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Query: UMLS:C0034065 (pulmonary embolism)
14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postmortem chest roentgenograms in approximately 3,500 cases of a random autopsy population were reviewed. Pneumothorax was found in 77 cases (2.2%). Simple pneumothorax was present in 38 cases, and tension pneumothorax or combined simple and tension pneumothorax was present in 39 cases. Only 40 of the 77 patients had been clinically diagnosed as having pneumothorax. Pulmonary conditions most often present in cadavers with pneumothorax were bacterial pneumonia, pulmonary emphysema, and pulmonary embolism, with or without infarcts and infarct abscesses. Procedures most frequently associated with pneumothorax were mechanical ventilation and attempts at cardiorespiratory resuscitation. Rib fractures (iatrogenic and noniatrogenic) were found in 23 of the 77 cases.
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PMID:Pneumothorax in a large autopsy population. A study of 77 cases. 69 69

Electromechanical dissociation (EMD) may be primary, due to disease of the heart muscle itself, or secondary to alterations in loading conditions of the heart. Factors such as internal hemorrhage, acute cardiac tamponade, tension pneumothorax, acute pulmonary embolism, and inflow or outflow obstructions of the heart may be responsible for changes in loading. Myocardial ischemia, myocardial depressant overdose, and other conditions may also contribute to secondary EMD. If detected early, these secondary forms of EMD may respond to treatment. Drugs for resuscitation of a patient with EMD include epinephrine, atropine sulfate, and, in selected instances, calcium.
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PMID:Electromechanical dissociation. Treatable causes of a dire cardiac emergency. 194 21

Clinical presentation of aortic dissection is similar to that of acute myocardial infarction (AMI). Clinical differential diagnoses from lethal chest pain in emergency department include AMI, aortic dissection, pulmonary embolism, tension pneumothorax, etc. Thrombolytic therapy for recanalization of thrombotic occluded coronary artery in AMI must be considered, but it is absolutely contraindicated for aortic dissection. However, AMI secondary to aortic dissection is a rare condition, which might be caused by compression of the coronary arteries by a hematoma or extension of the dissection into the coronary arterial wall. Surgery is the first choice for AMI secondary to aortic dissection caused by extension of dissection into the coronary arterial wall. We present a case of inferior wall AMI caused by type I aortic dissection with presentation of chest pain and hemiparaplegia of right lower limb.
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PMID:Acute myocardial infarction caused by aortic dissection. 1176 85

