CV 1 and 2

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Components of Blood: Plasma=55%
Blood cells=45%
Blood Cells: Erythrocytes, Leukocytes, Platelets
Plasma: Water, Electrolytes, Salts, Plasma Protein
Erythrocytes: RBCs that filled with hemoglobin, transport CO2
Leukocytes: Defense and immunity
Platelets: Initiate blood clotting
Hemostasis: Stops bleading, limits hemmorage: vascular spasm, platelet plug formation, clot formation
Platelet Plug Formation: Vessels are damaged and Platelet adhesion, platelet activation/release, aggregation: leads to stickiness/clot formation
How does PPF work: Prothrombinase, Thrombine, Fibrinogen, insoluable threads that form the clot
Fibronalysis: Disolving of unwanted clots once the vessel is repaired
Pathways of blood circulation: Systemic; Pulmonary; Corinary
Systemic Circulation: Carries Oxygen and nutrients to body tissues and removes wastes
Pulmonary: Carries deox blood to lungs, excretion of CO2, returns oxygenated blood to heart
Corinary: Sub-pathway of systemic; removes wastes
Chambers (four hollow) continuously filled with blood: R/L Atria: upper (recepticles for blood coming into heart from body)
R/L Ventricle: lower (push blood back into body)
Which system supplies blood directly to the heart?: Coronary circulation
Walls of blood vessels: Tunica externa
Tunica media
Tunica interna/intima
Tunica externa: Fibrous connective tissue
Tunica media: Smooth muscle and elastic tissue
Tunica interna/intima: Endothelial Tissue
Arteries: Carry blood away from the heart; two types: muscular and elastic (expand, receive blood during systole, recoil during diastole)
Arterioles: Smallest type of arteries; branch into capillaries (thin walls/single cell layer!); allows O2, nutrients from blood to cells
Valves of the heart: Prevent backflow of blood
AV Valves
Semilunar valves
Open and close according to pressure changes in chambers
Atrioventricular Valves: Separate atria and ventricles: tricuspid and mitral (R&L)
Semilunar Valves: Regulate outflow of ventricles
Cardiac cycle: Systole (contracts)
Diastole (relaxes)
Layers of the Heart: Three layers: epicardium (outer, epithelial), myocardium (middle, striated muscle), endocardium (inner, smooth)
Main vessels of the heart: Aorta and coronary arteries
Superior/Inferior vena cava
R&L pulmonary veins
R&L pulmonary arteries
Aorta and coronary arteries: Supply body and heart with oxygenated blood
Superior/inferior vena cava: Return deox blood to heart
Cycle of systemic circulation: Ox blood from lungs--> Pulmonary veins-->
Left Atrium--> Left Ventricle--> Aorta-->
Arterial system-->
Body's Tissues and organs
Cycle of pulmonary circulation: Deoxygenated blood from vena cava-->right atrium--> right ventricle-->pulmonary arteries-->lungs-->blood unloads CO2, picks up O2--> Left atrium-->systemic circulation
Cycle of coronary circulation: O2 blood carried thru coronary arteries-->capillaries in heart tissue -->deox blood --> cardiac veins-->coronary sinus-- right atrium
Cardiac Output: CO=HRxSV
Amount of blood ejected from the L or R ventricle each minute (mL/minute)
Nervous System Control of BP: Parasympathetic Stim (decreases HR & impulses)
Sympathetic Stimulation (increases HR & impulses
Cardia Muscle Cell Contraction: - Deplorization/ Repolarization triggers change in e` potential of cell membrane
-This releases a Ca Ion, which shortens cadiac cells
-Muscle contracts
Blood Flow Variables: Blood Pressure: Force exerted by flood on vessel walls
BP = CO x TPR
TPR: Total Peripheral Resistance: Sum of all opposition to blood flow from force of friction between blood and vessel walls
Hormonal Control of BP: Kidneys: nephrons filter blood and reabsorb H20
Renin-Angiotensin-aldosterone system (RAAS) regulates BP
Malfunctions of RAAS: Affect both cardiac output and peripheral resistance
RAAS Flow...: Decreased arterial pressure-->Renin (kidney)-->Angiotensin I-->Angiotensin II-->Leads to: Increase in Na/H20 Retention; in vasoconstriction; in system arterial pressure
Other hormones involved in PB control: ADH and ANP:
Antidiuretic hormone and Atrial Natriuretic Peptide
Aldosterone: Homrone that causes vasoconstriction and causes body to retain sodium and water, which means increased BP
HYPERTENSION: Inappropriately sustained elevation in BP
Optimal BP for adult is:: <120/80 mm Hg
JNC 7 Classification: Hypertension=BP>140/90
Prehypertension=BP between 120/80 and 139/89
Goal: to decrease elevated BP<140/90
Primary Hypertension: Over 95% of cases
Cause unknown
Secondary Hypertension: Causes: Renal, Adrenal, Other (oral contraceptives, narrowing of the aorta, hyperthyroidism)
Possible causes of Primary Hypertension: Genetics; fetal environment; increased activity of vasoconstrictor systems; renal Na retention; Vascular Hypertrophy; decreased activity of vasodilating systems; insulin resistance
Other factors possibly causing Primary Hypertension: Obesity; alcohol intake; physical activity; smoking
True or False: prevalence of hypertension increases with age: TRUE
More common in Men up to age 50; equal in gender between 50 & 74; after 74 more common in women (estrogen protective effect)
Hypertension is under___, under___, and poorly con___.: Underdiagnosed, undertreated, and poorly controlled.
