Acute Coronary Syndrome Treatment Essay Paper
Acute Coronary Syndrome Treatment Essay Paper
Acute coronary syndrome describes a range of conditions associated with sudden, reduced blood flow to the heart.
The blockage can be sudden and occur in one instant, or it may come and go over a period of time.
Acute coronary syndrome encompasses a collection of three acute processes related to myocardial ischemia. These include: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). Myocardial ischemia is caused by inadequate perfusion within the myocardial tissue due to oxygen demand exceeding oxygen supply.Acute Coronary Syndrome Treatment Essay Paper
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In a healthy person the amount of oxygen required by the myocardium (O2 demand) is determined by heart rate, myocardial contractility, myocardial wall stress, and afterload. As explained by Antman, et al (2012), “oxygen supply to the myocardium requires a satisfactory level of oxygen-carrying capacity of the blood (determined by the inspired level of oxygen, pulmonary function, and hemoglobin concentration and function) and an adequate level of coronary blood flow”. The coronary vessels have the ability to adjust their level of resistance to adapt to the increased oxygen demand required by the myocardium during certain times (such as during physical exertion).
Ischemic heart disease is typically caused by atherosclerosis, which is a buildup of plaque inside the lumen of the coronary vessels. The emergence of atherosclerosis in the vessels does not occur overnight. Antman, et al. (2012) found that “atherogenesis in humans typically occurs over a period of many years, usually many decades” and that “growth of atherosclerotic plaques probably does not occur in a smooth, linear fashion but discontinuously, with periods of relative quiescence punctuated by periods of rapid evolution”.Acute Coronary Syndrome Treatment Essay Paper
The process of atherosclerosis begins with an abundance of lipoproteins in the blood stream. These lipoproteins bind to the walls of vessels and are eventually deposited within the intima of the arteries. To counteract this process, phagocytes are sent into the vessel to attack these “foreign” particles (Antman et al., 2012). Once the phagocytes are within the intima, they mature into macrophages and become lipid-laden foam cells (Antman et al., 2012). As these plaques advance calcification occurs. This process is thought to be a key step in the formation of atherosclerotic plaques (Antman et al., 2012).
Normally this narrowing of the vessel lumen does not cause chest pain or discomfort. Eventually, however, these plaques may rupture. At this point platelet activation occurs, which eventually leads to clot formation at the sight of the plaque. This clot, or thrombus, may break off and lodge in a coronary vessel. These two processes are a common pathogenic finding with acute coronary syndrome (Lincoff, Califf, Anderson, Weisman, Aguirre, Kleiman, Harrington & Topol, 1997). A partial occlusion of the coronary vessels due to a ruptured plaque/platelet complex causes unstable angina or a NSTEMI. In this case, the oxygen demands of the heart cannot be met. A complete occlusion causes a STEMI (Anderson, Adams, Antman, Bridges, Califf, Casey Jr, Chavey II & Wright, 2011), which eventually leads to myocardial cell death.
Discussion/Analysis
The emergency department providers are often the first line of defense in the management of patients with chest pain. The ability to quickly evaluate whether or not the cause of chest pain is potentially fatal is of great importance. Critical chest pain can be broken down in to non-cardiac and cardiac causes. Non-cardiac causes include: pneumothorax, pulmonary embolism, and Boerhaave’s syndrome. Acute coronary syndrome is among several cardiac causes of emergent chest pain.
An accurate diagnosis of the cause of chest pain requires several key components. These include: patient history (including risk factors), physical examination, diagnostics, and labs.Acute Coronary Syndrome Treatment Essay Paper
History
History is instrumental during the evaluation of a patient with chest pain. Ischemic chest pain is often described as a severe “pressure” or “squeezing” and is classically described as the feeling of “an elephant sitting on my chest”. Typically this pain is described as substernal chest pain which radiates to the neck, jaw, or down the left arm. Additional details regarding the onset of chest pain can also serve as important clues. For example, pain on exertion that resolves with rest suggests stable angina, whereas new onset chest pain or chest pain at rest suggests unstable angina. A good method to differentiate cardiac from non-cardiac chest pain is whether the pain improves after administration of nitroglycerin (NTG). If the pain is relieved by NTG it is considered to be likely due to cardiac causes. Additional details suggesting cardiac origin are shortness of breath, nausea +/- vomiting, diaphoresis, and the presence of syncopal/near-syncopal episodes.
It is important to note that a patient with chest pain often have a silent or atypical presentation. This is especially true in elderly men (Woon & Lim, 2003) and diabetics (Tabibiazar & Edelman, 2003). A patient with an atypical presentation may present with shortness of breath but lack the classical symptom of angina pectoris which radiates to the jaw or left arm. Commonly these patients complain of a feeling of indigestion or epigastric discomfort. Thus it is very important to consider ACS in these patients.
Patients with a new diagnosis of acute coronary syndrome (ACS) often do not know a great deal about their disease, its treatment, or the lifestyle changes needed to prevent recurrence.1 Restenosis is common (39% of patients) after percutaneous coronary intervention.2 In addition, ACS recurrence lowers quality of life and is expensive.Acute Coronary Syndrome Treatment Essay Paper
Pharmacists have the ability to improve outcomes and increase the quality of life of their patients. Early, individualized education leads to better self-care and greater satisfaction with that care.1 Also, family and health care social support increases the perceived benefit,2 which improves adherence with self-care and thereby improves outcomes.2
Self-Care
Self-care (eg, smoking cessation, regular health checks, medication adherence, diet, exercise) can prevent recurrence of ACS, but long-term adherence to self-care is key. Adherence to self-care depends on a patient’s beliefs, disease knowledge, overall ability to function, emotions (eg, anxiety, depression), and outside influences (eg, social and health care networks). Disease knowledge includes knowing about ACS characteristics, risk factors, medications, and dietary and exercise needs. Knowing more does not affect a patient’s anxiety, depression, or valuation of the benefits of self-care.2
Self-efficacy, which includes the ability to manage one’s own medications, smoking, diet, and exercise, notably influences self-care. Encourage your patients to see past the likely occurrence of reduced body function. Help them understand there will be setbacks that increase the perception of barriers, which can be overcome with a positive attitude.2
Patients may not like hearing it, but improvements in diet, as well as exercise and smoking cessation, can help.
Most individuals will adhere to self-care for a month after they are given an ACS diagnosis, but adherence drops at about 6 months after discharge from the hospital.2 Smoking, combined with a lack of exercise or dietary restraint, for even 6 months after an ACS incident, increases nearly 4-fold the incidence of acute myocardial infarction, stroke, and death.2 Regular monitoring and education on the benefits of diet and exercise, can improve patient adherence to healthy behaviors. Acute Coronary Syndrome Treatment Essay Paper
Lack of exercise, including excessive sitting, increases cardiac morbidity and mortality.3 At least a half hour of moderate exercise 5 times per week is recommended for patients who have been cleared for exercise by their doctor.3 Even moving, rather than sitting for extended periods, has health benefits for everyone.3 Having a workout program increases the likelihood of continuing to exercise.2
It has repeatedly been shown that heart health can be improved and heart attacks prevented by having a healthy diet; engaging in physical activity; maintaining a healthy body weight, blood pressure and cholesterol levels; and reducing or eliminating alcohol and smoking. Healthy diets known to help patients with ACS, include the Mediterranean diet and a diet high in fruits, vegetables, whole grains, and seafood, with limited salt and sugar. Simply having a healthy diet and limiting alcohol reduces heart attack risk by onethird. The combination of a healthy diet, moderate alcohol use, moderate exercise (4-5 hours a week), smoking cessation, normal blood pressure and cholesterol levels, and a healthy body mass index decreases a woman’s chance of a first heart attac
The heart muscle needs a constant supply of oxygen-rich blood. The coronary arteries, which branch off the aorta just after it leaves the heart, deliver this blood. An acute coronary syndrome occurs when a sudden blockage in a coronary artery greatly reduces or cuts off the blood supply to an area of the heart muscle (myocardium). The lack of blood supply to any tissue is termed ischemia. If the supply is greatly reduced or cut off for more than a few minutes, heart tissue dies. A heart attack, also termed myocardial infarction (MI), is death of heart tissue due to ischemia. (See also Overview of Coronary Artery Disease.)
