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ischemic heart disease drugs
The effect of drugs on thrombolytric cardiac enzymes, creatine kinase and creatine phosphokinase-MB, myocardial infarction €
"The thrombolytric effect of drugs on the cardiac enzyme, creatine kinase and creatine phosphokinase-MB, myocardial infarction.
MYOCARDIAL INFARCTION
Myocardial infarction refers to a dynamic process by which one or more regions of experience cardiac muscle a severe and prolonged decline in oxygen supply due to coronary heart disease after necrosis or death of myocardial tissue occurs.
The launch process infarction attack may be sudden or gradual progression to complete event takes about 3 to 6 hours.
PREVALENCE
Myocardial infarction is the leading cause of death in the United States (USA), and in most industrialized countries in the world. Approximately 800,000 people in the United States are concerned and, despite a greater awareness of symptoms present, 250,000 die before their presentation to a hospital. 4 The survival rate of patients hospitalized with AMI U.S. is about 90% to 95%. This represents a significant improvement in survival and relates improvements in emergency response and medical treatment strategies.
In general, MI can occur at any age but its incidence increases with age. The actual impact depends on the risk factors predisposing to atherosclerosis, which is discussed below. About 50% of all IM in the United States occur in people under 65 years. However, in the future, demographic changes and the average age of the population increases, a higher percentage of patients with MI will be over 65 years.
Men are more likely than women but the risk is higher among women than among men after menopause.
Coronary arteries
Arteries coronary capillaries provide myocardial blood
The artery to right coronary artery (CDA) supplies the headset right ventricle and right, bottom left ventricular septal and posterior wall AV, SA, and nodes
Coronary artery left (ACG) is composed of two major branchiate left anterior descending (LAD) and circumflex (LCX).
LAD artery supplies below the left ventricular anterior wall, anterior septum and apex of the left ventricle.
The arterial blood supply LCX in the left lateral ventricle and posterior.
Cardiac enzymes
Cardiac marker levels increased overtime. Therefore, enzymes are taken on a number of general model in the home and more than 6.24 hours for 3 samples.
Enzymes are typically evaluated CK, CKMB, LDH, Troponin T & I
CK-MB ratio indicates the degree of deterioration of heart muscle. The higher the ratio, the more heart muscle damage. Troponins are preferred markers of myocardial injury or are very specific and cardiac believed to increase before permanent damage develops.
Increased levels of troponin should not be used by themselves to remove href = "http://www.labtestsonline.org/understanding/conditions/heart_attack.html"> heart attack. Troponin will remain high for 1-2 weeks after IM allows easy diagnosis if the patient presented with late myocardial infarction EC older than the others will not be identified, except reinfarction occurs.
The elevation of cardiac enzymes myocardial infarction
Rising enzyme Normalize peak CKMB value Normal value
CK 12 h 16-30hrs 3-5 days 35-232IU / L
CKMB 4.8 h 24 h 72 h <51IU / L <6%
3-6 hr troponin I 20 hours 14 days 0,0-0,4 ng / ml
Troponin T 2-4 hours 8-12 am 14 days 0.0-0.1 ng / ml
LDH 12 h 12-24 h 10 days 100-190 IU / L
PATHOPHYSIOLOGY
The most common sites of myocardial infarction in the left ventricle, the chamber of the heart that has the highest workload. Changes in tissue produced in the myocardium are related to the extent to which the cells were deprived of oxygen. Deprivation results in a total area of infarction in which cells die and become necrotic tissue.
Necrosis in this area is evident in the 5 to 6 hours after occlusion. In response to necrosis of the body increases its products of leukocytes, which helps eliminate dead cells. With the increase in collateral circulation, bringing the fibroblasts, which form a connective tissue scar in the area of infarction. In general, the formation of fibrous scar tissue is completed 2 to 3 months.
Near the zone of the infarct is an area less severely damaged injury. It may deteriorate and thus extending the area of infarction and an adequate collateral circulation, which can recover its function within 2 weeks.
The area outside of damage is ischemic zone bordering the site of injury. The cells in this area are low by decreasing the oxygen supply, but may return in the role usually 2 to 3 weeks after onset of occlusion.
