The diagnosis is “Coronary artery disease” Essay

The diagnosis is “Coronary artery disease. Acute inferior infarction”. There are several pathognomic symptoms, which can be used as the diagnostic criteria: chest pain, ECG changes (ST elevation in the inferior leads). Other information (hypotony and bradycardia) was provided in the case study can be useful for understanding of the severity of the condition.

There's a specialist from your university waiting to help you with that essay.
Tell us what you need to have done now!


order now

The risk of death is (heart rate x [age/10]2)/SBP=16.9, consequently the risk of death in the first 24 hours is up to 0.4%/ death at the hospital –1.5% and in 30 days – 1.9% (see Annex, tab. 1).

By the definition using in the MESH database, the myocardial infarction is a “gross necrosis of the myocardium, as a result of interruption of the blood supply to the area”. The interruption of blood supply often is caused by the thrombus appearing in the vessels damaged by the atherosclerotic process. The occlusion by the blood clot can be total or subtotal. An atheroma, the atherosclerotic plaque on the artery walls, changes mechanical resistance and elasticity of the vessel. This narrow spot will make the blockage of blood supply more likely. Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth. Thus the blood clot will form on the atheroma easier. Sometimes a clot forms in the cavity of the heart and goes in a coronary artery with the flow of blood.

Rarely myocardial ischemia can be caused by the spasm of the coronary arteries. Slowly accruing stenosis of epicardial coronary arteries may proceed to complete occlusion but do not usually lead to the myocardial infarction because of the development over time of a rich collateral network. With time the resultant thrombus can completely occlude the epicardial infarct artery. If there is an insufficient collateral supply, a wave front of myocardial necrosis begins within 15 minutes and spreads from the endocardium toward the epicardium. This may be modulated by the extent of collateral flow and determinants of myocardial oxygen consumption, affording opportunity for significant myocardial salvage.

Depending on the evidence of the myocardial lesion we can distribute all causes of an acute coronary syndrome in the following diagnoses: unstable angina, myocardial infarction without ST elevation (NSTE-MI) and myocardial infarction with ST elevation (STEMI) (see Annex, fig. 1).

The main determinants of acute myocardial infarctions are an acute parietal vascular lesion; local coronary vasoconstriction and a platelet and fibrin thrombus. The coronary spasm and the thrombotic cascade can be triggered by the parietal fissuration.

A key concept in the pathophysiology of acute myocardial infarction is ventricular remodeling – changing size, shape, and thickness of the ventricle walls involving both the damaged and intact segments of the ventricle. Acute dilatation and thinning of the area of infarction that is not due to additional myocardial necrosis is referred to as infarct expansion. An extraload is placed on the residual functioning myocardium, which results in compensatory hypertrophy. Thus inhibition of the renin-angiotensin-aldosterone system is is a key therapeutic maneuver in patients with infarction. Additional important pathophysiological concepts in patients with infarct include cardiac arrhythmias such as those that result from electrical instability, pump failure/excessive sympathetic stimulation, and conduction disturbances. Mechanical problems that result from dysfunction or disruption of critical myocardial structures (e.g. mitral regurgitation, rupture of the interventricular septum, ventricular aneurysm formation, and free wall rupture) may require a combination of pharmacological, catheter-based, and surgical treatments.

The acute infarction has several phases: 1) The Ischemic Insult Phase; 2) The Phase of Coagulation Necrosis; 3) The Healing Phase and 4) The Scarring phase. The Ischemic Insult Phase lasts 4 hours from the interruption of blood flow. It begins in the subendocardium within 20 min and progresses to necrosis in 60 minutes. An urgent reperfusion can save some myocardiocytes.

The Phase of Coagulation Necrosis lasts from 4-48 hours after the occlusive event. The reperfusion is ineffective in this stage. Damaged endothelium initiates inflammatory response. This condition is characterized by the increased rate of LKC, subfebrility and high platelets adhesion.

The Healing Phase begins 48 hours later and lasts up to a week. Next the Scarring Phase begins. Its duration depends on the size of the leisure. In this stage the necrotic cells are replaced by connective tissue. A tough fibrous scar is forming. In several years the scar disappears but remodeling of the ventriculus leads to developing the cardiomyopathy.

Simultaneously, the “zones of tissue damage” are forming-the zone of ischemia, the zone of injury and the zone of infarction. The zone of ischemia is the outer zone. The myocardiocytes are still viable but their repolarization is impaired. We can see it on ECG as dysrythmias and appearing of T-wave inversion and ST depression. The damage is reversible with reperfusion caused by the rest or use of antianginal medications (nitrates). The zone of injury is the middle layer of the infarction. This zone surrounds the area of infarction. Impaired processes of repolarization result in ECG phenomena: T-wave abnormalities and ST elevation. This signs can appear within 1-2 hours of the insult and resolve in 48-72 hours. The reperfusion reverses the pathological changes and improves the prognosis. The zone of infarction is the area of necrosis. ST elevation, after that development of the Q-wave, and finally T-wave inversion. There are ST-T wave abnormalities and Q and QS waves reflecting cell death.

