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The Killip classification is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify

them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class.[1]

[edit] The study


The study was a case series with unblinded, unobjective outcomes, not adjusted for confounding factors, nor validated in an independent set of patients. The setting was the coronary care unit of a university hospital in the USA. 250 patients were included in the study (aged 28 to 94; mean 64, 72% male) with a myocardial infarction. Patients with a cardiac arrest prior to admission were excluded. Patients were ranked by Killip class in the following way: Killip class I includes individuals with no clinical signs of heart failure. Killip class II includes individuals with rales or crackles in the lungs, an S3, and elevated jugular venous pressure. Killip class III describes individuals with frank acute pulmonary edema. Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).

[edit] Conclusions
The numbers below were accurate in 1967. Nowadays, they have diminished by 30 to 50% in every class. Within a 95% confidence interval the patient outcome was as follows: Killip class I: 81/250 patients; 32% (2738%). Mortality rate was found to be at 6%. Killip class II: 96/250 patients; 38% (3244%). Mortality rate was found to be at 17%. Killip class III: 26/250 patients; 10% (6.614%). Mortality rate was found to be at 38%. Killip class IV: 47/250 patients; 19% (1424%). Mortality rate 67% The Killip-Kimball classification has played a fundamental role in classic cardiology, having been used as a stratifying criteria for many other studies. Worsening Killip class has been found to be independently associated with increasing mortality in several studies. Killip class 1 and no evidence of hypotension or bradycardia, in patients presenting with acute coronary syndrome, should be considered for immediate IV beta blockade. Guideline: Non-ST-Elevation Myocardial Infarction (NSTEMI) - Unstable Angina > Manage My Condition Text Size: A A A Printer Friendly E-mail to a Friend

What used to be simply called a heart attack is more accurately known today as acute coronary syndrome or ACS. This is an umbrella term that covers the heart attack (known medically as a myocardial infarction) and unstable angina. There is a specific type of heart attack that is closely related to unstable angina; its called non-ST elevation myocardial infarction or NSTEMI. The ST segment refers to a specific portion of an electrocardiogram (ECG), which is a graphic representation of heart beats. The ST segment of the ECG suggests that a heart attack is occurring when it is elevated away from the baseline (so called ST-elevation MI or STEMI). However, more than half of all people experiencing a heart attack will not show this diagnostic elevation on their ECG, leaving them to be classified as NSTEMI. Angina is not a disease but rather a chronic condition characterized by discomfort in the chest, jaw, neck, shoulder, back, or arm, which occurs with exertion or emotional stress. It is usually a stable and fairly predictable symptom related to underlying coronary artery disease. A more serious type of angina is called unstable angina, which is chest pain or discomfort that is unexpected and usually occurs while at rest. The discomfort may be more severe and prolonged than stable angina and it may be the first time a person has angina. Unstable angina is often accompanied by shortness of breath, indigestion and/or dizziness. Unlike STEMI and NSTEMI, which cause muscle damage in the heart, unstable angina is not associated with muscle damage. However, unstable angina is very dangerous, may progress to a heart attack, and needs emergency treatment. Symptoms of Unstable Angina and NSTEMI: Chest pain, pressure, tightness, or heaviness. This discomfort may radiate to the neck, jaw, shoulders, back, or one or both arms; Indigestion or heartburn; nausea and/or vomiting associated with chest discomfort Persistent shortness of breath Weakness, dizziness, lightheadedness, loss of consciousness. Dial 9-1-1. Patients with symptoms should be transported to the hospital by ambulance rather than by friends or relatives. NSTEMI and unstable angina are often considered together because of their similarities in terms of patient management. Conversely, STEMI is often considered separately because of important differences in early hospital care. If you have been diagnosed with NSTEMI or unstable angina, the following guidelines and standards of care may apply to the management of your condition. It is important to remember that the recommendations presented here may not be appropriate for all patients. It is always prudent to discuss your particular situation with your personal physician. Early Management of Patients with Unstable Angina/NSTEMI 1. Patients with chest discomfort whose symptoms are not improved 5 minutes after taking nitroglycerin (NTG) are advised to call emergency medical service (EMS) before taking more NTG. Patients with chronic stable angina may take up to a maximum of three NTG doses, 5 minutes apart, if symptoms are significantly improved by the first dose of NTG. They should still call EMS if symptoms are not resolved completely. 2. An electrocardiogram (ECG) should be performed on the patient with chest pain within 10 minutes of arrival to the emergency department. 3. Several blood tests are available to help diagnose heart muscle damage, but some are better than

