1. Oxygen Needs Interference
with
O2 Transport

2. Case Study

3. Oxygen Needs Interference with O2 Transport
Coronary Artery Disease
Complications
Dysrhythmias
Pulmonary Embolism
Hypertension
Complication
Congestive Heart Failure
Peripheral Vascular / Arterial Disease

4. Oxygen Needs Interference with O2 Transport
Care of Patients with:
Coronary Artery Disease
Risk Factors
Myocardial Infarction
Alterations in:
Rate & Rhythm (Cardiac Conduction)
Effect on Cardiac Output

5. Content Approach Anatomy & Physiology Review Demographics/occurrence
Pathophysiology
Clinical Manifestation
Medical / Surgical Management
Nursing Process (APIE)
Assessment - Nursing Actions - Education

6. Anatomy & Physiology Right Heart Left Heart Systole Diastole
Valve Closure:
Diastole

7. Cardiac Circulation

8. Myocardium Anterior Posterior

9. Cardiac Cycle Passive Filling – preload
Atrial contraction – Aortic & Pulmonic semilunar valves close – S2
Isovolumetric ventricular contraction – all
valves closed
Ejection – ventricular systole – Mitral & Tricuspid valves close – S1 - afterload
Isovolumetric ventricular relaxation – all valves closed

10. Cardiac Cycle Phases

11. Heart Sounds & Stethoscope Placement

12. Coronary Arterial System

13. What is the impact of heart rate on coronary artery filling?
Physiology: Oxygen Supply to the Cardiac Muscle during the Cardiac Cycle
Coronary artery oxygen deficit
during ventricular contraction & ejection (systole)
Coronary artery filling
during ventricular filling (diastole)
What is the impact of heart rate on coronary artery filling?

14. Oxygen Supply to the Cardiac Muscle during the Cardiac Cycle
The actual time available for diastole shortens significantly as the heart rate increase
% of a Minute Heart Rate
70%
50%
33%
Results: Less time for ventricular filling & coronary artery filling + as HR increases, increased oxygen is needed each minute to eject the same volume of blood.
Stroke volume: volume ejected in one heart beat
Cardiac Output: volume ejected in one minute
Cardiac Output = Stroke Volume x Heart Rate

15. Factors Determining Myocardial Oxygen Needs
Decreased Oxygen Supply:
Noncardiac: Anemia, hypoxemia, pneumonia, asthma, COPD, low blood volume
Cardiac: Arrhythmias/dysrhythmias, congestive heart failure (CHF), coronary artery spasm, coronary artery thrombosis, valve disorders
Increased Oxygen Demand or Consumption:
Noncardiac: anxiety, cocaine use, hypertension, hyperthermia, hyperthyroidism, physical exertion
Cardiac: aortic stenosis, arrhythmias, cardiomyopathy, hypertension, tachycardia

16. CAD - Demographics

17. CAD - Demographics

18. Comparison of death by CV Disease and Breast Cancer – by Women’s Age

19. Coronary Artery Disease (CAD) Pathophysiology
ASHD, IHD, CVHD = CAD
AHA
1.1 mil Americans will have an MI in 2003
460,000 will die
About half of those deaths occur within 1 hour of the start of symptoms and before the person reaches the hospital.
Major cause: Atherosclerosis—focal deposit of cholesterol & lipids

20. CAD – Risk Factors
Unmodifiable: Age, Gender, Ethnicity, Genetic predisposition/family history
Modifiable Major: Dyslipidemia--Elevated serum lipids*, hypertension*, cigarette smoking, obesity—visceral/central obesity
Modifiable Contributing: Diabetes Mellitus*,
stressful lifestyle
* may have genetic predisposition

21. CAD – Risk Factors Metabolic Syndrome: Insulin Resistance
Hyperglycemia >110mg/dL
Hypertension - > 130/85
Increased triglycerides >110mg/dL
Decrease HDL <40 men; < 50 women
Central Obesity
men: waist > 40” women: waist > 35”

