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

A one-step CO2 rebreathing method for the determination of cardiac output and stroke volume (SV) has been evaluated by comparison with the direct Fick technique during recumbent exercise (10-90 W) in 13 patients. In an initial analysis, the influence of different rebreathing times and of correction for haemoglobin concentration was studied. The best correlation with the direct Fick technique was obtained with the longest analysis time, i.e. 21 s, and correction for variations in haemoglobin concentration further improved the correlation. Consequently, an analysis time of 21 s and correction for haemoglobin have been used. At low cardiac outputs, the CO2-rebreathing method overestimated the flow compared to the Fick technique. The correlation between the methods, however, was so good that a valid estimate of cardiac output could be obtained from the CO2 rebreathing method with appropriate corrections (Cardiac output, CO2 method = 2.7 + 0.77. Cardiac output, Fick; r = 0.91; Residual Standard deviation (SD res) = 0.77 l X min-1). Stroke volumes measured with the CO2 rebreathing method did not differ significantly from those obtained with the direct Fick technique, although there was a tendency to overestimate stroke volume with the CO2 rebreathing method (SV, CO2 method = 12 + 0.89 X SV, Fick; r = 0.82; SD res = 11 ml).
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PMID:Non-invasive assessment of cardiac output and stroke volume in patients during exercise. Evaluation of a CO2-rebreathing method. 309 12

Bilateral, cervical vagotomy in birds denervates, among other receptors, the carotid bodies. To test whether such neural section removes sensitivity to hypoxia, we measured respiratory, cardiovascular, and blood gas responses to hypoxia at 84-, 70-, and 49-Torr inspiratory O2 partial pressure (PIO2) in five pigeons with intact vagi and in five bilaterally, cervically vagotomized pigeons. Normoxic respiratory frequency (fresp) and expiratory flow rate (VE) were decreased after vagotomy. Intact pigeons showed large increases in VE in response to hypoxia, effected mostly by increases in fresp. VE also increased greatly in response to hypoxia in vagotomized pigeons, but increases were largely the result of tidal volume. O2 consumption, CO2 production, and respiratory exchange ratio increased slightly in all pigeons during hypoxia. Normoxic heart rate was greater after vagotomy; cardiac output increased in all pigeons in response to hypoxia, but stroke volume increased only in intact pigeons. During normoxia, arterial and mixed venous O2 partial pressure, O2 concentration, and pH were lower and arterial and mixed venous CO2 partial pressure was higher, after vagotomy. In all pigeons during hypoxia, arterial and mixed venous O2 and CO2 partial pressure and O2 concentration decreased and arterial and mixed venous pH increased; changes were roughly parallel in intact and vagotomized pigeons. The arteriovenous O2 concentration differences during normoxia and hypoxia were similar in all pigeons. We conclude that bilateral, cervical vagotomy in the pigeon causes hypoventilation and tachycardia during normoxia, but strong respiratory and cardiovascular responses to hypoxia are still present.
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PMID:Cardiorespiratory responses to hypoxia in intact and bilaterally vagotomized pigeons. 309 37

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat. 309 15

Cerebral CO2-reactivity was tested by transcranial Doppler sonography (Doppler CO2 test) in 232 patients. Time averaged flow velocity in the middle cerebral artery at the 40 mm Hg blood pCO2 level was taken as a reference point, and the relative increase of flow in hypercapnia of 46.5 mm Hg pCO2 was defined as "Normalized Autoregulatory Response" (NAR). A total of 82 patients with no evidence of cerebrovascular disease gave "normal" values for NAR (23.2 +/- 5.2 SD). In 150 patients with 233 stenoses and occlusions of the internal carotid artery NAR was significantly decreased in higher-grade stenoses (P = 0.01 for 80% diameter reduction, P less than 10(-6) for 90% or more). In such stenoses, patients with NAR less than 14 had suffered more frequently (P less than 0.01) from ipsilateral transient ischemic attacks and/or stroke during the previous 6 months than patients with "normal" NAR. Preoperative NAR less than 14 always improved to "normal" values following carotid surgery, while preoperative NAR greater than 19 remained unchanged (60 cases). The transcranial Doppler CO2 test is thought to be a reliable noninvasive method to detect hemodynamically critical carotid stenoses and occlusions. This may be of interest in selecting patients for superficial temporal artery-middle cerebral artery bypass and carotid surgery. For practical use 4 categories of NAR are suggested.
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PMID:Transcranial Doppler CO2 test for the detection of hemodynamically critical carotid artery stenoses and occlusions. 310 Feb 97

