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Residents' clinic Mayo Clin Proc. • August 2010;85(8):e52-e55 • doi:10.4065/mcp.2009.0548 • www.mayoclinicproceedings.come52 For personal use. Mass reproduce only with permission from Mayo Clinic Proceedingsa . 40-Year-Old Man With Nausea and Vomiting “Found Down” Residents' clinic R. Jay Widmer, MD, PhD*; Jeffrey B. Geske, MD*; and Ian P. Clements, MD† *Resident in Internal Medicine, Mayo School of Graduate Medical Education, Mayo Clinic, Rochester, MN. †Adviser to residents and Consultant in Cardiovascular Diseases, Mayo Clinic, Rochester, MN. See end of article for correct answers to questions. Individual reprints of this article are not available. Address correspondence to R. Jay Widmer, MD, PhD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905. © 2010 Mayo Foundation for Medical Education and Research A 40-year-old man with a history of prior closed head injury, insulin-dependent diabetes mellitus type 2, and nicotine dependence was evaluated at Saint Marys Hospi- tal, a Mayo Clinic–affiliated hospital in Rochester, MN, after being found unconscious at his home. On arrival at Saint Marys Hospital, the patient was lucid and relayed that earlier in the day he had experienced sudden-onset malaise while moving a mattress at his cousin’s home. After eating a sand- wich, he noted a finger-stick glucose reading of greater than 400 mg/dL. He proceeded to take 40 U of subcutaneous glargine insulin. When a recheck 1 hour later yielded an identical blood glucose, he administered an additional 40 U of glargine insulin. After this injection, he had an unwitnessed loss of consciousness. His family noted that, 3 years before presentation, he had sustained a closed head injury with residual “spells” in which he would seize before losing consciousness. His cousin found him down and called emergency medical services. On arrival, the paramedics found him to be responsive but confused and nauseated with bradycardia (heart rate, 45 beats/min). The patient was transported to a Mayo satellite facil- ity emergency department, where he reported symptoms of heartburn and nausea and experienced vomiting. The pa- tient was hemodynamically stable with a pulse of 80 beats/ min and a blood pressure of 121/60 mm Hg. While in the emergency department, he had episodic periods of altered consciousness lasting 10 to 15 seconds, during which he would become disoriented, agitated, nauseous, and combat- ive. Initial diagnostic evaluation included chest radiography, computed tomography of the head, a basic chemistry panel, blood glucose measurement, and a urine toxicology screen, findings on all of which were unremarkable. Initial treatment was limited to 125 mL/h of intravenous normal saline, 324 mg of aspirin, and 4 mg of ondansetron. Given his altered consciousness, he was transferred via helicopter to a higher level of care at Saint Marys Hospital. On arrival, the patient was experiencing sinus bradycardia (heart rate as low as 40- 50 beats/min, with systolic blood pressure ranging from 80 to 90 mm Hg. Physical examination revealed a moderately distressed and writhing patient with crackles at the bases of his lungs, a jugulovenous pulsation of 10 cm H 2 O, a pul- monary artery tap, 2+ pulses in all 4 extremities without edema, and a regular, quiet S 1 and S 2 without murmurs, rubs, or gallops. Shortly after arrival at Saint Marys Hospital, the patient experienced a sinus arrest and was treated with two 0.5-mg doses of atropine and 1 round of cardiopulmonary resuscitation. 1. Given the patient’s presentation, which one of the following is the most appropriate initial test? a. Magnetic resonance imaging (MRI) of the head b. Glycated hemoglobin measurement c. Serum toxicology screen d. Serial troponin assay e. D-dimer assay In a hemodynamically unstable patient with new ar- rhythmia, appropriate initial diagnostic evaluation is critical. Although increased intracranial pressure or stroke could manifest with altered mental status, nausea, and vomiting, unremarkable findings on computed tomogra- phy of the head performed before arrival make intracra- nial pathology less likely. The presence of hyperglycemia and recent high-dose insulin administration should alert the physician to constantly monitor blood glucose levels and treat appropriately. However, glycated hemoglobin is not the test of choice in an emergent situation1 because it reflects