RISK FACTORS
There two types of risk factors for heart attack, including
- Inherited factors
- Acquired factors
Factors hereditary
These are risk factors you are born with it can not be changed, but can be improved with a medical treatment and changes in lifestyle. After more risk —
- persons with inherited hypertension
- People who have inherited low levels of HDL or LDL-cholesterol
- with a family history of heart disease in aging men and women
- People with diabetes type [1]
- women after menopause, in general, men are at risk at an age earlier than women, but after the appearance of women have the same risk
Acquired factors
These are risk factors that are caused by activities that we chose to include in our lives that can be managed by changes in lifestyle and clinical care. After more risk —
- People with hypertension acquired
- People with low HDL cholesterol or high LDL cholesterol
- cigarette smokers
- People who are under stress
- person who lives a sedentary life
- Overweight 30% or more
Type of myocardial infarction
1. Different degrees of damage to heart muscle –
Area of necrosis: death of heart muscle due to lack by oxygen damage and complete, irreversible
Zone of injury: muscle region around the region the heart of necrosis, swollen and painful, but remains viable if sufficient oxygen can be restored.
Ischemic Area: area of heart muscle that surrounds the ischemic lesion and that is viable, not in danger of extinction if the extent of infarction is produced.
2. Under layers of heart muscle involved, MI may be classified as
Transmural infarction or Q – the vagus, area of necrosis occurs in the entire thickness of cardiac muscle. endocardial or transmural infarction, necrosis area is limited to the deepest layer of the heart muscle.
3. Location of MI was identified as the place muscle cardiac damage in the left ventricle inferior, anterior, lateral and posterior —
Left ventricle is the most frequent and dangerous for me because it is the main pumping chamber of the heart
Right ventricular infarction occurs frequently with me overcome the damage the lower wall and / or the posterior left ventricular
Region 4. Heart muscle is damaged determining coronary artery is blocked
Main coronary artery
Circumflex branch
Anterior ramus
Great cardiac vein
Middle cardiac vein
Right cardiac vein
CLINICAL MANIFESTATIONS
1) Chest Pain
- not relieved by rest vasodilator therapy on sublingual
- constant severe pain in the chest under the sternum of a crushing and pressing nature
- May radiate to the arm, neck, jaw and shoulders
- more than 15 minutes continuously
- can cause anxiety and fear
2) Sweating
3) hypertension or hypotension
4) Bradycardia or tachycardia
5) palpitations, severe anxiety, dyspnea
6) The disorientation, confusion and agitation
7) Loss of consciousness, marked weakness
Nausea, vomiting, hiccups
9) The atypical symptoms epigastric discomfort and abdominal pain, dull ache or tingling sensation, shortness of breath, fatigue scale
Ground since ASSESSMENT
1. Changes in ECG
They usually occur within 2 to 12 hours, but may take 72 to 96 hours.
Necrotic tissue injuries and ischemic depolarization and impaired ventricular repolarization
ST segment depression and the T wave of investment show a model of ischemia
ST elevation indicates a pattern of injury
- Previous small-V3 – Leads V4
- Previous V2 Extended – leads V5
- Anteroseptal leads V1-V3
- Posterior V1 – V2, R wave and ST depression gradually
- Anterolateral V4 – V6, I, AVL leads
- Apical V5 – V6 leads
- Lower Lead II, III and AVF [mutual]
2. Elevated enzymes and isoenzymes in serum:
The enzymes are extracted in a series model in general admission and every 6 to 24 hours for 3 samples are obtained. The activity after the enzyme is correlated with the degree of heart muscle damage
Enzymes are commonly evaluated are CK, LDH, CK-MB, AST, Troponin I, troponin T. [Figure 4]
LDH 2 is generally higher than LDH 1, except when the heart muscle is damaged is a reversal of
3. Other findings:
White blood cell count and sedimentation rate increases due to the inflammatory processes associated with damaged heart muscle.
