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PubMed1998

The hemodynamic effects of hypoxemia in anesthetized pigs: a comparison between right heart catheter and echocardiography.

UNLABELLED: During hypoxemia, hypoxic pulmonary vasoconstriction and tachycardia are often observed in association with increases in pulmonary artery pressure and cardiac output. Nevertheless, the hemodynamic consequences of hypoxemia have never been evaluated by echocardiography and simultaneously compared with invasive hemodynamic variables. Fourteen open-chest, anesthetized piglets (weight 29-36 kg) were submitted to progressive hypoxemia and reoxygenation. Usual invasive hemodynamic variables were obtained from peripheral and central heart catheters. Direct epicardial echocardiography was used to measure right and left ventricular areas on a short-axis view at mid-papillary level. The mean pulmonary artery pressure (MPAP) increased with pulmonary vascular resistance in a dose-related manner as the fraction of inspired oxygen (FIO2) declined from 0.5 to 0.12. The MPAP correlated with right ventricular end-diastolic area (RVEDA) only at FIO2 0.08. There was a 49% reduction in left ventricular end systolic wall stress (LVESWS) between FIO2 0.5 and 0.08. Left ventricular ejection fraction area (LVEFA) increased by 33% above baseline and correlated with the decrease in LVESWS. No correlation was observed between left ventricular end-diastolic area and pulmonary artery occlusion pressure or left atrial pressure and between cardiac output and LVEFA. Systemic vascular resistance underestimates the magnitude of changes in LVESWS but overestimates the afterload compared with LVESWS. This study demonstrates that, for the lowest FIO2 (0.08), changes in MPAP correlated with changes in RVEDA but not in pulmonary vascular resistance. Moreover, LVESWS decreases significantly in a dose-related manner under progressive hypoxemia and normalizes immediately after reoxygenation. This study also shows that, under hypoxemic conditions, echocardiography enhances understanding of hemodynamic changes compared with right heart catheterization alone. IMPLICATIONS: Acute hypoxemia in pigs is responsible for pulmonary vasoconstriction-induced pulmonary hypertension (which is restricted by the right ventricular failure), as well as a PaO2-dependent decrease in left ventricular afterload. These changes are better displayed by echocardiography than by right heart catheter.

Anesthesia↗
PubMed1999

Hemodynamic changes and catecholamine release during laparoscopic adrenalectomy for pheochromocytoma.

UNLABELLED: We investigated hemodynamics and plasma catecholamine concentrations in eight consecutive patients undergoing laparoscopic adrenalectomy for suspected pheochromocytoma. The same anesthesia protocol was used in all patients: a continuous infusion of sufentanil 0.5 microg x kg(-1) x h(-1) and isoflurane 0.4% (end-tidal) in 50% N2O/O2. Systolic arterial pressure was maintained between 120 and 160 mm Hg by adjusting an infusion of nicardipine, a calcium-channel blocker, while tachycardia (>100 bpm) was treated by 1-mg boluses of atenolol. Hemodynamics (thermodilution technique) and plasma catecholamine concentrations were measured before surgery, after the induction of anesthesia, after turning the patient to the lateral position, during pneumoperitoneum, during tumor manipulation, after adrenalectomy, and at the end of surgery. Two events resulted in significant catecholamine release: creation of the pneumoperitoneum and adrenal gland manipulation. As a consequence, a twofold increase in cardiac output was recorded. Adjustments of nicardipine infusion (2-6 microg x kg(-1) x min(-1)) minimized changes in mean arterial pressure. Beta-adrenergic blockade was necessary in six patients. In conclusion, laparoscopic adrenalectomy for pheochromocytoma results in marked catecholamine release during pneumoperitoneum and tumor manipulation. Titration of a nicardipine infusion allowed easy and quick control of the hemodynamic aberrancies related to these processes. IMPLICATIONS: Pneumoperitoneum during laparoscopy, now used for adrenalectomy, may complicate anesthetic management of patients with pheochromocytoma. In this study, laparoscopic adrenalectomy was associated with catecholamine release during the creation of pneumoperitoneum and tumor manipulation. Adjustments of a nicardipine infusion readily attenuated the subsequent hemodynamic aberrancies.