others. A cardiac-specific troponin test is preferred in patients presenting with symptoms consistent with ACS. 4. Patients with possible ACS, but with a normal ECG and normal blood tests over 12 to 16 hours should generally have a stress test performed prior to discharge from the hospital or within 72 hours of discharge. Patients with a low probability of coronary artery disease (CAD), for example younger patients and those without many risk factors for CAD, can be evaluated by a noninvasive coronary angiogram (CT angiography) in lieu of a stress test. HOSPITAL MANAGEMENT OF PATIENTS WITH UNSTABLE ANGINA/NSTEMI 1. Aspirin should be administered to patients with ACS as soon as possible (unless contraindicated) and continued lifelong. Patients with an aspirin allergy should be treated with clopidogrel (Plavix). Other antiplatelet medications and combinations of antiplatelet medications may be appropriate depending upon the overall treatment plan. 2. Nonsteroidal anti-inflammatory drugs (such as naproxen or ibuprofen) should be discontinued on admission to the hospital in a patient with ACS. 3. Hormone replacement therapy (HRT) should not be started in patients with ACS. Patients on HRT at the time of ACS should be advised to discontinue it. 4. Beta-blockers (a class of medications which slow the heart rate and reduce blood pressure) should be instituted within the first 24 hours in absence of contraindications. 5. Proceeding to coronary angiography is preferable in patients with ongoing symptoms or unstable vital signs. Patients who are free of ACS symptoms and are otherwise stable can be managed with medications alone. Proceeding to coronary angiography under these circumstances is based on physician and patient preference. Patients who are stable for 12-24 hours on medical therapy, should undergo stress testing prior to discharge from the hospital. 6. If significant blockages are discovered at the time of angiography, the choice to proceed to angioplasty, stent implantation or bypass surgery needs to be determined based upon individual patient characteristics and specific angiogram findings. 7. Opening up a completely blocked coronary artery in patients with nonST-elevation myocardial infarction (NSTEMI) does not appear to provide any benefit and should not be routinely pursued. MANAGEMENT AFTER DISCHARGE 1. The risk of death or recurrent heart attack in patients with NSTEMI is highest in the first 2 months and returns to a baseline by 3 months. Patients with NSTEMI should be seen in follow-up as early as 2 weeks to at most 6 weeks after discharge. 2. All patients with ACS should receive aspirin, statins, beta-blockers, and clopidogrel. Angiotensinconverting enzyme (ACE) inhibitors (or angiotensin-receptor blockers, ARBs) should be initiated in patients with abnormal left ventricular ejection fraction, high blood pressure, diabetes, or heart failure. These medications are best initiated in the hospital since the likelihood that they will be continued long-term is highest. The blood pressure goal should be less than 140/90 mm Hg for all patients and less than 130/80 mm Hg for patients with diabetes mellitus or chronic kidney disease. 3. Patients with diabetes should be treated to attain normal or near normal blood sugar levels.

