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PubMed2001

Can we use vertical bore magnetic resonance scanners for murine cardiovascular phenotype characterization? Influence of upright body position on left ventricular hemodynamics in mice.

High resolution magnetic resonance (MR) imaging is uniquely suited for cardiovascular phenotype characterization in transgenic mice. Experimental MR scanners with the high magnetic field strength are commonly built with a vertical bore design. The hemodynamic consequences of a prolonged upright body position in anesthetized mice are, however, unknown. Thus, the purpose of this work was to investigate the influence of a vertical body position on murine systemic blood pressure and left ventricular (LV) hemodynamics over time. We studied six C57Bl/6 mice at 14-16 weeks of age (body weight, 24-28 g) under isoflurane anesthesia. Positioned supine on a 37 degrees C warming pad, a microtip catheter was advanced via the right carotid artery into the left ventricle. Continuous registration of LV hemodynamics was performed at rest and after tilting of the table to a 90-degree vertical position. After tilting, there was a transient decrease of LV systolic pressure to 96% of initial values immediately after tilting with return to baseline level within 6 min. Tilting to vertical position had no influence on LV end-diastolic pressure, heart rate, maximal rate of left ventricular pressure increase, and maximal rate of left ventricular pressure decrease. Over a follow-up period of 60 min in vertical position, there were no significant changes in murine hemodynamics. An acute change of body position is fully compensated by a normal orthostatic response in anesthetized mice. Prolonged upright body position exerts no significant changes in murine LV hemodynamics. Hence, high resolution MR studies for cardiovascular phenotype characterization in transgenic mice performed on vertical bore MR scanners allow measurements under physiologic conditions.

Animals↗
PubMed2004

Hemodynamic maladjustment and disease progression in nephrosis with FSGS.

Idiopathic nephrotic syndrome (NS) associated with focal segmental glomerulosclerosis (FSGS) and severe renal function impairment is usually refractory to the conventional treatment and progresses to end-stage renal disease. Herein, we reported 10 patients with NS-FSGS who had initially had CCr 34 +/- 12 mL/min/1.73 m2 (normal 120 mL/min/1.73 m2), FE Mg 7.8 +/- 2.6% (normal 2.2%), 24-h urinary protein 3.1 g (normal <200 mg) and been followed up for over 10 years. The initial intrarenal hemodynamic study revealed a marked elevation of efferent arteriolar resistance (RE 17289 +/- 8636 dyne x s x cm(-5); normal 3000 dyne x s x cm(-5)), intraglomerular hypertension (PG 57 +/- 1 mm Hg; normal 52 mm Hg), hyperfiltration (FF 0.24; normal 0.2), marked reductions in GFR 35 +/- 17 mL/min/1.73 m2, renal plasma flow (RPF 159 +/- 61 mL/min/1.73 m2; normal 600 mL/min/1.73 m2) and peritubular capillary flow (PTCF 123 +/- 57 mL/min/1.73 m2; normal 480 mL/min/1.73 m2). Such a hemodynamic alteration indicated a hemodynamic maladjustment with a preferential constriction at RE. Treatment consists of multidrugs, namely angiotensin converting enzyme inhibitor, calcium channel blocker, antiplatelet and anticoagulant, with or without angiotensin II receptor antagonist. Following the treatment, correction of hemodynamic maladjustment has been achieved which is characterized by reductions in RE 6046 +/- 2191 dyne x s x cm(-5), PG 52 +/- mm Hg, FF 0.19 +/- 0.1 and increments in RPF 341 +/- 118 mL/min/1.73 m2, PTCF 280 +/- 106 mL/min/1.73 m2 and GFR 64 +/- 17 mL/min/1.73 m2. Coinciding with hemodynamic improvement, there has been a steadily increased creatinine clearance and improvement in FE Mg 4.3 +/- 2.6% and suppression of proteinuria 0.29 +/- 0.4 g/24 h after the period of follow-up of greater than 10 years.

Disease Progression↗
PubMed2003

Pressure-related hemodynamic effects of CO2 pneumoperitoneum in a model of acute cardiac failure.

