Clinical Presentation
The classic initial manifestations of an acute MI include prolonged substernal chest pain with dyspnea, diaphoresis, and nausea. The pain may be described as a crushing, pressing, constricting, vise-like, or heavy sensation. There may be radiation of the pain to one or both shoulders and arms or to the neck, jaw, or interscapular area. Only a few patients have this classic overall picture. Although 80% of patients with an acute MI have chest pain at the time of initial examination, only 20% describe it as crushing, constricting, or vise-like. The pain may also be described atypically, such as sharp or stabbing, or it can involve atypical areas such as the epigastrium or the back of the neck. “Atypical” presentations are common in the elderly.
The classic initial manifestations of an acute MI include prolonged substernal chest pain with dyspnea, diaphoresis, and nausea. The pain may be described as a crushing, pressing, constricting, vise-like, or heavy sensation. There may be radiation of the pain to one or both shoulders and arms or to the neck, jaw, or interscapular area. Only a few patients have this classic overall picture. Although 80% of patients with an acute MI have chest pain at the time of initial examination, only 20% describe it as crushing, constricting, or vise-like. The pain may also be described atypically, such as sharp or stabbing, or it can involve atypical areas such as the epigastrium or the back of the neck. “Atypical” presentations are common in the elderly.
The initial manifestations of an acute MI were more likely to include symptoms such as sudden dyspnea, acute confusion,
cerebrovascular events (e.g., stroke or syncope), acute CHF, vomiting, and palpitations. There is strong evidence that a substantial proportion of MIs are asymptomatic. That 28% of infarcts were discovered only through the appearance of new ECG changes (Q waves or loss of R waves) observed on a routine biennial study. These infarctions had been previously unrecognized by both patient and physician.
cerebrovascular events (e.g., stroke or syncope), acute CHF, vomiting, and palpitations. There is strong evidence that a substantial proportion of MIs are asymptomatic. That 28% of infarcts were discovered only through the appearance of new ECG changes (Q waves or loss of R waves) observed on a routine biennial study. These infarctions had been previously unrecognized by both patient and physician.
Physical Examination
For the patient with an “uncomplicated MI” there are few physical examination findings. The main purpose of the examination is to assess the patient for evidence of complications from the MI and to establish a baseline for future comparisons. Signs of severe left ventricular dysfunction include hypotension, peripheral vasoconstriction, tachycardia, pulmonary rales, an S3, and elevated jugular venous pressure. Preexisting murmurs should be verified. A new systolic murmur can result from a number of causes: papillary muscle dysfunction, mitral regurgitation as a result of ventricular dilatation, ventricular septal rupture, and acute severe mitral regurgitation due to papillary muscle rupture.
For the patient with an “uncomplicated MI” there are few physical examination findings. The main purpose of the examination is to assess the patient for evidence of complications from the MI and to establish a baseline for future comparisons. Signs of severe left ventricular dysfunction include hypotension, peripheral vasoconstriction, tachycardia, pulmonary rales, an S3, and elevated jugular venous pressure. Preexisting murmurs should be verified. A new systolic murmur can result from a number of causes: papillary muscle dysfunction, mitral regurgitation as a result of ventricular dilatation, ventricular septal rupture, and acute severe mitral regurgitation due to papillary muscle rupture.
Electrocardiography
The classic ECG changes of acute ischemia are peaked, hyperacute T waves, T wave flattening or inversion with or without ST segment depression, horizontal ST segment depression, and ST segment elevation. Changes associated with an infarction are (1) the fresh appearance of Q waves or the increased prominence of preexisting ones; (2) ST segment elevations; and (3) T wave inversions. It is important to recognize that with acute MI the ECG may be entirely normal or contain only “soft” ECG evidence of infarction.
The classic ECG changes of acute ischemia are peaked, hyperacute T waves, T wave flattening or inversion with or without ST segment depression, horizontal ST segment depression, and ST segment elevation. Changes associated with an infarction are (1) the fresh appearance of Q waves or the increased prominence of preexisting ones; (2) ST segment elevations; and (3) T wave inversions. It is important to recognize that with acute MI the ECG may be entirely normal or contain only “soft” ECG evidence of infarction.
