1. Chapter 28 Management of Patients With Myocardial Infarction
Dr. Maysoon S. Abdalrahim

2. Pathophysiology: Myocardial Infarction
Unstable angina
rupture of an atherosclerotic plaque  reduced blood flow in a CA (not completely occluded)  preinfarction angina.
Myocardial infarction
plaque rupture and thrombus formation Myocardial ischemia (complete occlusion of CA)  an area of the myocardium is permanently destroyed  myocardial death

3. Pathophysiology: Myocardial Infarction
Other causes of MI= intense imbalance between myocardial O2 supply and O2 demand
Vasospasm of a CA
decreased O2 supply (bleeding, anemia, or low BP)
Increased O2 demand (tacky cardia, thyrotoxicosis, cocaine)

4. Pathophysiology: Myocardial Infarction
The area of infarction develops over minutes to hours.
“time is muscle”: the urgency of appropriate treatment to improve patient outcomes.
The ECG identifies the type (STEMI, NSTEMI)and location of the MI(ant- inf- post- lat), and the timing (acute- evolving- old).
the goals of therapy are to prevent or minimize myocardial tissue death and prevent complications

5. Clinical Manifestations: Myocardial Infarction
Chest pain
sudden and continuous despite rest and medication
Patients may have sympathetic NS symptoms
shortness of breath
indigestion, nausea
Anxiety
cool, pale, and moist skin
Tachycardia-tachypnea

6. Diagnostic Findings: Myocardial Infarction
Patient History
The symptom
History of previous cardiac and other illnesses
Family history of heart disease.
The risk factors for heart disease

8. Diagnostic Findings: Myocardial Infarction
Electrocardiogram
For diagnosing an acute MI.
It should be obtained within 10 minutes from the time a patient reports pain or arrives in the ED.
serial ECG changes over time, the location, and resolution of an MI.
The classic ECG changes are
T-wave inversion
ST-segment elevation
an abnormal Q wave

9. Electrocardiogram :indicators
First myocardial injury signs in ECG is peaked T wave.
Then ST elevation more than 1 mm above isoelectric line in two contiguous leads.
Then ST depression or T inversion
Q wave develop within 1-3 days(0.04sec- 5mm-25% R wave).
Poor R wave progrossion

10. Diagnostic Findings: Myocardial Infarction
patients are diagnosed with one of the forms of ACS:
Unstable angina : typical symptoms, but ECG & cardiac markers shows no evidence of acute MI.
STEMI: ECG evidence of acute MI(changes in two leads)
NSTEMI: elevated cardiac biomarkers but no definite ECG evidence of acute MI.
During recovery from an MI, the ST segment is the first ECG indicator to return to normal (1 to 6 weeks).
Q-wave changes are permanent.
T large for 24 hr then inverts within 1-3 days to 2 weeks

11. Diagnostic Findings: Myocardial Infarction
Echocardiogram
to evaluate ventricular function when the ECG is nondiagnostic.
Detect hypokinetic and akinetic wall motion
Determine EF%

12. Diagnostic Findings: Myocardial Infarction
Laboratory Tests
Cardiac enzymes and biomarkers to diagnose an AMI.
myoglobin and troponin: analyzed rapidly
Creatine Kinase and Its Isoenzymes: CK-MB increase within a few hrs and peaks within 24hrs
Myoglobin: a heme protein (transport O2). starts to increase within 1 to 3 hrs and peaks within 12 hrs, not very specific for cardiac.
Troponin: a protein regulates the myocardial contraction that have 3 isomers : C, I, and T. (I&T)reliable and critical markers of MI. detected within a few hrs and remains elevated for 3 weeks

13. Diagnostic Findings: Myocardial Infarction

14. Diagnostic Findings: Myocardial Infarction
Cardiac Catheterization(in less than 60 min)

15. Medical Management: Myocardial Infarction
The goals are to minimize myocardial damage, preserve myocardial function, and prevent complications.
These goals are facilitated by the use of guidelines developed by the American College of Cardiology (ACC) and the AHA (Chart 28-7).

