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

The thoracocardiograph (TCG) displays cardiac oscillations transmitted to the external surface of the thorax through inductive plethysmographic transducers placed transversely around the thorax near or about the xiphoid process. Such signals, with the appearance of ventricular volume curves, were used to compute changes of stroke volume (SV) and cardiac output (CO) in normal subjects. Their values were compared with changes of SV and CO measured with the impedance cardiograph (IC). Increases of SV and CO were produced with subcutaneous terbutaline and there was excellent agreement between TCG and IC values, best from TCG transducers placed at the xiphoid process and 3 cm caudal to it, although TCG locations 6 cm caudad and 3 cm cephalad to the xiphoid were also satisfactory. Since the site 3 cm caudad to the xiphoid process is known to anatomically transect solely a segment of the left ventricle, it was designated the TCG-Reference location. Both TCG and IC derived SV were not altered during postural shifts about a horizontal axis. Neither TCG nor IC showed the expected large decreases of SV from supine posture to head-up tilt. With baseline TCG and IC measurements in 60 degrees head-up tilt. MAST suit application increased CO measured with TCG but not with IC. Neither TCG nor IC revealed alteration of CO with nasal CPAP up to 10 cm H2O despite a rise in functional residual capacity (FRC) level of 870 ml. This investigation indicates that TCG has promise as a near continuous, noninvasive monitor of SV and CO in normal subjects if postural axis is fixed and does not require highly trained personnel or labor-intensiveness for its operation.
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PMID:Thoracocardiography. Part 2: Noninvasive measurement of changes in stroke volume; comparisons to impedance cardiograph. 200 92

The OSA syndrome, described over 100 years ago, was rediscovered in 1966. It is a common disorder, especially among fat, middle-aged men. Stentorian snoring and diurnal somnolence are the cardinal manifestations and should always lead to an examination during sleep. That examination (polysomnography) can demonstrate the pathognomonic events--repetitive apneas occurring in sleep--which signal the failure of the sleeping brain to maintain the patency of the supraglottic airway. All evidence points to the problem being an abnormal pharyngeal airway, one which has a shape or size or compliance that allows inspiratory collapse as the normal loss of pharyngeal dilator muscle tone occurs with sleep. The apneas are asphyxic events terminated by arousals which fragment sleep continuity and lead to the daytime sleepiness. Because the snoring occurs during sleep, the arousals are unremembered, and the sleepiness can develop so gradually that the patient may forget what normal alertness is like. It is important to interview the patient's spouse or partner. Besides obesity and maleness, other risk factors for OSA are diseases that have an impact on the configuration or effective compliance of the pharyngeal passageway. Recent studies support the clinical intuition that sleep apnea is undesirable. Sleepiness leads to accidents. The hypoxemia occurring during apnea can lead to potentially fatal cardiac dysrhythmias. A number of reports suggest that snoring and sleep apnea are associated with an increased risk of stroke, myocardial ischemia, and infarction. Finally, there are now two papers showing a significantly decreased probability of 5-year survival in patients with symptomatic sleep apnea. The good news is that treatment with tracheostomy or NCPAP improves mortality rates to normal. Approximately 90 per cent of patients can tolerate a night's initial trial with CPAP. Long-term acceptance of CPAP has now been reviewed in a number of studies, and it appears to be about 65 to 70 per cent.
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PMID:Sleep disorders and upper airway obstruction in adults. 219 4

The role of altered end-expiratory pressure on total oxygen dynamics was studied prospectively in 18 patients with injuries and sepsis. Eight patients received high tidal volumes (12 to 18 ml/kg), continuous positive airway pressure, and intermittent mandatory ventilation (CPAP/IMV); 10 patients received low tidal volumes (8 to 10 ml/kg) with zero end-expiratory pressure and assist control mode of ventilation (ZEEP/A-CM). CPAP/IMV patients had better oxygen tension, reduced physiologic shunting in the lung (24% versus 18%), and an improved arterial tension: inspired oxygen concentration ratio. CPAP/IMV patients also had significantly higher central filling pressures that were associated with significant reductions in cardiac output (8.2 L/min versus 6.4 L/min). The reduced cardiac output appeared to be a result of a reduction in left ventricular stroke work index. Consequently, the total oxygen delivery was reduced for all 3 days following insult and for the cumulative data for all 3 days (266 versus 306 ml/min) in the CPAP/IMV patients. Oxygen consumption was also reduced in the CPAP/IMV patients; this reduction was not significant for each of the first 3 days but was significant when the data for the 3 days were added to the analysis (306 versus 272 ml/min). Future prospective randomized studies are needed to determine the most effective use of ventilatory support on total oxygen dynamics including oxygen delivery and oxygen consumption.
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PMID:Effect of end-expiratory pressure on total oxygen dynamics. 662 64