NHANES Data Stats: Not aware: 31.1%
Not treated: 41.6%
Not controlled: 46.9% (among treated patients)
Hypertension Diagnosis:: -No symptoms until it's progressed to the point of damaging organs
-BP eval; Clinical eval; Lab evals
BP Evaluations: -Baseline calculated by averaging cuff readins at 2 or more visits
-JNC7 recs f/u if initial pressure reading is found
Ambulatory (out of office) readings (BP evals): Verify white coat hypertensio; access antihypertensive treatments; improve compliance; reduce physician visits
Clinical Evaluations: -Medical History; Previous records; family; CV risk factors; signs/symptoms, concomitant medications
-Phyiscal exam: funduscopic; cardiac; arteries; phyiscal appearance
Laboratory Evaluations: Urinalysis (renal status); Blood chem eval (blood cell count, K, creatinine, LDL, glucose, BUN)
Electrocardiogram (cardiac status LVH; provide baseline pre therapy)
Consequences of Hypertension: 1. Endothelial Damage
2. Organ Damage
3. Atherosclerotic Plaques
Endothelial Damage: Hypertension damages endothelium of blood vessels: lining thickens; vessel narrows; flow impeded
Organ Damage: Eyes: hemorrhages, blurred, blindness
Heart: ventricular hypertrophy, atherosclerosis
Kidneys: decreased blood supply, renal disease
Brain: stroke, aneurysm rupture, TIA, embolus
Stroke: CVA: cerebrovascular accident
Occurs when O2 and nutrient flow to brain is interrupted b/c a blood vessel is blocked or burst
Two types: Ischemic (blocked blood vessel) and Hemorrhagic (burst blood vessel)
TIA: Transient Ischemic Attack: a mini-stroke.
Brief cerebral vascular ischemia causing focal neurological signs/symptoms lasting less than 24 hours; precursor to stroke
Atherosclerotic Plaques (clinical consequences of hypertension): Atherosclerotic plaques develop in people with high lipid levels: changes in plaque occur and blood flow obstructed
Walls of arterials: Tunica intima, media, externa
Dyslipidemia (defined): 1. Pressence of abnormal levels of lipids, lipoproteins in blood
2. Elevated levels of VLDL, LDL, IDL, TGs
3. Low levels of HDL
Chylomicrons: Chylomicrons: transport dietary TGs and C from small intestine to body tissues post meal
Blood Pressure equation: BP=COxPR
(Cardiac Output x Peripheral resistance)
Medical definition for hypertension: High blood pressure
Types of Lipoproteins: Chylomicrons; VLDLs; LDLs; HDLs
VLDLs: VLDLs: tranport lipids from liver to fat tissue; converted to LDLs
LDLs: LDLs: Tranport Cholesterol from liver to body tissue; increase risk for atherosclerosis
HDLs: Tranport excess Cholesterol from body tissue to liver; reduce risk for atherosclerosis
Friedewald Formula: Formual used to calculate LDL-C when TG are <400mg/dL:
LDL=TC - HDL - (TG/5)
Lipid Synthesis: Exogenous vs. Endogenous
Exogenous: Exogenous pathway: lipids obtained from diet
Endogenous: Endogenous pathway: lipids made by liver
Lipid sythesis (cont.): Decrease: LDO receptors and uptake of LDL
Increase LDL in blood and risk of atherosclerosis
Types of Lipid Disorders: Hyperlipidemia
Dyslipidemia
(Dys/Hyperlipidemia and hypercholesterolemia used interchangably by Drs)
Hyperlipidemia: Elevated levels of lipids, usually VLDL, LDL, IDL & TGs
Dyslipidemia: Elevated levels of bad lipids and low levels of HDL
Classifications of Dyslipidemia: Primary vs. secondary: based on cause of dyslipidemia
Fredrickson classification: based on patterns of lipid elevations
Genotypic classifciation: based on genetic causes of primary dyslipidemias
Clincial classification: based on which lipids are elevated/reduced
Hypertrophy: Increased size of a part caused by an increase in the size of its cells
