ST elevation myocardial infarction electrocardiogram
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| Myocardial infarction electrocardiogram Classification and external resources | |
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|---|---|
| Illustration of ST segment elevation with measurement of the magnitude of ST elevation 60 milliseconds after the J point. | |
| ICD-10 | I21.-I22. |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
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Overview
A primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. The 12 lead ECG is used to classify patients into one of three groups:
- Those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
- Those with ST segment depression or T wave inversion (suspicious for ischemia), and
- Those with a so-called non-diagnostic or normal ECG.[1]
A normal ECG does not rule out the presence of acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is instead the presence of a hyperacute T wave.[2] In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.[3] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.[4]
Definition of ST Elevation
The electrocardiographic definition of ST elevation MI requires the following: at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads.[1] While these criteria are sensitive, they are not specific as thromboctic coronary occlusion is not the most common cause of ST segment elevation in chest pain patients.[5]
Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis
ST Segment Elevation Does Not Always Signify a Myocardial Infarction. ST segment elevation should alert the clinician to the possibility of myocardial injury, however, there are a variety of conditions that cause ST segment elevation which are not associated with myonecrosis. Indeed, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead.[6] The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.[7][8][6]
Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of acute myocadial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads.[9] The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.[10]
Acute epicardial artery occlusion by thrombus is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following: (listed in alphabetical order) [6][11]
- Aneurysm of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.
- Balloon inflation in a coronary artery during percutaneous coronary intervention
- Coronary artery rupture during percutaneous coronary intervention
- Early repolarization is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by bradycardia.
- Hyperkalemia known as the "dialyzable current of njury" hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity
- Left bundle branch block is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.
- Myopericarditis can cause injury to the subepicardial myocytes and ST segment elevation.
- Myocarditis can cause injury to the subepicardial myocytes and ST segment elevation.
- Pericardiocentesis when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.
- Pericarditis can cause injury to the subepicardial myocytes and ST elevation.
- Prinzmetal's angina is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.
- Stroke Intracranial hemorrhage can in some cases cause ST segment elevation due to direct myocyte injury from a hyperadrenergic stimulation emanating from the central nervous system.
Differential Diagnosis of Causes of ST Segment Elevation in the Presence of Myonecrosis (STEMI)
While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rapidly identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: cocaine induced STEMI would not be treated with beta-blockers, and myocardial contusion would not be treated with an antithrombin. These conditions include the following:
| Cardiovascular | Aortic dissection more often extends to occlude the ostium of the right coronary artery
Aortic stenosis can cause subendocardial ischemia and infarction if demand grossly exceeds supply
|
| Chemical / poisoning | Carbon monoxide poisoning |
| Dermatologic | No underlying causes |
| Drug Side Effect | Oral contraceptive pills, particularly among women who smoke |
| Ear Nose Throat | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI |
| Endocrine | Thyrotoxicosis |
| Environmental | Blizzards and snow shoveling, and inhalation of fine particulate matter in areas with air pollution and high traffic have been identified as triggers of MI. |
| Gastroenterologic | A heavy meal has been associated with a 4 fold rise in the risk of MI, and it is not clear if this is mediated by hyperadrenergic tone [12]; |
| Genetic | Familial hypercholesterolemia |
| Hematologic | Disseminated intravascular coagulation (DIC) |
| Iatrogenic | Epinephrine overdose
Sudden withdrawal of Beta blockers or nitrates |
| Infectious Disease | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI
Infectious endocarditis may STEMI as a result of embolization |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | A heavy meal has been associated with a 4 fold rise in the risk of MI and it is not clear if this is mediated by hyperadrenergic tone[13];
Mucopolysaccharidoses or Hurler disease Thiamine deficiency has been associated with ST elevation and myonecrosis [14][15][16] |
| Obstetric/Gynecologic | Spontaneous coronary dissection in the setting of pregnancy |
| Oncologic | Radiation therapy can accelerate atherosclerosis particularly in the distribution of the left anterior descending artery; |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | Cocaine ingestion which may result in direct myocyte injury due to an adrendergic surge, vasoconstriction of the microvasculature or plaque rupture and thrombus formation;