Adrenal Gland Neoplasms↗
PubMed2000

The hemodynamic effects of endothelin receptor antagonism during a venous air infusion in dogs.

UNLABELLED: Endothelin (ET) is involved in the humoral component of the vasoconstriction during pulmonary embolism. We examined the effects of selective ET receptor antagonists on the hemodynamic and respiratory changes and on serum thromboxane B2 (TXB2) levels, during a continuous venous air infusion (VAI) in anesthetized mongrel dogs. The VAI (0.2 mL x kg(-1) x min(-1)) was initiated 5 min after an injection of saline (controls, n = 7), 1 micromol of the selective ET(A) receptor antagonist JKC-301 (group A, n = 6), or 1 micromol of the selective ET(B) receptor antagonist BQ-788 (group B, n = 6). Hemodynamic evaluation was performed every 15 min of VAI, and blood samples were drawn for blood gas analysis and TXB2 determinations. The increase in pulmonary perfusion pressure after 30 min of VAI was attenuated in Group A compared with the controls and Group B (Group A = 7+/-1 mm Hg; Group B = 16+/-1 mm Hg; controls = 14+/-1 mm Hg; P < 0.05). Pulmonary vascular resistance showed a similar behavior. TXB2 concentrations increased after 60 min of VAI in the controls and in Group B, but not in Group A (controls = 48%; Group B = 104%; Group A = 18%; P < 0.05 for controls and Group B). Similar decreases in Pao2 and Sao2 were observed in the three groups. We conclude that antagonism of ET(A) receptors attenuates the hemodynamic changes and blunts the increase in thromboxane A2 production during a VAI in dogs. IMPLICATIONS: We evaluated the effects of endothelin receptor antagonists during a venous air infusion in dogs. EndothelinA receptor antagonism attenuated the hemodynamic changes and blunted the increase in thromboxane A2 production in this setting.

Animals↗
PubMed2001

Hemodynamic-induced changes in aortic valve area: implications for Doppler cardiac output determinations.

UNLABELLED: Monitoring cardiac output (CO) by transesophageal echocardiography involves measurements of ascending aortic flow and an initial measurement of aortic valve area (AVA). Hemodynamic-induced changes in AVA are a potential source of error for this simplified method. Our goal was to quantify these changes in AVA and their effects on CO calculations. In 17 anesthetized patients, a dobutamine infusion was titrated to achieve a 50% increase in ascending aortic flow velocity (V(max)). Hemodynamic and echocardiographic variables, including V(max) and planimetry of AVA, were determined at baseline and at maximal dobutamine dose. Dobutamine produced a 3.0 +/- 1.4 L/min increase in CO, a 54.5% +/- 19.6% increase in V(max), and a 50.6% +/- 34.2% increase in systolic blood pressure. AVA increased by 4.3% +/- 2.6% during dobutamine infusion (P < 0.001). The simplified CO method, which does not account for increases in AVA, produced a 0.32 +/- 0.24 L/min underestimation of CO. This investigation demonstrates hemodynamic-induced changes in AVA. The use of a single AVA measurement for all subsequent CO calculations introduces a clinically acceptable degree of error, supporting a simplified CO protocol requiring less probe manipulation and reduced procedural time. IMPLICATIONS: An intraoperative dobutamine infusion was used to increase aortic blood flow and demonstrate hemodynamic-induced changes in aortic valve area. These valve-area changes affect the accuracy of Doppler cardiac output determinations.

Adult↗
PubMed2002

The efficacy of hemodynamic and T-wave criteria for detecting intravascular injection of epinephrine test dose in propofol-anesthetized adults.

