The effect of drugs on thrombolytric cardiac enzyme, creatine kinase and creatine phospho kinase-MB, myocardial infarction "

"The effect of drugs on thrombolytric cardiac enzymes, creatine kinase and creatine kinase-MB in phospho myocardial infarction.

MYOCARDIAL INFARCTION

Myocardial infarction refers to a dynamic process whereby one or more regions of the heart muscle experience a severe and prolonged decline in oxygen supply due to coronary artery Later, tissue necrosis, or death of a heart attack occurs.

Initiating the process of myocardial infarction may be sudden or gradual progression of the event takes about 3 to 6 hours.

PREVALENCE

Myocardial infarction is the leading cause of death in the United States (U.S.) and in most industrialized countries worldwide. Approximately 800,000 people in the United States are affected, and Despite a better understanding of the symptoms, 250,000 die before presentation to hospital. 4 The survival rate for patients hospitalized for MI U.S. is about 90% to 95%. This represents a significant improvement in survival and is bound to improve emergency medical services and treatment strategies.

In general, MI can occur at any age but its incidence increases with age. The actual impact depends on factors that influence the risk of atherosclerosis, which is discussed below. Approximately 50% of all adverse events U.S. occur in people under 65. However, in the future, the lever Demography and the average age of population increases, a higher percentage of patients IM will be over 65 years.

Men are more likely than women, but the risk is higher among women than men after menopause.

Coronary arteries

Coronary arteries supply blood capillaries of the myocardium

Artery right coronary artery (RCA) provides the right atrium and right ventricle, the bottom of the left ventricle, septum and posterior wall of the SA and AV nodes

The left coronary artery (ACL) consists of two major branchiate left anterior descending (LAD) and circumflex (LCX).

DAL artery below anterior wall of the left ventricle, interventricular septum and anterior left ventricular apex.

LCX artery supplies blood to left posterior lateral ventricle.

Cardiac enzymes

The cardiac marker levels increased overtime. Therefore, enzymes are established in a production model in general admission and up to 6-24 hours 3 samples are obtained.

Enzymes are commonly evaluated include CK, CKMB, LDH, troponin T & I

CK-MB ratio indicates the degree to damage the heart muscle. The higher the ratio, the more damage to the muscle heart. Troponins are preferred markers of myocardial injury or are very specific and the heart is thought to rise before permanent damage develops.

Increased troponin concentrations should not be used in themselves to exclude the heart attack. Troponin remains elevated for 1-2 weeks after MI for easy diagnosis if the patient presents later with an old MI EC others will not be measured except reinfarction occurs.

The cardiac enzyme elevation myocardial infarction

Enzyme The increase in normalized peak normal value report CKMB

CK 12 h 3-5 days 16-30hrs 35-232IU / L

CKMB 4-8 hours 24 hours 72 hours 51IU </ L <6%

Troponin I, 3-6 h 20 h 14 days 0,0-0,4 ng / ml

2-4 hours 8-12 am troponin T 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 are the left ventricle, the heart chamber that has the highest workload. Tissue changes that occur in the myocardium are related to the degree to which cells were deprived of oxygen. Total scores of poverty in an area infarction in which cells die and become necrotic.

Necrosis in this area is evident in the 5 to 6 hours after occlusion. Answering this necrosis of the body increases its products of leukocytes, which help remove dead cells. As the collateral circulation develops, brings fibroblasts forming a connective tissue scar in the infarct area. Generally, scar tissue formation is completed by 2 to 3 months.

Immediately all area of the infarct zone is less severely damaged injury. It can deteriorate and expand the area of infarction or adequate collateral circulation, can resume its role in 2 weeks.

The outermost regions of the zone along the area of ischemic damage of the wound. The cells in this area are weakened by oxygen has been reduced but the function may return more often within 2 to 3 weeks after onset of occlusion.

