ACS Presentation Year 4 Internal Medicine Notes OmpathStudy

ACS Presentation Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.2 / Ngugi -- Slide 1 coronary HEART DISEASES BY: JAEL CHEPKOECH & FREDRICK MUGAMBI Slide 2 ACUTE CORONARY SYNDROMES Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations that result from acute ischemic injuries to the myocardium, due to a sudden occlusion or reduction of blood flow in the coronary vessels. ACS includes the following pathologies; Unstable angina Non–ST-segment elevation myocardial infarction (NSTEMI) ST-segment elevation myocardial infarction (STEMI) Slide 3 etiology It is almost always associated with the rupture of an atherosclerotic plaque with subsequent partial or complete occlusion of the infarct-related artery by a thrombus. Stable coronary artery disease (CAD) may result in ACS in the absence of plaque rupture and thrombosis at times of exertion, emotional stress or physiologic stress (e.g., trauma, blood loss, anemia, thyrotoxicosis, infections, tachyarrhythmia) increases demands on the heart. Slide 4 . Slide 5 pathogenesis Slide 6 Atherosclerosis development: Atherosclerosis is a chronic inflammatory condition that underlies most cases of acute coronary syndromes (ACS). Endothelial dysfunction occurs due to risk factors like hypertension, smoking, and high cholesterol. Inflammation leads to adhesion of immune cells and LDL cholesterol accumulation in arterial walls. Over time, a fatty streak develops, progressing to a fibrous plaque with a lipid core. Slide 7 Plaque vulnerability: Plaques vary in stability; vulnerable plaques have thin fibrous caps and high lipid content. Inflammation plays a crucial role in plaque destabilization. Macrophages and T cells release enzymes that degrade the fibrous cap, weakening it. Plaque rupture or erosion: Rupture occurs when the fibrous cap is weakened beyond a critical point. Ruptured plaques expose their thrombogenic core to the bloodstream. Alternatively, plaques can erode, exposing the lipid-rich core directly. Slide 8 Thrombus formation: The exposed lipid core triggers platelet activation and aggregation at the site. Clotting factors are activated, leading to thrombus formation. Thrombi can partially or completely occlude the coronary artery. Ischemia and tissue damage: Blood flow to downstream heart tissue is compromised due to the occlusion. Ischemia leads to oxygen and nutrient deprivation, causing reversible injury initially. Prolonged ischemia results in irreversible damage to myocardial cells. Slide 9 Inflammatory response: Inflammatory cells infiltrate the injured area, including neutrophils and macrophages. These cells release cytokines and growth factors, further amplifying the inflammatory response. Microvascular dysfunction: Microvasculature can also be affected by inflammation and oxidative stress. Impaired dilation of smaller blood vessels contributes to ongoing ischemia. Slide 10 Potential outcomes: Unstable angina Myocardial infarction Healing and scar formation: Inflammatory response subsides as healing begins. Granulation tissue forms and collagen deposition leads to scar tissue. Scar tissue can impair heart function and increase the risk of arrhythmias. Slide 11 Unstable angina Unstable angina is chest discomfort or pain caused by an insufficient flow of blood and oxygen to the heart. Etiology: Plaque rupture: unstable angina is often triggered by the rupture of an atherosclerotic plaque in a coronary artery. This can lead to the formation of a blood clot (thrombus) and partial or temporary blockage of blood flow to the heart muscle. Dynamic coronary artery obstruction: in some cases, unstable angina may occur due to dynamic obstruction of the coronary arteries, such as coronary artery spasm (variant angina) or microvascular dysfunction. Inflammation: inflammation within the coronary arteries can contribute to plaque instability and trigger episodes of unstable angina. Slide 12 Myocardial infarction Major classifications are based on: Ecg findings Universal Definition of Myocardial Infarction(ACC/aha/whf/ESC) Slide 13 Based on ecg findings; Non-ST-segment elevation myocardial infarction (NSTEMI): Characterized by the absence of ST-segment elevation but is still indicative of myocardial damage. It typically results from a partial blockage or thrombus in a coronary artery. NSTEMI is a more severe condition than UA which results in myocardial damage and elevated cardiac biomarkers (troponin). ST-segment elevation myocardial infarction (STEMI): STEMI is characterized by the elevation of the ST-segment on the ECG. It indicates a complete blockage of a coronary artery, leading to significant myocardial damage. Q-wave MI (QMI) vs. Non-Q-wave MI (NQMI): After an MI, changes in the Q-waves of the ECG can be observed. Q-wave MI (QMI) indicates the presence of pathological Q-waves, suggesting a transmural infarct with significant myocardial damage. Non-Q-wave MI (NQMI) indicates an MI without significant Q-wave development