Radionuclide Imaging allows recognition of areas of decreased perfusion
Positron emission position determines the presence of reversible and irreversible injury heart muscle and tissue necrosis extending into the injured heart muscle responded to treatment may also be determined
MANAGEMENT
Treatment aims to protect ischemic tissue injury and preserve heart muscle function, reduce infarct size, and prevent death. The innovative ways to provide rapid restoration of coronary blood flow and the use of pharmacological agents in To improve the oxygen supply and demand, reduce and / or prevent disarrhythmias and inhibit the progression of artery disease coronary.
1. Treatment with opioid analgesics: Morphine is used to relieve pain, improve hemodynamic reducing cardiac preload and after load and relieve anxiety.
Meperidine [Demerol] is useful to treat pain in patients cons-indication to morphine or sensitivity to respiratory depression.
2. Agents Anxiolytics: Benzodiazepines are used in compound analgesics anxiety chest pain and its relief
3. Antiplatelet agents: aspirin interfere with the function of the enzyme cyclo-oxygenase and inhibits the formation of thromboxane A2. In some minutes the aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion
Other antiplatelet agents, clopidogrel, ticlopidine, dipyridamole, these agents, particularly clopidogrel may be useful for patients who have a true allergy to aspirin and may be used in combination with aspirin.
4. Supplemental oxygen: oxygen additional must be administered. The reason of the use is guaranteed that the erythrocytes is saturated at the maximum load capacity. Because MI impairs circulatory function of the heart, oxygen extraction by the heart and other tissues may be reduced.
5. Nitrates: Nitrates should be administered intravenously in MI, persistent ischemia, hypertension or a large anterior wall MI. Nitrates are metabolized to nitric oxide in vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates blood vessels light. Vasodilation, reduces both cardiac preload and after load, and reduces the need for myocardial oxygen. Vasodilation coronary arteries, improving blood flow in partially obstructed vessels and through collateral vessels. When administered sublingual or intravenous nitroglycerin has a rapid onset of action.
6. Adrenergic beta-blockers are recommended within 12 hours of symptoms of myocardial infarction and continued indefinitely. Beta-blockers reduce the rate and force of myocardial contraction and a decrease General demand for myocardial oxygen. During the acute phase of MI-blockers may be initiated intravenously
7. Heparin: UFH: unfractionated heparin intravenously is recommended to undergo percutaneous revascularization. It is also recommended for patients receiving fibrinolytics and nonselective agents such as fibrinolytic urokinase, streptokinase and anistreplace. Heparin inhibits the formation of new and thrombus propagation, effective when administered intravenously or subcutaneously.
Low-molecular-weight heparin: Can not manage IM clients treated with fibrinolytics
8. Fibrinolytic or thrombolytic agents: is fibrinolytic therapy indicated ST-segment elevation. Plasminogen activators restore coronary vessels by dissolving clots that block. Plasminogen activator was shown to restore blood flow in coronary flow by 50% 80% of patients with myocardial infarction. The successful use of fibrinolytic agents provides a survival benefit determined is maintained for years. Reteplase has been shown to produce slightly higher 60 – and 90-minute patency rate alteplase angiography, while the rate of adverse events were equal.
However, a higher rate of permeability Early did not translate into a survival advantage to 30 days of monitoring. The most critical variable in achieving successful fibrinolysis is the time to onset symptoms Drug Administration. A fibrinolytic is more effective when the "door to needle time" is 30 minutes or less.
9. Inhibitors of angiotensin converting enzyme: the oral ACE inhibitors are recommended in the first 24 hours after onset of symptoms of infarction, to reduce the burden through the myocardium after vasodilation.
10. Anti managers dysarrhythmic: Lidocaine reduces ventricular irritability, which normally occurs after MI.
11. Calcium channel Calcium: Improve the balance between supply and demand for oxygen by reducing heart rate, blood pressure and dilation of coronary vessels.
Diltiazem has been shown to decrease the incidence of reinfarction patients with non-Q-Wave MIS.