Primary dyslipidemia: Genetic/no ID'd cause
60-70% of LDL level is genetics
Due to complex interaction of gens: age, gender, saturated fat diet, physical activity
Secondary dyslipidemia: Known causes: Lifestyle; metabolid disorders; kidney; liver; hormonal; medications; pregnancy
Fredrickson classifcaiton: *Patients classified according to which lipids/lipoproteins are elevated
*I, IIa, IIb, III, IV, V
*Treatment often based on lipid phenotype
*Not based on HDL levels
Genotypic Classification: *Classifies lipid disorders according to known genetic cause (primary only)
*Homozygous familial hypercholesterolemia (FH): 2 mutated LDL receptor alleles
Heterozygous FH: having 1 mutated LDL receptor allele
Clinical Classification: Relies on results of blood tests for lipids
Four main catagories: 1. elevated cholesterol/ hypercholesterolemia
2. elevated TGs/hypertriglyceridemia
3. elevated cholesterol and TGs /mixed dyslipidemia
4. Low HDL
NCEP ATP III: *2001 published guidelines for classification of cho levels
*2004 addendum made to NCEP ATP III for those at very high risk
NCEP ATP III Classificatoin of Lipid Levels: Optional LDL: <70 mg/dL
Optimal LDL: <100
Desirable TOTAL C: <200
Low HDL: <40
High HDL: >60
Normal TGs <150
Epidemiology of Dyslipidemia: 105 million Americans have borderline high to high range of total cholesterol
Clinical consequences: Can lead to atherosclerosis, which lead to: Angina, MI, Stroke
Lipid Hypothesis: Evolved in last 50 years
Based on study data
Central to CHD, lowering lipeds lowers risk of CHD
Framingham Heart Study: *1948 in Framingham, MA
*5127 people 30-62 years old w/o diseases
*Study to show CHD are related to high lipids/lipoproteins
*CHD risk increases with increased total-C
MRFIT: Multiple Risk Factor Intervention Trial
*Random, multicenter, 7-yr study
*12,866 mid-age men w/ no CHD but w/ mutliple risk factors
*1% reduction in total-C-->2% reduction in CHD risk
Atherosclerosis: Buildup of fatty substances (plaque) on walls of arteries/reduces blood flow
May take decades for symptoms to show up
Protective Factors: HDL-C: removes C from arterial walls, tranports to liver for exretion
Exercise: weight control, incrase levels of HDL, lower BP, reduce risk of heart attack
Alcohol: moderate intake may protect against CHD & Athscl
Initiation of Atherosclerosis: 1. Chronic endothelial injury (from atherscl risk factors)
2. Accumulation of lipids at the site of the injury (prolif of muscle cells)
3. Oxidation/modification of LDL-C (inflammation response)
4. Formation and death of foam cells (fatty streaks)
Progression of Atherosclerosis: *Fatty streaks progress to atheromas: lesion-->lumen; soft lipid core, hard fibrous cap
*Growth of plaque is outward/positive remodeling
*Fibrous plaque grows/stable
Stable Plaques: *Thick fibrous cap, low inflammation, low lipid content
*Outcome: stenosis-->occlusion
*Symptoms: angina, claudication
Unstable plaques: Thin fibrous cap; high inflammation; high lipid content; may lead to thrombosis
Complications of Atherosclerosis: 1. Clots/Thrombi form around fissures in vessel walls
2. Fibrous cap can rupture; lipid core spilled into blood
Types of Thrombosis: 1. Mural: clot spreads along artery wall; doesn't occlude lumen
2. Occlusive: Clot fills lumen, obstructs blood flow; may cause MI
Stroke Epidemiology: *500,000/year in US experience 1st stroke
*200,000+/year exp 2nd stroke
*3rd leading cause of deathin in US and devel countries
*Leading cause of long-term disability
*Risk factors include those for atherosclerosis

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