FACTORS RISK

There are two types of risk factors for heart attack, including

1. Hereditary factors
2. Acquired factors

Hereditary factors

These are risk factors you are born that can not be changed, but can be improved by taking care medical and lifestyle changes. Here are more risk

• persons with inherited hypertension
• People inherited low levels of HDL cholesterol or high levels of LDL
• those men with a family history of heart disease and aging women
• people with diabetes mellitus type [] 1 diabetes
• women, after menopause begins in general, men are at risk at a younger age earlier than women, but after the emergence of women are also at risk

Acquired factors

These are risk factors that are caused by activities that we choose to include in our lives that can be managed by lifestyle changes and clinical care. Then are most at risk

• People with acquired hypertension
• people with low levels of HDL cholesterol or high LDL acquired
• cigarette smokers
• people who are in many stress
• individual who leads a sedentary life
• 30% overweight or more

  TYPE myocardial infarction

. 1 Different degrees of muscle damage heart

Area of necrosis, death of heart muscle caused by lack of oxygen that is broad and comprehensive permanent damage

Accident Area: the area of heart muscle that surrounds the area of necrosis, inflammation and injury, but still feasible if sufficient oxygen can be restored.

ischemia Area: region around the area of heart muscle injury, that is viable and nonischemic endangered unless the extent of infarction occurs.

2. For the layers of heart muscle concerned, may be classified as MI-

Transmural myocardial infarction or Q wave, necrotic area around the thickness of the heart. transmural myocardial muscle endocardial product or not, the area of necrosis is limited to the innermost layer of the heart muscle.

3. Location of the MI is identified as the location of the damaged heart muscle in the lower left ventricle, anterior, posterior-lateral

To the left ventricle is the most common and dangerous for MI because it is the main pumping chamber of the heart

Right ventricular infarction occurs frequently, I join the lower damage and / or ventricular posterior wall of the left

4. Region of the heart muscle is damaged by the determination of the coronary artery becomes blocked

Left main coronary artery

circumflex branch

Previous ascending limb

Great cardiac vein

Middle cardiac vein

right coronary vein

CLINICAL

1) chest pain

• that is not relieved by rest during vasodilator sublingual
• under intense constant pain in the chest of a sternum injury and pressing nature
• may radiate to the arm, neck, jaw and shoulders
• still more than 15 minutes
• can cause anxiety and fear

2) Sweating

3) hypertension or hypotension

4) The bradycardia or tachycardia

5) palpitations, severe anxiety, dyspnea

6) The disorientation, confusion and agitation

7) The faint, marked weakness

Nausea, vomiting, hiccups

9) with atypical symptoms such as epigastric pain, abdominal pain, dull ache or tingling sensations, fatigue, shortness of breath, large

EVALUATION DIGNOSTIC

1. ECG changes

Usually occurs within 2 to 12 hours but may take 72 to 96 hours.

Necrotic tissue damage and ischemic ventricular depolarization and repolarization change

ST segment elevation and T wave inversion indicates a trend of ischemia

ST-segment elevation indicates a type of injury

• Previous small V3 – V4 leads
• Previous vast V2 – V5 leads
• V1-V3 anteroseptal
• Back V1 – V2, R wave and ST segment depression progressive
• Anterolateral V4 – V6, I, led Avl
• Apical V5 – V6 leads
• Less lead ii, III and aVF] [mutual

2. Elevated serum enzymes and isozymes:

Enzymes are established in a production model in general admission and every 6 to 24 hours to 3 samples are obtained. The enzyme activity was correlated to the extent damage the heart muscle

Enzymes are usually evaluated include CK, LDH, CK-MB, AST, Troponin I, troponin T. [Fig 4]

LDH 2 is usually greater than 1, except LDH when the heart muscle is damaged there is a reversal

3. Other findings:

WBC and ESR student due to inflammatory processes associated with damaged heart muscle.