Marijuana ingestion has been identified as a trigger of MI. |
| Psychiatric | Anger, anxiety, bereavement, work-related stress, earthquakes, bombings and other psychosocial stressors have been identified as triggers of MI, and it is not clear if the mechanism is plaque rupture or hyperadrenergic tone;
Stress cardiomyopathy or Broken heart syndrome causes ST segment elevation most often in the anterior precordium and is thought to be due to direct myocyte injury from a hyperadrenergic stimulation emanating from the central nervous system. |
| Pulmonary | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI |
| Renal / Electrolyte | Homocystinuria |
| Rheum / Immune / Allergy | Takayasus |
| Sexual | Sexual activity has been identified as a trigger of MI |
| Trauma | Both penetrating and non-penetrating trauma to the heart or myocardial contusion, commotio cordis can be associated with ST elevation and myonecrosis. |
| Urologic | No underlying causes |
| Miscellaneous | Hypotension particularly if it is prolonged |
Limitations of the 12 lead ECG
While clinicians are widely familar with the 12 lead ECG, there are limitations to its sensitivity and specificity in detecting myocardial injury due to thrombotic vessel occlusion. A single static ECG represents a brief sample in time. In STEMI, the culprit artery is often opening and closing or "winking and blinking" due to cyclic flow variations with the clot dissolving and reforming again. Furthermore, patients with acute coronary syndromes often have rapidly changing supply versus demand characteristics. As a clinical example, one of the authors (CM Gibson) once saw a patient with 6 hours of chest pain who had non-specific ECG changes. 15 minutes later the patient complained of worsening chest pain, and at that time the ECG showed ST elevation. Had the second ECG with ST elevation been instead the first ECG that was reviewed, it would have been concluded that the patient was infarcting for over 6 hours, when instead, the artery was occluded for 15 minutes at most during the recent episode of chest pain. Because a single ECG may not accurately represent evolving myocardial injury, it is standard practice to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring.[17] While the standard 12 lead ECG is well designed to detect anterior ischemia, by virtue of the fact that it samples only electrical vectors from the front left chest wall, the 12 lead ECG may miss right ventricular and posterior infarctions. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG or ST segment depression in the anterior precordial leads. The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. Newer technologies such as the 80 lead ECG have demonstrated greater sensitivity in detecting RV and posterior infarcts compared with the 12 lead ECG. The failure to identify patients with ST elevation MI delays care and has a negative effect on the quality of patient care.[18]
Localization of the Culprit Artery Based Upon the 12 lead ECG
While the ECG leads that are involved with ST elevation and depression are often used to predict the potential location of the culprit artery, teh sensitivity and specificity of these techniques are often poor. New technologies such as 80 lead ECGs may prove to be more useful in this regard. Identification of the potential culprit artery can be important in guiding patient management. In particular, the ECG should be used to identify patients with a right ventricular infarct where nitrate administration is contraindicated. The 12 lead ECG can also be used to identify the most appropriate artery to perform angiography on first when performing primary angioplasty.
| Wall Affected | Leads Showing ST Segment Elevation | Leads Showing Reciprocal ST Segment Depression | Suspected Culprit Artery |
|---|---|---|---|
| Septal | V1, V2 | None | Left Anterior Descending (LAD) |
| Anterior | V3, V4 | None | Left Anterior Descending (LAD) |
| Anteroseptal | V1, V2, V3, V4 | None | Left Anterior Descending (LAD) |
| Anterolateral | V3, V4, V5, V6, I, aVL | II, III, aVF | Left Anterior Descending (LAD), Circumflex (LCX), or Obtuse Marginal |
| Extensive anterior (Sometimes called Anteroseptal with Lateral extension) | V1,V2,V3, V4, V5, V6, I, aVL | II, III, aVF | Left main coronary artery (LCA) |
| Inferior | II, III, aVF | I, aVL | Right Coronary Artery (RCA) or Circumflex (LCX) |
| Lateral | I, aVL, V5, V6 | II, III, aVF | Circumflex (LCX) or Obtuse Marginal |
| Posterior (Usually associated with Inferior or Lateral but can be isolated) | V7, V8, V9 | V1,V2,V3, V4 | Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX)) |
| Right ventricular (Usually associated with Inferior) | II, III, aVF, V1, V4R | I, aVL | Right Coronary Artery (RCA) |
Evolution of ST Segment Elevation
As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction.[19] Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred. Understanding the typical time course of ST changes in acute MI is critical in distinguishing STEMI from pericarditis and other conditions.
| Figure | change | |
|---|---|---|
| minutes | 
| hyperacute T waves (peaked T waves)
ST-elevation |
| hours | 
| ST-elevation, with terminal negative T wave
negative T wave (these can last for months) |
| days | 
| Pathologic Q Waves |
Measurement of the Magnitude of ST Elevation: 60 Milliseconds after the J point
The optimal time after the J point to measure ST elevation is debated. This example shows the technique of measuring the magnitude of ST elevation 60 milliseconds or 1.5 small boxes after the J point.
