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Myocardial Infarction

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Group AMI

on 23 April 2015

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Transcript of Myocardial Infarction

Affect the action potential of cardiac cells to restore normal rate and rhythm
Myocardial Infarction
The Case
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.

Atherosclerosis
John's past history related to Myocardial Infarction
Normal vs Dysfunctional state
Pathophysiology
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
Diabetes
Hypertension
Smoking
Pathophysiology
-Feeling of indigestion
Presentation by Ann, Eunjin, Pasha and Sherin
Diabetes
Smoking
Hypertension
Higher risk of heart disease
Changes blood vessels
Tobacco components
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
S-T segment of normal people
Normally the
S-T Segment
is flat
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
Potential Complications
Dysrhythmias
Further Myocardial Infarction
The S-T segment is a crucial sign on figuring out the state of an MI.
Investigations
pathological Q waves, results from the absent of electrical activity (scar)

ECG
Serum Cardiac Markers
ST elevation
T waves are large and symmetrical then inverted
www.studyblue.com
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 ?
dysfunctional state
Chronic stable Angina?
Difficulty in breathing/ Shortness of Breath
Tachycardia
Heart Failure
Drugs that affect blood coagulation : Management of MI
Antiplatelets
Anticoagulants
Thrombolytics
Prevent of unwanted thrombus formation by decreasing the platelet aggregation;
Anti platelet Agents
Clopidogrel
Prevent clot formation and extension
Anticoagulant Agents
Heparin
Warfarin
Works on the resolution of clots
decreased mobility

PCI complications

drugs adverse reactions
Decreased Mobility/Activity Intolerance/Immobility

- IDC complications

- pressure sores
- pneumonia
-loss of muscle mass
- decreased in cardiac reserve
- constipation
- UTI
Percutaneous Coronary Intervention (PCI) complications
dissection of the newly dilated coronary artery
rupture of coronary artery
cardiac tamponade
Ischeamia and infarction
decreased CO
coronary spasm
Abrupt closure
Restenosis
death
respiratory depression
Bradypnoea
hypoxia
Nausea and vomiting
headache
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
Thrombolytic agent:
Tenecteplase
Prevention of Reinfarction
Beta-blockers
-Metoprolol: short term 3 to 10 days after MI
-Propranolol: Long term 1-4 week after MI

Antiarrythemic agent
-Lignocaine
Antihypertensive agents
Treatment for hypertension; Lowering the degree of hypertension lowers the risk of developing MI
-ACE inhibitors:

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


REFERENCES
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?.
Retrieved from
http://www.nhlbi.nih.gov/health/health-topics/topics/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

Nursing Diagnosis
Evidenced by-
Ineffective cardiopulmonary tissue perfusion related to reduced coronary blood flow from coronary thrombus & atherosclerotic plaque
chest pain
HR, dyspnea
nausea, diaphoresis
Intervention-
Assess & document vitals
Chest pain (location, intensity, duration)
ECG
Rationale-
To determine cause & effect
To provide a baseline
Intervention
Assess the effect of chest discomfort on CV perfusion
to heart, brain & kidneys
Rationale-
CO & organ perfusion
MI myocardial contractility
Arrhythmia
Intervention-
Obtain a 12 lead ECG
Rationale-
Useful in the diagnosis of an extension of MI
Intervention-
Administer medication therapy
Rationale-
First line of defense in preserving myocardial tissue
Oxygen- supply to myocardium
Antithrombotics- prevent thrombus formation
Thrombolytics- clot busters
GTN- dilate coronary arteries
Nursing Diagnosis-
Acute pain related to tissue ischaemia
Evidenced by-
Radiating chest pain
Facial grimacing
changes to LOC
BP & pulse changes

Intervention-
Characteristics of pain, grimaces,
BP & HR changes
Rationale-
Pain triggers stress response
Release of stress induced catecholamines
HR & BP
Interventions-
Deep & slow breathing
Distraction techniques
Visualisation techniques
Rationale-
Helpful in perception of pain
Sense of control over situation
in attitude.
Intervention-
Administer pain medication
Rationale-
To decrease sympathetic stimulation
Morphinesulfate/ meperidone
Medical Intervention-
Suspected AMI referred to PCI
Open occluded artery- promote reperfusion.
Need for Cardiac catheterisation and staff.
Preparation for procedure

PCI- Percutaneous Coronary intervention
Nursing Diagnosis
Activity intolerance related to imbalance between oxygen supply and demand.
Evidenced by-
Changes in BP & HR with activity/exertion
Interventions-
Encourage rest initially.
Limit activity on basis of pain
Rationale-
myocardial workload & consumption
Reduces risk of complications
Intervention-
Cardiac rehabilitation program
Rationale-
Provides continued support & additional supervision
Recovery and well ness process
Nursing Diagnosis-
Impaired gas exchange related to fluid overload
Evidenced by-
Crackles & changes in breath sounds
SOB

Intervention-
Maintain a Fluid Balance Chart
Rationale-
Helps determine excess fluid volume
CO impaired kidney function
urine output
Intervention-
Administer diuretics
Rationale-
To correct fluid overload
UR Number: 1987102
Name: John Smith
D.O.B: 12/07/1964
Address: 42 Wallaby Way, Sydney.
Pharmacological interventions
Aspirin
Intervention-
Position client with head of bed elevated/Semi fowlers position
Rationale-
Reduces oxygen demand
Promotes lung expansion
Onset-Immediate
Onset-about 3 days
Antiplatelet Anticoagulant Thrombolytic
Contraindications





Adverse effects

Safety



Monitoring


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
Bleeding, Dyspnoea
Bleeding
Bleeding, Arrhythmia
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
Platelet level
Blood test
Vital signs,
Occurrence if cardiac arrhythmia

Contraindications



Adverse effects



Safety



Monitoring
Beta-Blockers
Hypersensitive to drug
An individual with bradycardia
NSQHS
Bradycardia, heart failure, rash, fatigue, hypoglycaemia
Always check apical pulse rate before administering drug
BGL
(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)
Catropril,Trandolapril
Beta-blockers
Yes! End of presentation!
Managing Potential complications
Sherin
Ann
Pasha
Eunjin
THANK YOU FOR LISTENING TO OUR PRESENTATION!
Arrhythmia
Hypertension
:(
imaginary 5th member
Prevent reinfarction by the supression of myocardial oxygen demand for a prolonged period
Treat hypertension
excitability of heart

CO

cardiac oxygen consumtion
lOWERS
BP
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
Full transcript