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Mrs. G is experiencing acute, severe, nonpleuritic chest pain. This presentation is associated with multiple “must not miss” diagnoses. The acuity of the pain is a pivotal point in this history. MI with and without ST elevations and unstable angina, as a group referred to as acute coronary syndromes, are the most common life-threatening causes of acute chest pain and need to be considered first. Aortic dissection also needs to be considered given the severity of the pain, the history of hypertension, and the radiation of the pain to the back. PE is another possible cause even though the chest pain is not pleuritic. Other alternative causes of this type of pain are esophageal spasm and pancreatitis (though it would be atypical for pancreatitis to begin so acutely). Table 9-5 lists the differential diagnosis.
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The patient takes enalapril for hypertension. She lives alone, is sedentary, and smokes 1 pack of cigarettes each day. She has an 80 pack-year smoking history.
On physical exam, the patient is in moderate distress. She thinks that she is having a heart attack. Vital signs are temperature, 37.0°C; BP, 156/90 mm Hg in both arms; pulse, 100 bpm; RR, 22 breaths per minute. Head and neck exam, including jugular and carotid pulsations, are normal. The lung exam is clear. Heart exam is notable for a normal S1 and S2 and a soft, II/VI systolic ejection murmur. Abdominal exam is unremarkable with no tenderness, hepatosplenomegaly, or bruits.
Is the clinical information sufficient to make a diagnosis? If not, what other information do you need?
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Leading Hypothesis: Acute MI
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Textbook Presentation
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The classic presentation of an acute MI is crushing substernal chest pressure, diaphoresis, nausea, shortness of breath, and a feeling of impending doom in a middle-aged man with risk factors for CAD. Even more than other “textbook presentations,” this description is often inaccurate because it does not take into account the frequency of MIs in women, younger and older patients, and the frequency of atypical presentations.
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MI occurs when there is a prolonged failure to perfuse an area of myocardium leading to cell death.
Most commonly occurs when a coronary plaque ruptures causing thrombosis and subsequent blockage of a coronary artery.
The universal definition of MI describes 5 subtypes of MI based on their clinical presentation:
Spontaneous MI due to a primary coronary event.
MI secondary to ischemia due to either increased oxygen demand or decreased supply, eg, coronary artery spasm, anemia, or arrhythmias.
Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia.
MI associated with PCI or stent thrombosis.
MI associated with CABG.
Acute MIs are classified as either ST segment elevation MI (STEMI) or non–ST segment elevation MI (NSTEMI).
ST elevations signify transmural ischemia or infarction.
NSTEMI
Are less severe, usually injuring only subendomyocardial tissue
Have a higher subsequent risk for STEMI than for patients who have had a STEMI
These 2 types of MI are managed differently. The discussion of STEMI is covered in this section while the management of NSTEMI is discussed in the next section on unstable angina.
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Evidence-Based Diagnosis
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The diagnostic criteria for acute MI have been clearly established. There are 5 criteria that vary somewhat, based partly on the subtype of MI. They are shown in Table 9-6.
Clinical findings suggestive of MI
Pretest probability
About 15% of patients who arrive at the emergency department complaining of chest pain are having an MI.
About 33% of patients admitted to the hospital with suspicion of an MI are found to be having one.
About 50% of patients admitted to the CCU with suspicion of an MI are found to be having one.
Historical and physical exam features are never sufficient to diagnose an MI and only (nearly) exclude MI in the lowest risk patients. Test characteristics for some common signs and symptoms appear in Table 9-7.
Types of chest pain that decrease the likelihood of MI include pleuritic pain, sharp or stabbing pain, or positional pain.
ECG findings suggestive of MI
All guidelines recommend an ECG be performed within 10 minutes of a patient’s arrival at a healthcare facility when an MI is suspected.
Patients with chest pain should have an ECG within 10 minutes of arriving at a healthcare facility.
Prevalence rates of MI among emergency department patients with chest pain and various ECG findings follow:
New ST elevation of 1 mm: 80%
New ST depression or T wave inversion: 20%
No new changes in a patient with known CAD: 4%
No new changes in a patient without known CAD: 2%
Table 9-8 shows the test characteristics for ECG findings in patients with acute chest pain. (Because numbers vary from study to study, these likelihood ratios should be treated as estimates.)
A patient with chest pain and ≥ 1-mm ST elevations in 2 contiguous leads or a new left bundle-branch block is having an acute MI and should receive immediate therapy.
Cardiac enzymes
As is clear from the diagnostic criteria, abnormal levels of cardiac enzymes define the presence of MI.
When an MI is suspected, creatine kinase MB subunit (CK-MB) and troponin should be ordered and processed immediately.