The new CPR guidelines are based on a scientific consensus which was reached by 281 international experts. Chest compressions (100/min, 4-5 cm deep) should be performed in a ratio of 30:2 with ventilation (tidal volume 500 ml, Ti 1 s, FIO2 if possible 1.0). After a single defibrillation attempt (initially biphasic 150-200 J, monophasic 360 J, subsequently with the respective highest energy), chest compressions are initiated again immediately for 2 min. Endotracheal intubation is the gold standard; other airway devices may be employed as well depending on individual skills. Drug administration routes for adults and children: first choice IV, second choice intraosseous, third choice endobronchial [epinephrine dose 2-3x (adults) or 10x (pediatric patients) higher than IV]. Vasopressors: 1 mg epinephrine every 3-5 min IV. After the third unsuccessful defibrillation attempt amiodarone IV (300 mg); repetition (150 mg) possible. Sodium bicarbonate (1 ml/kg 8.4%) only in excessive hyperkalemia, metabolic acidosis, or intoxication with tricyclic antidepressants. Consider atropine (3 mg) and aminophylline (5 mg/kg). Thrombolysis during spontaneous circulation only in myocardial infarction or massive pulmonary embolism; during CPR only during massive pulmonary embolism. Cardiopulmonary bypass only after cardiac surgery, hypothermia or intoxication. Pediatrics: best improvement in outcome by preventing cardiocirculatory collapse. Alternate chest thumps and chest compression (infants), or abdominal compressions (>1-year-old) in foreign body airway obstruction. Initially five breaths, followed by chest compressions (100/min; approximately 1/3 of chest diameter): ventilation ratio 15:2. Treatment of potentially reversible causes (4 "Hs", "HITS": hypoxia, hypovolemia, hypo- and hyperkaliemia, hypothermia, cardiac tamponade, intoxication, thrombo-embolism, tension pneumothorax). Epinephrine 10 microg/kg IV or intraosseously, or 100 microg (endobronchially) every 3-5 min. Defibrillation (4 J/kg; monophasic oder biphasic) followed by 2 min CPR, then ECG and pulse check. Newborns: inflate the lungs with bag-valve mask ventilation. If heart rate<60/min chest compressions:ventilation ratio 3:1 (120 chest compressions/min). Postresuscitation phase: initiate mild hypothermia [32-34 degrees C for 12-24 h; slow rewarming (<0.5 degrees C/h)]. Prediction of CPR outcome is not possible at the scene; determining neurological outcome within 72 h after cardiac arrest with evoked potentials, biochemical tests and physical examination. Even during low suspicion for an acute coronary syndrome, record a prehospital 12-lead ECG. In parallel to pain therapy, aspirin (160-325 mg PO or IV) and in addition clopidogrel (300 mg PO). As antithrombin, heparin (60 IU/kg, max. 4000 IU) or enoxaparine. In ST-segment elevation myocardial infarction, define reperfusion strategy depending on duration of symptoms until PCI (prevent delay>90 min until PCI). Stroke is an emergency and needs to be treated in a stroke unit. A CT scan is the most important evaluation, MRT may replace a CT scan. After hemorrhage exclusion, thrombolysis within 3 h of symptom onset (0.9 mg/kg rt-PA IV; max 90 mg within 60 min, 10% of the entire dosage as initial bolus, no aspirin, no heparin within the first 24 h). In severe hemorrhagic shock, definite control of bleeding is the most important goal. For successful CPR of trauma patients, a minimal intravascular volume status and management of hypoxia are essential. Aggressive fluid resuscitation, hyperventilation, and excessive ventilation pressure may impair outcome in severe hemorrhagic shock. Despite bad prognosis, CPR in trauma patients may be successful in select cases. Any CPR training is better than nothing; simplification of contents and processes remains important.
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PMID:[The new 2005 resuscitation guidelines of the European Resuscitation Council: comments and supplements]. 1691 4

Hypotension and shock can be classified as hypotension caused by reduced or maintained left ventricular (LV) ejection. Reduced left ventricular ejection can result from intrinsic left ventricular, aortic valve or mitral valve failure, which includes dilated or ischemic cardiomyopathy, left main trunk disease, acute myocarditis, etc. Acute and subacute severe aortic regurgitation can also cause shock. Echocardiography allows noninvasive diagnosis of infective endocarditis and Takayasu's arteritis to cause severe arotic regurgitation and can also be used to diagnose obstruction of the left ventricular outflow tract. Reduced left ventricular preload can be caused by pericardial effusion and right ventricular ejection failure, and can result from pulmonary embolism, tricuspid regurgitation, right ventricular infarction, tension pneumothorax, hypovolemia and others characterized by a small left ventricle with good ejection fraction. Normal left ventricular ejection may be associated with hypotension. Sepsis, anaphylactic shock and neural disorder are associated with hypotension and normal cardiac output. Pseudohypotension may result from aortic dissection, Takayasu's arteritis, arteriosclerosis obliterans and aortic coarctation. A right parasternal approach enables better visualization of the ascending aorta. Fundamental echochocardiographic scanning allows approximate yet useful diagnosis of hypotension and shock.
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PMID:[Easy echo diagnosis for hypotension and shock]. 1908 1

Cardiac arrest presenting as pulseless electrical activity (PEA) is associated with poor outcome. Its major underlying causes (e.g. cardiac tamponade, pulmonary embolism, tension pneumothorax or hypovolaemia) are difficult to detect reliably in an out-of-hospital setting. We here present a case of a 14-year-old girl suffering from PEA because of cardiac tamponade 4 weeks after surgical closure of a ventricular septal defect. Immediate focused echocardiography on scene by an emergency physician showed a large pericardial effusion that had led to cardiac tamponade and finally to a PEA cardiac arrest. Immediate pericardiocentesis was carried out. The girl progressed to complete neurological recovery. This case report demonstrates that focused emergency echocardiography may be useful for the diagnosis of pericardial tamponade leading to cardiac arrest and this diagnosis can be made out-of-hospital by an appropriately trained physician.
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PMID:Focused emergency echocardiography: lifesaving tool for a 14-year-old girl suffering out-of-hospital pulseless electrical activity arrest because of cardiac tamponade. 1921 56

