scholarly journals Acute Myocardial Ischemia Detection with a New ST Segment Monitoring Algorithm in an ICD

2011 ◽  
Vol 27 (Supplement) ◽  
pp. OP68_5
Author(s):  
Axel Kloppe ◽  
Dejan Mijic ◽  
Markus Zarse ◽  
Bernd Lemke
2002 ◽  
Vol 11 (4) ◽  
pp. 378-386 ◽  
Author(s):  
Barbara J. Drew

The electrocardiogram continues to be the gold standard for the diagnosis of cardiac arrhythmias and acute myocardial ischemia. The treatment of arrhythmias in critical care units has become less aggressive during the past decade because research indicates that antiarrhythmic agents can be proarrhythmic, causing malignant ventricular arrhythmias such as torsade de pointes. However, during the same period, the treatment of acute myocardial ischemia has become more aggressive, with the goal of preventing or interrupting myocardial infarction by using new antithrombotic and antiplatelet agents and percutaneous coronary interventions. For this reason, critical care nurses should learn how to use ST-segment monitoring to detect acute ischemia, which is often asymptomatic, in patients with acute coronary syndromes. Because the electrocardiographic lead must be facing the localized ischemic zone of the heart to depict the telltale signs of ST-segment deviation, the challenge is to find ways to monitor patients continuously for ischemia without using an excessive number of electrodes and lead wires. The current trend is to use reduced lead set configurations in which 5 or 6 electrodes, placed at convenient places on the chest, are used to construct a full 12-lead electrocardiogram. Nurse scientists at the University of California, San Francisco, School of Nursing are at the forefront in developing and assessing the diagnostic accuracy of these reduced lead set electrocardiograms.


2010 ◽  
Vol 43 (2) ◽  
pp. 113-120 ◽  
Author(s):  
Michael Ringborn ◽  
Jonas Pettersson ◽  
Eva Persson ◽  
Stafford G. Warren ◽  
Pyotr Platonov ◽  
...  

Heart Rhythm ◽  
2014 ◽  
Vol 11 (11) ◽  
pp. 2084-2091 ◽  
Author(s):  
Juan Cinca ◽  
Francisco Javier Noriega ◽  
Esther Jorge ◽  
Jesús Alvarez-Garcia ◽  
Gerard Amoros ◽  
...  

2019 ◽  
Vol 57 ◽  
pp. S110-S111
Author(s):  
Salah S. Al-Zaiti ◽  
Ziad Faramand ◽  
Christian Martin-Gill ◽  
Mohammad Alrawashdeh ◽  
Richard Gregg ◽  
...  

1987 ◽  
Author(s):  
R NIADA ◽  
R Porta ◽  
R Tettamanti ◽  
R Pescador ◽  
M Mantovani ◽  
...  

Defibrotide was able to prevent the hemodynamic and biochemical alterations caused by acute myocardial ischemia (AMI) induced by coronary occlusion in the cat when infused 3.5 h before and 5 h after left anterior descending coronary artery (LAD) occlusion. In the platelet perfused heart, Defibrotide was a selective stimulator of coronary vascular PGI^ but not of platelet thromboxane formation. The present study was designed both to investigate the effects of Defibrotide injected 30 min after the induction of acute myocardial ischemia (AMI) in the cat and to evaluate the ability of this drug to reduce infarct size. In the first set of experiments a permanent ligature (5 hours) was placed around LAD. ST segment from ECG, mean aortic pressure (MAP), heart rate (HR) and the pressure-heart rate index (PRI) were considered. Plasma and tissue creatine phosphckinase activity (CFK), tissue lactate and ATP were measured by enzymatic kits from Boehringer Biochemia. 30 min after coronary occlusion a loading dose of Defibrotide (32 ng Kg-1 ) was administered i.v. immediately followed by an infusion (32 ng Kg-1 h 4.5 h-1) MAP, HR and PRI were not modified either by AMI or by the infusion of Defibrotide. AMI-ST segment increases were reduced by Defibrotide from 0.5 h after the beginning of the treatment (—49% vs. AMI control) to the and of experiments (-83% vs. AMI control after 5 h occlusion period). Plasma CFK was reduced from 2.5 h after the beginning of the treatment (-29%) till the end of experiments (-52%). Ischemic tissue CFK, lactate and ATP were normalized by Defibrotide. In the second set of experiments the animals were infused with Defibrotide (50 or 200 mg Kg-1 h-1 , i.v.) starting 2 hours before coronary ligature. The infusion was maintained throughout the 5 h occlusion period. The risk and infarct areas were measured by Evans blu and nitroblue tetrazoliun staining. The 51 ± 3% of risk area was infarcted in AMI control cats. Defibrotide at the two tested doses significantly reduced these infarct areas to 42 ± 4% and 34 ± 2% of risk areas respectively. The beneficial effects of Defibrotide observed in AMI could be attributed both to its ability to enhance PGI2 release from vascular walls and to improved local tissue oxygenation and energy supplies. However it could be taken into account a direct cytoprotective action.


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