17. Medical Management: Myocardial Infarction
Pharmacologic Therapy
aspirin, nitroglycerin, morphine, an IV beta-blocker, and other medications
Patients should continue the beta-blocker throughout hospitalization
LMWH + platelet-inhibiting agents to prevent further clot formation.
NSAIDS may be discontinued because of SE on heart.
Analgesics: morphine in IV boluses :reduce pain& anxiety, preload & afterload, which decrease load on heart & relax bronchioles(↓BP, ↓RR)

18. Medical Management: Myocardial Infarction
Pharmacologic Therapy
Angiotensin-Converting Enzyme Inhibitors (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II BP decreases and diuresis (decrease O2 demand).so check BP-↑K-fluid balance-↓Na-UOP- KFT.
Thrombolytics: IV in a specific protocol (Chart 28-8). The purpose is to dissolve the thrombus in a CA
must be administered within 3 to 6 hours for patients with ECG evidence of acute MI, and should be initiated within 30 minutes of presentation to the hospital (door-to-needle time).

19. Chart 28-8

20. Medical Management: Myocardial Infarction
Emergent Percutaneous Coronary Intervention (PCI)
used to open the occluded CA increase O2 supply.
should be performed within 60 minutes (door-to-balloon time).
Coronary Stent is a tiny wire mesh tube used to prop open an artery during angioplasty. The stent stays in the artery permanently. The stent will also improve blood flow to the heart muscle and will relieve chest pain (angina).

21. Cardiac Rehabilitation: Myocardial Infarction
After the patient with an MI is free of symptoms
education, individual and group support, and physical activity.
The goal: to improve the quality of life.
limit the effects and progression of atherosclerosis
return to work and pre illness lifestyle
enhance psychosocial and vocational status
prevent another cardiac event.

22. Ng diagnoses
Ineffective cardiac tissue perfusion RT reduced coronary blood flow
Risk for imbalanced fluid volume
Risk for ineffective peripheral tissue perfusion RT decreased COP
Anxiety RT cardiac event
Knowledge deficiency about ACS self-care

23. Nursing Interventions: Myocardial Infarction
Relieving Pain and Symptoms of Ischemia
Balancing O2 supply with O2 demand
relief of chest pain is the top priority
O2 by nasal cannula in a rate of 2 to 4 L/min, saturation levels of 96% to 100%
Medication therapy
Vital signs

24. Nursing Interventions: Myocardial Infarction
Relieving Pain and Symptoms of Ischemia
Physical rest in bed with the back elevated to decrease chest discomfort and dyspnea.
Tidal volume improves
Drainage of the upper lung lobes improves.
venous return to the heart (preload) decreases

25. Nursing Interventions: Myocardial Infarction
Improving Respiratory Function
Regular assessment to detect early signs of pulmonary complications.
Monitor fluid volume status to prevent overloading
Encourage deeply breathing exercises
Change position frequently
Pulse oximetry

26. Nursing Interventions: Myocardial Infarction
Promoting Adequate Tissue Perfusion
Bed or chair rest to reduce O2 oxygen demand and remain until the patient is pain free and stable.
check skin temperature and peripheral pulses frequently to monitor tissue perfusion.

27. Nursing Interventions: Myocardial Infarction
Reducing Anxiety
To reduce the sympathetic stress  decrease O2 demand and relieve pain
Develop a trust and caring relationship
Provide information
Ensure a quiet environment, promote sleep, using caring touch, relaxation techniques, using humor, and providing spiritual support
An atmosphere of acceptance
Music therapy and pet therapy

28. Nursing Interventions: Myocardial Infarction
Monitoring and Managing Complications
the Plan of Nursing Care in Chart
monitor the patient closely for changes in cardiac rate and rhythm, heart sounds, BP, chest pain, respiratory status, urinary output, skin color and temperature, sensorium, ECG changes, and laboratory values.
Report rapidly any changes in the patient's condition

29. Nursing Interventions: Myocardial Infarction
Teaching patients self-care.
provide adequate education about heart-healthy living
facilitate the patient’s involvement in a cardiac rehabilitation program