1. Coronary Heart Disease
NUR -224

2. Coronary Heart Disease
Affects 16 million people
Causes more than 600,000 death annually
Caused by impaired blood flow to the myocardium
Accumulation of atherosclerotic plaque in the coronary arteries usual cause.
May be asymptomatic or may lead to angina pectoris, acute coronary care syndrome, myocardial infarction (MI/heart attack), dysrhythmias, heart failure and even sudden death

3. Coronary Atherosclerosis
Atherosclerosis is the abnormal accumulation of lipid deposits within arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium.

4. Coronary Heart Disease
Risk Factors
age (over 50)
heredity
smoking
obesity
high serum cholesterol levels
hypertension
diabetes mellitus

5. Angina Pectoris
Characterized by chest pain and usually precipitated by exercise and relieved by rest.
Myocardial oxygen needs are greater than partially occluded vessels can supply, myocardial cells become ischemic and shift to anaerobic metabolism 
produces lactic acid that stimulates the nerve endings in the muscle  pain
Pain subsides when oxygen supply meets myocardial demand.

6. Angina Pectoris
Chest pain  reduced coronary blood flow  temporary imbalance between myocardial blood supply and demand
This causes temporary/reversible myocardial ischemia.
More than 30 minutes of ischemia irreversibly damages myocardial cells (necrosis)

7. Types of Angina Stable angina Unstable angina Silent Ischemia
Variant angina (Prinzmetal’s angina)

8. Stable Angina Occurs with a predictable amount of activity or stress
Predictable and common
Occurs when the work of the heart is increased by physical exertion, exposure to cold, or by stress
Sensation may occur  neck, jaw, shoulders
Lasts for few minutes – 5/15 minutes
Relieved by rest and/or nitrates

9. Unstable Angina
Occurs with increasing frequency, severity and duration
Pain is unpredictable and occurs with decreasing levels of activity or stress and may occur at rest.
Patients at risk for myocardial infarction
May not be relieved by NTG or rest

10. Variant Angina (Prinzmetal’s)
Atypical angina that occurs unpredictably
Caused by coronary artery spasm with/out atherosclerotic lesion
Often occurs at night

11. Silent Ischemia
Occurs in the absence of any subjective symptoms (asymptomatic)
Patient reports no pain
May occur with either activity or mental stress

12. Clinical Manifestations
Chest pain
Precipitated by an identifiable event.
Classic sequence
Women frequently present with atypical symptoms of angina

13. Angina Pain Manifestations Chest Pain Quality
Associated manifestations
Atypical manifestations
Precipitating factors
Relieving factors

14. Assessment/Diagnostic Findings
Past medical history/family history
Comprehensive description of chest pain
Presence of risk factors
Electrocardiography
Echocardiography
Cardiac stress testing
Cardiac Angiography

15. Medical Management
Focus on maintaining coronary blood flow and cardiac function
Measures to restore coronary blood flow (later)
Pharmacologic therapy
* nitrates
* beta blockers
* calcium channel blockers
* aspirin

16. Nitrates SL NTG -> acute angina attacks (Buccal spray)
Acts within 1-2 minutes
Long acting nitroglycerin
Used to prevent attacks not treat an acute attack.
Headache, hypotension, nausea, dizziness
NTG, Nitrostat, Nitro-bid

17. Nitrates
Nursing Responsibilities
Patient Teaching

18. B –Adrenergic Blockers
Decrease myocardial contractility, HR, BP  which will reduce myocardial oxygen demand
Side effects  bradycardia, hypotension, wheezing, GI complaints.
Contraindicated for patient with asthma
Metoprolol (Lopressor), Atenolol(Tenormin), Carvedilol (Coreg)

19. Beta Blockers
Nursing Responsibilities
Patient Teaching

20. Calcium Channel Blockers
Decrease the workload of the heart
Relax blood vessels  decrease BP and increase coronary perfusion
Potent coronary vasodilator
Amlodipine (Norvasc), Diltiazem(Cardizem), Felodipine (Plendil)
Used to treat Variant Angina

21. Aspirin Prevent platelet aggregation/thrombus formation
Reduces the incidence of MI
mg of aspirin as soon as dx. is made
If patient is taking Tylenol – should continue to take aspirin
GI upset – H2 blocker, PPI

22. Nursing Diagnosis Ineffective Cardiac Tissue Perfusion
Deficient Knowledge
Risk for Ineffective Therapeutic Regimen Management

24. Acute Coronary Syndrome
Condition of unstable cardiac ischemia
Includes unstable angina and acute myocardial ischemia c/out significant injury of myocardial tissue
Coronary blood flow is acutely reduced, but not fully occluded. Myocardial cells are injured by the acute ischemia that results.
Most people have stenosis of one or more coronary arteries.

