rate were measured before (T‐5) and 5(T5), 10(T10), 15(T15) min after performance of caudal anesthesia. Results: In GA group, no significant hemodynamic alteration was observed in comparison with T‐5, except HR, which decreased by 7% at T15; In GA+CP group, compared with T‐5, HR decreased significantly at T5, T10 and T15, respectively, by 6%, 7% and 10%. And also CO decreased significantly at T15 by 8% compared with T‐5; In GA+CA group, no significant hemodynamic alteration was observed expect diastolic arterial blood, which decreased significantly at T15 by 10% compared with T‐5; At T15, the larger decrease of systolic arterial blood in GA+CP group and GA+CA group vs (GA) group (P < 0.05). Conclusions: The study shows the stability of hemodynamic variables during caudal anesthesia with Bupivacaine and with epinephrine‐added Bupivacaine in newborn infants.     

Hemodynamic effects of dobutamine and dopexamine after cardiopulmonary bypass in pediatric cardiac surgery*

Background: After surgical repair of congenital heart disease, inotropic support is sometimes necessary to wean from cardiopulmonary bypass. In pediatric cardiac surgery, dobutamine and dopamine are often used as inotropic support. Dopexamine is a synthetic catecholamine, which has positive inotropic and vasodilating properties. Because the hemodynamic effects of catecholamines are modified after cardiopulmonary bypass, the aim of this study was to investigate the effects of dobutamine and dopexamine on cardiac index and systemic vascular resistance index after cardiopulmonary bypass in pediatric cardiac surgery. Methods: The study was performed in a prospective, randomized, and double‐blinded cross‐over design. The investigation included 11 children for elective, noncomplex congenital heart surgery. After weaning from cardiopulmonary bypass and a 20‐min period of steady state, children received either 2.5 μg·kg^?1·min^?1 dobutamine or 1 μg·kg^?1·min^?1 dopexamine for 20 min. Cardiac index (transpulmonary thermodilution), mean arterial pressure, central venous pressure, stroke volume, systemic vascular resistance, and central venous oxygen saturation were determined. The primary outcome variable was cardiac index. Results: No difference in cardiac index was observed between the two groups (P = 0.594). Both drugs increased cardiac index, dopexamine from 3.9 ± 0.6 to 4.7 ± 0.8 l·min^?1·m^?2 (P = 0.003) and dobutamine from 4.1 ± 0.7 to 4.8 ± 0.7 l·min^?1·m^?2 (P = 0.004). During treatment with dobutamine, children presented with significantly higher mean arterial pressure (P = 0.003) and systemic vascular resistance index (P = 0.026). Conclusions: This trial demonstrates that low‐dose dobutamine and dopexamine both increase cardiac index during pediatric cardiac surgery but with different hemodynamic effects.     

Hemodynamic consequences of high- and low-pressure capnoperitoneum during laparoscopic cholecystectomy

Background: Peritoneal insufflation to 15 mmHg diminishes venous return and reduces cardiac output. Such changes may be dangerous in patients with a poor cardiac reserve. The aim of this study was to investigate the hemodynamic effects of high (15 mmHg) and low (7 mmHg) intraabdominal pressure during laparoscopic cholestectomy (LC) Methods: Twenty patients were randomized to either high- or low-pressure capnoperitoneum. Anesthesia was standardized, and the end-tidal CO₂ was maintained at 4.5 kPa. Arterial blood pressure was measured invasively. Heart rate, stroke volume, and cardiac output were measured by transesophageal doppler. Results: There were 10 patients in each group. In the high-pressure group, heart rate (HR) and mean arterial blood pressure (MABP) increased during insufflation. Stroke volume (SV) and cardiac output were depressed by a maximum of 26% and 28% (SV 0.1 > p > 0.05, cardiac output p > 0.1). In the low-pressure group, insufflation produced a rise in MABP and a peak rise in both stroke volume and cardiac output of 10% and 28%, respectively (p < 0.05). Conclusions: Low-pressure pneumoperitoneum is feasible for LC and minimizes the adverse hemodynamic effects of peritoneal insufflation. Received: 23 May 1997/Accepted: 11 March 1998     

Attenuation of arterial baroreceptor reflex response to acute hypovolemia during induced hypotension