The canine gastric response to acute dilatation, its correlation with selected systemic cardiovascular changes, and preliminary study of its modulation by membrane-stabilizing agents were studied in 21 Beagle dogs. Gastric mucosal damage and adverse cardiovascular sequelae were induced by inflation of an intragastric balloon to 60 mm of Hg in each anesthetized dog for 2.5 hours. At this time, dogs were given 1 of 4 treatments: control; lidocaine HCl, 2.2 mg bolus + 66 micrograms/min, IV; prednisolone succinate, 6.6 mg, IV; and zinc sulfate, 2.2 mg bolus + 66 micrograms/min, IV. After treatments were given, there was a 4-hour deflation period. Throughout the 6.5 hours, continuous measurements were made of stroke volume, arterial blood pressure, PaO2, PaCO2, and plasma HCO3- concentration. Gastric lesions, assessed by planimetric analysis of ulcer indices, were limited to the fundus and corpus and were significantly decreased by lidocaine administration. As seen by histopathologic examination, a sharply delineated transverse area bordering the corporeal-antral junction near the lesser curvature demonstrated minimal resistance to ulceration and showed mucus depletion. Plasma HCO3- concentration, base excess, and CO2 values were negatively correlated with development of gastric damage, indicating that plasma HCO3- concentration has a key role in mucosal resistance to ulcerogenesis.
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PMID:Topographic localization of gastric lesions and key role of plasma bicarbonate concentration in dogs with experimentally induced gastric dilatation. 310 3

The cardiac responses of male paraplegics to upper-body endurance training have been studied by M-mode echocardiography and CO2-rebreathing determination of cardiac output. Data for nine exercised subjects are compared with 5 controls. After 16 weeks of arm ergometer exercise, heart rates of trained individuals were 9 bt X min-1 lower during isometric handgrip effort (30% of MVC for 3 min), with a substantial decrease of rate pressure product (20%; p less than 0.05). In contrast (possibly because of greater anticipation) the control subjects developed a larger rate-pressure product with repetition of the standard isometric effort. Despite a significant increase of VO2 peak (19% and 31% after 8 and 16 weeks, respectively; p less than 0.05), echocardiographic LV mass, dimensions and indices of LV performance were unchanged by training, either at rest or during the isometric handgrip. Stroke volumes were significantly increased by 12-16% after training, both in isometric and in rhythmic work; at the highest intensity of arm ergometry, there was also a suggestion of increased cardiac output. We conclude that a short period of arm training is insufficient to induce cardiac hypertrophy, an increase of stroke volume with a decreased rate-pressure product but no change in echocardiographic indices of LV performance implies an improved myocardial efficiency. Possible explanations are a greater strength of the trained arms, and some increase of pre-loading (due to an increase of venous tone and more effective operation of the muscle pump after training).
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PMID:Cardiac effects of short term arm crank training in paraplegics: echocardiographic evidence. 310 34

Estimation of cardiac output by impedance cardiography (QZ) in exercise during normal breathing (NB) has been limited by motion artifact. Our objective was to obtain readable impedance cardiograms on five subjects during upright cycle exercise at 0, 50, 100, 150, and 200 W to permit comparisons of QZ during NB, expiratory breath hold (EXP) and inspiratory breath hold (INSP). Q was also determined using an equilibration CO2 rebreathing method [Q(RB)]. QZ during NB exceeded EXP QZ at 100, 150, and 200 W, and exceeded INSP QZ at 100 W (P less than 0.05). The low EXP QZ values were due to a significantly lower stroke volume at 100, 150, and 200 W (P less than 0.05). For the INSP QZ at 100 W, heart rate was lower than during EXP (P less than 0.05). Regression of QZ (NB) against Q(RB) resulted in a linear relationship (r = 0.93) over the range of Q = 7-26 1/min. The slope of the regression differed significantly from 1.0 (P less than 0.05). We conclude that QZ values obtained during EXP or INSP should not be assumed to represent QZ during NB, at least at work rates greater than 50 W. A consequence of the linear relationship between QZ(NB) and Q(RB) over the range of 0-200 W is that estimates of CO2 rebreathing cardiac output can be obtained by impedance cardiography if QZ is adjusted using an appropriate empirical factor.
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PMID:Cardiac output in exercise by impedance cardiography during breath holding and normal breathing. 310 80