The complications of acute coronary syndromes depend on how much of the heart muscle is damaged, which is a direct result of where a coronary artery was blocked and how long this artery was blocked. If the blockage affects a large amount of heart muscle, the heart will not pump effectively. If the blockage shuts off blood flow to the electrical system of the heart, the heart rhythm may be affected.Acute Coronary Syndrome Treatment Essay Paper
Pumping problems
In a heart attack, part of the heart muscle dies. Unlike muscle, dead tissue, and the scar tissue that eventually replaces it, does not contract. The scar tissue sometimes even expands or bulges when the rest of the heart contracts. Consequently, there is less muscle to pump blood. If enough muscle dies, the heart’s pumping ability may be so reduced that the heart cannot meet the body’s need for blood and oxygen. Heart failure, low blood pressure (hypotension), and/or shock develop. If more than half of the heart tissue is damaged or dies, the heart generally cannot function, and severe disability or death is likely.
Drugs such as beta-blockers and especially angiotensin-converting enzyme (ACE) inhibitors can reduce the extent of the abnormal areas by reducing the workload of and the stress on the heart (see table Drugs Used to Treat Coronary Artery Disease). Thus, these drugs help the heart maintain its shape and function more normally.
The damaged heart may enlarge, partly to compensate for the decrease in pumping ability (up to a point, a larger heart beats more forcefully). Enlargement of the heart makes abnormal heart rhythms more likely.
Rhythm problems
Abnormal heart rhythms (arrhythmias) occur in more than 90% of people who have had a heart attack. These abnormal rhythms may occur because the heart attack damaged part of the heart’s electrical system. Sometimes there is a problem with the part of the heart that triggers the heartbeat, so heart rate may be too slow (bradycardia). Other problems can cause the heart to beat rapidly or irregularly (for example, atrial fibrillation). Sometimes the signal to beat is not conducted from one part of the heart to the other, and the heartbeat may slow or stop (heart block).Acute Coronary Syndrome Treatment Essay Paper
In addition, areas of heart muscle that have poor blood flow but that have not died can be very irritable. This irritability can cause heart rhythm problems, such as ventricular tachycardia or ventricular fibrillation. These rhythm problems greatly interfere with the heart’s pumping ability and may cause the heart to stop beating (cardiac arrest). A loss of consciousness or death can result. These rhythm disturbances are a particular problem in people who have an imbalance in blood chemicals, such as a low potassium level.
Pericarditis
Pericarditis (inflammation of the two-layered sac that envelops the heart) may develop in the first day or two after a heart attack. Pericarditis is more common in people who have not had the blocked artery opened by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). People seldom notice symptoms of early developing pericarditis because their heart attack symptoms are more prominent. However, pericarditis produces a scratchy rhythmic sound that can sometimes be heard through a stethoscope 2 to 3 days after a heart attack. Sometimes, the inflammation causes a small amount of fluid to collect in the space between the two layers of the pericardium (pericardial effusion).
Post-myocardial infarction (Dressler) syndrome is pericarditis that develops 10 days to 2 months after a heart attack. This syndrome causes fever, pericardial effusion (extra fluid in the space surrounding the heart), inflammation of the membranes covering the lungs, pleural effusion (extra fluid in the space between the two layers of the pleura), and joint pain. Diagnosis is based on the symptoms it causes and on the time it occurs.Acute Coronary Syndrome Treatment Essay Paper
People who develop pericarditis are usually given a nonsteroidal anti-inflammatory drug. Colchicine is often rapidly effective. Even with treatment, the syndrome can recur. If post-myocardial infarction syndrome is severe, a corticosteroid or a different nonsteroidal anti-inflammatory drug may be needed for a short time.
Myocardial rupture
Rarely, the heart muscle ruptures under the pressure of the heart’s pumping action because the damaged heart muscle is weak. Rupture usually occurs 1 to 10 days after a heart attack and is more common among women. The wall separating the two ventricles (septum), the external heart wall, and the muscles that open and close the mitral valve are particularly susceptible to rupture during or after a heart attack.
Rupture of the septum results in too much blood being diverted to the lungs, causing accumulation of fluid (pulmonary edema). A rupture of the septum can sometimes be repaired surgically.
Rupture of the external wall almost always causes rapid death. Doctors rarely have time to attempt surgery, and even then, surgery is rarely successful.
If the mitral valve muscles rupture, the valve cannot function—the result is sudden and severe heart failure. Doctors can sometimes repair the damage surgically.Acute Coronary Syndrome Treatment Essay Paper
Ventricular aneurysm
The damaged muscle may form a thin bulge (aneurysm) on the wall of the ventricle. Doctors may suspect an aneurysm based on abnormal results of electrocardiography (ECG), but echocardiography is done to be sure. These aneurysms may cause episodes of abnormal heart rhythms and may reduce the heart’s pumping ability. Because blood flows more slowly through aneurysms, blood clots can form in the heart’s chambers. If heart failure or abnormal heart rhythms develop, the aneurysm may be removed surgically.
Blood clots
Historically, about 20% of people who have had a heart attack form clots inside the heart, over the area of dead heart muscle. More recently, clot formation is less common. In about 10% of these people, parts of the clots break off, travel through the bloodstream, and lodge in smaller blood vessels throughout the body. They may block the blood supply to part of the brain (causing a stroke) or to other organs.
Echocardiography may be done to detect clots forming in the heart or to determine whether a person has factors that make clots more likely to form. For example, an area of the left ventricle may not be beating as well as it should.
For people who have clots, doctors often prescribe anticoagulants (sometimes called blood thinners) such as heparin and warfarin. Heparin is given intravenously in the hospital for at least 2 days. Then, warfarin is given by mouth for 3 to 6 months. Aspirin also is taken indefinitely.Acute Coronary Syndrome Treatment Essay Paper
Numerous complications can occur as a result of an acute coronary syndrome and increase morbidity and mortality. Complications can be roughly categorized as
Electrical dysfunction (conduction disturbance, arrhythmias)
Mechanical dysfunction (heart failure, myocardial rupture or aneurysm, papillary muscle dysfunction)
Thrombotic complications (recurrent coronary ischemia, mural thrombosis)
Inflammatory complications (pericarditis, post-myocardial infarction syndrome)
Electrical dysfunction occurs in > 90% of MI patients (see also Arrhythmias and Conduction Disorders). Electrical dysfunction that commonly causes mortality in the first 72 h includes tachycardia (from any focus) rapid enough to reduce cardiac output and lower BP, Mobitz type II block (2nd degree) or complete (3rd degree) atrioventricular (AV) block, ventricular tachycardia (VT), and ventricular fibrillation (VF). Asystole is uncommon, except as a terminal manifestation of progressive left ventricular failure and shock. Patients with disturbances of cardiac rhythm are evaluated for hypoxia and electrolyte abnormalities, which can be causative or contributory.
Sinus Node Disturbances
If the artery supplying the sinus node is affected by an acute coronary syndrome, sinus node disturbances can occur; they are more likely if there is a preexisting sinus node disorder (common among the elderly).Acute Coronary Syndrome Treatment Essay Paper
Sinus bradycardia
Sinus bradycardia, the most common sinus node disturbance, is usually not treated unless there is hypotension or the heart rate is < 50 beats/min. A lower heart rate, if not extreme, means reduced cardiac workload and possibly reduced infarct size.
For bradycardia with hypotension (which may reduce myocardial perfusion), atropine sulfate 0.5 to 1 mg IV is used; it can be repeated after several minutes if response is inadequate. Several small doses are best because high doses may induce tachycardia. Occasionally, a temporary transvenous pacemaker must be inserted.
Sinus tachycardia
Persistent sinus tachycardia is usually ominous, often reflecting left ventricular failure and low cardiac output. Without heart failure or another evident cause, this arrhythmia may respond to a beta-blocker, given po or IV depending on degree of urgency.
Atrial Arrhythmias
Atrial arrhythmias (atrial ectopic beats, atrial fibrillation, and, less commonly, atrial flutter) occur in about 10% of patients who have had a myocardial infarction and may reflect left ventricular failure or right atrial infarction.
Paroxysmal atrial tachycardia is uncommon and usually occurs in patients who have had previous episodes of it.
Atrial ectopy is usually benign, but if frequency increases, causes, particularly heart failure, are sought. Frequent atrial ectopic beats may respond to a beta-blocker.Acute Coronary Syndrome Treatment Essay Paper
Atrial fibrillation
Atrial fibrillation is usually transient if it occurs within the first 24 h (see figure Atrial fibrillation). Risk factors include age > 70, heart failure, previous history of myocardial infarction, large anterior infarction, atrial infarction, pericarditis, hypokalemia, hypomagnesemia, a chronic lung disorder, and hypoxia.
Atrial fibrillation
Atrial fibrillation
Fibrinolytics reduce incidence.
Recurrent paroxysmal atrial fibrillation is a poor prognostic sign and increases risk of systemic emboli.
