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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen women were studied during elective diagnostic laparoscopy with CO2-insufflation to an intraabdominal pressure (IAP) of 2 kPa and Trendelenburg tilt to 30 degrees. They were allocated to either a halothane (Group I) or a balanced (Group II) anaesthesia with relaxation and controlled ventilation. Heart rate (HR), arterial pressure, stroke volume, CO2-elimination, end-tidal CO2 vol.% and total respiratory compliance (TRC) were the parameters measured, and mean arterial pressure (MAP), total peripheral resistance (TPR), stroke index (SI) and cardiac index (CI) were calculated. At maximum haemodynamic strain, SI and CI were on average reduced by 42% in both groups, without significant changes in HR and MAP. TPR increased by 50% in Group I and 100% in Group II. The reduction in SI was related to the changes in TRC. A small increment in CO2-elimination after CO2-insufflation was most pronounced in Group II. SI and CI did not reach the pre-insufflation values after return to the horizontal position and CO2-exsufflation. The haemodynamic differences between the two groups were small compared to the effects of the laparoscopy procedures.
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PMID:The effect of general anaesthesia on the haemodynamic events during laparoscopy with CO2-insufflation. 252 65

To determine the effects of beta blockade on hemodynamics during increasing levels of treadmill exercise, 10 healthy volunteers were studied after 1 week of placebo, and then after 1 week of treatment with oral propranolol, 80 mg twice daily, or dilevalol, 400 mg once daily. The study was randomized and double-blind, with a crossover sequence. Hemodynamics were measured by CO2 rebreathing at rest and at 25, 50, 75 and 100% of VO2 max. After placebo, cardiac output increased from 5.8 +/- 2.1 (rest), to 19.4 +/- 6.4 liters/min (100% VO2 max), mainly due to an increase in heart rate from 84 +/- 6 to 169 +/- 15 beats/min. Stroke volume increased from 70 +/- 27 (rest), to 137 +/- 65 ml (25% VO2 max), and then leveled off to 116 +/- 41 at 100% VO2 max. After both beta blockers, exercise cardiac output was maintained at 100% VO2 max: 20.1 +/- 9.3 liters/min with propranolol and 19.1 +/- 8.6 with dilevalol. However, a significant reduction versus placebo values was observed for cardiac output at 25% VO2 max, from 13.7 +/- 5.9 during placebo, to 9.4 +/- 2.5 during propranolol, and to 9.6 +/- 2.3 during dilevalol (both p less than 0.01 vs placebo). Maintenance of cardiac output with both beta blockers at higher levels of exercise came from an increased stroke volume (p less than 0.05 vs placebo), while heart rate (in beats/min) was greatly reduced (propranolol 61.6 +/- 9.4 rest, 90.1 +/- 10.7 at 100% VO2 max; dilevalol 70.8 +/- 6.4 rest, 99.2 +/- 11.8 at 100% VO2 max, p less than 0.01 vs placebo for each).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the Frank-Starling mechanism in maintaining cardiac output during increasing levels of treadmill exercise in beta-blocked normal men. 256 24

Non-biological descriptors such as jet feeding pressure and oscillator stroke volume are often used to describe HFV. This results in confusion and hinders acceptance of HFV. The goal of this paper is to show how physiological parameters which are valid during HFV can be monitored. Airway pressure measured in narrow tubes with high linear flow rates is underestimated. A relevant airway pressure must be measured well below the tracheal tube. Pressure measured higher up should be validated against peripheral pressure measurements. Minute ventilation and expired CO2 concentration can be determined with a ServoVentilator and a CO2 analyzer arranged at its exit port. Minute ventilation and CO2 elimination can thereby be continuously monitored during high frequency jet ventilation or so-called "combined high frequency jet ventilation" to prevent undetected disturbance of ventilation and perfusion. Physiological dead space can be studied for optimization of ventilatory pattern. The principle of gas analysis at the exit port of the ventilator may be used for FRC determinations with sulfur-hexafluoride.
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PMID:Monitoring of physiological parameters during high frequency ventilation (HFV). 264 35

