Your fifty five year old patient complains of chest pain radiating to the left arm you should first

A 35-year-old female presents with a 1-hour history of chest pain, which resolved spontaneously. The pain is described as a chest pressure radiating to both arms. The patient is a smoker but has no other risk factors (no family history of cardiac disease, hypertension, diabetes, hyperlipidemia, etc.). The patient is diaphoretic and has a normal blood pressure. Physical examination reveals that the patient has tenderness to palpation of the anterior chest wall that reproduces the chest pressure. She is now otherwise free of chest pain and all her lab assays, including cardiac enzymes, are normal.

Question 2.1.1 Which of the following is true about this patient's physical findings and history?

A) Pain radiating to both arms makes it unlikely that this patient's pain is cardiac.

B) The physical findings that are most highly associated with an acute myocardial infarction (AMI) include hypotension, diaphoresis, and a new S3 gallop.

C) The absence of risk factors makes it unlikely that this patient has cardiac disease.

D) The fact that the pain is reproducible on palpation of the chest wall effectively rules out cardiac disease.

E) Based on the information available, further cardiac evaluation is unnecessary.

Answer 2.1.1 The correct answer is "B." The findings that are most likely to be associated with an AMI are hypotension, diaphoresis, and a new S3 gallop. "A" is not true because pain radiating to both arms can still be associated with cardiac disease. In fact, compared with left arm radiation, right arm radiation or bilateral arm radiation doubles the likelihood of the pain being cardiac (LR 2.3 for radiation to the left arm vs. LR 4.1–4.7 for radiation to the right or bilateral arms). (JAMA. 2005;294(20):2623–2629.) Women with AMI often present atypically and may experience more chest pain radiating to the right arm/shoulder and the anterior neck or with abdominal pain as compared with men. "C" is incorrect. The absence of risk factors is only one consideration in the evaluation of this patient. Smoking, hypertension, family history, etc., do not change the prior probability of cardiac disease enough to allow them to be used to rule out or rule in cardiac disease. Of note, male gender and diabetes DO increase the pretest probability of coronary artery disease (CAD) (luckily our patient is a woman!). Evaluation of pretest probability is important in the diagnostic algorithm, but should be used in addition to, not in exclusion of, clinical judgment and findings. "D" is incorrect. It is true that chest pain reproduced by palpation of the chest wall makes cardiac disease less likely. However, 15% of patients with cardiac disease and 17% of patients with a pulmonary embolism (PE) will have their pain reproduced by chest wall pressure. This does not mean that you are making their cardiac pain worse. It is likely because of the patient's inability to discriminate between the types of pain (cardiac vs. chest wall).

You decide that further testing is warranted, including an ECG and cardiac enzymes.

Question 2.1.2 Which of the following statements is TRUE?

A) A normal initial ECG in the emergency department (ED) effectively rules out cardiac disease.

B) Creatine phosphokinase MB fraction (CPK-MB) is more sensitive but less specific than troponin.

C) Serum troponin is an unreliable marker of cardiac ischemia in patients with renal failure.

D) The serum troponin is 100% specific for myocardial infarction.

E) A normal troponin and CPK in the ED cannot be used to make decisions about who to admit.

Answer 2.1.2 The correct answer is "E." Except in cases where the chest pain has been continuous for over 12 hours, normal cardiac enzymes (troponin, CPK-MB) do not rule out cardiac disease. If they did, we would not admit patients for a "rule out" but would rather rely on the single level drawn in the ED. "A" is incorrect since 9% of patients with AMI will have a normal initial ECG in the ED. In fact, only about 50% of those with AMI have a diagnostic ECG in the ED. Even a normal ECG obtained during chest pain does not reliably rule out AMI (Acad Emerg Med. 2009;16:495). "B" is incorrect since the CPK-MB is overall less sensitive than a high sensitivity troponin. CPK-MB and myoglobin may become positive earlier than the troponin. However, CPK-MB and myoglobin add little, if anything, to the troponin; many labs no longer perform these assays in house. Eighty percent of AMIs will have one positive marker within the first 3 hours of ED arrival (but 20% will not). "C" is incorrect. Patients with renal disease may have a mildly elevated troponin at baseline due to poor clearance, but troponin can still be useful in these patients if it continues to rise. It may be useful to have knowledge of the patient's baseline troponin in renal failure, but this is NOT an indication to start drawing a baseline troponin on all of your patients with renal failure. "D" is incorrect because we now know that other processes, such as PE, can elevate the serum troponin.

