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Transcript of Myocardial Infarction
John is a 51 year old Salesman.
He was presented to ED with a one hour history of severe ongoing chest pain, as well as back, jaw and other areas of the upper body. As well as SOB.
When John started having chest pains, he took GTN to try to control the symptom but due to the severity of the chest pain his wife immediately called EMT.
John has had a previous case of MI and therefore has medication to
control and manage his symptoms.
John has history of diabetes, atherosclerosis and hypertension. He was previously a smoker.
John's family history includes a mother who had died from a myocardial infarction.
John's past history related to Myocardial Infarction
Normal vs Dysfunctional state
1. Cardiomycocytes in the heart
2. Plaque build up in the artery
3. Blood rushes and pumps faster
4. Rupture of plaque causes a thrombus
5. Interrupt the blood flow to the heart
6. Sends pain signals to the brain
7. Clot grows
8. Release of hormone known as adrenaline
9. Cardiomycocytes begin to die
10. Heart compensates
11. Leakage of protein called Troponin
12. Reach Hypoxia and ischemia
-Feeling of indigestion
Presentation by Ann, Eunjin, Pasha and Sherin
Higher risk of heart disease
Changes blood vessels
Body's response to smoking
Study shows smoking causes an increase of thrombus formation
Combination of HT and Diabetes
Increases risk of atherosclerosis
Force against arterial walls
S-T segment of normal people
S-T Segment elevation
Patient suffers with chest pain, difficulty in breathing, excessive sweating and syncope (sudden loss of consciousness).
Indicated area of injury
Amount of heart muscle damage
First sign of coronary occlusion
Isoelectirc section of ECG because it represents interval between ventricular depolarization and repolarization.
What is a S-T Segment
Further Myocardial Infarction
The S-T segment is a crucial sign on figuring out the state of an MI.
pathological Q waves, results from the absent of electrical activity (scar)
Serum Cardiac Markers
T waves are large and symmetrical then inverted
Creatinine Kinase (CK)
normal level: 25-200 U/L
in AMI: >200 U/L
Cardiac Troponin I (TnI)
very specific for cardiac injury
normal level: <0.08ug/L
Myocardial necrosis: level > 0.08ug/L
NSTEMI/ unstable angina ?
STEMI/ AMI ?
Chronic stable Angina?
Difficulty in breathing/ Shortness of Breath
Drugs that affect blood coagulation : Management of MI
Prevent of unwanted thrombus formation by decreasing the platelet aggregation;
Anti platelet Agents
Prevent clot formation and extension
Works on the resolution of clots
drugs adverse reactions
Decreased Mobility/Activity Intolerance/Immobility
- IDC complications
- pressure sores
-loss of muscle mass
- decreased in cardiac reserve
Percutaneous Coronary Intervention (PCI) complications
dissection of the newly dilated coronary artery
rupture of coronary artery
Ischeamia and infarction
Nausea and vomiting
Cazzolli, P. A. (1999), ALS Care Project.
Preventing and Treating Complications of Immobility in Peole with ALS
. Retrived from http://www.alscareproject.org/
Chisholm Institute (Ed.). (2012). HLT51607 Medical/Surgical Nursing (Version 2)
Brown, D., & Edwards, H. (2009). Lewis's medical-surgical nursing: assessment and management of clinical problems (2nd ed.). Australia: Luisa Cecotti
Prevention of Reinfarction
-Metoprolol: short term 3 to 10 days after MI
-Propranolol: Long term 1-4 week after MI
Treatment for hypertension; Lowering the degree of hypertension lowers the risk of developing MI
Lisa, M & Sanja, M (2012). Nursing & midwifery drug handbook (6th ed).
Lisa, M & Sanja, M (2012). Austraila New Zealand Nursing & midwifery drug handbook (6th ed). NSW:Sydney, Lippincott Williams & Wilkins
Lisa, M & Anecita, L (2014). Mckenna's pharmacology for nursing and health professionals (2nd ed). NSW:Sydney, Lippincott Williams & Wilkins
Cohen, B. J. (2012).
Memmler’s The Human Body in Health and Disease (
12th Ed). Philadelphia, PA: Wolters Kluwer Health.
Klabunde, R. E. (2007).
The Pharmacologic Treatment of Myocardial Infarction
. Retrieved from http://www.cvpharmacology.com/clinical%20topics/myocardial%20infarction
Gibbons, G.H. (2014).
What is Atherosclerosis?.
Global Diabetes Community UK (n.d)
Diabetes and Heart Disease
. Retrieved from http://www.diabetes.co.uk/diabetes-complications/heart-disease.html
Cleveland Clinic (2014)
. Diseases and Conditions: High Blood Pressure and Heart Attack.
Retrieved from http://my.clevelandclinic.org/health/diseases_conditions/hic_Hypertension_High_Blood_Pressure/hic_High_Blood_Pressure_and_Heart_Attack
Bolooki, H. M., & Askari, A. (2010). Acute Myocardial Infarction. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/acute-myocardial-infarction/Default.htm
Chiariello, M., & Indolfi, C. (1996). Circulation.
