06-CV4-MI.ppt
07/23/2009
Coronary Artery Disease
Coronary Artery Disease,
Angina and MI
? Most CAD nothing more than Atherosclerosis
in the coronary arteries
? Chronic leads to angina pectoris
? Acute is MI
¨C 700,000 new MIs in U.S.
¨C 500,000 recurrent MIs in U.S.
Risk Factors
? Major nonmodifiable
¨C Age/gender
¨C Family hx
? Major modifiable
¨C
¨C
¨C
¨C
¨C
¨C
¨C
Dyslipidemia
Hypertension
Smoking
DM, insulin resistance
Obesity
Sedentary
Atherogenic diet
? Nonconventional
¨C HS CRP
¨C Homocysteine
¨C Lp(a)
Coronary Arteries
? Coronary Arteries surround and then
penetrate the heart muscle
¨C Right coronary artery (RCA) (back of heart)
¨C Left (Main) coronary artery
? Left circumflex (Side)
? Left anterior descending (Front)
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Myocardial Ischemia
? Blood flow must be impeded before heart
metabolism is affected
¨C Absolute
¨C Relative
? Causes
Supply/Demand Considerations
? Oxygen supply
¨C
¨C
¨C
¨C
Cardiac output
Hemoglobin levels
Respiratory function
Fitness of muscle
? Oxygen demand
¨C Atherosclerosis, Vasospasm
¨C Hypotension, Arrythmias, Anemia, V/Q
¨C Work of the heart
? Contractility
? HR
¨C Hypertrophy of the heart
Myocardial Ischemia
? Myocardium becomes ischemic within 10
seconds of coronary occlusion
? Working cells remain viable for up to 20
minutes
¨C Anaerobic mechanisms kick in
? Lactic acid
? Free radical damage, esp after reperfusion
Cardiac Ischemia Manifestation
? Stable angina
¨C Chronic obstruction
¨C Chest pain with exertion
¨C May radiate, may have diaphoresis, SOB, pallor
¨C Relief with rest or nitrates
? Prinzmetal angina
? Silent ischemia
? Unstable angina
¨C May become a myocardial infarction
Evaluation
?
?
?
?
?
?
H&P
Lipids, BP, risk factor assessment
ECG
Stress test
Angiography
Unstable angina
¨C Cardiac enzymes (rule in/out for MI)
Treatment for Stable Angina
? Drug
¨C Nitrates
¨C Beta blockers
¨C Calcium Channel Blockers
¨C Atherosclerotic disease tx (HTN, Lipids)
? Surgery
¨C Bypass
¨C PCI (PTCA, Stent)
¨C Experimental
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Acute Coronary Syndrome
Acute Coronary Syndrome
Atherosclerotic Plaque
? Unstable Angina ¨C reversible ischemia
¨C Rupture of an unstable plaque
¨C Clots spontaneously resolve over time
¨C Damage depends on size of clot and rate of
dissolution vs. rate of clot formation
¨C Myocardial infarction
Stable Plaque
Unstable Plaque
Stable Angina
Acute Coronary Syndrome
Transient
Ischemia/
Unstable
Angina
Sustained
Ischemia
Myocardial
Infarction
Necrosis
MI Pathophysiology
? Plaque rupture --> Clotting cascade active
? Thrombus occludes vessel
? Myocardium becomes hypoxic
¨C Shift to Anaerobic Respiration
¨C Waste products release/hypoxic injury
¨C Cardiac output impaired
? Norepinephrine/Epinephrine Release
? Renin release
Ischemic Morphology
? Increased O2 demand: epinephrine, RAAS
? Hypoactive wall/Necrosis
¨C Transmural
¨C Subendocardial
? Conductile problems
¨C PVCs
¨C Dysrhythmias
Myocardial Changes
? Myocardial stunning
¨C Temporary loss of contractility that persists for
hours to days
? Myocardial hibernation
¨C Chronically ischemic; myocytes are hibernating to
preserve function until perfusion can be restored
? Myocardial remodeling
¨C Loss of contractility mediated by Ang II,
catecholamines, and inflammatory cytokines
ECG changes
? Conductile cells of heart are most sensitive to
hypoxia
? Classic: T-wave inversion, ST-elevation, Q waves
? Non-Q wave MI: no Q waves, possibly normal
ST segment
? R/O CANNOT be made with ECG alone!!!