Chest pain is one of the most frequently seen chief complaints in patients presenting to emergency departments, and is considered to be a "high-risk" chief complaint. The differential diagnosis for chest pain is broad, and potential causes range from the benign to the immediately life-threatening. Although many (if not most) emergency department patients with chest pain do not have an immediately life-threatening condition, correct diagnoses can be difficult to make, incorrect diagnoses may lead to catastrophic therapies, and failure to make a timely diagnosis may contribute to significant morbidity and mortality. Several atraumatic "high-risk" causes of chest pain are discussed in this article, including myocardial infarction and ischemia, thoracic aortic dissection, and pulmonary embolism. Also included are brief discussions of tension pneumothorax, esophageal perforation, and cardiac tamponade.
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PMID:High-risk chief complaints I: chest pain--the big three. 1993 1

Non-traumatic chest pain is a common symptom in patients who present in the emergency department. From a clinical point of view, it is important to differentiate cardiac chest pain from non-cardiac chest pain (NCCP). Among the plethora of potential causes of NCCP, life-threatening diseases, such as aortic dissection, pulmonary embolism, tension pneumothorax, and esophageal rupture, must be differentiated from non-life threatening causes. The majority of NCCP, however, is reported to be benign in nature. The presentation of pain plays an important role in narrowing the differential diagnosis and initiating further diagnostic management and treatment. As the benign causes tend to recur, and may lead to patient anxiety and great costs, a meticulous evaluation of the patient is necessary to diagnose the underlying disorder or disease.
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PMID:Imaging of non-cardiac, non-traumatic causes of acute chest pain. 2146 34

Echocardiography plays an important role in emergency medicine because this non-invasive method is universally available and provides crucial diagnostic findings for acute decision making. The cardiac etiology in the presence of acute chest pain, acute dyspnea, hemodynamic instability or shock, new heart murmurs, chest trauma, peripheral embolism and cardiac arrest can be determined by echocardiography in the emergency scenario. The analysis of left ventricular function documents myocardial ischemia and myocardial infarction. Analysis of right ventricular function documents right heart infarction, pulmonary embolism, tension pneumothorax and sequelae of chest trauma. Echocardiography differentiates between different entities of shock. The analysis of heart valves is a domain of echocardiography. Affections of the pericardium and the hemodynamic sequelae can also be determined. It is obvious that echocardiography with its multiple diagnostic applications can only be well performed, especially in emergency medicine after in-depth education and training in this method.
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PMID:[Echocardiography in emergency diagnostics]. 2283 2

The assessment of acute circulatory failure is a challenge in absence of solid gold standard. It is suggested that artifacts generated by lung ultrasound can be of help. The FALLS-protocol (Fluid Administration Limited by Lung Sonography) follows Weil's classification of shocks. Firstly, it searches for pericardial fluid, then right heart enlargment, lastly abolished lung sliding. In this setting, the diagnoses of pericardial tamponade, pulmonary embolism and tension pneumothorax, i.e. obstructive shock, can be schematically ruled out. Moreover, the search of diffuse lung rockets (i.e. multiple B-lines, a comet-tail artifact) is performed. Its absence excludes pulmonary edema, that in clinical practice is left cardiogenic shock (most cases). At this step, the patient (defined FALLS-responder) receives fluid therapy. He/she has usually a normal sonographic lung surface, an A-profile. Any clinical improvement suggests hypovolemic shock. The absence of improvement generates continuation of fluid therapy, eventually yielding fluid overload. This condition results in the change from A-profile to B-profile. Lung ultrasound has the advantage to demonstrate this interstitial syndrome at an early and infraclinical stage (FALLS-endpoint). The change from horizontal A-lines to vertical B-lines can be considered as a direct marker of volemia in this use. By elimination, this change indicates schematically distributive shock, while in current practice septic shock. The major limitation is the B-profile on admission generated by an initial lung disorder. FALLS-protocol, which can be associated with no drawback with traditional hemodynamic tools, uses a simple machine (without Doppler) and a suitable microconvex probe allowing for heart, lung and vein assessment.
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PMID:FALLS-protocol: lung ultrasound in hemodynamic assessment of shock. 2436 5


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