The beneficial haemodynamic effects of sequential atrioventricular (AV) pacing have been clearly established and are dependent on the AV delay and pacing rate. However, the optimal AV delay is difficult to determine in each particular patient. We used a modified impedance plethysmographic method to assess variations in stroke volume for different AV delay and pacing rate settings. Impedance measurements showed a good correlation with CO2 rebreathing stroke volume measurements in VVI patients. Impedance variations were then used to set the optimal AV delay at different pacing rates in DDD patients. The inverse relationship between the optimal AV delay and the pacing rate has been accurately identified in most of the patients but is not predictable. In all cases, the cardiac output was higher in DDD mode at the optimal AV delay than in VVI mode. In some patients with a damaged myocardium, the stroke volume appeared to be highly sensitive to multiple AV delay settings. Impedance plethysmography can permit such repetitive non-invasive quick measurements, increasing the accuracy of optimal AV delay determination and is well suited for routine examination of patients with cardiac dual chamber pacemakers.
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PMID:Assessment of the optimal atrio-ventricular delay in DDD paced patients by impedance plethysmography. 270 72

Anesthetized dogs were studied in two protocols to determine the effect of isoflurane on the extent of myocardial injury resulting from left anterior descending coronary artery (LAD) occlusion. In 22 dogs (11 treated with isoflurane 1% inspired, beginning 1 hr after LAD occlusion, and 11 control) myocardial infarct size measured postmortem after 6 hr of LAD occlusion was significantly less with isoflurane than without it, 23.4 +/- 3.8% vs 36.2 +/- 2.4% of left ventricle; regional myocardial blood flow (RMBF) did not differ between groups and hemodynamic differences were slight. Fifty-two other dogs underwent two 15-min periods of LAD occlusion separated by 1 hr of reperfusion. Without isoflurane (n = 12), hemodynamic, RMBF, and regional metabolic data did not differ between the two occlusion periods. When isoflurane 1.3% inspired was administered during one of the two occlusion periods by random assignment, coronary perfusion pressure, left ventricular stroke work index, and systolic left ventricular pressure decreased more than when isoflurane was not administered. Both oxygen (O2) consumption and supply in ischemic myocardium decreased proportionately during LAD occlusion, but more so with isoflurane. Neither lactate production, potassium release, glucose extraction, nor coronary venous carbon dioxide (CO2) or O2 content differed between LAD occlusion periods with and without isoflurane. Thus, isoflurane decreased the extent of myocardial necrosis produced by LAD occlusion but neither RMBF nor metabolic indications were improved during transitory ischemia.
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PMID:Effect of isoflurane on the extent of myocardial necrosis and on systemic hemodynamics, regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion. 280 93

Carbicarb is a mixture of Na2CO3/NaHCO3 that buffers similarly to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% O2/92% N2). Dogs with HLA (n = 28) were then treated with 2.5 meq/kg of either NaHCO3 or carbicarb over 1 hr. Measurements were made, after 1 hr of hypoxia and 1 hr of therapy, of: cardiac hemodynamics, blood gases, liver intracellular pH (pHi), oxygen consumption, and regional lactate production. After therapy, the arterial pH rose with carbicarb (7.22 to 7.27, p less than .01), and fell with NaHCO3 (7.18 to 7.13, p less than .01). Mixed venous PCO2 did not change with carbicarb but increased with NaHCO3 (p less than .05). Arterial lactates stabilized with carbicarb but rose with NaHCO3 (by 3.1 mmol/liter, p less than .005). Lactate use by muscle, gut, and liver all improved with carbicarb and decreased with NaHCO3. The liver pHi (normal = 6.99, hypoxia = 6.80) improved with carbicarb (to 6.92), but decreased further with NaHCO3 (to 6.40). Muscle O2 consumption rose with carbicarb, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (-12 vs -46 mm Hg, p less than .006) and the cardiac output was stable with carbicarb but decreased with NaHCO3 (from 143 to 98 ml/kg/min, p less than .004). Stroke volume also improved with carbicarb but there was no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis. 282 46

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.
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PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65

