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American College of Sports Medicine
Seven Factors
- Non Life Style Lifestyle
- 1. Age
- 2. Genetics
- 3. Type I
- Life Style
- 4. Hypocholsterolimia
- 5. Hypertension
- 7. Sedentary Lifestyle
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Coronary Artery Disease Factors
- Age
- Genetics
- Type I
- Hypertension
- Eating
- Excercise
- Smoking
- Sedentary Lifestyle
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Emulsifiction stage I
Fat enters the small intestine and sends out a hormone signal cholecyokinin to Gall Bladder to secrete bile into small intestine which surrounds the fat making it water soluble
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Emulsification Stage II
The pancrease secretes Lipases to breakdown fat into a smaller form called Monoglycerides surrounded by gile now called Micells.
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Emulsification III
Micells enter enterocytes by facillited diffusion and modified at he smooth endoplasmic reticulum and repackaged at the Golgi into CHYLOMICRON which is larger.
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Emulsification IV
Chylomicron enters lymphatic system via lymp lacteals into circulation for fat delivery
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Emulsification V
High density lipo protein (HDL) recognizes the Chylocicron remants after most of the delivery has been make and places a molecular tag on the remants for liver take up
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Emulsification VI
Liver repackages chylomicron remants into a new smaller form called VLDL and sent out for delivery
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Emulsification VII
HDL recognizes VLDL liver takes up and repackages into smaller IDL form sent out for delivery
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Emulsification VIII
HDL recognizes IDL liver take up repackaged into LDL sent out for delivery
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Emulsificaton iX
HDL recognizes LDL and liver takes up remants
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Lymphatic Safety Factors
- Tissue pressure -6mm/hg
- Lymphatic drain -7mm/hg
- Wash down of proteins -7mm/hm
Need to exceed -20mm/hg in order to have Edema
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Capillary Exchange Pressures
- Arteriol end
- BP out 30mm/hg Hydrostatic Pressure-heart pumping
- TP out -6mm/hg Hyrostatic Pressure into interstial space cells creating a sucking effect
- COPV in 28mm/hg osmosis toward albumin in vascular space
- COPT out 4mm/hg sosmosi toward protein in interstitial space
- Filtration
- Venule end
- BP out 10mm/hg muscle tonus
- TP out -6mm/hg Hyrostatic Pressure into interstial space cells creating a sucking effect
- COPV in 28mm/hg osmosis toward albumin in vascular space
- COPT out 4mm/hg sosmosi toward protein in interstitial space
- Osmosis
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Causes of Edema
- any increase of BP on either the Arteriol end or Venule end
- art-renal failure, hypertension
- ven-hd increasing P1 pressure, decrease muscle tonus
- decrease in COPV=decrease albumin
- Kwashiakov, protein malnutrition, renal disease
- natural way-histamine release by immune system creating local temporary edema for healing
- increases the gap between cells
- Lymphatic blockage-bacterial infection, elephantitus, surgical removal
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Tachycardia Drugs
Class II
- Beta receptors-blockers effect both heart and lungs
- beta blocker inhibit EPI decreasing Sympathetic NS and allowing Parasympathic to lower BP
- Increase HR- secrete EPI with Atropine blocking receptor onthe heart and lungs down regulating the parasympathetic NS
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Tachycardia Class I
- Inhibit, block or slow
- Na+ from entering cells extending depolarization
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Tachycardia III
- Inhibit, block or slow
- K+ from exiting cells during repolarization extending repolarization
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Tachycardia IV
- Inhibit, block or slow
- Ca2+ from entering cells during depolarization extending depolarization
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Tachycardia V
- Adensine
- Increase K+ ability to leave the cell during repolarization causing hyperpolarization
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Blood Flow
Into the right atrium-oxygen-poor
- The oxygen-poor blood flows from the right atrium through the tricuspid valve to the right ventricle.
- From the right ventricle, blood is pumped through the pulmonary valve into the blood vessel that goes to the lungs. This blood then picks up oxygen (becomes oxygenated or oxygen-rich).
- Oxygen-rich blood flows from the lungs through blood vessels back to the heart's left atrium.
- From the left atrium, blood goes through the mitral valve and into the left ventricle.
- The left ventricle pumps blood through the aortic valve to a major blood vessel called the aorta and out to the body.
- The blood delivers oxygen to the body, then returns through veins to the right atrium and repeats the blood flow cycle.
