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1. Coronary Artery Disease
Cardiac Pharmacology
Myocardial Infarction
Lecture 2
NUR240 Joy Borrero, RN, MSN 9/10 Angina PectorisAcute Coronary Syndrome
2. Coronary Artery Disease Etiology
Risk factors
Nonmodifiable vs. modifiable risk factors
Clinical manifestations
Goals of therapy
Medications
3. ATHEROSCLEROSIS
5. Angina Pectoris Episode of chest pain or pressure due to insufficient artery flow of oxygenated blood.
Myocardial 02 demand exceeds 02 supply. CAD is the most common cause.
One coronary artery branch becomes completely occluded; therefore, 02 is not perfused to the myocardium, resulting in transient ischemia and subsequent retrosternal pain.
6. Angina Pectoris Precipitating Factors: Warning Sign for MI
Clinical Signs & Symptoms: do not occur until lumen is 75% narrowed. Sternal pain: mild to severe. May be described as heavy, squeezing, pressing, burning, crushing or aching. Onset sudden or gradual. May radiate to L. shoulder and arm. Radiates less commonly to R. shoulder, neck, jaw. Pt may have weakness/numbness of wrist, arm, hands. pain usually short duration and relieved by removal precipitating factors,rest or NTG. Can be gradual (CAD) or sudden(vasospasm)
Associated Symptoms: dyspnea, N & V, tachycardia, palpitations, fatigue, diaphoresis, pallor, weakness, syncope, factors
7. Types of Angina Stable: There is a stable pattern of onset, duration and
intensity of sx, pain is triggered by a predictable degree of exertion or emotion.
Variant Angina (Prinzmetal's)
Cyclical, may occur at rest.
Ventricular arrhythmia, brady arrhythmia and conduction disturbances occur.
Syncope associated with arrhythmia may occur
Nocturnal Angina only at night. Possible associated with REM sleep.
Unstable Angina AKA Pre infarction angina
Pain is more intense, lasts longer
8. Assesment 1. Hx
2. Physical Exam
3. EKG
4. Exercise EKG
5. Thallium Scan
6. Coronary Angiography
7. Cardiac Enzymes
9. Medications for Angina
1. Nitrates decrease myocardial 02 demand via
peripheral vasodilation and reverse coronary artery spasm thus increase 02 supply to myocardial tissue.
2. Understanding how Nitrates Work: peripheral vasodilation results in:
-decreased 02 demand
-decreased venous return to heart
-decreased ventricular filling which results in decreased wall tension and thus
-decreased 02 demand
10. NTG Forms:
SL (Nitrostat)
Lingual Sprays - similar to SL in use (Nitrolingual)
Sustained release capsules/tablets (Nitrobid)
Ointments 2% (Nitrobid)- wear gloves when applying
Transdermal Patch (Nitro-Dur)
IV (Tridil) For attacks unresponsive to other tx
11. Side/Adverse Effects
Vascular HA (may be severe)
Hypotension (may be marked)
Tachycardia
Palpitations
12. Acute Angina Treatment
Goal: Enhance 02 supply to myocardium:
M- Morphine for pain
O- Oxygen 4-6L as ordered
N- NTG sublingual, repeat q5 minutes x3
A- Aspirin to prevent platelet aggregation
13. Angina Treatment The focus is to relieve acute attacks and prevent further attacks.
1. Activity/exercise tolerance - a regular exercise prescription is established after stress testing
and/or cardiac cath.
Baseline
Gradual increase
Avoid
Alternate
ADLS
NTG before exercise
14. Patient education
Lifestyle modifications for controllable risk factors. Support groups are helpful, Example: Weight watchers,
Smoke-enders, stress workshops, cardiac rehabilitation. Supply patients with information, name of contact person and phone numbers
Identify precipitating factors for Anginal pain
Medication compliance
15. Cardiac Pharmacology
16. Beta-adrenergic Blockers
Therapeutic effect - decrease the rate and force of the cardiac contraction (resulting in decreased 02 demand) and decrease vasoconstriction in the myocardium and vasculature.
Mechanism of Action - inhibit circulating catecholamines from stimulating beta receptor sites. There are two type of beta receptors (B1 & B2).
17. Beta-adrenergic Blockers
B1 receptor stimulation by catecholamines
results in increased HR & myocardial contractility so, blocking the B1 effect results in slowed HR & decreased myocardial contractility.
