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Acute Coronary Syndromes

Acute coronary syndromes (ACS) describes a group of conditions, including unstable angina, non-Q-wave myocardial infarction, and Q-wave myocardial infarction. ACS are conditions caused by coronary vessel obstruction and thrombotic occlusions from rupture or erosion of plaque.

The incidence of ACS is higher in males who are younger than age 70 ( although the incidence of angina at 15 years postmenopause is equal to that in men); however, mortality after a myocardial infarction (MI) is significantly higher among women than men up to age 75. That's because many prescribers tend to overlook signs and symptoms of ACS in women for all ages) because of the perceived cardioprotective effect of estrogen.

The higher risk of death among women may be explained partially by differences in medical history (such as diabetes), a lower rate of established treatment use in women, and clinical characteristics. Indeed, among patients under age 50, mortality for women is more than twice that for men. Thus, women are considered a high-risk group.

Causes

The predominant cause of ACS is due 10 atherosclerotic plaque disease. Coronary artery vasospasm is a less common cause. The most common cause of unstable angina is coronary artery disease (CAD) due to atherosclerosis. Fatty, fibrous plaques progressively narrow the coronary artery lumina, reducing the volume of blood that can flow through them and leading to myocardial ischemia.

As atherosclerosis progresses, Iuminal narrowing is accompanied by vascular changes that constrict the blood vessel and impair blood flow.

This causes a precarious balance between myocardial oxygen supply and demand, threatening the myocardium beyond the lesion. When oxygen demand exceeds what the diseased vessel can supply, localized myocardial ischemia results.

Myocardial cells become ischemic Within 10 seconds of a coronary artery occlusion. Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial function. Untreated, this can lead to tissue injury or necrosis. Within several minutes, oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism,leading to accumulation of lactic acid and reduction of cellular pH.

The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular function. The strength of contractions in the the affected myocardial region is reduced as the fibers shorten inadequately, resulting in less force and velocity. Moreover, wall motion is abnormal in the ischemic area, resulting in less blood being ejected from the heart with each contraction. Restoring blood flow through the coronary arteries restores aerobic metabolism and contractility. However, if blood flow isn't restored, MI results.

Other causes of MI include:

  • obesity
  • excessive intake of saturated fats
  • sedentary lifestyle
  • aging
  • stress or type A personality
  • drug use, especially cocaine and amphetamines.
  • hypertension
  • smoking
  • positive family history

MI results from occlusion of one or more of the coronary arteries. Occlusion can stem from atherosclerosis thrombosis, platelet aggregation, or coronary artery stenosis or spasm. If coronary artery occlusion causes ischemia lasting longer than 30 to 45 minutes, irreversible myocardial cell damage and muscle death occur. The site of the MI depends on the vessels involved. Occlusion of the circumflex branch of the left coronary artery causes a lateral wall infarction; occlusion of the anterior descending branch of the left coronary artery causes an anterior wall infarction. True posterior or inferior wall infarctions generally result from occlusion of the right coronary artery or one of its branches.

Right ventricular infarctions may also result from right coronary artery occlusion, can accompany inferior infarctions, and may cause right-sided heart failure. In Q-wave (transmural) MI, tissue damage extends through all myocardial layers; in non-Q-wave (subendocardial) MI, damage occurs only in the innermost and, possibly middle layers.

All infarcts have a central area of necrosis or infarction surrounded an area of potentially viable injury. This zone may be salvaged if circulation is restored or it progress to necrosis. The zone injury, in turn is surrounded by of viable ischemic tissue. (Although ischemia begins immediately, the size of the infarct can be limited if circulation is restored within 6 hours.

Signs and symptoms

The symptoms of ACS are due to myocardial ischemia, the underlying of which is an imbalance between supply and demand of myocardial oxygenation. Typically, angina is a symptom of myocardial ischemia. It is usually described as a sensation of the pressure, tightness, or heaviness that's produced by activities or conditions that increase myocardial oxygen demand. However, not all patient will experience chest pains. Some patient will experience chest pains. Some patients will present with neck, jaw, arm, or epigastric pain. Others may experience shortness of breath, light headedness or dizziness, nausea and vomiting, diaphoresis, or severe weakness, which may represent anginal equivalent symptoms.