12. Percutaneous coronary intervention [Fig-15]: the mechanical opening of the arteries coronary arteries can be done during a heart attack in progress. A balloon catheter is inserted by a guidewire within a coronary vessel with a non-calcified atherosclerotic lesions. The catheter balloon is inflated, causing the rupture of the intima and the development of atherosclerosis. The result is an increase in lumen diameter of the coronary arteries and improve blood circulation in the lesion.
Percutaneous coronary intervention is an alternative therapy to fibrinolysis restoration of coronary blood flow in an MI can be done mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as primary treatment as an alternative to fibrinolysis fibrinolysis when not clearly indicated or stated-cons. PCI can successfully restore coronary blood flow by 90% to 95% of patients myocardial infarction.
13. Revascularization surgery: new or urgent CABG is justified in the context of percutaneous intervention in patients with hemodynamic instability and coronary anatomy sensitive transplant surgery. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as septal defects, ventricular free wall rupture or mitral regurgitation acute. Coronary blood flow restoration emergency bypass surgery (CABG) can limit myocardial injury and cell death if it is done in 2 or 3 hours after onset of symptoms. Emergency coronary bypass surgery has a higher risk of perioperative morbidity (bleeding and extension MI) and mortality of elective CABG. The risk of operative mortality in CABG is higher in patients emergency, which are in cardiogenic shock, those with previous surgery CABG, and several ships. Furthermore, Emergency CABG confers a survival advantage in patients with ischemic recurrent post-MI whose coronary anatomy is unsuitable complete revascularization with PCI. Elective CABG improves survival in patients post-MI who have left artery disease main three-vessel disease or double-vessel disease is not capable of PCI. The timing of elective coronary bypass-MI is controversial, but retrospective studies indicate that when CABG is performed in post days 3 to 7-MI, the operative mortality is equivalent to bypass surgery coronary place outside of MI.
14. The stress test cardiac stress tests heart post-MI showed limited value in risk stratification and assessment of functional capacity. Stress testing is not recommended for several days after MI. Only sub-tests of maximal exercise should be performed in stable patients, 4 to 7 days after IM. The test effort to identify patients with residual ischaemia further efforts to revascularization. Exercise testing also provides information prognostic and acts as a guide to post-myocardial infarction and exercise prescription for cardiac rehabilitation.
15. Lipid Management: All post-MI patients should be the American Heart Association Step II diet (<200 mg cholesterol per day, <7% of total calories from saturated fat). Post-MI patients with LDL cholesterol> 100 mg / dL in a step II diet is recommended treatment medication to reduce levels of LDL cholesterol <100 mg / dL. Post-MI patients with low HDL-cholesterol <35 mg / dL in a step II diet is recommended to participate in a program of regular exercise and medication to increase HDL cholesterol. 4 Recent data indicate all MI patients should be treated with statins regardless of lipid levels or diet
16. Medication long term: Most oral medications up in the hospital when the IM will be maintained long term. Treatment aspirin and beta blockers is maintained indefinitely in all patients. ACE is continued indefinitely in patients with congestive heart failure, the fraction left ventricular dysfunction (ejection <0.40), hypertension or diabetes. A lipid-lowering agent, particularly a statin, in addition modification of food is maintained indefinitely
17. Cardiac Rehabilitation: Rehabilitation heart is a place of continuing education, return to the application of the modified lifestyle and compliance with a requirement to complete treatment for the recovery of MI, which includes training. Participation in cardiac rehabilitation programs post-MI is associated with reduced morbidity and mortality post-heart. Other benefits include improved quality of life, functional status and social support. A minority patients post-MI had actually participated in cardiac rehabilitation programs due to a lack of formal well-structured programs, medical recommendations, low patient motivation, noncompliance, or financial constraints.
NEED FOR STUDY
Reperfusion therapy, which include thrombolytic therapy and percutaneous coronary intervention (PCI), including angioplasty and stenting is the greatest advance in treatment of acute myocardial infarction
Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not. In addition, those who receive it time to administration of thrombolytic therapy, or "door-to-time the needle is often delayed, threatening attacks and leads to significant morbidity and mortality.