For atrial fibrillation, a heparin (unfractionated or low molecular weight) is usually used because systemic emboli are a risk.
IV beta-blockers (eg, atenolol 2.5 to 5.0 mg over 2 min to total dose of 10 mg in 10 to 15 min, metoprolol 2 to 5 mg q 2 to 5 min to a total dose of 15 mg in 10 to 15 min) rapidly slow the ventricular rate and are typically given when heart rate is > 100. Heart rate and BP are closely monitored. Treatment is withheld when ventricular rate decreases satisfactorily or systolic BP is < 100 mm Hg.
IV digoxin, which is not as effective as beta-blockers, is used cautiously and only in patients with atrial fibrillation and left ventricular systolic dysfunction. Usually, digoxin takes at least 2 h to effectively slow heart rate and may rarely aggravate ischemia in patients with recent acute coronary syndrome.
For patients without evident left ventricular systolic dysfunction or conduction delay manifested by a wide QRS complex, the IV calcium channel blockers verapamil or diltiazem may be used for rate control when beta blockers are contraindicated or if adequate ventricular rate control is not achieved with other agents. Diltiazem may be given as a continuous IV infusion to control heart rate for long periods.Acute Coronary Syndrome Treatment Essay Paper
If atrial fibrillation compromises circulatory status (eg, causing left ventricular failure, hypotension, or chest pain), urgent electrical synchronized cardioversion is done. If atrial fibrillation returns after cardioversion, IV amiodarone should be considered for patients who continue to experience symptoms (eg chest pain) or remain hemodynamically compromised.
The heart is primarily made up of the cardiac muscle.
The coronary arteries are responsible for supplying oxygen-rich blood to all the parts of the heart muscle.
The heart then contracts rhythmically, to pump blood into the different blood vessels, which carry it to different parts of the body.
If any of the coronary arteries become narrow or blocked, due to cholesterol build-up and fatty deposits (a condition also known as atherosclerosis), the blood supply to that part of the heart gets affected. That particular part of the heart does not receive enough oxygen, and the tissue therein is at a risk of dying, unless the blockage is quickly removed. If left untreated, it can lead to a heart attack or unstable angina.Acute Coronary Syndrome Treatment Essay Paper
A heart attack or myocardial infarction is caused when the blood flow to the heart, from the coronary arteries, completely stops due to a blockage. (The word infarction means death of some tissue due to a blocked blood vessel.)
Unstable angina occurs when the blood flow to the heart slows down due to narrow arteries caused by cholesterol and fatty deposits or even blood clots.
There is also a condition known as stable angina, which is caused by sudden exertion, for example, after some rigorous exercise. This condition normally lasts from 1 to 5 minutes and is not considered very serious. It normalizes after some rest.
Doctors do not use the term Acute Coronary Syndrome while interacting with an affected patient. They usually use the term amongst themselves or in medical literature.
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Who is prone to Acute Coronary Syndrome?
You are prone to ACS if you:
have a high cholesterol level
have high blood pressure/hypertension
have a family history of heart disease
are obese
suffer from diabetes
lead a sedentary lifestyle
smoke excessively
Tobacco consumption is a major concern, with almost 40% of the ACS patients in India being chain-smokers. 38% of the ACS patients suffer from hypertension, while 30% of them also suffer from diabetes.Acute Coronary Syndrome Treatment Essay Paper
What are the symptoms of Acute Coronary Syndrome? How is Acute Coronary Syndrome diagnosed?
The ACS patients almost always complain of symptoms such as:
severe chest pain, which gets worse with emotional stress or vigorous physical activity ( the pain can last from 15 mins to several hours)
sweating
breathlessness
palpitation
A few patients also complain of giddiness, vomiting and abdominal pain.
Diagnosis
ACS is diagnosed with the help of an electrocardiogram, which reveals whether you suddenly suffered from a heart attack or whether you have angina. The electrocardiogram tests the heart’s electrical activity and measures the impulses. These impulses are recorded in the form of a graph on paper. The doctor checks the graph to see whether the heart is getting enough blood from the coronary arteries.
What are the complications of Acute Coronary Syndrome?
The complications of ACS depend upon the location of the blockage in the coronary artery, the amount of time it is blocked, and the size of the blockage. Depending on these factors various complications may arise.Acute Coronary Syndrome Treatment Essay Paper
• Pump Failure
When the blood flow to the heart gets affected it may lead to a heart attack. In a heart attack parts of the heart muscle, which do not receive oxygen, withers and dies which is then replaced by scar tissue. The scar tissue cannot contract and pump blood. On the contrary, the scar tissue may swell out or expand, when the rest of the heart muscle contracts to pump the blood, putting more pressure on the active parts of the heart to pump blood. Less blood may get pumped as a result, leading to less oxygen circulation in the body.This may result in low blood pressure, heart failure and death.
• Cardiac Arrhythmias
Also called irregular heartbeat, cardiac arrhythmias is a condition where the heartbeat is irregular. It is either too fast or too slow. This can occur due to many reasons.
An impaired heart might enlarge itself to make up for the decreasing pumping ability. The enlarged heart then beats more forcefully to pump blood, which affects the natural rhythm of the heart.
Following a heart attack, the electrical impulses of the heart get affected which may cause the irregular heartbeats.Acute Coronary Syndrome Treatment Essay Paper
Some parts of the heart which experience less blood flow, may not be dead but just be irritable. These irritable parts interfere with the natural rhythm of the heart. This condition is also known as ventricular fibrillation or ventricular tachycardia.
At times, cardiac arrhythmias can lead to heart failure or cardiac arrest.
• Mechanical Complications
The mechanical complications after a heart attack or death of some tissue in the heart include:
a malfunctioning mitral valve, which can lead the blood to be pumped backwards, thus not supplying enough oxygen-filled blood to the body.
ventricular wall rupture, which stops the blood supply to the body.
left ventricular aneurysm, which is the swelling of a weak area in the wall of the left ventricle, the main pumping chamber of the heart. The swelling may block the passage leading to less blood flow to the body.
• Pericarditis
Pericardium is a tissue shaped like a two-layered thin sac which holds the heart in place, allowing it to perform its functions efficiently. The two layers have a small amount of pericardial fluid between them which keeps them from rubbing against each other. When pericarditis occurs the pericardium or the thin sac becomes inflamed and rubs against the heart. This causes chest pain and produces a rasping sound which is rhythmic that can be heard through a doctor’s stethoscope for around 2 days following a heart attack.
• Blood Clots
After a heart attack, blood clots form in the hearts of some people over the dead areas of the heart muscle. These blood clots can travel through the bloodstream and block passages impeding the blood supply to the rest of the body.Acute Coronary Syndrome Treatment Essay Paper
Other effects of ACS especially after a heart attack are shock, persistent depression and nervousness. A supportive family, breaking free from stress, and leading a healthy lifestyle goes a long way in managing and at times overcoming Acute Coronary Syndrome.
What is the treatment for Acute Coronary Syndrome?
Exercise
Following a regular regimen of exercise for just half an hour can be extremely beneficial for your heart health. Exercising strengthens and tones your muscles, which includes your heart, which is actually made of a muscle. It will keep your heart fit, helping it to pump blood and distribute it efficiently throughout your body.
It is advisable to consult with your cardiologist before starting an exercise regimen.
Medical Treatments
If only medicines do not suffice to restore normal blood flow through your arteries the doctor may suggest the following procedures:
Angioplasty: In this procedure, the doctor inserts a thin tube called catheter into your blocked, or narrow plaque-ridden artery. Then he inserts a wire with an attached deflated balloon through the catheter, into the blocked area. Once inserted, the balloon is inflated which forces open the blocked area as the plaque is pushed against the walls of the artery.
Coronary Intravascular Stent Placement: After the angioplasty procedure, a stent may be placed in the blocked area of the artery by the doctor, so that the area remains open and blood can flow through with ease. The stent is like a wire mesh tube, made of metal, which keeps the artery open at all times. Stents may be placed in multiple locations depending on the number of blocked arteries. The stents remain for life in the arteries.Acute Coronary Syndrome Treatment Essay Paper
Coronary Artery Bypass Graft: Not all blocks in the arteries can be treated with angioplasty. If you have multiple blocks or have blocks which are inconveniently placed, the doctor may advise coronary artery bypass grafting. This is a process in which the doctor will take a healthy artery, or vein, from any part of the body, including, legs, chest, or the wrist, and graft or connect, one end of it of the vein above the blocked artery, and the other end below the block. This way, the blood flows through the newly grafted artery and goes around, or bypasses the blocked part of the coronary artery, to reach the heart.