Topic diagnostics helps to assess the clinical situation and prognosis. The changes in the inferior lead (II, III and aVF) show that the inferior wall of the left ventricle is damaged. In that way it is a sign that the right coronary artery is blocked. Inferior myocardial infarction often presents with nausea, vomiting or an urge to defecate due to the stimulation of periphery nervous system. SA block and sinus bradycardia, atrial arrythmias and hypotension are common. The bradycardia origin is the ischemia of sinus node. Posterior infarction can occur along with inferior myocardial infarctions. There are several pathognomic symptoms: sinus bradycardia, the 1st & 2nd degree AV block, the reciprocal changes in leads V1-4 (ST depression and high R). In right ventricular infarctions there are involved the changes in II, III, aVF and V4-6 leads. This infarction can be confirmed by echocardiography. Anterior infarction results from occlusion of the left anterior descending artery. This localization of the infarction is characterized by affecting V1-V4 leads. The diagonal branches of the leFt anterior descending infarction can be involved also. In this case, I and aVL, V5-6 leads will be affected. Antero-lateral infarctions involve I and aVL leads and result from occlusion of the circumflex artery. There are AV left bunch branch blocks and congestive heart failure (CHF) resulting antero-lateral infarction.

A working diagnosis of an acute myocardial infarction can be made in the presence of clinical symptoms consistent with acute coronary syndrome and specific ECG changes. The cardiospecific enzymes could be useful for assessment of the dynamics of process. There are following ECG criteria of acute infarction:

ST elevation of ?0.2 mV in leads VI–V3 or ? 0.1 mV in other leads
ST segment depression consistent with posterior MI
Established MI (either old or recent) may be defined by the presence of Q waves of ?0.03 s in leads V1–V6 or II, aVL, aVF.
Tests following ECG are cardioselective enzymes (troponine, creatine kinase, lactate dehydrogenase, transaminases), concentration of myoglobine, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), serum sodium and potassium and chest radiograph. All they have different diagnostical value. There is an evidence that negative troponin T, troponin I, or CK-MBm result 9 to 12 hours after the beginning of symptoms practically exclude the diagnosis of the miocardial infarction. The ECG and myocardial markers (see Annex, tab.5, fig.2) change with the course of the disease : first there is an ST elevation, after that development of the Q-wave, and finally T-wave inversion. Typical increase in the concentration of serum cardiac troponins or creatine kinase isoenzyme containing M and B subunits (CK-MB) associated with at least one of the following:

symptoms of cardiac ischemia
recent pathological Q waves in the ECG
ischaemic ST segment changes in the ECG
coronary artery revascularization
ECG Diagnosis
In a T-wave infarction (non-Q-wave infarction), no classical Q waves are present, but the diagnosis is based on an increase of myocardial enzymes, chest pain, or ST-T changes. Classical Q-wave changes; ST elevations, and T inversions may be caused by various other diseases, which should be remembered in the differential diagnosis. An old infarction, bundle branch block, and early repolarization make the diagnosis difficult, in which case the change in ECG is important and an old ECG recording valuable. The diagnosis should be made without delay since early therapy improves the prognosis decisively.

Relying on above mentioned we can determine the following priorities in the management of acute myocardial infarction: to limit infarct size, treat arrythmias, and preserve function of the myocardium.

In the choice of the optimal scheme of the management of the myocardial infarction the use of evidence based approach is crucial. Evidence based practice can be determined as “the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research.” (D. Sacket, 1996). In other words, the evidence-based medicine is the process of systematically reviewing, appraising and using clinical research findings to aid the delivery of optimum clinical care to patients. (Bandolier, 2004)

To make the evidence based medicine more acceptable to clinicians and to encourage its use, it is best to turn a specified problem into answerable questions by examining the following issues:

Target person or population.
Intervention given.
Comparison (if appropriate).
Outcomes considered.
Every clinician, every nurse strives to provide the best possible care for patients. However, given the multitude of research information available, it is not easy task to choose the optimum intervention or diagnostic technique. Evidence is presented in many forms, and it is important to understand the basis on which it is stated. The value of evidence can be ranked according to the following classification in descending order of credibility:

I.                   Strong evidence from at least one systematic review of multiple well-designed randomised controlled trials.

II.                Strong evidence from at least one properly designed randomised controlled trial of appropriate size.

III.             Evidence from well-designed trials such as non-randomised trials, cohort studies, time series or matched case-controlled studies.

IV.             Evidence from well-designed non-experimental studies from more than one centre or research group.

V.                Opinions of respected authorities, based on clinical evidence, descriptive studies or reports of expert committees.