Elevated troponin levels may be due to conditions other than AMI, including heart failure, PE, burns, sepsis or other critical illness, stroke, and more.

The new ultra-sensitive troponin may be positive within 3 hours. You need to know what test your hospital is doing. Troponin levels peak in about 36 hours after an infarct and may stay elevated for 7 to 10 days, so the infarct may have occurred anywhere within this time frame. Follow the trend of the troponin to help determine when the infarct occurred.

Question 2.1.3 All of the following statements are true EXCEPT:

A) All myocardial infarctions present with chest pain.

B) Dyspnea may be the only presenting symptom of myocardial infarction.

C) Patients with myocardial infarction can present with syncope.

D) Females, the elderly, and diabetic patients are more likely to present with atypical symptoms of myocardial infarction.

Answer 2.1.3 The correct answer is "A." As the saying goes, "Never say never, and never say always." Many elderly and diabetic patients ("D") will present with atypical symptoms or painless, "silent" myocardial infarctions. In fact, up to 30% of myocardial infarctions are pain free. "B" is a correct statement because, especially in the elderly, dyspnea may be the only presenting symptom due to left ventricular failure secondary to ischemia. "C" is a correct statement because syncope (as well as lightheadedness and fatigue) can be presenting symptoms of a myocardial infarction.

Her ECG shows nonspecific ST-T changes.

Question 2.1.4 Which of the following drug(s) is/are indicated in the initial management of this patient?

B) Thrombolytic such as tPA or streptokinase.

D) Glycoprotein IIb/IIIa inhibitor (e.g., apciximab [ReoPro]).

E) All of the above.

Answer 2.1.4 The correct answer is "A." Immediate therapy in the ED requires ASA 325 mg orally (chewed). Since we are not sure that this patient has AMI or unstable angina, there is no indication for thrombolytic therapy ("B"), heparin ("C") or glycoprotein IIb/IIIa inhibitor ("D"). Since she is currently pain free, heparin carries more of a risk than a benefit at this juncture and is not recommended. However, all patients with possible angina or an AMI should have aspirin unless they are truly allergic (hives, anaphylaxis). "B" is incorrect because thrombolytics are indicated for acute ST elevation myocardial infarctions (STEMI), not for a simple chest pain evaluation.

Should "MONA (morphine, oxygen, nitroglycerin, aspirin) greet all patients," as the editors learned in med school? Per more recent 2010 Cochrane Database Systematic Review, the efficacy of oxygen in AMI has been questioned and may even be detrimental in those with a normal oxygen saturation (94% or greater, Cochrane Database Syst Rev. 2010;6:CD007160). So, withhold oxygen unless the oxygen saturation is <94%. Morphine should be used only after a patient fails specific therapy, such as aspirin and nitroglycerin. And nitroglycerin does not change infarct size.

Current use of warfarin or aspirin should not preclude the administration of aspirin in the ED for a patient with chest pain that may be cardiac in origin. You never know whether the patient is actually taking it or not. So, unless there is a real allergy to aspirin, it must be given to chest pain patients in the ED.

The patient tells you that she is allergic to aspirin, which causes hives and bronchospasm. She can, however, take other nonsteroidal anti-inflammatory drugs (NSAIDs) without difficulty. Oh, great. Now you need to go to plan B (no, not the "morning after pill").

Question 2.1.5 Which of the following is an acceptable substitute for aspirin in this situation?

Answer 2.1.5 The correct answer is "B." Clopidogrel in a loading dose of 600 mg can be used as a substitute for aspirin in the setting of unstable angina or AMI. "A" is incorrect because dipyridamole (in combination with aspirin) is indicated only for stroke prevention. Dipyridamole itself is a relatively weak platelet inhibitor. "C" is incorrect because ibuprofen and naproxen are reversible platelet inhibitors that do not give adequate platelet inhibition and have NOT been shown to be of benefit in angina/AMI. In addition, both ibuprofen and naproxen can block the effect of aspirin by making its binding sites on platelets unavailable. In fact, stopping NSAIDs in any patient being admitted for possible CAD is considered good practice; they increase the risk of a cardiac event. "D" and "E" are both incorrect because celecoxib and salsalate have not been shown to inhibit platelets to a significant degree and thus would be of no use in this situation.

