1. Imbalance Between Myocardial Supply and Demand
Irma B.Ancheta,PhD,RN.

2. Learning Guide:
Pathophysiology of atherosclerosis, arteriosclerosis, Acute Coronary Syndrome
Modifiable and non-modifiable risk factors for CAD (Coronary Artery Disease)
Anti-platelet medications:
aspirin
Plavix (clopidogrel)
Medications for dyslipidemia:
HMG Co-reductase inhibitors
Niacin
Fibric acid derivatives
Anti-anginal medications:
Nitroglycerin preparations
Beta blockers
Calcium channel blocke

3. Learning Guide:
Assessment of men and women presenting with s/s of angina, or ACS (Acute Coronary Syndrome)
Definitions and defining characteristics of:
Decreased cardiac output r/t ventricular damage, dysrhythmias
Acute pain r/t myocardial tissue damage from inadequate blood supply
Risk for bleeding r/t thrombolytic therapy
Risk for peripheral neurovascular dysfunction
Definition and Indicators of these NOCs:
Cardiac pump effectiveness
Tissue perfusion, peripheral
Review these NICs:
Cardiac Care
Cardiac care, acute
Circulatory precautions

4. Learning Objectives:
Describe assessment strategies (and related nursing care) for patients with ACS:
Stress tests, echocardiography, cardiac catheterization, ECG monitoring
Plan, implement and evaluate care for patients experiencing Unstable angina, NSTEMI, MI
Plan, implement and evaluate care for patients post interventional cardiology procedures
Describe interventional (cath lab)/surgical interventions for myocardial revascularization
Describe health promotion strategies (and teaching plans) for patients at risk of CAD/ACS.

5. Cardiac Review

6. A&P Review
Layers of the Heart Pericardium Epicardium Myocardium Endocardium

7. A&P Review
Cardiac Chambers Atria Ventricles

9. Cardiac Valves
Atrioventricular Valves Tricuspid and mitral Semilunar Valves Pulmonic and aortic

10. A&P Review
Conduction System Atria Sinoatrial node Internodal pathways Intraatrial bundle AV Node to Bundle of HIS Ventricles Right and left bundle branches Purkinjie fibers

11. Electrical Conduction System

12. A&P Review Coronary Blood Supply Coronary Arteries
Left coronary artery divides into left anterior descending and left circumflex
Right coronary artery perfuses the right side of the heart and in most people the SA and AV nodes
In 70% of the population the RCA perfuses the posterior coronary artery

13. Coronary Arteries
Right coronary
artery

14. A&P Review Venous Return from the Heart Coronary sinus
Thebesian vessels drain directly into the chambers of the heart and produce physiologic shunt

15. A&P Review Systemic Circulation Arterial system of resistance vessels
Capillary bed: tissue perfusion
Venous system of capacitance vessels

16. A&P Review Physiology Properties of cardiac tissue Excitability
Conductivity
Automaticity
Rhythmnicity
Contractility
Refractoriness

17. A&P Review
Electrical Activity
Action potential

18. A&P Review Cardiac Cycle Ventricular systole Ventricular diastole
Cardiac Output

19. A&P Review Regulation of Heartbeat Nervous control
Intrinsic regulation

20. A&P Review Control of Peripheral Circulation Intrinsic Control
Extrinsic control

21. Ejection Fraction

22. Ejection Fraction
Normal = 50% or higher Low = < 40%

23. Ejection Fraction
[1] MUGA (multiple-gated acquisition) Scan [2] echocardiogram [3] Cardiac Catheterization [4] Nuclear tests

24. Risk Factors associated with Coronary Artery Disease

25. Objectives: Definition of CAD Identifying risk factors (a) effects
(b) treatments
(c) management
Latest developments

26. Affects nearly 13 million people in the USA
CAD Statistics
Affects nearly 13 million people in the USA
Causes 500,000 deaths each year

27. Framingham Heart Study (FHS)

29. Definition of Coronary Artery Disease
A narrowing of the inside diameter of arteries that supply the heart with blood.
The condition arises from the accumulation of plaque and greatly increases the risk of having a heart attack or myocardial infarction (Cooley, 1996).