Preservation of the arterial baroreflex response is important to restore cardiac output and blood pressure by reflex sympathetic nerve activation in the event of sudden hypotension caused by acute blood loss during surgery. However, the arterial baroreflex may be significantly attenuated by both anesthetics and hypotensive agents. In isoflurane-anesthetized dogs, the authors investigated the arterial baroreflex response 1) to bolus injections of sodium nitroprusside (SNP), prostaglandin E1 (PGE1) and trimethaphan (TM); and 2) to rapid blood loss (5 ml/kg) before and during induced hypotension with SNP, PGE1, and TM by measuring mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Hypotension produced by both SNP and PGE1 was accompanied by an increase in RSNA and HR. The increase in RSNA and HR following the SNP bolus injection was significantly greater than that following injection of PGE1 (P less than 0.05). Trimethaphan was associated with a decrease in RSNA and HR. Rapid blood loss resulted in the same degree of MAP reduction (20 +/- 2 mmHg) before and during induced hypotension. Sensitivities of baroreflex, as evaluated by ratios of maximum changes in RSNA or HR to MAP (delta RSNA/delta MAP, delta HR/delta MAP), in response to rapid blood loss, were significantly suppressed during continuously induced hypotension, as compared with responses before induced hypotension. Despite the same degree of induced hypotension (70 +/- 5 mmHg of MAP), delta RSNA/delta MAP and delta HR/delta MAP in response to rapid blood loss were significantly greater with PGE1 than those with SNP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of dexmedetomidine sedation for CT imaging studies

Background: Dexmedetomidine sedation for radiological imaging studies is a relatively recent application for this drug. Previous studies have demonstrated some haemodynamic effects of dexmedetomidine, however, the effects remain poorly described in children. The aim of this study was to better define the effect of age on heart rate (HR) and blood pressure changes in children sedated for CT imaging with dexmedetomidine. Methods/materials: At our institution dexmedetomidine is given for sedation for CT imaging as a bolus of 2 mcg·kg⁻¹ over 10 min followed by an infusion of 1 mcg·kg⁻¹·h⁻¹ with a second bolus if required. Detailed quality assurance data sheets document patient demographics, sedation outcomes, adverse events, and hemodynamic data are recorded for each patient. Results: A total of 250 patients (range 0.1–10.6 years) received dexmedetomidine. anova revealed strong evidence for changes in HR and mean arterial blood pressure during bolus and infusion relative to presedation values (P < 0.001). These changes were apparent in each age group and similar between groups. During the first bolus and during infusion, 82% and 93% of patients respectively were within the age-based normal range for HR. For mean arterial blood pressure, 70% of patients were within the normal range during first bolus and 78% during infusion. Conclusion: In the pediatric population studied, intravenous dexmedetomidine sedation was associated with modest fluctuations in HR and blood pressure. Hemodynamic changes were independent of age, required no pharmacologic interventions and did not result in any adverse events. By anticipating these possible hemodynamic effects and avoiding dexmedetomidine in those patients who may not tolerate such fluctuations in HR and blood pressure, dexmedetomidine is an appropriate sedative for children undergoing CT imaging.     

Hemodilution significantly decreases tolerance to isoflurane-induced cardiovascular depression

Background: Hemodilution is used to reduce the need for allogenic blood transfusion. The aim of this study was to evaluate to what extent acute extreme normovolemic hemodilution affects the circulatory response to isoflurane. Methods: Ten midazolam-fentanyl-pancuronium anesthetized pigs were exposed to isoflurane at end-tidal concentrations of 0,0.5,1.0,1.5 and 2%, before and after extreme normovolemic hemodilution (hematocrit 33±3% and 11±1%, respectively). Systemic and myocardial hemodynamics and oxygen delivery and consumption were measured. Results: At zero end-tidal isoflurane concentration, hemodilution caused an increase in cardiac output (from 157±12 to 227±39 ml kg min^-1, P <0.01) a decrease in systemic vascular resistance (from 39±7 to 18±5 mmHg · L^-1 · min^-1, P <0.01) a decrease in mean arterial blood pressure (MAP) (from 130±13 to 91±13 mmHg, P <0.01) and a decrease in systemic oxygen delivery (from 23.1±2.7 to 11.8±1.7 ml · kg^-1 min^-1, P <0.01). When the end-tidal isoflurane concentration was increased from 0 to 2% after hemodilution, cardiac output decreased by 86±37 ml · kg^-1 · min^-1, as compared with 36±20 ml · kg^-1 · min^-1 (P <0.01) before hemodilution. Likewise, systemic vascular resistance decreased with increasing isoflurane concentrations; at 2%, the decrease was 7±4 mmHg·L^-1· min^-1 after hemodilution and 18±5 mmHg.L^-1 mid before hemodilution (P < 0.01). At an end-tidal isoflurane concentration of 2%, MAP had decreased to 43±6 mmHg after hemodilution, and to 61±15 mmHg before hemodilution (kO.01). After hemodilution, isoflurane concentrations above 1% decreased systemic oxygen delivery enough to cause delivery-dependent oxygen consumption and hyperlactemia; and at 2% isoflurane, myocardial blood flow became insufficient, as indicated by myocardial lactate production. Conclusions: isoflurane-induced cardiovascular depression had adverse effects on cardiac output and oxygen delivery during extreme hemodilution because: 1) The vasodilatory effect of isoflurane was insufficient to compensate for the myocardial depression, and also contributed to a critically low arterial blood pressure; 2) A decrease in cardiac output produced delivery-dependent oxygen consumption and hyperlactemia; and 3) A decrease in myocardial blood flow caused myocardial ischemia which may have exacerbated the myocardial depression.     