In the past infarcts were classified as transmural or subendocardial, depending of the presence of Q waves. This terminology has now been replaced by the terms Q-wave and non–Q-wave MI. This distinction has more clinical relevance, as several studies have indicated differences in etiology and outcome. The key differences between these two groups are as follows: (1) Q-wave infarctions account for 60% to 70% of all infarcts and non–Q-wave infarctions for 30% to 40%. (2) ST segment elevation is present in 80% of Q-wave infarctions and 40% of non–Q-wave infarctions. (3) The peak creatine kinase tends to be higher in Q-wave infarctions. (4) Postinfarction ischemia and early reinfarction are more common with non–Qwave infarctions. (5) In-hospital mortality is greater with Q-wave infarctions (20% versus 8% for non–Q-wave infarctions). In general, it is thought that the non–Q-wave infarction is a more unstable condition because of the higher risk of reinfarction and ischemia.
Laboratory Findings
Elevation of the creatine kinase muscle and brain subunits (CK-MB) isoenzyme is essential for the diagnosis of acute MI. In general, acute elevations of this enzyme are accounted for by myocardial necrosis. Detectable CK-MB from noncardiac causes is rare except during trauma or surgery. The peak level appearance of CK-MB is expected within 12 to 24 hours after the onset of symptoms; normalization is expected in 2 to 3 days. Therefore patients should have a CK-MB level determined on admission and every 8 to 12 hours thereafter (repeated twice). Reliance on a single CK assay in an emergency room setting to rule out MI is not sensitive and should be discouraged. Cardiac troponins (T and I) are newer markers for cardiac injury. The troponins first become detectable after the first few hours following the onset of myocardial necrosis, and they peak after 12 to 24 hours. Normalization of troponin T levels requires 5 to 14 days; troponin I levels requires 5 to 10 days.
Elevation of the creatine kinase muscle and brain subunits (CK-MB) isoenzyme is essential for the diagnosis of acute MI. In general, acute elevations of this enzyme are accounted for by myocardial necrosis. Detectable CK-MB from noncardiac causes is rare except during trauma or surgery. The peak level appearance of CK-MB is expected within 12 to 24 hours after the onset of symptoms; normalization is expected in 2 to 3 days. Therefore patients should have a CK-MB level determined on admission and every 8 to 12 hours thereafter (repeated twice). Reliance on a single CK assay in an emergency room setting to rule out MI is not sensitive and should be discouraged. Cardiac troponins (T and I) are newer markers for cardiac injury. The troponins first become detectable after the first few hours following the onset of myocardial necrosis, and they peak after 12 to 24 hours. Normalization of troponin T levels requires 5 to 14 days; troponin I levels requires 5 to 10 days.
Management Guidelines
The main priority for patients with an acute MI is relief of pain. The frequent clinical observation of rapid, complete relief of pain after early reperfusion with thrombolytic therapy has made it clear that the pain of an acute MI is due to continuing ischemia of living jeopardized myocardium rather than to the effects of completed myocardial necrosis.
The main priority for patients with an acute MI is relief of pain. The frequent clinical observation of rapid, complete relief of pain after early reperfusion with thrombolytic therapy has made it clear that the pain of an acute MI is due to continuing ischemia of living jeopardized myocardium rather than to the effects of completed myocardial necrosis.
Effective analgesia should be administered at the time of diagnosis. Analgesia can be achieved by the use of sublingual nitroglycerin or intravenous morphine (or both). Sublingual nitroglycerin is given immediately unless the systolic blood pressure is less than 90 mm Hg. If the systolic blood pressure is under 90 mm Hg, nitroglycerin may be used after intravenous access has been obtained. Longacting oral nitrate preparations are avoided for management of early acute MI. Sublingual or transdermal nitroglycerin can be used, but intravenous infusion of nitroglycerin allows more precise control. The intravenous dose can be titrated by frequently measuring blood pressure and heart rate. Morphine sulfate is also highly effective for the relief of pain associated with an acute MI. In addition to its analgesic properties, morphine exerts favorable hemodynamic effects by increasing venous capacitance and reducing systemic vascular resistance. The result is to decrease myocardial oxygen demand. As with nitroglycerin, hypotension may occur. The hypotension may be treated with intravenous fluids or leg elevation.
