Abstract Of This Case Study
Have you ever wanted to know what a Myocardial Infarction is and what its all about. Read on and find out through my eyes, about a patient I was caring for - what happened to him in both his body and mind.
The following will show what a Myocardial Infarction ( MI ) is, what happens in the patients body and what care is involved by the medical and nursing teams. All of this to ensure my patient would walk out of hospital and again feel like productive member of society that he most certainly was before his cardiac event.
Also within the body of this case study will be evidence based articles to support statements made. Congruent to this, will be reflection on how all that transpired with this man affected me and how my nursing practice has developed because of it.
This patients health related journey and the anonymous intimacy that took place, came to a happy conclusion for both nurse and patient. Judith Christiansen’s Nursing Partnership Model was published in 1990 and was developed in response to the knowledge gaps in the nursing system in New Zealand ( Taylor, 1995 ).
This partnership model is a theoretical framework for nursing practice. It has 3 major concepts – these being nursing partnership, the passage and the context. Anonymous Intimacy is one of 3 elements of the contextual facet of the partnership model – the other 2 being episodic continuity and mutual benevolence. According to Watson ( 1992 ) she perceives nursing as being continuous when in reality it is a series of episodes. Separate nurses in separate episodes contribute to a single patients health related journey ( Christensen, 1990, p.33 ). And to me each nurse has “ anonymous intimacy” with there patient. Each time I interacted with Mr T it was a privelege – he sanctioned personal closeness by a person he had not long met .
Sixteen New Zealanders die each day, or one person every 90 .
minutes, as a result of Coronary Artery Disease ( Hay, 2004 ).
Acute Coronary Syndrome accounts for approximately 7 million deaths annually in the world.
“In New Zealand, Cardiovascular Disease ( heart, stroke and blood vessel disease ) was the leading cause of death, accounting for 40% of all deaths in 2000 ”. 22% of those deaths were from coronary heart disease ( CHD ) with admissions to public hospitals totalling 29,456 in 2000 – 2001 ( 59% men and 41% women ). The death rate from CHD is more than twice as high for men than women – also across the age groups in New Zealand, deaths are highest for Maori, closely followed by Pacific people ( Hay, 2004 ).
Life means many things to many people but the common denominator for all appears to be that life is for living and enjoying. As heart disease is largely preventable, we can uptake the many resources available to ensure we can live a long and healthy life ( National Heart Foundation ).
Informed consent is a legal contract. It is when a patient gives consent for any nursing and/or medical treatment once full explanation, appreciation and understanding of his/her condition and the implications of any actions has been discussed between themselves and the medical/nursing team. Congruent to this the patient must be in possession of all of his/her faculties, and his/her judgment must not be impaired at the time of consenting (by sleepiness, intoxication by alcohol or drugs, other health problems, etc).
Mr T was consented for treatment, nursing care and his interventional procedure. This was done once all treatments, procedures, implications, complications and alternatives were comprehensively discussed with him.
- 61 year old Ice-Cream Factory Worker
- Works night shift so he can manage his son’s soccer team
- Married – lives in own home with wife, youngest son and 2 cats
Mr T has excellent family support once he returns home
- Non-Smoker/Social Alcohol
- Weight 110kgs – Body Mass Index is 34
- Height 178cms
Past Medical History
- Prostatism – details unknown
- Viral pneumonia one year ago requiring hospital admission
- Arthritis – details unknown
- No previous history of cardiac problems but has a strong family history of heart disease
- Father died @ 60 – had a Myocardial Infarction ( MI ) @40 years. Acute myocardial infarction is the rapid development of myocardial necrosis. This is caused by a crucial imbalance between the oxygen supply and demand of the myocardium. It usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium (Stahmer, 2005 )
- Sister had a Coronary Artery Bypass Graft x4grafts ( CABG ) Brother has heart problems but details unknown
This is a preview of the whole essay
- History of Chest Pain on minimal exertion for 3 – 4 days - relieved by rest. No shortness of breath ( SOB ), no nausea, no palpitations, no radiating pain.
