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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proximal aortic dissection is frequently associated with cardiac tamponade. The treatment sometimes is difficult. We present a 69-year-old female patient who after repeated episodes of syncope received an open drainage of pericardial effusion that ended in a fatal outcome. She was also known to have mural thrombi in the aorta. However, preanesthetic trransesophageal echocardiography revealed besides pericardial effusion, also dilatation of aortic root which compressed both atria. She developed sudden cardiovascular collapse following drainage of pericardial effusion to which she succumbed in spite of vigorous resuscitation. We suggest that the patients with cardiac tamponade complicated by aortic dissection must receive direct aortic repair together with intraoperative pericardial drainage. Selective or single pericardiocentesis should better be avoided.
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PMID:Acute cardiovascular collapse after pericardial drainage in a patient with aortic dissection. 1586 3

The Paleolithic-Threat hypothesis reviewed here posits that habitual efferent fainting can be traced back to fear-induced allelic polymorphisms that were selected into some genomes of anatomically, mitochondrially, and neurally modern humans (Homo sapiens sapiens) in the Mid-Paleolithic because of the survival advantage they conferred during periods of inescapable threat. We posit that during Mid-Paleolithic warfare an encounter with "a stranger holding a sharp object" was consistently associated with threat to life. A heritable hardwired or firm-wired (prepotentiated) predisposition to abruptly increase vagal tone and collapse flaccidly rather than freeze or attempt to flee or fight in response to an approaching sharp object, a minor injury, or the sight of blood, may have evolved as an alternative stress-induced fear-circuitry response. Such a stable (balanced) polymorphism for the hemodynamically "paradoxical" flaccid-immobility in response to these stimuli may have increased some non-combatants' chances of survival. This is consistent with the unusual age and sex pattern of fear-induced fainting. The Paleolithic-Threat hypothesis also predicts a link to various hypo-androgenic states (e. g. low dehydroxy-epiandrosterone-sulfate. We offer five predictions testable via epidemiological, clinical, and ethological/ primatological methods. The Paleolithic-Threat hypothesis has implications for research in the aftermath of man-made disasters, such as terrorism against civilians, a traumatic event in which this hypothesis predicts epidemics of fear-induced fainting.
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PMID:The human fear-circuitry and fear-induced fainting in healthy individuals--the paleolithic-threat hypothesis. 1594 75

The use of automated external defibrillator (AED) by persons other than paramedics and emergency medical technicians is advocated by several US- and European organizations. However, at the present time it is still unclear to identify public places with a high incidence of out-of-hospital cardiac arrest. There are few data on the potential impact of public access defibrillators on survival after out-of-hospital cardiac arrest in sporting arenas or water parks. Therefore, we studied prospectively incidence of out-of-hospital cardiac arrest in the LAGO-die Therme in Herne. This is one of the most important swimming parks in Europe and member of the European Waterpark Association EWA. Eight AEDs were placed in the waterpark LAGO-die Therme. The locations where the defibrillators were stored were chosen to make possible a target interval of 60 seconds from collapse to first defibrillation. Twenty waterpark officers were instructed in cardiopulmonary resuscitation and in the use of the AED. During November 16, 2001 and December 31, 2004, 2.05 Mio. visitors were counted in the LAGO. Out-of-hospital cardiac arrest occurred in none of them. AED were used in two visitors with non arrhythmogenic syncope, no shock was delivered. Questionaires were done in 588 visitors (336 males, 252 females, mean age 38+21 years) in 2002 and in 579 visitors (322 males, 257 females, mean age 37+/-25 years) in 2004. In 2002, 77% of the visitors noticed the AED and, therefore, 49% performed more sporting activities. In addition, in 2004, AED was noticed by 480 visitors (83%) and 277 visitors (48%) did more sporting activities. There were no significant differences between 2002 and 2004 (p=ns). Despite no out-of-hospital cardiac arrest in the waterpark during the 3 year follow- up, it seems reasonable to install AED in sporting places with thousands of visitors per year.
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PMID:[First responder defibrillation in the LAGO-die Therme--results and experiences]. 1599 57

Mutations in the cardiac ryanodine type 2 receptor (RyR2) gene are associated with catecholaminergic polymorphic ventricular tachycardia. We hypothesized that these mutations could be detected at autopsy in cases of exercise-triggered sudden death. Fourteen sudden death patients, eight males and six females, were studied at autopsy based on apparent sudden cardiac death, without significant anatomical abnormalities. The coding regions of arrhythmia genes were amplified by polymerase chain reaction and directly sequenced. Three novel RyR2 mutations, R414C, F2331S, and R2401L, were identified in three unrelated patients (two males and one female; mean age at death, 12 +/- 2 years), all performing strenuous activity at the time of death or collapse. These mutations were located in highly conserved regions where arrhythmia-linked RyR2 mutations clustered. Although G269S in the KVLQT1 gene was detected in a female with known family history of syncope and sudden cardiac death, no other mutations were found in any of the 14 cases, and no other mutations was found in 200 controls. The absence of structural cardiac disease in physical activity-induced sudden death and the finding of three novel RyR2 mutations suggest that mutation screening in such cases should include RyR2.
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PMID:Identification of novel missense mutations of cardiac ryanodine receptor gene in exercise-induced sudden death at autopsy. 1643 35