The clinical criteria and parameters of a single ECG is of limited value for the noninvasive diagnosis of myocardial reperfusion. Other methods, such as monitoring segment ST and the kinetic analysis of biochemical markers, may also be useful for early identification of the infarct artery related acute (), the activity of total CK, CK-MB isoenzymes appear to be biochemical markers of the most promising.
In addition, the proposed thresholds for the diagnosis of reperfusion are usually derived from time-to-peak values. This excludes a diagnosis early, because the values of CK plasma level occurs in average 9 – + 6 hours after thrombolysis.
Determination of plasma total CK and MB offers greater precision than any other method currently available for the diagnosis of acute myocardial infarction.
In addition to providing an accurate diagnosis of AMI, CK-MB quantitative analysis can also be used to obtain an accurate estimate infarct size. In recent years, the accuracy in diagnosis of acute myocardial infarction has gained importance even greater, since the election and when a variety of opportunities for diagnosis and treatment after admission to the unit coronary care depend on whether the race took place. In addition, the advent of thrombolytic therapy for acute myocardial infarction emphasized the need for biochemical markers of necrosis more sensitive in the early hours. The realization that ultimately the restoration of blood flow was the main mechanism to reduce infarct size has led to a therapeutic approach dominated by thrombolysis and, literally, by using interventions to open vessels and keep them open.
The key observation is that the profit margin on the use a drug could be demonstrated if the drug was given before the period of ischemia.
However, the greater benefit in treating patients with myocardial infarction has probably been the restoration of blood flow in the shortest time after occlusion
The purpose of this study is to identify the reperfusion injury exacerbated by thrombolytic drugs in myocardial infarction in the process of elevation of cardiac enzymes as vertices and reached normal levels within 24 hours, preventing injury and ischemia Prolonged myocardial tissue.
However, the objective was to prospectively evaluate the biochemical markers for early diagnosis permeability after coronary IV thrombolysis for acute myocardial infarction.
STATEMENT OF PROBLEM
"The effect thrombolytric drugs on cardiac enzymes, creatine kinase and creatine phosphokinase-MB, myocardial infarction.
OBJECTIVES
- To evaluate the effect of thrombolytic agents in cardiac enzymes.
- To compare the effect of thrombolytic drugs and without thrombolytic agents in cardiac enzymes
- To determine the importance of thrombolytics to a patient who suffered a myocardial infarction
- Propose guidelines for public education on quick search of medical assistance at the onset of chest pain.
DEFIITIONS OPERATIONAL
Result: Result or produce a result
Thrombolytic drugs: used to dissolve blood clots
KPC: cardiac enzyme released into the blood at high levels, when a injury occurs in the heart. It is also known as creatine kinase or creatine Phophokinase.
CK-MB: It is also reported an enzyme in the blood inside the heart muscle during cardiac damage
Myocardial infarction: a necrosis region of infarction caused by an interruption of blood supply to the heart, usually as a result of occlusion of a coronary artery.
HYPOTHESIS
"The fibrinolytic agents has an effect on reducing the maximum levels of cardiac enzymes, CK and CK-MB"
LIMITATIONS
Coronary Care Unit: Data from this research is applicable to the configuration of the unit coronary care.
Age: Clients Only selected persons between 35 and 65.
Myocardial infarction: This applies also to Customers who have been admitted to hospital within 6 hours of onset of chest pain with myocardial infarction who received Inj. Metalyse.
Acute coronary syndrome: Customers who are admitted 6 hours after onset of chest pain with acute coronary syndrome were included in the group witness.
METHODOLOGY:
This study was conducted by an experimental method of research design in the development of coronary care unit in hospital in Dubai, United Arab Emirates a consecutive series of patients receiving IV Metalyse [Tenecteplase] for MI May 2006 to November 2006 were included in this study.
DESIGN SEARCH:
This study uses comparative presentation.
Adjustments:
This study was conducted in patients regardless of age, sex and nationality, who were admitted to the Care Unit Coronary hospital through the emergency departments in Dubai, UAE United Arab Emirates
SAMPLE SIZE:
This study included 60 clients, men and women, regardless of nationality, aged between 35 and 65. Of the 60 clients, 30 were taken in the experimental group and 30 considered as controls.