Acute coronary syndromes include
Unstable angina
Non–ST-segment elevation myocardial infarction (NSTEMI)
ST-segment elevation myocardial infarction (STEMI)
These syndromes all involve acute coronary ischemia and are distinguished based on symptoms, ECG findings, and cardiac marker levels. It is helpful to distinguish the syndromes because prognosis and treatment vary.
Unstable angina (acute coronary insufficiency, preinfarction angina, intermediate syndrome) is defined as one or more of the following in patients whose cardiac biomarkers do not meet criteria for myocardial infarction (MI):
Rest angina that is prolonged (usually > 20 min)
New-onset angina of at least class 3 severity in the Canadian Cardiovascular Society (CCS) classification (see table Canadian Cardiovascular Society Classification System for Angina Pectoris)
Increasing angina, ie, previously diagnosed angina that has become distinctly more frequent, more severe, longer in duration, or lower in threshold (eg, increased by ≥ 1 CCS class or to at least CCS class 3)Acute Coronary Syndrome Treatment Essay Paper
ECG changes such as ST-segment depression, ST-segment elevation, or T-wave inversion may occur during unstable angina but they are transient. Of cardiac markers, CK is not elevated but cardiac troponin, particularly when measured using high-sensitivity troponin tests (hs-cTn), may be slightly increased. Unstable angina is clinically unstable and often a prelude to myocardial infarction or arrhythmias or, less commonly, to sudden death.
Non–ST-segment elevation MI (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
ST-segment elevation MI (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin or showing new left bundle branch block. Troponin I or troponin T and CK are elevated.
Both types of MI may or may not produce Q waves on the ECG (Q wave MI, non-Q wave MI).
Etiology
The most common cause of acute coronary syndromes is
An acute thrombus in an atherosclerotic coronary artery
Atheromatous plaque sometimes becomes unstable or inflamed, causing it to rupture or split, exposing thrombogenic material, which activates platelets and the coagulation cascade and produces an acute thrombus. Platelet activation involves a conformational change in membrane glycoprotein (GP) IIb/IIIa receptors, allowing cross-linking (and thus aggregation) of platelets. Even atheromas causing minimal obstruction can rupture and result in thrombosis; in > 50% of cases, pre-event stenosis is < 40%. Thus, although the severity of stenosis helps predict symptoms, it does not always predict acute thrombotic events. The resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about two thirds of patients; 24 h later, thrombotic obstruction is found in only about 30%. However, in virtually all cases, obstruction lasts long enough to cause varying degrees of tissue necrosis.
Rarer causes of acute coronary syndromes are
Coronary artery embolism
Coronary spasm
Coronary artery dissection
Coronary arterial embolism can occur in mitral stenosis, aortic stenosis, infective endocarditis, marantic endocarditis, or atrial fibrillation.Acute Coronary Syndrome Treatment Essay Paper
Cocaine use and other causes of coronary spasm can sometimes result in myocardial infarction. Spasm-induced MI may occur in normal or atherosclerotic coronary arteries.
Coronary artery dissection is a non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction. Dissection may occur in atherosclerotic or non-atherosclerotic coronary arteries. Non-atherosclerotic dissection is more likely in pregnant or postpartum women and/or patients with fibromuscular dysplasia or other connective tissue disorders.
Pathophysiology
Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted.
Myocardial dysfunction
Ischemic (but not infarcted) tissue has impaired contractility and relaxation, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock; usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Some degree of heart failure occurs in about two thirds of hospitalized patients with acute myocardial infarction. It is termed ischemic cardiomyopathy if low cardiac output and heart failure persist. Ischemia involving the papillary muscle may lead to mitral valve regurgitation. Dysfunctional wall motion can allow mural thrombus formation.
Myocardial infarction (MI)
Myocardial infarction is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue. MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria.Acute Coronary Syndrome Treatment Essay Paper
Infarction may be
Transmural: Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG.
Nontransmural (subendocardial): Nontransmural infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities.
Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG.
Necrosis of a significant portion of the interventricular septum or ventricular wall may rupture, with dire consequences. A ventricular aneurysm or pseudoaneurysm may form.
Electrical dysfunction
Electrical dysfunction can be significant in any form of acute coronary syndrome. Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T abnormalities), arrhythmias, and conduction disturbances. ST-T abnormalities of ischemia include ST-segment depression (often downsloping from the J point), T-wave inversion, ST-segment elevation (often referred to as injury current), and peaked T waves in the hyperacute phase of infarction. Conduction disturbances can reflect damage to the sinus node, the atrioventricular (AV) node, or specialized conduction tissues. Most changes are transient; some are permanent.Acute Coronary Syndrome Treatment Essay Paper
Symptoms and Signs
Symptoms of acute coronary syndromes depend somewhat on the extent and location of obstruction and are quite variable. Painful stimuli from thoracic organs, including the heart, can cause discomfort described as pressure, tearing, gas with the urge to eructate, indigestion, burning, aching, stabbing, and sometimes sharp needle-like pain. Many patients deny they are having pain and insist it is merely “discomfort.” Except when infarction is massive, recognizing the amount of ischemia by symptoms alone is difficult.
Symptoms of ACS are similar to those of angina and are discussed in more detail in sections on unstable angina and acute myocardial infarction.
Complications
After the acute event, many complications can occur. They usually involve
Electrical dysfunction (eg, conduction defects, arrhythmias)
Myocardial dysfunction (eg, heart failure, interventricular septum or free wall rupture, ventricular aneurysm, pseudoaneurysm, mural thrombus formation, cardiogenic shock)
Valvular dysfunction (typically mitral regurgitation)
Electrical dysfunction can be significant in any form of ACS, but usually, large parts of myocardium must be ischemic to cause significant myocardial dysfunction. Other complications of ACS include recurrent ischemia and pericarditis. Pericarditis that occurs 2 to 10 wk after an MI is known as post-MI syndrome, or Dressler syndrome.Acute Coronary Syndrome Treatment Essay Paper
Diagnosis
Serial ECGs
Serial cardiac markers
Immediate coronary angiography for patients with STEMI or complications (eg, persistent chest pain, hypotension, markedly elevated cardiac markers, unstable arrhythmias)
Delayed angiography (24 to 48 h) for patients with NSTEMI or unstable angina without complications noted above
Acute coronary syndromes should be considered in men > 30 yr and women > 40 yr (younger in patients with diabetes) whose main symptom is chest pain or discomfort. Pain must be differentiated from the pain of pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral separation, esophageal spasm, acute aortic dissection, renal calculus, splenic infarction, or various abdominal disorders. In patients with previously diagnosed hiatus hernia, peptic ulcer, or a gallbladder disorder, the clinician must be wary of attributing new symptoms to these disorders. (For approach to diagnosis, see also Chest Pain.)Acute Coronary Syndrome Treatment Essay Paper
The approach is the same when any ACS is suspected: initial and serial ECG and serial cardiac marker measurements, which distinguish among unstable angina, NSTEMI, and STEMI. Every emergency department should have a triage system to immediately identify patients with chest pain for rapid assessment and ECG. Pulse oximetry and chest x-ray (particularly to look for mediastinal widening, which suggests aortic dissection) is also done.
ECG
ECG is the most important test and should be done within 10 min of presentation. It is the center of the decision pathway because fibrinolytics benefit patients with STEMI but may increase risk for those with NSTEMI. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not for those with NSTEMI.
For STEMI, initial ECG is usually diagnostic, showing ST-segment elevation ≥ 1 mm in 2 or more contiguous leads subtending the damaged area (see figure Acute lateral left ventricular infarction).
Acute lateral left ventricular infarction (tracing obtained within a few hours of onset of illness)
There is striking hyperacute ST-segment elevation in leads I, aVL, V4, and V6 and reciprocal depression in other leads.Acute Coronary Syndrome Treatment Essay Paper
Acute lateral left ventricular infarction (tracing obtained within a few hours of onset of illness)
Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader’s attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing MI. Serial tracings (obtained every 8 h for 1 day, then daily) showing a gradual evolution toward a stable, more normal pattern or development of abnormal Q waves over a few days (see figure Inferior (diaphragmatic) left ventricular infarction) tends to confirm the diagnosis.
Inferior (diaphragmatic) left ventricular infarction (after the first 24 h)
Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF.
