Biomedical subjects

B Biber

Publications and source records attributed to B Biber.

At least 55 records · Page 3Linked to original sources

PubMed1995

Vasodilator effects of desflurane and isoflurane in the feline small intestine.

The influence of desflurane (DES) and isoflurane (ISO) on the intestinal vasculature was investigated in normoventilated cats (n = 10) during basal chloralose anesthesia (control). We measured heart rate, mean arterial pressure (MAP), and intestinal blood flow (optical drop flowmetry). Intestinal vascular resistance (IVR) was derived. To avoid changes in local vascular tone related to alterations in transmural pressure gradients, intestinal arterial pressure was controlled and kept constant by a variable aortic clamp. Measurements were performed during control and during the administration of DES (3.5% and 7.0% end-tidal) or ISO (0.8% and 1.6% end-tidal). Each animal was exposed to both agents, prior to and after intestinal postganglionic denervation. In the innervated intestine, both DES and ISO dose-dependently decreased IVR. At the high dose, DES (50 +/- 10% decrease in IVR) was a significantly more powerful vasodilator than ISO (37 +/- 12% decrease in IVR). In the denervated intestine, less pronounced vasodilations were produced by both DES and ISO, as compared to the innervated state, and there were, in this situation, no significant differences between agents concerning the magnitude of the vasodilation. As indicated by comparisons between the innervated versus the denervated state, both neurogenic and non-neurogenic mechanisms contributed to the vasodilator responses. The vascular relaxation at the high dose was for ISO associated with a significantly more powerful non-neurogenic vasodilation, and for DES associated with a significantly more powerful neurogenic vasodilation. This suggests that withdrawal of sympathetic neurogenic vasoconstrictor tone is more important for the vasodilation produced by DES than it is for ISO.

Anesthetics, Inhalation↗

PubMed1995

Oxygen metabolism changes and outcome in response to immediate colloid treatment in the endotoxaemic rat.

A colloid (Hespan) fluid regimen in a 4 h rat model of endotoxaemia was used to prevent the development of the early hypodynamic phase of shock. Groups (N = 10 each) of isoflurane-anaesthetized, male Sprague-Dawley rats received either 1) E. coli endotoxin (E, 20 mg.kg-1 BW, i.v.), 2) 0.9% saline (S), 3) endotoxin + Hespan (E + H), or 4) saline + Hespan (S + H). After a 30 min baseline, 15 ml of 6% hetastarch (Hespan) were infused over 1 h beginning 1 min after endotoxin or saline. Pulmonary artery wedge pressures suggested no fluid overload in the E + H or S + H groups. By the end of the study, there were six spontaneous deaths in the E group vs. no deaths in the other groups. However, despite successful prevention of the early hypodynamic response together with increased cardiac output, increased oxygen delivery, decreased oxygen extraction, and sustained normal oxygen consumption in the E + H group, this fluid regimen failed to prevent significant and progressive acidaemia and hyperlactataemia. Also, by 4 h the E + H group exhibited declining blood pressures, marked hypoglycaemia, and significant small intestinal damage. Our results indicate that the early hypotensive, hypodynamic period is not crucial for the development of significant pathology in endotoxaemia, and that early flow-dependency of whole body oxygen uptake is not inherent to the early response to endotoxin in this model.

Acidosis↗

PubMed1994

Hepatic artery occlusion and energy charge in rat liver tumour.

Hepatic artery ligation (HAL) is a model for inducing a vascular attack on liver tumours which causes a reduction in tumour growth. To determine in an experimental rat liver adenocarcinoma the duration and magnitude of changes in adenonucleotide concentration and energy charge (EC) after HAL, analyses of energy-rich nucleotides were performed at 1, 2, 24 and 168 hours after HAL or a SHAM procedure. There was a significant decrease of the ATP content and energy charge in the tumour one hour after HAL. Two hours after HAL this difference had decreased and with longer observation it was not detectable. Twenty-four hours of starvation did not significantly alter the effects of HAL on the tumour. HAL gives rise to a transient energy depletion of the tumour which is not completely compensated for by glycolysis after 1 hour, but is restored after 2 hours.