Oxygen
Supplemental oxygen is given to all patients with an acute MI. Hypoxemia in a patient with an uncomplicated infarction is usually caused by ventilation-perfusion abnormalities. When oxygen is used it is administered by nasal cannula or mask at a rate of 4 to 10 L/min. In patients with chronic obstructive pulmonary disease it may be wise to use lower flow rates.
Supplemental oxygen is given to all patients with an acute MI. Hypoxemia in a patient with an uncomplicated infarction is usually caused by ventilation-perfusion abnormalities. When oxygen is used it is administered by nasal cannula or mask at a rate of 4 to 10 L/min. In patients with chronic obstructive pulmonary disease it may be wise to use lower flow rates.
Thrombolytic Therapy
In addition to relieving pain and managing ischemia, thrombolytic therapy must be considered. Thrombosis has a major role in the development of an acute MI. Approximately 66% of patients with MIs have ST segment elevation, making it likely that the process is caused by an occlusive clot. The goal of thrombolytic therapy is reperfusion with a minimum of side effects. The most commonly used thrombolytic agents are streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), recombinant tissue-type plasminogen activator (rt-PA), urokinase, and pro-urokinase.
In addition to relieving pain and managing ischemia, thrombolytic therapy must be considered. Thrombosis has a major role in the development of an acute MI. Approximately 66% of patients with MIs have ST segment elevation, making it likely that the process is caused by an occlusive clot. The goal of thrombolytic therapy is reperfusion with a minimum of side effects. The most commonly used thrombolytic agents are streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), recombinant tissue-type plasminogen activator (rt-PA), urokinase, and pro-urokinase.
Early administration of thrombolytic therapy, within 6 to 12 hours from the onset of symptoms, has been associated with a reduction in mortality. Indications for thrombolytic therapy include typical chest pain >30 minutes but <12 hours that is unrelieved by nitroglycerin, and ST segment elevation in more than two contiguous leads (>1 mm in limb leads or >2 mm in chest leads) or ST segment depression in only V1 and V2 or a new left bundle branch block. Relative contraindications for thrombolytic therapy include history of stroke, active bleeding, blood pressure >180 mm Hg systolic, major surgery/ trauma in the last 3 to 6 months, recent noncompressible vascular puncture, and possible intracranial event/unclear mental status. Wright and colleagues56 present a summary of the major thrombolytic trials. Advances in this therapeutic modality during the past 5 years include new third-generation fibrinolytic agents and various strategies to enhance administration and efficacy of these agents. A number of ongoing trials are attempting to determine whether the combination of fibrinolytic therapy with low molecular weight heparin enhances coronary reperfusion and reduces mortality and late reocclusion. Also presented is a dose and cost summary of the available fibrinolytic agents.
Complications (Mechanical)
The most common complications of an acute MI are mechanical and electrical. Mechanical complications include those that are quickly reversible and those that are clearly life-threatening. Reversible causes of hypotension include hypovolemia, vasovagal reaction, overzealous therapy with antianginal or antiarrhythmic drugs, and brady- and tachyarrhythmias. Other, more serious etiologies include primary left ventricular failure, cardiac tamponade, rupture of the ventricular septum, acute papillary muscle dysfunction, and mitral regurgitation.
The most common complications of an acute MI are mechanical and electrical. Mechanical complications include those that are quickly reversible and those that are clearly life-threatening. Reversible causes of hypotension include hypovolemia, vasovagal reaction, overzealous therapy with antianginal or antiarrhythmic drugs, and brady- and tachyarrhythmias. Other, more serious etiologies include primary left ventricular failure, cardiac tamponade, rupture of the ventricular septum, acute papillary muscle dysfunction, and mitral regurgitation.