UNLABELLED: A recent study demonstrated 100% effectiveness of hemodynamic criteria during propofol anesthesia, when a full dose of an epinephrine (15 microg)-containing test dose was injected intravascularly. We designed this dose-response study to determine minimal effective epinephrine doses and efficacies of hemodynamic and T-wave criteria for detecting intravascular injection of the epinephrine test dose in propofol-anesthetized adults. Eighty healthy adult patients were randomly assigned to one of four groups according to a simulated IV test dose using propofol (133 microg center dot kg(-1) center dot min(-1)) and nitrous oxide (FIO(2) = 0.33) anesthesia after endotracheal intubation (n = 20 each). The Saline group received 3 mL of normal saline IV; the Epinephrine-15 group received 3 mL of 1.5% lidocaine containing 15 microg epinephrine; and the Epinephrine-10 and -5 groups received 2 and 1 mL of the test dose of the identical components, respectively. Heart rate (HR), systolic blood pressure (SBP), and lead II of the electrocardiogram were recorded continuously for 5 min after the IV injection of the study drug via a peripheral vein. Sensitivities and specificities of 100% were obtained based on the modified HR (positive if greater-than-or-equal to 10 bpm increase) and the T-wave (positive if greater-than-or-equal 25% in amplitude) criteria if greater-than-or-equal 5 microg of epinephrine was injected IV. Based on the SBP criterion (positive if greater-than-or-equal 15 mm Hg increase), however, 100% sensitivity and specificity were associated only with greater-than-or-equal 10 microg of epinephrine doses. These results suggest that the minimal effective epinephrine doses for detecting unintentional intravascular injection are 5 microg based on the HR and T-wave criteria, and 10 microg based on the SBP criterion in adult patients anesthetized with propofol and nitrous oxide. IMPLICATIONS: Accidental migration of an epidural catheter into a blood vessel is often detected by hemodynamic changes after injecting an epidural test dose containing epinephrine. Our results suggest that 5 microg of epinephrine is not adequate to reliably produce hemodynamic and T-wave alterations in adult patients during propofol anesthesia.

Adult↗
PubMed2002

Hemodynamic and hormonal responses to the sudden interruption of caval flow: insights from a prospective study of hepatic vascular exclusion during major liver resections.

UNLABELLED: Hepatic vascular exclusion (HVE) combines portal triad clamping and occlusion of the inferior vena cava. Although HVE has been performed for major liver resections during the last 2 decades, little is known about the mechanisms that explain its satisfactory hemodynamic tolerance. Consequently, we performed a comprehensive study of both hemodynamic and hormone responses to HVE. Twenty-two patients who underwent liver resection for secondary tumors developed in noncirrhotic livers were prospectively studied. Heart rate, arterial blood pressure, pulmonary artery pressure, mixed venous saturation, cardiac output, and left ventricular dimensions determined by transesophageal echocardiography were monitored in HVE patients. Blood concentrations of arginine vasopressin (AVP), epinephrine, norepinephrine, dopamine, and atrial natriuretic peptide and plasma renin activity (PRA) were measured before clamping; 5, 15, and 30 min after clamping; and 15 min after unclamping. Hemodynamic response to HVE was characterized by a significant (P < 0.05) decrease in left ventricular dimensions, fractional area change, and pulmonary artery pressure. We also observed a marked decrease in cardiac output (50%) and an increase in heart rate and systemic vascular resistance. After unclamping, there was peripheral vasodilation, assessed by a significant decrease in systemic vascular resistance from the preclamping value to unclamping. An acute and sustained increase in AVP and norepinephrine that returned to baseline after unclamping and the absence of modification in PRA concentrations were noted. The marked decrease in venous return that characterizes HVE is compensated for by an increase in vascular resistance secondary to an important activation of the AVP and sympathetic systems. The PRA system does not play an important role in maintaining arterial blood pressure during HVE. IMPLICATIONS: Hemodynamic and hormonal responses to the acute interruption of caval venous return to the heart were investigated in patients undergoing liver resection with hepatic vascular exclusion. A compensatory role for arginine vasopressin and sympathetic systems that provoked increased vascular resistance was demonstrated.

Aged↗
PubMed1983

Hemodynamic interactions of verapamil and isoflurane.

The hemodynamic interactions of verapamil and isoflurane were studied in eight dogs. Left ventricular function was analyzed using a right heart bypass preparation to permit rigid hemodynamic control. Hemodynamic studies were performed at 0.7, 1.05, and 1.40% isoflurane before and during the maintenance of two stable levels of verapamil, administered intravenously by combining a bolus dose (0.2 mg X kg-1) with an infusion (3.0 and 6.0 micrograms X kg-1 X min-1). Isoflurane produced a concentration-dependent depression of left ventricular function as indicated by dP/dt max, per cent systolic shortening, and left ventricular function curves. This depression was enhanced in a dose-plasma concentration-dependent manner by verapamil and was reversed by calcium chloride. Isoflurane alone and the combination of verapamil and isoflurane decreased systemic vascular resistance in a dose-dependent fashion that was antagonized partially by calcium chloride. Therefore, verapamil can enhance the hemodynamic effects of isoflurane in a dose-related manner that needs to be considered when both drugs are administered together.

