When a blood clot forms on a ruptured plaque in a coronary artery The condition is referred to as a N group of answer choices?
Overview. Myocardial ischemia occurs when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction).
What is it called when the heart cant maintain adequate cardiac output?
The problem in heart failure is that the heart isn’t pumping out enough blood each time it beats (low stroke volume). To maintain your cardiac output, your heart can try to: Beat faster (increase your heart rate).
What happens if the connection between the SA node and the AV node becomes blocked?
If the connection between the SA node and AV node becomes blocked, the ventricles will beat more slowly.
What happens if cardiac muscle is deprived of normal blood supply?
Insufficient blood flow to the heart muscle can lead to symptoms of chest pain (angina). If the coronary artery becomes completely blocked, it will cause a heart attack. During a heart attack, some of the heart muscle can die from a lack of oxygen.
How is atherosclerosis diagnosed?
Your doctor will order blood tests to check your blood sugar and cholesterol levels. High levels of blood sugar and cholesterol raise your risk of atherosclerosis. A C-reactive protein (CRP) test also may be done to check for a protein linked to inflammation of the arteries. Electrocardiogram (ECG or EKG).
How is plaque in arteries diagnosed?
The tests may include:
- Cholesterol screening.
- Chest X-ray.
- CT scan.
- Ultrasound.
- Echocardiogram and/or cardiac stress test.
- Electrocardiogram.
- MRI or PET scanning.
- Angiogram.
How does heart failure affect cardiac output?
Cardiac and Vascular Changes Overall, the changes in cardiac function associated with heart failure result in a decrease in cardiac output. This results from a decline in stroke volume that is due to systolic dysfunction, diastolic dysfunction, or a combination of the two.
What does the AV node do if the SA node is damaged?
When something goes wrong with the sinoatrial node, you may develop a consistently slow heartbeat (sinus bradycardia) or the normal pacemaker activity may stop entirely (sinus arrest). If sinus arrest occurs, usually another area of the heart takes over pacemaker activity. This area is called an escape pacemaker.
What happens if the AV node is damaged?
Disease of the AV node can cause either a delay or a partial or complete block in the transmission of electrical impulses from the atria to the ventricles, a condition known as heart block.
What happens to cells during myocardial infarction?
During myocardial infarction, cardiac myocytes in the ischemic zone die by both apoptosis and necrosis. Surprising, the magnitudes of each form of cell death remain unclear.
How does the immune system respond to cardiac injuries?
The lack of oxygen and nutrients causes the death of cardiomyocytes and leads to the exposure of danger-associated molecular patterns that are recognized by the immune system to initiate inflammation. Results: At the initial stage of post-MI inflammation, the immune system further damages cardiac tissue to clear cell debris.
Does the infarcted heart have M1 and M2 macrophages?
Although the infarcted heart contains subsets of macrophages, which have some similarities to M1 and M2 macrophages in terms of expression markers and functions, the cardiac macrophage profile is much more complicated and dynamic.
What is the pathophysiology of myocardial infarction (MI)?
Following myocardial infarction (MI), neutrophils are quickly recruited to the ischemic region, where they initiate the inflammatory response, aiming at cleaning up dead cell debris. However, excessive accumulation and/or delayed removal of neutrophils are deleterious.
What is the role of neutrophils in the pathophysiology of myocardial infarction?
Neutrophils are first-line responders of the innate immune system. Following myocardial infarction (MI), neutrophils are quickly recruited to the ischemic region, where they initiate the inflammatory response, aiming at cleaning up dead cell debris. However, excessive accumulation and/or delayed removal of neutrophils are deleterious.