Respiratory and circulatory (measured and calculated) variables were obtained at the same time in resting eels, during normoxia and after 1 h exposure to environmental hypoxia (water PO2 of 40 torr). In normoxia, values of respiratory and circulatory variables appeared less than those reported for most other fish. These differences could be partly explained by a lower level of standard metabolism and a greater uptake of O2 through the skin. Hypoxia caused a marked decrease in heart rate (40%), cardiac output (37%), ventral and dorsal arterial blood pressures (22% and 32%), associated with a constriction of prebranchial veno-venous shunt, and an increase in branchial vascular resistance (30%). Atropine treatment during hypoxia reduced, but did not abolish, bradycardia, and branchial vascular resistance remained unchanged. The lack of increase in cardiac stroke volume as well as the slowing of the heart in atropine-treated eel, could be regarded as metabolic effects of sustained hypoxia. The increase in branchial resistance and constriction of prebranchial veno-venous shunt could be regarded as a direct myogenic effect of hypoxia. Hypoxic exposure resulted in an increase in ventilatory water flow Vg (more than twofold), a decrease in gill O2 uptake (50%) and oxygen partial pressure in arterial (PaO2 80%) and mixed venous blood (PvO2 78%), and in increase in the transfer factor for O2 of the gills, TO2, (+66%). The ventilatory convection requirement increased (fivefold) while extraction (EwO2%) and effectiveness (Eff%) of gill oxygen transfer were maintained in spite of hyperventilation. Hypoxic hyperventilation reduced partial pressure of CO2 (PaCO2 from 3.4 to 0.7 torr) and markedly raised pH (pHa from 7.98 to 8.33) in arterial blood, thus causing a typical respiratory alkalosis, which resulted in increased O2 affinity and capacity of eel haemoglobin.
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PMID:Ventilatory and circulatory adjustments in the European eel (Anguilla anguilla L.) exposed to short term hypoxia. 292 Aug 10

Hemodynamic measurements were performed in 10 healthy women undergoing elective laparoscopy for the investigation of infertility. A standardized anesthetic technique which included the application of positive end-expiratory pressure (PEEP), 0.49 kPa (3.7 mmHg) was utilized. The following variables were studied: cardiac output, stroke volume and left ventricular ejection time (determined non-invasively with impedance cardiography), heart rate, blood pressure, total peripheral vascular resistance and end-tidal carbon dioxide (ET-CO2). The combination of 25 degrees head-down tilt and PEEP ventilation during laparoscopy was associated with a pressure response that restored arterial pressures to essentially pre-anesthetic levels. Net cardiac effects were small. With this regime low pressure 0.7-1.1 kPa (5-8 mmHg) intra-abdominal insufflation with CO2 was associated with only minor cardiovascular changes. There were no indications that 0.49 kPa PEEP during laparoscopy produced adverse cardiovascular effects. The application of PEEP reduced (P less than 0.001) ET-CO2. There was no net increase in ET-CO2 after CO2-insufflation compared to the measurement after induction of anesthesia. This is in contrast to earlier studies without PEEP where a significant net increase in ET-CO2 was reported after CO2-insufflation.
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PMID:Hemodynamic changes during laparoscopy with positive end-expiratory pressure ventilation. 297 54

The influence of different degrees of hyperventilation on stroke volume measured with a CO2 rebreathing method was studied in seven normal subjects and seven patients with aortic regurgitation. Hyperventilation was initially performed with a rebreathing rate of 30 min-1 and a tidal volume corresponding to 60% of the subject's vital capacity. The tidal volume was then randomly decreased or increased by 0.5 and 1.01 and the procedure was repeated with rebreathing rates of 25 and 35 min-1. The possible influence of habituation to repeated measurements was tested in seven of the subjects. No significant differences in response to hyperventilation of stroke volume, cardiac output or heart rate were found between normal subjects and patients. When the tidal volume was increased, there was a significant increase in heart rate and also an increase in cardiac output, which was significant when comparing measurements performed with the lowest and highest tidal volumes. When comparing initial and final measurements, there was a significant decrease in heart rate and a tendency to decrease in cardiac output. Stroke volume was not affected by variations in rebreathing rate from 25 to 35 min-1 or tidal volume changes of +/- 0.51 and was also unaffected by repeated measurements.
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PMID:The influence of hyperventilation on the measurement of stroke volume using a CO2 rebreathing method. 308 37


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