Maximum Change In Heart Rate Research Articles

Cardiovascular reflexes during treatment of social phobia with moclobemide

INTRODUCTION: Cardiovascular side-effects are less frequent with moclobemide than with tricyclic or monoamine oxidase inhibitor antidepressants. We performed a detailed assessment of cardiovascular reflexes in 15 patients meeting DSM-III-R criteria for social phobia, before treatment and whilst taking a stable dose of moclobemide for a median of 7 weeks. METHOD: Cardiovascular reflex responses to standing, deep breathing and the Valsalva manoeuvre were assessed using beat-by-beat blood pressure and heart rate recording. RESULTS: Moclobemide produced a statistically significant, but clinically modest, degree of improvement in social phobia symptoms. Only the maximum change in heart rate from supine to standing showed a change from before to after treatment, which was not statistically significant after Bonferroni correction, and there was no consistent pattern of altered sympathetic or parasympathetic function. CONCLUSION: Moclobemide is relatively devoid of cardiovascular autonomic effects in physically healthy subjects with social phobia. ( Int J Psych Clin Pract 2001; 5:27-31)

Effects of propofol and remifentanil on phrenic nerve activity and nociceptive cardiovascular responses in rabbits.

The effects of propofol, remifentanil, and their combination on phrenic nerve activity (PNA), resting heart rate (HR), mean arterial pressure (MAP), and nociceptive cardiovascular responses were studied in rabbits. Basal anesthesia and constant blood gas tensions were maintained with alpha-chloralose and mechanical ventilation. PNA, HR, MAP, and maximum changes in HR and MAP (deltaHR, deltaMAP) evoked by electrical nerve stimulation of tibial nerves were recorded. The comparative effects were observed for propofol at infusion rates from 0.05 to 3.2 mg x kg(-1) x min(-1) (group I) and remifentanil from 0.0125 to 12.8 microg x kg(-1) x min(-1) alone (group II), and during constant infusions of propofol at rates of 0.1 and 0.8 mg x kg(-1) x min(-1) (groups III and IV, respectively). Finally, the effect of remifentanil on propofol blood levels was observed (group V). The infusion rates for 50% depression (ED50) of PNA, deltaHR, and deltaMAP were 0.41, 1.32, and 1.58 mg x kg-(1) x min(-1) for propofol, and 0.115, 0.125, and 1.090 microg x kg(-1) x min(-1) for remifentanil, respectively. The ratios for the ED50 values of deltaHR and deltaMAP to PNA were 3.2 and 3.9 for propofol, and 1.1 and 9.5 for remifentanil, respectively. Analysis of the expected and observed responses and isobologrms showed that although their combined effects on PNA, resting HR, and MAP, and deltaMAP were synergistic for deltaHR, they were merely additive. Remifentanil had no effect on propofol blood levels. PNA was abolished by propofol and remifentanil, alone and in combination, before significant depression of nociceptive pressor responses occurred. Their combined effects on PNA, HR, MAP, and deltaMAP are greater than additive, ie., synergistic. Unlike propofol, remifentanil obtunded pressor responses more than the resting circulation.

Longitudinal follow-up of cardiovascular reflex tests in multiple sclerosis

Several studies have shown various degrees of autonomic dysfunction in patients with multiple sclerosis. Longitudinal follow-up studies are remarkably scarce up to now. We assessed autonomic dysfunction twice with an interval of 1 year in 20 relapsing remitting and 26 secondary progressive MS-patients. Autonomic function was assessed by the heart rate response during deep breathing, standing up and Valsalva manoeuvre. Only the maximum change in heart rate after standing up (in ms and beats/min) and the Max/Min ratio after standing up showed significant worsening over 1 year. The changes in EDSS scores also documented gradual deterioration of the neurological condition over the study period. We conclude that there is progression of autonomic dysfunction in MS over 1 year and that this could correlate with progression in clinical disability.

