1/10. A case of vasovagal syncope with convulsions--the effects of midodrine hydrochloride.A 42-year-old female had suffered from repeated syncope. She had vasovagal syncope with convulsions from vasodilatation and cardiac standstill which lasted for 9.8 sec. The 60 degrees head-up tilt test, nitroglycerin injection and isoproterenol infusion provoked vasovagal reaction. Although a beta blocker was not effective in preventing tilt-induced hypotension and bradycardia, midodrine hydrochloride (alpha-1 stimulant) or atropine prevented it. In this patient, insufficient constriction of capacitance vessels might have played an important role in activation of an inhibitory reflex from cardiopulmonary mechanoreceptors which caused hypotension and bradycardia.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/10. An unusual complication of coil embolization of a large coronary-pulmonary fistula.A 58-year-old man with hemoptysis was found to have a large fistula from his circumflex artery to the pulmonary system. Coil embolization was performed. This resulted in occlusion of the fistula, including a small branch likely supplying the sinus node. Following the procedure he developed junctional bradycardia but remained hemodynamically stable. He had a brief period of atrial fibrillation which, after 48 hours, reverted to a rhythm from an ectopic focus in the low right atrium. This case highlights an unusual complication of fistula embolization and emphasizes the need for caution when occluding vessels which may supply the sinus node.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/10. Parasympathetic hyperresponsiveness and bradyarrhythmias during apnoea in hypertension.Voluntary end-expiratory apnoea in a 23-year-old asymptomatic mild hypertensive patient consistently elicited bradyarrhythmias (complete heart block and sinus pause) and sympathetic activation to muscle blood vessels, indicating simultaneous sympathetic and parasympathetic activation during apnoea. The sympathetic bradyarrhythmic response to apnoea was potentiated by hypoxia and eliminated by atropine. baroreflex activation also attenuated the bradycardic response to apnoea. A 43-year-old hypertensive patient with sleep apnoea also exhibited bradyarrhythmias (sinus arrest for up to 10 s) and a fall in perfusion pressure to less than 50 mmHg during episodes of sleep apnoea. These cardiovascular changes were associated with a reduction in oxygen saturation to levels as low as 35%. Neither patient was on any medication. Simultaneous sympathetic and parasympathetic activation during episodes of apnoea may predispose to cardiovascular catastrophe. These chemoreflex mediated autonomic changes are inhibited by baroreflex activation. We propose that patients with impaired baroreflexes (patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnoea. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion and sympathetic activation during apnoea may predispose to sudden death.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/10. Sudden death caused by bradycardia and asystole in a heart transplant patient with coronary arteriopathy.The mechanism of death as a result of allograft ischemic heart disease is not well characterized. Ventricular tachycardia and fibrillation may not be the terminal events they often are in the general population. We report observations in a 41-year-old man with cardiac allograft arteriopathy who died suddenly while wearing an ambulatory monitor. The lethal rhythm was a progressive bradycardia terminating in asystole. autopsy revealed epicardial and small vessel intramyocardial, coronary arteriopathy, and only mild allograft rejection. It is our belief that ischemia caused the bradycardic sudden death. We would like to hypothesize that prophylactic permanent pacemaker implantation may prevent bradycardic sudden death and improve survival in heart transplant patients with coronary disease.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/10. Severe bradycardia following electrical cardioversion for atrial tachyarrhythmias in patients with acute myocardial infarction.bradycardia following electrical cardioversion is an uncommon complication. The present report describes three patients who developed life-threatening bradycardia following electrical cardioversion for atrial tachyarrhythmias in the setting of an acute myocardial infarction. All three patients had multivessel coronary artery disease with a totally occluded right coronary artery and a possibility of ischemic sinus node dysfunction. When electrical cardioversion is undertaken for new onset of atrial tachyarrhythmia in the setting of an acute myocardial infarction, measures for immediate, temporary pacing should be easily available.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