Cardio-selective
Excess blockade can result in bradycardia, heart block, heart failure and/or hypotension.
atenolol (Tenormin)
metoprolol (Lopressor, Toprol)
18. Beta-adrenergic Blockers
B2 receptor stimulation by catecholamines results in dilation of the bronchial tree, the coronary arteries and the peripheral vasculature
Blocking the B2 effect results in bronchoconstriction, coronary artery vasoconstriction and peripheral vascular constriction.
Drugs that have a B2 blockade effect are used cautiously/contraindicated in clients with COPD.
Non-selective Beta Blockers - Block B1 and B2 receptors
propanolol (Inderal)
carvedilol (Coreg)
19. Beta-adrenergic Blockers
Side Effects - many may be predicted based upon understanding the mechanism of action.
Hypotension Bradycardia
Heart Failure Weakness/Fatigue
Depression Impotence
Hypoglycemia Hallucinations
Patient Teaching:
Use with caution in clients prone to coronary artery spasm due to vasoconstrictive effects.
Contraindicated in clients with CHF and second or third degree heart block due to the rate slowing and reduction in contractility.
Non-selective beta blockers contraindicated with COPD.
Do not abruptly discontinue beta blockers
20. Calcium Channel Blockers Action - inhibit flow of Ca+ across cell membrane. Ca+ is essential for cardiac stimulation, conduction, contractility and relax vascular smooth muscle which results in decreased 02 demand and increased coronaryblood supply?
VASODILATION
Indications: angina, HTN, arrhythmia
Drugs-
verapamil (Calan, Isoptin)
diltiazem (Cardizem)
nifedipine (Procardia)
amlodipine (Norvasc)
21. Calcium Channel Blockers Side Effects of Calcium Channel Blockers
Constipation (with Verapamil)
Dizziness
Facial Flushing
HA
Edema of ankles/feet
Bradycardia
Hypotension
22. Epinenepherine (adrenalin) Vasoconstriction- Increase BP
Alpha, Beta 1 and Beta 2 agonist
Decrease congestion of nasal mucosa
Catacholamine- produced by
Tx of AV block and cardiac arrest
23. ACE INHIBITORS The prils Angiotensin Converting Enzymes Inhibitors
Action: Blocks production of Angiotensin II in kidneys
Indications: HF, HTN, MI, DM neuropathy
Causes: Vasodilation (mostly arteriole)
Decreased BP
Excretion of Na and H2O (but not K)
Ex.: captopril (Capoten)
enalapril (Vasotec)
fosinopril (Monopril)
ramapril (Altace)
SE : ortho hypotension, dry cough, hyperkalemia
24. Angiotensin Receptor Blockers- ARBs Action- Block the binding of Angiotensin II
to its receptor in the vascular and adrenal tissues
Examples: candesartan (Atacand)
losartan (Cozaar)
25. Cardiac Glycoside digoxin (Lanoxin) Action :+Inotropic effect
Increases force of myocardial contraction
- Chronotropic effect- decreases HR
Tx: heart failure, afib
Nsg: Apical Pulse for 1 full minute, hold for <60, same time daily
Monitor Dig levels 0.5-0.8 ng/ml
Monitor K levels
Monitor for Dig toxicity: anorexia, fatigue, weakness, vision changes (halos)
26. Myocardial Infarction Leading cause of death in US
Thrombosis in atherosclerotic artery causes 90% of MIs.
A region of the myocardium is abruptly deprived of blood supply due to restricted coronary blood flow
Ischemia results and may lead to necrosis within 6 hours
JCAHO Core Measures for AMI (4/10)
27. Gender Differences in MI Females, when compared to males:
-present with MI later in life
-have poorer prognosis and high morbidity
-are 2x as likely to die in the first weeks
-are more likely to die from the first MI
-have higher rates of unrecognized MI
-NSTEMI MI vs STEMI
28. EKG changes with MI
29. Location of MI Depends on which artery is affected
LV receives most of the CA supply and so it is the most affected
Left Anterior Descending (LAD)
Left Circumflex artery (LCA)
Right Coronary Artery (RCA)
30. General Types of MI Transmural-invades full thickness of myocardium
Subenedocardial-invades partial thickness
31. Collateral Circulation A network of blood vessels present at birth that can dilate and become functional a/r/o coronary artery occlusion and ischemia. collateral circulation
Natural bypass mechanism helps decrease the size of the MI
32. Risk Factors and Etiology CAD and its risk factors
Any situation requiring increased O2 in the presence of decreased O2 supply.