Diagnosis

The initial diagnosis of ACS is based almost entirely on the patient's medical and family history, risk factors and, to a lesser extent, an electrocardiogram (ECG). ECG is the most important diagnostic test for angina. It may show changes during symptoms and in response to treatment. It may show preexisting structural or ischemic heart disease (left ventricular hypertrophy, Q waves). An ECG may be normal between anginal episodes. A normal ECG or one that remains unchanged from baseline doesn't exclude the possibility that chest pain is ischemic in origin. Changes that may be seen during anginal episodes includes:

  • Stress testing may be performed to detect ST-segment changes during exercise or pharmacologic stress, indicating ischemia, and to determine a safe exercise prescription.
  • Coronary angiography reveals the location and degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing.
  • Intravascular ultrasound may be used to further define coronary anatomy and Iuminal narrowing.
  • Myocardial perfusion imaging with thallium-201 may be performed during treadmill exercise to detect ischemic areas of the myocardium; they appear as "cold spots," which normalize during rest, indicating viable tissue.
  • Stress echocardiography may show abnormal wall motion in ischemic areas.
  • Rest perfusion imaging with sestamibi may be used to rule out myocardial ischemia in the patient with a chest pain syndrome that isn't clearly cardiac in nature.

A diagnosis of MI is determined using the following tests:

  • Serial 12-lead ECG may reveal characteristic changes, such as serial ST-segment depression in non-Q wave MI (a more limited area of damage insufficient to cause changes in the pattern of ventricular depolarization) and ST-segment elevation in Q-wave MI (a larger area of damage, which causes permanent change in the pattern of ventricular depolarization). An ECG can also identify the location of MI, arrhythmia's, hypertrophy, and pericarditis.
  • Serial creatine kinase fraction (CK­MB) is the standard test for diagnosing MI.
  • Serial cardiac enzymes and proteins may show a characteristic rise and fall-specifically, CK-MB, the proteins troponin T and I, and myoglobin - that confirm the diagnosis of MI.

Treatment

The goals of treatment are to preserve patency of the coronary artery, increases blood flow through stenosed lesions, and reduce myocardial oxygen demand. Patients with severe unstable angina and ECG changes should be, admitted to a telemetry unit. All patients should receive anti platelet agents, and patients with ongoing ischemia should receive aggressive medical intervention until signs of ischemia resolve, as indicated on ECG and by lack of signs and symptoms.

The following drugs have been used to treat ACS:

  • Nitrates oppose coronary artery spasm and reduce myocardial oxygen demand by reducing preload and afterload.
  • Analgesics reduce pain, which decreases sympathetic stress and reduces preload.
  • IIB/ IIA antagonists with aspirin are standard antiplatelet therapy for a patient at high risk for unstable angina. Adenosine diphosphate (ADP) antagonists aren't considered standard therapy but may be useful in a patient who can't tolerate aspirin.

Treatment of an MI typically involves following the treatment guide. lines recommended by the American College of Cardiology/American Heart Association (ACC/ AHA) Task Force on Practice Guidelines. These include:

  • assessment of the patient with chest pain in the emergency department within 10 minutes of symptom onset because at least 50% of deaths take place within 1 hour of the onset of symptoms (Moreover, thrombolytic therapy is most effective when started within the first 3 hours after the onset of symptoms.)
  • oxygen by nasal cannula for 2 to 3 hours to increase blood oxygenation.
  • nitroglycerin sublingually or I.V. to relieve chest pain, unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 or greater than 100 beats/minute.
  • morphine or meperidine (Demerol) for analgesia because pain stimulates the sympathetic nervous system,leading to an increase in heart rate and vasoconstriction.
  • aspirin every day indefinitely to in habit platelet aggregation.
  • continuous cardiac monitoring to detect arrhythmia's and ischemia
  • I. V. fibrinolytic therapy for the patient experiencing chest pain for at least 30 minutes who reaches the hospital within 12 hours of the onset of symptoms (unless contraindications exist) and whose ECG shows new left bundle-branch block (LBBB) or ST­segment elevation of at least 1 to 2 mm in two or more ECG leads (The greatest benefit of such reperfusion therapy, however, occurs when reperfusion takes place within 3 hours of the onset of chest pain.)
  • I. V. heparin for the patient who has received fibrinolytic therapy to increase the chances of patency in the affected coronary artery.

Special considerations

Care for the patient who has suffered an ACS is directed toward detecting complications, preventing further myocardial damage. and promoting comfort, rest. and emotional well-being. Commonly, the patient with an MI receives treatment in the intensive care unit (ICU), where he's under constant observation for complications. Other considerations include:

  • On admission to the ICU, monitor and record the patient's ECG, blood pressure, temperature, and heart and breath sounds.
  • Assess and record the severity and duration of pain, and administer analgesics. Avoid I. M. injections; absorption from the muscle is unpredictable. and bleeding is likely if the patient is receiving fibrinolytic therapy.
  • Check the patient's blood pressure after giving nitroglycerin, especially the first dose.
  • Frequently monitor the ECG to detect rate changes or arrhytlunias. Place rhythm strips in the patient's chart periodically for evaluation.
  • During episodes of chest pain, obtain 12-lead ECG, blood pressure, and pulmonary artery catheter measurements and monitor them for changes.


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