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:
- 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.
Submission Instructions:
- Your initial post should be at least 500 words for each case study, formatted and cited in the current APA style with support from at least 2 academic sources other than your textbook
Case Study 2: Cardiovascular
- Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease (CAD) and Acute Myocardial Infarction (AMI):
Modifiable Risk Factors: a. Smoking: Mr. W.G.’s risk for CAD and AMI may be influenced by his smoking history, if applicable. Smoking is a significant modifiable risk factor as it contributes to the development of atherosclerosis and increases the risk of clot formation. b. Diet and Obesity: Poor dietary choices and obesity can raise cholesterol levels, blood pressure, and contribute to the formation of plaques in coronary arteries. c. Physical Inactivity: Lack of physical activity can lead to obesity and other risk factors, such as hypertension and diabetes. d. Hypertension: High blood pressure is a modifiable risk factor, and its control through lifestyle changes and medications can reduce the risk of CAD and AMI. e. Diabetes: Proper management of diabetes through lifestyle modifications and medications is essential to control blood sugar levels and reduce cardiovascular risk. f. High Cholesterol Levels: Elevated levels of LDL cholesterol can be managed through dietary changes and medication, reducing the risk of CAD and AMI.
Non-Modifiable Risk Factors: a. Age: Mr. W.G. is 53 years old, which is considered an age-related non-modifiable risk factor for CAD and AMI. Risk generally increases with age. b. Gender: Being male is a non-modifiable risk factor, as men tend to have a higher risk of CAD and AMI than premenopausal women. However, postmenopausal women catch up in risk. c. Family History: A family history of CAD or AMI can increase one’s risk, and it is a non-modifiable factor. d. Genetics: Genetic predisposition can play a role in CAD and AMI risk, and it is non-modifiable. e. Ethnicity: Some ethnic groups, including Caucasians, are at higher risk for CAD and AMI.
- EKG Findings for Mr. W.G. and Compatibility with Acute Coronary Event:
Given Mr. W.G.’s symptoms of crushing chest pain radiating to the neck and jaw, along with nausea, it is highly suspicious of an acute coronary event. On the EKG, we would expect to see the following findings: a. ST-Segment Elevation: Elevation of the ST-segment, specifically in the precordial leads (e.g., V1-V4), is indicative of an acute ST-elevation myocardial infarction (STEMI). b. T-Wave Changes: T-wave inversion or flattening may occur in the affected leads. c. Q-Waves: The development of pathological Q-waves in the same leads as ST-segment elevation indicates an established myocardial infarction. d. Arrhythmias: Arrhythmias such as ventricular tachycardia or fibrillation may develop in severe cases.
- Most Specific Laboratory Test for Confirming AMI:
The most specific laboratory test for confirming an AMI is cardiac troponin. Cardiac troponin is released into the bloodstream when cardiac muscle cells are damaged, making it highly specific to cardiac injury. Troponin levels typically rise within a few hours after the onset of myocardial infarction and remain elevated for several days, allowing for both early and late detection of cardiac injury. Other biomarkers like creatine kinase-MB (CK-MB) and myoglobin may be used in conjunction with troponin for additional diagnostic information, but troponin remains the most specific and sensitive marker for AMI.
- Increased Temperature after Myocardial Infarction and its Timing:
The increase in Mr. W.G.’s temperature after his myocardial infarction can be explained by the inflammatory response that occurs as a result of cardiac tissue injury. This inflammatory response is part of the healing process, but it can lead to a transient fever. This fever typically occurs within the first 24-48 hours after the myocardial infarction and can last for several days.
The pathophysiology behind this fever involves the release of proinflammatory cytokines and activation of the immune system in response to the cardiac injury. These inflammatory mediators can lead to an elevation in body temperature. The fever is often mild to moderate in intensity and is generally self-limiting.
- Explanation of Pain during Myocardial Infarction to Mr. W.G.:
Mr. W.G.’s chest pain during his myocardial infarction can be explained by the inadequate blood supply (ischemia) and subsequent damage (infarction) to the cardiac muscle tissue. The coronary arteries, which supply oxygen and nutrients to the heart muscle, become partially or completely blocked due to the formation of a blood clot (thrombus) in conjunction with atherosclerotic plaque rupture.
As a result of this blockage, the affected portion of the heart muscle does not receive sufficient oxygen and nutrients, leading to cellular injury and death. The pain Mr. W.G. experienced, described as a crushing sensation in the sternal area that radiated to his neck and jaw, is due to the following factors:
a. Ischemia: The initial lack of blood supply to the heart muscle causes ischemia, which is experienced as chest discomfort or pain.
b. Inflammation: The cardiac tissue becomes inflamed as part of the body’s response to injury, contributing to pain perception.
c. Irritation of Nerve Endings: The damaged cardiac tissue can irritate nerve endings, sending pain signals to the brain.
d. Referral Pain: The heart and its surrounding structures share pain-sensing nerves with other areas of the body, leading to the referred pain sensation in the neck and lower jaw.
It is important for Mr. W.G. to understand that prompt medical attention and treatment are crucial during a myocardial infarction to minimize further damage to the heart muscle and improve his chances of recovery.