- Visited local Accident and Emergency Clinic – was told ECG was “good“ and sent home. I was unable to determine what “ good “ meant as this information was unavailable. The following day went to GP with same history as above who then referred him to hospital( GP referral stated Crescendo Angina. Hx of chest pain with minimal exertion for 3 – 4 days. No hx of cardiac problems but strong family hx of heart disesae. Non-Smoker, BMI 34. ECG shows Sinus Rhythm, inverted T-Waves in Anterolateral leads ). An ECG allows the reader to determine the area of myocardium that has been damaged ( Houghton & Gray, 2003 ). As in Mr T’s case what was to follow later was major ECG changes in his antero-lateral leads – 1, aVl, V1 – V6.
- On admission to Emergency Care Centre ( ECC ) Mr T had 3/10 Central Non-Radiating Chest Pain with no SOB,nausea or palpitations. Palitations is a term often used to describe an irregular heart beat, or the sensation of skipped or extra heart beats
- His GCS was 15/15. The GCS – Glasgow Coma Scale is a scale which evaluates the patient's level of awareness. The scale rates three categories of patient responses; eye opening, best verbal response, and best motor response. The lowest score is 3 and is indicative of no response, the highest score is 15, indicates the patient is alert and aware of his or her surroundings.
- Medications given in ECC were: Asprin 300mg. Nothing else was given at this point.
Asprin works by inhibiting the blood’s ability to clot. It works by interfering with the action of Platelets - which are factors in the blood that affect coagulation, clotting and hemostasis. In response to injury, platelets begin to stick to each other and to the sides of the injured tissue to form a plug, blocking further blood loss. Aspirin has also been shown to inhibit the development of arthrosclerosis. Because of its benefits, aspirin is recommended for many heart and stroke patients (Hamby, R D’Agostino, R, 2005 ).
Numerous studies have shown that patients who take an aspirin within 30 minutes after their heart attack begin to limit the damage of the attack. In the second international study of Infarct Survival ( ISIS-2), asprin was found to be nearly as effective as streptokinase, reducing 30-day mortality 23% in 17,000 patients with acute MI (Berger & Orford, 2004).
It is said that chewing aspirin rather than swallowing a tablet whole achieves a faster effect ( Hamby, R D’Agostino, R, 2005 ).
There is 25% reduction in death, nonfatal re-infarction and stroke in patients who are maintained on prolonged Asprin post Myocardial Infaction ( Berger & Orford, 2004 ).
Much of our cardiovascular disease is preventable. Certain factors can increase your risk for heart disease and stroke. Some of these factors you cannot change (referred to as “nonmodifiable risk factors”), and some you can change to reduce your risk (referred to as “modifiable risk factors”)
( Medline Plus ) As a rule the more risk factors you have, the greater your risk for developing heart disease or stroke ( Jaggi, H Kearns, E, 2004 ).
As is with most people Mr T had some of the above risk factors ( as indicated below ) which were addressed within hospital and at the cardiac rehab classes he attended once he was discharged from hospital
Non-modifiable risk factors are things that you cannot change. These include: Age, gender, family history. Mr T certainly had family history, age and the fact that it is males >45years who are more at risk of coronary artery disease ( Jaggi, H Kearns, E, 2004 ).
Modifiable risk factors are things that you can alter by changing your lifestyle or taking medications to assist in reducing your cardiovascular risk. These include: Smoking, cholesterol, blood pressure, physical inactivity, obesity and diabetes ( Jaggi et al ). Only some of these modifiable risk factors pertained to Mr T. He never smoked with only social alcohol consumption. His diabetes, mild obesity, physical inactivity and stress levels were something Mr T had control over. These issues would be addressed at a later point eg cardiac rehabilitation and with his GP
On admission to Coronary Care Unit via ECC Mr T was diagnosed as having had a Non – ST – Elevated Myocardial Infarction ( NSTEMI ).A non stemi is a syndrome in which the symptoms of coronary artery and ischemic heart disease increase in frequency. This occurs because the heart muscle is starved of needed oxygen. It is difficult to distinguish between unstable angina and a NSTEMI based on symptoms alone. The differentiating feature is that patients with NSTEMI have abnormal blood enzymes ( Troponin – discussed below ) proving that a heart attack has occurred. For many patients, it takes 6-12 hours to complete a series of blood enzyme tests to diagnose a NSTEMI ( Levin, 2000 ).