Non atherosclerotic coronary artery occlusions
33. Effects of MI Cell death
Contractility in the affected areas reduced or absent
Electrical instability
34. Dysrhythmias occur in 90% of patients PVCs
V tach
V fib
Bradycardia
35. Complications of MI CHF
Mitral Valve Insufficiency
Dysrhythmias
Pericarditis
Post Infarction MI
Thromboembolic Complications
Rupture of Ventricular Wall
36. MI Precipitating Factors None in most cases
Severe exertion and stress
59% occur at rest or while asleep
37. Clinical Manifestations Angina-Chest Pain
Vital Signs
Heart and Lung
Associated S&S
38. Whats the difference? Angina Myocardial Infarction
39. Diagnosis of MI Based on 2 out of 3 criteria
Chest pain indicative of ischemic heart disease
Characteristic EKG changes (ST elevation)
Marked rise and eventual decline in serum markers of cardiac injury
40. Diagnostic studies EKG
Serum Enzymes/Cardiac Biomarkers
Cardiac Catheterization
Other lab tests
Echocardiogram
CXR
Pulse Ox
41. Goals Limit size of infarct/prevent further damage
Increase O2 supply and decrease O2 demand
Prevent and /or recognize complications early
Reduce pain
42. Nursing Diagnosis
43. Nursing InterventionsRemember: MONA and Oh Batman Obtain EKGs
Monitor mentation
Assess heart sounds
Assess lungs
Assess peripheral circulation/skin
Assess urinary output
Assess GI function
Assess pain
44. OH BATMAN! O
H
B
A
T
M
A
N
45. Nursing Interventions Activity
Safety
Reduce anxiety
Patient Education
Nutrition
46. Pharmacology Therapy for MI Thrombolytic Agents a/k/a Plasminogen Activators (Streptokinase, T-PA,Retavase)
-decrease infarct size
-improved ventricular function
-increased survival rates
Glycoprotein IIB and IIIA
47. Pharmacology Therapy ASA
Nitrates
Morphine Sulfate
Beta blockers
Calcium channel blockers
ACEs and ARBs
48. Antiarrhythmics Class IA- Na channel blockers
Class IB- Na channel blockers
Class II- Beta blockers
Class III- Amiodarone
Class IV- Ca Channel blockers
49. Anticoagulants Heparin
LMWH- Lovenox, Fragmin
50. Post MI Cardiac rehab Begins in acute phase and continues indefinitely as outpatient
Includes:
education
activity progression
counseling
medical management
51. Non-Pharmacologic Therapy Percutaneous transluminal coronary angioplasty (PTCA)
Dilates coronary arteries obstructed by plague. 30% restenosis rate within first 6 months.
Patient Criteria
Non-calcified lesions less than 2 cm. The ideal candidate would have less than a one year history of angina and be able to undergo coronary artery by-pass grafting if necessary. Patients with calcified lesions or lesions in branch vessels are not considered good candidates
52. Non-Pharmacologic Therapy
Cardiac Catheterization/ Balloon Angioplasty
Performed in the cardiac cath lab. A catheter with a balloon tip is passed into the obstructed artery and is alternately inflated and deflated to increase arterial diameter and perfusion.
Complications
Arterial rupture, spasm, emboli, MI
Post-procedure care
53. Other Procedures Coronary Artery Stents
Stainless steel mesh stent is placed in lumen to prevent restenosis after angioplasty. Requires anticoagulation and antiplatelet tx to prevent local-thrombosis.
Coronary Laser Surgery
Laser can destroy atherosclerotic plaque. Research is being conducted in transluminal laser angioplasty to coronary arteries.
Atherectomy - surgical removal of atheroma.
54. Coronary Artery By-Pass Grafting (CABG)
Procedure - Surgical revascularization to increase coronary blood flow.
Patients with severe disease may not be candidates. Longevity after surgery still being debated. Surgery does not cure atherosclerosis and patients must still control risk factors
55. Post-op CABG
Post-Operative Nursing Assessments & Care
Cardiovascular function
Respiratory function - pt may be on mechanical ventilator for short time.