Studies of the hemodynamic effects of nasal continuous positive airway pressure (n-CPAP) in normal subjects have had conflicting results. The largest study (n = 19) found no effect of up to 15 cm H2O on heart rate (HR), cardiac stroke volume (SV), or cardiac index. We hypothesized that n-CPAP, by increasing intrathoracic pressure, should decrease SV and cardiac output (CO) in a dose-dependent fashion in normal subjects. We also hypothesized that mouth position, i.e., open or closed, could affect intrathoracic pressure and thus SV and CO. Six normal subjects were tested with four levels of CPAP (5, 10, 15, and 20 cm H2O) under three mask conditions-face mask and nasal mask with the mouth open (mo) or with the mouth closed (mc). Noninvasive pulsed Doppler measurements of SV and HR were made under each condition. N-CPAP (mc) and face mask CPAP (f-CPAP) resulted in significant dose-dependent decreases of SV-24 +/- 5 ml (21%) and 33 +/- 5 ml (28%), respectively--from baseline to 20 cm H2O (p < 0.05). HR were unchanged and CO significantly decreased with n-CPAP(mc) and with f-CPAP, 1.6 +/- 0.38 L/min (23%) and 2.29 +/- 0.54 L/min (31%), respectively, from baseline to 20 cm H2O (p < 0.05). Esophageal pressure measurements verified increasing intrathoracic pressure with increasing levels of f-CPAP and n-CPAP (mc) but not with n-CPAP (mo). In conclusion, n-CPAP (mc) and f-CPAP resulted in significant and similar dose-dependent decreases in SV and CO.
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PMID:Hemodynamic effects of nasal and face mask continuous positive airway pressure. 800 20

In patients with severe heart failure due to acute myocardial infarction (AMI) breathing with PEEP can be of additional therapeutic value. This study was designed to assess the effects of CPAP through face mask with 15 cm H2O on left ventricular performance in AMI patients, using equilibrium radionuclide angiocardiography (ERA). In response to lung inflation, high levels of PEEP have been shown to decrease heart rate and stroke volume. The sum of the TPF pathological prolongation and the Mean-FR reduction suggests a decrease in the left ventricular compliance determined by the restriction imposed by the positive pressure. The global systolic performance is preserved.
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PMID:Evaluation of the left ventricular performance through equilibrium radionuclide angiocardiography. 890 31

There is clear evidence for obstructive sleep apnea as an independent cause of arterial hypertension. We report a case of intracranial hemorrhage with systemic hypertension resistant to antihypertensive medication, which could only be adjusted after effective treatment of coexisting sleep-disordered breathing. The 36 year old male (body mass index 31 kg/m2) was admitted to hospital three weeks before for intracranial bleeding at the left external capsule. Diagnosis of primary hypertension was made after extensive work-up in the acute hospital. Blood pressure was adjusted with five-fold antihypertensive medication at the time of admission to neurological rehabilitation, but was still elevated with "non-dipping" as determined by long-term measurement despite medications above the recommended dosages. Polysomnography confirmed the diagnosis of obstructive sleep apnea. 10 days after initiation of treatment with nasal CPAP blood pressure control was easier with normal dipping at night. Medication could be reduced during rehabilitation with further reduction after discharge. Moderate obstructive sleep apnea appears to be the cause of severe hypertension resistant to pharmacological therapy in this patient. The case underlines the impact of diagnosis and treatment of sleep-disordered breathing for the secondary prevention of stroke.
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PMID:[Obstructive sleep apnea syndrome. A probably cause of therapy refractory hypertension in intracerebral hemorrhage]. 1055 87