Inferior (diaphragmatic) left ventricular infarction (after the first 24 h)
Because nontransmural (non–Q wave) infarcts are usually in the subendocardial or midmyocardial layers, they do not produce diagnostic Q waves or distinct ST-segment elevation on the ECG. Instead, they commonly produce only varying degrees of ST-T abnormalities that are less striking, variable, or nonspecific and sometimes difficult to interpret (NSTEMI). If such abnormalities resolve (or worsen) on repeat ECGs, ischemia is very likely. However, when repeat ECGs are unchanged, acute MI is unlikely and, if still suspected clinically, requires other evidence to make the diagnosis. A normal ECG taken when a patient is pain free does not rule out unstable angina; a normal ECG taken during pain, although it does not rule out angina, suggests that the pain is not ischemic.
If right ventricular (RV) infarction is suspected, a 15-lead ECG is usually recorded; additional leads are placed at V4R, and, to detect posterior infarction, V8 and V9.Acute Coronary Syndrome Treatment Essay Paper
ECG diagnosis of myocardial infarction is more difficult when a left bundle branch block configuration is present because the ECG changes resemble changes due to STEMI (see figure Left bundle branch block). ST-segment elevation concordant with the QRS complex strongly suggests MI as does > 5-mm ST-segment elevation in at least 2 precordial leads. But generally, any patient with suggestive symptoms and new-onset (or not known to be old) left bundle branch block is treated as for STEMI.
Left bundle branch block
Left bundle branch block
CLINICAL CALCULATOR:
M.I. Prediction Decision TreeCalc icon
CLINICAL CALCULATOR:
Non Q Wave Myocardial Infarction Prediction icon
CLINICAL CALCULATOR:
M.I. Prediction Decision TreeCalc icon
Cardiac markers
Cardiac markers (serum markers of myocardial cell injury) are
Cardiac enzymes (eg, CK-MB)
Cell contents (eg, troponin I, troponin T, myoglobin)
These markers are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and specific and are now the markers of choice. Recently, several new, highly sensitive assays of cardiac troponin (hs-cTn) that are also very precise have become available. These assays can reliably measure troponin levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL).Acute Coronary Syndrome Treatment Essay Paper
Previous, less sensitive cTn tests were unlikely to detect cTn except in patients who had an acute cardiac disorder. Thus, a “positive” cTn test (ie, above the limit of detection) was very specific. However, the newer hs-cTn tests can detect small amounts of cTn in many healthy people. Thus, troponin levels detected with hs-cTn tests need to be referenced to the normal range, and are defined as “elevated” only when higher than 99% of the reference population. Furthermore, although an elevated troponin level indicates myocardial cell injury, it does not indicate the cause of the damage (although any troponin elevation increases the risk of adverse outcomes in many disorders). In addition to acute coronary syndromes, many other cardiac and non-cardiac disorders can elevate cTn levels (see table Causes of Elevated Troponin Levels); not all elevated levels detected with hs-cTn represent myocardial infarction, and not all myocardial necrosis results from an acute coronary syndrome event even when the etiology is ischemic. However, by detecting lower levels of troponin, hs-cTn assays enable earlier identification of MI than other assays, and have replaced other cardiac marker tests in many centers.
Patients suspected of having an ACS should have an hs-cTn assay done on presentation and 3 h later. Troponin should be measured at 0 and 6 h if a standard cTn assay is used.
An hs-cTn level must be interpreted based on the patient’s pre-test probability of disease, which is estimated clinically based on Acute Coronary Syndrome Treatment Essay Paper
Risk factors for ACS
Symptoms
ECG findings
A high pre-test probability plus an elevated level detected with an hs-cTn assay is highly suggestive of ACS, whereas a low pre-test probability plus a normal hs-cTn assay result is unlikely to represent ACS. Diagnosis is more challenging when test results are discordant with pre-test probability, in which case serial hs-cTn assays often help. A patient with low pre-test probability and an initially slightly elevated troponin level detected with hs-cTn that remains stable on repeat testing probably has non-ACS cardiac disease (eg, heart failure, stable coronary artery disease). However, if the repeat level rises significantly (ie, > 20 to 50%) the likelihood of ACS becomes much higher. If a patient with high pre-test probability has a normal troponin level detected with hs-cTn and that rises > 50% on repeat testing, ACS is likely; continued normal levels (often including at 6 h and beyond when suspicion is high) suggest need to pursue an alternate diagnosis.
TABLE
Causes of Elevated Troponin Levels icon
Coronary angiography
Coronary angiography most often combines diagnosis with percutaneous coronary intervention (PCI—ie, angioplasty, stent placement). When possible, emergency coronary angiography and PCI are done as soon as possible after the onset of acute myocardial infarction (primary PCI). In many tertiary centers, this approach has significantly lowered morbidity and mortality and improved long-term outcomes. Frequently, the infarction is actually aborted when the time from pain to PCI is short (< 3 to 4 h).
Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients with uncomplicated NSTEMI or unstable angina whose symptoms have resolved typically undergo angiography within the first 24 to 48 h of hospitalization to detect lesions that may require treatment.Acute Coronary Syndrome Treatment Essay Paper
After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that angiography be done before hospital discharge in STEMI patients with inducible ischemia on stress imaging or an ejection fraction < 40%.
Other tests
Routine laboratory tests are nondiagnostic but, if obtained, show nonspecific abnormalities compatible with tissue necrosis (eg, increased ESR, moderately elevated WBC count with a shift to the left). A fasting lipid profile should be obtained within the first 24 h for all patients hospitalized with ACS.
Myocardial imaging is not needed to make the diagnosis if cardiac markers or ECG is positive. However, in patients with myocardial infarction, bedside echocardiography is invaluable for detecting mechanical complications. Before or shortly after discharge, patients with symptoms suggesting an ACS but nondiagnostic ECGs and normal cardiac markers should have a stress imaging test (radionuclide or echocardiographic imaging with pharmacologic or exercise stress). Imaging abnormalities in such patients indicate increased risk of complications in the next 3 to 6 mo and suggest need for angiography, which should be done before discharge or soon thereafter, with PCI or CABG done as necessary.
Right heart catheterization using a balloon-tipped pulmonary artery catheter can be used to measure right heart, pulmonary artery, and pulmonary artery occlusion pressures and cardiac output. This test is not routinely recommended and should be done only if patients have significant complications (eg, severe heart failure, hypoxia, hypotension) and by doctors experienced with catheter placement and management protocols.Acute Coronary Syndrome Treatment Essay Paper
Prognosis
Global risk should be estimated via formal clinical risk scores (Thrombosis in Myocardial Infarction [TIMI], Global Registry of Acute Coronary Events [GRACE], Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy [PURSUIT]—1) or a combination of the following high-risk features:
Recurrent angina/ischemia at rest or during low-level activity
Heart failure
Worsening mitral regurgitation
High-risk stress test result (test stopped in ≤ 5 min due to symptoms, marked ECG abnormalities, hypotension, or complex ventricular arrhythmias)
Hemodynamic instability
Sustained ventricular tachycardia
Diabetes mellitus
PCI within past 6 mo
Prior CABG
LV ejection fraction < 0.40
CLINICAL CALCULATOR:
Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable Angina Non ST Elevation Myocardial Infarction icon
CLINICAL CALCULATOR:
Thrombolysis in Myocardial Infarction (TIMI) Score for ST Elevation Acute Myocardial Infarction icon
Prognosis reference
1. Boersma E, Pieper KS, Steyerberg EW, et al: Predictors of outcome in patients with acute coronary syndromes without persistent ST-segment elevation. Results from an international trial of 9461 patients. The PURSUIT Investigators. Circulation 101(22): 2557–2567, 2000.Acute Coronary Syndrome Treatment Essay Paper
Treatment
Prehospital care: Oxygen, aspirin, and nitrates and triage to an appropriate medical center
Drug treatment: Antiplatelet drugs, antianginal drugs, anticoagulants, and in some cases other drugs
Often, angiography to assess coronary artery anatomy
Often, reperfusion therapy: Fibrinolytics, percutaneous coronary intervention or coronary artery bypass surgery
Supportive care
Post discharge rehabilitation and chronic management of coronary artery disease
Treatment, including drug treatment, is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications. An acute coronary syndrome is a medical emergency; outcome is greatly influenced by rapid diagnosis and treatment.
Treatment occurs simultaneously with diagnosis.
Contributing disorders (eg, anemia, heart failure) are aggressively treated.
Because the chest pain of myocardial infarction usually subsides within 12 to 24 h, any chest pain that remains or recurs later is investigated. It may indicate such complications as recurrent ischemia, pericarditis, pulmonary embolism, pneumonia, gastritis, or ulcer.