Adenocarcinoma↗

PubMed1994

Cardiovascular depression by isoflurane and concomitant thoracic epidural anesthesia is reversed by dopamine.

Interactive effects between exogenous dopamine (DA) and isoflurane (I) combined with thoracic epidural blockade (TEA) were studied in dogs during chloralose anesthesia. The I-TEA intervention per se decreased heart rate (HR; 28%), mean arterial pressure (MAP; 63%), cardiac output (CO; 54%), left ventricular dP/dt (LVdP/dt; 75%) and LVdP/dt/systolic arterial pressure (SAP; 42%). Prior to the I-TEA intervention, dopamine increased MAP, CO, LVdP/dt, LVdP/dt/SAP and stroke volume (SV) already at the dose 10 micrograms.kg-1.min-1 and, additionally, increased mean pulmonary artery pressure (MPAP) at the dose 20 micrograms.kg-1.min-1. During the I-TEA intervention, the DA-induced increases in MAP and systemic vascular resistance (SVR) were significantly higher than prior to I-TEA, as indicated by significant ANOVA interactive effects. At the dose 10 micrograms.kg-1.min-1, DA restored MAP, CO, LVdP/dt, LVdP/dt/SAP and SV to levels found before the I-TEA intervention, while HR was restored first at the dose 20 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1, DA also increased MAP (39%), LVdP/dt (119%), LVdP/dt/SAP (73%), SVR (28%) and MPAP (70%) above levels prior to I-TEA. To conclude, exogenous dopamine effectively and dose-dependently counters cardiovascular depression induced by the anesthetic technique of combining I and TEA. The pressor and systemic vasoconstrictor actions of dopamine are potentiated by conjoint administration of I and TEA.

Anesthesia, Epidural↗

PubMed1993

Effects of endotoxemia on the redox level of brain cytochrome a,a3 in rats.

We conducted the present study to determine the effect of endotoxin challenge on brain oxidative metabolism, after finding evidence in previous studies suggesting early uncoupling of mitochondrial oxidative phosphorylation in the rat small intestine during endotoxemia. Twenty male Sprague-Dawley rats were divided into two groups (N = 10 each) which received E. coli endotoxin (20 mg/kg BW) or an equal volume of 0.9% saline (1 ml/kg) by i.v. bolus. Catheter implantation and the subsequent data collection were conducted using isoflurane anesthesia with controlled ventilation. Hemodynamic and metabolic data were recorded for 30 min before and 60 min after endotoxin or saline injection. Tissue oxidative metabolism was monitored in vivo using differential multiwavelength near-infrared spectrophotometry. Optrodes were positioned on either side of the rat's head (transillumination mode) to monitor the redox state of mitochondrial cytochrome a,a3 (AA3) as well as the supply of oxygen to the brain as reflected by tissue oxyhemoglobin (HbO2). In contrast to our previous results for the small intestine, where the decrease in AA3 oxidation level was disproportionately greater than the concomitant HbO2 decrease, we found that the endotoxin-induced impairment in blood flow to the head was associated with a decrease in brain AA3 redox level, which was proportional to the decrease in tissue HbO2. This finding of an apparent oxygen-dependent AA3 redox shift in the brain during endotoxemia is similar to previous findings of others in hemorrhagic hypotension and hypoxic hypoxia. Possible mechanisms for the different mitochondrial AA3 redox responses to endotoxin in the brain and small intestine are discussed.

Animals↗

PubMed1992

The effects of propofol, methohexitone and isoflurane on the baroreceptor reflex in the cat.

