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

The euthyroid sick ("low T3") syndrome occurs in circulatory collapse and could influence survival. To evaluate the role of T3 and rT3 in shock, 36 mongrel dogs were subjected to hemorrhagic shock. In 13 dogs 15 micrograms/kg of T3 was given after 60 min of hypotension and 15 micrograms/kg of rT3 was administered IV 30 min before hemorrhage in 10 dogs. An equal volume of saline was injected in 13 dogs for control study. These dogs were bled rapidly into a reservoir to a mean arterial pressure (MAP) of 40 mmHg. After 60 min of hypotension the reservoir line was clamped for 30 min. The shed blood was then reinfused over 30 min. T3 administration caused significant increases during the clamped period in cardiac output, stroke volume, MAP, right and left ventricular stroke work and systemic vascular resistance, with a decrease in pulmonary vascular resistance (PVR). In the group receiving rT3 the only significant hemodynamic-metabolic differences were PVR and mean arterial pH. In the control group, 6 of 13 dogs died, whereas 9 of 10 dogs given rT3 died (p less than 0.03) and only one of 13 T3 dogs died (p less than 0.05). This study strongly suggests that T3 improves survival by acting on cardiovascular receptors or via the hypothalamic-pituitary-thyroid axis and that exogeneous rT3 is detrimental during the stress of shock and may play a biologically causative role in the sick euthyroid syndrome.
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PMID:[The effect of triiodothyronine (T3) and reverse triiodothyronine (rT3) on canine hemorrhagic shock]. 320 Feb 34

To assess the dose-response effects of isoflurane and halothane anesthesia on hemodynamics and coronary artery reactivity, the authors studied myocardial hyperemic responses following brief single artery flow arrests in 21 open chest, isocapnic swine in which arterial blood pressures and cardiac outputs were recorded. A specially designed Doppler probe was used to measure the peak and time course of coronary blood flow velocity in the left anterior descending coronary artery (LAD) after 15-s LAD occlusions. The ratio of peak velocity of blood flow to resting velocity (coronary reserve), relative repayment of flow debt, and duration of hyperemic responses were studied. Surgery was performed at MAC end-tidal concentrations ([Et]isoflurane = 1.45%. [Et]halothane = 1.25%) of isoflurane (n = 7) or halothane (n = 7), and recordings were made after 15-min steady state [Et]agent at 0.5, 1, 1.25, 1.5, 1.75, 2 MAC, and further 0.5 MAC increments until the demise of each animal. To compare coronary reactivity at similar coronary pressures, an aortic snare was used to elevate arterial pressures in a third group of halothane anesthesized pigs (n = 7) to those in the previously studied isoflurane group at each MAC level. There were three major differences between halothane and isoflurane. First, cardiac depression (reduction in arterial pressure, cardiac output, and stroke volume) was less with isoflurane compared with halothane anesthesia. Second, with halothane anesthesia, there was a marked decrease in coronary reactivity independent of coronary perfusion pressures with marked, dose-dependent reductions in both coronary reserve and relative flow repayment. During isoflurane anesthesia, coronary reactivity and coronary reserve was well preserved within physiologic limits up to 1.75 MAC [Et]. Third, halothane anesthesized pigs died in cardiac collapse at much lower agent concentrations than with isoflurane (no animals survived 1.75 MAC halothane, whereas all animals survived 2.5 MAC isoflurane). Therefore, pigs anesthesized with isoflurane had greater coronary reserve, better preserved cardiac function, and greater tolerance to increasing agent concentration than pigs anesthesized with halothane.
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PMID:Comparative coronary vascular reactivity and hemodynamics during halothane and isoflurane anesthesia in swine. 334 77