Halothane anesthesia suppresses reflex tachycardia caused by calcitonin gene-related peptide in dogs

Calcitonin gene-related peptide (CGRP) is known to produce vasodilation, hypotension, and tachycardia. To investigate the interaction between CGRP and anesthetics, the hemodynamic response to infusions of CGRP was studied in dogs anesthetized with halothane or pentobarbital. In halothane-anesthetized dogs given 0.4 μg·kg⁻¹ of CGRP, mean arterial pressure (MAP) did not change significantly. However, there was a significant reduction in systemic vascular resistance (SVR) associated with significant increases in cardiac index (CI) and stroke volume index (SVI). Higher doses (4 and 40 μg·kg⁻¹) of CGRP produced dose-dependent decreases in MAP accompanied by a reduction in SVR. Further, both CI and SVI significantly increased at 4 μg·kg⁻¹ CGRP but remained unchanged at the 40 μg·kg⁻¹ infusion rate. Heart rate (HR) was not increased at all doses but was decreased at 40 μg·kg⁻¹. In pentobarbital-anesthetized dogs, CGRP at doses of 4 μg·kg⁻¹ produced a qualitatively similar cardiovascular responses as that observed in halothane-anesthetized dogs, but with one exception: HR was significantly increased. The results show that the hemodynamic profiles induced by CGRP during halothane or pentobarbital anesthesia are a decrease in MAP accompanied by a reduction in SVR and no consistent alterations in CI. However, CGRP effects on HR showed in a different way. The results also show that HR response differs depending on the anesthetics used: HR increases during pentobarbital anesthesia, while it does not increase during halothane anesthesia. This study was presented in part at the 39th annual meeting of the Japan Society of Anesthesiology, Fukuoka, April 1992, and at the annual meeting of the American Society of Anesthesiologists, New Orleans, October 1992     

Dose-related cardiovascular effects of amrinone and epinephrine in reversing bupivacaine-induced cardiovascular depression

Background: To ascertain the efficacy of amrinone and epinephrine in reversing bupivacaine-induced cardiovascular depression, we investigated the time course of recovery of cardiac function with 3 doses of both agents after bupivacaine administration. Methods: In sevoflurane-anaesthetized dogs, bupivacaine was infused intravenously at 1 mg . kg^?1 . min^?1 until mean arterial pressure fell to 60 mmHg or less. The 3 doses of amrinone (1, 2, and 4 mg . kg^?1) or the 3 doses of epinephrine (2, 5, and 10 μg . kg^?1) were administered as a bolus in randomized order in each dog. Results: Amrinone improved maximum left ventricular dP/dt, a time constant of left ventricular isovolemic relaxation and cardiac index persistently and dose-relatedly. Amrinone increased heart rate and decreased left ventricular end-diastolic pressure and systemic vascular resistance index. Amrinone at 1 and 2 mg . kg^?1 significantly increased mean arterial pressure, but amrinone at 4 mg . kg^?1 did not. Epinephrine increased mean arterial pressure, maximum left ventricular dP/dt, and systemic vascular resistance dose-relatedly. The duration of action of epinephrine, peaking at 1 min and subsequently decreasing by 10 min after administration, did not differ among the groups. Epinephrine at all doses failed to improve a time constant of left ventricular isovolemic relaxation and cardiac index. ECG evidence of serious ventricular dysrhythmias was seen in 1 out of 6 dogs after administrating each dose of amrinone and in 3, 3 and 5 out of 6 dogs after administrating 2, 5 and 10 μg . kg^?1 of epinephrine, respectively. Conclusion: Bolus amrinone may have a certain efficacy in reversing bupivacaine-induced cardiovascular depression, and improving cardiac contractility and relaxation dose-relatedly. In contrast to amrinone, bolus epinephrine remains indispensable for resuscitation, causing a rapid, massive, transient and doserelated rise in blood pressure. However, the use of amrinone may be limited predominantly by a decrease in systemic vascular resistance, while the use of epinephrine may be limited predominantly by the generation of serious ventricular dysrhythmias and lack of effectiveness on cardiac index and on cardiac relaxation.     