The effects of postoperative external heat supply on shivering, oxygen uptake, carbon dioxide production, ventilatory requirements and haemodynamic variables were studied postoperatively after aortocoronary bypass surgery in 24 men with stable angina pectoris. After hypothermic cardiopulmonary bypass (CPB) at 25 degrees C, the patients were rewarmed to a nasopharyngeal temperature of at least 38 degrees C, resulting in a rectal temperature of about 34 degrees C before termination of CPB. Twelve patients, forming the control group, were given no other external heat supply. In another group (n = 12), the "radiant heat supply group", additional external heat was provided postoperatively, the main source of which was a thermal ceiling supplemented with heated, humidified respiratory gases. In this latter group the postoperative rewarming was accomplished earlier and was converted into a mainly passive process. Shivering, oxygen uptake, CO2 production and ventilation volumes were significantly reduced compared with the control group. Cardiac index and stroke index were higher and systemic oxygen extraction was lower in the radiant heat supply group. Postoperative hypertension and vasoconstriction were greatly decreased, suggesting that residual hypothermia is an important cause of the postoperative vasoconstriction.
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PMID:Postoperative ventilatory and circulatory effects of heating after aortocoronary bypass surgery. Postoperative external heat supply. 311 49

1. The ventilatory and circulatory responses to electrically induced leg exercise (EEL) were studied in seven normal subjects and compared with the responses to performing the same exercise voluntarily (EV). 2. EEL was produced by surface electrode stimulation of the quadriceps and hamstring muscle groups. This produced a push-relax pattern of exercise against a spring load and was free of any pain or discomfort. EV, at the same level, was achieved by subjects copying a display of timing and force information on a storage oscilloscope. 3. Cardiac output was estimated using validated Doppler ultrasound measurements of the velocity in the ascending aorta, combined with an estimate of aortic cross-sectional area using M-mode echocardiography. 4. Data from EV and EEL exercise runs were matched, within subjects, for the increase in oxygen consumption during the first 30 s of exercise; there were no significant differences between the resting states prior to either form of exercise. 5. The first ten beats of exercise were used to study the circulatory on-transient. The cardiac output responses to both EV and EEL were similar; however, in EV alone there was an initial significant drop in stroke volume and a slightly greater rise in heart rate. 6. The first five breaths of the response were used to study the ventilatory on-transient, and by measuring cardiac output, stroke volume and heart rate throughout each breath, the relationship between circulatory and ventilatory variables could be assessed. Ventilation showed a significantly greater rise at the onset of exercise during EV than during EEL; PET,CO2 (end-tidal CO2 pressure) showed small but significant falls for both EV and EEL. 7. The circulatory changes on a breath-by-breath basis are similar for EV and EEL although the ventilatory changes differ. In both EV and EEL the average increase in ventilation at the onset of exercise is proportionally greater than the average increases in cardiac output. Individual exercise runs show no particular relationship between circulatory and ventilatory change. 8. The results provide no support in man during mild leg exercise for a 'cardiodynamic' drive to breathing.
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PMID:The early circulatory and ventilatory response to voluntary and electrically induced exercise in man. 311 4

An index of cerebral perfusion reserve (RES%), defined as the percent change of regional cerebral blood flow over baseline per mm Hg of end-tidal CO2 tension, was determined for each middle cerebral artery (MCA) territory in patients with unilateral carotid distribution transient ischemic attacks or minor cerebrovascular accidents and was compared with that of age-matched, neurologically normal volunteers. Vasodilator responses to induced hypercapnia were tested during inhalation of 5% CO2 in 95% O2 while regional cerebral blood flow was measured by fluoromethane inhalation positron emission tomography. Mean RES% for 24 normal MCA territories was 5.2 +/- 0.8%. Mean RES% for 15 patient nonischemic MCA territories was 3.8 +/- 1.3% and for 15 ischemic MCA territories was 2.8 +/- 1.9% (both p less than 0.001). Individual RES% values and symmetry ratios between ischemic and nonischemic regions were also determined and compared with angiographic data. Areas of diminished, asymmetric, or paradoxical (two patients) CO2 reactivity appear to correspond to areas of compensatory vasodilation. We found this technique to be a safe and reproducible method for defining and recording localized areas of cerebral tissue at apparent risk for hemodynamically related damage.
Stroke 1988 Jan
PMID:Cerebral perfusion reserve indexes determined by fluoromethane positron emission scanning. 312 75


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