Radionuclide imaging allows recognition areas of hypoperfusion

position emission tomography determined the presence of reversible heart muscle damage irreversible tissue or necrosis, which extends to the injured heart muscle has responded to treatment can also be determined

MANAGEMENT

Treatment is aimed at protection of ischemic heart tissue and injured to preserve muscle function, reduce infarct size and prevent deaths. innovative ways to provide rapid restoration of coronary blood flow and the use of pharmacological agents to improve the oxygen supply and demand, reduce and / disarrhythmias or prevent and inhibit the progression of coronary artery disease.

1. Treatment with opioid analgesics: morphine is used to relieve pain, improve cardiac hemodynamics by reducing preload and after loading and to relieve anxiety.

Meperidine [Demerol] is useful for controlling pain in patients cons morphine or susceptibility to respiratory depression.

2. Drugs for anxiety: Benzodiazepines are used painkillers when anxiety chest pain and its relief complicated

3. Antiplatelet agents: aspirin interferes with the functioning of the enzyme cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes, aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion

other antiplatelet agents are, clopidogrel, ticlopidine, dipyridamole, these agents, particularly clopidogrel may be useful for patients who have a true allergy to aspirin and may be used with the association with aspirin.

4. Oxygen Supplement: Supplemental oxygen should be administered. The justification for the use is confident that the erythrocytes are saturated in the maximum load. Because MI impairs the circulatory function of the heart of oxygen extraction by the heart and other tissues may be reduced.

5. Nitrates: Nitrates should be administered intravenously 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 the blood vessel lumen. Vasodilation reduces both cardiac preload and after load, and reduces oxygen demand infarction. Coronary artery vasodilatation improves blood circulation in partially obstructed vessels and collateral vessels. When administered nitroglycerin sublingual or intravenous injection has a rapid onset of action.

6. Beta-blockers: Beta blockers are recommended within 12 hours symptoms of MI and continued indefinitely. Beta-blockers reduce the frequency and strength of cardiac contraction and an overall decrease oxygen demand infarction. During the acute phase of MI beta-blockers may be initiated by intravenous

7. Heparin: Unfractionated heparin: unfractionated heparin intravenously is recommended percutaneous revascularization. It is also recommended in patients receiving therapy fibrinolytic and non-selective fibrinolytic agents such as urokinase, streptokinase and anistreplace. Heparin inhibits thrombus formation and propagation of additional, effective when administered intravenously or subcutaneously.

The low molecular weight heparin: it can give customers MI not treated with thrombolytic therapy

8. Fibrinolytic or thrombolytic agents: fibrinolytic therapy indicated elevation ST. plasminogen activators restore coronary vessel blockage by dissolving thrombi. Plasminogen activators have been shown to restore blood flow to coronary flow by 50% to 80% of patients with MI. The successful use of fibrinolytic agents provides a definite survival benefit is lasts for years. Reteplase has been shown to slightly higher 60 – and 90 minutes angiographic patency rate accelerated alteplase, whereas event rates were negative equal.

However, the long patency rate above does not result in any survival advantage at 30 days follow up. The variable more important to achieve successful thrombolysis is the start time symptoms of drug administration. Thrombolysis is most effective when the door " needle "time is 30 minutes or less.

9. Inhibitors of angiotensin converting enzyme: inhibitor Oral ACE recommended in the first 24 hours after symptom onset MI, myocardial infarction decreases after the load by vasodilation.

10. Dysarrhythmic Anti agents: Lidocaine reduces ventricular irritability, which usually occurs after MI.

11. Blockers of calcium channels: improved balance between supply and oxygen demand by decreasing heart rate, blood pressure and dilation of the coronary arteries.

Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-Wave MIS.

12. percutaneous coronary intervention [Fig-15]: the mechanical opening of the coronary arteries can be done during a heart attack in progress. A catheter balloon is inserted via a guidewire in a coronary vessel with a calcified atheromatous lesion. The catheter balloon is inflated, leading to disruption of the intima and the development of atheroma. The result is an increase in the diameter of the coronary vessel lumen and improved flow blood below the injury.

percutaneous coronary intervention is an alternative therapy to the recovery of fibrinolysis coronary blood flow in myocardial infarction can be achieved mechanically by percutaneous coronary intervention (PCI). mechanical revascularization ICP is used as primary treatment as an alternative to fibrinolysis when not clearly indicated or stated thrombolysis cons. PCI can successfully restore coronary blood flow by 90% to 95% of patients with MI.