Changes in carbon dioxide tension and oxygen saturation during deep sedation for paediatric cardiac catheterization

The purpose of this observational study was to determine whether hypercarbia or oxygen desaturation occurred during our current regimens of deep sedation or general anaesthesia of infants and children undergoing cardiac catheterization. Data were gathered prospectively from 50 consecutive infants and children aged 4 months to 12 years undergoing cardiac catheterization. Several anaesthetists used the following regimens, which were not randomized: 1) propofol. 1.5–2.0 mg·kg^?1 and fentanyl 1 μg·kg^?1 IV over 2 min for induction, followed by propofol infusion of 100–150 μg·kg^?1·min^?1; 2) fentanyl 2–3 μg·kg^?1 and midazolam 0.1–0.2 mg·kg^?1 IV over 10–15 min; 3) ketamine 8 mg·kg^?1 IM, or 4) same as regimens 1 or 2, plus pancuronium, intubation and controlled ventilation. Regimens 1, 2, and 3 were associated with spontaneous ventilation through the natural airway. End-tidal carbon dioxide tension (Petco₂), Spo₂, and respiratory rate were monitored for 60 min. The three regimens employing spontaneous ventilation through the natural airway were associated with both statistically and clinically significant increases in Petco₂ and decreases in Spo₂. This raises the possibility that acute exacerbation of PAP and PVR may occur in pulmonary hypertensive patients. In contrast, Petco₂ and Spo₂ did not change significantly from baseline in the controlled ventilation group.     

Foetal responses to acute haemorrhage under halothane anaesthesia

The effect of halothane anaesthesia on the foetal responses to acute haemorrhage was studied in chronically prepared ewes. An average of 27.9 ml·kg^-1of foetal blood was withdrawn resulting in an acute 20 per cent decrease in mean arterial pressure which returned toward the control value after 186 seconds. After the blood loss, cardiac output was reduced by 26.1 per cent and heart rate decreased by 26 per cent. Blood flows to the kidneys, placenta and musculoskeletal structures were reduced by 247, 38.2 and 35.3 per cent respectively but flow to the brain increased by 30 per cent. Reinfusion of lost blood, corrected flow reductions and the supply to the gastrointestinal organs increased above control values. This study showed that foetal lambs were able to tolerate an acute blood loss under halothane anaesthesia. An adequate perfusion pressure and blood flow to critical organs, such as the brain was maintained by increasing systemic vascular resistance. The compensation, however, was incomplete. Placental blood flow, maternal-foetal gas exchanges, and redistribution of cardiac output away from gastrointestinal tract and skin were impaired.     

Are the cardiovascular actions of dopamine altered by isoflurane?

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 ug · kg^-1 · min^-1. At the dose 20 μf · kg^-1 · min^-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 μg · kg^-1 · min^-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 μg · kg^-1 · min^-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+ 132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone. However, the increase in SVR (at the dose 20 μg · kg^-1 · min^-1) and MAP (at the 10 and 20 μg · kg^-1 · min^-1 doses) by DA was significantly more pronounced with ISO than without ISO. In conclusion, the pressor effects of DA seem to be potentiated by ISO. DA restores systemic arterial pressure during ISO anesthesia by attenuating the cardiac depressant effects of ISO and by increasing SVR above pre-ISO control levels.     

Cardiorespiratory effects of venous lipid micro embolization in an experimental model of mediastinal shed blood reinfusion

Background

Retransfusion of the patient's own blood during surgery is used to reduce the need for allogenic blood transfusion. It has however been found that this blood contains lipid particles, which form emboli in different organs if the blood is retransfused on the arterial side. In this study, we tested whether retransfusion of blood containing lipid micro-particles on the venous side in a porcine model will give hemodynamic effects.