30. Modifiable Risk factors
Life style factors
Smoking
Obesity
Physical Inactivity
Stress
Pathophysiologic factors:
Hypertension
Diabetes
Hyperlipidemia

31. Nonmodifiable risk factors
AGE
GENDER
RACE/ETHNIC BACKGROUND
HEREDITY

32. Emerging Risk Factors Homocysteine=
blocks NO production < elastic Blood vessels permit plaque formation
TTT= B complex Folic acid, Niacin
LDL-C = mechanical injury
Prothrombotic state (e.g., high fibrinogen or plasminogen activator inhibitor–1 in the blood)
Proinflammatory state (e.g., elevated C-reactive protein in the blood causes inhibition of NO)
Low Adiponectin levels increase CRP production

33. Five Major Risk Factors
1.Smoking
2.Hypertension
3.High cholesterol
4.Diabetes
5.Family History

34. Smoking
Effects of Smoking
Roughening effect of inside diameter of the arterial wall>formation of plaque,constriction of arteries>HPN
Increases heart rate and produces irregular heartbeats>clots>stroke
Decrease HDL levels and increase LDL > increase risk CAD

35. Management of Smoking
Quit Smoking
Avoid secondary smoke

36. Hypertension: Or high blood pressure.. SBP >120 mm Hg
..DBP>80 mm Hg
Indicates a problem in the mechanism that regulates blood pressure in the circulatory system
“hyper” too much “tension” pressure

37. Hypertension Effects of HPN
[Mechanical Injury] Causes thickening or hardening of the walls off the arteries>causes narrowing >decrease blood flow to coronary arteries>MI.
Thickening of left ventricle >decrease Cardiac output > causes CHF
> kidney damage>Renal dialysis
In the diabetic population, HPN>retinal damage(retinopathy)>BLINDNESS

38. New Features and Key Messages
For persons over age 50, SBP is a more important than DBP as CVD risk factor.
Starting at 115/75 mmHg, CVD risk doubles with each increment of
20/10 mmHg throughout the BP range.
Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN.
Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD (JNC 7, 2003)

39. New Features and Key Messages (Continued)
Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes.
Certain high-risk conditions are compelling indications for other drug classes.
Most patients will require two or more antihypertensive drugs to achieve goal BP.
If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic. (JNC 7, 2003)

40. Blood Pressure Classification
BP Classification
SBP
DBP
Normal
<120
and
<80
Prehypertension
120–139 or
80–89
Stage 1 Hypertension
140–159 or
90–99
Stage 2
Hypertension
>160 or
>100
(JNC 7, 2003)

41. Benefits of Lowering BP
Average Percent Reduction
Stroke incidence –40%
Myocardial infarction 20–25%
Heart failure %
(JNC 7, 2003)

42. BP Control Rates
Trends in awareness, treatment, and control of high blood pressure in adults ages 18–74
National Health and Nutrition Examination Survey, Percent II
1976–80
(Phase 1)
1988–91
(Phase 2)
1991–94
1999–2000
Awareness 51 73 68 70
Treatment 31 55 54 59
Control 10 29 27 34
Sources: Unpublished data for 1999–2000 computed by M. Wolz, National Heart, Lung, and Blood Institute; JNC 6.

43. Summary:

44. Treatment Overview Goals of therapy Lifestyle modification
Pharmacologic treatment
Algorithm for treatment of hypertension
Classification and management of BP for adults
Follow-up and monitoring (JNC 7, 2003)

45. Management of hypertension
Exercise
Proper stress management
Quit Smoking
Healthy diet
Decrease sodium intake.
Anti- HPN Medication

46. Lifestyle Change: What Difference Does it Make ?
Weight loss. (decreases SBP*1.6 mm Hg for each kg lost)
Dietary Approaches to Stop Hypertension: DASH diet:
(decreases systolic BP 8-14 mmHg)
Reducing salt in the diet.(decreases SBP 2-8 mmHg)
30-45 minutes daily aerobic exercise
(decreases systolic BP 4-9 mmHg)
Limit alcohol. (decreases SBP* 2-4 mm Hg)
Avoidance of tobacco products.
(*SBP = systolic blood pressure)
There are multiple lifestyle changes that can help reduce blood pressure. It is possible that those in the “prehypertension category can reduce blood pressure back into the optimal range by making some changes in the diet or exercise plan.
Weight loss can effect a reduction in blood pressure. Following the DASH diet, a diet high in fruits, vegetables and low fat dairy products can result in a blood pressure reduction of *.
A 30 minute walk on most days of the week can reduce the blood pressure *
There are multiple lifestyle changes that can help reduce blood pressure. It is possible that those in the “prehypertension” category can reduce blood pressure back into the optimal range by making some changes in the diet or exercise plan.
Weight loss can effect a reduction in blood pressure. Following the DASH diet, a diet high in fruits, vegetables and low fat dairy products can result in a blood pressure reduction.
A 30 minute walk on most days of the week can also reduce the blood pressure.