In patients with neurocardiogenic syncope, head-up tilt often evokes acute loss of consciousness accompanied by vasodilatation, increased plasma adrenaline and systemic hypotension. Since hypotension increases adrenaline levels and adrenaline can produce skeletal muscle vasodilatation by activating beta2 receptors, adrenaline might induce a positive feedback loop precipitating circulatory collapse. We hypothesized that propranolol, a non-selective beta-blocker, would prevent adrenaline-induced vasodilatation and thereby prevent syncope. Eight subjects with recurrent neurocardiogenic syncope and previously documented tilt-induced syncope with elevated plasma adrenaline levels participated in the present study. Subjects underwent tilt table testing after receiving oral propranolol or placebo in a double-blind randomized crossover fashion. Haemodynamic and neurochemical variables were measured using intra-arterial monitoring, impedance cardiography, arterial blood sampling and tracer kinetics of simultaneously infused [3H]noradrenaline and [3H]adrenaline. The occurrence of tilt-induced neurally mediated hypotension and syncope, duration of tilt tolerance, extent of the decrease in SVRI (systemic vascular resistance index) and magnitude of plasma adrenaline increases did not differ between the propranolol and placebo treatment phases. SVRI was inversely associated with fractional increase in plasma adrenaline during both phases. One subject did not faint when on propranolol; this subject's response is discussed in the context of central effects of propranolol. In this small, but tightly controlled, study, propranolol did not prevent tilt-induced vasodilatation, syncope or elevated plasma adrenaline.
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PMID:Failure of propranolol to prevent tilt-evoked systemic vasodilatation, adrenaline release and neurocardiogenic syncope. 1684 62

Vasovagal syncope is a common cause of sudden collapse. It results from inappropriate activation of left ventricular mechanoreceptors causing sudden vasodilation with bradycardia. Tilt testing is an inexpensive and non-invasive way of establishing a vasovagal diagnosis in unexplained syncope. If critical care nurses improve their understanding of the pathophysiology of vasovagal syncope and the procedure of tilt testing, their care of syncopal patients will be enhanced. This literature review discusses the pathophysiology and clinical presentation of vasovagal syncope. The procedure of tilt testing is explained and the treatment of vasovagal syncope is briefly reviewed.
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PMID:Tilt testing for syncope. 1694 8

Up till now, the presence of wave reflection of pressure and flow waves was not considered in studies on the cerebral circulation. This study tested the hypothesis whether the typical changes in cerebral blood flow velocity (CBFV) seen in patients during vasovagal syncope can be explained by the emergence of a wave reflection site in the cerebrovascular vessels. Continuous recordings of peripheral blood pressure (ABP, by Finapres) and CBFV (by transcranial Doppler) of 20 control subjects and 10 patients with syncope during tilt table testing were analyzed. Wave reflection analysis (WRA) consisted of a multivariate regression analysis with CBFV as dependent variable and simultaneous ABP as well as delayed ABP (by systematically varied time lags) as independent variables. The time delay yielding the best prediction of CBFV was interpreted as the reflection time. A univariate regression analysis with only simultaneous ABP as independent variable served as control method. In patients and controls CBFV during supine position could be explained sufficiently (explained variance=88-90%) by univariate regression without improvement by WRA. During syncope, multivariate regression improved the prediction of CBFV (explained variance=58% with univariate and 77% with multivariate regression) in 9 of 10 patients. The mean reflection time was 160 ms. The results can be explained by a collapse of the distal bridging veins during systemic hypotension giving rise to a pressure wave moving backward with a resulting distortion of the flow wave. In particular, the WRA model could account for the characteristic changes in the diastolic flow shape during syncope.
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PMID:Wave reflection analysis of the human cerebral circulation during syncope. 1697 26

Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPs) > or = 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPs, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPs was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPs was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPs and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension.
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PMID:Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. 1819 19

Vasovagal syncope refers to a reflex cardiovascular depression that gives rise to loss of consciousness with bradycardia and profound vasodilatation. This response commonly occurs during regional anesthesia, hemorrhage or supine inferior vena cava compression in pregnancy. The changes in circulatory response from the normal maintenance of arterial pressure to parasympathetic activation and sympathetic inhibition may cause severe hypotension. This change is triggered by reduced cardiac venous return as well as episodes of emotional stress, excitement or pain. Occasionally, these vasovagal responses may be unpredictable and may dramatically proceed to asystole with circulatory collapse, and may even result in death. In these circumstances, hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilatation. Regional anesthesia, decreased venous return, hemorrhage and abnormal fetal presentation cumulatively increase the risk of vasovagal syncope in cesarean section patients. When a vasovagal response occurs, ephedrine is the drug of first choice because of its combined action on the heart and peripheral blood vessels. Epinephrine must be used early in established cardiac arrest, especially after high regional anesthesia.
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PMID:Perioperative vasovagal syncope with focus on obstetric anesthesia. 1717 65

A previously asymptomatic 15-year-old boy was treated at our institution after an episode of chest pain, palpitation, and syncope while playing in a high school soccer game. The patient's resting electrocardiogram was normal. A transthoracic echocardiogram showed an anomalous left main coronary artery originating from the right sinus of Valsalva. Contrast-enhanced multidetector computed tomography demonstrated clearly that the anomalous vessel coursed between the aorta and the pulmonary trunk (interarterial subtype). Treadmill testing registered several nonsustained polymorphic ventricular tachycardias and transmural myocardial ischaemia in the early recovery phase (ST-elevation up to 5mm in CM5 and V2 leads). The patient underwent bypass grafting. One year later, he remains asymptomatic, and new treadmill tests have been normal. In this patient, severe transmural myocardial ischaemia was detected, possibly due to collapse or vasospasm of the anomalous vessel, triggering life-threatening ventricular arrhythmias.
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PMID:Anomalous coronary artery causing transmural ischaemia and ventricular tachycardia in a high school athlete. 1735 80


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