Animals↗
PubMed1987

Reduced narcotic requirement by clonidine with improved hemodynamic and adrenergic stability in patients undergoing coronary bypass surgery.

The authors examined the effect of clonidine, a preferential alpha 2-adrenergic agonist, upon narcotic requirements, hemodynamics, and adrenergic responses during the perioperative period in patients undergoing CABG surgery. Anesthesia was provided by sufentanil supplemented with isoflurane; sodium nitroprusside was given as needed for hemodynamic control. Ten patients received oral clonidine preoperatively at the time of premedication, and again intraoperatively by nasogastric tube. Another group of ten untreated patients were otherwise managed identically. Intergroup differences in required anesthetic and vasoactive drug doses and recovery times were measured and evaluated, as well as hemodynamics and plasma catecholamines prior to induction, after intubation, and at intervals intra- and postoperatively. Patients who received clonidine required less diazepam prior to induction, and received 40% less sufentanil during the anesthetic period, than did untreated controls. More control patients required the addition of isoflurane to prevent hypertension. Mean blood pressures and heart rates were elevated at many sampling points in patients not treated with clonidine. Four of the clonidine-treated group required atropine for treatment of bradycardia in the pre-incision period. Plasma catecholamines were significantly lower throughout most of the study period in patients treated with clonidine. After cardiopulmonary bypass and postoperatively, cardiac outputs were significantly higher in the treated group. Patients who had received clonidine were extubated significantly earlier, and fewer of them shivered postoperatively. We conclude that perioperative treatment with clonidine reduced narcotic and anesthetic requirements, improved hemodynamics, reduced plasma catecholamines, and shortened the period of postoperative ventilation in patients undergoing coronary artery surgery.

Anesthetics↗
PubMed1988

Anesthetic and hemodynamic effects of the alpha 2-adrenergic agonist, azepexole, in isoflurane-anesthetized dogs.

The authors studied the reduction in anesthetic requirement (MAC) and the hemodynamic effects of the highly selective alpha 2-adrenergic agonist azepexole in isoflurane-anesthetized dogs. Eleven male beagles were anesthetized with isoflurane in oxygen. After a 2-h equilibration period, they determined isoflurane MAC and baseline hemodynamic function. Azepexole (at 0.1, 0.3, and 1.0 mg/kg) was administered via a right atrial port over 15 min, while each dog was given isoflurane at the MAC dose for that animal. Twenty minutes after the end of infusion, at a time when hemodynamic variables were stable, they reassessed hemodynamic function. They then determined isoflurane MAC again. In other experiments, dogs were pretreated with either idazoxan (the alpha 2-adrenergic antagonist; n = 5) or naloxone (the opiate antagonist; n = 7) prior to the administration of azepexole. Isoflurane MAC was determined before and after each dose of azepexole. Isoflurane MAC decreased as the dose of azepexole increased, to the extent that at the highest dose (1 mg/kg) the decrement in MAC was more than 85%. This reduction of MAC caused by azepexole could be completely prevented by pretreatment with idazoxan, while naloxone was without effect. Azepexole did not change mean arterial blood pressure, but caused heart rate and cardiac output to progressively decrease. The MAC-reducing effect of azepexole appears to be mediated by alpha 2 adrenoreceptors. Given the extent of the reduction of MAC, it is unlikely that inhibition of central noradrenergic neurotransmission through agonism of presynaptic alpha 2 adrenoreceptors is the sole explanation, since complete disruption of central noradrenergic tracts decreases MAC by only 40%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1989

The effect of neuromuscular blockade with vecuronium on hemodynamic responses to noxious stimuli in the rat.

