1. Coronary Artery Disease and Acute Coronary Syndrome Myocardial Infarction (relates to Chapter 33, “Nursing Management: Coronary Artery Disease and Acute Coronary Syndrome,” in the textbook)

2. Description
Cardiovascular diseases are the major cause of death in Canada
Heart attacks are still the leading cause of all cardiovascular disease deaths and deaths in general

3. Etiology and Pathophysiology Developmental Stages
Complicated lesion
Final stage in development
The most dangerous
Plaque consists of a core of lipid materials within an area of dead tissue

4. Etiology and Pathophysiology Developmental Stages
Complicated lesion
With the incorporation of lipids, thrombi, damaged tissue, and accumulation of calcium, the growing lesion becomes complex

5. Etiology and Pathophysiology Collateral Circulation
Normally some arterial branching, termed collateral circulation, exists within the coronary circulation

6. Etiology and Pathophysiology Collateral Circulation
Growth of collateral circulation is attributed to two factors:
The inherited predisposition to develop new vessels
The presence of chronic ischemia

7. Etiology and Pathophysiology Collateral Circulation
When occlusion of the coronary arteries occurs slowly over a long period, there is a greater chance of adequate collateral circulation developing

8. Collateral Circulation
Fig. 33-5

9. Clinical Manifestations of CAD
Angina Pectoris
Acute Coronary Syndrome
Sudden Cardiac Death

10. Clinical Manifestations
Stable Angina
Results when the lack of oxygen supply is temporary and reversible

11. Clinical Manifestations
Acute Coronary Syndrome (ACS)
Develops when the oxygen supply is prolonged and not immediately reversible

12. Clinical Manifestations
ACS encompasses:
Unstable angina
Non-ST-segment-elevation myocardial infarction (NSTEMI)
ST-segment-elevation (STEMI)

13. Relationships Among CAD, Stable Angina, and MI
Fig. 33-8

14. Etiology and Pathophysiology
Myocardial ischemia:
O2 demand > O2 supply
Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis

15. Etiology and Pathophysiology
In CAD the coronary arteries are unable to dilate to meet increased metabolic needs because they are already chronically dilated beyond the obstructed area

16. Etiology and Pathophysiology
For ischemia to occur, the artery is usually 75% or more stenosed
In addition, the diseased heart has difficulty increasing the rate of blood flow

17. Etiology and Pathophysiology
Coronary spasm
The constriction is transient and reversible
Causes either subtotal or total narrowing

18. Etiology and Pathophysiology
Myocardial cyanosis occurs within the 1st 10 seconds of coronary occlusion
ECG changes
Total occlusion  anaerobic metabolism and lactic acid accumulation

19. Etiology and Pathophysiology
Myocardial Infarction
Occurs as a result of sustained ischemia, causing irreversible cellular death

20. Etiology and Pathophysiology
Myocardial Infarction
The degree of altered function depends on the area of the heart involved and the size of the infarct

21. Etiology and Pathophysiology
Myocardial Infarction
Contractile function of the heart stops in the areas of myocardial necrosis
Most involve the left ventricle (LV)

22. Etiology and Pathophysiology
Myocardial Infarction
Transmural MI
Involves the entire thickness of the myocardium

23. Transmural MI
Fig

24. Etiology and Pathophysiology
Myocardial Infarction
Subendocardial MI
The damage has not penetrated through the entire thickness

25. Etiology and Pathophysiology
Myocardial Infarction
Infarctions are described by the area of occurrence

26. Etiology and Pathophysiology Healing Process
Within 24 hours, leukocytes infiltrate the area of cell death
Enzymes are released from the dead cardiac cells (important indicators of MI)

27. Etiology and Pathophysiology Healing Process
Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by 2nd or 3rd day
Development of collateral circulation improves areas of poor perfusion

28. Etiology and Pathophysiology Healing Process
Necrotic zone identifiable by ECG changes and nuclear scanning
10 to 14 days after MI, scar tissue is still weak

29. Etiology and Pathophysiology Healing Process
By 6 weeks after MI, scar tissue has replaced necrotic tissue
Area is said to be healed

30. Etiology and Pathophysiology Healing Process
Ventricular remodeling
In an attempt to compensate for the infarcted muscle, the normal myocardium will hypertrophy and dilate

31. Types of Angina Silent Ischemia
Up to 80% of patients with myocardial ischemia are asymptomatic
Associated with diabetes mellitus and hypertension

32. Types of Angina Prinzmetal’s Angina
When spasm occurs:
Pain
Marked, transient ST segment elevation with angina (unlike with AMI; ↑ST = MI)
May occur during REM sleep

33. Clinical Manifestations Myocardial Infarction
Pain
Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration
The hallmark of an MI

34. Location of Chest Pain
Fig

35. Clinical Manifestations Myocardial Infarction
Nausea and vomiting
Can result from reflex stimulation of the vomiting center by the severe pain

