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

A case of shock and pulmonary embolism in a 57-year-old woman is described in which hemodynamics were unresponsive both to usual therapy (volume loading, dobutamine, thrombolysis) and then to norepinephrine. Epinephrine proved to be effective, above all by strong beta 1-inotropic effect.
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PMID:Efficacy of epinephrine therapy in shock complicating pulmonary embolism. 832 96

Left ventricular end diastolic (LVEDP) and mean right atrial (RAP) pressures were recorded simultaneously in 30 patients with shock (14 acute myocardial infarction, 10 acute pulmonary embolism or severe bronchopulmonary disease, and 6 sepsis). Myocardial infarction was characterized by a predominant increase in LVEDP, pulmonary disease by a predominant increase in RAP, and sepsis by a normal relationship between LVEDP and RAP. In all three groups a significant positive correlation was noted between RAP and LVEDP, with the regression line in cor pulmonale deviated significantly toward the RAP axis and the regression line in myocardial infarction exhibiting a zero RAP intercept at an elevated LVEDP.Low cardiac outputs with elevated LVEDP in myocardial infarction indicated severe left ventricular failure. Low outputs with elevated RAP in cor pulmonale were consistent with right ventricular overload. Although cardiac outputs often were normal in sepsis, low outputs with elevated cardiac filling pressures in some patients were consistent with a hemodynamic or humoral-induced generalized depression of cardiac performance.Vasoconstrictor and inotropic drugs often produced a functional disparity between the two ventricles, with the gradient between LVEDP and RAP increasing, apparently because of an increase in left ventricular work or an inadequacy of left ventricular oxygen delivery. Acute plasma volume expansion with dextran in patients with pulmonary vascular disease resulted in a somewhat more rapid rise in RAP than in LVEDP. In septic and myocardial infarction shock, however, LVEDP and RAP usually rose proportionally, with the absolute rise of LVEDP surpassing that of RAP. Although the absolute level of the central venous pressure thus may not be a reliable indicator of left ventricular function in shock, changes in venous pressure during acute plasma volume expansion should serve as a fairly safe guide to changes in LVEDP.
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PMID:Studies in clinical shock and hypotension: VI. Relationship between left and right ventricular function. 1669 56

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

Cardiac arrest and sudden cardiac death remain major causes of mortality. Early intervention has been facilitated by emergency medical response systems and the development of training programs in basic life support and advanced cardiac life support (ACLS). Despite the implementation of these programs, the likelihood of a meaningful outcome in many life-threatening situations remains poor. Pharmacotherapy plays a role in the management of patients with cardiac arrest, with new guidelines for ACLS available in 2005 providing recommendations for the role of specific drug therapies. Epinephrine continues as a recommended means to facilitate defibrillation in patients with pulseless ventricular tachycardia or ventricular fibrillation; vasopressin is an alternative. Amiodarone is the primary antiarrhythmic drug that has been shown to be effective for facilitation of defibrillation in patients with pulseless ventricular tachycardia or fibrillation and is also used for the management of atrial fibrillation and hemodynamically stable ventricular tachycardia. Epinephrine and atropine are the primary agents used for the management of asystole and pulseless electrical activity. Treatment of electrolyte abnormalities, severe hypotension, pulmonary embolism, acute ischemic stroke, and toxicologic emergencies are important components of ACLS management. Selection of the appropriate drug, dose, and timing and route of administration are among the many challenges faced in this setting. Pharmacists who are properly educated and trained regarding the use of pharmacotherapy for patients requiring ACLS can help maximize the likelihood of positive patient outcomes.
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PMID:Pharmacotherapy considerations in advanced cardiac life support. 1712 34

An 18-year-old healthy woman with no previous history of coagulation disorders underwent general anesthesia for tonsillectomy. The procedure was uneventful. After the surgery, she was ordered to rest on bed overnight. The next day, the patient experienced transient syncope followed by hypotension (< 60 mmHg) and severe dyspnea. Epinephrine 2 mg administration restored the blood pressure promptly, yet dyspnea persisted. The lung-perfusion scintigraphy showed upper-lobe perfusion defect in the left lung and she was diagnosed as having pulmonary embolism. She received low-molecular-weight heparin and warfarin therapy and recovered fully. The postoperative laboratory analysis did not show thrombophilic disorders or prothrombotic state. The pulmonary embolism was speculated to have occurred due to deep vein thrombosis which developed after postoperative immobilization. The prophylactic maneuvers such as elastic stockings were not applied to the patient preoperatively, who had been considered unlikely to develop deep vein thrombosis. Although deep vein thrombosis in children and adolescence are rare, postoperative children should be monitored carefully for thrombotic complications. Postoperative bed rest should be minimized in terms of prevention of thrombosis.
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PMID:[Case of postoperative pulmonary embolism after tonsillectomy in a healthy young woman]. 1787 53

We studied changes in platelet aggregation and fibrinogen levels during thrombolysis with massive or submassive pulmonary embolism. Fifteen patients were randomized into ultrahigh-dose streptokinase (UH-SK n = 8) or alteplase (tPA n = 7) groups. Arterial blood samples were taken before and after thrombolysis every 4 h between 4 and 36 h, and once daily between 2 and 30 days. In-vitro platelet aggregation was examined as spontaneous (0.9% NaCl) and induced aggregation with adrenaline 10 micromol/l, collagen 2 microg/ml and ADP 10 micromol/l. D-dimer and fibrinogen were measured every 8 h on first day, and later as above. In the UH-SK group, adrenaline-induced platelet aggregation decreased at 4 and 8 h compared with baseline (P < 0.03). Adrenaline-induced platelet aggregation was significantly lower in the UH-SK group than in the tPA group at 36 h and on day 3 (P < 0.03). Platelet aggregation induced by ADP was lower at 4 h than at baseline in the UH-SK group (P < 0.05). Collagen-induced platelet aggregation was lower at 4 and 8 h than at baseline (P < 0.05) in the UH-SK group. Compared with baseline, fibrinogen levels decreased in both groups after thrombolysis. D-dimer levels were elevated in both groups at 8 h (tPA group, P < 0.0004; UH-SK group, P < 0.05). Spontaneous platelet aggregation, major bleeding or re-embolism was not documented. Platelet aggregation decreased after thrombolysis with UH-SK for 12 h, in comparison tPA caused an insignificant decrease. Fibrinogen level decreased with UH-SK treatment for 5 days but in case of tPA we could not measure significant changes. According to our findings, tPA is a more suitable drug but streptokinase is also effective because of its cost-benefit ratio.
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PMID:Time course of platelet aggregation during thrombolytic treatment of massive pulmonary embolism. 1789 Sep 54

Adrenal cell carcinoma is a rare tumor and more than 70% of patients present with advanced stages. Adrenal cell carcinoma is an aggressive tumor with a poor prognosis. Surgical intervention is the gold standard treatment and mitotane is the only drug approved for the treatment of adrenal cell carcinoma. Until recently in 2012, the etoposide, doxorubicin, cisplatin plus mitotane are approved as first-line therapy based on response rate and progression-free survival. This case illustrates a case of advanced adrenal cell carcinoma in a young girl who presented with huge adrenal mass with inferior vena cava thrombosis and pulmonary embolism. Multi-approach of therapy was used to control the tumor size and metastasis. Therefore, it may prolong her survival rate for up to 5 years and 4 months.
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PMID:Multi-Target Approach to Metastatic Adrenal Cell Carcinoma. 2763 Nov 84