The effect of neuromuscular blockade with vecuronium on the hemodynamic responses to a noxious stimulus was investigated in male Sprague-Dawley rats. The rats were anesthetized with either halothane (group 1, n = 10), or isoflurane (group 2, n = 10). The maximum values for heart rate and mean arterial pressure during the noxious stimulus (base-tail clamp) were measured, and the maximum changes in these values (maximum minus prestimulation) were calculated. The responses were measured at two different anesthetic concentrations (0.6 X MAC, 0.75 X MAC), before and after vecuronium 1.0 mg.kg-1 iv. It was found that neuromuscular blockade with vecuronium did not reduce any of the hemodynamic responses measured, at either anesthetic concentration, in either the halothane or the isoflurane group. However, increasing the anesthetic concentration from 0.6 X MAC to 0.75 X MAC produced statistically significant (P less than 0.01) reductions in several of the responses measured. The inability of vecuronium to reduce hemodynamic responses to noxious stimuli in this study suggests that neuromuscular blockade does not alter anesthetic depth in the rat. A knowledge of this "absence of effect" may be important for investigators who need to induce muscle relaxation in laboratory animals prior to examining the effect of anesthetic agents on hemodynamic responses to noxious stimuli. The results also question the ability of neuromuscular blockade to reduce anesthetic requirement, and support the view that neuromuscular blockade does not contribute to the anesthetic state.

Anesthesia, Inhalation↗
PubMed1990

Relationship of regional wall motion abnormalities to hemodynamic indices of myocardial oxygen supply and demand in patients undergoing CABG surgery.

To investigate the hemodynamic correlates of perioperative regional wall motion abnormalities (RWMA), we measured wall motion continuously via transesophageal echocardiography (TEE), and related RWMA to continuously measured hemodynamic indices of myocardial oxygen supply and demand (heart rate [HR] and systemic and pulmonary arterial blood pressures). Fifty patients undergoing coronary artery bypass graft (CABG) surgery were studied throughout the prebypass postbypass, and intensive care unit (ICU) periods. Only 28% of TEE episodes (RWMA suggestive of ischemia) were preceded by acute changes in any hemodynamic parameter. Specifically, 7% of TEE episodes were preceded by increases in HR (20% deviation from control), 14% by increases in systolic blood pressure (SBP), 13% by decreases in diastolic blood pressure (DBP), and 9% by increases in pulmonary artery diastolic pressure (PAD). Twelve per cent of TEE episodes were associated with increases in rate-pressure product (RPP) to greater than 12,000, and 27% were associated with decreases in mean arterial pressure (MAP)/HR to less than 1 at the onset of TEE episodes. Comparison among periods revealed that postbypass TEE episodes were more frequently associated with either increases in demand or decreases in supply than were prebypass episodes (53% vs. 25%, P less than 0.05). ECG ischemic episodes also were infrequently (30%) associated with acute changes in HR, SBP, DBP, or PAD. We conclude that perioperative TEE episodes are infrequently triggered by changes in hemodynamics, suggesting that a primary decrease in myocardial oxygen supply may be an important mechanism for most perioperative RWMA. In addition, neither pulmonary artery catheter pressure measurements nor specialized indices (RPP and MAP/HR) appear to be useful in predicting TEE episodes.

Adult↗
PubMed1991

Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog.

The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. Systemic and coronary hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.25 and 1.75 MAC desflurane, isoflurane, halothane, and enflurane. Desflurane (+79 +/- 12% change from control) produced greater increases in heart rate than did halothane (+44 +/- 12% change from control) or enflurane (+44 +/- 9% change from control) at 1.75 MAC. Desflurane preserved mean arterial pressure to a greater degree than did equianesthetic concentrations of isoflurane. This result was attributed to a smaller effect on peripheral vascular resistance as compared to isoflurane and greater preservation of myocardial contractility as evaluated by peak positive left ventricular dP/dt and the rate of increase of ventricular pressure at 50 mmHg (dP/dt50) compared to other volatile anesthetics. Increases in diastolic coronary blood flow velocity (+19 +/- 6 and +35 +/- 12% change from control at 1.75 MAC, respectively) and concomitant decreases in diastolic coronary vascular resistance (-41 +/- 12 and -58 +/- 6% change from control at 1.75 MAC, respectively) were produced by desflurane and isoflurane. In the presence of autonomic nervous system blockade, the actions of desflurane and isoflurane were nearly identical with the exception of coronary vasodilation. After autonomic nervous system blockade, isoflurane increased coronary blood flow velocity, but desflurane did not. Furthermore, both desflurane and isoflurane continued to produce less depression of myocardial contractility than did halothane and enflurane. In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.

