Findings that elevate suspicion of MI

1. EKG: after an MI, you should see flipped or flattened! waves, ST segment elevation, and/or Q waves in a segmental distribution (e.g., leads II, III, and aVF for an inferior infarct).

2. Pain characteristics: usually described as crushing, poorly localized substernal pain that may radiate to the shoulder, arm, or jaw; not reproducible on palpation. Pain usually does not resolve with nitroglycerin (as it often does in angina). Pain visually lasts at least a half-hour.

3. Laboratory values: a patient with a possible MI should have serial determinations of creatine kinase (the MB isoenzyme) or troponin I/P (usually drawn every 8 hours times 3 before MI is ruled out), lactate dehydrogenase (I.HI I) elevation and flip (I.DHt > LDH7) also may be used, especially if the patient presents after 24 hours. Aspartate aminotransferase is also elevated but not used clinically for MI. X-ray may show cardiomegaly and/or pulmonary congestion; echocardiography may show ventricular wall motion abnormalities.

4. Physical exam: pulmonary rales in the absence of other pneumonia-like symptoms, distended neck veins, S3 or S4, new murmurs, hypotension, and/or shock should make you think along the lines' of an MI. Patients are often diaphoretic, tachycardic, and pale; nausea and vomiting may be present.

5. History: patients with Ml often have a history of angina or previous chest pain, murmurs, arrhythmias, or risk factors for CAD. Some are taking heart medications (digoxin, furosemide, antihypertensives, cholesterol medications).

Treatment for an Ml involves hospital admission to the intensive care or cardiac care unit with adherence to several basic principles:

1. Early thrombolysis (usually less than 6 hr after pain onset) if the patient meets strict cri teria for use; PTCA (percutaneous transluminal coronary angioplasty) may be used if thrombolysis contraindicated.

2. EKG monitoring: if ventricular tachycardia develops, use lidocaine (do not use prophylactically).

3. Give Q} by nasal cannula (maintain 02 saturation > 90%).

4. Pain control with morphine (which may help with pulmonary edema if present)

5. Nitroglycerin

6. Beta blocker (on which patient should remain for life if no contraindications are present; proven to reduce incidence of second MI)

1. Aspirin (and possibly low-dose heparin)

8. Soft diet or NPO and. stool softeners

9. Begin anticoagulation with IV heparin in patients with cardiac thrombus, large area of dyskinetic ventricle, or severe congestive heart failure (CHF).

10. Patients with CHF (ejection fraction < 40%) should be started on an angiotensin-con-verting enzyme inhibitor, which has been shown to reduce mortality in this setting.

Note: Remember that the patient can reinfarct on the same hospital visit, even with adequate medical management.

Other causes of chest pain and clues to diagnosis:

1. Gastroesophageal reflux disease and peptic ulcer disease: relation to certain foods (spicy, chocolate), smoking, caffeine, lying down; relieved by antacids or acid-reducing medications; positi ve for Helicobacter pylori (peptic ulcer disease only).

2. Stable angina: pain begins with exertion or stress and remits with rest or calming down; relieved by nitroglycerin. EKG shows ST segment depression with pain, then reverts to normal when pain stops; pain lasts less than 20 minutes

3. Chest wall pain (costochondritis, bruised or broken ribs): reproducible on palpation and well localized.

4. Esophageal problems (achalasia, nutcracker or esophageal spasm): difficult differential. Question will probably mention a negative work-up for MI; look for barium swallow (achalasia) or esophageal manometry abnormalities. Treat achalasia with pneumatic dilatation; treat nutcracker/esophageal spasm with calcium channel blockers, then my otomy if calcium channel, blockers are ineffective

5. Pericarditis: look for viral upper respiratory infection prodrome. EKG shows diffuse ST segment elevation. Other signs include elevated erythrocyte sedimentation rate and low-grade fever.lire most common cause is viral (coxsackie virus); others include tuberculosis, uremia, malignancy, and lupus or other autoimmune diseases.

8. Pneumonia: chest pain due to pleuritis. Patients also have cough, fever, and/or sputum production, with possible sick contacts.

Unstable angina usually presents with normal cardiac enzymes and EKG changes (ST depression) with prolonged chest pain that does not respond to nitroglycerin initially (like MI). Pain often begins at rest. Treat like an MI, but use IV heparin to anticoagulate and consider PTCA emergently if pain does not resolve. Almost all patients have a history of stable angina and CAD risk factors. In strict terms, unstable angina is defined as a change from previous st able angina; thus, if a patient who used to get angina once a week now gets it once a day, he or she has unstable angina.

Variant (Prinzmetal's) angina is rare and associated with anginal pain at rest with ST elevation (cardiac enzymes, however, are normal).The cause is coronary artery spasm. Variant angina re sponds to nitroglycerin; long-term treatment usually is will) calcium channel blockers.

Note: 25% of Mis are silent, meaning that they present without chest pain (especially in diabet ics, who have neuropathy). Such patients present with CI II', shock, or confusion/delirium (especially elderly patients).

0 0

Post a comment