Intro to Cardiology Module 1 Guide Part 10

Angina pectoris: a prominent symptom of myocardial ischemia, is chest pain as a result of the imbalance between myocardial oxygen demand and supply. It is typically caused by the inability of atherosclerotic coronary arteries to perfuse the heart under conditions of increased myocardial oxygen consumption (demand). Angina pectoris is specifically the uncomfortable sensation felt in the chest and neighboring structures as a result of inadequate blood supply. It is usually triggered by exercise, emotion, or physiological stress. It is typically relieved by rest or by cessation of stimulus. The pain may radiate to the left arm, shoulder, neck, and jaw. (angina pectoris, can be termed as stable angina, unstable angina, variant angina, silent ischemia, and syndrome x) Stable angina, also referred to as typical angina, the pattern tends to be chronic and extremely predictable, precipitated by exertion or emotional stress. It is typically caused by fixed and obstructive plaque in one or multiple arteries. In general, the pattern of symptoms is related to the progress of the underlying disease. The location of the pain is typically diffuse rather than localized, occurring most often behind the middle or upper part of the sternum (i.e., substernal area). It can radiate to other parts of the chest (usually on the left side) or to the lower jaw, the neck, left arm, and shoulder. Individuals with stable angina experience a retrosternal tightness or pressure that does not vary with movements of the chest (e.g., breathing). An important indicator of typical angina is its duration: an attack is rarely longer than 10 minutes. During the attacks there are often characteristic changes in the ECG: temporary ST depression without permanent myocardial damage. Stable angina is relieved within a few minutes by rest or by administration of nitroglycerin (venodilator). Unstable Angina: When stable angina suddenly exhibits an increase in frequency and duration of episodes and is precipitated by a lesser degree of exercise, even possibly occurring at rest, it is termed unstable angina. In many cases, myocardial infarction follows shortly after; therefore, unstable angina requires timely treatment. Usually patients with unstable angina have had a history of stable angina related to severe atherosclerosis. Variant angina, also called Prinzmetal’s angina, is a random episode of chest pain (often at rest and associated with ST segment elevation) caused by the spasm of a coronary artery that has no significant atherosclerotic lesion. It is speculated that the spasm (which is extreme enough to induce myocardial ischemia at rest) occurs as a result of increased sympathetic activity in conjunction with endothelial dysfunction. Typically, the episodes of variant angina are selflimiting but they can be prevented or terminated by nitrates or calcium channel blockers. The diagnosis of variant angina can be confirmed by injecting ergonovine (a potent vasoconstrictor) under carefully controlled conditions during coronary arteriography in the cardiac catheterization laboratory. Silent ischemia occurs in the absence of noticeable discomfort (asymptomatic). It may occur in patients that also suffer from symptomatic angina. In some instances it may be the only sign of CAD and require detection by laboratory and electrocardiography techniques. The occurrence of symptomatic versus asymptomatic angina is not completely understood. Syndrome X is typical chest pain of seemingly ischemic origin (may show laboratory signs of ischemia)in the absence of significant arteriosclerosis. It is speculated that the basis for the pain is: ● Inadequate vasodilator reserve of the coronary resistance vessels ● Microvascular dysfunction, vasospasm and hypersensitivity to pain There is a better prognosis for patients with Syndrome X angina than evident atherosclerosis disease. Evaluation and Diagnosis of Chronic Stable Angina Patients rarely arrive at a hospital or clinic with active chest; therefore, it is important for the Cardiology Technologist to inquire about the patient’s history to evaluate ischemic heart disease. This can be done by asking the patient for a description of the quality and location of the angina episodes. The patient may describe the pain as "pressure," "tightness," or "heaviness." It may be described as a strangling discomfort, which can be referred to as Levine signs. To differentiate from musculoskeletal pain, angina is not described as a sharp or stabbing pain and as mentioned before it rarely lasts longer than 10 minutes but is always longer than a few seconds. Angina is usually a diffuse retrosternal pain that often radiates to the left side. It may be accompanied with other symptoms: for example, tachycardia, diaphoresis, nausea, dyspnea, weakness, and fatigue. There are also resulting transient left ventricular regional wall motion abnormalities. Angina is exacerbated by increased myocardial oxygen demand, such as during exercise, a large meal, cold weather, emotional stress, and excitement. As previously mentioned, angina is typically relieved shortly after rest or more quickly with nitroglycerine. Patients tend to modify their activity based on their experience with angina so in some cases