BACKGROUND: The adverse effects related to CO2 pneumoperitoneum (PP) have been well documented. Although these effects in the state of cardiac failure have not been investigated, it appears to be common current clinical practice to use low-pressure PP in this clinical setting, assuming it to be safer. OBJECTIVE: The aim of our study was to compare the hemodynamic changes with the application of conventional 15 mm Hg PP versus low-pressure 10 mm Hg PP in control and acute cardiac failure (ACF) animal models. METHODS: We studied changes in cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR), applying 10 mm Hg and 15 mm Hg CO2 PP in control and, following the pharmacological induction of acute cardiac failure, in 10 domestic pigs. RESULTS: In control, the application of 10 mm Hg PP did not cause any significant hemodynamic changes compared to baseline parameters. The use of 15 mm Hg PP in the model with normal cardiac function, however, produced a significant change in the tested hemodynamic values: CO decreased from 3.8L/min to 2.8L/min (P =.0018); SV declined from 38 mL to 30 mL (P =.046); SVR increased from 1677 dyne.s.cm-5 to 2414 dyne.s.cm-5 (P =.049) compared to baseline. In the model of ACF induced by the intravenous infusion of sodium pentobarbital, the application of either 10 mm Hg or 15 mm Hg PP was found to have a similar hemodynamic trend: CO, 1.65 L/min vs. 1.41 L/min; SV, 23.2 L vs. 20.9 L; SVR, 2487 dyne.s.cm-5 vs. 2597 dyne.s.cm-5 (P = NS for all). CONCLUSIONS: The application of low-pressure 10 mm Hg PP, compared to conventional 15 mm Hg PP, in the animal model of ACF does not appear to have any hemodynamic advantages.

Acute Disease↗
PubMed1996

Comparison of the respiratory and hemodynamic responses of healthy subjects to exercise in three different protocols.

Although the importance of exercise testing has been well established, standardization of protocols is lacking. In the current study three protocols were compared with respect to respiratory and hemodynamic variables at submaximal and peak exercise. Fifteen healthy young men underwent three maximal exercise tests using the following protocols: (I) an increase of 30 Watt, every three minutes; (II) an increase of 10 Watt, every minute; (III) a continuous load increase of 10 Watt/min. Respiratory measurements were made of oxygen uptake (VO2), carbon dioxide output (VCO2), minute ventilation (VE) and tidal volume (VT). Hemodynamic measurements were made of ECG, heart rate (HR), blood pressure and stroke volume (SV). The latter variable was measured by means of electrical impedence cardiography (EIC). There were no differences in mean maximum load or peak-VO2 between protocols I, II and III. The course of SV was similar in all protocols, i.e. an increase of about 30% until 100 Watt, with a subsequent stabilization until maximum load. All other hemodynamic measurements were similar in both protocols, too. Significant differences were found in submaximal values of VO2 and VCO2. There were no differences in other gas-exchange variables at any moment during exercise. With respect to the VO2max or the hemodynamic response to exercise, any protocol can be used. For the evaluation of submaximal exercise, the protocol that has been used has to be taken into account. Differences at these levels are not related to differences in hemodynamic responses.

Adult↗
PubMed1996

Hemodynamic consequences of obstructive sleep apnea.

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.

Adult↗
PubMed1992

Effect of calcium replacement on the hemodynamic changes associated with high dose interleukin-2 therapy.

Administration of high-dose IL-2 results in hemodynamic changes that are similar to those seen in septic shock. These include a decrease in systemic vascular resistance (SVR) with a resultant drop in mean arterial pressure (MAP). Hypocalcemia is seen in septic shock and with IL-2 administration. Calcium replacement in septic shock has been reported to result in hemodynamic improvement; we therefore administered calcium to patients receiving high dose IL-2 to correct ionized hypocalcemia. Five consecutive patients underwent invasive hemodynamic monitoring before and during IL-2 administration. Calcium chloride was administered to correct ionized hypocalcemia, and hemodynamic parameters were monitored before and after calcium administration. Ionized hypocalcemia was associated with an elevation in parathyroid hormone levels. There was no toxicity related to the administration of calcium. An improvement in the MAP and SVR was seen early and late (after a dose of IL-2 was held) in the IL-2 treatment cycle; there were minimal effects at other points. Because of the potential hemodynamic benefit of calcium replacement, we recommend that ionized hypocalcemia be corrected in patients receiving high-dose IL-2.

