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 having 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. In route to the hospital, the patient was placed on 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 Questions
For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarct, describe the modifiable and non-modifiable risk factors.
What would you expect to see on Mr. W.G. EKG and which findings described on the case are compatible with the acute coronary event?
Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarct, which would be the most specific laboratory test you would choose and why?
How do you explain that Mr. W.G temperature has increased after his Myocardial Infarct, when that can 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 Infarct. Elaborate and support your answer.
Full Answer Section
- Diabetes mellitus: Strict glycemic control is important.
- Dyslipidemia: Managing cholesterol and triglyceride levels is key.
- Stress management: Techniques like meditation or yoga can be helpful.
Non-Modifiable Risk Factors:
- Age: Risk increases with age, particularly for men over 50 and women over 65.
- Family history: Positive family history for coronary artery disease increases risk.
- Gender: Men generally have a higher risk than women before menopause.
- Ethnicity: Some ethnicities have higher risk due to genetic and socioeconomic factors.
- Expected EKG Findings and Compatible Case Features:
Mr. W.G.'s symptoms raise suspicion for an acute coronary event, likely a myocardial infarction (MI). On his EKG, we might expect to see:
- ST-segment elevation: Indicates ischemia or damaged heart tissue.
- Q waves: May be present in a later-stage MI, indicating dead heart tissue.
- T-wave inversion: Can indicate ischemia or injury.
- Arrhythmias: Tachycardia (fast heart rate) or bradycardia (slow heart rate) are possible.
The case details compatible with an acute coronary event include:
- Angina-like chest pain: Crushing, radiating to neck and jaw, not relieved by deep breathing.
- Nausea and diaphoresis: Common autonomic symptoms during an MI.
- History of risk factors: Age, gender, possible dietary and exercise habits.
- Most Specific Laboratory Test for Confirming MI:
While troponin levels are the gold standard for confirming MI, if only one test can be ordered, CK-MB (creatine kinase-MB) would be the most specific choice in this scenario.
- Troponin: Highly sensitive and specific for myocardial injury, but levels rise slower, peaking at 24-48 hours. Delaying treatment based on a negative early troponin could be detrimental.
- CK-MB: More specific for cardiac muscle damage than total CK, rises faster than troponin (peaking at 12-24 hours), making it quicker for initial diagnosis.
- Elevated Body Temperature after MI:
Mr. W.G.'s fever can be explained by the inflammatory response triggered by the myocardial injury. This "febrile response" is common after an MI and typically peaks within 12-24 hours, gradually resolving within 3-5 days.
- Pain Mechanisms in Myocardial Infarction:
Mr. W.G.'s chest pain during his MI can be attributed to several factors:
- Ischemia: Reduced blood flow to the heart muscle due to a blocked coronary artery, causing oxygen deprivation and pain.
- Inflammation: Tissue damage triggers an inflammatory response, releasing chemicals that sensitize pain receptors.
- Stretching of the pericardium: The inflamed heart muscle can stretch the surrounding pericardium, a membrane with pain receptors.
- Activation of autonomic nervous system: Sympathetic nerve stimulation during stress or pain can aggravate discomfort.
These combined factors contribute to the characteristic crushing, oppressive chest pain radiating to the neck and jaw, often experienced during an MI.
Remember, this analysis is based on the provided information and does not constitute medical advice. Mr. W.G. should consult with a qualified healthcare professional for diagnosis and treatment.
I hope this information provides a comprehensive understanding of Mr. W.G.'s case and the complexities of cardiovascular events.