Coronary Artery Disease Cardiac Pharmacology Myocardial Infarction Lecture 2 NUR240 Joy Borrero, RN,...

Coronary Artery DiseaseCardiac PharmacologyMyocardial Infarction

Lecture 2

NUR240

Joy Borrero, RN, MSN 9/10

Angina PectorisAcute Coronary Syndrome

Coronary Artery DiseaseEtiologyRisk factorsNonmodifiable vs. modifiable risk factors

Clinical manifestationsGoals of therapyMedications

ATHEROSCLEROSIS

START

END

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

Angina PectorisEpisode 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.

Angina PectorisPrecipitating Factors: Warning Sign for MIClinical 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

Types of Angina Stable: There is a stable pattern of onset,

duration andintensity 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

Assesment 1. Hx 2. Physical Exam 3. EKG 4. Exercise EKG 5. Thallium Scan 6. Coronary Angiography 7. Cardiac Enzymes

Medications for Angina1. 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

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

Side/Adverse Effects

Vascular HA (may be severe)Hypotension (may be marked)TachycardiaPalpitations

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

Angina TreatmentThe 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.

BaselineGradual increaseAvoidAlternateADLSNTG before exercise

Patient educationLifestyle 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

Cardiac Pharmacology

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).

Beta-adrenergic BlockersB1 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)

Beta-adrenergic BlockersB2 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)

Beta-adrenergic BlockersSide Effects - many may be predicted based upon understanding the mechanism of action.

Hypotension BradycardiaHeart Failure Weakness/FatigueDepression ImpotenceHypoglycemia 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

Calcium Channel BlockersAction - 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

VASODILATIONIndications: angina, HTN, arrhythmiaDrugs-

verapamil (Calan, Isoptin)diltiazem (Cardizem)

nifedipine (Procardia) amlodipine (Norvasc)

Calcium Channel BlockersSide Effects of Calcium Channel Blockers

Constipation (with Verapamil) Dizziness Facial Flushing HA Edema of ankles/feet Bradycardia Hypotension

Epinenepherine (adrenalin)Vasoconstriction- Increase BPAlpha, Beta 1 and Beta 2 agonistDecrease congestion of nasal mucosaCatacholamine- produced by……Tx of AV block and cardiac arrest

ACE INHIBITORS –The “prils”

Angiotensin Converting Enzymes InhibitorsAction: Blocks production of Angiotensin II in kidneys

Indications: HF, HTN, MI, DM neuropathyCauses: 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

Angiotensin Receptor Blockers- ARBsAction- Block the binding of Angiotensin II

to it’s receptor in the vascular and adrenal tissues

Examples: candesartan (Atacand) losartan (Cozaar)

Cardiac Glycoside digoxin (Lanoxin)

Action :+Inotropic effect Increases force of myocardial contraction

- Chronotropic effect- decreases HR

Tx: heart failure, afibNsg: 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)

Myocardial InfarctionLeading cause of death in USThrombosis 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)

Gender Differences in MIFemales, 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

EKG changes with MI

Location of MI

Depends on which artery is affectedLV 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)

General Types of MITransmural-invades full thickness of myocardium

Subenedocardial-invades partial thickness

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

Risk Factors and EtiologyCAD and its risk factorsAny situation requiring increased O2 in the presence of decreased O2 supply.

Non atherosclerotic coronary artery occlusions

Effects of MICell deathContractility in the affected areas reduced or absent

Electrical instability

Dysrhythmias occur in 90% of patientsPVCsV tachV fibBradycardia

Complications of MI

CHFMitral Valve InsufficiencyDysrhythmiasPericarditisPost Infarction MIThromboembolic ComplicationsRupture of Ventricular Wall

MI Precipitating Factors None in most casesSevere exertion and stress59% occur at rest or while asleep

Clinical ManifestationsAngina-Chest PainVital SignsHeart and LungAssociated S&S

What’s the difference?