47. Medications for HPN Diuretics Beta-Blockers Calcium channel Blockers
ACEI
Vasodilators

48. Diabetes Causes vasoconstriction of coronary arteries
>decrease blood flow > decrease oxygen supply
>increase risk of heart attack or MI

49. Management of Diabetes
Healthy diet. Exercise Stress Management Medications Check Blood sugar regularly

50. CHOLESTEROL Effects of Increased Cholesterol levels
Causes plaguing of the
coronary walls,
narrows coronary arteries,
creates blockage of coronary
arteries
less blood flow to heart cells
>MI

51. Cholesterol
LDL cholesterol
HDL cholesterol
Total cholesterol
Triglycerides

52. Serum cholesterol levels
LDL Cholesterol –Primary Target of therapy <100 Optimal Near optimal/above optimal Borderline high High 190 > Very High Total cholesterol < 200 Desirable Borderline 240 > High HDL <40 Low >60 High (NCEP/ATP III Guidelines, 2004)

53. Management of Cholesterol Levels
DIET MEDICATION NON-SMOKING EXERCISE

54. Family History
Parent or sibling that died of CAD less than 60 years of age...

55. Medications for CAD
[1] Anti-platelet medications [2] Medications for dyslipidemia [3] Anti- anginal medications

56. Anti-platelet medications
[1] Aspirin [2]Clopidogrel (Plavix)

57. Medications for dyslipidemia
HMG CoA-reductase inhibitors Nursing Interventions (statins) [1] Rosuvastatin No grapefruit [2] Simvastatin Monitor liver enzymes [3] Atorvastatin Instruct pts. mm tenderness [4] Pravastatin Take at night Niacin [1] Niaspan,Niacin With meals/Flushing/?med Fibric Acid Derivatives [1] Lopid 30 minutes before or with meals [2] Zetia

58. Anti- anginal medications
[1] NTG preparations [2]Beta-blockers [3] Calcium channel blockers

59. Summary of risk factors for CAD
[1] ? [2] ? [3] ? [4] ? [5] ?

60. How many risk factors for CAD do you have?

61. Coronary Artery Disease

62. Coronary Artery Disease (CAD)
CAD is a broad term that includes stable angina pectoris and acute coronary syndromes. When blood flow through the coronary arteries is blocked, ischemia or infarction of the myocardium may result.

63. Ischemia and Infarction
Ischemia occurs when insufficient oxygen is supplied to meet the requirements of the myocardium
Infarction (necrosis of the cells, cell death) occurs when sever ischemia is prolonged and irreversible damage to tissue results.

64. Acute Coronary Syndromes
Angina- coronary ischemia- a temporary imbalance between the coronary arteries ability to supply oxygen and the cardiac muscle’s demand for oxygen (no permanent damage to myocardial tissue).
Stable Angina- predictable; fixed lesions
Unstable Angina- more intense, may occur at rest or with exertion and causes marked limitations of activity. Attacks increase in intensity and pain. Includes new-onset angina, variant (Prinzmental’s) angina, pre-infarction angina and crescendo angina

65. Angina Location Duration Quality Radiation Precipitating Factors
Medication Relief

66. Myocardial Infarction
Irreversible necrosis due to an abrupt decrease or total cessation of coronary blood flow.
Plaque rupture
New thrombus in coronary artery

67. Process of Infarction Tissue Ischemia Hypoxemia
Autonomic Nervous System Influences
Metabolic Derangement
Acid-base imbalances
Hemodynamic disturbances
Electrolyte disturbances
Fiber stretch

68. Zone of Infarction Dependent on Three Factors: Collateral circulation
Anaerobic metabolism
Workload demands

69. Types of Infarction Subendocardial Infarction (non-Q wave)
(multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI. )
Transmural Infarction (Q wave)
(involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%).
Physiologic response = ventricular remodeling (change in shape and size of L ventricle causing decrease L V F leading to HF)