Animals↗
PubMed1992

Drug interactions with sufentanil. Hemodynamic effects of premedication and muscle relaxants.

Induction of anesthesia with synthetic opioids is occasionally accompanied by undesirable hemodynamic changes such as tachycardia and hypertension, or bradycardia and hypotension. We hypothesized that drug interactions cause many of these adverse responses. Therefore, we conducted a randomized double-blind study to investigate the interactive effect of premedication and muscle relaxants on the hemodynamic response to induction with intravenous (iv) sufentanil 10 micrograms.kg-1. Eighty patients with left ventricular ejection fraction greater than or equal to 0.40, undergoing elective coronary artery surgery, were premedicated with either morphine 0.1 mg.kg-1 and scopolamine 6 micrograms.kg-1 intramuscularly, or lorazepam 60 micrograms.kg-1 orally, and paralyzed with either pancuronium 0.1 mg.kg-1 or vecuronium 0.1 mg.kg-1 iv. The four treatment groups were SP (morphine-scopolamine + pancuronium), LP (lorazepam + pancuronium), SV (morphine-scopolamine + vecuronium), and LV (lorazepam + vecuronium). Hemodynamics were recorded at three time periods: 1) control, 2) induction, and 3) intubation. Premedication-relaxant interactions significantly affected hemodynamics. In group SP, mean heart rate (HR) increased significantly on induction (56 +/- 11 to 69 +/- 13 beats.min-1), while mean arterial pressure (MAP) and cardiac index (CI) were unchanged. HR, MAP, and CI were significantly higher after induction in group SP compared to the other three groups. In group LP, mean HR increased less than in group SP (56 +/- 8 to 62 +/- 14 beats.min-1), whereas MAP and CI declined significantly. In group SV, HR and CI were unchanged, but MAP declined significantly. In group LV, HR was stable, whereas both MAP and CI declined significantly. The incidence of pharmacologic interventions during the study period also differed significantly among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

The pharmacokinetics and hemodynamic effects of intravenous and intramuscular dexmedetomidine hydrochloride in adult human volunteers.

BACKGROUND: Dexmedetomidine is an alpha 2 agonist with potential utility in clinical anesthesia for both its sedative and sympatholytic properties. METHODS: The pharmacokinetics and hemodynamic changes that occurred in ten healthy male volunteers were determined after administration of dexmedetomidine 2 micrograms/kg by intravenous or intramuscular route in separate study sessions. RESULTS: The intramuscular absorption profile of dexmedetomidine, as determined by deconvolution of the observed concentrations against the unit disposition function derived from the intravenous data, was biphasic. The percentage bioavailability of dexmedetomidine administered intramuscularly compared with the same dose administered intravenously was 73 +/- 11% (mean +/- SD). After intramuscular administration, the mean time to peak concentration was 12 min (range 2-60 min) and the mean peak concentration was 0.81 +/- 0.27 ng/ml. After intravenous administration of dexmedetomidine, there were biphasic changes in blood pressure. During the 5-min intravenous infusion of 2 micrograms/kg dexmedetomidine, the mean arterial pressure (MAP) increased by 22% and heart rate (HR) declined by 27% from baseline values. Over the 4 h after the infusion, MAP declined by 20% from baseline and HR rose to 5% below baseline values. The hemodynamic profile did not show acute alterations after intramuscular administration. During the 4 h after intramuscular administration, MAP declined by 20% and HR declined by 10%. CONCLUSIONS: The intramuscular administration of dexmedetomidine avoids the acute hemodynamic changes seen with intravenous administration, but results in similar hemodynamic alterations within 4 h.

Adrenergic alpha-Agonists↗
PubMed1994

The effect of adenosine-induced hypotension on systemic and splanchnic hemodynamics during halothane or sevoflurane anesthesia in the rat.