Another classification is used mainly in European countries (see also the Annex, tab.2-4):

A.    Strong research-based evidence. Multiple relevant, high-quality scientific studies with homogeneous results. (Level I – see above)

B.     Moderate research-based evidence. At least one relevant, high-quality study or multiple adequate studies. (Level II)

C.     Limited research-based evidence. At least one adequate scientific study. (Level III, IV)

D.    No research-based evidence. Expert panel evaluation of other information. (Level V)

For collecting/selecting evidence we can use the hand-search of published literature (i.e. journal, articles, books, manuals etc) and search of electronic databases (i.e. OVID, MEDLINE, HINARI, the Cochrane database of systematic reviews, EMBASE and the Database of Abstracts of Reviews (DARE) etc). The Cochrane Library brings together a number of regularly updated evidence-based medicine databases, including the Cochrane Database of Systematic Reviews, The Database of Abstracts of Reviews of Effects (DARE), The Cochrane Central Register of Controlled Trials (CENTRAL), The Cochrane Methodology Register, The NHS Economic Evaluation Database, Health Technology Assessment Database and The Cochrane Database of Methodology Reviews (CDMR). Unfortunately Cochrane Heart Group did not produce any systematic review on the issues of the acute infarction management. (The Cochrane Library Issue 4, 2004). There were only some Cohcrane protocols about the evidence of use of beta-blockers and some secondary treatment (herbs, magnesium) in the patients with myocardical infarction.

Another source of evidence based practice is Critically Appraised Trials (CATs). But there were no trials on the issue of the evidence based nursing in the acute infarction at the specialized web-sites (e.g. http://www.eboncall.org). During the search in MEDLINE using a tool “Clinical queries” there were retrieved 44 articles. Search history: “(infarction nursing) AND systematic [sb]”. Only 5 articles were selected for future analysis.

Recent Kelly’s publication in the British Journal of Nursing was dedicated to the issue of evidence-based care of a patient with a myocardial infarction. Author considers that holistic approach to the management of is an important myocardial infarction is a key element of quality nursing care. This review based on the case reports and its level of evidence is “D” only. Swallwood A. and Chadwick R. insist that nurse-initiated thrombolysis is one way to safely achieve the standards of the acute infarction management. Hand H. from the School of Nursing and Midwifery of the University of Sheffield recommends integrating the National Service Framework for Coronary Heart Disease into nursing practice. The goal of the National Service Framework for Coronary Heart Disease was that by April 2002, 75% of eligible patients should receive thrombolysis within 30 minutes of arriving at hospital. A district general hospital introduced a strategy to improve door to needle times. In the first phase (1989-1995), patients with suspected acute myocardial infarction, referred by general practitioners, were assessed in the coronary care unit; all other patients were seen first in the accident and emergency department. In the second phase (1995-1997), all patients with suspected acute myocardial infarction were transferred directly to a fast track area within the coronary care unit, where nurses assess patients and doctors started treatment. In this program the median door to needle time was significantly reduces during these phases. In the third phase (1997-2001), all patients with suspected acute myocardial infarction were transferred directly to the fast track area and assessed by a “coronary care thrombolysis nurse.” If electrocardiography confirmed the diagnosis of acute myocardial infarction, the nurse could initiate thrombolytic therapy (subject to guidelines and exclusions determined by the consultant cardiologists). The implementation of this practice shorten median door to needle time for 3 of 15 minutes (range 5-70 minutes), with 80% of patients treated within 30 minutes. Systematic clinical review showed no cases in which a nurse initiated inappropriate thrombolysis (Qasim A, et all) and thrombolysis started by nurses is safe and effective in patients with acute myocardial infarction. It may provide a way by which the national service framework’s targets for door to needle times can be achieved.

By the Cook N.F. et all. “through analysis of the patient’s health status, with frequent reference to pathophysiology, the nurse can perform an accurate nursing assessment and so determine immediate priorities for nursing care. The priority objectives were identified as pain control, management of cardiogenic shock, reperfusion of the myocardium, cardiac monitoring for complications of AMI and the effects of treatment, and management of anxiety”. This article is based on the case reports and has the level of evidence “C”.

Let’s discuss these priorities. Pain relief is an important element in the early management of the patient with ST-elevation myocardial infarction. Morphine is generally recommended for pain control. Recent randomized clinical trial (MEMO study (metoprolol-morphine)) compared the analgesic effect of metoprolol and morphine in patients with chest pain due to suspected or definite acute myocardial infarction after initial treatment with intravenous metoprolol. Researchers found that in suspected acute myocardial infarction, if chest pain persists after intravenous beta-adrenergic blockade treatment, standard doses of an opioid analgesic such as morphine will offer better pain relief than increased dosages of metoprolol (Everts B et all., 1999, level of evidence B). Thus, morphine sulfate (2 to 4 mg IV with increments of 2 to 8 mg IV repeated at 5- to 15-minute intervals) is the analgesic of choice for management of chest pain associated with acute myocardial infarction.

Data of other trials show that intravenous administration of atenolol significantly reduces mortality (6 lives saved per 1000 treated), and must be considered as part of the first-line treatment of AMI (ACC/AHA Practice Guideline). But in the analysing case patient has bradycardia and low blood pressure, which are the contraindications to the use of beta-blockers. Patients with early contraindications within the first 24 hours of the myocardial infarction with ST elevation should be re-evaluated for candidacy for beta-blocker therapy. (Level of Evidence: C)

Morphine lessens anxiety and decreases the catecholamine response and has a vasodilator effect as well. It’s recommended to use morphine in the dose 5-15 mg by slow intravenous injection titrated against the response (ACC/AHA Practice Guideline).