Adult↗
PubMed1986

The hemodynamic and clinical responses to terazosin, a new alpha blocking agent, in congestive heart failure.

To determine the hemodynamic effects of a new alpha 1 blocker, terazosin, in congestive heart failure, six patients with this condition underwent hemodynamic testing (at rest and during exercise) before and after dosing. Doses of 2, 5, and 10 mg were examined in sequence over 3 days to define dose-response characteristics. Terazosin, in these doses, decreased pulmonary and systemic vascular resistances and right atrial and pulmonary capillary wedge pressures. Terazosin increased stroke volume and cardiac output, presumably through afterload-reduction, without altering heart rate. These aforementioned responses were apparent both at rest and during exercise. While a direct relationship existed between dose and plasma concentration, a similar relationship was not observed for dose (or plasma concentration) and hemodynamic response; no differences were noted between the hemodynamic responses to the three doses. Improvement in hemodynamics persisted and the clinical status and exercise capacity improved in the four patients chronically treated (over 2 months) with terazosin. Treating the heightened tone of the sympathetic nervous system in congestive heart failure with the alpha 1 blocker, terazosin, may be of benefit to some patients afflicted with this disorder.

Adrenergic alpha-Antagonists↗
PubMed1986

Acute hypercalcemia and cardiac autotransplantation in dogs: long-term hemodynamic adaptability.

Cardiac autotransplantation (excision and reimplantation) is a unique model that isolates totally the cardiac afferent and efferent neural pathways and results in hemodynamic misadaptability to many provocative tests. Since the cardiovascular response to acute hypercalcemia is modulated by numerous factors among which the autonomic innervation plays a major role, the hemodynamic response to bolus administration of calcium gluconate was compared in normal and cardiac autotransplanted dogs. Twenty-two animals underwent an autotransplantation while a sham procedure was performed in 18 animals. Each dog was equipped with an electromagnetic flow probe positioned around the ascending aorta and with central venous and aortic catheters. Hemodynamic data were collected daily during 1 month, before and during rapid intravenous administration of calcium gluconate (0.90 mEq). Baseline hemodynamic studies indicate that for both groups myocardial failure is evident in the immediate postoperative period; despite progressive recovery, the autotransplants always show lower cardiovascular performance. Calcium administration elicits transient positive inotropism, which is more important in presence of myocardial failure; this is true for both control and autotransplanted dogs. In the early postoperative period, hemodynamic adaptability to this stress is impaired in the autotransplants. However, long-term results indicate that minimal differences subsist over time in response to calcium administration, and when they are observed, they result from interferences in baroreceptor regulation and reflexes.

Animals↗
PubMed1995

Transcatheter closure of ventricular septal defects: hemodynamic instability and anesthetic management.

The technique of transcatheter ventricular septal defect (VSD) device closure may be associated with significant hemodynamic instability. The anesthetic records and catheterization data of 70 consecutive transcatheter VSD closures between February 1989 and September 1992 were reviewed, and risk factors associated with hemodynamic instability evaluated. In 28 of 70 procedures (40%), hypotension (> 20% decrease in systolic blood pressure from baseline) occurred; 12 responded to administration of fluids intravascularly alone, whereas 16 patients required additional acute resuscitation. Significant dysrhythmias occurred during 20 (28.5%) anesthetics associated with hypotension and requiring treatment or catheter withdrawal. ASA physical status, precatheterization indication for device placement, and patient size were not predictive of hemodynamic instability during the procedure. Blood transfusions were necessary in 38 (54.4%) cases and were size-related, with patients weighing less than 10 kg requiring a significantly larger transfusion volume (25.1 +/- 12.4 mL/kg). After 35 procedures (50%) patients were admitted directly to the intensive care unit (ICU) due primarily to hemodynamic instability or procedure duration; 24 (68%) required mechanical ventilation. No deaths occurred; there was no late morbidity due to catheterization-related events. Intravenous sedation was used for the initial catheterizations, maintained with a combination of midazolam, ketamine, and morphine. Subsequently general intravenous or inhaled anesthesia was predominantly used during transesophageal echocardiography and internal jugular vein cannulation. We conclude that hemodynamic instability is common during device closure of VSDs, and is likely to be an inescapable feature of these procedures in many patients because of the technique necessary for device placement.

