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

The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5-75 micrograms/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.
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PMID:The immediate haemodynamic and electrophysiological response to prenalterol during fixed rate pacing in patients with chronic ischaemic heart disease. 395 93

This study was carried out in order to investigate possible side-effects of thoracic epidural morphine on cardiac electrophysiology, haemodynamics and metabolism. In pentobarbital-anaesthetized dogs, intracardiac conduction times were determined by His bundle electrography, and refractoriness by programmed electrical stimulation; monophasic action potential recordings were obtained from the right ventricle by the suction electrode technique. Cardiac output, left ventricular and aortic blood pressures were measured, as well as plasma concentrations of morphine, free fatty acids, glycerol, glucose and lactate. Thoracic epidural morphine (0.12 mg X kg-1) reduced spontaneous heart rate, prolonged atrioventricular nodal conduction time and refractoriness, and reduced left ventricular dP/dt max. Bilateral vagotomy reversed these effects. Intra-atrial, His Purkinje and intraventricular conduction times, atrial and ventricular refractoriness and action potential duration, stroke volume and mean aortic blood pressure, as well as the metabolic variables, were not significantly influenced by thoracic epidural morphine with or without vagotomy. Peak plasma morphine levels of 12-25 ng X ml-1 were measured 10 min after morphine injection. In conclusion, this study demonstrates depressive side-effects of epidural morphine on cardiac function, mediated by an increased vagal activity.
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PMID:Cardiac effects of thoracic epidural morphine caused by increased vagal activity in the dog. 396 75

In a prospective randomized study of treatment for early-stage Hodgkin's disease presenting above the diaphragm, 76 patients had staging by laparotomy (Group I) and 28 had staging by closed techniques (Group II). Treatment consisted of involved-field radiotherapy alone (44 patients), involved-field radiotherapy followed by chemotherapy (38 patients), total nodal radiotherapy alone (15 patients), or total nodal radiotherapy followed by chemotherapy (seven patients). On presentation, both groups had similar clinical features and similar treatment distribution. With similar follow-up (87 months), no significant differences in remission or survival were observed between Groups I and II: remission 59 versus 68 percent; survival 74 versus 92 percent; p value 0.27 and 0.09, respectively. Multiple areas of relapse were more frequently observed in Group I (11 of 32 had relapse) as compared with Group II (none of nine had relapse, p less than 0.082). In Group I, relapse in the abdomen was observed as an isolated event or as part of disseminated relapse in 12 percent of patients compared with 3 percent (one patient) in Group II with abdominal relapse alone. Seven patients in Group I and two patients in Group II died with Hodgkin's disease. Six other patients in Group I died with complete remission of non-Hodgkin's lymphoma (one patient), leukoencephalopathy (one patient), sepsis during chemotherapy (two patients), myocardial infarction (one patient), and cerebrovascular accident (one patient). Three other patients in this group had other secondary malignancies successfully controlled (histiocytic lymphoma, squamous cell carcinoma of the cervix, and malignant schwannoma). No second primary lesions or death with complete remission were observed in Group II. Staging laparotomy with splenectomy in early-stage Hodgkin's disease did not improve the duration of remission or survival or decrease the number of abdominal relapses compared with closed staging.
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PMID:Staging laparotomy and splenectomy in early Hodgkin's disease. No therapeutic benefit. 638 Feb 86

The haemodynamic and electrophysiologic responses to rapid intravenous injection of digitoxin (0.6 mg over 5 min) were measured in 6 patients with chronic coronary heart disease without clinical heart failure. Two minutes after end of injection peripheral resistance increased and stroke volume fell, while peak dP/dt in the right ventricle showed minimal increase. AV nodal conduction velocity decreased markedly. Thereafter, the peripheral resistance remained unchanged, stroke volume and peak dP/dt in the right ventricle increased slightly, while AV conduction remained stable. In 2 control patients stable values were found during 60 min. We conclude that digitoxin given intravenously as a single bolus injection induces an abrupt slight increase in peripheral resistance. Thereafter, a gradual increase in inotropy is found. The effect on the AV node appears rapidly and remains stable.
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PMID:Effect of intravenous digitoxin on inotropy, haemodynamics and P-Q interval in ischaemic heart disease. 648 88