36. Clinical Manifestations Myocardial Infarction
Sympathetic nervous system stimulation
 catecholamines released during initial phases of MI
Results in diaphoresis and vasoconstriction

37. Clinical Manifestations Myocardial Infarction
Fever
May  within 1st 24 hours up to 100.4°
May last as long as 1 week

38. Clinical Manifestations Myocardial Infarction
Fever
Systemic manifestation of the inflammatory process caused by cell death

39. Clinical Manifestations Myocardial Infarction
Cardiovascular manifestations
 BP and heart rate initially
Later the BP may drop from  CO

40. Clinical Manifestations Myocardial Infarction
Cardiovascular manifestations
 urine output
Crackles
Hepatic engorgement
Peripheral edema

41. Complications of Myocardial Infarction
Arrhythmias
Most common complication
Present in 80% of MI patients
Most common cause of death in the prehospital period

42. Complications of Myocardial Infarction
Congestive heart failure
A complication that occurs when the pumping power of the heart has diminished

43. Complications of Myocardial Infarction
Cardiogenic shock
Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure
Requires aggressive management

44. Complications of Myocardial Infarction
Papillary muscle dysfunction
Causes mitral valve regurgitation
Condition aggravates an already compromised LV

45. Complications of Myocardial Infarction
Ventricular aneurysm
Results when the infarcted myocardial wall becomes thinned and bulges out during contraction

46. Complications of Myocardial Infarction
Pericarditis
An inflammation of the visceral and/or parietal pericardium
May result in cardiac compression,  LV filling and emptying, and cardiac failure

47. Complications of Myocardial Infarction
Dressler syndrome
Characterized by pericarditis with effusion and fever that develops 1 to 4 weeks after MI

48. Complications of Myocardial Infarction
Pulmonary embolism
Source of the thrombus may be the roughened endocardium or leg veins

49. Diagnostic Studies Myocardial Infarction
History of pain
Risk factors
Health history
ECG: ST elevation, greater than 1 mm above PR Interval; T Wave inversion (flipped T Waves); Pathological Q-wave (Q wave greater than ¼ size of R wave)
Serum cardiac markers:
CK-MB: indicates muscle damage (rises 3-12 hours post AMI – returns to normal 2-3 days)
Triponen: is a myocardial muscle protein (rises as quickly as CK; remains elevated for 2 weeks)
Myoglobin: rises 3 hours after AMI; lacks cardiac specificity

50. Collaborative Care Angina
Percutaneous coronary intervention
Surgical intervention alternative
Performed with local anesthesia
Ambulatory 24 hours after the procedure

51. Collaborative Care Angina
Stent placement
Used to treat abrupt or threatened abrupt closure and restenosis following PCI

52. Collaborative Care Angina
Atherectomy
The plaque is shaved off using a type of rotational blade
Decreases the incidence of abrupt closure as compared with PCI

53. Collaborative Care Angina
Laser angioplasty
Performed with a catheter containing fibers that carry laser energy
Used to precisely dissolve the blockage

54. Collaborative Care Angina
Myocardial revascularization (CABG)
Primary surgical treatment for CAD
Patient with CAD who has failed medical management or has advanced disease is considered a candidate

55. Collaborative Care Angina
MIDCABG procedure
Minimally invasive direct coronary artery bypass grafting (MIDCABG)
Alternative to traditional CABG

56. Collaborative Care Myocardial Infarction
Fibrinolytic therapy
Cardiac catheterization
Percutaneous coronary intervention

57. Collaborative Care Myocardial Infarction
Drug Therapy
IV nitroglycerin
Antiarrhythmic drugs
Morphine

58. Collaborative Care Myocardial Infarction
Drug Therapy
-Adrenergic blockers
Angiotensin-converting enzyme inhibitors
Stool softeners

59. Collaborative Care Myocardial Infarction
Nutritional Therapy
Diet restricted in saturated fats and cholesterol
Low sodium

60. Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Acute Intervention
Morphine
Continuous ECG
Frequent vital signs
Rest and comfort

61. Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Acute Intervention
Anxiety
Emotional and behavioral reactions
Communicate with family
Provide support

62. Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Ambulatory and Home Care
Rehabilitation
Cardiac rehabilitation
Physical exercise

63. Nursing Management Angina and Myocardial Infarction Nursing Implementation: MI
Ambulatory and Home Care
Resumption of sexual activity
Emotional readiness
Physical training

64. Nursing Management Angina and Myocardial Infarction Evaluation
Pain level
Cardiac pump effectiveness
Anxiety control
Energy conservation
Health orientation

65. Women and Coronary Artery Disease
About 500,000 deaths occur in women per year
Kills almost 10 times more women than breast cancer

66. Women and Coronary Artery Disease
Manifest CAD 10 years later in life than men
Most have symptoms of angina rather than MI

67. Women and Coronary Artery Disease
Diabetes mellitus found to be the single most powerful predictor of CAD in women