Methods

Seven adult pigs were used. A shed blood surrogate containing 400 ml diluted blood and 5 ml radioactive triolein was produced to generate a lipid embolic load. The shed blood surrogate was rapidly (<2 minutes) retransfused from a transfusion bag to the right atrium under general anesthesia. The animals' arterial, pulmonary, right and left atrial pressure were monitored, together with cardiac output and deadspace. At the end of the experiment, an increase in cardiac output and pulmonary pressure was pharmacologically induced to try to flush out lipid particles from the lungs.

Results

A more than 30-fold increase in pulmonary vascular resistance was observed, with subsequent increase in pulmonary artery pressure, and decrease in cardiac output and arterial pressure. This response was transient, but was followed by a smaller, persistent increase in pulmonary vascular resistance. Only a small portion of the infused triolein passed the lungs, and only a small fraction could be recirculated by increasing cardiac output and pulmonary pressure.

Conclusion

Infusion of blood containing lipid micro-emboli on the venous side leads to acute, severe hemodynamic responses that can be life threatening. Lipid particles will be trapped in the lungs, leading to persistent effects on the pulmonary vascular resistance.     

Etomidate,alfathesin and thiopentone as induction agents for coronary artery surgery

In 24 premedicated patients about to undergo coronary artery bypass surgery, anaesthesia was induced with either etomidate 0.3 mg kg^-1, alfathesin 0.07 ml kg^-1 or thiopentone 3.0 mg · kg^-1, in combination with fentanyl. Detailed haemodynamic studies were made including measurements of arterial pressure, right atrial pressure, pulmonary artery and pulmonary capillary wedge pressure, heart rate, cardiac output and monitoring of the lead V5 electrocardiogram. Cardiovascular data were recorded in the awake patient and one, three and five minutes after induction of anaesthesia. Following fentanyl 0.01 mg · kg^-1 and suxamethonium 1.0 mg · kg^-1 the trachea was intubated and further measurements were made immediately and five minutes after intubation. Induction of anaesthesia using the new non-barbiturate agent etomidate was associated with a remarkable cardiovascular stability. No major changes in heart rate, arterial blood pressure, cardiac index, pulmonary artery pressure, right and left ventricular filling pressure or total peripheral resistance occurred. The addition of fentanyl decreased heart rate and cardiac index slightly and was associated with a significant reduction of the rate-pressure product. The cardiovascular effects of thiopentone were very similar to those of etomidate, except for a small increase in heart rate with thiopentone. Alfathesin produced a significant fall in arterial pressure, cardiac index and stroke index, while heart rate increased. The rate-pressure product remained unchanged. The combination of alfathesin with fentanyl produced an additional decrease in blood pressure and cardiac index. None of the three induction procedures was associated with cardio-vascular stimulation during laryngoscopy and tracheal intubation. Our findings suggest that either thiopentone or etomidate combined with fentanyl are acceptably safe in cardiac patients while alfathesin with fentanyl appears to be more detrimental to the circulation.     

Cerebrovascular effects of small volume resuscitation from hemorrhagic shock: comparison of hypertonic saline and concentrated hydroxyethyl starch in dogs

To determine if hypertonic and hyperoncotic resuscitation solutions exerted comparable effects on cerebral hemodynamics following hemorrhagic shock, we compared randomly assigned, equal volumes (6.0 ml/kg) of hypertonic (7.2%) saline (HS) and hyperoncotic (20%) hydroxyethyl starch (HES) for resuscitation from acute experimental hemorrhage in 12 anesthetized dogs. Regional cerebral blood flow (radiolabeled microspheres), intracranial pressure (cisternal catheter), and systemic hemodynamics were recorded. Rapid hemorrhage reduced the mean arterial pressure to 45 mm Hg for 30 min. Resuscitation fluids were infused over 5 min. Both fluids restored mean arterial pressure and cardiac output equally. However, at 60 min following resuscitation, cardiac output decreased in the HS group in comparison to the HES group (1.7 +/- 0.1 vs. 3.1 +/- 0.2 L/min, p <0.05). Cardiac output rapidly declined, however, in the HS group in comparison to the HES group (p <0.05 60 min following resuscitation). Intracranial pressure and cerebral perfusion pressure were similar at all intervals. Regional cerebral blood flow was similar following both fluids. Neither fluid restored cerebral oxygen transport to baseline values. Based on these data, the authors conclude that, following severe hemorrhagic shock of brief duration, systemic and cerebral hemodynamic values are restored equally well by highly concentrated colloid or by hypertonic saline, although hypertonic saline only transiently improves cardiac output.     