25. Acute Coronary Syndrome
Cardinal manifestation
Chest pain – substernal/epigastric
Dyspnea
Diaphoresis
Pallor
Cool skin
Tachycardia
Hypotension

26. Acute Coronary Care Syndrome
Diagnosis
ECG
Cardiac Markers
*Cardiac muscle troponins (sensitive indicators
of myocardial damage)
* Creatine Kinase (CK) & CK-MB (specific to
myocardial muscle)

27. Medications Reduce myocardial ischemia Reduce risk for blood clotting
Nitrates
Beta blockers
Antiplatelet (po/IV)

28. Oral Antiplatelet -Medication
Aspirin
Clopidogrel (Plavix)
Ticlopidine (Ticlid)
Suppress platelet aggregation, prevents the development of thrombus.
Nursing responsibilities
Patient Education

29. IV Antiplatelet Tirofiban (Aggrastat) Eptifibatide (Integrilin)
IV antiplatelets more effective than oral administered meds but the risk of bleeding is greater

30. Heparin Prevents the formation of new clots
Reducers the occurrence of MI
IV bolus/then continuous infusion
Infusion based on PTT – times the normal PTT value (25-35 sec.)
LMWH – Lovenox/Fragmin
All increase the risk of bleeding : bleeding precautions

31. Revascularization Procedures
Several procedures may be used to restore blood flow and oxygen to ischemic tissue.
Nonsurgical techniques:
percutaneous coronary revascularization
coronary atherectomy
intracoronary stents
coronary artery bypass graft (surgical procedure may be used)

32. Percutaneous Coronary Revascularization
Is recommended for patients:
Fail medical management
Have left main coronary artery/three vessel disease
Are not candidates for PCI
Have failed PCI with ongoing chest pain

33. Percutaneous Coronary Intervention
Goal: open the affected artery within 90 minutes of arrival to a facility
Advantages:
Alternative to surgical intervention
Performed with local anesthesia
Patient is ambulatory 24 hours after the procedure
Hospital stay shorter
Patient can return to work

34. Percutaneous Coronary Revascularization
A balloon-tipped catheter is threaded over the guide wire
Balloon is inflated for about 30 sec.-2 minutes to compress the plaque against the arterial wall
The stent is then placed over a balloon catheter and expanded as the balloon is inflated
It remains in the artery when the balloon is removed.

35. Percutaneous Coronary Intervention
Post procedure care:
Assess vital signs
Bedrest/ flat in bed
Affected leg straight
Pressure dressing applied
Monitor for bleeding/hematoma
Resume self-care activities/ambulation few hours after procedure

36. Percutaneous Coronary Revascularization

37. Atherectomy Remove plaque from the identified lesion
Catheter shaves the plaque off vessels walls using a rotary cutting head - retaining the fragments in it compartment and removing them from the vessel.
Rotation catheter pulverize the plaque into particles small enough to pass through the coronary microcirculation.

39. CABG
Involves using a section of a vein /artery to create a connection (bypass) between the aorta and the coronary artery beyond construction.
This allows blood to perfuse the ischemic portion of the heart.
Internal mammary artery in the chest/saphenous vein from the leg are the vessels most commonly used.

40. CABG Surgery Internal mammary artery – is commonly used.
Remains palliative treatment and not a cure.
Improves quality of life/patient outcomes
Postoperative complications/mortality increase as a function of age.
Women have a higher mortality rate than men

42. CABG

43. Patient teaching Lifestyle changes and reduction of risk factors
Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of ischemia
Teaching regarding disease process
Cardiac rehabilitation
Stress reduction
When to seek emergency care

45. Myocardial Infarction
An area of the myocardium is permanently destroyed  necrosis of the myocardial cells. If circulation to the affected myocardium is not promptly restored , the heart loses the ability to maintain effective cardiac output.
Life-threatening event
May lead to cardiogenic shock and death

46. Myocardial Infarction
Annually 785,000 experience their first MI
Majority of deaths from MI occur during the initial period after symptoms begin:
60% within the first hour
40% prior to hospitalization
Medical treatment and training in CPR are vital to decrease deaths due to MI.

