Setting: ED
CC: “My chest hurts, Doc.”
VS: R: 23 breaths/minute; BP: 144/94 mm Hg; P: 104 beats/minute; T: 99.8°F
HPI: A 68-year-old man who has had crushing, substernal chest pain for the past 15 to 20 minutes arrives at the ED. He immediately called 911 for an ambulance right after the pain began. He has had “chest discomfort” a few times before when walking up stairs in his home, but it was a “vague soreness” that lasted 1 to 2 minutes and stopped right after he got to the top of the stairs. Today, the pain was more severe in intensity and did not stop.
PMI:
Hypertension
Tobacco smoking—quit 5 years ago
Hyperlipidemia
Medications:
Nifedipine
Vitamins
PE:
Cardiovascular: normal
Lung sounds normal
Head, ears, eyes, nose, throat (HEENT): normal
On the CCS, choose parts of the physical examination based on what could be abnormal.
Initial Orders:
ECG
Creatine kinase myocardial band (CK-MB)
Troponin
Myoglobin
Aspirin
Nitroglycerin sublingual
Morphine
All patients admitted to the hospital need complete blood counts (CBCs), urinalysis (UA), basic metabolic panels, and chest x-rays.
As the clock is moved forward 15 to 20 minutes, the CK-MB, troponin, and myoglobin levels all revert to normal. The ECG shows ST-segment elevation in leads V2 through V4. The patient describes his pain as “sore, squeezing, and pressure-like.” He is somewhat short of breath.
What test becomes abnormal first?
a. CK-MB
b. Troponin
c. Myoglobin
Answer c. Myoglobin
Myoglobin level increases as early as 1 to 4 hours after the onset of myocardial damage. Elevation of myoglobin level is absolutely not specific to cardiac muscle. You do not see an elevated myoglobin level because of its specificity to heart tissue. You order a myoglobin test because a normal test at 4 hours strongly excludes a current infarction. CK-MB and troponin levels do not begin to increase until 4 to 6 hours after the onset of damage.
What is the mechanism of the drug you should add?
a. Blockade of P2Y12 adenosine diphosphate (ADP) receptor
b. Potentiation of antithrombin III
c. Thrombin inhibition
d. Plasmin inhibition
e. Dihydropyridine receptor inhibition
Answer a. Blockade of P2Y12 ADP receptor
All patients with unstable angina (acute coronary syndrome [ACS]) need two antiplatelet medications. A second drug is added to aspirin. Clopidogrel, prasugrel, and ticagrelor work through inhibiting the ADP receptor on the platelet. Heparin is not as useful in an acute ST-segment elevation myocardial infarction (MI) as it is in unstable angina or non-ST segment elevation MI (NSTEMI).
• Potentiation of antithrombin III = heparin
• Thrombin inhibition = argatroban, lepirudin
• Plasmin inhibition = aminocaproic acid (This is always wrong in coronary syndromes.)
• Dihydropyridine receptor inhibition = CCB
Aspirin and clopidogrel are started. Nitroglycerin, morphine, ACE inhibitor, metoprolol, and a statin are given as well. Medications on CCS are considered to be administered as soon as you verify them on the electronic order system. There is no time delay to drug administration on CCS. There is a modest improvement in pain and no change in vital signs. Angioplasty is superior to thrombolytics in terms of outcomes such as mortality, incidence of CHF, and recurrences of chest pain. Only 20% of hospitals in the United States can do urgent angioplasty with intervention. Your question will clearly tell you if the catheterization laboratory is close enough to get the balloon inflated within 90 minutes of the patient with chest pain arriving at the ED.
Up to how long after the onset of chest pain should thrombolytics be given?
a. 30 minutes
b. 90 minutes
c. 3 hours
d. 4.5 hours
e. 12 hours
Answer e. 12 hours
Thrombolytics are useful for an ST-segment elevation MI for 12 hours after the onset of pain. They do not work for NSTEMI. Use them for 3 to 4.5 hours for a stroke. It is very easy to confuse the question “how long after onset of pain” with “how long after coming to the ED” should thrombolytics be used. Once in the ED, you should have thrombolytics in the patient’s needle within 30 minutes of coming to the door.
Tissue plasminogen activator (TPA) is good for 12 hours after onset of chest pain.
TPA is used only for chest pain with ST elevation and new left bundle branch block (LBBB).
The patient is at a hospital with an interventional cardiac catheterization laboratory. Percutaneous coronary intervention (PCI) is performed. A sirolimus-coated stent is placed and the vessel diameter is increased in size from 2 mm to 4 mm.
What is the increase in the amount of flow with this increase in vessel size?
a. 2×
b. 4×
c. 8×
d. 16×
Answer d. 16×
Use Poiseuille’s equation: Flow is proportional to the radius raised to the fourth power. So a doubling in radius or diameter will increase flow by 2 × 2 × 2 or 16 times. Flow is inversely proportional to the length of the tube and the viscosity of the liquid. Length and viscosity cannot be changed in coronary syndromes.
This equation explains why interventions that increase the interior lumen diameter are the ones that improve flow and mortality. Beta-blockers such as metoprolol lower mortality, but they are not as dependent on time. In other words, although it is urgent to deliver anticoagulants and PCI, you are not pressed for time in administering beta-blockers.
Mortality Benefit in Myocardial Infarction
• Aspirin
• Second antiplatelet drug
• Angioplasty
• Thrombolytics
• Beta-blockers
• Statins