BACKGROUND: It has been suggested that the liver may be at risk for ischemic damage during adenosine-induced hypotension. This notion, however, is somewhat inconsistent with the understanding that adenosine is a powerful vasodilator of the splanchnic circulation. To help clarify the effect of adenosine-induced hypotension on splanchnic hemodynamics, we studied the systemic and splanchnic hemodynamic responses to adenosine, both alone and in the presence of halothane or sevoflurane. METHODS: Systemic and splanchnic hemodynamics were determined during the infusion of adenosine in 36 rats allocated randomly to one of three study groups: (1) awake, (2) halothane anesthesia (1.0 MAC), or (3) sevoflurane anesthesia (1.0 MAC). Adenosine was infused at a rate sufficient to decrease the mean arterial pressure by 35-38% from awake control values. Cardiac output and organ blood flows were measured using the radiolabeled microsphere technique. RESULTS: Adenosine infusion produced stable hypotension of rapid onset due to a reduction in systemic vascular resistance. Stroke volume increased, but cardiac output remained unchanged in the awake and sevoflurane groups because of a decrease in heart rate. Infusion of adenosine during halothane anesthesia increased cardiac output enough to compensate for the decrease in cardiac output due to halothane alone. In the splanchnic circulation, there was an increase in portal tributary (42%, P < 0.01) and hepatic arterial (38%, P < 0.05) blood flows during adenosine infusion in awake rats. This resulted in an overall increase in total liver blood flow (42%, P < 0.01). Halothane anesthesia was associated with a decrease in portal tributary blood flow (28%, P < 0.05). In contrast, sevoflurane anesthesia was associated with an increase in hepatic arterial flow (35%, P < 0.05) but with no change in portal tributary blood flow. During halothane anesthesia, adenosine infusion increased portal tributary (90%, P < 0.01) and hepatic arterial (37%, P < 0.05) blood flows, thereby increasing total liver blood flow to values similar to those in awake adenosine-infused rats. During sevoflurane anesthesia, adenosine infusion increased portal tributary blood flow (48%, P < 0.01), but hepatic arterial blood flow did not increase beyond the values observed during sevoflurane anesthesia alone. CONCLUSIONS: These findings demonstrate that adenosine is a potent vasodilator of portal tributary and hepatic arterial vasculature in the rat and that the splanchnic hemodynamic effects of adenosine predominate over those of halothane and sevoflurane.

Adenosine↗
PubMed1994

Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and abnormal ventricular function.

BACKGROUND: Transesophageal echocardiography (TEE) is used to diagnose hypovolemia despite the lack of validation studies. The objective was to determine the effects of acute graded hypovolemia on TEE and conventional hemodynamic determinants of left ventricular (LV) preload in anesthetized patients with normal and abnormal LV function. METHODS: Determinants of LV preload derived from TEE and hemodynamic monitoring were measured serially in 35 anesthetized cardiac surgical patients without valvular heart disease. Patients were stratified into two groups: those with normal LV function (group 1, n = 17) and those with LV wall motion abnormalities (group 2, n = 13). Patients in groups 1 and 2 were subjected to graded hypovolemia produced by collecting 6 aliquots of blood, each equal to 2.5% of their estimated blood volume (EBV). A third group of patients (group 3, n = 5), not subjected to graded hypovolemia, were studied to test for time-dependent changes. RESULTS: Group 2 had a significantly greater baseline (mean +/- SD) pulmonary artery occlusion pressure (17 +/- 6 vs. 11 +/- 6 mmHg), LV end-diastolic area (23 +/- 5 vs. 18 +/- 4 cm2), LV end-diastolic wall stress (23 +/- 10 vs. 14 +/- 6 x 10(3) dyne.cm-2), and smaller fractional area change (35 +/- 13 vs. 59 +/- 7%). In groups 1 and 2, the LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress decreased linearly in response to blood loss in the range of 0-15% of the EBV. No significant changes in the measured parameters occurred in group 3. A significant decrease in the central venous pressure, pulmonary artery occlusion pressure, and LV end-diastolic area was detected in response to a 2.5% EBV deficit (approximately 1.75 ml.kg-1) in groups 1 and 2. The mean change in LV end-diastolic area (0.3 cm2/1.0% EBV deficit) in response to equivalent EBV deficits was the same in groups 1 and 2. In contrast, the mean change in cardiac output and LV end-diastolic wall stress was less in group 2 despite a greater decrease in pulmonary artery occlusion pressure. Compared to group 1, a greater EBV deficit (7.5% to 12.5% vs. 2.5% to 5%) was required in group 2 to cause a significant decrease in the cardiac output, stroke volume, mixed venous oxygen saturation, and LV end-diastolic wall stress. CONCLUSIONS: TEE and hemodynamic determinants of LV preload detected changes in LV function caused by acute blood loss. Acute blood loss caused directional changes in LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress even in patients with LV wall motion abnormalities. Changes in LV end-diastolic wall stress, derived from both TEE and hemodynamic measurements corresponded to changes in cardiac output, stroke volume, and mixed venous oxygen saturation that occurred during acute blood loss.