Sampling Technique:
The samples are selected as appropriate sample into two groups, experimental and control group. Customers received thrombolytics within 6 hours after onset of chest pain were selected in the experimental group, and patients late after 6 hours of the onset of chest pain and did not receive thrombolytic therapy are selected in the control group. All patients received diagnosis of myocardial infarction confirmed by the subsequent elevation of creatine kinase [CK] and levels of CK-MB isoenzyme. Metalyse IV is administered at a dose of 6000 units to 9000 units by weight of patients. Patients who suffered a myocardial infarction in acute phase were admitted to the coronary care unit for more than 6 hours after onset of pain were also included.
The data collection procedure:
The study data are collected by an instrument, which consists of 22 items, including sample number, age and sex. Religion, nationality, occupation, habits, style Living life onset of pain, the date and time of admission, signs and symptoms, vital signs, type of myocardial infarction, protocol thrombolytic therapy, the levels of cardiac enzymes, post thrombolytic therapy, medications received and the release date.
A survey revealed that most customers who had MI was the Indian subcontinent, which constitute 63.3% and minorities represent only 1.6%, Great Britain and Turkey. 3.3% of customers were Egyptians and Syrians. Composed Bangladesh, 6.6% and 21.6% were Pakistanis. Only 9.9% customers had MI were citizens of Dubai. Among them, 46.6% of clients were aged 46 to 55 years and 41.6% of clients were aged between 36 to 45 and the remaining 11.6% of clients have between 56 to 65 years of age.
36.2% of clients had an acute coronary syndrome and do not receive thrombolytic therapy. Left instant messaging client is true and most of them were thrombolysed. However, all customers who have undergone angioplasty coronary. Apart from these customers one customer had normal coronary vessels, two were with mild coronary stenosis to medical treatment and conservative 4 customers three major blocs vessels CAP have been published. Other clients are treated by percutaneous coronary angioplasty to LAD [50%], ARC [21.6%] and circumflex [13.5%].
Is also evident in the study that most Indians are affected by a myocardial infarction and main factors are smoking, stress and lack of knowledge on the disease state.
Based on Chi-square difference association between Standardization of cardiac enzyme levels in the study groups are as follows —
In the experimental group, 30 clients received Inj. Metalyse. between them, except for 4 clients, customers of 26 other reports given cardiac enzymes were normal in 24 hours after admission and administration of a thrombolytic agent.
In the control group of 30 client reports of blood for normalization of cardiac enzymes were anlysed where there are 27 more customers high levels of cardiac enzymes after 24 hours of admission.
- Critical value 14.56, p value <0.05 to reject the hypothesis null
Inj. Metalyse has a good effect on the heart muscle always critical value 14.56, the probability <0.05, as evidenced by the decrease the maximum cardiac enzyme CK and CK-MB within 24 hours after receiving thrombolytic agent.
DISCUSSION
Tenecteplase [Metalyse] Fibrin is a recombinant plasminogen activator specific. It binds to the fibrin component of thrombus and converts selectively fixed thrombus plasminogen into plasmin, which degrades the fibrin matrix of thrombi. Tenecteplase was withdrawn from circulation by binding to specific receptors in the liver, followed by catabolism of small peptides.
After a single intravenous bolus of tenecteplase in patients with myocardial acute infarction, tenecteplase antigen exhibits biphasic plasma elimination. No dose-dependent clearance of tenecteplase in the range of doses therapeutic.
The dominant middle initial is 24 + _5.5 [mean = /-SD] min. terminal half-life is 129 + _87 minutes and the plasma clearance is 119 + _49 Ml / min
The main finding of this study is the beginning of the peak total CPK and CK-MB
isozymes were identified after successful reperfusion therapy Metalyse. CPK peaked at 12 hours and CK-MB levels were taken within 6 hours. The study reveals that levels of cardiac enzymes peaked and normalized in time of 24 hours in the pilot group who received thrombolytic agents within 6 hours of onset chest pain. Once this is done 3 to 5 days for peak enzyme levels in the control group customers who did not receive thrombolytic agents because of late arrival to the hospital, causing more damage to the myocardium.