Silent Myocardial Ischemia in Patients With Diabetes Mellitus
. 93, 2089-2091. doi: 10.1161/01.CIR.93.12.2089
Nesto, R. W., & Zarich, S. (1998). Circulation.
Acute Myocardial Infarction in Diabetes Mellitus
. 97, 12-15. doi: 10.1161/01.CIR.97.1.12
Creager, M. A., Luscher, T. F., Cosentino, F., & Beckman, J. A. (2003). Diabetes and Vascular Diease.
Pathophysiology, Clinical Consequences, and Medical Therapy: Part I
. 108, 1527-1532. doi: 10.1161/01.CIR.0000091257.27563.32
Litton, K. (2002).
Left vs. Right Ventricular MI: Which is it?
Retrieved from http://www.modernmedicine.com/modern-medicine/content/left-vs-right-ventricular-mi-which-it?page=full
Kulick, D. L., Marks, J.W., & Davis, C. P. (2014)
. What are the complications of a heart attack?
Retrieved from http://www.medicinenet.com/heart_attack/page6.htm
Grasso, A. W., & Brener, S. J. (2014).
Complications of Acute Myocardial Infarction
. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/complications-of-acute-myocardial-infarction/Default.htm
Tidy, C. (2014).
Complications of Acute Myocardial Infarction.
Retrieved from http://www.patient.co.uk/doctor/complications-of-acute-myocardial-infarction
Primary Nursing Goals
Promote pain relief
Promote adequate oxygenation & tissue perfusion, decrease myocardial workload
Promote comfort, relief from anxiety
Ineffective cardiopulmonary tissue perfusion related to reduced coronary blood flow from coronary thrombus & atherosclerotic plaque
Assess & document vitals
Chest pain (location, intensity, duration)
To determine cause & effect
To provide a baseline
Assess the effect of chest discomfort on CV perfusion
to heart, brain & kidneys
CO & organ perfusion
MI myocardial contractility
Obtain a 12 lead ECG
Useful in the diagnosis of an extension of MI
Administer medication therapy
First line of defense in preserving myocardial tissue
Oxygen- supply to myocardium
Antithrombotics- prevent thrombus formation
Thrombolytics- clot busters
GTN- dilate coronary arteries
Acute pain related to tissue ischaemia
Radiating chest pain
changes to LOC
BP & pulse changes
Characteristics of pain, grimaces,
BP & HR changes
Pain triggers stress response
Release of stress induced catecholamines
HR & BP
Deep & slow breathing
Helpful in perception of pain
Sense of control over situation
Administer pain medication
To decrease sympathetic stimulation
Suspected AMI referred to PCI
Open occluded artery- promote reperfusion.
Need for Cardiac catheterisation and staff.
Preparation for procedure
PCI- Percutaneous Coronary intervention
Activity intolerance related to imbalance between oxygen supply and demand.
Changes in BP & HR with activity/exertion
Encourage rest initially.
Limit activity on basis of pain
myocardial workload & consumption
Reduces risk of complications
Cardiac rehabilitation program
Provides continued support & additional supervision
Recovery and well ness process
Impaired gas exchange related to fluid overload
Crackles & changes in breath sounds
Maintain a Fluid Balance Chart
Helps determine excess fluid volume
CO impaired kidney function
To correct fluid overload
UR Number: 1987102
Name: John Smith
Address: 42 Wallaby Way, Sydney.
Position client with head of bed elevated/Semi fowlers position
Reduces oxygen demand
Promotes lung expansion
Onset-about 3 days
Antiplatelet Anticoagulant Thrombolytic
Significant bleeding tendency
Significant bleeding tendency
Significant bleeding tendency
hypersensitive to drug
hypersensitive to drug
hypersensitive to drug
Should not be given if Hypertension is uncontrolled
Caution if given with other antiplatelet agent, anticoagulant or thrombolytic
Caution if heparin given with oral anticoagulants
Caution if given with antiplatelet agents, or anticoagulant
Occurrence if cardiac arrhythmia
Hypersensitive to drug
An individual with bradycardia
Bradycardia, heart failure, rash, fatigue, hypoglycaemia
Always check apical pulse rate before administering drug
(Mentioned throughout presentation-written form)
Clinical Handover- Case study and presented condition
Patient identification- Check UR number and ensure correct patient
Medication safety- Correct procedure in medication administration (monitoring vitals)
Yes! End of presentation!
Managing Potential complications
THANK YOU FOR LISTENING TO OUR PRESENTATION!
imaginary 5th member
Prevent reinfarction by the supression of myocardial oxygen demand for a prolonged period
excitability of heart
cardiac oxygen consumtion
Matt, V (2014), Nursing Care Plans. Retrieved from http://nurseslabs.com/7-myocardial-infarction-heart-attack-nursing-care-plans/
Heart and Stroke Foundation, 2015, Percutaneous Coronary Intervention, retrieved from http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3831925/k.4F32/Heart_disease__Percutaneous_coronary_intervention_PCI_or_angioplasty_with_stent.htm
Maureen, F., Suzanne, C., & Brenda, G., (2005), Smeltzer & Bare's Textbook of Medical Surgical Nursing (1st ed). Australia, Lippincott Williams & Wilkins
last 1-14 days
>13 days: may develop ventricular aneurysm