4. Return to activity should be guided by an exercise tolerance test. Exercise training can begin within 1-2 weeks after coronary revascularization. 30-60 minutes of physical activity daily, such as walking, is encouraged. Patients with an uncomplicated NSTEMI or unstable angina can return to driving within 1 week of discharge unless prohibited by state law. Individuals with more complicated heart attacks should delay driving for 2-3 weeks. LONG TERM LIFESTYLE MODIFICATIONS An acute event, such as a heart attack or unstable angina, is an opportunity to re-evaluate your lifestyle, including aggressive risk factor modification. Patients and their families should learn how to manage their cholesterol, blood pressure, and diabetes. Physicians and their staff can provide valuable information on diet, weight control, physical activity, tobacco cessation, and other appropriate lifestyle modifications. Diabetes greatly increases risk of future events, which means lifestyle changes are especially important if diabetes is present or there is a strong family history of diabetes. 1. Smoking greatly increases the risk of fatal and nonfatal heart attacks in both men and women. Women who smoke and use oral contraception have an even greater risk of heart attacks and strokes. The good news: 1 year after you quit smoking, your risk of a heart attack drops to about half that of current smokers, and continues to decline over time. Nicotine replacement therapies include gum, lozenges, inhalers, nasal spray, and nicotine patches. Non-nicotine prescription drugs are also available and they reduce the severity of nicotine cravings and withdrawal symptoms. The likelihood that you will successfully quit smoking is increased further with participation in a stop smoking program; these are offered at many local hospitals and health centers. Besides stopping smoking, individuals who have had a heart attack or experienced unstable angina should avoid second-hand smoke, too. 2. Patients with an acute coronary syndrome/unstable angina should achieve and maintain a body mass index (BMI) between 18.5 and 24.9. BMI is a measure of a persons weight in relationship to their height. There are many tools available online to calculate BMI, including our own tool here on CardioSmart.org. BMI should be assessed regularly. Weight maintenance/reduction should be attained through an appropriate balance of physical activity, reduced caloric intake, and formal behavioral programs, when indicated. 3. Waist circumference is another important measurement, and can point to the presence of metabolic syndrome (a group of several risk factors that greatly increases the risk of future heart problems. A waist circumference greater than or equal to 35 inches (89 cm) in women or 40 inches (102 cm) in men is especially worrisome. When waist measurements are in this range, it is important to initiate lifestyle changes and consider treatment strategies for metabolic syndrome, if present. Men can develop metabolic syndrome when their waist circumference is only slightly increased (e.g., 37-40 inches [94102 cm]). Waist circumference should be assessed regularly. 4. The ACC/AHA guidelines strongly recommend that patients with any acute coronary event should live their lives in a CardioSmart manner. All of the following are importantweight control; increased physical activity; moderation of alcohol consumption; limited sodium intake; and maintenance of a diet high in whole grains, fresh fruits, vegetables, and low-fat dairy products. You should reduce your intake of saturated fats (found mostly in animal products) to less than 7% of total calories, greatly reduce intake of trans fats (also in animal products and most snack foods), and limit cholesterol intake to less than 200 mg per day. (Note: 3.5 ounces of beef has 70 mg of cholesterol; 3.5 ounces of chicken has 60 mg of cholesterol; and one boiled egg has 225 mg of cholesterol.) The guidelines also encourage anyone who has experienced an acute coronary syndrome to increase their consumption of omega-3 fatty acids, found in fish and in supplement form. 5. At minimum, low-density lipoprotein cholesterol (LDL) should be reduced to below 100 mg/dl. Indeed, it is reasonable to attempt to reduce LDL to less than 70 mg/dl. There is a wealth of evidence