the frequency of pain might not be accurate. An inquiry into the limitation of daily activities is important. It is also important to uncover various risk factors that may predispose the patient to atherosclerosis. Pericarditis, costochondral syndrome, cervical radiculitis, biliary colic, esophageal spasm, and gastroesophageal reflux can all be mistaken for angina pectoris. A detailed history is necessary to assist the physician in making a differential diagnosis. Gastrointestinal causes can be mistaken as cardiac in origin; these are generally instigated by particular foods and have no correlation to exercise. Alternatively, musculoskeletal discomfort can be localized and more superficial, and in some cases vary with respiration. Physical signs that accompany an angina attack may include: ● Increased blood pressure and heart rate ● Bulging impulse upon left chest palpitation due to severe mitral regurgitation (MR) ● S4 heart sound due to decreased ventricular compliance Note: In the absence of angina there maybe no abnormal findings. Several diagnostic tests can be performed to confirm the presence of ischemia. Diagnostic test Electrocardiogra m Notes ● Obtained during an episode of ischemia ● ST segments and T wave changes ● Acute ischemia = transient horizontal and downsloping ST depression and T wave flattening/inversion ● Transmural myocardial ischemia = ST segment elevation ● ST deviations normalize with relief from symptoms (acute MI changes do not resolve with relief from symptoms) Stress testing ● Exercise is used to provoke angina, with progressively increased workloads ● Test is positive if patient experiences typical reproducible angina or abnormalities consistent with ischemia (> 1mm horizontal or downsloping ST depression) ● Test is extremely positive if ECG abnormalities in the first 3 minutes of exercise persist 5 minutes after rest, ST segment depression is > 2 mm, drop in systolic blood pressure with exercise, ventricular arrhythmias or poor exercise tolerance due to cardiopulmonary limitations ● Medications that reduce heart rate should be withheld for 24 to 48 hours prior to the study Nuclear imaging ● Radionuclide imaging increases the sensitivity and specificity of the exam by overlooking conduction abnormalities that cause ST abnormalities (i.e., hypertrophy and bundle branch blocks) or when stress test results are inharmonious with clinical suspicion ● It is particularly useful for differentiating between ischemia, infarction, and hibernating myocardium Exercise echocardiograph y ● Ultrasound images are taken prior to and immediately post exercise ● Inducible myocardial ischemia is represented by wall motion abnormalities on the ECG Pharmacological stress testing ● Performed using agents (i.e., Persantine/Dypyridamole or Dobutamine) that increase myocardial oxygen demand and mimic exercise or vasodilators ● Followed by nuclear imaging ● Can be performed with pre and post echocardiography Coronary angiography ● Gold standard for diagnosis of CAD ● Radiopaque contrast dye is injected via catheters and radiographic images are used to identify focal narrowings and stenosis of the coronary arteries ● Used in patients where anti-anginal therapy is inadequate; there is unstable presentation or the result of other diagnostic tests indicate the need for revascularization Pharmacological Treatment In all cases, the goal of anti-anginal therapy is to reduce the frequency of attacks. When experiencing acute angina, it is important that the patient stop physical activity and administer nitroglycerine sublingually. Nitrates have two functions: they act quickly as a venodilator and as a dilator of the coronary vasculature. Long-term treatment to prevent attacks rely on organic nitrates, beta blockers, and calcium channel blockers. - Organic nitrates relieve ischemia, primarily through venodilation and coronary vasodilation. They can be used during an acute attack, prophylactically or long acting, depending on the preparation. - Beta blockers decrease myocardial oxygen supply by decreasing ventricular contractility and heart rate. - The action of calcium channel blockers depends on the individual drugs used. However, in general, they decrease oxygen demand through venodilatation and increasing myocardial oxygen supply via coronary dilatation. Acute Coronary Syndrome acute coronary syndrome occurs as a consequence of two factors: the disruption of atherosclerotic plaque following platelet aggregation and formation of the intracoronary thrombus. However, it can be caused by non-atherosclerotic causes, such as emboli from mechanical valves, vegetations from infected valves, congenital coronary artery anomaly, acute vasculitis, coronary trauma or aneurysm, conditions that cause increased blood viscosity, cocaine abuse, and rarely, coronary artery spasm. The disruption of plaque can result in either a partial or completely obstructed coronary artery. Unstable angina and non-ST elevated myocardial infarction (NSTEMI, also referred to as non-Q wave MI) can occur as a result of a partial obstruction. Unstable angina does not result in myocardial necrosis, whereas NSTEMI can result in myocardial necrosis. A complete obstruction causes a larger area of necrosis and presents on the ECG as an ST elevation, termed