Hypotension and shock associated with heart block and other forms of atrioventricular (AV) dissociation frequently accompany right ventricular infarction ( RVI ). Such patients do not invariably improve with ventricular pacing. We evaluated the relative effects of AV dissociated rhythms (ventricular pacing or nodal rhythm) and AV synchronous rhythms (atrial pacing, AV sequential pacing, or return to normal sinus rhythm) in seven patients with RVI complicated by AV dissociation, who had hypotension or shock. Hemodynamic monitoring demonstrated the characteristic features of RVI in all patients. Restoration of AV synchrony resulted in a highly significant (p less than or equal to 0.001) increase in systolic blood pressure (88.0 +/- 16.5 mm Hg to 133.0 +/- 21.8 mm Hg), cardiac output (3.8 +/- 0.9 L/min to 5.7 +/- 0.9 L/min), and stroke volume (40.5 +/- 6.9 cc to 61.0 +/- 10.0 cc). We conclude that restoration of normal AV synchrony has a marked effect on stroke volume in this setting and that atrial or AV pacing can reverse hypotension and shock in RVI complicated by AV dissociation.
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PMID:Reversibility of hypotension and shock by atrial or atrioventricular sequential pacing in patients with right ventricular infarction. 673 Dec 82

In nine patients (pts.) with recurrent SVT, we have performed a combined electrophysiological and hemodynamic study. Five pts. showed reciprocating nodal tachycardia and 4 pts. reentry tachycardia associated with WPW syndrome (2 with Kent bypass tract and 2 with James bypass tract). Hemodynamic parameters were recorded during sinus rhythm (SR), atrial (AP) and ventricular pacing (VP) and following the initiation of SVT. The arrhythmia was induced by rapid atrial pacing or with atrial or ventricular premature stimuli. Hemodynamic data were then compared. Our results point out a greater hemodynamic deterioration during SVT than during AP or sinus tachycardia at similar rates. We have often observed in SVT, and constantly in A-V nodal reentrant (AVN) cases, the appearance of giant waves in the right and left atrium. This finding confirms hypothesis of the primary role of the changes in atrioventricular contraction sequence during SVT, especially in AVN tachycardias, with subsequent reduction in stroke volume and cardiac output.
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PMID:Hemodynamic changes induced by supraventricular tachycardia. 715 84

Diltiazem (DT), a potent slow channel blocker, has been found to be clinically useful for treatment of coronary vasospasm, hypertension, and tachyarrhythmias. Nevertheless, only limited data are available on the hemodynamic and electrophysiologic effects of DT. Atrial, His, right ventricular apex, aortic, and Swan-Ganz thermodilution catheters were used in 10 anesthetized dogs, and recordings were made during control period and after each of four infusions of DT (0.01, 0.02, 0.04, and 0.08 mg/kg/min) each lasting 30 minutes. Results showed that heart rate, pulmonary capillary wedge pressure, stroke volume, and HV interval did not change significantly. However, two dogs had second-degree AV block and a third had escape junctional rhythm during DT 0.08 mg/kg/min. Mean aortic pressure (AP), corrected sinus node (SN) recovery time, and systemic vascular resistance (SVR) were significantly reduced, whereas AH interval, AV functional and effective refractory periods were prolonged by DT. AV nodal refractory periods and AH interval were the only parameters significantly affected at DT 0.02 mg/kg/min. SN recovery time was significantly shortened at DT 0.04 mg/kg/min, whereas AP and SVR tell significantly at DT 0.08 mg/kg/min. DT had significant electrophysiologic effects at low doses, whereas hemodynamics were significantly altered only at high doses. Further, major electrophysiologic effects were on the AV node with lesser effects on SN function. Therefore, at a dose when antiarrhythmic effects are evident, the safety of diltiazem is corroborated by lack of adverse hemodynamic effects.
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PMID:Electrophysiologic and hemodynamic actions of diltiazem: disparate temporal effects shown by experimental dose-response studies. 721 68