that cholesterol-lowering therapy reduces the risk of future cardiovascular events. 6. While LDL is probably the best known of the lipids that occur naturally in the body, there are other measurements obtained in a standard lipid profile: total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG) levels. There are even different sizes and types of cholesterol particles that affect cardiovascular health, such as very low density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL). While LDL-C is an important risk factor, in some patients nonHDL cholesterol (non-HDL-C) may be better to use as a treatment goal. Your non-HDL-C is simply your total cholesterol minus HDL, or put another way, it is the sum of your bad cholesterol levels: LDL, VLDL, and IDL. If triglyceride levels are between 200 and 499 mg/dl, for example, non HDL-C should be less than 130 mg/dl. Further reduction of nonHDL-C to less than 100 mg/dl may also be reasonable. 7. Haemoglobin A1c (commonly written as HbA1c) is a blood test which reflects the average blood sugar level over a 3-month period. In patients with diabetes and coronary artery disease, lifestyle efforts and medications should be used as necessary to achieve a normal or near-normal HbA1c (less than 7%). OTHER 1. Every year in the United States, influenza (the flu) causes more than 36,000 deaths and 225,000 hospitalizations. Individuals with chronic conditions, such as cardiovascular disease or diabetes, are particularly vulnerable to complications of the flu. Vaccination during the flu season has a critical but under appreciated role in the prevention of death or hospitalization. Thats why the guidelines now suggest that any child or adult with cardiovascular disease should have an annual flu shot. 2. Antioxidant vitamin supplements (e.g., vitamins E, C, or beta carotene) have NOT been shown to be beneficial in reducing risk in NSTEMI or UA patients. Nor is there evidence supporting the use of folic acid, with or without B6 and B12, for secondary prevention. However, it is reasonable to increase consumption of omega-3 fatty acids in the form of fish or in capsule form (1 gram per day) for risk reduction. For treatment of elevated triglycerides, the guidelines suggest that higher doses of omega-3 fatty acids (2 to 4 grams per day) may be used for risk reduction. GUIDELINE-BASED STANDARDS OF CARE: WHAT YOU SHOULD KNOW The American College of Cardiology (ACC) and the American Heart Association (AHA) work together on an ongoing basis to publish Guidelines addressing standards of care for the diagnosis, management and prevention of cardiovascular disease. The ACC/AHA Guidelines represent a consensus of expert medical opinion, with the goal of establishing a standard on which to base cardiovascular care decisions, serving the patients best interests. The guidelines are intended to help health care providers and patients make informed, best-possible decisions regarding care for specific clinical circumstances. The ACC strongly believes that adoption of these standards leads to higher quality cardiovascular care, cost-effectiveness, and most importantly, better outcomes for patients. Please note that the ACC/AHA Guidelines attempt to define practices that meet the needs of most patients in most circumstances. However, everyone is unique, and the extent to which the guidelines apply specifically to you should be a key point of discussion between you and your cardiologist or health care provider. The ultimate judgment regarding your care must be made by you and your healthcare provider together, in light of circumstances specific to you as a patient. Although all ACC/AHA Guideline documents are freely available, and can be downloaded from the

ACCs Cardiosource web site, these documents are often extremely long, and written primarily for the healthcare provider. Here at CardioSmart you will find a summary of the key points from the Guidelines, written specifically with the patient in mind. We urge you to review these key points, print them out if you like, and engage your healthcare provider in a discussion of how the guidelines relate to you and your condition. That is, after all, what being CardioSmart is all about being empowered to work with your physician in managing your care to assure the best possible outcome! If youd like to read the full guidelines from which this summary is derived, please click on either of the links below. Please note that these documents are large, so please have patience while they load.

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Unstable angina and NSTEMI: The early management of unstable angina and non-STsegment-elevation myocardial infarction
The term 'acute coronary syndromes' encompasses a range of conditions from unstable angina to STsegment-elevation myocardial infarction (STEMI), arising from thrombus formation on an atheromatous plaque. This guideline addresses the early management of unstable angina and non-STsegment-elevation myocardial infarction (NSTEMI) once a firm diagnosis has been made and before discharge from hospital. If untreated, the prognosis is poor and mortality high, particularly in people who have had myocardial damage. Appropriate triage, risk assessment and timely use of acute pharmacological or invasive interventions are critical for the prevention of future adverse cardiovascular events (myocardial infarction, stroke, repeat revascularisation or death). The guideline does not cover the management of STEMI or specific complications of unstable angina and NSTEMI such as cardiac arrest or acute heart failure. Assessment and classification of people presenting with undifferentiated chest pain are covered in 'Chest pain of recent onset' (NICE clinical guideline 95)[1]. The guideline will assume that prescribers will use a drug's summary of product characteristics to inform decisions made with individual patients. This guideline recommends some drugs for indications for which they do not have a UK marketing authorisation at the date of publication, if there is good evidence to support that use. Unlicensed or offlabel use is indicated by a footnote. Throughout the guideline, the term 'angiography' refers to invasive angiography.