The effects of propofol (P), methohexitone (M) and isoflurane (I) on the baroreceptor reflex were studied in a cat model in which the blood pressure in a bilateral isolated carotid sinus preparation was artificially varied between 50-200 mmHg. The influence from aortic and cardiopulmonary baroreceptors was excluded by vagotomy. With basal chloralose anaesthesia as control, the investigated anaesthetics were used in doses corresponding to MAC 0.5 and 1.0. The maximum change in systemic mean arterial pressure (MAP) and heart rate (HR) following a defined increase in carotid sinus pressure was used as an index of baroreceptor reflex sensitivity. Compared to control, M and I anaesthesia were associated with significant depression of baroreceptor reflex sensitivity at the high dose (corresponding to MAC 1.0), and during I anaesthesia also at the low dose (MAC 0.5). The baroreceptor reflex sensitivity was maintained during propofol anaesthesia. The carotid sinus pressure interval at which the maximum changes in MAP could be elicited, was significantly higher during M than during P. This indicates resetting of the baroreflex.

Animals↗

PubMed1991

Rapid reduction of intestinal cytochrome a,a3 during lethal endotoxemia.

In vivo near-infrared spectrophotometry was used to determine whether lethal endotoxemia impairs small intestinal oxidative phosphorylation as reflected by the redox state of mitochondrial cytochrome a,a3 (AA3). Adult male Sprague-Dawley rats were anesthetized with 2.1% isoflurane in 30% O2:70% N2O, and the small intestine was partially exteriorized for spectrophotometric monitoring (OMNI-3). By 5 min after an iv bolus of Escherichia coli endotoxin (40 mg/kg, LD90, n = 7) a significant shift toward reduction in intestinal AA3 had occurred in association with hypotension and a marked fall in both superior mesenteric artery blood flow (SMAF) and cardiac output. In a separate group (n = 7) SMAF was kept at the baseline level by periodic infusions of donor rat plasma begun 1 min after endotoxin injection, and the reduction in AA3 was again found despite the fluid loading intervention which successfully maintained not only organ blood flow, but also cardiac output and mean arterial pressure in their normal ranges. Further experiments (n = 34) measuring SM vascular bed oxygen consumption indicated that intestinal VO2 remained unchanged during early endotoxemia. These findings suggest a rapid impairment of oxidative phosphorylation by endotoxin which seems to occur through direct (and/or indirect) toxic cellular effects rather than through impaired tissue perfusion.

Animals↗

PubMed1991

Interactive effects of isoflurane and amrinone in the feline intestinal and renal circulation.

Interactive effects of the phosphodiesterase-III inhibitor amrinone and isoflurane were investigated in cats. Cardiac output (thermodilution method), and intestinal (IBF) and renal (RBF) blood flows (optical flowmetry) were measured. Intestinal (IVR) and renal (RVR) vascular resistances were derived. To discriminate between pressure-related local myogenic vascular responses and primary vascular drug effects, intestinal and renal perfusion pressures (50 mmHg; 6.7 kPa) were controlled. The protocol included steady-state recordings with and without isoflurane in a randomized order, both before and after the administration of amrinone (2 mg.kg-1 i.v. + 2 mg.kg-1.h-1 i.v.. Amrinone induced no significant changes in IVR or RVR during basal chloralose anesthesia. During administration of 0.8% isoflurane, amrinone produced decreases in IVR and RVR, which were more pronounced than the vasodilator responses induced by this dose of isoflurane alone. On the other hand, with 1.6% isoflurane, amrinone did not add to the vasodilation. The cardiac effects of isoflurane and amrinone were small. Our data indicate that the vascular tone before administration of amrinone could be crucial for the vascular response of the drug and that isoflurane can significantly influence the regional circulatory effects of amrinone.

Amrinone↗

PubMed1991

Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog.

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor-mediated mechanisms, dopamine effects were investigated in nine chloralose-anesthetized dogs. The circulatory response to dopamine (0-40 micrograms.kg-1.min-1) was studied before and during TEA, and during TEA after introducing the alpha 1-antagonist prazosin (0.3 mg.kg-1), the alpha 2-antagonist rauwolscine (0.3 mg.kg-1), and the beta 1-antagonist metoprolol (0.5 mg.kg-1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine-induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre-TEA levels at 10 micrograms.kg-1.min-1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the beta 1-blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding beta 1-blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre-TEA values by dopamine at 5-10 micrograms.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1991

Local vascular effects of isoflurane during regional intestinal hypothermia in cats.