Hemodynamic changes during laparoscopic cholecystectomy monitored with transesophageal echocardiography

Although pneumoperitoneum has been well tolerated in a predominantly healthy population, there is concern that an increased intraperitoneal pressure may be poorly tolerated in patients with marginal cardiopulmonary function. The purpose of this study was to demonstrate noninvasively the hemodynamic effects of carbon dioxide pneumoperitoneum utilizing biplane transesophageal echocardiography.Fourteen otherwise-healthy patients undergoing nonemergent laparoscopic cholecystectomy were studied using bi-plane transesophageal echocardiography under a standardized anesthetic protocol utilizing isoflurane, fentanyl, and vecuronium bromide. Endtidal CO₂, oxygen saturation, cardiac rhythm, temperature, and blood pressure were monitored noninvasively. Minute ventilatory volume was adjusted as needed to keep end-tidal CO₂ less than 38 mmHg. Data were recorded at baseline, following abdominal insufflation to 15 mmHg with CO₂, with head-up tilt of 20°, following exsufflation, and with the patient level. Significance was determined using a paired Student t-test.Insufflation to 15 mmHg decreased cardiac index (C.I.) by 3% (3.34 to 3.23 l/min/m²) while both heart rate (HR) and mean arterial pressure (MAP) increased (by 7% and 16%), respectively, and stroke volume index decreased by 10% (from 51.6 to 46.6 ml/beat/m²). Head-up tilt of 20° further decreased CI to 2.98 l/min/m² (–11%) and SVI to 40.3 ml/beat/m² (–22%) while HR increased by a total of 14% and MAP by 19%.As laparoscopic techniques are applied to a broader population, the impact of small but significant decrements in cardiac function become increasingly important. This study demonstrates that the combination of CO₂ pneumoperitoneum and the reverse Trendelenburg position does adversely effect cardiac output.Presented at the annual meeting of the Society of American Gastrointestinal Endoscopic Surgeons (SAGES), Nashville, Tennessee, USA, 18–19 April 1994     

Hemodynamic Effects of Hemodialysis and Hemofiltration

The hemodynamic effects (n=8) of hemodialysis (HD) and hemofiltration (HF) were compared in the same group of dialyzed patients. The two procedures induced the same decrease in body weight, total blood volume, and blood pressure; however, hemodynamic alterations were different. Cardiac index and stroke index decreased markedly with HD and did not change significantly with HF, and peripheral resistance remained stable after HD and decreased significantly after HF.
These results suggest that the maintenance of a high cardiac output may account for the lack of acute hypotensive episodes Reported during HF. The reduction of blood pressure after HF is related to the decrease in total peripheral resistance. Thus, the arterial vasodilator effect induced by HF might explain the improvement of severe hypertension on long-term treatment with HF, as Reported previously.     

Redistribution of intraorgan blood flow in acute, hyperdynamic porcine endotoxemia

In a standardized porcine model of acute, hyperdynamic endotoxemia the distribution of intraorgan blood flow within heart, kidney and brain was analyzed. Twelve pigs received either short-term (23 min) or long-term (205 min) continuous intravenous infusion of endotoxin (Salmonella abortus equi). A high cardiac output/low peripheral resistance state was maintained throughout the 3.5 h observation period. Total organ blood flow in heart, kidney and brain remained high; however, already small amounts of endotoxin provoked a significant redistribution of intraorgan blood flow within the left ventricle and the kidney. These characteristic alterations were absent in a control group of 5 animals subjected to the same protocol, but receiving 0.9% saline instead of endotoxin. Deterioration of respiratory function developed exclusively after continuous intravenous endotoxin infusion over 205 min, indicating incipient organ failure. Using electron microscopy, endothelial cells swelling and entrapment of blood cells in capillaries of the midmyocardium as well as severe ultrastructural damage in the kidney could be demonstrated already after 90 min of endotoxemia in two additional animals. It is concluded that already in the initial phase of acute endotoxemia, in the presence of high cardiac output and high global organ blood flow microcirculatory deterioration and organ failure develops. As small amounts of endotoxin are capable of inducing these alterations, earliest possible diagnosis of endotoxemia should be achieved in critically ill patients.