Renal Function
Neurologic Function
Peripheral Vascular Function
Fluid & Electrolyte Balance
Pain management
Psychological Status
Safety - Pt may be restrained to present self extubation
56. Cardiac Tamponade of CABG
Etiology - heart is compressed by fluid within the pericardial sac. Ventricular filling is thus impaired resulting in decreased cardiac output and circulatory collapse.
Clinical Signs
Pulsus Paradoxus Blood Pressure
Neck Veins Heart Sounds
Respirations Mental Status
Pain
Treatment
Thoracotomy Pericardiocentesis
57. NCLEX TIME Modifiable risk factors associated with CAD include:
age, weight, cholesterol level
Smoking, diet, BP
Family hx, weight, BP
Blood glucose, activity level, family hx
58. NCLEX TIME A patient has just returned from cardiac cath. Which nursing intervention is most appropriate?
Assist pt to ambulate to the BR
Restrict fluids
Monitor peripheral pulses
Insert an indwelling catheter
59. NCLEX TIME A 63 man is resuscitated successfully after cardiac arrest. Blood studies show that he is acidotic. Why?
Decreased tissue perfusion causes lactic acid production
The pt typically has an irregular heart beat
The pt was treated inappropriately with Na Bicarb
Fat forming ketoacids are breaking down
60. NCLEX TIME Rosie is preparing her client for discharge following his inpatient stay with angina, which is now stable. Rosie is reviewing both modifiable and nonmodifiable risk factors. Select all factors below that are nonmodifiable.
A.Age
B.Gender
C.Obesity
D.Family history
E.Hypertension A, B, DA, B, D
61. NCLEX TIME Following her inferior wall MI, Mrs. Green is quiet, reserved, and avoiding contact with her family. Understanding the psychosocial aspects of ACS, which intervention would be best for the nurse to do first?
A.Have the clients cardiologist write for a psychiatric referral.
B.Provide an atmosphere of acceptance.
C.Foster mechanisms to suppress anger and hostility.
D.Provide factual information to the clients family alone. BB
62. NCLEX TIME When Rosie is assessing her client with chest pain, she is evaluating whether or not the client is suffering from angina or MI. Which symptom would be indicative of an MI?
A.Substernal chest discomfort
B.Chest pain brought on by exertion or stress
C.Substernal chest discomfort relieved by nitroglycerin or rest
D.Substernal chest pressure relieved only by opioids DD
63. NCLEX TIME All of the following clients are being cared for on the coronary care stepdown unit. When making client assignments, which client will be best for the charge nurse to assign to a new graduate RN who has completed 6 months of orientation to the unit?
A.A client who has a new diagnosis of heart failure and needs discharge teaching about medications
B.A client who has just returned to the unit after having a coronary arteriogram and has orders for vital signs every 15 minutes
C.A client with a history of angina who is requesting nitroglycerin for left anterior chest pain
D.A client who has many questions about the electrophysiology studies that are scheduled bb
64. NCLEX TIME 4.An RN and an LPN who both have several years of experience in the intensive care unit are caring for a group of clients. Which task will be most appropriate for the RN to delegate to the LPN?
A.Obtaining pulmonary artery wedge pressures every hour for a client admitted with pulmonary edema
B.Monitoring vital signs and assessing the catheter insertion site for a client who returned from a coronary arteriogram an hour ago
C.Teaching the family members of a client who is scheduled for myocardial nuclear perfusion imaging about the procedure
D.Completing the admission assessment for a client admitted to the unit with acute coronary syndrome BB
65. NCLEX TIME The nurse is caring for a client who has been admitted with chest pain of unknown etiology. All of the following laboratory tests are obtained. Which test results require the most immediate action by the nurse.
A.Troponin T is elevated.
B.Creatinine kinase is decreased.
C.Myoglobin is increased.
D.High-density lipoproteins are decreased. AA
66. Cardiac Case Study A 57yo male is admitted to your unit c/o dull pain in the left side of his chest and radiating to his neck. Theres no diaphoresis or SOB. Risk factors include hypercholesteremia and a 70 pack year hx of smoking.
PE reveals BP 140/86, HR 110, normal heart sounds and clear lungs bilat. Cardiac markers drawn ˝ hour after the onset of pain show Myoglobin 45mcg. Troponin I at 0.01ng/mL and CPK-MB of 10u/L. EKG shows nonspecific ST wave changes in the anterior leads.