22. One of the Major Modifiable
Risk Factors
One of the Major Modifiable
Physical Inactivity

23. Types of Plasma Lipoproteins
HDL –
Contain more protein and less lipid
Carry lipids away from arteries to liver for metabolism
This process prevents lipid accumulation within arterial walls
Higher levels are desirable
LDL –
Contain more lipids than any other lipoproteins
Affinity for arterial walls
Increased levels correlate closely with an increased
incidence of atherosclerosis
Lower levels are desirable
VLDL
Contain of triglycerides
Correlation with heart disease is uncertain

24. Plasma Lipoproteins

25. Atherosclerosis Elevated serum lipids Cholesterol > 200mg/dl
Triglyceride > 200mg/dl
HDL
< 35 mg/dl – major risk
45-59 mg/dl – average risk
> 60 mg/dl – negative risk
LDL
< 130 – desirable
130 – 159 mg/dl – borderline risk
> 160 mg/dl – high risk

26. Progressive Atherosclerosis

27. Drug Therapy for Dyslipidemia
Bile Acid Sequestrants (Questran) - Binds with bile salts
Niacin - Inhibits synthesis of VLDL & LDL
Fibric Acid Derivatives (Atromid)– Decrease VLDL
HMG CoA Reductase Inhibitors (Statins - Lipitor, Pravachol, Zocor) – Block synthesis of cholesterol
Cholesterol Absorption Inhibitor (Zetia)– Inhibits intestinal absorption of cholesterol

28. Natural Lipid Lowering Agents
Niacin - < LDL levels
Omega-3 fatty acids – fish/flaxseed oil - <Triglycerides & > HDL levels
Milk thistle – Silymarin - > HDL levels
Fiber - < Cholesterol
Phytosterols - < Cholesterol
Soy - < Cholesterol absorption from GI tract
CoEnzyme Q10 – HMG CoA reductase inhibitors – natural statins

29. Coronary Thrombogenesis

30. During an Acute Coronary Syndrome

31. Angina

32. Clinical Manifestations Angina – Chest Pain
Stable Angina Pectoris – intermittent, same pattern of onset, duration, intensity of symptoms mins.
Silent Ischemia – 80% of patients with ischemia are asymptomatic
Prinzmetal’s Angina – variant – not precipitated by physical activity – may be due to spasm
Nocturnal Angina – occurs at night but not necessarily during sleep or in recumbent position
Angina Decubitis – recumbent position – relieved by standing
Unstable Angina – Unpredictable or may evolve from stable angina – increasing frequency, duration, intensity

33. CAD Clinical Manifestation – Diagnostics
History & Physical Examination
EKG / Echocardiogram / Stress Echocardiogram
Thallium Stress Test (perfusion scanning) cold spots where tissue is inadequately perfused cardiac tissue
CAT scan- calcium score/CT coronary angiogram
MUGA (Multiple gated radioisotope scan) – left ventricular function
MRI of the heart
PET (Positron emission computed tomography) – evaluate coronary artery patency

34. Normal Thallium Stress Test

35. Abnormal Thallium-Stress Test

36. CAD - Clinical Manifestation Invasive Diagnostics
Cardiac Catheterization
Right sided:
Catheter through the femoral vein through the vena cava into right atrium and right ventricle – pulmonary artery – wedge pressure
Left sided:
Catheter through the femoral artery through the aorta into the left atrium and left ventricle / openings of the coronary arteries
Coronary arteriography: Injected dye with video & x-rays

37. CAD - Clinical Manifestation Invasive Diagnostics
Cardiac Catheterization
Potential Complications
Catheter looping/breaking, dysrhythmias, allergic reaction to contrast medium, arterial thrombosis, myocardial infarction, hemorrhage, infection.
Patient Preparation
Informed consent; allergies – shellfish/iodine; NPO x 6 hrs; explanation “flushed/tingling”; supine – absolutely still
Postprocedure Care