EFFICACY OF EPIDURAL TEST DOSE IN THE ELDERLY DURING GENERAL ANESTHESIA

S322 Heart rate (HR) responses to beta-adrenergic agonists are known to be suppressed in the elderly patients. [1] This study was designed to determine the efficacy of epidural test dose (ETD) to detect intravascular injection in healthy elderly patients during sevoflurane anesthesia. METHODS: Following IRB approval and informed consent, 20 ASA class 1 patients, >65 yrs of age, undergoing abdominal surgeries were randomly assigned to either control group or ETD group (n=10 each). No premedication was given. After performing epidural anesthesia at Th7/8 interspace using 1.5% lidocaine with epinephrine (1:200,000) solution and confirming analgesia at or above Th4, general anesthesia was induced with thiamylal 3 mg/kg and fentanyl 2 [micro sign]g/kg IV. Endotracheal intubation was facilitated with IV vecuronium, and anesthesia was maintained with end-tidal sevoflurane 1%, 67% N2 O in oxygen in all patients. When reinforcing dose of epidural lidocaine was necessary at the discretion of attending anesthesiologists, either ETD consisting of 1.5% lidocaine 3 mL plus 15 [micro sign]g epinephrine or saline 3 mL was injected IV over 5 sec. Then, continuous record of HR and systolic blood pressure (SBP) were obtained, from which HR and SBP were analyzed at 20-sec intervals. Sensitivities, specificities, and positive (+PV) and negative predictive values (-PV) were calculated based on the conventional (Delta HR>or=to20 bpm) and the modified (Delta HR>or=to10 bpm) HR criteria, and the SBP criterion (Delta SBP>or=to15 mmHg). RESULTS: Mean age of the patients was 71 +/- 4 (mean +/- SD) yrs. Maximum changes in HR and SBP of the ETD group were 16 +/- 12 bpm and 48 +/- 20 mmHg, respectively. (Table 1)Table 1CONCLUSIONS: Regardless of the criteria, peak HR change is an unreliable indicator to detect intravascular migration of the epidural catheter in the elderly patients during sevoflurane anesthesia, whereas peak SBP change appears to be more sensitive.

The relationship between maximum cardiac output and swimming performance in northern squawfish, Ptychocheilus oregonensis: the effect of coronary artery ligation

The objective of this study was to determine whether experimental reductions in maximum cardiac output would reduce the swimming performance of northern squawfish, Ptychocheilus oregonensis. The reduction in maximum cardiac output was accomplished using ligation of the coronary arteries, and the effectiveness of the ligation depended upon fish size. Maximum cardiac output was significantly reduced in coronary-ligated fish greater than 320 g, but was unchanged in smaller fish. The reduction in maximum cardiac output was due to a significant decrease in maximum stroke volume, with no change in maximum heart rate. Despite the significant reduction in maximum cardiac output in the larger fish, there was no significant reduction in critical swimming speed.

Reliability and Validity of the Beats Above Baseline Index: A New Measure of Task Difficulty

The Beats Above Baseline Index (BABI) is mathematically based on the integral of effort (estimated by instantaneous heart rate increase) across the time interval for task completion. This is equivalent to the number of heart beats occurring during a task minus the number of beats that would have occurred during the same time interval at the baseline rate. We assessed the test-retest reliability and construct validity of the BABI using 19 normal subjects accomplishing a stair-climbing task. Subjects completed the task under normal conditions (N), with a knee immobilizer and cane (CANE), and using crutches (CRUTCH). Reliability of the BABI was high within (ICC 0.84, 95% CI 0.70-0.92) and between sessions (ICC 0.91, 95% CI 0.77-0.97). Individual BABI values for all 19 subjects conformed to the underlying construct, namely N < CANE < CRUTCH. In contrast, two commonly used alternative measures, namely maximum change in heart rate and time for task completion, showed inferior concordance to the construct.