Mr T’s blood results were:
- ( Peak Troponin - 0.22 )
Troponin is a protein that is released into the blood stream as a result of myocardial damage. It isn’t present in healthy people so even minute amounts indicate damage ( WDHB Protocols ).The troponin test is usually ordered when a patient first comes into the emergency room – as did occur with Mr T. It is ordered again at 6 and 12 hours ( Peaking at 12 hours ) to assess trends of the enzyme. (American Association for Clinical Chemistry). It also is done to separate it from chest pain that may be due to other causes eg heart failure, stroke, pulmonary embolus, sepsis, myocarditis – to only mention a few ( WDHB Protocols – author unknown ).
- ( Creatinine Kinase - CK - 188 )
CK is located in skeletal muscle and is not specific for myocardial injury. CKMB is more specific to cardiac muscle and usually dissipates in 1 to 3 days. Elevations thereafter are indicative of another event – as was the case with Mr T ( American Association for Clinical Chemistry ).
LOOK up other blood results such as K
Sinus Rhythm ( SR ) with inverted T-Waves in Antero-Lateral Leads (later to become ST Elevation in these same leads ).
According to Palatnik ( 2001 ) heart rate and blood pressure depend greatly on a balance between the sympathetic and the parasympathetic responses of the autonomic nervous system. Understanding how cardiac drugs work in the body allows you to anticipate ordered treatments and accurately assess your patients response to them.
Palanik goes on to say that if a patient has ACS ( Acute Coronary Syndrome ) shae has cardiac ischemia which is often associated with atherosclerosis. When a arthrosclerotic plaque ruptures or is disrupted platelets adhere to it signalling other platelets to adhere to it – thus a clot forms.Depending on the size of the clot blood supply to the heart muscle distal to the occlusion may be completely or partially cut off causing a MI or ischemia.
There is a plethora of drugs and treatments given to improve blood flow and oxygenation to the heart ( about to be discussed ). These drugs are given to increase and/or decrease cardiac output. Look up SAAB
Mr T on admission to CCU was commenced on Clexane as well as a cocktail of other medications.
Mr T was given 4 doses of Clexane – within a 48hour period.
Clexane also known as Enoxaparin is a medicine known as a low molecular weight heparin. Heparin consists of chains of polysaccharides of varying lengths – Clexane being a low molecular weighted heparin has short chains of polysaccharides and the unfractioned heparin has longer chains and therefore parameters must be monitored very closely to prevent over- or under-anticoagulation.
It is an anti-clotting or anticoagulant medicine, and works by interfering with the body's natural blood clotting mechanism (Rutherford et al ).
It is used as prophylaxis in situations that lead to a high risk of thrombosis. Clexane inactivates a compound in the clotting pathway called thrombin thus preventing the formation of blood clots – thrombosis. Blood clots are dangerous as they can travel in the blood vessels and potentially block off blood supply to the heart, lungs and/or brain
… so Mr T was given the clexane to reduce his risk of thrombosis
Research shows that subcut Clexane given at least for 48hrs before Angiogram/PCI with out additional unfractionated or low molecular weighted heparin during or after Angio/PCI was both safe and effective in high risk patients ( Zhonghua, 2003 ).
- Commenced on a ACE Inhibitor.
Ace-Inhibitors block an enzyme in the body that is necessary to produce a substance that causes blood vessels to tighten. As a result, they relax blood vessels. This lowers blood pressure and increases the supply of blood and oxygen to the heart ( Medline Plus ). A meta-analysis of trials has confirmed that ACE Inhibitors improve survival when given both early and late after MI. Giving the ACE Inhibitors early gave a much larger mortality at 1 year of 32%, with only half as much benefit derived from late administration, more than 48 hours post MI. However, it was shown that the benefits of late therapy did increase with extended follow up, with 25% reduction in 2-year mortality and 24% reduction in a 3 year mortality ( Rodrigues, 2003 ).
Overall, results demonstrated that the use of ACE inhibitors following MI was associated with a 30% reduction in mortality among all patients, including those with clinical evidence of heart failure ( Rodrigues, 2003 ).