6/10. Enteral and intranasal treatment for vasopressor-dependent hypotension in C1 tetraplegia.A complete traumatic C1 spinal cord lesion leads to bradycardia and temporary hypotension until fluid administration can restore blood volume and pressure to the autosympathectomized capacitance vessels. In spite of adequate volume status, however, our patient required intravenous pressor agents to maintain adequate arterial and central venous pressure several weeks after injury. Using oral pseudoephedrine and occasional nasal phenylephrine, intravenous lines could be removed with maintenance of arterial pressure and resolution of bradycardia.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
7/10. Reperfusion arrhythmia: a marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction.We studied the effects of coronary recanalization on arrhythmogenesis in patients undergoing intracoronary thrombolysis during the early hours of myocardial infarction. catheterization, ventriculography, coronary angiography, and intracoronary streptokinase infusion were performed in 22 patients. Twenty-one of 22 had thrombotic total occlusion of the infarct-related transient thrombolysis with reocclusion by the end of the procedure. In 12 of these 17 patients, restoration of antegrade coronary flow was accompanied by transient arrhythmia. In these 12 patients coronary angiography within seconds of onset of arrhythmia showed vessel patency in a previously totally occluded coronary artery. Two additional patients developed arrhythmias during streptokinase infusion but after reperfusion had already been established. accelerated idioventricular rhythm was most often noted. Sinus bradycardia and atrioventricular block with hypotension occurred during restoration of flow in arteries supplying the inferoposterior left ventricle. These arrhythmias may be useful noninvasive markers of successful reperfusion during thrombolytic therapy in acute myocardial infarction.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
8/10. Coronary reperfusion and Bezold-Jarisch reflex (bradycardia and hypotension).This study reports the occurrence of bradycardia and hypotension (Bezold-Jarisch reflex) induced by myocardial reperfusion. Among 92 patients undergoing interventional catheterization for intracoronary thrombolysis in an early phase of acute myocardial infarction, left anterior descending, right coronary, and left circumflex (LC) arteries were identified as the "infarct vessel" in 44, 41, and 7 cases, respectively. The Bezold-Jarisch reflex occurred in 15 of 23 patients (65%) after right coronary recanalization and in 1 of 34 patients after left anterior descending recanalization. The reflex also was observed in 4 (22%) of 18 patients with nonoccluded or nonrecanalized right coronary arteries. The average time from onset of symptoms to right recanalization was significantly shorter (p less than 0.01) among patients in whom the reflex did not develop. atropine, postural changes, or temporary pacing, or all 3, were generally sufficient to control symptoms. The findings of this study are substantially parallel to those reported by others and confirm that reperfusion of the inferoposterior myocardium is capable of stimulating a cardioinhibitory reflex. Follow-up data available in 15 patients with occluded and recanalized right coronary arteries indicate that the occurrence of the Bezold-Jarisch reflex after reperfusion is not a reliable predictor of myocardial salvage.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
9/10. Cardiac arrest after oxymetazoline nasal spray.oxymetazoline nasal spray is a potent alpha 1-adrenergic agonist commonly used to vasoconstrict blood vessels in the nasal mucosa. In this incident, oxymetazoline nasal spray 0.025% was administered to a 2-year-old patient during general anesthesia for nasal endoscopy. Severe hypertension with reflex bradycardia progressed to sinus arrest and was successfully treated with alropine and cardiopulmonary resuscitation. Decreasing the dose of oxymetazoline and pretreatment with an anticholinergic is recommended.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
10/10. Midtrimester genetic amniocentesis of a twin gestation complicated by immediate severe fetal bradycardia with subsequent associated fetal anomalies.We present an unusual complication of midtrimester genetic amniocentesis of a monochorionic twin gestation in which prolonged fetal bradycardia of 60 to 80 beats per minute sustained over two hours was associated with multiple subsequent fetal anomalies. These included: microcephaly, bilateral closed-lip schizencephaly, duodenal atresia, and complete paresis of the left upper extremity. Etiology of the fetal bradycardia was unclear. Fetal hemorrhage was not visualized despite targeted, continued real-time ultrasonography and was therefore considered an unlikely etiology. Although the bradycardia and associated hypoperfusion could alone explain the fetal outcome, destabilization of hemodynamics of a communicating vessel, resulting in a possible (although unproven) acute twin-twin transfusion induced at the time of amniocentesis due to decreased intra-amniotic pressure in association with a velamentous umbilical cord insertion could have led to this unusual occurrence.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
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