Prehospital care
Oxygen
Aspirin
Nitrates
Triage to appropriate medical center
A reliable IV route must be established, oxygen given (typically 2 L by nasal cannula), and continuous single-lead ECG monitoring started. Prehospital interventions by emergency medical personnel—including ECG, chewed aspirin (325 mg), pain management with nitrates (see table Drugs for Coronary Artery Disease), early thrombolysis when indicated and possible, and triage to the appropriate hospital where primary PCI is available—can reduce risk of mortality and complications.Acute Coronary Syndrome Treatment Essay Paper
Although opioids have long been used to treat pain in patients with acute coronary syndromes, new data suggest that morphine attenuates activity of some P2Y12 receptor inhibitors and may contribute to worse patient outcomes (1, 2).
Early diagnostic data and response to treatment can help determine the need for and timing of revascularization when primary percutaneous coronary intervention is not possible.
Heart Attack: An Acute Coronary Syndrome
Acute Coronary Syndrome is a name given to three types of coronary artery disease that are associated with sudden rupture of plaque inside the coronary artery:
Unstable angina
Non-ST segment elevation myocardial infarction or heart attack (NSTEMI)
ST segment elevation myocardial infarction or heart attack (STEMI).
The location of the blockage, the length of time that blood flow is blocked and the amount of damage that occurs determines the type of acute coronary syndrome. These life-threatening conditions require emergency medical care.
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Unstable Angina
Unstable angina is a new symptom or a change from stable angina. The angina may occur more frequently, occur more easily at rest, feel more severe, or last longer. Although this angina can often be relieved with oral medications, it is unstable and may progress to a heart attack. Usually more intense medical treatment or a procedure is required. Unstable angina is an acute coronary syndrome and should be treated as a medical emergency.
Heart attack: Non-ST segment elevation myocardial infarction (NSTEMI)
This heart attack, or MI, may not cause changes on an electrocardiogram (ECG). However, chemical markers in the blood indicate that damage has occurred to the heart muscle. In NSTEMI, the blockage may be partial or temporary, and so the extent of the damage relatively small.Acute Coronary Syndrome Treatment Essay Paper
Heart attack: ST segment elevation myocardial infarction (STEMI)
This heart attack, or MI, is caused by an abrupt and prolonged blocked blood supply. It affects a large area of the heart muscle, and so causes changes on the ECG as well as in blood levels of key chemical markers.
Other terms associated with a heart attack:
Stunned Myocardium
If blood flow is returned to an area of heart muscle after a period of ischemia (lack of blood supply), the heart muscle may not pump normally for some time. This is called “stunned” heart muscle or myocardium.
Hibernating Myocardium
If deprived of adequate blood supply for a long period of time, some areas of heart muscle stop working as they should. Some areas will have permanent damage. Other areas are able to return to their normal function if blood flow is returned to that area (by medications or a procedure). Hibernating myocardium is heart muscle that is “resting” or “sleeping” and may possibly return to normal function if treated appropriately.
Cleveland Clinic cardiologists specialize in prompt diagnosis and treatment of heart attack and acute coronary syndromes. If you do not find what you are looking for about heart attacks, contact us. We would be happy to help you.
Acute coronary syndrome (ACS) is the leading cause of death in the Western world. In the United States, approximately one in seven deaths is secondary to coronary heart disease. It is estimated that more than one million Americans experience a myocardial infarction (MI) every year, which in effect means that one American experiences an MI every 24 seconds [1].
Diagnostic and treatment modalities have vastly evolved over the years. Since this disease entity was first reported by Herrick in 1912 [2], adjuvant and pharmacological modalities for the management of ACS have evolved greatly and resulted in better pain relief and mortality reduction after cardiac events. Presently, use of a few drugs such as aspirin, heparin, or P2Y12 inhibitors is mandatory to treat ACS.Acute Coronary Syndrome Treatment Essay Paper
Unfortunately, the mnemonic MONA (morphine, oxygen, nitrates, and aspirin) continues to be used as a teaching tool in universities, on websites, and in educational videos. It must be stated here that a few less experienced professionals who learn this mnemonic might in fact be doing harm to their patients because strict adherence to only MONA may cause underestimation of the importance of other drugs not contained in MONA.
In this article, we discuss historical and technical aspects of the pharmacological treatment used in the management of ACS and the use of this mnemonic and investigate whether MONA continues to be relevant in the contemporary management of ACS.
The presence of risk factors plays an important role in the evaluation of chest pain, especially in a patient with known disease. The landmark Framingham Heart Study showed that cardiac risk can be influenced by diet, lifestyle, and familial risk factors (Oppenheimer, 2005). The more risk factors that a person carries, the greater their risk of developing ischemic heart disease. These risk factors are generally grouped into two categories: those that are modifiable and those that are not. Risk factors amendable are as follows:Acute Coronary Syndrome Treatment Essay Paper
Tobacco smoke (American Heart Association, 2012)
High blood cholesterol (AHA, 2012)
High blood pressure (AHA, 2012)
Physical inactivity (AHA, 2012)
Obesity and overweight (AHA, 2012)
Diabetes mellitus (AHA, 2012)
Risk factors that cannot be changed include:
Age- 82% of people who die of coronary heart disease are >65 (AHA, 2012)
Male sex (AHA, 2012)
Heredity- this includes both family history and race (AHA, 2012)
Risk is higher among Mexican Americans, American Indians, native Hawaiians and some Asian Americans (AHA, 2012)
Patients presenting with unstable angina or NSTEMI have variable levels of risk of cardiac death and ischemic cardiac events (Antman, Cohen, Bernink, McCabe, Horacek, Papuchis, Mautner & Braunwald, 2000). The trial conducted by Antman et al. (2000) set out to “develop a simple risk score that has broad applicability, is easily calculated at patient presentation, does not require a computer, and identifies patients with different responses to treatments for UA/NSTEMI”. In doing so, the TIMI risk score was created. The scores are calculated using a score of 1 for each risk factor (7 total categories) assigned to a given patient. According to Antman, et al (2000) the score determines the patient’s risk of death, myocardial infarction, or severe ischemia. Antman, et al. (2000) found 7 prognostic variables that increase a patients risk. These are:
Age 65 years or older
At least 3 risk factors for coronary artery disease (male, dyslipidemia, smoking, hypertension, diabetes mellitus, obesity & family history)Acute Coronary Syndrome Treatment Essay Paper
Prior coronary stenosis of 50% or more
ST-segment deviation on ECG at presentation
At least 2 anginal events in prior 24 hours
Use of aspirin in prior 7 days
Elevated serum cardiac markers
In TIMI 11B/ESSENCE, event rates increase significantly as the TIMI-score increases (Antman et al., 2000). A score of 0/1 showed a 4.7% event rate; 8.3% for 2; 13.2% for 3; 19.9% for 4; 26.2% for 5; and 40.9% for 6/7. This landmark pair of trials allows practitioners a quick assessment of a patient’s risk of suffering a serious cardiac event.
Physical Exam
Physical exam is also a key component in the evaluation of a patient with chest pain, as many clues can suggest acute coronary syndrome. Unstable vital signs can be an important hint that the patient has suffered an MI. A general examination may reveal a patient who is diaphoretic and/or using accessory respiratory muscles. The cardiovascular exam could reveal a new murmur, S3/S4 gallop, or JVD. Finally, during the pulmonary exam rales may be heard upon auscultation.
Diagnostics
Diagnostic testing is an essential part of the evaluation of a patient presenting with chest pain. Several important diagnostic tools were introduced to the emergency department in the latter half of the 20th century that greatly improved the diagnosis and care of acute coronary syndrome.Acute Coronary Syndrome Treatment Essay Paper
Electrocardiogram
The introduction of coronary care units in the 1960’s allows physicians to utilize the electrocardiogram (ECG) to monitor potential fatal arrhythmias in patients with acute myocardial infarction (Julian, 1987). Shortly thereafter the portable electrocardiogram became commonplace within the emergency department to assist in diagnosing complications of acute coronary syndrome (Drew, et al, 2004). A patient presenting with myocardial ischemia will typically have symmetrically-inverted T waves in leads V2-V6 (Dubin, 2000). As the name suggests, a STEMI is an ST-segment elevation myocardial infarction, though ST-segment elevation can occur with Prinzmetal’s angina in absence of an infarction (Dubin, 2000). Additionally, the ECG allows us to evaluate necrosis of the heart in the form of the presence of “Q-waves”. Q-waves are the first downward deflection of the QRS complex (Dubin, 2000). As Dubin (2000) explains, a positive Q-wave MI must:
Lack a preceding spike in the QRS complex
Be at least 1 mm wide
or
Have an amplitude of 1/3 the QRS complex
An additional benefit of the ECG is that it allows the practitioner to identify the location of an acute event. Each lead corresponds to a particular location of the heart. For example, leads II, III, and AvF are the inferior leads and reflect the inferior portion of the heart.
