Myocardial Ischemia & Infarction - PDF

NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Myocardial Ischemia Partial blockage of one or more branches of the left or right coronary artery Causes Coronary atherosclerosis (coro...

NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Myocardial Ischemia Partial blockage of one or more branches of the left or right coronary artery Causes Coronary atherosclerosis (coronary artery disease) Repetitious endothelial injury with the resulting inflammatory response in the blood vessel wall results in a buildup of fibrous caps and plaque, which restricts blood flow to coronary arteries. Other causes/contributing factors include: Vasospasms of coronary artery (called Prinzmetal or variant angina) Decreased oxygen supply to myocardium (e.g., hypoxemia, anemia) Increased myocardial demand (increased heart rate or CO) Pathophysiology Coronary atherosclerosis results in myocardial ischemia Oxygen demand of ventricle exceeds oxygen supply in the coronary arteries 1  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Clinical Consequences Decreased ventricular contractility Conduction disturbances Ischemic Pain Stable angina pectoris Intermittent chest pain occurring with the same pattern of onset, duration and intensity Chest pain that lasts for a few minutes and is relieved by rest, position change, when precipitating factor has stopped (activity, stress, etc.), and/or nitroglycerin Pain is often described as a tightness, pressure, squeezing, or heartburn Pain can radiate (arms, shoulders, jaw) Unstable angina pectoris Chest pain lasting 15 to 20 minutes not relieved by rest, position change, or nitroglycerin Often described as crushing, pressure, tightness or burning Pain often radiates (arms, shoulders, jaw) Sign of an impending myocardial infarction 2  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Myocardial Infarction Severe reduction of coronary artery blood flow leading to myocardial cell death Causes Coronary atherosclerosis (coronary artery disease) Other less common causes include: Coronary artery emboli Aortic dissection with retrograde involvement of the coronary arteries Coronary vasospasm Coronary artery trauma Cocaine and other illicit drug use Prescription and over-the-counter medications Precipitating conditions include factors that increase metabolic demand: Extreme physical demand Hypertension Aortic stenosis Precipitating conditions include factors that reduce the oxygen content of the blood: Hypoxemia (altitude, pulmonary disease) Anemia 3  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Types There are several schemes used to classify types of MI for the purpose of directing treatment. (Don’t memorize) Classification Description of Categories Morphologic Transmural: necrosis extends throughout the entire wall of the myocardium Non-transmural: necrosis is limited to the endocardium or subendocardium (most frequent), or a segment of the myocardium. STEMI vs. NSTEMI STEMI: MI in the presence of ST segment elevation on the ECG NSTEMI: no ST segment elevation Fourth Universal Myocardial Injury: Elevated troponin with at least one value > 99 %ile Definition of Type 1: MI related to acute athero-thrombosis of artery feeding the Myocardial Infarction infarcted myocardium (2018) Type 2: Supply-demand mismatch unrelated to acute athero-thrombosis Type 3: Cardiac death in patients with symptoms suggestive of myocardial ischemia and presumed new ischemic EKG changes before troponin levels available or abnormal Type 4a: MI associated with percutaneous coronary intervention Type 4b: MI related to stent thrombosis Type 4c: MI related to restenosis Type 5: MI related to CABG Pathophysiology Infarction of an atherosclerotic coronary artery generally occurs due to the following circumstances: Thrombus forms on the rough surface of the plaque Wall of an atherosclerotic coronary artery ruptures Long-term obstruction of coronary artery by plaque Plaque embolus obstructs coronary artery 4  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Hypoxic injury Within 10 seconds of infarction, see hypoxic injury to myocardial cells. Consequences of anaerobic metabolism include decreased ATP production & lactic acid formation. Anaerobic metabolism is insufficient - after 20 minutes of complete occlusion, irreversible injury and cell death begins in the affected areas. Inflammation Neutrophils release a myriad of inflammatory mediators, some of which can cause myocardial cell injury (e.g., NO, IL-1, TNF, etc) Neutrophils also release reactive oxygen species (ROS) and lysosomal enzymes during phagocytosis, which also contributes to myocardial cell injury Reperfusion injury If the hypoxic myocardial tissue is reperfused (thrombolytic therapy or percutaneous coronary intervention), further cardiac injury occurs due to oxidative stress. Introducing oxygen to tissue that has been hypoxic causes the formation of reactive oxygen species (i.e., free radicals) Note: Microvascular (capillary) obstruction due to microthrombi, small plaque fragments, lipids, and or endothelial injury can reduce effectiveness of reperfusion. 5  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Repair and resolution Coagulative necrosis develops at site of infarct. Inflammation leads to scar tissue deposition at the site of infarct (and other changes in the surrounding tissue described on the next page). Clinical Consequences Functional impairment depends on location and severity of infarct Decreased ventricular (and atrial) contractility Conduction disturbances Ischemic pain 6  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes Laboratory Evaluation – Cardiac Biomarkers Troponin I & T Cardiac troponin I and T are proteins unique to myocardial muscle cells, and are only released into circulation after myocardial cell injury. Elevated (positive) troponin levels (cardiac TnI and TnT via immunoassay) are considered diagnostic of an acute MI (best sensitivity and specificity of the cardiac biomarkers) Levels rise within 2-3 hours after onset of chest pain, peak within 12 to 48 hours, and remain elevated for 4-10 days. Note: Elevated troponin levels in the absence of ECG changes (e.g., without ST elevation) is a risk factor for dying from a future cardiac event CK-MB (Creatine Kinase – muscle and brain type) Enzyme found primarily in myocardial muscle cells that is released after cell injury Sensitivity of test is improved by using the CK-MB/total CK index (ratio > 5 indicates cardiac source of CK-MB) Rises 4-6 hours after the MI, peaking in 24 hours, and disappearing in 2-3 days. Myoglobin An intracellular protein similar to hemoglobin that is released after myocardial cell injury Rises in myoglobin are very sensitive, but not very specific to acute MI 7  NURS 7053 Advanced Pathophysiology I for DNP Students Alterations of Cardiovascular Function II - Class Notes C-Reactive Protein (CRP) Plasma protein (acute phase reactant) that is released by the liver during inflammation Elevations greater than 1 mg/L are associated with increased risk of cardiovascular disease. Any level > 3 mg/L is associated with a high risk for heart disease Elevated CRP is a reliable predictor of degree of heart failure and mortality following an AMI, but lacks specificity because it is a general marker for inflammation. Lactate dehydrogenase (LDH) LDH is an intracellular enzyme (present in the cytoplasm of all cells) that catalyzes the process of converting pyruvate to lactate. It is also found in the plasma. LDH-1 is an isoenzyme of LDH that is primarily found in cardiac muscle cells. LDH-2 is the isoenzyme primarily found in the plasma. An elevation of LDH-1 (or an increase in the ration of LDH-1 to LDH-2) is indicative of myocardial cell injury. Sensitivity is high, but specificity is not as good as troponin I. Rises at 24-72 hours, peaks at 3-4 days, returns to normal within 8-14 days. FYI - Other Lab Findings Elevated glucose CBC – Elevated WBC count Chemistry – Elevated potassium Lipid profile – see ‘atherosclerosis’ 8