47. Myocardial Infarction
The area of infarction develops over minute to hours.
Cellular ischemia  affects conduction and myocardial contractility
Myocardial contractility decreases, increasing the risk for dysrhythmias, subsequently reducing cardiac output, B/P, and tissue perfusion

48. Myocardial Infarction
When a larger artery is compromised, collateral vessels connecting smaller arteries in the coronary system dilate to maintain blood flow to the cardiac muscle.
The degree of collateral circulation determines the extent of myocardial damage.
Occlusion of coronary artery without any collateral vessels  massive tissue damage and death

49. Clinical Manifestations
Pain – sudden and usually not associated with activity
Women/older adults atypical chest pain, elevated BP & HR initially, then ↓’es
Nausea/vomiting
Fever
Dyspnea, shortness of breath
Anxiety , sense of impending doom

52. Collaborative Care Goals Relieve chest pain
Reduce the extent of myocardial damage
Maintain cardiovascular stability
Decrease cardiac workload
Prevent complications

53. Assessment/ Diagnostic Findings
ECG
Laboratory tests— serum cardiac biomarkers
CK-MB
Myoglobin
Troponin
CBC
Echocardiogram

54. Laboratory Tests Serum Cardiac Markers
Are proteins released into the blood from necrotic heart muscle
They occur after cellular death indicates cardiac damage
Creatine kinase (CK-MB) and troponin are measured to diagnose an MI.

55. Serum Cardiac Markers Creatine kinase (CK )
Important enzyme for cellular function
Found mainly in cardiac muscle (skeletal muscle/brain)
Begin to rise rapidly with damage to these tissues at about 4/6 hours after an MI , peak at about 12/24 hours and return to normal within 36/48 hours
CK correlates with the size of the infarction

56. Serum Cardiac Markers CPK-MB Subset of CK specific to cardiac muscle
Most sensitive indicating of MI
Elevated CK –alone is not specific for MI
Elevated CPK-MB  positive indicator of MI
Does not normally rise with chest pain from angina or other causes other than MI

57. Serum Cardiac Markers Troponin
Regulates the myocardial contractility process
Proteins released during myocardial infarction – are sensitive indicators of myocardial damage.
Necrosis of cardiac muscle, troponins are released and blood levels rise.
Is a highly cardiac specific indicator of an MI
Increases with 4-6 hours during an acute MI, remains elevated for a long period -- 3 weeks

58. Serum Cardiac Markers Myoglobin Helps transport oxygen
Found in cardiac and skeletal muscle
Levels start to increase within 1-3 hours of symptom onset return to normal within 24 hours after onset of symptoms.
Is one of the first cardiac markers to appear after MI, it lacks cardiac specificity.
Kidneys rapidly excrete it in urine  blood levels return to normal range within 24 hours.

59. Ischemia, Injury , Infarction

60. COMPLICATIONS Heart failure Cardiogenic shock
Dysrhythmias and cardiac arrest

61. Interdisciplinary Care
Immediate treatment goals for the MI
Relieve the chest pain
Reduce the extent of myocardial damage
Decrease the cardiac workload
Prevent complications

62. Treatment of Acute MI
Obtain diagnostic tests including ECG within 10 minutes of admission to the ED
Oxygen
Aspirin, nitroglycerin, morphine, beta-blockers
fibrinolytic therapy
Revascularization Procedures
As indicated: IV heparin, LMWH
Bed rest

63. Nursing Interventions
Pain stimulates the SNS, increasing cardiac work. Pain relief is a priority.
Acute Pain
Assess for verbal and nonverbal signs of pain
Administer oxygen2-5L/min via nasal cannula
Promote physical and psychologic rest
Titrate IV nitroglycerin as ordered
Administer morphine by IV push for chest pain as needed

64. Nursing Interventions
Ineffective Tissue Perfusion
Assess and document vital signs
Assess for changes in LOC
Auscultate heart and breath sounds
Monitor ECG Administer antidysrhythmic medications
Monitor oxygen saturation