Anesthesia↗
PubMed1997

Early hemodynamic effects of left atrial administration of epinephrine after cardiac transplantation.

We studied the hemodynamic effects of left atrial (LA) administration of epinephrine in 10 patients after cardiac transplantation, using a prospective, randomized, double-blind, cross-over design. After allograft implantation, a LA catheter was inserted and epinephrine infusion commenced at 100 ng.kg-1.min-1. Each trial period consisted of 20 min, with the LA and right atrial (RA) lines switched over between each period; hemodynamic measurements were taken after each time period. Whether epinephrine was administered via the RA or LA did not significantly alter hemodynamics (RA versus LA): mean (SD) arterial blood pressure 67 (7.5) vs 64 (9.5) mm Hg (P = 0.16), mean pulmonary artery pressure 22 (4.0) vs 21 (9.4) mm Hg (P = 0.67), cardiac index 3.2 (1.1) vs 3.2 (1.1) L.min-1.m-2 (P = 0.83), pulmonary vascular resistance index 308 (157) vs 345 (157) dynes.s.cm-5/m-2 (P = 0.30) or right ventricular ejection fraction 35% (11%) vs 32% (9.8%) (P = 0.23). Arterial epinephrine plasma levels were similar (P = 0.16). There was no significant pulmonary extraction of measured catecholamines. We observed no hemodynamic benefit of LA epinephrine administration. It may be that the cardiac transplantation population reacts differently compared with other cardiac surgical patients (possibly because pulmonary extraction of catecholamines is reduced). Because we did not observe a hemodynamic advantage in patients immediately after cardiac transplantation, we would not recommend the use of LA epinephrine at the dose studied.

Adult↗
PubMed1998

Unplanned tracheal extubation outside the operating room: a quality improvement audit of hemodynamic and tracheal airway complications associated with emergency tracheal reintubation.

UNLABELLED: The incidence of hemodynamic and airway complications associated with tracheal reintubation after an unplanned extubation has not been established. Patients whose tracheas were emergently intubated outside the operating room were reviewed over a 27-mo period via a quality improvement vehicle to evaluate hemodynamic and airway complications. Data from a subset of patients (n = 57) who underwent tracheal reintubation after unplanned (self-) extubation were collected for analysis. Of the reintubations, 93% took place within 2 h of self-extubation. Of the patients, 72% had hemodynamic alterations and/or airway-related complications, including hypotension (35%), tachycardia (30%), hypertension (14%), multiple laryngoscopic attempts (22%), difficult laryngoscopy (16%), difficult intubations (14%), hypoxemia (14%), and esophageal intubation (14%). In addition, one surgical airway and one case of "cannot ventilate, cannot intubate" leading to cardiac arrest and death were recorded. These findings suggest that patients requiring reintubation will likely do so soon after self-extubation and that reintubation can be fraught with significant hemodynamic and airway complications. Less than one third of patients undergo a mishap-free reintubation. Strategies to decrease the self-extubation rate in the intensive care unit are needed to improve patient safety and to lessen the potential impact of emergency airway management. IMPLICATIONS: Self-extubation by patients requiring mechanical ventilation can be life-threatening, and replacing the breathing tube often leads to hemodynamic and airway complications. Using this quality improvement audit, 57 self-extubating patients and the complications associated with replacing the breathing tube, which are numerous and can lead to significant morbidity and mortality, were analyzed.

Adolescent↗
PubMed1998

The effect of magnesium sulphate on hemodynamics and its efficacy in attenuating the response to endotracheal intubation in patients with coronary artery disease.