Note that the loading dose of clopidogrel has been increased from 300 to 600 mg. But either is likely an acceptable answer on the board examination (and in practice). Newer antiplatelet agents, such as prasugrel (Effient) and ticagrelor (Brilinta) are becoming more widely used as loading agents. However, bleeding risks are higher with the newer agents.

Of the NSAIDs (except aspirin), naproxen appears to carry the lowest cardiac risk. However, it has more GI side effects. Cox-2 inhibitors, such as celecoxib, and diclofenac are GI friendly but have more adverse cardiac events. Ibuprofen acts more like naproxen (Lancet. 2013;382(9894):769–779). Guidelines suggest stopping all NSAIDs (except aspirin) upon admitting a patient for ACS or a question of ACS. Please do not use ketorolac to treat chest pain as this is also an NSAID.

Well, not all chest pain is cardiac, and this patient may have another cause for hers.

Question 2.1.6 Which of the following is TRUE?

A) Giving a "GI cocktail" (e.g., combination of Maalox and viscous lidocaine) can reliably differentiate cardiac from esophageal/GI causes of chest pain.

B) A normal chest radiograph and symmetrical pulses in the upper extremities reliably rules out a thoracic aortic dissection.

C) Most patients with a spontaneous pneumothorax should be treated with a chest tube.

D) If nitroglycerin relieves the chest pain, then the pain is certainly cardiac.

E) Pain is a finding in only about 60% of patients with a PE.

Answer 2.1.6 The correct answer is "E." Only a small majority (59%) of patients with pulmonary emboli have pain as a feature. "A" is incorrect because about 20% of patients with cardiac pain will have their pain relieved by a GI cocktail. Conversely, "D" is incorrect because nitroglycerin can relieve pain from esophageal spasm as it is a nonselective smooth muscle relaxer. "B" is incorrect because only 50% of patients with an aortic dissection will have unequal pulses and blood pressures, and only 75% will have an abnormal chest x-ray. The consideration of an aortic dissection mandates a chest CT scan with contrast, transesophageal echo, or angiogram. Remember that about 20% of the population will have unequal blood pressures in the upper extremities at baseline. "C" is incorrect because most patients with spontaneous pneumothorax can be treated with a "pigtail" catheter with a Heimlich valve. This type of treatment reduces the morbidity associated with a chest tube.

Chest x-ray findings in patients with thoracic aortic dissection may include widened mediastinum, obliterated aortic knob, pleural "capping," tracheal deviation, depression of left main stem bronchus, esophageal deviation, and loss of the paratracheal stripe.

The patient's pain recurs in the ED. You suspect that she is having a myocardial infarction, but do not yet have unequivocal proof, such as ECG changes or elevated cardiac enzymes. The patient becomes markedly hypotensive in response to another dose of sublingual nitroglycerin.

Question 2.1.7 Which of the following is TRUE?

A) Intravenous nitroglycerin is contraindicated in this patient.

B) Hypotension caused by nitroglycerin is usually unresponsive to IV saline.

C) Hypotension caused by nitroglycerin may be indicative of a right ventricular infarction, which is most commonly associated with an inferior wall myocardial infarction (IAMI).

D) Hypotension caused by nitroglycerin is diagnostic of cardiogenic shock, suggesting that this patient will have a poor outcome.

Answer 2.1.7 The correct answer is "C." Hypotension in response to nitroglycerin may be indicative of a right ventricular infarct, which is most commonly associated with an inferior wall MI (IAMI). Since the right ventricle is dependent on filling pressure (preload), nitroglycerin, which drops the preload, will frequently result in hypotension in those with a right ventricular infarct. "A" is incorrect because hypotension from sublingual nitroglycerin is not a contraindication to additional nitrates once the patient's blood pressure is stable. A typical sublingual dose is 400 μg (0.4 mg). A typical IV dose starts at 20 μg/min. Thus, the sublingual dose is quite a bit larger than the IV dose. In such a situation, you could consider starting IV nitroglycerin at 10 to 20 μg/min and titrating up as the blood pressure allows. "B" is incorrect because hypotension from nitroglycerin will generally respond to a saline bolus. "D" is incorrect. Certainly, patients with cardiogenic shock will be hypotensive, but hypotension with nitroglycerin is a common result of the drug itself and does not define cardiogenic shock.

