1. Chapter 21: Acute Myocardial Infarction

2. Pathophysiology of Atherosclerosis
Endothelium of artery is damaged
3 known causes:
High cholesterol and triglycerides
Hypertension
Cigarette smoking
Unsmooth lining attracts cholesterol, calcium, fibrin
Atheroma
Decreased blood flow
Injury to blood vessel attracts WBCs, platelets, smooth muscle cells
Endothelium matrix thickens
Fibrous plaque becomes necrotic
Hemorrhage and calcification
Prone to blockage with thrombosis

3. Collateral Blood Flow

4. Inflammatory Markers Used in Assessment of Risk for Heart Disease
Highly sensitive C-reactive protein (hs-CRP)
hs-CRP <1.0 mg/dL: low risk
hs-CRP 1.0 to 3.0 mg/dL: moderate risk
hs-CRP >3.0 mg/dL: high risk

5. Major Risk Factors for Heart Disease
Nonmodifiable
Age
Sex
Genetic influence
Race
Modifiable
High blood pressure
Cigarette smoking
High cholesterol
Weight and inactivity
Diabetes

6. Contributing Risk Factors
Influence of stress and unhealthy behaviors
Link of alcohol with high BP, heart failure, and stroke
Metabolic syndrome (3 or more factors)
Fasting blood sugar 100 mg/dL or more
HDL <40 mg/dL in males, <50 mg/dL in females
Triglycerides 150 mg/dL or more
Increased waist circumference
BP 130/85 mm Hg or higher

7. Classification System of Angina
Class of Angina
Assessment Findings/ Treatment
Stable angina
(chronic stable, classic, exertional angina)
Chest pain occurs with activity or emotional stress.
Treatment: rest, nitrates
Unstable angina
(preinfarction or crescendo angina)
Chest pain occurs at rest. Pain lasts longer and is more severe than stable angina.
Treatment: emergent; risk for MI, dysrhythmias, cardiac arrest
Variant angina - form of unstable angina
(Prinzmetal’s or vasospastic angina)
Chest pain occurs at rest from midnight to 8 A.M.
Treatment: emergent; usually severe disease in at least one vessel; vasospasms occur near area of blockage

8. Pathophysiology of Angina
O2 demand
O2 supply
Reduced blood flow: 3 Causes
Atherosclerosis (CAD)
Coronary artery spasm
Vessels constrict
Narrowing of vessels
Arterial inflammation
Supply of O2 does not meet demands
Compensatory mechanisms fail
(anaerobic metabolism)
Ischemia occurs
Chest pain develops

9. Pathophysiology of Myocardial Infarction
Change in endothelium of vessel
Mechanism (CAD, spasm, inflammation)
Narrowing of vessel with plaque formation
Plaque ruptures
(Obstructs blood flow to myocardium)
Thrombus formed
Area of ischemia, injury, infarction
(subendocardial layer)
Can spread through thickness of myocardial wall (Necrosis)
Ventricular remodeling

10. Atherosclerotic Plaque in Acute Coronary Syndromes

11. Comparison of Angina and Myocardial Infarction (MI)
Assessment Findings
Diagnostic Test Results
Angina
Chest pain can be relieved with rest and/or nitrates.
Pale, clammy skin
May have tachycardia, hypertension
(ECG): T-wave inversions and ST depression
Dysrhythmias - temporary MI
Prolonged chest pain not relieved with rest or nitrates
Diaphoresis, dyspnea
May have GI symptoms
(ECG): May or may not have ST elevation, Q wave
Elevations in troponin
Dysrhythmias – can be more persistent

12. Evolution of MI

13. Acute Lateral Wall MI See Figure 21-10.

14. Acute Inferior Wall MI See Figure 21-11.

15. Acute Anterior Lateral Wall MI

16. Acute Right Ventricular MI

17. Biochemical Markers Used to Diagnose MI
Creatinine kinase (CK-MB)
Appears 3 to 12 hrs after MI
Peaks in 24 hrs after MI
Returns to normal 48 to 72 hrs after MI
CK-MB2 to CK-MB1 ratio is >1
Troponin
Troponin T
Troponin I

18. Question
A client is admitted with a diagnosis of rule out MI. Which diagnostic test will provide the most specific information that the client has had a MI? A. Myoglobin level B. CK-MM level C. Troponin T and I levels D. Total CK level 18

19. Answer
C. Troponin T and I levels Rationale: The most specific test for MI is troponin T and I. Myoglobin is released earlier than CK from ischemic muscle but is not specific to the myocardium, so it is not specific for the diagnosis of MI. Myoglobin is also released from skeletal muscle. CK-MM bands are specific to skeletal muscle. CK-MB is specific to myocardial muscle. The overall CK level is influenced by muscle damage anywhere in the body. 19

20. Caring for the Patient Receiving Thrombolytic Therapy
Establish 2 or 3 18-gauge peripheral IV lines.
Assess for signs of reperfusion:
Chest pain resolves
ST segments return to normal
Reperfusion dysrhythmias
Monitor for complications:
Internal bleeding
Symptoms of reocclusion of coronary artery

21. Question
A client just received thrombolytic therapy for an acute inferior wall MI. Which of the following assessment findings suggest that the client is experiencing reperfusion? A. Bouts of ventricular tachycardia on the monitor B. Chest pain rated 3/10 C. Elevated ST segments in leads II, III, aVF D. Decrease in level of consciousness

22. Answer
A. Bouts of ventricular tachycardia on the monitor Rationale: Reperfusion dysrhythmias include ventricular tachycardia, accelerated idioventricular rhythm, and AV heart block. Other signs of reperfusion include absence of chest pain, normal ST segments, and hemodynamic stability (mentation is clear and vital signs are stable). Decreased level of consciousness could be a sign of internal bleeding into the brain. Other signs of a bleed into the brain might include a severe headache and seizures.

23. Caring for the Patient After an Acute MI
Maximize cardiac output and minimize cardiac workload
Cardiac monitor with ST-segment monitoring
Lead selection according to area of damage
Serial ECGs and serial cardiac biomarkers
Pulse oximetry and oxygenation
NPO until pain-free
Avoid Valsalva maneuver

24. Caring for the Patient After an Acute MI (cont.)
ACE inhibitors within 24 hrs
Anterior wall MI
Pulmonary edema
Ejection fraction <40%
Maintain blood glucose in normal range
Correct electrolyte imbalances
IV beta-blocker followed by oral therapy
Anticoagulation for high-risk patients

25. Cardiac Rehabilitation
Education and counseling
Risk factor modification
Smoking cessation
Diet
Weight management
Exercise program
Monitored
Maintenance

26. Question
24 hours after an acute MI, a client develops a new-onset loud holosystolic murmur with a thrill palpated at the parasternal area. The nurse recognizes that this is most likely _________ and the first action is to _________. A. Cardiogenic shock; improve oxygenation B. Left ventricular wall rupture; institute life-support measures C. Ventricular septal wall rupture; give fluids and inotropic support D. Pericarditis; give anti-inflammatory agents 26

27. Answer
C. Ventricular septal wall rupture; give fluids and inotropic support Rationale: The client with a ventricular septal wall rupture will have a loud holosystolic murmur with a thrill palpated at the parasternal area and worsening dyspnea, tachycardia, and pulmonary edema. The oxygenated blood in the left ventricle is being shunted to the right ventricle. The client needs fluid and inotropic support and afterload reduction to buy time until an emergent angiogram and surgery can be done. The client may need IABP. The other answers are correct for the specific complication given, but the symptoms do not match this scenario. 27