13. Revascularization: emerging or coronary bypass surgery urgent surgery is justified in the context of failure of percutaneous intervention in patients with hemodynamic instability and coronary anatomy suitable for transplant surgery. Surgical revascularization is also indicated in the context of mechanical complications of AMI and rupture septal defect ventricular free wall, or acute mitral regurgitation. Restoration of blood flow in coronary artery bypass graft coronary artery (PAC) can limit myocardial damage and cell death if is done in 2 or 3 hours of symptom onset. Emergency CAP has a higher risk of perioperative morbidity (bleeding and extension MI) and mortality than elective CAP. The risk of emergency CABG operative mortality is increased in patients in cardiogenic shock, those with previous CABG, and with multiple vessels. Moreover, emergency CABG confers a survival advantage in patients with recurrent ischemia post-MI whose coronary anatomy is not suitable for complete revascularization with PCI. CABG improves survival in post-MI patients who have left main artery disease, three vessel disease or two-vessel disease not amenable to PCI. The time of the election of the CAP post-AMI is controversial, but retrospective studies indicate that when CABG is performed within 3 to 7 days post-infarction, operative mortality is equivalent to coronary bypass surgery performed in non-MI.

14. cardiac Stress Testing: Heart Test posttraumatic stress set the value of MI risk stratification and assessment of functional capacity. Stress testing is not recommended in the days post-stroke. Only submaximal Stress Tests should be performed in stable patients 4 to 7 days after MI. Stress testing identifies patients with ischemic Additional efforts residual revascularization. Exercise testing also provides prognostic information and acts as a guide for prescribing post-MI exercise and cardiac rehabilitation.

15. Lipid Management: All post-MI patients should be in an American Heart Association Step II diet (<200 mg of cholesterol per day, <7% of total calories from saturated fat). Postinfarction patients with LDL-cholesterol over 100 mg / dL to a Step II diet is recommended to take medication to lower LDL-C <100 mg / dL. Post-MI Patients with levels of <HDL-cholesterol 35 mg / dL on a Step II diet is recommended to participate in a program of regular exercise and drug treatment to increase HDL cholesterol. 4 Recent data indicate all MI patients should be treated with statins regardless of lipid levels or diet

16. Long-term medication: Most oral medications to the hospital at the time of MI will continue long term. Treatment by aspirin and beta-blockers remains indefinitely in all patients. IEC is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (fractional ejection <0.40), hypertension or diabetes. A lipid-lowering agent, particularly a statin, in addition to diet modification continues indefinitely  

17. Cardiac rehabilitation: Cardiac rehabilitation provides a place for continuing education, returns to the application of the change in lifestyle and compliance with a prescribed course of treatment for recovery from myocardial infarction, including training exercises. Participation in cardiac rehabilitation programs post-infarction is associated with a decrease in cardiac morbidity and mortality later. Other benefits include improved quality of life, functional capacity and social support. A minority of post-MI patients participated in cardiac rehabilitation Formal due to lack structured programs, medical referrals, the patient's motivation to small, non-compliance, or financial.

NEED ANALYSIS

reperfusion therapy, which include thrombolysis and percutaneous coronary intervention (PCI), including angioplasty and stent is the greatest advance in the treatment of acute myocardial infarction

Studies have shown that many patients with AMI who are eligible for therapy reperfusion do not. In addition, those who receive it time for the administration of thrombolytic therapy, or "door-needle time" often is delayed, thereby jeopardizing infarction and leads to greater morbidity and mortality.

The clinical and ECG parameters have a value simple limited to the diagnosis of noninvasive assessment of myocardial reperfusion. Other methods, such as monitoring and kinetic analysis of ST segment biochemical markers may also be the value of early identification IRA () infarction related artery, the total CK, CK-MB isoenzymes appear to be most promising biochemical markers.