Consider holding beta-blockers in inferior wall acute MI (IAMI), as these patients often have bradycardia and heart block. Also, beware of atypical presentations of IAMI such as nausea, vomiting, and other GI symptoms. Hold beta-blockers in those with hypotension, heart block or heart failure.

Question 2.1.8 Which of the following is TRUE of patients with an IAMI?

A) They will likely continue to have problems with right ventricular functioning in the future.

B) They will need to increase their salt intake in order to increase preload and right ventricular filling pressure.

C) Their right ventricular function should return to normal or close to normal following their infarction.

D) A and B.

Answer 2.1.8 The correct answer is "C." Most patients will have return of right ventricular functioning following a myocardial infarction. "B" is incorrect because there will be no need to increase right ventricular filling pressure (which is what IV saline does acutely) once right ventricular function returns to normal.

The patient's pain continues despite treatment with nitroglycerin, and you obtain another ECG (Fig. 2-1).

FIGURE 2-1. ECG for patient in question 2.1.9.

Question 2.1.9 Which of the following is TRUE regarding this ECG?

A) This injury pattern on ECG is most consistent with an anterior wall MI.

B) In this situation, intervention in the cath lab with percutaneous transluminal coronary angioplasty (PTCA) and stent placement is superior to tPA or other thrombolytic.

C) This injury pattern on ECG is most consistent with pericarditis.

D) This injury pattern on ECG proves that this patient does not have an aortic dissection.

E) This pattern on ECG is totally fine. What, me worry?

Answer 2.1.9 The correct answer is "B." Intervention in the cath lab with PTCA and/or stent placement is superior to thrombolytic therapy in the treatment of AMI, provided that the "door to balloon" time is 90 minutes or less. In cases where the patient is located in a facility without a cardiac catheterization laboratory, the patient may receive thrombolytic therapy. "A" is incorrect because this pattern is indicative of an inferior wall, not an anterior wall, MI. You will note that this ECG shows ST elevations in leads II, III, and aVF (inferior leads) along with reciprocal ST segment depression in leads V1 and V2. An anterior wall MI is defined by ST elevations in leads V3, V4, and V5, and an anteroseptal MI shows ST elevations in leads V1, V2, and V3. For IAMI concerning for RV infarction, consider "right-sided chest leads." "D" is incorrect because patients with pericarditis should have ST elevations in all leads (although an ECG is only 80% sensitive for pericarditis). "D" is incorrect because patients with an aortic dissection can present with an abnormal ECG that looks similar to an infarct pattern. So, ECG changes do not prove that the patient does not have an aortic dissection. "E" is just plain wrong and you should be worried if you see this pattern!

You now have all the evidence that you need to show that this patient is indeed having an ongoing myocardial infarction. Since your rural hospital is "just around the corner from nowhere," stenting is not going to happen within 90 minutes. You decide to initiate thrombolytic therapy.

Question 2.1.10 All of the following are true statements EXCEPT:

A) Patients who are candidates for thrombolytics must have at least 1 mm of ST-segment elevation in at least 2 contiguous limb leads or at least 1 to 2 mm of ST-segment elevation in at least 2 contiguous precordial leads.

B) Patients who are candidates for thrombolytics must have an absence of prior history of hemorrhagic stroke within the past year.

C) Patients who are candidates for thrombolytics should have no active bleeding, including menstrual bleeding.

D) Patients who are candidates for thrombolytics should have no history of recent head trauma.

E) Patients who are candidates for thrombolytics should not be pregnant.