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Chronotropic
- Changes that effect the heart rate
- SA node sets regular rhythm
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Resting membrane potential
- electric stability
- brief isoelectric line at -70 mv
- K+ leak
- Na+ bully
- Na+/K+ pump
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Threshold
- minimum valve needed to depolarize the nerve
- dotted isolectric line at -50mv
- set by channels of depolarization
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Trigger Zone
- distance electrically from RMP to threshold
- represented by the line from RMP to threshold
- Na+ leak channel
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Depolarization
- generation of electricity
- distance from threshold to peak of amplitude
- Ca2+ voltage gate channels
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Repolarization
- reset electric potential back to RMP
- distance electrical from end of depolarization until reaching RMP
- K+ voltage gated channels
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Blood flow control
Pre capillary sphincters smooth muscle collar at the end of arteries which can either vasoconstric or vasodialate hooked to CNS to control flow
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Systemic Circulation
- arranged in parallel
- provide equal delivery
- ablility to regulate flow
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Pulmonary circulation anatomy
- rt heart, atrium, ventricle
- pulmonary artery and lungs
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Systemic Circulation Anatomy
- pulmonary veins
- left heart, atrium, ventricle
- all tubing
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Poiseuille's Law
- 4th Power law
- change the diameter of the tube the flow rate changes by the 4th power
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Iontropic
- increase of heart contraction
- increase intercelluar Ca2+ release causing more actin myosin crossbridging
- natural-release of EPI-binds to beta 1 receptors causing increasing intercellular Ca2+
- cardiac glycosides-digitalis - digitoxin inhibitsa very small portion of Na+/K+ pump causing an increase in intracellular Na+
- Na+ inhibits Na+/Ca2+ exchange increaseing intracellular Ca2+ increasing contraction strength
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EKG
electrical representation of how electricity travels through the electrical conduction tissue SA node, AV node, bundle of hiss, bundle branches and perkiji fibers
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Components of EKG
- P-wave-electricity as it travels through the SA node representing atrial contraction
- QRS complex- electricity as it travels through AV node, bundle of hiss, bundle branches and perkinji fibers ventrical contraction
- T-wave-electrical tissue of the QRS complex repolarizing ventrical relaxation
- atrial relaxation not seen masked by QRS complex
- PR interval time between atrial contraction and ventrical contraction
- QT time between ventrical contraction and ventrical relaxation
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Cardiac Cycle Diagram
- Stage I-Diastasis-Atrial&ventricular contraction relaxation filling with blood 75% ventricle at this time
- Stage II-Atrial Systole-atrium contraction- atrial kick
- Stage III Ventricular contraction-increase in left ventricular pressure with no change in volume-before aortic valve opens
- Stage IV 2nd part of ventricular contraction-rapid ejection
- Stage V Isovalumic relaxation-decrease in left ventricular pressure no change in left vent volume-beginning of relax b4 mitral valve opens
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Cardiac Function Evaluation using cardiac cycle
- 1 determine stage effected
- 2 EKG effected?
- 3 pressure changes
- 4 volume changes
- 5 heart sounds
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Compensation from Edema
- any increase in P1 pressure leads to Edema
- any decrease in P3 pressure leads to Edema via renin release
- any decrease in P3 pressure leads too LVH leading to CHF or chronic heart failure
- heart rate increases ventilation rate increases
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cholesterol measures
- total measures all chrylomicrons, vldl, idl, ldl
- Individual-LDL less than 100mg/dl, HDL greater than 35mg/dl
- Ratio-3:1 total vs HDL
- Tri 130mg/dl
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Atherosclerosis process
- How plaque happens in arteries
- turbulent flow causes Eddy currents
- Eddy currents damage epithial lining and immune system activated for healing
- LDL answer the call invaginating into the damaged epithial cells
- macrophages engulf LDL and encapsulate them causing an inward hypertrophy toward the lumen decreasing the diameter
- anthroma protective cap is placed over tissue creating a positive feedback system
- thrombus-a piece breaks off
- complete occlusing-blocked
- spasm- cocaine binding
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atherosclerosis signs and symtoms
- 60-70% blockage-no symtoms
- 80%-at excercise
- 90%- at rest and excercise
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atherosclerosis therapy
- diet and excercise-decreasing blood pressure and turbulent flow through excercise
- decrease HCT by plasma volume increase
- decrease viscosity
- increase HDL
- decrease LDL
- decrease animal fat intake
- increase veggies and fruit
- eat more fiber
- lower salt
- take pharma
- surgery-stent, shave, laser, angioplasty
- CAB
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Cardiac measures after heart attacks
- creatine kinase enzyme measures
- PCR+H+ +ADP
- Skeletal muscle CK-mm
- Nervous tissue CK-BB
- Cardiac muscle CK-mb 8-24 hrs
- Tripoinin Complex Protein
- 12-24 hrs
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