The influence of isoflurane on intestinal blood flow (IBF) during regional intestinal hypothermia (28 degrees C intraluminal temperature) was investigated in cats (n = 12) during basal chloralose-nitrous oxide anesthesia. A jejunal segment, which was dissected free in situ and intermittently cooled in a saline bath, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio-venous shunt. Intestinal perfusion pressures were controlled by adjusting the shunt flow. IBF was measured (optical drop-recording) during regional normothermia and hypothermia. The protocol included steady-state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% isoflurane. During normothermia, IBF levels were higher during isoflurane anesthesia than during basal chloralose anesthesia. Regional intestinal hypothermia induced no significant changes in IBF during basal chloralose anesthesia. However, the intestinal vasodilator effects of isoflurane, as shown during normothermia, were efficiently countered by regional cooling of the intestinal segment to 28 degrees C. Accordingly, hypothermia IBF levels were similar, regardless of whether isoflurane was administered or not. This could have an impact on the choice of anesthetic techniques.

Anesthesia, Inhalation↗

PubMed1991

Dose-related reduction of intestinal cytochrome a,a3 induced by endotoxin in rats.

Dose-related, endotoxin-induced changes in oxidative metabolism were investigated in vivo using near-infrared spectrophotometry. Sixty fasted male Sprague-Dawley rats were randomly allocated to groups (N = 10 each) receiving saline, 0.08, 0.3, 1.25, 5, or 20 mg/kg Escherichia coli endotoxin by i.v. bolus (1 ml/kg volume). Isoflurane anesthesia with controlled ventilation was used for surgery and the subsequent collection of hemodynamic and metabolic data. Approximately half the length of the small intestine was exteriorized for continuous spectrophotometric monitoring of tissue oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), and mitochondrial cytochrome a,a3 (AA3) redox state. Hemodynamic parameters included arterial and central venous pressures, cardiac output, and superior mesenteric artery blood flow (SMAF). Intestinal AA3 exhibited a marked and sustained shift toward reduction in those groups (1.25, 5, and 20 mg/kg) which developed significant blood pressure and blood flow decreases. However, the AA3 reduction did not seem to reflect tissue hypoxia, since 1) the simultaneously measured tissue HbO2 levels remained essentially constant, 2) the AA3 redox shift did not reverse upon recovery of intestinal blood flow in the 1.25 mg/kg group, which exhibited only a transient decrease in SMAF, and 3) systemic oxygen consumption was unchanged in any group. Endotoxin-induced lethality was tested in six separate groups (N = 10 each) and was significant (60%) only in the 20 mg/kg group. These results suggest that endotoxin may induce a direct (or rapidly mediated indirect) impairment of cellular oxidative phosphorylation.

Animals↗

PubMed1990

Influence of pentobarbital and chloralose on metabolic and hemodynamic changes in liver ischemia.

Hemodynamic and metabolic consequences of a 90-minute period of liver ischemia followed by 120 minutes of reperfusion were studied in rats that were awake during most of the experiment and in rats anesthetized with either pentobarbital (40 mg/kg body weight) or chloralose (30 mg/kg X hour) during the complete length of the experiment. Ischemia was induced by occluding the blood vessels to the left and median liver lobes with a small vascular clamp, which was removed after 90 minutes. Protein synthesis rate was determined by measuring incorporation rate of 14C-leucine into protein in incubated liver slices. At the end of the ischemic period, adenosine triphosphate levels in liver tissue and protein synthesis rate were reduced by 80% to 90%, with no significant differences among groups. During reperfusion, energy levels and protein synthesis rate remained depressed in the anesthetized animals, but improved, although not to normal values, in the awake rats. Hepatic tissue water increased during ischemia, probably reflecting hepatocellular membrane injury. The increase in hepatic tissue water was more pronounced in the chloralose group than in the other groups of rats. During reperfusion hepatic tissue water remained increased in the anesthetized rats but was normalized in the awake group. Mean arterial blood pressure was stable during ischemia and reperfusion in the pentobarbital anesthetized rats, while a progressive decrease in blood pressure during the experiment was noted in the chloralose group. The results suggest that hemodynamic and metabolic responses to liver ischemia and reperfusion can be influenced by anesthetics. Chloralose may be less suitable than pentobarbital for anesthesia when liver ischemia is inflicted.