Beta-blockers block the effect of the sympathetic nervous system, that is they block the effect of the hormone adrenaline so that the heart rate is reduced, myocardial contractility is reduced , systemic blood pressure is lower and myocardial workload is reduced by way of reducing the hearts need of oxygen and improves the blood supply to the heart muscle. They also reduce the risk of ventricular arrhythmias especially post MI. Research shows by way of the Miami Trial that patients treated early with beta-blockers had lower rates of re-infarction and recurrent ischaemia
( Herlitz, ? date ).
No beta-blockers were given as yet to Mr T’s due to his pulse rate being 45bpm – we did not want his heart rate to go even lower than it was.
Mr T was also:
Because of Mr T’s presenting symptoms it was detemined that a Coronary angiogram was necessary. So therefore Mr T was: ( FIND A REFERENCE FOR THIS )
- Consented for in patient Angiogram.
An angiogram is an x-ray image of blood vessels after they are filled with a contrast medium. A coronary angiogram is the "gold standard" for the evaluation of coronary artery disease and can be used to identify the exact location and severity of CAD ( Lee, 2005 ).
Although the above picture is not a film of Mr T’s arteries this is to show how occluded his arteries were. Results to be discussed later.
- Also seen by Cardiac Nurse Specialist re Cardiac Rehabilitation
The New Zealand Heart Foundation believes that cardiac rehabilitation and secondary prevention programmes should be made available to every patient that has had a MI, CABG, Angioplasty and/or any other cardiac event. Mr T was referred to our Cardiac Nurse Specialist and was present at the rehabilitation classes post admission. I, also was present at one where Mr T was present.
Two days days later Mr T was transferred to the ward while he was waiting for his inpatient angiogram. It was at this point I became involved with his care and just happened to be the nurse looking after him on the day when he had his next cardiac event.
Another 2 days went by ( now his 4th day in hospital ) and Mr T developed 4 -5/10 central chest pain. He appeared pale and clammy. Chest Pain management protocols ( WDHB ) were adhered to. There were no acute changes on the ECG and observations were stable. His pain dropped to 2-3/10 - his blood pressure and pulse were low. Only 1 spray of GTN was given due to sensitivity to GTN in CCU (bradycardia). Five minutes later this patients pain developed into 9/10 central chest pain. The ECG showed 3 – 4mm ST Elevation in the anterior and inferior leads and his pulse rate was noted to be @ 40bpm. Pain relief ( Morphine ) given - 16mg in total by the time he was again painfree.
Morphine is a potent narcotic. The term narcotic is derived from the greek word narkotikos, meaning “benumbing or deadening” ( Wikipedia,2006 ) and its primary use is in the management of moderately severe and severe pain.
Mr T was then transferred back to CCU with a Antero-Lateral STEMI. As indicated above Mr T had 3 – 4mm ST Elevation in the anterior and inferior leads.
ST Segments is a transient period where no further electrical current can be passed through the myocardium and is measured from the end of the S Wave to the beginning of the T Wave. ST segment elevation can represent anything from a potentially life threatening condition to a normal variation, thus making it very important to diagnose what the cause of the ST Elevation is. Prompt diagnosis and treatment is essential ( Houghton & Gray, 2003 ).
Part of the treatment for acute myocardial infarction is thrombolysis. However, one has to determine whether thrombolysis is indicated:
According to ( WDHB Protocols ) indications for thrombolysis is
- patients experiencing prolonged chest pain >30 minutes
- ECG changes: significant ST Elevation
- 2mm chest leads in 2 or more continuous leads
- 1mm limb leads in any 2 continuous leads
- New onset LBBB
On going 8-9/10 Pain
Bradycardia - Secondary to ischaemia
Pathophysiology of a Myocardial Infarction
The most common cause of an MI is narrowing of the coronary blood vessels due to arthrosclerotic plaques. Atherosclerosis — a disease in which fatty material is deposited on the wall of the arteries. This fatty material causes the arteries to become narrow and it eventually restricts blood flow.