Answer 2.1.10 The correct answer is "C." While active internal bleeding is a contraindication to the use of thrombolytics, menstrual bleeding is not. While there are no controlled trials, anecdotal evidence suggests that thrombolytics are safe with menstrual bleeding. "A" is correct. In addition to these ECG criteria, the presence of a new complete left bundle branch block (LBBB) with characteristic MI pain also indicates that the patient may benefit from thrombolysis. Patients with only ST-segment depression or a normal ECG, even with symptoms, do not benefit. "B," "D," and "E" are all true statements. Patients are not candidates for thrombolytics if they have recent head trauma, are pregnant, or have had a hemorrhagic stroke in the last year. There are additional criteria for and contraindications to the use of thrombolytics. See Tables 2-1A and 2-1B.

TABLE 2-1AACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION

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TABLE 2-1A ACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION

Class 1 recommendations for the use of thrombolytics in myocardial infarction include any ONE of the following three ECG findings:

• ≥1 mm of ST-segment elevation in at least 2 contiguous limb leads

• 1–2 mm of ST-segment elevation in at least 2 contiguous precordial leads

• New complete bundle branch block that obscures the ST segment analysis plus a history suggestive of MI

And

• Presenting 12 hours since the onset of pain, age <75 years (although treating those >75 years of age is still a class 2 recommendation below)

Class 2 recommendations for the use of thrombolytics in myocardial infarction include any ONE of the following:

• ≥1 mm of ST-segment elevation in at least 2 contiguous limb leads and age >75 years OR presenting 12–24 hours after onset of infarction

• 1–2 mm of ST-segment elevation in at least 2 contiguous precordial leads and age >75 years OR presenting 12–24 hours after the onset of infarction

• Blood pressure of >180 mm Hg systolic and >100 mm Hg diastolic in a patient with a "high-risk" myocardial infarction (e.g., the high risk of the MI mitigates the warning about thrombolytic use in uncontrolled hypertension)

TABLE 2-1BACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION

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TABLE 2-1B ACC/AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH ST-ELEVATION MYOCARDIAL INFARCTION

"Facilitated PCI," that is, administration of thrombolytics with the intent to perform PCI within 2 or more hours of giving thrombolytics has very mixed (and mostly negative) data. Outcomes are worse (and not just because PCI is a "rescue" technique at this point). It certainly is NOT the standard of care and, in fact, is no longer considered as part of the treatment algorithm. If thrombolytics versus primary PCI is being considered, it is valuable to contact the cardiologist at the cath center to determine whether he/she would like thrombolytics before transfer—timing (both from symptom onset and for transfer) is central to the decision making process. "Rescue PCI" for failed reperfusion after thrombolytic therapy should be performed as soon as logistically possible, ideally within the first 24 hours, but NOT within the first 2 to 3 hours postthrombolytic therapy.

Remember to repeat the ECG after thrombolytics to prove that ST elevations have resolved. Evidence of successful reperfusion after thrombolytics is suggested by: nearly sudden and complete relief of chest pain, >70% ST elevation resolution in the index lead showing the greatest degree of elevation, plus or minus the presence of reperfusion arrhythmia.

After conferring with your closest cath center, you give a thrombolytic—and cross your fingers. Unfortunately, the patient develops a new LBBB. In addition, the ECG shows evidence of a first-degree heart block (a prolonged PR interval), although the heart rate remains normal at 80 bpm.

Question 2.1.11 The proper response to this is to:

A) Insert a Swan–Ganz catheter to monitor central pressures.

B) Insert a temporary pacemaker regardless of the heart rate.

C) Administer atropine to this patient.

D) Administer isoproterenol to this patient.

E) Do nothing, other than observe this patient.

Answer 2.1.11 The correct answer is "B." For patients with an AMI, a transvenous pacemaker should be inserted if she develops (1) complete heart block, (2) second-degree heart block type II (Mobitz II), or (3) new LBBB with first-degree AV block. See Tables 2-2 and 2-3 for more on arrhythmia and pacemakers in the setting of AMI. "A" is incorrect because a Swan-Ganz catheter will be of no help in arrhythmias. "C" is incorrect because atropine is indicated for symptomatic bradycardia and not for a bundle branch block. "D" is incorrect for the same reason as "C." In addition, isoproterenol is arrhythmogenic and is no longer recommended. "E" is incorrect because the patient may rapidly progress into a complete heart block. Of note and importantly, the placement of a transvenous pacemaker should not delay transfer for catheterization since a pacemaker may be placed in the cath lab. However, apply an external pacemaker as required.

