[Acute massive pulmonary embolism]. / Az akut masszív tüdoembólia.

To establish the diagnosis of the acute massive pulmonary embolism is critically urgent for the doctors, because the life saving causal therapy should be introduced as soon as possible. The combined use of the estimated clinical probability and the results of one or more noninvasive examinations increase the accuracy in confirming the diagnosis of embolism. The most important methods to confirm or rule out the suspicion of pulmonary embolism are the noninvasive perfusion pulmonary isotopic scanning, spiral CT, echocardiography and the invasive "gold standard" pulmonary angiography. The life saving causal therapy means the urgent recanalization of the obstructed pulmonary arteries. The surgical embolectomy is a high risk intervention, but the invasive radiological methods are also capable of destroying the emboli mechanically and very effectively. The different thrombolytic treatment methods mean causal therapy too, and these protocols can be used in every hospital. There is no alternative treatment in patients with sudden clinical death caused by acute pulmonary embolism: the drug administration during reanimation should be completed with thrombolysis.

Lack of a hypotensive effect with rapid administration of a new aqueous formulation of intravenous amiodarone.

Hypotension is the most frequent adverse event reported with intravenous amiodarone. Hypotension has been attributed to the vasoactive solvents of the standard formulation (Cordarone IV) and is not dose related, but related to the rate of infusion. Drug labeling calls for intravenous amiodarone to be administered over 10 minutes. A new aqueous formulation of amiodarone (Amio-Aqueous) does not contain vasoactive excipients and may be administered safely by rapid administration without hypotension. This hypothesis was tested using combined data of 4 clinical trials; each assessed the development of hypotension prospectively. Hypotension was defined as a 25% decrease in systolic blood pressure (BP), with the development of a systolic BP of <90 mm Hg or a systolic BP that decreased to <80 mm Hg. In all, 358 Amio-Aqueous and 225 lidocaine boluses were administered to 278 patients; 246 had ventricular tachycardia (VT) during drug administration. Hypotension developed in 11% of patients on Amio-Aqueous versus 19% on lidocaine (p = NS), all during VT; most resolved spontaneously with VT termination. With both drugs, hypotension persisted after VT termination in 1% of patients; the incidence of drug-related hypotension occurred in 2% of patients (1% had hypotension requiring treatment). The Amio-Aqueous was discontinued in 1% of patients, and lidocaine was discontinued in 2% of patients because of hypotension. We conclude that Amio-Aqueous is at least as safe as lidocaine in terms of causing hypotension when administered rapidly. This is a significant advantage over the standard amiodarone formulation, because Cordarone cannot be administered by rapid bolus owing to excipient-related hypotension.