Classification of patients with acute MI.
Class 1: Patients with uncomplicated infarction without evidence of heart failure as judged by the absence of rales and an S3.
Class 2: Patients with mild to moderate heart failure as evidenced by pulmonary rales in the lower half of the lung fields and an S3.
Class 3: Patients with severe left ventricular failure and pulmonary edema.
Class 4: Patients with cardiogenic shock, defined as systolic blood pressure less than 90 mm Hg with oliguria and other evidence of poor peripheral perfusion.
Class 1: Patients with uncomplicated infarction without evidence of heart failure as judged by the absence of rales and an S3.
Class 2: Patients with mild to moderate heart failure as evidenced by pulmonary rales in the lower half of the lung fields and an S3.
Class 3: Patients with severe left ventricular failure and pulmonary edema.
Class 4: Patients with cardiogenic shock, defined as systolic blood pressure less than 90 mm Hg with oliguria and other evidence of poor peripheral perfusion.
Cardiogenic shock has emerged as the most common cause of inhospital mortality of patients with an acute MI. Despite advances in medical therapy, cardiogenic shock has a dismal prognosis (80–90% mortality). The management of patients with cardiogenic shock includes adequate oxygenation, reduction in myocardial oxygen demands, protection ofischemic myocardium, and circulatory support. The potential for myocardial salvage with emergency reperfusion should be considered in all cases.
Complications (Electrical)
The past 30 years has seen major developments in the recognition and treatment of arrhythmias. The most common include the brady- and tachyarrhythmias, AV conduction disturbances, and ventricular arrhythmias. Organized treatment protocols have been developed for each of these dysrhythmias.
The past 30 years has seen major developments in the recognition and treatment of arrhythmias. The most common include the brady- and tachyarrhythmias, AV conduction disturbances, and ventricular arrhythmias. Organized treatment protocols have been developed for each of these dysrhythmias.
Post-MI Evaluation
Recommendations for pre- and postdischarge evaluations of patients with an acute MI recommendations for testing exercise tolerance and strategies to determine those who would benefit from medical or surgical intervention. These recommendations include a submaximal ETT at 6 to 10 days and at 3 weeks to determine functional capacity.
Recommendations for pre- and postdischarge evaluations of patients with an acute MI recommendations for testing exercise tolerance and strategies to determine those who would benefit from medical or surgical intervention. These recommendations include a submaximal ETT at 6 to 10 days and at 3 weeks to determine functional capacity.
Rehabilitation
The goal of cardiac rehabilitation includes maintenance of a desirable level of physical, social, and psychological functioning after the onset of cardiovascular illness. Specific goals of rehabilitation include risk stratification, limitation of adverse psychological and emotional consequences of cardiovascular disease, modification of risk factors, alleviation of symptoms, and improved function. Risk stratification is accomplished by exercise tolerance testing. Additionally, high-risk patients include those with CHF, silent ischemia, and ventricular dysrhythmias. All patients should undergo an evaluation to reduce risk factors (smoking, hyperlipidemia, and hypertension). Risk modification of these factors has been associated with significant reduction in subsequent cardiac events. Enrollment in a cardiac rehabilitation program with particular emphasis on exercise has been shown to reduce cardiovascular mortality.
The goal of cardiac rehabilitation includes maintenance of a desirable level of physical, social, and psychological functioning after the onset of cardiovascular illness. Specific goals of rehabilitation include risk stratification, limitation of adverse psychological and emotional consequences of cardiovascular disease, modification of risk factors, alleviation of symptoms, and improved function. Risk stratification is accomplished by exercise tolerance testing. Additionally, high-risk patients include those with CHF, silent ischemia, and ventricular dysrhythmias. All patients should undergo an evaluation to reduce risk factors (smoking, hyperlipidemia, and hypertension). Risk modification of these factors has been associated with significant reduction in subsequent cardiac events. Enrollment in a cardiac rehabilitation program with particular emphasis on exercise has been shown to reduce cardiovascular mortality.
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