Standard therapy with any complaints of chest pain includes oxygen supply. Usual dose is 4 lters per minute by facemask or nasal prongs. Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO 2 less than 90%). (Level of Evidence: B). It is reasonable to administer supplemental oxygen to all patients with uncomplicated ST-elevation myocardial infarction during the first 6 hours. (Level of Evidence: C)

There is evidence that oral acetylsalicylic acid (Aspirin, ASA) at dosage ? 162 mg as first line therapy significantly reduces mortality in patients with acute myocardial infarction. If there are no contraindications, acetylsalicylic acid (ASA, aspirin) and a beta-blocker should be started for all patients. Aspirin (dose 162to 325 mg) should be given on the first day 1 of and in the absence of contraindications should be continued indefinitely on a daily basis there-after at a dose of 75 to 162 mg. (Level of Evidence: A). A thienopyridine (clopidogrel or Plavix) should be administered to patients who are unable to take aspirin because of hypersensitivity or major gastrointestinal intolerance. (Level of Evidence: C)

Low molecular weight heparins (LMWH) and platelet glycoprotein IIb/IIIa inhibitors are not effective in the myocardial infarctions with ST elevation.

Thrombolytic therapy should be given as early as possible in all cases with a clinical picture of the myocardial infarction and corresponding ECG changes (ST elevation). Thrombolytic therapy is indicated:

if the pain has lasted less than 6 to 12 (24) hours and there is at least a 2-mm elevation in the ST segment in at least two chest leads, or
a 1-mm elevation of ST in at least two leads in the extremities, or
a reciprocal ST depression in V1-V4, or
a recent left bundle branch block
Alteplase is preferred to streptokinase as it provides superior coronary patency and clinical benefits and a lower incidence of adverse effects. Newer fibrinolytic drugs (reteplase, tenecteplase) are convenient as they can be given as a bolus. The most important complication of fibrinolytic therapy is bleeding, in particular intracranial haemorrhage. Uncontrolled hypertension (especially above 170/100) is a strong risk factor for intracranial haemorrhage. It is a contraindication for fibrinolytic drugs and should be controlled before fibrinolytic therapy. Patients with contraindications should be considered for immediate transfer to a unit equipped for PCI. The contraindications for thrombolytic therapy must always be considered (see Annex, fig.1). Indications for fibrinolytic therapy include:

Class I

1. In the absence of contraindications, fibrinolytic therapy should be administered to STEMI patients with symptom onset within the prior 12 hours and ST elevation greater than 0.1 mV in at least 2 contiguous precordial leads or at least 2 adjacent limb leads. (Level of Evidence: A)

2. In the absence of contraindications, fibrinolytic therapy should be administered to patients with ST-elevation myocardial infarction (STEMI) with symptom onset within the prior 12 hours and new or presumably new LBBB. (Level of Evidence: A)

Class IIa

1. In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to STEMI patients with symptom onset within the prior 12 hours and 12-lead ECG findings consistent with a true posterior MI. (Level of Evidence: C)

2. In the absence of contraindications, it is reasonable to administer fibrinolytic therapy to patients with symp-toms of STEMI beginning within the prior 12 to 24 hours who have continuing ischemic symptoms and ST elevation greater than 0.1 mV in at least 2 contiguous precordial leads or at least 2 adjacent limb leads. (Level of Evidence: B)

Class III

1. Fibrinolytic therapy should not be administered to asymptomatic patients whose initial symptoms of STEMI began more than 24 hours earlier. (Level of Evidence: C)

2. Fibrinolytic therapy should not be administered to patients whose 12-lead ECG shows only ST-segment depression except if a true posterior MI is suspected. (Level of Evidence: A)

The reduction in mortality with fibrinolytic therapy is present regardless of sex, presence of diabetes, blood pressure (if less than 180 mm Hg systolic), heart rate, or history of previous infarcts. The mortality benefit is greater in the setting of anterior STEMI, diabetes, low blood pressure (less than 100 mm Hg systolic) or tachicardia (greater than 100 bpm).

The earlier therapy begins, the better the outcome, with the greatest benefit decidedly occurring when therapy is given within the first 3 hours. Benefit occurs, however, up to at least 12 hours from the onset of symptoms. Unfortunately, the absolute benefit is less with inferior infarctions, except for the subgroup with associated right ventricle infarction or anterior ST-segment depression indicative of a greater area at risk.

Unfractionated heparin admistrating intravenously is recommended in patients with myocardial infarction who undergo fibrinolytic therapy with alteplase or percutaneous revascularization. Intravenous unfractionated heparin is also recommended in patients with an infarct who receive fibrinolytic therapy with a non-selective fibrinolytic agent (urokinase, streptokinase, anistreplase) and are at increased risk for systemic emboli.

