It showed no significant improvement in survival ( 13) but case reports and meta-analysis suggested using thrombolysis combined with heparin as a successful therapy during prolonged CPR in pulmonary thromboembolic (PTE) patients ( 14, 15). In a randomized, multicenter TROICA trial, all patients with asystole and pulseless electrical activity immediately underwent thrombolytic therapy with tenecteplase alone. So, diagnosis and treatment of these two main etiologies should also be considered when there are no directly related echocardiographic findings, but other etiologies are ruled out. study two of fifty arrests were suspected of pulmonary emboli. study, five pulmonary emboli out of one hundred arrests were diagnosed by echocardiography and in Hayhurst et al. The review of the literature reveals that transthoracic echocardiography is highly specific but not highly sensitive to detect pulmonary embolism and few prospective studies have been conducted to evaluate the accuracy of the transthoracic echocardiography to detect pulmonary emboli in a cardiac arrest setting ( 11, 12). Diagnosis of an acute ischemic stroke is possible by echocardiographic evaluation of ventricular wall function but in the setting of cardiac arrest, it becomes difficult and requires more studies. 70% of all cardiac arrests are caused by acute myocardial ischemia or massive pulmonary embolism ( 10). The proximate mechanism for failure of electromechanical coupling is abnormal intracellular calcium metabolism, intracellular acidosis and adenosine triphosphate depletion that can occur because of acute myocardial ischemia, which is the major cause of cardiac arrest, toxins, and electrolyte imbalance. In primary PEA, none of those obvious mechanical factors is present, and ventricular muscle fails to produce an effective contraction despite continued electrical activity. Echocardiography during CPR is beneficial to detect secondary causes that include easily treatable, reversible pathologies associated with PEA ( 9). The secondary form includes the causes that result from an abrupt cessation of cardiac venous return, such as massive pulmonary embolism, acute malfunction of prosthetic valves, exsanguinations, and cardiac tamponade. PEA underlying causes are separated into primary and secondary forms. Another approach is application of additional therapeutic strategies for pseudo-PEA patients when echocardiography does not determine specific causes of arrest and does not guide us to more effective key procedures. Some studies focused on the terminating prolonged resuscitation in true PEA subjects. Pseudo-PEA patients have a higher potential of ROSC compared to true PEA while therapeutic strategies in both cases are similar. Echocardiography could help the definite diagnosis of an underlying cause in some PEA cases and lead to appropriate intervention but it failed as a targeted intervention in a subset of patients and no study showed improvement in the outcome of these patients ( 2- 5).Īs an important result, these studies revealed that in a noticeable proportion of patients with the diagnosis of PEA or asystole, the echocardiography demonstrates cardiac motion (pseudo-PEA) and these patients have higher survival rates ( 4, 6- 8). Therefore, studies and trials focusing on performing echocardiography alongside ACLS to access this goal were conducted to assay the utility of echocardiography in cardiac arrest. The focus of treatment in ventricular fibrillation is delivering shock treatment of underlying etiology comes in the next stage, whereas in PEA, primary and timely diagnosis of the underlying cause is acknowledged. While substantial efforts on an understanding of ventricular fibrillation (VF) pathophysiology have reduced deaths from ventricular fibrillation and ventricular tachycardia ( 1), pulseless electrical activity (PEA) during years have been associated with poor outcome.
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