38. Right Heart Catherization

39. Left Heart Catheterization

40. Coronary Angiography Coronary Blockage - LAD

41. Cardiac Catheterization Post Procedure Care
Assess:
VS q15 mins. x 2 hrs; q30 min x 2 hrs
Monitor cardiac rate and rhythm
Check site for bleeding
Extremity: Peripheral pulse check, temperature, color, sensation, mobility
Assess for chest pain, dizziness, dyspnea
Nursing Action:
Straight at groin x 24 hours; pressure at site x 30 mins.
Maintain IV KVO for 2 hrs; IV capped x 2 hrs; then d/c
Encourage oral fluids
Patient/Family Education:
Rationale for all nursing actions
No squatting, sitting, lifting for 24 – 48 hours++
Report bleeding, swelling, discoloration, drainage
Change dressing after 24 hours – small dressing to bandaid

42. Clinical Manifestation Myocardial Infarction Lab Diagnostics
Cardiac Protein – Troponin T
More sensitive than CK
Elevates 3 hr – peak hrs; normal 5-14 days
Cardiac Enzyme – Creatine kinase (CK-MB)
Released when cardiac cells die
Elevates 3 hrs – peak hrs; normal 2-3 days
Cardiac Marker - Myoglobin
First to elevate
Lacks cardiac specificity
Normal range within 24 hours

43. Serum Cardiac Markers after MI

44. CAD – Angina Relationship
Coronary Artery Disease
/ \
Stable Angina Acute coronary syndrome
/ / \
Unstable Angina > Myocardial Infarction ST-elevated MI
Non-ST-elevated MI

45. CAD & Acute Coronary Syndrome

46. Heart With Muscle Damage and a Blocked Artery

48. Myocardial Infarction

49. Myocardial Infarction Acute Coronary Syndrome
Location correlates with coronary circulation involved
Inferior Wall – Right coronary artery
Anterior Wall – Left anterior descending
Lateral, posterior or inferior – left circumflex
Healing Process
Within 24 hours – leukocytes & enzymes
Third day – collateral circulation developing
10-14 days – scar tissue is still weak
Vulnerable time – unstable state of healing + increased activity
6 weeks – scar tissue replaces necrotic tissue
Normal myocardial tissue may compensate – ventricular remodeling – can cause late congestive heart failure

50. Coronary Artery Collateral Circulation

51. Angina Medical Management
A Aspirin / Antianginal therapy / ACE Inhibitor
B b-Adrenergic blocker / blood pressure
C Cigarette smoking / Cholesterol
D Diet / Diabetes
E Education / Exercise

52. Angina- MI Medical Management
B-Adrenergic Blockers – decreases rate, contractility, afterload
Nitrates – peripheral vasodilation decreasing preload and afterload / coronary artery vasodilation
Calcium Channel Blockers – Coronary & peripheral vasodilation, decreases AV conduction and myocardial contractility
Morphine – analgesic – reduces preload & myocardial oxygen consumption
Angiotensin-Converting Enzyme Inhibitors – Vasotec / Capoten - prevents Angiotensin I conversion to Angiotensin II – HTN, CHF

53. Antiplatelet and Anticoagulant Agents in unstable angina and NSTEMI
Oral anti-platelet agent
Aspirin Initially 300 mg p.o. then mg daily
Clopidogrel (Plavix) Initial loading dose of 300 mg then 75 mg daily
• Increased bleeding risk
Heparins
Heparin Sodium: Bolus: 60 U/kg IV bolus to a maximum of 4,000 units
Drip: 12 units/kg/h infusion to a maximum of units/h
• Monitor PTT: keep at seconds
Low-molecular-weight heparin - Enoxaparin 1 mg/kg subcut q12 hr
Precautions: • Peptic ulceration • Aspirin allergy • GI bleeding