In the analyzing case patient’s BP is 102/58 and pulse rate 48 bpm. The presence of sinus bradycardia needs the administration of atropine. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, such as ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis, preclude use of atropine without careful medical supervision.

The pharmacological treatment of bradycardia and AV conduction disturbances during the myocardial infarction with ST elevation is a therapeutic measure. Pharmacotherapy centers on the use of atropine at doses of 0.6 to 1.0 mg intravenously repeated every 5 minutes until there is the desired effect or a total dose of 0.04 mg/kg has been reached. When there is infranodal block, however, atropine may increase the sinus rate without affecting infranodal conduction, and so the effective ratio of conduction may decrease, and the ventricular rate may decrease.

Nitrate administration in acute myocardial infarction has been viewed as a means of providing an exogenous source of nitric oxide that may help replenish or restore the actions of an endothelium-derived relaxing factor (EDRF). The primary action of nitrates is vasodilation, which is attributable primarily to nitrate-induced relaxation of vascular smooth muscle in veins, arteries, and arterioles. Generally, the recommendations for intravenous Nitroglycerin are following (ACC/AHA guideline, 1999):

Class I

For the first 24 to 48 hours in patients with acute myocardial infarction and congestive heart failure, large anterior infarction, persistent ischemia, or hypertension.
Continued use (beyond 48 hours) in patients with recurrent angina or persistent pulmonary congestion.
Class IIa

None.

Class IIb

For the first 24 to 48 hours in all patients with acute myocardial infarction who do not have hypotension, bradycardia, or tachycardia.
Continued use (beyond 48 hours) in patients with a large or complicated infarction.
Class III

Patients with systolic pressure less than 90 mm Hg or severe bradycardia (less than 50 bpm).
There is a dilemma for nitrates administration in the case of acute coronary syndrome with symptoms of SA block. On the one hand, nitrates administration should be avoided in the presence of marked bradycardia (less than 50 bpm). On other hand the chest pain is direct indication for use of the nitrates. It does correspond to the class III of the recommendations for intravenous nitroglicerine administration. By the ACC/AHA guideline nitrates should not be administered to patients with systolic blood pressure less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, severe bradycardia (less than 50 bpm), tachycardia (more than 100 bpm), or RV infarction. (Level of Evidence: C).

An effective substitute of nitroglycerine is isosorbide dinitrate. Nitrates could not be used as a substitute for narcotic analgesia that is usually required to manage pain associated with acute myocardial infarction.

Hence, analysis of complaints, status praesens objectivus, ECG changes show that in the case of acute inferior infarctions the main priorities of the disease management are limiting infarct size, treat arrythmias and preserve function of the myocardium. These goals can be achieved by the applying of the principles of evidence based practice in nursing. Registered nurse should provide proper pain control, management of cardiogenic shock, reperfusion of the myocardium, cardiac monitoring for complications of AMI and the effects of treatment, and management of anxiety. He/she should provide care correspondingly to the highest standards of evidence based medicine, prevent complications and promote recovery.

The acute inferior myocardial infarction can be complicated with left ventricle insufficiency, SA and AV block, cardiogenic shock, myocardial ruptures… Early beginning of measures on pain relief, administration of antiplatelet drugs and trombolytical therapy is an important element of the successful treatment and secondary prevention. Nurse can use for control of the effectiveness of applied interventions data of physical examination, dynamics of changes at ECG and carcdiac biomarkers dynamics (see. Annex, fig.2, tab. 5).

The medications of choice in the case study are morphine, oxygen, aspirine, tissue pasminogen activator (e.g. anteplase) and atropine. After normalization of heart rate we can add beta-blockers. All contraindications for chosen medications should be taken in the account. Nursing care should be provided by individuals certified in critical care, with staffing based on the specific needs of patients and provider competencies, as well as organizational priorities. Optimally, the nursing staff should have a skill set similar to the nurses of cardiovascular care unit so that they may evaluate and respond to any deterioration of a patient with acute infarctions. Developing of the guidelines of evidence based nursing could be useful to achieve better results of health care.

References:

ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction–Part V http://www.americanheart.org/presenter.jhtml?identifier=1864
ACC/AHA Practice Guidelines http://www.acc.org/clinical/guidelines/amiIndex.htm
Antman EM, Grudzien C, Sacks DB: Evaluation of a rapid bedside assay for detection of serum cardiac troponin T. Journal of the American Medical Association 1995; 273 (16): 1279-1282
Arone C. Management of the acute coronary syndromes Australian Prescriber 2001;24:56-8 http://www.australianprescriber.com/index.php?content=/magazines/vol24no3/coronary.htm
Cook NF, Melby V. Acute MI: analysing health status and setting immediate priorities. Br J Nurs. 1999 Feb 11-24;8(3):150-2, 154, 156-8.
de Winter RJ, et al: Value of myoglobin, troponin T and CK-MB (mass) in ruling out an acute myocardial infarction in the emergency room. Circulation 1995; 92: 3401-3407
Everts B, Karlson B, Abdon NJ, Herlitz J, Hedner T. A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction–the MEMO study. J Intern Med. 1999 Feb;245(2):133-41.
Evidence based medicine: Bandolier http://www.jr2.ox.ac.uk/bandolier/painres/download/whatis/ebm.pdf
Gillespie M, Melby V. Assessing acute myocardial infarction. Emerg Nurse. 2003 Sep;11(5):26-9.
Hand H. Myocardial infarction: Part 1. Nurs Stand. 2001 May 23-29;15(36):45-53
Kelly J. Evidence-based care of a patient with a myocardial infarction. Br J Nurs. 2004 Jan 8-21;13(1):12-8.
Qasim A, Malpass K, O’Gorman DJ, Heber ME. Safety and efficacy of nurse initiated thrombolysis in patients with acute myocardial infarction. BMJ. 2002 Jun 1;324(7349):1328-31.
Sackett D.L. Evidence-based medicine : how to practice and teach EBM Churchill Livingstone 2000
Sayre MR, et al: Measurement of cardiac troponin T is an effective method for predicting complications among emergency department patients with chest pain. Annals of Emergency Medicine 1998; 31: 539-549
Scheinman MM, Thorburn D, Abbott JA. Use of atropine in patients with acute myocardial infarction and sinus bradycardia. Circulation. 1975 Oct;52(4):627-33.
Smallwood A, Chadwick R. Nurse-initiated thrombolysis in coronary care. Nurs Stand. 2000 Sep 27-Oct 3;15(2):38-40.
Morrow DA, Antman EM, Giugliano RP, et al. A simple risk index for rapid initial triage of patients with ST-elevation myocardial infarction: an InTIME II substudy. Lancet 2001 Nov 10;358:1571–5

Annex:

Table 1. Risk index scores (quintiles) and mortality risks for patients with ST elevation myocardial infarction (derivation data set)[1]

Risk index scores
Mortality risk
24 hours
in hospital
30 days
12.5
0.2%
0.6%
0.8%
;12.5 to 17.5
0.4%
1.5%
1.9%
;17.5 to 22.5
1.0%
3.1%
3.3%
;22.5 to 30
2.4%
6.5%
7.3%
;30
6.9%
15.8%
17.4%
(Heart rate x [age/10]2)/systolic blood pressure.

Fig. 1 Contraindications for trombolysis.

Tab. 2 Levels of Evidence[2] (UK)
Grade of recommendation
Level of Evidence
Therapy: Whether a treatment is efficacious/ effective/harmful
Therapy: Whether a drug is superior to another drug in its same class
Prognosis
Diagnosis
Differential diagnosis/symptom prevalence study
Economic and decision analysis
A
1a
SR (with homogeneity*) of RCTs
SR (with homogeneity**) of head-to-head RCTs
SR (with homogeneity*) of inception cohort studies; CDR† validated in different populations
SR (with homogeneity*) of Level 1 diagnostic studies; CDR† with 1b studies from different clinical centres
SR (with homogeneity*) of prospective cohort studies
SR (with homogeneity*) of Level 1 economic studies
1b
Individual RCT (with narrow Confidence Interval‡)
Within a head-to-head RCT with clinically important outcomes
Individual inception cohort study with ; 80% follow-up; CDR† validated in a single population
Validating** cohort study with good††† reference standards; or CDR† tested within one clinical centre
Prospective cohort study with good follow-up****
Analysis based on clinically sensible costs or alternatives; systematic review(s) of the evidence; and including multi-way sensitivity analyses
1c
All or none§

All or none case-series
Absolute SpPins and SnNouts††
All or none case-series
Absolute better-value or worse-value analyses‡‡
B
2a
SR (with homogeneity*) of cohort studies
Within a head-to-head RCT with validated surrogate outcomes ‡‡‡
SR (with homogeneity*) of either retrospective cohort studies or untreated control groups in RCTs
SR (with homogeneity*) of Level ;2 diagnostic studies
SR (with homogeneity*) of 2b and better studies
SR (with homogeneity*) of Level ;2 economic studies
2b
Individual cohort study (including low quality RCT; e.g., ;80% follow-up)
Across RCTs of different drugs v. placebo in similar or different patients with clinically important or validated surrogate outcomes
Retrospective cohort study or follow-up of untreated control patients in an RCT; Derivation of CDR† or validated on split-sample§§§ only
Exploratory** cohort study with good ††† reference standards; CDR† after derivation, or validated only on split-sample§§§ or databases
Retrospective cohort study, or poor follow-up
Analysis based on clinically sensible costs or alternatives; limited review(s) of the evidence, or single studies; and including multi-way sensitivity analyses
2c
“Outcomes” Research; Ecological studies

“Outcomes” Research

Ecological studies
Audit or outcomes research
3a
SR (with homogeneity*) of case-control studies
Across subgroup analyses from RCTs of different drugs v. placebo in similar or different patients, with clinically important or validated surrogate outcome

SR (with homogeneity*) of 3b and better studies
SR (with homogeneity*) of 3b and better studies
SR (with homogeneity*) of 3b and better studies
3b
Individual Case-Control Study
Across RCTs of different drugs v. placebo in similar or different patients but with unvalidated surrogate outcomes

Non-consecutive study; or without consistently applied reference standards
Non-consecutive cohort study, or very limited population
Analysis based on limited alternatives or costs, poor quality estimates of data, but including sensitivity analyses incorporating clinically sensible variations.