Due to the relatively high specificity but low sensitivity of the 12 lead ECG in diagnosis of acute coronary syndrome, a group of researchers in Canada recently set out to enhance ischemia detection by conducted a trial which added a new criteria using a three vessel specific leads derived from the traditional 12 lead ECG (Horacek, Mirmoghisi, Warren, Wagner & Wang, 2008). This trial showed a statistically significant improvement in the ability of the vessel specific lead protocol to detect ischemia (Horacek et al., 2008). Horacek et al. (2008) found the following sensitivity and specificity for conventional STEMI criteria versus that of the vessel specific leads (VSL):Acute Coronary Syndrome Treatment Essay Paper
Vessel
Sensitivity
Specificity
Left Anterior Descending
74% conventional, 91% VSL
97% conventional, 97% VSL
Right Coronary Artery
60% conventional, 70% VSL
94% conventional, 94% VSL
Left Circumflex Artery
36% conventional, 71% VSL
100% conventional, 100% VSL
Totals Set
60% conventional, 76% VSL
96% conventional, 96% VSL
Based on these results, Horacek et al. (2008) concluded that using vessel specific leads “can identify acute ischemia better than existing STEMI criteria”. While a STEMI criteria using vessel specific leads has yet to become a mainstay within the standard emergency room protocol, this study provides exciting new improvements in the detection and management of patients with ACS.
Serum Biomarkers
The use of biochemical markers to detect cardiac cell death significantly evolved in the 1980’s and 1990’s. Initially, nonspecific markers such as aspartate transaminase and total creatinine kinase were used to detect myocardial necrosis (Lewandrowski, Chen & Januzzi, 2002). During the mid-1990’s the more cardiac specific enzymes CK-MB became the gold standard for detection of myocardial injury (Lewandrowski et al., 2002). CK-MB, which commonly rises 4-9 hours after the onset of angina, was not without its shortcomings. CK-MB may be falsely elevated due to several different causes, including recent strenuous exercise or skeletal muscle damage, or renal failure (Vivekanandan & Swaminathan, 2010). In the late 1990’s a more predictable biomarker, troponin I, was introduced for more accurate detection of acute coronary syndrome (Heeschen, Goldmann, Moeller & Hamm, 1998). According to Heeschen et al. (1998), Troponin I can be evaluated at the bedside in the emergency room and “has a higher diagnostic sensitivity for the detection of acute myocardial infarction (60% vs 48%)” when compared to CK-MB. The reason for this improvement in accuracy is that troponin I is not found in skeletal muscle tissue or renal failure (Heeschen et al., 1998). As Heeschen et al. (1998) demonstrated in a head to head study that “cTnI test systems produced no positive results in patients with end-stage renal failure and acute or chronic skeletal muscle injury, whereas 30% and 71% of the patients, respectively, had increased CK-MB mass concentrations”. One disadvantage of troponin I, however, is that it has a lower sensitivity for the detection of acute myocardial infarction compared to that of CK-MB (Heeschen et al., 1998). This is due to an increased level of cTnI in patients with unstable angina (Heeschen et al., 1998). For this reason, a typical workup for a patient with chest pain in the emergency room includes both cTnI and CK-MB assays, which are drawn at presentation and every 3-6 hours thereafter (Ross, Bever, Uddin & Hockman, 2000).Acute Coronary Syndrome Treatment Essay Paper
Imaging
A common component of a chest pain protocol is a chest x-ray. This is normally either a standard AP/lateral series or a portable chest x-ray if the patient is unable to get out of bed. The chest x-ray is useful to eliminate other possible causes of chest pain, such as an aortic aneurism or a pneumothorax.
Contrast-enhanced computed tomographic angiography, or CTA, has become an integral part of the management of acute coronary syndrome due to its high sensitivity and specificity (Hoffman, Truong, Schoenfeld, Chou, Woodard, Nagurney, Pope & Udelson, 2012). According to the ROMICAT-I study performed by Hoffman et al., (2012), CTA is an effective way to rule out myocardial infarction or ischemia as well as major cardiovascular events over the next 2 years from presentation. The data presented in ROMICAT-I showed that patients undergoing CTA decreased their hospital stay by 7.6 hours compared to standard therapy (Hoffman et al., 2012). Additionally, 50% of CTA patients were discharged from the hospital within 8.6 hours of presentation versus only 10% of patients undergoing standard therapy (Hoffman et al., 2012). Finally, the mean time to diagnosis was significantly decreased with the CT group versus the standard group (Hoffman et al., 2012). Overall, CTA was shown to reduce time spent in the hospital and time to diagnosis when compared to standard therapy for acute coronary syndrome. This is important to note considering the importance of quick coronary reperfusion of STEMI patients (Trost &Lange, 2011). An additional observation was that these benefits were achieved without an increase in the cost of care (Hoffman et al., 2012). There was no overall difference between the groups in incidence of myocardial infarction 30 days after initial presentation (Hoffman et al., 2012). It is important to note that a patient undergoing a CTA is exposed to increased radiation. Additionally, patients undergoing CTA were more likely to undergo invasive coronary procedures when compared to standard evaluation.
Based on this data, a question arises as to whether every patient presenting with possible acute coronary syndrome should undergo a CTA. The population studied in ROMICAT-I consisted of low to intermediate risk patients. Overall, CTA was shown to decrease the time to diagnosis and hospital stay for patients with possible ACS. In contrast, CTA increases a patient’s exposure to radiation and increases the likelihood that these patients will undergo an increase in invasive coronary procedures. These factors should all be considered when evaluating a patient presenting with chest pain.Acute Coronary Syndrome Treatment Essay Paper
Treatment
Pharmacologic
Aspirin: Early aggressive aspirin (ASA) therapy (162-325mg followed by 81-162mg daily) is currently recommended for all patients with acute coronary syndrome, unless contraindicated (Kirk, Kontos & Diercks, 2011).
Plavix (Clopidogrel): According to the CURE trial Clopidogrel has been shown to provide “a 20% reduction in cardiovascular death, MI, or stroke” for NSTEMI patients with positive biomarkers or ischemic ECG changes (Kirk et al., 2011). It is important to note that the significant anti-platelet benefits of Clopidogrel administration should also be weighed against the increased risk of bleeding events if the patient may be a candidate for coronary artery bypass surgery.
Antianginal Agents:
Nitroglycerin (NTG): NTG is commonly administered by EMS respondents but can also be ordered once the patient arrives in the emergency department, typically sublingually or in the form of Nitropaste. Nitroglycerin dilates the coronary arteries, which reduces myocardial oxygen demand (Trost & Lange, 2011). For this reason, it is important to evaluate the patient’s baseline blood pressure. If SBP is less than 100, caution should be used.
Morphine: Intravenous morphine may be given in the event that chest pain is not relieved by NTG administration. Morphine reduces ventricular preload, thereby decreasing myocardial O2 demand (Trost & Lange, 2011).Acute Coronary Syndrome Treatment Essay Paper
Beta-Andrenergic Blockers: Beta-blockers decrease demand on the heart by decreasing heart rate, blood pressure, and myocardial contractility (Trost & Lange, 2011). In a patient presenting with ACS, IV Lopressor is typically the agent of choice. These are especially effective agents in patients with elevated blood pressure or tachycardia. It is important to evaluate relevant contraindications to beta-blocker therapy, such as: HR<45bpm, 2° or 3° AV block, uncompensated heart failure, SBP<100, cardiogenic shock, sick sinus syndrome without pacemaker, pheocromocytoma, or peripheral vascular disease (Epocrates, 2012).
Calcium-Channel Blockers: Diltiazem and Verapamil improve cardiac O2 supply by vasodilation of the coronary vessels, reduce O2 demand by reducing afterload, and reduce heart rate and contractility (Trost & Lange, 2011). Calcium-channel blockers are 2nd line treatments for ACS and are typically reserved for patients who are unable to take a beta-blocker (Trost & Lange, 2011). Contraindications include: sick sinus syndrome, 2° or 3° AV heart block, hypotension, acute MI with pulmonary congestion, atrial fibrillation or flutter with accessory bypass tract, and ventricular tachycardia, severe left ventricular dysfunction, and cardiogenic shock (Epocrates, 2012).
Antithrombotic therapy: Antithrombotic therapy is recommended in a patient with suspected ACS, unless contraindicated (Trost & Lange, 2011).