long-term glycemic control and will not alter emergent management. Evaluation for intoxication is a reasonable test in a patient found down; however, a serum toxicology screen is not likely to add substantial diagnos- tic value in this patient with a negative urine toxicology screen. Levels of serial cardiac biomarkers, namely tro- ponins, are likely to be elevated in the setting of recent cardiopulmonary resuscitation. That said, trending these markers is needed to evaluate for ischemia in the setting of a life-threatening cardiac arrest. Pulmonary embolism should be considered in patients with acute hemodynamic instability; however, this patient’s Wells score for pul- monary embolism was zero.2 In the setting of recent car- diopulmonary resuscitation, an elevated D-dimer level is expected and thus is not likely to be of value in diagnostic evaluation. Residents' clinic Mayo Clin Proc. • August 2010;85(8):e52-e55 • doi:10.4065/mcp.2009.0548 • www.mayoclinicproceedings.com e53 For personal use. Mass reproduce only with permission from Mayo Clinic Proceedingsa . Initial electrocardiography revealed sinus bradycardia, minimal ST-T abnormalities, and no T-wave inversion or peaking (Figure 1). Computed tomography revealed no aortic dissection or pulmonary embolism. The patient was admit- ted to the cardiac care unit, where hemodynamic instability persisted, with worsened hypotension (blood pressure, 80/50 mm Hg), persistent bradycardia (heart rate, 40 beats/min), and continued nausea and vomiting. The patient denied any chest discomfort. Findings on the initial troponin T assay were positive (0.82 ng/mL), but findings on the serum electrolyte panel and the complete blood cell count were unremarkable. 2. Which one of the following is the most appropriate next diagnostic step in this case? a. Await the results of serial troponin assays b. Perform cardiac MRI c. Perform transesophageal echocardiography d. Place right-sided and posterior electrocardiographic (ECG) leads e. Perform an adenosine-sestamibi scan Given the patient's hemodynamic instability and clini- cal decline without a clearly identified etiology, further urgent evaluation is needed. Awaiting further blood tests to trend the patient’s troponins will likely result in delayed diagnosis and treatment. Cardiac MRI may very well show wall motion abnormalities in high resolution, especially when gated to ECG. However, the patient is too unstable to be transported to such a time-intensive test. Echocar- diography can be useful in showing right ventricular (RV) dysfunction in an RV infarct, but images can be difficult to obtain and can delay angiography.3 Bedside transthoracic echocardiography would likely be the test of choice in this unstable patient because transesophageal imaging is not likely to add substantial benefit and will require sedation. Right-sided and posterior electrocardiography are current- ly a class I recommendation by the American Heart Asso- ciation/American College of Cardiology 2007 guidelines in patients with suspected right-sided myocardial infarc- tion.4 These diagnostic tools are 78% sensitive5 and have a specificity of over 85%, making placement of right-sided and posterior ECG leads the most appropriate next diag- nostic step in this patient. In this case, right-sided and pos- terior ECGs revealed no evidence of ischemia. In addition, nuclear imaging is not feasible in this patient given time restraints. Emergent bedside echocardiography revealed a left ventricular ejection fraction of 56%, no regional wall motion abnormalities, and a relatively unremarkable RV systolic pressure of 24 mm Hg (systolic pressure at the time of examination was 93 mm Hg) despite the physical finding of a pulmonary artery tap. Ultimately, positive findings on initial troponin assays in a high-risk patient in the setting of hemodynamic instability should lead to the decision to send the patient to the cardiac catheterization laboratory. 