Adenine Nucleotides↗

PubMed1990

Clinical evaluation of an ensemble-averaging impedance cardiograph for monitoring stroke volume during spontaneous breathing.

Simultaneous determination of stroke volume (SV) with an ensemble-averaging impedance cardiograph (AIGG) and the thermodilution technique (TD) was compared in 10 patients scheduled for major vascular surgery. A small, successive increase in SV was achieved by a step-wise infusion of dextran-70 and elevation of the patient's legs. The patients were allowed to breathe normally during the measurement procedures. There was no difference between the ability of AICG and TD to monitor changes in SV and the correlation coefficient for the measurement of changes in SV by the two methods was 0.88. There was no difference between the reproducibility of AICG- (4.6 ml) and TD- (9.2 ml) determined SV or between the coefficient of variation for AICG (4.8%) and TD (9.9%). The mean difference between AICG- and TD-determined SV at the different measurement points (range 1.3-4.2 ml) was well within acceptable limits. In conclusion, the ensemble-averaging impedance cardiograph described in this study was found to be reliable for monitoring changes in SV during uninterrupted, spontaneous breathing.

Aged↗

PubMed1989

[Silent ischemia in long-term ECG in the early post-infarct period].

101 consecutive patients (73 m, 29 f; 48 AMI, 53 IMI) under 70 years were assigned to 24 hour-Holter monitoring in the third week after first transmural infarction. ST-segment analysis could be performed in 88 patients (89%). 18 patients (20%) had episodes of ischemia which were silent in 95%. One third of these episodes occurred in the absence of physical exercise. Ischemic events displayed a circadian rhythm with a maximum between 6 and 12 a.m. There was no correlation between ischemia and the occurrence of ventricular arrhythmia. In addition, we show that visual control of automatic ST-segment analysis is a prerequisite for routine use in clinical practice.

Aged↗

PubMed1989

Respiratory and cardiovascular effects of thyrotropin-releasing hormone as modified by isoflurane, enflurane, pentobarbital and ketamine.

Thyrotropin-releasing hormone (TRH) possesses significant arousing and cardio-respiratory stimulant actions. The effects of a 2 mg/kg i.v. bolus dose of TRH on respiration and systemic hemodynamics were compared in conscious, freely-moving rats and during anesthesia with 4 different anesthetics. Fifty-four male Sprague-Dawley rats weighing 285 +/- 4 g (mean +/- S.E.M.) were divided into 5 groups: conscious, enflurane (2%), isoflurane (1.4%), pentobarbital (8 mg/kg/h i.v.), and ketamine (60 mg/kg/h i.v.). Anesthetized rats were intubated and breathed oxygen or anesthetic/oxygen spontaneously. Aortic blood pressure, heart rate, cardiac output, respiratory rate, arterial blood pH, blood gases, lactate and glucose were measured, and data were collected over a 20 min baseline period and for 130 min post-TRH. TRH increased respiratory rate in all groups; concomitant changes in arterial PCO2 indicated increased minute ventilation in the inhalation agent groups but not in the i.v. anesthetic groups or in the awake group. Significant respiratory depression in the enflurane group was rapidly reversed by TRH. The respiratory stimulant and arousing effects of TRH were smallest with ketamine anesthesia. The hemodynamic responses to TRH were consistent with a pattern of sympathoadrenalmedullary activation and were relatively uniform across groups despite anesthetic-induced alterations in baseline values. TRH or its analogues may prove useful as an analeptic in clinical anesthesia.

Animals↗

PubMed1989

Effects of isoflurane on feline intestinal blood flow during hemorrhage-induced hypovolemia.