an ST elevated MI (also referred to as a Q-wave MI). Pathogenesis of Coronary Thrombosis Thrombus formation is a major cause of atherosclerosis and contributes to it in two ways. ● Plaque rupture ● Endothelial dysfunction On some occasions, acute coronary syndrome can be triggered by emotional or physical stress. Unstable angina and non-ST-elevated MI can be differentiated by certain blood serum markers, such as troponin levels and creatine kinase MB isoenzyme. Myocardial infarction is the result of inadequate oxygen supply to the heart causing necrosis of the heart muscle cells (myocytes). It can be further divided into transmural and subendocardial infarcts. As the name implies, transmural extends through the entire width of the wall, whereas subendocardial penetrates only the inner layer. The amount of damage that the heart muscle sustains during an acute MI depends on several factors, which include the: ● ● ● ● mass of muscle perfused by the coronary artery that is occluded amount of time and magnitude of the blood flow obstruction requirement for oxygen at the infected region availability of collateral arteries distal to the effected site Diagnosis of Acute Coronary Syndromes Unstable angina, NSTEMI, and STEMI are diagnosed based on symptoms, acute ECG changes, and the detection of specific serum markers. ECG: An ECG should be performed by an experienced professional such as a Cardiology Technologist and reviewed by a physician within 10 minutes of patient arrival in the case of an acute MI. If inconclusive, serial ECGs should be performed at 5 to 10 minute intervals. Serum Levels: Cardiac Troponins – Troponin I and T are specific to the heart and absent in the healthy individual. They offer superior sensitivity and specificity to that of creatine kinase. The pattern of troponin serum levels is as follows: ● Rise for 3 to 4 hours ● Peak at 18 to 36 hours ● Detected for up to 10 to 14 days Creatine Kinase – Creatine kinase is found in many body organs, muscles and tissues, which makes it less specific than troponin. The isoenzyme CK-MB is found primarily in the heart and increases specificity. The pattern of creatine kinase serum levels is as follows: ● Rise for 3 to 8 hours ● Peak at 24 hours ● Normalize in 48 to 72 hours Serial laboratory biomarker measurements can be used to provide evidence of reperfusion to infarct. Imaging An x-ray can be useful in differentiating acute MI from aortic dissection. A portable echocardiogram may be useful in the diagnosis of acute MI. In summary, unstable angina presents with chest discomfort at rest or new onset of severe angina. The ECG demonstrates ST depression and/or T wave inversion and there is no elevated blood serum biomarkers. NSTEMI and STEMI present classic chest pain that is more intense in duration and severity. Laboratory results indicate elevated blood serum levels. ECG changes indicate ST depression and/or T wave inversion in the case of NSTEMI. Conversely, STEMI shows ST elevation with Q wave development. Treatment of ST-segment Elevation MI Routine management strategies include the administration of oxygen, nitroglycerine, morphine (pain), aspirin, heparin (unfractionated or low molecular weight heparin), clopidogrel (Plavix), calcium channel blockers, ACE inhibitors and beta-blockers, in addition to fibrinolytic or primary percutaneous coronary intervention. The American College of Cardiology (ACC) and American Heart Association Guidelines for reperfusion strategy suggest that the major deciding factor on how to treat a patient with fibrinolysis versus primary percutaneous coronary intervention (PCI) depends on the time of presentation. At the Royal Jubilee Hospital, physicians refer to the critical time from the onset of symptoms to invasive treatment as the 'golden hour.' Within 90 minutes of the onset of symptoms, PCI is generally the reperfusion treatment of choice. However, after 90 minutes there is no significant benefit of PCI versus fibrinolytic treatment. The time required to arrive at a medical site that offers PCI is often the limiting factor. Commonly used fibrinolytic treatments include: ● ● ● ● Streptokinase Alteplase Reteplase Tenecteplase Treatment of Unstable Angina with non ST-segment Elevation MI The ACC and AHA treatment guidelines for ACS indicate the following therapies: nitrates, morphine, beta-blocker, calcium channel blockers, ACE inhibitors, antiplatelets (aspirin, clopidogrel, GP IIb/IIIa inhibitors), and heparin (UF or LMWH), in addition to oxygen. Management varies slightly depending on whether a conservative (patient at low risk) or percutaneous coronary intervention (patient at high risk) approach is taken. Early conservative treatment is pharmacologically based and requires surveillance through serial ECGs and blood serum markers to ensure an invasive approach (PCI) is not warranted. Complications Complications from unstable angina include death and progression to MI. Infarction patients are exposed to many possible complications. These complications include: ● ● ● ● ● Recurrent ischemia Arrhythmia (i.e., VF, SVT, heart block) Myocardial dysfunction (CHF, cardiogenic shock) Right ventricular infarction Mechanical complications (papillary muscle rupture, rupture, aneurysm) ● Pericarditis ● Thromboembolism