65. Nursing Interventions
Fear
Acknowledge the client’s perception of the situation
Encourage questions/ provide consistent, factual answers
Encourage self-care
Administer anti-anxiety medications as ordered
Teach non-pharmacologic methods

67. HEART FAILURE

68. Heart Failure
Complex syndrome resulting from cardiac disorders that impair the ventricles’ ability to fill and effectively pump blood
Inability of the heart to pump sufficient blood to meet the metabolic demands of the body.
5.7 million people in the US have heart disease.
HF is increasing in incidence and prevalence.
Primarily a disease of older adults.
HF is associated with high morbidity/mortality rates

69. HEART FAILURE
Heart failure develops  cardiac output falls  decrease in tissue perfusion.
Is a disorder of cardiac function
Hypertension and CHD are the leading causes of heart failure
The prognosis for the client with heart failure depends on the underlying cause and how effectively the precipitating factors can be treated.
Most clients with heart failure die within 8 years of the diagnosis.
Ejection fraction – provides information about the (L) ventricle during systole. Normal 55-65%.

70. Pathophysiology
Decrease cardiac output activation of compensatory mechanisms neurohormonal response decrease in renal perfusion & increase vasoconstriction  sodium and water retention  fluid overload increase the workload of the heart

72. Etiology CAD and advancing age are the primary risk factors for HF
CAD is found in more than 60% of patients
Other factors: hypertension, diabetes, cigarette smoking, obesity,

73. Manifestations of Heart Failure
CHD/hypertension are common causes of
L-sided heart failure whereas R- heart failure caused by conditions that restrict blood flow to the lungs (acute/chronic pulmonary disease).
Left sided heart failure can lead to right sided heart failure.

74. Classification of Heart Failure
Left-sided heart failure
Most common form of HF
LV cannot pump blood effectively to the systemic circulation. Pulmonary venous pressures increase and result in pulmonary congestion with dyspnea, cough, crackles, and impaired oxygen exchange.
This increase pulmonary pressure  pulmonary congestion and edema

75. Types of Heart Failure
Manifestation of L-sided heart failure result from pulmonary congestion (backward effects) and decreased cardiac output (forward effects).
Fatigue and activity intolerance
Dizziness and syncope
Pulmonary congestion
Cyanosis
Rales/wheezing

77. Types of Heart Failure Right sided heart failure
Causes a back up of blood to the ( R) atrium
RV cannot eject sufficient amounts of blood into the pulmonary circulation  blood backs up in the venous system.
Increase venous pressure causes abdominal organs to become congested /peripheral edema develops
This results in peripheral edema, ® upper quadrant pain, ascites, anorexia, nausea, weakness, and weight gain.

79. Multisystem Effects of Heart Failure
Neurologic
Respiratory
Cardiovascular
Gastrointestinal
Genitourinary
Integumentary
Metabolic

80. Diagnostic Studies BNP levels – key diagnostic indicator of HF
Serum electrolytes
Liver function tests
Echocardiogram
Chest x-ray
Electrocardiogram

81. Heart Failure Hemodynamics Monitoring
Used to assess cardiovascular function in the critically/unstable client and evaluate their interventions
Hemodynamic parameters  heart rate, arterial blood pressure, central venous pressure, pulmonary pressure and cardiac output

83. Management of Heart Failure
Eliminate or reduce etiologic or contributory factors.
Reduce the workload of the heart by reducing afterload and preload.
Optimize all therapeutic regimens.
Prevent exacerbations of heart failure.
Medications are routinely prescribed for heart failure.

84. Medications Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Beta-blockers
Diuretics
Digitalis
Other medications

85. Other Treatment Surgery Circulatory assistance Cardiac transplantation
Hemodynamic Monitoring

86. Complications Compensatory Mechanism Hepatomegaly/splenomegaly
Dysrhythmias
Pulmonary problems

87. Nursing interventions
Decreased Cardiac Output
Excess Fluid Volume
Activity Intolerance
Diet

89. ACUTE CORONARY SYNDROME
ACS  occurs when ischemia is prolonged and not immediately reversible resulting in myocardial cell death .
The spectrum of ACS encompasses: unstable angina(UA), non-ST-segment-elevation MI (NSTEMI), ST-segment-evaluation MI (STEMI).