UNLABELLED: Laryngoscopy and endotracheal intubation may produce adverse hemodynamic effects. Magnesium has direct vasodilating properties on coronary arteries and inhibits catecholamine release, thus attenuating the hemodynamic effects during endotracheal intubation. We studied 36 patients with coronary artery disease (CAD) scheduled for elective coronary artery bypass grafting to evaluate the hemodynamic effects of magnesium and its efficacy in attenuating the response to endotracheal intubation. Patients received either 0.1 mL/kg (50%) magnesium sulfate (50 mg/kg) (Group A, n = 19) or isotonic sodium chloride solution (Group B, n = 17) before the induction of anesthesia and 0.05 mL/kg of isotonic sodium chloride solution (Group A) or lidocaine 2% (1 mg/kg) (Group B) before intubation. The hemodynamic variables were recorded before induction, after the trial drug, after induction, and after endotracheal intubation. Automatic ST segment analysis was performed throughout the study period. Magnesium sulfate administration was associated with increased cardiac index (P < 0.01), a minimal increase in heart rate, and a significant decrease in mean arterial pressure (MAP) and systemic vascular resistance (SVR) (P < 0.001). None of the patients in the magnesium group had significant ST depression compared with three patients in the control group. The magnesium group patients had a significantly lesser increase in MAP (P < 0.05) and SVR (P < 0.01) compared with the control group patients who received lidocaine before endotracheal intubation. Thus, magnesium is an useful adjuvant to attenuate endotracheal intubation response in patients with CAD. IMPLICATIONS: Endotracheal intubation produces adverse hemodynamic effects, which may be more detrimental in patients with coronary artery disease than in healthy patients. The present study shows that magnesium administered before endotracheal intubation can attenuate this response better than lidocaine.

Anesthetics, Local↗
PubMed1999

Cardiovascular autonomic dysfunction and hemodynamic response to anesthetic induction in patients with coronary artery disease and diabetes mellitus.

UNLABELLED: Autonomic neuropathy is a major complication of diabetes mellitus and is reported to be associated with increased perioperative hemodynamic instability. We investigated the relationship between autonomic dysfunction and hemodynamic response to anesthetic induction in diabetic and nondiabetic patients with coronary artery disease. We studied 60 patients scheduled for coronary artery surgery, 30 suffering from diabetes mellitus. Preoperative evaluation included traditional cardiovascular autonomic function tests (coefficient of variation of 150 beat-to-beat intervals in heart rate at rest, heart rate response to deep breathing, and heart rate and arterial blood pressure response to standing), spectral analysis of blood pressure and heart rate variability (HRV), and the computation of spontaneous baroreflex sensitivity. After premedication with clorazepate, anesthesia was induced with sufentanil (0.5 microg/kg), etomidate (0.1-0.2 mg/kg), and vecuronium (0.1 mg/kg). Heart rate and blood pressure before anesthetic induction and before and after tracheal intubation were compared between groups. Autonomic function tests, spectral analysis of HRV, and spontaneous baroreflex sensitivity revealed significant differences between patient groups. Most diabetic patients (n = 23) had one or more abnormal test results, in contrast to most nondiabetic patients, who did not show signs of autonomic neuropathy (n = 23). There was no relationship between cardiovascular autonomic function and hemodynamic behavior during anesthetic induction. The blood pressure response to anesthetic induction was not different between patient groups, even when comparing the subgroups with and without abnormal autonomic function tests. These findings indicate that increased hemodynamic instability during anesthetic induction is not obligatory in patients with diabetes mellitus and autonomic dysfunction. IMPLICATIONS: This study indicates that increased hemodynamic instability during anesthetic induction is not obligatory in patients with coronary artery disease and autonomic dysfunction.

Adult↗
PubMed1999

Small-dose inhaled nitric oxide attenuates hemodynamic changes after pulmonary air embolism in dogs.

UNLABELLED: Inhaled nitric oxide (NO) has been used to treat pulmonary hypertension. Experimental studies have suggested therapeutic effects of NO after pulmonary microembolism. We evaluated the protective effects of NO in dogs during a pulmonary air embolism (PAE). NO (3 ppm) was administered to six anesthetized mongrel dogs (NO group) but not to the seven dogs in the control group. After 20 min, each dog received a venous air injection of 2.5 mL/kg. Hemodynamic evaluation was performed, and blood samples were drawn for blood gas analysis before and after NO inhalation and 5-60 min after the PAE. Both arterial blood pressure and cardiac output were decreased in the control group for >15 min after PAE, whereas NO-treated animals showed only transient hypotension. NO attenuated the pulmonary hypertension after PAE, as demonstrated by small (P < 0.05) increases in pulmonary artery pressure and pulmonary vascular resistance index in NO-treated animals (90% and 135%, respectively) compared with the controls (196% and 282%, respectively). These hemodynamic effects of NO were associated with higher mixed venous O2 tensions and saturations in the NO group compared with the controls. We conclude that small-dose NO (3 ppm) attenuated the hemodynamic changes induced by PAE in dogs. This protective effect of NO on hemodynamics is not accompanied by improvement in pulmonary oxygenation in this setting. IMPLICATIONS: In this study, we evaluated the protective effects of inhaled nitric oxide in a pulmonary air embolism setting. Nitric oxide attenuated the hemodynamic changes induced by pulmonary air embolism without improving pulmonary oxygenation.

