Heartburn other diagnostic studies

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2] Ahmed Elsaiey, MBBCH [3] Cafer Zorkun, M.D., Ph.D. [4]

Other Diagnostic Studies

Overview

Other diagnostic findings present in heartburn and consistent with diagnosis of gastroesophageal reflux disease (GERD) is the presence of acidic reflux in the esophagus through the ambulatory reflux monitoring.

Other diagnostic studies

Ambulatory reflux monitoring

  • GERD is mostly diagnosed clinically by the presenting typical symptoms which include heartburn, regurgitation, and dysphagia.
  • Correlation of the GERD symptoms with confirmed acid presence by the ambulatory reflux monitoring is strongly suggestive of GERD.
  • Ambulatory reflux monitoring is recommended by the American College of Gastroenterology (ACG) as the only laboratory test to determine the presence of acidic reflux in the esophagus.[1]
  • Indications of ambulatory reflux monitoring include the following:[2]
    • GERD diagnosis if it is not confirmed
    • Determine the time of reflux occurrence
    • Refractory GERD symptoms
    • Preoperative for non-erosive disease
  • Ambulatory reflux monitoring is performed in either two ways which include:
    • Telemetry capsule (48 hours monitoring)
    • Transnasal catheter (24 hours monitoring)

Upper Gastrointestinal (GI) Series

A series of x-rays of the upper digestive system are taken after drinking a barium solution. These can demonstrate reflux of barium into the esophagus, which suggests the possibility of gastroesophageal reflux disease. More accurately, fluoroscopy can be used to document reflux in real-time.

Biopsy

A small sample of tissue from the esophagus is removed. It is then studied to check for inflammation, cancer, or other diseases.

Electrocardiogram

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.[3]

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.[4] In clinical practice, hyperacute T waves are rarely seen, because they exists for only 2-30 minutes after the onset of infarction.[5] Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia.[6]

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.[3] 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.[7]

ST Depression

ST depression in the anterior leads might either represent reciprocal changes on EKG[8] or might be pathologically caused by either anterior ischemia in the context of a patent artery[9] or posterior infarct due to the complete occlusion of a coronary artery.[10]

References

  1. Katz PO, Gerson LB, Vela MF (2013). "Guidelines for the diagnosis and management of gastroesophageal reflux disease". Am J Gastroenterol. 108 (3): 308–28, quiz 329. doi:10.1038/ajg.2012.444. PMID 23419381.
  2. 2.0 2.1 Katz PO, Gerson LB, Vela MF (2013). "Guidelines for the diagnosis and management of gastroesophageal reflux disease". Am J Gastroenterol. 108 (3): 308–28, quiz 329. doi:10.1038/ajg.2012.444. PMID 23419381.
  3. 3.0 3.1 "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.
  4. Somers MP, Brady WJ, Perron AD, Mattu A (2002). "The prominant T wave: electrocardiographic differential diagnosis". Am J Emerg Med. 20 (3): 243–51. PMID 11992348. Unknown parameter |month= ignored (help)
  5. Smith SW, Whitwam W. "Acute Coronary Syndromes." Emerg Med Clin N Am 2006; 24(1): 53-89. PMID 16308113
  6. "The clinical value of the ECG in noncardiac conditions." Chest 2004; 125(4): 1561-76. PMID 15078775
  7. Smith SW, Whitwam W (2006). "Acute coronary syndromes". Emerg. Med. Clin. North Am. 24 (1): 53–89, vi. doi:10.1016/j.emc.2005.08.008. PMID 16308113. Unknown parameter |month= ignored (help)
  8. Norell MS, Lyons JP, Gardener JE, Layton CA, Balcon R (1989). "Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty". J Am Coll Cardiol. 13 (6): 1270–4. PMID 2522957.
  9. Gibson CM, Chen M, Angeja BG, Murphy SA, Marble SJ, Barron HV; et al. (2002). "Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery". J Thromb Thrombolysis. 13 (1): 9–12. PMID 11994554.
  10. Pride YB, Tung P, Mohanavelu S, Zorkun C, Wiviott SD, Antman EM; et al. (2010). "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". JACC Cardiovasc Interv. 3 (8): 806–11. doi:10.1016/j.jcin.2010.05.012. PMID 20723851.