Post on 24-May-2015
transcript
Arteriosclerosis
and
Atherosclerosis
Problems With Oxygen
Transport
LIPIDS = FATS
TRIGLYCERIDES
PHOSOPHOLIPIDS
STEROIDS
CHOLESTEROL
Wax like substance
Structural component of
cell membranes
Hormones, Vit D, Bile Acids
Produced in Liver
COMPLEXES
Lipoproteins
LDL
HDL
VLDL
Serum Lipids
HDL
High density lipids
“good cholesterol”
Protective effect against atherosclerosis
LDL
Low density lipids
“bad cholesterol”
Increased incidence of atherosclerosis
VLDL
Very low density lipids
Transport triglycerides
Increase risk of premature atherosclerosis
TRIGLYCERIDES
Stored body fat
Serum Lipids
Arteriosclerosis
Hardening and of elasticity
of arterial walls
Most common arterial
disease
Normal aging process
Hypertension
Diabetes
Atherosclerosis
Formation of obstructive lipid deposits
Affects arteries
Lipid metabolism disorder
Obstruction of blood flow organs
Underlying cause of CAD, MI,
CVA, aneurysms and arterial
vascular disease
Normal and
atherosclerotic arteries
ETIOLOGY
AGE & SEX
GENETICS
PRE EXISTING CONDITIONS
SMOKING
DIET
EXERCISE OR LIFE STYLE
ATHEROSCLEROTIC LESIONS
Fatty streak
Raised fibrous plaque
Atheroma - irreversible
Commonly Affected Sites
Coronary arteries
Vascular bifurcations or
branch areas
Abdominal aorta
Iliac arteries
Femoral arteries
Progression of
Atherosclerosis
INCIDENCE & RISK
MALE vs FEMALE UNTIL MENOPAUSE
BLACK vs WHITE IN MEN AND WOMEN
FAMILY PREDISPOSITION
HIGH SERUM LIPIDS
SMOKING
OBESITY - LIFESTYLE
PRE EXISTING CONDITIONS
RISK FACTORS
HIGH SERUM LIPIDS
SMOKING
OBESITY - LIFESTYLE
PRE EXISTING CONDITIONSHTN
DIABETES
ATHEROSCLEROSIS
SERUM LIPID STUDIES
WHAT DO MY
CHOLESTEROL LEVELS MEAN???
AMERICAN HEART ASSOCIATION
HANDOUT
MANAGEMENT
Dietary FATS
Saturated
Polyunsaturated
Monounsaturated
Hydrogenated
HX & NUTRITIONAL FACTS
Calories vs. Fats
Cooking recommendations
Alcohol consumption
Exercise
DRUG THERAPY
Statins: Lipitor, Zocor
HMG-COA Reductase Inhibitors:
Mevacor
Bile acid sequestrants: Questran
Nicotinic Acid: Niacin
Fibric Acids: Atromid, Lopid
LET’S TAKE A LITTLE BREAK!!
CORONARY ARTERIES
Vessel spasm
Tachycardia
Blood diseases
Bradycardia
FACTORS THAT O2 SUPPLY
TO THE
Heart rate increase
Contractibility
Afterload
Hypertrophy of Left
Ventricle
FACTORS THAT O2 DEMAND
ON THE
RISK FACTORS
MODIFIABLE
CHOLESTEROL
LEVEL
BP
SMOKING
OBESITY
NTG + VIAGRA
ETOH
HOMOCYSTEINE
UNMODIFIABLE
AGE
SEX
RACE
FAMILY HX
DIABETES
RISK RATIO
ANGINA PECTORIS
Temporary imbalance between O2 supply and demand
Symptom not a disease itself
Pain results from Lactic Acid
ANGINA PECTORIS
Stable Angina
Unstable angina
Silent Ischemia
Variant or Prinzmetal’s
Angina
STABLE ANGINA
Precipitated by exertion
Impaired blood delivery due to 75%
block
Predictable pattern
No change in symptoms over time
Pain relieved by rest or NTG
UNSTABLE ANGINA
Occurs at rest or without O2
demand
Preinfacrtion Angina
Can be > 90% blockage
Extreme pain
Last longer than 10 minutes and poor
relief from NTG or rest
SILENT ISCHEMIA
No pain
+ ECG
+ Cardiac Enzymes
VARIANT ANGINA
Arterial Spasms
No precipitating
factors
Rare
Occurs at rest
ASSESSMENT OF SXS
P = PRECIPITATES
Q = QUALITY
R = RADIATES
S = SEVERITY and
SYMPTOMS
T = TIMING
Characteristics of angina
CHEST PAIN
Different for men and women
: squeezing, fullness or
pressure in the center of your
chest.
: stabbing, pulsating, or sharp
Characteristics of angina
Vise squeezing chest
Heavy weight placed on their chest
Extend to the arm, especially the left arm,
neck, jaw, shoulder or back.
Nausea, fatigue, shortness of breath,
anxiety, sweating or dizziness
Crescendo effect – builds up and
gradually fades away
LAB TESTS
Cardiac Enzymes
Lipid profiles
CBC & Lytes
NTG Test
ECG
Stress Tests
Cardiac Scans (Thallium, MUGA, PET, LVEF)
Echo (TEE)
Cardiac Cath
PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY
NURSING
INTERVENTIONS
TEACH REFER
MEDICATIONS
ASA
NITRATES
BETA ADRENERGIC BLOCKERS
ACE INHIBITORS
CALCIUM CHANNEL BLOCKERS
ANGIOTENSIN II RECEPTOR BLOCKERS
THROMBOLYTIC THERAPY
ETIOLOGY