70. Zones of Infarction
Zone of Ischemia = T-wave inversion Zone of Injury = ST elevation Zone of Necrosis = Abnormal Q wave

72. Classification of MI by Location
Inferior: Abnormalities that appear in leads II, III, and F (called the inferior leads) indicate pathology on the inferior or diaphragmatic surface of the heart. Lateral: Leads I, F, and V5-V6 are called lateral leads. Abnormality in these leads indicates pathology on the lateral, upper surface of the heart. Anterior: Anterior pathology is seen in leads V1-V4, and often in lead I. Posterior: Problems on the posterior surface of the heart are difficult to diagnose using the standard 12 ECG leads. The pathology may be seen as “reflected” through V1 and V2. Combination: Abnormalities may not be limited to one of the four areas above. Inferolateral damage will show up in a combination of the inferior and lateral leads. Anterolateral damage will be seen in both the anterior and the lateral leads.

73. Normal 12 lead EKG

74. ? MI????

76. Identify which coronary artery is affected?
[1] severe crushing chest pressure/pain/radiating to neck [2] chest pressure/pain with radiation to L arm [3] chest pressure radiating to the back/scapula.

77. Cultural Considerations
Black and Hispanic women have a higher incidence of CAD risk than white women with comparable socioeconomic status
Native Americans/American Indians/Alaskan Natives >18 years of age have greater incidence of HTN, smoking, high cholesterol, excess weight, and/or diabetes mellitus
Leading cause of death in men and women in the most prevalent ethnic groups is cardiac disease even though there are genetic predispositions to develop risk factors (AHA, 2003)

78. Cultural Considerations
Higher incidence of HTN in Black community and in whites in the South
Black individuals experience longer delays in seeking treatment
Symptom may be dyspnea and not chest pain
Symptoms in older adults may not be associated with acute chest pain

79. Women and Heart Disease
More women than men have angina but many women experience atypical angina.
What does atypical mean?
Women have MI at older ages than men
Lack of education in women that CAD is the leading cause of death in women
Pathophysiology in women is different than men i.e. smaller vessels, less collateral circulation than men
Impaired glucose tolerance seriously increase risk

80. Heart Disease: The Leading Cause of Death for American Women
500,000+ women die annually from cardiovascular disease
2. More than from cancer, lung disease, osteoporotic fractures, AIDS and accidents all combined
There are 50 million American women in the USA today, who are over the age of 50 so we can anticipate these numbers continuing to increase.
Eight million women are living with heart disease.
American Heart Association

81. Cardiovascular Disease Mortality Trends United States: 1979-2001
Since 1984, more women have died from heart disease each year than men (graph AHA)
Over 500,00+ women die annually in the USA from CVD this translates to 1 death every minute (AHA Circ 2004)
Black women have the highest CVD mortality among ethnic minority groups
13% of women age 45 and over have had a heart attack ( WomenHeart Fact Sheet)
Source: CDC/NCHS.

82. Why The Gender Gap?
Women present to emergency rooms or chest pain centers 1- 2 hours later than men.
Do the multiple roles a woman takes on delay care because of her responsibilities to others?
Do women delay care because they perceive that heart disease is something that happens to one’s father, brother, or spouse?
1.Women tend to delay seeking medical care and thus we see:
2.50% more women die within the hospital from a heart attack (acute MI) than men.
Twice as many women die within 1 year post Coronary Artery By-Pass Surgery (CABG)than men. With hospital mortality for young women < 50 2x greater than women 50 –70 yrs of age.
(Vaccarino, Viola, M.D et al, Circulation Feb. 18, 2002)
Women presenting to the emergency room with acute coronary syndrome have more co-morbid diseases including diabetes and hypertension.
(Redberg, Rita. M.D., Coronary Artery Disease in Women: Understanding the Diagnostic and Management Pitfalls. Med Genmed 1 (3). 2000

83. Differences in Heart Attack Symptoms
Women
Pain in chest, upper back, jaw or neck
Shortness of breath
Flu-like symptoms: nausea or vomiting, cold sweats
Fatigue or weakness
Feelings of anxiety, loss of appetite, malaise
Men
Sub-sternal chest pain or pressure
Rest pain
Pain down left arm and shoulder
Weakness
These symptoms do not always occur with the drama of a “Hollywood heart attack.” It is common for a heart attack victim to deny actual pain and admit only to an uncomfortable fullness, pressure, or burning sensation. This can be falsely perceived as discomfort from gastrointestinal cause.