In addition, the proposed thresholds for the diagnosis of reperfusion were generally time-to-peak in values. This excludes the early diagnosis because the peak plasma CK values are reached, on average 9 – + 6 hours after thrombolysis.

Determination of total plasma concentration of CK-MB provides precision than any other method currently available for the diagnosis of acute myocardial infarction.

In addition to providing an accurate diagnosis of acute myocardial infarction, CK MB quantitative tests can also be used to obtain an estimate infarct size accurately. In recent years, accuracy in the diagnosis of acute myocardial infarction has become even more important as the choice and when a variety of options for diagnosis and treatment after admission to the coronary care unit depend on whether the attack occurred. Moreover, the emergence thrombolytic therapy of acute myocardial infarction emphasized the need for more sensitive biochemical indicators of necrosis in the early hours. The eventual realization that the recovery of blood flow is the dominant mechanism for the reduction of infarct size has led to a therapeutic approach dominated by thrombolysis and literally by the use of interventions to initiate and maintain open vessels.

The key observation is that the benefits of using a drug could be demonstrated if the drug was administered before ischemia time.

However, the greatest benefit in the management of patients with myocardial infarction has undoubtedly been the restoration blood flow as soon as possible after occlusion

The aim of this study is to determine the reperfusion injury exacerbated by drugs thrombolytics in myocardial infarction through the process of elevation of cardiac enzymes that culminates and comes to normal within 24 hours, injury prevention and prolonged myocardial ischemia.

However, the objective was to prospectively evaluate the biochemical markers for the diagnosis of coronary thrombolysis permeability IV early after acute myocardial infarction.

THE PROBLEM

"The effect of drugs on the enzymes thrombolytric Cardiac creatine kinase and creatine kinase-MB phospho in myocardial infarction.

OBJECTIVES

• To evaluate the effect of thrombolytic agents in cardiac enzymes.
• To compare the effect of thrombolytic agents and thrombolytic drugs in non-cardiac enzymes
• To determine the importance of thrombolytics for myocardial infarction patients
• Provide guidance on the teaching of population Prompt medical attention on the principle of chest pains.

OPERATIONAL DEFIITIONS

Effect: The result or outcome

Thrombolytic drugs: Drugs used to dissolve blood clots

CK: A cardiac isoenzyme released into the bloodstream at high levels during an injury to the heart. Also known as creatine or creatine kinase Phophokinase.

CK-MB: isoenzyme is also found in blood from the heart of the heart muscle during a heart injury

Myocardial infarction, necrosis of a region of infarction caused by an interruption of blood supply to the heart, usually as a result of occlusion of a coronary artery.

HYPOTHESIS

"Thrombolytic agents has an effect in reducing maximum levels of cardiac enzymes, CK and CK-MB "

LIMITATIONS

Coronary Care Unit: Data for this research is applicable in the parameters of the coronary care unit.

Age: customers select only 35 to 65 years of age.

Myocardial infarction: This also applies to customers who have been admitted to hospital within 6 hours after onset of chest pain, myocardial infarction who received Inj. METALYS.

Acute coronary syndrome: Customers were admitted after 6 hours of onset of chest pain with acute coronary syndrome are included in the control group.

METHODOLOGY:

This study was conducted by an experimental method of research design in the parameters of the coronary care unit Hospital in Dubai, United Arab Emirates a consecutive series of patients receiving IV METALYS [tenecteplase] for MI May 2006 to November 2006 were included in the study.

Research Design:

This study uses a design comparison.

Parameters:

This study was conducted in patients regardless of age, sex and nationality, who were admitted to the coronary care unit in the emergency department at Dubai Hospital, UAE

SAMPLE SIZE

This study included 60 clients, men and women, regardless of nationality, between 35 and 65. Of the 60 clients 30 were taken in the group experimental and 30 others regarded as control group.