Using non-invasive methods, haemodynamic responses to antagonism of pancuronium (Pc) and alcuronium (Ac) block were compared in patients anaesthetized with thiopental-N2O-fentanyl and undergoing minor surgery. Neuromuscular block (90%) was maintained with Pc in 10 patients and Ac in 10 patients. After surgery, atropine 0.015 mg kg-1 and neostigmine 0.03 mg kg-1 (AN) were given simultaneously. The rate of reversal of the block was equal in the two groups. Between 4 and 16 min after AN, the decrease of heart rate (HR) was more pronounced in patients who had received Pc. The mean of the lowest HR was 43.2 beats min-1 in the Pc group, compared with 62.0 beats min-1 in the Ac group. The bradycardia was associated with a moderate decrease in arterial pressure in patients treated with Pc. However, due to an increase in stroke volume, mean cardiac output (CO) was not lower in the Pc group. Some patients treated with Pc developed a temporary nodal rhythm after AN and this was associated with a considerable decrease in CO. It is concluded that, in spite of marked bradycardia during antagonism of Pc block, circulation is well maintained, provided that sinus rhythm is present.
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PMID:Haemodynamic responses to antagonism of pancuronium and alcuronium block. 729

In the treatment of refractory ventricular tachyarrhythmias antiarrhythmic drugs must sometimes be combined. An electrophysiologically appropriate combination is lignocaine and procainamide and, when needed, a beta-blocking agent. The hemodynamic effects of this treatment were studied in 6 patients in the acute phase of myocardial infarction. After a control period, an infusion of lignocaine was started and 1 h later procainamide/placebo was added in a double-blind system and finally also practolol/placebo. The drugs were given intravenously in ordinary doses. Hemodynamics were studied by bedside catheterization. During triple treatment heart rate and aortic pressures fell significantly whereas right atrial mean pressure increased compared to the control period. Stroke volume, cardiac output and pulmonary artery pressures were unchanged. Most of the changes appeared when practolol was added. Following the procainamide injection a transient fall in aortic pressures was noted. Lignocaine gave no hemodynamic effects. The number of ventricular premature beats was reduced in all patients and no patient had ventricular tachycardia during treatment. In these patients it was possible to combine lignocaine, procainamide and practolol in the acute phase of myocardial infarction. However, 3 patients developed hypotension, 1 sinus bradycardia and 1 had a short run of nodal tachycardia. It is concluded that this kind of combined treatment, because of its potential risks, should be restricted to critical clinical situations and then it ought to be hemodynamically controlled.
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PMID:Hemodynamic effects of combined treatment with lignocaine, procainamide and practolol in acute myocardial infarction. 738 52

Atrial fibrillation affects approximately one million persons in the United States, making it the most common cardiac arrhythmia seen in clinical practice. Its prevalence increases with age, and occurs in up to 10% of the population in the eighth decade of life. Unlike coronary heart disease, atrial fibrillation affects men and women approximately equally and, in an increasingly elderly population, will become an increasing burden to the health care system. The management of atrial fibrillation has undergone significant change in recent years. Large randomized controlled trials have shown that anticoagulation markedly reduces the risk of stroke, and a number of new antiarrhythmic agents are available for the restoration and maintenance of sinus rhythm. Furthermore, physicians have become more aware of the potential proarrhythmic side effects of all antiarrhythmic drugs. Finally, new procedures such as radiofrequency ablation of the atrioventricular junction and permanent pacing are playing increasing roles in the management of this arrhythmia. In this review, the identification of underlying causes and/or precipitating factors of atrial fibrillation, methods to control the ventricular response with atrioventricular nodal blocking drugs, the questions of whether restoration of sinus rhythm is a possible or desirable goal and how best to maintain sinus rhythm, should sinus rhythm be restored, and the importance of long-term anticoagulation with warfarin or antiplatelet therapy with aspirin are discussed.
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PMID:The management of atrial fibrillation. 921 52


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