AnginaMyocardial Infarction

Diagnosis of MI

Based on 2 out of 3 criteria1. Chest pain indicative of ischemic

heart disease2. Characteristic EKG changes (ST

elevation)3. Marked rise and eventual decline

in serum markers of cardiac injury

Diagnostic studiesEKGSerum Enzymes/Cardiac BiomarkersCardiac CatheterizationOther lab testsEchocardiogramCXRPulse Ox

Goals Limit size of infarct/prevent further damage

Increase O2 supply and decrease O2 demand

Prevent and /or recognize complications early

Reduce pain

Nursing Diagnosis

Nursing InterventionsRemember: MONA and Oh BatmanObtain EKGsMonitor mentationAssess heart soundsAssess lungsAssess peripheral circulation/skinAssess urinary outputAssess GI functionAssess pain

OH BATMAN!OHBATMAN

Nursing Interventions

ActivitySafetyReduce anxietyPatient EducationNutrition

Pharmacology Therapy for MI

Thrombolytic Agents a/k/a Plasminogen Activators (Streptokinase, T-PA,Retavase)

-decrease infarct size-improved ventricular function-increased survival ratesGlycoprotein IIB and IIIA

Pharmacology TherapyASANitratesMorphine SulfateBeta blockersCalcium channel blockersACEs and ARBs

AntiarrhythmicsClass IA- Na channel blockersClass IB- Na channel blockersClass II- Beta blockersClass III- AmiodaroneClass IV- Ca Channel blockers

AnticoagulantsHeparinLMWH- Lovenox, Fragmin

Post MI Cardiac rehabBegins in acute phase and continues indefinitely as outpatient

Includes: education activity progression counseling medical management

Non-Pharmacologic Therapy Percutaneous transluminal coronary angioplasty (PTCA)

Dilates coronary arteries obstructed by plague. 30% restenosis rate within first 6 months.

Patient CriteriaNon-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

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.

ComplicationsArterial rupture, spasm, emboli, MI

Post-procedure care

Other ProceduresCoronary Artery StentsStainless steel mesh stent is placed in lumen to prevent restenosis after angioplasty. Requires anticoagulation and antiplatelet tx to prevent local-thrombosis.

Coronary Laser SurgeryLaser can destroy atherosclerotic plaque. Research is being conducted in transluminal laser angioplasty to coronary arteries.

Atherectomy - surgical removal of atheroma.

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

Post-op CABG

Post-Operative Nursing Assessments & Care

Cardiovascular functionRespiratory function - pt may be on mechanical ventilator for short time.

Renal FunctionNeurologic FunctionPeripheral Vascular FunctionFluid & Electrolyte BalancePain managementPsychological StatusSafety - Pt may be restrained to present self extubation

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 PainTreatment Thoracotomy Pericardiocentesis

NCLEX TIMEModifiable risk factors associated

with CAD include:A. age, weight, cholesterol levelB. Smoking, diet, BPC. Family hx, weight, BPD. Blood glucose, activity level,

family hx

NCLEX TIMEA patient has just returned from

cardiac cath. Which nursing intervention is most appropriate?

A. Assist pt to ambulate to the BRB. Restrict fluidsC. Monitor peripheral pulsesD. Insert an indwelling catheter

NCLEX TIMEA 63 man is resuscitated successfully

after cardiac arrest. Blood studies show that he is acidotic. Why?

A. Decreased tissue perfusion causes lactic acid production

B. The pt typically has an irregular heart beat

C. The pt was treated inappropriately with Na Bicarb

D. Fat forming ketoacids are breaking down

NCLEX TIMERosie 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.AgeB.GenderC.ObesityD.Family historyE.Hypertension

NCLEX TIMEFollowing 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 client’s 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 client’s family alone.

NCLEX TIMEWhen 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 discomfortB.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

NCLEX TIMEAll 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

NCLEX TIME4.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

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.

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. There’s 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 ½ 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.