Arthrosclerosis
Ischemia Infarction Collateral Circulation
Ethnic background
Hypertension
Impaired glucose tolerance Obesity Physical inactivity Stress Diabetes Oral Contraceptives
The major underlying cause is atherosclerosis. Atherosclerosis is a slow, progressive disease which begins in childhood and takes decades to advance
Pathogenesis of Atheroma
1. Fatty streak development 2. Atheromatous plaque development 3. Thrombus development
Dr. Enos and Holmes reported on autopsis of 2000 dead soldiers in Korean War average age 22.
35% had fatty streaks in coronary arteries 42% had had established atheroma
Initiation of atheroma by damage to endothelium which becomes more porous to lipids and monocytes
Monocytes from blood stream pass through endothelium into blood vessel wall
Bacteria
Hypertension
Homocysteine
Smoking
Diabetes
Oxidized LDL
Cytokines
Initiation of Monocyte attachment with activation of endothelial transcription nuclear factor Kb (TNF-Kb) by oxidized low density lipids, cytokines, and glycolated end products seen in diabetes.
VACM-1
VACM-1
VCAM-1 and chemokine monocytic chemotactic protein I localizes monocytes in vessel wall.
Low Density Lipids (LDL) pass through damaged endothelium into blood vessel wall
O LDL LDLO
O LDL LDLO
LDL O LDLO
Low density lipids (LDL) oxidized in vessel wall
LDLs are oxidized and then induce production of bio active molecules such as Interleukin 1, Interleukin 6, matrix metalloproteases, Prostaglandins.
Monocytes trigger chronic inflammatory reaction with lymphocytes and this results in tissue necrosis and fibrosis
LDLO Bacteria MMP Prostaglandins Cytokines LDLO Cytokines Cytokines LDLO MMP
Circulating bacteria and cytokines add to inflammation. This leads to Atheromatous plaque formation
HDL are a heterogeneous lipoproteins produced in the liver and small intestine. HDL contains 70% phospholipid and protein, 25% cholesterol, 5% triglycerides. HDL has 2 antioxidant enzymes
Paraoxonase Platelet activating factor acetyl hydrolase Apolipoprotein A-1 stabilizes paraoxonase
Enzymes associated with HDL apolipoproptein (apoAL) and paraoxenase (PON) protect by destroying the oxidized pro-inflammatory lipids from LDL
PON also inhibits LDL induced Monocyte Migration.Periodontitis may cause reduction in Apo AI and PON and so increase the level of oxidized lipids and monocytes in blood vessels walls.
HDL
LDL
O LDL HDL
LDL HDL
LDL HDL
Blood vessel wall becomes distended and continues to accumulate cholesterol, some areas become calcified
THROMBUS DEVELOPMENT
Coronary Artery with stable atheroma. Inflamation and necrosis have replaced the smooth muscle but there is a dense layer of collagen next to lumen (arrows)
Bacterial Proteases
MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP MMP
MMP s from macrophages and proteases from circulating bacteria can destroy collagen to form an unstable atheromatous plaque
Blood vessel wall can rupture and then get thrombus formed at region of ulceration
Thrombus formation
Oral Bacteria
Thrombus formation on atheromataous plaque. Slits of cholesterol crystals seen in vessel wall.
Oral Bacteria
lumen
Calcification (blue area) and distended vessel wall with narrowed lumen of Coronary Artery.
Ultrafast CAT Scan of Thorax Showing Cross-Section of Heart. Calcified Tissues Stained Pink.
Note: Calcified Atheromatous Plaques in Coronary Arteries
thrombus
Myocardial infarct with replacement of necrotic myocardium with inflammatory cells and fibroblasts
Age
Hispanic Asian Native Black White Amer. 99 870 224 1128 426 244
2181 2079
Cardiovascular Assessment
Subjective Data: Personal/Familiar HX, CP, Dyspnea, weight changes etc. Physical Assessment: Skin, extremities, BP, JVP, Lungs, Precordium Objective Data: Labs: CPK/ troponin Hypo/ Hyperkalemia Hypocalcemia Serum Na
Acute Coronary Syndrome Unstable angina S/S Squeezing pressure, ache, or heaviness Aching tooth neck or jaw Aching back/arms Feeling of choking, gas Pale, sweaty skin Myocardial infarction
Pathophysiology of Infarction Automaticity and ectopy are enhanced Catacholamines (epinephrine and norepinephrine) released in response to hypoxia and pain Increases the hearts rate and contractility and after load
Pathophysiology of Infarction Increase in O2 requirements in tissue O2 deprived tissue. Infarct extend into areas of injury and ischemia This depends on 3 factors:
Collateral circulation, Anaerobic metabolism Work load demands of the myocardium
Subendocaardium (subendocardial MI) - not total wall less severe Transmural - spread to the epicardium or all three layers of cardiac muscle
Effects the wall motion and cardiac output.
Pathophysiology of Infarction
Physical Changes
6 hours 48 hours infarct area appears blue and swollen infarct turns gray with yellow streaks as neutrophils invade the tissue and begin to remove the necrotic cells. the necrotic area eventually develops into a shrunken, thin firm scar.
8-10 days
2-3 months granulation tissue forms at the edges of the necrotic tissue.