C
4
Case-series (and poor quality cohort and case-control studies§§ )
Between non-randomised studies (observational studies and administrative database research) with clinically important outcomes
Case-series (and poor quality prognostic studies ***)
Case-control study, poor or non-independent reference standard
Case-series or superseded reference standards
Analysis with no sensitivity analysis
D
5
Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles”
Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles”; or non-randomised studies with unvalidated surrogate outcomes
Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles”
Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles”
Expert opinion without explicit critical appraisal, or based on physiology, bench research or “first principles

Tab. 3 Levels of evidence (AU)

Level of Evidence
Feasibility F(1-4)
Appropriateness A(1-4)
Meaningfulness M(1-4)
Effectiveness E(1-4)
Economic Evidence EE(1-4)
1
SR of research with unequivocal synthesized findings
SR of research with unequivocal synthesized findings
SR of research with unequivocal synthesized findings
SR (with homogeneity) of Experimental studies (eg.  RCT with concealed allocation)

Or 1 or more large experimental studies with narrow confidence intervals
SR (with homogeneity) of evaluations of important alternative interventions comparing all clinically relevant outcomes against appropriate cost measurement, and including a clinically sensible sensitivity analysis
2
SR of research with credible synthesized findings
SR of research with credible synthesized findings
SR of research with credible synthesized findings
Quasi-experimental studies (eg. without randomization)
Evaluation of important alternative interventions comparing all clinically relevant outcomes against appropriate cost measurement, and including a clinically sensible sensitivity analysis
3
SR of text/opinion with credible synthesized findings
SR of text/opinion with credible synthesized findings
SR of text/opinion with credible synthesized findings
3a. Cohort studies (with control group)

3b. Case-controlled

3c Observational studies without control groups
Evaluation of important alternative interventions comparing a limited number of outcomes against appropriate cost measurement, without a clinically sensible sensitivity analysis
4
Expert opinion without explicit critical appraisal
Expert opinion without explicit critical appraisal
Expert opinion without explicit critical appraisal
Expert opinion without explicit critical appraisal, or based on physiology, bench research or consensus
Expert opinion without explicit critical appraisal, or based on economic theory
Cited from http://www.joannabriggs.edu.au/pubs/approach.php?mode=TEXT

Tab. 4 Grading of Recommendations (AU)[3]

Grade of Recommendation
Feasibility
Appropriateness
Meaningfulness
Effectiveness
A
Immediately practicable
Ethically acceptable and justifiable
Provides a strong rationale for practice change
Effectiveness established to a degree that merits application
B
Practicable with limited training and/or modest additional resources
Ethical acceptance is unclear
Provides a moderate rationale for practice change
Effectiveness established to a degree that suggests application
C
Practicable with significant additional training and/or resources
Conflicts to some extent with ethical principals
Provides limited rationale for practice change
Effectiveness established to a degree that warrants consideration of applying the findings
D
Practicable with extensive additional training and/or resources
Conflicts considerably with ethical principals
Provides minimal rationale for advocating change
Effectiveness established to a limited degree
E
Impracticable
Ethically unacceptable
There is no rationale to support practice change
Effectiveness not established

Analysis
Normal Range
Total creatinine phosphokinase (CPK)
30-200 U/L
CPK, MB fraction
0.0-8.8 ng/mL
CPK, MB fraction percent of total CPK
0-4%
CPK, MB2 fraction
< 1 U/L
Troponin I
0.0-0.4 ng/mL
Troponin T
0.0-0.1 ng/mL
Tab. 4 Normal values of blood tests to detect myocardial infarction[4]

Fig. 2 Cardiac biomarkers in ST-elevation myocardial infarction (STEMI).

The medications recommended in acute myocardial infarction (ACC/AHA guideline):

Acute Adjunctive Medications

Antiplatelets, such as aspirin (ASA) and clopidogrel (Plavix®)
Beta blockers, such as metoprolol (Lopressor®), acebutolol hydrochloride (Sectral®), atenolol (Tenormin®), pindolol (Visken®), bisoprolol fumarate (Zebeta®), betaxolol hydrochloride (Kerlone®), carteolol hydrochloride (Cartrol®), carvedilol (Coreg®), esmolol hydrochloride (Brevibloc®), labetalol hydrochloride (Normodyne®, Trandate®), metoprolol succinate (Toprol XL®), nadolol (Corgard®), penbutolol sulfate (Levatol®), propranolol hydrochloride (Inderal®, Betachron ER®), sotalol hydrochloride (Betapace®), timolol maleate (Blocadren®) ?
Nitrates ?
Unfractionated heparin(UFH) or low-molecular-weight heparin (LWMH)
Oral anti-arrhythmics (amiodarone, lidocaine)
Note: Prophylactic use of lidocaine has been shown to be harmful and should be avoided. Lidocaine may be useful in treating arrhythmias associated with significant myocardial infarction and reperfusion (thrombolysis). No other antiarryhthmics are indicated for treatment of acute myocardial infarction.