The sampling technique:

The samples were selected as a convenience sample in two groups, experimental and control groups. Customers who have received thrombolytics within 6 hours after onset of pain chest were selected as experimental group, and final customers were presented after 6 hours of onset of chest pain and did not receive thrombolytic therapy are selected in the control group. All patients with the diagnosis of myocardial infarction confirmed by the subsequent elevation of creatine kinase [] CK and CK-MB isoenzyme. METALYS IV is administered at a dose of 6000 units to 9000 units depending on the weight of patients. Patients with acute myocardial infarction who were admitted to cardiology service more than 6 hours after onset of pain are also included.

  DATA Collection procedure:

The study data were collected by an instrument, which consists of 22 elements, whose number shows the age and sex. Religion nationality, occupation, eating habits, lifestyle, the onset of chest pain, the date and time of admission, signs and symptoms, vital signs, the rate of myocardial infarction, thrombolytic treatment protocol, cardiac enzyme levels after thrombolytic therapy, medication and received a release date.

A study reveals that most IM clients was the Indian subcontinent, which constitute 63.3% and the minority who constitute only 1.6% of the Greater Columbia and Turkey. 3.3% of customers were the Egyptians and Syrians. Bangladesh was 6.6% and Pakistanis were about 21.6%. Only 9.9% of customers who had MI citizens of Dubai. Among them, 46.6% of patients were aged between 46 and 55 years and 41.6% Customers has between 36 to 45 years and the remaining 11.6% of clients were between 56 to 65 years of age.

36.2% of clients with acute coronary syndrome and were not thrombolytic therapy. Rest of customers have been with the IMF and most of them were thrombolysed. However, all customers who have undergone coronary angioplasty. Of these customers a customer had normal coronary vessels, two were diagnosed with mild coronary stenosis, a conservative treatment and clients with major vessel block 4 triples It has been shown that for CABG. The rest of the customers has been treated with percutaneous coronary angioplasty to LAD [50 %],]] RCA [circumflex and 21.6% [13.5%.

It is also clear from the study that most Indians suffer from myocardial infarction and the main factors are smoking, stress and lack of knowledge on the state of the disease.

On the basis of the association Chi-square difference between the normalization of the heart enzyme levels in the study groups are as follows-

In the experimental group, 30 patients received Inj. METALYS. of them except for 4 clients 26 clients taking into account that the reports cardiac enzymes normalized within 24 hours of admission and administration of thrombolytic agent.

In the control group, 30 reports of clients Normalization of blood cardiac enzymes were analyzed, where we found 27 reports showed that customers higher levels of cardiac enzymes after 24 hours of admission.

1. Critical value 14.56, p <0.05 and assuming no

Inj. METALYS has a good effect on the heart muscle is supplied with critical value 14.56, the probability value <0.05, as shown by the highest fall of cardiac enzymes CK and CK-MB within 24 hours after receiving thrombolytic agent.

DISCUSSION

Tenecteplase [METALYS] is an activator recombinant plasminogen fibrin-specific. It binds to fibrin component of thrombus and converts plasminogen to plasmin selectively bound thrombus, which degrades fibrin matrix of thrombi. Tenecteplase is removed from circulation by binding to specific receptors in the liver, followed by catabolism of peptides small.

After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase sample antigen elimination biphasic plasma. No dose tenecteplase dependence involved in the therapeutic dose range.

The first half of life is dominant 24 + _5.5 [mean = / Min]-SD. half-life is 129 + _87 minutes and the plasma clearance is 119 + _49 ml / min

The main finding of this study is the first peak in the level total CK and CK-MB

isoenzymes successfully identified after reperfusion therapy METALYS. CPK levels peak in 12 hours and CK-MB have been displaced in 6 hours. Study reveals that cardiac enzyme levels peaked and returned to normal within 24 hours of time in the experimental group who received thrombolytic agents at 6 hours after onset of chest pain. When it was 3 to 5 days for peak enzyme levels to clients in the control group who received no agents thrombolytic therapy because of late arrival to the hospital, causing more damage to the myocardium.