( National Women's Health Information Centre ). When the plaque ruptures, platelet aggregation occurs and a thrombus forms. This results in partial or complete occlusion of the vessel and the ensuing myocardial ischemia occurs. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial death, but reperfusion within this period can retrieve the myocardium and reduce morbidity and mortality (Stahmer, 2005 )
Allergy Status – Intolerant to beta-blockers ( severe bradycardia)
- Hytrin ( Terazosin ) 5mg PO Nocte
- Candyl-D ( Piroxicam ), 10mg PO Daily
- Losec ( Omeprazole ) 20mg PO Daily
- As above – as well as
- Asprin - Enteric Coated 100mg PO Daily
- Simvistatin ( Lipex ) 40mg PO Nocte
- Cilazapril 1mg PO Daily
- Clexane (S/C) 12 hourly 100mg
- Metformin 250mg PO twice daily
- Non-Regular PRN Medications
- GTN Spray
- Morphine 2.5 – 5mg Q1/2Hrly/PRN
- Maxalon 10mg Q6hrly/PRN
- Paracetamol 1gm Q4hrly/PRN
- Mylanta Suspension 20mls TDS/PRN
- Hytrin 50mg PO Nocte 1 Month
- Candyl-D 10mg PO Daily 1 Month
- Losec 20mg PO Daily 1 Month
- Asprin EC 100mg Daily 1 Month
- Simvistatin 40mg PO Nocte 1 Month
- Cilazapril 1mg PO once daily 1 Month
- Metformin 250mg PO BD 1 Month
- GTN 400mcg/1 Dose Sublingual Spray, 1 - 2 Puffs, SL PRN, 1 Month
Hay,DR, Cardiovascular Disease in New Zealand 2004. Technical Report No 82, October 2004
National Heart Foundation
Zhonghua Nei Ke Za Zhi ( 2003 ) The Safety and Efficacy of pre-treatment With Enoxaparin In Acute Coronary Syndrome Patients Undergoing Percutaneous Coronary Intervention; 42(2):91-3
Teasdale G., Jennett B., LANCET (ii) 81-83, 1974
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FLORIDA INSTITUTE FOR NEUROLOGIC REHABILITATION, INC
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, D.O., FACC
Houghton, A R Gray, D ( 2003 ) Making Sense of the ECG – A Hands on Guide 2nd ed, London, Arnold.
Levin, T ( 1999 – 2000 ) West Suburban Cardiologists, Ltd
Stahmer, S ( 2005 ) Myocardial Infarction
Picture Gallery of emedicine.com
American Association for Clinical Chemistry ( 2001–2006)
Jaggi, H Kearns, E ( 2005 ) Risk Factors in Coronary Artery Disease, Missouri
Coronary Artery Disease Risk Factors
Lee, D ( 2005 ) Coronary Angiogram
National Heart Foundation - Cardiac Rehabilitation
Definition of Informed Consent
Berger, P B, Orford, J L ( 2004 ) Acute Myocardial Infarction
Few would argue that prompt reperfusion improves survival in patients with suspected STEMI. The problem is: which reperfusion therapy is best – surgery, thrombolytic therapy, or primary catheter-based intervention? While the debate continues, so do studies indicating that reperfusion therapy is underutilized and often not administered soon after presentation.
Title: Thrombolysis: How and Who in 2005?
Interviewee: Dr. Freek W. A. Verheugt
Interviewer: Magnus Ohman, MD
Herlitz, J Karlson, BW Hjalmarson, A
Retrieved on 16.02.06
Taylor, M ( 1995 ) Nursing Partnership: A Model for Nursing Practice, in Beginning Journeys, Christchurch Polytechnic.
Christensen, J ( 1990 ) Nursing Partnership: A Model For Nursing Practice. Daphne Brasell Associates Press, Wellington.
Rodrigues, E ( 2003 ) Meta-Analysis of Trials of Ace Inhibitors. American Journal of Medicine; 115: 473 – 479.
Watson, J. ( 1988 ) Nursing: Human Science and Human Care ( pp. 32 – 33 ). New York, NY:National League for Nursing.
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This is an extremely well researched case study. 1. The referencing is good and the inclusion of information from primary sources excellent. 2. The report is well structured though its subheadings. 3. The use of key terms is outstanding. 4. Avoid the use of running commentaries. *****