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Long-term outcomes in survivors of early ventricular arrhythmias after acute ST-elevation and non-ST-elevation myocardial infarction treated with percutaneous coronary intervention. PubMed Article Google Scholar. Masuda, M. Priori, S. Otherwise, oral beta-blocker therapy is given in the acute setting. It is important to refrain from giving beta-blockers if there are signs of cardiogenic shock, such as hypotension or pulmonary edema on chest X-ray.
Long-term lifetime therapy has been shown to reduce MI incidence and improve mortality. Caution must be used in the acute setting to avoid hypotension, which can worsen myocardial ischemia. When LV function returns to normal and the patient does not have diabetes, the benefits are less clear. ARBs are generally given only if ACE inhibitors cannot be tolerated due to cough or other side effects. A class effect is likely present; therefore, spironolactone is frequently used instead of eplerenone due to cost concerns, although there is no direct data to support this practice.
The nondihydropyridine calcium channel blockers diltiazem and verapamil can be used when there is a contraindication to beta-blockers, such as in asthma, and no HF or significant LV systolic dysfunction are present. Sublingual nifedipine is contraindicated due to a reflexive increase in the sympathetic nervous system, which can be harmful.
There are quite a few mechanical and nonmechanical complications of STEMI, many of which are life-threatening.
This results in end-organ hypoperfusion and potentially multi-system organ failure and can be fatal. Most commonly, the apex of the heart is involved; however, the inferior wall can form an aneurysm as well. There are four main concerns in patients with LV aneurysm. The most common cause of pre-hospital death during STEMI is ventricular fibrillation; the widespread availability of automated external defibrillators, or AEDs, has been of benefit in this situation.
Ventricular tachycardia also commonly occurs as well during and after STEMI and can be life-threatening. This is a benign, hemodynamically stable rhythm, and no treatment is necessary. Below is one ECG example. Note the AV dissociation in the rhythm strip in lead V1 at the bottom; this is diagnostic for VT in the setting of a wide QRS complex tachycardia, but not always seen.
Rapid control of heart rates is crucial to limit the extent of ischemia. Recall that oxygen demand increases as heart rate increases. Emergent cardioversion and amiodarone therapy are frequently needed in the setting of atrial fibrillation and STEMI. When infarction of the interventricular septum occurs, this area can thin with the remodeling process and, on occasion, a complete defect between the right and left ventricles can develop.
This results in left-to-right shunting of blood and can be life-threatening when acute. A holosystolic murmur at the left lower sternal border occurs. The ventricles are good at adapting to hemodynamic stress when gradually introduced, as in worsening aortic regurgitation; however, when acute, ventricular failure and shock occurs — as is present with acute VSD formation.
Emergency surgical repair is warranted in this setting. Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute MI can occur as a complication of an inferior MI right coronary artery supply , as the posteromedial papillary muscle is the most likely to rupture. There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply — from the left anterior descending coronary artery and the left circumflex coronary artery — in most individuals, whereas the posteromedial papillary muscle receives its sole blood supply from the right coronary artery.
Complete infarction of the posteromedial papillary muscle can occur during an inferior MI but only partial, or no, damage will be done to the anterolateral papillary muscle during an anterior left anterior descending or lateral circumflex infarction, as there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture. Emergent surgical repair or replacement of the mitral valve is indicated.
As a bridge to surgery, intraaortic balloon counterpulsation can be helpful hemodynamically to reduce afterload and lessen the mitral regurgitation.
After MIs, especially anteriorly, the myocardial stunning that occurs can result in blood pooling toward the akinetic segment — frequently the cardiac apex — resulting in thrombus formation. Embolization of this thrombus can cause a stroke. This is a fatal complication of MI and occurs when thinning of the left ventricular free wall occurs as a part of remodeling. A complete defect results in blood from the left ventricle filling the pericardium.
This usually occurs rapidly, resulting in cardiac tamponade, pulseless electrical activity, or PEA, and death. Treatment is emergent surgical repair. When obstructed, the portion of the heart muscle serviced by that artery will quickly suffer from a lack of oxygen, called ischemia. Chest pains angina are often the first signs of this. If the obstruction is extensive enough, some of the heart muscle will begin to die, resulting in myocardial infarction. ACS is categorized by the level of obstruction and the resulting damage to the heart muscle:.
Regardless of how an ACS event is classified, it is still considered a medical emergency since unstable angina and NSTEMI are often early warning signs of a major heart attack.
STEMI will typically result in intense pain or pressure in or around the chest, often radiating to the neck, jaw, shoulder, or arm. Profuse sweating, breathlessness, and a profound sense of impending doom are also common. At times, the signs may be far less obvious, manifesting with nonspecific or generalized symptoms such as:.
As a general rule of thumb, anyone at significant risk of a heart attack should pay close attention to any unusual symptom arising from above the waist. A review of symptoms, accompanied by the evaluation of the ST segment on the ECG, is usually enough for a doctor to begin treatment. A review of cardiac enzymes may also help but usually arrives well after acute treatment is started.
It is important to stabilize the person as quickly as possible. In addition to pain and distress, STEMI can cause sudden death due to ventricular fibrillation a serious disturbance of the heart rhythm or acute heart failure when the heart cannot pump enough blood to properly supply the body. After a heart attack has run its course, the muscle itself may be left with substantial permanent damage.
Chronic heart failure is a common consequence of this, as is the increased risk of dangerous cardiac arrhythmias irregular heartbeats. In addition to administering drugs to stabilize the heart muscle including morphine, beta-blockers , and statin medications , efforts will be made to immediately reopen the blocked artery.
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