Thus it is clear that the extent of damage to the myocardium and demand oxygen is lower in the experimental group of customers.

Finally, you can use as a surrogate endpoint for demonstration of angiography

permeation studies in future clinical reperfusion therapy. improve the diagnostic yield when the analysis was limited to patients older than 6 hours after onset of symptoms.

CONCLUSION

Clinical studies of fibrinolytic therapy show myocardial infarction, thrombolytic therapy first begins at 6 hours after onset of chest pain, significantly reduced the risk of other damage and myocardial oxygen demand, by the process of low levels of the maximum levels of cardiac enzymes in 24 hours.

Inj. It reached its METALYS peak cardiac enzymes early in the experimental group showed the artery open infarct-related, the clot is dissolved by Inj. METALYS This means that we have a thrombolytic effect good, so we have reached a peak in the early stages.

Early identification patients with occlusion persisting after thrombolyis during

Acute myocardial infarction is also important because it can pave the way for life-saving interventions such as rescue percutaneous transluminal coronary angioplasty or repeated thrombolysis.

Implications for nursing NURSES:

SERVICE

Determine the intensity of angina customers

Observe signs and symptoms

Place the patient in a comfortable position

Administer oxygen if necessary

vital signs every 15 minutes for 2 hours, every half hour to an hour and

every hour for two hours and then necessary

Get a 12-lead ECG

Monitor for pain relief

Monitor patient response to drug treatment

Institute continuous cardiac monitoring and watch-reperfusion arrhythmias, changes in rhythm, bradycardia and tachycardia

Interpreting rhythm strips

View Complaints of headaches with the use of nitrates

Beware of recurrence of pain. Reinforce the importance of notifying the nursing staff each time the pain is felt.

Administer medications to alleviate patient anxiety as directed, such as sedatives and tranquilizers

Provide complete bed rest for 24 hours

Determine the level of activity that precipitated the pain of angina occurs.

Identify specific activities of the patient can perform below the level at which anginal pain

Preparation for angiography diagnosis and treatment, as coronary PTCA [percutaneous transluminal] coronary angioplasty

EDUCATION

Advocate on risk factors and changes lifestyle such as-

Stress reduction methods such as biofeedback and relaxation techniques

Low in cholesterol content diet low

Avoid excessive caffeine consumption

Do not use diet pills, nasal decongestants

Follow-up visits to control diabetes and hypertension

Educate patients and families in relation to-

Prevention of recurrence of pain

Regular use of drugs

The risks of smoking

Other factors contributing Prevention

Regular monitoring

Importance of changes in diet

Avoid activities that cause angina, such as sudden exertion, walking against the wind, extreme temperatures, stress emotional, to refrain from physical activity for 2 hours after meals, reducing the weight, etc.

appropriate use of medicines

Adverse Medicines

Administartion

Lead interdisciplinary intervention programs

Education nursing students and staff

Provide nursing education in service

Maintenance of records and reports

Maintenance statistics

Develop policies and procedures

Monitoring and evaluation of staff performance

Recommendations for consideration

Most of patients after MI did not really participate in formal cardiac rehabilitation or because the lack of structured, physician

references the patient's motivation to small, non-compliance and financial constraints.

Cardiac rehabilitation is a place of learning, creating

lifestyle modification and full compliance with the requirements of

therapies for the recovery of MI, including training exercises.

Participation in cardiac rehabilitation programs after instant messaging with a decrease

subsequent morbidity and cardiac mortality.

adequate education in hospitals and work on the causal factors and contribute to the prevention of heart attacks and return stroke is needed.

All forms of reperfusion, depending on local services should be available for patients. Protocols must be written and agreed for the reperfusion strategy to be implemented in a network. Early diagnosis of elevation myocardial infarction ST is essential and is best done by recording the ECG Rapid Interpretation of First Contact with a doctor if 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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