Distinguishing Early Repolarization and Other Normal Variants from Pathologic ST Elevation
Early repolarization is an electrocardiographic pattern that can mimic the changes of ST elevation myocardial infarction. It is often seen in younger males. As the example below shows, there is often a notch (shown in red) where the QRS and ST segments join.
EKG Examples
 The evolution of an infarct on the ECG. ST elevation, Q wave formation, T wave inversion, normalization with a persistent Q wave |
 Pathologic ST elevation |
 12-lead electrocardiogram (ECG) showing acute inferior ST segment elevation MI (STEMI). Note the ST segment elevation in leads II, III, and aVF along with reciprocal ST segment depression in leads I and aVL. |
 Acute inferior myocardial infarction with RV involvement. |
 Same case. Right precordial leads. |
 Acute inferior MI |
 Acute inferoposterior MI: ST elevation in II, III, AVF (in III > II). ST depression in I, AVL, V2. Tall R in V2, otherwise normal QRS morphology. |
 Acute inferior MI |
 Acute posterolateral MI |
 Acute inferolateral MI: ST depression in V1, V4, tall R in V2. ST elevation in II, III, AVF, V5 and V6. |
 Acute anterior MI. Loss of R waves throughout the anterior wall (V1-V6). QS complexes in V3-V5. ST elevation in V1-V5 with terminal negative T waves. |
 Sinus bradycardia with first degree AV block and inferior-posterior-lateral myocardial infarction. |
 Sinus bradycardia with inferior-lateral myocardial infarction. |
 Acute anterior MI. LAD artery occlusion |
 Sinus rhythm with anteroseptal myocardial infarction. |
 Sinus rhythm with left bundle branch block, comparison with an old EKG is mandatory to evaluate whether the LBBB is new (a sign of myocardial infarction) or old. |
 Inferior-posterior myocardial infarction with complete AV block and ventricular excape rhythm with RBBB pattern and left axis, followed by sinus rhythm. |
 Acute anterior myocardial infarction and left anterior hemiblock. Image courtesy of Dr Jose Ganseman |
 Old anterior myocardial infarction and bifascicular block (RBBB and LAHB) Image courtesy of Dr Jose Ganseman |
 Acute MI with proximal LAD occlusion |
 A 2 days old anterior infarction with Q waves in V1-V4 with persisting ST elevation, a sign of left ventricular aneurysm formation. |
 A 2 weeks old anterior infarction with Q waves in V2-V4 and persisting ST elevation, a sign of left ventricular aneurysm formation. |
 ECG on admission: A large anterior wall infarction |
 Detail for conduction times. |
 The heart rate increases and there are two extra systoles short after each other. Then, a chaotic rhythm develops: ventricular fibrillation. |
 Atrial fibrillation and inferior-posterior myocardial infarction. |
 Same patient's 2. EKG; This EKG shows clear ST elevation in the right precordial leads. A coronary angiography revealed a proximal right coronary artery occlusion. |
 Inferior-posterior-lateral myocardial infarction with a nodal escape rhythm |
 Patient with RBBB and inferior MI. Note to left axis deviation. |
 Lead V4R in the same patient with RBBB and inferior MI clearly shows ST elevation. |
 The same patient before acute MI developed. Horizontal axis. |
 Acute myocardial infarction in in a patient with a pacemaker and LBBB. Concordant ST elevation in V5-V6 are clearly visible. There is discordant ST segment elevation > 5 mm in lead V3. |
 The same patient as in the first example 2 months before the myocardial infarction. Normal LBBB pattern. |
 Acute MI in a patient with LBBB |
 Atrial fibrillation with inferior-posterior-lateral myocardial infarction and incomplete right bundle branch block. Lead I shows ST depression, suggestive of right coronary artery involvement. |
Sources
- The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction [23]
- The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction [24]
References
- ↑ 1.0 1.1 "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 8: Stabilization of the Patient With Acute Coronary Syndromes." Circulation 2005; 112: IV-89 - IV-110.
- ↑ Somers MP, Brady WJ, Perron AD, Mattu A (May 2002). "The prominant T wave: electrocardiographic differential diagnosis". Am J Emerg Med 20 (3): 243–51. PMID 11992348.
- ↑ Smith SW, Whitwam W. "Acute Coronary Syndromes." Emerg Med Clin N Am 2006; 24(1): 53-89. PMID 16308113
- ↑ "The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775
- ↑ Smith SW, Whitwam W (February 2006). "Acute coronary syndromes". Emerg. Med. Clin. North Am. 24 (1): 53–89, vi. doi:10.1016/j.emc.2005.08.008. PMID 16308113.