Administration, Inhalation↗
PubMed1999

The relationship among carbon dioxide pneumoperitoneum, vasopressin release, and hemodynamic changes.

UNLABELLED: We assessed the role of vasopressin (VP) for the hemodynamic response to pneumoperitoneum in pigs. Four groups of anesthetized pigs were investigated. Nine pigs were intraabdominally insufflated with CO2 and eight were intraabdominally insufflated with argon; eight pigs received an i.v. injection of 1 mg/kg SR 49059, a VP antagonist, before CO2 insufflation; and six pigs received SR 49059 alone. Hemodynamics, plasma concentrations of VP and vasoactive hormones, and Paco2 were measured. Data were analyzed by using analysis of variance, Student's t-test, and Mann-Whitney U-test. Five minutes after insufflation, changes in systemic vascular resistance (SVR) were significantly correlated with changes in VP (r = 0.72; P = 0.005) but not with changes in epinephrine, norepinephrine, renin activity, or Paco2. SVR increased during CO2 insufflation but not during argon insufflation or CO2 insufflation with a preceding infusion of SR 49059. The SR 49059 injection itself resulted in increases in heart rate and cardiac output and decreases in blood pressure and SVR. We conclude that, during CO2 pneumoperitoneum in pigs, absorbed CO2 initiates a pathophysiological process that stimulates VP release. Hence, VP most likely plays a key role in the hemodynamic response to a CO2-induced pneumoperitoneum. IMPLICATIONS: Intraabdominal insufflation of CO2 is associated with hemodynamic and hormonal changes. Investigating CO2 and argon-insufflated pigs and using a vasopressin antagonist, we found that CO2 insufflation released vasopressin, which, in turn, induced hemodynamic perturbances.

Animals↗
PubMed2002

The effects of age on neural blockade and hemodynamic changes after epidural anesthesia with ropivacaine.

UNLABELLED: We studied the influence of age on the neural blockade and hemodynamic changes after the epidural administration of ropivacaine 1.0% in patients undergoing orthopedic, urological, gynecological, or lower abdominal surgery. Fifty-four patients were enrolled in one of three age groups (Group 1: 18-40 yr; Group 2: 41-60 yr; Group 3: > or=61 yr). After a test dose of 3 mL of prilocaine 1.0% with epinephrine 5 microg/mL, 15 mL of ropivacaine 1.0% was administered epidurally. The level of analgesia and degree of motor blockade were assessed, and hemodynamic variables were recorded at standardized intervals. The upper level of analgesia differed among all groups (medians: Group 1: T8; Group 2: T6; Group 3: T4). Motor blockade was more intense in the oldest compared with the youngest age group. The incidence of bradycardia and hypotension and the maximal decrease in mean arterial blood pressure during the first hour after the epidural injection (median of Group 1: 11 mm Hg; Group 2: 16 mm Hg; Group 3: 29 mm Hg) were more frequent in the oldest age group. We conclude that age influences the clinical profile of ropivacaine 1.0%. The hemodynamic effects in older patients may be caused by the high thoracic spread of analgesia, although a diminished hemodynamic homeostasis may contribute. IMPLICATIONS: Analgesia levels after the epidural administration of 15 mL of ropivacaine 1.0% increase with increasing age. This is associated with an increased incidence of hypotension in the elderly, although an effect of age on the hemodynamic homeostasis may have contributed. It appears that epidural doses should be adjusted for elderly patients.