TABLE 2-2TYPE OF HEART BLOCK ASSOCIATED WITH INFARCTION

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TABLE 2-2 TYPE OF HEART BLOCK ASSOCIATED WITH INFARCTION

TABLE 2-3CLASS I INDICATIONS FOR PACEMAKER IN PATIENTS WITH AN ACUTE MYOCARDIAL INFARCTION

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TABLE 2-3 CLASS I INDICATIONS FOR PACEMAKER IN PATIENTS WITH AN ACUTE MYOCARDIAL INFARCTION

New left bundle branch block + first-degree AV block

New right bundle branch block + left anterior or posterior fascicular block + first-degree AV block

Mobitz type II heart block

Third-degree heart block

Symptomatic bradycardia unresponsive to atropine.

The patient requires heparin with the thrombolytic that you choose (and is indicated, by guidelines, for a minimum of 48 hours and preferably for the duration of the index hospitalization, up to 8 days or until revascularization is performed).

Question 2.1.12 Which of the following dosing regimens is the best accepted for use in AMIs?

A) Enoxaparin 30 mg subcutaneously (SC) every 12 hours.

B) Enoxaparin 1 mg/kg SC every 12 hours.

C) Heparin 5,000 units bolus and a drip at 1,000 units per hour.

D) Heparin 100 unit/kg bolus with a drip at 25 units/kg/hr.

E) None of the above represents the best dosing option in this situation.

Answer 2.1.12 The correct answer is "B." For anticoagulation in AMI, the dose of enoxaparin is 1 mg/kg SC every 12 hours. "A" is incorrect since 30 mg SC every 12 hours is the dose for DVT prophylaxis, not for anticoagulation. "C" is incorrect. This is the classic way that heparin has been dosed but it is not the best option listed. "D" is incorrect as well. The correct dose for heparin when given with a thrombolytic is 60 units/kg bolus (maximum of 4,000 units) with a drip of 15 units/kg/hr (maximum dose of 1,000 units/hr), with rate adjusted to achieve an activated partial thromboplastin time (aPTT) of 1.5 to two times control (for 48 hours or until revascularization). The bottom line here is that either enoxaparin or heparin can be used in this setting, and they are more or less equivalent. If you choose to use heparin, do not use fixed dose heparin but rather weight-based dosing. Also, keep in mind that in the United States, it is likely that most interventional cardiologists would prefer heparin over enoxaparin, due to both familiarity with dosing as well as drug pharmacology in the cath lab.

Did you know that for ST-elevation MI, an initial dose of 30 mg of IV enoxaparin (that's right—intravenous) should be given with the first (and only the first) dose for those age <75 years. The IV dose should be given at the same time as the first 1 mg/kg subcutaneous dose. Do it!

The patient receives her thrombolytic, enoxaparin, and transvenous pacing, and she is admitted to the hospital to a monitored bed. You get a call from the nursing staff 5 hours later. The rhythm strip shows 3 PVCs per minute. Your patient remains pain free and is hemodynamically stable.

Question 2.1.13 The nurse (who has more than a few gray hairs) would like an order for lidocaine. Your response is:

A) "Do it. Give the lidocaine."

B) "Give amiodarone—it works better than lidocaine."

C) "Give no antiarrhythmic at this point in time."

D) "Check labs including potassium and magnesium."

E) C and D.

Answer 2.1.13 The correct answer is "E." The use of lidocaine in this setting incurs no benefit and is proarrhythmic. The same is true for prophylactic amiodarone, which can cause torsades de pointes, albeit at a lower frequency versus other antiarrhythmics (such as quinidine, procainamide, sotalol, and newer Class III antiarrhythmic agents). In the setting of AMI, antiarrhythmics may be indicated only for complex arrhythmias (PVC couplets, triplets, nonsustained ventricular tachycardia [<30 seconds], or >10 PVCs per minute). More than 90% of patients will have isolated PVCs in the peri-infarct period, and there is no association with increased mortality. Correcting hypokalemia and hypomagnesemia can help to reduce arrhythmias, and checking these labs is prudent.

The patient remains pain free while in the hospital. She is ready to be discharged 4 days later.

Question 2.1.14 Which of the following tests is the most appropriate for this patient prior to discharge?