Ecg Dx of acut coronary syndrome


This article is part of a series on the electrocardiogram (ECG) diagnosis of acute coronary syndrome and myocardial infarction (MI) mimics. This article covers the typical ECG diagnosis and the less wellknown ECG indications of myocardial ischemia, injury, and infarction. Infarction mimics involving Q waves were presented in Vol 18, No. 4 (Oct-Dec 2007); infarction mimics that involve the ST segment or T wave will be presented in a subsequent issue. The Normal ECG A detailed description of a normal ECG and of each of the 12 leads can be found in any book on electrocardiography. For the purposes of this issue, normal is defined as no significant Q waves, ST segment at the isoelectric line, and normal T waves in all 12 leads. Small Q waves (ie, <0.04 second wide and <25% the height of the QRS complex) can be normal in all leads except V1, V2, and V3; and lead AVR is often a QS complex normally. T waves can be slightly inverted in the right precordial leads (V1 and V2), and should be inverted in AVR in normal ECGs. Figure 1 shows which leads of the 12lead ECG face the different surfaces of the heart and where those leads are located on a standard 12lead ECG. Myocardial ischemia, injury, and infarction are diagnosed on the ECG by the presence of ECG changes in leads facing the involved area of the myocardium. Figure 1. No caption available.

Acute Coronary Syndrome The term acute coronary syndrome (ACS) refers to the pathophysiologic continuum that begins with plaque rupture in a coronary artery and ultimately results in total occlusion of the artery by thrombus unless the process is arrested. Three distinct phases of this continuum are unstable angina (UA), nonST elevation MI (NSTEMI), and ST elevation MI (STEMI).1 Patients presenting with chest pain and ST elevation on the ECG are classified as STEMI. Patients presenting with chest pain, no ST elevation on the ECG, and normal cardiac biomarkers are classified as UA. Patients with elevated biomarkers are classified as NSTEMI. Patients in whom cardiac biomarkers are elevated, regardless of the presence or absence of ST elevation, are ultimately diagnosed with either Q-wave MI or non-Q-wave MI based on the presence or absence of Q waves on the ECG. ECG Signs of Myocardial Ischemia Ischemia occurs when there is a mismatch between myocardial O2 supply and demand and can occur with either decreased O2 supply or increased O2demands. Ischemia is a reversible process if blood

flow is restored to the myocardium before permanent cell damage occurs. Patients presenting early in the ACS process often have ECGs that show changes in the ST segment or T wave that are consistent with myocardial ischemia, because ischemia precedes myocardial cell injury, and injury precedes myocardial cell death (necrosis or infarction). The most familiar ECG patterns of ischemia are horizontal or downsloping ST segment depression of 1 mm or more and T-wave inversion.2-4 These signs of ischemia can be isolated to ECG leads overlying the involved myocardium and thus suggest localized ischemia, or they can be present in many ECG leads, suggesting more widespread ischemia. There is a correlation between the number of ECG leads that show ST deviation and the extent and severity of coronary artery disease.4 If ST segment depression occurs in 8 or more leads along with ST elevation in AVR and V1, there is a high risk of either left main coronary artery disease or severe triple vessel disease.5Figure 2 is a 12-lead ECG of a patient who presented with chest pain unrelieved by his usual dose of nitroglycerin in the emergency department (ED). His cardiac biomarkers (creatine kinase-MB [CK-MB] and troponin I) were normal, but his ECG showed ST depression in leads I, II, III, AVF, and V3-V6, and ST elevation in AVR and V1. This pattern placed him at high risk for either left main or triple vessel disease and indicates the need for antiplatelet and anti-ischemic therapy and a trip to the catheter laboratory to evaluate coronary anatomy and possible intervention. Because his ECG does not show ST elevation and his biomarkers are normal, his diagnosis is UA. Figure 2. No caption available.