Adolescent↗
PubMed1991

The effects of the stereoisomers of the alpha 2-adrenergic agonist medetomidine on systemic and coronary hemodynamics in conscious dogs.

The alpha 2-adrenergic agonist medetomidine produces systemic hemodynamic effects that are mediated by both peripheral and central nervous system actions. The current investigation was designed to characterize coronary and systemic hemodynamic effects of the D- and L-stereoisomers of medetomidine in conscious, chronically instrumented dogs with and without autonomic nervous system blockade. Dogs were instrumented for measurement of aortic pressure, coronary blood flow velocity, cardiac output, left ventricular pressure, rate of change in pressure (dP/dt), and subendocardial systolic shortening. Administration of the D-isomer of medetomidine (doses of 1.25, 2.5, and 5.0 micrograms/kg, each administered over 10 min, with 60 min between doses) significantly altered systemic hemodynamics, in a biphasic fashion. A decrease in respiratory rate without change in arterial blood gas tensions occurred. With the 5 micrograms/kg dose of D-medetomidine, an initial pressor response was followed by secondary, significant (P less than 0.05), and dose-related decreases in heart rate (74 +/- 3 to 57 +/- 4 beats per min), mean arterial pressure (109 +/- 2 to 100 +/- 3 mmHg) and the rate-pressure product (10.5 +/- 0.4 to 7.0 +/- 0.5 beats.min-1.mmHg.10(3] accompanied by a reduction in plasma concentrations of norepinephrine. No changes in left ventricular end diastolic pressure or coronary blood flow velocity occurred. In contrast to the D-isomer, the L-isomer (1.25, 2.5 and 5.0 micrograms/kg) produced no changes in hemodynamics or plasma concentrations of norepinephrine. In dogs pretreated with hexamethonium (20 mg/kg), propranolol (2 mg/kg), and atropine methylnitrate (3 mg/kg) to produce autonomic nervous system blockade, D-medetomidine also produced an initial pressor response, but no secondary reduction in heart rate or arterial pressure occurred. The results indicate that the D-isomer of medetomidine is stereospecific for alterations in hemodynamics: the active D-isomer produces decreases in heart rate, arterial pressure, and the rate-pressure product via diminished sympathetic and/or augmented parasympathetic tone. This conclusion is supported by the absence of these changes after pharmacologic blockade of the autonomic nervous system.

Adrenergic alpha-Agonists↗
PubMed1992

Premedication with oral dexmedetomidine alters hemodynamic actions of intravenous anesthetic agents in chronically instrumented dogs.

Dexmedetomidine (the D-stereoisomer of medetomidine), a highly selective alpha 2-adrenoceptor agonist, has been demonstrated to produce analgesia and sedation and attenuate hemodynamic responses to emergence from inhalational anesthetics, which suggests a potential use for this drug as a premedicant for general anesthesia. The authors examined hemodynamic interactions between dexmedetomidine and three commonly used intravenous anesthetic agents with markedly different hemodynamic effects. Conscious, chronically instrumented dogs received intravenous induction doses of ketamine, propofol, or etomidate, followed by continuous infusions of each drug at four different doses for 15-min intervals on different days. Studies in six separate groups (range, 9-12 dogs/group) with and without pretreatment with oral dexmedetomidine (20 micrograms/kg) were completed. Heart rate, arterial pressure, left ventricular pressure, rate of increase of left ventricular pressure at 50 mmHg (dP/dt50), and cardiac output were continuously recorded. Dexmedetomidine administration caused a significant (P less than 0.05) decrease in heart rate, rate-pressure product, left ventricular dP/dt50, and cardiac output. Dexmedetomidine abolished or attenuated the increase in heart rate, rate-pressure product, cardiac output, and arterial pressure produced during induction of anesthesia with ketamine. After the dexmedetomidine pretreatment, continuous infusion of ketamine caused no increase in heart rate or rate-pressure product. However, ketamine significantly reduced left ventricular dP/dt50 compared to control in dogs premedicated with dexmedetomidine. Except for a significant reduction in systemic vascular resistance, dexmedetomidine did not significantly affect the hemodynamic response to induction of anesthesia with propofol. Similarly, dexmedetomidine did little to alter the hemodynamic response to induction of anesthesia with etomidate.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