Therefore, it is clear that the extent injury to the myocardial oxygen demand is lower in the experimental group of customers.
Finally, it can be used as end point substitute for angiographic demonstration
permeability in future clinical trials of reperfusion therapy. Improving the diagnostic performance when the analysis was limited to patients older than 6 hours after onset of symptoms.
CONCLUSION
Clinical studies of fibrinolytic therapy in myocardial infarction show that early thrombolytic treatment begins within 6 hours Start pain, significantly reduces the risk of damage and oxygen demand of the myocardium, through the process of falling in the maximum enzyme levels heart in 24 hours.
Inj. Metalyse has a peak cardiac enzymes early in the experimental group, reflecting artery opening stroke, the clot dissolves by Inj. Metalyse which means they will have a thrombolytic well, so we have reached historical levels.
Identification Early patients with persistent occlusion after being thrombolyis
Acute myocardial infarction is also important because it can pave the way for the rescue as a rescue percutaneous transluminal coronary angioplasty or repeated thrombolysis.
Implications for Nursing:
SERVICE
To determine the intensity of angina customer
Observe signs and symptoms
Place the patient in a comfortable position
Administer oxygen if necessary
Obtain vital signs every 15 minutes to 2 hours, every half hour for an hour and
every hour for two hours, then if necessary
Get a 12-lead ECG
Monitor pain relief
Monitor patient response to drug treatment
Institute continuous cardiac monitoring and observation of reperfusion, arrhythmias, changes in rhythm, bradycardia and tachycardia
Interpretation rhythm strips
Pay attention to complaints of headache with the use of nitrates
Watch the recurrence of pain. Reinforce the importance report the caregivers when they feel pain.
Administer drugs to relieve patient anxiety as indicated, as sedatives and tranquilizers
Keep complete bed rest for 24 hours
Determine level of activity that precipitated angina pain occurs.
Identify the specific activities of patients can perform below the level which produces angina
Prepare for the diagnosis and treatment procedures such as coronary angiography and PTCA [percutaneous transluminal coronary angioplasty]
EDUCATION
The lawyer of the risk factors and changes in lifestyle such as: —
The methods of reducing stress as the feedback Biological and relaxation techniques
The low cholesterol diet and low fat
Avoid excessive caffeine
Do not use diet pills, nasal decongestants
Follow-up visits to monitor diabetes and hypertension
Educate patients and families on —
Preventing the recurrence of pain
Regular use of drugs
Dangers of Smoking
Prevention of other factors that contribute
Regular monitoring of
Importance of dietary changes
Avoid activities that cause anginal pain as a sudden effort, walking against the wind, extreme temperatures, emotional stress, to refrain from physical activity for 2 hours after eating, weight reduction, etc.
The proper use of medicines
Drug Side Effects
Administartion
Outreach programs interdisciplinary
The education of nursing students and staff
Provide continuing education for nursing service
Recordkeeping and reports
Keep statistics
Develop policies and procedures
Supervision and appraisal Staff
Recommendations for further studies
Most e-MI patients not actually participated in formal rehabilitation heart due to the absence of well-structured programs, physician
references, poor patient motivation, failure and stress Financial.
Cardiac rehabilitation provides a forum for continuing education, strengthening
modification of lifestyle and life compliance requirements complete
therapies for the recovery of MI, including training exercises.
Participation in rehabilitation programs cardiac, post AMI with decreased
subsequent morbidity and cardiac mortality.
Proper education in hospitals and workplaces on the causal factors and contributing, preventive measures for heart attack and stroke suffered, is necessary.
All forms of reperfusion, depending on local services should be available for patients. The protocols must be in writing and by reperfusion strategy to implement in a network. Early diagnosis of myocardial infarction without ST-segment elevation is essential and is best achieved record Rapid interpretation of the ECG and medical contact first, if such contact occurs.
About the Author
Pushpa Latha, MSN, Vinayaka Missions University, Selam, Madras, India E-Mail keerthiraksha@yahoo.co.in Ph- 00971504277926
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