1. acute coronary syndrome ACS
Fall Semester
Nur 221

2. Myocardial Infarction (MI)
myocardium is permanently destroyed. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.
Other causes are vasospasm of coronary artery, decrease O2 supply, increase O2 demand
The term “acute coronary syndrome” includes unstable angina and myocardial infarction.

4. Types of MI:
ST segment elevation, non-ST segment elevation
According to the injury of the ventricular wall ( Anterior, posterior, inferior, lateral)
Point of time in which infarction occur (acute, evolving, old)
C\M:
Chest pain ( sudden, continuous)
S.O.B, indigestion, nausea, anxiety
Cool, pale, moist skin
Increase HR and RR

5. Clinical manifestations
cardiovascular: chest pain or discomfort (sudden, continuous), palpitations (S3, S4) and early onset of murmur. BP elevated due to sympathetic stimulation. ST-segment and T-wave changes. ECG shows tachycardia, bradycardia, dysrthmias.
Resp: SOB, tachypnea, dyspnea, crackles, pulmonary edema may be present.
GI: nausea and vomiting,
Urinary: dec urinary output,
Skin: cool and clammy skin, diaphoretic and pale appearance, dependent edema,
Neurologic: anxiety, restlessness, light headedness, dec contratability and cerebral oxygenations, headache, visual disturbances, altered speech, altered motor function.

6. Assessment and Diagnostic Tests
Pt HX (presenting symptoms, past Hx, family Hx for heart disease, risk factors)
ECG (obtained within 10m pt reported pain or arrives to ER)
Lab test (Myoglobin, Troponin, CK)
Echocardiogram (to evaluate ventricular function& EF)

7. Laboratory tests: Serum markers of acute MI
CK (creatine kinase) with elevation of isoenzymes and lactic dehydrogenaze (LDH) levels, this is used to identify cardiac event.
Creatine kinase and its isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), CK-BB (brain)
CK-MB: is found in cardiac cells and released when damaged to heart occur. Starts to increase a few hours and peak within 24 hours of an MI.
Myoglobin: a heme protein that helps to transport O2 like CK-MB released on cardiac damage; starts to increase 3 hours after MI and then peaks within 12 hours of the onset of symptoms. Not very specific indicator of cardiac event
**Troponin: protein found in cardiac regulated the MI contraction process. Three isomer (C, I, T ), increase at the same time of CK-MB but last for at least three weeks after the symptoms.

9. ECG changes in MI Hyper acute T wave, then inversion of T wave
ST segment elevation
Appearance of abnormal Q wave
In some person no persistent ECG changes, MI diagnosed with cardiac biomarkers.

10. ST Segment
The point at which the ST segment “takes off” from the QRS complex is called the J point
Figure D 10

11. Pt diagnosed with one of the ACS:
The spectrum of ACS is:
USA: C\M of coronary ischemia present, no ECG or biomarkers changes
ST segment elevation MI: ECG changes of acute MI (significant myocardial damage),
Non- ST segment elevation MI: pt biomarker elevated, no ECG changes.

12. Major Goals For Medical Management
Minimize myocardial damage
Preserve myocardial function
Manage complications

13. Pharmacological therapy
Thrombolytic/fibrinolytics:
purpose: dissolve and lyse the thrombus in CA
Indication: less than 6hr’s from onset of pain with ST segment elevation
C\I:
Active bleeding
Hx of hemorrhagic stroke
Recent major surgery
Uncontrolled HTN
pregnancy

14. Nursing interventions with thrombolytic
Minimize number of skin punctures
Avoid IM injections
Start at least 2 IV lines
Monitor for signs and symptoms of bleeding
Monitor for reperfusion dysrhythmias
Monitor for allergic reactions with Streptokinase
Treat bleeding with direct pressure and notify physician

15. Morphine sulfate, IV bolus Used to decrease pain and anxiety
Most used thrombolytic agent: ateplase ( t-PA, Activase), reteplase (r-PA, TNkase)
Analgesic:
Morphine sulfate, IV bolus
Used to decrease pain and anxiety
Reduce preload and afterload, relax bronchiole to enhance oxygenation
S\E: decrease BP and RR
ACE inhibitors:
prevent conversion of angiotesein I to II, thus BP decrease, the kidney excrete Na and fluid, decrease O2 demeaned on the heart
S\E: hypotension, hyponatremia, hypovolemia, hyperkalemia
angiotensin-converting-enzyme inhibitor

16. PCI (percutaneous coronary intervention)
Used to open the occluded coronary artery to promote reperfusion
Effective more than thrombolytic agent
See Chart 27-9
Other treatment CABG

17. PCI (percutaneous coronary intervention)

18. Nursing Process: The Care of the Patient with MI: Assessment
A vital component of nursing care!
See Chart 27-6.
Assess all symptoms carefully and compare to previous and baseline data to detect any changes or complications.
Assess IVs.
Monitor ECG.

19. Diagnosis
Ineffective cardiac tissue perfusion R\T reduced coronary blood flow from coronary thrombus
Risk for imbalance fluid volume
Risk for ineffective peripheral tissue perfusion R\T decrease CO
Death anxiety
Deficient knowledge (post MI self care)

20. Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade

21. Planning Goals include:
the relief of pain or ischemic signs and symptoms,
prevention of further myocardial damage,
absence of respiratory dysfunction,
maintenance of or attainment of adequate tissue perfusion,
reduced anxiety,
adherence to the self-care program,
absence or early recognition of complications.

22. Nursing interventions:
administer medication immediately
Administer O2 therapy (nasal cannula, 2-4 L/min is usually adequate to elevate O2 saturation to %.
Monitor vital signs
Bed rest and elevation of bed to decease tension on heart and drainage of the upper lung lobes improves
Assess resp status
Promote adequate tissue perfusion: limit the patient to bed and chair
Reducing anxiety: reassurance, emotional support