Coronary Artery Bypass↗
PubMed1995

Halothane impairs the hemodynamic influence of endothelium-derived nitric oxide.

BACKGROUND: The endogenous vasodilator endothelium-derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow. METHODS: Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW-nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats. RESULTS: NW-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 +/- 2 (P < 0.001) and 20 +/- 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 +/- 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW-nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats. CONCLUSIONS: Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.

Animals↗
PubMed1996

Long-term angiotensin-converting enzyme inhibitor treatment attenuates adrenergic responsiveness without altering hemodynamic control in patients undergoing cardiac surgery.

BACKGROUND: The sympathoadrenal and the renin-angiotensin systems are involved in blood pressure regulation and are known to be markedly activated during cardiac surgery. Because unexpected hypotensive events have been reported repeatedly during anesthesia in patients chronically treated with angiotensin-converting enzyme (ACE) inhibitors, the authors questioned whether renin-angiotensin system blockade would alter the hemodynamic control through attenuation of the endocrine response to surgery and/or through attenuation of the pressor effects of exogenous catecholamines. METHODS: Patients with preserved left ventricular function undergoing mitral valve replacement or coronary revascularization were divided into two groups according to preoperative drug therapy: patients receiving ACE inhibitors for at least 3 months (ACEI) group, n = 22) and those receiving other cardiovascular drug therapy (control group, n = 19). Anesthesia was induced using fentanyl and midazolam. Systemic hemodynamic variables were recorded before surgery, after anesthesia induction, during sternotomy, after aortic cross-clamping, after aortic unclamping, as well as after separation from cardiopulmonary bypass (CPB) and during skin closure. Blood was sampled repeatedly up to 24 h after surgery for hormone analysis. To test adrenergic responsiveness, incremental doses of norepinephrine were infused intravenously during hypothermic CPB and after separation from CPB. From the dose-response curves, pressor (defined as mean arterial pressure changes), and vasoconstrictor (defined as systemic vascular resistance changes) effects were analyzed, and the slopes and the dose of norepinephrine required to increase mean arterial pressure by 20% were calculated (PD(20)). RESULTS: At no time did the systemic hemodynamics and the need for vasopressor support differ between the two treatment groups. However, for anesthesia induction, significantly less fentanyl and midazolam were given in the ACEI group. Although plasma renin activity was significantly greater in the ACEI group throughout the whole 24-h study period, plasma concentrations of angiotensin II did not differ between the two groups. Similar changes in catecholamines angiotensin II, and plasma renin activity were found in the two groups in response to surgery and CPB. The pressor and constrictor effects of norepinephrine infusion were attenuated markedly in the ACEI group: the dose-response curves were shifted to the right and the slopes were decreased at the two study periods; PD(20) was significantly greater during hypothermic CPB (0.08 micro/kg in the ACEI group vs. 0.03 micro/kg in the control group; P < 0.05) and after separation from CPB (0.52 micro/kg in the ACEI group vs. 0.1 micro/kg in the control group; P < 0.05). In both groups, PD(20) was significantly less during hypothermic CPB than in the period immediately after CPB. CONCLUSIONS: Long-term ACE inhibitor treatment in patients with preserved left ventricular function alters neither the endocrine response nor the hemodynamic stability during cardiac surgery. However, a significantly attenuated adrenergic responsiveness associated with incomplete blockade of the plasma renin-angiotensin system supports the hypothesis that inhibition of angiotensin II generation and of bradykinin degradation within the vascular wall mediates some of the vasodilatory effects of ACE inhibitors.

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