A) Coronary angiography.

B) Submaximal stress test.

C) Full Bruce protocol, symptom limited, stress test.

D) Spiral CT to assess for coronary artery calcification.

E) Family Medicine Board Examination.

Answer 2.1.14 The correct answer is "B." Submaximal stress testing is considered the standard of care. Patients with a positive submaximal stress test should be referred for catheterization. Patients with a borderline stress test can be sent for a radionuclide study. Coronary angiography is not routinely recommended for all patients who have had a myocardial infarction unless they are considered to be at high risk (continued symptoms, positive screening test such as submaximal stress test, heart failure, cardiogenic shock, etc.). "C" is incorrect because a symptom-limited, full-protocol stress test should be done only 14 to 21 days after an infraction. Finally, spiral CT ("D") to assess for coronary artery calcification has no role in risk stratification after a myocardial infarction … their risk is 100%! Also, keep in mind that the weight of the clinical evidence favors transfer for early catheterization, especially for higher risk patients. "E" is the test YOU are studying for … right? Disoriented already? It's only Chapter 2!

Question 2.1.15 The patient passes her stress test with flying colors (and you pass your Board Examination). Patients after a myocardial infarction should be routinely discharged on all of the following medications EXCEPT:

B) Beta-blocker.

C) Continuous nitroglycerin (e.g., patch or isosorbide).

D) HMG-CoA reductase inhibitor ("statin").

E) Sublingual nitroglycerin for PRN use.

Answer 2.1.15 The correct answer is "C." There is no benefit to scheduled nitrates unless needed for a specific indication (e.g., recurrent angina). All postmyocardial infarction patients should be discharged on aspirin, beta-blocker, statin, nitroglycerin PRN, and an angiotensin-converting enzyme (ACE) inhibitor (if tolerated, of course). Also, per ACC NSTE-ACS guidelines, individuals treated with an ischemia-guided strategy (vs. early invasive strategy), a P2Y12 inhibitor should be continued for up to 12 months if there are no contraindications (options include clopidogrel 75 mg daily, ticagrelor 90 mg BID). Finally, per ACC guidelines, all patients with ST-elevation MI or non-STEMI/unstable angina should be discharged on an intensive lipid-lowering regimen with an HMG-CoA reductase inhibitor ("statin"), such as atorvastatin 40 to 80 mg per day.

In patients with a history of acute coronary syndrome (ACS), statin therapy lowers the risk of recurrent MI, stroke, CAD-related death, and the need for coronary revascularization. Statin therapy after ACS is beneficial in ALL patients, including those with a baseline LDL <70 mg/dL. Discharge ACS patients on a statin.

Question 2.1.16 If this patient had a STEMI (or "Q-wave" MI), which of the following statements would be TRUE?

A) Patients with a non-STEMI have the same, or perhaps a bit worse, outcomes long term than do patients with a STEMI.

B) Patients with a non-STEMI have worse in-hospital outcomes when compared with patients with a STEMI.

C) Unstable angina and non-STEMI can be readily differentiated from one another on presentation.

D) None of the above is true.

Answer 2.1.16 The correct answer is "A." Patients with a non-STEMI actually have the same, or perhaps even slightly worse, outcomes long term as do patients with a STEMI. This makes sense; there is still myocardium left to infarct after a non-STEMI. As to the other answers, patients with a STEMI do have worse in-hospital outcomes, and unstable angina and non-STEMI look similar on ECG with T-wave inversion, etc., but without the ST elevations that are classically seen in a transmural infarction.

Objectives: Did you learn to…

• Define the accuracy of the initial history, ECG, and labs in the diagnosis of cardiac disease in the ED or office?

• Recognize the role and significance (or lack thereof) of risk factors, such as diabetes, family history, smoking, and hypertension, in the decision of whether or not to admit a patient to the hospital for chest pain?

• Generate a differential diagnosis of chest pain?

• Identify the roles of various diagnostic tests in the evaluation of chest pain?

• Treat a patient with an AMI?

When treating a patient with chest pain pressure or discomfort you should first?

How myocardial infarction causes chest pain?

Which of the following signs is commonly observed in patients with right sided heart failure?

What is the most common complaint of patients with cardiac compromise?