Assessment /ClinicalManifestations
Pain P where is pain Point to it. Q uality sharp/dull R adiation jaw, neck, arm S everity 1-5 T ime how long
Precipitating and relieving factors
SOB
Diaphoresis
Nausea/Vomiting
Signs of shock
Angina pain
Associated symptoms
Assessment /Clinical Manifestations Vitals Rhythm Psychosocial Distal pulses Skin temp
Silent MI
15 -20% painless or atypical MI
Toothache
Pain in jaw/arm
Lipid management and control of other coronary risk factors in post menopausal women
J. Womens Health and Gender related Med. 9:235,2000
African American and Hispanic women at greater risk than Caucasian women
First myocardial infarction in women is more severe and more lethal than they are in men
Womens mortality rate at 6 months post myocardial infarction double that of men
Coronary artery bypass surgery operative mortality 4.5% women, 2.6% men
Post menopausal hormonal therapy gave 53% reduction in death from CHD in study using 121,700 registered nurses
Framingham Study. Risk of coronary artery disease doubles with onset of menopause
20 centers with 2,763 post menopausal with C.H.D. average age 67 years. Hormone group got 0.6625mg conjugated estrogen, 2.5mg medroxyprogesterone acetate daily. Hormones gave no significant decrease in C.H.D. events - infarct or death hospitalization angina revascularization, congestive heart failure, stroke, ischemia or ventricular arrhythmia Another study on same population showed hormone group had increased rated of venous thrombo-embolism and biliary tract surgery. 261 deaths compared to 239 in controls
Grady, D. et al JAMA 2002, 288:49
Heart Disease and Women #1 risk. Early knowledge with first MI Underrepresented in clinical trials for cardiovascular drugs Studies predominately middle-aged men
Statistics
Number 1 killer of women 12 times more die of CVD than breast cancer Rate of CVD has risen over last 2 decades 2/3 of women who die suddenly from CHD had no previously recognized symptoms Within 6 years of an MI 35% have another MI 11% have a stroke 6% experience sudden cardiac death.
Cardiovascular risk factors DM Hypertension Obesity Family history Pregnant Birth control pills Menopause
Symptoms Disparities
Sex differences Different signs and symptoms Women Men Classic symptoms are far less common in women
Diagnostic Differences
Suspected CHD - Not tested Coronary vessels Atherosclerosis Test interpretation ST-segment elevation False positive test results.
Psycho-social Assessment
Men and women
Denial Fear Anxiety Anger
Lab
Diagnostic Tests
Troponin T and I Creatinine kinase MB (CK-MB) Myoglobin
Stress test Medication stress testing adenosine (Adenocard) dobutamine (Dobutrex) Myocardial perfusion imaging Thallium scans Dipyridamole (Persantine) Radioisotope imaging MRI Cardiac Catheterization
Diagnostic Tests
Prognosis
30 -40 % expire before reaching hospital 80% reach hospital survive Of 20% that expire occurs usually in 3-4 days of admission. arrhythmias 30 year olds ignore especially with DM
ICU /Telemetry unit Emergency angioplasty Pain relief Thrombolytic agents Aspirin 160 325mg on day 1 and then indefinitely thereafter. Antiplatelet agents Oxygen Rest and more rest
Medical Treatment
Nitroglycerin Increases collateral blood flow, Vasodilation. SL, Spray, Patch, IV Oral Isosorbide dinitrate (Isordil, Iso-Bid), Isosorbide Mononitrate (Imdur) Extended release After 5 minutes recheck pain assessment if BP less than 100 systolic or 25mm lower than the previous reading lower the head of the bed
Drug Therapy
Drug Therapy
SL Nitroglycerin - vasodilation Total of 3 pills in 5 minute increments Under tongue Relief time Storage Self life Tingle Vital Signs
Drug Therapy
Nitroglycerin Paste AM/PM IV nitro - slow initial infusion Check BP and pain every 3-5 minutes dose is increased until pain is relieved BP falls excessively or the max dose is reached SE: Headache
Drug Therapy
Morphine
Chest pain unresolved by Nitro. Action: Dose: 2-10mg IV every 5-15 minutes until max dose Side Effects Toxicity
Drug Therapy
Beta Adrenergic Blockers Decrease the size of the infarct, ventricular dysrhythmias, and mortality rates in clients with an MI. Cardioselective BB Noncardioselective BB Wean off or rebound MI may occur
Drug Therapy
Ace Inhibitors Prevent ventricular remodeling and the development of heart failure (first 48 hours) Survival rate Nursing Intervention: Potassium effects
Drug Therapy
Calcium Channel Blockers
Clients with Angina. Vasodilation and myocardial perfusion. Angina use Monitor the client
Drug Therapy
Calcium Channel Blockers
Nifedipine ( Adalat, Procardia (XL)) Verapamil (Calan Isoptin) - (slows SA and AV conduction) Diltazem ( Cardizem ) Amlodipine ( Norvasc) Nicardipine (Cardene)
Drug Therapy
Anti-platelet Agents Action ASA Dosing Aspirin 81- 650mg/day SE: Clopidogrel (Plavix) Ticlopidine (Ticlid)
Drug Therapy
Thrombolytic Therapy
Dissolve thrombi IV or Intracoronary during cath Indications CP > 30 min unrelieved by nitro with indications of transmural ischemia and injury on EKG Chest pain <6 hours, Contraindications recent abdominal surgery, stroke, recent trauma
Drug Therapy
Thrombolytic Therapy Dissolve thrombi IV or Intracoronary during cath Indications CP > 30 min unrelieved by nitro with indications of transmural ischemia and injury on EKG Chest pain <6 hours, Contraindications recent abdominal surgery, stroke, recent trauma
Drug Therapy
Thrombolytic Therapy Post procedure Vital signs Neuro status Assess bleeding external and internal Clotting studies Successful?
Drug Therapy
Fibrinolytics Dissolve blood clots that have formed in certain blood vessels. Given only by or under the direct supervision Tissue Plasma activator t-PA, Retavase, TNKase
Drug Therapy
Fibrinolytics
Streptokinase Anisoylated plasminogen activator Urokinase