The experimental and early clinical experience with percutaneous valvuloplasty using trefoil and bifoil balloon catheters (Schneider Shiley) and a long introducer sheath with a new back-up wire are reported. The trefoil balloon consists of three and the bifoil balloon of two angioplasty balloons mounted in parallel on a single catheter. Inflated, they form a rosette allowing for some blood flow through the spaces between the individual balloons. These small balloons are more pressure tolerant than one large balloon. The hemodynamic advantage of these balloons compared to single balloons could be demonstrated in animal experiments (healthy valves and surgically created stenoses). In 31 consecutive patients with trefoil-bifoil balloon valvuloplasty, there was no inhospital mortality. The results of trefoil valvuloplasty in twelve patients with pulmonary stenosis compared favorably to those of patients treated with single balloons. There were no technical failures or complications. There were two unsatisfactory results (severely dysplastic valve). In the aortic valve, the results with calcified stenoses were satisfactory at first but disappointing during follow-up. There were no technical failures but one of nine patients suffered an embolic myocardial infarction. In the mitral valve, there were two failures (one deficient equipment, one stroke during balloon positioning). In one case, insufficient balloon size led to an inadequate result. One patient needed surgical drainage for a pericardial tamponade. In two patients, mitral regurgitation was significantly increased. A 17F long sheath was developed to further facilitate balloon valvuloplasty. It guides the balloon catheter across the valve (and across the septum in case of the mitral valve), stabilizes it during inflation, and serves as a second pressure line to continuously monitor the transvalvular pressure gradient. It prevents bleeding at the puncture site during the intervention and presumably reduces the trauma to the artery. Because of its thrombogenic potential, heparinization of the patients is essential. The largest balloon accepted by the sheath is a 2 X 19 bifoil balloon which was the reason to use a bifoil balloon in some mitral valves. Trefoil balloons put in place through a long sheath provide some theoretical advantages over conventional single balloons introduced over guidewires that need to be evaluated by larger clinical studies. Although they do not prevent circulatory collapse during initial inflation in tight stenoses, they permit transvalvular flow when fully unfolded.
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PMID:Valvuloplasty with trefoil and bifoil balloons and the long sheath technique. 337 40

Improvements in mechanical support for profound circulatory collapse have resulted in increasing survival of these critically ill patients. Since 1980, 27 patients aged 3 days to 69 years (mean 34.9 years) who required mechanical circulatory assistance have been followed up after discharge from the hospital. The refractory cardiogenic shock necessitating mechanical support occurred postoperatively in 22 patients (coronary artery bypass in nine, valve replacement in four, correction of congenital heart defects in nine) and with end-stage cardiomyopathy in five. Fourteen patients were supported with a Pierce-Donachy ventricular assist device (left ventricular assist in seven, right ventricular assist in three, both in four); nine were supported with extracorporeal membrane oxygenation, two with a Medtronic centrifugal left ventricular assist pump, one with biventricular Biomedicus pumps, and one with a Novacor left ventricular assist system. The duration of support ranged from 8 hours to 91 days with a mean of 3.5 days in patients supported for postoperative shock. Major complications occurred in 18 patients (67%), including bleeding that necessitated operative exploration in 14, serious infection in five, renal failure in two, and stroke in two. The five patients with cardiomyopathy underwent cardiac transplantation. The remaining 22 patients who had postoperative cardiogenic shock were weaned from support. There have been four late deaths: two cardiac related at 6 months and two of cancer at 46 and 53 months (one patient was in New York Heart Association class I and the other in class II before death). The remaining 23 survivors have been followed up for 3 to 79 months (mean 29 months) and at last examination 17 (74%) were in class I, two (9%) were in class II, three (13%) were in class III, and one (4%) was in class IV. Eight patients are employed full time, three are retired, four attend school, three are in preschool, one is a housewife, and one is unemployed but free of symptoms. Only four patients have significant cardiac disability, and one of these still works. In conclusion, mechanical circulatory assistance allows adequate support to permit satisfactory long-term survival in patients with refractory cardiogenic shock.
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PMID:Follow-up of survivors of mechanical circulatory support. 338 94

1. Although heat stroke is a frequent cause of death in both humans and animals as a result of climatic or exercise-imposed stress, underlying mechanisms are understood poorly. In order to develop more effective strategies for prevention and treatment of this cause of death and suffering, controlled experiments were conducted on a small number of sheep to examine cardiovascular involvement in the thermoregulatory failure of heat stroke. 2. Sheep were studied in a hot environment at rest and then during exercise until collapse. 3. With exercise, mean arterial pressure (MAP) increased slightly, cardiac output (CO) increased markedly and total peripheral resistance (TPR) decreased slightly. As collapse was imminent, MAP increased but CO and TPR did not change significantly. On collapse, MAP and TPR increased markedly and CO decreased markedly. 4. Radioactive microsphere measurements demonstrated during exercise a redistribution of blood flow (BF) away from abdominal viscera and torso skin, to muscles involved in exercise, respiratory muscles, myocardium, fat, limb skin and nasobuccal tissues. With progressively increasing heat stress and exercise, BF increased in exercise muscles and decreased in limb skin and fat. As collapse was imminent, there were sharp increases in BF in exercise muscles, brain and spinal cord. On collapse, BF decreased markedly in exercise and respiratory muscles and fat. 5. It is concluded that collapse and ultimately heat stroke are not due primarily to cardiovascular 'failure' but, rather, to consequences of high body temperatures resulting from thermoregulatory failure attributable to demands for blood pressure regulation dominating requirements for body temperature regulation.
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PMID:Circulatory changes associated with heat stroke: observations in an experimental animal model. 344 49