Unfractionated heparin is easy to administer (IV) and is rapidly reversible with protamine in the event of bleeding. (Trost & Lange, 2011). As with any antithrombotic, there is a risk of bleeding so these patients require close monitoring.
Low molecular weight heparin is more predictable, has a lower incidence of thrombocytopenia, and does not require monitoring (Trost & Lange, 2011). LMWH is the preferred agent for a more conservative, ischemia-guided strategy to prevent in hospital death or myocardial infarction (Trost & Lange, 2011).Acute Coronary Syndrome Treatment Essay Paper
Bivalirudin is an antithrombotic agent that does not cause thrombocytopenia (Trost & Lange, 2011). It has been shown to be equally as effective as unfractionated heparin or LMWH but with a significantly lower rate of bleeding (Trost & Lange, 2011).
Oxygen administration should be administered for patients who are short of breath, showing signs of shock, or O2 saturation <94% (O’Connor, Brady, Brooks, Diercks, Egan, Ghaemmaghami, Menon & Yannopoulos, 2010).
Next Step for NSTEMI or Unstable Angina Patients
If a patient is considered to be high risk, such as a patient is at risk of future ischemia or infarction, an early invasive strategy is recommended (Trost & Lange, 2011). For these patients, cardiac catheterization should be performed within 24-48 hours of admission (Trost & Lange, 2011). In a low risk patient, a more conservative treatment is typically recommended. For these patients, catheterization is only recommended if recurrent or provocable ischemia occurs (Trost & Lange, 2011). TIMI scores are a valuable tool to assess the patients risk and to guide the practitioner on the appropriate next step.Acute Coronary Syndrome Treatment Essay Paper
Next Step for STEMI Patients
Prompt coronary reperfusion is paramount in patients presenting with STEMI (Trost & Lange, 2011). A “door-to-balloon” time of less than 90 minutes is considered to be the goal (Trost & Lange, 2011). If the patient presents to a facility without a percutaneous coronary intervention facility the patient should be either:
Treated with fibrinolytic therapy if not contraindicated (Trost & Lange, 2011)
Or
Transferred to a nearby PCI facility (Trost & Lange, 2011).
Conclusion
Acute coronary syndrome is spectrum of diseases typically caused by atherosclerotic disease. Emergency department practitioners must be able to rapidly diagnose and manage ACS patients in order to potentially preserve precious heart muscle. While treatments for ACS have improved dramatically over the past 30 years, several recent innovations have brought upon exciting new possibilities for the care of these patients. These include new vessel specific ECG leads, cardiac specific biomarkers, and the use of computed-tomographic angiography to assess patients with possible ACS.
One component of the management algorithm that has not changed is the need for a strong history and physical examination to aid in diagnosis. Urgency in obtaining diagnosis cannot be stressed enough, and patients presenting with STEMI should be rapidly sent for PCI or transferred to a facility with PCI capabilities.
The condition occurs due to the buildup of fatty deposits in and on the walls of the coronary arteries. These arteries are responsible for delivering oxygen and nutrients to heart muscles.
Heart muscles need a steady and constant supply of oxygen-rich blood to function. A blood clot is the most common cause of a blocked coronary artery.Acute Coronary Syndrome Treatment Essay Paper
Types
Man holding chest
Angina and heart attacks are types of acute coronary syndrome.
Acute coronary syndrome is used to describe three types of coronary artery disease:
Unstable angina
Non-ST-segment elevation myocardial infarction or heart attack (NSTEMI)
ST-segment elevation myocardial infarction or heart attack (STEMI)
If the supply of oxygen to the cells becomes too low, the cells of the heart muscles can die.
The lack of blood supply to any tissue is called ischemia. The death of the cells results in damage to muscle tissue, and this is a heart attack or myocardial infarction.
In some cases, the cells do not die, but damage due to an inadequate supply of oxygen results in heart muscles that do not work correctly or efficiently. The problem may be temporary or permanent. Unstable angina is the term used to describe the condition when acute coronary syndrome does not lead to cell death.
The location of the blockage, the length of time that the blood flow is blocked, and the amount of damage that occurs determines the type of acute coronary syndrome. Doctors classify the coronary syndromes based on:
The presence of certain substances in the blood released by the damaged heart
Symptoms
Electrocardiography (ECG) results
Proper classification is especially important when it comes to choosing the right treatment.Acute Coronary Syndrome Treatment Essay Paper
Everything you need to know about angina
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Symptoms
Large man smoking
Risk factors associated with acute coronary syndrome include smoking and obesity.
The signs and symptoms of acute coronary syndrome generally begin quickly, sometimes without warning, and can alert a person that something is wrong. Common symptoms include:
Chest pain or discomfort
Pain or discomfort in one or both arms, the back, jaw, neck, or stomach
Shortness of breath
Dizziness or feeling lightheaded
Indigestion
Nausea or vomiting
Sweating
These symptoms are very serious and a person should seek emergency treatment immediately. Chest pain caused by acute coronary syndromes can come on suddenly without warning, which occurs during a heart attack.
In other cases, the pain can be unpredictable and get noticeably worse even after rest, which is a symptom of unstable angina. Chest pain or discomfort is typically the most common symptom of acute coronary syndrome, but signs and symptoms vary depending on age, sex, and the presence of other medical conditions.
Risk factors
There are certain risk factors associated with acute coronary syndrome that people should be aware of. Risk factors include:
Older age – men of 45 years or older, women aged 55 years or older
High blood pressure or cholesterol
Smoking
Lack of physical activity
Unhealthy diet, obesity, or overweight
Diabetes
Family history
Diagnosis
To make a quick and accurate diagnosis, a doctor will perform tests as well as inquire about any symptoms and previous medical history. Typical tests include:Acute Coronary Syndrome Treatment Essay Paper
Electrocardiogram (ECG): This test measures the electrical activity in the heart via electrodes attached to the skin. Abnormal or irregular impulses may indicate poor heart function due to a lack of oxygen to the heart. Certain electrical signal patterns may also help to indicate the location of a blockage.
Blood tests: Certain enzymes may be detectable in the blood if cell death results in damage to the heart tissue. A positive result indicates a heart attack.
Cardiac perfusion scan: This scan can show if the heart is getting enough blood and can check areas of damage after a heart attack.
Information from these tests, as well as the actual signs and symptoms, are used to help diagnose acute coronary syndrome and determine whether it should be classified as a heart attack or unstable angina.
Doctors may use other tests to determine if additional treatment is needed or if there are additional heart problems present.
Some doctors may order a person to wear a Holter monitor, which records the heart’s electrical activity for 24 hours. The monitor helps to detect whether the person has abnormal heart rhythms or periods of inadequate blood supply that may not have any symptoms.
Additional tests may be ordered to rule out other causes as well as help to treat the person better.
Treatment
Ambulance
Acute coronary syndrome is a medical emergency and medical attention should be sought immediately.
This is a medical emergency. Immediate treatment is ordered for acute coronary syndrome. The short-term goals include relieving pain and improving blood flow to help restore heart function as quickly as possible.
Long-term goals include improving overall heart function, managing risk factors, and lowering the risk of a heart attack. Typical treatment includes a combination of medical drugs and surgical procedures.Acute Coronary Syndrome Treatment Essay Paper
Medications include:
Nitroglycerin
Antiplatelet drugs
Beta blockers
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin receptor blockers (ARBs)
Statins
People who call the emergency services may be instructed to take or be given aspirin in the ambulance. If medications fail to alleviate the problems and restore proper blood function, angioplasty and stenting as well as coronary bypass surgery may be necessary.
Lifestyle changes
In some people, acute coronary syndrome may be prevented. Heart disease can lead directly to acute coronary syndrome, but those who do not have heart disease can protect themselves by practicing a healthy lifestyle:
Following a heart-healthy diet: Eating a diet that includes fruits, vegetables, whole grains, and lean protein.
Not smoking: Those who smoke can try medicines and counseling to help them quit.
Being active: Engaging in regular exercise to stay physically fit. People should aim for moderate exercise at least 2-3 hours a week.
Paying attention to the numbers: People should know their blood pressure and cholesterol levels and understand what the numbers mean as well as the optimum range.
Maintaining a healthy weight.
Drinking alcohol in moderation: Drinking more than one or two alcoholic drinks per day can raise blood pressure.
People who have had problems such as a heart attack in the past may also be instructed to take one baby aspirin in addition to their daily medication. Aspirin helps to prevent platelets from forming clots and helps to reduce the risk of a second heart attack by around 22 percent.
With lifestyle changes and the right medication, it is possible to prevent acute coronary syndrome or to treat it and lead a normal life. Acute Coronary Syndrome Treatment Essay Paper
