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Coronary Artery Disease
Cardiac Pharmacology
Myocardial Infarction
Lecture 2
Joy Borrero, RN, MSN 9/10
Angina Pectoris
Acute Coronary Syndrome
Coronary Artery Disease
 Etiology
 Risk factors
 Nonmodifiable vs. modifiable risk factors
 Clinical manifestations
 Goals of therapy
 Medications
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 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.
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
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
Assesment
 1. Hx
 2. Physical Exam
 3. EKG
 4. Exercise EKG
 5. Thallium Scan
 6. Coronary Angiography
 7. Cardiac Enzymes
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
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)
 Tachycardia
 Palpitations
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 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
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
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 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)
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)
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
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)
Calcium Channel Blockers
Side Effects of Calcium Channel Blockers
 Constipation (with Verapamil)
 Dizziness
 Facial Flushing
 HA
 Edema of ankles/feet
 Bradycardia
 Hypotension
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
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
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)
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)
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)
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
EKG changes with MI
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)
General Types of MI
 Transmural-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 Etiology
 CAD and its risk factors
 Any situation requiring increased O2 in the
presence of decreased O2 supply.
 Non atherosclerotic coronary artery occlusions
Effects of MI
 Cell death
 Contractility in the affected areas reduced or
absent
 Electrical instability
Dysrhythmias occur in 90% of patients
 PVCs
 V tach
 V fib
 Bradycardia
Complications of MI
 CHF
 Mitral Valve Insufficiency
 Dysrhythmias
 Pericarditis
 Post Infarction MI
 Thromboembolic Complications
 Rupture of Ventricular Wall
MI Precipitating Factors
 None in most cases
 Severe exertion and stress
 59% occur at rest or while asleep
Clinical Manifestations
 Angina-Chest Pain
 Vital Signs
 Heart and Lung
 Associated S&S
What’s the difference?
Angina Myocardial Infarction
Diagnosis of MI
Based on 2 out of 3 criteria
1. Chest pain indicative of ischemic heart disease
2. Characteristic EKG changes (ST elevation)
3. Marked rise and eventual decline in serum
markers of cardiac injury
Diagnostic studies
 EKG
 Serum Enzymes/Cardiac Biomarkers
 Cardiac Catheterization
 Other lab tests
 Echocardiogram
 CXR
 Pulse 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 Interventions
Remember: 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
OH BATMAN!
 O
 H
 B
 A
 T
 M
 A
 N
Nursing Interventions
 Activity
 Safety
 Reduce anxiety
 Patient Education
 Nutrition
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
Pharmacology Therapy
 ASA
 Nitrates
 Morphine Sulfate
 Beta blockers
 Calcium channel blockers
 ACEs and ARBs
Antiarrhythmics
 Class IA- Na channel blockers
 Class IB- Na channel blockers
 Class II- Beta blockers
 Class III- Amiodarone
 Class IV- Ca Channel blockers
Anticoagulants
 Heparin
 LMWH- Lovenox, Fragmin
Post MI Cardiac rehab
 Begins 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 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
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
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.
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 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
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
NCLEX TIME
Modifiable risk factors associated with CAD include:
A. age, weight, cholesterol level
B. Smoking, diet, BP
C. Family hx, weight, BP
D. Blood glucose, activity level, family hx
NCLEX TIME
A patient has just returned from cardiac cath. Which
nursing intervention is most appropriate?
A. Assist pt to ambulate to the BR
B. Restrict fluids
C. Monitor peripheral pulses
D. Insert an indwelling catheter
NCLEX TIME
A 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 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
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 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 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
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
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
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.

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ACS Lecture.ppt

  • 1. Coronary Artery Disease Cardiac Pharmacology Myocardial Infarction Lecture 2 Joy Borrero, RN, MSN 9/10 Angina Pectoris Acute Coronary Syndrome
  • 2. Coronary Artery Disease  Etiology  Risk factors  Nonmodifiable vs. modifiable risk factors  Clinical manifestations  Goals of therapy  Medications
  • 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 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
  • 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
  • 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 1. Chest pain indicative of ischemic heart disease 2. Characteristic EKG changes (ST elevation) 3. 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
  • 43. Nursing Interventions Remember: 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
  • 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: A. age, weight, cholesterol level B. Smoking, diet, BP C. Family hx, weight, BP D. Blood glucose, activity level, family hx
  • 58. NCLEX TIME A patient has just returned from cardiac cath. Which nursing intervention is most appropriate? A. Assist pt to ambulate to the BR B. Restrict fluids C. Monitor peripheral pulses D. Insert an indwelling catheter
  • 59. NCLEX TIME A 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
  • 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
  • 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 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.
  • 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
  • 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
  • 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
  • 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.
  • 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. 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.