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MI Manifestations
? Prodromal
¨C Symptoms usually appear 24-72 hours before
¨C Malaise, Tiredness, Weakness fatigue
¨C Visual disturbance
? Acute Phase
¨C Symptoms: Chest Pain, Dyspnea, Nausea,
Diaphoresis, weakness, fatigue, anxiety
¨C Signs: Gray/ashen, gasping, clutching, loss of
consciousness, confused, ECG changes,
tachycardia, tachypnea
Eval & Tx
? ECG
? Cardiac Enzymes X 4
¨C If Ruled in
? Anticoagulation, antiplatelet
? Thrombolytic Therapy
? Cath lab, Emergency bypass
¨C If Ruled out
? Stress test
? Angiogram
Nitroglycerine
? Vasodilating actions
¨C Primarily acts on veins and large arteries
¨C Uptake by VSM cells and converts to active form:
NO
? Therapeutic uses: Stable Angina
¨C Decreases preload decreases contraction
oxygen demand
¨C Does not dilate coronary arteries
? MONA: Morphine, O2, Nitrates, ASA
Nitrates
? Kinetics
¨C Highly lipid soluble: can be given PO, IV, SL,
transdermal
¨C Rapid inactivation by organic nitrate reductases
¨C Half-life 5 ¨C 7 minutes
¨C PO: most drug is destroyed in liver before reaching
systemic circulation
? Adverse Effects
¨C Headache
¨C Orthostatic Hypotension
¨C Reflex tachycardia
Nitrates
? Interactions
¨C Other hypotensive drugs
¨C Beta blockers, verapamil, diltiazem
¨C Sildenafil (Viagra) ¨C life threatenening: 25 mmHg
drop
? Tolerance
¨C Most common in high dose, continuous therapy
¨C Prevent by using lower dose intermittent therapy:
8 hour drug free time
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Nitrates
? Preparations
¨C Sublingual: works in 1 ¨C 3 minutes; lasts an hour; expires within
6 months of opening
¨C Translingual spray
¨C Topical Ointment
¨C Transdermal patch
¨C PO Sustained release capsules or tablets: higher doses d/t first
pass effect (isosorbide mononitrate, dinitrate)
¨C IV infusion: glass bottle, special (vented) tubing
? Nursing implications
¨C Check BP before and after administering
¨C Assess for headache
¨C Discontinue slowly if patient has been on it for a while
Immediate Post MI Tx
? Most common cause of death within 72 hours
of MI is ________________
¨C Must be monitored
?
?
?
?
Reduce myocardial workload
Prevent Remodeling
Reduce chances of reocclusion
Reduce oxidative stress (reperfusion injury)
Post MI Evaluation
? Stress test
? Angiography
? Symptoms
Post MI Treatment
? Lifestyle
¨C Diet
¨C Exercise ¨C Cardiac Rehab
¨C Stress management
? Drugs
¨C Antiplatelet: ASA, clopidogrel, persantine
¨C Beta blocker
¨C Statin medication
¨C Treat risk factors (HTN, lipid, smoke, etc.)
¨C Sometimes coumadin
Clot Review
? Platelet aggregation
¨C Become sticky
¨C Activate GP IIb/IIIa
receptors
¨C Chemicals
? Prostaglandins
? Thromboxanes
? ADP
? Clot Stabilization
¨C Activation of
fibrinogen
¨C Binds to GP IIb/IIIa
¨C Chemicals
? Clotting cascade
Thrombin
Fibrinogen activation
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