Electrocardiographic Prediction of Acute Left Main Coronary Artery Occlusion
Rostoff P, Piwowarska W, Gackowski A, et al. Amer J Emerg Med 2007;25:852-855.
This isn’t new news to anyone that’s been attending advanced ECG workshops (e.g. FHC!) or keeping up with some of the ECG literature, but just one more publication on the utility of lead aVR, the lead I refer to as the “forgotten 12th lead” or the “Rodney Dangerfield lead.” The authors wrote this brief report in response to an article we published in November 2006 pertaining to lead aVR.1 In that article, we discussed that ST-segment elevation (STE) in lead aVR in patients with acute cardiac ischemia has been found to be highly specific for acute occlusion of the left main coronary artery (LMCA). Why should we worry more about ACS with LMCA involvement vs. any other ACS case? Very simple...the literature indicates that when a patient has ACS involving the LMCA, they carry a 70% risk of developing cardiogenic shock or dying, and the only treatment that has been demonstrated to improve outcomes in patients with LMCA occlusion is rapid PCI (or often they will need CABG). No medical therapies have been found to reliably improve the prognosis, including thrombolytics. This is not just applicable to patients with STEMI…it also applies if the patient has an ST-depression ACS.
The authors performed an analysis of published data and report that STE in lead aVR during ACS is 77.6% sensitive, 82.6% specific, and 81.5% accurate for LMCA occlusion. These authors don’t specifically comment on what degree of STE is required (0.5 mm? 1.0 mm?), but in our evaluation of the literature there are three patterns that appear to predict LMCA occlusion: (1) STE in lead aVR which is greater in magnitude than the STE in lead V1; (2) STE in lead aVR with simultaneous STE in lead aVL; or (3) STE in lead aVR > 1.5 mm. Also, it is important to bear in mind that these findings only apply when there is evidence of ischemia or infarction in other leads as well, so this is really not applicable to non-ACS patients. For example, some patients with SVT will develop STE in lead aVR, and this is not clinically predictive of LMCA disease.
For anyone wondering why STE occurs in lead aVR, apparently it’s not completely clear. The authors cite one theory that “it is caused by transmural ischemia of the basal part of the interventricular septum, where the injury’s current is directed toward the right shoulder” thus producing STE in lead aVR. Sounds good to me. The bottom line is this: when a patient has evidence of ischemia or infarction on the ECG, take a special look at lead aVR. If there is STE there, the first thing you need to do is to get on the phone and find a cardiologist that will take the patient for PCI. And if you have to transfer the patient and have a choice of where to send the patient, opt for a center that also has cardiac surgeons available for CABG. They will often be needed.
1. Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med 2006;24:864-874.
A Randomized Study of Out-of-Hospital Continuous Positive Airway Pressure for Acute Cardiogenic Pulmonary Oedema: Physiological and Clinical Effects
Over the past couple of years in this series we’ve reviewed articles demonstrating the utility of non-invasive ventilation (NIV) in the early management of cardiogenic pulmonary edema (CPE). Various studies have demonstrated that NIV is associated with decreased intubation rates, ICU utilization and length of stay, decreased hospital costs, and even decreased mortality. One key, though, is that NIV must be used early in the course of treatment. Logically, one would then assume that application of NIV by prehospital care providers would be very beneficial. Plaisance and colleagues evaluated this assumption in the Paris EMS system. They conducted a randomized, prospective study in which they compared in various combinations early CPAP (during the first 15 minutes), late CPAP (between 30-45 minutes of treatment), medical treatment alone (the loop diuretic bumetanide; NTG added if SBP > 100 mm Hg à 400 mcg SL followed by infusion at 1 mg/hr [pretty low!]; and nicardipine infusion was added for afterload reduction if SBP remained > 160 or DBP > 90 mm Hg despite NTG), and combinations of medical treatment with early or late CPAP for patients with CPE. The primary endpoints they were evaluating was the effect of early CPAP on a dyspnea clinical score and on ABGs after 45 minutes; and the secondary endpoints were the effects of early CPAP on tracheal intubation rates, need for inotropic support, and in-hospital mortality. CPAP pressures were 7.5 cm H2O. 124 patients were enrolled.
The researchers found that patients receiving early CPAP had greater improvements than patients receiving either medical treatment alone or medical treatment plus late CPAP in terms of dyspnea scores, PO2 levels, and tracheal intubation rates; and patients with early CPAP also had a trend towards lower in-hospital mortality (P=0.05, nearly statistically significant). Additionally, fewer patients in the early CPAP group needed inotropic support. Overall, the efficacy of CPAP was so significant that the authors did not observe any clear benefit of adding medical treatment if CPAP was applied early, whereas the addition of late CPAP to medical treatment was associated with significant improvements.
There are two major takeaway points here. First, NIV appears to be the best early therapy for CPE. Second, NIV works best when it is applied early. This study demonstrated that even a short 15 minute delay was associated with significant effects on patient outcomes. The authors suggest that the delay in initiation of NIV in patients with CPE might be equated to the delay in aggressive resuscitation of patients with septic shock in terms of outcomes. This paper certainly makes a strong argument for pushing for more prehospital systems to include NIV in their CPE protocols!