Thirty-six patients aged 2 months to 14 years were observed. Noninvasive assisted ventilation of the lungs (NAVL) was performed through Respironix Inc. masks (USA) with Puritan-Bennet 7200, Bear 1000, and Bear 750 respirators in the SIMV + PS, CPAP + PS modes with manual regulation of the supporting pressure level. Respiratory rate, heart rate, respiratory volume, pO2, pCO2, SpO2, stroke volume, and minute volume of the heart were evaluated. During development of central respiratory failure in the early postoperative period or in case of forced deep medicamentous neuroplegia NAVL normalized the external respiration function and promoted adequate ventilation of the lungs; in the majority of cases with development of restrictive respiratory failure (RF) it improved ventilation of the lungs and therefore no intubation of the trachea and transfer to forced ventilation was needed. NAVL is indicated as a component of multiple-modality treatment for obstructive RF.
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PMID:[Use of noninvasive assisted lung ventilation in children in intensive care units]. 1076 65

Obstructive Sleep Apnea(OSA) is associated with an increased prevalence of cardiovascular complication such as systemic hypertension, ischemic heart disease and stroke, which may lead to unexpected or early death. Sleep in patients with OSA demonstrates a pattern of recurrent arousals, hemodynamic changes, and sympathetic neural activity that have been associated with adverse carviovascular events following awakening in the morning. Neurologic problems in patients with OSA include cognitive impairment, poor memory, and high risk for cerebral infarction. These central nervous system symptoms might be due to hypoxemia and sleep fragmentations. The vascular endothelial damage, platelet aggregation, and hemodynamic changes during sleep apnea are influenced by changes in oxygen and carbon dioxide tension inducing alterations of vascular tone. The cerebral hemodynamics in relation to apneas may not only influence daytime cerebral symptoms but may also have implications for the generation of cerebrovascular disease in OSA. These changes resulted from OSA might play an important role in pathophysiological aspects of the central nervous system. And these changes will be improved after CPAP application.
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PMID:[Abnormality of blood congulation]. 1094 24

In the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of repetitive episodes of hypoxia, hypercapnea, arousals, and a striking surge in sympathetic excitation, and altered baroreflex control during sleep. Obstructive sleep apnea (OSA) may lead to the cardiac arrhythmias and myocardial ischemia and it is a possible risk factor for stroke. We confirmed that nasal CPAP has been shown to lower blood pressure in some hypertensive OSA patients. Early recognition and treatment of sleep-apnea may improve cardiovascular function.
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PMID:[Hypertension and altered cardiovascular variability associated with obstructive sleep apnea]. 1094 41

The immediate transition from positive pressure mechanical ventilation to spontaneous ventilation may generate significant cardiopulmonary hemodynamic alterations based on the mode of weaning selected, particularly in individuals with preexisting cardiac dysfunction. The purpose of this study was to compare hemodynamic responses associated with the initial transition to 3 modes of ventilator weaning (spontaneous ventilation/T-piece, pressure support [PS], and continuous positive airway pressure [CPAP]). Right ventricular hemodynamic responses were evaluated with a thermodilution pulmonary artery catheter; while left ventricular hemodynamic responses were measured by a transducer-tipped Millar catheter and conductance catheter. Two groups of canines were studied. Group 1: normal biventricular function (n = 10) and group 2: propranolol-induced biventricular failure (n = 10). Dependent variables were measured at baseline on controlled mechanical ventilation (MV) and following the initial transition to each of 3 randomized spontaneous ventilatory conditions: T-piece, PS 5 cmH2O, and CPAP 5 cmH2O. Both groups significantly increased cardiac output in response to T-piece. Right ventricular stroke work was also significantly increased with T-piece and CPAP in both groups of subjects. Left ventricular response depended on baseline ventricular function. Baseline ventricular function influenced hemodynamic response to the immediate transition from mechanical to spontaneous ventilation. There were also differential hemodynamic responses based on the ventilatory mode. Consideration of baseline cardiac function may be an important factor in the selection of an appropriate mode of spontaneous ventilation following controlled MV.
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PMID:A comparison of hemodynamic changes during the transition from mechanical ventilation to T-piece, pressure support, and continuous positive airway pressure in canines. 1123 4


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