The influence of isoflurane on intestinal reflex vasoconstriction during hemorrhage was investigated in cats (n = 10) during basal chloralose-nitrous oxide anesthesia. Intestinal blood flow (IBF) was studied in a model with controllable intestinal perfusion pressures to exclude local myogenic vascular responses related to changes in intraluminal pressure. A jejunal segment, which was dissected free in situ, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio-venous shunt. Intestinal perfusion pressure was controlled by adjusting the shunt flow. IBF was measured (optical drop-recording) before and after hemorrhage (8% of estimated blood volume). The protocol included steady-state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% (MAC 1.0) isoflurane. IBF levels were consistently higher during isoflurane anesthesia than during basal chloralose anesthesia in the perfusion pressure range 75-150 mmHg (10.0-20.0 kPa). During basal anesthesia, a hemorrhage-induced decrease in IBF was demonstrated throughout the perfusion pressure range 50 to 150 mmHg (6.7-20.0 kPa). The magnitude of the hemorrhage-induced decrease in IBF was not significantly influenced by the addition of isoflurane. Thus, IBF, following hemorrhage, was significantly higher during isoflurane anesthesia than during basal chloralose anesthesia at perfusion pressures 50, 100, 125 and 150 mmHg (6.7, 13.3, 16.7 and 20.0 kPa).

Anesthesia, Inhalation↗

PubMed1989

Effects of dopamine on intestinal hemodynamics and motility during epidural analgesia in the cat.

The effects of dopamine on intestinal blood flow (IBF) and intestinal contraction rate (ICR), and on mean arterial pressure (MAP) and heart rate (HR) were studied in eight cats before and during epidural analgesia (EDA). Before EDA, dopamine 5 and 10 micrograms.kg-1.min-1 had no effect on IBF, MAP and HR, but the higher infusion rate decreased ICR by 71 +/- 19% (mean +/- 1 s.e.mean) (P less than 0.01). EDA significantly increased IBF when intestinal arterial pressure was maintained at an unchanged level by means of a pump, and transiently increased ICR and intestinal tone, but reduced MAP by 46 +/- 8% (139 +/- 11 to 75 +/- 9 mmHg, P less than 0.01) and HR by 26 +/- 3% (248 +/- 7 to 184 +/- 8 beats.min-1, P less than 0.01). During EDA, dopamine increased IBF further, the response being similar at both infusion rates. 5 micrograms.kg-1.min-1 increased HR by 26 +/- 7 beats.min-1 (P less than 0.01) and MAP by 19 +/- 9 mmHg (ns). The corresponding values at 10 micrograms.kg-1.min-1 were 65 +/- 14 beats.min-1 (P less than 0.01) and 35 +/- 8 mmHg (P less than 0.01), respectively, Vascular autoregulation appeared to be unaffected by dopamine and EDA. The effect of dopamine on ICR was not significantly different to what was seen before EDA. It is concluded that the effects of dopamine on IBF, MAP and HR were markedly different during EDA as compared to before the block and that ICR was reduced by dopamine, while it was transiently increased by EDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia, Epidural↗

PubMed1989

Problems of sensing tachyarrhythmias by an antitachycardia pacemaker (Symbios 7008).

Atrial burst pacing is an effective method of terminating supraventricular tachycardia. In the patient presented in this report, a Symbios 7008 pacemaker (Medtronic Inc., Minneapolis, MN, USA) was implanted for two reasons: (1) severe AV conduction defect (AH, 230 msec; HV, 150 msec) and bifascicular block following anterior myocardial infarction; and (2) paroxysmal atrial flutter. The conduction defect ruled out programming other than atrial burst in DDD mode. Activation of burst pacing required appropriate programming of the "tachycardia detection window" on the basis of the cycle length of the flutter waves. In the case reviewed, episodes of atrial flutter with variable cycle lengths of 230 to 280 msec necessitated reprogramming of the AV interval, the refractory period, and the upper rate interval. The use of an antitachycardia device in automatic mode may be limited by variations in tachycardia cycle length.

Aged↗