54. Antiplatelet Drugs used in unstable angina and NSTEMI
Intravenous
tirofiban (Aggrastat), eptifibatide (Integrilin)
New class, GP IIb/IIIa inhibitors
Abciximab (ReoPro) 0.25 mg/kg IV bolus min before PCI, than 10 μg/min IV - Infusion for 12 h
Precautions:
• Thrombocytopenia • Bleeding disorder • Surgery < 6 weeks
• Abnormal bleed < 30 d • Active GI ulceration
• Puncture of a non-compressible • Prior stroke, organic CNS pathology
• Any systolic BP > 180 mmHg during the acute event

55. Thrombolytic Drugs Drugs that break down, or lyse, preformed clots
Tissue plasminogen activator
plasminogen-streptokinase activator complex (APSAC)
streptokinase (Streptase)
alteplase (t-PA, Activase)
reteplase (Retavase)

56. Angina - MI Invasive Medical Management
Percutaneous Coronary Intervention – PCTA – Percutaneous transluminal coronary angioplasty
Balloon-tipped catheter passed through just beyond the lesion – balloon inflated – atherosclerotic plaque is compressed
Reduction in lesion size by >50% in 90% of patients
Used in conjunction with thrombin inhibitors

57. Angina- MI Invasive Medical Management
Stent Placement – may be placed during PCTA – expandable meshlike structures to maintain vessel patency – placed over the angioplasty site to hold the vessel open
* Stents are thrombogenic –
IV antiplatelet agents
ASA/Plavix
Atherectomy – plaque is shaved away from the coronary artery wall
Limited to use in larger portions of vessels
Laser Angioplasty – “cool” laser – no heat

58. Coronary Artery Stent Placement

59. Coronary Atherectomy

60. Angina - MI Invasive Medical Management
Complications
Abrupt closure of angioplasty site
Stent thrombosis / embolization
Hemorrhage / vascular damage
Coronary spasm, Acute MI
Need for emergent coronary artery bypass graft (CABG)

61. Fibrinolytic Contraindications
Absolute Contraindications
Active internal bleeding, active inflammatory bowel disease, active peptic ulcer disease, acute pericarditis, GI/GU bleeding within 6 months, Hx of hemorrhage CVA, Neurosurgical procedure within 2 months, Pregnancy, Suspected aortic dissection, Uncontrolled HTN, >180/110
Relative Contraindications
Bacterial endocarditis, chronic Coumadin Therapy, Diabetic hemorrhagic retinopathy, Poorly controlled HTN

62. Angina - MI Surgical Management
Coronary Artery Bypass Graft
(CABG)
construction of new vessels between the aorta to beyond the obstructed coronary artery
(or arteries)
Saphenous vein or internal mammary artery
Palliative treatment for CAD – not a cure
Postoperative care: Care of cardiac patient with chest tubes / sternotomy; pain management; short ventilator support; early ambulation; 4-5 day hospital stay

63. Coronary Artery Bypass

64. Coronary Artery Bypass

65. Complications of MI
Arrhythmias – lethal PVC’s within 4 hours of onset of chest pain
Congestive Heart Failure
Cardiogenic Shock – severe left ventricular failure – intra-aortic balloon pump & vasoactive medications
Papillary Muscle Dysfunction – Mitral valve regurgitation – treat dyspnea, pulmonary edema & decreased CO
Ventricular Aneurysm Pericarditis – 1-3 days post MI; pleural friction rub & fever
Dressler Syndrome – pericarditis with effusion & fever 1- 4 wks post MI; elevated WBC & Sed Rate. Tx-Steroids
Pulmonary Embolism

66. Acute Coronary Syndrome Pair Share
Discomfort or a heavy feeling in the chest can signal a heart attack. A. True B. False
Women do not frequently experience heart attacks. A. True B. False
African-American women die of heart attacks at the same rate as white women. A. True B. False
Some people who are experiencing the symptoms of a heart attack may wait hours or even days before seeking needed medical care. A. True B. False
Being treated within about an hour of the first symptoms can make a significant difference. A. True B. False