84. Postmenopausal Hormone Therapy (HT)
Postmenopausal HT is no longer recommended as a strategy to prevent heart disease.
Hormone therapy, generally short term, may still be used to treat symptoms of menopause - this is a decision between a woman and her healthcare provider.
For many years, it was generally thought that the use of hormone therapy after menopause lowered a woman’s risk of heart disease. More recent studies have not shown this, and in fact, have shown that the risk of hormone therapy outweighs the benefits in terms of disease prevention.
Short term hormone therapy still has a place for the management of the symptoms of menopause. This is a decision that should be made after careful consultation between a woman and her health care provider. Research continues in this area.

85. The Red Dress Campaign

86. Cardiac Management

87. Collaborative Management
History
Pain Assessment
Cardiovascular Assessment
Psychosocial Assessment
Laboratory Assessment
Radiographic Assessment
Other Diagnostic Assessments

88. History/ Pain Assessment
Historical data
If chest pain present, describe and find out for how long (time is muscle)
Attempt to differentiate between angina pain and infarction pain
Associated symptoms patient describes i.e. N/V, diaphoresis

89. Cardiovascular and Physical Assessment
Vital signs
Monitor for dysrhythmias
Distal peripheral pulses
Heart and Lung sounds

90. Cardiac Auscultation

91. Psychosocial Assessment
Denial
Fear
Anxiety
Anger

92. Laboratory Assessment
Troponin T and I- myocardial muscle protein released into the bloodstream with injury to the myocardial muscle (not found in healthy clients)
Creatine kinase- MB (CK-MB) is an enzyme specific to cells of the brain, myocardium and skeletal muscle. Indicates tissue necrosis or injury, Cardiac specificity is determined by measuring the isoenzyme activity CK-MB is found in myocardial muscle CK-MM (skeletal) CK-BB (brain)
Myoglobin early marker of MI is a low-molecular-weight heme protein found in cardiac and skeletal muscle, appears as early as 2 hours after an MI with rapid decline after 7 hours
C-Reactive Protein is a marker of inflammation. Any inflammatory process can increase CRP in the blood

93. Additional Laboratory Tests
Homocysteine
Serum Lipids
PT, PTT, INR
Arterial Blood Gases
Serum Electrolytes
CBC

94. Radiographic and Other Diagnostic Tests
Chest X-ray
ECG- what are we looking for?
Stress Tests- exercise tolerance testing with or without pharmacologic agents
Myocardial Perfusion Imaging- Thallium scans
Cardiac Catherization

95. Cardiac Catherization
This procedure is performed to determine the extent and exact location of obstruction of the coronary arteries. Helps to identify course of therapy for patients i.e. PTCA/stent or CABG

98. Nursing Diagnosis & collaborative problems .
Acute pain related to biologic injury agents
Ineffective tissue perfusion related to interruption of arterial blood flow
Activity intolerance related to fatigue
Ineffective coping related to effects of acute illness and major changes in lifestyle
Potential for dysrhythmias
Potential for heart failure
Potential for recurrent symptoms and extension of injury

99. NICs/NOCs NIC NOC Pain Management Drug Therapy
Ineffective Tissue Perfusion- expect to have adequate blood flow to maintain heart function
Ejection fraction
Pulmonary wedge pressure
Apical heart rate
Systolic and diastolic blood pressure

100. Collaborative Management
MONA-
M=morphine
O= oxygen
N= nitroglycerine
A= aspirin
Thrombolytic Therapy
Beta Blockers or Calcium Channel Blocker)
ACE Inhibitors
Antiplatelet Agents- ASA, Plavix, Ticlid

101. Potential Complications and Interventions
Dysrhythmias- ventricular in origin
Ventricular Failure- Class I- IV
Cardiogenic Shock- Intra-Aortic Balloon Pump (IABP)
Thrombolytic Therapy- Fibrinolytics and/ or Glycoprotein IIb/IIIa inhibitors
PTCA