Figure 3 shows widespread T-wave inversion, which is another familiar sign of ischemia. There is Twave inversion in the inferior leads (II, III, AVF) and in all of the precordial leads (V1-V6). If the cardiac biomarkers are normal, the diagnosis is UA; if they are elevated, the diagnosis is NSTEMI. Figure 3. No caption available.

More Subtle Signs of Ischemia In addition to the well-known ST depression and T-wave inversion, other ECG changes can also indicate coronary insufficiency and be an early indicator of ischemia. These include a horizontal ST segment that forms a sharp angle with the ascending limb of the T wave6 and U wave inversion following an upright T wave.3,6,7Table 1 illustrates several patterns of myocardial ischemia. ST segment and T wave changes are often nonspecific and can occur in a variety of conditions, but they should be considered as possible indicators of ischemia in patients presenting with chest pain. Figure 4 shows an ECG with U wave inversion in V4-V6 in a patient presenting with chest pain but no other obvious ECG changes.

Figure 4. No caption available.

Table 1: Patterns of Ischemia

ECG Signs of Myocardial Infarction ECG changes of infarction include ST elevation (indicating injury), Q waves (indicating necrosis), and T-wave inversion (indicating ischemia and evolution of the infarction). These changes are called the indicative changes of infarction and occur in leads facing the damaged tissue. Reciprocal changes are the mirror image of the indicative changes and are often seen in leads recording from the opposite area of the heart. Reciprocal changes include taller-than-normal R waves (mirror image of Q waves), ST depression (mirror image of ST elevation), and tall T waves (mirror image of T-wave inversion). Table 2 shows the leads in which indicative and reciprocal changes are recorded with different types of MI. Table 2: Leads Showing ECG Changes of MI

The earliest ECG changes that occur with acute coronary artery occlusion are tall, peaked, and often wide-based T waves.6,8 This sign is rarely seen in the clinical setting because patients are usually not having a 12 lead ECG recorded at the moment their artery occludes. The first ECG change seen clinically is usually ST segment elevation, which indicates myocardial injury in tissue underlying the electrodes. The American College of Cardiology/American Heart Association Task Force on Practice Guidelines for management of STEMI define significant ST elevation as 1 mm or more in 2 contiguous leads (eg, 2 neighboring leads facing the same area of the heart).9Figure 5 is a 12-lead ECG of STEMI in the inferior wall (ST elevation is present in leads II, III, and AVF); reciprocal ST depression is present in most other leads. The presence of large R waves and ST depression in V1-V3 indicates that the posterior wall is also involved in the infarct. Figure 6 is a 12-lead ECG of STEMI in the anterior wall (ST elevation is present in leads V1-V5); there are no reciprocal changes in other leads.

Figure 5. No caption available.

Figure 6. No caption available.

Q waves are the indicative change of infarction (necrosis). Many leads can record normal Q waves, which are less than 0.03 seconds in width and usually small (no more than 25% the height of the following R wave).2,8,10 Significant Q waves are more than 0.03 seconds wide and often 25% or more the height of the following R wave. Other conditions can also cause abnormal Q waves on the ECG, but in a patient with chest pain and ST elevation, Q waves are considered diagnostic of infarction. Q waves usually appear within 8 to 12 hours of ST elevation if the artery is not reperfused; however, some patients do not develop Q waves until days after the MI.8 If an artery is reperfused early, Q waves may disappear in subsequent ECGs. In Figure 5, there are significantly wide Q waves in leads III and AVF, indicating inferior wall infarction. Other ECG Signs of Injury In addition to ST elevation, other ECG changes can indicate acute injury, including an ST segment that pulls up to the peak of the T wave with no obvious J point visible; tall, peaked T waves; and symmetrical T-wave inversion. Table 3 shows acute injury patterns. Some ECG changes can indicate either ischemia or injury (eg, T-wave inversion), and most of the ECG changes that occur in ischemia and injury can also be seen in other conditions (eg, electrolyte imbalances, other cardiac disease processes). The ECG is not specific in diagnosing anything other than the rhythm, but it remains a useful diagnostic tool, especially in the patient presenting with ACS. Table 3: Acute Injury Patterns

