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| ==Overview==
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| There are no [[ECG]] findings associated with [[heartburn]].
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| The [[ECG]] may be useful in the diagnosis of cardiac causes of [[heartburn]] such as [[acute coronary syndrome]]s.
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| ==Electrocardiogram==
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| * There are no ECG findings associated with GERD. However, [[EKG]] can be performed in cases of GERD that present with atypical chest pain that can mimic [[angina pectoris]] [[pain]].<ref name="pmid234193812">{{cite journal| author=Katz PO, Gerson LB, Vela MF| title=Guidelines for the diagnosis and management of gastroesophageal reflux disease. | journal=Am J Gastroenterol | year= 2013 | volume= 108 | issue= 3 | pages= 308-28; quiz 329 | pmid=23419381 | doi=10.1038/ajg.2012.444 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23419381 }}</ref>
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| In case of heartburn due to [[acute coronary syndromes]], the [[12 lead ECG]] is used to classify patients into one of three groups:
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| *Those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with [[thrombolysis|thrombolytics]] or primary [[percutaneous coronary intervention|PCI]]),
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| *Those with ST segment depression or T wave inversion (suspicious for ischemia), and
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| *Those with a so-called non-diagnostic or normal ECG.<ref name="ECC_2005_ACS">"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.</ref>
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| 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]].<ref name="pmid11992348">{{cite journal |author=Somers MP, Brady WJ, Perron AD, Mattu A |title=The prominant T wave: electrocardiographic differential diagnosis |journal=Am J Emerg Med |volume=20 |issue=3 |pages=243–51 |year=2002 |month=May |pmid=11992348 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735675702921935}}</ref> In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.<ref name="ACS_Clin_NA">Smith SW, Whitwam W. "Acute Coronary Syndromes." ''Emerg Med Clin N Am'' 2006; '''24(1)''': 53-89. PMID 16308113</ref> Hyperacute T waves need to be distinguished from the peaked T waves associated with [[hyperkalemia]].<ref name="ECG_Noncardiac">"The clinical value of the ECG in noncardiac conditions." ''Chest'' 2004; '''125(4)''': 1561-76. PMID 15078775</ref>
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| ====ST Elevation====
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| 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.<ref name="ECC_2005_ACS"/> While these criteria are sensitive, they are not specific as thrombotic coronary occlusion is not the most common cause of ST segment elevation in [[chest pain]] patients.<ref name="pmid16308113">{{cite journal |author=Smith SW, Whitwam W |title=Acute coronary syndromes |journal=Emerg. Med. Clin. North Am. |volume=24 |issue=1 |pages=53–89, vi |year=2006 |month=February |pmid=16308113 |doi=10.1016/j.emc.2005.08.008 |url=}}</ref>
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| ====ST Depression====
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| ST depression in the anterior leads might either represent reciprocal changes on EKG<ref name="pmid2522957">{{cite journal| author=Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R| title=Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. | journal=J Am Coll Cardiol | year= 1989 | volume= 13 | issue= 6 | pages= 1270-4 | pmid=2522957 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2522957 }} </ref> or might be pathologically caused by either anterior ischemia in the context of a patent artery<ref name="pmid11994554">{{cite journal| author=Gibson CM, Chen M, Angeja BG, Murphy SA, Marble SJ, Barron HV et al.| title=Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery. | journal=J Thromb Thrombolysis | year= 2002 | volume= 13 | issue= 1 | pages= 9-12 | pmid=11994554 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11994554 }} </ref> or posterior infarct due to the complete occlusion of a coronary artery.<ref name="pmid20723851">{{cite journal| author=Pride YB, Tung P, Mohanavelu S, Zorkun C, Wiviott SD, Antman EM et al.| title=Angiographic and clinical outcomes among patients with acute coronary syndromes presenting with isolated anterior ST-segment depression: a TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) substudy. | journal=JACC Cardiovasc Interv | year= 2010 | volume= 3 | issue= 8 | pages= 806-11 | pmid=20723851 | doi=10.1016/j.jcin.2010.05.012 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20723851 }} </ref>
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