These tests are highly reliable in diagnosing MI. (Note that the definition of MI is based on enzyme results whenever they are available.)
Troponin: sensitivity, 95%; specificity, 98%; LR+, 47; LR-, 0.3.
Serial CK-MB: in the first 24 hours—sensitivity, 99%; specificity, 98%; LR+, 50; LR-, 0.1.
Troponin levels in patients with kidney disease
Patients with kidney disease often have elevated troponin levels raising the risk of false-positive tests for MI.
Patients with elevated troponin levels at baseline will still have a diagnostic rise and fall with MI.
In patients with chronic kidney disease, higher baseline troponin levels are predictive of poor cardiovascular outcomes.
MI in women
Presentation
Acute MIs present differently in women than in men.
Women often report prodromal symptoms such as fatigue, dyspnea, and insomnia.
Women are more likely to present without chest pain than men (42% vs 30.7%). This difference becomes less pronounced as patients age (as both men and woman present more frequently without chest pain).
Just under half of women suffering an MI have a chief complaint other than chest pain.
Dyspnea, weakness, and fatigue are the other common presenting symptoms.
Outcomes
Women who suffer an MI are more likely to die. Recent data show an in-hospital mortality rate of 14.6% for women and 10.3% for men.
The cause of this disparity is multifactorial but includes the fact that patients without chest pain receive delayed and less aggressive care.
The mortality difference becomes less pronounced and eventually reverses as patients age.
Unrecognized MI
Although the combination of symptoms, ECG findings, and enzymes make most MIs easy to diagnose, about 2% of patients with acute MI are not diagnosed and are discharged from the emergency department.
Failure to recognize an MI results in worse outcomes for patients and serious medicolegal issues.
MIs most commonly go unrecognized when they present in unusual ways or in people not expected to have MI.
A patient with an MI or unstable angina who is mistakenly discharged is most likely to:
Be a woman younger than age 55
Be non-white
Have a chief complaint of shortness of breath
Have a nondiagnostic ECG
The most common alternative presentations of MI are listed below. MI should at least be considered in patients being discharged from the emergency department with 1 of these diagnoses:
HF
Stable angina
Arrhythmia
Atypical location of pain
Central nervous system manifestations (symptoms of cerebrovascular accident)
Nervousness, mania, or psychosis
Syncope
Weakness
Indigestion
MI can present in many different ways. A high index of suspicion should always be present. Certain groups of patients (elderly, women, minorities, diabetics) are most likely to be misdiagnosed.
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Once an MI is diagnosed, therapy must be initiated immediately. The following applies to the treatment of STEMI:
Medications
Antiplatelet agents: aspirin, P2Y12 receptor blockers (eg, clopidogrel) and, in patients undergoing primary PCI, a glycoprotein IIb/IIIa inhibitor
Beta-blockers
Oxygen
Nitroglycerin
High intensity HMG-CoA reductase inhibitors (statins)
Other therapy based on presentation
(1) Opioids for patients in pain
(2) Atropine for patients with pathologic bradycardia
(3) Antiarrhythmic agents
Reperfusion with either systemic thrombolysis or primary PCI.
Although not universally available, primary PCI is the preferred option.
Primary PCI is associated with
Lower mortality (even in patients who must be transferred—albeit quickly—to a hospital with the capability)
Significantly lower risk of serious bleeding complication. Hemorrhagic stroke is not a potential complication as it is with systemic thrombolysis.
The ability to do primary PCI depends on the presence of an interventional cardiology team who can rapidly (within 90 minutes) bring the patient to the catheterization laboratory.
Primary PCI with stent placement is the most efficacious treatment.
Both primary angioplasty and thrombolysis are most effective when completed within 12 hours of symptom onset.
Once the culprit vessel has been opened, various medications have been shown to improve survival after acute MI.
Beta-blockers
ACE inhibitors
Aspirin
P2Y12 receptor blockers (duration based on intervention and risk of bleeding)
HMG-CoA reductase inhibitors, dosed to achieve an LDL < 70 mg/dL.
Glycoprotein IIB/IIIA inhibitors are recommended for patients with MIs who undergo stenting.
An exercise test is also recommended within 3 weeks of an MI in patients not undergoing PCI or angiography for information on prognosis, functional capacity, and risk stratification.
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Mrs. G’s ECG shows ST depression in leads II, III, AVL, and V3–V6. The chest radiograph is normal.
Have you crossed a diagnostic threshold for the leading hypothesis, acute MI? Have you ruled out the active alternatives? Do other tests need to be done to exclude the alternative diagnoses?