All resuscitation attempts outside hospital attended by the Auckland life support unit ambulances during 1983 were reviewed. There were 405 attempted resuscitations during the 12 month period. Of the 344 patients who arrested before the life support unit arrived, 189 (55%) had cardiopulmonary resuscitation initiated by bystanders and 34 (10%) by conventional ambulance personnel. Sixty one patients suffered their arrest after the arrival of the life support unit. One hundred and ninety two patients (47% of the total 405 patients) died at the scene of collapse, 95 patients (24%) died in accident and emergency departments and 46 (11%) died in hospital. Eighteen of the 213 patients successfully resuscitated and transported to hospital had complications related to cardiopulmonary resuscitation. Of the 72 patients discharged, 65 (90%) were alive one year after discharge. Of all patients in whom resuscitation was attempted, 75% were males. This male predominance was present in all age groups and disease categories except subarachnoid haemorrhage and stroke. Myocardial infarction and other ischaemic heart disease accounted for the great majority of cases, followed by asthma and a variety of other conditions. Below 30 years of age the causes of collapse were predominantly noncardiac, and with age increasing above 30 years there was increasing likelihood of a cardiac cause for the collapse.
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PMID:Resuscitation outside hospital in Auckland. 346 71

Six athletes were examined immediately after collapsing from heat stroke during exercise, and then followed for several weeks. At the time of collapse most of the patients were sweating profusely, their rectal temperatures being more than 42 degrees C. All recovered within a few hours. The renal function was not disturbed more than expected during heavy exercise, serum levels of liver enzymes were, however, increased for several weeks. Electrolyte homeostasis was undisturbed but for a transient hypercalcemia that can not be fully explained. The marked increments in plasma levels of catecholamines, vasopressin and renin were as expected after heavy exercise. We conclude that as heat stroke presents as a continuum of clinical pictures, biochemical evidence of liver cell injury is a sensitive and important parameter for the diagnosis.
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PMID:Heat stroke in endurance exercise. 353 1

Eighty experiments were performed with nine awake dogs to study the changes of phasic-pleural pressure with exercise. The increased minute volume with exercise was obtained by more frequent pleural pressure swings and by a substantial extension of the pressure swings in both directions. The cyclic changes of stroke volume following the pressure swings support the hypothesis that alterations of pleural pressure affect the stroke volume and can act, if necessary, as a secondary pump for the circulation. Mean pleural pressure during exercise fell by 2.5 cm H2O from the rest value of 12.1 cm H2O. The absolute right atrial pressure during exercise (-2.69 mm Hg) was not different from that at rest (-2.39 mm Hg). However, the transmural right atrial pressure of 7.6 mm Hg during exercise was higher than the pressure of 6.2 mm Hg at rest because during exercise the right atrium was perfused by 38% higher blood flow than that at rest. The phasic pattern of right atrial pressure shows that there is good reason to assume that during inspiration the extrathoracic veins are collapsed at their entrance into the chest, but this collapse is removed during expiration. There is no reason to assume an effective, sustained collapse of extrathoracic veins. Rather we can visualize a rhythmical change of flow in extrathoracic veins from transient limitation to transient acceleration.
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PMID:Changes of phasic pleural pressure in awake dogs during exercise: potential effects on cardiac output. 366 49

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.
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PMID:Hemodynamics of hemorrhage in the conscious rat and chicken. 377 12

The hemodynamic effects and ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity after partial inferior vena cava occlusion were investigated in anesthetized dogs (n = 12). Partial occlusion of the inferior vena cava resulted in a 12% decrease in mean arterial pressure, a 62% decrease in cardiac output, a 66% decrease in stroke volume, and a 135% increase in systemic vascular resistance. Bupivacaine, 20 mg/kg intravenously, resulted in cardiovascular collapse in all animals. The resuscitation time for animals without partial caval occlusion was 2.1 +/- 0.5 min, whereas that for animals with partial caval occlusion was 22.2 +/- 6.9 min (P less than 0.05). Significantly increased amounts of epinephrine and NaHCO3 were required to resuscitate the animals with caval occlusion. We conclude that partial inferior vena cava occlusion can significantly alter the ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity.
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PMID:Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion. 395 8


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