Comparative effects on blood pressure and heart rate of dynorphin A(1–13) in anterior hypothalamic area, posterior hypothalamic area, nucleus tractus solitarius, and lateral cerebral ventricle in the rat

The objective of this study was to explore the effects of the endogenous opioid peptide dynorphin A(1–13) on the CNS regulation of blood pressure and heart rate. Wistar rats, anesthetized with pentobarbital and halothane, received dynorphin A(1–13) microinjected into the anterior hypothalamus area (AHA), the posterior hypothalamic area (PHA), the nucleus tractus solitarius (NTS), or the lateral cerebral ventricle (ICV). Dynorphin A(1–13), 20 (12 nmol) or 30 μg ICV, produced significant ( p < 0.05) reductions in blood pressure and heart rate. Naloxone, 50 μg/kg ICV, completely prevented the blood pressure response and significantly ( p < 0.05) blunted the heart rate response to the highest dynorphin concentration, 30 μg ICV (18 nmol). Dynorphin A(1–13), 5 μg, in the NTS significantly ( p < 0.05) decreased systolic and diastolic blood pressure and heart rate with the response being evident 10 min and persisting for 30 min after injection. In contrast, the same dose of dynorphin A(1–13) in the AHA produced an immediate, marked, and significant ( p < 0.05) decrease in systolic and diastolic blood pressure and heart rate that attained its maximum 1–3 min and returned rapidly towards baseline levels. Dynorphin A(1–13), 5 or 10 μg in the posterior hypothalamic area, was not associated with any change in blood pressure or heart rate. Injection of the diluent at any site was not associated with any changes in blood pressure or heart rate. The maximum change in blood pressure with dynorphin was greater in the AHA than NTS, and the maximum change in heart rate was greater in the NTS than AHA. These data indicate a potential role for dynorphin as a modulator of the CNS regulation of blood pressure and cardiac rate, and this is mediated in part through different areas in the brain that maybe localized to the anterior hypothalamic area and nucleus tractus solitarius but not the posterior hypothalamic area.

Relationship between heart rate, left ventricular output, and stroke volume in preterm infants during fluctuations in heart rate.

The relationship between changes in heart rate, left ventricular output, and left ventricular stroke volume was studied in 18 preterm infants, with mean gestational age 29 wk (range 26-33 wk) and mean postnatal age 10 d (range 1-21 d). To yield left ventricular output, the blood flow velocity in the ascending aorta was measured by range-gated Doppler technique and multiplied by the aortic cross-sectional area measured by cross-sectional and M-mode echocardiography. Stroke volume was calculated by dividing left ventricular output by heart rate. The individual mean left ventricular output correlated poorly with heart rate (r2 = 0.17), and, accordingly, there was a closer relationship between stroke volume and left ventricular output. In only four of the 18 infants was a significant correlation between heart rate changes and left ventricular output found. Substantial changes in stroke volume were seen in most infants, and in 13 of the 18 infants the changes exceeded 25%. These variations in stroke volume were closely related to left ventricular output. In 15 of the 18 infants, the maximum heart rate change was associated with a stroke volume change in the opposite direction. The group average of the maximum heart rate increase in each individual, 24 bpm (18%), corresponded to a decrease in stroke volume of 0.15 mL.kg-1 (9%) (p less than 0.05) and an increase in left ventricular output of 22.7 mL.min-1.kg-1 (9%) (p less than 0.05). A reciprocal relationship was seen between afterload and left ventricular output.(ABSTRACT TRUNCATED AT 250 WORDS)

A Clinical Study of Sensitivity to Sodium Nitroprusside during Controlled Hypotensive Anesthesia in Young and Elderly Patients

