- For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarction, describe the modifiable and non-modifiable risk factors.
- What would you expect to see on Mr. W.G.'s EKG and which findings described in the case are compatible with the acute coronary event?
- Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarction, which would be the most specific laboratory test you would choose and why?
- How do you explain that Mr. W.G's temperature has increased after his Myocardial Infarction, when can that be observed, and for how long? Base your answer on the pathophysiology of the event.
- Explain to Mr. W.G. why he was experiencing pain during his Myocardial Infarction. Elaborate and support your answer.
Cardiovascular
Cardiovascular
Mr. W.G. is a 53-year-old white man who began to experience chest discomfort while playing tennis with a friend. At first, he attributed his discomfort to the heat and had a large breakfast. Gradually, however, discomfort intensified to a crushing sensation in the sternal area and the pain seemed to spread upward into his neck and lower jaw. The nature of the pain did not seem to change with deep breathing. When Mr. G. complained of feeling nauseated and began rubbing his chest, his tennis partner was concerned that his friend was having a heart attack and called 911 on his cell phone. The patient was transported to the ED of the nearest hospital and arrived within 30 minutes of the onset of chest pain. En route to the hospital, the patient was placed on a nasal cannula and an IV D5W was started. Mr. G. received aspirin (325 mg PO) and 2 mg/IV morphine. He is allergic to meperidine (rash). His pain has eased slightly in the last 15 minutes but is still significant; was 9/10 in severity; now7/10. In the ED, chest pain was not relieved by 3 SL NTG tablets. He denies chills.
Case Study 2 Questions:
Sample Solution
Case Study 2: Mr. W.G. and Acute Myocardial Infarction
1. Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease and Acute Myocardial Infarction:
Modifiable:
- Smoking
- High cholesterol
- High blood pressure
- Physical inactivity
- Obesity
- Diabetes
- Unhealthy diet
- Stress
Non-Modifiable:
- Age
- Sex (male)
- Family history of cardiovascular disease
2. Expected Findings on Mr. W.G.'s EKG and Compatible Findings:
Expected EKG Findings:
- ST-segment elevation in leads V1-V6 and I and aVL, indicating injury to the
Full Answer Section
- Possible Q waves, suggesting necrosis (tissue death) in the affected area.
Compatible Findings:
- Crushing chest pain radiating to the neck and jaw, a classic symptom of angina pectoris or myocardial infarction.
- Nausea and diaphoresis, common autonomic symptoms associated with pain and anxiety.
- Elevated blood pressure, a compensatory mechanism in response to decreased cardiac output.
- Lack of relief from chest pain with nitroglycerin (NTG), further suggesting a larger event beyond angina.
3. Most Specific Laboratory Test for Acute Myocardial Infarction:
Troponin: This cardiac-specific protein is released into the bloodstream when heart muscle is damaged. Troponin levels typically remain elevated for several days after an acute myocardial infarction, making it the most specific and sensitive test for confirming this diagnosis.
4. Explanation for Mr. W.G.'s Potential Temperature Increase:
Fever is not a typical symptom of acute myocardial infarction. However, a slight increase in temperature (up to 101°F) can occur within the first 24-48 hours due to several factors:
- Inflammatory response: The body's natural response to tissue damage, including the damaged heart muscle, can trigger the release of inflammatory mediators that elevate body temperature.
- Stress and anxiety: The emotional stress associated with a heart attack can also contribute to a temporary rise in temperature.
- Secondary infection: While not common, in severe cases, tissue damage after a heart attack can lead to secondary infections, causing fever.
5. Explanation for Mr. W.G.'s Pain During Acute Myocardial Infarction:
The crushing chest pain experienced by Mr. W.G. during his myocardial infarction originates from several factors:
- Ischemia: When a coronary artery is blocked, blood flow and oxygen supply to the heart muscle are compromised. This ischemia leads to the buildup of metabolic waste products, triggering pain receptors in the heart.
- Inflammation: The damaged heart muscle triggers an inflammatory response, further contributing to pain and sensitivity.
- Nerve activation: The pressure and tension in the heart wall due to ischemia and inflammation can stimulate pain-sensitive nerves surrounding the heart, radiating the pain to the chest, neck, and jaw.
Mr. W.G.'s pain was likely not relieved by nitroglycerin because it primarily helps with angina pectoris, which is caused by temporary narrowing of the coronary arteries. In his case, the complete blockage due to a myocardial infarction requires more immediate intervention like stenting or bypass surgery to restore blood flow and stop the tissue damage.