3. Given this patient’s symptoms, rhythm disturbance, and symptoms, which one of the following would be the expected finding on coronary angiography? a. Left circumflex coronary artery occlusion b. Left anterior descending coronary artery occlusion c. Right coronary artery occlusion d. Aortic dissection e. Ventricular septal rupture Myocardial infarction typically presents with anginal chest pain but can manifest with alternative symptoms, particularly in patients with diabetes.4 Even with no evi- dence of ischemia on initial electrocardiography (Figure 1), the patient’s positive troponin assay, arrhythmia, mul- tiple risk factors, absence of alternative diagnosis, and continued hemodynamic deterioration should prompt immediate evaluation for coronary artery disease. Left circumflex occlusions rarely present with conduction dis- turbances because the circumflex supplies the sinoatrial node, atrioventricular node, or His bundle only 10% to 40% of the time. ST-T changes in anterior leads would correspond to a left anterior descending artery distribu- tion, which is not consistent with this patient’s presen- tation. Inferior infarction most typically corresponds to right coronary artery occlusion and predominantly affects the right ventricle. This patient displays typical signs and symptoms (ie, sinus arrest, nausea, and vomit- ing) of an inferior myocardial infarction, usually involv- ing the myocardium of the right ventricle.6 Aortic dis- section might cause some of these symptoms; however, the presentation would be much more dramatic in terms of hemodynamic changes. Septal wall rupture would not present with these hemodynamic parameters and would be visible on echocardiography. FIGuRE 1. Routine left-sided electrocardiogram obtained because patient was experiencing bradycardia and nausea. Sinus bradycar- dia is noted, with no significant ST-T abnormalities. Residents' clinic Mayo Clin Proc. • August 2010;85(8):e52-e55 • doi:10.4065/mcp.2009.0548 • www.mayoclinicproceedings.come54 For personal use. Mass reproduce only with permission from Mayo Clinic Proceedingsa . Coronary angiography revealed an acute, fully occluded proximal right coronary artery lesion with thrombus (Fig- ure 2, left). Catheter-directed thrombus extraction, balloon angioplasty, and placement of a drug-eluting stent were performed. Postintervention images are shown in the right panel of Figure 2. 4. Given the patient’s diagnosis and hemodynamics, which one of the following additional therapies should be recommended in the short term? a. β-blockade b. Nitroglycerin infusion c. Reduction of myocardial oxygen demand with morphine d. Intravenous fluid administration e. Afterload reduction with an angiotensin-converting en zyme inhibitor Physicians should use extreme caution when using preload-reducing agents such as β-blockers, nitroglycer- in, and morphine in the preload-dependent state of right- sided myocardial infarction because doing so may cause systemic pressures to plummet.6,7 Ultimately, there is one primary means by which to treat this type of myocardial infarction—intravenous fluids. This treatment is known to increase preload in the right ventricle and allow cardi- ac output to be maintained.8 Afterload reduction with an angiotensin-converting enzyme inhibitor has been shown to be beneficial after myocardial infarction but should also be used with caution so as not to reduce preload as in the case of β-blockade. However, this contraindication is not as strong as it is with β-blockade and nitroglycerin. Thus, initial treatment, both before and after catheteriza- tion, should consist of intravenous fluid administration.6 The patient returned from the cardiac catheterization lab to the cardiac care unit in stable condition. He received a total of 1.2 L of intravenous fluid resuscitation. 5. Given this patient’s diagnosis, which one of the follow- ing is the highest predictor of mortality? a. Myocardial infarction size b. ST elevation in lead V4R c. Age d. Time to presentation e. Pacemaker implantation The diagnosis of RV infarction portends a poor prognosis for patients, with mortality increased by as much as 50% in patients who have LV infarcts that also involve the RV.4 Infarct size can serve as an indicator of mortality when discussing overall infarct prognosis. However, those who survive the ini- tial event show a favorable long-term outcome.9 ST-elevation in lead V4R increases in-hospital mortality (31% vs 6%)5 but not to the extent that age does. Patients older than 75 years have an increased in-hospital mortality (47%),10 which is the greatest indicator of morbidity and mortality in RV infarcts. This increase in morbidity and mortality is mostly due to cardiogenic shock and interventricular rupture.10 Delayed presentation to a hospital can adversely affect survival,11 yet differences seen in trials may be related to the nature of early intervention (thrombolysis vs angiography). Pacemaker implantation is a common consequence associated with RV infarcts; however, pacemaker dependence does not impart substantially higher mortality, and indeed pacemaker therapy serves to improve survival.5 Thus, age is the primary determi- nant of prognosis in patients with RV infarcts. The patient was discharged in less than 1 week, after adjustment to his blood pressure medications and insulin regimen and tobacco cessation counseling. Discussion Although the outcome in this patient was good, right-sided in- farcts have the potential to catch physicians off-guard because FIGuRE 2. Coronary angiography demonstrated a completely occluded right coronary artery (left). After thrombectomy and drug-eluting stent deployment, patency of the vessel was noted with TIMI-III flow (right). Residents' clinic Mayo Clin Proc. • August 2010;85(8):e52-e55 • doi:10.4065/mcp.2009.0548 • www.mayoclinicproceedings.com e55 For personal use. Mass reproduce only with permission from Mayo Clinic Proceedingsa . of their nontypical presentation and the special circumstances surrounding the management of such infarcts. Right ven- tricular infarcts are seen in 10% to 50% of inferior infarcts, with occlusion of the proximal right coronary artery typically the culprit lesion.9 The classic presentation of hypotension, increased jugulovenous pressure, and clear lung fields are typically described during RV involvement, and this triad is fairly specific for the presentation of this type of infarct. These findings are due to the acute failure of the RV, which causes an elevation in the right atrial and vena caval pressures and a concomitant decrease in cardiac output to the pulmonary and systemic vascular beds. The Bezold-Jarisch reflex, hypopnea, and bradycardia can also be seen with right-sided infarcts.6 However, as this patient demonstrated, the presentation can include chest pain–free patients with nausea and vomiting. On physical examination, RV infarction classically pres- ents with Kussmaul sign (increased jugulovenous distention with inspiration), pulsus paradoxus (decrease in systolic blood pressure of >10 mm Hg with inspiration), an RV heave, a pul- monary artery tap, an RV S 3 or S 4 , and a positive hepatojugular reflex.6 The likelihood of detecting these physical findings in our patient was considerably compromised because of his nausea, vomiting, and agitated state. Although some elevated jugulovenous pulsations and an RV heave were noted, heart sounds were distant and his writhing prevented evaluation of the hepatojugular reflex and pulsus paradoxus. Diagnostic evaluation should include electrocardiography with right- sided and posterior leads, as well as measurement of cardiac biomarker levels.4 A greater ST elevation in lead III than lead II is often indicative of a right coronary artery occlusion manifesting as an RV infarct. Likewise, right-sided precordial lead V4R demonstrates the greatest sensitivity and specificity for an RV infarct.4 Although other diagnostic tools, such as invasive hemodynamic assessments, echocardiography, and nuclear imaging, may be helpful in diagnosing an RV infarct, typically time does not allow for these formal studies and the patient should be referred for cardiac catheterization if the clinical suspicion of an RV infarct is high.9 In the setting of an RV infarct, the clinician must be cognizant that hemodynamic complications could lead to a low cardiac output state (eg, bradyarrhythmias), hypotension from low filling pressures, increased incidence of ventricular tachyarrhythmias, and mechanical complications such as tricuspid regurgitation.8 Initial management should include early reperfusion and maintenance of RV preload with intra- venous fluids.6 There are no good data to indicate the amount of fluid needed, but current thought is to titrate to accept- able mean arterial pressure or up to 15 mm Hg pulmonary capillary wedge pressure if Swan-Ganz catheter insertion is deemed necessary.7,8 Inotropic therapy may be necessary early in the treatment of RV infarcts to maintain cardiac out- put, and dopamine is preferred over afterload reduction, with RefeRences 1. 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Zahn R, Schiele R, Gitt AK, et al; Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) Study Group; Myocardial Infarction Registry Study Group. Impact of prehospital delay on mortality in patients