67. Acute Coronary Syndrome Pair Share
Many heart attack victims say their heart attack wasn’t what they’d expected. A. True B. False
A family member, such as a spouse, can persuade a loved one having a heart attack to seek help immediately. A. True B. False
Calling for chest pain alone would probably turn out to be a waste of the emergency medical personnel’s time. A. True B. False
Most heart attacks occur in people over 65. A. True B. False The major issue in delay is how long it takes for emergency medical personnel to find the address and deliver the patient to the hospital. A. True B. False

68. Nursing Diagnoses
TOP 4
?????

69. Nursing Process Nsg Dx: Acute Pain related to Cardiac Ischemia
Assess: Chest pain—intensity, location, duration, precipitating, alleviating factors; Monitor cardiac rate & rhythm; effect of pain medication; peripheral pulses; VS; Pulse Oximetry
Nsg Action: Administer O2 NC; IV access; position of comfort
Patient Education: Rationale for all procedures; pain scale; instruct to report pain

70. Nsg Dx: Ineffective Tissue Perfusion related to Myocardial Injury
Assess: VS & Pulse Oximetry qh; continuous cardiac monitoring; respiratory status if Morphine IV is used; fluid balance – strict I&O peripheral edema; heart & breath sounds
Nsg Action: Rest periods; Administer meds & oxygen as ordered
Patient Education: Rationale for rest; energy conservation

71. Nsg Dx: Anxiety related to perceived or actual threat of death
Assess: verbal & nonverbal queues
Nsg Action: Calm, reassuring approach; encourage verbalization of feelings, fears, perceptions; family involvement;
Patient Education: Relaxation techniques; simple instructions

72. Nsg Dx: Ineffective therapeutic regimen management related to lack of knowledge
Assess: Current knowledge level & readiness to learn; family dynamics
Nsg Action: Assist pt in identifying small successes; Assist pt is identifying lifestyle that needs to be changed; Community referrals—smoking cessation, cardiac rehab, support groups,
Patient Education: Lifestyle changes, Medications—desired effect/side effects; comprehensive discharge plan—continuity with community cardiac rehabilitation

73. Nsg Dx: Activity Intolerance related to fatigue & chest pain
Assess: Monitor patient’s response to medications, activity tolerance as increased; Cardiac rate, rhythm, respiratory effort
Nsg Action: Include family; advance activity as tolerated; supplement oxygen as needed
Patient Education: Teach patient energy conservation – activity/rest – activities that will promote independence and decrease oxygen consumption; Cardiac Rehab: exercise & sexual activity

74. Patient Education: Exercise Guidelines post MI
Type of Exercise – regular, rhythmic & repetitive – using large muscle groups
Intensity – determined by patient’s HR – should not exceed 20 beats per min > resting HR
Duration – Build to mins
Frequency x/week
Warm-up/Cool-down – 5 mins before and after aerobic exercise. Exercise should not be stopped abruptly

75. Cardiac Rehab – Metabolic Equivalents of Energy Expenditure

76. Patient Education: Sexual Activity post MI
Plan of resumption of sexual activity should correspond to activity prior to MI
Physical training improves physical response to coitus
Food & alcohol < prior to sexual activity
Familiar & relaxed surroundings; positions of comfort
Avoid hot or cold showers
Foreplay is desirable – gradual increase in heart rate prior to orgasm
Prophylactic use of nitrates decreases angina
Orogenital sex places no undue strain on the heart
Anal intercourse may cause undue cardiac stress – vasovagal response

77. Emotional & Behavioral Response to Acute MI
Denial – Ignores symptoms; minimizes severity; ignores activity restrictions
Anger – “Why did this happen to me?”
Anxiety & Fear – Fear of death & disability –apprehension, tachycardia, restlessness, hypochondria, projection of feelings
Dependency – reliant on staff; hesitant to leave ICU or hospital
Depression – Mourning period; realizes seriousness of situation
Realistic Acceptance – Focuses on optimum rehabilitation; plans changes compatible with cardiac function