Magnesium
Calcium channel blockers, such as diltiazem (Cardizem®, Cartia XT®, Tiazac®, Dilacor XR®), verapamil (Calan®, Isoptin SR®, Verelan®, Covera-HS®), amlodipine (Norvasc®), bepridil (Vascor®), felodipine (Plendil®), isradipine (DynaCirc®), nicardipine (Cardene®), nifedipine (Adalat®, Procardia®, Nifedical®), nisoldipine (Sular®)
Glycoprotein IIb-IIIa platelet inhibitors, such as abciximab (ReoPro®), eptifibatide (Integrilin®), tirofiban (Aggrastat®)
Chronic Adjunctive Medications

Antiplatelets
Beta-blockers
Angiotensin-converting enzyme (ACE) inhibitors, such as fosinopril sodium (Monopril®), lisinopril (Prinivil®, Zestril®), captopril (Capoten®), enalapril maleate (Vasotec®), benazepril hydrochloride (Lotensin®), moexipril hydrochloride (Univasc®), perindopril erbumine (Aceon®), quinapril hydrochloride (Accupril®), ramipril (Altace®), trandolapril (Mavik®)
Calcium channel blockers
Oral nitrates
Low-molecular-weight heparin
Warfarin (Coumadin®)
Oral antiarrhythmics
Statins, such as atorvastatin calcium (Lipitor®), fluvastatin sodium (Lescol®), lovastatin (Mevacor®), pravastatin sodium (Pravachol®), simvastatin (Zocor®)
Tobacco cessation, such as bupropion and/or nicotine patch
Glycoprotein IIb/IIIa platelet inhibitors

Invasive Measures

Cardiac catheterization
Coronary angiography (emergency, if necessary)
Primary percutaneous coronary intervention (PCI) such as percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass graft (CABG)
Secondary Prevention/Cardiac Rehabilitation

Risk factor counseling, risk factor modification (e.g., smoking cessation, diet, exercise, lifestyle modification, control of hypertension and targeting low-density lipoprotein-cholesterol)
Phase I, inpatient, cardiac care unit
Phase II, outpatient monitored
Phase III, outpatient, non-monitored
Phase IV, outpatient cardiac rehabilitation maintenance of functional capacity
Diagnosis of Acute Myocardial Infarction Complications

2-D echocardiography
Electrocardiography
Doppler color flow imaging
Treatment of Acute Myocardial Infarction Complications

Atropine sulfate
Transcutaneous cardiac pacing
Dopamine hydrochloride (Intropin®)
Epinephrine (adrenaline chloride, Epipen®, Sus-Phrine®)
Isoproterenol hydrochloride (Isuprel®)
Temporary or permanent pacemaker
Cardioversion
Beta-blockers
Type I anti-arrhythmics, such as intravenous amiodarone
Digoxin
Adenosine (Adenocard®)
Diuretics
Vasodilators
Oral or intravenous diltiazem
Long-acting nitrates
Calcium channel blockers
Anti-inflammatory agents
Intravascular volume expansion
Swan-Ganz catheter insertion
Intraaortic balloon pump insertion (IABP)
Surgical repair of heart ruptures
Early coronary angiography
Pericardiocentesis, preferably guided by echocardiography

MAJOR OUTCOMES CONSIDERED
Morbidity and mortality from acute myocardial infarction
Incidence of nonfatal recurrent myocardial infarction
[1] Cited by http://ebn.bmjjournals.com/cgi/content/full/5/3/90?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=infarct&andorexactfulltext=and&searchid=1099351545958_3474&stored_search=&FIRSTINDEX=0&sortspec=relevance&resourcetype=1&journalcode=ebnurs
[2] Cited from http://www.eboncall.org
[3] Cited from http://www.joannabriggs.edu.au/pubs/approach.php?mode=TEXT
[4] (http://www.clevelandclinicmeded.com/diseasemanagement/cardiology/acutemi/acutemi.htm)

Free Essays
Bullying and People Essay

Bullying- everyone knows about it, but a lot of people don’t realize why it’s serious. Bullying can be defined as unwanted, aggressive behavior among school aged children that involve a real or perceived power imbalance. About 30% of teens in the U.S have been involved in bullying. People should care …

Free Essays
Most difficult aspects of learning English Essay

I studied English language at school and in university, but when I started to work in Russian-American it-company I met several difficulties with my English. I understood that my English wasn’t perfect and I need study more to build my career,, because in this company and generally you have to …

Free Essays
Cell Phone Essay

Many kids these days have cell phones. You often see teenagers talking on their phones, or, just as often, texting. It has become a part of everyday life, and a part of our society. It is encouraged socially, especially among teenagers, to have a phone. Cell phones can be very …

x

Hi!
I'm Terry

Would you like to get such a paper? How about receiving a customized one?

Check it out