Case Study A 61-year-old woman with mild epigastric pain and nonradiating chest pressure, which she described as being 2 on a 10-point scale (0, no pain; 10, worst possible pain), presented to the emergency department (ED). She had a history of hypertension and high cholesterol and was a smoker. Her medications included atenolol (Tenormin), omeprazole (Prilosec), premarin, and atorvastatin (Lipitor). Her blood pressure was 134/68 mm Hg, heart rate 56 beats per minute, and respiratory rate 16/min.

Figure 7 is her admission ECG. Cardiac biomarkers (CK-MB and troponin I) were both normal, and a sestamibi scan was negative. Figure 7. No caption available.

Do you see anything suspicious for myocardial ischemia, injury, or infarction on her ECG? She was sent home, where she continued to have pain for the next few hours. She returned to the ED when her pain worsened. On readmission, her pain was 8 on a scale of 1-10 and radiated to her jaw and left shoulder. She was nauseated and lightheaded, and her blood pressure was 98/60 mm Hg. Figure 8 is her ECG on readmission to the ED. Her CK-MB was 6 U/L (normal 0-5 U/L), and her troponin I was 1 ng/ml (normal <0.7 ng/ml). Figure 8. No caption available.

Do you see anything suspicious for myocardial ischemia, injury, or infarction on her ECG now? Which artery is the culprit? What is her rhythm? Her cardiologist was notified and she was sent immediately to the cardiac catheter laboratory, where she was found to have a totally occluded right coronary artery (RCA). She was started on heparin and Integrilin and received two stents to her RCA. Four hours later, her CK-MB was 661 U/L and her troponin I was 13.2 ng/ml. Figure 9 is her ECG taken the morning after her stent insertion. Figure 9. No caption available.

What signs of infarction are present on her postprocedure ECG? Her postprocedure recovery was uneventful and she was discharged 2 days later with clopidogrel (Plavix), atorvastatin, metoprolol, and premarin prescribed. Discussion The admission ECG (Figure 7) was interpreted as normal. There are no abnormal Q waves of infarction and there is no ST segment elevation indicating injury. There is a horizontal ST segment with a fairly sharp angle between the ST segment and the ascending limb of the T wave in leads I, II, and V3-V5. There is suspicion of an inverted U wave in V5 and V6. On return to the ED, her ECG (Figure 8) showed ST elevation in leads II, III, and AVF with reciprocal ST depression in all other leads. Based on the presence of ST elevation, her diagnosis was STEMI of the inferior wall. She had not yet developed Q waves in the inferior leads. Her rhythm was type I second-degree AV block (Wenckebach), which is not unusual with inferior infarction because the RCA that supplies the inferior wall also supplies the AV node in most people. The postprocedure ECG shows resolution of the ST segment elevation, Q waves, and T-wave

inversions in leads II, III, and AVF, all signs of an evolving MI. The Q waves indicate that some myocardial necrosis did occur although the artery was opened with stents. The ST-T angle is more gradual and normal looking, and the hint of U-wave inversion is gone. There is a large upright T wave in V2 with a fairly large R wave, which could indicate involvement of the posterior wall in the infarction. This is a good example of the value of a chest pain monitoring unit. If the patient had been observed for several hours instead of being sent home, changes of ischemia might have been detected before injury could occur and treatment might have been initiated before myocardial damage could result.

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