- ↑ 6.0 6.1 6.2 Wang K, Asinger RW, Marriott HJ (November 2003). "ST-segment elevation in conditions other than acute myocardial infarction". N. Engl. J. Med. 349 (22): 2128–35. doi:10.1056/NEJMra022580. PMID 14645641.
- ↑ Brady WJ, Chan TC, Pollack M (January 2000). "Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction-left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy". J Emerg Med 18 (1): 71–8. PMID 10645842.
- ↑ Brady WJ, Perron AD, Chan T (April 2001). "Electrocardiographic ST-segment elevation: correct identification of acute myocardial infarction (AMI) and non-AMI syndromes by emergency physicians". Acad Emerg Med 8 (4): 349–60. PMID 11282670.
- ↑ Sgarbossa EB, Pinski SL, Barbagelata A, et al (February 1996). "Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators". N. Engl. J. Med. 334 (8): 481–7. PMID 8559200.
- ↑ Brady WJ, Syverud SA, Beagle C, et al (October 2001). "Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic analysis of the ST segment". Acad Emerg Med 8 (10): 961–7. PMID 11581081.
- ↑ Ako J, Honda Y, Fitzgerald PJ (March 2004). "Conditions associated with ST-segment elevation". N. Engl. J. Med. 350 (11): 1152–5; author reply 1152–5. doi:10.1056/NEJM200403113501118. PMID 15014192.
- ↑ Lipovetsky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS. Heavy meals as a trigger for a first event of the acute coronary syndrome:a case-crossover study. Isr Med Assoc J. 2004;6:728 –731.
- ↑ Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS (December 2004). "Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study". Isr. Med. Assoc. J. 6 (12): 728–31. PMID 15609883.
- ↑ Kawano H, Koide Y, Toda G, Yano K (June 2005). "ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi". Intern. Med. 44 (6): 578–85. PMID 16020883.
- ↑ Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954.
- ↑ Read DH, Harrington DD (June 1981). "Experimentally induced thiamine deficiency in beagle dogs: clinical observations". Am. J. Vet. Res. 42 (6): 984–91. PMID 7197132.
- ↑ Selker HP, Zalenski RJ, Antman EM, et al (January 1997). "An evaluation of technologies for identifying acute cardiac ischemia in the emergency department: executive summary of a National Heart Attack Alert Program Working Group Report". Ann Emerg Med 29 (1): 1–12. PMID 8998085.
- ↑ Masoudi FA, Magid DJ, Vinson DR, et al (October 2006). "Implications of the failure to identify high-risk electrocardiogram findings for the quality of care of patients with acute myocardial infarction: results of the Emergency Department Quality in Myocardial Infarction (EDQMI) study". Circulation 114 (15): 1565–71. doi:10.1161/CIRCULATIONAHA.106.623652. PMID 17015790.
- ↑ Namba Y, Bando M, Takeda K, Iwata M, Mannen T (June 1991). "[Marchiafava-Bignami disease with symptoms of the motor impersistence and unilateral hemispatial neglect]" (in Japanese). Rinsho Shinkeigaku 31 (6): 632–5. PMID 1934778.
- ↑ Novotný T, Sisáková M, Floriánová A, et al (September 2007). "[QT dynamicity in risk stratification in patients after myocardial infarction]" (in Czech). Vnitr Lek 53 (9): 964–7. PMID 18019666.
- ↑ Jensen BT, Abildstrom SZ, Larroude CE, et al (April 2005). "QT dynamics in risk stratification after myocardial infarction". Heart Rhythm 2 (4): 357–64. doi:10.1016/j.hrthm.2004.12.028. PMID 15851335.
- ↑ Chevalier P, Burri H, Adeleine P, et al (March 2003). "QT dynamicity and sudden death after myocardial infarction: results of a long-term follow-up study". J. Cardiovasc. Electrophysiol. 14 (3): 227–33. PMID 12716101.
- ↑ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK (August 2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction)". Circulation 110 (9): e82–292. PMID 15339869.
- ↑ Antman EM, Hand M, Armstrong PW, et al (January 2008). "2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee". Circulation 117 (2): 296–329. doi:10.1161/CIRCULATIONAHA.107.188209. PMID 18071078.
See Also
Additional Resources
- Tanel RE. ECGs in the ED. Pediatr Emerg Care. 2008 Jan; 24 (1): 62-3. PMID 18212616
External links
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to date resource of Cardiovascular Research
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