Aging has important effects on the cardiovascular system; baroreceptor reflex function decreases and the elderly are more resistant to both β-receptor agonists and antagonists. The purpose of the present clinical study was to determine the relationship between age and sensitivity to sodium nitroprusside in 16 patients during deliberate hypotensive anesthesia by determining the blood pressure changes in young and elderly patients to incremental increases in dose of sodium nitroprusside. A dose-response curve relating change in mean blood pressure to dose of sodium nitroprusside (μg·kg−1·min−1) was constructed for each patient; the slope of this line is a measure of “sensitivity.” The change in mean arterial blood pressure per μg·kg−1·min−1 nitroprusside dose (i.e., slope), showed a significant correlation with age (r = 0.766, P < 0.001), demonstrating that sensitivity to sodium nitroprusside increases with advancing years. The maximum change in heart rate produced by nitroprusside showed a reciprocal correlation with age (r = −0.791, P < 0.001). There was no significant correlation between age and maximum change in plasma norepinephrine or epinephrine concentrations during nitroprusside infusion. The increased sensitivity to nitroprusside might have been due to 1) diminished baroreflex activity, 2) resistance of cardiac adrenergic receptors to catecholamine stimulation, or 3) alteration in sensitivity to the direct vasodilating effects of sodium nitroprusside. Whatever the mechanism, however, this clinical study has shown that lower doses of nitroprusside should be used in elderly patients to achieve the same degree of hypotension achieved in younger patients.

A Clinical Study of Sensitivity to Sodium Nitroprusside during Controlled Hypotensive Anesthesia in Young and Elderly Patients

Aging has important effects on the cardiovascular system; baroreceptor reflex function decreases and the elderly are more resistant to both beta-receptor agonists and antagonists. The purpose of the present clinical study was to determine the relationship between age and sensitivity to sodium nitroprusside in 16 patients during deliberate hypotensive anesthesia by determining the blood pressure changes in young and elderly patients to incremental increases in dose of sodium nitroprusside. A dose-response curve relating change in mean blood pressure to dose of sodium nitroprusside (microgram X kg-1 X min-1) was constructed for each patient; the slope of this line is a measure of "sensitivity." The change in mean arterial blood pressure per microgram X kg-1 X min-1 nitroprusside dose (i.e., slope), showed a significant correlation with age (r = 0.766, P less than 0.001), demonstrating that sensitivity to sodium nitroprusside increases with advancing years. The maximum change in heart rate produced by nitroprusside showed a reciprocal correlation with age (r = -0.791, P less than 0.001). There was no significant correlation between age and maximum change in plasma norepinephrine or epinephrine concentrations during nitroprusside infusion. The increased sensitivity to nitroprusside might have been due to diminished baroreflex activity, resistance of cardiac adrenergic receptors to catecholamine stimulation, or alteration in sensitivity to the direct vasodilating effects of sodium nitroprusside. Whatever the mechanism, however, this clinical study has shown that lower doses of nitroprusside should be used in elderly patients to achieve the same degree of hypotension achieved in younger patients.

Pyridostigmine as an antagonist of d-tubocurarine-induced and pancuronium-induced neuromuscular blockade.

In an evaluation of the clinical effectiveness of pyridostigmine as an antagonist of d-tubocurarine-induced and pancuronium-induced neuromuscular blockade in patients anesthetized with a neurolept-nitrous oxide (N2O) technic, 60 adults received either d-tubocurarine (dTc) (N equals 30) or pancuronium (N equals 30). The pancuronium-dTc potency ratio with neurolept-N2O anesthesia is 4.85:1. The mean doses of pyridostigmine necessary for 50 percent recovery of control twitch height and sustained tetanus were 5.72 plus or minus 0.45 (S.E.) mg. and 11.6 plus or minus 0.88 mg., respectively, for dTc, and 4.05 plus or minus 0.24 mg. and 8.27 plus or minus 0.41 mg., respectively, for pancuronium. There was no correlation between the amount of pyridostigmine necessary for relaxant antagonism and the total dose of relaxant used. In 24 patients, neuromuscular blockade was reversed by an intravenous injection of pyridostigmine and either 0.6 mg. or 1 mg. of atropine. Within 2 minutes, patients given 1 mg. of atropine had a significantly faster heart rate than those given 0.6 mg of atropine (p smaller than 0.0001). There was no correlation between control heart rate and maximum changes in heart rate. No cardiac arrhythmia or bronchospasm was observed in patients with either pancuronium or dTc following atropine-pyridostigmine mixtures. The cardiac muscarinic effects of pyridostigmine could be modified by simultaneous administration of 1 mg. of atropine.