Angina Pectoris Acute Coronary Syndrome

1. Angina PectorisAcute Coronary Syndrome Coronary Artery Disease Cardiac Pharmacology Myocardial Infarction Lecture 2 NUR240 Joy Borrero, RN, MSN 9/10

2. Coronary Artery Disease • Etiology • Risk factors • Nonmodifiable vs. modifiable risk factors • Clinical manifestations • Goals of therapy • Medications

3. ATHEROSCLEROSIS START END

4. STATINS aka: (COENZYME INHIBITOR) • Mevacor, Zocor, Lipitor • BLOCKS BIOSYNTHESIS OF CHOLESTEROL • HIGH FIRST PASS EFFECT • *MONITOR LFT • SIDE EFFECTS • N/V/D & ABDOMINAL CRAMPS • MYALGIA, ARTHRALGIA,Cataracts • HEADACHES, DIZZINESS, INSOMNIA • Liver and kidney dysfunction

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 Anginaonly at night. Possible associated with REM sleep. • Unstable AnginaAKA 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 it’s 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. What’s 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